Government of India

CENTRAL INSTITUTE OF PSYCHIATRY

SEMINAR
DISORDERS OF MEMORY
Chairperson : Dr.A.K. Bakhla
Presenter : Dr. Archana Singh
Discussant : Dr. Sathishkumar S V

1. Introduction 6. Types Of Memeory Disorders

2. Classification Of Memory A. Amnesia
3. Processes Of Memory Formation B.Paramnesia
4. Models Of Memory Processing C. Hyperamnesia
5. Clinical Assessment of Memory 7. Conclusion

INTRODUCTION
The ability to store and recall information is one of the most amazing capacities of higher organisms. As human
adults, we can remember events that happened in our earliest childhood. We can recall skills learned far in the
past. Our memories encapsulate our sense of personal identity, our cultural identities, and the meaning of our
lives. We can even be influenced by memories that we cannot explicitly remember. However, we all remember
—of that there can be no doubt. Whether we remember accurately or inaccurately, in detail or in abstract, are
questions that researchers have investigated for many years.

Disturbance of memory is always of significance for the sufferers; sometimes, however, forgetting is equally
important and is an active process. The memory disturbance was a specific feature following head injury and
other conditions was recognised in various writings in mid 19 th century. The earliest detailed study of disordered
memory from a psychological perspective was by Ribot (1882). Korsakov (1890) subsequently described his
eponymous condition, pointing out that gross disorder of memory may occur in patients in whom other
intellectual functions and judgement are preserved (Oyebode, 2008).

CLASSIFICATIONS OF MEMORY
 BASED ON DURATION
 SENSORY MEMORY
 SHORT TERM MEMORY
N
O
G
S
L
H
T
R
A
B
S
E
D
N
O N
O
Y
R
 LONG TERM MEMORY
 WORKING MEMORY M
R
E
T
D
A
R
E
M
U
T N
O
I
Y
R
 BASED ON INTEGRITY OF
INFORMATION
O
E
M Y
R
 IMMEDIATE MEMORY
 RECENT MEMORY
 REMOTE MEMORY

SENSORY MEMORY
Sensory memory is the ability to retain impressions of sensory information after the original stimulus has
ceased. It refers to items detected by the sensory receptors which are retained temporarily in the sensory
registers and which have a large capacity for unprocessed information but are only able to hold accurate images
of sensory information momentarily. Sensory memory corresponds approximately to the initial 200–500
milliseconds after an item is perceived (Morgan et al., 1993). The two types of sensory memory that have
been most explored are iconic memory and echoic memory. Visual sensory memory is more commonly referred
to as iconic memory and auditory sensory memory is known as echoic memory. This type of memory cannot
be prolonged via rehearsal.

SHORT TERM MEMORY

Short-term memory (or "primary" or "active memory") is the capacity for holding a small amount of
information in mind in an active, readily available state for a short period of time. The duration of
has a limitless
L
T
M
R
E
O
D
S
C
N
P
G
Y
H
U
A
I
V
short-term memory is believed to be in the order of seconds. Estimates of short-term memory capacity
are 7 plus or minus 2 units. Short term memory is memory that holds information received from
sensory register for up to about 30 seconds. Baddeley, (1986) defined working memory as "A system
for the temporary holding and manipulation of information during the performance of cognitive task
such as comprehension, learning and reasoning (Sims, 2003). Short-term memory is believed to rely
mostly on an acoustic code for storing information, and to a lesser extent a visual code.

LONG TERM MEMORY (LTM)

When
have
memories
been
rehearsed in short
term memory, they
are encoded into
long term memory.
Long Term Memory
(LTM), provides
lasting retention of
information and
skills from minutes
to a lifetime and

capacity. Encoding is the process of placing information into what is believed to be a limitless memory reservoir
or LTM, can occur for specific stimuli as well as for the general memory (Casey and Kelly, 2007). ). The storage of
material in long-term memory allows for recall of events from the past and for the utilization of information
learned throughout life.

Divisions Of Long Term Memory

Long-term memory is commonly divided into two major types -'declarative' and 'non-declarative (Oyebode,
2008).
 Declarative memory also termed as explicit memory, encompasses all the information that we
can consciously describe or report. . It has been further subcategorized into:
(a) Semantic memory which concerns memory for meaning, the storage of abstracts and general facts.
(b) Episodic memory or autobiographical memory is memories based upon a personal experience
relating to self and is linked to a particular time and place in life.

 Non Declarative memory refers to skills, habits or other manifestation of learning that can be
expressed without an awareness of what has been learned. It is heterogeneous collection of
nonconscious or implicit memory abilities.
Subtypes
Procedural
Simple classical conditioning
Priming
Procedural memory, also known as implicit memory, is memory system that retains information
we cannot readily express verbally-for example, information necessary to perform skilled motor
activities like riding a bicycle (Baron, 2005). Although we retain these skills and abilities we are
often completely unable to introspect upon or describe how we do them. Procedural memory is
very resistant to forgetting and is also resistant to brain damage that eradicates other forms of
memory like seen in anterograde amnesic patients who forget simple events or verbal instructions
after a few moments.
Simple Classical Conditioning is another type of non-declarative memory that generally occurs in
the presence of conscious awareness of conditioned stimulus (CS) and unconditioned stimulus
(UCS) contingency, but can occur without awareness also (Budson,2001).
Priming
When an object has just been perceived or processed, there is a tendency for that object to be
perceived more easily the next time, a temporary facilitation that is something like a warm-up
effect. Such priming operates across a wide range of sensory and motor systems, occurring at a
range of different processing levels. For example, presenting a picture of an airplane will make it
easier for a subject to identify a highly fragmented version of the picture as an airplane when it is
presented shortly afterwards. In general, priming tends to be very specific, as though some aspect
of the perceptual system has been facilitated by being used recently. As mentioned earlier, priming
is usually preserved in amnesic patients good explicit learning do not influence implicit learning,
 and vice versa. Another feature of implicit learning is the way in which it appears to bypass
conscious awareness.

The diagram indicates various neural structures thought to be important for different types of
declarative and non declarative memory.

SEMANTIC MEMORY
Semantic memory refers to a person’s conceptual knowledge about the world. It includes knowledge of the
meaning of words, objects and other stimuli perceived through the senses, as well as a rich abundance of facts
and associated information. Semantic memory is immensely important because it constitutes the knowledge
base that allows us to communicate, use objects, recognize foods, react to environmental stimuli and function
appropriately in the world. Semantic memory does not break down in an all-or-none fashion. Patients may know
some words but not others, may recognize one exemplar of an object but not another, and may retain partial
information about a concept while other information is lost(Snowden, 2002).

WORKING MEMORY
The concept of working memory (WM) was initially proposed by Baddeley and Hitch (1974) and developed by
Baddeley (1986), and is characterised by the assumption that short-term storage of information must be
considered as part of a more complex system involved in the execution of a specific task. The information is
stored in the WM as long as necessary, and the structure need not be defined only in terms of the dichotomy
between short- and longterm information storage. On the contrary, this system has the ability to store and
process information simultaneously (Cornoldi & Vecchi 2003).

CLINICAL CLASSIFICATION

For clinical descriptive purposes, memory is often subdivided into three basic types— immediate,
recent, and remote—distinguished by the time interval between presentation of the stimuli and
retrieval. Immediate memory may refer to the registration of information as a memory trace for
several seconds or more, corresponding to both sensory and sometimes short-term memory described
earlier. Recent memory assumes some period of memory storage, and might include a person’s recall
of day-to-day events, and may refer to information learned hours, days, or even weeks ago. Remote
memories typically include memories of events or knowledge learned years ago, usually premorbidly or
before a brain injury (Strub and Black, 2000 ).

PROCESSES OF MEMORY FORMATION

 Description of the requirement for memory is chiefly referable to long term memory and can be
subdivided phenomenologically into the following five functions (Oyebode, 2008).

 Registration or encoding is the capacity to add new information to the memory store.
 Retention or storage is the ability to maintain knowledge that can subsequently be returned to
consciousness.
 Retrieval is the capacity to access stored information from memory by recognition, recall or by
demonstrating that a relevant task is performed more efficiently as a result of prior experience.
 Recall is the effortful retrieval of stored information into consciousness at a chosen moment. It requires an
active complex search process. It is influenced by primacy and recency effects.
 Recognition is the retrieval of stored information that depends on the identification of items previously
learned and is based on either remembering (effortful recollection) or knowing (familiarity based
recollection).

Seven stages in memory: Following Welford, memory can be isolated in seven stages (Hamilton, 1984).
These are
1. Adequate perception, comprehension and response to the material to be learned.
2. Short-term storage mechanism.
3. Formation of a durable trace.
4. Consolidation in which traces are often modified or simplified by subsequent learning.
5. Recognition that certain material needs to be recalled.
6. Isolation of the relevant memory.
7. Using the recalled material in new situation.

MODELS OF MEMORY PROCESSING

1) Atkinson-Shiffrin model
Atkinson and Shiffrin considered memory to have three major constituents. In the Atkinson-Shiffrin theory,
memory starts with a sensory input from the environment which is held for a very brief period in the sensory
register associated with the sensory channels like
vision, hearing and touch etc. information that is
attended to and recognized in the sensory register is
passed on to short term memory where it is held for
about 20-30 seconds. Some of the information reaching
short term memory is processed by being rehearsed
and may then be passed along to long term memory;
information that is not processed is lost. When items of information are placed in long term memory they are
organized into categories. It was assumed that the longer an item is held in the short term memory, the more
likely it is to go into long-term memory (Morgan et al., 1993).

