Psychiatry All-in-one

Psychiatry All-in-one
Neuroscience 2

General Adult Psychiatry 19

Substance Abuse and Addictions 180

Childhood and Adolescent Psychiatry 222

Psychogeriatrics 260

Psychiatric Diagnostic Interview 303

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Neuroscience
What is the Brain 3
Brain Topography 3

Brain Networking 4

Diffuse modulation systems 5

Sensory Cortices 6

Inner Model of the World 6

Motor System 7

Prefrontal System 7

The Brain and Psychiatry 8

“Triune” Brain Model 8

Embryology of Brain 8

Major Brain Functions 9

Assessing Salience 9

Arousal & Activation 10

Reaction to Harm/ Danger 12

Learning: Conditioning 13

Sensory Perception 14

Decision making, Thinking, Planning, Inhibition 15

Memory 16

Thalamus 17

Cerebellum - Automatic Processing 17

Summary 17

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What is the Brain

- The brain is probably the most complex object in the universe
- There are 100 billion neurons in the brain, which is the same no. of stars in our galaxy
- The brain accounts for 2% of body weight but 20% of daily energy expenditure

Brain Topography
Topographic Classification
- Lobes: Frontal Lobe, Parietal Lobe, Temporal Lobe, Occipital Lobe
- Cortical Sulci
• Lateral aspect: Uses Central Sulcus as index
• Medial aspect: Uses Corpus Callosum as index

- Brodmann’s Areas
• Functional classification
• A total of 52 Brodmann’s areas
• Classical examples incl. Broca’s area (BA44), Wernicke’s area (BA22)

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Brain Networking
Types of networking structure
- Feed-forward network
• i.e. multiple inputs + bias → single output
• Feedback system to correct weighting of different input to facilitate output
- Auto-associative network
• i.e. use external inputs → output & auto-regulation
• aka distributive network; signifying that information is encoded by a redundant number of
neural units (neurons) so that there is buffer when a minority of these units are damaged
• Similar theory in Alzheimer’s Disease

Feed-forward network Auto-associative network

Examples of Brain networking

Association fibres
- i.e. connections within the same hemisphere
- Arcuate fibres/ Short association fibres: between intra-lobar gyri
- Longitudinal fasciculi/ Long association fibres: between intra-hemispheric lobes
• e.g. Arcuate fasciculi: Broca’s area & Wernicke’s area
• e.g. Superior Longitudinal fasciculus: Frontal & Occipital lobe
• e.g. Inferior Longitudinal fasciculus: Occipital & Temporal lobe
• e.g. Fornix: Hippocampus & Mammillary body

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Diffuse modulation systems

Dopaminergic systems
- Mesocortical pathway
• by A10 Dopaminergic neurons
• Originate from Ventral Tegmental Area (VTA)
• Projects to Prefrontal Cortex (DLPFC, OFPFC, VMPFC)
- Mesolimbic pathway
• by A10 Dopaminergic neurons
• Originate from Ventral Tegmental Area (VTA)
• Projects to Ventral Striatum/ Nucleus accumbens, Amygdala
- Nigrostriatal pathway
• by A9 Dopaminergic neurons
• Originate from Substantia nigra Pars compacta (SNpc)
• Projects to Dorsal Striatum (Caudate + Putamen)
- Tuberoinfundibular pathway
• Originate from Infundibular/ Arcuate nucleus of Hypothalamus
• Projects to Medial eminence of Anterior Pituitary Gland (APG)

Serotonergic system (5-HT)

- Accounts for general and sustained arousal
- Originate from Hypothalamus and Raphe nuclei
- Projects to Cerebral cortex, Thalamus, Cerebellum and Spinal cord

Noradrenergic system (NE)

- Accounts for general and short term arousal
- Originate from Locus coeruleus
- Projects to Spinal cord, and to Cerebral Cortex via Dorsal adrenergic bundle

Cholinergic system (ACh) Memory loss in Alzheimer’s is

- Accounts for memory; a/w Dementia e.g. Alzheimer’s Disease attributed to neuronal death in
- Origin is difficult to identify; a ill-defined area in brain basal forebrain and ACh deficit

(aka Septal Area/ Basal Forebrain)

- Projects to Cerebral cortex and Hippocampus (acts on NMDA receptor)

***These systems interact for complex functions

e.g. Arousal involves α1, M1, H1, 5HT2A/C receptors

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Sensory Cortices
Visual system
- “Top-Down” processing of visual information
• i.e. Interpret information from a contextual point
• c.f. “Bottom-up” processing that interpret from details to a full picture
• Serves to make visual predictions based on existing information
(i.e. to make sense of multiple visual inputs)
• Disruption in the processing pathway accounts for Visual hallucination

Inner Model of the World

Language

Face recognition
- Human can recognise a large number of faces
- Proposed to be a evolutionary advantage as humans are group animals that need to recognise
enemies and friends
- Responsible by the Fusiform gyrus

Voice recognition
- Neuroscientists found that the number of voices we can recognise is ~1-2 dozens
- Responsible by the Fusiform gyrus

Person recognition
- Integrate Face and Voice recognition for a comprehensive recognition of a person
- Responsible by the Fusiform gyrus
- Disrupted Fusiform gyrus causes misidentification symptoms e.g. Capgras, Fregoli delusions

Affect recognition
- Accounted by Striate cortex (SCx), Fusiform face area (FFA), SC

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Motor System
Pyramidal system
- i.e. Motor cortex → Corticospinal tract in Cerebral peduncle → Pyramid in Pons → Corticospinal
tract in Anterior & Lateral spinal columns → Motor neuron

Extrapyramidal system
- Disruption → Parkinsonism

Cerebellum
- Account for
• Fine-tuning of movement
• Planning of movement
• Some cognitive functions?

Mirror Neurons
This mechanism is found in various cortical functions:
- Empathy/ Sympathy
• Emotional mimicry can induce emotion
• e.g. You see others smile → You smile despite not happy yourself → You become happy
- Language
- Automatic imitation
- Understanding intention (Theory of mind)
- Motor mimicry

Prefrontal System
Supplementary Motor Area (SMA)
- Accounts for connection between Motor command and conveying this information to visual/
somatosensory areas
- Damage to SMA causes “Alien Hand Syndrome” in neurology, or “Delusion of Control/ Passivity”
in psychiatry - i.e. visual system do not know that action is mediated by motor area; so interpret
that as controlled by others

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The Brain and Psychiatry

- Humans have big brains, and high brain-to-body ratio
- The Cerebral cortex is particularly well developed in humans that accounts for the large size

“Triune” Brain Model

- Neuroscientist Paul MacLean formulated the Triune brain mode that
propose a 3-layer organisation of human brains
1. Neomammalian Complex/ Neocortex - the human brain
2. Paleomammalian Complex/ Paleocortex - the old mammal brain
3. Reptilian Complex - the lizard brain
- Higher centres are responsible for behaviour/ thoughts that are
conscious, rational and complex
- Lower centres are responsible for behaviour/ thoughts that are
unconscious, instinctive and simple
- It was later found to be more organised than it proposed

Triune Brain Model Correspond to Functions

Rational thoughts
Neomammalian Complex Cerebrum, Basal Ganglia
Language, Abstraction, Planning, Perception

Paleomammalian Complex Limbic System Process emotions

Reptilian Complex Cerebellum, Brainstem Survival response

Embryology of Brain
- Upper Neural Tube has a Cephalic end and 3 swellings
- The 3 swellings develop into Forebrain, Midbrain and Hindbrain
Telencephalon Cerebrum, Basal ganglia
Forebrain
Diencephalon Epithalamus, Thalamus, Subthalamus, Hypothalamus

Midbrain Mesencephalon Midbrain

Metencephalon Pons, Cerebellum

Hindbrain
Myelencephalon Medulla Oblongata

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Major Brain Functions

Principles: Receive input → Internal processing → Produce output

Domains of input/ output

- Sensations
- Perceptions
- Emotions
- Memories
- Thinking
- Decision making
- Movements
- Homeostasis

Complex Brain processes

- Assessing salience (i.e. to detect significance of objects or events)
- Arousal and activation (i.e. to become ready for action)
- Reacting to harm/ dangers/ threats (to avoid imminent harm / death)
- Learning and memory (to predict what actions are safe / rewarding)
- Sensory Perception (i.e. to integrate and interpret big sensory data)
- Express one’s mood/ Assume an emotional state (to adapt to the prevailing environment)
- Decision making/ Prioritisation of competing activities
- Inhibition (i.e. to stop primitive impulses with harmful consequences)
- Concentration/ Attention to processes relevant to prioritised activities
- Thinking and planning (to deal with novel situations)
- Motor Coordination (to execute precise and effective movements)

Assessing Salience
- Salience is the extent that a stimulus demands immediate attention and response
- Sensory modalities
• Visual: Retina has direct projections to the superior colliculus (aka optic tectum)
• Other sensory modalities also have projections to the brainstem
- Relative to cortical projections, these projections convey relatively “crude” information, but
enough to signal “significant” objects or events in the environment

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Arousal & Activation

- Arousal is triggered by Dangers (e.g. predator) or Rewards (e.g. food),
which leads to instinctive immediate response to triggers, which help
animals to survive
- Degree of arousal is related to performance (Yerkes-Donson model)
- Mediated by 2 main regions A trigger of arousal,
• Brainstem: Ascending Reticular Activating System (ARAS) as a predator of human,
• Hypothalamus, which react to Body’s internal state or a food to Chinese

Ascending Reticular Activating System (ARAS)

- ARAS is composed of multiple Monoamine arousal systems
3 major pathways in ARAS
- Serotonergic (5-HT) pathways - General, sustained arousal
- Noradrenergic (NE) pathways - General, short term (Now)
- Dopaminergic (DA) pathways - Specific, action (Do)

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Hypothalamus
- Hypothalamus is responsible for maintaining homeostasis in body by neuro-hormonal signals
- Signals are mediated by chemical signals (e.g. Leptin, Orexin) in blood, sent to Hypothalamus at
regions that lack effective blood-brain barrier
Example: Satiety and Recuperation
- Leptin
• Leptin interacts with Serotonergic system to control appetite
• Damage to Hypothalamus will cause Anorexia or Hyperphagia (Obesity)
- Orexin (aka Hypocretin)
• During hunger (an energy-deficient state) → ↑ Arousal and craving for food
• This phenomenon is mediated by ↑ Hypothalamic Orexin, which acts on monoamine systems
and medial frontal cortex
• After heavy food intake → ↓ Hypothalamic Orexin → Induce satiety & ↓ Arousal
(which is why people have “Food coma”/ 飯氣攻⼼心 after meal)
• Orexin deficiency will cause Narcolepsy (persistently ↓ arousal)
• Lesions at Pedunculo-pontine (PPT) and Latero-dorsal tegmental (LDT) nuclei are also a/w
Narcolepsy

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Reaction to Harm/ Danger

- As mentioned above, arousal can be triggered by Harm or Danger, be it actual or imminent
- Upon receiving innately fearful stimuli e.g. Visual input to Superior colliculi,
the response to Harm or Danger, is mediated by
• Midbrain: Peri-Aqueductal Gray (PAG), which control subconscious reactions
• Amygdala, which associate danger-stimuli to Stress response, which is in turn mediated by
- Sympathetic nervous system (SNS)
- Hypothalamic-Pituitary-Adrenal axis (HPA)
• Prefrontal Cortex and Limbic system, which process conscious aspect of fear and anxiety

Peri-Aqueductal Gray (PAG)

Actions of PAG
- Inhibit ascending nociceptive signals (that’s why people don’t feel pain when excited)
- Activating freeze, flight or fight reactions
- Connects with Amygdala

Stress response
Actions of SNS
- ↑ HR, ↑ RR
- Divert blood from gut to muscles
- Promote inflammation/ repair
Actions of HPA axis
- Release glucocorticoid → ↑ Blood glucose, Dampen inflammation
HPA axis malfunction
- Prolonged stress response
→ Depletion of brain monoamines and neuronal dysfunction → Anxiety and Depression
- The sensitivity to stress (or Resilience) is reflecting the reactivity of HPA axis
• Determined by genetic, epigenetic, and
environmental factors
• e.g. Severe childhood stress
→ Hypersensitivity of HPA axis
• e.g. Mild intermittent childhood stress
→ Hyposensitivity/ Resilience of HPA axis

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Learning: Conditioning
- Animals can learn the salience of a non-salient/ neutral stimulus if
it consistently occurs before a salient one (Classical Conditioning)
- Animals can also learn to associate a particular response to
salient effect (Operant Conditioning)
- The learning process is controlled by Striatum and Midbrain
(Substantia nigra)

Striatum
- Striatum acts in two pathways in response to stimulus
- During operant conditioning, Ventral Striatum (Nucleus
Accumbens) associates reward with action and context, leading
to purposeful actions that depends on reward value of stimulus
- After repeated reinforcement (i.e. conditioned already),
Dorsal Striatum (Caudate, Putamen) takes over, leading to
automatic actions in response to context, independent of the
reward value of stimulus

Midbrain
- Substantia nigra release dopamine to alter the salience of stimulus
and mediate the shift from Ventral to Dorsal Striatum
- One theory suggests that psychosis is the result of aberrant salience
signals from midbrain to Striatum. This may explain positives symptoms
incl. delusion, thought disorder, loosening of association and ambivalence

Classical Conditioning
- Refers to the association of a neutral stimulus to salient stimulus,
so that the neutral stimulus acquires the effect(s) of the salient stimulus
- Eventually, the neutral stimulus produce the same subconscious response to a
salient stimulus
- e.g. Pavlov’s dog: Associating “image of food” to “food intake”, so that seeing
“image of food” will induce salivation in dogs
- This concept is applied in exposure/ desensitisation therapy for phobia, by
dissociating a fearful stimulus with actual harm, so that the fearful stimulus
eventually is not perceived fearful

Operant/ Instrumental Conditioning/ Positive Reinforcement

- Law of Effect: “responses that produce a satisfactory effect in a
particular situation become more likely to occur again in that
situation, and responses that produce a discomforting effect become
less likely to occur again in that situation”
- e.g. Skinner box:
• Associating “pressing the green light” to “food appearing”, so that
the mouse purposefully “press the green light” even without the
actual reward
• Associating “pressing the red light” to “electric shock”, so that the
mouse purposefully avoid “pressing the red light” even without
“being shocked after pressing it”
- This concept can explain the shift of drug use in abusers from
occasional to habitual, and eventually to a compulsive state
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Sensory Perception
- i.e. to integrate and interpret large sensory data
- Previously mentioned, sensory input to Brainstem is subject to rapid processing,
and leads to relative simple or automatic responses
- In contrast, sensory input to the Cerebral cortex is subjected to more sophisticated processing,
and leads to more complex behaviour
- Processing of sensory input is by Sensory cortex and Association cortices

