There’s something in my head (but it’s not me).

The complex relationship between

the built environment and schizophrenia

- from aetiology to recovery.

Papers and exegesis submitted for the degree

Doctorate of Philosophy

Sydney University, June 2012

Jan Golembiewski, BFA, BArchS, MArch

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 DECLARATION

This work is original and wholly the work of the candidate, Jan Golembiewski, including

all the enclosed papers, except where duly cited.

Supervisor Dr. Peter G. Armstrong (FADP, U. Syd).

Other expert guidance and associate supervision also received from:

Dr. Rena Archer (FADP, U. Syd.), Dr. Michael Robertson (Medical Ethics and the Law,

Psychiatry, U. Syd.), Dr. Arne Dietrich (Neuroscience American University of Beirut),

Dr. Branka Spehar (Psychology, UNSW) and Dr. Richard White (Psychiatry, U. Syd.), Dr.

Martes Alison.

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CONTENTS

CONTENTS  .............................................................................................................................................  3  

ABSTRACT  .............................................................................................................................................  8  

ACKNOWLEDGEMENTS  ...................................................................................................................  10  

THANKS  .................................................................................................................................................................  13  

FOREWORD:  READING  A  RHYZOMIC  THESIS.  ..........................................................................  16  

INTRODUCTION:  THE  EXECUTIVE  SUMMARY  .........................................................................  21  

PURPOSE  STATEMENT  ....................................................................................................................  25  

POTENTIAL  SIGNIFICANCE  ............................................................................................................  26  

INCIDENCE  RATES  ................................................................................................................................................  29  

SOCIO-­‐ECONOMIC  COSTS  ....................................................................................................................................  33  

RESEARCH  QUESTIONS  ...................................................................................................................  34  

QUESTION  1:  SPECIALIST  PSYCHIATRIC  FACILITIES  TO  HELP  PEOPLE  WITH  SCHIZOPHRENIA  ..............  35  

QUESTION  2:  WHAT  IS  SCHIZOPHRENIA?  .......................................................................................................  41  

QUESTION  3:  THE  ROLE  OF  THE  BUILT  ENVIRONMENT  IN  THE  AETIOLOGY  AND  SYMPTOMS  OF  

SCHIZOPHRENIA  ...................................................................................................................................................  44  

HOW  THIS  RESEARCH  MAY  HELP  ................................................................................................  47  

METHODOLOGY  .................................................................................................................................  50  

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THESIS  INCLUDING  PUBLICATION:  LIMITATIONS  AND  ADVANTAGES  ...........................  56  

PAPERS,  PRESENTATIONS  AND  INCOMPLETE  ARTICLES    NOT  INCLUDED  ....................  59  

QUESTION  ONE:  HOW  CAN  SPECIALIST  PSYCHIATRIC  FACILITIES  IMPROVE  THE  WAY  

THEY  HELP  PEOPLE  WITH  SCHIZOPHRENIA?  .........................................................................  61  

START  MAKING  SENSE:  APPLYING  A  SALUTOGENIC  MODEL  TO  ARCHITECTURAL  DESIGN  FOR  

PSYCHIATRIC  CARE.  .............................................................................................................................................  62  

SO  YOU’RE  GOING  TO  DESIGN  A  MENTAL  HEALTH  FACILITY?    HOW  TO  MAKE  IT  FUTURE-­‐PROOF.  .......  97  

MENTAL  ILLNESS  AND  THE  URBAN  ENVIRONMENT  ..........................................................  125  

DETERMINISM  AND  DESIRE:  SOME  NEUROLOGICAL  PROCESSES  IN  PERCEIVING  THE  DESIGN  OBJECT.

 ..............................................................................................................................................................................  126  

A  TAXONOMY  OF  THE  NEURO-­‐CORRELATES  OF  PERCEPTION,  ACTION  AND  DESIRE.  .............................  129  

Affordances;  the  heart  of  perception  and  the  automation  of  action.  ...................................  130  

Behaviour-­‐settings:  the  context  of  affordances  and  the  automation  of  inhibition.  ........  132  

Creativity  and  awareness:  the  deliberate  extension  of  affordances  and  behaviour-­‐

settings.  ............................................................................................................................................................  135  

WHAT  DRIVES  ENGAGEMENT?  THE  FACTORS  OF  SALIENCY.  .....................................................................  138  

USING  THEORY  IN  PRAXIS:  DETERMINISM  ....................................................................................................  149  

CONCLUSIONS  .....................................................................................................................................................  156  

GENERAL  HOSPITAL  DESIGN  ......................................................................................................  158  

THE  NEUROLOGICAL  BASIS  OF  SALUTOGENIC  HEALTHCARE  DESIGN.  ......................................................  159  

A  BROADER  APPLICATION  OF  THE  SALUTOGENIC  METHODOLOGY  IN  MENTAL  

HEALTH  SERVICES  .........................................................................................................................  182  

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MOVING  FROM  THEORY  TO  PRAXIS  ON  THE  FLY:  INTRODUCING  A  SALUTOGENIC  METHOD  TO  EXPEDITE  

MENTAL  HEALTH  CARE  PROVISION  IN  DISASTER  SITUATIONS.  .................................................................  183  

2.   QUESTION  TWO:  WHAT  IS  SCHIZOPHRENIA?  ..............................................................  199  

SCHIZOPHRENIA  AND  PERCEPTUAL  EXPERIENCE  .............................................................  200  

THE  RIDDLE  OF  PSYCHOTIC  PERCEPTION  RESOLVED:    THE  INTEGRATED  FINDINGS  OF  AN  IN-­‐DEPTH  

ANALYSIS    OF  CURRENT  HYPOTHESES  FOR  SCHIZOPHRENIA.  .....................................................................  204  

Healthy  salience  ...........................................................................................................................................  210  

The  neural  architecture  of  healthy  attention  .................................................................................  238  

The  emergence  of  symptoms  ..................................................................................................................  257  

Summary:  Solving  the  aberrant  salience  riddle  .............................................................................  284  

Appendix  I:  The  psychotic  spectra  continuum  ................................................................................  286  

Appendix  II:  Refuting  noise  theories  ....................................................................................................  289  

Appendix  III:  Notes  on  data  sources  for  table  3.  ............................................................................  293  

3.   QUESTION  THREE:  WHAT  IS  THE  ROLE  OF  THE  BUILT  ENVIRONMENT  IN  THE  

AETIOLOGY  AND  SYMPTOMS  OF  SCHIZOPHRENIA?  ...........................................................  295  

LOST  IN  SPACE:  THE  ROLE  OF  THE  ARCHITECTURAL  MILIEU  IN    THE  AETIOLOGY  AND  TREATMENT  OF  

SCHIZOPHRENIA.  ................................................................................................................................................  296  

EMOTIONAL  AFFORDANCES  .............................................................................................................................  307  

Physical  affordances  ...................................................................................................................................  309  

Identification  affordances  ........................................................................................................................  310  

Narrative  affordances  ...............................................................................................................................  312  

Addressing  bottom-­‐up  attention  deficits  ...........................................................................................  323  

Aesthetic  and  natural  engagement:  ....................................................................................................  325  

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Environmental  generosity  .......................................................................................................................  327  

Dealing  with  top-­‐down  superfluity  ......................................................................................................  329  

ARE  DIVERSE  FACTORS  PROXIES  FOR  ARCHITECTURAL  INFLUENCES?  A  CASE  FOR  ARCHITECTURE  IN  

THE  AETIOLOGY  OF  SCHIZOPHRENIA.  .............................................................................................................  336  

AUTOMATIC  AND  OPPORTUNISTIC  PSYCHOTIC  BEHAVIOURS  ......................................  356  

COMMON  PSYCHOTIC  SYMPTOMS  CAN  BE  EXPLAINED    BY  THE  THEORY  OF  ECOLOGICAL  PERCEPTION.

 ..............................................................................................................................................................................  358  

Ecological  perception  ................................................................................................................................  361  

PSYCHIATRIC  VIOLENCE  ..............................................................................................................  372  

INTRODUCING  THE  CONCEPT  OF  REFLEXIVE  AND  AUTOMATIC  VIOLENCE:  A  FUNCTION  OF  ABERRANT  

PERCEPTUAL  INHIBITION.  ................................................................................................................................  373  

Automatic  perception  and  reflexive  action  ......................................................................................  379  

Deficits  of  perceptual  inhibition  ............................................................................................................  382  

Automatic  triggers  and  delusional  rationalizations:  ..................................................................  386  

PSYCHIATRIC  SUICIDE  ..................................................................................................................  396  

FURTHER  RESEARCH  ....................................................................................................................  398  

GLOSSARY  OF  TERMS  ........................................................................................................................................  401  

AUTHOR  AND  KEYWORD  INDEX  ...............................................................................................  425  

BIBLIOGRAPHY  ...............................................................................................................................  433  

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Callan Park, in Rozelle, Sydney is typical of the buildings designed by

John Soan for Tomas Storey Kirkbride, a Quaker in the mid nine-

teenth Century who advocated the moral treatment of the insane. This

thesis is not a historical account. The intentions of Kirkbride can be

read into my own approach. I see the environment as no less active

than the social environment or even psychotropic medications. Like

Kirkbride, I believe that architects, clinicians and researchers have a

moral responsibility to the patients who our efforts will serve.

(Source: Simon Fieldhouse)

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ABSTRACT

This thesis explores schizophrenia and the dynamics it has with the built environment.

In doing this, three research questions are addressed. The answers are all delivered in

article format – most of which have been published.

Question one: ‘what can architects do with the design of specialist psychiatric facilities

to help people with schizophrenia?’ required a greater depth of the understanding of

schizophrenia than is available in print. My need to know not only what schizophrenia

is (the psychogenesis), but what it does to perception (the phenomenology) drove a

second research question; ‘What is schizophrenia?’ The answer to this question is a

cogent integrative meta-hypothesis, spanning and integrating datasets and ideas from

areas of science that are rarely connected.

Findings in this research led to speculation on the possible role of the built environment

beyond the treatment of the syndrome - possibly even as an aetiological factor. As such,

the thesis finishes with the question three: What is the role of the built environment in

the aetiology and symptoms of schizophrenia?

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Pithy answers to the questions are:

Q.1) Designing with a view to fostering a sense of coherence promises that design

decisions will firstly ‘do no harm’. Further, by building opportunities for patients to

explore the sensibilities of meaning, comprehensibility and by providing for

manageability, facilities themselves may assist with recovery.

Q.2) Schizophrenia appears to be a syndrome where bottom-up perception diminishes

and top-down perception becomes over stimulated and over focused. This combination

gives rise to eight syndromes. These syndromes can explain all the symptoms of

schizophrenia.

Q.3) The role of the built environment in schizophrenia is found to be at least as

significant as any other major known epidemiological factors. But the many functions

of the built environment are complex, leaving several possibilities worthy of future

exploration.

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ACKNOWLEDGEMENTS

I must dedicate this thesis to my father, Olek (Alex) Golski because a thesis must

explore a gap and his death forced me to learn about impossible gaps and have the

courage to span them.

My father knew gaps like few others. As a young boy he was cast into one of the most

fabled gaps of history: one of Hitler’s concentration camps. The gap I have chosen to

explore is also fabled and for many of the same reasons. Like the holocaust,

schizophrenia is better described as an abyss than a gap. And like the holocaust,

schizophrenia has claimed untold numbers of lives to a madness that few of us have the

courage to attempt to understand.

It is not just a poetic metaphor – it’s a central premise of this thesis that the edge of a

cliff demands a leap. I discovered this precipice in 2006 while designing a new mental

health facility for the New South Wales Health Department and I was unsatisfied with

the regulatory guidelines that drove the project and still drives similar projects. Like

many other architects faced with similar jobs, I intuitively felt that there is a relationship

between mental illness and the built environment. But it was a commercial necessity to

ignore that relationship because knowledge is time consuming and difficult to come by.
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Little did I know then that it’s not psychiatrists or psychologists but architects that do

almost all the research that ever goes into the design of better psychiatric facilities, and

if we have a problem with the guidelines, it’s ours (as a profession) to fix. I did my best

then, but no sooner had the project come to a close, and I returned to university and to

address that gap.

The research component of my Master’s degree was far from sufficient. To return to my

metaphor, the research I did for the Master’s was really just scouting around the edge.

My leap occurred only when I arrived at Sydney University at the beginning of 2009, to

commence this PhD.

I have a lot of people to thank for this privilege. Nobody could have been more kind and

supportive than Dr. Bem Le Hunte, my wife. Without her constant support, her training

and her pressure to complete this project in good time (‘have you finished yet?’ became

a daily chant, well before the thesis was even due), I would have never made this leap,

much less found my way to the other side.

I also have to thank my supervisor, Dr. Peter Armstrong. In a supervision meeting, very

early on, Peter and I were discussing the scope of this project and the time it may take in

achieving my goal. Peter leaned back and said, “It’s an awfully big gap isn’t it?” Once I

admitted that neither he, nor I knew the half of it, he added. “Well, if I’ve ever met a

man who can pull a rabbit out of a hat, it’s you.” I don’t know, Peter, if this thesis is a

rabbit exactly. To me it resembles a jumbo-jet, but whatever – you deserve thanks for

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the continual support you have given me and for helping me through the trials I’ve had

on the way. I’ve always suspected that you kept me on a loose rein because you (like

me) intuitively felt that there is another horizon, and that the world could be a better

place if I find it. Only recently, schizophrenia claimed your sister’s life. I know it’s

presumptuous but I felt, throughout the entire period, that it was her experience that you

reflected on when reading and hearing about my discoveries. I hope, that in some way,

this thesis helps you better understand your sister’s trial – her gap – the great

unexplained algebra of the schizophrenia diagnosis.

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Thanks

My mother, Kathy Golski, for feeding and helping me when I’ve been pressed for time.

My supervisors – Dr. Peter Garth Armstrong, my principle supervisor from the outset.

There are many times when I may have looked well out of my depth. Thanks for

bearing with me and taking this journey to the end.

Dr. Branka Spehar, Dr. Arne Dietrich and Dr. Michael Robertson. All of you had deep

insight into the mechanisms of the human mind and were able to steer me out of the

deep end. Thanks for your time and patience.

Dr Rena Czaplinska Archer, Thank you for finding me a place in the faculty. With a

project as peculiar as mine, it was difficult to find someone willing to say “I’ll do it,”

and you were my hero at the moment when that counted.

Dr. Richard (Dick) White and Dr. Anthony Harris. Thanks for taking the time to read

through my work and be of assistance, even for the short periods you were available.

Tuesday (Martes Alison) for being a sounding board particularly as I gathered

hypotheses and data on the psychogenesis of schizophrenia.

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To my friends and colleagues at the Schizophrenia Research Institute, the Schizophrenia

International Research Society, The International Academy for Design and Health and

the countless other researchers elsewhere who provided the stepping-stones I needed to

cross this gap.

My kids, for all the time I should have been doing stuff with them – and especially

Taliesin who, when I’ve been stuck was always great at explaining basic scientific

principles that evaded my memory.

The university staff; Joanna, Penny, Kim, Suzanne, Jennifer and others who beaver

away in secret, sorting out all the paperwork that proliferates at the university. The

librarians: Tom, Rosemary, Bill, Tina and others for teaching me Endnote, finding

obscure documents deep in storage and for locating books in faraway places. Bruce for

the hundreds of times he’s helped me out when I’ve lost my keys, and to Leslie, Ben,

Julius and Ken for all their technical assistance.

To other students and academics, both at Sydney and other universities, who have kept

me on track and inspired. Some deserve a special mention – those who have reviewed

my work (often doubly blinded) and who have always given valuable feedback.

I also want to acknowledge my starting point as I reach for my terminal degree. As a

boy, Peter Muller took it upon himself to be my mentor and to teach me the basic

principles of architecture. I was only in my mid teens when he taught me how to cut

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sections and draw plans. This work is much more theoretical than those practical

origins, but in everything I write, I hope that its applicability to praxis is always present.

To all of you, a big and heartfelt thanks.

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

FOREWORD: READING A RHYZOMIC THESIS.

This thesis was written to be useful. It was to have broad and practical application but

this came at the expense of the tight and cogent narrative structures that PhD theses

traditionally aspire to. The thesis is largely composed of separate articles, each with its

own practical focus.

I wanted a PhD degree, but a tome gathering dust in the Fisher Library like a medieval

manuscript was not my objective. I always wanted to do my PhD by publication and

viva voce as my colleagues have done in Cambridge and Berkeley, but that’s not

currently allowed at University of Sydney. I fancifully considered writing an article on

the background for my study, another on my literature review, an article about my

methodology and another on my findings, but this goal is not particularly practical, nor

is it very likely to succeed. Every article needs its own literature search, methodology

and findings – otherwise they have little value and won’t get published, and even if they

did, their usefulness would be questionable. What good is a literature review that covers

a gap as broad as mine? Instead the thesis became a collection of mini-theses. And

there’s the possibility that it’ll be read that way – as a fractured document that says

many things rather than honing in on the archetypal single gap and approaching it with

new empirical studies the way a thesis normatively is expected to.

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The perception that the thesis might be fractured is also driven by a second reason – it

set out to cover a cavernous knowledge gap. Thus some articles were conceived as

scaffolding for others: (Golembiewski, in review-d) provides support for other articles

such as (2013), for example. Sure this logic is linear, but a reader can equally trace other

linear tracks through the thesis to come to other conclusions. (2010b) Provides a

scaffolding and a methodology for (2012e), but more complex still, the basis of (2010b)

is analysed on a neurological level in (in review-d) and (2012e) provides a foundation

for (2010b). As jumbled as it all sounds, each of these threads is coherent. But this

thesis can be read any number of other ways – and should be, depending on what a

reader wishes to take from it.

Instead of tracing a singular narrative from the front to the back, the logic of my thesis

is more like an academic book than a fairy-tale. It’s intended to be read in parts, entered

and exited at any point, by people who are interested in the subject matter and want to

find out more but not in material that is of peripheral interest, indeed it’s intended to be

read principally as separate articles. Thus the thesis structure is in a fundamental way

quite rhizomic, as Deleuse and Guittari proposed that academic writing should be.

But the Deleusian model doesn’t apply in full. I’m not a post-modernist and the thesis

can also be taken as a whole. In its completeness it is more than the sum of its parts. The

thesis is thus also arbourescent, and its structure is ultimately very simple – although

still non-linear. Each of the three research questions make a section, and these are

sandwiched between the front and back matter of the exegesis:

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Part 1: Background, Aims, Methodology etc.

Part 2: Question One: How can architects improve specialist psychiatric

facilities for people with schizophrenia?

Part 3: Question Two: What is Schizophrenia?

Part 4: Question Three: What is the Role of the Built Environment in the

Aetiology and Symptoms of Schizophrenia?

Part 5: Further Research, Index and bibliography.

In a single-minded reading, the thesis is an exploration of the influence of the

architectural environment on schizophrenia. And ultimately, the findings are singular

also: Schizophrenia is conceived as a diagnosis given to the bizarre behavioural

symptoms that follow an imbalance within the perceptual system. But it’s really a

coincidence that my aims and findings actually link up well. At the top level, the thesis

looks broadly at the phenomenology of schizophrenia, because when perception is

awry, phenomenal experience suffers. The behavioural peculiarities of schizophrenia

sufferers are not disingenuous but are genuine reactions to a very odd take on the world.

This is particularly important in the architectural context because the built environment

is usually all that is left once the social environment is depleted (as is always the case in

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any valid diagnosis of schizophrenia by American Psychiatric Association, 1994, p. 285

criteria.)

This is a very important reading of the thesis, and it would be lovely if academics and

practitioners would take note and change their perspectives because of it. But I’m

sceptical about whether academics and practitioners ever consult theses, much less

change their opinions because of what they read therein. Even published books are a

little old fashioned, and it’s my belief that people are more likely to read journals – so

in the interests of effective dissemination, my chosen mode is the academic article.

Realistically, how the thesis is to be read depends on what (and how much) a reader

needs to know and why. If you are a health architect, you’ll find it really useful to know

how patients tick, and what kinds of interventions may be useful for given situations.

You may also want to know the implications for healthy people. For you, question 1

will be recommended reading. In this case the papers in the later sections of the thesis

provide only empirical support, which you’d only bother with if you were sceptical. If

you were a clinical psychologist wanting to understand patient symptoms, question 2

would be your target. If you wanted to understand patient behaviour, question 3 might

also be useful. An epidemiologist would start with question 3 and might go no further.

The result is, that the reading of the thesis is a very personal experience. The writing

was too. The process consumed me for several years, and there can be no denying my

passion for the subject and my findings. This is reflected in my writing style. Criticise it

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as you may, it’s a fallacy that the academic can be truly extricated from their work. So I

don’t hesitate to insert my personal viewpoint into my articles nor this exegesis. Where

there is no first-person voice, you can assume that reviewers have been through and

whitewashed the content to create the false veneer of impassive neutrality.

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INTRODUCTION: THE EXECUTIVE SUMMARY

If asked, what is the single most important contribution this thesis makes to knowledge,

I would like to assert that ‘the Riddle…’ (from page 204) is the only comprehensive

hypothesis for schizophrenia. It’s an outlandish claim, considering that the subject has

been scrutinised for a century or so by thousands of researchers the world over - the

keyword ‘schizophrenia’ turns up in over 6000 citations per year in a Medline search

(see p. 206).

I never anticipated pulling such a body of data together. In fact, I never even realised

that I was even trying to do so. It’s just that I naïvely thought that there must be

someone who already had, and I thought I was trying to locate something that had surely

been cognised before – some pearl of wisdom, while I write up what I find.

I knew that schizophrenia hadn’t been understood to the level where the effect of the

environment meant, and I saw that as my job: a relatively appropriate step to take as a

PhD project. But another Medline review of nearly 2000 articles carrying the keywords

“schizophrenia AND hypothes*” revealed that at best, authors would focus on just one

side of the syndrome (either the negative signs or just the positive symptoms) and

ignore the other, yet in the schizophrenia diagnosis both sides of the syndrome are
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ubiquitous, even if they are not directly observed by a clinician (American Psychiatric

Association, 1994, p. 277). More often, authors hone in on a single gene or neuron and

offer no cogent explanation why save saying that ‘it was implicated in schizophrenia.’

(Eg. Welch et al., 2011) Notable exceptions such as Gray, Feldon, Rawlins, Hemsley

(1991), Fletcher and Frith (2009) and Kapur (2003) were inevitably also profoundly

skewed, but at least all of these made some attempt to pull themselves from the mire of

partially digested data and explain schizophrenia more holistically. It is like this small

number of authors apparently spent enough time staring at the broader field of data

(like some great random dot autostereogram) to discern some really relevant patterns,

but still they missed the big picture. Like the autostereogram, the data on schizophrenia

is apparently plagued by random data with produces definable patterns but no clear

picture. It’s only after staring at it and going wall-eyed (that is seeing everything in

inversed perspective) that a holistic 3D image becomes suddenly evident.

In three years of reading the most notable hypotheses and literally thousands of other

findings, I suddenly saw that every one of the thousands of articles I read, as well as

every diagnostic criteria and other symptom actually does make sense – and not only in

a scattered way, but with a singular cogence. It was a bit like seeing the big image in the

aforementioned autostereogram. Methodologically, it was like the payoff of a grounded

theory approach, but not situated among people, but ideas and data. Like in a

Hollywood movie, it happened not during my studying hours, but during a vivid dream.

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The exploration was intended to provide for better questions about the relevance of the

built environment in schizophrenia, not to be the heart of the thesis, but there it was. If

ever I needed to advance new knowledge, here was my opportunity. I had discovered

something quite unexpected. As an architect I should have ignored it – the aetiology and

psychopathology of schizophrenia was none of my business. But do you ignore the

diamonds you find in a gold mine, just because you’re a gold-miner? I very nearly

jumped boat and abandoned the hunt for ‘gold’ and made this question alone my PhD

topic, but I was restricted by formal constraints. I was in the Faculty of Architecture,

Design and Planning and my supervisor was an architect with no more than a flirting

interest in schizophrenia. So I had to plough on and pursue the question of the built

environment.

Even so, the model for schizophrenia that I present is quite literally the heart of the

thesis, making up the whole of section 2 (from p. 204). It serves as a wonderful

foundation – allowing my assertions about the environment to be translational rather

than being based on original empirical studies. The theory I developed was that

schizophrenia is fundamentally an illness of the perceptual system and that all

perceptual stimulation must either make the condition more severe or incrementally

better.

Fortunately this finding was very relevant to the built environment because the built

environment is a ubiquitous a source of perceptual stimuli, and one that profoundly

affects phenomenal experience.

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In this context, the built environment (on all scales) reflects a concentration of many

potentially active percepts, with each individual building offering a range perceptual

opportunities – some of which are good, others harmful. Effectively this makes the built

environment aetiologically culpable as a likely transmission pathway – in itself innocent

an innocent agent, except as it carries dangerous psycho-agonists: like water for cholera.

The two other sections effectively emerged from the second: the first (question 1, from

page 62) is how tailored environments should be shaped to mitigate the effects of

schizophrenia. These articles are not about aetiology, but are about treatment.

The articles in the third section are about the culpability of designed objects,

architecture and the urban environment in the aetiology of schizophrenia and related

mental illnesses. This section (from page 296) finds the stimulation provided by the

built environment culpable twice over. Firstly, for a lack of consideration of how it

stimulates the formation and maintenance of delusions and hallucinations. But perhaps

more importantly there’s the other side – the failure of architecture to stimulate where it

can and should.

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PURPOSE STATEMENT

It is my aim to discover what influence the architectural

environment has on schizophrenia.

Ultimately I want this work will reveal new architectural innovations and affordances

that will assist: a) in urban planning to avoid schizophrenia onset and b) to assist in the

treatment and management of schizophrenia.

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POTENTIAL SIGNIFICANCE

Schizophrenia is a debilitating and deadly illness that can strike in any social context

anywhere in the world – although epidemiology of schizophrenia is subject to enormous

variation (Kirkbride, Fearon, et al., 2007). The normative opinion among researchers is

that schizophrenia not uncommon but reliable figures on schizophrenia incidence show

only that it is subject to extreme variation. The fact is that 0.2% of Australia’s

population had a diagnosis of schizophrenia in 2001 (a simple calculation extrapolated

from reported figures (Carr et al., 2002) and the Australian population at the same time

(Australian Bureau of Statistics, 2011)). Thus even the incidence of schizophrenia is a

subject worthy of in-depth research.

For an analysis of incidence, please see p.29: Incidence of

schizophrenia

Schizophrenics lose their ability to interact meaningfully with society. They lose their

somatogenic perception, meaning the connection with the senses that inform them about

pain, hunger, comfort and other essentials is lost or unusually poor. People with

schizophrenia also lose their abilities to manage day-to-day tasks. (Osmond, 1966;

Searles, 1960; S. Williams, 2002b). Finally, and most famously, the ability to perceive

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the outside world is hampered by interference from delusions, internal projections and

hallucinations (Fletcher & Frith, 2009).

For hypotheses explaining the symptoms, signs and other

consequences of schizophrenia, please see the articles

starting on p. 204, p.358 and p.373.

Furthermore, schizophrenia should be considered a deadly illness. About 5 to 8.5% of

schizophrenics die by suicide (Harris & Barraclough, 1997; Palmer, Pankratz, &

Bostwick, 2005), and a similar number by accident or unspecified violence (Ösby,

Correia, Brandt, Ekbom, & Sparén, 2000). An estimated 2% die from catatonic

complications (Wyatt, Alexander, Egan, & Kirch, 1988) and many others die from

comorbid illnesses that would be treatable in healthy people but are difficult to treat in

schizophrenia because of negativism, poor comprehension and compliance.

Comorbidities lower life expectancy by about 9 years (Dembling, Chen, & Vachon,

1999). Overall, diagnosed schizophrenics have a life expectancy that is much lower

than the general population, with two thirds of excess mortality being from ‘natural

causes’ including heart disease and poorly managed diabetes (Auquier, Lançon,

Rouillon, & Lader, 2007).

I propose that much of the suicide and accidental and violent

death of schizophrenic patients (as well as the occasional

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violent death of others) is automatic opportunism. Please see

psychiatric suicide on p. 396.

Medication, the main mode of treatment, is well recognised as being ineffective in about

30% of cases (H. M. Jones, 2004), and when it is effective, it only treats some

symptoms (Golembiewski, in review-d) (Page 199-). Psychotropic medication is thus is

better understood as symptom management than treatment. Medication is rarely a

perfect fit for patients and it causes an incredible array of undesirable side effects, some

of which are permanent (S. Williams, 2002a). Psychotherapy is normatively considered

useless for schizophrenics (S. Williams, 2002a) although clinicians sporadically report

good results with various forms of talk therapy (Searles, 1960, 1965), CBT (cognitive

behavioural therapy), physical therapy (Vancampfort et al., 2012) and even placebo

treatment even though the efficacy of psychotropic medications is apparently decreasing

(D. H. Freedman, 2010).

Although it has been suspected for a long time that modifications to the environment

will improve the well-being of the schizophrenics (Foley & Lacy, 1967; Osmond,

1966), very little research has been done to discover what those changes could be. This

area of research has more or less vanished with the growth of other areas of focus - most

schizophrenia research currently focuses on genetics and pharmacology.

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Incidence rates

Schizophrenia can develop anywhere, in any population and demographic. Despite this,

its incidence is far from even. The most commonly reported figure for the worldwide

average incidence is 1% over the course of a lifetime, but the reality is that the figure

seems to be far lower, although in some locations at some points in history the figures

have crept up and even exceeded this figure. The 1% is a ‘strategic’ number,

presumably intended to bring attention to this very important cause, in the tradition of

Florence Nightingale, who manipulated statistics to dramatize causes of preventable

deaths and bring attention to her new methods of healthcare (H. Woodbury, 2008). A

meta-analysis of 1,458 rates taken from 33 countries suggests that the incidence spans a

distribution curve running from 7.7 to 43.0 cases per 100 000 people (i.e., 0.0077% to

0.043%) (J. J. McGrath, Saha, et al., 2004).

But the heterogeneity of rates is far more extreme than normalization curves would have

us believe because the incidence is subject to extreme fluctuation based diagnostic

criteria and paradigms (even before on social and physical environment are considered).

At the moment, the sober figure mentioned by McGrath et al is modified by the removal

of pellagra, scurvy, syphilis and hyperthyroidism from the diagnosis by the

identification of distinct pathologies and by the removal of bipolar disorder, various

forms of developmental disorder, affective psychoses and geriatric dementias by

reclassification (American Psychiatric Association, 1994; Berrios, Luque, & Villagrán,

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2003; Boyle, 2002; Hoffer & Osmond, 1963). As many as 1% of the population were

committed in psychiatric hospitals and estimates of uncommitted and undiagnosed cases

were estimated to make up 3% of the entire population of the USA in 1957 (Campbell,

1958).

Although schizophrenia was thought to have a relatively even distribution in terms of

population-wide levels at that time, this opinion was based on assumptions rather than

methodological empiricism (Campbell, 1958) and even on much smaller scales, the

variation of incidence was already known to be enormous (Faris & Dunham, 1939).

Since then, incidence patterns must have changed radically. The removal of nosological

conditions from the schizophrenia diagnosis had marked huge changes in distribution of

incidence patterns. Until the mid twentieth century, pellagra was common in the USA

for instance. Especially in rural areas of the southern states where the diet (being based

on maize) had no natural vitamin A. It’s possible that the inner city prevalence of

schizophrenia at the time was also a product of diet – as poor people were removed

from natural sources of vitamin C, it is conceivable that incidence of scurvy rose,

although by the time of Faris and Dunham’s study, the cause of scurvy was well known

and should not have been reflected in the data they collected.

With increasingly narrow diagnostic criteria, the heterogeneous incidence patterns of

schizophrenia have become more predictable. As mentioned earlier, incidence tends to

increase with exposure to urban settings. Against this backdrop, there is only one known

outlier to this rule: the incidence in Chandigarh, a modern city designed by Le

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Corbusier, in the state of Punjab, (India) which has lower incidence than its surrounding

rural areas (Varma et al., 1997; Wig et al., 1993). The reason for this, like anything

about schizophrenia, is unknown and has not been formally hypothesised. Chandigarh is

an interesting case however, because it is exception it’s the exceptions that explain

bigger patterns.

The conditions for the design of Chandigarh are discussed in

depth in my paper: Determinism and Desire: A neurological

language for architectural design (Golembiewski, 2013)

(starting on page 126). This paper does not focus on

schizophrenia, but it does outline why Chandigarh may be an

exceptional case.

Other known exceptions are high incidence rates among rural populations (their

relationship with the nearest cities has not yet been tested to my knowledge). These

occur in the north west of Ireland, in rural Scandinavia (especially in the north), and in

Istria, a peninsula jutting into the Adriatic, currently part of Croatia, on the Italian and

Slovenian border.

The placement of Istria is traditionally in the warpath of just about every major

European conflict. And being in close proximity to Italy, Slovenia, Austria, Germany,

Hungary and Bosnia-Herzegovina, its population has never recovered from the wars of

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the twentieth Century and most of its buildings are still in ruins. Rather than mark an

anomaly, the conditions in Istria possibly marks a local statistical aberration.

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Socio-economic costs

Schizophrenia represents a huge social and financial burden to society – but not evenly

distributed over the whole of society. Rather the strain is patchy and uneven because of

inconsistent models of care, and because the greatest burden is usually handled by the

families of those who suffer (Beecham & Knapp, 2001). Incidence and recovery rates

also vary from region to region. But as a whole, the cost to Australia in 2001 alone was

estimated to be $1.85 billion (about 0.5% of the GDP). Over a third of this was borne by

families, and another $661 million in direct costs to the healthcare system and finally

the indirect costs at $772 million in lost income and increased morbidity etc. (Carr et al.,

2002).

To estimate the potential financial impact on this figure by the research that was

conducted for this thesis will be a futile process because we cannot guess at the impact

that my work may have. This thesis affects three domains: urban planning (where

outcomes are intended to reduce the epidemiology of schizophrenia), psychiatric facility

design (where outcomes are intended to improve treatment) and in the general

understanding of the syndrome (which promises more abstract, but high-level impacts).

Just how much does it help to have someone understand the syndrome? Will that

improve medical and social treatment? It is conceivable. Will this understanding also

help hone the broad study of schizophrenia to more practical outcomes? Once again, it’s

conceivable but immeasurable.

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RESEARCH QUESTIONS

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Question 1: Specialist psychiatric facilities to help people with

schizophrenia

Originally “How can specialist psychiatric facilities be improved in the way they

help people with schizophrenia?” was to be my one and only research question. An

extraordinarily naïve one too – loaded with assumptions that somewhere someone may

not only know what schizophrenia was, but also may know what may help.

The research question that asks about the design of specialist

facilities is largely explored in pages 61-198.

I started out by researching suitable models to understand how innovation in the built

environment may improve the wellbeing and health outcomes of schizophrenic patients.

I had previously worked on mental healthcare design and had been frustrated by the

scarcity of tools for designers who are tackling the problems that come with designing a

psychiatric facility – unless they are designing a dementia facility, in which case there’s

a fair amount of quality information available (largely due to the efforts of John Zeisel,

Ian Forbes and a few others) but Alzheimer’s and other old age dementias don’t share a

lot with schizophrenia, certainly not on a neurological level. Where dementia is defined

by the loss of memory, schizophrenia is better defined by losses of awareness of the

‘unexpected’ coupled with intense awareness of expected events (see the section on

schizophrenia, page 204 onwards).

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I approached my problem as an architect, with a concern for praxis. I wanted to create a

tool that would be easy and fast to use and would generate better outcomes regardless of

theoretical concerns about the relationship between schizophrenia and the built

environment.

Other design researchers pointed the way. In the first decade of the 21st century, a

number of authors started to write about a salutogenic approach to healthcare design

(Bahrs et al., 2003; Dilani, 2008; Edvardson, Sandman, & Rasmussen, 2005; Eriksson

& Lindsrom, 2008; Eva Langeland et al., 2005; Eva Langeland, Wahl, Kristoffersen, &

Hanestad, 2007). These papers brought my attention to Aaron Antonovsky’s psycho-

social model for understanding the parabolic continuum that spans the theoretical states

of perfect health and death (Antonovsky, 1987, 1996). These researchers used the term

‘salutogenics.’ They also roughly sketched out the principles of salutogenesis and its

benefits over other models of psycho-supportive design. But I turned the theory into a

methodology, designed, as I needed it, for use in design praxis.

The method isn’t only applicable for architectural praxis, but

for anyone who has to make decisions about other people’s

well being on the fly. In 2009 I demonstrated this in a

symposium held to look at rural emergency management

(Golembiewski, 2009a), and in 2012 the conference paper

was published in the Australian government bulletin:

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Australian Journal of Emergency Management

(Golembiewski, 2012b) (starts on page 148).

There are any number of studies that demonstrate the relative strength of salutogenic

theory, but how the theory works is relatively obscure. Antonovsky did explore this

question, but he did so in the mid 1970’s to the mid 1980’s and what was acceptable

then (in terms of psychological explanation) seems weak now. At any rate, I had to dive

deeper than the theory of salutogenics. And in order to find substance to make my terms

of reference deeper, I had to look at schizophrenia itself. How could I know how the

environment affects schizophrenia (and vice versa) until I knew what schizophrenia

actually was? As it happens, I was eventually led to make associations between the

principles of salutogenic theory and the psychogenesis of schizophrenia (Golembiewski,

in review-d) (Starts on page 204). This is a paper that returns to salutogenic theory to

find neurological causes: ‘The neural basis for the salutogenic method of healthcare

design.’ It is presented here from page 159.

In the outset, the possibility that salutogenic theory may present answers to what

schizophrenia actually is was not on the horizon. Another serendipitous association

came from the depths of architectural theory.

While studying undergraduate architecture, I came across the ecological theory of

perception in Lang’s textbook on theoretical drivers for architecture (1987). It was one

of my associate supervisors, Dr. Spehar who directed me back to it, suggesting it may

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have relevance. This theory, whilst relatively well known among perceptual

psychologists, is virtually unknown among clinical psychologists, yet it did seem

relevant. Already some fringe areas of medicine were picking up on the theory to

explain the ‘mirror neuron’ phenomena that was being observed in interpersonal

communications. The ecological theory of perception essentially proposes that

perception is direct and directly stimulates action and such a model could explain a lot

that cognitive models of perception can’t. It seemed plausible that schizophrenia – when

conceived as a dysfunction of perception, may be partly a dysfunction of ecological

perception. I have explored this possibility in several papers, most notably ‘The Riddle

of Psychotic Perception Resolved,’ (reprinted here from p.204), ‘Common Psychiatric

Symptoms…’ (reprinted on p.358), and ‘Lost in Space…’ (Reprinted from p.296.)

Because of these lines of enquiry, and because of my dissatisfaction with the dismal

lack of understanding of the phenomenology of schizophrenia, the question “what is

schizophrenia” became my second, but most important research question.

My work on the nature of schizophrenia is where my deepest research has taken place,

and where my breakthroughs have been most profound. I thus consider my work on

schizophrenia itself to be the heart of my thesis. I would have been happy to let my

findings about the nature of schizophrenia be the topic and substance of this thesis.

I attribute any success I have had in neuro-psychological enquiry to my architectural,

rather than scientific training. Architects must address wicked problems on a regular

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basis, and they learn to be comfortable with the unknown and unresolved. Furthermore,

there are reasons why many scientists would not be able to approach the subject of

schizophrenia as I have. Scientists have a commonality in their training and language,

they have common normative values and frequently researchers emerge from under a

focused umbrella of enquiry that is dominated by their supervisors. None of these

factors affected me. In effect I was freed by my independence and lack of awareness of

the dogmas that are so prevalent in the scientific method.

For the articles I have published or am publishing in this

space please see ‘Common symptoms…’ (Golembiewski,

2012a, in review-b) page 358, for presentations see

(Golembiewski, 2009b; Jan Golembiewski, 2010a; Jan

Golembiewski, 2010), for peer reviewed online discussions

see (March, Kirkbride, Veling, & Golembiewski, 2009; Volavka

et al., 2011) – (Presentations and on-line discussions have not

been reprinted here, except as they are cited in more

significant works.)

I have yet to see whether my principle work on this subject

shall be published, but it is enclosed here (Golembiewski, in

review-d) starting on page 204.

It was the demand from healthcare architects planners and facility managers have made

it impossible to put questions about psychiatric design off until I finished my PhD – in

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effect it was industry that has kept me focused on my original question. It was little

things that kept me to my original question – the need for designers to know more, the

questions raised by my colleagues in the Faculty of Architecture Design and Planning,

and the opportunities I was given such as a paper on how my neurological findings may

be applied generally and deterministically to any design project, from object design, to

buildings to urban scale design.

The paper was produced and presented. It is now in press:

Determinism and Desire… (Golembiewski, 2013) (Starts on

page 126).

I was then asked to present a paper to a symposium on mental healthcare design

(Golembiewski, 2011b). This opened a floodgate, and the pressure for me to produce

more and more of this material is evident, several more offers of plenary addresses at

conferences have accelerated the interest in this material. I started to get approached by

the health departments around Australia and by several prominent architecture firms

who work in this space; HASSELL Healthcare, Bates Smart, BVN, Woods Bagot and

MAAP (UK). I have been asked to guest edit an edition of Facilities on the subject and

also to write a piece for the Australian Journal of Psychiatry.

In short, I had little choice but to return to the space I had started out in: health design.

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Question 2: What is schizophrenia?

The great algebra of what schizophrenia is and what may cause it has dominated the

three years of my PhD research. Originally it was because the depth of answers I needed

(about the relationship between schizophrenia and the environment) could only emerge

from a very deep understanding of the phenomenology of schizophrenia itself. I could,

perhaps have spent time with a sizable number of schizophrenia patients and conducted

an ethnographic methodology, but this approach never felt right, and besides, I never

had a means to access to a significant numbers of patients in diverse environmental

contexts. Professor Perkins (in review) relates his experience doing just that. The

findings that he and his students and colleagues discovered are very reasonable and

offer great depth to his field of enquiry (landscape design for psychotic patients). The

principles Perkins et al. devised are intimately related to the salutogenic methodology I

published and present in this thesis, but the issue of the life-world of schizophrenic

patients is one that Perkins et al. wisely skirted around. Indeed, his work makes no great

distinction between the phenomenology of schizophrenia and the phenomenology of

other mental illnesses.

In any case, I did not choose an ethnographic methodology but a speculative enquiry

through literature. It was not going to be sufficient to rely on other’s hypotheses, simply

because the vast bulk of them just didn’t ring true. And besides, many were useless for

understanding how schizophrenia interacts with the built environment and vice-versa.
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Schizophrenia is not an illness as such, but a diagnosis based on loose but cohesive sets

of symptoms. There are significant diagnostic differences between some of the

published diagnostic system (such as the DSM-IV and the ICD-9), and on a finer level

there is a range of different sets of symptoms apparent even within a single diagnosis. It

is hardly surprising, then, that the established knowledge base about schizophrenia is

subject to a few contradictions and huge open-ended questions.

At a minimum I had expected to find that research and practice might be unified by a

common theory – or at least a common hypothesis. But what I found was that every one

of tens of thousands of researchers and clinicians harbour their own heuristic ideas. Of

these, few reach far beyond the very limited scope of their own very limited areas of

enquiry. Because the definition of schizophrenia is so nebulous, theoreticians take

permission to break the illness into component parts and address the bits, while

dismissing the holistic presentation of the illness. The pet interests of the theorists only

exacerbate the problem; the very ephemerality of the question means that answers

appear to be skewed to match or prove a-priori agendas. Examples include beliefs that

human consciousness is a delusion (Taylor, 2010), or that heeled shoes have a knock-on

effect that causes mental illness (Flensmark, 2004), or that thin people are have a

territorial nature (Kellett, 1973). If I had tailored practical solutions to such limited

hypotheses, it is unlikely that they would be of much use. An analogy that we can all

understand it that the schizophrenia researchers of the world are apparently attempting

to draw a 1:1 scale map of the world of schizophrenia, but are ignoring the mountains,

lakes and forests as they concentrate on the contours of bits of gravel.

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So I persevered, placing a great deal of interest in the hypotheses that focused on what I

figured may ‘bridge’ the individual mind and the world we all live in. This meant I

prioritised hypotheses that focused on perception such as (Fletcher & Frith, 2009; Gray,

Feldon, Rawlins, Hemsley, & Smith, 1991; Kapur, 2003). As useful as they were, these

hypotheses held a consistently naïve model of perception. Certainly the models of

perception they employed were never as sophisticated as the ecological theory of

perception, developed by James J Gibson (1979). The discoveries I have made, with the

question “what is schizophrenia” at least partly involves matching schizophrenic

phenomenology to the ecological theory of perception.

My working hypothesis for schizophrenia is my second

question and is largely contained within a single article. See

the section running from p.199-294.

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Question 3: The role of the built environment in the aetiology and

symptoms of schizophrenia

Contrary to the views of many researchers, to me it seems obvious that the aetiology of

schizophrenia cannot be meaningfully separated from the symptoms. There is a twofold

reason for this: firstly because schizophrenia is a diagnosis and not a nosological

condition. The diagnosis is based on symptoms, absences of normal behaviour it is thus

a behavioural expression. And whenever pathogens or other nosological conditions are

discovered that cause these symptoms (or similar ones), they are automatically

exempted and re-classified, because the diagnosis of schizophrenia is specifically

invalidated when and if nosological disorders are identified (American Psychiatric

Association, 1994). In the past many other causes of schizophrenic-like

symptomatologies have thus been excluded. They include pellagra, scurvy, syphilis,

hyperthyroidism, autism and drug abuse (American Psychiatric Association, 1994;

Boyle, 2002; Hoffer, 1970; Hoffer & Osmond, 1963).

The other reason that the aetiology and symptomatology of schizophrenia cannot be

disentangled is that genetic and environmental factors that come into play do so because

they create a predisposition for schizophrenia and a context into which schizophrenia is

expressed: the environmental and genetic factors thus moderate and mediate the

symptoms through moderating and mediating experience. This is reflected in behaviour

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and thus also in diagnosis. Like genetics, the environment cannot be considered as

directly causal, but it does inextricably contribute to the diagnostic symptomatology.

As an illustration of this point, a patient of Dr. H. Searles remarks (while trying to

express what it means to experience schizophrenia) “how would you like to have square

eyes?” at this point Searles realised that the patient was being quite literal. The

experience of having ‘square eyes’ demonstrated a lack of differentiation with the

external physical environment. The square eyes the patient complained of were the

windows of Searles’ office (Searles, 1960, p. 51).

The very inability to disentangle schizophrenia from the environment is very interesting

from the perspective of an architect because this viewpoint involves the built

environment in the very aetiology and psychogenesis of schizophrenia and can be

spotted in cross-sectional epidemiological studies.

One of the most interesting findings about schizophrenia is that it is predominantly an

urban syndrome. The incidence of schizophrenia grows with exposure to urban centres

(Kelly et al., 2010). This was first observed nearly a century ago (Faris & Dunham,

1939). But there are few hypotheses that lend themselves to understand this

phenomenon. Some say that cities are places of greater social anxiety (Selten & Cantor-

Graae, 2005, 2007), places of social ghettoization and stigma (Kirkbride, Fearon, et al.,

2007; Kirkbride et al., 2006; Kirkbride, Morgan, et al., 2007; March et al., 2009), places

where noise and air pollution are rife (Halpern, 1995), others have suggested that one of

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the symptoms of schizophrenia is urban drift, and that people end up in the cities in

search of cheaper accommodation (Evans, 2003; D. Freeman, 1994; Lapouse, Monk, &

Terris, 1956), some arguments have been rejected by cross-sectional studies (the noise

and air pollution proposals for example) but for most, the jury is still out (March et al.,

2008).

I was part the debate about this question in an online

conversation (peer reviewed and edited) on Schizophrenia

Research Forum. (March et al., 2009)

My third question is: “what role does the built environment itself play in the

aetiology and epidemiology?” The strong relationship between the built environment

and schizophrenia means that this question remains valid, even if the popular

hypotheses (that don’t point to the physical environment as an aetiological factor) are

found to be true. Minimally, the built environment makes up the context within which

schizophrenia is experienced.

Importantly to me, a designer, the question has a suffix: what does the correlation

between schizophrenia and place mean for us, the designers of the built environment –

whether we design psychiatric units, cities, or the buildings that they are built from?

These questions are tackled in the section of the thesis that

runs from page 295 to page 397.

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HOW THIS RESEARCH MAY HELP

It is the central premise of this thesis that the relationship between psychotic conditions

and the built environment is inextricable.

The reason is an argument in logic: Both schizophrenia and bipolar-1 are diagnoses

based on behaviour. As mentioned earlier, the moment a nosological disorder is

identified, which presents similarly to schizophrenia (or bipolar), it is withdrawn from

the diagnosis by a general exclusion of other identifiable disorders (American

Psychiatric Association, 1994). This effectively means that these psychoses cannot be

considered as illnesses. These conditions can be no more than behavioural

manifestations – that is distinctive sets of florid symptoms and deficit signs. As

psychotic illness is defined by behaviour, the built environment is the ubiquitous

context for that behaviour.

Behaviour reflects experience:

1. Somatogenic experience, which is opaque to observers.

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2. The internal experience of a common context (the phenomenology of the outside

world), this may be noticeable by others.

Behaviour is the outward expression of experience (called symptoms when the

behaviour is especially unusual), and behaviour occurs within a common context. All

behaviour reflects the context in which it is expressed, both by interaction and also by

expectations of appropriateness. By interaction I mean that there is a big difference in

sitting on the floor of a Japanese room with tatami mats and sitting in the muck of a

pigsty. An example of contextual expectations is in the rowdiness, which is expected in

a schoolyard, but not in church. All behaviour is, at least in equal part, environmental.

But logic aside, epidemiological studies consistently find the 'urban milieu' to account

for about 30% of all incidence, even once all other known factors are accounted for

(Kelly et al., 2010; Krabbendam & van Os, 2005).

If this evidence is insufficient, then the Camberwell walk study can be called in; a study

of 17 paranoid psychiatric patients undertook a PANSS test before and after a 10-

minute walk through the busy Camberwell High Street of London. The test showed that

paranoia and other psychotic scales were increased after this short 'dose' of urban life

(Ellett, Freeman, & Garety, 2008). Even without going into my PhD research into why

this may be so, the evidence is amply triangulated. The environment is an inextricable

factor in psychosis and we, as the designers and planners of the environment are

culpable.

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Just as a building has to have foundations on the earth, psychosis is an expression of the

mind as it meets experience. And for most of us, most of the time, that experience is of

the built environment.

Now that we know how implicated the environment is in psychotic conditions, it is time

to look back at the environments we prescribe for psychotic patients. Could they be

better? How would I feel if I were 'on the edge' and in this space? Are there any

provisions to improve a patient's sense of coherence? (See the research question on p.35

and how it is addressed starting on p. 62)

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METHODOLOGY

My methodology has been unorthodox. What started as naïvely pursuing very diverse

research questions – over a period became my guiding methodology. Over the last three

years, I have discovered that one line of questioning gives perspective to the other.

Typically scientific enquiry is approached in very small steps and with close guidance

from a supervisor who is doing research in a closely related field. The resulting research

findings will be published in a small collection of papers with the supervisors name on

the right and the student as the first or second author. The process taken by a PhD

student called Melissa Green typified this trajectory, right here at Sydney University.

Her topic was specific, doable, and likely to produce publishable results: ‘Facial affect

processing in delusion-prone and deluded individuals: a continuum approach to the

study of delusion formation’ (Green, 2001). The research questions addressed little gaps

and solidly filled them with new findings using established lab-based methodologies. If

I had been in the psychology department (as Green was) my thesis question would not

have been accepted, much less my far more expansive research questions. But in the

faculty of Architecture, Planning and Design, my supervisor wasn’t to know that I had

taken on a subject that is normatively taken to be impossible.

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But I’m not at all upset that I took this route because it yielded results. My approach

meant that I had to come to understand schizophrenia using very broad-brush strokes,

and then to refine the knowledge I acquired. This is the opposite of the normative

approach, which is to learn first-up that the solution is not in sight and that a researcher

has to focus on one little piece of the puzzle. Forget schizophrenia – look at delusions.

The researcher then reads everything about delusions, but focus their own studies on a

single piece of that puzzle. There’s no doubt – that method works, and it’s far less risky,

but I more or less did the opposite.

Architects are practical people, yet people that are able and trained to address wicked

problems (Kunz & Rittel, 1972) and find practical solutions. This is, in fact possibly the

most useful talent architects possess and there is a whole research school in Stanford

(The D School) to study ‘Design Thinking’ (R. Buchanan, 1992). Architects are trained

to find the simple bits of information that are needed allow them to make lateral

innovations that solve many problems. My approach to PhD research followed this

practical approach, only I didn’t ask simple questions. At first I just wanted to know

what schizophrenia was, so I could establish solid design guidelines for an incredibly

vulnerable and marginalized population, so I started reading. As I went, I wrote one

hypothesis after another. As and when they became coherent, I sent them off to be

published. Inevitably, most were rejected, but rarely without some sound advice: look at

this or that. Sometimes my associate supervisors gave similar advice: look at this or

that. As they got more refined, my papers started being reviewed, and usually still

knocked back. The reviewers’ advice was always well considered and to the point. But
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none ever suggested that I should abandon my questions. So I continued. I resolved

difficult issues, I integrated disparate seams of knowledge and my hypothesis for what

schizophrenia is became more and more cogent.

But it seems that there aren’t many people who do approach schizophrenia research

with such a design-thinking approach. Green’s PhD topic is normatively considered to

be expansive and an ideal question to consider for three to six years. In the last few

decades there have been very few comprehensive hypotheses for the illness – and all

have somehow lacked the integrative holism that I sought. Out of all of them, Gray,

Feldon, Rawlins, Hemsley, & Smith was in 1991 (Gray et al., 1991). It was by far, the

hypothesis with the broadest reach, and it has also remained remarkably good over the

last 20 years, but since it was published, another 75 000 or so related articles have come

off the press (MacDonald & Schulz, 2007). In many ways, my own hypothesis

(Golembiewski, in review-d) which starts on page 204, is very compatible, although it

comes to the argument from a completely different route, and is naturally more up-to

date on its sources. Gray et al. 1991 was an uncharacteristic leap, stretching far further

than any hypothesis since. Subsequent broad stroke hypotheses include (Kapur, 2003),

for instance. Despite it’s reputation for being an ‘extravagantly comprehensive

synthesis’ (H. M. Jones, 2004), the author himself defends it as a hypothesis for no

more than ‘psychosis within schizophrenia’ (Kapur, 2004). Far from the reach of Gray

et al, this putatively explains but a handful of symptoms from the ‘complex

constellation of schizophrenia’(American Psychiatric Association, 1994). A last opus

magnum on schizophrenia was Fletcher and Frith’s 2009 Bayesian hypothesis (Fletcher
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& Frith, 2009), that studiously avoided mention of Kapur 2003, yet didn’t reach far

beyond it. But typically the authors marched knowledge forward incrementally; they

very cleverly synthesized the growing consensus to the Bayesian understanding of

Friston (2003).

My method was two pronged, and indeed, the rigor and substance I was able to bring to

the theory of design from my scientific discoveries has been well received, and as I

write, have been accepted into press or published in several international journals. My

scholarship has also been awarded with many prizes and even a guest editorship in

Facilities Journal.

In terms of formal methods, I’m not ashamed to say that all my research has been

conducted with an integrative literature review methodology employing logical

argumentation (Groat & Wang, 2002). Exactly the same method was used by (Gray et

al., 1991) in their landmark thesis. The decision to take this approach was based on the

advice of Dr. Peter Armstrong (my supervisor) and Professor Hemsley (in personal

conversation, at the IoP in 2011). Despite this heritage, the method is sure to attract

negative attention. Once again, there is a normative expectation (at least in the sciences)

that PhD theses will generate new empirical data. Here there is another great benefit in

being in architecture. Architecture is not a science, and so the requirement for new data

can be dismissed without further thought. But even so, I feel compelled to refute this

expectation. I did take (and methodologically analyse) a dataset, only it was not one of

my making.
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Although there is a cavernous gap of knowledge around the spatial and material needs

for psychiatric patients, there is too much knowledge about schizophrenia, and these

opposites are complimentary. In 2007 there were 4400+ articles and other publications

of schizophrenia related issues published. That’s up from about 4200 in 2006 and 3700

in 2005. This steady upward climb has continued since at least 1987 (MacDonald &

Schulz, 2007). The data isn’t up to date, but at the same rate of growth, estimates are

that this year will see about 7000 – about 52 articles a week. If there ever was a data

feed that is really comparable to drinking from a fire-hose, this is it.

It was from my emersion in this data that I noticed patterns and brought them to light.

Methodologically this is very similar to a Grounded Theory method (Corbin & Strauss,

1990; Strauss & Corbin, 1990), except that instead of grounding myself in a social

milieu, I grounded myself in published data. Where a Grounded Theorist typically takes

noted on observed behaviour until saturation has been achieved, I took notes on data.

Where a Grounded Theorist diligently ignores what people say they are doing (to

observe the reality of their actions), I ignored what authors said their findings were, to

focus on what they materially discovered.

Inevitably my methodology will not please everyone and for those who remain critical

about it, it’s worth remembering what a methodology is for. It is a routine, an accepted

road-map to approach a gap in knowledge. Methodologies are not only useful for

pointing a researcher the right way, so they make their discoveries efficiently, they are

particularly useful for justifying failures. If a PhD student were to finish their tenure
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without discovering anything, they had better be able to explain what they did, that they

could find so little. If their approach was systematic (such as taking half the rooms in a

mental health unit, painting them in different colours and comparing the in and out

PANNS scores over time), and still the study found nothing conclusive, then the

researcher could safely write: ‘the colour of rooms appears to make no difference to the

PANNS scores of patients over time.’ It is thus safe, and useful, even when an

experiment fails to have a highly structured methodology.

I had intentions of undertaking such a methodological approach (I intended to do

grounded research within a mental health unit, ethics permission allowing it), but I

didn’t because I started making discoveries about the time I started applying for ethic

permission. As I was aware that I would not need to justify a failure post-hoc because

my findings looked like they would be ample, I knew that I wouldn’t need to undertake

a massive design intervention or some similar new empirical study.

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THESIS INCLUDING PUBLICATION:

LIMITATIONS AND ADVANTAGES

Among first-rank universities around the world, it is now de rigeuer that a PhD can be

granted by publication and a viva voce. Unfortunately University of Sydney hasn’t made

this step, and instead, a PhD may be given to a series of publications that are

accompanied by an exegesis.

What an exegesis is, and what form this PhD including publication takes is all but clear.

Professor Adrian Snodgrass once said, “all I want to see in an exegesis is one short

sentence: ‘It’s all in the papers.’” On the other hand, some still feel there is value in the

traditional tome.