2) Working memory model- Baddeley and Hitch

In 1974 Baddeley and Hitch proposed a working memory model which replaced the concept of general short
term memory with specific, active components. In this model, working memory consists of three basic stores:
the central executive, the phonological loop and the visuo-spatial sketchpad. In 2000 this model was expanded
with the multimodal episodic buffer. The central executive essentially acts as attention. It channels information
to the three component processes: the phonological loop, the
visuo-spatial sketchpad, and the episodic buffer. The
phonological loop stores auditory information by silently
rehearsing sounds or words in a continuous loop: the articulatory
process.
The visuospatial sketchpad stores visual and spatial information.
The episodic buffer is dedicated to linking information across
domains to form integrated units of visual, spatial, and verbal
information and chronological ordering. The episodic buffer is
also assumed to have links to long-term memory and semantical
meaning. The working memory model explains many practical
observations, such as why it is easier to do two different tasks (one verbal and one visual) than two similar tasks
(e.g., two visual).

3) Levels of processing model- Craik and Lockharts

Craik and Lockhart (1972) argued that the previous view of a short-term memory store relying on
speech coding and feeding a long-term memory store was inappropriate. They suggested that the
more deeply information is processed; the more likely it is to be retained (Baron , 2005). They argued
that all of these processes would lead to some long-term learning, but that the amount of learning
depended on the type of processing, with "deep" processing in terms of meaning leading to much
better retention than "shallow" processing. Maintenance rehearsal might keep material available, but
would not enhance long-term learning.

Memory Disorders

Memory disorders may affect the ability to recall both past events (retrospective memory) and future events
and intentions (prospective memory)
The two major brain regions that have generally been implicated in human memory dysfunction include the
diencephalon and the hippocampi (Emilien et al., 2005). The dysmnesic syndromes that involve these structures
include impairment of long-term data storage, disruption of the encoding of short-term into long-term storage,
or a loss of decoding or access to the long-term data storage. Dysmnesia is the preferred term describing a
partial memory loss, in contrast to the term amnesia, which implies a total memory loss. Amnesia may be
viewed as an extreme on a broad continuum of dysmnesic syndromes where mild dysmnesic illnesses occur
more commonly than total amnesia.
There can be varied presentation of memory impairments. A patient can have memory impairment in single
memory domain, e.g. working memory, or can have deficit in different domains simultaneously (Lishman, 2004).

Memory disorders can be broadly classified into -

AMNESIAS (loss of memory)

PARAAMNESIAS (distortions of memory)

HYPERAMNESIAS

THE AMNESIAS

Amnesia is a general term meaning temporary or permanent impairment of some part of the memory system.
The term amnesia is typically applied to a deficit of long-term episodic memory, involving an impaired capacity
for new learning (anterograde amnesia), and/or a deficit in access to old memories (retrograde amnesia). The
classic amnesic syndrome involves impaired episodic memory, but with preserved intellect, normal working
memory and access to semantic memory, although new semantic learning is likely to be impaired. Implicit
memory is likely to be preserved, with patients able to acquire motor and perceptual skills, to show perceptual
priming, to be capable of classical conditioning, and of non-associative learning.

Its origin may be organic or psychogenic.

 Psychogenic Amnesias:
Psychogenic amnesias may appear without any organic disease present but the presentation of
organic brain disease is always modified by psychogenic factors, (Oyebode, 2008).

Childhood amnesia- Freud used the concept of repression to account for childhood amnesia. He said that we
are unable to retrieve childhood memories because they are associated with the forbidden, guilt arousing sexual
and aggressive urges. These urges and their associations are repressed and cannot be retrieved; they are
forgotten because being aware of them would result in strong feeling of guilt or anxiety. Another interpretation
of childhood amnesia stresses over difference in the ways young children and older people encode and store
information (Morgan et al., 1993).

Dream amnesia-Freud’s interpretation of dreams was based on repression. He considered dreams to be

expression of forbidden sexual and aggressive urges. Other interpretation stress the differences in the
symbol system used in dreaming and waking, the memory-symbol network in waking life are different from
those of dreaming so it is difficult to retrieve dreams in waking state (Morgan et al., 1993).

Defensive amnesia-This form of amnesia is usually considered to be a way of protecting oneself from the
guilt or anxiety that can result from intense, intolerable life situations or conflicts. People with this form of
amnesia may forget their names, place of living, occupation and many other important details of their past
life. Amnesic episode can last for weeks, months, or years (Morgan et al., 1993).

Anxiety amnesias- Anxiety amnesia occurs when there is anxious preoccupation or poor
concentration in disorders such as depressive illness or generalized anxiety. More severe forms of
amnesia in depressive disorders resemble dementia and are known as depressive pseudo dementia.
Amnesias in anxiety and depressive disorders are generally caused by impaired concentration and
resolve once the underlying disorder is treated (Casey and Kelly, 2007).
Katathymic amnesia- also known as motivated forgetting. It is the inability to recall specific painful
memories and is believed to occur due to defense mechanism of repression. Though the term is
often used interchangeably with dissociative amnesia, katathymic amnesia is more persistent and
circumscribed than dissociation in that there is no loss of personal identity (Casey and Kelly, 2007).
Dissociative or hysterical amnesia- is a sudden amnesia that occurs during periods of extreme trauma
and may be concerned about the stressful or traumatic life events that may last for hours or even
days. The amnesia will be for personal identity such as name, address and history as well as for
personal events, while at the same time the ability to perform complex behaviors is maintained
(Casey and Kelly, 2007). Dissociation may be associated with a fugue or wandering state in which the
subject travels to another town or country, and is often found wandering and lost. Four types of
amnesia are been described.
 Localized amnesia being the commonest type, have inability to recall the events over
circumscribed period of time corresponding to stressor.
 Selective amnesia related to only selective events of a particular period related to stressful
life event without impairment of memory in other events of same time period.
 Continuous amnesia, inability to recall all the personal events from the time of stressful
situation till present time.
 Generalized amnesia, rarest inability to recall whole life in face of stressful life event (Ahuja,
1999).

Organic amnesias
Organic impairment of memory is referred to as true amnesia and can affect different functions of memory.
There can be impairment of registration, retention, retrieval or recall, or recognition.

 Acute brain disease -In these conditions memory is poor owing to disorders of perception and attention.
Hence there is a failure to encode material in long-term memory. In acute head injury there is amnesia,
known as retrograde amnesia that embraces the events just before the injury. Anterograde amnesia is
amnesia for events occurring after the injury; these occurred most commonly following accidents and
are indicative of failure to encode events into long-term memory. Blackouts are circumscribed periods of
anterograde amnesia experienced particularly by those who are alcohol dependent during and following
bouts of drinking. They indicate reversible brain damage and vary in length but can span many hours.
They also occur in acute confusional states (delirium) due to infections or epilepsy (Casey and Kelly,
2007).

 Subacute coarse brain disease- The characteristic feature of this disorder, is an amnestic state in which
the patient is unable to register new memories leading to inability to learn new information
(anterograde amnesia),and the inability to recall previously learned material (retrograde amnesia).
However, memories from the remote past remain intact, as does recall of over learned material from
the past and immediate recall. As improvement occurs, the amnestic period may shrink and recovery
may sometimes be total (Casey and Kelly, 2007).

 Chronic coarse brain disease- Patients with a progressive chronic brain disease have an amnesia
extending over many years, though the memory for recent events is lost before that for remote events.
This was pointed out by Ribot and is known as Ribot's law of memory regression (Casey and Kelly, 2007).

THE AMNESIC SYNDROMES

Korsakoff’s syndrome

Korsakoff ’s syndrome results from prolonged and excessive alcohol intake. The thiamine (B1) deficiency has a
direct effect on the brain, specifically on the medial thalamus and possibly on the mammillary bodies of the
hypothalamus (Victor et al., 1989).The most common symptoms associated with this syndrome include
anterograde as well as retrograde amnesia, confabulations, and a general sense of apathy. Korsakoff ’s
syndrome has long been recognized the prototype of diencephalic amnesia, although it is now recognised that
Korsakoff ’s syndrome commonly involves cortical atrophy, especially the frontal lobes and damage to other
brain regions (Parkin, 1991 ). In addition to their Anterograde memory deficit, Korsakoff ’s syndrome patients
have severely impaired retrograde memory. In Korsakoff ’s syndrome memory for events in the more distant
past preserved relative to memory for more recent events (Butters & Granholm, 1987; Parkin, 1991). Patients
with Korsakoff’s syndrome have a striking anterograde and retrograde amnesia, often with marked
confabulation but preserved attention, personality, social functioning, STM, and nondeclarative memory.
Korsakoff patients, like other amnesics, exhibit severe impairments in the ability to learn new information.
Transient global amnesia

In most cases of amnesia, the severity of the memory deficit remains stable over a period of years, but there are
conditions such as transient global amnesia where recovery occurs. Global amnesia is characterized by a
relatively circumscribed deficit in LTM for new information. It appears that transient global amnesia may be
caused by temporary bilateral dysfunction of medial temporal lobe structures, including the hippocampus,
entorrhinal cortex, and parahippocampal gyrus (Fisher, 1982). This dysfunction is most likely due to ischaemia,
perhaps caused by vertebrobasilar hypoperfusion or migrainous vasospasm of vertebrobasilar vessels (Caplan et
al., 1981; Crowell et al., 1984). This type of amnesia is characterised by a patient’s inability to learn new
material, by their repeated asking of questions that have been answered and being able to recall events that
antedate the onset of the episode. Transient global amnesia occurs in middle aged and elderly men more
commonly than women (Fisher and Adams, 1964). The condition, which is still not clearly understood, can
emerge in times of severe stress, pain, or emotion, and has been attributed to migraine, epilepsy, drug use,
hypoglycaemia, stroke, and neoplasms but is still not clearly understood. Fortunately, these patients normally
improve spontaneously, within a few hours, and are neurologically normal the following day. In the clinic,
transient global amnesia is typically assessed by means of recall and recognition tests that require retrieval of
recently learned information. Patients with global amnesia also manifest retrograde amnesia. Frequently,
remote memories are better preserved than memories for events that occurred shortly before brain injury.