Association Cortices
- Most higher cognitive functions results from processing in
association cortices
- Association cortices can be classified as
• Motor/ Pre-Frontal Cortex (PFC)
• Sensory/ Parietal-Occipital-Temporal Cortex (POT)
- Prime examples of sensory and motor association cortices
• Language comprehension: Wernicke’s Area
• Language formulation: Broca’s Areas
• Representation of self: Precuneus
• Internal state: Insula
• Emotion: Anterior Cingulate Cortex (ACC)

Precuneus
- A part of Parietal Association Cortex
- Located in medial parietal cortex above Posterior Cingulate
cortex, between Somatosensory and Visual cortices
- Responsible for creation of “representation of self”
(i.e. the way people see themselves)
- Touch is probably the sensory modality most important for
the early development of a representation of one’s body in
relation to the external world

Insular Cortex & Anterior Cingulate Cortex

- Insula: Receives sensory information concerning self (Internal state, Pain, and Distress)
- ACC: Effect autonomic response and conscious emotions, and social behaviour
- Insular degeneration is observed in Frontotemporal Dementia (FTD)
→ Alexithymia (i.e. deficiency in understanding, processing and describing emotion)
- Also implicated in Autism, Mood disorders, and Tourette Syndrome

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Decision making, Thinking, Planning, Inhibition

Prefrontal Cortex
- PFC is the Motor association cortex responsible for a number of higher cognitive functions:
• Working memory
• Abstract reasoning and planning
• Inhibition or moderation of primitive impulses
- PFC is divided into 3 areas namely Ventromedial (VMPFC), Orbitofrontal (OFPFC), and
Dorsolateral (DLPFC)
• VMPFC and OFPFC: Social cognition and behaviour
• DLPFC: Working/ Short-term memory, Cognitive flexibility, Planning, Inhibition, and
abstract reasoning
PFC pathology
- Hypofrontality (i.e. loss of Frontal cortex) → Antisocial behaviour
e.g. Phineas Gage, a capable foreman before the accident that penetrates his PFC, became a
childish man and changed job to care for horses
- Hypo-activity of Dopamine pathway in PFC → Negative symptoms in Schizophrenia e.g.
Affect flattening, Asociality, Cognitive impairment

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Memory
Classification of memory
Types of memory Stored by

Sensory memory
Temporal lobe
i.e. the retained sensory information
Parietal lobe
e.g. Iconic (Visual), Echoic (Auditory), Haptic (Tactile)

Short-term/ Working memory

i.e. Temporarily held information Prefrontal Cortex
Important for decision-making and planning

Episodic memory
i.e. Personal events in time that Hippocampus
Explicit/ Declarative can be retrieved to re-experience
memory
i.e. Memory that are Semantic memory
Long-term consciously available i.e. Knowledge about facts about Hippocampus
memory the general world, and literal Medial Temporal lobe
meaning of words

Cerebellum
Implicit/ Procedural memory
Basal ganglia
i.e. Unconscious memory, usu. for performance of tasks, skills
Striatum

Episodic Memory: Hippocampus

- Episodic Memory is formed by brain activities during a particular time, including representations
of objects, place and temporal order
- Hippocampus’s neuronal architecture is ideal for the encoding and retrieval of episodic memory
- Cortex send certain cues to Hippocampus → Retrieve episodic memory → Project back to
Cortex to recreate the pattern of neuronal activities similar to that when the episode occurred
[Cortico-hippocampo-cortical loop]
- Formation of memory is inhibited in Alcoholism → Blackouts

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Thalamus
- Thalamus receives multimodal input sensory and has
extensive reciprocal connections with all parts of the
cerebral cortex
- It may represent a “super hub” in the overall brain network,
to increase the efficiency of network connectivity and to
coordinate and/or prioritise the activities of different brain
regions

Cerebellum - Automatic Processing

- Roles of Cerebellum
• Receive order from Cerebral cortex, who delegate
cerebellum to to perform precise but automatic actions
• Enable movements to become increasingly automatic
and fluent with practice
• Automatic processes in perception, cognition and
emotional control
- Cerebellar pathologies
• Cerebellar Ataxia: Vertigo, Ataxia, Nystagmus, Intentional
tremour, Slurred speech etc
• Cerebellar Cognitive-Affective Syndrome (CCAS): Cortico-Hippocampo-Cortical loop
Cognitive decline, Blunted affect, Inappropriate behaviour

Summary
High mental functions Survival benefit Responsible brain structure

Retina → Superior colliculi

To detect significance of objects or
Assessing salience Other sensory → Brainstem
events automatically
Learnt by Midbrain (Substantia nigra)

Arousal and activation To become ready for action ARAS, Hypothalamus

Reacting to harm To avoid actual or imminent harm PAG, Amygdala, SNS, HPA axis

Sensory Cortex, Association Cortices

To integrate and interpret big - Self-representation: Precuneus
Sensory perception - Language comprehension: Wernicke’s
sensory information
- Internal state: Insula
To excuse precise and effective Motor Cortex, Cerebellum
Motor coordination - Language expression: Broca’s
movements

To adapt to the prevailing PFC, Limbic System

Mood and emotion - Emotional expression: ACC
environment

To predict what actions are safe/

Learning/ Conditioning Striatum, Midbrain (Substantia nigra)
rewarding

Episodic memory To recall Hippocampus

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To prioritise competing activities
Decision making
To deal with novel situations
Thinking, Planning PFC
To stop primitive impulses with
Inhibition
harmful consequence

ARAS: Ascending Reticular Activating System; PAG: Peri-Aqueductal Gray; SNS: Sympathetic
nervous system; HPA axis: Hypothalamic-Pituitary-Adrenal axis; PFC: Prefrontal Cortex; ACC:
Anterior Cingulate Cortex

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General Adult Psychiatry

Introduction to Psychiatry 22 Benzodiazepines and Z drugs 56

Mental Illnesses 22 MOA of BDZ 56

Examples of BDZ 57
Prevalence of Mental Illnesses 22
Common psychiatric indications 57
Aetiology of Mental Illnesses 23
ADR of BDZ 58
Clinical Features of Mental Illnesses 24

Classification of Mental Illnesses 25 Other Anxiolytics 59

Diagnosis of Mental Illnesses 27 Z Drugs 59

Complications of Mental Illnesses 28 Barbiturate 60

Somatisation of Mental Illnesses 29 Buspirone 60

Spectrum of Somatisation 29 Antidepressants 61

Pathogenesis of Somatisation 32 MOA of Antidepressants 61

**Approach to Somatisation** 32 Examples of Antidepressants 62

Management of Somatisation 33 Common psychiatric indications 67

Mental Illnesses and Suicide 34 ADR of Antidepressants 68

Definitions & Terminology 34 Mood Stabilisers/ Stabilising Agents 70

Epidemiology of Suicide 34 Lithium 70

Aetiology of Suicide 34 Valproate (Epilim®) 71

Suicidal Risk Assessment 35 Lamotrigine (LG)(Lamictal®) 71

Methods used in Completed Suicide 37 Carbamazepine (CBZ)(Tegretol®) 72

Misconceptions about Suicide 37 Quetiapine 73

**Approach to Suicidality** 38 Olanzapine 73

Ethics in Psychiatry 40 Mood Stabilisers in Pregnancy 73

Consent and Refusal of Treatment 40 Antipsychotics 74

Capacity 41 Common psychiatric indications 74

Decision-making in absence of capacity 42 First Generation Antipsychotics (FGA) 75

Compulsory Detention and Treatment 44 Second Generation Antipsychotics (SGA) 76

Confidentiality 45 FGA vs SGA 78

Mental Health Ordinance 47 ADR of Antipsychotics 79

Assessment of ADR of Antipsychotics 81

Aims of MHO 47

Legal definitions 47 Mood Disorders 82

Mental Health Review Tribunal 47 Depressive Disorders 82
Mental Health Ordinance Form 1-12 48 Spectrum of Depressive Disorders 82
Basics in Psychotherapy 49 Epidemiology of Depressive Disorders 83

Introduction to Psychotherapy 49 Aetiology of Depressive Disorders 84

Classification of Psychotherapy 49 Pathogenesis of Depressive Disorders 85

Psychoanalysis 50 Clinical presentation of Depressive Disorders 87

Freudian Concepts 51 Diagnosis of Depressive Disorders 89

Jungian Analysis/ Analytical Psychology 51 **Approach to Depression** 93

Hierarchy of Defence mechanisms 52 **Approach to Postpartum Mood** 94

Cognitive Behavioural Therapy (CBT) 53 Antidepressants 95

Psychiatric Pharmacology 56
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Non-Pharmacological Management of Depressive Management of Anxiety Disorders 137
Disorder 96
Generalised Anxiety Disorder 138
Bipolar Disorders 98
Clinical presentation of GAD 138
Spectrum of Bipolar Disorders 98
Diagnosis of GAD 138
Epidemiology of Bipolar Disorders 99
Approach to GAD 139
Aetiology of Bipolar Disorders 99
**Approach to Anxiety** 140
Clinical presentation of Bipolar Disorders 100
Panic Disorder 141
Diagnosis of Bipolar Disorders 102
Clinical presentation of Panic Disorder 141
**Approach to Mania** 105
Diagnosis of Panic Disorder 142
Misdiagnosis of Bipolar Disorders 106
**Approach to Panic Disorder** 143
Management of Bipolar Disorders 107
Management of Panic Disorder 144
Prognosis of Bipolar Disorders 109
Phobic Anxiety Disorders 145
Screening of Bipolar Disorders 110
**Approach to Phobia** 145
Psychotic Disorders 111
General Management of Phobic Anxiety disorders 145
What is Psychosis? 111
Agoraphobic 146
Spectrum of Psychotic Disorder 111
Clinical presentation of Agoraphobia 146
Epidemiology of Psychotic Disorder 112
Diagnosis of Agoraphobia 146
Early Intervention Paradigm 112
Social Phobia 148
Schizophrenia 113
Clinical presentation of Social Phobia 148
History of Schizophrenia 113
Diagnosis of Social Phobia 148
Epidemiology fo Schizophrenia 113
Specific Phobia 149
Aetiology of Schizophrenia 114
Clinical presentation of Specific phobia 149
Pathogenesis of Schizophrenia 116
Diagnosis of Specific Phobia 149
Clinical presentation of Schizophrenia 119

Diagnosis of Schizophrenia 123

Post-Traumatic Stress Disorder 150
Spectrum of Trauma-and Stressor-related Disorders 150
**Approach to Psychotic symptoms** 125
Epidemiology of PTSD 150
Management of Schizophrenia 128
Aetiology of PTSD 150
Prognosis of Schizophrenia 129
Pathogenesis of PTSD 150
Brief Psychotic Disorder 130
Diagnosis of PTSD 151
Clinical presentation of Brief Psychotic Disorder 130
**Approach to PTSD** 152
Diagnosis of Brief Psychotic Disorder 130
Management of PTSD 153
Schizophreniform Disorder 131
Acute Stress Disorder/ Reaction 154
Diagnosis of Schizophreniform 131
Diagnosis of Acute Stress Disorder 154
Schizoaffective Disorder 132
Adjustment Disorder 154
Clinical presentation of Schizoaffective Disorder 132
Diagnosis of Adjustment Disorder 154
Diagnosis of Schizoaffective Disorder 132
Obsessive-Compulsive Disorder 155
Delusional Disorders 133
Epidemiology of OCD 155
Clinical presentation of Delusional Disorder 133
Aetiology of OCD 155
Diagnosis of Delusional Disorder 133
Clinical presentation of OCD 156
Anxiety and related Disorders 134
**Approach to OCD** 157
Epidemiology of Anxiety Disorders 134
Diagnosis of OCD 158
Risk factors of Anxiety Disorders 134
Management of OCD 158
Pathogenesis of Anxiety Disorders 134
Sleep-Wake Disorders 159
Clinical presentation of Anxiety Disorders 136
Spectrum of Sleep-Wake Disorders 159
Spectrum of Anxiety Disorders 137
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**Approach to Sleep-Wake Disorders** 159

Sleep Investigations 160

Physiology of Sleep 160

Normal Sleep Architecture 161

Sleep Deprivation 162

How much sleep is enough? 162

Insomnia Disorder 163

Aetiology of Insomnia Disorder 163

Classification of Insomnia Disorder 163

Pathogenesis of Insomnia Disorder 163

Clinical presentation of Insomnia Disorder 164

Diagnosis of Insomnia Disorder 164

Management of Insomnia Disorder 166

Hypersomnolence Disorders 167

What is Sleepiness 167

Sleepiness Assessment 168

Narcolepsy 169

Breathing-Related Sleep Disorders 170

Obstructive Sleep Apnoea 170

Parasomnias 171
NREM Parasomnia 171

REM Parasomnia 173

Dreaming 173

Movement-related Sleep Disorders 174

Restless Leg Syndrome (RLS)/ Periodic Limb Movement
Disorder (PLMD) 174

Circadian Rhythm Sleep-Wake Disorder 175

Delayed sleep-wake phase disorder (DSWPD) 175

Personality Disorders 176

Personality 176

DSM-5 vs ICD-10 176

DSM-5 Criteria of different PD 177

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Introduction to Psychiatry
Mental Illnesses
- aka Mental Disorders, Psychiatric Disorders
- They are disorders of the brain, described in different ways in different schools of thoughts
• Complex cognitive and emotional responses
• Interaction with the person’s life experience (Lebenswelt)
• Centralised rather than peripheral system (Wernicke)
• Complex partial modular system
• Information disorders

Prevalence of Mental Illnesses

- Common Disorders (15-20%)
• Depression
• Anxiety
• Bipolar
• Schizophrenia
- Severe Disorders (5%)
- Dementia (15%; mostly >70yo)
- Developmental Disorders (10%)
- ADHD (5%)

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Aetiology of Mental Illnesses

- Mostly are multifactorial with multiple aetiologies or risk factors

Types of risk/ aetiological factors (3P model)