There are advantages either way. The ‘by papers’ route exposes a candidate to the

rigours of the international academy early. Internationally accepted experts review

papers as they are produced and the candidate (me in this case) gets to work on their

advice. At the same time the candidate builds a portfolio of publications and a

reputation in their field before the PhD is even granted – these benefits serve the

university too.

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The disadvantage of this approach, as I see it, is that when papers are collected into a

tome (as mine have), they can sometimes be a bit repetitive: sometimes the same

arguments are employed in two or more papers, and if one paper draws on another, they

may recap on findings. Furthermore, the thesis is likely to lose its monolithic narrative

structure. If you as a reader find these problems in the published works of this thesis,

please forgive me. Rather than re-write the papers to fit the tome, I have kept them

much as they were published, excepting only changing the language to The Queen’s

English, whenever a work was written to be published in an American Journal.

Another thing I have noticed is that ideas do move on. Data emerges that is

contradictory, logical fallacies are discovered in retrospect, etc. Knowledge is

capricious, and an idea that has enough validity to be published need not be future-

proof. Although publishing gives knowledge an aura of finality, it doesn’t stop it from

being falsified. Indeed this has happened in my own papers. My finding that negativity

motivates common psychotic symptoms (Golembiewski, 2012a) (reprinted here from

page 358) is at least partly falsified by my work on the psychogenesis of schizophrenia,

(Golembiewski, in review-d) (also reprinted here from page 204). The reasons are

detailed on page 356, but in a traditional tome contradictions like these would probably

not be acceptable. Once again, here I must present my papers much as they are being

read by others, not with an apology (I shouldn’t need to apologise for publishing after

all) but with a note to explain the odd U-turn or logical contradiction over a series of

works. Believe me I am aware of these, and it is my intention that readers of this

exegesis should be also.

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Finally the exegesis with publications doesn’t follow a logical linear structure that one

may expect from a thesis. Obviously since Nietzsche, Wittgenstein and with

postmodernity, the days of the singular narrative are a bit passé anyway, but I do see the

value in in-depth linear analysis, and for all those who are inclined to agree, the

enclosed paper “The Riddle…” (from page 204), is nearly 20 000 words, plus another

5 000 if citations are included, you are welcome to take that as the thesis and ignore the

rest!

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PAPERS, PRESENTATIONS AND INCOMPLETE ARTICLES

NOT INCLUDED

A neurological language for determinism in design. Seminar presented at HASSEL,

Melbourne (19 April, 2012). (Also presented at AAA seminar series)

Schizophrenia and Violence, Case Not Closed. Volavka, J., M. Large…Golembiewski,

JA et al. Schizophrenia Research Forum. Edited Live Discussions. V. Wilcox (ed.),

Schizophrenia Research Forum (2011).

The dopamine-mediation of perception hypothesis and the implications for

schizophrenia. Australian and New Zealand Journal of Psychiatry (2010) 44, A51.

(Paper presented at the ASC2010 Molecules to Mind Conference, Schizophrenia

Research Institute, Sydney, September 2010)

Design for disability lecture for the Masters studio, Faculty of Architecture, Design and

Planning, University of Sydney (2010)

Environment in Psychiatric Research Outstanding Challenges and Future Directions.

Live Discussions. V. Wilcox (ed.), Schizophrenia Research Forum (2009).

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Perception, attention, working memory and the dopamine salience hypothesis.

Cognitive Neuropsychiatry. (Awaiting resubmission after review).

We are our architecture. Science and Non-duality Conference. San Rafael, California,

Centre for Consciousness Studies, (University of Arizona) (2009). SND29-315 DVD

3/3. (Also presented at AAA seminar series)

There’s something in my head (but it’s not me): The complex relationship between the

built environment and schizophrenia. Paper presented at the Research Visions

Conference, University of Sydney.

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QUESTION ONE: HOW CAN SPECIALIST

PSYCHIATRIC FACILITIES IMPROVE THE WAY

THEY HELP PEOPLE WITH SCHIZOPHRENIA?

The salutogenic methodology for the design of psychiatric facilities

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Start making sense: Applying a salutogenic model to architectural design

for psychiatric care.

Published in: Facilities (2010), 28(3/4), 100-117. Doi: 10.1108/02632771011023096

Winner of the Emerald Literati Outstanding Paper Award 2010.

Abstract

Purpose

This paper aims to look into the significance of architectural design in psychiatric care

facilities. There is a strong correlation between perceptual dysfunction and psychiatric

illness, and also between the patient and his environment. As such, even minor design

choices can be of great consequence in a psychiatric facility. It is of critical importance,

therefore, that a psychiatric milieu is sympathetic and does not exacerbate the psychosis.

Design/methodology/approach

This paper analyses the architectural elements that may influence mental health, using

an architectural extrapolation of Antonovsky’s salutogenic theory, which states that

better health results from a state of mind which has a fortified sense of coherence.

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According to the theory, a sense of coherence is fostered by a patient’s ability to

comprehend the environment (comprehensibility), to be effective in his actions

(manageability) and to find meaning (meaningfulness).

Findings

Salutogenic theory can be extrapolated in an architectural context to inform design

choices when designing for a stress-sensitive client base.

Research limitations/implications – In the paper an architectural extrapolation of

salutogenic theory is presented as a practical method for making design decisions (in

praxis) when evidence is not available. As demonstrated, the results appear to reflect

what evidence is available, but real evidence is always desirable over rationalist

speculation. The method suggested here cannot prove the efficacy or appropriateness of

design decisions and is not intended to do so.

Practical implications

The design of mental health facilities has long been dominated by unsubstantiated

policy and normative opinions that do not always serve the client population. This

method establishes a practical theoretical model for generating architectural design

guidelines for mental health facilities.

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Originality/value

The paper will prove to be helpful in several ways. First, salutogenic theory is a useful

framework for improving health outcomes, but in the past the theory has never been

applied in a methodological way. Second, there have been few insights into how the

architecture itself can improve the functionality of a mental health facility other than

improve the secondary functions of hospital services.

Start making sense: Applying a salutogenic model to architectural

design for psychiatric care.

There is growing evidence that the design of a healthcare facility will directly affect the

health outcomes of patients (Ulrich, 2006). But designing a healthy psychiatric unit is a

difficult task as the patients are prone to distorted perceptual systems that make them

especially vulnerable to confusing building forms and layouts, or even to a lack of

tactile, acoustic, temporal, olfactory or visual stimulus (E. T. Hall, 1975). This article

analyses various aspects of design, ranging from apparently minor interior choices such

as texture, decoration and finishes through to the enveloping architectural form. By

doing this we should be able to see how design decisions may affect patients’ health

outcomes. To establish these links, the analysis looks at the transactional nature of

perception and applies a salutogenic framework to assess design choices (largely

recommendations drawn from literature) for psychiatric health facilities. It is hoped that

this methodology will be useful for making informed decisions in circumstances where

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there is no empirical evidence available and when architectural decisions have to be

made regardless.

There is a reasonable body of literature about the design of hospitals and related

buildings, and even about mental healthcare facilities, but the material is severely

limited when compared to the complexity of problems that an architectural team faces.

Without specific studies into the specific questions that an architect has to face hundreds

of times a day, how are architects and other team members to know that the choices he

or she has made are the best for the subject group? There are no studies on the

psychological benefits for basic design elements that are mandatory in mental health

facilities. And it is the moral obligation of all facility planners’ to question any details

that may not be in the best interests of the facilities reason d’être, which is to assist

patients in recovery. How do architects know how a space with cushioned vinyl walls

and floors will affect the wellbeing of patients inhabiting that space?

As it happens, the architect is often given little choice about the layout and finishes of

standard rooms within a programme as standards and codes have already pre-empted

any decision-making. “The Australian Health Facility Guidelines” (HCAMC & CHAA,

2007) for example, specifies the layout and finishes of most of the spaces within a

mental healthcare unit.

Facility planning teams will also have to resolve occasional contradictory findings or

opinions – many of these will not be impartial. One study that observes the benefits of

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opening up nurses’ stations and other spaces in mental wards (Whitehead, Polsky,

Crookshank, & Fik, 1984), is contradicted by another article calling for the same wards

to be ‘locked down’ and made more secure (Osmond, 1958; Sine, 2008)1. It’s important

that the lead architect is proactive and has perspective; architects have to pose a

question to others on the design team; “Who are we designing for, why, and how will

this decision help to do that job well?”2 A strong guiding theoretical hypothesis makes

rational decision-making easier where there are no relevant empirical studies to provide

support. For this reason salutogenics – a theory gaining interest in recent literature

reviews for linking the environment to health outcomes (Dilani, 2008; Schweitzer,

Gilpin, & Frampton, 2004) may prove to be useful for formulating robust principles for

the design of psychiatric units.

1
Mr. David Sine, the author, is president of Safety Logic Systems, a company that may

well have vested interests in locking patients down.

2
Of course the diverse needs of clinical and non clinical staff, of facility directors, local

governments and other involved people are also very important, but great care must be

taken that their needs do not come before those of the patients. (Osmond, 1958) These

negotiations won’t be easy, as empowering the patients will to some degree mean

wrestling control from staff some of who may well be part of the planning team.

(Searles, 1960).

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Figure 1: Dr Osmond writes that the seclusion room must not be

merely pleasant, but the best room of any ward (Osmond 1958). The

rooms he describes have hardly changed since 1958 and are better

used for storing dangerous chemicals than treating distressed and

vulnerable patients. This room was designed according all the rec-

ommendations of the 2007 Australasian Health Facilities Guidelines

(ACAMC & CHAA 2007).

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Spaces not dissimilar from this have been shown in repeated tests to

cause hallucinations even among people with ‘normal’ perceptual

abilities. Scatological, violent or apsophilic behaviour in such an en-

vironment is a defence against psychosis.

Salutogenics is a psychosocial study of what keeps people healthy, starting from the

perspective that illness and health are different points on the same continuum. Where

treatment may be required when one is ill, a supportive environment is always required

to assist and maintain good health. The primary premise of salutogenic theory is that a

‘sense of coherence’ (SOC) is strongly linked to better resistance to illness. A strong

SOC is supported by feelings of comprehensibility, manageability and

meaningfulness. Ultimately a SOC builds a dynamic feeling of confidence that one’s

internal and external environments are predictable and that there is a high probability

that things will work out as well as can reasonably be expected (Antonovsky, 1987;

Bahrs et al., 2003).

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Generalised Resistance Resources (GRR’s)

{
Sense of coherence derived from:
Meaning, comprehensibility and manageability
and other treatment Generalised resistance deficits (GRD’s)
Active forces

such as inabilities, illnesses and

stresses

Deterioration Better health

DEATH LIFE
State of well being

The salutogenic effect

Figure 2: The concept that a state of health or well-being is a point on

a continuum is central to salutogenic theory. Forces that support bet-

ter health are called generalised resistance resources. They include

treatment and a sense of coherence. Illnesses, inabilities and other

generalized resistance deficits work the other way.

The idea that the environment has a direct effect on health through psychology is both

intuitive and well supported in research. As Ulrich writes ‘the concept of stress provides

a credible departure point for understanding why design should affect health

outcomes…’ (Ulrich, 1997). Ulrich and others have created a model associating

psychological stress to poor health outcomes; the maxim is that anything likely to

increase stress levels is to be avoided in health design. The stress model is simple and in

most instances it is appropriate for healthcare design and especially for mental health.

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But the stress model is not comprehensive nor specific, and it does come under criticism

by Antonovsky who points out that there are times when stress can have a salutogenic

effect; that is when a person is subjected to stressors whilst receiving high levels of

environmental support the result can be fortifying. Furthermore in the salutogenic

model, stress is understood to be omnipresent and not just a feature or an absence of

the environment (Antonovsky, 1987; Bahrs et al., 2003). Lawton and Nahemow support

this viewpoint by observing that an environment that lacks challenges leads to atrophy,

but then too much challenge can be damaging (Lawton & Nahemow, 1973). They add

that patients have a reduced capacity to adapt when they are ill or infirm. Aside from

this caveat, the salutogenic model seems an appropriate broad framework in which to

locate the stress model because it supports the stress model with much needed substance

– effectively filling the causation gap between action and effect.

Understanding the environment from a salutogenic perspective.

From the perspective of architectural design, the salutogenic framework is compelling,

as it understands the environment as a source of meaning, as a sphere of influence3 and

for its readability4. From the point of view of mental health design, the salutogenic

framework provides a direct link between architectural language and psychiatry.

3
Being able to influence the surrounding environment is the basis of manageability.
4
Readability is an architectural simile for comprehensibility.

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What is interesting about salutogenics from the psychiatric point of view is that in this

model the relationship between a patient and the environment is understood as being

transactional, not fixed; the environment effectively changes according to the subject’s

sensory and perceptual abilities and conditioning (E. T. Hall, 1990). Perception is a

complex neurochemical process that is highly reactive to the surrounding environment

and yet it is the only channel for receiving new information of any sort5. It has been

postulated that a great deal of mental health problems occur because of imbalances and

distortions in the perceptual system, causing hallucinations, instability, unpredictability

and delusions. Thus, the act of perception itself can trigger psychotic events (E. T. Hall,

1975, 1990; Maeissner, Perry, Dorr, & Rowan (Ed.), 1965; Osmond, 1957, 1958, 1966;

Searles, 1960; Weckowicz, 1957).

5
It is conceivable that old information (memory) is stored and retrieved through non-

perceptual means, but this is not the area of this study.

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Knowledge (epistemology)
a b
Perceptual Ability
Sensation

Memory

Culture
(sight, smell etc.)
Experience
Object Object as
experienced

Subject

The process of object cognition

Figure 3: When Searles reported a woman who genuinely experienced

people as trees he is not suggesting that people are trees or that peo-

ple are like trees but that, for this woman, people are experienced as

trees. This effect is because object comprehension is not a one-way

process. Cognition is manufactured through the filters of memory, cul-

ture and a pre-existing epistemology. Thus we understand the envi-

ronment through association with familiar concepts, languages, ob-

jects, forms, materials, textures, emotions and expectations. Under

normal circumstances a is similar enough to b that problems don’t

occur, but perceptual problems, lack of experience, knowledge gaps

and cultural norms can undermine experience. (E. T. Hall, 1990;

Searles, 1965)

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Comprehensibility – reading the environment.

The importance of making sense of experience cannot be underestimated (Searles, 1960;

M. Woodbury & Woodbury, 1969), and in the case of psychiatric patients, this may

mean making sense of a living nightmare (M. Woodbury & Woodbury, 1969). It is

therefore important that all decision makers in design teams for psychiatric wards

understand that hallucinatory experience is very real to those who suffer from it and that

the environment we create may either intensify or elevate such experiences.

Hallucinations are stressful and often spiral into a vicious cycle of disorienting

experience, which in turn is stressful (Searles, 1960; M. Woodbury & Woodbury,

1969). There may be cases when there is a well informed psychologist within the team

who will take responsibility for relevant design decisions, but it cannot be assumed that

those on the client side will always understand the sensitivity of this issue or the

complexity of behavioural psychology (Philip, 1996).

If we accept that perception (whether visual, acoustic, haptic, temporal or olfactory) is

synthetic, (there are arguments either way, but there is little doubt that sensory ‘data’

must at some point be translated onto neurochemicals and electrical impulses, implying

at least some level of post-experiential synthesis (Ames & Princeton University

Psychology Research Center, 1955; Collerton, Perry, & Ian, 2005; Grossberg, 2003a;

Ullman, 1980)) then the relationship between comprehensibility and the environment

that we draw experience from is personal. Not all people will gather the same

information from the same experience (E. T. Hall, 1990; Searles, 1960). However, in

normal circumstances, the ‘gap’ between a subjective experience and the reality of the
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objective world is acceptable and is resolved without consideration. But with

schizophrenics the disjuncture between the experiential reality and objective reality is

confusing for the patient (Searles, 1965; Weckowicz, 1957). For this reason it is

important that the environment is designed to reduce the possibility of perceptual

distortion. Size perspective, for example, is a ‘natural’ effect whereby the apparent size

of an object reduces as it retreats into the distance. The severity of a schizophrenic

episode is illustrated by just how much the patient thinks an object has shrunk rather

than moved backwards in space (Weckowicz, 1957). The distortion caused by size

perspective can be limited by keeping spaces small and to comfortable proportions

(Osmond, 1957).

There are a number of other perceptual functions that are also subject to distortion,

misreading or loss. These functions include very basic skills such as the understanding

of distance, relative dimensions, mass, spatial orientation, the passage of time etc. (E. T.

Hall, 1990). Cognitive scientists have counted at least thirteen distinct ways that people

comprehend the relative depth of space visually and several other ways when we

include the various tactile, thermal and acoustic perceptual systems. Whilst I shall not

discuss them in any depth here6 some provision can be embedded into the environment

to assist patients in these tasks. Hall notes that where one sensory ability might fail,

6
A handy summary is found in the appendix of Hall (1990) and in more depth in James

Gibson’s original texts.

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

there are others that will provide support (Osmond, 1957). Textured surfaces assist with

textural perspective7. Horizontal courses in masonry or timber assist linear

perspective8. Various objects (outside; the presence of trees, landscape features; and

inside; pieces of furniture, paintings, rugs, light fittings etc.) assist with size

perspective9, the various perspectives of parallax10 and other perspectives11 (E. T. Hall,

1990; Osmond, 1957, 1958, 1966; Searles, 1960). As all these perspectives support the

same cognitive function, that is the measuring and comprehension of space, the more

provisions for these functions the better for reducing the likelihood of misreading and

hallucination.

7
The density of texture appearing to increase as space recedes.
8
Parallel lines appear to converge to a vanishing point.
9
Relative size apparently decreasing with distance.
10
The angular difference as seen from one eye and the other; (binocular vision) and

motion parallax where distant objects appear to move slowly, but objects up close move

quickly relative to the viewer.

11
Including blur perspective, aerial perspective, relative upward location in the visual

field, textural shifts when one object is placed before another, completeness of outline

and changes in light and shade.

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Figure 4: This hospital corridor in Argenteuil, France could be any-

where, not just because there are no windows to connect the interior

to the exterior, but also because the corridor is typical of these spaces

in hospitals around the world. These spaces are disorientating; it is

difficult to tell the walls from the floor from the ceiling. Bare drab

spaces provide no sense of meaning and they offer no opportunities to

affect any change to the environment. From a salutogenic perspective

it is hardly any wonder such spaces bring out the worst in mental

health patients. Source: Julie Kertesz (release granted).

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

Comprehensibility isn’t only a matter of spatial cognition, however. Understanding

what objects are and what they are for is also of great importance. But the purpose of a

place or an object is not directly cognised. Object comprehension is manufactured

through the filters of memory, culture and a pre-existing epistemology (E. T. Hall,

1990; Searles, 1965). Thus we understand the environment through association with

familiar concepts, languages, objects, forms, materials, textures, emotions and

expectations. For this reason it is important, as far as possible, to provide a familiar

environment for psychotic patients to increase the likelihood of comprehension and to

reinforce messages that aren’t likely to increase stress levels or paranoid delusions. For

this reason Osmond, Elliot and Bayes Friba recommend that the typology of a

psychiatric facility is not institutional; instead it should present as something both

ubiquitous and desirable; a cosy and safe home (Elliot & Bayes Friba, 1972; Linebaugh,

2002; Osmond, 1957).

Searles points out that all mental illnesses affect perceptual cognition although

schizophrenia does so most dramatically (Searles, 1960). It’s therefore imperative that

the design team considers visual, acoustic, haptic, temporal and olfactory sensibilities in

their designs, not just to avoid excessive sensory pollution (such as street sounds and

kitchen smells,) but to avoid distortion generally. Echoes have been found to be

disturbing to patients who hear voices anyway. Excessive or repetitive noise can also be

disturbing, especially for patients with neurotic complications. A sense of real time to

treat temporal distortion can be promoted by including elements that track time such as

clocks, calendars, up-to-date magazines and judicious use of TV (Osmond, 1957).

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

Beyond perceptual distortion, facility designers need to be aware of environmental

symbolism that might be amplified, de-contextualised or misunderstood by sufferers of

a broad range of mental illnesses (Halpern, 1995). Though there haven’t been a great

deal of studies into this effect in mental institutions12, problems have been found in how

patients interpret the symbolism inherent in nurses’ uniforms, which have on occasion

been found to bring back wartime memories and other paranoid delusions (Richardson,

1999). When designing a mental facility, aesthetic choices and forms need to be

carefully critiqued. Is the design reminiscent of schools, prisons, courts, orphanages,

religious institutions or hospitals?

12
Halpern’s observations were in the wider community.

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

Figure 5: This hospital in San Lorenzo, Italy shows an attempt to open

this corridor to the outside and provides a clear sense of destination.

As such it is a great improvement to the traditional hospital corridor.

Care still has to be taken to ensure the space is readable. The red

stripes, texture-less and colourless surfaces and cut ceilings don’t re-

late to any traditional forms and could prove very confusing to a pa-

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tient suffering from spatial disorientation. Source: Gualtiero Bertoldi

(release granted)

In order to maximise comprehensibility, ambiguity should be avoided (Osmond, 1957).

Objects should look, sound and feel like whatever they are (except, of course for

institutions, which should have charm and personality and should be the functional

equivalent of a ‘home’ (Chrysikou, 2009; Osmond, 1957)). Thus a door should be

‘door-like’ and should have a comfortable thud when closed (Osmond, 1958). Needless

to say, there are a range of other details that have not been tested and therefore where an

understanding of salutogenics becomes useful in lieu of proper evidence. Questions

about whether walls have to be solid and run perpendicular to the ground or whether

they should have coved skirtings can be tested against salutogenic criteria; in this case,

against likely impacts on comprehensibility. If details may pose a challenge to patients’

perceptual abilities then the team might consider other available options. The choice of

sliding glazed doors for example. Because sliders are walls, doors and windows all at

the same time this could pose a problem to patients with categorisation impairments (a

symptom13 of schizophrenia (American Psychiatric Association 1994)). Other things

that could come under scrutiny for comprehensibility might be the material palette. Can

13
Technically a symptom is positive and refers to an unusual phenomenon.

Categorisation impairment is the opposite; a sign. As it is negative - an absence of

normal ability.

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

the team avoid the use of ambiguous materials? Could materials appearing to be

something other than what they are such as veneer or printed timber patterns are

confusing to some patients? Perhaps there are other advantages still for choosing real

exposed timber, stone, natural carpet and quality pressed brick; being ubiquitous the

world over, they will resonate with a wider range of cultural backgrounds. Natural

materials are also replete with textures to assist with difficulties in perceptual cognition.

A design team that adopts salutogenics as a guiding theory might find the framework at

odds with architectural fashion. In the interests of promoting comprehensibility, some

architectural mannerisms might not be appropriate. Postmodern double readings,

façadism, deconstructionalism and tectonic expressionism are all deliberately confusing,

but do not necessarily need to be abandoned altogether. These are decisions the team

will have to make. Dr. Sivadon found that the practice of gradually exposing

schizophrenic patients to more and more complex social environments was an effective

treatment (Baker, Llewelyn, & Sivadon, 1959; E. T. Hall, 1975). The medical

specialists on the team may propose that something similar is done with the built

environment.

Other fashions are much clearer in terms of intentions and can also be considered with

care; Modernist chic tends to plainness and mechanical functionality, both of which

have been identified as undesirable for schizophrenic patient populations (American

Psychiatric Association, 1994). Woodard Smith recognises this and points out that

advances in engineering have enabled plasticity of form, giving bad designers scope to
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extend worst practice past the restrictions of traditional construction techniques. When it

comes to form, mental institutions benefit from the strong structural grid and small

spaces associated with traditional building methods (Woodard Smith, 1959).

Manageability; the importance of being able to make a difference.

Architectural form itself can amplify or deny power. If one questions the validity of this

major psychological effect, then consider the effect of Albert Speer’s Reich

Chancellery, related in The Edifice Complex. Sudjic tells how it was the disempowering

‘architectural stage set’ of Nazi architecture in 1939 that caused Emil Hácha,

Czechoslovakia’s president, to hand over his state to Germany without even engaging

the ‘well equipped Czech army with modern artillery, technologically advanced aircraft

and Skoda tanks’ that were waiting to defend Czechoslovakia’s border. From the broad

architectural grammars of form and space through to minute details of door-handles,

architecture can work with us or against us.

The second of the principles of salutogenics is manageability. The feeling that a person

is in control of his or her environment and life circumstances is very fortifying. And, as

illustrated by Sudjic, the feeling that you are totally out of control is absolutely

disempowering. All patients are subject to loss of control in the hospital system, with

those who forfeit control being seen by staff as ‘good patients’ and those who struggle

to maintain control as being ‘bad’ (Sloan Devlin & Arneill, 2003). This is even more

true for psychiatric patients than any other group; as patients are overtaken by mental

illness, control (manageability) is one thing that is lost entirely, not just because of
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pressure from the hospital staff or the disempowering nature of the hospital

environment, but also because they lose trust in their own perceptions, memories, their

own selves. With this loss goes all social support; patients frequently lose their old

lives, their jobs, their sense-of-self and their perceptual abilities (Searles 1960). For this

reason it is imperative that the shreds of control that patients still have left are

supported and not withheld (Osmond, 1958). Interpersonal relationships

There are a host of things facility planners and architects can do to nurture a patient’s

sense of control and ability to be effective. Right up on top of the list is keeping unit

numbers small and making arrangements so that numbers are never bigger than those of

the archetypal human community; the nuclear family. More than five or six patients

should not have to come into contact if they don’t wish to (Osmond, 1966). The

tendency of institutions to put people together in large dayrooms, dining rooms, living

rooms and other spaces is well known for exacerbating psychotic symptoms, because

the number of human interactions compounds with every extra person present. And at a

time when the capacity to relate to one another is hampered anyway, this equates to a

direct loss of control (Osmond, 1958). Consider that control in a social setting relies on

an awareness of your ‘place’. In which case, two people will have one relationship. In

other words, they only have to maintain an awareness of one another. Three people will

have three dynamics. They maintain awareness of each other and of a single new

dynamic, which is the relationship between the other two. Four people already have six

dynamics to maintain an awareness of, and seven people have twenty. By the time there

are fifty people, a setting plays host to one thousand two hundred and twenty five
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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

relationships (Osmond, 1966). Any resulting confusion is further complicated by the

delusions of the patients, which will make even a simple set of relations potentially

deleterious14. Interpersonal relationships

14
It is normal for schizophrenic patients to attribute non-human qualities to themselves

or to other patients, objects or even to perceive themselves as being several

disconnected entities. (Osmond, 1957)

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

2:1 3:3 4:6

5:10 6:15 7:20

Chart showing the compounding numbers

of relationships among small groups.
The first figure shows the number of participants (p),
the second the number of relationships (r) in the dynamic (d).

Figure 6: Consider that control in a social setting relies on an aware-

ness of your “place” among all the possible one – to – one relation-

ships in the milieu: two people will have a single dynamic; that is they

have to maintain an awareness of each other. Three people will have

three dynamics. They are aware of one another and each is aware of a

single new dynamic, which is the relationship between the other two.

Four have 20. By the time there are 50 people, a setting plays host to

1225 one to one interpersonal relationships.

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

The problem of overcrowding leads to one of the classic issues that define mental health

problems in the public imagination: the ‘madman in the cupboard.’ E. T. Hall (1975)

relates this anecdote of Dr. Woodbury

“…In one of the violent ‘back’ wards, where most of the communication was

spatial… the ‘currency’ of the ward was space. Woodbury observed that the

organization of the ward was territorial rather than social. In terms of hierarchy

of freedom of movement, the dominant patient could go anywhere. Below this

patient were two patients, each of whom could move freely in his own half of the

ward. Each of these dominated the territory of other patients who were

restricted to increasingly smaller areas. At the bottom of the hierarchy was a

patient who slept under a bench and was not permitted even to use the spit hole

in the centre of the floor. His so-called ‘incontinence’ was a function of the fact

that the toilet was not in his territory and therefore he was not permitted to use

it.’ (M. A. Woodbury, 1958)

As control of the environment is lost, psychiatric patients frequently need to be re-

taught everything: how to wash, how to cook, clean, or use a toilet (Osmond, 1957). For

this reason provisions for these basic tasks should be very simple. It should be very easy

to maintain personal hygiene and for a patient to clean up if mistakes are made

(Osmond, 1957). The relearning of these ordinary tasks is now generally considered as

part of the therapeutic process and is both empowering and essential for life outside of

an institution. For this reason one of the beneficial innovations over the last half-century
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in psychiatric architecture is the reintroduction of ordinary facilities that are essential in

the outside world, such as kitchens, laundries, baths, telephones15 etc. ADL (Activities

of Daily Living) facilities (as they are called,) are now a part of the normal programme

for a new institution and there are recommended guidelines for their design (Osmond,

1957). Unfortunately the ADL facilities are usually in locked rooms and don’t actually

serve real-life functions; that is, they are only for structured lessons or diagnosis.

Planning teams should consider placing the ADL kitchens centrally and having them

open (even if the ovens etc. have to be locked to prevent accidents,) to replicate a

domestic environment as recommended by Elliot and Bayes Friba (1972). In the same

spirit there are many other tools that are present outside of institutions that people

should be able to exercise their control over, lest patients’ abilities atrophy. Opening

windows and adjustable heating and cooling are very obvious examples. Such features

will assist in maintaining successful control of the environment and will have the

additional benefit of deinstitutionalising the milieu (Osmond, 1957).

It has been observed that sports such as table tennis have a salutogenic effect for mental

patients, (not just for the players, but for the greater patient populations) as the events

assist in structuring and re-engaging human relationships, developing coordination and

15
ADL (Activities of Daily Living) services are usually used as teaching and diagnostic

facilities with the supervision of staff

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perceptual abilities and tackling apathy and boredom, both of which lead to skills

atrophy (1972).

There are other ways to humanise mental hospitals and make them more manageable

and comprehensible. Unhomely corridors and unnecessarily enlarged spaces should be

avoided as they exacerbate the worst aspects of schizophrenia (Osmond, 1957). Physical

retreats must be provided (Elliot & Bayes Friba, 1972; Osmond, 1957, 1958, 1966);

Furniture should be movable, but solid enough to feel secure (Osmond, 1957). Of

course there are many other details that will also be useful but are more simply

recognised with a basic understanding of salutogenic principles rather than being listed

here.

Meaning: a reason for seeing.

Meaning, it seems, is essential to the maintenance of life (Antonovsky, 1987; Frankl,

1963) and is therefore the most significant ingredient of a sense of coherence. And

while meaning is found in the environment, it is illusive and difficult to provide for, as

questions of meaning steer pretty quickly to philosophical and cultural/social debate

rather than to the simple cause and effects so desirable in the physical sciences. Of all

the sources of environmental meaning, there is little doubt that it is primarily found in

the social environment – in love and communication, in family, friendship and in sexual

relations. But the one thing that is common to all mental patients with no exceptions – is

that they have experienced a rupture in interpersonal relationships resulting in

alienation from the greater community and they are to a greater or lesser extent socially
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isolated (Osmond 1957). Even so, good facilities for receiving social support must be

considered to enable recovery The current practice of affording space meet up with

family and old friends (HCAMC & CHAA, 2007) is very important and, in the interests

of fostering meaning, might even be extended with the provision of extra facilities for

friends and family to stay over. (Gutkowski, Ginath, & Guttmann, 1992; Osmond, 1966;

Whitehead, Ellison, Kerpen, & Marshall, 1976; Whitehead et al., 1984; M. Woodbury

& Woodbury, 1969)

A salutogenic perspective means that affordances for pets may be considered. They

have been shown to radically improve mental well-being (Searles, 1960, 1965, 1986;

Wells, 2007) and while affordances for cats and dogs may be too difficult, too

dangerous and raise any number of health issues including the possibility of allergies, it

must be remembered that relationships with pets are often of more significance to the

mentally ill than relationships with other humans and are often important stepping

stones for re-establishing human relationships and other milestones for recovery such as

the development of self awareness and moral conscience (Searles 1960).

When interpersonal relationships have broken down the material environment can be of

life saving significance (Searles 1960). Mental patients regularly place huge importance

and feel very emotional about things and places, with schizophrenics frequently

confusing their environments and themselves. Searles relates dozens of anecdotes about

how the material environment waxes in importance as social relationships collapse.

One patient spoke poignantly during therapy about having lost herself. During the
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session it emerged that the ‘self’ she was referring to was the home she used to live in.

Her identity was inextricably linked her childhood home and all it meant to her and it

was when she left the house she started experiencing mental problems. Another case

Searles reported was of critical melancholia; a man who preferred to spend his life in

bed, not doing anything lest he should see someone caring for a garden. He was

overwhelmed with grief about the loss of his closest companion: his own garden. The

same man refused to leave therapy sessions. It turned out that Searles’ telephone

reminded him of one that he had owned.

Whilst these fixations might sound trivial to people who don’t suffer from psychosis, it

must be remembered that schizophrenic patients don’t speak figuratively. These

experiences are very real, not poetic interpretations and they are symptomatic of a very

deep and painful ontological crisis (Searles, 1960, 1962, 1965) A designer must be

aware of how meaning and its inverse (meaninglessness) may be structured into the

environment. The negative effects an ugly and dehumanising space can have on such a

patient cannot be underestimated (Osmond, 1966). And neither can the reassurance that

comes with a space that is highly refined and aesthetically considered. As De Botton (a

popular philosopher) suggests, architecture really only comes into its own when we

have to plumb life’s deepest questions; when we have to deal with pain, grief and

confusion, and it is at these times that no pill can help (De Botton, 2006).

Ulrich has made some very important associations between accessibility of the natural

environment and better health outcomes. Whilst it hasn’t been explicitly noted in his
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papers, it is likely that the health benefits derived from access to a natural landscape

occurs because meaning is so easily found in nature (Ulrich & Parsons, 1990).

It seems that meaning is fostered through environmental richness; through complexity,

order and aesthetic considerations (Bachelard & Orion Press (Tr.), 1958, 1964 (Tr.)).

The more afflicted the patient, the more significant it is that the spaces they use are truly

beautiful. Obviously such a term raises all kinds of prickly issues, (like who is to be the

final arbiter of taste,) but the point, (raised by Osmond,) is not so much about the

aesthetic of the final solution, but that the ‘usual’ drabness of hospital architecture is

avoided. The detailing of mental facilities should be more considered (aesthetically)

than a ‘nice’ home because it is only when patients’ expectations are exceeded that they

will feel a sense of ease (Osmond, 1958). Currently there is a long way to go; the

surroundings in mental health wards hark back to their genealogy; as lockups,

dungeons, and more recently as asylums (Osmond, 1966; Sine, 2008). These

associations must be rejected entirely as there should be no sense of ‘punishment’

embodied in health architecture.

Bare, drab spaces directly affect perception (even of healthy individuals,) in a very

dramatic way. A reduced environment causes hallucinations, delusions, confusion, the

impairment of organised thinking, oppression and depression, even for healthy people

(Hebb, Heath, & Stuart, 1954; Osmond, 1966; Searles, 1965; Solomon, Leiderman,

Mendelson, & Wexler, 1957) and the inverse; a multi-sensory environment that is rich

in complexity, has been linked to improvements in emotional, cognitive and immune

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system functions (Schweitzer et al., 2004; Woodard Smith, 1959). To this end, Osmond

suggests that spaces for psychiatric care should be exceptionally generous in the way

they’re decorated and finished (Huntoon, 1959; Osmond, 1957, 1958), even going so far

as recommending fresh cut flowers in the private spaces. Any fears about patients’

scatological and autoerotic behaviour (presumably the reason for vinyl surfaces in the

first instance,) can be largely allayed. According to Osmond, a patient is only likely to

resort to ‘apsophilic activities, touching the staff and painting the walls with faeces’

when left with no other more acceptable sensory gratification (Osmond, 1958).

Although nostalgia can be a symptom of schizophrenia, Searles (1960) describes how it

can also be a very important transitional fixation in the process of re-engagement with

the outside world. It is very important that patients aren’t separated from their pre-

existing lives, as this completes a disjuncture that is already a serious problem for

mental health. Patients should be able to bring in photos and to stick them on their walls

(Osmond, 1966; Searles, 1960). Ideally they will have some kind of music system in

their rooms also, so they can listen to their favourite tunes (Osmond, 1958). Of course

these things can give rise to melancholy, but they can also be restorative as they remind

a patient that there is meaning in life; be it love, desire, friendship or something else

more pertinent (Searles, 1960).

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Figure 7: CCTV Surveillance of seclusion rooms in Kansas City. It is

hardly any wonder that patients indulge in apsophilic and scatologi-

cal behaviour in such a sensory void, painting the walls with faeces

and masturbating are the only available options for sensory gratifica-

tion. Such acts are the last resort in preventing further mental deterio-

ration. Research shows that people with no history of psychosis will

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soon start to hallucinate in such an environment Source: Victor Van

Hee (release granted).

Conclusion

Under normal circumstances people have a great deal of ability to adapt to new

surroundings – even in stressful situations – and such changes can actually support the

overall robustness of wellbeing. However, when environmental factors start to erode a

general sense of coherence – when meaning, control and comprehensibility are lost –

resistance to disease weakens and perceptual difficulties are exacerbated, often creating

a vicious circle of increased vulnerability and anxiety.

It is imperative, therefore, that health facility planning teams carefully scrutinise plans

for anything that may not be in the patient’s interests. A basic understanding of what

makes an environment supportive in order to assist and maintain good health will

provide a useful framework for this critique. To this end, Salutogenic theory is a

particularly useful tool as it is specific16 and easily applied to an architectural

application.

Essentially the theory proposes that a ‘sense of coherence’ (SOC) is an integral part of

the natural healing process and that a strong SOC is supported by feelings of

16
A hypothesis about the specific effects of each decision can be established with

relative ease.

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comprehensibility, manageability and meaningfulness, all of which have architectural

ramifications. Of course the use of a salutogenic framework does not mean that no

further research is required and nor does it insure that all the choices the design team

makes will be the very best decisions in the given circumstances, but in providing a

basis for making purposeful decisions about any aspect of the design on the fly, it

means that the architectural teams are empowered to design the very best facilities they

can, given restricted time and budgets and a the general paucity of useful empirical

evidence.

There are many things that can be done with the architecture of a facility that may

alleviate mental symptoms, lessen the likelihood of future psychotic episodes, alleviate

stress and assist with basic cognitive functions. These innovations can be broken into

three categories in an architectural extrapolation of salutogenic theory:

Designing to foster a sense of coherence through:

1. Comprehensibility; making sure that perceptual cues are present to assist percep-

tual processes. These include attention to texture and materiality, controlling the

size of spaces and the numbers of patients and expressing environmental fea-

tures in a normal way.

2. Manageability: that is allowances for patients to exercise control of the envi-

ronment, details such as opening windows and the provision of ADL and sport-

ing facilities.

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3. Meaningfulness: enriching the environment with complexity, order and aesthetic

considerations as well as providing good spaces for visitors special personal be-

longings and possibly even for pets.

All of these approaches come together to create an architecture that really serves the

needs of mental health patients, fortifying their overall sense of coherence and mental

wellbeing and improving recovery.

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So you’re going to design a mental health facility?

How to make it future-proof.

Published in: World Health Design Scientific Review, (2012); Psychiatric Design: Using

a salutogenic model for the development and management of mental health facilities.

5(2), 74-79.

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Abstract

The prevailing model of psychiatric design (the world over) does not fulfil its potential

in supporting the healing process. In order to design for future usability, design teams

must have a vision beyond current paradigms and understand the direction healthcare is

going. More importantly still, models of care that will actually improve mental health

outcomes instead of just managing patient behaviour must be considered.

To create this vision, a methodological salutogenic approach can be employed for the

project development and management phases – from design of the buildings through to

the design of the models of care. This approach advocates taking an interdisciplinary

and collaborative approach to actively improve a sense of coherence for all users

including patients and staff. This can be done at every decision point by choosing to

foster manageability, comprehensibility and most importantly meaning.

How to plan for psychiatric recovery through more supportive design?

The current paradigm of the design of psychiatric facilities has a long history. But many

historical approaches to the treatment of mental illness were not supportive to healing

process. Even today vestiges of the ancient traditions of imprisonment and punishment

of psychiatric patients can still be found in the buildings that healthcare designers are

presenting today – and these are for current models of care and for units that are

expected to be in place for a generation at least. In many other healthcare typologies

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there is a lot of value to be retained in existing models of care and paradigms of design.

The same cannot be said for mental healthcare. To move into the future, we have to

escape the past.

This paper does not take aim at the worst aspects of psychiatric care. It isn’t necessary

to be explicit about the shortfalls of seclusion and other compromising methods that are

maintained in current paradigms. To designers, facility managers and directors,

magistrates, nursing staff, clinicians, politicians and local community groups – the

problem areas of the psychiatric milieu are quite obvious and need no elaboration.

Instead, this paper outlines a challenge and a methodology for achieving this

appropriate goal – to design a mental health facility that is appropriate for the task and

supportive of the healing process.

The challenge is paradigmatically new – but is familiar nonetheless. In several years of

in-depth study of the psychiatric milieu, I have seldom met anyone who doesn’t already

feel the challenge tapping away at their consciences. The challenge is to bring

humanity, aesthetics, love and meaning back into the psychiatric milieu to address the

cause of mental illness – not only to manage the symptoms.

This is the methodology that medicine has to adopt in order to become sustainable.

Obscure, as it is now, the salutogenic method will become universal over the years to

come if mental units are to be of service in the future.

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

The future of healthcare

The current escalation of healthcare costs is financially, socially and environmentally

unsustainable. Even in places that are highly dependent on private health insurance,

government subsidies to the healthcare industry are a major economic problem. The

reason is because it is very expensive to treat an illness once it has become critical. The

cost of keeping a person alive when they are suffering from the failure of a major organ

is enormous.

Antonovsky visualized health as a continuum and the progress of disease as entropic

(Antonovsky, 1987) pp. 71-72), meaning the fall from a state of health accelerates. The

more entrenched illness becomes, the more energy is required to arrest that fall. For this

reason 80% of a country’s health budgets are spent trying to prevent the inevitable – the

hospitalisation and treatment costs that arise in the last year of life from preventable

disease (Sylvan, 2012). And this cost is increasing.

With limited resources we must reverse the entropy of disease much earlier, while it is

still affordable. In many cases, this can take place before disease ever occurs. Not only

is early intervention much cheaper, but the benefits are not only economic but social

and environmental also. Worldwide vaccination programmes and similar massive scale

interventions have already tested this approach and found them to be spectacularly

successful.

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A number of remarkable studies show how minor and apparently non-causal

interventions can improve health outcomes and shorten hospital stays. There have been

hundreds of such studies. These studies identify views of nature, passive plants, hand-

washing, single bedrooms, designed soundscapes, appropriate lighting and a number of

other interventions (Ulrich, 2006). Even in mental health, small things like the décor of

a unit reduce stays by 25% (Vaaler, Morken, & Linaker, 2005). But can such

interventions occur earlier still? Before a patient ever gets sick by preventing the risk

factors that are embodied in the built environment?

Antonovsky shows that they can – and it’s never too late, although the best time is

before pathologies arise. The principles he proposes are called salutogenics.

Salutogenics

The theory of salutogenics is critical of the current model of illness. An illness doesn’t

occur with the development of a distinct pathology, but well before, with any slippage

from an idealised state of health. In this model the state of health is a continuum, with

an idealised state of perfect health and well-being at one end, and with illness at the

other. The only point of definition is at the far end of illness, and it is death – the point

of no return (see

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Generalised Resistance Resources (GRR’s)

{
Sense of coherence derived from:
Meaning, comprehensibility and manageability Generalised resistance deficits (GRD’s)
and other treatment There are no absolute GRD’s.
Active forces

GRD’s are any forces that erode the ability to cope.

Typically these include under- or overloads.

Deterioration/Pathogenesis Better health/Salutogenesis

DEATH LIFE
State of well being

Antonovsky’s salutogenic theory (1987)

Figure 8).

Generalised Resistance Resources (GRR’s)

{
Sense of coherence derived from:
Meaning, comprehensibility and manageability Generalised resistance deficits (GRD’s)
and other treatment There are no absolute GRD’s.
Active forces

GRD’s are any forces that erode the ability to cope.

Typically these include under- or overloads.

Deterioration/Pathogenesis Better health/Salutogenesis

DEATH LIFE
State of well being

Antonovsky’s salutogenic theory (1987)

Figure 8: The principles of Salutogenics as visualised by Antonovsky.

Two sets of forces that affect the state of well-being compete, with

generalised resistance resources (GRR’s) promoting health and gen-

eralised resistance deficits (GRD’s) exerting a deleterious influence.

The GRD’s are entropic – without GRR’s, there is not homeostasis,

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but decline into inevitable illness and death (Antonovsky, 1987;

Frankl, 1963).

This continuum has competing forces working in either direction. The forces driving a

person toward health are called generalised resistance resources (GRR’s) and those that

drive toward illness and ultimately to death are generalised resistance deficits (GRD’s).

Both GRR’s and GRD’s are the same thing – they are life events. But it is not what they

are – it is how they are dealt with that is important to designers and facility staff. A

stressor may push one person over the edge, and another may not notice the stressor at

all – they may even treat it as a challenge.

The difference lies in what Antonovsky called the sense of coherence (SOC). “The

confidence that, as in the past, things by and large, work out well” (Antonovsky, 1987),

p. 133). Three engines power the SOC: Manageability, comprehensibility and meaning.

The GRD’s on the other hand, reflect inabilities in dealing with situations, paralysis in

the face of life’s continual challenges. These reflect deficits in comprehensibility,

manageability and/or meaning.

A strong SOC provides motivation for action and an understanding of the situation at

hand, but a weak SOC is paralysing. There is no impetus to act, nor knowledge of

what’s at stake or what action to take in any case. Thus very similar circumstances have

very different effects on different people. In Antonovsky’s time this was difficult to

prove. Questionnaires like the ones used by Antonovsky could show no more than

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correlations, because individual circumstances could never exactly be the same and

variables in real life situations are impossible to control - even inside a lab. To get

around this, some scientists created a virtual reality experiment where people were

given a virtual experience of a trip on the London Underground (D. Freeman &

Freeman, 2008). In this way, the expressions and behaviours of every passing stranger

could be guaranteed to be identical, and strictly neutral. The virtual reality experiment

showed that even healthy people interpreted the same circumstances very differently

and behaved differently accordingly. Where one subject said things like “It was nice –

much nicer than a real experience. I thought they (the virtual commuters) were pretty

friendly,” another subject said, “there was something dodgy about that guy. Like he was

about to do something – assault someone, plant a bomb, say something not nice to me,

be aggressive (D. Freeman & Freeman, 2008) pp. 71-72). These reactions depend

hugely on the SOC.

Evidence-based design, research-based design, or design guideline-based design?

Very recent reviews of all the mental health units in New South Wales (Australia) and

the Australian Health Facilities Guidelines (CHAA, 2009) found that the decisions

embodied into existing units and even the guidelines themselves were based on little or

no evidence at all. In many cases, the units and the guidelines contrasted starkly to

existing evidence (Barach & Potter-Forbes; forthcoming). Fortunately (and possibly as a

result) the Department of Health Infrastructure in New South Wales made a statement

that the guidelines are “only guidelines” and that the reliance on them is being “rolled

back” (Rust, 2012). This will improve the healthcare design, because it liberates design
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17
teams to employ evidence-based design (where it exists – for a brief review see

(Shepley, Pasha, & Huffcut, in review). But perhaps more importantly, it allows the

teams to reach for non-targeted research to inform their decision-making in what is

called research-based design. Approaches can be very methodical. An example is the

salutogenic method for psychiatric healthcare design, which is currently the only,

published evidence-informed design methodology specifically for psychiatric unit

design (Jan Golembiewski, 2010b) (reprinted here from page 62).

The architect’s problem

As every architect knows, a hundred decisions have to be made every day. Some of

these will be critical – like in writing the functional program; but most of the decisions

will be small; which cornice, which colours, textures, finishes and specs. As the virtual

reality experiment above demonstrates, it isn’t only critical things that people with a low

SOC will react to (everybody reacts to those!) How can we make even these tiny

decisions in the best interests of the end-users?

The answer isn’t as difficult as it may seem. But before we go into the specifics of the

salutogenic method, we must acknowledge that the patients who are going to use the

facilities we design are likely to be there because in some ways, it’s too late to rely only

17
The term evidence-based design (EBD) is often regarded as a marketing tool and

certification programme – the term ‘research-based design’ does not have these

connotations, nor are the research criterion so formulaic.

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on salutogenics, because many of those patients are going to be suffering acutely before

they even arrive.

Customisation

Most mental disorders don’t have known pathologies, and for these there are no

universally effective treatments. Psychotropics suppress some symptoms, cognitive

behavioural therapy (CBT) and other therapies help patients to get themselves on their

feet – but none offer a cure. This means that a lot is left for the environment to do and

that’s a big responsibility. But it’s one we designers should embrace.

A very important starting point is to understand the treatment profile of the patients who

are expected to use the facility. I recommend dedicated units for specific psychotic

disorder spectra– these can be roughly classed into two:

Those who are depressed, with dementia and mood disorders; and those who are hyper-

aroused, with psychosis and mania.

Institutional resistance

As a single cog in a big wheel, you’d be justified in fearing resistance to the

introduction of new ideas – especially if they are the foundational ones that are seldom

questioned. Institutional change is difficult to achieve because it carries the inertia of

habit. But there’s reason to be positive that change will be received well. In the years I

have studied the design of mental health facilities, the only people who are happy with

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the current paradigm are those who sell anti-ligature hardware, vandal-proof windows

and other products that are customised for the current paradigm (eg, Sine, 2008). The

list of those who know that structural changes are needed include everybody from

patients, clinicians, nurses, ancillary staff, family and even politicians.

To some extent the fear that a new paradigm may be mistaken is mitigated by the reality

that mistakes are already well entrenched, and short of a reversal to total barbarism,

with a bit of common sense we could hardly do worse.

Positivity from the start

Negativity and positivity are both processed differently, and in different regions of the

brain. This is possibly why early judgements are very slow to reverse, so first

perceptions are pivotal on how a new unit will be accepted. A positive initial

experience will mean that users will be forgiving of a few mistakes. A bad start, on the

other hand, will mean that a unit may never be loved – despite having brilliant vision

and innovations (Golembiewski, 2012a, 2012c) (Articles are included on pages 358-

and 159-.)

A positive first experience is essential for all new users of a new facility, whether they

are clinical, non-clinical, patients or visitors.

Although negativity and positivity are processed differently in the brain, they both use

the same neurotransmission system: the dopamine receptors in the mesolimbic

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dopamine pathways. Here we run into one of the most difficult complications in

predicting the experience of someone with mental illness. Dopamine dysfunction is

central to the psychopathology of most mental illness – and the inhibition of dopamine

transmission is the central task of all anti-psychotic medications (Ginovart & Kapur,

2010). Meanwhile anti-depressants and anti-Parkinsonian medications excite the same

neurotransmitters (Dunnett & Bentivoglio, 2005; Pei et al., 2010).

Being one of the four central neurotransmission systems of the mammalian physiology,

dopamine serves many functions. One of these, and possibly the most relevant in this

context, is that the dopamine receptors moderate attention. This means that the subject

of experience (engagement, attentional focus) is largely determined by a system that is

dysfunctional in most mental illness (Golembiewski, in review-d) (p. 204- q.v.) The

focus of mental health patients is frequently bizarre and unpredictable. Having said this,

the diagnoses of mental illnesses are very useful for drawing generalisations, because

the standardised diagnoses are largely based on symptoms that reflect the specifics of

attentional dysfunction rather than by pathology.

The attentional biases of various mental disorders can be understood in simplified terms

according to Table 1.

Top-down Bottom-up
Superfluity Hyper-arousal, mania, paranoid psychosis Hyper-arousal
Deficits Depression Flat affect
Forgetfulness Poor self-awareness

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Table 1: The attentional biases of various mental illnesses can be un-

derstood in terms of attentional dysfunctions. Top-down attention is

intent and habit driven, and bottom-up attention is stimulus driven.

Many mental illnesses are the combination of two dysfunctions. Para-

noid schizophrenia, for instance, is likely the superfluity of top-down

attention with a simultaneous deficit of bottom-up attention

(Golembiewski, in review-d) (Page 204- q.v.)

Neutral perception

As the virtual reality experiment of Freeman and Freeman (2008) above demonstrates,

there’s no such thing as a neutral perception. This is a reflection of the fact that affective

positivity and negativity are processed differently on a neurological level (also above).

In practice, neutral is processed either as positive when it occurs in a positive context, or

as negative when neutrality occurs in a negative context. With healthy people, all

perception, including personal communication, carries a natural affective positive bias,

meaning that the ambiguity of so-called ‘neutral’ perceptions is taken as positive by

default. This bias is reversed in psychotic conditions (other psychiatric conditions have

yet to be tested), meaning that an entrenched negative bias tends to dominate in

psychiatric conditions (Golembiewski, 2012a) (See article on p. 358 q.v.) The result is

that everyone and the environment must work hard to counter this bias. For psychiatric

patients, ambiguity is much harder to resolve and is much more likely to be taken badly.

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Person to person communication is particularly important to analyse in the context of

the polarisation of perception, because it touches the sorest points of paranoid thinking

(Chadwick, 1992; Freeman & Freeman, 2008). Psychiatric patients are often bizarrely

unaware of their surroundings unless they relate in some small way to the underlying

narratives of their delusional scripts. At which point, they become highly attuned. If

patients are paranoid (a very high proportion of schizophrenics, bipolar, substance

related psychosis and dementia patients are), then ambiguous or negative

communication will not go unnoticed, even if it is very subtle. It is easy to scoff at the

idea that patients will pick up on any subtleties at all, when the circumstances of their

existence deny the fact so completely. Schizophrenic patients are frequently oblivious to

the fact that their shoes are on the wrong feet, and the fact that they sleep in between six

lanes of traffic, so how could they pick up on nuances that most of us would miss?

Several studies demonstrate that schizophrenic patients are an order of magnitude more

sensitive to expected stimuli than healthy controls, especially when those expectations

relate to delusional ideas (Brennan & Hemsley, 1984; Dakin, Carlin, & Hemsley, 2005;

Shergill, Bays, Frith, & Wolpert, 2003).

Negativity in communication is ubiquitous. Carrere and Gottman (1999); Gottman

(1996); Gottman, McCoy, and Coan (1996) are able to identify ten common negative

communication behaviours within three minutes of any conversation. It’s important that

staff are trained to identify their own negative words and actions, lest negativity is

present in communication with patients, because if they are, the architecture cannot
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come to the rescue. The common negative communications are: contempt, disgust,

defensiveness, belligerence, stonewalling, domineering, anger, whining, sadness and

fear. There is ample evidence that communication failures frequently lead to the use of

coercive measures such as sedation or seclusion (Hoekstra, Lendemeijer, & Jansen,

2004). One of the recommended ways to dispose of these facilities is to, “Try to gain

trust: suit the action to the word and the word to the action (and…) try to get in touch

with patients by talking to them and showing genuine interest… Don’t shy away from

physical contact with patients.” (Hoekstra et al., 2004, p. 282) In other words, to train

staff in appropriate and ultra-humane communication.  

Design and treatment fit

Many healthcare units are high reliability organisations where a small practitioner error

can have sudden and catastrophic consequences. In these circumstances the fit between

spatial design and the routines established in clinical praxis are critical to the

functioning of the facility (Sanchez & Barach, 2012).

A major shift in models of care will be required before equivalent spaces in the mental

healthcare milieu can be developed because these facilities are essentially domestic. The

main treatment rooms in a mental health facility include bedrooms, courtyards, living

rooms and rooms that can be used to retrain patients in the use of normal activities of

daily life (ADL) including kitchens, bathrooms, and laundries. Other clinical spaces also

serve normal human functions and thus are best if they are human in scale and layout:

consultation and assessment rooms, rehabilitation gyms, and spaces for other person-to–
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person treatments. The exact details of these seldom matter, aside from good acoustic

privacy, appropriate lighting, and the inclusion of practitioner escape routes.

The spaces in existing units that are possibly the most design sensitive are seclusion and

medication rooms. Both are useful only when models of care have failed.

Consultation or interactive collaboration?

Consultation is an attempt to engage interest groups in the design process. How this

works depends a lot on the all those involved, but it’s rare that consultation is a two-way

conversation – unless those on the design side see the opportunity for a PR exercise.

Certainly it’s rare that a genuine dialogue evolves that requires an on-going

commitment from those that are consulted. Collaboration, on the other hand, requires

that both problems and solutions be shared, and with a deep level of responsibility. As

counter-intuitive as it sounds, we should not seek opinions and ideas of the stakeholders

to guide the project, but rather seek out representatives of the interest groups who are

willing to take the whole journey, sharing the responsibility for both successes and

failures. With this approach, you’ll find people who are going to understand – at a

depth, why things turn out one way or another. This is where people are engaged just

enough that they feel they have been heard. They have handed over their opinions and

ideas, but most people have no idea just how complex architectural problems are, and

that some concepts must get lost in the design and building process. When the finished

product inevitably doesn’t reflect their input, people feel deceived and unheard, and this

breeds negativity – even if the opinions and ideas were worthless or not implementable.
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It’s important that everyone knows that the project is aiming to be the best and future-

proof, which means it cannot rely on current models of care or design paradigms. But

this short paper is not the place to lay down a methodology for effective collaboration

and project development. Consider engaging a change management expert and see for

more guidance (Plsek & Wilson, 2001).

The Salutogenic method

In 2010 a method was published especially for addressing the salutogenesis of mental

health patients to give a good basis for decision making, wherever evidence is hard to

locate or simply doesn’t exist (Golembiewski) (Article on p.62 q.v.) The method aims to

make every decision support the SOC in some way. Generally speaking these will have

a holistic effect on the coherence of the entire facility.

To do this all decisions, however minor, should be subjected to close scrutiny for how

they assist the ability to manage, comprehend or find meaning. They should then be

checked for how they might erode the sense of coherence by taking away

manageability, comprehensibility and meaning.

Ideally the more important decisions should be referred to a collaborative committee so

that the critical decisions can be ratified from other perspectives (Plsek & Wilson,

2001).

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Figure 9: Salutogenic theory treats the state of well-being as a con-

tinuum, with death at one end and a more meaningful, more fulfilled,

more connected life at the other. The sense-of-self in this model is the

core of experience. Beliefs are the anchors we use to connect to the

greater world, but beliefs are plastic and changeable to suit any situa-

tion – or delusion. Only beliefs that are grounded in reality are non-

delusional.

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In this model a state of paranoid psychosis is a contraction from

greater social concerns because of a loss of meaning and comprehen-

sibility.

The hierarchy of meaning

“The absence of the things that make life manageable has obvious consequences,

although they are not as significant as we tend to assume. Lack of food, water

and shelter will be a source of stress that will make outcomes worse, but with

their meaning and comprehensibility needs looked after; people can go a long

time without basics. As Frank Lloyd Wright famously said, “give me the

luxuries of life, and I’ll gladly go without the necessities.’” (Golembiewski, in

review-b) (Article on p.159 q.v.)