Visual memory-deficit amnesia

Vision and visual imagery play a central role in a variety of memory tasks (Rubin, 1995). Biographical memory
appears to rely on visual imagery to a much greater extent than other sensory modalities. A form of amnesia
called visual memory deficit amnesia, caused by damage to areas of the visual system that store visual
information, has been described (Rubin & Greenberg, 1998). Because it is caused by a deficit in access to stored
visual material and not by an impaired ability to encode or retrieve new material, it has the otherwise infrequent
properties of a more severe retrograde than anterograde amnesia with no temporal gradient in the retrograde
amnesia.

Paramnesia (Distortions of memory)

This term was coined by Emil Kraepelin (1887) in analogy of terms such as paranoia, paraphasia, and
paraphrenia, as a general term to explain illusions and hallucinations of memory (Burnham, 1889). This is the
falsification of memory by distortion. This can occur in normal subjects due to the process of normal forgetting
or due to proactive and retroactive interference from newly acquired material and is also seen in persons
suffering from emotional problems or other organic states.

It can be divided into Distortions of recall

Distortions of recognition

Distortions of recall

Retrospective falsification
Retrospective falsification refers to the unintentional distortion of memory that occurs when it is filtered
through a person's current emotional, experiential and cognitive state (Casey and Kelly, 2007).Though it can
occur in any psychiatric illnesses, it is often found in those suffering from depressive illness and hysterical
personality and is invariably related to the insight of the patient as well as to suggestibility.

Retrospective delusions
Retrospective delusions are found in some patients with psychoses who backdate their delusions in spite of the
clear evidence that the illness is of recent origin (Casey and Kelly, 2007). Thus, the person will say that they have
always been persecuted or that they have always been evil.

Delusional memories
Primary delusional experiences may take the form of memories and these are known as delusional memories,
consisting of sudden delusional ideas and delusional perceptions. Delusional memories are variously defined,
some authorities believing them to be delusional interpretations of real memories (Pawar & Spence, 2003),
while others such as the Present State Examination (PSE) suggest that they are experiences of past events that
did not occur but which the subject clearly remembers. There are two components to a delusional memory, i.e.
the perception (either real or imagined) and the memory.

Confabulation
Confabulation is the falsification of memory occurring in clear consciousness in association with organic
pathology. It manifests itself as the filling-in of gaps in memory by imagined or untrue experiences that have no
basis in fact. There are two broad patterns (Bonhoeffer, 1901), the embarrassed type in which the patient tries
to fill in gaps in memory as a result of an awareness of a deficit and fantastic type in which the lacunae are filled
in by details exceeding the need of the memory impairment. The confabulation diminishes as the impairment
worsens.
Some related disorders include
 Pseudologia fantastica
Pseudologia fantastica or fluent plausible lying (pathological lying) is the term used to describe the confabulation
that occurs in those without organic brain pathology such as personality disorder of antisocial or hysterical type.
Typically the subject describes various major events and traumas or makes grandiose claims and these often
present at a time of personal crisis, such as facing legal proceedings. Although it seems that the person with
pseudologia believes their own stories and there is a blurring of the boundary between fantasy and reality,
when confronted with incontrovertible evidence these individuals will admit their lying (Casey and Kelly, 2007).
Minor varieties of this occur in those who falsify or exaggerate the past in order to impress others.
 Vorbeireden or approximate answers
Vorbeireden or approximate answers is seen in patients with hysterical pseudodementia, named after Ganser
who, in 1898 described four criminals showing several common features (Casey and Kelly, 2007). Prominent
features present in such patients include: clouding of consciousness with disorientation, auditory and visual
hallucinations (or pseudo-hallucinations), amnesia for the period during which the symptoms were manifest,
conversion symptoms and recent head injury, infection or severe emotional stress. Approximate answers
suggest that the patient understands the questions but appears to be deliberately avoiding the correct answer,
for instance, to avoid a court appearance .It is distinguished from pseudodementia in which consciousness is
clear. Many now believe that the Ganser syndrome is indicative of either an organic or a psychotic state rather
than hysteria as originally believed .Ganser syndrome and malingering/factitious disorder are often confused in
spite of the conscious basis for the latter. Vorbeireden is also found in acute schizophrenia, usually the
hebephrenic type.
 Munchausen's syndrome
It is a variant of pathological lying in which the individual presents to hospitals with bogus illnesses, complex
medical histories and often multiple surgical scars. A proxy form of this condition has been described in which
the individual, usually a parent, produces a factitious illness in somebody else, generally their child. The
diagnosis of Munchausen’s by proxy is itself a controversial diagnosis.

 False memory
False memory is the recollection of an event (or events) that did not occur but which the individual subsequently
strongly believes did take place (Brandon et al, 1998). The syndrome refers not to distortion of true memories,
as in normal forgetting, but to the actual construction of memories around events that never took place (Casey
and Kelly, 2007). Memory distrust syndrome is a type of false memory which originates from the person's own
fundamental distrust of their memory known as 'source amnesia'. This source amnesia arises because of
difficulty remembering the source from which the information was acquired, whether from one's own recall or
from some external source as recounted by others.

 Screen memory
This is a recollection that is partially true and partially false; the affected individual only recalls part of the true
memory because the entirety of the true memory is too painful to recall (Casey and Kelly, 2007). It is difficult to
find out precisely which elements of such memories are true and which is false.

 Multiple personality disorder (W .H .0,1992 ; Oyebode,2008)

This disorder is rare, remains controversial due to lack of reliable information, unclear prevalence, selection bias
and psychopathological imprecisions (Oyebode, 2008). The essential feature is the apparent existence of two or
more distinct personalities within an individual, with only one of them being evident at a time. Each personality
is complete, with its own memories, behaviour, and preferences: these may be in marked contrast to the single
premorbid personality. In the common form with two personalities, one personality is usually dominant but
neither has access to the memories of the other and the two are almost always unaware of each other's
existence. Change from one personality to another in the first instance is usually sudden and closely associated
with traumatic events.

 Cryptamnesia
Cryptamnesia is described as 'the experience of not remembering that one is remembering, (Oyebode,2008).For
example a person writes a witty passage and does not realize that they are quoting from some passage they
have seen elsewhere rather than writing something original. There is no indication as to whether this is a
common phenomenon or whether it is associated with any specific psychiatric disorder (Casey and Kelly, 2007).

 State-dependent memory
State dependent memory is the recall of events or learned material only when the person is in the same drug or
medication-induced state under which the event was experienced or the material learned. Patients with
psychosis or severe mood disorder experience this phenomenon and, when well, will not recall dramatic
experiences that occurred when ill. When ill again, the memories are again accessible and recalled (Murphy-
Eberenz et al. 2006).

Distortions of recognition

Déjà vu is not strictly a disturbance of memory, but a problem with the familiarity of places and events. It
comprises the feeling of having experienced a current event in the past, although it has no basis in fact.

Jamais vous is the knowledge that an event has been experienced before but is not presently associated with
the appropriate feelings of familiarity.
Déjà entendu, the feeling of auditory recognition.

Déjà pense, a new thought recognized as having previously occurred, is related to déjà vu, being different only
in the modality of experience. These experiences occur occasionally in normal persons but they may
become excessive in temporal lobe lesions.

Misidentification
This may occur in confusion psychosis and in acute and chronic schizophrenia. Misidentification may be

 Positive misidentification
 Negative misidentification
 Positive misidentification:
The patient recognizes strangers as his friends and relatives. Some patients assert that all of the people whom
they meet are doubles of real people. In acute schizophrenia, it can be based on a delusional perception.

 Negative misidentification:
The patient denies that his friends and relatives are people whom they say they are and insists that they are
strangers in disguise. Leonhard has suggested that negative identification could result from an excessive
concretization of memory images, so that the patient retains all the minute details of the characteristics of the
people whom he encounters. When he sees the same person again he compares the new perception with the
exact memory image.

The Basic Misidentification Syndromes

Capgras Syndrome
It was first described by capgras and Reboul-Lachaux in 1923. The essential feature of this syndrome is
hypoidentification. Patients insists that a particular person (or persons), usually somebody with whom
the patients is emotionally linked, is not the person he claims to be but is really a double; is often
accompanied by depersonalization and occurs in a paranoid setting. The commonest cause of capgras
syndrome is schizophrenia and less common causes include involutional depression and hysteria.
Amphitryon illusion: in this patients believe that their spouses are doubles.
Sosias illusion: In this patients believe that other people as well as the spouse are doubles (Hamilton
1984) .

Fregoli syndrome
It was first described by courbon and Fail in 1927. In fregoli syndrome hyperidentification takes place.
The patient identifies a familiar person (usually his persecutor) in various strangers, who are therefore
fundamentally the same individual.