- Predisposing factors (i.e. what makes the individual more liable/ vulnerable to disease)
• Biological and Psychological predispositions
• Previous experience
- Precipitating factors (i.e. what triggers the disease e.g. stress trigger VZV reactivation)
• Key incidents on self or others around
• Increased awareness of physiological changes associated
- Perpetuating factors (i.e. what maintains the disease)
* some alleviating attempts may actually be perpetuating the disease e.g. excessive rests to
reduce pain and fatigue

Liability-Threshold Model
- Applied to multifactorial diseases e.g.
Alzheimer Disease Diathesis-Stress Model
- Liability of an individual = Total effect of all - Applied to partly genetic + partly environmental
aetiological factors in that individual diseases e.g. Depressive Disorder
• Each aetiological factor is given a weight/ - Liability of an individual = Diathesis (vulnerability)
score of liability + Stress (circumstances of individual)
• Combination of factors gives a sum of the - Vulnerability is inherited or distal factors
score (may have synergism or which are relatively stable over the life span
antagonism?) - Stress is proximal factors which are fluctuating
- The distribution of aetiological factors (i.e. depending on circumstances of the individual
Liability of population) becomes bell-shaped - Stronger the diathesis, the weaker the stress
- Theoretically, individuals with liability necessary for triggering the disorder
exceeding a certain threshold will develop
the disorder

Genetics Heritability
Disorders of high heritability: - Concerns the relative contributions of genetic and
- Bipolar Disorder environmental factors to the variation in liability in
a population
- Schizophrenia - Defined as: proportion of total variance
- Alzheimer Disease accounted for by genetic factors
Behaviours of high heritability: (Genetic variance divided by Genetic +
- Cocaine use disorder Environmental variance)
- Estimated from
- Anorexia Nervosa • Population risk
- Alcoholism • MZ concordance rate
Mechanism of genetics • DZ concordance rate
- However, in diseases with
- Neurotransmitter receptors high heritability, current
e.g. Monoamine Oxidase A (MAOA) which understanding of their genetic mutations cannot
dominates NE, Adrenaline, 5-HT, Dopamine explain the large effect of heritability
• Patients have reduced fecundity (i.e. ability to
• Coded by X-linked gene give birth to abundant offsprings)
• Nonsense mutation of MAOA causes • Mutation with large effect size would be
aggressive and antisocial behaviour in subject to strong negative selection pressure
males • Only mutations with small effect size can be
common
• Rare variants may have larger effect sizes

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Sex
- Male: More prone to Intellectual Disability, Autism-Spectrum Disorder, Conduct Disorder,
Substance use disorder
- Female: More prone to childhood Emotional disorder, Anxiety and Depression

Substance use
- Prolonged and heavy usage of psychoactive substances can increase risk of mental disorders
- Alcohol: Psychosis, Dementia
- Amphetamines: Psychosis
- Cannabis (i.e. Marijuana, Weed): Psychosis

Social Support
- Good social support is protective against and helps to maintain remission from mental disorders
- High expressed emotions (i.e. hostility, over-involvement, critical comments) from family
members can increase risk of relapse of Schizophrenia

Resilience
- People with more positive attitudes and better coping skills are more able to live through
difficulties w/o becoming mentally ill
- Study of positive mental attributes is known as “Positive Psychology”

Life events
- Adverse life events (e.g. Bereavement, Divorce, Injury, Illness, Unemployment or Loss of wealth,
Humiliation) can trigger mental disorders e.g. Depression, Mania, and Schizophrenia

Clinical Features of Mental Illnesses

- Dominated by subjective experiences, but still measurable in terms of type, severity, duration,
clinical significance
- Experiences would be defined as abnormal if
• cannot exist in reality (e.g. hallucination, delusion) or
• excessive, irrational, uncontrollable (e.g. anhedonia)
- Symptoms are very individualised with high complexity, and informational significance

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Classification of Mental Illnesses

Pros of classification
- Bring order into great diversity of phenomena encountered in clinical practice
- Give suitable treatment with predicable outcome
- Diagnosis are made using valid and reliable assessment but not “look like”

Cons of classification
- Labelling and stigmatisation
- Misunderstand severity
- One term can have different meaning to different people
- Arbitrary cut-off makes no sense
- Patients who cannot fit nearly into available categories need to “NOS” or unclassified
- Distract one from the understanding the problem unique to the individual

Types of classification systems

- Categorical
• e.g. Schizophrenia, Depressive disorder
• Familiar, easy to understand, to remember and to use, ready to action
- Dimensional
• e.g. Mood disorder; Anxiety disorder; Obsession etc
• Convey more information, more flexible, do not imply the presence of unproven qualitative
differences, do not impose boundaries

What makes a good classification system?

- High validity
- High reliability
- High utility
- Easy to use
- Applicable across settings and cultures
- Meet the needs of various users

General classification
- Disorder of Perception
- Disorder of Thought and Speech
- Disorder of Memory
- Disorder of Emotion
- Disorder of Experience of the self
- Disorder of Consciousness
- Disorder of Motor control

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Commonly used classification systems in Psychiatry:
- Diagnostic & Statistical Manual of Mental Disorder (DSM)
• by American Psychiatric Association (APA), updated every 13 years
• Definitions are mostly descriptive
• Theoretical statements are avoided
• Aetiology is included only when clearly demonstrable
• DSM-4 (2000) has a multi-axial system consisted of 5 axes which fully describe an individual’s
mental illness
• DSM-5 (2013): Removed the multi-axial system but adopted both dimensional and categorical
type of classification systems
- International Classification of Diseases (ICD)
• by World Health Organisation (WHO), updated every 10 years
• ICD-10 (1990) - Chapter V focuses on "mental and behavioural disorders" and consists of 10
main groups

ICD-10 Classification (Chapter V)

- F0: Organic, including symptomatic, mental disorders
- F1: Mental and behavioural disorders due to use of psychoactive substances
- F2: Schizophrenia, schizotypal and delusional disorders
- F3: Mood [affective] disorders
- F4: Neurotic, stress-related and somatoform disorders
- F5: Behavioural syndromes associated with physiological disturbances and physical factors
- F6: Disorders of personality and behaviour in adult persons
- F7: Mental retardation
- F8: Disorders of psychological development
- F9: Behavioural and emotional disorders with onset usually occurring in childhood and
adolescence
- In addition, a group of "unspecified mental disorders”.

DSM-4 Classification
- Axis I: Clinical Disorders (all mental disorders except Personality Disorders and Mental
Retardation)
- Axis II: Personality Disorders and Mental Retardation
- Axis III: General Medical Conditions (must be connected to a Mental Disorder)
- Axis IV: Psychosocial and Environmental Problems (for example limited social support network)
- Axis V: Global Assessment of Functioning (Psychological, social and job-related functions are
evaluated on a continuum between mental health and extreme mental disorder)

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DSM-5 Classification
DSM-5 groups Examples

Disorders usu. first diagnosed in infancy, childhood or adolescence Intellectual Disability, ADHD

Delirium, Dementia, Amnesia and other cognitive disorders Alzheimer's Disease

Mental disorders due to a general medical condition AIDS-related Psychosis

Substance-related disorders Alcohol abuse

Schizophrenia and other psychotic disorders Schizophrenia, Delusional disorder

Major Depressive Disorder

Mood disorders
Bipolar Disorder

Generalised Anxiety Disorder

Anxiety disorders
Social Anxiety Disorder

Somatoform discorders Somatisation Disorder

Factitious disorders Munchausen Syndrome

Dissociative disorders (aka Conversion disorder) Dissociative Identity Disorder

Dyspareunia, Gender Identify

Sexual and gender identify discorders
Disorder

Eating disorders Anorexia nervosa, Bulimia nervosa

Sleep disorders Insomnia

Impulse control disorders not elsewhere classified Kleptomania

Adjustment disorderrs Adjustment Disorder

Personality disorders Narcissistic personality disorder

Other conditions that may be a focus of clinical attention Tardive Dyskinesia, Child abuse

Diagnosis of Mental Illnesses

Examples of Structured Interviewing Schedules
- Structural Clinical Interview for the DSM-IV (SCID)
- Present State Examination (PSE)
- Mini Mental State Examination (MMSE)

Common elements in a diagnostic criteria

- Cluster of symptoms
• Core symptoms e.g. Depressed mood and Loss of interest in Depressive disorder
• Associated symptoms e.g. Sleep disturbance, Reduced appetite, Poor concentration etc
- Characteristic feature(s)
- Minimal duration of symptoms
- Distress or impairment in function
- Exclusion criteria e.g. Drug, Medical condition, Another mental illness

Hierarchy for diagnostic ascertainment

Organic/ Substance abuse > Psychotic Disorders > Major Mood Disorders > Anxiety Disorders
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Complications of Mental Illnesses

- Suicide
- Shortened life expectancy
- Poor functioning
- Social isolation
- High global disease burden
- Distress and poor QoL

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Somatisation of Mental Illnesses

- Mental illnesses may present as Medical problems
- aka Psychosomatic, Somatisation, Somatoform, Abnormal illness behaviour, Hysteria,
Neurasthenia, Medically unexplained symptoms, Functional symptoms etc
- Somatic symptoms can be the main or secondary symptoms of some mental illnesses
e.g. 60% of Depressed patients report pain at time of diagnosis
- Classical definitions:
• Bodily disorder arising as the expression of a deep-seated neurosis (Stekel)
• Tendency to experience, conceptualise and/or communicate psychological states or contents
as bodily sensations, functional changes, or somatic metaphors, and to seek medical help for
them (Lipowski)

Spectrum of Somatisation
Clinical presentation DSM-5 ICD-10

Somatic symptoms Somatisation Disorder

Somatic Symptom Disorder
Pain symptoms Persistent Somatoform Pain Disorder

Excessive fear of being ill Illness Anxiety Disorder Hypochondriacal Disorder

Excessive perceived defect

Body Dysmorphic Disorder
of physical appearance

Factitious Disorder
Made up symptoms - Imposed on self (Munchausen Syndrome)
due to mental disorder - Imposed on others (Munchausen Syndrome by proxy)
Made up symptoms
Malingering
for secondary gain

Somatisation Disorder (ICD-10)

- ≥ 2yr of multiple and variable physical symptoms with no adequate physical explanation found
- Pre-occupation with the symptoms causes persistent distress and leads to seeking repeated
consultations or sets of investigations
- Persistent refusal to accept medical reassurance
- Some degree of impairment of social and family functioning
- Characterised by a combination of GI, CVS, UG, skin and pain symptoms (total of 6 or more
from the list, at least 2 separate groups)

Persistent Somatoform Pain Disorder (ICD-10)

- Predominant complaint is of persistent, severe and distress pain
- Cannot be explained fully by a physiological process or a physical disorder
- Occurs in association w/ emotional conflict or psychological problems
- Chronic: Duration of ≥6 months and continuously on most days

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Somatic Symptom Disorder (DSM-5)
A. 1 or more somatic symptoms that are distressing or result in significant disruption of daily life
B. Excessive thoughts, feeling, behaviours related to the somatic symptoms or asso. health
concerns as manifested by at east one of the following
1. Excessive thoughts, feelings, behaviours related to the somatic symptoms
2. Disproportionate and persistent thoughts about the seriousness of one’s symptoms
3. Excessive time and energy devoted to these symptoms or health concerns
C. Although any one somatic symptom may not be continuously present, the state of being
symptomatic is persistent (typically more than 6 months)
Features
- Commoner in women
- Chronic but fluctuating course that rarely remit completely
- Propensity of doctor shopping
- Risk of iatrogenic complications from numerous tests, procedures, and medications
- Potential of drug misuse (Opioids, BDZ)
- Common to have co-morbid Axis I diagnosis e.g. Depression, Dysthymia, Anxiety disorder,
Substance abuse/ dependence; as well as Axis II diagnoses e.g. underlying personality
difficulties

Illness Anxiety Disorder (DSM-5)/ Hypochondriacal Disorder (ICD-10)

Features
- Excessive & disproportionate preoccupation with having or acquiring a serious illness
- Somatic symptoms are absent or only mild
- High level of anxiety about health and easily alarmed about personal health status (normal are
often interpreted as abnormal and distressing)
- Performs excessive health-related behaviours or exhibits maladaptive avoidance
- For at least 6 months
- Can be care-seeking or care-avoidant type
- The belief is not of delusional intensity
- Equally common in men and women
- High medical use and high potential for iatrogenic damage from repeated Ix
- They believe that good health is a relatively symptom-free state, and that symptoms means
disease

Somatic Symptom Disorder Illness Anxiety Disorder

Somatic symptoms Significant, Distressing Minimal if not absent

Excessive and disproportionate

preoccupation with
Excessive thoughts, feelings having or acquiring a serious illness
Mental symptoms
related to somatic symptoms High level of anxiety about health
Easily alarmed about personal health
Believe that symptoms = disease

Excessive health-related behaviours

Excessive behaviours related to somatic (Care-seeking) or
Behaviour
symptoms Exhibits maladaptive avoidance
(Care-avoidant)

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Body Dysmorphic Disorder
Features
- Preoccupation with perceived defects or flaws in physical appearance that are not observable
or appear slight to others
- Performed repetitive behaviours or mental acts in response to the appearance concerns
- Onset is typically in adolescence
- Most common complaints involve facial appearance, and less common complaints about hair,
breasts, genitalia, other body parts
- May seek attention from a plastic surgeon or dermatologist
- Sometimes difficult to determine whether complaint is an over-valued idea or somatic delusion
- Psychological dysfunction is often profound, with social withdrawal and decreased functioning
- usu. chronic course, with few symptom-free intervals
Somatic Symptom
Factitious Disorder Malingering
Disorder

Insight None Yes

Feels ill; Feels ill; Does not feel ill;

Illness
Unconscious Conscious process; Conscious process;
behaviour
process Intentional Intend to look ill and/ or have needs met

Secondary gain
e.g. Retreat from responsibility, acquiring
Motivation To assume sick role
controlled substances, food, shelter,
compensation

Factors that arise suspicions of Malingering

- Patient presentation has a medico-legal context
- Marked discrepancy between patient’s claims of disability or distress and objective findings
- Vague reports, loaded with overgeneralisation, seemingly rehearsed
- Once objective achieved, symptoms seem to take on less significance
- Rejects all form of treatments that do not include psychoactive medications
- Exhibits lack of cooperation with medical diagnostic interventions
- Poor compliance with treatment interventions
- Possible antisocial personality disorder associated