Not all interventions and decisions are equal. There is a distinct hierarchy of meaning,

with meaning and connections with society and the greater world as the foundational

basis for meaning, followed by understanding and comprehensibility and finally by

basic needs. This inverts Maslow’s well-known logic that basic needs are pivotal for

maintaining human life and that self-actualisation a final luxury once all other needs are

in place.

The mental health unit is also a forum for the competing needs of the various users: the

clinical, legal, non-clinical, patients and visitors. Each has a claim on limited resources

such as space, sunlight and proximity to the centre of the building/s. But more

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importantly still, clinical and legal staff can claim the basic freedoms of patients. These

freedoms are essential to the maintenance of a sense of meaning, yet all too often

psychiatric facilities are designed to make manageability for the staff extremely

efficient, while taking power from patients. This is all too easy with architecture, which

has a long tradition of amplifying power to some and denying it to others (Jan

Golembiewski, 2010b)(Article on p.62 q.v.) Such games must be avoided because it

works against the very raison d’ etre of the unit: to empower and enable patients

enough that they can handle life on their own once they leave. Great care should be

taken to make sure that the patient’s well-being and sense of meaning is always

protected. In the context of the mental health facility, this principle harks back to the

Hippocratic oath “I will apply measures for the benefit of the sick according to my

ability and judgment; I will keep them from harm and injustice.” (Edelstein, Temkin, &

Temkin, 1987), p. 6)

Manageability

This is what hospital architecture does best. Support for manageability means providing

the basics to support life; food, shelter, medication, security, activities to occupy the

mind etc. (Golembiewski, 2012b) (See article on p.183- q.v.) it is also the focus of a lot

of the treatment; managing pain, managing patients etc. But at every step, the role of the

unit in managing on behalf of patients should be rolled back to allow patients to manage

on their own. It may be impractical, but giving the less critical patients access to a

kitchen and groceries could be an important step in enabling independence. “The feeling

that a person is in control of his or her environment and life circumstances is very
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fortifying” (Golembiewski, 2010, p. 107) (In this thesis, p.82). Things that support

manageability for patients will include provisions for their health, security and comfort,

and even more importantly, provisions for the patients to make decisions for themselves

and as far as possible, to take action accordingly.

Comprehensibility

Comprehensibility is the way an individual understands the situations they’re in. It is

information of every kind. In a mental health facility context, that means knowing why

they are there, how to negotiate the facility and its routines and how to do things,

including how to leave. It also means knowing about the diagnoses and medications

they’re being given, their rights etc. and the context of the greater world, including the

formal laws or informal social mores of the world.

Comprehensibility is more important than manageability, because it’s much easier to

cope with adversity if people can understand their circumstances: if people know what

is going on and why.

Psychiatric patients often have a very hard time understanding the basis of how things

work and why things are like they are. In fact, it is widely hypothesised that attempts to

rationalise beliefs about how things work are the basis of delusions. (D. Freeman,

Garety, Kuipers, Fowler, & Bebbington, 2002; Garety & Freeman, 1999; Garety,

Kuipers, Fowler, Freeman, & Bebbington, 2001; Startup, Freeman, & Garety, 2008)

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Things that may improve comprehensibility for patients are clear way-finding, simple

typologies, lots of relevant information, lessons, transparency in methods of care and

decision making and as little ambiguity as possible. Ambiguity may be fun for healthy

people, but it is generally dangerous for psychiatric patients (Osmond, 1957). A

doorknob should look like a doorknob and a shower like a shower.

Meaning

Only a rich sense of meaning will be of assistance when manageability and

comprehensibility is lost. With meaningfulness, one can face dire circumstances –

starvation, pain, illness and the worst demonstrations of human antipathy and feel

confident, that in the long run everything will turn out for the best (Antonovsky, 1987;

Frankl, 1963). In psychotherapy, it is only when meaning is established that there is

ever release, resolution and recovery (Clarkson, 2006), thus it is reasonable to assert

that the fostering of meaning is the single most important role of the mental health

facility. It is also the hardest task to accomplish because efforts cannot be prescriptive.

Meaning is deeply personal and the product of an individual journey.

One of the great problems of health facility design and management is the problem of

suicide. The creation of meaning is the only way suicidal ideation can be reliably

treated. If anti-ligature fittings, CCTV and constant monitoring work at all, it is only

while a patient is locked into a unit. As long as patients are free to leave, suicidal

patients can always throw themselves in front of a passing car. When a patient discovers

something to live for, suicidal thoughts will lose their power to turn into action.
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To foster meaning, emotional connections are very important. Meaning is built on

anything that is of greater importance than the individual self; friends, family, society,

the planet, pets – all these are likely areas of concern on which meaning can be fostered.

Religion can also fit into this group, but belief is infinitely plastic – in other words,

belief is infinitely flexible and adaptable to current circumstances. Unless belief is

grounded and validated by some level of external reality, it loses its purpose and is as

worthless as any delusion. What belief is useful for is to create real and meaningful

links with the greater society, world and cosmos. Remember that one of the

fundamental reasons that the principles of salutogenics work, is because they enable

action rather than paralysis. If I believe God loves me because I care for the

environment, I will actively care for the environment, and those positive actions form

the basis of an affectively positive connection with the environment. A basis for

meaning.

Delusional beliefs don’t do this. Delusional beliefs support passive or negative

behaviours. If I were to believe that it doesn’t matter, I can’t make a difference anyway;

I would be suffering from a passive delusion. If I were to believe that a random shopper

was evil, and the best thing I could do is to slay her (such an event took place recently in

Tenerife) this would be a negative delusion (Golembiewski, in review-b) (Article from

p.373 q.v.)

External reality is, for the best part, very unforgiving. People can be very savage –

especially to people who behave strangely like many mental patients do (Goffman,
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1963). But there are ways that patients can connect with external reality meaningfully,

with little risk of failure.

This is not the place to detail all the ways of encouraging meaningful connections to the

external world, but here are some ideas:

To encourage pet ownership

Many patients with mental illnesses have pets – especially dogs, and in the context of

mental health recovery, pets should be considered as more important than any

contributor to manageability or comprehensibility (Beck & Katcher, 1983; Katcher &

Beck, 1983; Searles, 1960). When designing a unit, it is wise to provide at least some

rooms – separate if necessary – that welcome pets.

Arts

The arts form important and traditional associations – they can be a meaningful way of

linking mental patients with society. This is particularly relevant because there is a

common perception that mental patients are frequently geniuses. Regardless of whether

or not this is true, everything that could encourage artistic and literary endeavours

should be encouraged: poetry, music, painting, drawing, sculpture, dance and

performance are all wonderful for promoting a sense of meaning. And if you are

concerned (like many others are) about handing patients carving tools, bear in mind that

the use of woodcarving tools are increasingly common even in forensic mental health

units (yes, where patients are sectioned because of extreme psychiatric violence) in New

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Zealand, and the impacts on improved mental health and behaviour are really good. I’ve

also heard concerns that patients will paint on walls and write obscene and threatening

material. My answer to those concerns it to let them, and even to encourage it, but give

the patients washable materials! That way the invective and obscenities can be washed

clean before the next patient takes the room.

Meaningful activity

It’s hard to find meaningful activity for patients who cannot even look after themselves,

but an effort should be made. One of the most meaningful things a patient can do is

share their recovery by helping out the more critical patients (Alomes, 2009). There was

a short period between 1850 and 1860 when less critical tasks used to be routinely given

to patients. Patients used to milk cows and work gardens, and the products of their

labours used to end up on the tables in the evening, by all accounts, it was a

spectacularly successful (E. T. Hall, 1975; Yanni, 2007).

Meaning takes time and effort to build, but can vanish in minutes. The thing that is most

damaging to meaning is meaninglessness. Meaning is incrementally destroyed by any

reason that someone may want to hate the world and society: cruelty, meanness, broken

promises, deception, stonewalling, and contempt. Unfortunately sedation and seclusion

fit into this category. This is not to say anti-psychotics are bad. In most cases they are

essential. But the use of sedation as a management tool puts the management needs of

staff before the patient’s need for meaning.

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Conclusion: an example of how a finished salutogenic unit might look and function.

A number of examples and explorations of these ideas are included in (Jan

Golembiewski, 2010b; Golembiewski, 2012a, 2012b, 2012e, 2013, in review-a, in

review-b, in review-c, in review-d) (reproduced throughout this thesis), and every

facility will be different, but to conclude this article, I would like to present the

phenomenology of a patient’s experience of a new salutogenic psychiatric unit.

Frank is brought in a police van. It’s 2am. He’s been through this before because the

past few years he has spent more time in short stay mental health facilities than out. He

has been diagnosed with chronic Bipolar (type I) with frequent substance induced

psychotic episodes. Frank is aware that he was smoking cannabis earlier in the night,

but he’s furious because he didn’t do anything wrong – until the police arrived. It’s just

that someone tried to steal his car and beat him up and stripped him as a final

humiliation.

When the van door opens, Frank hurls abuse at his captors, the police. But he steps out

somewhere unexpected. It’s not a prison cell, nor a mental health facility; it’s nice. It

looks like the back veranda of a country home. The lights are low, and there are a

couple of people sitting, chatting on a sofa having a drink and a cigarette. One gets up

and meets Frank at the bottom of the steps. “Hi. I’m Lloyd,” He says.

“Those x*$# pigs! Roughed me up!” Frank replies.

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“Yeah. Looks like it.”

“When we picked him up, he was vandalising a car in a parking lot…” one of the

policemen start to report. Frank doesn’t realise that the staff at the salutogenic unit have

all the information the police can give already. They were contacted twenty minutes

ago, and that’s why they are out here on the veranda at 2am!

“Put it in all your report, and kindly leave. This feller is naked, unhappy, and needs to

relax.” Lloyd says to the policeman, who is slightly affronted but gets back into the van,

and drives off. Lloyd leads Frank onto the veranda. “Do you want a dressing gown? A

drink or a cigarette?” Lloyd asks. Veranda, nice person, dressing gown, cigarette,

drink? Have I gone to heaven? Frank thinks to himself as he volunteers an arm for

Lloyd to dress him.

Over the next fifteen minutes, Frank debriefs to Lloyd and Zaha on the sofa, with a

glass of lemon, lime and bitters (not his personal choice – but that’s what was there)

while he is introduced to the e-cigarette for the first time. “…Not allowed to smoke real

ones here,” Zaha explains, handing Frank the e-cigarette. “But this is much the same.

It’s still smoking, and it’s still nicotine, only you can use it indoors, and it’s not

cancerous. Have it, it’s yours.” Frank is asked if he has pets or anything he has to collect

from home in the morning…

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Soon Frank is led to his bedroom. The short corridor has a polished hardwood floor,

with a long and deep runner rug to muffle footsteps. Paintings (some donated by an art

school and some by other guests, he is told) hang off a picture rail. His room has a big,

heavy wooden door with a brass handle. Inside, the room is simple. A heavy wooden

bed with old-fashioned sheets and blankets is made up. The window has open louvers

and a mosquito screen. There is a heavy wooden desk, with paper, crayons and pens laid

out on it (they are washable, but John hasn’t been told that). The dimmed wall-mounted

wash lighting casts a warm yellow glow. A fern sits in a small pot on the table. There

are picture and dado rails, and an abstract painting hangs from them. As a precaution

against suicide attempts, a few of the features – the curtains, the picture rail and the

toilet roll holder in the bathroom are suspended by strong magnets, but the unit is still

new, and nobody has tried yet, so these features just look normal, fancy even.

The story continues…so long as the designer is willing and belief can be sustained –

materialised even, into something incredibly meaningful.

This is a snippet of my vision of how psychiatric units will look and function in the

future: always cognisant that the healing process of mental illness involves humanity,

aesthetics and everything else to foster a sense of meaning, comprehensibility,

manageability and total coherence.

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MENTAL ILLNESS AND THE URBAN ENVIRONMENT

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Determinism and Desire:

Some neurological processes in perceiving the design object.

In press, The International Journal of Design in Society, Year/Volume: 2013 Issue: 6

Winner CG Publisher’s research excellence award, 2012

Abstract

The environment moderates behaviour using a subtle language of ‘affordances’ and

‘behaviour-settings’. Affordances are environmental offerings. They are objects that

demand action; a cliff demands a leap and binoculars demand a peek. Behaviour-

settings are ‘places;’ spaces encoded with expectations and meanings. Behaviour-

settings work the opposite way to affordances; they demand inhibition; an introspective

demeanour in a church or when under surveillance. Most affordances and behaviour-

settings are designed, and as such, designers are effectively predicting brain reactions.

Affordances are nested within, and moderated by behaviour-settings. Both trigger

automatic neural responses (excitation and inhibition). These, for the best part cancel

each other out. This balancing enables object recognition and allows choice about what

action should be taken (if any). But when excitation exceeds inhibition, instinctive

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action will automatically commence. In positive circumstances this may mean laughter

or a smile. In negative circumstances, fleeing, screaming or other panic responses are

likely. People with poor frontal function, due to immaturity (childhood or

developmental disorders) or due to hypofrontality (schizophrenia, brain damage or

dementia) have a reduced capacity to balance excitatory and inhibitory impulses. For

these people, environmental behavioural demands increase with the decline of frontal

brain function.

The world around us is not only encoded with symbols and sensory information.

Opportunities and restrictions work on a much more primal level. Person/space

interactions constantly take place at a molecular scale. Every space we enter has its own

special dynamic, where individualism vies for supremacy between the opposing forces

of affordance-related excitation and the inhibition intrinsic to behaviour-settings. And in

this context, even a small change – the installation of a CCTV camera can turn a circus

to a prison.

This paper draws on cutting-edge neurological theory to understand the psychological

determinates of the every day experience of the designed environment.

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Determinism and Desire

Some neurological processes in perceiving the design object.

Watching children on a 6th floor balcony, I couldn’t help but notice the way they

searched for objects to throw over the balustrade. The promise of such a large fall yells:

“Jump. Jump. JUMP!” It is only when an inhibitory reflex kicks in that a battle with a

self-preservation instinct ensues. The winner is a holistic sense-of-self, of inner

coherence, and the urge is diverted. And the children harmlessly throw apples over the

edge in place of themselves.

The precipice, the apples – every opportunity the environment provides, calls for action.

But why? This article presents a framework of neurological mediators of perception and

action in an attempt to establish a cross-sectional theory of desire.

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A taxonomy of the neuro-correlates of perception, action and desire.

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Affordances; the heart of perception and the automation of action.

We don’t just perceive a compilation of colours and shapes (‘sense data’), then figure

out what it all means, and then act on that knowledge as a serial process. The perception

of the actions that an object allows (Gibson, 1979), occurs with the first phase of

perception, prior even to the recognition of features such as colour and shape (Yantis,

2000). This is an evolutionary necessity. An animal that is slow to react when

threatened will be the first to be eaten, and action must therefore commence before

perception even reaches a declarative (conscious) stage (Stephen Kaplan, 1992). When

we hear a loud roar, a range of automatic actions take place; our legs may start running

and we may grab a weapon. The blood pressure and heart rate increases, plasma levels

of adrenaline increase and our senses are piqued (Ekeberg, Kjeldsen, Greenwood, &

Enger, 1990). All this occurs even before we know where the roar has issued from.

The instinctive reach for tools and escape paths is just one of many hints informing us

that perception revolves around opportunities to act, for better or for ill. These

opportunities are called ‘affordances’ and are a central premise of Gibson’s Ecological

Theory of Perception (Gibson, 1979; Withagen, de Poel, Araújo, & Pepping, 2012).

Action-opportunities (objects) are the primary stimulants for attention (the first phase of

perception), but even so, they are subject to pre-existing environmental restrictions

(Yantis, 2000). These issue from behaviour-settings. Individuals have a sense of

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contextual awareness, a sense of what is possible and what is the right thing to do in

most given circumstances, and these are deliberately embodied in the physical milieu.

Because the perception of behaviour-settings is automatic, people in good mental health

rarely ‘act now and think later:’ such impulsiveness is unusual and is frequently a sign

of psychiatric illness (American Psychiatric Association, 2000) or the immature conduct

that you’d expect in children and adolescents (Quay & Quay, 1965).

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Behaviour-settings: the context of affordances and the automation of

inhibition.

A behaviour-setting is an environment that highly correlates with the behaviour that is

expected to take place there, that is the standing patterns of behaviour (mores,) that take

place in a congruent milieu (Barker & Wright, 1954). The behaviour-setting of a

football field invites the affordance of ball play, but restricts the play to specific rules

(Lhermitte, 1986). Most behaviour-settings are designed to reflect the mores that will

take place within.

A behaviour-setting restricts the possibilities of an affordance within it. For example,

the affordance of an apple in a store (a behaviour-setting) is different to the same apple

at home. At home you can just pick it up and eat it without breaking with convention.

Behaviour-settings restrict behaviour to the limits previously learned, so it should come

as no surprise that the inhibitory reflexes imposed by behaviour-settings will tend to

reflect normative limits of social acceptability. The behaviour-setting of a church, for

instance, demands an introspective demeanour and the behaviour-setting imposed by

surveillance demands introspective self-monitoring (Foucault, 1977). Behaviour in

keeping with the milieu is a primary automatic response and is neither creative nor

individualistic. This doesn’t mean that behaviour-settings are bad – or even good. Just

that they exist ubiquitously and that they modify the potential behaviour that an

affordance will trigger.

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Normally healthy adults are particularly good at voluntarily resisting the temptation to

act. This inhibitory phase of perception extends the automatic inhibition provided by the

behaviour-setting. But some people have neither choice to act, nor to resist action. They

must act – even against specific and authoritative instructions. These people include

children, whose frontal lobes are not yet fully developed, but even more so patients with

organic brain damage (Lhermitte, 1986; Lhermitte, Pillon, & Serdaru, 1986).

During a clinical study investigating the effects of organic brain damage on behaviour,

one patient (a 52 year old housewife who had been given a partial frontal lobectomy to

remove a cancerous tumour) attempted to give her doctor an injection, just because a

syringe was handy. Another patient (a 51 year old engineer who had also had a

lobectomy for cancer) picked up a gun, and because it was unloaded, found the

appropriate cartridges. The doctor had to intervene to confiscate the weapon (Lhermitte,

1986). Like the patient with the syringe, the man would have had no choice but to shoot

the doctor. This bizarre behaviour, absolutely lacking in autonomy, is caused by the

excitatory presence of a perceived opportunity. The perception of opportunity was

involuntary in both the cases mentioned above. They are examples of how the constant

stream of action and thought that we humans are engaged in is completely co-opted by

affordances if the organ that is responsible for inhibiting impulses and enabling alternate

actions ceases to function. The same impulse to act occurs even in healthy individuals,

but what is bizarre about the attempted actions of the lady with the syringe and the man

with the gun, is the absence of normal neural reactivity, a product of the very same

organ that also moderates the functions of self-reference (Northoff & Bermpohl, 2004;
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Northoff et al., 2006) and creativity (Dietrich, 2004; Dietrich & Kanso, 2010). In other

words, reactivity, self-awareness and creativity are all closely linked.

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Creativity and awareness: the deliberate extension of affordances and

behaviour-settings.

Not all action is automatic, especially for healthy adults. Given a context, we have two

choices; we can act as we please within the tight behavioural limits set for us by

learning. That means we can act on the automatic action cues imbedded within

affordances as they are modified by the automatic initiatory limits prescribed by

behaviour-settings (see Figure 10). But we can also break convention and extend those

limits. So if a person has learned to adopt a certain demeanour in church, this will be the

automatic mode of action when in church. But, by an act of wilful defiance, a person

may dance down the isle. This is a creative act, originating in the prefrontal cortex, the

seat of creativity (Golembiewski, 2012a). Creative acts of this kind will extend the

limits of automatic activity, by modifying associated schemata (Johnson Abercrombie,

1960); once you have danced down the isle once, it will be hard to return to the demure

demeanour that was once automatic.

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Automatic limbic processes Affective / hedonic pre-judgement

1a. Narrative/affective monitoring – +

Automatic (mesostriatal) processes Creative (frontal) reprocessing

1b. Latent restrictions from
behaviour settings (inhibition) 2. Expanding possibilities of
behaviour settings (excitation)
Behaviour limits
3. Opportunities of
Affordances (excitation) 4. Choice to react against
– affordances (inhibition)
+
}}
5. Potential range of final action
(mediated by the striatum)

Figure 10: The Choices We Make.

In this model, excitatory and inhibitory forces compete to establish the

range of potential action. The mesencephalon is the source of auto-

matic responses and the frontal cortex the source of creative repro-

cessing. 1. Behaviour limits are automatically set. 2. These are con-

sciously and defiantly extended. 3. The initial excitation of affordanc-

es is also automatic. 4. This is already inhibited (to some degree) due

to the behaviour-setting (1) but may be consciously restricted further.

The result is the scope of action that may take place.

• If affordances are negative, this inhibition is normally so complete that

no action takes place (see factors of saliency: worth).

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• When patients have frontal damage, the behaviour-setting limitations

and affordances are automatic.

• Automatic responses are learned from creative responses.

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What drives engagement? The factors of saliency.

The levels of perceptual engagement that affordances trigger are uneven. The reason is

that the level of perceptual engagement (activation potential) that they capture is uneven

and subject to competing forces. Live studies on monkeys, where sensors were wired

directly to monkey neurons (for obvious reasons not repeated on humans) isolate three

factors that contribute to how much engagement an affordance or behaviour-setting will

trigger (Schultz, 1998; Schultz, Apicella, & Ljungberg, 1993; Schultz, Dayan, &

Montague, 1997). All three factors are types of attentional salience; and the higher the

salience, the more likely the attention of a subject will be engaged 18. The three factors

are described below from numbers 2-4. The first factor was discovered by

experimentation on humans.

Opportunity: People instinctively find themselves attracted to an opportunity to act just

because it’s an opportunity to act. There may be the attraction of a nice smell, a

beautiful hue, a lovely texture (an individual may find themselves touching, looking,

reacting appropriately) (Gibson, 1979).

18
The terms prominence, significance and worth are used in place of the more common,

but less specific term; salience.

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Prominence: This is the prominence of the physical qualia of the object or setting.

Noisy, sudden sounds, flashing lights and bright colours etc., are highly prominent and

therefore demand reaction. High contrasts and perceptual simplicity contribute to

perceptual prominence (Ljungberg, Apicella, & Schultz, 1992).

Significance; the importance of the whole concept that is being recalled. There are three

things that increase the significance of an affordance or setting according to importance:

a) anything that helps build meaning, b) anything that contributes to understanding, and

c) anything that may needed to sustain existence (Golembiewski, 2009a; Jan

Golembiewski, 2010b). In other words, we react to affordances that are important. If

your work demands that you react in a certain way, you do so.

Worth, This is a quantitative measure of desirability. The promise of positive experience

generates a much greater impact than the threat of a negative one (Mirenowicz &

Schultz, 1996; Schultz, 1998). This is the graded pleasure principle. There’s a big

difference in human reaction to bland food and delicious food, even though the two may

be equally healthy.

The presence of an affordance may be informed by any of the above four saliency

factors. For example, someone may pick a rose because it’s there to be picked

(opportunity) it catches their eye (prominence), they want to gift it to someone they love

(significance) or because that rose is a particularly beautiful (worth). Beyond initial

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attention, another set of neurological processes commence, these involve an enormous

range of neurotransmitters and processes that are beyond the scope of this article.

The salience of sensory opportunity

As a driver of engagement, sensory opportunity may be unique to humans. Certainly

humans have rich taxonomies for every kind of sensation and are easily absorbed in

sensory experiences of all kinds. We hoard opportunities for sensory exploration in the

same way that a squirrel hoards acorns. Sensory opportunities are not a quantitative

measure of anything. They are the potential quality of an experience. Affordances of

this kind are invitations to explore and interact with the world in a sensual way (Gibson,

1979). A sensory opportunity may be found in the quality of a curve in a body (not only

because the curve is prominent or bright or significant). It is found in the texture of a

cashmere sweater, but also in the roughness of a fence-post.

From birth, babies will actively engage with the perceptual environment. They will

imitate expressions (Meltzoff & Moore, 1977), grasp a graspable object, and with age

they will want to touch textures, run fingers down Brancusi’s sculptures, absorb

themselves in colours and scents, feel the curvature and warmth of surfaces, immerse

themselves in tastes, experiment with sounds, etc. They will want to squeeze bubble-

wrap and juice cartons, just to hear them pop. They light sparklers to see the sparks fly

off in all directions; they burn incense to scent the air, and climb snowy mountains, just

to feel the rush of zooming down again. None of these engagements are especially

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useful. But they are enjoyable, and possibly even fortify one’s mental health

(Golembiewski, 2009b, 2011b).

With familiarity, sensory affordances appear to be temporarily extinguished (there are

limits on how much bubble-wrap one can pop). Anecdotally it appears that sensory

pleasures are renewed unless they are recast in a negative light, so the desire to eat fish,

for example might be repeated, but may be extinguished after a night of food poisoning.

Designers deliberately use sensory affordances all the time, and undoubtedly it makes

their projects more successful. From the crackle of pop-candy to the sweet-water

fountains of Rome, little sensory treats are difficult to resist, but do enrich experience in

a positive way. The architect, Louis Kahn appeared to be aware of this, and made his

use of affordances to create behaviour-settings explicit, using the terms availabilities in

a similar way to the way Gibson used affordances, and the term agreement to describe

the congruency of behaviour-setting, affordance and mores. It was his view that the

milieu should be designed in agreement with the mores that would take place there

(Kahn, 1971).

The salience of prominence

Prominence or as architects say, ‘spectacularity’ is a quantitative measure of the

difference between qualia and expectations. It is a measure of novelty - the unexpected.

As such, salience is subject to extinction with familiarity. Someone dressed in orange

will catch your eye, but if you see them in orange all the time, then they take on

background status (they become less salient). Technically, the dopamine neurons that
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are activated by prominence lose their activation potential with familiarity (Berns,

Cohen, & Mintun, 1997; Mirenowicz & Schultz, 1994). Familiarity is comfortable and

is an essential feature of a behaviour-setting, but one that gradually extinguishes

prominence (Schultz, 1998).

One very important fact about prominence is that, in the dopamine neurons that mediate

saliency, it has a short bursting (phasic) action which temporarily dominates the

underlying rhythmic ‘tonic’ action that moderates other forms of saliency (Jan

Golembiewski, 2010a; Golembiewski, in review-d; Grace, Floresco, Goto, & Lodge,

2007). Prominent perceptions may therefore displace other perceptions and thoughts

along with all other contents of the working memory (Lavie, 2010; Theeuwes, Kramer,
19
Hahn, & Irwin, 1998) . In real terms this will mean that prominent perceptions take

possession of the mind and generate enormous but temporary interest, in the same way

that a tiger would, if you suddenly discovered one in your home. It is as if the brain only

recognises prominence as potentially important, and closes perception off to it once it

has been fully assessed and found to be benign.

The importance of prominence for architects and other designers is that prominence gets

a lot of attention quickly. But it is difficult to maintain interest unless other saliency

19
It should be remembered that working memory is a hotly debated construct with

several competing models, none of which has universal acceptance.

(Miyake & Shah, 1999)

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factors support it. The focus of human attention travels logically from an initial phase of

exploration of novelty and difference, to familiarity and the exploration of further

opportunity, to significance and worth. With greater familiarity, the exploration of

potential opportunity will also be extinguished, leaving only significance and worth.

This truism has frustrated many an egotistical designer. An architect may design a

prominent and forward-thinking building, only to see it rejected and all of its great

innovations ignored. Big exceptions occur when the project is somehow identified as

being genuinely important. This happens whenever the building serves mores, in which

case prominence is at least remembered as people go about their business. For example,

someone working next to Sydney’s Opera House may see it from their window daily, so

the initial shock of the new – the curves, bright white tiles and stylistic ambition – is

maintained by a generalised engagement with the Opera House. The interest we have in

new and delightful designs will only remain as long as those designs continue to be

useful and/or foster meaning and serve worthy mores.

The salience of significance

Significance and worthiness are essentially two axes of the same concept. In the

commercial world, this is the ‘what’s in it for me?’ question that drives many a

marketing effort. Worthiness is a quantitative value (where something stands in the

spectrum between good or bad) and significance is what the worthiness qualifies. As an

example, cuisine can be described according to whether it is delicious or bland

(worthiness) but what is significant is that it will feed you. Significance is the potential
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for an affordance to enrich or diminish the quality of our lives. ‘What’s in it for me?’

Well, with this example, you’ll get fed.

Significance A: Meaning. Things that imbue life with the richness of meaning are

significant even if they don’t serve any direct function as such. These things often

transcend the pedestrian notions of good or bad because they are essential. These are the

things we live and die for. And like all other forms of saliency, can be attributed to both

object/affordances and places/behaviour-settings. One needs to look no further than

religious artefacts and places for evidence of the importance of these settings and the

mores that surround them. Take the Temple Mount for the Jews, the Church of the Holy

Sepulchre for many Christians and the Al-Aqsa Mosque for Islam. Places and artefacts

need not be religious or even commonly acknowledged to be deeply meaningful.

Meaning is also very personal (Antonovsky, 1987; Golembiewski, 2012b).

Significance B: Comprehensibility. Another dimension of significance is

comprehensibility. We engage with things that help us understand the situations we find

ourselves in, for example, some people may find astrology interesting as it gives them

insight into people and behaviour and even into themselves. The desire to find out more

is the basis of a rich personal ontology and provides a foundation for independence

(Antonovsky, 1987).

Significance C: Manageability. Manageability, the things that make a person’s

existence manageable right now may also be significant (Antonovsky, 1987). But here

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we have a caveat; you must have a simultaneous corollary need. Things that enable

manageability alone are in themselves not very enriching, yet they are essential – but in

an opposite way to meaningful ones. Affordances that contribute to manageability are

basic shelter from the weather, food etc. Manageability is frequently the only

consideration designed into the built environment, particularly in institutional design

(Jan Golembiewski, 2010b). And while things that enable existence are important, they

are of no interest when the need does not present itself (preparations for future needs

being a product of comprehensibility) (Golembiewski, 2009a). How much consideration

does one give to an anorak during mid-summer? It doesn’t register as an affordance at

all. Yet, in mid-winter it becomes very important indeed as it yells ‘put me on!’

The salience of worth

At first glace, affordances that appear to be positive draw more attention than negative

ones. Technically, this appears to be due to one of the functions of the medium spiny

striatal dopamine neurons. Empirical studies of these neurons show that, in healthy adult

populations, they are reliably more easily excited by positive stimulus than negative

(Northoff et al., 2004; Schultz, 1998). The judgement of worthiness is among the first

of a series of automatic reactions. And in general terms, positive affordances are far less

subject to reactionary inhibition. For example, smiles, laughter, warm fuzzy feelings

and cause automatic and unrestricted engagement beyond the a-priori automatic

restrictions imposed by the behaviour-setting. Put another way, the choice to engage in

positive experiences is a normal feature of robust mental health, but so too is the ability

to restrain oneself to be appropriate in a given context. In many psychiatric conditions,

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this positive bias is far less apparent or is even inversed in fact ‘affective flattening’ or

catatonia, are common in clinical pathologies (American Psychiatric Association, 2000;

Golembiewski, 2012a).

Figure 11: Excitability of Negative, Positive and Neutral Stimulus for

Catatonic, Paranoid and Healthy People. (from Golembiewski

(2012a) and based on data from (Northoff et al., 2004)), shows results

from a clinical study of three groups. The first group: C) were akinetic

catatonic patients, three of whom were diagnosed with schizophrenia,

and seven with bipolar disorder. The second group: P) had seven par-

anoid schizophrenic patients and three bipolar. In the third group: H)

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there were ten people who had never been diagnosed with a mental

disorder.

The numbers (graphed) show the net excess of neural excitatory reac-

tions after all concurrent inhibitory reactions has been subtracted. All

groups were exposed to negative stimulus (pictures of horrific things;

black), positive stimulus (pictures of lovely things; white) and neutral

stimulus (grey card; grey). As you can see, in the negative condition,

there was such a minor excess of excitation in the healthy group that it

was not chartable (0.63%). The patients however, were unable to bal-

ance negative perceptions. On the other hand, positive perceptions

were not so strongly balanced out (although some inhibition had taken

place – not graphed). The healthy group had about double the positive

reaction than the paranoid group and about a third greater positive

reaction than the akinetic catatonic patient group. This demonstrates

how negative affordances are balanced out in healthy people as op-

posed to psychiatric patients.

Unless negative affordances are very prominent, an individual will react against them,

effectively reducing their activation potential to nearly nothing (here only 21 more

excitatory neurons fire than inhibitory ones. In psychiatric conditions the excitation is

much higher - as much as 1385 among the paranoid group. See Figure 11.)

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An interesting correlate is that when healthy people start perceiving something with a

negative sentiment, they avoid further exploration and continue to reject the affordance,

behaviour-setting and all it entails (Golembiewski, 2012a). This pervasive bias is

automatic and therefore requires conscious and creative intervention to reverse. For

example, neighbours may complain about the construction of an absolutely glorious and

useful building because the construction meant cutting down a beautiful forest on the

site. To get the neighbours to appreciate the building is going to be difficult, as they

have decided to explore the ‘affordance’ no further. One very important thing to note

here, is that a very small design change can have a disproportionate effect on the

‘worth’ of an affordance or behaviour-setting. A neutral space can very easily adopt the

negative associations implied by objects therein; a CCTV camera or surface dirt.

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Using theory in praxis: determinism

Intuitive observations of behaviour around affordances and behaviour-settings have

traditionally played a major role in the design industries, but observations have seldom

reached into neuroscience to find explanations. For affordances, determining how an

object will be engaged with is relatively simple; an object is perceived for what it offers.

Thus a Zippo® lighter is attractive because of its sensory opportunities; it is graspable,

flickable and pocketable. It provides an opportunity for discrete engagement (a

plaything in a pocket), even when circumstances (behaviour-settings, mores) prevent the

lighter to be used. The Zippo® may also have significance; it is presentable, meaning it

serves a need for meaning (social status), and also for the occasional function

(manageability) need for fire.

The main complication with affordances is that they are subject to change given

different behaviour-settings. An apple says, ‘Eat me!’ when it is in a bowl on a kitchen

bench. It says, ‘Pick me!’ when hanging, ripe from a bough. And it says, ‘Buy me!’

when it is displayed in a supermarket.

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Figure 12: Jeff Koons (1985). Three Ball 50/50 Tank (Two Dr. J Sil-

ver Series, One Wilson Supershot). MOMA. New York. Glass, painted

steel, distilled water, plastic, and three basketballs, (154 x 123.9 x

33.6 cm).

In Three Ball 50/50 Tank and in others, Koons explored how af-

fordances shifted with new settings in his works.

But behaviour-settings not only represent complications for affordances, they also

complicate design problems. The manipulation of human behaviour through design is

called determinism. For small objects (affordances), this is done intuitively and with

relative success, but for big objects – buildings in particular, the variables are more

complex and success is far harder to predict.

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The concept of architectural determinism has fallen to disrepute and the term is usually

considered dismissive due to a history of disappointment (Broady, 1966; Lang, 1980).

There are a number of reasons why authors criticise deterministic thought – for the fact

that it privileges the power of the environment and neglects psychology – the individual

and social reaction with the environment. This introduction of a neuropsychological

basis for design determinism attempts to redress this shortcoming.

In brief, typical criticisms of determinism include the following:

Sometimes deterministic failure is put down to normative effects such as beliefs of the

designer:

Determinists are accused of overestimating the value and power of the their own ideas –

for example, the innovative vertical corridors in the Pruitt-Igoe complex were thought

by reviewers to be fabulous, but many of the people who lived in the complex were far

less enthusiastic (Franck, 1984; Lang, 1980). In other words, the mere presence of

opportunity within the environment does not ensure that will be noticed, appreciated or

even used (Lang, 1980; Newman, 1996).

Determinists are accused of a naïve belief that environmental effects on behaviour are

always direct (Franck, 1984). For example, Hellmuth, Yamasaki and Leinweber (later

reincorporated as Hellmuth, Obata, Kassabaum Inc.) the architects of the Pruitt-Igoe

complex provided common rooms for suites of several apartments in the belief that they

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would create informal communities. The stark reality is that the provision of a common

room doesn’t create a community. The common room is just a space until mores match

it. And a space without positive mores has a tendency to turn to a negative space

(Jacobs, 1961). In this case, Pruitt-Igoe was famously criticised for a lack of passive

surveillance and defensive opportunities (Newman, 1996).

Determinists are accused of believing that people are passive in their interactions with

the environment and are not driven by their own autonomous goals and choices (Franck,

1984).

They are also accused of assuming that the environment is an immutable entity that will

not be modified by inhabitants (Franck, 1984).

Determinists may also be cynical of knowledge that they don’t have – for example an

architect who doesn’t know anything about colour theory might dismiss it without

exploring its potential.

There is a possibility that deterministic design may fail because designers employ faulty

or inappropriate psychological theories. These are input errors:

The psychology used by determinists may have been developed to explaining a

phenomenon, but for unknown reasons may not be applicable for predictive design.

Psychological theory is largely derived from empirical studies that are performed in

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controlled circumstances, which may not reflect reality in a holistic way. People don't

necessarily behave as they do in a psychological experiment (Philip, 1996).

Input errors may occur because a designer has embraced part of an unresolved debate.

The psychological literature on behaviour contains unresolved debates, incomplete

models and oxymorons, which may occasionally be contradictory (Lang, 1980).

Sometimes the motivations, values and competence levels of populations are not

properly considered when designing behaviour-settings. This may affect the usability of

designs (Lang, 1980).

All of the above factors play a part in limiting the effectiveness of deterministic design;

after all, there are many ways to judge success or failure and many more ways that

something may be right or wrong about a design. But possibly the most significant

factor is that a behaviour-setting must be congruous with the mores that take place

therein, and whilst architects can design the milieu, they cannot design mores. In

other words, when designing a behaviour-setting, architects may design just one side of

a complex interaction; the other side is largely social and neurological and cannot be

‘designed’ – certainly not in the way that buildings can be. As Louis Kahn may have

said, the building is not in agreement (Kahn, 1971). This is not to say that revolutionary

ideas cannot work. It’s just that any new scheme still needs to be matched with mores in

order to be fully functional. Wherever the customary mode is abandoned, any effort to

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make a scheme engaging will encourage users to make the commitment to adapt to the

new space and way of doing things.

Of course both the physical environment and behaviour is subject to adaption. But

accordingly, behaviour patterns are only likely to change incrementally when

transferred to a new but familiar milieu. But if the design is congruent with a major shift

in the mores, then radical innovations may also be embraced.

In support of this hypothesis, many of the well-accepted examples of (socially)

successful radical architecture are matched by equally radical social change. Niemeyer

and Costa’s city of Brasília reflected the major social, industrial and political changes of

Brazil that occurred during the highly popular reformist presidency of Kubitscheck.

Even before the foundation stone was laid, the city had been long awaited. The

construction of the new capital was a fundamental election promise, reflecting a

decision that had been written into the constitution six generations earlier (Avila, 2008).

Similarly another modernist and innovative city that has been continually praised, is

Chandigarh, planned by Le Corbusier, which was built to re-house the Punjab capital

after Lahore was lost to Pakistan during the partition of India. India’s first Prime

Minister, Nehru, personally oversaw the project seeing it as a symbol of India’s new

independence and self-determination (Lang, 2005). But not all ambitious rationalist

schemes of similar genres and scales are so well received.

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The twentieth century saw a list of great architectural ideas being bulldozed (and

occasionally blown up) there are many reasons for the failure of architectural

determinism, as outlined earlier, but especially when inhabitants’ don’t engage with the

new schemes. Remember, here we present engagement as a neurological problem, not

an abstract one.

The archetypal example of failure was the aforementioned Pruitt-Igoe public housing

development in St. Louis. This development was originally praised for its innovations –

especially for the creation of common balcony areas, each servicing twelve apartments

of 1-4 bedrooms each. These would run off the common areas to either side or

immediately above or below. These were intended to create ‘individual

neighbourhoods’ within the larger monolithic building (Lopez, 1956). Apart from these

common spaces, there was no common horizontal circulation within the buildings.

The relative successes and failures of Pruitt-Igoe are still hotly debated with fashionable

opinions swinging one-way and then the other (see (Freidrichs, 2011) for comparison).

With a project as iconic and complex as Pruitt-Igoe, it’s hardly a surprise. Even so, it’s

reasonable to assert that projects like this that could benefit from greater insight into the

neuropsychological systems that underlie the desire to engage and perceive.

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Conclusions

Affordances and behaviour-settings are at once designed objects and are also designed

physical interventions to the human neuropsychology. Put in simple neurological terms,

affordances automatically trigger excitatory reactions, and behaviour-settings

automatically trigger inhibitory ones. Beyond these, the range of potential behaviours

that are associated with these design-objects can be expanded or contracted through

choice by engaging the creative centre of the brain. This action has the benefit of

fostering individuality and a sense-of-self, which is incidentally one of the major factors

in combating a range of important mental health problems (Kean, 2009; Sass & Parnas,

2001; Searles, 1966).

Affordances are relatively intuitive to design because they are simple. As long as there

are provisions for one or more forms of salience, the affordance (the object) will be in

the running to engage people. But the design of behaviour-settings is a wicked problem

and is much more difficult. The problems are open ended and you can always ‘do

better’ (Kunz & Rittel, 1972). Furthermore the problem isn’t improved by the

complexity of human/object interactions; the congruency between humans and their

habitats is easy to misread. Certainly, behaviour-settings will predetermine the limits of

affordances. But it is a mistake to think that people will be content with prescribed

behaviour patterns. The strong correlations between the way people behave and the

milieu where the behaviour takes place does not mean that architecture determines
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behaviour – even if it appears that way. Equally, it is mistaken to say that mores

determine human behaviour. A behaviour-setting still inhibits behaviour when only one

person is present. We don’t stop being social beings just because nobody else is around.

Behaviour-settings will continue to suggest mores when people are not present at all.

When a shop is opened up in the morning, shoppers will behave very much as they did

the day before, even though there was nobody there to continue the behaviour

overnight.

Behaviour-settings are more than the limitations on how a space can be used. A

cathedral may offer enough space to play football, but this behaviour is not suggested

by the architecture (curiously sports stadiums have been used as churches during events

such as World Youth Day, but how these exceptions have been achieved are a study of

their own). Behaviour-settings do not only limit behaviour, they suggest it also.

Effectively, every behaviour-setting is an affordance also.

However it is considered, a behaviour-setting is a dynamic and organic relationship

between designed place, the mores that it enables and the neurology and psychology of

the users. A new setting can change those mores, but only incrementally, as much as

people will individually allow. The adoption process can be sped up if the mores are

already in a state of positive flux. Under these conditions, people are more willing to

change.

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GENERAL HOSPITAL DESIGN

There is a growing interest in my work on salutogenics and mental health research,

because most of the research into health facility design is limited to studies involving

direct evidence. These studies, though very valuable, only serve to prove or disprove

very specific hypotheses in a very controlled setting. Typically, such a study will

involve the modification of one element of the environment and then records of hospital

stays or consumer satisfaction will be gathered. There is a growing frustration with this

approach. Designers, researchers and commissioning bodies need and want more. They

need to understand the psychological implications of their decisions. Traditionally it has

been difficult to apply such knowledge and even more so to assess outcomes. The in-

depth knowledge provided by an understanding of neurological mechanisms is therefore

refreshing, especially as this fine-grained approach is backed up by a broad-brush

methodology, which picks up the pieces to allow a holistic approach to design.

An understanding of some of the mechanisms involved in mental illness is applicable

across the board. With this in mind, I was invited to present the following paper on

general hospital design as an invited plenary address at the Design and Health

Australasia Symposium: Global Perspectives, Local Identities, UTS, Sydney 29th

March 2012.
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The neurological basis of salutogenic healthcare design.

In Press: World Health Design, 5(4) October 2012

This paper was received a highly commended award in the 8th World

Congress for Design and Health (2012), in Kuala Lumpur, Malaysia.

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Abstract

Objectives

The theory of salutogenics has a basis in the empirical testing and ideas of Antonovsky,

which state that health outcomes improve when a sense of coherence is fostered. A

sense of coherence in turn, depends on the net resources that support meaning,

comprehensibility or manageability. The reason that manageability is important for

health is obvious, but why abstractions like meaning and comprehensibility are

important is more difficult to understand.

Methods

Salutogenic abstractions are traced to back to current neurological models to locate the

endocrinal and neural mechanisms that underpin them.

Results

Meaningfulness, comprehensibility and manageability functionally correlate with triune

brain theory. Meaning is managed by the neomammalian frontal cortex;

comprehensibility by the hippocampus and amygdalae within the paleomammalian

limbic region and the association cortices; and manageability by the reptilian brain: the

mesencephalon and primary perceptual cortices. In general, the slower, but more

evolved frontal functions take precedence. But the paleomammalian organs continually

monitor the comprehensibility of phenomenal events. If events fit within a positive

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narrative, the neomammalian processes are allowed to continue, but if things ‘look

bad,’ instincts regulated by the reptilian brain take over. The result includes a wide

range of deleterious somatic and behavioural changes.

Conclusions

Healthcare architecture is not a neutral container for healthcare facilities. All

architecture embodies narratives that may either support or work against a state of good

health. A salutogenic approach to design attempts to include support for meaning,

comprehensibility and manageability, and to avoid their antithesis – meaninglessness.

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The neurological basis of salutogenic healthcare design.

Architecture mediates almost all experience and moderates a great deal of behaviour.

For the best part, the moderation effect that architecture plays is qualitatively even. The

ubiquity of vertical walls and orthogonal layouts with very similar features for similar

typologies guarantees this. Is there a qualitative difference in a right turn over a left

one? Does it mater whether a window is a sash-cord or a casement? Either way the

actions these decisions prescribe are radically different, but on a qualitative level, the

experiences are nearly identical.

But architecture can be genuinely manipulative, and herein lies the qualitative

differences in the phenomenology of architectural experience. Sudjic (2006) describes

how architecture is used as a weapon, to defeat an enemy before a shot has ever been

fired; Snodgrass (1990) describes architecture that is used as a vehicle for religious and

spiritual revelation; and Jencks (1999) makes a solid attempt to relate how architecture

can thrill its visitors. But when it comes to healthcare design, architecture is rarely so

focused on psychology. Somehow architecture all too often loses its considerable

manipulative power as it becomes subservient to its parts: future expansion, structure,

models of care, functional programme, efficiencies, sightlines, infection control and the

needs of a diverse group of users. There’s no question; all these things are critical, but to

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let functional and structural issues lead design is to let the cart lead the horse. So is it

possible to harness the considerable manipulative power of architecture for better health

outcomes?

Architecture – a building, or better still, an entire environment can amplify emotions,

especially when they are already vulnerable. Sudjic (2006) proposes that the endless

gallery leading to Hitler’s chambers in Albert Speer’s Neuen Reichskanzlei, and the

grandiosity and sheer scale of his suite so amplified the helplessness of the 1939

president of Czechoslovakia, Dr. Emil Hácha, that he not only surrendered his nation,

but also suffered a cardiac arrest in Hitler’s presence.

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Figure 13: The Neuen Reichskanzlei in 1941. A grandiose gallery

leading to Hitler’s chamber takes up most of the building. Photograph

by Heinrich Hoffmann.

From a medico-legal paradigm, it seems impossible to prove that the Neuen

Reichskanzlei (Figure 13) had anything to do with the state of Dr. Hácha’s heart, but

from a salutogenic perspective, the relationship is un-missable. The same can be said for

architectural interventions that are designed to improve health outcomes – correlations

don’t mean causation. But architects and healthcare planners should not be dismissed so

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easily. Reviews of healthcare design research show there are now thousands of relevant

studies, many of which have been shown to make a substantial difference in health

outcomes (Ulrich et al., 2008). But these studies invariably focus on single details,

frequently drawing on abstract aetiological mechanisms such as the general concept of

‘stress’. The salutogenic methodology is both more holistic and more specific: for

Antonovsky (1987) the stimulation we call stress isn’t just noise, it’s information. And

our ability to cope with the flood of information – be it good or bad – is ultimately what

determines our generalised state of health.

The theory of salutogenics has a basis in the empirical testing and ideas of Antonovsky

(1987), which find that health outcomes improve when a sense of coherence is fostered.

A sense of coherence (SOC) in turn, depends on the net resources that support

meaning, comprehensibility or manageability. Put simply, all of these things help us

make the best of life’s circumstances. They help us cope.

Almost all healthcare interventions (medicine, care, architecture) focus on

Manageability: the physical resources needed to keep on going. It’s paradigmatic that

this is virtually all healthcare is obliged to do: to treat the sick and keep them warm, fed

and dry while they recover from a point of critical illness or injury.

Comprehensibility is a function of knowledge. Information about the life situations

people find themselves in builds a sense of comprehensibility. For healthcare

information will include facts about the nature of the illness, how long a stay will be,

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what treatments are available, who will be involved and how, information about side

effects and what resources will assist in recovery. In the healthcare sector, things are

improving for comprehensibility and there are a few ‘islands in the sun,’ but

information communication is something which health facilities have traditionally been

bad at (Cleland, Ross, Miller, & Patey, 2009; Wistow, 2012).

Meaningfulness enriches and gives quality to life. It is the sum of all the best reasons

people have to keep on living (Antonovsky, 1987; Jan Golembiewski, 2010b;

Golembiewski, 2012b, 2012e). Generally speaking, hospitals don’t consider the

fostering of meaning to be their role, but when people are beleaguered with anxiety

about their state of health and about the future, it’s hard to imagine that any other

psychological interventions could be more significant than developing reasons to hang

in there and believe that everything is going to be okay in the long-run (Antonovsky,

1987, 1996; Jan Golembiewski, 2010b; Golembiewski, 2012b, 2012e). A caveat is due

here; salutogenic needs do change with the intensity of pathology – comprehensibility is

more important (in the short term) than meaningfulness whenever ‘things are not

looking good’ for a patient, and they know it - in cases of primary myocardial infarction

(cardiac arrest), for instance (Bergman, Malm, Ljungquist, Bertero, & Karlsson, 2012),

and we shall soon see why.

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The neurology of salutogenic healthcare design

The reason that manageability is important for health is obvious and doesn’t need

further elaboration here, but why abstractions like meaning and comprehensibility are so

important can be difficult to understand.

The brain can be seen as an organ that perceives, creates and manages meaning. The

most basic level of this is manageability. Even the most simple of creatures need to

manage the needs of survival: sustenance, protection and reproduction. The bulk of the

relevant processes to manage these needs are automatic in most creatures. The areas of

the brain that are wired for manageability are within the reptilian complex; a simple

system that implements a simple formula; if it’s food, eat it, if it’s danger, flee and if it

secretes sex hormones, mate it (Bargh & Dijksterhuis, 2001).

Comprehensibility is a step more complicated because it involves perception, that is, a

cognitive, interpretive step. And this presents a problem: how is sense-data interpreted.

The internal representations we have of external objects cannot be true to reality. This is

firstly because reality offers a richness that humans simply cannot experience: humans

don’t even share the same sensory range as one another (some have better high

frequency hearing, others are colour blind etc.), and certainly we have very different

sensory ranges to other animals. Bats can hear pitches of up to 115kHz, and humans

only about 17 kHz, humans can feel light of 300-400 tHz range as heat, but poecilia

reticulata (the common freshwater guppy) can see and taste the same spectrum. But

what humans lack in terms of sensory ability, we make up for in cognitive ability. We
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have an extraordinary ability to identify the differences between just about everything,

and this information is stored in vast lexical ontologies. At a glance we can tell the

difference between a Nokia and an iPhone, between a painting by Modigliani and one

by Picasso or a song by Jimi Hendrix and a religious hymn. Not all this information is

immediately relevant, but it is our nature to store and use such information as needed.

Information becomes critical only when required: “I need medical attention – where’s

Emergency?” Or “If I take this medicine will I get side effects?”

The cerebral cortex is used for associations, in other words, the links between pieces of

information – the basis of comprehensibility. Learning is the generation of these links,

and knowledge is their retrieval. Although learning takes place over a globally

distributed network (Baars & Franklin, 2007), the main place that somatic (sensual,

physical) associations are paired with meanings is in the primary perceptual cortices

(Grossberg, 2009). A paleomammalian (limbic) organ called the thalamus mediates the

somatic nervous and sympathetic nerve impulses and distributes them to the appropriate

perceptual areas of the brain. These are then associated with one another and more

abstract meanings in the higher perceptual association cortices and with actions in the

motor cortex (all are subsections of the cerebral cortex).

Comprehensibility doesn’t have to reflect ‘truth’. Comprehension can be delusional.

Delusional subjects generally have relatively low SOC scores, due to poor

manageability and meaningfulness scores. But recovery from delusional states only

reduces SOC scores further – particularly for comprehension, implying that the
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underlying SOC is challenged by having to comprehended the world afresh (Bergstein,

Weizman, & Solomon, 2008).

Meaning is an order more complex again, and in this evolutionary step, the anterior

hemisphere of the cerebral cortex swells to make a distinctly neomammalian shape, one

that is far more defined in humans than in any other species – it is the neomammalian

complex, incorporating a highly developed anterior cingulate cortex (ACC) and

prefrontal cortex (PFC). These organs process choice, insight, creativity, the sense-of-

self and other complex cognitive processes to establish appropriate actions for

situations for which there are no ready responses (Dietrich, 2004; Northoff et al.,

2006). The use of the neomammalian complex definitively separates humans from all

other animals, and makes us what we are: more human 20.

Like other advanced mammals, the folds of the neomammalian complex contain a thick

network of dopamine neurons. What differentiates ours from those of all other animals

is that most of the neural receptors in the human frontal cortex are of the D1 type with

higher densities of D2 type receptors deeper, in the paleomammalian regions (see the top

section of Figure 15). In contrast, D2 receptors remain ubiquitous throughout the entire

20
Note that some neuroscientists question the validity of the free-will concept, but neu-

roscientists who do believe in the freedom of will usually link the concept to creativity,

and the ‘most human’ of organs, the prefrontal cortex (Searle, 2001).

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mesofrontal region in other mammals – from the reptilian middle brain right through to

the prefrontal cortex (Nichols, 2010; Prante, Dörfler, & Gmeiner, 2010). The difference

is not subtle. The D1 receptor is excitatory, meaning that when it fires, it activates the

neo-mammalian complex. This means that some perceptions will activate the centre of

consideration, thoughtfulness and creativity. D2 is inhibitory, so when it fires, it restricts

activations in the same region. This enables faster judgements, but at the expense of

consideration, thoughtfulness and creativity. This explains what we all know already;

that humans are naturally more considered in their actions than any other animals.

Animals, on the other hand, are more instinctive.

Each evolutionary iteration of the brain must process increasingly complex information,

but like a computer the more complex information is, the slower it is to work through.

Unfortunately evolutionary theory doesn’t favour slow reactions, so to maintain quick

reflexes, the more evolved areas don’t replace the primitive ones. The more developed

layers of the brain fold around the more primitive, and mechanisms have been

developed that allow the primitive/instinctive areas to spring back into action whenever

speed is required. In advanced mammals, reflexes are regulated by the amygdalae (used

to monitor emotional context) and the hippocampi (to monitor schemata and narrative

context). Together these set up thresholds for automatic inhibitory responses and

excitatory overrides, so if a surprise occurs, appropriate instincts will be already

approximately set for appropriate action in a given situation (Golembiewski, 2013) (see

Figure 14).

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#Automatic#limbic#processes# Affective$/$hedonic$preCjudgement
1a.$Narrative/affective$monitoring – +

Automatic#(mesostriatal)#processes Creative#(frontal)#reprocessing
1b.$Latent$restrictions$from
behaviour$settings$(inhibition) 2.$Expanding$possibilities$of$
behaviour$settings$(excitation)
Behaviour#limits
3.$Opportunities$of
Affordances$(excitation) 4.$Choice$to$react$against
– affordances$(inhibition)
+
}}
5.#Potential#range#of#final#action
(mediated#by#the#striatum)

Figure 14. The reptilian complex (orange) mediates instinctive ‘event

management’ responses – there is either instinctive/learned action or none.

Paleomammalian organs (the hippocampi and amygdalae) monitor experience

for narratives that impart an affective or hedonic value (i.e., “it’s good or bad

for me”) the sense of “where I am in this story” roughly corresponds to the

salutogenic notion of comprehensibility (green). In positive circumstances, the

neomammalian complex (blue) is engaged and is able to expand the possibilities

of action or restrict them according to a person’s own sensibilities and context.

(Image from (Golembiewski, in review-c))

Behaviour settings are pre-set expectations of behaviour in a given

environmental setting. Affordances are perceived opportunities to act (Barker

& Wright, 1954; Gibson, 1979; Golembiewski, 2013).

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Sometimes surprises are good and welcome – jokes for instance, and the automatic

reactions include laughter, smiles and happy feelings. These are good and don’t need to

be managed. But a negative shock will solicit screaming (sounding an alarm to others)

and even more basic self-protection instincts: the release of stored energy to enable

flight, and the defensive withdrawal of blood from the periphery of the body (to prevent

certain death, should a snake or bear bite a limb). All of these reactions commence in

the reptilian complex, and their activation inhibits the activation of the neomammalian

complex (Golembiewski, 2012a).

The withdrawal of peripheral circulation protects the body from physical shocks. It is a

primary function of the hypothalamus, the pineal gland and adrenal cortex. Together,

these secrete hormones, which inhibit peripheral circulation by metabolising quickly to

cortisol (Steptoe & Kivimaki, 2012). It’s fast, but not an ideal solution because cortisol

has a number of undesirable side effects: It overrides healthy limits on blood sugar,

blood pressure and heart rate (the tip of the iceberg: there are other negative side effects

also). In non-emergencies, cortisol synthesis doesn’t occur and essential hormones are

produced from the same primary compound (cholesterol) instead. These maintain

happiness and appropriate healthy bodily function; they include progesterone,

dihydrotestosterone (DHEA) “the joie de vivre hormone” (Gluck & Edgeson, 2010),

testosterone and oestrogen, to name only a few (see lower section of Figure 15).

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Chemical
Neuronal-Excitatory

Key
Neuronal-Inhibitory (’shuts down’ target)
Neuronal-Axon (base)

CREATIVITY Anterior caudal Prefrontal Premotor/motor

D1 GABA
cingulate cortices cortices
The “free-will*” The “automatic” ACTION

Glu
pathway D1

D2
pathway

Parahippocampal Ventral tegmental Nucleus

gyrus area accumbens

Adrenocorticotropic hormone
Hippocampus Oxytocin

Hypothalamus Posterior pituitary Adrenal gland

Anterior pituitary
Amygdala
Corticotropin releasing hormone FEELINGS
and Arginine vasopressin Oxytocin Cortisol
References: Swenson, R. (2006) Review of clinical and functional neuroscience
Steptoe, A. and M. Kivimaki (2012) Nature Reviews Cardiology Other hormones
Rossato, J., L. Bevilaqua, et al. (2009) Science
Oei, N. and I. Veer, et al. (2012) Social Cognitive and Affective Neuroscience
Goldman-Rakic, PS. (1987) Handbook of Physiology
Golembiewski, JA. (2012) Medical Hypotheses

Figure 15: The automatic vs. creative action pathways – the thresholds

for conscious choice and deliberate behaviour are moderated by the

combined amygdalae and the hippocampi in the limbic region of the

brain. If circumstances are perceived as going beyond a reasonable

threshold of control, these organs trigger the hypothalamus to override

neomammalian processes. Associated feelings occur in parallel - nega-

tive events triggering cortisol – a hormone associated with non-specific

anxiety. Cortisol bypasses normal hormonal regulation.