Syndrome of Subjective Doubles

It is characterized by delusions of doubles exclusively of the patient’s own self. The misidentification
can be either hallucinatory or delusional.

Syndrome of Intermetamorphosis
In this syndrome patient believes that others have changed their physical appearance.

Reduplicative paramnesia
In reduplicative paramnesia, patients believe that a physical location has been duplicated.
Hyperamnesia
The opposite of amnesia and paramnesia can also occur and is termed hyperamnesia, or exaggerated
registration, retention and recall. Flashbulb memories are those memories that are associated with intense
emotion. They are unusually vivid, detailed and long-lasting. Flashbacks are sudden intrusive memories that are
associated with the cognitive and emotional experiences of a traumatic event such as an accident. It may lead to
acting and/or feeling that the event is recurring. It is regarded as one of the characteristic symptoms of post-
traumatic stress disorder but is also associated with substance misuse disorders and emotional events (McGee,
1984). It is also likely to be a term that is used inaccurately and should not be confused with intrusive
recollections, which lack the emotional familiarity of flashbacks. Flashbacks involving hallucinogenic experiences
can occur in association with hallucinogenic drugs and possibly cannabis use after the short-term effects have
worn off. These incorporate visual distortions, false perceptions of movement in peripheral fields, flashes of
color, trails of images from moving objects, after-images and halos, as well as classical hallucinations. Eidetic
images represent visual memories of almost hallucinatory vividness that are found in disorders due to substance
misuse, especially hallucinogenic agents.

CLINICAL ASSESSMENT OF MEMORY

Tests for memory (Strub & Black, 2000)

Valid memory testing presumes that the patient is reasonably attentive, can relate to and cooperate with the
examiner, and has no defect that impairs language comprehension or expression.

Immediate recall (short term memory)

Immediate memory usually tested by digit repetition.

Recent memory: Tested for constantly changing facts. Indian adaptation (max score=5):

1. कल आपने रात के खाने में क्या खाया?

2. आज सब
ु ह आपने नाश्ते में क्या खाया?
3. इस महिने का क्या नाम है ?
4. आज कौन-सा दिन है ?
5. कल आपसे कौन-कौन मिलने आया या कल आप किस किस से मिलने गये?

Remote memory

These evaluate the patient’s ability to recall personal and historic events. Personal events must be verified from
a reliable source other than the patient, and performance on the recall of historic information must be
interpreted in light of the patient’s premorbid intelligence, education, and social experience.
Indian adaptation: The following items to be enquired-

1. आपकी उम्र कितनी है ?

2. आपका जन्म कहाँ हुआ?
3. आपकी शादी कब हुई?/आपने नौकरी या व्यसाय करना कब से चालु किया?/आपने पढ़ना कब छोडा या हाई-स्कूल
कब पास किया?
4. आपके सबसे छोटे बच्चे या भाई बहिन की उम्र कितनी हौ?
5. आप इस विभाग में पहली बार अपने इस इलाज के लिये कब आये?
6. पिछलि बार आप इस विभाग कब आये थे?
Each correct answer to be scored one thus a maximum score of 6. (Pershad & Wig, 1988)

Four unrelated words

Instructions: Tell the patient, “I am going to tell you four words that I would like you to remember. In a few
minutes, I will ask you to recall these words”. To ensure that the patient has heard, understood, and initially
retained the four words, have him or her to repeat the words immediately and to correct any errors. Older
patients may require several trials to learn the words.
Then he is asked to recall the words at 5, 10 and 30 minutes. To eliminate possible mental rehearsal,
interference should be used between presentation and recall of words.

Scoring: Normal persons accurately recall 3-4 words after a 10-minute delay. In some, after being
reminded of the correct words i.e., by verbal cues, whether he/she recognizes the appropriate word
from the series of words and improve their performance after 10 and 30 minutes may be seen, but
patients with dementia cannot improve even on subsequent trials.

Indian adaptation: (Pershad & Wig, 1988)

Set 1 छाता, फूल, घडी, तस्वीर, Set 2 मछली, लैंप, रुपया, ताज, खिलैना
पैंसिल

Verbal story for immediate recall

Instructions: tell the patient, “I am going to read you a short paragraph. Listen carefully, because when
I finish reading, I want you to tell me everything that I told you.” A short paragraph is read out to the
patient which he is required to reproduce immediately. As the patient retells the story the number of
items recalled is indicated. The normal individual is expected to produce at least 10 of these items,
though this number decreases with age. If recall is good then he may be asked for another recall after
30 minutes.

Indian adaptation:

There are three sentences of increasing length. First sentence is read slowly, distinctly and at a uniform
rate and note down the recalled sentence verbatim or each of the correctly recalled clauses. One mark
for each clause correctly reproduced. (Pershad & Wig, 1988)

1. राम कुर्सी से उठा, दरवाजा खोला और घर चला गया।

2. रोगी को मेज पर लिटाया, उसको दे खा, दवा लिखी और कल आने के लिए कहा।
3. मोहन के घर पानी नहीं था, उसने बाल्टी उठाई, बाजार के नल पर गया, पानी भरा और वापिस लौट आया।

Visual memory (hidden objects) (Strub & Black, 2000)

Five small, commonly used, easily recognizable objects are hidden in the patient’s vicinity while he is
watching. Each item is named while being hidden. Then interfering stimuli is provided for 5 minutes.
After this period he is asked to name and indicate the location of each hidden object. Finding out fewer
than three objects indicates impaired visual memory.

Paired associate learning

Instructions: Tell the patient, “I am going to read you a list of words, two at a time. Listen carefully
because I will expect you to remember the words that go together. When the patient understands the
directions, continue as follows: “Now listen carefully to the words as I read them.” The patient is read
out a list of paired words at the rate of one pair every 2 seconds. Then he is given the first words from
the pairs, one after another and given 5 seconds for each response. After completion of the first recall
list the second presentation list is provided after a 10 second interval and proceeded in the same way.

A normal person under 70 years is expected to recall the two easy paired associates and at least one of
the hard associates of the first recall trial and to recall all paired associates on second trial. Some
patients can learn the paired words with strong natural associations but cannot learn the pairs without
such associations which indicate an inability to learn new material that cannot be associated with
memories already in storage.
Indian adaptation: (Pershad & Wig, 1988)

Retention for similar pairs For dissimilar pairs

पेड़ फूल मेज काला
मीठा नमकीन पेड़ ऊँचा
आदमी औरत लैंप खुरदरा
दिन रात बच्चा कड़वा
काला सफेद सपना गहरा

CONCLUSION

Our memories reflect the accumulation of a lifetime of experience and, in this sense, our memories are who we
are. We learn to walk, to dance, to drive a car, to throw a ball, and to play a video game—a myriad of acquired
skills we come to take for granted. We learn to fear dangerous situations, to appreciate particular types of music
and styles of art—a broad range of aversions and enjoyments we have assumed as elements of our preferences
and personality. We learn world history, and we learn our own family tree and personal autobiography—all of
these, and much, much more, compose the vast contents and intricate, complex organization of memories that
make each of us a unique human being. Disorders of memory may present as discrete dysfunction or as part of
psychiatric syndrome. There are various clinical and neuropsychological tools to assess these and hence early
interventions to manage these can be used.

DISCUSSION

Discussion will be covered under following headings:

TYPES OF MEMORY: ARE THEY REPRESENTING SEPERATE SYSTEMS?

MODELS OF MEMORY: A BRIEF CRITICAL APPRAISAL

NEUROBIOLOGY OF MEMORY

EPISODIC LEARNING, REMEMBERING, FORGETTING AND KNOWING

AMNESIA IN THE CURRENT NOSOLOGY

AGING, MILD COGNITIVE IMPAIRMENT AND DEMENTIA

MEMORY DYSFUNCTION IN PSYCHIATRIC DISORDERS

MEMORY DISORDERS IN EPILEPSY

DRUG INDUCED MEMORY ALTERATION

MEMORY DISTURBANCES AND ECT

AGING AND MEMORY IMPAIRMENT

EMOTIONAL AND SOCIAL CONSEQUENCES OF MEMORY DISORDERS

MEMORY REHABILITATION

CONCLUSION

TYPES OF MEMORY: ARE THEY REPRESENTING SEPERATE SYSTEMS?

Memory researchers have hypothesized a range of separate memories that deal in different
ways with the incoming information from the external world. The oldest division hypothesized
was between primary and secondary memory, which was proposed by William James (1890).
He distinguished between what one remembered from current consciousness which he called
primary memory and secondary memory which involved the knowledge about what had been
absent from consciousness. This can be considered as the beginning of the working
memory / long term memory distinction.

During 1960s this distinction was elaborated into a theory of short term and long-term
memory (Atkinson and Shiffrin, 1968) and later modified into a theory of working memory
model (Baddeley, 1986) in which an account of the mechanism and support system for
processing was given. Working memory model introduced several subdivision of short term
memory. There is a central executive, responsible for the processing of the incoming
information, the articulatory loop that can hold a couple of seconds of speech like
information, temporarily freeing the central executive of their load and the visuo-spatial
sketchpad that can similarly retain spatial information for a short time.

Prior even to the central executive, other very short-term, sensory memories have been
postulated on the basis of the ability for apparently large amounts of visual and acoustic
information to be held briefly. A visual iconic memory store was initially postulated by
Sperling (1960) and later a related acoustic memory was proposed by crowder and morton
(1969). Though there are robust demonstration of the accessibility of much that has been
presented visually or verbally for brief intervals. Usually less than 1 second, there have been
disputes over their interpretation (Haber, 1983;Coltheart, 1983).