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Pathogenesis of Somatisation
- Physiological
• Autonomic arousal
• Muscle tension
• Hyperventilation
• Physiological effects of inactivity
• Sleep disturbance
- Psychological
• Perceptual factors
• Believes
• Mood
• Personality factors
- Interpersonal
• Reinforcing actions of relatives and friends
• Healthcare system
• Disability system

e.g. Hypochondriacal Disorder is triggered by some information/ event/ illness/ image initially, but
then maintained by endogenous interpretation of body sensation and/or signs as indicating severe
illnesses

**Approach to Somatisation**
- Physical complaint(s) of patient
- Time period (>6 months?)
- Previous investigations/ doctors/ treatments
- What patient thinks of previous treatment/ doctors
• Definitive diagnosis? Refuse to accept reassurance?
• Doctor shopping?
- How the patient treat the complaints
• Spend much time visiting doctor?
• Pain → Abuse analgesics?
- Comorbid depression e.g. Low mood, Loss of interest, Lack of energy
- Substance abuse
- Distress/ Functional impairment
- Assess risk of suicide
- Soothing statements:
• 「有些⼈人係壓⼒力力之下有些徵狀狀係好難解釋既，我相信你既感受係真實既，其實呢個情況都好常
⾒見見 如果你可以講多啲比我聽，我可以幫到你多啲」
• 「我絕對係相信你講既野係你真實既感受，只係想了了解你多啲，等我可以幫到你 」

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Management of Somatisation
- Explain that symptoms are real and familiar to doctor
- Provide positive explanation, incl. how behavioural, psychological, and emotional factors may
exacerbate physiologically based somatic symptoms
- Offer opportunity for discussion of their worries
- Arrange regular FU and review
- Identify and treat mood or anxiety disorder
- Protect patients from iatrogenic (usu. surgical) problems
- Minimise polypharmacy
- Provide specific treatment when indicated
- Discuss and agree on treatment plan
- Change social dynamics
- Reduce our expectation of cure and instead aim for containment and damage limitation
- Encourage return to normal activity and work (coping and not curing)
- Recognise and control negative reactions, beware of counter-transference

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Mental Illnesses and Suicide

Definitions & Terminology

Self-inflicted death with evidence (either explicit or implicit) that the
Suicide/ Committed Suicide
person intended to die

Self-injurious behaviour with a non-fatal outcome accompanied by

Suicide Attempt
evidence (either explicit or implicit) that the person intended to die

Wilful self-inflicting of painful, destructive, or injurious acts

Deliberate Self-Harm (DSH)
w/o intent to die

Parasuicide (Ambiguous term that should better be avoided)

Categories of Suicidal behaviours

(Gardner & Cowdry 1985)
- Likely with an underlying mental illness esp. Depression
- Characterised by intense melancholia and despair
True Suicidal Acts - A wish for relief from emotional pain
- Intent to die (⼀一⼼心求死)
- Highest likelihood of careful planning & risk of completed suicide
- Characterised by impulsiveness, vengefulness
Retributive Rage - Constricted capacity to see other immediate options (走投冇路路)
- Often repetitive, tinged with strong dependency needs
Parasuicidal Gesturing - Appears to be a form of communication
- To extract a response from a significant other (求關注)
- Serves the purpose of relieving dysphoria (⾃自娛)
Self-Mutilation - A form of “indirect self-destructive behaviour”

Epidemiology of Suicide
- Suicide rate in HK was 12.5 per 100,000 in 2016
• Male (17.6) > Female (8.2)
• Higher in older age groups
- The previous peak of suicide rate was in 2003
(Ref.)

Aetiology of Suicide
Diathesis-Stress Model of Suicidal Behaviour
- Diathesis: Genetic predisposition, Early life experiences, Personality characteristics, Chronic
illness, Chronic substance abuse
- Stress: Acute intrinsic psychiatric illness, Acute substance abuse, Acute medical illness, Acute
family and social stresses

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Suicidal Risk Assessment

- Psychiatrists cannot predict who will commit suicide but can reduce or eliminate suicide risk
- Purpose: Identify and treat acute risk factors and to identify and mobilise protective factors in
management

Demographics
- Age
• Higher the age, higher the suicide rate is
• Suicide among the elderly is particularly a/w depressive disorder, physical illness, functional
impairment and social isolation
- Sex
• Women: More suicidal attempts and depressive disorders
• Men: Higher suicidal mortality rate
- Sexual orientation
• Individual with minority sexual orientation (LGBT) have increased suicide risk
- Marital status
• Suicide rate: Divorced > Widows > Never married > Married
- Social class and employment
• Factors a/w increased risk of suicide: Unemployment, Retirement
• Occupations a/w increased risk of suicide: Dentists (5.4X), Doctors (2.3X), Nurses (1.6X),
Social workers (1.5X), Mathematicians/ Scientists, Lawyers, Professors, Artists

Previous Hx of attempts
- If have Hx of attempt
• 100X risk of general population
• 1% will have committed completed suicide within 12 months of index attempt
• 3-4% will have committed complete suicide eventually
- Accounts for 25-50% of those who completed suicide

Current psychiatric/ physical symptoms

- Disorders with high standard mortality ratio for suicide:
Eating disorder, Major depression, Sedative abuse, Mixed drug abuse, Bipolar disorder, Opioid
abuse, Dysthymia, OCD, Panic disorder, Schizophrenia, Personality disorder, AIDS, Alcohol
abuse, Epilepsy, Child & adolescent, Cannabis abuse, Spinal cord injury, Neurosis, Brain injury,
Huntington’s chorea, Multiple sclerosis, Malignant neoplasms
- Reduced mortality ratio: Mental retardation
- >80% of suicided were retrospectively diagnosed to have ≥1 psychiatric diagnosis in HK
- However, <50% of the cases had never begin contact with mental health services
- Depressive Disorders:
• Account for 50% of suicide patients
• 1970 data: 15% committed suicide (Narrow definition, only include severe cases)
• 2000 Mayo Clinic: 2-9% committed suicide
• Current data: 6.7%
• Higher risk when mood is improving, around discharge
- Schizophrenia:
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• 5% completed suicide, 25-50% attempted suicide
• Could be due to active psychotic symptoms e.g. command hallucinations, persecutory
delusions during acute psychotic phase
• A window of high risk exists in the first few years after diagnosis
• Also highest risk within a few days after discharge from hospital
- Substance abuse
• 20% subjects who completed suicide were probably intoxicated with drugs or substances, incl.
alcohol at their deaths
- Personality disorders
• Traits like impulsivity, aggressiveness, liability of mood
• a/w comorbidity e.g. Depression, Substance abuse
- Other risk factors
• Higher cognitive ability (c.f. Intellectual disability is protective)
• Awareness of loss of function (imposed by illness)
• Difficulty accepting decline in socioeconomic status

Extent of lethality of recent suicidal attempt and thoughts/ ideas

- Passive suicidal idea can quickly become active suicidal idea
- Probability of transitioning from suicidal idea to plan: 34%
- Probability of transitioning from suicidal plan to attempt: 72%

Future: Is there anything going to change?

- Modifiable and treatable suicide risk factors
• Depression, Anxiety, Panic attacks, Psychosis, Sleep disorders, Substance abuse
• Impulsivity, Agitation, Physical illness/ symptoms, Situations (e.g. family, work), Lethal means
(e.g. guns, drugs), Drug effects (e.g. akathisia)
- Possible protective factors
• Having children in a family
• Sense of responsibility to family Poor prognostic factors in Suicidality
- Male
• Pregnancy
- Advanced age (>60yo)
• Religiosity - LGBT
• Life satisfaction - Poor marital status (Divorced, Single)
• Positive coping skills - Living alone, Lack of social support
• Positive social support - Unemployed or Retired
• Positive therapeutic relationship - Certain occupations
- Hx of Suicidal attempts, thoughts/ idea
- Genuine Intent to die
- Mental illnesses
• Depression (esp. in remission)
• Hallucination (derogatory, criticising, about death)
• Delusion (guilt, death, persecutory)
• Unstable mood (anxious, panic, fear)
- Other chronic illnesses esp. pain
- Substance abuse/ dependence e.g. Alcohol, Drug
- Personality traits/ disorders (Antisocial, Borderline)
- FHx of Suicidal completion
- Absence of protective factors e.g. have children
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Methods used in Completed Suicide

(HK 2016 Data: Ref.)
1. Jumping/ Jump from height (JFH) (54.9%) - more popular in young completer
2. Hanging (23.3%) - more popular in old (≥65yo) completer
3. Charcoal burning (11.8%) - more population in adult completer
4. Poisoning (3.5%)
- Common drugs used in overdose:
• Readily available OTC medications: Paracetamol, Cold-remedies, Herbal hypnotics, Rat-
poison (probably Warfarin-containing)
• Prescribed medications: Antidepressants, Benzodiazepine, other hypnotics in known
psychiatric patients, Other prescribed or left-over medications at home
- Medications w/ particular high risk of life-threatening complications in overdose should be
avoided in patients with high suicidal risk e.g. TCA (also substantial cardiac risks)
- Balance between risk and benefits e.g. Lithium (Risk of toxicity in overdose vs Lowering
suicidal risk)
5. Others (5.3%)

Misconceptions about Suicide

Myth: Suicidal patients are very determined and will die anyway
Fact: Suicidal patients are often ambivalent. Timely intervention can save precious lives

Myth: Once patients feel less depressed, it implies that they are less troubled with their problems
and will be less likely to attempt suicide
Fact: Depressed patients who show improvement may in fact be more at risk - may have regained
the energy which the once lacked to commit suicide

Myth: Asking patients about suicide may provoke them to carry out the plan
Fact: In the context of empathetic understanding and concern, asking patients about suicide will
often make patients feel understood and relieved - physicians’ caring questions show them that
someone wants to help

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**Approach to Suicidality**
Framework
- Present 現在
• This attempt (Reason, P&P, C&C, Methods, Perceived lethality)
• Current psychiatric/ physical symptoms
- Past 過去
• Demographics (Age, Occupation, Marital status)
• Previous attempts (Reason, P&P, C&C, Methods, Perceived lethality)
- Future 未來來
• Is there anything going to change?
• Protective factors

Important notes
- Empathetic statements
- Fewer “Why” but more “How”, “What”, “Where”, “Which”
- Non-judgemental
- Preparatory statements, generalisation
- Act and ask professionally

Patient Demographics
- Name
- Age
- Occupation
- Marital status, No. of children, Family relationship
- Pregnancy
- Religiosity

Present
- General mood/ feeling about current medical condition 依家⼼心情如何?
- Negative thoughts/ cognition e.g. Guilt, Hopelessness, Life worthlessness
有冇負⾯面嘅想法, 例例如內疚、對將來來冇希望、⽣生冇可戀?
- Suicidal thoughts/ idea 有冇想完結⽣生命嘅想法? (passive idea) 想⾃自殺? (active idea)
- Reason for suicide
• Intent to die? 想了了結⽣生命?
• Retributive rage? 走投冇路路?
• Para-suicidal gesturing/ Attention-seeking? 等⼈人發現/ 關注?
• Self-mutilation? 只想傷害⾃自⼰己?
- Preparation & Precaution
• Preparation e.g. saving up pills, buying charcoal, writing wills, letters, saying goodbye
有冇準備? 例例如搵地點、買⼑刀、買炭、買藥
有冇交代後事? 例例如寫遺書、立遺囑、買保險、安排⼈人地照顧仔女

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• Precaution (prevent from being stopped/ found) e.g. lock doors, wait till no one’s around
有冇咩做啲咩唔俾⼈人發現/ 阻⽌止?
- Communication & Concealment
• Communication e.g. suicide note, seek help/ tell plan to others directly/ indirectly
有冇同⼈人提過?
• Concealment 有冇特登隱瞞?
- Method(s) ⽤用咩⽅方法⾃自殺? 例例如跳樓、燒炭、吊頸、跳海海、割脈
• Reason for choosing that method(s) 點解會選擇呢個⽅方法? 想真係結束⽣生命、嚇⼈人?
• Perceived lethality of method(s) 覺得呢個⽅方法有幾成機會成功?
e.g. laymen usu. think paracetamol OD is non-lethal and Benzodiazepine OD is lethal
- Suicidal attempts (What) 事發經過、(When) 時間、(Where) 地點、(Who) 附近⼈人物? 邊個發現/
送你去醫院?

Past
- Previous deliberate self-harm 曾經傷害⾃自⼰己?
- Previous suicidal attempts (e.g. within 2yr) +/- Reason, P&P, C&C, Method 曾經試過⾃自殺? 幾
多次? ⽤用咩⽅方法? 結果如何? (hospitalisation) 講講情況最壞⼀一次嘅經歷
- Recent loss e.g. significant other, job, money, reputation, status, image 最近⽣生活轉變?
- Recent stress e.g. exam, life event, interpersonal conflict 最近嘅壓⼒力力? 困難? 解決到?
- Stress-coping skills, Social support 感到困擾時搵邊個幫助或傾訴?
- Alcohol or Substance dependence 有冇食煙、飲酒或者吸食藥物嘅習慣?
- Family member/ Peer completed suicide 有冇家⼈人朋友⾃自殺過左⾝身?
- Chronic illness (pain, physical, mental) 有冇長期病?

Future
- Patient’s view on suicidal attempts e.g. remorseful, non-remorseful 依家有咩睇法?
- Future suicidal idea/ preparation? 仲有冇⾃自殺嘅想法、有冇計畫?
- Any protective factors?
• Positive stress-coping skills 遇到唔開⼼心/困難, 通常會點樣解決?
• Positive social support ⾝身邊有冇會幫助你嘅⼈人?
• Positive therapeutic relationship 同醫⽣生關係點?
• Something to miss 如果真係離開左 最唔捨得係咩?

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Ethics in Psychiatry

Consent and Refusal of Treatment

Why we need consents?
- Consent from patient is legally necessary before we perform any examination or procedure
- Based on the respect for autonomy, the law protects a person's right to self-determination
- As stated in law, for consents to be valid, the patient must:
1. Be given relevant information relating to the nature and purpose of the treatment and its
risks and benefits
2. Have the capacity to make the decision
3. Give consent voluntarily: able to exercise choice, free from manipulation or undue
influence

What is a consent?
- Consent may be express (e.g. saying ‘yes’ clearly) or implied (e.g. holding an arm out and
rolling up his sleeve when asked to have a blood test)
- “Consent form"
• The law actually does not require consent to be in written form
• Having a signed consent form does not automatically mean a patient has given consent
• It is only evidence, and may be questioned in court

How to get a consent?