It is important to note that cortisol is not stress and stress is not cortisol, although the

two are commonly confused. Cortisol can be a useful medicine when used wisely.

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Cortisone (synthesised cortisol) is used to suppress the immune system (during allergies

or asthma attacks, for instance). But in natural circumstances, cortisol is a by-product of

automatic self-preservation systems that only kick in when:

a) The neomammalian complex is bypassed. This area is used to process the

primary salutogenic resource: meaning.

b) People find themselves in situations, which they associate with lurking danger (a

hippocampal function, which correlates to another salutogenic resource:

comprehensibility).

c) The environment is perceived as being aversive (a function of the amygdalae,

which also correlates to comprehensibility). Note that amygdalae don’t have a

‘neutral’ function. Neutral stimuli are emotionally ambiguous, so they are

polarised into negative or positive following narrative cues from the

hippocampi.

d) Automatic behaviours commence before cortisol even reaches the bloodstream.

These include instinctive and learned behaviours, but the problematic ones are

only noticed in negative circumstances: they are stereotypical behaviours,

screaming, fleeing, sudden violence, confused thinking patterns and

perseverance (when in excess, all of these are associated with mental illness)

(Golembiewski, 2012a) (See p. 358- q.v.).

It begins to become clear that the failure of comprehensibility triggers the reflexes in the

reptilian brain to produce cortisol and other unwanted reactions. This is apparently a

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‘last-ditch effort’ to maintain the last and most primitive of the salutogenic resources:

manageability.

If asked if Dr. Hácha’s experience in the Neuen Reichskanzlei could have caused a

heart attack, there is no doubt that the building was an essential factor in rapidly increas-

ing his vulnerability. The design of the Neuen Reichskanzlei worked (as intended) to

defeat adversaries. The narrative of immense power was written into the masonry. And

when this was combined with the generalised negativity that Dr. Hácha must have

sensed as he approached his nemesis, his creative and adaptive resources would have

been reduced. Instead of using his neomammalian brain to test creative solutions, the

negativity inherent in his situation (reinforced by the architecture and social milieu)

must have triggered alternative automatic behaviour pathways, thereby reducing his

thoughts to testing established fears for himself and his country. It’s easy to imagine Dr.

Hácha thinking thoughts along the lines of: ‘Perhaps they have invaded already, and

they are keeping me here so I’m not there to rule my country in its hour of need?’ (Note

the paranoid thinking). Meanwhile, on a physiological level, Dr. Hácha’s cortisol levels

will have soared, causing his blood pressure to increase. When extreme this reaction can

cause transient myocardial ischemia, an atypical cause of cardiac arrest: the heart stops

because of the sudden swelling of the heart tissues (Steptoe & Kivimaki, 2012).

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Figure 16: A patient reads the morning paper on one of the many

abundantly green spaces of the Khoo Teck Puat Hospital in Singa-

pore. (Designed by CPG Consultants Pte Ltd and landscaped by Pe-

ridian Asia Pte Ltd – photo credit CPG Consultants Pte Ltd)

Thus architecture can be a powerful weapon. But can it be an equally powerful ally?

The hippocampi/amygdalae coupling sets up automatic response thresholds that are

already likely to be low for people entering a healthcare setting, so as healthcare

designers, our first task is to maintain comprehensibility (Bergman et al., 2012). To do

this, the embedded narratives within the environment must be managed. That means

taking great care that the typology and patient experience is recognisably and

indisputably positive. The first step is to distance the style of the new facility from those

ubiquitously seen in medical dramas. That means design teams should look for
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functional alternatives to white walls, vinyl floors, strip lighting, typical services and

even the design of surgical scrubs and nurses’ uniforms (Richardson, 1999). Bring in

masses of glorious plants and fresh air like in the Khoo Teck Puat Hospital in Singapore

(Figure 16), and consciously design the soundscapes, lighting, and patient experience.

Perhaps the most alarming features of modern hospitals are the monitors, which set off

alarms when a patient’s vital signs are irregular. There is no question that these

machines are essential, but the alarms no longer need to sound right by a patient’s

bedside. Current technology allows the alarms to be routed directly to communications

devices that are carried by medical staff. Healthcare lighting should be natural and

electric light should be low -glare, and be of a ‘warm’ temperature (Tammes & Burnett,

in review). Windows should look out to gardens and plants and art should adorn patient

rooms. Many interventions of this kind have already been studied and found to be

useful, even on their own, once again see (Malkin, 2008; Ulrich et al., 2008) for handy

reviews.

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Figure 17: When in a state of robust health, a person’s attention is pri-

marily focused on the aspects of life that provide meaning; family,

friends, the world around etc. and not only focused on survival. In this

diagram blue represents the locus of attention, and green peripheral at-

tention.

The next step is to enrich meaning. Meaning is to be found whenever humans engage in

concerns beyond their own (even if these are very abstract); the well-being of family

and friends, in the greater good of society, in protecting animals and the environment,

even in protecting the security of the cosmos (Figure 17). Designing environments that

foster meaning isn’t easy because what makes life worth living is intrinsically personal,

but design decisions that should be avoided are more universal. At the top of this list,
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unsurprisingly, is meaninglessness. Meaninglessness causes bizarre and frightening

expressions such as mutism, emotional shutdown or severe mental illness

(Golembiewski, 2009b, 2012b; Reach Out, 2009; Searles, 1966). As mentioned earlier,

it can also be traced to physiological breakdown as demonstrated by Dr. Hácha’s heart

attack. Meaninglessness must be avoided in all scales from typology to detail. Yet

meaninglessness is ubiquitous in traditional hospitals: Kafkaesque corridors that go on

and on, rooms without windows, machines that make alarming sounds and have

flashing lights (the staff appear to ignore them and never explain what they are for).

Large wards, where patients may feel like objects not people. More important still are

the subtleties of approaches to care: Staff that don’t look you in the eye, don’t seem to

care, or have mean dismissive or haughty attitudes are measurably deleterious

(Gottman, 1996). Unsurprisingly, evidence suggests that the same innovations that

improve health outcomes also improve social relations (L. Larsen, Adams, Deal,

Kweon, & Tyler, 1998). It doesn’t always take much to change these details, and the

differences will be very profound.

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Figure 18: A meercat photographed in the ambulatory waiting room of

the Royal Children’s Hospital, Melbourne. In this project, the archi-

tects (Bates Smart and Billard Leece) up the ante: hospitals can be

places to be enjoyed. (Photo credit: John Gollings.)

It seems ironic, but hospital stays are shortened by better hospital experiences. Thus,

designers are wise to concentrate on making a patient want to stay. The ‘-care’ in the

term: ‘healthcare’ is axiomatic for better health because care supports the amygdaloid/

hippocampal coupling. If the environment says, “everything possible is being done to

help and it’s all going to be okay,” then the scene is set for the ideal health-building be-

haviour and thought patterns to kick in. Furthermore, unhelpful by-products such as cor-

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tisol will be reduced, meaning the endocrine system can naturally regularize.

Ultimately, the healthcare designer has to juggle two narrative concerns. On one hand

vigilance is needed to avoid any typologies, symbols and settings that may be associated

with negative outcomes. On the other hand, the team should look for opportunities to

imbed positive experiences for all the facility users. Not only are all good things ex-

pected to improve the outcomes for patients, but to improve the environment for the en-

tire facility including the staff and guests.

Already some industry leaders are pushing far beyond the statutes and guidelines to

make exceptional hospitals by focusing on the patient and staff experience. Simple con-

cepts like comfort, cosines, joy and aesthetics have had no place in traditional twentieth

century hospitals, yet they are the psychological bricks and mortar of all healthy build-

ings, whether or not they are healthcare facilities. The architects who designed the Roy-

al Children’s Hospital in Melbourne, Billard Leece Partnership and Bates Smart, put in

a giant touch screen – like a huge iPod, for kids to play with. There’s a multi-level

aquarium, a great adventure playground and even a meercat enclosure. CPG Architects

ensured that Khoo Teck Puat Hospital in Singapore departed from the twentieth century

hospital paradigm by introducing an abundance of greenery, fresh air and 100 varieties

of butterflies. The payoff is that patients feel that things are going to be better than ex-

pected, and surely they are right.

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A BROADER APPLICATION OF THE SALUTOGENIC

METHODOLOGY IN MENTAL HEALTH SERVICES

After completing ‘Start Making Sense’ (from page 62), I could see that the salutogenic

methodology may have application outside the walls of the mental health facility, even

for treating mental health disorders. To test and see if it was acceptable to the many

people involved in mental health services delivery, I presented the following paper to

the Australian Rural and Remote Mental Health Symposium in Canberra, 2nd

November 2009. It was subsequently published in the Australian Journal of Emergency

Management, 27(2), 42-47.

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Moving from theory to praxis on the fly: Introducing a salutogenic method

to expedite mental health care provision in disaster situations.

Presented to the Australian Rural and Remote Mental Health Symposium in Canberra,

2nd November 2009. Subsequently published in the Australian Journal of Emergency

Management (2012), 27(2), 42-47.

Abstract

Not a lot is known about most mental illness. Its triggers can rarely be established and

nor can its aetiological dynamics, so it is hardly surprising that the accepted treatments

for most mental illnesses are really strategies to manage the most overt symptoms. But

with such a dearth of knowledge, how can worthy decisions be made about psychiatric

interventions, especially given time and budgetary restrictions?

This paper introduces a method, extrapolated from Salutogenics; the psychosocial

theory of health introduced by Antonovsky in 1987. This method takes a normative

stance (that psychiatric health care is for the betterment of psychiatric patients,) and

applies it to any context where there is a dearth of workable knowledge. In lieu of

guiding evidence, the method identifies reasonable alternatives on the fly, enabling

rational decisions to be made quickly with limited resources.

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Figure 19: The principles of salutogenic theory based on the model by

(Antonovsky 1987).

An emergency psychiatric response is the sort of time critical intervention that might

not be well informed by enough evidence to proceed quickly but must regardless.

Whatever the nature of the emergency, it is the very nature of catastrophe that they

catch people unprepared; in recent history we’ve seen bushfires, floods, earthquakes,

tsunami’s, storms, volcanoes, landslides and winds the events are diverse in nature, but

the effect on people is consistent and devastating.

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Figure 20: The San Francisco Earthquake. Source: Records of the

Office of the Chief Signal Officer. (1906) National archives and Rec-

ords Administration (Public access).

It is the nature of emergencies that they are sudden and catastrophic (Galambos, 2005).

A swift turn of events means that some people lose their lives and other lives are put on

tenterhooks. The initial damage tends to be physical and material, but mental health

issues follow close behind. Whatever the emergency event: be it tsunami, bushfire,

storm, flood or earthquake, the initial impact of the disaster only spells the beginning of

the catastrophe. Because of supply interruptions provisions for basic needs such as

communication, shelter, food, sanitation and water as well as health services and social

networks, matters tend to deteriorate after the initial shock. It is at this early stage when

mental health issues begin to compound a disaster.

It is a conceit to think of mental and physical health as separate issues. Although they
21
are distinct, the two are intimately related. One will exacerbate the other . That is,

21
This is true in situations where the emergency was an unusual occurrence. In

situations where emergencies are regular and expected, such as in the North East of

NSW, which is subject to frequent flooding, events cause some psychological stress, but

probably don’t trigger mental illness as such. (Little 2009)

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mental stress tends to make physical illness worse and vice versa. For this reason it is

imperative that service providers address mental issues as quickly and appropriately as

possible after a catastrophic event, just as they will food, shelter and sanitation.

Delays in the provision of all forms of emergency care can be caused by indecision

about what is suitable action. The question of appropriateness always calls for

normative decisions based on subjective opinion – and those opinions are difficult to

justify in life and death situations – especially when providing a limited resource to one

person might mean someone else will go without. The outcome, sadly, is that decisions

sometimes aren’t made and this only makes matters worse. It is for the psychological

comfort of the decision makers that they (we) want to rely on evidence to make

decisions. Evidence based decisions are easily justified and move the burden of decision

making to scientists elsewhere. And fair enough. There’s little doubt that empiricism is

the most suitable way forward in the circumstances where empirical evidence exists and

is available at hand (Galambos 2005). This is, sadly, rarely the case.

The scientific method is very specific and conclusions can only be proven if they are

drawn in isolation from any confounding variables that might otherwise influence the

data. Not just is this clinical approach divorced from reality, but also more significantly,

the findings tend to be incremental and as such there isn’t enough empirical data to

answer most basic real world problems. I am an architect and I specialise in mental

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health design 22. Like emergency services provision, there is a huge onus on evidence

to generate any innovations in this area of the profession. As with emergency services

provision, evidence is time consuming to locate and analyse, and in many cases it turns

out to be irrelevant in any case. There are few clients who are willing to encumber their

design bills with much time for research, and yet, decisions need to be made constantly

because architectural problems are incredibly consequent. One minor change here will

affect something else elsewhere. Like the problems that face providers for emergencies,

the problems we face are incredibly complicated and open ended, often with no clear

solutions. Thus we usually have two ways forward. To continue to do things the way

they have always been done – even if we suspect those methods are dated or plain

wrong. Or we have to take risks and improvise. But I have been faced with these

problems and have tried both methods and found them both deficient – So I developed a

methodology that allows reasonable decisions to be made on the fly. And the same

methodology can be easily adapted to enable quick and appropriate decision making for

various logistical tasks in emergency situations.

22
I also have some experience with emergency services provision; I was part of

Bangun, a UNSW effort to assist survivors of the 2004 Boxing Day Tsunami.

(Golembiewski, Ho & Wong 2004)

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Firstly it is important to understand that every provision means the denial of something

else because resources are always limited in some way. It’s like going and ordering at a

restaurant. Out of the twenty dishes presented you’ll only get to choose one. If the

choice is yours, there’s a fair chance it will be the best choice. If the choice is left to

someone else – your spouse for example, you might be disappointed. The defence that

‘beggars can’t be choosers,’ is unhelpful. It is not the spirit of fine dining to be classed

as a beggar! Significantly, the more victims of emergencies can be spared a similar

attitude the better.

Aaron Antonovsky’s salutogenic theory (1987) demonstrated that the distinction

between sickness and health is indistinct and a person’s level of well-being will be

somewhere on the continuum between death and a theoretical state of perfect health.

Antonovsky found that a person’s state of health reflects a person’s sense of coherence.

The more a person feels they understand and make a contribution to the world around

them the stronger their resistance to illness.

Antonovsky breaks down a sense of coherence into three domains of importance. A

strong sense of coherence is supported by feelings of comprehensibility, manageability

and meaningfulness (Jan Golembiewski, 2010b) (See p.62 q.v.) Ultimately a SOC

builds a dynamic feeling of confidence that one’s internal and external environments

are predictable and that there is a high probability that things will work out as well as

can reasonably be expected (Bahrs et al., 2003). These categories can be extrapolated to

find easy application in emergency situations as a salutogenic method. When applied to

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emergency care, comprehensibility is the matter-of-fact understanding of the

situation a subject finds him or herself in. In a disaster situation this can mean

information: who, why, what, where, how and when. Manageability, the next of the

principles of salutogenic theory extrapolates to mean action and empowerment and in

an emergency situation it will be the things that enable survival, things like food, water,

communication, shelter and things that can be done to lessen the impact of the disaster.

Meaning is the most illusive of all the salutogenic principles, yet it is in many ways the

most important. Meaning always comes into question during disasters, yet it is the

hardest issue to address. Meaning is the subject of the big question; “but why?” If

meaning can be sustained, then survival in the most difficult and horrific circumstances

becomes possible (Frankl, 1963). This kind of survival gives others hope. It is the stuff

of miracles, and it through these miracles that meaning is fostered in others.

A salutogenic methodology for emergency care ensures that the best interests of the

victims of disasters are always maintained with a holistic perspective, even when

dealing with the minutiae of service provision. It is an approach to understanding the

individual’s needs holistically and in such a way that the effort isn’t likely to interfere

with the psychosocial needs of the subjects. This method is intended to be used by

communication officers through to people at the cold face because it is simple to

remember and easy to apply. It’s just a matter of keeping three things at the forefront of

mind: Comprehensibility, manageability and meaningfulness, and having an idea of how

these concepts work on the ground. With more complex projects (such as architecture or

emergency service provision,) each decision can be analysed with respect to the three
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salutogenic categories to see how elements relating to a sense of coherence can be

incrementally supported. It is important to remember that this method is designed for

use on the fly and mistakes are okay, to make an error of judgement using a salutogenic

theory is better than having no theoretical basis whatsoever.

Comprehensibility is maintained when people are kept abreast of what’s

happening. In the case of the Victorian fires, there was a need for information about

where the fires were heading and at what velocity. Information is also needed about the

emergency response. When will help arrive? People need to know who is dead and who

survived. They need to know about the safety of their family, friends, pets and livestock.

They need to know if their homes are in danger or if there is anything left of them.

These are all very profound issues and quality information is an extremely important

tool for the maintenance of a sense of coherence. The inverse is also true. Rumours and

lies are harmful (Freyd, Klest, & Allard, 2005). And so too can be ‘shielding’ survivors

from the truth (although this is a complex issue in itself because the truth is rarely

definitive and hope must also be maintained as much as possible.) It might be really

tough to tell a mother that her child has died, but if it is absolutely and unavoidably true,

there is no protecting her from that fact. Yes, sympathy is called for and it might be ‘the

last straw, ‘ but it is an inevitable last straw, and at the very least it shouldn’t come with

added ugliness from deceit and distrust (Meyer, 1969).

When information is given in an emergency, accuracy and honesty is imperative. Under

promising allows expectations to be exceeded, carrying a strong message of hope and

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that everything is working out as well as possible. Disappoint on the other hand might

be taken as betrayal. The art of making promises has implications for higher levels of

coherence. When stressed, people might be excused for making unreasonable demands.

They might, for instance, extract promises that are difficult or impossible to keep. Who,

after all, wants to deny someone who is desperate and might have his or her life in

danger? Who wouldn’t prefer to lie and say, ‘don’t worry. Everything will be fine?’ But

a hastily made guess that ‘someone will be there to help in a couple of hours,’ can start

doing damage at 120 minutes and 1 second (Alomes 2009). The reason is because the

promise suddenly becomes questionable, and at his point meaning starts to erode

(Golembiewski, 2009a, 2009b).

Whether it is the provision of food, water, shelter, blankets or medical services, most

aid and emergency provisioning focuses on improving manageability – usually

helping people to help themselves. Its critical, but the obviousness of this area of

concern tends to dominate emergency provisioning. Needs – physical ones are the

squeaky wheel of emergency care. Information and material support enables people to

act. And when people act, and feel that they can do something, their overall sense of

coherence improves. This is good for health outcomes, and having people move from

stunned/disabled mode to being an active participant in the rescue effort means another

hand (with local knowledge) at the helm.

The absence if the things that make life manageable has obvious consequences,

although they are not as significant as we tend to assume. Lack of food, water and
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shelter will be a source of stress that will make outcomes worse, but with meaning and

comprehensibility needs looked after, people can go a long time without basics. As

Frank Lloyd Wright famously said, “give me the luxuries of life, and I’ll gladly go

without the necessities.”

Meaning is the most difficult aspect of the salutogenic theory to understand and to

provide for, but it is nevertheless the most important. Meaning is the glue of life. It

is what makes lives whole and fulfilled. In psychotherapy, it is only when our life’s

narratives are revealed to be meaningful that there is release and resolution (Clarkson

2006). Meaning is the force that binds social groups together and is a major purpose of

religious belief (Durkheim, 1975; Obeyesekere, 1981). All aesthetics, literature, art, and

all other ubiquitous abstracts of human endeavour relate to and contribute to meaning.

Meaning gives people the power to withstand inhuman conditions, starvation, illness,

and extreme conditions (Frankl 1963). There are theories about why and how meaning

gives people such tenacity, but it is not the purpose of this paper to go into these debates

(For more information, see (Golembiewski, 2011a, in review-d) (see article on p.204).

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Figure 21: Meaning trumps concerns for hunger and comfort. Source:

Ponting, H. (Rights expired).

Whilst meaning is associated with arts and the complexities of culture, there is no

suggestion that reading poems will be of any use to someone who has just lost their

family in a bushfire (on the other hand, it might happen to be just what’s needed!) In

emergency situations meaning can be defined as whatever is of critical importance to

the subjects. It means concern for life, for the people they care about, and sometimes for

significant cultural constructions like religion, history and tradition. Meaning is what

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creates the desire to stay alive. And the desire to stay alive keeps people alive. Meaning

comes from anywhere and everywhere, but there are some sources that are especially

potent. Sometimes the emergency effort itself can contribute meaning; after all, being

needed is a big one. Emergencies are situations where the people who are needed, are

needed to the extreme. Thus involvement in the rescue operation is a good way to help

people through their grief and hardship. This is true to the extent that fire-fighter’s have

commonly been found to be arsonists, lighting fires, so they can fight them and feel

significant as humans. By fighting fires, the arsonists found camaraderie and intense

personal narratives, both of which are critically important contributors to a sense of

meaning (Australian Institute of Criminology, 2005).

Under normal circumstances meaning is a stable constant for most people. It waxes and

wanes a bit, but in circumstances of extreme displacement it becomes mobile. Meaning

is based on a personal ontology – a holistic foundation of connections, meaningful

associations and distinctions and narratives that are created throughout a person’s entire

life. As things are found to ‘make sense’ they contribute to this holistic body of

knowledge and order. And things that don’t make any sense and cannot be understood

directly challenge a person’s ontology, causing severe disturbances until everything

makes sense again (Golembiewski, 2012b) (see article on p. 183). In emergency

circumstances meaning can be a double-edged sword. The power of meaning to do good

by maintaining a person’s psyche can suddenly come under fire. The elusiveness of

meaning means that it is particularly susceptible to inversion. Meaning can suddenly

become meaninglessness – especially in extreme circumstances. And meaninglessness

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undermines a salutogenic framework like nothing else can. This causes bizarre and

frightening expressions such as mutism or emotional shutdown (Reach Out, 2009). In

fact, there is every possibility that the atomisation of an ontological framework is the root

cause of every single case of mental illness – especially the psychoses (Golembiewski,

2012b; Searles, 1966).

The capacity for the ontology to flip makes the protection of meaning the single most

important function of the emergency caregiver. The well-accepted model proposed by

Maslow (the hierarchy of needs model,) places meaning as a ‘higher’ need that can only

be considered once the stability of ‘lower’ needs such as shelter or food is established.

This truism is false. Rather it is the ontology the ‘highest need,’ that is the foundation

upon which everything is known. The ontology is the product of self-actualisation.

Without a strong ontology, a person loses the capacity to think, feel, or even act. But

people can go without basic needs or make do indefinitely if the struggle is meaningful.

There is meaning in place and even in the narrative of hanging in there against the odds.

Of course the maintenance of someone else’s body of wisdom and experience isn’t

possible because we still have no means to occupy somebody else’s mind. So how can

we help? We can be on the lookout. As we know that emergencies trigger ontological

challenges we can encourage people to find direction when they most need it. Getting

survivors active and involved in the emergency effort when they look like they might

otherwise take a turn for the worse can be a good idea. We can be encouraging, helping

the survivors of disaster understand that all that is humanly possible will be done and
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that the things will work out as well as can reasonably be expected. It is important,

however not to overplay this, as dashed promises or misinformation are often the

tipping point to despair (Alomes 2009). In catastrophes, the survivors must be allowed

to feel that they can trust the providers and care they are getting. Consider the anger

after Hurricane Katrina when misinformation about looting caused the mobilisation of

armed troops with orders to shoot. The McLeod Commission noted that the greatest

failure of the bushfire response was the misinformation that the response team

disseminated in good faith (McLeod, 2003).

Frequently ontological shifts mean that old spiritual models will be dismissed. In these

circumstances missionaries for various faiths can do a lot of good, even as they prey on

the victims of disaster. Rigid belief systems offer support when it is most needed, like a

crutch, but have a tendency to fail people down the track (Antonovsky 1987). In

emergencies missionary activity can be a double edged sword of its own – often

missionaries are very experienced and generous caregivers who ask nothing in return,

but cultural suitability of service provision is an issue that cannot be overlooked.

Culture is a very important source of meaning and is a context for our life’s narratives.

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Figure 22: Nero fiddles while Rome burns. Quo Vadis. (1924). (Rights

expired)

When Nero famously played the fiddle while his city burned, was he mad or was he

reaching for the thing that gave him meaning and a sense of control at a time of extreme

disempowerment and inevitable death? In emergency situations even empirically tested

and well-accepted theory and information may not apply. Catastrophes both change the

normal order of things and the speed with which decisions have to be made. So it is

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essential that people who are to go out and face emergencies are equipped to make

clever decisions on the fly. An extrapolation of salutogenics (a salutogenic method,) is a

fine tool for such circumstances, because it is easy to guess how little efforts might be

amplified once projected onto a simple salutogenic framework; how does an action

affect manageability, comprehensibility and the sense of meaning? Is the sum force on

the coherence continuum likely to be life supporting or not?

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2. QUESTION TWO: WHAT IS SCHIZOPHRENIA?

This second question is largely answered by a single paper “The Riddle of Psychotic

Perception Revealed…” (p.204).

This section should be read with the following however, because the aetiology cannot

be easily separated from the syndrome. Thus the first papers in the third section “Are

diverse factors proxies…” (p.336-) and “Common Psychotic Symptoms can be

Explained…” (p.358-) should be taken to address both research questions.

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SCHIZOPHRENIA AND PERCEPTUAL EXPERIENCE

The question about the relationships between schizophrenia and the environment are

complex and answers have to be built on both a robust understanding of schizophrenia

and also the built environment. Both are complex in their own right, but lines of enquiry

are further complicated by the unknowable common mechanism: the human mind. In

the case of built form, the idea that buildings are form and space created by people out

of material stuff is very tempting but is only half the story – and probably not even half

because architecture is not only to protect people from bad experience (the weather,

dangers etc.) but also to improve experience.

Experience is a composite process in that it draws on all previous experience to

establish an a-priori framework of understanding. Experience is therefore a unique

analogue process that affects everything we perceive. In as much as our experiential

referents differ, we cannot experience the same space in the same way. It is common to

discuss the quality of experience among friends, precisely because experience is not

universal and yet a social experience is one that is shared. “It’s beautiful, don’t you

think?”

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Even the experience of a single building draws on knowledge that has been gathered on

approach. Short of arriving in a coma, we cannot separate the experience of the interior

spaces from the experiences of the exterior as we draw near. If we arrive with the

building in full view, we have the opportunity to access it typographically. We get a

sense of what it is and what it will be like when it is still a postage sized representation

on the back of the retina. If we arrive in the back of a paddy wagon, we will be

delivered to an unloading bay, and presumably rushed through an uncomfortable and

frightening arrivals process that denies normal opportunities of assessment. We arrive

with the distinct impression that out safety is in immediate jeopardy, because we don’t

know where we are.

Perceptual experience is sequential and composite. Under normal conditions we will see

first, then we will usually see and hear by this stage we will have greater faculties of

sight, perhaps we will get a sense of depth in parallax and perspective. We might also

have a glimpse of some textural qualities. The first sounds will be deep or loud ones.

Later we will smell, then feel and perhaps at some later stage again taste. Although the

opportunities for sight will generally come much earlier than those for smell or taste, the

latter senses do not shut out the first. Perception becomes more complex as it becomes

increasingly polymodal. Complex as polymodal perception is, it is anything but rich

without the backup of a deep ontology.

Physically our perceptual abilities are very limited. Out of the potentially infinite array

of available information, we genuinely perceive only the tiniest sample of the stimulus
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that we are exposed to. Let’s consider the sight, the primary modality for humans. When

we see, we do so over a very limited focal range, depending on how close an object is,

the range might be as short as a couple of centimetres (reference needed). We also only

truly see whatever is in an arc of about 1.5° (E. T. Hall, 1990). This limited information

is restricted to the capacity of the human eye, the fovea allows us to see finest details

but even then we can’t see objects or textures smaller than about 0.1 mm3 without

assistance. The cone sampling rate drops precipitously with increasing retinal

eccentricity (D. Williams, 1986). Furthermore, with increased eccentricity, the lattice

becomes more irregular (D. Williams, 1986). By the periphery, the eye sees very little –

some colour information and a sense of ‘presence’ generally – but not enough detail to

distinguish shapes. Thus the images we receive from the periphery are highly abstract,

and whatever is in the foveal area is specific. Effectively we don’t get to see a lot with

any certainty, but memory and ontology fills the gaps maintaining the sense of

consistency. This reduces the perceptual demands on the brain. We maintain a notional

‘visual image’ of what is behind our heads also. This is maintained by auditory haptic

and olfactory supplementary information. But our other senses aren’t much better. We

hear unevenly – with a better horizontal range than vertical. The human capacity for

hearing tone seldom reaches its limits of 20hz – 17khz. Even then, we can only focus on

one sound at a time. Humans cannot hear volumes less than 1dB and have difficulty

detecting sounds less than 10dB, and even then, those sounds need to be in the middle

of the human spectrum to be heard at this level.

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Ultimately, the information we gather from the environment has little new information

and is supplemented by what we expect already. By ‘expect,’ I mean information that

fits within a normal range of expectations given similar criteria in the past, these

sensory inputs are constructed from meaning, instinct and memory. The mechanism is

identical to the one used to draw meaning from writing and language. A symbolic

representation draws on the ontology to find and express meaning. The sensory inputs

only relate to the physical as a point of reference, like a written word triggers the

meaning response, but doesn’t embody it. (Meaning is only ever an approximation

(Popper, 1970)) Thus architecture, like all else, as it is experienced, exists primarily in

the mind. Occasionally architectural expressions use our relative inability to perceive;

the architecture of adventure rides in theme parks for example. When sight is

suppressed with darkness and sound masked by sound-scapes, the architectural

environment can shift and change in order trigger false a-priori decisions about the

likely narrative – the likely content of the ride.

The sense of concreteness and reality that is associated with architecture obviously has

some reality beyond experience – but my concern is not for what is, but how it is

constructed from our ontological models of physicality, which is confirmed using the

perceptual systems: Constructs of memory, meaning and desire. These intangibles are

highly subject to change, to reinterpretation.

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The riddle of psychotic perception resolved:

the integrated findings of an in-depth analysis

of current hypotheses for schizophrenia.

The following paper presents a hypothesis for schizophrenia that draws together many

disparate strands of evidence. It is currently being read a third time by Psychological

Bulletin, after significant changes to the last draft.

Abstract

After generations of enquiry, and currently around 6150 papers being published

annually (mostly focusing on the minutiae of the syndrome) there is a normative

expectation that the pathogenesis of schizophrenia will never be unearthed.

This in-depth review of all the prominent hypotheses of schizophrenia reveals that none

can account for the heterogeneous presentations of the syndrome, especially one that

‘reaches beyond the categorical definitions to recognize the ‘constellation’ of

schizophrenia features’ as the DSM-IV instructs. But by integrating and developing

these hypotheses (including competing ones like the glutamate vs. dopamine hypothesis

rivalry), the reams of data appear to congeal into a remarkably coherent meta-

hypothesis. For the first time since the DSM-IV diagnostic criteria was published, a

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comprehensive and holistic explanation of all the symptoms and signs (as well as other

findings known to the scientific community) is presented.

The role that the striatal D1/D2 heteromers have in modulating saliency and mediating

both bottom-up and top-down perception is expanded, bearing in mind that the

switching of the striatal D1/D2 heteromers from a low affinity state (D2Low), to high

(D2High) is already putatively the root of schizophrenia. Here links are found that

associate top-down attention with presynaptic tonic dopamine synthesis and the function

of D2High. Bottom-up attention, on the other hand, is given to powerful phasic synthesis

– the action of D2Low.

All attentional modes are essential to healthy perception and the functions that depend

on perception, and as bottom-up attention subsides and top-down attention increases,

eight very closely related syndromes can be identified, each with a distinct presentation

and psychogenesis. These converge roughly into the main schizophrenia subtypes.

The meta-hypothesis that emerges from this review is highly triangulated and supported

by robust published evidence.

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The riddle of psychotic perception resolved:

an in-depth analysis of aberrant salience hypotheses for schizophrenia

By its narrowest definition, psychosis is a delusional and/or hallucinatory experience

(American Psychiatric Association, 1994). Psychosis (thus defined) occurs in a number

of conditions, but when psychotic symptoms are particularly bizarre and enduring, they

characterize the most prominent symptoms of schizophrenia (Schneider, 1959). Next to

schizophrenia, other psychoses simply aren’t as bizarre. The causes of schizophrenia

have never been resolved and debate abounds from disciplines as diverse as linguistics

and genetics about what mechanisms may be involved. A Medline review reveals 6146

articles since last year alone23. All heuristically use normative hypotheses, but these are

fragmented and their findings ad-hoc: they study one facet of the disorder or another

and produce new hypotheses to explain their findings – the few comprehensive

hypotheses are notable exceptions. These are discussed below but their explanations

invariably fall far short of plausibility considering quite how bizarre, debilitating and

heterogeneous schizophrenia is. This paper traverses several prominent hypotheses and

integrates diverse streams of data to present a cogent meta-hypothesis to draw together

all the diagnostic criteria listed in the DSM-IV to a single molecular dysfunction.

1. Topics: schizophrenia, period: 2011-2012

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This model first picks up on a number of perception-based hypotheses. These conceive

perception as an input and behaviour as an output. Psychotic symptoms are thus output

errors, caused by the dysfunction either within perception, working memory, or any

number of other areas of cognition, depending on the model. One class of hypotheses

with an enduring legacy is that symptoms are caused by an inability to filter out

(attenuate) perceptions of little or no importance resulting in a tendency to make

irrelevant observations (Frith, 1979; Gray et al., 1991; Kapur, 2003). More recently, one

of these hypotheses has gained particular attention; because it links dopamine – a

known active agent in psychosis, to the front end of the perceptual process, that is

perceptual saliency (Heinz & Schlagenhauf, 2010; Howes & Kapur, 2009; Kapur, 2003;

Kapur, Mizrahi, & Li, 2005; Schwartz, Wiggins, Naudin, & Spitzer, 2005). In the

aberrant saliency models, a salient event is a perception marked by significance

(something of importance relative to other percepts). In elaborating his hypothesis,

Kapur posits that the importance or saliency of the event is tagged by the stimulation of

the D2 receptors within the striatal dopamine neurons. The tagging process ensures that

selective attention is directed to the percept that has been tagged as important.

Salient events (those that have been tagged as important) should reflect normal

perception and the gamut of common reality as experienced by healthy people.

Dopamine-saliency hypotheses propose that a functional oversupply of dopamine may

harness attention independently of cue and context (Kapur et al., 2005). As an example,

Kapur refers to Bowers & Freeman (1966), who recall a patient describing his

symptoms thus:
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‘I developed a greater awareness… my senses were sharpened. I became fasci-

nated by the little insignificant things around me.’

Aberrant saliency is presumed to cause disorganized thought, hallucinations and subse-

quent delusions. The pathogenesis is explained by a competing hypothesis, which is

similar in many details: Fletcher & Frith’s Bayesian attenuation failure hypothesis

(2009). In this model, normality is a state where familiar events go unnoticed – in other

words they are attenuated. That is, people get so used to normality that they fail to no-

tice it. However, when there is an attenuation failure, normal experiences appear uncan-

ny, and essential cognitive processes are aborted and left unresolved. Essentially Kapur,

Fletcher & Frith are in agreement here.

While the prima facie evidence appears to bind dopamine, saliency and psychosis into a

tight relationship, these hypotheses are bereft of details and need exploration. This is

especially important because the hypotheses are used to advocate specific treatments

and account for serious conditions such as schizophrenia. But before we can discuss the

implications of a dysfunctional system, a better understanding about the nature of the

healthy system is needed, and for the purposes of this article, four research questions

have been posed.

Firstly, we need to ask exactly what saliency is. How much do we know about the

neurological and perceptual processes involved in directing attention to important

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information? Only once these questions have been covered, can we ask questions that

are more pertinent to the aberrant saliency model.

Secondly, if aberrant saliency is the basis for florid psychotic symptoms (hallucinations,

delusions, etc.) as both Fletcher & Frith (2009) and Howes and Kapur (2009); Kapur

(2003); Kapur et al. (2005) assert, then what are the deficit symptoms – the distinct lack

of responsiveness that was once thought to be at the core of the schizophrenic diagnosis

(Bleuler, 1950; Parnas, 2011)?

Thirdly, must aberrant salience (the mis-tagging of important events) equate to over-

stimulation – or even dopamine oversupply? Certainly, this is what Fletcher & Frith and

Kapur both propose (Fletcher & Frith, 2009; Kapur, 2003; Kapur et al., 2005), yet about

a third of schizophrenia cases don’t respond to dopamine antagonists (H. M. Jones,

2004), and how can this be explained?

Lastly, is aberrant saliency restricted to saliency, as the concept is traditionally defined?

That is, solely to stimulus-led perception, or does it also affect intention-led perception?

In other words, does it only affect attention that is stimulated by bottom-up, unsought

stimuli – or are there other events that may also trigger saliency responses - even when

stimuli are not unanticipated?

The answers to these questions will help us not only to better understand schizophrenia,

but will shed light on the processes of perception more generally.

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Healthy salience

The concept of salience is based on the assumption that we selectively attend to a

limited number of competing streams of information by filtering out or de-prioritizing

irrelevant information (Milstein, Dalley, & Robbins, 2005). In this general framework,

saliency is the measure of the influence that a singleton (a technical term for a single

potential percept, prior to it actually being singled out and declaratively perceived) has

in gaining attention. At most, a single percept can dominate thought. It can, quite

literally, ‘take possession of the mind’ (James, 1890, p. 404). At a minimum, the percept

may remain latent; that is, beyond the threshold of declarative consciousness

(Duckworth, Bargh, Garcia, & Chaiken, 2002; Hassin, Bargh, Engell, & McCulloch,

2009; Hassin, Bargh, & Zimerman, 2009). In between these two points, a singleton

might make a partial incursion on working memory, occupying one or more ‘places’ of

what is often reckoned to be a limited capacity system. (The capacity is dependent on

the model for working memory that you find most compelling. Most models allow four

to seven items in active awareness (Cowan, 2005) and others extend working memory

to a further ‘behind the scenes’ implicit level of awareness (Baars & Franklin, 2003;

Hassin, Bargh, Engell, et al., 2009).)

The factors of saliency

Saliency refers to those properties of a singleton that attract selective attention – that is

the directed awareness of the perceiver. But saliency is not a unitary concept. In vivo

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studies of monkeys reveal that at least three factors will capture attention

(Golembiewski, 2013) (Article reprinted from p.126). Because all three are referred to

as salience, a new taxonomy is proposed to distinguish exactly why information is

tagged as important:

Prominence

High contrasts of the singleton against the setting (noisy, sudden sounds, flashing lights

and bright colours etc.) are highly prominent and demand reaction (Ljungberg et al.,

1992). As a subject learns about the presence of a prominent object, the initial burst of

saliency immediately begins to wane - eventually to the point of extinction (Berns et al.,

1997; Mirenowicz & Schultz, 1996). It appears that prominence is moderated

automatically through the glutamatergic and cholinergic neurotransmission systems

(Carlsson, 1995; Corringer, Changeux, Bronner, Edelstein, & Smit, 2008) these then

gate the secondary dopaminergic system (more about that below).

The kind of arousal that prominence evokes is highly automated, instinctive and is

central to orientation reflexes (Ward, 2008). This form of salience must be non-

cognitive because it generally survives states of hypoarousal such as vegetative comas

(Laureys, 2005; Schiff et al., 2002) it will also activate both excitatory and inhibitory

synapses of layer 2/3 of pyramidal neurons even in vitro – the result being a rhythmic

oscillation in the gamma frequency – one that is widely recognised as relating to

sensory processing (Feldmeyer, 2010).

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Significance

This form of salience is highly cognitive. It is the potential importance of the concept

(schemata) that is being recalled. There are three things that increase the significance of

a singleton: a) anything that helps build meaning, b) anything that contributes to

understanding, and c) anything that may needed to sustain existence (Jan

Golembiewski, 2010b; Golembiewski, 2011b) (Articles on p. 62 and p.296 q.v.) In other

words, we react to perceptions that are significant concepts, not only prominence.

Worth

Salience has a pre-cognitive affective or hedonic bias (Barrett & Bar, 2009). Monkeys

responded to stimuli according to their desirability. The promise of a rewarding

experience generates a much greater impact than the threat of a negative one

(Mirenowicz & Schultz, 1996; Schultz, 1998). Worth should further be broken down

into affective and hedonic subcategories. Affective worth is how a singleton makes you

feel, whereas hedonic worth relates to an expectation of reward or sensual punishment.

Worth appears to be mediated by the amygdala, and its function appears to remain

either intact or slightly under engaged in schizophrenia (Anticevic et al., 2012; Becerril

& Barch, 2010). This contrasts with affective psychoses like bipolar disorder, in which a

large body of literature reports over-engagement of the amygdalae (S. B. Perlman et al.,

2012).

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A fourth saliency factor should also be added to the list. This factor was not identified

using the same series of animal experiments, possibly because it is peculiar to healthy

humans.

Opportunity

This is response to stimuli just for the sake of it, sometimes just because we are active

beings and need to do something. This is engagement – just for sensory variation, for

stimulation, but not necessarily for affective or hedonic gratification. It seems that no

other animals have a go at things without good reason or choose to avoid a favourite

food, just to try something different. Such behaviour is very compelling for humans, and

is therefore undeniably salient on some highly intellectual level, yet it doesn’t fit into

the categories mentioned above. Nor does it behave the same way: opportunity is

engagement with experience; it is not led by saliency cues and is not normally coercive

(except perhaps as it builds habits through Hebbian processes). Opportunity is the

salience of choice. The choice to try something off-putting, for no reason other than the

fact that it’s possible.

The modes of perception and attention.

The psychological canon allows for two modes of selective attention (see Table 2.)

There is top-down attention, which is the deliberate focus of declarative resources; and

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bottom-up attention, which refers to the attention that is brought to a subject by the

interruption of top-down attention. As attention turns to attend to the interruption of an

unexpectedly salient singleton, top-down intent changes. We abandon our prior

engagements and focus on the rude intruder. What is it? Does it have relevance? How

does it fit into what I know (the ontology)? If the transfer of focused attention to a new

stimulus is automatic and unavoidable, then intent plays no part and is thus called

bottom-up (Theeuwes, Atchley, & Kramer, 2000). This use of the term ‘bottom-up’ is

thus a bit ambiguous, because it refers to the top-down attention that is given to bottom-

up stimuli. To resolve this ambiguity the terms listed in column 2 of Table 2 are used.

Canonical Mode Action Saliency factors

term
Raw Potentially fills perception with undefined Prominence (stimulates
richness. gamma band inhibitory
Bottom-up/ feed-back

and excitatory
oscillations) and if
strong enough, NDMA
triggers the D1
receptors
Bottom- Identification and experience of novelty, Prominence: mismatch
up aberrance, data mismatches. detection (when D1 has
been already activated.)
Worth (negative) – not
dopaminergic
•General engagement, occupation of interest, Opportunity
Top-down/ feed-forward

turns opportunities into actions and brings

Active

attention to bottom-up stimuli that are neither

anticipated, nor beyond the range of probability.
•Brings attention to ‘non-critical’ interests such
as aesthetics.
•The basis of most experience.
Top-down Recognition of expected targets, data matches. Significance
‘The bingo’ experience. Worth (positive)- not
Experience that is intended or worse than dopaminergic
anticipated.

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Table 2: The modes of attention. Introducing a new taxonomy. The

canonical terms: bottom-up and top-down both miss the basis of most

experience, and the term ‘bottom-up’ is unclear about whether it re-

fers to a precognitive or cognitive phase of perception.

Raw attention

If there is such a thing, in its purest form, bottom-up attention must be a non-cognitive

observation of unprocessed perceptual stimulus. Theoretically, in this raw state, nothing

could be salient, because it would completely lack any kind of definition or ontological

associations. Even so, automatic bottom-up attentional processes continue to monitor

prominence, even during vegetative states, anaesthesia, deep sleep, and in vitro

(Feldmeyer, 2010; Laureys, 2005; Schiff et al., 2002) implying that this raw data feed

bypasses cognition. This form of bottom-up attention is referred to as raw attention.

Bottom-up attention

The cognitive attention given to anything that is not driven by intention, such as

prominence and negative feedback, is widely known as bottom-up attention.

Singletons that are picked up by bottom-up attention are those that stand out as different

from expectations (for example, you crack an egg and it smells bad – you weren’t

expecting it, but you notice). In bottom-up attention, saliency is primarily a response to

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the unexpected, the undefined, misplaced and unanticipated, in other words mismatches

between singleton-data and related schemata; Functionally this means that bottom-up

attention is a response to difference and novelty, and this is how the term is normally

used (Theeuwes et al., 2000).

Mismatch identification appears to be a Bayesian process, meaning that singletons are

noticed when they don’t fit expectations, and are otherwise ignored (Clark, 2012 - in

press; Friston, 2003; Stephan, Penny, Daunizeau, Moran, & Friston, 2009). In another

body of literature, another feedback mechanism called error related negativity (ERN) is

also proposed. This is a feedback loop specifically for negative affective or negative

hedonic feedback – ERN occurs when an event is worse than expectations (Falkenstein,

Hohnsbein, Hoormann, & Blanke, 1990; Holroyd & Coles, 2002). ERN is Bayesian too

– but it isn’t driven by bottom-up attention because the negative event happens within

the general range of expectations – ERN therefore fits in another category: active

attention. An example of a bottom-up Bayesian mismatch detection is when you see a

red poppy in a green field or a tiger on your lawn, the former is inconsequential, the

latter critical.

Bottom-up attention isn’t only given to external stimuli; it’s give to any unanticipated

stimuli. Bodily (somatogenic) signals like hunger, tiredness, pain etc. would normally

stimulate endogenous bottom-up stimuli because they are unsolicited: we do not usually

ask ‘am I hungry, tired or in pain?’ because we will feel hungry or tired spontaneously.

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Initially these signals are received using raw attention, but are modulated with bottom-

up attention.

It must be noted that top-down attention can be directed to somatogenic stimuli,

therefore while somatic and other bottom-up experience is normally bottom-up, it may

occasionally be modulated by top-down intention.

Top-down attention

Top-down attention is the mode of attention where percepts are anticipated. For

example, if I am hunting for truffles I ignore stones, but when I see something that

matches my expectation of a truffle, it will elicit recognition salience: a ‘bingo!’

response. The top-down mode of attention has an exclusive domain of interest: the

known. It is only concerned with recognizing significance saliency and only the

correspondence between a singleton and expectations (Coull, 2005). Unlike bottom-up

attention, top-down attention is not Bayesian, because of its tight focus. Because top-

down attention assesses only matches against intentions, top-down attention yields only

positive feedback (you don’t have an interest in things that you weren’t looking for –

these can only be noticed by other modes of attention.) This sets up a confirmation bias

(Nickerson, 1998). Things that are actively sought trigger top-down recognition

reactions easily, yet negative outcomes are referred to the bottom-up system, and will

only be regarded if it is salient in its own right (usually prominent) or significant in

some way.

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There are two levels of top-down attention; focal and incidental. If we want to do

something, we may focus on it intensely, in which case intention is highly deliberative.

In such cases saliency is only used for positive feedback. On the other hand, the

attention we give simple and well learned tasks is incidental. Here top-down attention

that is incidental is reclassified as active attention.

Active attention

When a bottom-up singleton interrupts a deliberate (top-down) action, it comes as a

distraction. But such encroachments are not regular (and may even be rare, depending

on one’s lifestyle) because they depend on bottom-up stimuli, which may or may not be

present. Despite this, we are not totally driven by intent (as other animals might be). In

real terms, for humans, there is a large and undefined grey-area that separates the top-

down and bottom-up modes of attention. If bottom-up attention is limited only to

detecting prominence, and top-down attention covers only significance, then what of the

rest? What of ERN? When things are noticed when they are worse than expectations but

are generally within the range of unconsidered probability – such as when someone

reaches into a fire and gets burned? Another whole range of experience is awareness on

the edge of latent automaticity, which is nevertheless still noticed. When we do any

routines we know well – such as drive, we do so automatically for the best part, yet we

remain more or less aware as we do so.

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There are many opportunities that we choose to engage in, just because they are there.

Likewise, events are noticed but neither because we are looking for them, nor because

they are prominent. Active attention is a term to describe the middle ground between

bottom-up and top-down. It may be environment led, yet without the sharpness of

novelty. Active attention is where top-down intention directs a ‘fuzzy’ search or where

bottom-up attention reveals something that you had an interest in, but had not been

looking for. Active attention is not driven by saliency, and isn’t a mode of attention in

its own right, but complex combinations of bottom-up and top-down processes, which

are led by habits of engagement, by choice and simply by the availability of resources.

And as such, active attention doesn’t sit comfortably with the assumed dynamics of the

canonical model of attentional salience.

Attention is an expansive resource that doesn’t retreat and become passive when it’s not

engaged in any clear intent or with salient environmental stimuli. If anything, the

opposite: Active attention is the awareness that accompanies the continual activity of

the mind and body, on the lookout for something to do, to experience and to think

about. Indeed, studies have demonstrated that when environments are depleted of

natural stimuli and opportunities for active attention, even healthy people start to

hallucinate them (Grassian, 1983; Weckowicz, 1957) or fabricate them using whatever

material is available – even human faeces (Osmond, 1958).

The behaviour that takes place around active perception is largely automatic and

involves stereotypical actions that are associated with whatever an object suggests – or
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affords the perceiver, thus objects of engagement are called affordances (Gibson, 1979;

Withagen et al., 2012). An example is when you find yourself eating a cookie that you

found when doing something altogether different. It wasn’t an intentional act, but

neither was it unintentional, it was just automatic.

Active-perception is very basic and instinctive because it links opportunity directly to

action and in evolutionary terms, this is the primary role of perception. Simple creatures

must act according to opportunities offered to them, but they don’t have the cognitive

apparatus to intellectualize or otherwise make that action declarative (Bargh &

Dijksterhuis, 2001). Active perception is evident in children too:

‘From birth, babies will actively engage with the perceptual environment. They will

imitate expressions (Meltzoff & Moore, 1977), grasp a graspable object, and with age

they will want to touch textures, run fingers down Brancusi’s sculptures, absorb

themselves in colours and scents, feel the curvature and warmth of surfaces, immerse

themselves in tastes, experiment with sounds, etc. They will want to squeeze bubble-

wrap and juice cartons, just to hear them pop. They light sparklers to see the sparks fly

off in all directions; they burn incense to scent the air, and climb snowy mountains, just

to feel the rush of zooming down again.’ (Golembiewski, 2013) (p. 126 q.v.)

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Parallel model of bottom-up and

top-down selective attention
Salience
Prominence
!
Bottom-up
Significance attention
★

Worth
Top-down Working
Intention attention memory

✓
Feedback

An integrated model of active attention

Salience

! Prominence Active
awareness
★ Significance Working
memory
BU
☺ Opportunity TD
Attention
Worth + –

Figure 23: Here the traditional parallel model of attention is con-

trasted with an integrated model that incorporates active attention.

Saliency is mediated by the active nature of awareness, not by a prop-

erty of the stimulus. Saliency isn’t unitary as commonly thought either.

The various factors of saliency show different patterns of behaviour

although they ultimately end up using a top-down or bottom-up path-

way to achieve declarative awareness.

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Systems that depend on attention

Perception is the most tangible link between the shared reality and personal experience.

A lot depends on it and this brief section cannot even address all the facets of the psyche

that are affected by attentional dysfunction, much less do them justice. Even so, it’s

important to sketch out the interconnected systems of perception, automaticity, the

sense-of-self and learning are needed because the most characteristic symptoms of

schizophrenia can be explained as dysfunctions of these downstream functions all of

which require attentional salience to function (see Figure 24).

The ontology
(schemata)

Sense-
Automaticity Learning
of-self

Perception
Hebbian antiHebbian
(‘dumb’) (considdered)
learning learning
Raw
perception

Figure 24: Perception is informed by new raw data and also by

learned schemata stored in memory (the ontology). This is constructed

using a ‘dumb’ but efficient Hebbian processes ‘cells that fire together

wire together’ (Shatz, 1996). New knowledge isn’t learned this way,

but associations are strengthened. This process creates the automatic

ontology – processes that can be enacted without much consideration.

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New knowledge is processed through anti-Hebbian processes in which

aberrance is detected and considered thoughtfully. The whole ontolo-

gy is used to process all perception, but the ontology itself is opaque –

it is perceived as something else – ‘the self’.

Perception

Even with robust attentional salience, perception is never perfect. Raw perceptual data

is filtered and interpreted by our gross perceptual mechanisms. The sensory world is

experienced through the available senses, so it is neither directly nor fully experienced.

Human sight is the experience of reflections or luminosity of a narrow bandwidth (400-

790 tHz) of vibrations, 1-400 tHz is experienced as warmth (Gibson, 1979; Matlin,

1988), and the 17Hz-17kHz range as sound and pressure (Moore, 1997), but bats hear

frequencies up to 115kHz (Heffner, 1983) and guppy fish can see light down to 300tHz

(E. J. Smith et al., 2002). To sense these and other frequencies, humans have to use

specialized equipment (such as radios or hyperspectral cameras), which translate

frequencies into our native sensitivity range of visible light and audible sound.

The next task ‘of the brain… can seem impossible: it must discover information about

the likely causes of impinging signals without any form of direct access to their source’

(Clark, 2012 - in press, p. 6). Sensations must be iteratively interpreted and experienced

through cortical processes. Information from the sensory organs travels to a series of

perceptual cortices which process information of increasing complexity and abstraction.

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The later cortices (such as V4 and V5) are globally integrated to enable the processing

of unknown, unpredictable and abstract stimuli. All the senses have lower-order

processing areas and share the higher order ones – although even primary inputs are

shared to some degree (Foxe et al., 2002).

A bottom-up process is required to modulate raw perceptual data of the environment

(including the body), but these stimuli can only be known and used in translation; that is

through the top-down process of learning: decoding and recoding, creating and

remodelling schemata. The heavy reliance on top-down processes doesn’t mean that

what we experience isn’t real – but it does mean that experience is highly mediated and

a partially inferred best guess (Sanders, 2004). The implications of this are broad:

1. The fact that all perception is in some way translated into electrical and chemical

impulses before it is reinterpreted as sensory perception should modify the way

we understand hallucinations. In a profound way, all we know is, in some way

hallucinated. I don’t suggest that healthy experience is just as unreal as

psychiatric hallucinations, but wish to point out that the qualifier of

‘hallucination’ is the departure from common and grounded sense of reality, and

not the extension of experience into fantasy.

2. Perception will be distorted if the ontology (which informs perception) is

dysfunctional.

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3. The ontology is informed by personal experience, structured into schemata

(including lexical schemas) and is fact-checked through a cultural lens. These

form the basis of perception. This is reflected in the DSM-IV:

‘Ideas that may appear to be delusional in one culture (e.g., sorcery and

witchcraft) may be commonly held in another. In some cultures, visual or

auditory hallucinations with a religious content may be a normal part of

religious experience (e.g., seeing the Virgin Mary or hearing God's voice). In

addition, the assessment of disorganized speech may be made difficult by

linguistic variation in narrative styles across cultures that affects the logical

form of verbal presentation.’ (American Psychiatric Association, 1994, p. 285).

4. The imperfect match between perception and experience means that all people

have the capacity to be fooled by what they believe they perceive. This leads to

one of the most commonly accepted hypotheses for hallucinatory experience –

the illusion-hallucination continuum (eg, Brébion et al., 2000; Frith & Done,

1988; Harvey, 1987; Johns et al., 2001). While direct studies of this

phenomenon do demonstrate significant illusion/hallucination correlations, and

therefore a possible role in psychosis, the effect size is still too small to explain

psychotic symptoms (Aleman, Böcker, Hijman, de Haan, & Kahn, 2003;

Woodward, Menon, & Whitman, 2007).

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5. The higher the reliance on top-down and active attentional processes are (that is,

the higher the top-down vs. bottom-up sampling rate is), the more likely that

perception will be distorted from reality, because sampling loses its fact-

checking facility and negative feedback tends to get ignored, creating a

confirmation bias. This perspective is known in philosophy as the intellectualist

position (A. D. Smith, 2007).

Theorists who take an intellectualist stance on perception have an easy time

understanding hallucinatory experience, because, for them the problem is resolved by

asserting that top-down attention leads perception, therefore, a dysfunctional top-down

attentional system will cause hallucinations. These models don’t acknowledge the

possibility of direct perception. Intellectualist models only outline the higher order

experience of knowing (a top-down function): they understand perception as a cognitive

process that employs raw perception only as feedback.

Current intellectualist models argue along the following lines: The brain is modelled as

an organ that assigns meaning to raw perception. On one hand, raw perception is

sensed, but sensory information remains meaningless until it is associated with

schemata within ontology. Clark (2012 - in press) and Fletcher and Frith (2009)

emphasize that this follows an anti-Hebbian, Bayesian logic in order to maintain

efficiency. In their models, singletons are only noticed when they are aberrant, at which

point learning must take place. Grossberg (2009) is interested in the cytoarchitecture of

perception. His model is Hebbian and distinctly not Bayesian, but is no less
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intellectualist. He proposes that the very laminar structure of the neocortical neurons

match raw data to schemata by matching predictive representations of the world with

raw bottom-up stimuli. The model Grossberg proposes is that neither top-down

intentions nor raw bottom-up stimuli will trigger a neuronal excitatory reaction

(recognition salience) on their own, except in psychosis (Grossberg, 2003b). It is when

two inputs: a tonic top-down intention and the other, a raw bottom-up singleton come

together, that a saliency signal is transmitted horizontally (from one neuron column to

another) through dendrites and vertically (to other brain regions) through axonal

connections. In this model, intent quite literally works in a top-down fashion, because it

stimulates the first layer of the neocortex. This tonic stimulation primes perception to

receive appropriate input. Bottom-up perception works the opposite way around, from

the sixth layer upwards. This tonically primes the neuron too, but the excitatory

potential of the neuron is only achieved when both top-down and bottom-up stimulation

occurs.