Beyond the short intervals covered by sensory and working memories, the possible
subdivisions of longer-term memory have been controversial. However, the distinction
between explicit and implicit memory has been generally incorporated into the accepted
conceptual anatomy of memory research.

The implicit/explicit memory distinction is justified by data that fit the defined distinction,
but argument continues over whether the phenomena of implicit and explicit memory implies
that there are two separate memory systems. Similar disputes occur-over the other major
divisions of longer-term memory. The terms episodic, semantic, autobiographical,
prospective, declarative, propositional and procedural memories provide useful concepts to
aid the understanding of memory even if they do not, necessarily, represent structurally
separate parts of the cognitive system (Morris and Gruneberg, 1994).

The episodic- semantic distinction was introduced by Tulving (1972) and can be useful in
describing the detailed content of losses from the long term memory store.

A further distinction is made between declarative and procedural memory and has
particular relevance to the classic amnesic syndrome. The phenomenon of “priming” probably
also falls within the domain of procedural memory i.e., the capacity to profit from prior
exposure to cues such as previously perceived or partially completed words in the execution
of a task. Again this represents ‘unconscious memory’ manifested in behavior. Thus there
appear to be several independent memory systems possibly tied to different neural networks
within the brain (Lishman, 2004).

Tulving proposed (Cohen, 2008) a number of criteria whereby separate systems could be
distinguished: -

1.Different memory systems have different functions and handle different types of
information.

2. Different systems may employ different processes but need not necessarily do so.

3. Different systems are mediated by different brain structures or mechanisms.

4 Different systems have developed at different evolutionary stages.

5 Different systems may have different forms of representation.

Applying these criteria Tulving identified five separate but interacting memory systems: -

1. Procedural memory, which is involved in skills, actions, and simple conditioning.

2. The Perceptual Representation System, which is involved in perceptual priming of the

identification of objects - -

3. Short-term memory, which includes working memory.

4. Semantic memory, for general knowledge of the world.

5 Episodic memory, for conscious recollection of personal experiences.

Each of these fine major systems includes multiple subsystems, as yet not fully identified
however, although there is a general agreement that memory includes different systems and
subsystems, there is no consensus about what these are and how they are related to and
interact with each other.

For the purpose of clinical description a somewhat arbitrary division is made into
immediate, recent and remote memory.
The immediate memory span (or ultra short-term memory) is reflected in the reproduction of
material such as brief digit sequences which fall within the span of attention. Clinically it
provides evidence that registration is intact.

Recent memory is reflected in ability to acquire and retain new knowledge (current
memorizing. new learning) and requires a process of consolidation in addition to registration.

Remote memory is reflected in the ability to recall information acquired after a considerable
distance in time, and certainly before the onset of the memory difficulties, it therefore
represents a process of retrieval of material which has been held in long term storage. In
every day clinical practice it is convenient to employ the terms- immediate, recent and
remote. Unfortunately however, considerable confusion can arise over some of the terms
used in referring to memory mechanisms, particularly when attempting to translate the
experimental literature to clinical practice. Short term for example is often used by
psychologists as synonymous with immediate, and often in medical practice as broadly
congruent with recent memory (Lishman, 2004).

MODELS OF MEMORY: A BRIEF CRITICAL APPRAISAL

Atkinson and Shiffrin’S Model (1968): The model by Atkinson and Shiffrin (1968) was
criticized as being too rigid and simplistic as information must flow in both the directions
since there is good deal of interaction between various stores, for example we tend to pay
attention to relevant information from the sensory register but this relevance must be stored
in a long term way. It also does not take into account the types of information taken into
memory as some items seemed to flow into Long Term Memory (LTM) far more readily than
others. It also ignores factors such as the effort and strategy subjects may show while
remembering and why information changes in coding from one memory store to another (Hill,
1998).

Craik and Lockharts Model:In the ensuing years researchers while analyzing Craik
and Lockharts deep processing model found out that the complex semantic processing
produced better cued recall than simple semantic processing and called this mechanism as
elaboration. Eyesenck and Eyesenck (1980) found even words processed phonetically were
better recalled if they were distinctive or usually labelled and termed it as distinctiveness.
Tyler et al. (1979) found better recall for words presented as difficult anagrams like OCDTRO
than simple anagrams like DOCTRO and termed it effort. Rogers et al. (1977) found better
recall for those questions which have personnel relevance (e.g. describes you) than general
semantic ones (e.g. means) (Hill, 1998).

Baddeley and Hitch Model (1974): There remain problems in defining deep processing
and further clarifying as to why it is so effective as semantic processing does not always lead
to better retrieval. It was the working memory model of Baddeley and Hitch (1974) which
then gave further insights into the memory processing and its revised model of 1990 is
currently the most accepted models in memory processing (Hill, 1998).

Miyake and Shah Model (1999): In their recent comprehensive review of working
memory models, Miyake and Shah (1999) proposed that working memory “is those
mechanisms or processes that are involved in the service of complex cognition, including
novel as well as familiar, skilled tasks”. This definition differentiates working memory from
short-term memory because it suggests that working memory goes beyond simply keeping
information “in mind”; rather working memory brings or keeps information online in a goal-
directed fashion (Kay and Tasman, 2006), though both the term (STM and working memory)
are used interchangeably.

NEUROBIOLOGY OF MEMORY

According to current views, information from the senses is temporarilly stored in various
areas of the prefrontal cortex as working memory. It is also passed to the medial temporal
lobe, and specifically to the parahippocampal gyrus. From there, it enters the hippocampus
and is processed in a way that is not yet fully understood. From the hippocampus it leaves
via the subiculum and the entorhinal cortex and somehow binds together and strengthens
circuits in many different neocortical areas, forming over time stable remote memories that
can now be accessed by many different cues (Ganong, 2005).

Figure below shows the brain regions thought to be critical for the formation and storage of
declarative memory. The entorhinal cortex in the major source of projections to the
hippocampus, and nearly two-thirds of the cortical input to the entorhinal cortex originates
in the perirhinal and parahippocampal cortex. The entorhinal cortex also receives direct
connections from the cingulate, insula, orbitofrontal, and superior temporal cortices. (Ken
and Larry, 2005).

midline thalamic nuclei hippocampal region

dorsomedial thalamus
entorhinal cortex
anterior thalamus
perirhinal parahippocampal
mammillary nuclei cortex cortex

frontal sensory
association association
areas areas

EPISODIC LEARNING

Stage1 Sensory, motor and other information, comprising the episode/event-to-be

remembered,activate a number of nodes in the trace system (filled circles).
Stage 2 Through the trace system a set of link nodes is activated, possibly within less
than a second. If the episode is sufficiently new or interesting, the modulatory
system will be activated. This will allow strengthening of connections between
activated link nodes and trace nodes shown by the thickening of the connections.
Stage 3 This stage represents the initial consolidation process. Repeated activation
takes place, leading to the gradual formation of trace–trace connections. These are
initially weak, but grow in strength with each consolidation episode. The repeated
reactivation of already learned representations is a random process that is initiated by
randomly activating a number of nodes in the link system. Consolidation occurs by
further strengthening of the trace–trace connections (trace–link connections are not
strengthened further at this time; this follows one the model of cholinergic processes
in the hippocampus.( Hasselmo,1995, 1999).
Stage 4 In the final stage of consolidation, trace–trace connections have become very
strong and retrieval has become independent of the link system. In both the link and
trace system, the learning of new memory representations will result in the gradual
overwriting of older representations (i.e. forgetting). This interference process is more
evident in the link system compared to the trace system, however, because the link
system has a lower capacity and higher plasticity.

REMEMBERING, FORGETTING AND KNOWING

Gardiner and Richardson-Klavhen (2000) defined remembering as intensely personal

experiences of the past ,those in which we seem to recreate previous events and experience
with the awareness and experiences mentally. The process of remembering has four parts-
registration, retention, retrieval and recall.

Knowing is referred to experience of the past in which we are aware of knowledge that we
process but in a more impersonal way without awareness of reliving them mentally or
familiarity of facts (Kopelman, 2002).

Forgetting refers to the apparent loss of information already learned and stored in long term
memory. Much is forgotten but enough enters so that we have a sketchy record of our lives.
Much of what we think we have forgotten does not really qualify as “forgotten” because it was
never encoded and stored in the first place. (Morgan et al. 2007) .

Intereference theory

Forgetting is a result of some memories interfering with others.

Proactive interference: Old memories interfere with ability to remember new memories.

Retroactive interference : New memories interfere with ability to remember old memories.

Intereference is stronger when material is similar .

AMNESIA IN THE CURRENT NOSOLOGY

Amnesia forms the core component or a part of symptomatology of a number of psychiatric

disorders in the current nosological system. The diagnostic categories in the current
nosological systems with amnesia as the core component of the diagnosis include:

ICD-10: The ICD-10(World Health Organization ,1992), provides two diagnostic categories for
describing amnesic disorder depending on the etiology of the disorders rather than the
symptomatology. The lCD-10 differentiates amnesia due to organic conditions from amnesia
due to use of substance — single or multiple. The diagnostic categories are:

F 04: Organic Amnesic Syndrome not induced by alcohol and other psychoactive substances

F1x.6: Mental and Behavioral disorder dun to use of psychoactive substances — Amnesic
Syndrome.