The treating doctor should:
1. Ensure the 3 components of a valid consent are in place
2. Give appropriate information using simple, clear, jargon-free language in broad terms
1. Nature of problem
2. Treatment recommended and its pros and cons
3. Alternatives and their pros and cons
3. Ensure patient has capacity and is voluntary

Limitation of a consent
- Consent could be invalid if there is material change in situation
- Do not do more than what is consented to, even if additional treatment is of benefit to patient,
except in life-saving situations

When is consent not required?

- Lack capacity to make decision
- Mental illness - act according to Mental Health Ordinance for detention, observation and
treatment of a person with a mental disorder
- Infectious diseases: Quarantine and Prevention of Disease Ordinance

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Capacity
- Related to a person's abilities to make that decision (functional approach)
- Decision-specific and Time-specific
- NOT determined by the outcome of the decision - a person is not to be treated as unable to
make a decision merely because he makes an unwise decision
- NOT determined by a person's diagnosis or status but may be diminished by illness, false
assumptions, misinformation or overbearing influence by another person

Legal definitions of Capacity in HK

- Common law - Relevant abilities for refusal of treatment:
• Understanding the information
• Believing the information
• Weighing the information in balance to arrive at a choice
- Mental Health Ordinance section 58ZB (2)
• Mentally Incapacitated Person (MIP)
- i.e. Adults (>18yo) with a mental disorder or mental handicap (e.g. dementia, brain
injured, mental illness, mental retardation)
- Defined by diagnosis/ condition
• Incapacity for consent to treatment
- i.e. Inability to understand the general nature and effect of the Tx or special Tx
- Defined by inability to understand (context specific)
- Not all MIPs lack the capacity for consent to treatment
e.g. A women with depression can still give consent for blood taking

Assessment of capacity
- Understanding the information
• Ask patient to recall the information and paraphrase it using own words
• Ability to understand is related to general intelligence and cognitive function
• Can be affected by mental disorders
- Believing the information
• Not factual information but more like insight
• Ability to apply the information realistically to oneself
• Ask about beliefs about the disorder (mental or physical)
• Ask if they believe they are ill
• Ask about beliefs about treatment
• Note cultural variations that affect patients' believes
- Weighing the information in balance to arrive at a choice
• Ability to process the treatment information, given his or her preferences
• Assessment concentrates on reasoning process, how the information was used, and how
the decision was reached

Indication of capacity assessment

- Mental illness
- Disagreement about management
- Significant (financial/ medical/ welfare) implications
- Any case you feel uncomfortable about
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Decision-making in absence of capacity

- Principle of “Best interests”
i.e. the treatment will save the life of the patient, or prevent damage or deterioration, or bring
about an improvement to his/her physical/ mental health and wellbeing
- If possible, include consideration of previously expressed wishes and adopting the least
restrictive alternative

How to make decision on treatment?

- Urgent? → Treat in patient’s best interests by the principle of necessity
- Non-urgent
• Non-MIP → Assume capacity for consent
• MIP with Guardianship → MHO Part IVB → Resort to Guardian’s consent
• MIP with Guardianship → Cannot reach Guardian → Treat in patient’s best interests
• MIP w/o Guardianship → MHO Part IVC → Treat in patient’s best interests
**Consent by next of kin has no legal authority**

Durable Power of Attorney for Health Care

- i.e. to appoint a health care proxy/ attorney to make decision regarding patient’s health care
when he/she is physically incapable of making decisions
- A type of Advanced directive with legal validity in HK (c.f. Living will has no legal validity in HK)
- Can only be appointed by the patient when he/she is mentally capable

Guardianship
- Takes months to process and is not indicated in most cases
Indications of Guardianship application
- Disagreement between family members and healthcare team or within family
- MIP strongly resists treatment that is in his/her best interests
- Doctors are unwilling to provide treatment without a guardian’s proxy consent
Powers of guardian
- Reside patient at a specific place
- Bring patient to a specific place using reasonable force
- Require patient to attend for treatment/ occupation/ education/ training
- Consent to treatment
- Require access to patient
- Receive/ pay a specified monthly sum for maintenance or other benefit (currently max at
$16,500/month)

Court Approval
Indications for application of court approval
- Guardian wrongfully refuses to give consent
- Controversial treatments
e.g. withdrawal of life-sustaining treatment, when there is overwhelming resistance from family
members, existence of a dubious advance directive
- Special treatments
e.g. organ donation, sterilisation (that cannot be consented by Guardianship)
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Compulsory Detention and Treatment

Detention
Reasons
- Protect the person detained from further harm e.g. detention of actively suicidal patients,
detention of patients in serious state of self neglect
- Protect society from the person detained e.g. convicted killers, rapists etc
- Both

Patients under observation

Grounds for admission
- Suffering from mental disorder of a nature or degree which warrants his detention in a mental
hospital for observation (or for observation followed by medical treatment) for at least a limited
period
- Ought to be so detained in the interests of his/her own health or safety or with a view to the
protection of other persons
Steps to admission
- Form 1: Filled by a relative, or a doctor
- Form 2: Filled by a doctor (with training in psychiatry)
- Form 3: Filled by a district judge or magistrate
Remarks
- Patient has a right to request to see the district judge or magistrate
- This period of observation may be extended if applied for by a doctor with special experience
in the diagnosis or treatment of mental disorders (approved doctor)

Certified patient
Grounds for admission
- Suffering from mental illness, amounting to mental disorder of a nature or degree which makes
it appropriate for him to receive medical treatment in hospital; and
- it is necessary for the health or safety of the patient or for the protection of other persons that he
should receive such treatment and it cannot be provided unless he is detained under this
section.
- Need at least one recommendation from approved doctor

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Confidentiality
- Confidentiality is important
- Patients might not seek help if the information they give doctors are not kept secret
- Autonomy and respect for privacy:
- There is an implied ‘promise’ that a doctor will keep patient information confidential
- BUT there is often conflict between confidentiality and the interests of others e.g. dangerous
patient

Relevant cases
- Tarasoff (1976, California): A patient told a psychologist that he intend to kill his ex-girlfriend. The
psychologist informed his superior and the police. However, no action was taken to warn the ex-
gf who eventually was killed by the patient. The family sued the psychologist and won.
- W vs Egdell (1990, England Court of Appeal): A patient (W), who is detained in hospital and a
risk to the public, applied a mental health review from Dr. Egdell, who wrote a report opposing
the application. W withheld the report and refuse to send a copy to the hospital. Dr. Egdell
forwarded a copy to the hospital and advised the hospital to forward to Home Secretary. W sued
Dr. Egdell and lost.
Conclusion: Public interest > Individual interest

When can we breech confidentiality?

- When public interest is threatened
• Immediate danger to self or others
• Child abuse cases (after referral to and consultation with medical social workers)
• Serious crime e.g. murder, manslaughter, rape, gunshot wound victims, multiple chop wound
• Sexual abuse or battered spouse: Referral to MSW or report to Police with victim’s consent
• Under 13 pregnancy
- In the course of investigating a crime by police or other law enforcement agencies under
very restricted circumstances
• Factual information: Section 58 Exemption
• Clinical information: Search warrant issued

Type of information
- Factual information
• e.g. Name, Age, Sex, Date of birth, HKID no., Hospital number, Address, Next-of-kin
particulars, Admission/ Discharge date, Ward/ Bed number
• Protected by Personal Data (Privacy) Ordinance
• Can only be disclosed without patient’s consent if statutory exemptions under the PDPO are
applicable, required by statute or under compulsion of law
• Request must be made by a person of Inspector rank or above and endorsed by an officer of
the rank of Superintendent or above
• Must certify that the request is for a purpose specified in section 58 of the Personal Data
(Privacy) Ordinance
- The prevention and detection of crime
- the apprehension, prosecution or detention of offenders
- the prevention, preclusion or remedying (including punishment) of unlawful or seriously
improper conduct, or dishonesty or malpractice, by persons…
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- Clinical information
• Means the patient’s medical information
• Protected under both PDPO and common law duty of confidentiality
• Can only be disclosed w/o patient’s consent if
- A search warrant has been issued
- Disclosure of such is in the public interest (e.g. in cases involving commission of a serious
crime, where the is a genuine risk to the public)
• The police has the responsibility to justify the request and provide sufficient background
information to facilitate the HA’s consideration

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Mental Health Ordinance

Aims of MHO
- Address care and supervision of mentally incapacitated persons (MIP)
- To provide for the management of the property and affairs of MIP
- To provide for the reception, detention and treatment of MIP who are mentally disordered
persons or patients
- To provide for the guardianship of MIP (incl. patients who are mentally disordered) generally
- To make provision for the giving of consent for treatment or special treatment in respect of
MIP who have attained 18 years of age

Legal definitions
Patient A person suffering or appearing to be suffering from mental disorder

Lack of capacity due to Mental disorder or Mental handicap

Mental Excludes
Incapacity - Promiscuity or other immoral conduct
- Sexual deviancy
- Dependence on alcohol or drugs
- Mental illness
- A state of arrested or incomplete development of mind which amounts to a
significant impairment intelligence and social functioning which is asso. with
Mental
abnormally aggressive or seriously irresponsible conduct on part of the person
Disorder
concerned
- Psychopathic disorder or
- Any other disorder or disability of mind which does not amount to mental handicap

A persistent disorder or disability of mind (whether or not including significant

Psychopathic
impairment of intelligence) which results in abnormally aggressive or seriously
Disorder
irresponsible conduct on the part of the person concerned

Mental Sub-average general intellectual functioning which deficiencies in adaptive

Handicap behaviour

Sub-average
An IQ of 70 or below according to the Wechsler Intelligence Scales for Children or
general intellectual
an equivalent scale in a standardised intelligence test
functioning

Any place declared to be a mental hospital in accordance with provisions of section 3

Mental hospital
i.e. Castle Peak Hospital, Kwai Chung Hospital, PYNEH, Tai Po Hospital

Mental Health Review Tribunal

- A statutory body to protect the rights of patients.
- Appeal may be lodged by the patient or his relative
- Automatic appeal lodged by Hospital head if no appeal after a period of detention for 12 months
- Power to discharge patient either absolutely or subject to conditions

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Mental Health Ordinance Form 1-12

Title Applicant

Relative of patient, or
Application for removal of a patient to a mental hospital
Form 1 Doctor, or
for the purpose of detention and observation
Public officer of SWD

Certificate of a mental practitioner in support of

Form 2 application for removal of a patient to a mental hospital Doctor with training in psychiatry
for the purpose of detention and observation

Order by a district judge or magistrate authorising the

District judge, or
Form 3 removal of a patient to a mental hospital for the purpose
Magistrate
of detention and observation

Certificate of medical practitioners for extension of

Form 4 Doctor
period of detention for observation

Relative of patient, or
Form 5 Application for admission into guardianship Doctor, or
Public officer of SWD

Certificate of a mental practitioner in support of

Form 6 Doctor with training in psychiatry
application for guardianship

Form 7 Certificate of medical practitioners as to mental disorder 2 Doctor

Form 8 Notice of revocation of permission to be absent on trial Medical superintendent of hospital

Certificate that a patient who is absent on trial need not

Form 9 Medical superintendent of hospital
be further detained

Relative of patient, or
Form 10 Application for discharge of a patient before recovery
Friend of patient

Form 11 Certificate of refusal to discharge a patient Medical superintendent of hospital

Form 12 Notice of recall of a conditionally discharged patient Medical superintendent of hospital

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Basics in Psychotherapy

Introduction to Psychotherapy
Rathusand Nevid (1999):
Psychotherapy may be defined as a systematic interaction between a therapist and a client that
brings psychological principles to bear on influencing the client’s thoughts, feelings, or behaviour in
order to help the client to overcome psychological disorders, adjust to problems in living, or
develop as an individual

Jerome Frank, Psychiatrist, Johns Hopkins Hospital:

The relief of distress or disability in one person by another, using an approach based on a
particular theory or paradigm, and a requirement that the agent performing the therapy has had
some form of training in delivering this. It is these latter two points which distinguish psychotherapy
from other forms of counselling or caregiving

Jeremy Holmes, Psychiatrist and Consultant Psychotherapist, UCL:

Psychotherapy is a form of treatment based on the systematic use of a relationship between
therapist and patient as as opposed to pharmacological or social methods - to produce changes in
cognition, feelings and behaviour

Classification of Psychotherapy
by number of patients per session
- Individual
- Couple
- Family
- Group

by schools of thoughts
- Psychoanalysis
- Psychodynamic psychotherapy
- Behavioural Therapy
- Cognitive-Behavioural Therapy (CBT)
- Other new schools e.g. Interpersonal Psychotherapy (ITP), Acceptance and Commitment
Therapy (ACT), Cognitive Analytical Therapy (CAT), Mentalisation-based Therapy (MBT),
Dialectical Behavioural Therapy (DBT), Interpersonal and Social Rhythm Therapy (IPSRT),
Cognitive Remediation Therapy (CRT), Metacognitive Therapy, Narrative Therapy, Emotional
Focus Psychotherapy, Hypnotherapy, Logotherapy, Grief Therapy, Mindfulness based PT/ CBT

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Psychoanalysis
- The first ever well-documented specific school of psychotherapy, popularised by Sigmund Freud
in early 20th century after the publication of Interpretation of Dreams in 1900
- Very popular in the past, now gradually fading out

Techniques
- Method of investigating unconscious psyche in order to understand and “cure” mental illness
- Insight-oriented and aim at recovering and interpreting information
- Typically take place with patient lying in a relaxed position on couch and analyst sitting
behind patient
- Common psychoanalysis techniques:
Patient is asked to talk about everything that may come to his/ her mind – in order to
facilitate a free-flow of conscious and preconscious content. The Analysts’ job is to pick
Free Association up on ‘slips’, ‘symbolic’ content, or other important content and interpret these to try and
understand the unconscious processes that determine neurotic behaviour. Facilitates
healthy regression.