On their own, intellectualist approaches are limited. A distinction is not made between

knowing and experience. Intellectualist approaches must face a very valid criticism; ‘I

think is not I am, unless by thought I can equal the world’s concrete richness.’ (Merleau

Ponty, 1943), This is not a critique of the reductive efficiency of Descartes, Bayes,

Hemholtz or their inheritors (like Clark, Fletcher, Frith, Friston or Grossberg), but a

critique of the lack of richness of experience that such approaches imply.

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As it happens, an automatic form of perception continues when top-down attention

ceases, even in conditions such as a vegetative coma (Laureys, 2005; Schiff et al., 2002;

Zeman, 2003), when sleep-walking (Plazzi, Vetrugno, Provini, & Montagna, 2005) or

even in vitro (Feldmeyer, 2010). This means that raw perceptual processes are

independent of any form of top-down attention, confirming Grossman’s assertion that

attention and perception work in parallel. Habitual engagement (active attention)

integrates the two. In this model, raw awareness provides a non-cognitive backdrop to

experience: a richness and fullness instead of a perceptual vacuum. During active

perception, raw sense data is not disposed of, just because it’s understood, nor is it

disposed of merely because it is not. On the contrary, these conditions are when we may

really start to enjoy experience. When we look at a painting and discover the subject,

the richness in how the figures are presented doesn’t evaporate. The active-attention

model accepts the intellectualist models of perception, but also the concept of direct

perception, thereby lowering the threshold for experience. The active attention model

proposes that experience becomes declarative iteratively, exactly as perceptions are

engaged with and acted on iteratively. At the most fundamental (pre-cognitive) level,

action is automated, not necessarily by attention, but by habits that have formed direct

associations with perceptual activations and actions: given familiar singletons, it isn’t

necessary to recognize them before actions commence. We do not see a flat, hard

surface and think; ‘hey – I can walk on that.’ We just walk (Bargh & Dijksterhuis,

2001; Gibson, 1979). The factors of salience will determine how much attention a

singleton is given as a parallel process (See The factors of saliency p.210).

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In agreement with Clark, prominence (mismatches between expectations and

experience) is a factor. But other factors (significance, worth and opportunity – see p.

212-213) also capture attention, and all are important. The mechanics of opportunity are

especially interesting in the context of active attention because we do engage through

action, but our awareness of such engagement may be implicit (Hassin, Bargh, Engell,

et al., 2009).

The associations that intellectualist models emphasize are plastic and changeable and

thus are intrinsically vulnerable. Grossberg recognizes this and insists that a resonance

between the raw data of reality and intentions is essential to create stability of meaning,

to prevent it from being re-written with every new perception (Grossberg, 2003b).

Meaning cannot survive (long) when sensory cortical inter connectivity is lost, even if

bottom-up sensory perception continues. Dementia within the association cortices

causes the singletons of perception to vanish, leaving behind nothing but a full, but

unintelligible jumble of sensory indistinctness. In some cases, patients with specific

dementia in the higher visual cortices cannot even distinguish between the categories of

visual information – between colours, lines and shapes, much less pick out contents of a

view, even though the raw visual information is still omnipresent (Sacks, 2010).

The sense-of-self

The sense-of-self is normatively considered irrelevant or only of peripheral interest to

perception, but this viewpoint is difficult to defend. All the modes of attention serve a

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single perspective, and this is experienced as the locus of the sense-of-self; I am the

centre of my experience. There are many possible reasons for this, including (at a

minimum):

1) Because all the organs of perception report to a single brain (although nominally to

different parts of the brain);

2) Because perception is served, and serves a single and personal ontology;

3) Because the actions perception triggers all occur within a single physiology (Braund,

in preparation);

4) Because all of these functions unite a single sense of identity and ego (Shoemaker,

1968).

5) Because we have narratives of existence (R. A. Jones, 2010)

6) Because we act on self-knowledge and a sense of coherence emerges from these

actions (Deci & Ryan, 1991);

7) We find anything that contributes to meaning, comprehensibility and manageability

perceptually significant and salient (Antonovsky, 1987)

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The holism these interconnected and interdependent systems generates normally taken

for granted, but it is vulnerable. The person (as philosophically conceived here) is an

ego-centric composite of a body, perceptual system and ontology, and for the best part,

the sense-of-self doesn’t atomize when these constructs do – blindness, injury and

ignorance are all undoubtedly risk-factors, but for the best part, the phenomenological

sense-of-self is relatively robust in these domains. An experiment was conducted where

the visual first person perspective was challenged, in this study the participants’ eyes

were masked and all sight was channelled through monitor glasses with a wireless

closed circuit video feed. The camera was put at a fixed angle in the corner of the room,

creating the illusion that ‘my body is there – not here.’ Even in these circumstances, the

sense-of-self was generally maintained; when participants wrote, the writing faced the

camera, not the body, but the participants had a choice – they could also choose to

engage their proprioception rather than visual modality, meaning that their writing faced

their bodies (Mizumoto & Ishikawa, 2005). This suggests that the self-perspective is

maintained by all the senses and can survive major disruptions. What is more vulnerable

is the ability to reflect on the narratives and actions that we associate with the constructs

of self, identity and self-agency. These narratives are sometimes oppositional: ‘I am x

because I am not y’ (Festinger & Carlsmith, 1959). They are sometimes affirmative: ‘I

am x because my actions are x-like’ (Bem, 1967). Both arguments rely on perception for

the basic information to know what x and y are, and on narratives to contextualize x and

y. Within these narratives, the sense-of-self is established relative to actions and

thoughts, whether they are oppositional or reconciliatory.

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I contend that both positions are valid, certainly in terms of contemporary neuroscience,

because the more deliberate actions are, the more resistance: neural excitation and

inhibition occur together, except during highly automated tasks, which are far more

parsimonious, and don’t necessarily engage attention at all (Bargh & Dijksterhuis,

2001). Sometimes excitation and inhibition are in equal measure, in which case the

balance suggests that no actions take place, but the greater the excess of excited

neurons, the more spontaneous action occurs (Golembiewski, 2012a) (see p.358 q.v.) It

might be resistance to action (inhibition) that is recognized as self-agency, rather than

actions themselves, whether successful resistance as in Festinger & Carlsmith’s model

or unsuccessful as in Bem’s. If this is the case, active attention will be insufficient to

maintain a sense-of-self.

Learning

The human search for comprehensibility and meaning appears to be endless. Every

unexpected singleton is met with top-down questions about why, who, what and when –

even when dreaming we are constantly trying to figure things out. This process involves

linking singletons to the lexical and motor schemata that are most challenged by the

new singleton (robin fits with birds, superhero side-kicks; with rhymes bobbin and

coffin; with names and other people called Robin like Robin Hood, with similar names

such as Robert and so on.) This is a logical process that has been adopted to simulate

intelligence in computing and has been adapted for very diverse models of learning

(Baars & Franklin, 2003; Clark, 2012 - in press; Grossberg, Carpenter, & Ersoy, 2005;
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Johnson Abercrombie, 1960; McClelland, McNaughton, & O'Reilly, 1995; Rumelhart,

McClelland, & UCSD PDP Research Group, 1986). If concepts defy knowing, they

may still be placed into abstract schemata. Concepts like God, love and infinity are

unknowable, but nevertheless have many associations across the global neural network.

Abstract schemata are sometimes less grandiose but no less vague. If a singleton doesn’t

initially appear to be of personal significance (i.e., few significant associations), it may

be bundled with other concerns for someone-else to deal with.

Regardless of whether their nature is specific or abstract, concepts and their associations

become schemata and are useful for defining other singletons (Johnson Abercrombie,

1960). This is an intrinsically antiHebbian process, because it wrestles apart automatic

associations and creates finer and finer distinctions within the ontology. But there is also

‘dumb’ learning, which follows Shatz’ (1996) aphorism to describe Hebb’s rule of

synaptic plasticity; ‘cells that fire together, wire together.’ Where real learning creates

associations, Hebbian learning reinforces them through long term potentation (ie,

usage). The mechanisms are highly complex, but recent reviews link automatic

functions to the strength of associations in the striatal association area (Ashby, Turner,

& Horvitz, 2010). Under normal circumstances, Hebbian and antiHebbian systems work

together. Whereas the anti-Hebbian system is primarilly used for initial learning (as

described by Clark and others), the associations that are generated are strengthened by

Hebbian processes, the oppositeis also true; disuse leads to synaptic loss and sometimes

dementia.

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Schemata that have been committed to memory for long periods are known to lump

together with similar concepts, if they can be recalled at all. This is demonstrated when

people are given several stories and asked to relate them after only a short period and

again after a long one. The phenomenon does not occur if subjects consider the stories

regularly; instead, the stories develop details and a new character of their own (Johnson

Abercrombie, 1960). This can be taken as preliminary evidence that the longer elements

of the ontology are left without focal attention, the more tacit they become. The more

focus they receive, on the other hand, the more explicit (Gulick, 2006). Tacit knowledge

is difficult to express because meanings are personal and hermetic, and the

communication of knowledge requires explicit knowledge, not vague concepts. For

example, someone who has forgotten their primary school science may say ‘light works

because of electricity.’ The person is not wrong, but the information lacks specificity

and isn’t very useful. Without regularly scanning knowledge for errors using a system

similar to the one described by Clark or Friston (Clark, 2012 - in press; Friston, 2003),

knowledge must become more tacit.

Tacit awareness of well known schemata and routines appears to be an ideal level of

awareness to allow associated actions to take place automatically.

Automation

Attention isn’t needed to trigger automatic actions such as well-learned motor behav-

iours. No deliberate attention needs to be given to walking, unless you are still a baby,

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and the skill is new. Having said that, intention (a distinct top-down form of attention)

can both trigger and inhibit automations. Automation is mentioned here because atten-

tion is variously helpful, destructive, or irrelevant to automatic performance at seeming-

ly unpredictable times (Willingham, 2001). Giving focal attention to automatic tasks

can cause ‘choking,’ the unintentional inhibition of that activity (Baumeister &

Showers, 1986; Dijksterhuis & van Knippenberg, 2000; Willingham, 2001).

Attention is an inhibitory response to a singleton. It pauses or arrests both automatic

actions and cognitive processes while the singleton is attended to. It will shortly be

demonstrated that there are two pathways that moderate attention: one is directly

inhibitory and the other excitatory – yet, because of their functional routes, they both

end up inhibiting automations – to differing degrees. The lower declarative awareness

levels associated with the troughs in tonic dopamine activity and associated with active

attention (see Figure 27), is likely to be the ideal level of awareness to enable automatic

tasks. This latent level of awareness allows automatic actions to be so efficient (Ashby

et al., 2010). Greater awareness, particularly bottom-up awareness (the phasic bursts in

Figure 27), as it invades working memory inhibits (that is, interrupts or even

terminates) actions whether they are automatic or not, by exciting the possibilities that

the action may precipitate and a range of alternatives (Dijksterhuis, Aarts, Bargh, & van

Knippenberg, 2000). This is presumably a function of the ACC and frontal cortex

through the activation of NMDA/D1 excitatory afferents (more about that shortly). But

even too much top-down attention can do the same (the peaks of tonic action in Figure

27), not because the ACC and frontal cortex are excited but the opposite: because the
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inhibitory D2 neurons bring awareness directly to the automatic functions, thereby

lifting awareness out of the ideal latent state. The classic example is with professional

sports players – when they ‘think too much’ they ‘choke’ – the automatic fluidity of

their actions fail (Willingham, 2001).

Automatic actions can be deliberately triggered by top-down intention (Ashby et al.,

2010), but for the best part, automatic actions are excited directly by affordances. This

sometimes even occurs in states of very low arousal as mentioned above; for instance

sleep-walkers will engage in automatic behaviours that relate to real and hallucinated

objects and environments: they have been known to drive, cook and occasionally act in

violent ways, especially if disturbed (Plazzi et al., 2005). When imaged using single

photon emission computed tomography (SPECT), sleepwalkers show profoundly

decreased regional blood-flow to the frontoparietal cortices, confirming that there is no

self awareness in this state (Bassetti, Vella, Donati, Wielepp, & Weder, 2000).

The typical sleepwalking patterns suggest a relevant issue for this argument; automatic

activity can be stimulated by top-down intention or simply by well-established links

between actions and the raw electro-chemical representations of perceived opportunity;

effectively bypassing all cognitive architecture (including the frontal cortex and ACC).

The implication is that intent is implicit within knowledge and that once knowledge is

established, it becomes an automatic reflex (Heidegger, 1981). For example, the

knowledge that an apple is edible prompts an intention to eat it (Bargh & Dijksterhuis,

2001). Any attention given to automatic actions has an inhibitory effect, but this is
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processed in parallel. For healthy people, inhibition balances latent ‘intentions’, thereby

moderating automatic actions to make them context appropriate.

The same cannot be said for schizophrenic or bipolar (I) patients, who don’t sufficiently

inhibit affordances, meaning that stereotypies and other automations go unchecked

(Golembiewski, 2012a) (reprinted here from p.358). For this reason, the inhibitory

properties of salience (when applied to automatic functions) must be considered as an

essential element of robust mental health.

The attention that healthy people give to their environmental context, automatically

establishes latent restrictions on behaviour – even on automatic behaviour. For

example, in a church or a temple, people automatically tone down their behaviour,

unless they have not learned the behavioural associations associated with the milieu

(babies for instance). This effect is known in environmental psychology as the influence

of the behaviour setting (Barker & Wright, 1954; Golembiewski, 2013). It is this latent

form of inhibition24 that prevents actions from occurring whenever an affordance is

present. A person will automatically assess the context, and will act only within the

restrictions imposed by the context unless they wilfully choose to be deliberately

defiant, or if they suffer a mental pathology of some kind.

24
. The inhibitory effect of the behavior setting should not be confused with latent inhi-

bition, a decrement in learning about notionally familiar circumstances (Lubow, 1973)

that became a pivotal part of the hypothesis of Gray et al. (1991).

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The neural architecture of healthy attention

Neurotransmitters and receptors

The neural processes involved in attention have been of interest for some time and

scientists have identified a range of systems and subsystems that may be involved.

Within this general field, the very lateralization into two dissimilar hemispheres has

been identified (Toga & Thompson, 2003). Four neurotransmission systems are also of

interest: acetylcholine, noradrenalin (norepinephrine), glutamate, and dopamine. There

is also a lot of research into specialized neural architecture, including larger scale region

analysis and the study of neurons and their components. All of these specialist interests

are growing fields, except perhaps lateralization, which, for all its promise, no longer

attracts the interest it did twenty five years ago (McGilchrist, 2010). In this chorus of

opinions, the striatal dopamine system is consistently singled out as the force that shifts

attention from one thing to another (Coull, 2005). Striatal dopamine is also linked to

salience perception (like in the above hypotheses (Fletcher & Frith, 2009; Howes &

Kapur, 2009)), to bottom-up attention (Hickey, Chelazzi, & Theeuwes, 2010; Holroyd

& Coles, 2002) and to reward salience – the way that attention is drawn to rewarding

stimuli (Berridge & Robinson, 1998, 2003; Bromberg-Martin & Hikosaka, 2009;

Mirenowicz & Schultz, 1994). The striatal dopamine pathways have also been

empirically linked to attention system more broadly and this will be discussed in further

depth shortly.

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The noradrenalin systems appear to support the dopamine function by selectively

inhibiting activity that is not task specific (especially somatosensory inputs) and by the

moderation of baseline levels of arousal (Coull, 2005), the cholinergic system, on the

other hand, appears to sustain interest beyond the initial turning of selective attention

(Aston-Jones, Rajkowski, & Cohen, 1999; Coull, 2005) It also serves a very important

role in communicating somatosensory impulses to the brain (Corringer et al., 2008)

along with glutamate (Carlsson, 1995). While all these processes are highly relevant to

the topic of attention, only dopamine, acetylcholine and glutamate appear to be active in

the early phases of perception. Because our interest here is particularly in the earliest

phase of attention - selective attention, the other transmission systems will not be

discussed further here.

A viable functional model is that salience is not unitary, and that most somatosensory

inputs are moderated by glutamate, acetylcholine or both and that these moderate

prominence. Cognitive saliency (significance and opportunity), on the other hand, is

almost certainly moderated primarily by dopamine. The saliency of worth is moderated

not by receptors, but by association organs – the left and right amygdalae.

The glutamatergic attentional system appears to monitor prominence, but glutamatergic

activations don’t normally invade awareness unless an event is prominent enough to

trigger the N-methyl D Aspartate (NMDA) receptors (Kleckner & Dingledine, 1988). At

this point the dopaminergic (cognitive) attention system becomes engaged in bottom-up

attention. People are profoundly unaware of glutamatergic activity until the NMDA
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receptors are activated, at which point the ‘winner takes all’ and working memory is at

least temporarily dominated by this new stimuli (Ward, 2008). The activation of the

NMDA receptors requires both a surge of voltage and particular connections, meaning

the receptor gates any activity that continues below the receptor ionization threshold

(Kleckner & Dingledine, 1988). Until this point, glutamatergic activity will continue

while a subject is utterly oblivious, meaning the deliberate blockade of NMDA

receptors can even be used to induce non-associative anaesthesia (Marek et al., 2010).

The cognitive (dopaminergic) and somatic (glutamatergic) selective attentional systems

are well integrated through networks of interconnected striatal neurons known as

mosaics (Cepeda, André, Jocoy, & Levine, 2010; Fuxe, Marcellino, Guidolin, Woods,

& Agnati, 2010; Gerfen, 1992; Gerfen, Baimbridge, & Thibault, 1987; Shen &

Surmeier, 2010). The functions of these can realistically only be understood in

simplified terms because mosaic patterns are often inconsistent and their distribution

patterns are heterogeneous (Gerfen, 1992). But within the mosaics, there are specific

dissimilar interconnections known as heteromers, which occur where two dissimilar

receptors are collocated (whether they are on separate neurons or the same doesn’t

appear to matter (Seeman, 2008a)). Relevant heteromers to the study of psychosis

include NMDA/D1 and D1/D2. These are of further interest because some have been

found to be up- or downregulated in a broad range of mental illnesses (Pei et al., 2010).

As we shall see, the D1/D2 heteromers are almost certainly involved in the moderation

of cognitive saliency (Seeman, 2010).

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There are a number of dopamine receptor types and these fall into two families: the D1

(excitatory) and D2 (inhibitory). But the ones that have been singled out as being

responsible for saliency tagging are the striatal D2 receptors, although the literature

rarely differentiates one type of saliency against another. The reasons for identifying the

striatal D2 receptors, according to Ginovart and Kapur (2010), are because psychotic

patients read far more significance into the environment than is evident to the greater

majority, and it is primarily these D2 receptors that are blocked by all anti-psychotic

medication. Thus, the prevailing hypothesis is that a psychotic episode is caused by a

functional over-availability of dopamine or of the D2 receptors (Laruelle & Abi

Dargham, 1999).

Seeman and others have also identified a particular formation of heteromers that render

the D2 receptors far more reactive. These are the D2High receptors. These are thought to

be responsible for psychosis for two reasons: not only are there more D2High receptors in

animal models of psychosis and in vitro studies of psychosis, but these receptors are

very easily stimulated and require very little dopamine to fire (Ginovart & Kapur, 2010;

Samaha, Seeman, Stewart, Rajabi, & Kapur, 2007; Seeman, 2010; Seeman & Kapur,

2000; Seeman et al., 2006). The other formation of the same receptors is D2Low. This

requires an order of magnitude more dopamine to fire (Seeman et al., 2005).

The conversion between D2High and D2Low (and vice versa) is caused by the presence of

an activated coupled D1 receptor. D1 is sensitive to a number of chemical agents

including nicotine and a range of psychostimulants. It is also activated by inputs from

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other neurons especially NMDA gated glutamatergic ones which are sensitive to the

same stimulants (Cepeda & Levine, 2000; Novak, Seeman, & Foll, 2010; Seeman,

2010; Seeman, Guan, & Hirbec, 2009). If the D1 receptor is stimulated before the

coupled D2, then the D2 receptor is in a D2Low state. In other words it is far less

susceptible to stimulation. If the D1 receptor does not fire before the D2, then the state is

D2High at the time it fires. It would appear that in psychosis, the D1 receptor is not

properly activated, leaving an unusual amount of D2High receptors to synthesize the

dopamine in the striatum.

There are a number of tell-tale signs that the D1 receptors are not properly activated in

schizophrenia. In humans, the identification of receptors activation in vivo is very

limited, but it has been known for some time that the axons of the human prefrontal

(PFC) and anterior cingulate cortices (ACC) are particularly abundant in D1 receptors.

These are 4-7 times more abundant in this region than any other receptor types and in

humans more so than in any other animals (Goldman-Rakic, Castner, Svensson, Siever,

& Williams, 2004; Nichols, 2010; Okubo et al., 1997). But these neurons are

significantly diminished in schizophrenia when compared with controls (Akil et al.,

1999; Okubo et al., 1997). The anterior dopamine pathway (the ACC and frontal cortex)

is under-activated during attentive tasks in schizophrenia, relative to healthy controls

and other types of psychosis (MacDonald et al., 2005). These findings consistently

correlate to the negative symptoms scales of schizophrenia (See review, Goldman-Rakic

et al., 2004; Javitt, 2009; Okubo et al., 1997). Another signature of under-activation of

D1 receptors in schizophrenia is an overabundance of D2High heteromers. In this state,

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the D1/D2 heteromers contain an un-activated D1 receptor. The overabundance of D2High

has not been adequately measured in schizophrenic patients and controls, but in animal

models of psychosis they are found to increase by 250% for amphetamine induced

psychosis 180% for phencyclidine induced states and up to 900% for certain gene

deletions (Seeman, 2008a).

But where do concepts of attention fit into this neurological model? I speculate that the

D2Low receptors mediate bottom-up attention because they only fire occasionally (how

often do we see an aberration in the environment – a tiger on the front lawn?) and

because the activated D1 receptors enable the ACC and frontal areas to consider matters
25
insightfully, as one must to understand the significance of aberrant events . D2Low is

excitatory, so its reaction is stronger – perhaps strong enough to turn attention from a

top-down focus to a prominent but possibly unimportant singleton. Finally D2Low draws

more dopamine, so it doesn’t leave a functional oversupply in the striatum.

25
. Unfortunately, the exact dynamics of the frontal activation is complex and

unclear (Dietrich & Kanso, 2010) so here the abstract paradigm of generalized

frontal activation (areas along the rostral axis from the striatum – notably the ACC

and PFC) as have been shown in the majority of the studies on insight) has to be

used as a proxy for a subject that cannot yet be resolved.

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Salient cue
Layer I (dendrite) D2
Striatal Excitation
La
cell Bottom-up
ye
Learning
r II
D1 Neocortical cell attention
/III Layer VI (axon)

D2Low configuration

Salient cue
Layer I (dendrite) D2 Inhibition
Striatal Familiar routines Active and
cell top-down
D1 Neocortical cell attention
D2High configuration

Figure 25: a D1/D2 heteromer in the striato-frontal pathway. Heter-

omers are bistable – they modulate two functional outcomes (Fuxe et

al., 2010). The D1/D2 heteromer modulates sensitivity to dopamine,

and is subject to change rapidly from a high affinity state (D2High) to a

low one; D2Low. The transformation is triggered by external stimula-

tion (either through direct chemical stimulation or through indirectly

through interneuronal connections (Seeman, 2010)). It is hypothesized

here that the D2Low configuration allows greater declarative aware-

ness to be brought to events by engaging the frontal neocortex. This is

useful for figuring things out, considering implications, developing

normative stances on ideas, and other learning tasks. The D2High, on

the other hand, limits the same awareness, enabling the conditions for

automatic action (Dijksterhuis & van Knippenberg, 2000).

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Consequently, the D2High receptors are probably responsible for top-down and active

attention, because these modes of attention are continuous, and usually follow well-

established routines. These are the modes of attention that are used constantly in normal

life (we’re always active, playing with the sugar, seeking out something, etc.). As a

result, they require less dopamine to fire, but they must fire more or less constantly.

Such a pattern has been repeatedly demonstrated in animal experiments.

In-vivo studies of macaca fascicularis monkeys and a number of rat species were

conducted by implanting microelectrodes directly onto the target dopamine neurons in

the striatum. Regardless of species, the studies repeatedly demonstrate two ranges of

dopamine firing in the striatum, in keeping with the above hypothesis. On one hand,

there is the occasional phasic burst, which is activated by unexpected rewards (Grace et

al., 2007); and a low level rhythmic tonic action which remains more or less active

unless it is interrupted (Grace, 2000; Schultz, 1998) (see Figure 26 and Figure 27).

Logically, the phasic burst must be modulated primarily by D2Low receptors because

they fire only occasionally, and only when the stimulus is unexpected. The tonic action,

on the other hand, fires in a continual but low amplitude rhythmic pattern (between 7-

30hz) (Grace et al., 2007; Seamans & Durstewitz, 2008). The implication is that tonic

action is modulated primarily by D2High receptors.

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1. Unexpected reward

Reward

2. Conditioned reward

Pavlovian
Conditioning

3. Conditioned (no reward)

Time (Seconds) 0 1 2

Tonic waveform Phasic burst / tonic depression

Figure 26: In vivo studies of Pavlovian conditioning in macaca fas-

cicularis monkeys. Here microelectrodes inserted into the axons of

mesocortical dopamine neurons (Ljungberg et al., 1992) demonstrate

three ranges of dopamine activity; a saliency response to an unex-

pected reward without Pavlovian stimulus; the tonic ‘background’

pattern and a ‘tonic depression’, or a gap in the normal tonic pattern,

as seen in condition 3 when the Pavlovian response occurs, but the

reward is not given, thereby appearing to tag disappointment. (Data

taken from Schultz, 1998; Schultz et al., 1997)

Heinz, Romero, Gallinat, Juckel, and Weinberger (2003); Heinz and Schlagenhauf

(2010) and Grace (1991); Grace et al. (2007) have noticed that both tonic and phasic

dopamine activation patterns are affected by saliency, but their findings vary from paper

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to paper. What is striking is that all their studies appear to be sound. It seems the

reported inconsistent findings reflect the non-unitary nature of salience, not poor

methodologies. Salience can be simultaneously increased in phasic bursting and

decreased in tonic actions and vice versa, notwithstanding the interrelationships that

clearly exist between the two.

There can be no doubt that tonic and phasic mechanisms are very interconnected: a)

They occupy the same neural pathways and stimulate the same neurons (Schultz, 1998).

They are thus only distinguishable by amplitude and oscillatory frequency (Grace, 1990,

1991). b) Whenever either receptor type fires, dopamine is generated as a response

(Strange, 1992), thereby incrementally increasing the baseline levels of dopamine

supply.

There are also patterns that do the opposite of phasic bursts. These are called tonic

depressions. They are gaps in the otherwise regular rhythmic tonic activity, and they

occur whenever a time-related event is conditioned and set to occur but doesn’t happen.

This is most likely due to harmonic desychronization of α-activity (Klimesch,

Doppelmayr, Russegger, Pachinger, & Schwaiger, 1998). For example in Figure 26

when the monkey in condition 1 is given an unexpected reward, there is an obvious

phasic burst. In condition 2, the monkey is given a reward but only after a Pavlovian

conditioning signal, which the monkey has already learned means a reward is coming

next. In condition 3, the monkey is given the same signal, setting up an expectation, but

the reward never appears. Instead, there is a gap in the tonic waveform exactly when the
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reward was due (Schultz, 1998). Similar findings have been widely replicated using

other methods and subjects, including humans (Grace et al., 2007).

It appears that tonic depressions are mismatch induced; meaning that tonic dopamine

also occasionally processes mismatches, but only occur when they are between top-

down expectations and how those expectations pan out in reality. Expectation

mismatches in a top-down process cause tonic depressions (condition 3); just as positive

mismatches produce phasic bursts (condition 1) in a bottom-up process.

High

b
f
Awareness

h
d e
a c
Low

D2High D2Low g

Figure 27: Proposed features of dopamine reactions: D2High is pro-

posed as the mediator of tonic dopamine wave patterns, and D2Low, the

mediator of phasic bursting. These actions bring attention from a la-

tent state (the grey background) to declarative awareness (white

background).

It’s not known what moderates the baseline levels of declarative

awareness, but being an organic phenomenon, it’s not likely to be lin-

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ear. A number of studies point to α-frequency desychronization

(Klimesch et al., 1998) – this is modulated both by higher cortical

arousal and also by amygdala function (W. R. Perlman, Webster,

Kleinman, & Weickert, 2004), thereby implicating worth-saliency in

the modulation of baseline awareness.

• Tonic dopamine firing makes low amplitude, regular (α - β

frequencies).

• Phasic bursts are irregular, stimulus induced and of high am-

plitude. These are gated by afferents from the glutamatergic

NMDA receptors.

• Tonic depressions are periods with no activity at all. This des-

ychronization could be a harmonic effect of α-frequency desy-

chronization, which also follows expectations (Klimesch et al.,

1998).

• The waxing ‘intent’ period of top-down attention.

• The attenuation of tonic excitation.

• The attenuation of phasic bursts.

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

• Waxing interest – the active attention phase.

• A body of evidence suggests that the discharge phase of dopa-

mine activity is dependent on Ca2+ (calcium ions) (Grace,

1990; Grace et al., 2007).

Saliency and meaning: it’s all in the neurons

Kapur et al. (2005, p. 61) hypothesize that ‘the normal process of context-driven novelty

and salience attribution is usurped by an endogenously driven assignment of novelty

and salience to stimuli… without cue or context.’ This line of thought attempts to escape

the obvious fact that these saliency signals occur within specific neurons, and that they

bring attention to the singletons that are associated with those neurons. It seems

axiomatic that in schizophrenia there is some confusion about what is salient and what

is not, but this process cannot be random as Kapur et al. suggests.

Even if aberrance is identified using an anti-Hebbian, Bayesian logic, it is still through

Hebbian learning processes that the ontology is constructed; ‘Cells that fire together,

wire together’ (Shatz, 1996, p. 604). If this aphorism of Hebb’s rule of neural plasticity

is valid, then the connections that are stimulated by a saliency event is not random at all,

but a distinct and meaningful association, even if that meaning is indecipherable to

anyone but a single psychiatric patient. Meanings need not be rational for instance: they

may be phonically (rhyme, alliteration etc.) associated (a phenomena known as clang or

jargonaphasia), or associated through irrelevant narratives (or delusions).

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A compelling model for how neurons are specifically associated with meanings

(discussed in the section on learning on page 232 in this article) is conceptually

described by Grossberg (2009) and confirmed by Feldmeyer (2010). The specifics both

authors relate are somewhat different, but this is only to be expected because when

analysing cells, scientists are forced to use idealized models to understand a

heterogeneous reality (Gerfen et al., 1987). The concept is that the outer dendritic layer

(I) of the neocortex process perceptual stimulus, whereas the inner axonal layer (VI)

processes top-down associations. As these match, the arbors of the middle layers (II-III,

IV, V) connect to other cells horizontally and diagonally across a distributed network

(Baars, 2005). Grossberg asserts that under normal circumstances, neither top-down, nor

bottom-up perceptual processes are sufficient to stimulate a recognition response in the

cell, but when both top-down and bottom-up stimuli match, an event potential spreads

to associated cells through the arbors.

This model is conceptualized for physical perception, but endogenous perception

(identified as aberrant by Kapur et al, 2005), is no different. The phonological loop and

the visuo-spatial sketchpad (the resources of endogenous perception identified by

Baddeley, 2003) are hypothesized to use the same mechanics, and largely in the same

areas of the brain (Grossberg & Kazerounian, 2011).

Even with the most basic level of bottom-up perception, perception requires an

endogenous chemical (such as acetylcholine) or electrical signal to function as a proxy

to represent an external sensation (see perception, p.223). This means that the most
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basic divisions in perceptual processes: between bottom-up top-down or between

endogenous vs. exogenous are not dissimilar. They’re only differentiated by whether

they are the subject or object of observation (and this permits confusion if the sense-of-

self were to unravel, as it frequently does in schizophrenia (Kean, 2009; Sass & Parnas,

2001)). The difference is relative – where the proxy for the object is processed in the

cortical dendrites, whereas the subject (self-perspective and intentions) is processed in

the axons.

The higher-order our awareness becomes, the more abstract. Indeed, we can even

become aware of our intentions, meaning that even intentions may be regarded as a

bottom-up phenomenon (dendritic stimulation), whereas, in lower-order perception,

intentions are the basis of top-down (axonal) perception.

Dysfunction of the attention system: aberrant salience

Both Fletcher and Frith (2009) and Howes and Kapur (2009); (Kapur, 2003; Kapur et

al., 2005) agree that the upregulation of dopamine and the correlated upregulation of
26
perceptual salience causes the positive symptoms of schizophrenia . Frith didn’t

always have this view. In 1978, Frith first floated the idea that schizophrenia may be

understood as a shortage of perceptual attention – a kind of cognitive blindness that

26. Technically Fletcher and Frith use a different terminology: they write of attenuation

failure rather than aberrant salience, but these are the same.

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stunts the cognitive component of perception (Frith, 1979; Joseph, Frith, &

Waddington, 1979). But because an empirical basis for the hypothesis was weak and

further studies only produced equivocal results, the hypothesis was subsequently

withdrawn (Frith, 1987; Frith & Done, 1988). Even so, the idea continued to find

support in modified hypotheses, such the neurophysiology hypothesis of schizophrenia

(Gray et al., 1991) and the attention deficit model for recurrent complex visual

hallucinations (Collerton et al., 2005). In keeping with Frith’s reversal, the aberrant

salience hypothesis and the Bayesian attenuation failure hypothesis do not take the view

that attention in schizophrenia is deficient, rather, that it is in surplus (Fletcher & Frith,

2009; Kapur, 2003). But Frith’s reversal is somewhat justified.

Distinctions between modes of attention allow for both a deficit and a surplus to co-

exist. This may partly explain the division in the schizophrenia diagnostic criteria,

where on one hand, diagnosis by the more florid of the so-called positive symptoms

(Symptoms A1: delusions, and A2: hallucinations, etc.) appear to be caused by

attentional superfluity, whereas the negative signs (Symptom A5: absences of normal

behaviours – akinesia etc.) appear to be caused by attentional deficits, and others such

as catatonia (Symptoms A3 and A4: disorganized speech and gross disorganization)

appear to be caused by both.

I propose that the core symptomatology of schizophrenia depends on Frith’s paradox. It

also solves a number of other prominent riddles: schizophrenia can be understood as a

functional surplus of top-down and active attention due to a presynaptic and subcortical
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upregulation of dopamine and the simultaneous deficit of bottom-up attention because

of a shortage of striato-frontal activations which would be triggered by phasic

(postsynaptic) dopamine.

Because of the known reliance on glutamatergic NMDA receptors to stimulate D1

receptors (Seeman, 2008b), this model directly explains another prominent paradox. It is

the problem of the glutamate hypothesis. The blockade of glutamatergic NMDA

receptors (using NMDA antagonists like ketamine or phencyclidine) mimics the

negative signs of schizophrenia like no other psychotropic intervention (Javitt, 2009),

yet no significant losses of glutamate are found in schizophrenia (losses range from 0%

to -5%) (Tamminga, Holcomb, Gao, & Lahti, 1995).

This hypothesis also solves another question that has plagued researchers for decades:

the combined tonic surpluses when added to the phasic deficits would explain why

striatal dopamine synthesis is found to be only moderately upregulated in schizophrenia

27
(Fusar-Poli & Meyer-Lindenberg, 2012) even though all anti-psychotics work by

reducing dopamine synthesis (Ginovart & Kapur, 2010).

27. A meta-analysis of 11 studies of dopamine synthesis capacity, covering cases of first

episode chronic, and catatonic schizophrenia showed that the average upregulation of

dopamine synthesis in schizophrenia was a moderate 14%, but with a telling variation –

at the lowest, three datasets showed very insignificant upregulation over the normal

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

Converging evidence also points to the same finding: tonic D2 receptor activity is

generally increased in schizophrenia – and to a significant level28 (d=0.79) (where 0

would mean that patients were matched to controls), yet these increases are not

ubiquitous (Howes et al., 2012). The heterogeneity in the data suggests that in some

cases presynaptic D2 activity is decreased – this is presumably in the aforementioned

rarer presentations of catatonic schizophrenia – the condition most resistant to

medication.

Finally this hypothesis will also explain why anti-psychotic medications are ineffective

in about 30% of patients with schizophrenia (H. M. Jones, 2004). (Note that while this

level 0%, 0.02% and 0.05% (Av =101.3) all were for cohorts with catatonic

schizophrenia. On the other end of the spectrum, upregulation reached as much as 40%

in one study, but this outlier was found to be non-significant during post-hoc analysis.

The other studies showed an average upregulation of 15.4% over a total of 81 cases of

schizophrenia (undifferentiated by presentation), the only study looking at first episode

schizophrenia exclusively, measured 18% upregulation above controls (Fusar-Poli &

Meyer Lindenberg, 2012).

28. Data from a meta-analysis of SPECT and PET studies of drug-naive patients with

matched controls.

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

observation lends support for the argument that schizophrenia is two syndromes (Crow,

1980). This logic is untenable because the functional surplus of striatal D2 receptors

inevitably downregulates over the course of schizophrenia, and this represents a

deterioration of the syndrome, not another nosology.)

To take this hypothesis further, the above outline of what (little) we know about the

healthy attentional system should prove a good starting point. The next step is to drill

down to the specifics of salience, to make informed predictions about what aberrant

saliency should mean.

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The emergence of symptoms

Level A Biochemical, neuronal Interneuronal interactions:

D1-D2 heteromers
Excitatory receptors
Inhibitory receptors
Level B Neuropsychological The modes of attention and combinations of:
processes top-down attention superfluity
top-down attention deficits
active attention superfluity
active attention deficits
bottom-up attention superfluity
bottom-up attention deficits
Dependent systems:
Perception
Epistemological processes
Automaticity
The sense-of-self
Contextual inhibition
Level C Psychological syndromes Tunnel focus
Undermined automaticity
Confirmation bias
Hebbian degradation of the automatic ontology
Positive feedback distortion
Subcortical confinement
Deficits in bottom-up attention
Behavioural negativity
Level D Behavioural symptoms and DSM-IV Class A symptoms:
signs (A1) Delusions
(A2) Hallucinations
(A3) Disorganized speech (e.g., frequent derailment
or incoherence)
(A4) Grossly disorganized or catatonic behaviour
(A5) Negative symptoms, i.e., affective flattening,
alogia, or avolition
Class B symptom: Social/occupational dysfunction

Table 3: Translations. Linking symptoms biological dysfunctions

through the modes of attention.

So far this paper has discussed the molecular biochemistry, and how it affects attention

through neuronal interactions (See level A of Table 3). These interactions are then

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linked to psychological processes; the modes of attention (top-down, bottom-up and

active. See level B). The next section of the paper explores the psychological syndromes

that the molecular dysfunctions, combinations of imbalances of the modes of attention

and dependent cognitive processes generate (Level C). A number of important cognitive

processes are directly affected including: attentional focus, perception, the ontology

(epistemological processes), automaticity, the sense-of-self and contextual inhibition.

Finally this hypothesis is putatively held to explain behavioural symptoms and signs of

schizophrenia - the ‘constellation’ as the DSM-IV refers to it (American Psychiatric

Association, 1994, pp. p. 274, 277), thereby linking the effect of molecular

neurotransmission to specific symptoms (level D).

Which came first is a chicken and egg argument, and it is still difficult to say which

came first. Some symptoms correlate with an up-regulation of top-down and active

attention and others because of the down-regulation bottom-up processes, but at its most

parsimonious, all the symptoms; positive and negative, acute or chronic and rare or

common are caused by confluence of these two interdependent dysfunctions and eight

interdependent but distinct syndromes this confluence causes. The patterns equate

roughly to the three main schizophrenia subtypes. There is the paranoid type (295.30)

which is where tunnel focus, undermined automaticity, and confirmation bias

syndromes are dominant because of a surplus of striatal dopamine; there is the

disorganized type (295.10) which manifests because of Hebbian degradation of the

automatic ontology, positive feedback distortion and subcortical confinement

syndromes. These are predominantly the combination of upregulated dopamine along

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with bottom-up attentional deficits; and there is the catatonic type (295.20), which

manifests because of bottom-up attention deficits and behavioural negativity

syndromes. The psychogenesis of the catatonic type is when bottom-up attention is in

severe deficit, especially when dopamine is no longer upregulated.

(Cantor-Graae, Nordström, & McNeil, 2001; Davidson & Heinrichs, 2003; Goldman, Hien, Haas, & Sweeney, 1992; J. A. McGrath

et al., 2009; Parnas, Handest, Jansson, & Sæbye, 2005)

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Putative explanation
Paranoid Disorganized Catatonic

Positive feedback

attention deficits
Confirmation bias
Diagnostic tool

Degradation of
DSM page

automaticity
Automaticity
Tunnel focus

Undermined

Subcortical

bottom-up

Behavioral
Frequency

negativity
Reference

distortion
Sample

arousal
Notes
Symptom
General criteria
D,E,F B A,C

Minimum term of active phase 100% 2 1 0 0 0 0 0 1 0

Social or occupational dysfunction (Criterion B) 100% 2 2 2 2 3 3 3 1 2

Not not better accounted for by other diagnoses (D,E, F) 100% 2 3 2 2 2 1 1 2 3

Positive Symptoms
Distortions or exaggerations of inferential thinking (A1: delusions) 89% 980 Castle etal. 3,4,5 DSM-III/DIP 1 3 1 3 1 0 2 0
Erroneous beliefs/misinterpretation 275-276 3% 923 McGrath etal. 5 DSMIII/DSMIV 2 0 1 0 0 0 0 0
Bizarre 82% 152 Goldman etal. 10 DSM-III 3 0 2 0 1 1 2 0
Persecutory; being persecuted, followed, tricked, spied on, ridiculed. 275-276 87% 1175 McGrath etal. DSMIII/DSMIV 1 1 1 2 1 0 0 0
A1

Referential; environmental cues (press etc.) are directed at the patient. 275-276 78% 1091 McGrath etal. DSMIII/DSMIV 1 1 1 2 1 0 0 0
Somatic; Loss of control over mind and body 275-276, 279 25% 1031 McGrath etal. 4 DSMIII/DSMIV 3 2 3 2 2 1 1 2
Grandiose or religious 55% 1103 McGrath etal. DSMIII/DSMIV 1 0 1 0 2 0 0 0
Distortions or exaggerations of perception (A2: hallucinations) 274-275 73% 980 Castle etal. DSM-III/DIP 2 3 3 3 1 1 2 0
Auditory 82% 1175 McGrath etal. DSMIII/DSMIV 2 0 2 0 1 2 3 3
Two or more voices or running commentary 0 0 0 0 1 2 3 3
Visual 41% 1067 McGrath etal. DSMIII/DSMIV 0 0 0 0 1 2 3 3
Multimodal no data 2 0 2 0 1 2 3 3
Monomodal no data 0 0 0 0 2 0 1 0
Olfactory or gustatory 15% 1079 McGrath etal. DSMIII/DSMIV 0 0 2 0 2 3 1 0
A2

15% 1079 McGrath etal. DSMIII/DSMIV

Tactile 13% 350 McGilchrist etal. RDS (Spritzer etal.) 0 0 3 0 1 2 1 0
Somatic 275, 279 19% 1043 McGrath etal. 8,5,4 DSMIII/DSMIV 3 3 2 3 1 1 1 2
Thought insertion 21% 911 McGrath etal. 5,4 DSMIII/DSMIV 1 0 1 0 1 3 2 2
Thought withdrawal 11% 911 McGrath etal. 5,4 DSMIII/DSMIV 3 0 2 0 2 0 1 0
25% 1031 McGrath etal. DSMIII/DSMIV
Delusions of control 24% 350 McGilchrist etal. 5,4 RDS (Spritzer etal.) 0 0 2 2 2 0 1 2
53% 1007 McGrath etal. DSMIII & DSMIV
Distortions of language, thought disorder (A3: disorganized speech) 274-276 76% 151 Parnas et al. 6 ICD-10 2 2 2 1 1 1 2 0
A3

Derailment no data 2 2 2 1 1 1 2 0
Tangenitality no data 3 3 2 1 1 1 3 0
loose associations to incoherence spectrum 53% 887 McGrath etal. DSMIII/DSMIV 3 3 2 1 1 1 3 0
Distortions behavioral monitoring (A4: grossly disorganized or catatonic behavior)274-275 58% 923 McGrath etal. DSMIII/DSMIV 3 2 0 1 1 1 3 3
Childlike silliness no data 0 2 3 1 1 1 3 0
Unpredictable agitation no data 0 3 0 1 1 1 3 2
Difficulties in goal-directed action, Activities of Daily Living no data 3 1 0 1 1 1 2 0
Deshevelled appearance no data 2 2 3 3 2 1 1 0
dress in an unusual manner (e.g., wearing too much on a hot day) no data 2 2 1 3 2 3 1 0
inappropriate sexual behavior (e.g., public masturbation) no data 2 0 3 0 3 0 2 1
A4:

unpredictable and untriggered agitation (e.g., shouting or swearing) no data 0 0 2 3 0 0 3 1

Catatonic behaviours - a marked decrease in reactivity to the environment 11% 1103 McGrath etal. DSMIII/DSMIV 0 0 0 3 3 1 1 1
Catatonic stupor (total lack of responsiveness to environment) no data 0 0 0 0 0 1 1 1
Catatonic rigidity (maintaining a rigid posture and resisting efforts to be moved) no data 0 0 3 3 3 1 1 1
Catatonic negativism (active resistance to instructions or attempts to be moved) no data 0 0 3 3 3 2 1 1
Catatonic posturing (the assumption of inappropriate or bizarre postures) no data 0 0 3 2 2 1 1 1
Catatonic excitement (purposeless and unstimulated excessive motor activity) no data 0 0 2 2 2 1 1 1
Negative Symptoms
Affective flattening 275, 277 55% 1127 McGrath etal. 3 0 0 0 0 2 1 0
A5:

Alogia (manifested in brief, laconic, empty replies) 275, 277 34% 923 McGrath etal. DSMIII/DSMIV 3 0 0 3 3 1 1 0
Initiation of goal-directed behavior (avolition, apathy) 275, 277 69% 935 McGrath etal. 0 0 0 3 3 1 1 0
Associated features and disorders (Unspecified, not for diagnosis)
gross impairment in reality testing (loss of insight) 50% 980 Castle etal. DSM-III/DIP 0 0 0 0 2 1 1 0
Loss of ego boundaries 75% 151 Parnas etal. 1 Unspecified 0 0 3 1 2 1 1 3
Depersonalisation no data 0 0 3 1 2 1 1 3
Derealisation no data 0 0 3 1 2 1 1 3
Attention dysfunction (Poor concentration) 29% 980 Castle etal. 7 DSM-III/DIP 3 2 3 2 2 2 1 0
Anhedonia (loss of interest or pleasure) 44% 1031 McGrath etal. DSMIII/DSMIV 0 0 0 3 2 1 1 0
Dysphoric mood (depression, anxiety, or anger) 73% 980 Castle etal. DSM-III/DIP 2 3 0 3 3 1 1 0
Disturbance to sleep patterns no data 2 0 3 0 0 1 1 3
Lack of interest in eating as a consequence of delusional beliefs no data 1 3 0 3 1 0 1 0
Psychomotor abnormalities (e.g., pacing, rocking, or apathetic immobility) no data 0 3 0 3 3 1 2 1
Confusion, disorientation, memory impairment no data 2 2 0 3 2 1 1 0
Suicide risk 45% 1139 McGrath etal. DSMIII/DSMIV 1 3 1 3 1 2 1 2
Comorbidity with substance abuse 40-60%
Metaanalysis Cantor-Graae etal. 9 Mixed 2 0 2 1 3 0 2 2

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Table 4: The symptoms of schizophrenia, as listed in the DSM-IV,

incidence and putative explanations. (The notes on the data appear

in appendix 3, p.293). The putative explanations are detailed thus:

0=little/no importance to the pathogenesis of the symptom, 1= Possi-

bly or somewhat involved: 2= This syndrome can be responsible for

the symptom.

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In untreated schizophrenia, there is frequently a moderate to high increase in striatal

dopamine synthesis (Metadata of 11 studies show a minimum of 0% increase, a

maximum of 40% and an average of 14% higher levels than healthy controls (Fusar-Poli

& Meyer-Lindenberg, 2012)). This surplus can be explained by a deficit of D2Low

activations, because D2Low consumes about ten times more available dopamine, so when

the heteromers are switched to a high affinity mode, there will be a natural surplus of

dopamine, of D2High and a deficit of D2Low. Many environmental conditions may cause

this switch, including the deactivation of interconnected cortical NMDA receptors, the

presence of corticosteroids or certain gene morphologies (Seeman et al., 2006). The

surplus dopamine is consumed by presynaptic activations of the highly reactive D2High

receptors. As these fire, they engage in the mechanisms of the striatum: the well-learned

habits, schemata and routines of active attention as well as positive top-down saliency

cues. Some of these naturally follow intentions. But the rest take place without any real

intentions to match them against. Both create symptoms that are particularly noticeable

in paranoid type schizophrenia.

Paranoid schizophrenia subtype (295.30)

The following syndromes: tunnel focus, undermined automaticity and confirmation bias

are all common in paranoid type schizophrenia: and these have the best overall

prognosis (Deister & Marneros, 1994; Kobayashi, 2001) this is because all these

syndromes maintain intent, and by doing this, a thread of meaning (however bizarre) is

kept. This prevents the deterioration into the disorganized type or catatonic subtypes,

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which occur when meaning is abandoned (see the specific subheads dealing with these

subtypes on p. 267-on page 284 below).

Tunnel focus

Where intentions exist, the attention they harness is intensified, especially as bottom-up

distractions are weakened. This non-bizarre symptom is particularly prevalent in early

and in paranoid psychosis, and whilst it is very common, is not unique to schizophrenia.

Top-down superfluity creates a single but intense range or ‘tunnel focus’ of interest that

defies distraction (Chadwick, 1992). The maintenance and single-mindedness of

thoughts is significantly higher in schizophrenic groups than controls (Leonard et al.,

2012).

Undermined automaticity

As mentioned earlier, focused attention undermines automatic actions, regardless of

whether the attention is bottom-up or top-down (Baumeister & Showers, 1986;

Dijksterhuis & van Knippenberg, 2000; Willingham, 2001) Only active attention

completely spares automatic functions. When top-down intention brings too much

focus to activities, intended regular routines will become more difficult, frustrating, time

consuming and prone to error (Semkovskaa, Bédard, Godboutc, Limogec, & Stip,

2004). Too much attention to functions that should be automatic, such as speech and

behaviour can make them seem mildly disorganized. A phenomenal example is familiar

to healthy people when trying to remember (a top-down process) a word or name that is

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‘in the tip of the tongue’. An example is taken from a first person account: ‘… I was left

with a nagging, pulling sensation in the middle of my brain…’ (Hayne & Yonge, 1997,

p. 316)

Confirmation bias

This syndrome occurs when surplus dopamine is consumed to register recognition

saliency events. If there are any intentions, these ‘bingo,’ ‘this is important’ and ‘just as

I expected’ cues will be matched up with intentions to set up a confirmation bias

(Nickerson, 1998). Because Hebbian learning is not disrupted in schizophrenia (Morris,

Griffiths, Le Pelley, & Weickert, 2012), patients will readily learn irrelevant

associations. The results of this nonsense become part of the automatic ontology and are

reinforced by Hebbian processes.

These new associations only make tunnel focus worse, because the weakest points of

evidence will be enough to constitute proof. And a deficit of bottom-up attention (due to

the downregulation of D2Low) means that there is a shortage of inhibitory negative

feedback to keep judgments context appropriate or maintain any standards of evidence.

The habit of jumping to conclusions has been found (in a meta-analysis) to occur in 40-

70% of studies of delusional patients (Garety & Freeman, 1999). This symptom gives

rise to paranoid and grandiose delusions (A1), and when it gets severe, it can present as

derailment – a particular form of disorganized speech (A3) also.

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The over-focus on prior expectations has been found in a series of experiments that

were conducted to establish where miscommunication between schizophrenic patients

and others occurred. The studies (which I won’t detail) found that patients relied so

heavily on prior expectations that they failed to regard obvious sensory evidence.

Predictably, it was noticed, that this effect correlated strongly with the severity of the

florid symptoms (Chambon et al., 2011).

Confirmation biases are also commonly reported in phenomenal accounts. Here is an

example of the exaggeration of unrelated information in the formation of paranoid

delusions:

‘A little girl… looked at me and then said to her mother, “Is that man possessed

by the Devil Mummy?” Her mother also looked at me and replied, “Yes dear”.

This coincidence just when I was thinking this very thought, was enough to

“prove” to me…’ (A case of paranoid schizophrenia, in Chadwick, 1993, p. 244)

Derailment – a symptom of disorganized speech can also begin to occur due to intense

tunnel focus. The following account about Phil; a patient known to have a delusion

involving Stephen Hawking and bikies. This is a third person recount account of a

psychiatric interview. Grace is an intern; the author is presumably a registrar:

‘So, could you, please, just tell me what’s been troubling you over the last

couple of days?’

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Phil was slow to answer. ‘Nothing at all… They can stay out of trouble… If they’re in

time.’

‘Sorry,’ Grace said. ‘When you say “They”, who do you mean? Who is it that

can stay out of trouble?’

‘Bikies.’ Phil was silent for ten seconds, then finished with, ‘everyone really.

Because of Stephen King.’

‘Do you mean Stephen Hawking?’ Grace asked.

‘Yes, Stephen King,’ he nodded. He paused, then continued, ‘He’ll put the bikies

in another time force if they make trouble…’ (From a case of schizophrenia-

probably disorganized type, in Pridmore, 2010, p. 17)

In this account, Phil’s attention has narrowed to the point that he can only focus on

subjects that relate to his delusion. This is principally a symptom of tunnel focus. The

questions posed by Grace are unable to steer Phil from his rut-like delusional course. An

association that would normally be very loose, the relationship between Stephen King

and Stephen Hawking appears to be indisputable and absolutely settled. For Phil, they

are one and the same because top-down saliency cues are triggered by the phonic

similarity (jargonaphasic) between the names. Here you can see the effect of a

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confirmation bias. To anyone else, this evidence would be far from acceptable they

apparently share no more than similar names and careers as famous authors.

Pridmore’s recount also gives some insight into the nature of paranoia. Paranoia, once

again is a state of exceptional focus given to the unacceptable evidence of loose

associations. If negative ideas are the subject of over-intense focus, these will lead to a

state of paranoia, because evidence to prove that people are conspiring against you will

become ubiquitous and thought patterns will inevitably lead eventually to catastrophe

(D. Freeman & Freeman, 2008; D. Freeman et al., 2002; D. Freeman, Pugh, & Garety,

2008).

In some cases, positive, egoistic ideas may be overvalued, especially if bottom-up

attention has not completely atrophied. This may present as grandiosity and religiosity.

Disorganized schizophrenia subtype (295.10)

Because the causal mechanisms of all of these syndromes are very similar, it is difficult

to perfectly distinguish one syndrome from another. Certainly this makes distinguishing

the schizophrenia subtypes complex. Not all disorganized symptoms are caused by the

following syndromes (as demonstrated immediately above), but the following

syndromes will make disorganization the main presentation of schizophrenia.

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Hebbian degradation of the automatic ontology

Whenever there are no intentions, but there is still a surplus of dopamine and D2High, the

confirmation bias will still continue, but the ‘bingo’ signals (recognition salience) will

be aberrantly matched to irrelevant routines, habits, schemata and ways of thinking

(hunches, superstitions, suspicions, and magical thinking patterns), instead of

meaningful associations. Naturally, these will also be subject to Hebbian reinforcement.

The outcome is that the quality of the ontology deteriorates, and habits will become

entrenched.

Positive feedback distortion

A lack of new knowledge from bottom-up channels causes experience to become

increasingly stereotyped, but doesn’t mean experience is dismissed as being absurd or

bizarre. On the contrary, it is taken to be highly salient because of the confirmation bias

and the decline of negative feedback. The conditions that are created are exactly

analogous to the Larsen effect (the bizarre positive feedback patterns that occur when an

amplifier amplifies it’s own signal) (See Figure 28). This distortion amplifies

stereotypical thought patterns, behaviours and even physical actions. (Even motor

functions are maintained in the greater ontology (Donchin & Shadmehr, 2002)). The

results are genuine thought and gross motor disorders (A3, A4). Normally there are

three mechanisms to prevent this positive feedback pattern, and the D2Low channel

moderates all of them. The first is the bottom-up enrichment of the ontology with new

understanding. Another is that the D2Low channel balances positive feedback with

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negative feedback – a fact-checking mechanism to ensure that perception always

adequately reflects raw reality (Holroyd & Coles, 2002). The last mechanism is that the

channel is inhibitory and therefore ‘gain’ (the amplification of intent) is reduced.

A classical sign of poor negative feedback processing is in addictive behaviours,

particularly gambling; a gambling habit will be fed by the expectation of wins and the

failure to notice losses (Fletcher & Frith, 2009). Gambling is a common co-morbidity in

schizophrenia (Desai & Potenza, 2009), but it is largely mitigated by a loss of interest in

profits because of the advance of avolition and anhedonia and by confusion about the

process and reasons to gamble in the first instance (alogia).

As this positive feedback loop develops, the lexical ontology (speech and thought) will

start to take on skewed and hermetic meanings and conventions. Nuances may well

become primary meanings. Neologisms may need to be developed to explain the

profoundly important but deeply personal experiences a patient has. Associations may

lateralize, meaning that the associations of such irrelevancies as rhyme or meter may

become more important than the traditional target concept (e.g. Rail may be taken to

mean jail, simply because they rhyme) (Chaika, 1977, 1982; Chaika & Lambe, 1989).

Jargonaphasia

The effects of positive feedback distortion can be seen in the Oberrealschul Student case

(presented by Kraeplin):

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‘The patient I will show you today has almost to be carried into the room, as he

walks in a straddling fashion on the outside of his feet. On coming in, he throws

off his slippers, sings a hymn loudly, and then cries twice (in English), “My

father, my real father!…” The patient understands perfectly, and has introduced

many phrases he has heard before into his speech… He speaks in an affected

way’ (Spitzer, Gibbon, Skodol, Williams, & First, 2004, pp. 495-497).

Input (+) feedback Input (+) feedback (+) feedback

R R R

Input
intent

& habit
intent

intent
Hebbian Hebbian
Hebbian
O O O
! AntiHebbian
(-) feedback
A A
hypothesis checking A

Bottom-up perception Top-down perception Hallucinatory conditions

Figure 28: Raw perception (R) is ultimately our primary link with the

outside world and the purpose of our ontologies (O) is to understand

what raw perception is telling us about the world we live in and to

make that information useful. But what we see in raw perception is

mediated by what we know already: We match our perceptions with

intent - what we expect to perceive. If things seem to match (✓), a pos-

itive salience cue fires and our attention (A) is brought to the fact

(positive feedback). Meanwhile the saliency event enforces the expec-

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tation in a Hebbian way. With well learned routines and expectations,

there isn’t much need for fact checking, but bottom-up perception

steps in when perception doesn’t meet expectations. It stimulates at-

tention and excites the cognitive apparatus that is needed to identify

what is wrong. This approach is inefficient, but it yields real infor-

mation, and builds the ontology in a meaningful (antiHebbian) way.