DSM-IV-TR: The DSM-lV-TR (American Psychiatric Association,1994) categorization of

amnesic disorders bears resemblance to the lCD-10 except for the fact that the two
diagnostic categories are clubbed under one roof as Amnestic disorders with further
categorization into that due to general medical condition, substance induced end unspecified.
The amnestic disorders are labelled under axis-I disorders with a description of the
underlying medical condition to be provided under the axis-Ill category wherever applicable.
The diagnostic categories are:

294.0: Amnestic disorder due to a general medical condition

Substance induced persisting amnestic disorder (Specific substances to be coded as 291.1

Alcohol induced persisting amnesic disorder,

292.83 Secobarbital induced persisting amnestic disorder and the likewise) 294.8 Amnestic
disorder not otherwise specified.

AGING AND MEMORY IMPAIRMENT

Both physical and cognitive functions change as we get older. Fluid intelligence and the
capacity to respond rapidly end flexibly gradually diminishes, while crystallised intelligence,
the residue of prior learning, continues to show a small but steady increase. In general,
memory deteriorates, but is to some extent compensated by the increased use of knowledge,
memory aids, and strategies. In the case of working memory, the phonological loop is
reasonably robust, the visuo-spatial sketch pad somewhat less so, while at least some
executive processes tend to decline. In the case of long-term memory, episodic memory shows
 a slow but steady decline from the twenties onwards, with memory for names being
particularly sensitive to the effects of ageing. Semantic memory continues to grow, but speed
and reliability of access declines. Implicit learning shows a mixed pattern, with some types of
learning being relatively preserved, but others deteriorating. As age advances, we find it
harder to maintain performance against distraction, particularly under levels of high arousal.
Nutritional factors may also influence the elderly more, as they are less able to maintain
blood glucose leave during the gaps between meals, resulting in poorer memory performance
(Baddeley, 1999).

MILD COGNITIVE IMPAIRMENT

A large group of elderly cognitively impaired subjects do not meet the criteria for dementia or
other specific neurological and psychiatric disorders.
Several descriptors including MCI, incipient dementia, and isolated memory impairment have
been used.
The terminology “mild cognitive impairment” refers to subjective memory disturbances
verified by objective deficits of memory at testing.
DEMENTIA
The Clinical features related to the three symptomatic domains that characterize
dementia is as follows -

Neuropsychological impairment Psychiatric symptoms/ Inability to perform

activities of daily life
Behavioral disturbance

 Amnesia-loss of memory Psychiatric symptoms Deficits in

 Aphasia-impairment of instrumental activities
language, most commonly  Depression
apparent on direct questioning,  Anxiety  Handling money
when asking a person to name  Hallucinations  Shopping
objects; a nominal aphasia.  Delusions  Driving
 Agnosia- inability to recognize  Euphoria  Using the telephone
or associate meaning to a sensory  Misidentifications  Doing the laundry
perception Behavioural disturbances  Preparing meals
 Executive dysfunction-  Managing medication
disturbances in judgment,  Agitation Deficits in basic
planning and abstraction.  Aggression activities, e.g.
Other deficits  Aberrant motor
behavior  Dressing
 Acalculia- inability to perform (pacing,wandering,irritability)  Eating
arithmetic
 Using the toilet
calculations Apathy  Personal hygiene
 Agraphia- inability to write  Sexual disinhibition
 Alexia-inability to read  Sleep abnormalities
 Increased appetite/
Change in eating habits

Dementia was initially thought of as a unitary behavioural syndrome, characterised by a

homogeneous decline in intellectual functions, regardless of aetiology.
Dementia is defined as decline of memory and other cognitive functions in comparison with
the patient’s previous level of function, implying a change between two or more assessment
points (McKhann et al., 1984).
ALZHEIMER’S DISEASE
The dementia of AD typically includes anterograde and retrograde amnesia early in its
course.
Deficits in recent memory are typically the first symptoms of AD and may be clinically
reported as misplacing objects, repeating questions and statements, and forgetting names.
Impairments in visuospatial memory are often experienced as getting lost. This anterograde
amnesia reflects impaired encoding and consolidation of the material. (Greene et al., 1995;
Sagar et al., 1988).
Several hypotheses have been proposed to account for this impairment of episodic
memory in AD, which might affect both encoding and retrieval of information, and would
result from attentional deficiencies, working memory dysfunction, semantic difficulties, or
neglect of contextual information (Van der Linden, 1994).
It has also been suggested that recent memories are more vulnerable than remote
memory especially in dementia(Ribot law).
 In general, remote memory remains relatively intact early in the course of AD. With
disease progression, a slight temporal gradient becomes evident. The remote memory
impairment in AD is a temporal gradient, with recall of recent events being more severely
impaired than recall of more remote events (Beatty & Salmon, 1991). In moderate to severe
AD, the temporal gradient disappears and patients show marked retrograde amnesia for all
decades of life (Butters et al., 1995). This general pattern of impairment has been
demonstrated for memory for famous faces and public events, visuospatial information, and
autobiographical information.

Semantic memory Naming

A naming disturbance has been recognised as one of the core clinical features of AD (Wilkins
& Brody, 1969). The anomia tends to be a relatively early manifestation of the disease. It
progressively worsens over the disease course and is strongly correlated with overall
dementia severity (Chertkow & Bub, 1990).

SEMANTIC DEMENTIA
Semantic dementia is a recently documented syndrome associated with non-Alzheimer
degenerative pathology of the polar and inferolateral temporal neocortex with relative sparing
(at least in the early stages) of the hippocampal complex (Hodges et al., 1992).
Core features of semantic dementia
1. Selective impairment of semantic memory causing severe anomia, impaired spoken and
written single-word comprehension, reduced generation of exemplars on category fluency
tests, and an impoverished fund of general knowledge about objects, persons, and the
meaning of words.
2. Relative sparing of other components of language output and comprehension, notably
syntax and phonology.
3. Normal visuo-perceptual and spatial skills, working memory, and non-verbal problem-
solving abilities.
4. Relatively preserved autobiographical and day-to-day (episodic) memory.
(Hodges et al., 1992).
Meta-memory
Meta-memory is the subjective judgment about one’s own memory capabilities. It is
influenced by the present state of emotion. Patients who are depressed subjectively
experience their performance to be worse than in fact, while those in manias or with the
frontal lobe disinhibited syndrome experience their performance to be better than in fact.
Patients with temporal lobe epilepsy overestimate their memory capacities and their self-
monitoring is less accurate for verbal or non-verbal recall depending on the side of the
seizure focus.

MEMORY DYSFUNCTION IN PSYCHIATRIC DISORDERS

The most common psychiatric disorders in which memory impairment may be seen are
schizophrenia, depression, and anxiety. The objective cognitive impairment is often mild with
alterations in such functions as attention, STM, and speed of processing.

SCHIZOPHRENIA

Memory deficits observed in schizophrenia are not restricted to a single element of memory
but strike different systems, such as declarative memory, short term, and working memory
(Goldberg et al., 1993).There are deficits in long-term memory, including evidence of impaired
retrieval in both recall and recognition. There is also evidence of impaired short term
memory. Furthermore, there is evidence of impairment of working memory and semantic
memory but procedural or implicit memory remains intact (McKenna et al., 2002). Cognitive
impairment is a central manifestation of the schizophrenic illness that impacts on the quality
of life of the patient.
ANXIETY

The presence of distracting, task-irrelevant thoughts is a common feature of anxiety. As

worry occupies some of the limited capacity available to the working memory system, this
negatively impacts tasks that rely heavily on the working memory system. The adverse effects
of anxiety will be evident on tasks carried out in conjunction with a task treated as more
“primary”, as this reduces the capacity available for further tasks.

DEPRESSION
STM or the retention of small amounts of information over very short durations has been
found to be unaffected among depressive patients (Austin et al., 1992; LTM seems to be more
prone to impairment. Depression is associated with a number of deficits in episodic memory
and learning. There is involvement of both explicit verbal and visual memory in patients with
both melancholic (endogenous) and non-melancholic (nonendogenous) depression (Austin et
al., 1999).Impaired delayed memory as opposed to preserved immediate recall has also been
found among depressive patients (Cohen et al., 1982).People with major depressive disorder,
including those who have recently attempted suicide, have difficulty retrieving specific
autobiographical memories in response to cue words (Williams, 1996).

Obsessive compulsive disorder

Obsessive compulsive disorder (OCD) is characterized by recurrent unwanted thoughts and

repetitive, ritualistic behaviors that lead to severe impairments in daily functioning. There are
deficits in learning and memory, especially for non verbal information in OCD patients
(Dirson et al., 1996). The difficulty in retrieving specific autobiographical memories exhibited
by OCD patients might reflect excessive cognitive capacity consumption due to preoccupation
with intrusive thoughts typical of major depression.

Panic disorder

Patients with panic disorder have a defect in fear-relevant episodic memory, and their panic
attacks arise from automaticity in recollecting fear-relevant emotional–automatic clusters.
The cluster as a component of fear appears to have been dissociated from cognitive structure,
episodic or informative memory trace, or from information structures.

Post-traumatic stress disorder

Post-traumatic stress disorder (PTSD) is a specific anxiety disorder of significant prevalence

and morbidity that develops following exposure to extreme emotional trauma. Three
symptoms clusters characterise the disorder, all of which represent direct or indirect effects
of memory processes:

(1) persistent re-experience of the traumatic event,

(2) persistent symptoms of increased arousal,

(3) persistent avoidance of stimuli associated with the trauma that may include amnesia for
an important aspect of the traumatic event.