Play Therapy Substituted of Free Association in child psychoanalysis, proposed by Melanie Klein

Interpretation of symbolic content of dreams to understand aetiology

Dream Analysis
Usually initiated alongside the free association technique

As exploration/ interpretation take place, patients’ internal resources put up a

Analysis of ‘resistance’ to avoid experiencing the anxieties associated with them. Some forms of
Resistance resistant include long silences, missing appointments and changing the topic. Analysts
try and explore these resistances to understand the patient.

The process of exploration/ analysis creates an emotional environment where the

patient unconsciously starts relating to the therapist the way he/ she did in the past
with an important figure, and relives and re-experiences all the associated feelings.
Transference Transference is thus reacting to the analyst in session as though he/ she were a person
from one’s past. It is the analysts’ job to encourage the patient to explore these feelings
in the safe environment of the session. The resolution of transference plays a key role
in ‘cure’. Transference interpretation are considered powerful interventions.

The emotional response of the therapist to the patient and the material the patient
Counter-
brings to therapy. Analysis of CT often provides clues to the patient’s problems, but
transference
the therapist needs to be award of his/ her personal contribution, conscious or
(CT)
unconscious, to the process. Interpretation of CT is often not necessary.

Analysis & Analysis of parapraxes (unintentional acts, such as a slip of the tongue or the pen), and
Interpretation their interpretation is another crucial element in the process of recovery.

3 main phases
- Establishment of therapeutic alliance/ rapport
- Stage of transference and its resolution
- Termination

Outcome
- Psychoanalysis is a gradual process which may result in years of treatment
- Interpersonal issues, Neurosis, Some personality disorders are best treated by
psychoanalysis
- Many shorter variations introduced in recent years

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Freudian Concepts
- As his attempt to understand psychiatric symptomatology, Sigmund Freud developed a theory
that link symptoms to unconscious mental processes, and emphasised the role of sex drive,
libidinal energy in their development and presentation

Structural and Topographic model

- Human mind is composed of 3 parts
• Id = The part of mind where innate instinctive impulses
and primary processes manifest e.g. Sex, Aggression
• Ego = The part of mind that mediate between conscious
and unconscious; responsible for reality testing and
sense of personal identity
• Superego = The part of mind that acts as self-critical
conscience; reflect socialised moral/ ethical/ cultural/
religious standards/ virtue taught during development
- Human mind expresses in 3 levels
• Conscious = Aware, reality of the external world
• Preconscious = Free floating, where ego is
• Unconscious = Majority; content Id

Psychosexual Stages of Development

- Oral stage: 0-18mo (Feeding)
• Stagnation in this stage → Oral fixation, Lead to oral activities in adult e.g. Smoking
- Anal stage: 18-36mo (Toilet training, Sphincter control)
• Stagnation in this stage → Anal retentive, Obsessive cleanliness e.g. OCD
- Phallic stage: 3-6yo (Sibling rivalry)
• Oedipus complex: Boys develop a deep unconscious sexual desire for their mothers, and
compete with their fathers for her attention
• Electra complex: Girls compete with their mother for father’s attention
• Resolution of stage leads to children relating to same sex parents
• Unsuccessful resolution:Neurosis, Homosexuality, Paedophilia
- Latent stage: 6yo-puberty (socialisation with opposite sex)
- Genital stage: Puberty onwards (Sexual urge towards opposite sex)

Jungian Analysis/ Analytical Psychology

- Carl Jung, a student of Sigmund Freud, proposed another explanation of people’s unconscious

Theories
- Introversion and Extraversion (i.e. the two basic traits of human personality)
- Complex (i.e. a pattern of emotions, memories, perceptions, and wishes in the personal
unconscious, organised around a common theme)
- Collective unconscious 集體潛意識 (i.e. the organised collection of all personal experiences)
- Synchronicity as an alternative to causality

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Hierarchy of Defence mechanisms

Denial 否認 Refuse to accept/ Ignore external realities
Narcissistic/
Delusional projection Delusions about external reality
Pathological
Distortion 扭曲 Gross reshaping of external reality to meet internal needs

Projection 向外投射 Attributing own unwanted thoughts/ behaviour onto someone else

Displacement 轉移 Redirection of aggression onto powerless substitute target

Splitting 分裂 aka Black-and-white thinking

Passive aggression
Indirect expression of hostility
被動侵略略

Direct expression of an unconscious wish or impulse in action,

Acting out 付諸⾏行行動
Immature without conscious awareness of the emotion

Replicate behaviours, attributes, or other fragments of the

Introjection 向內投射 surrounding to provide illusion of maintaining relationship at the
cost of loss of self

Withdrawal 退縮 Escape from or avoid situations that are challenging

Somatisation ⾝身⼼心病 Experience somatic symptoms in psychological distress

Fantasy 幻想 Gratifying frustrated desires by imaginary achievements

Subconscious# attempt to repel desires toward pleasurable

Repression 抑制
instincts, caused by a threat of suffering if the desire is satisfied

Temporary drastic modification of one’s personal identity to avoid

Dissociation 抽離
emotional distress

Displacement 遷怒怒 Shifts impulses to a more acceptable or less threatening target

Keep unwelcome thoughts and feelings from forming associative

Isolation 隔離 links with other thoughts and feelings so that the unwelcome
thought is rarely activated
Neurotic
Rationalisation 合理理化 Logically justify immoral, deviant, or unacceptable behaviours

Reaction formation Convert unconscious, dangerous/ unacceptable wishes or

反應形成 impulses into their opposites

Try to cancel out/ remove an unhealthy, destructive or threatening

Undoing 撤銷
thought or action by engaging in contrary behaviour

Cover up weakness, frustrations, desires, or feelings of

Compensation 補償
inadequacy through gratification or excellence in another area

Identification 東施效顰 Taking on the characteristics of someone viewed as successful

Conscious# decision to delay paying attention to a though,

Suppression 抑制
emotion, or need in order to cope with the present reality

Transformation of unhelpful emotions or instincts into healthy

Sublimation 昇華
actions, behaviours, or emotions
Mature
Altruism 利利他 Service others to brings pleasure and personal satisfaction

Humour 幽默 Overt expression of ideas and feelings that pleasure others

Anticipation 預期 Realistic planning for future discomfort

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Cognitive Behavioural Therapy (CBT)

- First advocated by Aaron Beck, a psychiatrist who published a psychological model of
depression, suggesting that thoughts play a significant role in the development and maintenance
of depression
- CBT is a psychotherapeutic approach which addresses dysfunctional emotions, maladaptive
behaviours and cognitive processes, and contents through a number of goal-oriented, explicit
systematic procedures
- CBT is problem-focused and action-oriented therapy; during which the therapist would assist
the client in identifying, selecting and tackling specific goals using different coping strategies
- A time-limited therapy with a clear goal conducted under a structured form
- Involves patient working on goal directed tasks “homework” that could involve cognitive or
behavioural aspects relating to the goal

Key concepts
- Collaborative empiricism
- Scientific approach
- Hypothesis-testing
- Guided discovery

Core principles of CBT

- CBT Triangle
• Thoughts, Behaviours, Emotion
• Describe the interlinked relationship between what
we think, feel and do on each other
- ABC of CBT
• Activating events, Belief, Consequence
e.g. Failing an exam (A) → “I am useless” (B) → Depressed and cry (C)
• CBT aims at identification and addressee maladaptive cognitions along this pathway
e.g. Failing an exam ≠ Useless
- Beck’s Cognitive Therapy: 3 levels of cognition
• Core beliefs, Dysfunctional assumptions, Automatic thoughts
e.g. “I am useless” → “If I am useless. I am not life worthy” → “I did not pass. I am useless”
• Automatic thoughts are negative and vicious in the presence of cognitive distortion
e.g. Jumping to conclusion that “I am useless” from “failing one exam”

6 phases of CBT
- Psychological assessment (intake session)
- Reconceptualisation (cognitive part of CBT)
- Skills acquisition
- Skills consolidation and application training
- Generalisation and maintenance
- Post-treatment assessment follow-up

Outcome

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- Best for Depression, Anxiety Disorders (e.g. OCD, PTSD, Panic, Agoraphobia), Bipolar Disorder,
Schizophrenia, Eating disorders, Substance use disorder, Chronic pain, Body dysmorphic
disorder

Pros & Cons

Pros Cons

Comparable efficacy with drug interventions

Favourable long term efficacy Relies heavily on patient commitment and involvement

Cost effective

Does not dynamically resolves underlying causes e.g.

Goal and action oriented, focusing on current unhappy childhood
problems
Does not address wider problems in systems or families

Structured and instructive Due to structured nature of CBT, it may not be suitable for
people who have more complex mental health needs, or
Short term (average 16 sessions) learning difficulties

Cognitive Distortions/ Errors

- Systemic errors in reasoning → Negative misinterpretation of experience
Always being right 我⼀一定啱 Being wrong is unthinkable and try to prove one is correct

Blaming 永不⾃自責 Assume others are held responsible

Personalisation 過度⾃自責 Assume responsibility for things that have little/ nothing to do with oneself

Fallacy of change 改變繆誤 Expect others to change when encouraged or pressured 逼⼈人地變

Fallacy of fairness 公平繆誤 Expect life to be extremely fair 公平撚

Global labelling/ Mislabelling Use only 1-2 encounters as a general assumption of someone's
標籤/ 錯誤標籤 personality or behaviour

Jumping to conclusion/ Use only 1-2 encounters as a general assumption of someone's

Arbitrary inference 妄下判斷 personality or behaviour

Overgeneralisation 以偏概全 Draw a general conclusion on the basis of a single incident

Emotional reasoning 感情⽤用事 Focus too much on emotional rather than common sense

Mental filtering/ Selective

Focus on a detail and ignoring more important features of a situation
abstraction 斷章取義

Discounting/ Disqualifying the

positive 唔理理正⾯面

Polarised thinking/ Splitting/ Evaluating the self, as well as events in life in extreme terms, as either all
Black-or-white thinking 非⿊黑即⽩白 good or all bad, either black or white, nothing in between

Magnification and minimisation

Exaggerate the negative and minimising the positive in evaluating oneself
放⼤大化和最⼩小化

Catastrophising 災難未來來 Predict the future negatively w/o considering other more likely outcomes

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Cognitive model of Mood disorder

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Psychiatric Pharmacology
Benzodiazepines and Z drugs
- Benzodiazepines, Z drugs and Barbiturates all exert similar action on GABAA receptor. However,
they bind to different sites and thus technically are different classes of drugs.

MOA of BDZ
GABAA receptor complex
- GABA = Ɣ-Aminobutyric acid
Binders to receptor
- GABA binds to GABA-binding site (interface
between α and Ɣ subunits) on receptor complex
→ Opening of chloride channel
→ Influx of chloride
→ Hyperpolarisation of neuronal membrane potential
→ Inhibitory effect
- BDZ binds to regulatory site (interface between α
and Ɣ subunits) on receptor complex
→ ↑ affinity of GABA to GABAA receptor
→ Enhance inhibitory effect of GABA
(w/o GABA, BDZ has no effect on chloride channel)
- Z drugs (Zolpidem and Zopiclone), Flumazenil (Z drug antagonist) and Barbiturates bind to
different sites on the receptor complex
Effect
- Anxiolytic
- Hypnotic (induction of sleep)
- Sedative (calmness)
- Reduce muscle tone (Anti-tetanus effect)
- Impair coordination
- Anti-convulsant
Classification of receptors
- NOT all GABAA receptors show affinity to BDZ
• High-affinity GABAA receptors (80%)
• Low-affinity GABAA receptors (10%)
• No-affinity GABAA receptors (10%)
- High-affinity GABAA receptors are subdivided by affinity to Zolpidem
• Type I (ω1 receptor): High affinity to Zolpidem
• Type II (ω2 receptor): Low/ no affinity to Zolpidem

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Examples of BDZ
Absorption rate/ Duration of Parent drug Metabolic Active metabolite
Examples
Onset action t1/2 (h) phase t1/2 (h)

Diazepam (Valium®) Rapid 20-100 I + II 30-90

Flurazepam Rapid 2 I + II 30-120

Clonazepam Rapid Long

Chlordiazepoxide
Intermediate 5-30 I + II 30-90
(Librium®, Librax®)

Rapid (IV)
Lorazepam (Ativan®) 10-20 II only \
Intermediate (PO)
Intermediate
Alprazolam Intermediate 5-15 I + II \

Nitrazepam Intermediate 24 I + II 30-90

Midazolam (Dormicum®) Rapid (IV) 1-4 \

Short
Triazolam Intermediate 1.6-5.5 \

Zolpidem
Rapid Short 2 II only \
(Imovane®)
Z drugs
Zopiclone
Rapid Short 3-4 I + II 3-6
(Stilnox®)

Common psychiatric indications

Psychiatric Disorder/ Clinical use Remarks Examples

Alprazolam
Chlordiazepoxide
Anxiety Disorders Long t1/2 preferred to avoid withdrawal
Clonazepam
i.e. Anxiolytics NOT the 1st line Rx (1st is SSRI)
Diazepam
Lorazepam

Triazolam
Shorter t1/2 preferred for sleep Temazepam
Sleep Disorders induction (induction insomnia) Flurazepam
i.e. Hypnotics/ Sedatives or other BDZ at high dose

Longer t1/2 preferred for early morning

Zopiclone
awakening

Alcohol Withdrawal Long t1/2 preferred to avoid withdrawal

Diazepam
Status Epilepticus
Rapid onset preferred Lorazepam
i.e. Anticonvulsant
Midazolam

Agitation/ Restlessness
e.g. Acute Dystonia, Akathisia BEWARE of paradoxical reaction of BDZ
due to Antipsychotics

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ADR of BDZ
Frequency ADR

Drowsiness/ Hangover/ Daytime sleepiness (Mx: Z-drug)

Dizziness
Common
Psychomotor impairment/ Motor incoordination
Dependence/ Withdrawal symptoms

Blurred vision
GI upset
Occasional Headache
Respiratory depression
Falls (in elderly)

Amnesia/ Poor memory

Paradoxical reaction (Restlessness, Disinhibition, Agitation, Aggression)
Rare
Respiratory arrest
Convulsion on abrupt withdrawal

Tolerance
Potential Drug of abuse
Dependence syndrome (intoxication s/s, withdrawal e.g. paranoid idea)

Dependence/ Drug of abuse

Benzodiazepine Withdrawal Symptoms

Clinical presentation
- Agitation
- Insomnia
- Sweating
- Restlessness
- Seizure
Management
- Taper down dosage
- Switching to longer acting BDZ
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Other Anxiolytics