Hallucinatory conditions occur when new information stops enriching

the positive feedback loop. Representations of reality are always lost

in translation, but when perception is based on intent, and intent is

based on perception, losses are compounded while the stereotypical

qualities of perception are amplified. Without raw enrichment, the on-

tology will shrink into ever more limited repertoire of stereotypical

patterns.

Subcortical confinement

When D2Low receptors are really depleted, a patient may effectively loose all frontal and

ACC connectivity, thereby confining their awareness to over stimulated subcortical

functions.

Excitatory receptors are needed to trigger event potentials in the parts of the brain that

are used to process ideas (normal arousal), and the deficit of excitatory dopaminergic

receptors (D2Low) in schizophrenia means this won’t happen, especially as the ACC is

further subject to the inhibitory activations of D2High. In order to enable automatic

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actions, the main cause of awareness (the phasic surges of bottom-up attention) must be

quickly inhibited. This is done through the same critical pathway – the striatal D2High

receptors. When these fire, they do create a limited awareness – particularly if they

follow top-down intentions, but they also limit the engagement of the higher-order

cognitive areas because they are inhibitory.

Importantly, a large number of neurons are activated nevertheless, because rather than

have a small amount of excitatory neurons branch laterally to activate the frontal cortex

and ACC, a much larger amount of inhibitory neurons shut it down. This creates the

opposite of the ‘flight of ideas,’ inflated ego, euphoria, dysphoria and other signs of

expansiveness of a manic episode (American Psychiatric Association, 1994), but the

large amount of activations still creates an event potential of sorts, although wholly

within the striatum (Figure 29).

The striatum isn’t used for insight or to make the abstract leap from symbols to

meaning. This involves higher-order areas; the ACC and areas of the frontal cortex

(Dietrich & Kanso, 2010) the striatum is, however strongly implicated in automaticity

and the other structural elements of thought: it is better connected to manage the well-

learned routines of lexica, grammar, schemata and other procedural resources than more

rostral areas are. The striatum has inputs and outputs to the sensori-motor cortex for

mediating movement; the association cortex, to mediates environmental stimuli and

behavioural responses; the inferior temporal visual cortex which mediate the visuo-

spatial sketchpad of working memory; the ventral striatum (including the nucleus
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accumbens) that receives input the amygdala and hippocampus: these modulate

emotions and narratives (Rolls, 1994).

It is conceptually bizarre that awareness can shift to focus on the building blocks of

thought, without awareness of meaning, because for most of us the opposite is the only

way we think. For most people meaning comes first, and the means to communicate

meaning, action or even thought follows automatically. But in terms of evolutionary

theory, the opposite must be the case – because if people stop to consider an impending

danger, they may well just get eaten (Dijksterhuis & van Knippenberg, 2000).

More than any other syndrome, this syndrome addresses the inability of severely

regressed schizophrenic patients to understand other people’s thoughts, abstractions like

identity and first person accounts report that even their own thoughts become

unintelligible (Kean, 2009). These symptoms (classed as theory of mind (ToM)

dysfunctions) are already of interest and are well known to occur in schizophrenia and

autism spectra disorders. Until now, no hypothesis has been presented that makes sense

of these dysfunctions (H. Gallagher & Frith, 2003). In support of this hypothesis, ToM

studies universally find activations of the most anterior region of the ACC – the

paracingulate cortex (H. Gallagher & Frith, 2003) or, in the case of severely regressed

schizophrenia – deactivations in this region (Brune et al., 2008).

A lot can be gleaned from first person accounts into this bizarre syndrome, and so the

insights from just spending dedicated time with patients is telling. Searles (an old-

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school psychiatrist who sat with his patients for an hour a week, for years on end)

counted dozens of other old-school therapists who discovered that schizophrenic

patients were frequently unable to escape concretistic thought. And he personally

observed: ‘I had worked with schizophrenic patients for several years before I came to

realize that a schizophrenic individual has, subjectively, no imagination. The moment

that something that we would call a new concoction of fantasy, a new product of his

imagination enters his awareness, he perceives this as being actual and undistinguished

from the world around him.’ (Searles, 1962, p. 37) This passage pre-empts and distils

this hypothesis beautifully because it is the imagination – the ability to think abstractly

that is paradigmatically so important about the ACC.

When you know what you are looking for, direct examples abound. When reading the

following extract, you cannot help but be aware of the lack of meaning; despite of a

cohesive logic in in linking the cross-section of associated schemata (i.e.. Metabolism

→ illness → distemper → cats → my cat → colour of my cat → black and white →

goldfish → clown (fish) → down (rhyme)): jargonaphasia

‘…Speeds up the metabolism. Makes your life shorter. Makes your heart bong.

Tranquilizes you if you've got the metabolism I have. I have distemper just like

cats do, ‘cause that's what we all are. Felines [pause]. Siamese cat balls. They

stand out. I had a cat, a manx, still around somewhere. You'll know him when

you see him. His name is G-I Joe. He’s black and white. I had a little goldfish

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too like a clown [pause]. Happy Halloween Down…’ (Chaika & Lambe, 1989,

pp. 411-412)

Sometimes the inability to raise ones awareness from the processes and schemata that

underlie thought and action are noted by patients with rare flashes of lucidity29:

‘I’m concentrating so much and trying to listen to what they are saying and I

lose track of the conversation’ (Chapman, 1966, p. 237)

‘…While I was blinking at a traffic signal light, remembering in it something

familiar, something which had a meaning I couldn’t recall, a wave cascaded on

the beach. A physical sensation, it arose in the back of my head and drifted

forward in a pleasant way, like a light gentle wash of sea froth. The waves fell,

disappeared into the sands, and left on the beach a thought. I remembered

suddenly the purpose of traffic signals and what the red and green lights meant.’

(B. J. Freedman, 1974, p. 336)

7. Occasional coherence indicates that schizophrenic symptoms may constantly

fluctuate with availability and consumption of dopamine.

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

{
1 x D2Low
Synthesis of 10 Normal
DA molecules + Activates
more cells =
arousal

Synthesis of 10
10 x D2High { ~
DA molecules - More cells
activated
Atypical
= arousal

Figure 29: The subcortical confinement syndrome. D2Low is excitato-

ry, so it excites target neurons, and D2High inhibitory, so they terminate

the excitatory sequence, but D2High is about 10 times more sensitive to

dopamine and therefore, 10 times more neurons will fire to synthesize

the same dopamine. The result, in terms of numbers of cells activated,

may be approximately equivalent, or even higher. The differences are

the location of these cells and what they do. In D2Low conditions, exci-

tation is in the ACC (and other more rostral areas), whereas in the

D2High condition (being presynaptic) are situated within the striatum,

with afferents to the ACC and beyond.

The catatonic subtype of schizophrenia 295.20

Dopamine isn’t always upregulated in schizophrenia. Sometimes psychotropic

intervention has been effective in consuming excess dopamine, and in other cases, time

has taken its toll and hyperdopaminergia has naturally settled. When this happens, the

symptoms that are driven by excess dopamine will also settle and the distinct absences

of normal behaviours become more obvious. But because these symptoms are caused by

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deficits of D2Low and bottom-up attention, they are expected to underlie all cases of

schizophrenia, even if they are subtle not immediately obvious alongside other more

florid symptoms.

Deficits of bottom-up attention:

The decrease of bottom-up attention will mean a decreased ability to notice things

including attention to somatic impulses, affect and social connection. Not only are these

symptoms very common in schizophrenia (Andreasen, 1985; Manscreck & Maher,

1991), it is also a feature of other psychoses including bipolar type I disorder and the

dementias (American Psychiatric Association, 1994; Spitzer et al., 2004).

‘The patient sits with his eyes shut, and pays no attention to his surroundings…

In the hospital he was almost dumb, was cataleptic, gave his hand stiffly and

jerkily, and almost entirely refused to eat. His expression was generally

indifferent, though sometimes cheerful, and visits from his relations made no

impression at all on him.’ (Kraeplin, the Oberrealschul Student case.

Subsequently re-diagnosed as schizophrenia - disorganised type. In Spitzer et al.,

2004, pp. 495-497)

It is hard to ascertain from the third person perspective why patients like the

Oberrealschul Student may have such an indifference to other people, the environment

or even somatic needs (such as hunger). This inability is not because of distracting

‘noise’ as many theorists propose (eg, Corlett, Frith, & Fletcher, 2009; Heinz &
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Schlagenhauf, 2010; Howes & Kapur, 2009; Juckel et al., 2006)(See appendix II, p.

289), but because unsought perceptions will not attract attention and therefore they must

simply go unnoticed or will appear distant, unconnected or irrelevant when bottom-up

attention is grossly deficient. This condition becomes so extreme that patients may fall

over obvious obstacles and the instinct to block the fall may not be triggered (McDiven,

2011).

Because bottom-up attention also mediates negative feedback (Clark, 2012 - in press;

Holroyd & Coles, 2002) any unsolicited feedback (from other people or from the

environment or from bodily experience) will go unnoticed. Without reality testing,

perceptual errors can compound, causing experience itself to diverge from the common
30
experience of reality. Many authors speculate that this or similar ideas (Collerton et

al., 2005; Friston & Frith, 1995; Grossberg, 2000, 2003b; Stephan, Friston, & Frith,

30. A related concept is the corollary discharge error (CDE) model for

hallucinations, which that was first described by Feinberg (1978), and further

popularized by Frith (1979- and onwards) This model claims that an individual

carries a record; ‘the efference copy’ of all endogenous actions, and once actions are

complete, the record is ‘discharged.’ Errors in this process are perceived as

hallucinations. The problem with this model is that it attempts to explain bizarre

hallucinations as if they were simple illusions, and goes no further in explaining

other bizarre symptoms of schizophrenia.

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2009) can explain hallucinations, but not for schizophrenia because schizophrenic

hallucinations can become very bizarre in a very short period and this cannot be

explained by lack of feedback or breakdowns in feedback processing or other similar

hypotheses.

What deficiencies of negative feedback will cause, is reckless, disinhibited or otherwise

antisocial behaviour to go unchecked, and this is important because it sets up a

definitive symptom of schizophrenia (symptom class B) the loss of social contact. An

obliviousness of social cues often results in the habit of invading other people’s

personal space.

A well-known area of schizophrenia research involves testing for Mismatch negativity

deficits. These are usually tests of auditory bottom-up attention. In mismatch negativity

studies, a repeated sound is interrupted with an unexpected discordant sound. So a tune

is interspersed with aberrant notes, etc. A meta-analysis identifies (on an average taken

over 32 studies) one standard degree of deviation between bottom-up attention in

schizophrenic patients against healthy controls (Keshavan, Tandon, Boutros, &

Nasrallah, 2008). Interestingly, and predictably, dopamine-blocking (antipsychotic)

medications don’t appear to improve this inability to notice aberrant notes (Michie,

2001).

The reason that anti-psychotics cannot be used to treat mismatch negativity deficits or

any other dysfunctional bottom-up phenomena is because the blockade of dopamine

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receptors cannot improve bottom-up attention, because bottom-up processes are

mediated by D2Low receptors. As it is, this configuration of the dopamine heteromers

already requires far more dopamine to fire, meaning that less available dopamine will

either make no difference, and may even make this symptom worse. Although D2Low has

a much lower affinity for dopamine, its affinity to known antagonists are equal

(Seeman, 2008a; Seeman et al., 2006). Nicotine, on the other hand is known to stimulate

both D1 and prime the NMDA gateway receptors that gate its activation (Aramakis &

Metherate, 1998; Seeman, 2008a) – it could be that the comorbidity between

schizophrenia and smoking is because smoking is literally self-medicating.

The bottom-up deficit syndrome will also present as a decline of emotions and the

overall sense of holism. Somatogenic, affective and hedonic impulses will all recede,

resulting in an affliction of disconnectedness. Patients lose awareness of basic bottom-

up experiences such as hunger, pain, physical discomfort, tiredness or awareness of

basic and obviously disagreeable experiences; they may dress in many layers in hot

weather, go naked in the cold, eat putrid food and express other signs of anhedonia,

until the associated urges become overwhelming. Most of these symptoms are well

observed in schizophrenia and they fall under the general diagnostic categories that best

define disorganized schizophrenia: A4, gross disorganization and A5, negative or

deficit signs (American Psychiatric Association, 1994).

The flattened affect that is so characteristic of schizophrenia is caused by poor

somatogenic awareness also. The cliché, ‘taking time to smell the roses,’ refers to a
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known correlation between bottom-up attention and feelings of joy. When talking of

family or friends, most healthy people subtly perk up (Pridmore, 2010). But this

reactivity is restricted in many cases of schizophrenia as it is in depression, although it’s

rarely restricted in other psychoses (American Psychiatric Association, 1994). Again,

one of the known side effects of antipsychotic medications is the progression of

anhedonia (S. Williams, 2002a; Wise, 1982). This stands to reason, because, once again,

if emotions were mediated by bottom-up attention, the medications that decrease

dopamine supply can only make the condition worse.

When bottom-up attention is debilitated over an extended period, the deficit signs – the

notable absences of normal behaviour in schizophrenia – will start to manifest.

Stimulus-driven perceptions will wane; negative outcomes and other unintended

percepts will be discarded. Somatoparaphrenic syndrome might ensue, where patients

don’t recognize their body parts and bodily processes (Coltheart, Langdon, & McKay,

2007). Symptoms like this are distinctly bizarre, and may be classed as somatic

delusions (A1) or as hallucinations (A2). The biological (somatogenic) signals that

depend on bottom-up attention (hunger, tiredness etc.) will go unnoticed until they have

reached extreme levels of intensity, manifesting as severe self-neglect. Examples are

most obvious among schizophrenic patients who live rough (Pridmore, 2010). A meta-

analysis of studies of schizophrenic homeless people suggests that about 11% of all

schizophrenic patients live on the streets (Folsom & Jeste, 2002). This figure, derived

largely from US data, is 11-12 times higher than the US national average (including the

schizophrenic homeless). It is conceivable that this isn’t only due to gross

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disorganization, but also because bottom-up events are so much more intense ‘in the

rough’ and this could be an attempt to maintain some form of bottom-up awareness.

Behavioural negativity

Many of the disorganized symptoms are hypothesized to be the product of excessive

inhibition of automatic functions and routines, resulting from excesses of focal attention

inhibiting them. But automaticity has a complex relationship with attention, and while

low levels of attention enables automaticity, too much automaticity is an unwanted

symptom.

People automatically inhibit their behaviour according to their contextual awareness or

behaviour setting (see automation, p. 234). But the awareness of the behaviour setting is

bottom-up, and this will be diminished in schizophrenia, bipolar disorder and some

other illnesses31. Healthy people always limit their behaviour to some degree – but they

tend to limit unwanted, negative behaviour completely – except where circumstances

are well beyond expectations, when they will scream or flee.

8.
This symptom occurs in schizophrenia, but is more marked in bipolar psychosis

because the amygdala, the organ that monitors positivity and negativity is overactive

in this disorder (S. B. Perlman et al., 2012) in this condition, negative affordances

appear to trigger psychosis (Golembiewski, 2012a) whereas positive ones do not. In

schizophrenia there is less distinction.

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

The kinds of negative behaviours that would be stopped in healthy people, but not in

psychosis include stereotypy, perseveration, and other unwanted habits and negative

routine thinking patterns. When exposed to negative stimulus, healthy controls show

balanced inhibition against activation (meaning no automatic action) and far less

inhibition than psychiatric patients did for positive stimuli, when the total inhibitory

activations were subtracted from the excitatory ones. The resulting activation of

excitatory and inhibitory neurons in each area was recorded and published (Northoff et

al., 2004) and analysed, post hoc by (Golembiewski, 2012a) (see article from p.358).

When patients become aware of these automatic actions, they won’t always recognize

their own role in them, giving rise to non-bizarre delusions.

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Summary: Solving the aberrant salience riddle

When formulating a comprehensive hypothesis for schizophrenia, an important

argument that has been raised by sceptics of schizophrenia diagnosis should be

addressed: How can a singular psychogenesis be discovered for something that cannot

even be defined, bearing in mind that the set of observables used for diagnosis are so

broad that at some point in the past, syphilis, scurvy, pellagra and hyperthyroidism have

been included (Berrios et al., 2003; Boyle, 2002; Hoffer, 1970)? Even the DSM-IV

notes that the diagnostic guidelines are insufficient tools to tackle the task. To lead

clinicians toward grounds for consensus, the DSM-IV stipulates a number of explicit

taxonomic conditions and exclusions (criteria C-F). But this is not enough: the DSM-IV

instructs ‘individuals with appropriate clinical training’ to reach beyond the categorical

definitions, and to recognize the ‘constellation’ of schizophrenia features, that is, not to

construct a diagnosis out of the symptoms, like ingredients in a ‘cookbook’ (American

Psychiatric Association, 1994, pp. xxiii, p. 274, 277).

It is tempting to ignore this advice and deal with schizophrenia in parts. But the

applicability of such hypotheses are limited to the features they address. The hypothesis

presented in this paper is not intended to dismiss the others, but to follow through on

their leads and selectively integrate them in a holistic way.

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In order to present an authoritative and comprehensive hypothesis for schizophrenia,

this paper has addressed each diagnostic criterion within the DSM-IV. And has done so

inductively, by first recognizing the ‘constellation’ of schizophrenia as instructed. In

doing so, a strict adherence to the DSM-IV (American Psychiatric Association, 1994)

was essential because schizophrenia is not defined by its pathology, but by the

correlations between its presentation and the diagnostic criteria. Without the DSM-IV

(or an equivalent protocol), a definition of schizophrenia is invalid.

By focusing in on a single set of relationships starting on a molecular level and ending

in specific symptoms, this meta-hypothesis triangulates hundreds of findings against

each other, against every one of the diagnostic criteria listed in the DSM-IV and against

other observations that are otherwise largely held to be ubiquitous. These include many

symptoms and signs that have (despite the avalanche of papers being published) hitherto

remained mysterious and unexplained.

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Appendix I: The psychotic spectra continuum

The DSM-IV, currently divides delusions (A1) and hallucinations (A2) into bizarre and

non-bizarre subcategories, with bizarreness currently carrying more diagnostic weight,

although both occur in schizophrenia. The DSM also notes that disorganized speech

(A3) can be relatively normal, provided it is not ‘severe enough to substantially impair

effective communication.’ (American Psychiatric Association, 1994). This division of

symptoms into bizarre and non-bizarre is likely to change next year with the release of

DSM-V (Tandon & Carpenter, 2012). This is unfortunate, because the hypothesis for

schizophrenia presented here explains why experience can be so bizarre in schizophre-

nia, but not in the continuum of psychotic experience, and therefore an important diag-

nostic nuance will be lost.

The psychotic continuum into healthy populations is well known (Hanssen, Bak, Bijl,

Vollebergh, & van Os, 2005; Johns et al., 2004; Nuevo et al., 2012; van Os, Hanssen,

Bijl, & Vollebergh, 2001; van Os, Linscotta, Myin-Germeys, Delespaula, &

Krabbendam, 2009). In a meta-analysis of random interviews of the general population,

a mean 3.1% report psychotic symptoms (van Os et al., 2009), but this finding is subject

to enormous variance. In Nepal, for instance, 45.8% of 8822 subjects have at least one

psychotic symptom (Nuevo et al., 2012). Hay (1994) reports numbers that are higher

again (potentially 60% of randomly interviewed subjects) if culturally encoded religious

and numinous experience is to be counted as hallucinatory or delusional – although

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these are specifically excepted by DSM-IV criteria (Saver & Rabin, 1997). When

compared with the experiences of schizophrenic patients, these numbers are low, but

this is due in part to a fallacious quantification: Few people (with or without mental

illness) believe that their experiences are hallucinatory or delusional, and neither are

they necessarily be aware of their speech disorders. Because inductive methods (self-

reporting) are typically the method used to assess psychotic spectra symptoms in the

community, it’s fair to assume that the data gathering takes place while the subjects are

feeling comfortable, secure, well and with their consent. In contrast, the diagnosis of

symptoms during the first meeting with a clinician is going to be deductive, enforced,

and generally occur at a time when a lot is at stake.

While this should be a concern for the authors of the DSM-V and for clinicians, it is

mentioned here to point out that the symptoms listed in the DSM-IV as not being psy-

chotic per sé. Delusions are extremes of belief and hallucinations employ the mecha-

nisms of normal perception (such as the phonological loop and visuo-spatial sketchpad).

It is not the presence, but the nature of the symptoms that should be a concern for clini-

cians, because the difference between psychotic experiences and those of the communi-

ty (and also from those of other mental illnesses) are quantitative and qualitative and not

absolute. In dementia with Lewy bodies for instance, hallucinations are very common,

possibly more so than in schizophrenia, yet the underlying pathology is putatively with

decreased dopamine synthesis (Gold, 2009). As it happens, these hallucinations are

quite distinct from schizophrenic ones; they tend to be visual and are rarely threatening

(Collerton et al., 2005) whereas schizophrenic patients tend to suffer a multisensory and
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threatening hallucinations, for example, someone appears on the TV to directly abuse

the patient (Chadwick, 1992). Schizophrenic delusions may be both bizarre and non-

bizarre, but they are usually polythematic. The monothematic delusions common in oth-

er conditions are rare in schizophrenia. This means that schizophrenics will believe a

diverse range of things (John Nash, a Nobel laureate mathematician, believed that he

would become Emperor of Antarctica, that he was the left foot of God on Earth, and that

his name was really Johann von Nassau), but dementia patients or patients with a cere-

bral lesion is more likely to have monothematic delusions like Capgras’ (the belief that

a close other has been replaced by a stranger) (Coltheart et al., 2007).

Other fundamental differences in the experiences of schizophrenic vs. healthy controls

are that in schizophrenia, a high proportion of hallucinations and delusions are

emotionally negatively charged (Garety et al., 2001). A study by Honig et al. (1998)

with 18 schizophrenic patients and 15 controls, point out that negativity is ubiquitous

(100% vs. 53%), fear is very common (78% vs. 0%) and interference with daily life is

also ubiquitous (100% vs. 20%). Another difference is closely related: the feeling of

being out of control. All healthy subjects report that they maintain control during

hallucinations, against a mere 12% of schizophrenic patients. Another qualitative

difference is that half the schizophrenic patients experience voices in the third person –

whereas only a quarter of healthy hallucinators report third person voices.

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Appendix II: Refuting noise theories

The DSM-IV lists ‘problems with focusing attention or distractibility due to

preoccupation with internal stimuli’ a non-diagnostic associated feature of

schizophrenia (American Psychiatric Association, 1994, p. 279). This informs the

heuristic belief that symptoms are a product of neural noise (Fletcher & Frith, 2009;

Heinz & Schlagenhauf, 2010; 2009; Rolls, Loh, Deco, & Winterer, 2008). The

hypothesis presented here locates a preoccupation with internal stimuli, but rejects the

notion that this is a distraction preventing focused attention. In fact distraction possibly

plays no greater part in schizophrenic perception (at least for paranoid subtypes) than it

does in healthy perception.

‘Noise’ hypotheses are apparently well supported by evidence, but this reflects a

common flaw in experiment design and analysis and is not an inclusive picture of all

available evidence (perhaps a confirmation bias?) Nearly 2000 articles report

distractibility in schizophrenia, and predictably, most found a pattern of misattribution

of attention to irrelevant stimuli (E.g., Martins Serra, Jones, Toone, & Gray, 2001;

Moran, Owen, Crookes, Al-Uzri, & Reveley, 2008; Oades, Zimmermann, & Eggers,

1996). When questioning these findings, a similar experiment ruled out the possibility

that this effect was caused by learning difficulties – only strengthening the distractibility

hypotheses (Morris et al., 2012). But no studies addressed the possibility that attention

given to irrelevant stimuli may have been deliberate – and caused by an admixture of

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the feeling that no information is irrelevant and a general disinterest in being

psychologically tested. Both are natural products of tunnel focus (q.v.) To clarify this

issue, other experiments demonstrate that the undue attention given to distracters in the

abovementioned papers may be a feature of greater focus, not greater distractibility.

Indeed, not all abilities are subject to loss in schizophrenia. While bottom-up attention

tags mismatches, top-down attention tags matches, whether they are true or not. If tasks

are well defined, avoid unexpected (bottom-up) challenges and complications that will

require creative and insightful solutions, tasks should be easier for patients with

increased top-down attention than for controls, after all, paranoid schizophrenics should

be less distractible than controls. A task was given to a group of schizophrenia patients

and two other control groups; a clinical control group, which included patients with bi-

polar, personality and severe affective disorders (some of them also showed psychotic

symptoms); and another healthy control group. The task was simple: to match two

patterns, where distracting fuzzy marks surrounded the target. Subjects were instructed

on the task and told to ignore the distracter stimuli. In experiment test 87% of the

schizophrenic cohort outperformed the best result shown by the combined controls.

Meanwhile, the differences between the two other control groups were insignificant

(Dakin et al., 2005). In another experiment, pairs of words were given in succession;

some had no correlation, others were genuine pairs. Paranoid schizophrenic patients

performed especially well at picking the pairs, particularly when the words were

pertinent to paranoia (victim, killer; secret, spy). Chronic schizophrenics with no

positive symptoms (catatonic subtype) performed particularly badly (Brennan &

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Hemsley, 1984; Hemsley, 1987). Once again, those with positive symptoms maintained

exceptional focus.

In a third study, schizophrenic patients outperformed controls in an experiment designed

to assess and match physical force, by reciprocating the force applied by a lever. In this

study, all subjects underestimated their own efforts, but schizophrenic patients

underestimated by only 27.5%, whereas controls underestimated by 43.5% (Shergill,

Samson, Bays, Frith, & Wolpert, 2005).

Not only do these results contradict the abovementioned distractibility studies, but these

results also appear to be in conflict with widely cited studies that demonstrate deficits in

attention drawn from Stroop tests and Wisconsin Card sorting tests. These tests measure

a combination of top-down and bottom-up attention and cognitive ability, rather than

measuring top-down attention alone. Naturally almost all the results show schizophrenic

patients lagging far behind controls in performance and accuracy (Chan et al., 2010;

Zihl, Gron, & Brunnauer, 1998). The Stroop test involves presenting the name of a

colour (RED) in dissimilar (green) ink, and assessing performance of subjects with a

battery of measures including time, accuracy and neuroimaging. The Wisconsin Card

Sorting Test similarly offers a range of contradictory triggers. In this test, the patient

must arrange cards, which can be sorted by any of four criteria, but with every match,

there is also a mismatch. They are not instructed on a correct method, although they are

told whether they are right or wrong. In other words, both tests are puzzles that assess

higher-order processing (Damasio, 1994; Goldman-Rakic, 1991; Zihl et al., 1998). And
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there is no question that higher-order functions are badly debilitated in schizophrenia

(Damasio, 1994; Goldman-Rakic, 1991).

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Appendix III: Notes on data sources for table 3.

(Table 3 is on p.257)

1. The ubiquity of this symptom reflects that it is a minimum diagnostic criterion;

failure to meet this means a schizophrenia diagnosis is invalid.

2. The nature of delusions typically changes in different cultural milieus (Ndetei &

Vadher 1984).

3. It can be difficult to differentiate between delusions and hallucinations, because one

is putatively thought to cause the other. The higher occurrence of delusions than the

hallucinations that are thought to cause them may reflect the difficulty clinicians have in

differentiating these symptoms.

4. It is not known how much crossover or under-reporting there is with this symptom

and related symptoms (e.g. delusions with hallucinations).

5. These values are combined because it is impossible to assess these values separately

(Chika, 1982).

6. How this was assessed was not reported. Several studies show better concentration

among schizophrenic patients, many show worse.

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7. This figure should not be lower than for subgroups.

8. This figure is very complex because of heterogeneity of substance, the ubiquity of

abuse in the community, and cultural and other factors including increased negative

automaticity and lack of negative feedback.

9. The authors found that the group with bizarre delusions was the same group that had

other severe positive symptoms, and yet interrater confidence in what constituted

bizarreness was not as high. For this reason the authors recommended against inclusion

of this qualifier in the Opportunistic psychotic behaviour

A lot of the behaviour that is most feared by psychiatric clinical staff is opportunistic.

The following two articles attempt to explain this phenomenon.

The first, ‘All common psychotic symptoms can be explained by the theory of

ecological perception.’ Has been published in Medical Hypotheses, (2012: 78, 7-10.

doi: 10.1016/j.mehy.2011.09.029)

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3. QUESTION THREE: WHAT IS THE ROLE OF

THE BUILT ENVIRONMENT IN THE AETIOLOGY

AND SYMPTOMS OF SCHIZOPHRENIA?

The third research question looks at aetiological issues and at symptoms, as they are an

expression of and express the built environment.

If the above hypotheses and evidence aren’t enough to convince sceptics of the

relationship between schizophrenia and the environment, then the following arguments

may.

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Lost in Space: The role of the architectural milieu in

the aetiology and treatment of schizophrenia.

In review for a special issue of Facilities,

Expected to be published in mid 2013.

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Abstract

Purpose: Psychological and epidemiological literature suggests that the built

environment plays both causal and therapeutic roles in schizophrenia, but what are the

implications for designers?

Methodology: A translational exploration of the dynamics between the built

environment and psychotic illness, using primary research from disciplines as diverse as

epidemiology, neurology and psychology.

Findings: The built environment is conceived as being both an agonist and as an

antagonist for the underlying processes that present as psychosis. The built environment

is implicated through several means: Through the opportunities it provides. These may

be physical, narrative, emotional, hedonic or personal. Some opportunities may be

negative, and others positive. The built environment is also an important source of

unexpected aesthetic stimulation, yet in psychotic illnesses, aesthetic sensibilities

characteristically suffer from deterioration.

This paper focuses on the role the built environment plays in psycho-environmental

dynamics, in order that negative effects can be avoided and beneficial effects

emphasised in architectural design.

Limitations and implications: The findings presented are based on research that is

largely translated from very different fields of enquiry. Whilst findings are cogent and

logical, much of the support is correlational rather than empirical.

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Social implications: The WHO claims that schizophrenia destroys 24 million lives

worldwide, with an exponential effect on human and financial capital. Because evidence

implicates the built environment, architectural and urban designers may have a role to

play in reducing the human costs wrought by the illness.

Originality/value: Never before has architecture been so explicitly implicated as a

cause of mental illness. This paper was presented to the Symposium of Mental Health

Facility Design, and is essential reading for anyone involved in designing for improved

mental health.

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Lost in Space: The place of the architectural milieu in the aetiology

and treatment of schizophrenia.

The environment is repeatedly found to be a very significant factor in the psychogenesis

of mental illnesses – especially with non-affective psychoses. This article is a

theoretical discussion. It draws on the evidence that links the designed and constructed

environment to psychosis – and translates this evidence in a way that helps to inform

future design practice.

Mental illnesses aren’t homogenous. They share some similarities, but also have very

significant differences. In some cases, interventions that promote well-being in one

disorder may do the opposite in another (Pei et al., 2010). In fact, not only are mental

disorders heterogeneous, the symptoms that they present are, too (American Psychiatric

Association, 1994). Hallucinations, for example, range from very normal experiences

through to utterly bizarre and frightening ones. Hay (1994) reports that as many as 60%

of people will have experiences that could be classed as hallucinatory if religious and

numinous experience were to be counted. ‘Normal’ hallucinations and those associated

with dementia are often meaningful and are usually experienced in a single modality – a

person may see or hear a deceased relative or angels for instance, but they rarely see

and hear. Shizotypal experience, on the other hand, is far less common: it’s usually out

of control, malevolent and is usually multimodal –the visual and aural experience of

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having God appear on the TV to command them to commit suicide, for example

(Chadwick & Birchwood, 1994; Golembiewski, in review-d; Honig et al., 1998).

Despite the complexity of mental illness, the current evidence available to direct design

decision-making is mundane, predictable and offers little insight into the psychological

and phenomenal impacts of prescribed designs. Psycho-phenomenology of design

hasn’t had much attention since (Elliot & Bayes Friba, 1972; E. T. Hall, 1975, 1990;

Osmond, 1958, 1966). But since then, designers haven’t kept up with the explosion of

knowledge about the psychology and neurology of mental illnesses.

Other papers on the design of psychiatric design take a few distinct methodologies, and

all have limitations, particularly when it comes to understanding findings. Some are

based on post-occupancy studies of units that have been renovated (Eg. Hurst, 1960;

Sloan Devlin, 1992; Vaaler et al., 2005). These cannot extend beyond the working

principles of the design team and are further limited by the evaluation criteria of the

post-occupancy assessors. Another methodology is based on expert opinions rather than

identifiable empirical support (Eg. Davis, Glick, & Osow, 1979; Foley & Lacy, 1967;

Gross, Sasson, Zarhy, & Zohar, 1998; Gutkowski et al., 1992; 1957, 1958, 1966).

Some researchers ask the patients when seeking design solutions. This approach is

effective, with qualifications. Valid questions hover over the usefulness of patient

opinions when patients are typically confused about basic reality. Also, all patient

cohorts cannot be represented – the more critical patients who have ‘lost touch with

reality,’ (the disorganised or catatonic type schizophrenic patients in particular) are

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unlikely to give meaningful answers at all, whereas it may be hard to contain the

opinions of patients with manic disorders. For this reason, patient questionnaires are

rare. Where useful findings can be uncovered using this approach, they still lack insight

into the dynamics of the environment on the syndrome’s aetiology. Instead they tend to

gauge patient satisfaction with one choice or another (Middelboe, Schjødt, Byrsting, &

Gjerris, 2001) (Eg. Barnhart, 1996; L. S. Larsen, 1992; Perkins, in this issue). As

examples, Barnhart (1996) found that schizophrenic patients generally prefer garden

settings than constructed ones and L. S. Larsen (1992) found that schizophrenic patents

preferred garden settings that were extremely naturalistic, highly enclosed by shrubbery

and extremely complex in contrast to controls who preferred more open gardens, less

complexity and more manicured gardens.

Another approach in the literature is to inform design through models of health, illness,

stress and psychosocial needs. These methods provide a welcome richness for designers

because they focus on broad principles. But these methods are still limited to the

specifics of the overarching models. Is a study on an Alzheimer’s unit applicable to

schizophrenia for instance? The neurology, symptoms and apparent phenomenology of

Alzheimer’s dementia is totally different from schizophrenia, so the applicability of

Zeisel’s studies on the environments for Alzheimer’s patients (Zeisel, 2005, 2007;

Zeisel & Raia, 2000; Zeisel et al., 2003) cannot be naïvely superimposed. Even so,

some of the eight principles and sixteen dimensions of Alzheimer’s care of (Zeisel)

remain relevant. This draws us toward another approach: the development of design

principles that transcend the specifics of illnesses, and are based on models of sickness

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and health. Examples include: Jan Golembiewski (2010b); (2012e, 2012f); S. Kaplan

(1995); Lawton and Nahemow (1973), but where focusing on specific disorders may be

too specific, approaches based on principles may be too generalised.

The approach taken here is not to address problem behaviour (ie. boredom, getting lost,

wandering etc.) but to identify specific aspects of the built environment that appear to

be aetiologically related to psychosis, so designers may understand how the built

environment may actually foster or settle psychotic experience.

Background

Attempts to alleviate the symptoms of schizophrenia by altering the built environment

reflect widely held and well-supported hypotheses that perception is dysfunctional in

schizophrenia (Fletcher & Frith, 2009; Kapur, 2003; Kapur et al., 2005; Searles, 1960).

These beliefs are supported by the prevalence of hallucinations in 73% (n=980) of

diagnoses (Castle et al., 2006) and by a general lack of responsiveness in others (69%,

n=935 (J. A. McGrath et al., 2009)). Attempts to improve symptoms by altering

environments are not uncommon but are usually guided by naïve models of perception.

Changing finishes does not change the way things are perceived. A green-coloured

bicycle is functionally no different from a peach-coloured one and likewise, peach or

green paint on the walls of a day-room cannot change the walls in a meaningful way,

even if it does make the place noticeably more cheerful to a healthy visitor. Yes,

replicated evidence does suggest that interior decorations, if significant enough, may

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improve mental health outcomes, lower vandalism rates, and shorten stays (Hurst, 1960;

Sloan Devlin, 1992; Ulrich & Parsons, 1990; Vaaler et al., 2005). These outcomes are

welcome, and these innovations may guide designers to make better choices, but

because superficial approaches are unlikely to affect the psychogenesis that underlies

psychotic states, there’s promise for much better results yet.

It’s heretical to suggest that the built environment has a causal effect on schizophrenia,

but the facts are bare: when other known factors are discounted – ‘urbanicity’ at the

time of birth correlates to an increase in schizophrenia incidence by 28-34.3% (above

the null hypothesis) once genetic factors have been discounted (Kelly et al., 2010).

Furthermore, epidemiological studies consistently point to a similar figure – assuming

that all other factors are even. Data from meta-analyses suggest that urbanicity at any

time of life correlates with a 48% increase in schizophrenia incidence. This number is

one of the highest and most stable epidemiological factors for schizophrenia (van Os,

2004). Ultimately, this builds a compelling argument that the urban environment has a

causal effect on psychotic conditions.

The idea that urbanicity is psycho-toxic has been tested, but the reasons are elusive.

Ellet et al (Ellett et al., 2008) conducted ‘the Camberwell Walk Study,’ which found

that even a few minutes of exposure to the urban environment has a significant negative

impact on psychotic patients. A ten minute walk along the dilapidated but busy

Camberwell High Street (South London) resulted in a significant effect on a battery of

psychological tests, including Positive And Negative Symptoms Scores (PANSS)

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(anxiety t (14) = –3.57 (p = 0.003); and paranoia t = –2.69 (p = 0.017, negative scores

represent deterioration).

The finger points squarely at the urban environment, but what features of the

environment are culpable? Is the urban environment itself a problem, or is it a proxy for

something else? Can ‘urbanicity’ represent particular social mores, the prevalence of the

built environment, for indoor living? For the psychic pressure of too many people? For

richness of opportunity?

Attempts to identify specific environmental psycho-agonists have looked at how genetic

influences are multiplied by environmental interactions (van Os, Kenis, & Rutten, 2010;

van Os, Rutten, & Poulton, 2008) or social dynamics (Selten & Cantor-Graae, 2007).

Collip, Myin-Germeys, and van Os (2008) suggests that the urban environment may

represent a concentration of both these factors and more: an increased likelihood of

exposure to whatever it is that a patient is sensitised to. This approach seems wise, but it

still fails to identify anything specific. The key to identifying environmental psycho-

agonists (at the level of detail required by designers) is in the relationship between

perception and action.

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Ecological perception:

understanding the action/behaviour expressway.

Mental illnesses are not defined by pathology but by behavioural symptoms. If the

symptoms aren’t disingenuous, then symptoms must be the expressions of a state of

mind and reflect natural responses to perceived stimuli, whether they are hallucinatory

or real. Certainly delusions (the most prevalent symptom in schizophrenia (J. A.

McGrath et al., 2009)) are best understood as being very genuine expressions of a state

of mind that is informed by a perceptual bias (Garety & Freeman, 1999). But how can

perception be so disordered that a patient can, in all honesty, mistake people for trees or

genuinely believe that the TV is broadcasting personal messages to them?

In order to understand schizophrenic experience, we must first abandon naïve models of

perception. Even a lot of scientific literature makes the mistake of assuming that

perception is a process where colour, shape, texture and other qualia (sensory

information; colours smells etc.) are separated and recombined in the mind to form the

objects of knowledge, but this is not a tenable position. We simply don’t have the

computing power to recognise every perception from all available data (Clark, 2012 - in

press). Certainly such a process must occur in healthy perception wherever objects are

unrecognisable, but in most instances, perception is direct and active. One of the best

models for understanding this kind of perception is the Ecological Theory of

Perception. This theory doesn’t immediately promise all the answers to the complex

questions surrounding psychotic illness, but it does provide valuable insight into

phenomenology – the presumed basis for psychotic experience. The principle is that we

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perceive ‘affordances:’ opportunities to engage and to act in well-learned or instinctive

ways (Bargh & Dijksterhuis, 2001). The cue-behaviour dynamic occurs in a very

mechanical way – much as a transplanted heart will automatically start thumping when

exposed to warm blood. We notice (and involve ourselves with) things we can directly

recognise, manipulate and use (For empirical evidence, see Gibson, 1979). Meanwhile,

colours, sounds and other raw sense data are easily missed or immediately forgotten.

Superficial changes do not affect the opportunities a space provides. People act when

they recognise affordances, and while colour and shape information may make an

affordance more or less recognisable, people don’t act on qualia (sense information) as

such. The primary task of perception is to initiate action (Bargh & Dijksterhuis, 2001;

Gibson, 1979). There are different types of affordances and each has its own lexica of

action-responses. Although not all are relevant to architecture as such, they all become

relevant to the dynamics within the designed milieu.

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Emotional affordances

Some perceptions have direct emotional (affective) meaning. This kind of engagement

is very important for humans. Humour automatically solicits laughter, friendship solicits

happiness, betrayal solicits anger, and disappointment solicits resentment etc. But

psychotic conditions often prevent emotional affordances from eliciting a normal range

of responses. This is particularly so for those with affective psychoses such as bipolar

type 1 disorder or symptoms of paranoia (note that paranoid schizophrenia is a

technical term that does not necessarily denote the presence of paranoia as such

(American Psychiatric Association, 1994)). In fact, symptoms can be induced by

exposure to circumstances that are rich in emotional affordances.

This was found using an image study. The subjects were 17 psychotic patients

(catatonic schizophrenia, n=3; akinetic type 1 bipolar disorder, n=7; paranoid

schizophrenia, n=3; and type 1 bipolar 1, n=7) and ten healthy controls. All subjects

had their frontal cortices scanned using functional magnetic resource (fMRI) imaging

methods at the same time as they were shown a series of pictures. Some pictures were

generically negative and others positive. One finding was that the psychiatric patients

showed very aberrant activation and inhibition patterns when compared to the controls

(Northoff et al., 2004). Another was more specific: where the healthy controls perfectly

balanced their neural excitations and inhibitions in response to the negative images, the

patients’ neural reactions were out of control. Aberrant excitation correlates with

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excessive thought and activity. And where healthy controls showed some control for the

positive images, the psychiatric patients showed excessive inhibition, indicating that

they were unable to ‘let go’ and enjoy a healthy experience. These dysfunctional

perceptual reactions appear to explain a wide range of psychotic symptoms including

stereotypy and negative thinking patterns (Golembiewski, 2012a).

Emotional affordances are, by and large embodied in the social environment (including

pets), but they are also to be found within the arts. The emotional affordances are the

product of aesthetic qualities such as beauty and sublimity. Since antiquity beauty has

been recognised as a quality of architecture (Vitrivius, circa 15BC) – although the last

century has largely disposed of this legacy. Other arts, including the visual arts and

music remain very important sources for emotional affordances.

HEDONIC AFFORDANCES: Anything that is known to stimulate hedonic pleasure can

become a hedonic affordance. These include substances; ‘recreational’ drugs and

alcohol – and behaviours; gambling, sex, and sometimes theft and violence. In the

context of health facilities, violent behaviour is a significant issue, but other habitual

behaviours are largely prevented through lack of opportunity.

Among healthy people, the moderation imposed by neural inhibition renders many

hedonic affordances acceptable but without healthy neural inhibition, the use of hedonic

stimulants becomes a mental illness in its own right, commonly known as an abuse or

addiction (American Psychiatric Association, 1994; Golembiewski, in review-b).

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Physical affordances

A very common symptom of schizophrenia is that patients will drink when a glass is

offered, even if they aren’t thirsty. The symptom seems innocuous, but the subsequent

overconsumption of water has been associated with acutely low sodium levels and there

have been published hypotheses suggesting that this may be the cause of schizophrenia

(American Psychiatric Association, 1994; Reeves, 2004; Wyatt et al., 1988). While this

hypothesis is simplistic and untenable, the symptom draws attention the lack of control

that patients demonstrate around physical affordances. Physical compulsions are

common in a range of organic neurological disorders (Lhermitte et al., 1986). The

presence of a syringe solicits a jab, a gun solicits a shot and flowers solicit smelling and

picking (Lhermitte, 1986). Louis Kahn also observed that building materials have

intrinsic affordances: a brick wants to be built into an arch (1982).

Environments may be rich or starved of affordances. If the affordances are negative,

that might be a good thing. But if people are deprived of positive affordances, not only

is a beneficial opportunity lost, but the absence of positive affordances could also

contribute to the pathogenesis of the illness.

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Identification affordances

Another critical area where the designed environment plays a part in schizophrenia is in

the formation of the sense-of-self. There is no consensus about what creates a holistic

sense-of-self; but whatever it is, one of the most alarming phenomena in schizophrenia

is that the sense-of-self is lost (Kean, 2009; Sass & Parnas, 2001; Searles, 1966).

Symptomatically this is classed as a bizarre delusion that is particularly characteristic of

schizophrenia (American Psychiatric Association, 1994).

A number of prominent theories emphasise the effect of personal choice in the

formation of a sense-of-self, although there is considerable dispute about why we make

those choices (Eg. Bem, 1967; Deci & Ryan, 1991; Festinger & Carlsmith, 1959).

Arguments aside, our choices are universally accepted as being important in

establishing a sense-of-self. But the sense-of-self is absent when choices are automatic.

You don’t choose how to bring a cup to your lip, nor do you peg your identity on this

action. You don’t choose how to drive either (once these basic functions have been

learned), and if you did, it would be a signal to others that the way you drive is an

important expression of self. While automatic choices may define others’ impressions of

you, your sense-of-self is defined by the choices you choose to make and by those you

choose not to.

The designed environment is possibly the most prominent context for personal choice

making, in this regard it is likely to eclipse the social environment in importance – after

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all, the designed and constructed environment is ubiquitous, whereas the social

environment comes and goes. The constructed environment can therefore be understood

as being an important domain for self-expression and therefore for the establishment of

a sense-of-self. Choices abound in the negotiation of the built environment and many of

them are definitively associated with the sense-of-self. Many of these choices revolve

around affordances. What we choose to do, given the opportunity. The major product is

what we call ‘home’ (Golembiewski, 2009b).

In a diminished environment, alternatives (and therefore choices) are restricted. The

choice to sit in front of the television usually has little to do with choice, if there’s

nothing else to do. Television may even be harmful because it trains passivity in the

face of virtual opportunities and also a sense of unlikely narrative through the storylines

of television shows, and this may structurally reinforce delusional patterns of thought

(see below).

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Narrative affordances

Paranoid psychotic patients (the most common subtype of the psychotic spectrum) have

a predisposition (a trait, perhaps) to believe that a narrative is being constructed around

them in which they are the unwitting protagonist (S. Gallagher, 2007). These delusional

narratives hold that all events ultimately relate to the self. Exposure to any place with

strong symbolic loadings and omens of impending disaster or evil must stimulate these

delusions – and such omens will be concentrated wherever people and their symbols are

concentrated: whether it be the glint in someone’s eye, an unusual concentration of

police or the odd name of a street.

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Figure 30: The odd name of a street may be enough to trigger para-

noid thinking - Orpheus St, on the Camberwell walk – in an area with

extremely high schizophrenia incidence.

Some environments might be particularly loaded with affordances that lend themselves

to delusional narratives. This was demonstrated by the Camberwell Walk Study (Ellett

et al., 2008) described on page 303. Camberwell is known for its extremely high

incidence of schizophrenia – as much as 9 times the incidence of areas that are nearby

(Kirkbride et al., 2006). My methodology was not scientific and cannot be reported as

such, but I retraced the area where the study had taken place. My route took me across

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an Orpheus Street (Figure 30), past the Pre-Loved store (Figure 31), and went past

several signs from the Black Katz real estate agent (Figure 32). In one place there was a

gathering of at least thirty police. These examples are just a few of many more odd and

suggestive narrative cues that I experienced in my ten-minute walk. Other notable non-

verbal omens I saw included stray dogs, graffiti, pits in the street, ladders leaning over

walkways, Zeus brand motorbike helmets, and ominous posters for games and

superhero movies, and a number of extreme an cultish looking places of worship.

Figure 31: The Pre-loved store, Camberwell

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Exactly what triggers a delusional quest shall not be discussed here, but once it has

commenced, there’s little doubt that the urban environment will contain more salient

stimuli in which emotional, physical and narrative cues are present. Without robust

inhibition, these will exacerbate delusional beliefs and hallucinations (for an

explanation see Golembiewski, 2012a). It has yet to be tested, but this alone seems

sufficient to explain complex patterns of schizophrenia incidence, particularly the

increase in urban areas as compared to rural ones. A rural lifestyle is simply going to be

less symbolically loaded, more regular, and more benevolent in general.

Figure 32: Black Katz

real estate agents.

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Given the richness in urban narrative subject matter, it seems that a rural setting could

be beneficial for patients, simply because of the decreased concentration of these

agonists. The theory that the country is healthier than the city is one that dates back two

hundred and fifty years, and has taken form in some archetypal asylums: the York

Retreat and the Kirkbride units that were constructed in the nineteenth Century (Yanni,

2007).

But confusingly, circumstantial evidence demonstrates that schizophrenic patients

appear to be attracted to the city. Healing though the country may be, schizophrenic

patients show a tendency to drift into the 24/7 red light areas of the big metropolises,

where they sleep rough in doorways, traffic islands and in areas often recognised for the

highest levels of substance induced violence. Psychiatric migration isn’t huge; but

schizophrenic people tend to flow to the centre rather than into the more calming

environments of small towns and the country. A traditional (but still current) argument

links this psychiatric migration to poverty (Read, 2010). But where city centres were

once cheap, the opposite is usually the case now – yet wanderers still roll in. So another

hypothesis is proposed: that the frenetic action of inner city life may provide comfort,

even though quietness and security comforts most other people. And although frenetic

city life may indeed increase the symptoms, it may also provide relief to a particularly

troubling symptom: the loss of the ability to experience anything other than troubling

delusions and hallucinations. Here I suggest that psychiatric migration is based on

decisions a person makes, rather than following some sort of unconscious process. But

to understand how the hustle and bustle of city life might provide relief from

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hallucinations and delusions, it’s necessary to look at another aspect of perception: this

time at selective attention theory. This theory also explains another gamut of psychotic

phenomenology that is relevant to designers.

Selective attention

The tendency to live rough in noisy and uncomfortable places suggests that

schizophrenic patients may want or need more external stimulation. As just noted, this

could provide relief from relentless delusional thought patterns because it stimulates

bottom-up attention, one of the two kinds of attention in the perceptual psychology

canon: Bottom-up attention is drawn to all stimuli that are unexpected and unsought.

The opposite, top-down attention is given to expected or intended phenomena.

Affordances (discussed above) are perceived only through top-down attention.

Affordances are automatic actions that follow a known pattern of behaviour. For

example, a glass of water affords the familiar action of drinking. Bottom-up attention

can’t trigger behaviour, as its stimuli is not yet associated with set behavioural

responses. For example, we recently had a morning in Sydney where the air was red as

if it had been dyed (Figure 33). Nobody knew how to respond, so instead we enquired

(turning on the radio, etc). Enquiry (rather than action) is triggered by bottom-up

stimuli. Thus action-responses to bottom-up perceptions aren’t automatic. Events that

draw bottom-up attention beg answers, not actions. Unusual opportunities, awe and

unexpected experiences are brought to attention by bottom-up processes.

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Figure 33: In 2009 Sydney awoke to a bright red sky. Nobody seemed

to know why or what it meant. People asked one another, tuned to the

radio and news and invented theories. Some alarmist people suspected

it was the fallout from a nuclear holocaust. Photograph credit: Mans-

ke, Magnus.

Where top-down attention is stimulated very easily and requires little stimuli, bottom-up

attention requires momentous events to draw attention. These include significant

mismatches with normal expectations, sudden contrasts and jolts from prominent sense

data and information (Golembiewski, in review-d; Theeuwes et al., 1998).

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Both the bottom-up and top-down modes of attention appear to be moderated by

dopamine (Grace et al., 2007), a neurotransmitter that is dysfunctional in schizophrenia,

Parkinson’s disease, depression and most other mental illnesses. There are two different

types of dopamine dysfunction. Put simplistically, too much dopamine causes an excess

of top-down attention (so called ‘positive’ symptoms of delusions, hallucinations,

disorganised speech and thought and grossly disorganised behaviour (American

Psychiatric Association, 1994). A deficit of dopamine (in the simplest terms) causes

symptoms associated with bottom-up attention failure – the so called ‘negative’ signs

such as the noticeable absences of normal behaviour that are very difficult to treat

pharmacologically – such as staring blankly or catatonia (Golembiewski, in review-d).

For reasons that can’t be discussed here, dopamine is sometimes in short supply in one

part of the brain and in surplus elsewhere, meaning that positive symptoms and negative

signs frequently present together.

What this means in schizophrenia is that prominent, awesome or unexpected things tend

to go unnoticed, even when they are plainly obvious. Bottom-up attention deficits are

not easy to observe as an outsider, but may be the most severe and troubling symptoms

of schizophrenia and other mental illnesses. These deficits present a whole host of

problems, not least of all a tendency to not to notice the glaringly obvious (Broome et

al., 2007). The inability to engage with awe (even if only occasionally) is possibly

sufficient to cause depression, debilitate good judgement, erode a sense of well-being

and contract the perception of time, so that it always feels like it’s running out (Rudd,

Vohs, & Aaker, 2012). Other bottom-up perception abilities are even more critical; the

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ability to listen to internal messages that tell us we’re hungry, tired, happy or miserable:

the signals that guide us socially and monitor whether our behaviour is appropriate or

not, etc.

Deficits of bottom-up attention seem to give rise to very worrisome symptoms. Social

dysfunction, isolation, hunger and confusion can all be traced to this deficit. This

hypothesis proposes that schizophrenic migration to the most stimulating parts of town

may occur in order to stimulate bottom-up attention. To force real feelings – to have real

experience.

Facility designers should be aware that patients with bottom-up attention deficits will be

especially prone to accidents – they are prone to get lost and fail to notice aesthetic

concerns such as time and beauty (Golembiewski, in review-d). Reflexively designers

and faculty managers may want to restrict movement and behaviour to prevent accidents

and harm (See Chrysikou, - in this issue). But equally so, environments that don’t

challenge bottom-up attention with opportunities for discovery or aesthetic stimulation

are in danger of causing further atrophy of bottom–up attention. So a careful balance is

required – improved safety measures must be balanced with aesthetic generosity, and

opportunities for discovery and to act in a fulfilling and positive way (See Perkins, - in

this issue). Decision makers may want uniform and bright lighting, but should be

warned that variation is important, especially as it reinforces diurnal rhythms.

The combination of top-down oversensitivity and bottom-up deficiency exacerbates

symptoms, especially delusions because patients overvalue unimportant, but expected

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perceptions (Chadwick, 1992; D. Freeman & Freeman, 2008) while missing contrary

facts. This phenomena, known as a confirmation bias, is very common even outside of

mental illness, but in paranoid states it is ubiquitous (Broome et al., 2007; Nickerson,

1998). Most people with face-to-face experience of schizophrenic and bipolar type I

patients recognise this syndrome and recall patients who may be standing there, wearing

two left shoes, claiming that they have re-cognised Einstein’s theory of relativity. The

patient’s claims are reinforced by top-down oversensitivity (the false ‘eureka

experience’). At the same time their bottom-up deficiency makes them oblivious to the

fact that they are wearing two left shoes.

Where a patient’s delusions and hallucinations are often a worry for other people, they

contribute to a sense of comprehensibility for the patient themselves – at least the

patient is sure about what’s going on and why (even when they’re wrong) (Bergman et

al., 2012). This knowledge may not be much use to negotiate the world, but it does add

to an overall sense of coherence, and that is certainly beneficial (Golembiewski, 2012e)

and delusions should not be treated as a problem, but as a coping strategy when

formulating a model of care (the functional program) for a facility.

Bringing the theory to praxis: the architectural milieu

When discussing opportunities to address schizophrenic dysfunction with architecture, a

caveat is required. Any changes to safety, security and operational systems need to

reflect and parallel changes to the model of care. Furthermore, support from all

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stakeholders should also be in place (Plsek & Wilson, 2001). There can be no doubt that

security and operational features are essential for the function of a psychiatric facility

and arguments against their removal will include fears that opportunities for self-harm,

violence and vandalism may increase. Having said this, the possibility that safety

concerns are in conflict with health issues is also real (L. Bowers, Banda, & Nijman,

2010; Chrysikou, in this issue), and in the interests of good practice, must be discussed

with all stakeholders in a frank and open way. Some patients are not at risk of suicide,

and others are. Patients are individuals and so are their circumstances (For a review of

specific factors see L. Bowers et al., 2010). Some provisions that are essential for one

patient will be detrimental for another, and as such, a diversity of spaces and provisions

should be designed for. Alternatively, units should be customised for the individual

conditions that they are to treat.

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Addressing bottom-up attention deficits

If bottom-up atrophy can be successfully addressed, the deficit signs of schizophrenia

will definitively show improvement. As it stands, pharmacological treatment for the

deficit signs is “at best modest… results have been largely disappointing” (Buckley &

Stahl, 2007, p. 93). This leaves a huge onus on alternative treatments, including

improved environments. But how bottom-up attention may be stimulated in a positive

way without stimulating top-down attention is a difficult problem.

Converging lines of evidence suggest deficits of bottom-up attention are partly caused

by the built environment, but there’s little doubt that the same symptoms diminish an

architect’s toolkit to deal with it. Bottom-up attentional deficiencies mean that design

features may simply go unnoticed, and if they are, top-down attentional surpluses mean

that features may only be noted only because they feed on-going delusions. For

example, a red feature may be noticed, not because of the prominence of the colour in

the context, but because red is interpreted to mean power or some other such delusion

(Reina, 2010).

Eventually a tailored in depth longitudinal study will be needed to pinpoint more

specifics of causal relationships that the built environment have with schizophrenia, but

evidence is already strong enough to justify assuming causality. In the same way, WHO

advises caution with mobile phones because they are linked to the recent glioma

epidemic, although the mechanism has not yet been identified (WHO & IARC, 2011).

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There is still every possibility that the removal of psychosis agonists and provisions

intended to counteract deficit signs will not reverse schizophrenia, but because even

insubstantial environmental changes improve outcomes, a targeted and informed

approach should be tested because it may yield remarkable results. Interventions may

work directly or assist natural recovery.

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Aesthetic and natural engagement:

Because positive bottom-up attention is engaged by aesthetics, it follows that good,

beautiful, natural and especially awe-inspiring design is likely to be restorative.