Adult PTSD patients often report a wide range of cognitive problems in memory,
concentration, attention, planning, and judgment.

PTSD may be conceived as a clinical condition that involves both memory intensification for
the core traumatic event and memory impairment for the context surrounding the trauma.
The latter comprises dissociation of the experience from ordinary autobiographical memory.

MEMORY DISORDERS IN EPILEPSY

Patients with epilepsy frequently complain of memory difficulties.In some cases this is
secondary to problems of concentration and attention and may therefore not be a memory
defect per se. For patients with temporal lobe abnormalities,memory may be selectively
affected. Seizures may have an acute effect on memory but this is usually transient and does
not affect prospective memory .But poor memory of patients with temporal lobe epilepsy does
not correlate with seizure frequency. In patients who are undergoing temporal lobectomy
careful testing of memory function prior to surgery is mandatory,and deficits may occur
following removal of offending lobe.

DRUG INDUCED MEMORY ALTERATION

Some drugs that may impair or improve memory

Drugs

IMPAIRED MEMORY Type of memory

impaired/improved
Lorazepam and diazepam Explicit and Implicit
Memory
Methylenedioxymethamphetamine Verbal and visual
(MDMA or “Ecstasy”) Memory

Ethanol and temazepam LTM

 IMPROVED MEMORY

Citicoline Facilitates recovery

of function and
cognition after
traumatic brain
injury
Over the past three or four decades,there has been increasing interest in
neuropharmocological regulation of memory.Some drugs have been identified as cognitive
enhancing agents or ‘’SMART DRUGS’’.these group of drugs have displayed memory-
enhansing effects in experimental settings through diverse mechanism of actions.important
mechanisms includes cholinergic agonists at the muscarinic and nicotinic
receptors,cholinesterase inhibitors such as physostigmine,CCB’s like
nimodipine,neurotransmitters such as norepinaphrine,GABA-B receptor blockers,peptides
like vasopressin corticotropin,glucose etc.(Beversdorf et al.,1998).

Lithium usually causes mind slowing(bradyphrenia) and cognitive deficits are more when
used along with ECT.

Anticholinergics mainly affects short term memory especially encoding and storage of
information.

Ethanol acute ingestion induces BLACKOUT AMNESIA which refers to profound STM deficits
and it may be associated with hypoglycemia, hypomagnesemia etc.chronic ingestion causes
korsakoff’s psychosis where we can see the memory deficits as confabulation as the patient
tries to fill the memory gaps with unnecessary details.

Beta blockers may produce poor memory particularly for emotionally valent
information(Cahill et al.,1994).

Corticosteroids causes memory impairment mainly by its deleterious effects on

hippocampus.(Sapolsky et al 1990).

Barbiturates tend to impair acquisition and interfere with retention of learned behavior.

Antiepileptic drugs may exacerbate pre existing memory problem by affecting

concentration,attention and psychomotor abilities.Phenyton and primodone are associated
with cognitive decline.

Topiramate causes word finding difficulties.

Cognitive enhancers(cerebroactive drugs).There are various drugs claimed to be having

cognitive enhansing property.But as per the Cochrane review there is no definitive evidence.

Cholinergic activators:Donepezil,Rivastigmine,Galantamine,Tacrine.

Glutamate(NMDA) antagonist:Memantine

Miscellaneous cerebroactive drugs:Piracetam,Pyritinol,Dihydroergotoxine,Piribedil,

Ginkgo biloba .

MEMORY DISTURBANCES AND ECT

Memory disturbances are seen occurring immediately after ECT and includes short lived
impaired learning ability, defective retrievals along with permanent loss of memories of
events (especially autobiographical memories) preceding immediately to ECT treatment.
These deficits are proportional to strength of current ,duration of electrical stimulus, number
of sessions given to the individual, the area of the brain where the current pulse is given
(dominant or non-dominant area of the brain) and finally bilaterality of ECT. Therefore ECT if
applied unilaterally, in non-dominant side of the brain not only hastens recovery but also
causes less post ictal amnesia, confusion and memory disturbances. However amidst various
ongoing controversies regarding the ECT generated memory deficits the effects do not seem to
last more than six months and some researchers currently have pointed out that ECT does
not cause more than a temporary disturbance in memory (Oyebode, 2008).

EMOTIONAL AND SOCIAL CONSEQUENCES OF MEMORY DISORDERS

These are acquired neuropsychological disorders fall within the domain of psychosocial
functioning.Emotional responses occur within the context of an individual’s personality
structure and their environment underlying stable traits, and transient fluctuations in
emotional affective and mood states, which occur in response to day to day events. Those
with fairly circumscribed memory disorders are well placed to harness their intelligence and
other neuropsychological strengths and implement compensatory strategies to circumvent
the memory disorders. This enables them to access a range of life otherwise it will be difficult
to achieve—productive work, independent lifestyles and a regular social life in the presence of
other neuropsychological impairments in addition to memory disorder makes it difficult to
attribute any emotional or social disturbance to the memory disorder itself, as opposed to
some concomitant neuropsychological problem that the person may experience, such as
aphasia, executive impairment, attention deficit and so forth.The literature regarding
emotional and social consequences for people with a range of neuropsychological problems is
relevant and important, given that, as Wilson (1991) observes, the majority of adults who
experience acquired memory disorder also have additional neuropsychological impairments.
(Prigatano, 1992).

MEMORY REHABILITATION

How are the memory difficulties manifested in everyday life?

• What problems cause most concern to the family and the memory-
impaired person?
• What do we know about the cultural background and level of
support available?
• What coping strategies are used?
• Are the problems exacerbated by depression or anxiety?
• Is this person likely to be able to return to work (or school)?
• Can this person live independently?
• What kind of compensatory aids did this person use premorbidly?
• What kind of memory compensation strategies are being used
now?
• What is the best way for this person to learn new information?

Ten Key Memory Tips

Take it easy
1. Try not to do too many things at once.
2. Anxiety and tiredness can affect memory, so try to avoid stressful situations.
Be positive and have regular breaks.
3. If you do forget something, don’t get too upset about it. Stay calm and think of
connections that may jog your memory.
Be well organized
4. Keep to a fixed routine, with set things at set times of the day and on set days
of the week.
5. Be systematic: Have a place for everything and put everything back in its place.
Put labels on drawers and files.
Concentrate better
6. If you have to do something, do it now rather than later: “Do it or lose it.”
7. Try not to let your mind wander: Keep on track.
8. If you have to remember something such as a message or a name, go over it in
your mind at regular intervals.
9. Try to find meaning in things you have to remember (e.g., by making
associations or linking things together). (from Narinder Kapur).
10. Use memory aids
External memory aids are effective in improving everyday memory functioning, and this
benefit is particularly evident in the area of prospective memory.
1. An electronic diary to keep a record of appointments.

2. An alarm which provides auditory cues, with or without text information, at preset,
regular or irregular times.
3. A temporary store for items such as shopping lists, messages, etc.
4. A more permanent store for information such as addresses, telephone numbers, etc.
5. In more expensive models, a communication device that can receive and send information,
such as reminders and factual knowledge.

CONCLUSION

Memory is not a unitary phenomenon. Capacities to remember vary for the different senses
and perceptions. When individuals with extraordinary memories complain of memory loss,
ordinary memory tests may be inadequate to detect their deficits, as their relative memory
loss may have reduced their capacities to a point within the range of most normal people.

REFERENCES
American Psychiatric Association(1994) Diagnostic and Statistical Manual of Mental
Disorder(4th ed)(DSM-IV).Washington DC ,APA..

Sims,A.. (2003). Disturbance of memory.In Symptoms in the Mind :An Introduction to

Descriptive Psychopathology,3rd ed,pp.63-76.Philadelphia,Saunders.

Baddeley, A., Emslie, H., Nimmo-Smith, I. (1996). The door and people test. Bury St.
Edumuinds: Thames Valley Test Company, Suffolk As cited in Mayes AR. The
Assessment of memory disorder. In Baddeley AD, Wilson BA, Wattas FN, 1 st eds.
Handbook of Memory Disorders. New York: John Wiley & Sons Inc.

Baddeley, A.D. (1999). Aging and memory. In essential of human memory. Taylor and
Franscis Routledge, pp251-272.

Baddeley, A.D., Koppelman, M.D., Wilson, B.A. (2002) The handbook of memory disorders
2nd ed., pp.145-667, John Wiley & Sons Ltd.

Budson, A.E., Price, B.H (2001). Memory: Clinical Disorders In .Encyclopedia of life sciences,
Macmillan Publishers Ltd, Nature Publishing Group / www.els.net

Casey, P.R. & Kelly, B. (2007) Fish’s Clinical Psychopathology: Sign and Symptoms in
Psychiatry,3rd ed., pp. 55-64.London, RCPsych Publications.

Cohen, G. (2008). Overview: conclusion and speculations. In Memory in the real world..3 rd
ed.,pp381-408.New York Psychology Press.

Coughlan, A.K., Hollows, S.E. (1996). The adult memory and information processing battery.
AK Coughlan, Psychology Department, St. James University Hospital, Leeds.
1985. As cited in Mayes AR. The Assessment of memory disorders. In Baddeley
AD, Wilson BA, Watts FN. 1 st ed. Handbook of Memory Disorders. New York:
John Wiley & Sons.