Z Drugs
e.g. Zopiclone (Imovane®), Zolpidem (Stilnox®), Zaleplon

Pharmacokinetics
- Zolpidem
• Extensively inactivated by liver CYP enzymes
• Excreted in urine and bile, <1% active drug excreted in urine
- Zopiclone
• Racemic mixture of 2 enantiomers that are metabolised at different rates
• Activated by liver CYP enzymes (oxidation, methylation, decarboxylation)
to produce active metabolite which accounts for 11% of metabolism
• Excreted in urine
• Characteristic bitter taste (窮⼈人食苦藥)
- Zaleplon
• Resembles Zolpidem
• Rapid onset and short duration of action
• (Not available in HK)

MOA
- Binds selective to BZ1 subtype GABA-receptors
- Facilitate GABA-mediated chloride influx and neuronal inhibition
- Antagonised by Flumazenil (competitive antagonist of binding site)

ADR
- Ataxia
- Nightmares
- Agitation
- Headache
- GI upset
- Dizziness
- Daytime drowsiness
- Confusion
- Zolpidem: Sleepwalking
- Zopiclone: Methaemoglobinaemia

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Barbiturate
- Obsolete class of drug due to numerous side effects
- Narrow therapeutic window

Examples
- Ultra-short-acting (10-20min): Thiopental/ Thiopentone
- Short-acting (2-8hr): Pentobarbital, Amobarbital, Secobarbital
- Long-acting (1-2d): Phenobarbital

MOA
- Binds to Barbiturate receptor (α & β subunit) on GABAA receptors
- ↓ AMPA-R
- Pentobarbital, at anaesthetic conc. → ↓ high-frequency NaC → ↓ Neuronal activity

ADR
- Drowsiness
- Motor incoordination
- REM sleep suppression
- Respiratory depression
- Coma (at toxic dose)
- Tolerance
- Physical dependence
- Severe Withdrawal symptoms
- CYP450 enzyme inducer

Buspirone
- BuSpar®
- Indicated in Generalised Anxiety Disorder (GAD)

MOA
- 5-HT1A agonist
- D2 receptor antagonist
- 5-HT2A agonist

ADR
- Headache, Dizziness
- Nausea, GI upset
- Restlessness
- Palpitation, Tachycardia
- Hypothermia
- Hyperprolactinaemia, Acromegaly

DDI
- Rifampicin (enzyme inducer to shorten t1/2)
- Erythromycin (enzyme inhibitor to lengthen t1/2)
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Antidepressants

MOA of Antidepressants
Basis of Antidepressants
- Old model: Monoamine Deficiency Hypothesis
• Depression is proposed to be due to deficiency in monoamines
• Related targets in Antidepressants:
- Monoamine oxidase (MAO)
- Serotonin (5-HT) receptor
• 5-HT1AR antagonism: Hormones, Depression, Anxiety, Cognition, Pyramidal inhibition
• 5-HT2AR antagonism: Sleep, Hallucination, Dopamine inhibition, Glutamate excitation,
Pyramidal excitation
• 5-HT2CR antagonism: Obesity, Mood, Cognition, Regulation of Dopamine and NE release
- Noradrenaline (NE) receptor
- Dopamine (DA) receptor

- New model is classifying antidepressants clinically instead of according to receptor profile

Serotonin Receptors
Classification
- 5-HT1 (1A, 1B, 1D, 1E, 1F)
- 5-HT2 (2A, 2B, 2C)
- 5-HT3
- 5-HT4 (4A)
- 5-HT5 (5A)
- 5-HT6
- 5-HT7

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Examples of Antidepressants

Classes of Antidepressants
* based on receptor profiles
Class MOA/ Receptor profiles

Monoamine Oxidase Inhibitor (MAOI) Inhibit MAO, no receptor binding

SRI, NRI
5-HT2A, 5-HT2C antagonism
H1 antagonism
Tricyclic/ Tetracyclic Antidepressants (TCA)
α1 antagonism
M1 (mACh) antagonism
Na channel (type 1A) blocker

Selective Serotonin Receptor Inhibitors (SSRI) SRI only

Selective Serotonin Norepinephrine Receptor Inhibitor (SNRI) SRI, NRI

SRI
5-HT2A, 5-HT2C antagonism
Serotonin Antagonist and Reuptake Inhibitor (SARI)
H1 antagonism
α1 antagonism

α2-Adrenergic Antagonist/ Norepinephrine Antagonist-Serotonin 5-HT2A, 5-HT2C antagonism

Antagonist (NASA)/ α1, α2 antagonism
Noradrenaline Selective Serotonin Antagonist (NaSSA) H1 antagonism

Norepinephrine Reuptake Inhibitor (NRI)/ NRI

Norepinephrine Dopamine Reuptake Inhibitor (NDRI) DRI

Melatonin Receptor Agonist (MRA)/ MT1, MT2 agonism

Noradrenaline Dopamine Disinhibitor 5-HT2C antagonism

SRI
New SSRI: Multi-modal Antidepressants e.g. Vortioxetine 5-HT3 & 5-HT7 antagonism → Cognition
5-HT1A agonism

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Monoamine Oxidase Inhibitor (MAOI)
- Non-selective MAOI e.g. Phenelzine (for Phobia), Tranylcypromine
- Selective MAOAI/ Reversed Inhibitor of MAOA (RIMA) e.g. Moclobemide (for Phobia)
MOA
- Inhibit MAO (MAO inactivate monoamines in pre-synaptic neurons) → ↑ 5-HT, NE, Dopamine
• MAOA is responsible for breakdown of 5-HT, NE, Adrenaline, Dopamine and Tyramine
• MAOB is responsible for breakdown of Dopamine, Phenylethylamine, Tyramine - more
selective action in Parkinsonism
ADR
- ↓ Breakdown of Tyramine in gut → Hypertensive crisis → ICH, Heart attacks
- Orthostatic/ Postural hypotension
- Weight gain
- Insomnia
- Restlessness
- Confusion
Food-Drug interaction
- Caution with Tyramine-rich food e.g. Processed meat, Poultry, Fish, Vegetable, Dairy, Beverages
(Alcohol), Avocados, Bananas, Pineapple, Eggplants
- Thus rarely prescribed anymore
DDI
- SSRI, SNRI, TCA → Serotonin Syndrome → Mild to lethal symptoms
- Serotonergic antidepressants should be discounted for at least 2 week before prescription of
MAOI (and vice versa) esp. in Fluoxetine (long t1/2) which should be discounted for 4-5 weeks

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Tricyclic/ Tetracyclic Antidepressants (TCA)
e.g. Amitriptyline, Clomipramine, Imipramine, Nortriptyline, Prothiaden, Dothiepin
Indications
- Depression
• Previous 1st line antidepressant for depression
• Now replaced by SSRI due to less ADR with comparable efficacy
• Only used in refractory depression to SSRI
- Panic Disorder (Imipramine)
- OCD (Clomipramine)
- Migraine
• Previous 1st line
• Now replaced by Sumatriptan
- Post-herpetic neuralgia
• Previous 1st line
• Now replaced by Gabapentin
- Narcolepsy
- Nocturnal enuresis
MOA
- TCA is a non-selective monoamine reuptake inhibitors and Na channel
blocker
antagonists; main action in Depression is inhibiting reuptake of
5-HT, NE, DA
- Receptor profile
• H1 antagonist
• α1 adrenergic antagonist
• M1 (ACh) antagonist
• SRI (Serotonin reuptake inhibitor)
• 5-HT2A & 5-HR2C antagonist
• NRI (Noradrenaline reuptake inhibitor)
ADR
- Sexual dysfunction
- Blurred vision, Dry mouth, Drowsiness, Urinary retention, Constipation
- Postural hypotension, Sedation
- Cardiotoxicity (Long QT, Arrhythmia, SCD esp. in Clomipramine)
- TCA Overdose:
• NaC blockage → Wide QRS complex, Long QT
• Antidote: Gastric lavage, Activated Charcoal, IV NaHCO3 bolus, Benzodiazepine
Cons
- More ADR, Poor tolerability
- Overdose is lethal
- Difficult to use
- Serious drug-drug interactions

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Selective Serotonin Reuptake Inhibitor (SSRI)
- Fewest ADR (usu. transitory, mild-moderate), Safe overdose, Cheap
Examples
- Paroxetine (Paxil®, Seroxat®) - Shortest t1/2, most withdrawal symptoms, CYP2D6 inhibitor
- Fluoxetine (Prozac®) - t1/2 lengthens with use, CYP2D6 inhibitor; DDI with TCA; NO increase
in suicidal risk in young patients
- Citalopram (Cipram®, Celexa®) - Cardiotoxicity
- Escitalopram (Lexapro®, Cipralex®) - Least DDI
- Sertraline (Zoloft®, Lustral®) - for PTSD
- Fluvoxamine (Faverin®, Luvox®) - CYP3A4 inhibitor; DDI with Diltiazem
- Vortioxetine - Novel SSRI that improve both depressive and cognitive symptoms
MOA
- SRI: Inhibit reuptake of Serotonin by pre-synaptic neuron → ↑ Synaptic Serotonin conc.
- Vortioxetine: SRI + 5-HT1A agonist + 5-HT1B partial agonist + 5-HT1D, 5-HT3 & 5-HT7 antagonist
Delayed onset for efficacy
- Require 4 weeks for benefit to take place
- Monoamine Hypothesis: SSRI inhibit 5-HT
reuptake in Raphe nuclei in Brainstem
→ Excess 5-HT bind to auto-receptors
→ -ve feedback on 5-HT production
→ Gradual down-regulation of auto-receptors &
restored cell firing and 5-HT release
→ SSRI can now inhibit 5-HT reuptake in
synaptic cleft
- Cortisol Hypothesis: Suppressed BDNF by high
cortisol take time to go from gene to protein
ADR
- Early agitation, mild restlessness
→ Covered by mild Benzodiazepine to control
early ADR in early phase of SSRI treatment
- SIADH → Dilutional HypoNa
- GI upset: Nausea, Diarrhoea
- Sexual dysfunction
- Coagulopathy, Bleeding tendency
- Vasoconstriction (inhibited nitric oxide synthase)
- Citalopram: Cardiotoxicity (Sinus Tachycardia, Long QT, Wide complex, Right axis deviation)
DDI
- CYP2D6:
• CYP2D6 inhibitor: Fluoxetine, Paroxetine
• CYP2D6 substrate: TCA, Warfarin, Risperidone
- CYP3A4
• CYP3A4 inhibitor: Fluvoxamine
• CYP3A4 substrate: Diltiazem (exaggerated bradycardia and hypotension)
- Less CYP interactions in the rest
- Least CYP interaction in Escitalopram

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Norepinephrine Reuptake Inhibitor (NRI)/
Norepinephrine-Dopamine Reuptake Inhibitor (NDRI)
- Relatively new class of antidepressant
e.g. Atomoxetine, Maprotiline, Reboxetine, Bupropion
ADR (Adrenergic effects)
- Raised BP
- Initial Tachycardia, Later Reflex Bradycardia
- CNS activation e.g. Insomnia, Anxiety, Agitation

Serotonin Norepinephrine Reuptake Inhibitor (SNRI)

e.g. Venlafaxine (Effexor®), Duloxetine (Cymbalta®), Des-
venlafaxine, Milnacipran, Mirtazapine (Rameron®)
MOA & ADR ~SSRI + NRI

Serotonin Antagonist and Reuptake Inhibitor (SARI)

- A relatively new class of antidepressant
e.g. Trazodone (Desyrel®), Nefazodone (Serzone®)
MOA
- 5-HT2A receptor antagonist (most potent pathway)
- SSRI effect
- Produce meta-chloro-phenylpiperazine (mCPP) which is a 5-
HT1A receptor agonist
ADR
- ~SSRI
- Trazodone specific ADR: Priapism, Tardive Dyskinesia

Norepinephrine Antagonist and Serotonin Antagonist (NASA)/

Noradrenaline Selective Serotonin Antagonists (NaSSA)
e.g. Mianserin, Mitrazapine
MOA
- Binds to α2 adrenergic receptor → ↓ NE transport in pre-
synaptic neuron → Remove auto-inhibition on pre-synaptic
neuron and ↑ NE release → ↑ 5-HT level
- 5-HT2A & 5-HT2C antagonist
ADR
- Sedation
- Dry mouth
- Dizziness
- Vertigo
- Specific ADR: Leukopenia, Weight gain

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Melatonin Receptor Agonist (MRA)/
Noradrenaline Dopamine Disinhibitor
e.g. Agomelatine (Valdoxan®)
MOA
- Synthetic Melatonin → MT1 & MT2 agonism
→ ↑ intracellular signalling for BDNF (improve depression) and
sleep-wake phase (improve sleep)
- 5-HT2C antagonisms → Dis-inhibiting release of Dopamine and
NE at Frontal cortex
- Increase concentration of NE, Dopamine but NOT Serotonin
ADR
- Dizziness
- Fatigue
- Drowsiness
- Hyperprolactinaemia
- Specific ADR of Agomelatine: Elevated liver enzymes (ALT, AST)
• FDA recommend LFT monitoring at 3rd, 6th, 12th, 24th week of treatment at start or when
dose increased to 50mg → Discontinue if ALT and/or AST >3X ULN

Common psychiatric indications

Psychiatric Disorder/ Clinical use Action

Depressive Disorders

Anxiety Disorders

Post-Traumatic Stress Disorder

Obsessive-Compulsive Disorder

Sexual Disorder
- Increase 5-HT, Dopamine, NE
Bulimia Nervosa - Unwanted actions?
(Fluoxetine only, approved since 1996) • Anti-histaminergic: Sedative, weight gain
• 5-HT: Weight gain, Delayed or premature ejaculation
Smoking cessation
(Bupropion, since 1997)

Premenstrual dysphoric disorder

Neuropathic pain, Fibromyalgia

Insomnia (Off-label use: Fluoxetine,

Trazodone, Mirtazapine)

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ADR of Antidepressants
- ADR can be deduced by their receptor profiles
- Some antidepressants have specific ADR
- 5-HT1AR antagonism: Hormones, Depression, Anxiety, Cognition, Pyramidal inhibition
- 5-HT2AR antagonism: Sleep, Hallucination, Dopamine inhibition, Glutamate excitation, Pyramidal
excitation
- 5-HT2CR antagonism: Obesity, Mood, Cognition, Regulation of Dopamine and NE release
5-HT2A 5-HT2C α1 & H1 M1
Class SRI NRI Others
antagonism antagonism antagonism antagonism