Unfortunately, there’s no easy guideline that will ensure good and beautiful results, and

just about any attempt to do so will incur extra costs in construction. This objective will

also prove difficult to quantify because bottom-up attention is notoriously difficult to

assess (Theeuwes et al., 2000) as are aesthetics, which are subjective. The objective of

aesthetic appeal in architecture has a long tradition – perhaps older than man’s ability to

build. It is the third of Vitruvius’ classical qualities of good building; “firmitas, utilitas,

venustas,” that is, the importance of the delight that architecture can evoke (Vitrivius,

circa 15BC).

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Figure 34: Aesthetic and Natural Engagement: It’s Morning. A pa-

tient reads the paper in one of the many abundantly green spaces at

Khoo Teck Puat Hospital in Singapore (designed and photographed

by CPG).

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Environmental generosity

When bottom-up attention atrophies, synaptic plasticity is reduced. In other words, the

interconnections between neurons are thinned, leading to difficulties with learning,

spatial cognition, information and logic handling, as well as other cognitive functions

that lead to dementia (Schultz & Dickinson, 2000; Stephan, Friston, et al., 2009).

Similarly, a socially and materially deprived environment has also been shown to cause

synaptic atrophy – at least in rats, which are easier to observe and test ethically than

humans (F. Hall et al., 1998). Whether these losses occur for humans or if they are

associated with the psychogenesis of mental illnesses is still unknown, but should be

considered. And any positive or neutral enrichment of the environment should improve

synaptic plasticity. If this proves to be the case, environmental richness will directly

assist recovery – once again, this is a hypothesis that is well worth testing.

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Figure 35: Boxed for native birds are attached to trees and the walls

of Roseberry Park Mental Health unit (UK) designed by Medical Ar-

chitecture. Image courtesy of Medical Architecture. The intent is to

make the environment more positive and more generous.

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Dealing with top-down superfluity

Another approach to take in design intervention for psychotic conditions is to enrich

spaces with positive affordances. Top-down attention is a mode that is concerned only

for engagement. For this reason, designers should focus on what positive activity and

entertainment the space can provide and they should avoid the opposite – negativity and

passive environments.

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Figure 36: A photograph of a meercat, taken from an ambulatory

waiting room in The Royal Children’s Hospital in Melbourne. This

room, and the ones around it look into a meercat enclosure. A good

method to channel excessive top down attention positively. The Royal

Children’s Hospital was designed by Billard Leece and Bates Smart.

Photograph by John Gollings.

The biggest scale of architectural intervention will be at the level of typology. Typology

is the classification of function according to appearance; (a house that looks like a

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house, a bank that looks like a bank etc.) the main function of typology is information:

it informs people about the nature of the place they are visiting. As Kahn puts it, “rooms

suggest their use without a name” (Kahn, 1971). Strong typology simplifies

understanding, orientation and way-finding (Lynch, 1992). But not all typology is equal.

Typology is symbolically and phenomenologically loaded, and so sensitivity needs to

be given to types that may have negative meanings. Negative typologies may include

prisons, hospitals, schools, courts, psychiatric facilities, seclusion rooms and other

institutional buildings (Jan Golembiewski, 2010b).

Spatial arrangement within an environment is important because it has a direct effect on

how people navigate and use the space. This becomes increasingly important as skills

and cognitive abilities atrophy. For best effect, space should be logical, non-repetitive

and well marked with memorable objects and functions.

Opportunities for engagement also exist at a smaller scale. We don’t regularly engage in

walls, and although we do constantly engage with the floor, it’s only because the ground

beneath us is as ubiquitous as the prevalence of gravity. For the best part, we use the

ground automatically, not as a matter of active engagement. We may be more inclined

to engage in architectural elements if they offered us something more, like if they have

to be negotiated in some way. Aalto had people engage with the floor by bringing it up

closer to the eye level of a seated person – he created step-down living spaces. Walls

would come alive with washable crayons and licence to scribble. It’s true that given a

chance, some paranoid patients will use the opportunity to write threats and draw

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obscenities. But if these expressions were easily erased, even this kind of expression

may still be helpful – at least it shows engagement and is a distraction from more

harmful pursuits (Golembiewski, 2012e).

We engage with objects, particularly interesting ones (is not engaging a synonym of

interesting?) more than we do with basic building elements. Our bodies are designed to

interact with movable objects and moving parts. Light switches, venetian blinds,

knickknacks and furniture are the sorts of ordinary moving objects in the built

environment that we regularly engage with. Architectural elements like these are

designed for our bodies and actively invite engagement. We fill our homes, hotels and

workplaces with such things – probably because they fortify mental well-being.

Ironically, the few places that are stripped of physical affordances are the places that

need them in abundance - prisons and psychiatric facilities - because such facilities are

designed with safety as a priority over healing. This is exemplified by the overuse of

anti-ligature devices - showerheads that don’t direct the water properly, doorknobs that

can’t be grasped, tap-less basins, and furniture that can’t be moved because it’s blind-

bolted to the floor. Institutional strip-lighting is recessed and secured and blinds are

often secured behind tempered glass. It is not unusual for anything that moves to be

controlled remotely by nurses. The intention behind the installation of these components

is clear; to restrict possible affordances for self-harm, but the result is that the

affordances of the environment are restricted to an absolute minimum.

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Top-down attention (the relevant mode for the engagement in affordances) is driven by

the tonic dopamine system, which is thought to be overexcited in schizophrenia (Grace

et al., 2007; Heinz & Schlagenhauf, 2010). This means that psychotic patients have a

stronger drive to engage than healthy people do, even though the drive may be masked

by catatonic symptoms or deficit signs (Northoff et al., 2004; Sass & Parnas, 2001) The

‘irresistible’ drive to engage is demonstrated in the emotional image study detailed on

page 307. In this context, the removal of physical affordances is predicted to only

frustrate patients and aggravate symptoms, if not the underlying pathology of the

disorder. Given the removal of positive affordances, negative intentions are likely to

become only more focused. It is important to note that even healthy people start having

hallucinatory and delusional experiences when all affordances are taken away

(Grassian, 1983; Weckowicz, 1957). To counter this, Osmond (1957, 1958) (an

experienced clinician and one of the leading authors on the subject of the design of the

psychiatric milieu) recommended movable furniture, the provision of equipment to play

music, to write etc. Now we should go further: design teams should actively think about

the creation of positive affordances: the provision of a multisensory environment filled

with relatively harmless but fun toys, sports equipment, drawing tools, opening

windows, doors that have a pleasing sound when closed, adjustable lighting, heating and

ventilation etc. Sensory rooms have already been found to be successful in a psychiatric

milieu for engaging patients and helping to manage undesirable behaviour (McGann).

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Conclusion

Ascertaining what is ‘bad’ and what is ‘good’ in an architectural context is not

particularly difficult, but it’s subjective and there’s no established scientific method for

such assertions. Moreover, there will always be specific exceptions for particular

patients, particularly if they suffer from paranoia. In such an ambiguous context, it is

dangerously seductive for designers to rely on ‘neutral’ design options. However,

neutrality in the design of psychiatric facilities will only serve to amplify the negativity

or positivity of the environment. On a neurological level there’s no such thing as

‘neutral’ engagement – it’s either positive or negative. Thus exactly the same ‘neutral’

affordances can be taken either way, depending on whether circumstances are judged as

aversive (D. Freeman & Freeman, 2008).

The image study described on page 307 used generic emotive photographs to solicit

emotional responses. Designers can also use the same methods to elicit specific

emotional responses – for example, use paintings or images with generically happy

themes rather than resort to the safety of artistic abstractions. Ulrich identified views of

trees as positive (Ulrich, 1991; Ulrich & Parsons, 1990), and current projects that

employ these concepts have been spectacularly successful (see Figure 34). The ability to

engage with plants to touch them and lie under them is likely to be an even stronger

positive affordance, although there is a reticence to plant trees in or around psychiatric

facilities due to a risk of self-harm. Other architects have been experimenting with the

inclusion of animal enclosures in their hospitals, also with wonderful feedback (Figure

35 and Figure 36). But the beneficial potential of architectural care goes far beyond

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trees, animals and emotive pictures. All positive affordances are likely to support the

recovery from all mental illnesses, where negative ones appear to make the conditions

worse. There are affordances everywhere, seats to sit on, apples to eat, windows to

open, books to read. Most of these are positive, but care should be taken, because

potential negative associations aren’t always obvious because of superstitious and

symbolic encoding (eg. the thirteenth room along a corridor) or linguistic associations

(eg. the association between Lucifer and Lucite; a brand of transparent acrylic used in

skylights) etc.

Any opportunities that engage in personal choice are particularly important because

they will contribute to a sense-of-self. But the most elusive opportunities are those that

will have the strongest beneficial effect (if any effect can be evoked at all) – sublimity

and abundant beauty. The response to unintended delight is one of the most profound

atrophies in schizophrenia and one, what’s more, that is currently untreatable using

pharmacological interventions.

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Are diverse factors proxies for architectural influences?

A case for architecture in the aetiology of schizophrenia.

This article has been submitted to Cureus.

Abstract

The last half-century of epidemiological enquiry into schizophrenia can be characterized

by the search for neurological imbalances and lesions, for genetic factors. The growing

consensus that these directions have failed, means there is a growing interest in

psychosocial models and developmental aetiological models. Another area of recent

interest is in epigenetics – the multiplication of genetic influences by environmental

factors.

In the flood of data that is being produced around the schizophrenia epidemic, one of

the most consistent findings is that schizophrenia is an urban syndrome. Once

demographic factors have been discounted, between a quarter and a third of all

incidence can still be traced to urbanicity. This prospect has been taken to threaten the

psychosocial, genetic and developmental models.

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This paper explains that the environment is an inextricable factor in all the above

models, and sketches out the arguments for the built environment to be considered as a

valid epidemiological factor. It maps all these models and demonstrates how they

appear to miss the mark.

The reason the built environment hasn’t already become a de rigueur area of

epidemiological research is possibly trivial – it just doesn’t attract enough science, and

lacks a hero to promote it alongside other hypotheses.

Are diverse factors proxies for architectural influences?

A case for architecture in the aetiology of schizophrenia

Ever since John Snow successfully combined statistics and mapping to identify the

Broad Street pump as the source of London’s cholera epidemic of 1854, attempts have

been made to do the same for other illnesses. Like the Broad St. Pump study, the

research of Faris and Dunham into the incidence of insanity in Chicago also found a

locus of concentration – the inner city slum area (Faris & Dunham, 1939). But neither

pump, nor pathogen was found. Instead, the authors pointed to various ‘breeder’ factors:

race, migration status, poverty and access to sunlight. To make sure this was not a case

of the ‘cum hoc ergo procter hoc’ fallacy (for confusing correlation with cause), Faris

and Dunham gave evidence to counter the ‘drift effect ‘ caused by downward (affected)

social mobility. They found that parents of the ‘insane’ are equally likely to inhabit the

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slums. The possibility that upward (unaffected) social mobility out of these areas may

increase concentrations was not raised for many years (H. L. Freeman & Alpert, 1986).

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Figure 37: Cholera mapping. By charting of deaths in places of resi-

dence (black marks), John Snow revealed that cholera clustered

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around the Broad Street pump in the Barbican, London, 1854.

Source: Snow, J. (Rights expired).

Social Urban Pathogen

environment environment

Living Geographic
Cholera
environment environment

Figure 38: The epidemiology of the Broad St Pump charted the urban

(in this case the public infrastructure; the streets and the pump itself)

and the living environment (the quarters of the deceased) in order to

trace the effect of an unknown pathogen to a known illness (cholera).

The mapped areas are marked here in grey, and the finding – the

pathogen in black. The interplay of other factors (background) were

very significant; the social and geographic environments in particu-

lar, but knowledge of the contaminated water table and the way the

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social environment clustered around it was only made clear after the

cause of the cholera was identified.

Nearly a century later, similar methods are still being used to identify similar findings,

albeit with better controls for drift. But even with new methodological approaches,

tighter definitions (insanity has been restrictively redefined as schizophrenia) and

different cohorts, studies are still identifying lack of sunlight and social dysfunction as

‘risk factors’. The problem is that effect sizes are universally small and therefore cannot

identify causality. The multifactor hypothesis attempts to explain how small effect ‘risk

factors’ will compound to cause the illness (van Os et al., 2010). In some instances,

factors don’t only add together, they seem to multiply.

A well-documented example is a case of multiple factors compounding together is

ecogenetic (genetic x ecological factors (van Os et al., 2008)). This involves the

catechol-O-methyltransferase (COMT) gene and exposure to cannabis in adolescence

(age being another factor which is at once social, biological and environmental). All

people have the COMT gene, which is expressed in one of three functional states:

Met/Met, Val/Met and Val/Val. Whichever functional state a person inherits makes very

little difference in the likelihood of developing schizophreniform disorder as an adult.

When isolated, cannabis use also represents a relatively small risk factor for adult

schizophreniform disorders (OR 1.13, CI 95%). But individuals with the Val/Val

polymorphism were found to have a high risk factor (OR 10.9, CI 95%), if they were a

cannabis user during adolescence. This contrasts to the Val/Met variation (OR 2.5, CI
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95%) and to Met/Met individuals who showed no additional likelihood of developing

the disorder (OR 1.1, CI 95%), a risk factor that was statistically insignificantly lower

than the factor of cannabis alone (Caspi et al., 2005).

As the authors of the COMT x cannabis x age study (quoted above) made explicit in

their findings, statistical analyses that are used to identify causal relationships are at risk

of cum hoc ergo propter hoc (correlation or false cause being taken as cause) fallacies

being made in the interpretation of data. To protect against epiphenomenal confounding,

there is an increasing obligation to link data with biological mechanisms that are known

to be active in schizophrenia; this often involves atypical morphologies of dopamine or

glutamate neurons. Scientists often go further, with animal studies that inevitably

produce peculiar behaviour, which is declared to be an animal equivalent of

schizophrenia. The fact that there are dozens of such models, and each quite different

should be alarming (Kilts, 2001; Marcotte, Pearson, & Srivastava, 2001). This allows

for post-hoc strategies, where the animal model of schizophrenia is developed –

apparently to prove the hypothesis. These strategies don’t disprove the hypothesis, but

neither do they prove them. An example is the developmental Vitamin D Deficiency

Schizophrenia animal model, which was generated apparently to justify the Vitamin D

deficiency model of diagnosable schizophrenia (J. J. McGrath et al., 2010; J. J.

McGrath, Saari, et al., 2004). This model manifests “abnormal motor responses to

psychomimetic agents… and (b) cognitive deficits” (Eyles et al., 2009, p. S252).

Attempts to reverse engineer schizophrenia in animals run the risk of complicating data

with comparison fallacies; the diagnosis of human schizophrenia is subtle and great care
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has to be taken that it is not confused with other human psychoses (American

Psychiatric Association, 1994), much less with induced psychoses of other mammals –

even if they are primates. Furthermore, these strategies do not protect against other

fallacies such as information biases. Epidemiological mapping always contains such

biases, because inclusion criteria must be chosen prior to a study being undertaken.

These inclusions will be based on what is already known or suspected, and on what is

readily measurable. This means that larger factors may well be ignored because they

haven’t yet been considered, are difficult to control, to identify, justify or are not prone

to clustering and therefore to study.

One of the most widely replicated data in schizophrenia incidence is the influence of

‘urbanicity’ in the aetiology of schizophrenia. When tested against a null hypothesis

and when controlled for other known factors, meta-analyses of epidemiological data

show the influence of the urban environment as place of birth turns increases the odds

of developing schizophrenia significantly, and can be traced back to 28-34.3% of all

cases once genetic factors have been factored out (Kelly et al., 2010). This does not

have to be taken as evidence that the urban environment has an effect on schizophrenia

(this assumption would be fallacious), but is definitely a robust enough finding to

dismiss the automatic scepticism that abounds when this possibility is addressed.

Personally, I hypothesize that the urban environment has no effect on schizophrenia, per

se – but rather that it exerts a negative salutogenic influence – in other words, it fails to

protect against the forces that cause schizophrenia.

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Whilst ecological effects may be able to multiply a genetic predisposition, there’s no

reason to reject the possibility that all other factors may also be subject to

multiplication. This is speculated to occur in a social context, for instance, where risk

factors for schizophrenia such as low IQ, poor hearing or immigration status are

multiplied by social discrimination (Selten & Cantor-Graae, 2007)32. There are other

areas where multi-factor compounding takes place, which may be obscure because of

information biases. Of these, on occasion when it has been studied, the urban landscape

has consistently and evenly been shown to have a dose-dependent, raised incidence of

schizophrenia (Krabbendam & van Os, 2005). This appears to be causal because urban

birth and upbringing precedes the development of the disorder (Krabbendam & van Os,

2005).

The effects of many urban factors have been noted to be significant; social cohesion

(Kirkbride et al., 2008; Selten & Cantor-Graae, 2007), the quality of urban fabric

(Curtis, 2008), urban density (Curtis, 2008), the ethnic makeup of the area (Coid et al.,

2008), the geographical location (Torrey, Mortensen, Pedersen, Wohlfahrt, & Melbye,

32
Please note that the evidence of a poor IQ is weak – a recent meta-analysis appears to

demonstrate the opposite. A high IQ (prior to the prodrome) is positively correlated to

the development of the syndrome – 93% of 1007 subjects had good/fair high school

results (J. A. McGrath et al., 2009).

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2001) etc., but like genetic factors on their own, each factor has a relatively small effect

size, which appears to multiply collectively in the urban milieu.

The urban environment is a melting pot for many external factors, implying that multi-

factor relationships take place in the urban milieu. But the living environment (home)

provides the principal filter for the ecological effects of urbanicity and the factors that

urbanicity draw together: society, civic services, poverty, atmosphere, geography and

collective identity. The living environment is also – and possibly more importantly, the

melting pot for internal factors because it is the primary milieu for self-development and

for behaviour, especially during childhood, or in a depleted social network, as is usually

the case in schizophrenia. These personal development factors are very difficult to

measure directly, but they have already been implicated in the expression of

schizophrenia (Golembiewski, 2012a) (p.358- q.v.). It remains to be seen whether

‘urbanicity’ is a proxy for the built environment – and whether the etiological influence

of the urban setting may be as it is mediated by the architectures of home, or work and

of other places where day-to-day life takes place.

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Genetic Personal Social Urban

factors factors environment environment

Biological Living Geographic

Schizophrenia
factors environment environment

Historical Atmospheric
pathology environment

Figure 39: The multiple factors of schizophrenia epidemiology appear

to come together in schizophrenia itself rather than in any identifiable

epidemiologically distinct milieu. Having said this, of all the ‘path-

ways,’ the living environment (grey) is the most implicated because it

has important relationships with the social environment, the urban

environment and other epidemiologically significant factors, such as

geography. The high implication of the urban environment in the in-

cidence of schizophrenia (28-34%) may be in how closely it relates to

the living environment (and not vice versa).

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Genetic Personal Social

factors factors environment

Schizophrenia

Figure 40: Factors that are mapped for the social defeat hypothesis

(Selten & Cantor-Graae, 2007) pinpoint a single psychological mech-

anism (social defeat). This is the product of the compounding of genet-

ic factors (racial appearance, hearing impediments), social factors

(competition) and personal factors (use of illicit drugs, low IQ10, hear-

ing impediments).

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Genetic Personal
factors factors

Biological
Schizophrenia
factors

Atmospheric
environment

Figure 41: Factors that are mapped for the vitamin D hypothesis pin-

point a biological mechanism (vitamin D deficiency due to long north-

ern European winters). They also take account of some genetics (UV

reflectivity of skin) and personal factors (dietary vitamin D).

The Vitamin D hypothesis reduces many environmental variables to the supply of

vitamin D at various critical points of a person’s life: specifically to availability of

sunlight, the most universal supply of ultra violet-B spectrum of light (UVB), which is
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the precursor for vitamin D synthesis. For this reason, theorists predicted that people

born in the northern winters, where and when there is virtually no sun, would make

them susceptible to schizophrenia later in life. The hypothesis also suggests that the

high incidence of schizophrenia among immigrants from Africa and the Caribbean is

because the skin colour of these immigrants is dark and therefore reflects more UVB. In

addition, in the cold European climates, the reduction of UVB is compounded by the

need to wear heavier clothing. Other factors that affect vitamin D supply are dietary,

that is, they follow the consumption of fish and mushrooms (which is naturally high in

dietary vitamin D,) but also of vitamin D supplements (Kinney et al., 2009).

There’s no doubt, these associations tend to concur with the vitamin D deficiency

hypothesis once outliers are excluded. But despite the linear graphs that Kiney et al

present, the relationships are nonlinear and are marked by exceptions. The exceedingly

high schizophrenia clusters in North West Ireland, where the risks at (17.4/1000) are

among the highest in the world, appears to be one such exception (D. Freeman, 1994;

Torrey, 1987). This population is presumably largely fair skinned and has a strong

fishing industry (The Irish Department of Agriculture Fisheries and Food, 2009). It is

speculated that exceptions like these must be complicated by increased genetic risks of

an unidentified nature (i.e.. not skin colour genes) (Torrey et al., 2001). Other secondary

elaborations that are used to round up the outliers (frequently by some of the same

authors) is exposure to the feline parasite, toxoplasma gondi (Kinney et al., 2009;

Torrey, Bartko, & Yolken, 2012; Yolken, Dickerson, & Fuller Torrey, 2009) and

poverty, which is linked to an inability to provide youngsters with supplements (Kinney

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et al., 2009). Genetics, infections and parasites are just a few of many factors that also

appear to create a predisposition for schizophrenia that have no clear relationships with

vitamin D. Poverty may have a lot to do with vitamin D deficiency, but surely this is

very speculative.

Architectural factors are no less fuzzy. There are many architectural factors that may

affect people to predispose them to schizophrenia – these should be looked at as

seriously as fish consumption, and perhaps more seriously after all, the entire

schizophrenia research community is shooting in the dark when it comes to

schizophrenia aetiology and we should look seriously at all factors that show high

incidence rates. What about the quality and tenure of housing, workplace and facilities

for leisure – what direction do buildings face? Do they collect sunlight or reject it? Is

the air quality good or is it ionised or polluted? Are surfaces hard or soft? Are living

places comfortable or not? There are other ecological factors too; Are these

environments prone to fungal or bacterial growth? Are pets, vermin or other animals

present? And the quality of interior light: does the spectrum include UV? Is it bright

enough to trigger cones, or do people get by only using rod-vision? With all of these

other factors, add the effects of varying amounts of daylight, of temperature and

humidity, and the question of how clusters occur become very difficult to resolve.

In order to clarify whether Vitamin D deficiency is epiphenomenal or causal, Eyles et

al. undertook a study of vitamin D deprived rats. The researchers took a population of

pregnant rats and removed Vitamin D from their diets and the diets of their pups. The
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researchers were careful that the lighting was balanced, (light for 12 hours/day, dark for

12 hours) but with no ultraviolet spectrum to prevent natural synthesis of Vitamin D.

Other rats were kept in similar conditions, but were fed with vitamin D supplements

(Eyles et al., 2009). The results of this study were impressive, with the rats developing

certain key morphologies that relate to schizophrenia: these include a sensitization to

glutamate antagonists; minor distortions of brain shape; increased lateral ventricle

volumes; reduced differentiation; diminished expression of neurotropic factors; and

peculiar behaviours that are speculated to be ‘schizophrenic like.’ But the assumption

that induced rodent psychosis is equivalent to schizophrenia is difficult to support. Even

human schizophrenia is not a correlate of human psychosis and findings such as

ventricle size are not diagnostic criteria. Certainly they are common correlates – and

may even be directly due to vitamin D deficiency, but they, like so many other

correlations are tendencies that are not ubiquitous (Rosa et al., 2010). Psychosis is but

one set of defining symptoms, and one that is excluded if there is no marked decrease in

social function (American Psychiatric Association, 1994). The rats that were subject to

this study had no noticeable social dysfunction (Eyles et al., 2009) and were therefore

definitively not schizophrenic. The study is once again suggestive, but proves only that

the target has somehow been missed.

The complexity of data can be read a number of ways; either that the aetiology of

schizophrenia is itself complex, with multiple compounding causal factors as suggested

by (Muller & Dursun, 2010; Rutten & Mill, 2009; van Os et al., 2010; van Os et al.,

2008), alternatively the same variation may point be because we are close to the target,
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but still a little way off. Surely John Snow also noticed increasing incidence of illness

and death as he approached Carnaby Street (Figure 37)? Compare Figure 40 and Figure

41 with the bigger picture presented in Figure 39. High, but not absolute correlations are

expected from the social environment and from biological factors, but unless they show

a 1:1 correlation, the high variation appears to be the reflection of correlations,

epiphenomenal and co-morbid effects. If this is the case, the aetiology of schizophrenia

may still be parsimonious and singular but somewhere that hasn’t been studied properly.

The physical built environment is sufficiently complex to be such an illusive target. Just

because it cannot be as easily unravelled and analysed as the human genome and it can’t

be put into a lab and studied under microscopes doesn’t mean it’s not the bull’s-eye

we’re all looking for.

The effect the physical environment has on human psychology is often overlooked as a

causal factor. The physical environment has a powerful influence on the social milieu

and also on other possible aetiological factors, including civic, geographical,

demographic, personal and other ecological influences. In fact, the physical milieu has

an influence on nearly every factor that has ever been targeted in the search for an

aetiology of schizophrenia so far – the primary exception being genetics. This idea has

been scoffed at in the past33, and to this day, receives little scientific attention. The

33
Specifically, Professor John McGrath’s answers to my question after his presentation

at the Australiasian Schizophrenia Conference in Sydney, 22-24 Sept 2010

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reasons for this are twofold; Firstly it is difficult to control environmental conditions for

human subjects and therefore difficult to study. Secondly, environmental aetiologies

reach outside of the traditional domain of psychiatry and into architecture, non-clinical

psychology, anthropology and sociology.

Evidence of the etiological effect of the environment is in its infancy, but already

preliminary findings are no less coherent than those of alternative hypotheses – and are

possibly better. My paper ‘Lost in space: The role of the architectural milieu in the

aetiology and treatment of schizophrenia.’ (Q.V.) starts to show some correlations and

possible mechanisms.

The statistical variables raised by the vitamin D case can be explained by the physical

environment: In this model, low levels of vitamin D is an indicator of reduced exposure

to the sun because of being indoors. Even in a brightly lit milieu, light through glass is

filtered of most UV. The idea that vitamin D deficiency is an indicator of environmental

factors supported by other data – statistical data gathered in various boroughs of South

London show extreme variation in the incidence of schizophrenia. From one borough to

another contiguous one, incidence may increase by several times (Kirkbride, Fearon, et

al., 2007). Even accounting for ethnicity and other demographic data, the increased odds

ratio remains extreme (Kirkbride et al., 2008; Kirkbride, Fearon, et al., 2007; Kirkbride

et al., 2006; Kirkbride, Morgan, et al., 2007).

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The same data can be used as evidence of a completely different hypothesis. And one

that makes sense of a different set of data on the epidemiology of schizophrenia. Is it

possible that schizophrenia is the product of general stimulation or environmental

poverty? A childhood lifestyle characterized by housing estates and run-down

neighbourhoods, with overworked and stressed parents and too much babysitting by the

TV. But in spite of this variation, environmental poverty, like schizophrenia, can be

found even in the most salubrious homes and well-manicured suburbs, in countries

where sunshine – and therefore vitamin D, is bountiful. This paper poses the question:

could a vitamin D deficiency in early childhood point to a lack of sunshine, which

further implies (but doesn’t mean) a lack of stimulation? This would mean that the

aetiology for schizophrenia is psychological and possibly sociological, but not

biological, at least in the developmental stage.

Epidemiological studies of schizophrenia find that financial poverty and schizophrenia

have a close relationship, but like vitamin D, the correlation reflects an impressive

tendency, but still not a one to one relationship. The studies find the children of

migrants have particularly high (Beebe et al., 2005) incidence of schizophrenia in later

life. The data of (J. J. McGrath et al., 2010) suggests that this may be due to maternal

and neonatal Vitamin D deficiency in the ‘new country’ (Eyles et al., 2009). Whilst this

is a very worthy argument, the same data may mean that the kids are brought up with

little more than a TV for company and stimulation while the parents try to get ahead in

their new life.

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Schizophrenia is strongly associated with poor lifestyle, but the question about whether

poor lifestyle is the product of schizophrenia or predisposed people to it dates right back

to Dunham and Ferris.

McGrath asks “Is it time to trial Vitamin D supplements to prevent schizophrenia?” (J.

J. McGrath, 2010) To this question, the answer must surely be yes, but this doesn’t have

to be at the expense of taking care that the environments in which we rear our children

are rich and rewarding.

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AUTOMATIC AND OPPORTUNISTIC PSYCHOTIC BEHAVIOURS

There is a prevalent normative view that the physical stuff of existence – literally the

bricks and mortar around us has little to do with mental illness. This is a leftover from

Descartes, who argued that the mind and body were intrinsically separated (Bolton,

2008). My own findings refute this logic.

An important step in relating the symptomatology of mental illness to the environment

is directly addressed in the following paper.

In retrospect I have one problem with this article: the principle data source I cite

(Northoff et al., 2004), doesn’t differentiate between bipolar and schizophrenia when

the symptoms these syndromes express are the same (i.e.. Paranoia, catatonia). Whilst

this is reasonable, I regret this lack of specificity and strongly suspect that schizophrenic

automatic behaviours will not reflect the same negative bias. My reason is that the

identification of experience as negative is currently figured to be a product of the

amygdala, and amygdala function is considerably greater in bipolar patients than in

healthy controls (S. B. Perlman et al., 2012; Watson et al., 2012), whereas in

schizophrenia amygdala function is reduced or unchanged (Anticevic et al., 2012). This

argument is followed in (Golembiewski, 2012d) (see article from p.159 q.v.)

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Regardless, the paper is what it is: a useful tool for heuristically understanding the

relationship between the environment and psychotic conditions.

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Common psychotic symptoms can be explained

by the theory of ecological perception.

Originally published in Medical Hypotheses in 2012 (78, 7-10. doi:

10.1016/j.mehy.2011.09.029).

Abstract

The symptoms of psychiatric illness are diverse, as are the causes of the illnesses that

cause them. Yet, regardless of the heterogeneity of cause and presentation, a great deal

of symptoms can be explained by the failure of a single perceptual function: the

reprocessing of ecological perception.

It is a central tenet of the ecological theory of perception that we perceive opportunities

to act. It has also been found that perception automatically causes actions and thoughts

to occur unless this primary action pathway is inhibited. Inhibition allows perceptions to

be reprocessed into more appropriate alternative actions and thoughts. Reprocessing of

this kind takes place over the entire frontal lobe and it renders action optional. Choice

about what action to take (if any) is the basis for the feeling of autonomy and ultimately

for the sense-of-self. When thoughts and actions occur automatically (without choice)

they appear to originate outside of the self thereby providing prima facie evidence for

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some of the bizarre delusions that define schizophrenia such as delusional

misidentification, delusions of control and Cotard’s delusion.

Automatic actions and thoughts are triggered by residual stimulation whenever

reprocessing is insufficient to balance automatic excitatory cues (for whatever reason).

These may not be noticed if they are neutral and therefore unimportant whereas actions

and thoughts with a positive bias are desirable. Responses to negative stimulus, on the

other hand, are always unwelcome, because the actions that are triggered will carry the

negative bias.

Automatic thoughts may include spontaneous positive feelings of love and joy, but

automatic negative thoughts and visualisations are experienced as hallucinations. Not

only do these feel like they emerge from elsewhere but they carry a negative bias (they

are most commonly critical, rude and are irrationally paranoid).

Automatic positive actions may include laughter and smiling and these are welcome.

Automatic behaviours that carry a negative bias, however, are unwelcome and like

hallucinations, occur without a sense of choice. These include crying, stereotypies,

perseveration, ataxia, utilization and imitation behaviours and catatonia.

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Common psychotic symptoms can be explained

by the theory of ecological perception.

INTRODUCTION

Psychiatric illness may strike anywhere and in any demographic. And even though

some syndromes are somewhat treatable, they are often utterly debilitating. For

generations researchers and clinicians have been attempting to grapple with these

syndromes. The effort is impressive, and with more than 7000 peer-reviewed articles for

schizophrenia alone being published per year, (Schizophrenia Research Forum, 2011)

there is no shortage of high quality empirical data. But like the data, most hypotheses

relate to a small aspect of a single syndrome – a single symptom perhaps. Very few

hypotheses or studies look broadly at psychiatric disorders, despite the murky

boundaries between the syndromes and the reoccurrence of common symptoms in

diverse conditions. Take imitation behaviour for instance. This is common in conditions

as diverse as biological lesions, schizophrenia, and Alzheimer’s disease. (American

Psychiatric Association, 1994; Lhermitte et al., 1986)

Psychotic disorders:

The effect of unmoderated Ecological Perception

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Ecological perception

Until mirror neurons were first explained using the ecological theory of perception,

(Gibson, 1979; Rizzolatti, Fabbri-Destro, & Cattaneo, 2009) the theory had no traction

at all in neuroscience or medicine, even though the theory has robust support and is

relatively well accepted in the field of perceptual psychology. (Bargh & Dijksterhuis,

2001) But mirror neuron theory remains a relatively isolated curiosity in medicine,

where naïve belief in serial and qualia oriented perception still dominates. As long as

this belief is maintained, it is hard to imagine that the Descartian divide between the

studies of ‘mental’ psychotic states and ‘physical’ stereotypies will be bridged or that

the overlap of symptoms of psychiatric illness will ever be understood holistically.

The ecological theory claims that perception is action. (Gibson, 1979) A person doesn’t

just interpret sense-data (qualia) to compile an array of conclusions – the senses work

holistically to excite or inhibit the actions and thoughts that we find ourselves

continually engaged with. A ‘delicious’ smell is delicious because it invites eating. A

smell is repulsive when, prior to any subsequent rationalisation, an impulse to retreat is

triggered. A chair isn’t a composite of visual and tactile information; it is foremost an

opportunity to sit, the colour and shape of the chair may never even register.

Evolutionarily advanced animals are able to moderate action/thought perceptions with

‘self-control,’ a secondary process that allows a person to moderate (accept or

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transform) perception/action. The ability to choose how we react forms the basis for

autonomy (as much as there is such a thing.) (Searle, 2001) Simple creatures have no

such discretion. For them perception does not suggest nor demand behaviour, it is

indistinguishable from behaviour. A frog has no choice but to eat a moving object of a

certain size, and a barnacle has no choice but to stick to a hard surface, at which point it

begins to consume its own brain. (Bargh & Dijksterhuis, 2001)

Just as a cue for action is automatic, so too is self-control, at least for animals that have

a frontal lobe which is developed enough to enable self-control. (Bargh & Dijksterhuis,

2001) In healthy adults, the force of self-control opposes undesirable automatic

behaviour with an equal opposite. In most cases, reprocessing is so well balanced that

people will not realize when they have ‘acted’ or ‘behaved’ (refrained from action).

People sometimes notice after the fact: for example when they have just swallowed the

strawberry that was meant to decorate a cake. People may also recognize the impulse

‘telling’ them to jump when they reach a cliff’s edge, but equally so, they recognize the

impulse to self-control: the recoil of alarm at the thought of plummeting of a cliff, or the

guilty thought: ‘I couldn’t resist,’ regarding the strawberry for the cake. As Gibson

points out, the ecological theory makes sense of impulses triggered by perception:

“Fruit says ‘eat me’”. (Gibson, 1979, p. 140) And a cliff says, “jump!”

An ecological hypothesis for

the symptoms of psychiatric disorders

Because the laws of physics govern action, they should also govern ecological
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perception because perception is active. Newton’s third law is particularly pertinent in

this instance; to discharge an action/perception, an equal and opposite self-

control/reaction is required. Perception always triggers action, although those actions

may be transformed into alternative responses. Self-control can transform inappropriate

action/perception impulses into alternative thoughts, feelings, desires or actions, just as

energy can be transformed.

Stimulus may be desirable (positive), neutral or undesirable (negative). And

untransformed actions should reflect these qualities. A raucous positive action may be

permissible in specific contexts (a party for instance). It may be tempered to meet a

social milieu, but the reprocessing of a positive stimulus need only be partial. Likewise

for neutral stimulus – action resulting from positive or neutral stimulation will rarely be

harmful and unwanted. Negative stimulus, on the other hand, needs complete

transformation, lest unwanted, unintended and unmoderated actions and thoughts occur.

Although organic brain damage (particularly to the frontal lobe) may prevent

reprocessing, (Lhermitte, 1983, 1986; Lhermitte et al., 1986) a Bayesian system

moderated by the dopamine system (Fletcher & Frith, 2009) also appears to be in place

to restrict autonomous action in emergencies, (Das et al., 2007) allowing automatic

behaviour free rein. (Cowan, 2005) Because automatic processes are fast and accurate,

the evolutionary purpose for this bypass function is presumably to allow much faster

fight and flight instincts when needed. (Stephen Kaplan, 1992)

Unmoderated reactivity is definitively automatic, regardless of whether a patient is

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aware of their behaviour or not. Because all unmoderated actions originate outside of

the autonomous domain, they will appear to originate elsewhere. If primarily physical,

unmoderated reactivity will present as stereotyped behaviours. Unmoderated thoughts

are experienced as hallucinations when thoughts (internal voices) and visualisations

(imagery) are experienced without the context of autonomy. The experience of

continual automaticity will erode a sense-of-self, because actions are genuinely not

autonomous. The primary exceptions being cases of severe frontal damage, where the

sense-of-self cannot exist at all (Northoff & Bermpohl, 2004; Northoff et al., 2006), but

neither can choice (Lhermitte, 1986). Aside from these extreme situations, many of the

bizarre beliefs and experiences that are common among psychiatric patients, and

characterise schizophrenia are related to the loss of autonomy of thought and action.

(See Table 5, on p. 368.)

When automatic reactions are predominantly physical, they will be classed as catatonic

(DSM-IV 295·20). When excess automaticity primarily causes misidentification of

action and thought, the paranoid classification is most appropriate (DSM-IV 295·30). If

automatic behaviours interfere with normal trajectories of reason or behaviour, a

disorganised classification (DSM-IV 295·10) will be applied. If perceptual reprocessing

is overly applied to positive stimulus, schizoaffective disorder and affective flattening

may be the diagnosis (DSM-IV 295·70). Thus, one solution addresses all the primary

symptoms of psychiatric disorders.

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Evidence

Reprocessing of action/perception is thought to occur over the entire frontal lobe of the

brain. This area is subject to decreased connectivity in schizophrenia (Das et al., 2007),

and is also the primary site for the processing of creativity, choice (Dietrich & Kanso,

2010) and the sense-of-self (Northoff & Bermpohl, 2004; Northoff et al., 2006). The

function of the frontal lobe in reprocessing of information is evident because whenever

there is frontal damage, some degree of unusual automatic behaviour is ubiquitous. A

study of fontal lesions showed that 100% eventually eventuated in imitation behaviour

or a more severe disorder involving loss of autonomy (4%, n=1), (n=29). (At the time

the study was conducted, there was one exception, whom presented with headaches.

This patient developed imitation behaviour shortly after the study period.) (Lhermitte et

al., 1986)

The reprocessing of negative stimulus was imaged by Northoff and colleagues

(Northoff et al., 2004). In this study, akinetic catatonic patients (DSM-IV 295·20, n=3;

bipolar 1 DSM-IV 296·54c, n=7), psychiatric patients (paranoid schizophrenia DSM-IV

295·30, n3; bipolar 1 DSM-IV 296·54, n7) and healthy controls where exposed to

emotionally positive, neutral and negative stimulus in the form of pictures (from the

International Affective Picture System) while undergoing fMRI scans of their entire

frontal lobes. For positive and neutral stimulus, all subjects showed processing

imbalances (eccentricity) where excitation (+) exceeded inhibitory reprocessing (-). For

negative stimulus, however, only the psychiatric cohorts showed any eccentricity. They

were all unable to balance the negative impact of the stimulus over the areas the frontal
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lobe (the orbitofrontal, anterior cingulate, medial prefrontal, lateral prefrontal, premotor

and motor cortices). In contrast, healthy controls did this nearly perfectly

(variation=0·63% n=21, p<0·05). All cases of eccentricity are speculated to relate to

automatic behaviours, but this does require further testing using experiments based on

the model developed by Northoff and his colleagues (Northoff et al., 2004). At this

stage it is difficult to monitor hallucinatory or delusionary thought, but in further

experiments, care should be taken to monitor for physical tics and mannerisms. To see

just how much they correlate with the neuronal eccentricity.

Conclusions and predictions

This hypothesis explains a broad spectrum of symptoms, from hallucinations and

delusions to disorganisation and catatonia; and wherever the symptoms present –

whether they occur in organic lesions, onset dementias or in psychotic illnesses.

It appears that any dysfunction within the frontal cortex (regardless of specific region)

will cause automatic and unintended action (imitation behaviour or a more severe

disorder also involving the loss of autonomy). But the frontal cortex must still be largely

functional for these automatic actions to be experienced as hallucinations or lead to

delusions. Without a functional frontal cortex it is unlikely that self-reflection can occur

at all, although this doesn’t mean that automatic expressions of happiness and sadness

are disingenuous. On the contrary, insincerity is one of the inhibitory functions that are

debilitated. The declarative experiences of patients are likely to be more genuine than

those of healthy individuals who are better equipped to voluntarily moderate their
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behaviour and take ownership of it. In many ways this explains some of the most vexing

questions about psychotic behaviour. When patients blame others for making the world

a bad place, their delusions are very genuine. And a diminished sense-of-self may easily

turn to selflessness and when actions are unpredictably automatic, sometimes the results

are very nasty indeed. (Volavka et al., 2011)

Not only does this hypothesis predict much of the bizarre experience and behaviour

associated with psychotic illness, it also predicts a measurable neurological correlate. If

inhibitory processes in the frontal lobe are insufficient to balance excitatory impulses, it

would follow that the primary inhibitory neurotransmitter within the frontal lobe (ϒ-

amniobutyric acid – GABA) will reflect this with moderate down-regulation, moderate,

because only negative impulses are properly balanced in healthy adults and also because

positive impulses are inordinately inhibited in severe psychotic conditions. Current

evidence seems to point this way, but has hitherto remained unexplained. (Li,

Kellendonk, Simpson, Kandel, & Gao, 2011)

It is hoped that this hypothesis will allow scientists and doctors to understand some of

their science in a more human way. To understand that an excited neuron has a corollary

action, and that the Newtonian laws even apply to the minds we live in.

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Symptom Explanation
DELUSIONS
Delusions of control, thought insertion Automatic (non-autonomous) actions, esp.
delusions and other misattribution delusions when experienced alongside hallucinations.
Grandiose delusions Hallucinations with positive bias.
Paranoid delusions Perception with negative bias due to
Somatic delusions improperly reprocessed negative stimulus
(Figure 42 and 43).
Delusions associated with automatic (non-
autonomous) body functions and hallucinated
experience.
HALLUCINATIONS
Voices Automatic (non-autonomous) thoughts, esp.
Visual hallucinations ones with negative bias.
Automatic (non-autonomous) visualisation,
esp. images with negative bias.
DISORGANISED SPEECH
Disorganised thought, derailment, Automatic thoughts interfere with normal
tangentality, communication difficulties, alogia sequence of logic and narrative structure.
GROSSLY DISORGANISED BEHAVIOUR
Disorganised behaviour, attention deficits, Automatic actions and thoughts interfere with
agitation, stereotypy, perseveration, normal sequence of behaviour.
behavioural monitoring peculiarities, agitation,
inappropriateness, silliness
NEGATIVE SIGNS
Affective flattening Attempts to reprocess negative stimulus
Negativity indiscriminately causes flattening. Some
positive automaticity is lost with the negative.
(See the reduced positive reactivity in Figure
42)
Incomplete negative reprocessing causes
negative bias.
CATATONIC SYMPTOMS
Catatonia and other deficit signs Evidence demonstrates that these symptoms
are caused by greater affective impact of
action/perception alongside a strong
reprocessing eccentricity. See figures 42 and
43 (Northoff et al., 2004).

Table 5: Most of the symptoms and signs listed in the DSM-IV for

schizophrenia and related disorders can be explained using the eco-

logical perception model.

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Overall impact (activation vs inhibition voxels) 2807

2181

1484
Amplitude

-796

-1595 -1463
C P H
Negative stimulus

Figure 42: Overall impact and excitatory eccentricity (deviation from

balance) caused by negative stimulus

C: Cataleptic (DSM-IV 295·20, n=3; Bipolar 1 DSM-IV 296·54c,

n=7) P: Psychiatric (Paranoid schizophrenia DSM-IV 295.30, n3; bi-

polar 1 DSM-IV 296·54, n7) H: Healthy controls

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Excitatory Eccentricity
0
C P H
Neg 1212 1385 21
Pos 598 470 881
Neu 812 539 198
Eccentricity (all stimulus)

Figure 43: Overall eccentricity caused by all stimulus: Note the in-

version in responses. Where healthy people are able to attenuate neg-

ative stimulus and are able to ‘express’ positive responses, the oppo-

site is true for both psychiatric cohorts.

The overall impact of exposure to negative stimulus (from the Interna-

tional Affective Picture System) measured by activation (+) and inhi-

bition of neurons (-) throughout the frontal lobe. Numbers represent

the sum activity of orbitofrontal, anterior cingulate, medial prefrontal,

lateral prefrontal, premotor and motor cortices.

Grey areas show the extent of deviation from equanimity.

C: Cataleptic (DSM-IV 295·20, n=3; Bipolar 1 DSM-IV 296·54c,

n=7) P: Psychiatric (Paranoid schizophrenia DSM-IV 295.30, n3; bi-

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polar 1 DSM-IV 296·54, n7) H: Healthy controls (Based on Northoff

et al., 2004).

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PSYCHIATRIC VIOLENCE

The concept presented in Medical Hypotheses 2012 can be used to understand not only

bizarre behaviour, but also psychiatric violence. The following paper was written for a

special issue of the APA journal, Psychiatric Violence, on technology and violence. It

was rejected principally because it was the only article that didn’t conceive technology

in terms of computers. The paper was subsequently reviewed by the journal and

returned for changes. I haven’t had the chance to make these changes and try again.

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Introducing the concept of reflexive and automatic violence:

a function of aberrant perceptual inhibition.

Abstract

It is commonly thought that psychiatric violence is motivated by delusions. In the

reflexive violence model, delusions are formed concurrently or subsequently to

rationalize the motivational power of an object.

The reflexive violence model proposes that perceptual stimuli trigger unwanted actions,

hallucinations and delusions. The model is based on one of the central tenets of the

theory of ecological perception. Here the opportunities enabled by an object (to a

perceiver) are cues to act. As an apple triggers a desire to eat, a gun triggers a desire to

shoot. These affordances (as they are called) are part of the perceptual apparatus, they

allow the direct recognition of objects – and in emergencies they enable the fastest

possible reactions.

Even under normal circumstances, the presence of a weapon will trigger inhibited

violent impulses. The presence of a victim will also, but under normal circumstances,

affordances of this kind don’t turn into violence because negative action impulses are

concurrently totally inhibited whereas in psychotic illness – and possibly in other mental

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illnesses also, negative affordances are treated as emergencies, and then far exceeds the

inhibition threshold, and what would have been recognition becomes blind, automatic

actions.

A range of mental illnesses from substance abuse to schizophrenia and biological

lesions can cause the inhibitory impulse to be exceeded. At it’s most innocuous, this

causes both simple hallucinations (where the motivational power of an object is

misattributed), but the act of perception may have the power to trigger very serious

violent acts also. This kind of violence is devoid of motives or any planning and is often

shrouded in amnesia or post-rational delusions.

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Introducing the concept of reflexive and automatic violence:

a function of aberrant perceptual inhibition

As part of an observational study, two patients were invited (separately) into the

apartment of their doctor, the investigator for the study. The patients were to be exposed

to a few tableaus (a made bed, a sideboard laid out with food etc.) and their behaviour –

already known to be bizarre – was to be recorded. One of the patients, a 52-year-old

housewife, was presented with was a syringe and vial of saline. Without hesitation, she

drew the saline and attempted to give the doctor an injection.

The other patient, a man this time, was a 51-year-old engineer was presented with a

painting sitting on the ground. A hammer and nail were nearby. The patient used the

tools to hang the painting. The patient was led into a bedroom. He stripped and hopped

into bed. A gun lay out on a tabletop. When the patient spotted it, he headed to it with

an expression of sheer delight. The patient picked it up and spun the barrel. There were

no cartridges, so he searched until he found some, then he loaded the gun… and the

experiment had to be called off. The doctor had to intervene to confiscate the weapon.

The patent was not angry, he had no prior homicidal intentions but would have had no

choice but to shoot the doctor just as the woman has no choice but to inject him with

saline. The gun was ‘telling’ the man to shoot (Lhermitte, 1986). Neither patient

suffered delusions because they lacked the self-reflexive criticality required to consider

their actions. What they did experience, however, were simple ‘non-bizarre’

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hallucinations. Somehow, these inanimate objects were able to speak and with enough

authority to motivate action: their instructions to act came from thoughts that arose

when they were in the excitatory presence of an object.

The issues of interpersonal and (self-inflicted) violence are a wicked problems (Kazdin,

2011); they abound with open-ended questions, shifting goalposts, compromised

solutions for an open number of stakeholders, and any number of other confounding

problems that prevent resolution. A characteristic of wicked problems is that they

embed other wicked problems (Kunz & Rittel, 1972). One of these is the problem of

psychiatric violence. At some point violence may become the product of a psychiatric

illness, and not of rationally considered alternatives (Alderman, 1916). This article

attempts to shed light on some of the processes involved and normative explanations for

them so that psychiatric violence can be better understood and identified more readily

and to ascertain to what extent violence is compos mentis (in right mind).

Although the issues of psychiatric violence are definitively wicked, current debate about

focuses on delusional intentions – not only is this a single and relatively contained

perspective, but it is also a case of ignoratio elenchi logic, because it leads nowhere. To

date, there is no cogent and well-accepted hypothesis for delusions, and of the strongest

models available, post-experiential explanations or post-experiential meta-logic is taken

to be their common source – for a review see (Garety & Freeman, 1999).

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The delusory intentions hypotheses are nevertheless relatively well accepted (De Pauw

& Szulecka, 1988; Richard-Devantoy et al., 2008), despite being poorly developed – if

anything there is evidence that delusional patients don’t act on their delusional beliefs

See review (A. Buchanan, 1993), but rather that delusions occur to explain actions that

are otherwise inexplicable (Startup et al., 2008). This is a parallel of Bem’s self-

perception theory: ‘Individuals come to “know” their own attitudes, emotions, and other

internal states partially by inferring them from observations of their own overt

behaviour and/or the circumstances in which this behaviour occurs.’ (Bem, 1972, p. 2).

Delusional intentions are roughly classed thus: paranoiac-defensive narratives, where

violence occurs in the belief that it is in self-defence. Grandiose and manic-delusional

narratives are where violence is motivated by a swollen sense-of-self-empowerment or

sense of entitlement; and altruistic narratives, where violence is regrettable, but believed

to be essential for the greater good (Richard-Devantoy et al., 2008; Richard-Devantoy et

al., 2009; Volavka et al., 2011). In these paradigms the delusionary motivations for

violence are considered to be a product of psychiatric illness, but the mechanism that

turns perception into action is not questioned. In this paper, the case for violence as a

product of perception is introduced. In this model, post-rationalised delusions are

separated from delusional intentions. They are presented as rationalizations of reflexive

actions that occur as part of the perceptual process.

In any violence, technology is usually conceptualized as a tool. The reflexive action

model presents the violence–technology relationship as being prior to or at the very

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least concurrent with any subsequent delusional ideation, because the technology is not

just a means, but part of the very hallucinatory experience that drives delusional

narratives.

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Automatic perception and reflexive action

There is a long history of debate about how people (and animals) perceive, and models

abound. I refer readers to some of the literature, but will not enter the debate in this

paper. For reviews on the many models and their strengths and weaknesses, see

(Baldwin, 2007; Clark, 2012 - in press; Golembiewski, in review-d) and perhaps a text

book also. Instead, this article hypothesizes about the implications of the ecological

theory of perception (one of the prominent theories of perception) when applied to the

question of intrapersonal or self-inflicted violence. The ecological theory of perception

is not always useful for understanding perceptual phenomena – in particular it has a

weakness when it comes to perceiving unrecognizable phenomena (Ullman, 1980).

Despite this weakness, the theory has demonstrated strengths for understanding how

recognizable objects and opportunities are identified (Bargh & Dijksterhuis, 2001;

Gibson, 1979; Ullman, 1980)(Peer commentary); (Withagen & van Wermeskerken,

2010).

The concept of ecological perception is that objects and opportunities are recognized by

the actions they enable. An object is recognized by the thoughts that commence as part

of the process of perception; once it is familiar, a syringe is not recognized by its colour

or shape – it is recognized by impulses that revolve around the potential opportunities it

enables. Equally an apple says eat me (Gibson, 1979), and a gun says shoot me. In

humans and animals with more developed frontal cortices, these impulses are not

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always acted on because of a pre-existing inhibitory reflex, which is primed by social

and physical contexts as suggested by the milieu (Proshansky, Ittelson, & Rivlin, 1972).

A useful term for contextual inhibition is found in foundational environmental

psychology literature: it is the behaviour setting (Barker & Wright, 1954).

In the ecological theory of perception, perception is not understood as a cognitive

system, but a desire/action management system, and is thus more visceral. It is a stab of

hunger or a proto-desire for a taste that causes the recognition of food – not an analysis

of available sense data. This means impulses will progress into action if a decision to

engage with an object is ever made. In healthy people and more evolved animals,

decisions are made at the moment of recognition whether to engage, and accept the

impulse as a declarative desire, or to ignore it and choose another course of action

altogether. Impulses are limited by context (the behaviour setting, and further by

choice). But in a number of conditions including hypofrontality, the choice is never

made and actions are automatic (Golembiewski, in review-b, in review-d) (Articles on

p.373 and p.204 q.v.). Simple creatures such as a barnacle that have no frontal cortex

have no choice but to act according to their perceptions (Bargh & Dijksterhuis, 2001).

Behaviour is inextricably related to opportunities, even from an evolutionary

perspective (Withagen et al., 2012). Objects that contain such opportunities and thus

demand action are called affordances. (Bargh & Dijksterhuis, 2001; Gibson, 1979).

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Neither behaviour settings, nor affordances appear in isolation. Just as perception is

continuous, so too are affordances (Clark, 2012 - in press). All animals engage in

affordances because they are always on the lookout to recognize them. One is connected

to another in series, and likewise behaviour settings are connected similarly.

Affordances will build on one another. In the study above, the doctor offered a

complimentary affordance to the syringe and the gun – because given the context of one

affordance, he became the natural complimentary affordance; he became a target. His

status changed from doctor to target only once the syringe or gun had been

automatically engaged with.

Reflexive violence is hypothesized to occur when the constant stream of action and

thought that we humans are continually engaged in, is completely co-opted by a series

of automatic negative affordances, when either in a setting that allows such action, or

(more likely) when there are deficits of the automatic inhibition imposed by the

behaviour setting. These may be symptomatic of psychotic or biological conditions or

substance abuse.

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Deficits of perceptual inhibition

The patients with the gun and the syringe were showing symptoms of a spectrum of

utilization behaviour disorders, all of which erode personal autonomy. These are

utilization behaviour, imitation behaviour and environmental dependency syndromes. In

one study, these were found to be ubiquitous in cases of frontal lesions; 100% of the 29

patients with frontal lesions that were studied developed these behaviours to some

degree (Lhermitte et al., 1986). 52% (n=15) of these patients developed utilization

behaviour, where engagement in affordances cannot be prevented, even against

authoritative contrary instructions (Lhermitte, 1983); Other behaviours included

environmental dependency syndrome which is where a patient depends on behavioural

cues from the milieu (Lhermitte, 1986); and imitation behaviour, where patients

automatically imitate the behaviour of others, for example, if they are watching

someone else putting on a pair of glasses, they will try to do so themselves, even if they

are already wearing glasses (Lhermitte, 1983). Only one patient at the time of the study

showed none of these syndromes, but he developed them three weeks after the study

was complete. These syndromes, bizarrely lacking in autonomy, are presumably caused

by the excitatory presence of an affordance (perceived opportunity) when the inhibitory

neurons of the frontal cortex have been severed (Golembiewski, in review-b, in review-

d; Lhermitte, 1986). This makes the perception-action pathway automatic, and in

extreme cases, functionally identical to the perceptions of a barnacle, except for a much

larger and expandable ontology, and therefore more programmed reflexive actions.

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The utilization behaviour spectrum disorders seem to occur wherever frontal

connectivity is lost. The report of Lhermitte et al. (Lhermitte, 1986) also identifies other

conditions that sometimes cause utilization behaviour – these include various other

focal lesions, Parkinson’s disease, progressive supraneuclear palsy, Alzheimer’s

disease, and multiple vascular accidents.

Utilization behaviour-like patterns are also common in non-biological psychotic

conditions. These are more complex than biological lesions, and are thus not strictly

speaking the same. In psychotic disorders at least, the inhibition of perceptual stimuli

appears to depend on the emotive nature of the stimuli, with percepts that have a

positive affective bias being over-inhibited and affectively negative ones being

extremely under-inhibited. This was found in a sample of 10 akinetic psychiatric

patients, 10 more common psychiatric patients1 and ten healthy controls. All

participants were shown emotive images while undergoing fMRI scans of their frontal

lobes. The emotional bias of the images was generic and indisputable, regardless of

acculturation. Negative pictures included things like a mangled face, positive ones a

happy baby. A neutral condition was also added – it was a piece of grey card (Northoff

et al., 2004). Among other findings, it was noticed that in the negative condition healthy

controls showed equal inhibitory and excitatory activity, thus cancelling each other out.

Psychiatric patients, on he other hand, showed very low levels of inhibitory activation

relative to neural excitation for negative stimuli, thereby replicating utilization

behaviour spectra conditions, albeit specifically in emotionally negatively charged

circumstances (Golembiewski, 2012a) (see article from p.358- q.v.). Thus patients with
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schizophrenia and other psychoses may also present with automatic and uncontrollable

behaviours, but only when the objects of perception are seen as negative

(Golembiewski, 2012a).

It may be difficult to assess what constitutes negativity, but affective qualities are often

relatively universal, despite the undeniable fact that subjective opinions are based on

culturally encoded schemata. And different schemas will evoke different responses - if

the ‘object’ of attention is situational, negativity may mean harmful, threatening or

wrong. In a social situation negativity may be linguistically encoded, and communicated

through words and deeds. Social expressions of negativity may include expressions of

contempt, disgust, defensiveness, belligerence, dominance, stonewalling, anger,

whining, sadness, tension or fear (Carrere & Gottman, 1999). It’s important to note that

these affective cues are subtle and function on an automatic and precognitive level (if

cognition strictly speaking plays a role at all), and thus may never be declarative. Social

negative affect, for instance, is typically not declaratively noticed by participants, but

can be identified by psychologists trained in the Specific Affect Coding System

(SPAFF) (Gottman et al., 1996). Furthermore, with automatic actions, the time lag

between impulse and action is virtually non-existent, as such automatic actions cannot

be considered to be premeditated (Bargh, 1997). This is supported by the close

examination of the psychologist’s reports from a French courthouse, which recorded

210 homicides committed between 1975 and 2005. Of these 14 were identified as being

potentially psychiatric. Schizophrenic patients committed all, and all shared distinctive

features; none of the 14 homicides appear to have been premeditated, all were
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committed alone, and all used available means (e.g. bare hands) (Richard-Devantoy et

al., 2009).