Crook, T.H., Larrabee, G.J. (1998). A self rating scale for evaluating memory in everyday life.
Psychology and Aging 1990; 5:448-57. As cited in Larrabee GJ, Crook TH. The
ecological validity of memory testing procedures: Developments in the
Assessment of Everyday memory. In. Sbordone RJ, Long CJ. Ecological validity
of Neuropsycholoygical Testing. New York, St. Lucie Press,pp 225-242.

Delis, D.C., Kramer, J.H., Kaplan, E., Ober, B.A. (1996). California Verbal Learning Test. The
psychological Corporation, San Antonio, 1987. As cited in Mayes AR. The
Assessment of memory disorders. In Baddeley AD, Wilson BA, Watts FN. eds.
Handbook of memory Disorders, New York: John Wiley & Sons Inc.

Einstein GO, McDaniel MA. Normal aging and prospective memory. J Exp Psychol Learn
Mem Cogn 1990; 16:717-726.
Ganong, W.F. (2005). Higher function of the nervous system, conditional reflex, learning and
related phenomenon, In review of medical psychology 22 nd ed. New York, The
McGraw Hill Company, pp259-270.

Golden, C.J, Hammeke, T.A., Purisch, A.D. (1988). The Luria-Nebraska Neuropsychological
Battery. Los Angeles; Western psychological services. As cited in: Assessment of
memory functioning. In. Kapur RL, Memory Disorders in Clinical Practice.
London: Butterworths.

Hamilton, M. (1984) Fish’s Clinical Psychopathology : Sign and Symptoms in Psychiatry, 4 th

ed., pp.63-69. John Wright Publication.

Hill, G. (1998) Advanced Psychology through diagrams, 1 st ed.,pp.64-72. Oxford University

Press

Howard, D., Patterson, K. (2003). The pyramid and Palm Test. Bury St. Edmunds: Thames
Valley Test Company, 1992. As cited in Bradley V, Kapur, N.
Neuropsychological Assessment of Memory Disorders. In Halligna PW, Kischka
U, Marshall JC. eds. Handbook of Clinical Neuropsychology, New York: Oxford
University Press, pp147-166.
Kay, J. & Tasman, A. (2006). Cognitive neurosciences and neuropsychology:In essential of
psychiatry, pp161-165.

Ken, A.P. & Larry, R.S. Biology of memory in Kaplan & Sadock Comprehensive Text boom of
psychiatry 8th edition. Lippincott Williams & Wilkins, pp 560-580.

Kopelman, M., Wilson, B., Baddeley, A. (1989). The autobiographical memory interview: a
new assessment of autobiogreaphical and personal semantic memory in
amnesic patients. Journal of Clinical and Experimental Neuropsychology, 11,
pp724-744.

Kopelmem, M.D. (2002). Disorder of memory. Brain;125, 2152-2190.

Kvavilashvili, L. (1998). Remembring intentions: Testing a new method of investigation.

Applied Cognitive Psychology; 12, 533-554.

McDaniel, M.A., Einstein, G.O. (2000). Strategic and automatic processes in prospective
memory retrieval: A multiprocess framework. Applied Cognitive Psychology,14,
127-144.

Lishman, W.A. (2004). Organic psychiatry the psychological consequences of cerebral

disorder, 3rd ed., pp28-31. Blackwell Publishing Company.

Morgan,C.T., King, R.A., Weiss, J.R., Schopler, J. (1993) Introduction To Psychology,7 th ed.,
pp.181-223,New York, Tata Mcgraw Hill Book Co.

Morris, E.P. & Grusberg, M. (1994). Theoretical aspect of memory. Routhedge, New Felter
Lane, London,pp 34-36.

Oyebode, F. (2008) Sims‘ Symptom in the Mind: An introduction to Descriptive

Psychopathology,4th ed,.pp 65-79. Elseviers Limited.

Petrides, A. Milner, C. (1998). Self ordered pointing test. In. Spreen O, Strauss EA.
Compendium of Neuropsychological Tests, New York: Oxford University Press.

Powell, H.D., Kaplan, E.F, Whitla, D. Microcog: Assessment of cognitive functioning (Version
2.1). Computer Software, San Antonio, TX: The Psychological Corporation As
cited in Elwood RW, Microcog: Assessment of cognitive functioning.
Neuropsychology Review 2001 ;11 : 89-100.

Ropper, A.H., Brown, R.H. (2005) Adams and Victors Principles of Neurology,8 thed, pp-
370.McGraw Hill Publications.

Sborodone, R.J., Hall, S.B., Towner, L.W., Cripe, L. (1996). The validity and reliability of the
shordone Hall Memory Battery. Presented at the annual meeting of the
International Neuropsychological Society, San Diego, California, 1985. In
Computers and Memory, As cited in Grant I, Adams KM, eds.
Neuropsychological Assessment of Neuropsychiatric Disorders, new York
Oxford.

Smith, E.E., Jemdles, J. Working memory in humans: neuropsycnological evidence. In

Gazzaniga MS, ed. The New Cognitive Neuroscieences. Cambridge: MTT Press,
1995, 797-804.

Strub, R.L., & Black, F.W.(2000) The Mental Status Examination in Neurology,4 th ed,,pp. 41
—189. Jaypee Brothers Medical Publisher (P) Ltd. New Delhi,

World Health Organization (1992). The ICD-10 Classification of Mental and Behavioural
Disorders :Clinical descriptions and diagnostic guidelines(10 th ed)Geneva World Health
Organisation.

Barbara A. Wilson Memory rehabilitation: integrating theory and practice .2009.1.Memory

disorders 2.Memory 3.Memory disordes-patients-Rehabilitation.

Austin, M. P., Ross, M., Murray, C., O’Carrol, R. E., Ebmeier, K. P., & Goodwin, G. M. (1992). Cognitive function in major
depression. Journal of Affective Disorders, 25, 21–30.
Bonhoeffer, K.(1901) [Die akuten Geisteskrankheiten der Gewohnheitstrinker] in psychiatry Jena in Fish’s Clinical
Psychopathology: Signs and symptoms: Gustav Fischer .

Butters, N., & Granholm, E. (1987). The continuity hypothesis: Some conclusions and their implications for the etiology and
neuropathology of alcoholic Korsakoff ’s syndrome. In O. A. Parsons, N. Butters, & P. E. Nathan (Eds.), Neuropsychology of
alcoholism: Implications for diagnosis and treatments. New York: Guilford Press.

Caplan, L., Chedru, F., Lhermitte, F., & Mayman, C. (1981). Transient global amnesia and migraine. Neurology, 31(9), 1167–
1170.

Cohen, R. M., Weingartner, H., Smallberg, S. A., Pickard, D., & Murphy, D. L. (1982). Effort and cognition in depression.
Archives of General Psychiatry, 39, 593–597.

Fisher, C. M. (1982). Transient global amnesia: Precipitating activities and other observations. Archives Neurology, 39(10),
605–608.

Fisher, C. M., & Adams, R. D. (1964). Transient global amnesia. Acta Neurologica Scandinavica, 40(Suppl. 9), 1–83.

Goldberg, T. E., Torrey, E. S., Gold, J. M., Ragland, J. E., Bigelow, L. C., & Weinberger, D. R. (1993). Learning and memory in
monozygotic discordant for schizophrenia. Psychological Medicine, 23, 71–85.

Hamilton, M. (1984) Fish’s Clinical Psychopathology: Signs and symptoms in psychiatry, 4 th Ed. Bristol, John Wright & sons,
63-69.

Hodges, J. R., Patterson, K., Oxbury, S., & Funnell, E. (1992). Semantic dementia: Progessive fluent aphasia with temporal
lobe atrophy. Brain, 115, 1783–1806.

McKenna, P.J., Ornstein, T., Baddeley, A.D. (2002) Schizophrenia. In Baddeley, A.D., Kopelman, M.D. and Wilson, B.A. (eds)
The Handbook of Memory Disorders, 2nd Ed., Chichester, John Wiley, 413-435.

Morgan, C.T., King, R.A., Weiss, J.R., Schopler, J. (1993) Introduction to Psychology, 7 th Ed., New York, Tata McGraw-Hill
Companies, 181-223.

Oyebode, F. (2008) Sims’ Symptoms in the Mind: An Introduction to Descriptive Psychopathology, 4 th Ed. Elsevier
Publication, 65-79.

Pawar, A. V. & Spence, S. A. (2003) Defining thought broadcast: Semi-structured literature review. British Journal of
Psychiatry, 183, 287–291.

Rubin, D. C. (1995). Memory in oral traditions: The cognitive psychology of epic, ballads and counting-out rhymes. New
York: Oxford University Press.

Rubin, D. C., & Greenberg, D. L. (1998). Visual memory-deficit amnesia: A distinct amnesic presentation and etiology.
Proceedings of the National Academy of Sciences of the United States of America, 95, 5413–5416.

Williams, J. M. G. (1996). Depression and the specificity of autobiographical memory. In D. Rubin (Eds.), Remembering our
past: Studies in autobiographical memory, Cambridge: Cambridge University Press.

Snowden, J.,(2002) disorders of semantic memory, In: the handbook of memory disorders , Ed,
baddeley,AD.,Kopelman.MD.,&Wilson BA ,2nd ed, John Wiley &sons, Wiltshire, UK: pp 293

Cornoldi C & Vecchi T (2003)., working memory ,in visuo-spatial working memory and individual differences., Hove and
NewYork: pp6
APPENDIX- 1

Budson, E.A., Price, B.H. (2001). Memory: Clinical Disorders. ENCYCLOPEDIA OF LIFE
SCIENCES, Macmillan Publishers Ltd. / www.els.net