In a grounded study of 30 women in extremely abusive relationships, all reported that

attacks appeared to occur unpredictably, suggesting that much domestic violence may

also be unpremeditated. The caveat here is that both the author of the study attributes a

motivation to this unpredictability; “Instilling the sense of fear that a physical attack is

possible at any moment is one way battering men control their partners” (Langford,

1996)p. 372). Like the observations of Richard-Devantoy et al. (2009), these attacks

appear to be spontaneous and unpremeditated, because assailants ‘mostly’ used

available means – victims were ‘hit with objects such as telephones, lamps, chairs’

(Langford, 1996), p. 374). To link these assailants to the psychiatric ones further,

victims reported noticing symptoms that are characteristic of severe psychiatric

conditions, such as “psycho eyes” and degraded speech patterns (Langford, 1996), p.

376). Abnormal eye gaze and is not useful for diagnosis of psychotic disorders, but they

are sufficiently common that they have been the subject of many studies and are thus

recognized as associated symptoms of schizophrenia. Degraded speech on the other

hand, is a characteristic symptom of active phase schizophrenia (American Psychiatric

Association, 1994).

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Automatic triggers and delusional rationalizations:

If an affordance is charged with a negative affect, the chance the perceptual proto-

desires will turn to actions is increased in psychotic conditions. Psychosis doesn’t need

to be a symptom of a primary psychotic disorder, however – it can equally be caused by

substance abuse (Caton et al., 2005), and in reality substance abuse is single the most

common factor of any violence outside of war (Langevin & Hardy, 1987; Langford,

1996).

It appears that automatic actions somehow bypass whatever it is that tags a sense-of-

self-agency, this may be experienced three ways; as a hallucination, where the action-

demanded by an affordance is misattributed (Golembiewski, 2012a); as an episodic

amnesia, where events cannot be remembered because they were never properly

experienced; or as delusions because actions are concurrently or retrospectively

rationalized (D. Freeman et al., 2002; Startup et al., 2008); much the same way as

individuals come to develop a self identity based on their own actions, functionally as if

they were outside observers (Bem, 1972). Indeed, detailed first-hand accounts of

schizophrenia sometimes provide insight into the retrospection involved in fostering

delusions:

“A little girl said to her mother, ‘Is that man possessed by the Devil Mummy?’

Her mother also looked at me and replied, ‘Yes dear.’ This coincidence just

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when I was thinking this very thought, was enough to prove (it to me)… I had to

make sense, any sense, out of all these uncanny coincidences. I did it by

radically changing my conception of reality.” (Chadwick, 1993), pp. 244-245)

Cases of amnesia may be more common than cases of delusions. In one London-based

study complete or partial episodic amnesia was claimed in 20 out of 50 homicides.

While this data may have been confounded somewhat by criminals who wish to avoid a

guilty sentence, the high number is also reflected in various conditions that made such

claims plausible; biological injury, psychosis and intoxication (O'Connell, 1959). In

some of these cases, the assailant handed themselves in, knowing they were prone

extreme actions without remembering them.

Unlike the lady with the syringe and the man with the gun, the negative charge provided

by the negative affordances and violence may provide an impression of deliberate

purpose, but only after or during the act because the motivation to act was never

intentional. It comes from recognition of the weapon or a victim, and didn’t exist any

earlier, yet actions are very convincing proof of intention even to the assailant. But

sometimes no plausible motive can be found – or even hallucinated. In such cases,

actions may be amnesic:

‘A young married man, following an enforced starvation of three days,

murdered, for no reason, one of his children with whom he had been on the best

of terms. He had no memory of his actions’ (O'Connell, 1959) p. 270)

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In May 2011, in Tenerife (the Canary Islands), a homeless man (presumed to be

schizophrenic, but more likely to be bipolar) grabbed a knife from a supermarket shelf,

and spontaneously decapitated a nearby tourist. He was apparently unprovoked and his

violence was almost certainly not premeditated. The only time the assailant had ever

met the tourist before was just a few moments earlier. The victim had complained to a

security guard about being harassed, and the assailant had been moved on. He

immediately returned to the supermarket and killed the tourist (Neild, 2011). Although

it is far from clear why the tourist was victimized, there’s no doubt that her presence

caused the assailant to become rapidly aroused. In this case, the convergence of the

negative affordance suggested by the by the tourist (‘target me’) and the no less horrific

negative affordance suggested knife (‘kill with me’) came together in a particularly

tragic way. The assailant’s delusions must have implicated the tourist in a very specific

way, because the he took her severed head out to the street and declared; “I am God's

avenger and I come to mete out justice!” The delusional narrative that this quotation

speaks to has a mythological quality – and draws on common culture, but nevertheless

must have developed with – or after, the events it related to –it couldn’t have developed

earlier, because the assailant and the victim had never met.

Typically delusions are formed on layers of complimentary affordances, which have

special (often encoded) meaning for the patient. These build quickly on themselves

following a single line of logic that is either imperceptible or irrelevant to others

(Coltheart et al., 2007). These become delusional narratives, which leave little

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reasonable forensic evidence, even though they make complete sense of the

circumstances to the patient (Chadwick, 1993).

Random homicides by psychotic strangers are very rare (Nielssen et al., 2011), and for

this reason, data is poor, but in a cross sectional study of homicides between 1978 and

1983, 1418 homicides were analysed and 108 were identified as having been committed

by psychiatric patients. Of these only 19 (17.6%) of the victims were strangers.

Obviously sudden and impulsive violence doesn’t always involve strangers, but

circumstances that do involve strangers are particular because they usually lack any

reasonable motive. Of the stranger homicides, 16 (14.8%) were utterly unprovoked

(Langevin & Hardy, 1987). Other evidence that suggests that violent impulses are

somatogenic to the assailant come from cases where no reasonable motive can be found:

“…The couple were on the very best of terms. There had been occasional sexual

intercourse and no major quarrels… On one occasion, for no apparent reason, he

had seized her by the throat but had relaxed his grip without harming her. She

had agreed to forget the incident and to continue their acquaintanceship. On the

night of the murder they had spent the evening together listening to the radio at

his home… As the girl rose to go he suddenly seized her by the throat and

strangled her, placing the body under the bed and then notifying the police.”

(Stafford-Clark & Taylor, 1949), p. 326)

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“He was in love with the girl and wished to marry her… Having met the girl one

evening to discuss marriage arrangements, he suddenly and without any warning

felled her with a heavy piece of wood and stabbed her in the neck with his clasp

knife.” (Stafford-Clark & Taylor, 1949)p. 326)

The events of the Tenerife homicide appear to be qualitatively similar, as all these cases

(and may more) suggest that psychiatric homicides can occur by circumstance rather

than choice. Attacks are rarely remembered by the assailant (O'Connell, 1959; Stafford-

Clark & Taylor, 1949). If events are apparently remembered, what may appear to be a

memory may in fact be a delusion or hallucinatory (Gibbens, 1958). The Tenerife

homicide may well be a case in point as the statement, “I am God’s avenger and I come

to mete out justice!” implies. This statement appears to match the assailant’s actions

(carrying the victim’s head by her hair, while clutching a knife in the other hand), but

not the assailant’s intentions – because he clearly had none. Delusions are like a fire,

kindled out of perceived events, opportunities and objects. The availability of a knife in

the Tenerife case was not premeditated, and neither was picking it up. The opportunity

to use the knife was also involuntary, even as a delusional narrative may have been

growing during the quick series of tragic events.

The relationship between technology and action is direct. Even the most simple of

animals perceive external objects as affordances, automatically triggering instinctive

action. A barnacle drift in the ocean until it hits a hard surface that it will then attach

itself to (Bargh & Dijksterhuis, 2001). A hard surface is a very limited form of
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technology, but as life becomes more complex, so too does the technology it can

engage. The sea eagle’s uses stones to break eggshells, and there are any number of

animals that will make good use of a hollow tree. Obviously for humans technology is

far more complex again, and human technology enables a potential range of affordances

that may be either specific (such as a custom part of an engine), or incredibly diverse

like a computer. But the complexity of human technology does not make it dissimilar to

a surface for a barnacle. Once the meaning of the object is known to the point that its

use is automated, it triggers action in very much the same way – although the barnacle

has no capacity to reprocesses information or to learn, and thereby cannot behave

differently (Bargh & Dijksterhuis, 2001). Choice is an evolutionarily advanced process,

which given some conditions, isn’t even ubiquitous in humankind, much less in simple

life. Thus technology, once its function has been learned, is part of the process of

thought and action.

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Figure 44: David slays Goliath by Caravaggio Oil on board, 1609-10.

As the image of the assailant and his words testify, the homicide in

Tenerife reflected an automatic action and a culturally familiar sche-

ma, not a conscious intention.

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It appears that the knife used in the Tenerife homicide was not just a weapon. It served

an important role in the psychological process that led to the attack. In premeditated

violence, the technology involved is a tool that is chosen after a decision to commit the

act of violence is made. This presupposes a motive and a desire to cause harm, which

was clearly the case in Tenerife, where the alleged assailant had not met the victim so

much as ten minutes earlier. But technology, firearms in particular, do trigger violence

that otherwise would never have occurred, whether or not there is a psychiatric

condition. In the USA, about 40% of the deaths caused by firearms are accidental and

involve children or teenagers (Edwards, 1972). This should come as no surprise;

automatic reflexive inhibition in the frontal cortex is low for children (8-10yrs) and

lower still for adolescents (14-18yrs) (Luna et al., 2001). A picture begins to emerge,

where the perception of the opportunity that enables violence suggests violence. But

more commonly, in cases of sudden psychiatric violence, the opportunity is not

suggested by the weapon, but rather by the presence of a vulnerable victim. Violence of

this sort is sudden, unplanned and direct – usually the attack is done with bear hands

(Alderman, 1916; Langevin & Hardy, 1987; Richard-Devantoy et al., 2009). Although

these circumstances are more common, in either case – the violence emerges

spontaneously from the perception of an opportunity.

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Discussion

The issue of violence is a broad subject, and only part of the whole problem will be

caused by reflexive action. This part is expected to be quite small overall, although it is

likely to explain most psychosis related violence. One of the features of schizophrenia

and type 1 bipolar disorder is that deliberation becomes very difficult, as is reflected in

the endless Wisconsin card sorting and Stroop tests that have been performed on

schizophrenic patients (Bora, Yücel, & Pantelis, 2010). The implication is that planning

violent action will be difficult in this condition. Furthermore, the conditions that make

reflexive action likely are present in these conditions (Golembiewski, 2012a). Beyond

this, becomes more difficult to further identify a group that suffers from reflexive

violence, except to say that these symptoms are likely to be far more common in

untreated psychosis, particularly first episode (about 80% of cases, in statistical meta-

analysis), when insight is poor (about 40% of cases) and when associated with self-harm

(approximately 90% of cases) (Large & Nielssen, 2011).

Several etiological options are presented here that may give rise to reflexive violence.

Of these, all are associated with reduced frontal inhibition, particularly when

circumstances or communication are perceived as being negative. Analyses of specific

forms of violence have been linked to cases of paedophilia, for instance, and in these

cases at least, frontal lesions are clearly evident in positron tomography studies. But it is

premature to assert causality. Paedophilia is a form of violence that is universally

regarded as negative, offering some support for the reflexive action hypothesis, but this

support carries no external validity and low numbers of studies and subjects mean that
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even internal validity is notional. Having said this, it is interesting to note that

utilization behaviour was found to be a common comorbidity along with all the

paraphilia’s including paedophilia etc. (Mendez, Chow, Ringman, Twitchell, & Hinkin,

2000).

Ultimately the greatest risk of reflexive violence is not for unknown victims, but for the

patient themselves. The reflex to jump, when at a cliff’s edge is noticeable, even for

many healthy people. And when an affordance to commit violence is observed, the fact

that schizophrenic patients spend most of their time alone means that they are most

likely to turn any violent impulses in on themselves.

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PSYCHIATRIC SUICIDE

“And I find it kinda funny, I find it kinda sad

The dreams in which I'm dying are the best I've ever had

I find it hard to tell you, I find it hard to take

When people run in circles it's a very very

mad world mad world” Roland Orzabel ‘Mad World’

The issue of suicide in all mental illness is very pertinent to any consideration of the

psychiatric milieu. The suicide rates of schizophrenic patients have a standard mortality

ratio (as calculated from meta-analyses) internationally of around 8.5% of all those with

a diagnosis. This figure has an incredibly high variation: from 0.8 to 115 times the

standard mortality ratio. One of the reasons for variation is in the time the study is

taken. The rate is at its peak at the time of first medication and admission to psychiatric

treatment (Harris & Barraclough, 1997; Palmer et al., 2005). Other psychiatric

conditions are higher – Bipolar disorder at about 15%, and major depression 20.5%

(Harris & Barraclough, 1997). The figure for opportunistic suicide is unknown, but it is

probably very high, especially among bipolar patients.

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The cost of keeping patients from self-harm is very high. Psychiatric facilities go to

incredible lengths to keep patients physically safe – even if these efforts are at the cost

of the patients’ best interests. Anti-ligature fittings (fittings that people cannot possibly

hang themselves on) are normally standard, windows are fixed and louvers are behind

bulletproof glass. Anti-ligature lighting is often barred strip lighting, which is so

desperately nasty that they make the lights in any other facilities look positively

pleasant.

Some of the implications of the risks of psychiatric suicide are

discussed in:

So you’re going to design a mental health facility? How to

make it future-proof. World Health Design Scientific Review,

5(2), 74-79. (Q.V.) (Starts on p. 97-)

Lost in space: The role of the environment in the aetiology of

schizophrenia. Facilities. (Q.V.) (Starts on p. 296- in this

volume.)

Introducing the concept of reflexive and automatic violence:

A function of aberrant perceptual inhibition. Psychology of

Violence. (Q.V.) (Starts on p. 373, in this volume.)

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FURTHER RESEARCH

Other Methodological Approaches:

I can’t say I left the big questions until last. But I have covered a lot of ground very

quickly, and sometimes the view has been obscured by my dust-cloud. One of the things

I missed during the research for this thesis is grounded research – that is, research

grounded in anything other than literature and the world of my own ideas. I didn’t spend

time with psychiatric patients and to ask them what they thought – well, that’s not

entirely true, but for ethical reasons, I cannot use the data I acquired this way in my

thesis or for academic purposes.

My reasons for not doing grounded research may have been valid: I figured that asking

patients would be unlikely to reveal especially useful information. Perhaps little more

than John Snow’s questions to his dying patients in the Barbican. Just because you are

afflicted, doesn’t mean you have all the answers – just ask someone who is suffering

from an undiagnosed allergy. The question itself can be frustrating! But even so,

perhaps I should have tried…

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The research itself has opened up several prospects. One of the projects I have

commenced is guest-editing a peer-reviewed volume on psychiatric facilities. One of the

papers I have reviewed for it tells of this exact approach. Professor Nathan Perkins, of

the University of Guelph, in Ontario, Canada, his students and his colleagues did some

studies of facilities that were grounded in patient participation. Quite apart from the

social capital this approach engendered among patients, these studies identified nine

design imperatives, all of which in some way ground the salutogenic paradigm I have

developed: the principles he identifies are: diversity, complexity, discovery,

engagement, connection, ceremony, control, manipulation, and achievement (Perkins, In

Press). Although I doubt that you would have managed to get such comprehensible

answers from regressed schizophrenic patients, the idea of doing these grounded studies

is quite inspiring.

Other areas of engagement

Looking back, I can see that the Medical Hypotheses and ‘Riddle of psychotic

perception’ articles both start to flesh out a much broader framework for understanding

mental illness than just schizophrenia alone. As such, I’m tempted to pursue the

neurological line of enquiry to understand bipolar, depression and even more

importantly to construct a theory of mental illness.

There’s still a lot to be learned about healthcare settings, and mental health facilities, but

I’ve discovered that the method of approaching a subject laterally seems to work. I think

that a lot could be learned from in-depth research into forensic facilities, because I think
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that a lot of the pain-points of psychiatric facility design are embodied by this quasi-

legal, quasi-medical hybrid.

I am also interested in looking at specific cultures and cultural understandings of mental

health and psychiatric facilities that are tailored to specific cultural archetypes. Some

time ago I started a dialogue with Paul Memmott at University of Queensland about

facilities for Aboriginal people with mental illness. Since then the conversation has

grown and others are getting involved. This may turn to something – who knows?

The aetiology of schizophrenia – continued

I find the ideas I have been sketching out (included in this thesis) on the aetiology of

schizophrenia deeply interesting and very important for architectural praxis and urban

design too. I’d like to resolve some of the mysteries surrounding this area too.

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Glossary of terms

Acetylcholine (ACh): A neurotransmitter involved with proprioception, somatogenic

perception. ACh activations frequently lead perceptual processes, with attention

following.

Activities of Daily Living (ADL): A normative set of daily tasks used to assess

executive dysfunction in mental illness. ADL activites are frequently retaught to

patients in psychiatric care using ADL facilities like kitchens bathroms, telephones,

laundries etc.

Active attention: A term to describe the middle ground between bottom-up and top-

down attentional processes. It may be environment led, yet without the sharpness of

novelty. Active attention is where top-down intention directs a ‘fuzzy’ search or where

bottom-up attention reveals something that you had an interest in, but had not been

looking for. Active attention is not driven by saliency, and isn’t a mode of attention in

its own right, but complex combinations of bottom-up and top-down processes, which

are led by habits of engagement, by choice and simply by the availability of resources.

See page 218.

Aetiology (US. Etiology): The causal circumstances for a syndrome or illness beyond

the pathology or psychopathology. For cholera, the aetiology is how water came to be

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infected and how people came to drink that water. The pathology of cholera relates

specifically to the pathogen.

Affect: A technical term for all emotion – happy or sad.

Affordance: The perceived opportunity an object or a situation provides. See pages

305-317.

Alogia: ‘An impoverishment in thinking that is inferred from observing speech and

language behavior. There may be brief and concrete replies to questions and restriction

in the amount of spontaneous speech (poverty of speech}. Sometimes the speech is

adequate in amount but conveys little information because it is over concrete, over

abstract, repetitive, or stereotyped (poverty of content)’ (American Psychological

Association, 1994, 764).

Alzheimer’s disease: A progressive mental deterioration, due to generalized

degeneration of the brain.

Amygdala: The twin amygdalae are parts of the limbic system and are pared with the

hippocampi. The amydalae function appears to moderate a sense of worth, or a sense of

a circumstance’s relevance to me. The amygdalae remain either intact or slightly under

engaged in schizophrenia (Anticevic et al., 2012; Becerril & Barch, 2010). This

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contrasts with affective psychoses like bipolar disorder, in which a large body of

literature reports over-engagement of the amygdalae (S. B. Perlman et al., 2012)

Anhedonia: a psychological condition characterized by inability to experience pleasure.

Anterior cingulate Cortex (ACC): a region of the frontal cortex, between the corpus

callosum and the prefrontal cortex. It is well situated between the striatum and the

prefrontal cortex thought to mediate deliberative action, and attention. The dopamine

receptors in the ACC and PFC are largely of the D1 type in humans.

Anti-ligature (anti-lig): An architectural term for devices that are designed to prevent

hanging. These are used in psychiatric facilities and jails.

Apsophilia: Scatological behaviour.

Automaticity: Automatic actions, either well-learned or instinctive that take place with

minimal declarative awareness. Examples are actions that take place while sleepwalking

or otherwise with minimal arousal. Some neurological conditions cause automatic

behaviour, particularly conditions that reduce prefrontal and ACC activity.

Avolition: ‘An inability to initiate and persist in goal-directed activities. When severe

enough to be considered pathological, avolition is pervasive and prevents the person

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from completing many different types of activities (e.g., work, intellectual pursuits, self-

care)’ (American Psychological Association, 1994, 764).

Awe: The aesthetic experience of the sublime.

Bayesian: a statistical method where meaning is derived from data that defies statistical

normalization.

Behavioural negativity: A neologism for a syndrome identified in this thesis.

Behavioural negativism relates closely to negativism, a catatonic symptom of

schizophrenia. See page 282.

Behaviour settings (US. behaviour settings): A neologism coined by Barker and

Wright (1954) to describe environmental settings that contain pre-set mores and

expectations of behaviour. (We are expected to swim in a swimming pool, pray in a

church etc.) See page:132.

Bottom-up attention: attention that is given to unexpected and sometimes unknown

singletons. Bottom-up attention also mediates somatogenic awareness and social

awareness. It is hypothesised that Bottom-up attention is moderated by dopamine

phasis. See page 215.

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Built Environment: The environment as it is constricted and designed by mankind,

including designed objects, buildings, landscaped areas, parks, roads and urban plans.

Catatonia: Marked motor abnormalities including motoric immobility (i.e., catalepsy or

stupor), certain types of excessive motor activity (apparently purposeless agitation not

influenced by external stimuli), extreme negativism (apparent motiveless resistance to

instructions or attempts to be moved) or mutism, posturing or stereotyped movements,

and echolalia or echopraxia (American Psychological Association, 1994, 764).

Clang: a form of psychotic jargonaphasia where words (and apparently meanings) are

derived from alliteration, rhyme and other poetic devices.

Cognitive behavioural therapy (CBT): A method of talk therapy that avoids the

supposed pathology and works directly on mitigating symptoms.

Confirmation bias: a condition (ubiquitous even outside of mental illness) where

there’s a notable bias to confirm ideas about perceived events rather than reject them.

This syndrome is particularly prominent in schizophrenia. In this thesis it is associated

with the paranoid subtype, though it is probably ubiquitous in the condition. See page

264.

Corollary discharge error (CDE): a hypothesis for hallucinations, which that was first

described by Feinberg (1978), and further popularized by Frith in many subsequent

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works. This model claims that an individual carries a record; ‘the efference copy’ of all

endogenous actions, and once actions are complete, the record is ‘discharged.’ Errors in

this process are perceived as hallucinations. The problem with this model is that it

attempts to explain bizarre hallucinations as if they were simple illusions, and goes no

further in explaining other bizarre symptoms of schizophrenia.

D1: A class of excitatory dopamine receptors, which are ubiquitous in the ACC and PFC

in humans. The D1 class consists of D1 and D5 receptor subtypes.

D2: A class of inhibitory dopamine receptors, which are ubiquitous in the striatum and

limbic areas in human brains. In rats they are also the most common type in the ACC

and PFC. The D2 class consists of D2, D3 and D4 receptor subtypes.

D2Low: A dopaminergic heteromer when in its low affinity state (see D2High above).

They are speculated to drive postsynaptic, phasic dopamine activity, and be closely

associated with the high levels of attention that is given to declaratively aware tasks.

See page 238 onwards.

D2High: A dopaminergic heteromer when in its high affinity state. These heteromers are

commonly overabundant in the striato-frontal pathway in schizophrenia, but they are

bistable – that is, they modulate two functional outcomes. The D1/D2 heteromer

modulates sensitivity to dopamine, and is subject to change rapidly from a high affinity

state (D2High) to a low one; D2Low. The transformation is triggered by external

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stimulation (either through direct chemical stimulation or through indirectly through

interneuronal connections). They are speculated to drive presynaptic, tonic dopamine

activity, and be closely associated with the low levels of attention that is given to

automatic tasks. See page 238 onwards.

Delusions: A false belief based on incorrect inference about external reality that is

firmly sustained despite what almost everyone else believes and despite what constitutes

incontrovertible and obvious proof or evidence to the contrary. The belief is not one

ordinarily accepted by other members of the person's culture or subculture (e.g., it is not

an article of religious faith). When a false belief involves a value judgment, it is

regarded as a delusion only when the judgment is so extreme as to defy credibility.

Delusional conviction occurs on a continuum and can sometimes be inferred from an

individual's behavior. It is often difficult to distinguish between a delusion and an

overvalued idea (in which case the individual has an unreasonable belief or idea but

does not hold it as firmly as is the case with a delusion).

Delusions are subdivided according to their content. Some of the more common types

are listed below:

Bizarre: A delusion that involves a phenomenon that the person's culture would

regard as totally implausible.

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Delusional jealousy: The delusion that one's sexual partner is unfaithful.

Erotomanic: A delusion that another person, usually of higher status, is in love

with the individual.

Grandiose: A delusion of inflated worth, power, knowledge, identity, or special

relationship to a deity or famous person…

Delusions of control: A delusion in which feelings, impulses, thoughts, or

actions are experienced as being under the control of some external force rather

than being under one's own control.

Delusions of reference: A delusion whose theme is that events, objects, or other

persons in one's immediate environment have a particular and unusual

significance. These delusions are usually of a negative or pejorative nature, but

also may be grandiose in content. This differs from an idea of reference, in

which the false belief is not as firmly held nor as fully organized into a true

belief.

Persecutory: A delusion in which the central theme is that one (or someone to

whom one is close) is being attacked, harassed, cheated, persecuted, or conspired

against.

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Somatic: A delusion whose main content pertains to the appearance or

functioning of one's body.

Thought broadcasting: The delusion that one's thoughts are being broadcast

out loud so that they can be perceived by others.

Thought insertion: The delusion that certain of one's thoughts are not one's

own, but rather are inserted into one's mind.’ (American Psychological

Association, 1994, 765)

(Note: Some delusions such as ‘thought insertion’ are difficult to distinguish

from hallucinations.)

Determinism (architectural): Maurice Broady (1966) coined the term to describe the

dubious practice of asserting that designs, once constructed will affect people in a

predictable and positive way.

Disorganised symptoms: Two classes of disorganised symptoms are listed for

schizophrenia in the DSM-IV (American Psychological Association, 1994, 276) they

are disorganized thinking and disorganized behaviour.

Disorganized thinking: ‘(“formal thought disorder,” “loosening of

associations”) has been argued by some (Bleuler, in particular) to be the single

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most important feature of Schizophrenia. Because of the difficulty inherent in

developing an objective definition of “thought disorder,” and because in a

clinical setting inferences about thought are based primarily on the individual's

speech, the concept of disorganized speech (Criterion A3) has been emphasized

in the Schizophrenia diagnosis.

The speech of individuals with Schizophrenia may be disorganized in a variety

of ways. The person may “slip off the track” from one topic to another

(“derailment” or “loose associations”); answers to questions may be obliquely

related or completely unrelated (“tangentiality”); and, rarely, speech may be so

severely disorganized that it is nearly incomprehensible and resembles receptive

aphasia in its linguistic disorganization (“incoherence” or “word salad”).

Because mildly disorganized speech is common and nonspecific, the symptom

must be severe enough to substantially impair effective communication. Less

severe disorganized thinking or speech may occur during the prodromal and

residual periods of Schizophrenia.’ (See Jargonaphasia also).

Grossly disorganized behavior: is peculiar ‘behavior that may manifest itself in

a variety of ways, ranging from childlike silliness to unpredictable agitation.

Problems may be noted in any form of goal-directed behavior, leading to

difficulties in performing activities of daily living such as organizing meals or

maintaining hygiene. The person may appear markedly disheveled, may dress in

an unusual manner (e.g., wearing multiple overcoats, scarves, and gloves on a

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hot day), or may display clearly inappropriate sexual behavior (e.g., public

masturbation) or unpredictable and untriggered agitation (e.g., shouting or

swearing).’ (American Psychological Association, 1994, 276)

Dopamine: A neurotransmitter that is highly implicated in schizophrenia and many

other mental illnesses. The implication stems from the reality that all the medications

that are used to treat psychosis affect dopamine transmission in some way. It is

speculated in this thesis that dopamine is used to moderate attention through two

frequencies, the phasic and tonic.

Efference copy: See Corollary Discharge Error.

Epidemiology: the branch of medicine that deals with the incidence, distribution, and

control of illness and epidemics.

Error related negativity (ERN): This is a perceptual feedback loop specifically for

negative affective or negative hedonic feedback – ERN occurs when an event is worse

than expectations.

Evidence-based design (EBD): an approach to design that relies on empirical data for

decision-making, much as random-controlled studies are used to drive approaches to

medicine. EBD is historically a reaction against architectural determinism. The

approach has become popular in Healthcare Architecture, but it is widely criticised

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because of the narrowness of its methods and its impracticality when thousands of

decisions are constantly being made in praxis.

Generalised resource deficits (GRD): Part of salutogenic theory. GRD’s are entropic

forces that work against a state of better health. See diagram on page 114.

Generalised resistance resource (GRR): Part of salutogenic theory. GRR’s are forces

that work to build a state of better health. They include anything that contributes to a

sense of coherence. See diagram on page 114.

Gross disorganization: See disorganisation.

Hallucinations: ‘A sensory perception that has the compelling sense of reality of a true

perception but that occurs without external stimulation of the relevant sensory organ.

Hallucinations should be distinguished from illusions, in which an actual external

stimulus is misperceived or misinterpreted.

Types of hallucinations include

Auditory: A hallucination involving the perception of sound, most commonly of

voices.

Gustatory: A hallucination involving the perception of taste…

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Olfactory: A hallucination involving the perception of odor.

Somatic: A hallucination involving the perception of a physical experience

localized within the body (such as a feeling of electricity). Somatic

hallucinations are distinguished from real physical sensations and from a tactile

hallucination.

Tactile: A hallucination involving the perception of being touched or of

something being under one's skin. The most common tactile hallucinations are

the sensation of electric shocks and formication.

Visual: A hallucination involving sight, which may consist of formed images,

such as of people, or of unformed images, such as flashes of light. Visual

hallucinations must be distinguished from illusions, which are misperceptions of

real external stimuli.’ (American Psychological Association, 1994, 767)

Hebbian degradation of the automatic ontology: A new term for a syndrome

identified in this thesis, where automatic behaviours are relearned wrongly. See page

268.

In vitro: studies conducted in severed tissue.

In vivo: studies conducted in live animals.

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Jargonaphasia: Symptoms of disorganised speech where patterns are identifiable, but

they are bizarre, as they do not communicate meaning in the normal way. These include

rhyme, clang, alliteration and other ‘poetic’ devices. See disorganised symptoms.

Manageability: The generalised resistance resource in salutogenic theory that makes

life liveable on the most basic level. Things like food and shelter. See page 116.

Meaning: The generalised resistance resource in salutogenic theory that enriches life

though engagement with other people, other life and the world and cosmos beyond

ourselves. Things like art and the environment. See page 118.

Mismatch Negativity (MMN): The neural failure to pick up on perceptual discordance.

Mismatch negativity deficits are well observed in schizophrenia, but are less common in

other mental illnesses. In this thesis MMN is taken as a deficit in bottom-up attention.

Models of care: The routines, rules and staffing patterns of a health facility.

Negative Signs: Also known as deficit symptoms: ‘account for a substantial degree of

the morbidity associated with schizophrenia,’ yet these are the most treatment resistant

symptoms. Three negative symptoms used for diagnosis: affective flattening, alogia,

and avolition, but there are also other negative symptoms (e.g., anhedonia). In this thesis

the negative signs are taken to be deficits in bottom-up attention (American Psychiatric

Association, 1994, 276).

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Negativism: A catatonic symptom characterised by apparent refusal to cooperate.

NMDA (N-Methyl-D-aspartate) receptors: Receptors within the glutamate system

that have a ‘gated’ effect. Stimulation has to be of significant intensity to activate the

glutamate neuron. It is speculated herein the NMDA receptors moderate prominence.

Noise Theory: The heuristic belief that symptoms are a product of excessive neural

noise. The theory is that irrelevant perceptions or internal chaotic neuronal reactions are

too overwhelming to extract meaningful information. This thesis also locates a

preoccupation with internal stimuli, but rejects the notion that this is a distraction

preventing focused attention. See page 289.

Noradrenalin (AKA noradrenaline or in the US., Norepinephrine) (NA): A

neurotransmission system that is implicated in attention. Noradrenalin appears to

support the dopamine function by selectively inhibiting activity that is not task specific

(especially somatosensory inputs) and by the moderation of baseline levels of arousal.

Parallax: A function of perspective where there is differential displacement in

the apparent position of an object when viewed along two different lines of sight.

Things that are further away seem to mode more slowly due to the effect of parallax.

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Paranoia: A symptom (usually related closely to delusions) where a person has a

tendency to catastrophise and imagine the worst outcomes of a given situation will

come true. Paranoia must be distinguished from paranoid type schizophrenia.

Paranoid Type schizophrenia: The most common subtype of the DSM schizophrenia

diagnosis. ‘”Paranoid Type” is assigned whenever there is a preoccupation with

delusions or frequent hallucinations are prominent.’ (American Psychological

Association, 1994, 286). See page 262 for explanation according to the hypothesis

presented in this thesis.

Phasic reception (of neurotransmitters): The postsynaptic bursting action of a

receptor. As opposed to a tonic action. The phenomenal effects of phasic and tonic

dopaminergic activity is profound (see pages 238 onward). It is speculated that

dopamine phasis regulates bottom-up attention and dopamine tone regulates top-down

attention. See diagram on page 248.

Phonological loop: One of the constructs in Baddely’s (2003) working memory

hypothesis. The phonological loop is used to manage semantic and aural resources.

Positive feedback distortion: A neologism for a syndrome identified in this thesis,

where a lack of new knowledge from bottom-up channels causes experience to become

increasingly stereotyped. The conditions that are created are exactly analogous to the

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Larsen effect (the bizarre positive feedback patterns that occur when an amplifier

amplifies it’s own signal). See page 268.

Prodrome: The undefined period prior to a mental illness being officially diagnosable.

The prodrome of schizophrenia is often marked by some symptoms, but not to the level

where a diagnosis is permitted. Because schizophrenia has a period of symptoms

condition, the term ‘prodrome’ often refers to that period. Although symptoms are

normatively thought to be similar in the prodrome, first person accounts often tell

another story. Where the symptoms of schizophrenia are generally horrific, the

hallucinations and delusions of the prodrome are often extremely exciting (Bowers, &

Freedman,1966; Anonymous, 2010).

Prominence: A form of perceptual saliency. Also known as spectacularity in

architecture. Prominence is speculated to be first moderated by the cholinergic, and

glutamatergic systems. See page 211.

Psychiatric spectra continuum: A state of psychosis (as loosely defined) marks one

end of a spectrum, with as much as 60% of some populations having numinous and

otherwise ‘unreal’ experience if religious experience were to be counted. Psychotic

perceptions normatively only occur in less than 3% of the population over the course of

a lifetime. See the appendix starting on page 286.

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Psychogenesis: A polite and less ambiguous term for psychopathology - the

pathological moment in the development of a mental disorder.

Psychopathology: The term isn’t used much because it is too easily confused with the

definition and phenomena of psychopaths. See psychogenesis (above).

Psychosis: “The narrowest definition of psychotic is restricted to delusions or

prominent hallucinations, with the hallucinations occurring in the absence of insight into

their pathological nature. A slightly less restrictive definition would also include

prominent hallucinations that the individual realizes are hallucinatory experiences.

Broader still is a definition that also includes other positive symptoms of Schizophrenia

(i.e., disorganized speech, grossly disorganized or catatonic behavior).” (American

Psychiatric Association 1994, 770)

Despite the narrow terms of definition of psychosis in the DSM, the term ‘psychosis’ is

used very liberally. Examples given in (Howes and Kapur 2009; Kapur 2003; Kapur,

Mizrahi, and Li 2005) neither refer to prominent hallucinations nor delusions, nor even

lack of insight, and is thus not even psychosis as the DSM-IV defines the term.

Certainly the application of the broadest definition (all the positive symptoms of

schizophrenia, if not the whole syndrome) is unjustified. Psychosis is to schizophrenia

as a cough is to influenza.

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Psychotropic: A psychoactive drug that affects the central nervous system. Such drugs

are often used to treat schizophrenia, but they are ineffective for many symptoms and in

many cases are of little use whatsoever.

Raw attention: Attention given to perceptions prior to any kind of automatic or

cognitive processing. Theoretically, in this raw state, nothing can be salient, because it

must completely lack any kind of definition or ontological associations. Even so,

automatic raw attentional processes continue to monitor prominence, even during

vegetative states, anaesthesia, deep sleep, and in vitro (Feldmeyer, 2010; Laureys, 2005;

Schiff et al., 2002) implying that this raw data feed bypasses cognition. See page 215.

Recognition salience: The saliency event triggered by a match between expectations

and events. This is low-level and thought to be driven by tonic dopamine reception. A

trigger for top-down attention.

Salience: In the literature saliency means a number of very different things to do with

the triggers for attention. From page 210 in this thesis a more specific taxonomy of

salience is proposed.

Salutogenisis/ salutogenics: A theory proposed by Aaron Antonovsky (1987) which

morels health and illness as a continuum. See the sections starting on the following

pages: 70 and 101.

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Scatology: An obsession with excrement and other bodily wastes. Fear of scatological

behaviour (including painting with faeces) is entrenched in mental health facilities.

Schemata: A nugget of knowledge, either well-learned or instinctive that can be

accessed automatically. Schemata are likely to be maintained by the striatum.

Seclusion: A method or restraint commonly used in mental health facilities. Seclusion

rooms, which are also known as quiet rooms or isolation rooms (there are sometimes

variations, depending on the model of care) typically are spaces where the furniture is

fixed to the floor and there are no affordances for patients to harm themselves or others.

This usually means the spaces are very bare. Seclusion is usually used to punish bad

behaviour such as violence, anger or scatological behaviour.

Sense of Coherence: The sum of all generalised resistance resources (the total

manageability, comprehensibility and meaningfulness) in salutogenic theory. See page

70.

Significance: One of the forms of salience in the taxonomy proposed within this thesis.

See page 143.

Somatogenic: relating to the physical body. Somatogenic perception is of hunger,

tiredness, sexual desire etc.

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Somatoparaphrenic syndrome: A condition where patients don’t recognize their body

parts and bodily processes.

Striatum: The part of the brain associated with automatic and autonomic functions. The

striatum is particularly rich in D2 and glutamatergic receptors and is implicated in many

mental illnesses. It is situated between the mesencephalon (mid-brain) and the larger

limbic area, the amygdalae, hippocampi and the corpus callosum.

Subcortical confinement: A neologism for a syndrome identified in this thesis.

Subcortical confinement is associated with the ‘disorganised subtype of schizophrenia’,

where D2Low receptors are severely depleted and a patient effectively looses all frontal

and ACC connectivity, thereby confining their awareness subcortical functions such as

the activation of schemata more or less randomly. See page 271.

Sublime: The aesthetic experience of an immense order: nature, intense beauty and

religious experience.

Tonic reception (of neurotransmitters): The presynaptic rhythmic action of a

receptor. As opposed to a phasic action. The phenomenal effects of phasic and tonic

dopaminergic activity is profound (see pages 238 onward). It is speculated that

dopamine phasis regulates bottom-up attention and dopamine tone regulates top-down

attention. See diagram on page 248.

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Top-down attention: The attention that is given to expected outcomes. These are

generally low level and little to get ‘excited about’ in normal circumstances. Top-down

attention is hypothesised to be moderated by tonic dopamine reception. See page 217.

Tunnel-focus: As the name implies, is the kind of top-down attention that excludes all

‘irrelevant’ stimuli, especially as bottom-up distractions are weakened. This non-bizarre

symptom is particularly prevalent in early and in paranoid psychosis, and whilst it is

very common in paranoid type schizophrenia, it is by no means unique to

schizophrenia, nor indeed to mental illness. In extreme conditions tunnel-focus can

become an identifiable syndrome, which is recognisable See page 263.

Typology: The messaging a building projects through associations. Typology is a

language of tectonic form, materials, size and situation. Using the language of typology,

it is usually easy to identify a church, a garage or a town-hall.

Undermined automaticity: Another new term for a syndrome identified in this thesis,

which is associated with the paranoid subtype of schizophrenia. Undermined

automaticity occurs when top-down intention brings too much focus to activities and

makes intended routines more difficult and prone to error. Too much attention to

automatic functions, such as speech and behaviour can make them seem mildly

disorganized. A phenomenal example is familiar to healthy people when trying to

remember (a top-down process) a word or name that is ‘in the tip of the tongue’. See

page 263.

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Visuo-spatial sketchpad: One of the constructs in Baddely’s (2003) working memory

hypothesis. The visuo-spatial sketchpad is used to manage images, visual imagination

and visual resources.

Way-finding: A term from the architectural lexicon, developed by Kevin Lynch (1992)

to understand how people find their way about a landscape using nodes, landmarks,

edges and pathways.

Wicked problems: Wicked problems are those that abound with open-ended questions,

shifting goalposts, compromised solutions for an open number of stakeholders, and any

number of other confounding problems that prevent resolution. A characteristic of

wicked problems is that they embed other wicked problems (Kunz & Rittel, 1972).

Working memory (WM): a construct of Baddley (1992) to model the limits of

declarative awareness. WM can be broken down into two essential roles; firstly WM is

the domain and the limit of declarative consciousness (Baars & Franklin, 2003). The

second role is the WM in its capacity as an information processor. This later function is

a multifaceted activity, linking an a priori organised ontology to the phonological loop

and a visuo-spatial sketchpad, and to perceptual inputs, desires, needs and learning

processes (Baars, 2007; A. Baddeley, 2003).

WM is a common subject of study for Sz researchers, but in this field, it is also a

controversial topic. On one hand, we are told that poor WM function is a strong

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indicator of schizophrenia and patients first-degree relatives, to an often touted ‘one

standard degree’ of variation (Becerril & Barch, 2010; Bora, Yücel, & Pantelis, 2010;

Goldman-Rakic, 1994; Haenschel & Linden, 2010; Klemm, Schmidt, Knappe, & Blanz,

2006; Pantelis et al., 1997; Simon et al., 2007; G. Williams & Goldman-Rakic, 1995b;

H. J. Williams, Owen, & O’Donovan, 2007; Wirgenes et al., 2010). Yet, studies aimed

at the genetic variants that underpin WM processes are sometimes inconsistent and in

other studies, even proven false (Nieratschker et al., 2010). Dramatic differences like

these may be caused by the lack of consensus about what WM actually is (Cowan,

2005).

It is commonly accepted that there are limits on how much declarative information the

WM can simultaneously handle, with different models contradicting one another on the

number of items that can be simultaneously handled. Some also include a ‘non-

declarative’ level of working memory, with an unlimited capacity (Cowan, 2005; Bargh,

1997).

Worth: One of the subtypes of salience defined in this thesis. Worth measures affective

or hedonic value to ‘me’. It is hypothesised to be moderated by the amygdalae. See page

145.

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AUTHOR AND KEYWORD INDEX

A   Baddeley,  241,  392  

Bahrs,  27,  60,  62,  177,  392  

Aboriginal,  380  
Baker,  72,  392  
ACC  (Anterior  Cingulate  Cortex),  157,  225,  226,  
Barach,  95,  102,  448  
232,  233,  259,  260,  261,  262,  264  
Barch,  202,  390,  394,  434  
Affect,  366  
Bargh,  155,  200,  210,  218,  219,  222,  225,  226,  296,  
Affective  flattening,  351  
343,  344,  361,  363,  366,  373,  393,  405,  406,  
Affordances,  119,  121,  128,  133,  144,  160,  270,  
421,  422  
363,  426,  463  
Barrett,  202,  393,  414,  461  
Alzheimer's  disease,  26,  290,  343,  365,  465  
Bayes,  68,  77,  78,  217,  407  
Ames,  65,  390  
Bayes  Friba,  68,  77,  78,  407  
Amygdala,  270,  390,  444  
Behavioural  negativity,  247  
Andreasen,  265,  390  
Bem,  221,  222,  299,  360,  368,  394,  395  
Antonovsky,  27,  28,  54,  60,  62,  79,  91,  92,  93,  94,  
Bipolar  disorder,  113,  270,  352,  353,  376,  444  
95,  109,  133,  149,  153,  154,  172,  173,  177,  185,  
Bleuler,  199,  396  
220,  390  
Bolton,  338,  396  
Architecture,5,  42,  50,  151,  152,  284,  432,  435,  

455,  461   C  
Arneill,  73,  454  
Camberwell  walk  study,  40,  293,  301,  302,  303  
Automatic  action,  226,  341,  351  
Cantor-­‐Graae,  37,  249,  293,  326,  329,  398,  453  

B   Carlsmith,  221,  222,  299,  409  

Carlsson,  201,  229,  398  

Baars,  156,  200,  222,  241,  391,  392  
Carpenter,  222,  274,  420,  457  
Bachelard,  81,  392  
Carr,  18,  24,  399  
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Caspi,  324,  399   D  

Castle,  292,  399  
D1  Receptor,  158,  194,  204,  225,  230,  231,  232,  
CBT  (Cognitive  Behavioural  Therapy),  20,  97  
233,  234,  244,  268,  415,  440,  442  
CCTV  (Closed  Circuit  Television),  84,  109,  120,  
D2  Receptor,  158,  194,  197,  226,  230,  231,  232,  
137  
233,  234,  245,  246,  433,  445,  452  
Cepeda,  230,  232,  400  
D2High  Receptor,  194,  231,  232,  234,  235,  238,  250,  
Choice,  341,  373  
256,  260,  264  
Choking,  394  
D2Low  Receptor,  194,  231,  233,  234,  235,  238,  250,  
Cholera,  321  
252,  257,  259,  260,  264,  265,  268  
Chrysikou,  71,  308,  401  
Dakin,  101,  278,  403  
Clark,  206,  213,  216,  217,  219,  222,  223,  224,  266,  
Damasio,  279,  404  
295,  361,  363,  401  
Dayan,  127,  450  
Cognition,  64,  406,  421,  422  
Deci,  220,  299,  404  
Cohen,  130,  229,  390,  391,  395,  434  
Deficits  in  bottom-­‐up  attention,  247  
Coid,  326,  402  
Delusions,  247,  266,  275,  299,  300,  351,  372  
Collerton,  65,  243,  266,  275,  402  
Dementia,  219,  396,  414  
Coltheart,  269,  276,  370,  402  
Depression,  100  
Comprehensibility,  10,  54,  60,  62,  65,  71,  72,  85,  
Design,  42,  43,  50,  54,  88,  102,  118,  146,  148,  287,  
86,  89,  94,  104,  106,  109,  111,  116,  133,  134,  
377,  398,  401,  406,  416,  417,  435,  448,  456,  
149,  150,  153,  154,  155,  156,  159,  162,  163,  
458,  459,  464  
164,  177,  180,  187,  220,  222,  307  
Dietrich,  124,  157,  233,  260,  347,  405  
Confirmation  bias,  247,  252,  253,  440  
Dijksterhuis,  155,  210,  218,  222,  225,  226,  234,  
Consciousness,  51,  412,  421,  439  
251,  261,  296,  343,  344,  361,  363,  373,  393,  
Consultation,  103  
405,  406  
Coull,  207,  228,  229,  403  
Dilani,  27,  58,  406  
Cowan,  200,  346,  403  
Donchin,  256,  406  
Crow,  246,  403  
DSM  (APA  Diagnostic  and  Statistical  Manual),  274,  
Culture,  185  
389  

Duckworth,  200,  406  

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Dunnett,  99,  406   Frith,  19,  35,  45,  101,  197,  198,  199,  215,  216,  217,  

Durkheim,  181,  406   228,  242,  243,  257,  261,  265,  266,  277,  279,  

292,  306,  346,  403,  409,  411,  412,  425,  426,  

E   453,  454,  456  

Fuller  Torrey,  331,  465  

Edvardson,  27,  407  
Fusar-­‐Poli,  244,  245,  250,  412  
Emergency,  28,  156,  170,  171,  416  
Future,  50  
ERN  (Error  related  negativity),  206,  208,  410  

Expectation,  238  
G  
Experience  (see  Phenomenology  also),  175,  189,  

204   Gao,  244,  349,  401,  433,  457  

Eyles,  324,  332,  336,  408,  437   Garety,  40,  109,  253,  255,  276,  295,  360,  407,  411,  

413,  455  
F   Gibson,  35,  66,  121,  122,  127,  128,  130,  160,  210,  

213,  218,  296,  343,  345,  362,  363,  414  

Faris,  22,  37,  320,  408  
Ginovart,  99,  231,  244,  414  
Feinberg,  266,  408  
God,  110,  215,  223,  276,  289,  370,  372  
Feldmeyer,  201,  205,  218,  241,  409  
Goffman,  111,  414  
Festinger,  221,  222,  299,  409  
Gold,  275,  414,  433  
Fletcher,  19,  35,  45,  198,  199,  216,  217,  228,  242,  
Goldman-­‐Rakic,  232,  279,  414,  415  
257,  265,  277,  292,  306,  346,  403,  409,  443  
Grace,  130,  235,  236,  237,  238,  240,  254,  255,  313,  
Folsom,  269,  409  
418  
Foucault,  123,  409  
Grandiose,  351,  360  
Frankl,  79,  94,  109,  178,  181,  410  
Gray,  35,  44,  45,  197,  227,  243,  277,  419,  436  
Franklin,  156,  200,  222,  392  
Green,  42,  44,  419  
Freedman,  20,  263,  396,  410  
Grossberg,  65,  156,  216,  217,  219,  222,  241,  266,  
Freeman,  38,  40,  95,  100,  101,  108,  197,  253,  255,  
419,  420  
295,  306,  314,  320,  331,  360,  368,  403,  407,  
Guttmann,  79,  420  
410,  411,  413,  455  

Freidrichs,  143,  411  

Friston,  45,  206,  217,  224,  266,  310,  411,  456  

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H   Irwin,  130,  457  

Ittelson,  362,  445  

Hall,  56,  63,  64,  65,  66,  68,  72,  76,  112,  191,  263,  

310,  420,  421   J  

Hallucinations,  64,  67,  247,  266,  288,  351  
Javitt,  232,  244,  410,  425  
Halpern,  37,  69,  421  
Jencks,  151,  425  
Harris,  14,  19,  376,  404,  421,  462,  463  
Jones,  20,  44,  199,  220,  245,  277,  402,  426,  429,  
Hassin,  200,  219,  421,  422  
436,  437  
Hebb,  82,  223,  240,  422  

Hebbian  degradation  of  the  automatic  ontology,  

K  
247,  248,  256  

Hedonic,  298,  395   Kahn,  129,  142,  215,  298,  389,  426  

Heidegger,  226,  423   Kaplan,  121,  290,  346,  427  

Heinrichs,  249,  404   Kapur,  35,  44,  99,  197,  198,  199,  228,  231,  240,  

Heinz,  197,  236,  265,  277,  313,  423,  426   241,  242,  244,  266,  292,  306,  414,  424,  427,  

Hemsley,  35,  44,  45,  101,  279,  397,  403,  419,  423,   448,  452  

425   Kelly,  37,  40,  293,  325,  428  

Hoekstra,  102,  423   Keshavan,  267,  428  

Holroyd,  206,  228,  257,  266,  424   Kirkbride,  7,  18,  31,  37,  303,  304,  326,  335,  402,  

Honig,  276,  424   429,  435  

Howes,  197,  199,  228,  242,  245,  266,  424   Krabbendam,  40,  274,  326,  430,  460  

Huffcut,  96,  453   Kuipers,  109,  411,  413,  425  

Huntoon,  82,  424  

L  
Hypotheses,  244,  263,  282,  340,  355,  379,  409,  

416   Lahti,  244,  457  

Lang,  29,  139,  140,  141,  143,  430,  431  

I  
Large,  50,  167,  375,  432,  441,  461  

Incidence,  3,  18,  21,  24   Laruelle,  231,  432  

Inhibition,  227,  341   Laureys,  201,  205,  218,  432  

Lavie,  130,  432  

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

Lawton,  62,  291,  433,  465   Miller,  154,  402,  428  

Learning,  156,  222,  406,  411,  420   Mirenowicz,  128,  130,  201,  202,  228,  439  

Levine,  230,  232,  400   Monk,  38,  431  

Lhermitte,  122,  123,  124,  298,  343,  346,  347,  359,   Montagna,  218,  444  

364,  365,  433   Moore,  129,  210,  213,  438,  439  

Light,  312,  456   Morgan,  37,  335,  399,  428,  429,  435  

Limogec,  252,  453   Morris,  252,  277,  394,  440  

Linebaugh,  68,  434   Myin-­‐Germeys,  274,  294,  402,  460  

Ljungberg,  127,  201,  236,  434,  450  

Ljungquist,  155,  395  

N  

Llewelyn,  72,  392  

Narrative,  300  

Nasrallah,  267,  428  

M  
negative,  71,  270  

Maher,  265,  435   Neurotransmitters,  228  

Malkin,  165,  435   Neutral,  100,  162  

Manageability,  62,  73,  86,  94,  107,  133,  154,  177   Newman,  140,  440  

Marcellino,  230,  412   Nichols,  158,  232,  440  

March,  31,  37,  38,  147,  435,  449   Nickerson,  207,  252,  306,  440  

Matlin,  213,  436   NMDA,  (N-­‐Methyl-­‐D-­‐aspartate  receptor)  

Meaning,  79,  109,  110,  112,  132,  133,  149,  157,    225,  229,  230,  232,  239,  244,  250,  268,  390  

166,  177,  180,  182,  183,  192,  219   Noise,  277  

Meltzoff,  129,  210,  438   Northoff,  124,  134,  135,  157,  271,  297,  313,  315,  

Memmott,  380   338,  346,  347,  351,  354,  365,  441  

Menon,  215,  464  

Mental  Health  Services,  4,  170  

O  

Merleau  Ponty,  217,  438  

Obeyesekere,  181,  442  
Metadata,  250  
Osmond,  18,  20,  21,  36,  57,  58,  59,  63,  65,  66,  68,  
Meyer-­‐Lindenberg,  244,  250,  412  
69,  71,  74,  75,  77,  78,  79,  81,  82,  83,  109,  209,  
Michie,  267,  438  
289,  313,  424,  443  

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 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

P   Richard-­‐Devantoy,  360,  367,  374,  446  

Richardson,  69,  165,  446  

Paleomammalian,  159  
Rittel,  43,  144,  359,  430  
Pantelis,  374,  396  
Rizzolatti,  343,  447  
Paranoia,  255,  338,  410  
Robinson,  228,  395,  433  
Paranoid,  100,  251,  278,  300,  351,  352,  353  
Rolls,  261,  277,  447  
Parnas,  144,  199,  242,  249,  299,  313,  443,  449  
Romero,  236,  423  
Parsons,  81,  292,  315,  454,  459  
Rumelhart,  223,  448  
Pei,  99,  230,  288,  443  
Rutten,  293,  333,  448,  459,  460  
Perception,  29,  51,  63,  67,  122,  188,  190,  212,  213,  
Ryan,  220,  299,  404  
214,  247,  296,  343,  345,  351  

Perkins,  33,  290,  379,  444   S  

Perlman,  202,  239,  270,  338,  444  
Sacks,  219,  448  
Perry,  63,  65,  402,  435  
Safety,  57,  391,  402  
Phasic,  dopamine  reception  239,  418  
Saha,  21,  437  
Popper,  192,  445  
Salience,  127,  202,  237,  242,  423  
Positive  feedback  distortion,  247,  256  
Salutogenic,  4,  54,  85,  104,  105,  149,  170  
Positivity,  98,  270  
Sass,  144,  242,  299,  313,  449  
Poverty,  332  
Schemata,  224  
Prante,  158,  445  
Schlagenhauf,  197,  236,  266,  277,  313,  423,  426  
Pridmore,  254,  255,  269,  445  
Schultz,  127,  128,  130,  134,  201,  202,  228,  235,  
Proshansky,  362,  445  
236,  237,  238,  310,  434,  439,  449,  450  
Psychosis,  196,  270,  333,  368,  427,  435,  452  
Seamans,  235,  450  

Q   Searle,  157,  344,  451  

Searles,  18,  20,  37,  58,  63,  64,  65,  67,  68,  69,  74,  
Questionnaires,  95  
79,  80,  81,  82,  111,  144,  167,  184,  262,  292,  

299,  451  
R  
Seeman,  230,  231,  232,  233,  234,  244,  250,  268,  

Recognition  salience,  204   441,  448,  451,  452  

430
 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

Serdaru,  123,  433   Toga,  228,  457  

Shadmehr,  256,  406   Tonic  dopamine  reception,  239  

Shergill,  101,  279,  453,  454   Torrey,  326,  331,  458,  461  

Significance,  3,  18,  127,  132,  133,  202,  204   Tunnel  focus,  247,  251  

Sloan  Devlin,  73,  289,  292,  454  

Smith,  35,  44,  72,  82,  213,  216,  419,  438,  454,  463  
U  

Snodgrass,  151,  455  

Ullman,  65,  361,  458  
SOC  (Sense  of  Control),  60,  85,  94,  96,  104,  153,  
Ulrich,  56,  61,  81,  92,  153,  165,  292,  315,  458,  459  
157,  177  
Undermined  automaticity,  247,  251  
Social/occupational  dysfunction,  247  

Somatogenic,  39,  268   V  

Spatial,  311  
Vaaler,  92,  289,  292,  459  
Spitzer,  197,  258,  265,  450,  455  
Variation,  244  
Srivastava,  324,  436,  452  
Varma,  23,  460,  462  
Staff,  58,  77,  167,  454  
Veling,  31,  435  
Startup,  109,  360,  368,  455  
Villagrán,  21,  396  
Strange,  237,  456  
Violence,  50,  355,  374,  377,  404,  417,  428,  432  
Striatum,  233  
Visual,  351  
Subcortical  confinement,  247,  259  
Vitamin  D,  324,  330,  332,  336,  337  
Sudjic,  73,  151,  152,  456  
Volavka,  31,  50,  349,  360,  461  
Surmeier,  230,  453  

Svensson,  232,  415  

W  

T   Waddington,  243,  426,  428  

Walls,  312  
Tacit  knowledge,  224  
Weckowicz,  63,  65,  209,  313,  461  
Tamminga,  244,  457  
Weickert,  239,  252,  440,  444  
Tandon,  267,  274,  428,  457  
Whitehead,  57,  79,  389,  462  
Taylor,  34,  371,  372,  417,  421,  455,  457  
Wicked  problems,  398  
Theeuwes,  130,  204,  206,  228,  310,  423,  457  
Wiggins,  197,  450  
431
 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

Wilcox,  50   Yantis,  121,  122,  464  

Williams,  18,  20,  191,  232,  258,  269,  404,  415,   Yolken,  331,  458,  465  

455,  462,  463   Yonge,  252,  422  

Wisconsin  Card  Sorting  Test,  279  

Wise,  269,  463  

Z  

Woodbury,  21,  64,  76,  79,  464  

Zeisel,  26,  290,  465  
Wyatt,  19,  298,  464  
Zeman,  218,  466  

Zihl,  279,  466  

Y  

Yanni,  112,  304,  464  

432
 SCHIZOPHRENIA AND THE BUILT ENVIRONMENT

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