MAOI

TCA ✔ ✔ ✔ ✔ ✔ ✔ NaC Blocker

SSRI ✔

NRI/ NDRI ✔ DRI

SNRI ✔ ✔

SARI ✔ ✔ ✔ ✔

NASA/ NaSSA ✔ ✔ ✔ α2 antagonism

MT1 agonism
MRA ✔
MT2 agonism

5-HT1A agonism
5-HT1B partial agonism
Vortioxetine ✔
5-HT1D, 3, 7
antagonism

Receptor profiles Drug class ADR

Serotonin Syndrome

SSRI Discontinuation Syndrome

ALL
Anti-depressants Sexual side effects (Least in Bupropion)
Serotonergic
except - Female: Decreased libido, Anorgasmia
NRI and MRA - Male: Decreased libido, Delayed ejaculation, Retrograde
ejaculation, Erectile dysfunction

Weight gain

Anticholinergic/
Dry mouth, Constipation, Urinary retention, Blurred vision,
Anti-muscarinic/ TCA
Visual accommodation problem, Acute angle closure (glaucoma)
M1 Antagonism

Anti-adrenergic/ α1: Priapism#, Postural hypotension*

α1/2 Antagonism TCA α2: Dizziness, Reflex tachycardia
SARI
Anti-histaminergic/ NASA Weight gain, Sedation/ Drowsiness
H1 Antagonism

* Priapism is due to α1 adrenergic receptor blockade; Reference: Link, Link

* Postural hypotension is indeed due to α1 adrenergic receptor blockade; Reference: Medscape

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Specific ADR
Cardiotoxicity
- Wide complex (QRS >100ms) in Lead II
TCA - RAD: Prominent R wave in aVR
SSRI - Citalopram - Sinus tachycardia (due to Anticholinergic and α-blocking effect)
- Long QT
- Sudden cardiac death esp. in Clomipramine
Priapism (i.e. persistent painful erection)(due to α1 antagonism)
SARI - Trazodone
Tardive dyskinesia or Idiosyncratic dystonia

NASA e.g. Mianserin Leukopenia, Weight gain

SNRI - Venlafaxine Hypertension

NRI Hypertensive crisis if MAOI + Tyramine-rich food or sympathomimetics

Elevated liver enzymes (ALT, AST)

MRA - Agomelatine FDA recommend LFT monitoring at 3rd, 6th, 12th, 24th week of treatment at start
or when dose increased to 50mg → Discontinue if ALT and/or AST >3X ULN

BLACK BOX Increased risk of suicidality in patients <25yo except Fluoxetine

WARNING (However, benefits of using Antidepressants in young patients still outweigh risk)

Serotonin Syndrome
- Common occurs in MAOI+SSRI, MAOI+TCA, Tramadol overdose
Clinical presentation
- Cognitive: Headache, Agitation, Hypomania, Delirium, Convulsion, Hallucinations, Coma
- Autonomic: Hyperthermia, Diaphoresis, Nausea, Vomiting
- Motor dysfunction: Tremour, Hypertonia, Ankle Clonus, Hyperreflexia, Babinski’s sign
Diagnosis: Hunter’s Criteria
1. Spontaneous clonus
2. Inducible clonus + Agitation or Diaphoresis
3. Ocular clonus + Agitation or Diaphoresis
4. Inducible or Ocular clonus + Hypertonia + Hyperthermia
5. Tremour + Hyperreflexia

Antidepressant discontinuation syndrome

- Basically means withdrawal symptoms of Antidepressants
- But not exactly the same because it is high-dose dependent and antidepressants are not
considered a “substance”
Clinical presentation
- A: Agitation, Anxiety
- B: Balance problems, Bad Dreams
- C: Concentration problems
- D: Dizziness, Diarrhoea, Nausea, Vomiting
- E: Electric shock-like sensation
- F: Flu-like symptoms
- Others: Psychosis, Confusion, Excitement
- Guideline: Reduce dose gradually over at least 4w period (better 2m)

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Mood Stabilisers/ Stabilising Agents

Lithium
Indications
- Epilepsy (Anti-epileptic drug/ Anticonvulsant)
- Acute Manic episodes (Anti-manics) of Bipolar Disorder
• Old but important drug - the ONLY mood stabiliser to reduce suicide
• 1st line in Acute Manic episodes, 80% response rate
• Maximal effectiveness require 2 weeks of treatment
• Cons: Numerous DDI with common drugs, Narrow therapeutic margin (esp. in elderly)
• In Acute Manic episodes, start with 250-500 mg/d to reach therapeutic conc. of Lithium
(0.6-1.0 mmol/L)
- 1st line for Prophylaxis in Cluster Headache

MOA
- Inositol mono-phosphatase (IMP) inhibition
- Glycogen synthase kinase (GSK) 3-β inhibition
- Up-regulation of mitochondrial BCL-2

ADR
- Nausea, Polydipsia, Polyuria, Fatigue, Fine tremour, Hair loss/ Alopecia
- Renal dysfunction (Nephrogenic DI, RTA, ?MCD) → eGFR Q3month
- Hypothyroidism → TFT Q6month (also used when antithyroid medication contraindicated but
have thyroid storm/ crisis)
- Weight gain (?Hypothyroidism) → Monitor BMI
- Teratogenicity (Ebstein’s anomaly in 1st trimester exposure, Neonatal goitre) → C/I
Pregnancy
- Cognitive impairment/ Poor memory
- Long QT (usu. benign, may exacerbate pre-existing LQTS)

DDI
- Diuretics
- NSAID
- CCB
- ACEI

Lithium Toxicity [Medical Emergency]

- Ax: DDI, Dehydration
- Early s/s: Coarse tremour, Anorexia, Nausea, vomiting, Diarrhoea, Dehydration, Lethargy
- Neurological s/s: Restlessness, Muscle Fasciculation/ Myotonic jerks, Hypertonia, Slurred
speech, Seizure, Coma
- CVS: Hypotension, Arrhythmia, Circulatory collapse
- Mx: Stop Lithium immediately, High fluid intake, Forced osmotic diuresis by IV NS,
Haemodialysis (repeated HD for redistributed Lithium)

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Valproate (Epilim®)
- Well-tolerated with few DDI
- May work faster with Lithium
- Start with 500mg/d

Indications
- Acute Manic or Acute Depressive episodes of Bipolar Disorder
- Prophylaxis for Bipolar Disorders
- Broad-spectrum Anti-Epileptic drug
• Effective against Primary GTCS, Absence seizure, Myoclonic seizure
• 2nd line for Partial seizure
- 2nd line for Cluster headache

MOA
- Histone deacetylase (HDAC) inhibition → Block voltage-gated Na channel

ADR
- Subjective effects: Nausea, Vomiting, Diarrhoea, Tremour, Sleepiness
- Systemic effects: Weight gain, Deranged LFT, Leukopenia,
Thrombocytopenia, Hair thinning or loss, PCOS ADR of Valproate
- Teratogenicity (Spina bifida, Valproate Syndrome, Intelligent Vomiting
disability) Anorexia
Liver toxicity
DDI Pancreatitis
- Aspirin Rash
- Warfarin Ovary (PCOS)
- Other Anti-epileptics e.g. Lamotrigine Alopecia
Teratogenicity
Excessive weight gain
Lamotrigine (LG)(Lamictal®)
- Good tolerability and wide therapeutic window

Indications
- Acute Depressive episode of Bipolar Disorder
• Start with 25mg/d in first 2 week
• If combine with Anticonvulsants, start with 12.5mg/d
• Otherwise 50-200mg/d
• Tailor the dose according to response
- Broad-spectrum Anti-Epileptic drug
• Effective against partial seizures, GTCS
• Preferred as 1st line AED in elderly patients

MOA
- Inhibition of voltage-gated Na channel
- Inhibition of glutamate release

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ADR
- Subjective effects: Headache, Fatigue, Dizziness, Dry mouth
- Systemic effects: Rash, Steven Johnson Syndrome (SJS)

DDI
- Other anti-epileptics e.g. Valproate
- OC pill (↑ LG clearance)

Carbamazepine (CBZ)(Tegretol®)
Indications
- Anti-Epileptic Drug
• Effective against Partial Seizure, GTCS
• NOT effective and even exacerbate Absence seizures, Myoclonic seizures

MOA
- Inhibition of voltage-gated Na channels
- Adenosine receptor antagonism

ADR
- Dose-related neurotoxicity/ Cerebellar ataxia (Diplopia, Dizziness, Headache, Nausea,
Somnolence)
- Allergic morbilliform rash (can progress to SJS esp. HLA-B*1502 positive)
→ Compulsory checking of HLA-B*1502 before starting CBZ
- Reversible leukopenia
- SIADH (HypoNa)
- Toxic hepatitis
- Orofacial dyskinesia
- Cardiac arrhythmia
- Severe idiosyncratic blood dyscrasia (rare)

DDI (CBZ is CYP3A4 induction)

- Oestrogen-containing OC pills (OC pills become ineffective)
- Haloperidol
- Benzodiazepine
- Other Anti-epileptic e.g. Phenytoin (↓ plasma level)
- Theophylline
- Steroid
- Warfarin

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Quetiapine
Indication
- Acute Depressive episodes of Bipolar Disorder
• ~200-400 mg/d for mild cases, up to 800 mg/d for severe cases
• Tailor dose according to response
- Schizophrenia
- Delirium

ADR
- Subjective effect: Dry mouth, Sleepiness
- Systemic effect: Weight gain, Metabolic syndrome, T2DM, Dyslipidaemia

Olanzapine
- Indicated in Anorexia Nervosa for its weight gaining effect
- Start with 5mg/d
- Aim at 10-20mg/d
- Tailor the dose to response

ADR
- Subjective effect: Sleepiness
- Systemic effect: Weight gain, Metabolic Syndrome, T2DM, Dyslipidaemia, Highest risk among
atypical antipsychotics

Mood Stabilisers in Pregnancy

- No drugs are really “safe”
- Most mood stabilisers belong to class C or D according to the FDA classification
- However, potential benefits may still warrant use despite potential risks
• Toxicity is dose dependent
• Stopping drug will increase the chance of relapse, even higher if stopped abruptly
• High risk of relapse during Postpartum period/ Puerperium

Commonly “non-safe” mood stabilisers

- Class C - i.e. adverse effect on foetus in animal studies; risk cannot be ruled out
• Lamotrigine, Topiramate - low risk of Cleft lip, Cleft palate
• Quetiapine, Olanzapine
• SSRI
- Class D - i.e. positive evidence of human foetal risk
• Lithium - 3X abnormalities of all types, 7X cardiac abnormalities (e.g. Ebstein’s anomaly)
• Valproate - Congenital malformation (Spina bifida, Facial dysmorphism), Developmental
delay (Low IQ)
• Benzodiazepine - 2X risk of Cleft lip, Cleft palate, Facial dysmorphism, Cardiac
abnormalities, Floppy Baby Syndrome

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Antipsychotics

Common psychiatric indications

Schizophrenia
- Antipsychotics are Dopamine antagonists against D2R, the mainstay of treatment of
Schizophrenia based on Dopamine Hypothesis
i.e. Increased pre-synaptic dopamine synthesis in Striatum
→ Hyper-dopaminergic transmission → Manifestations of Psychosis
- Exert effect via inhibition of Mesocortical dopaminergic pathways
Dopamine pathways
Functions Role in Schizophrenia

1. Mesolimbic hyper-dopaminergic
Motivation
VTA → Limbic System Accounts for Positive symptoms
Emotion
(Nucleus Accumbens/ Ventral e.g. Delusion, Hallucination
Reward
Striatum, and Amygdala)

VMPFC & OFPFC: Accounts for Negative symptoms

Social Cognition e.g. Affect Flattening, Avolition,
2. Mesocortical hypo-dopaminergic Anhedonia, Alogia, Asociality
VTA → PFC DLPFC:
Thinking, Planning, Accounts for Cognitive impairment
Working memory e.g. Memory loss

3. Nigrostriatal
ADR of Antipsychotics:
SNpc → Dorsal Striatum Motor Control
Extrapyramidal side effects (EPSE)
(Caudate, Putamen)

4. Tuberoinfundibular
Inhibit tonic Prolactin ADR of Antipsychotics:
Infundibular nucleus of Hypothalamus
release Hyperprolactinaemia
→ Medial eminence of APG

VTA = Ventral Tegmental Area; PFC = Prefrontal Cortex; VMPFC = Ventromedial PFC; DLPFC =
Dorsolateral PFC; SNpc = Substantia nigra Pars compacta; APG = Anterior Pituitary Gland

Dopamine receptors
- 5 Dopamine receptors; divided into D1-like & D2-like
families that antagonist each other
• D1-like family (D1R, D5R): ↑ intracellular cAMP
• D2-like family (D2R, D3R, D4R): ↓ intracellular cAMP
- D2R is the only one a/w psychotic symptoms
• Most concentrated in Cortex, Striatum, Limbic
System, Basal Ganglia, APG, Hypothalamus (i.e.
Mesolimbic & Mesocortical pathways)
• Blockade of Mesocortical & Mesolimbic pathways
→ Antipsychotic effect
• Blockade of Nigrostriatal pathway → Extrapyramimdal Syndrome (EPS)/ Extrapyramidal Side
Effects (EPSE)
• Blockade of Tuberoinfundibular pathways → Hyperprolactinaemia

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Outcome in Schizophrenia
- >80% patients with first episode of psychosis (FEP) respond to antipsychotics in their FEP
- High risk of relapse
• Major cause: Non-adherence to antipsychotics
• Recommend at least 1-2yr of maintenance treatment after positive symptom remission in FEP
- Withdrawal symptoms e.g. Tardive Dyskinesia, Nausea, Vomiting, Anorexia, Anxiety, Agitation,
Restlessness, Insomnia, Psychosis (?relapse)
- Tolerance due to skipping dose

Off Label Use of Antipsychotics

- Agitation (e.g. nervousness)
- Various headache conditions
- Anxiety disorders (limited trials, no effect, not FDA approved)
- To suppress hiccups
- Control various involuntary motor disorders e.g. Tourette syndrome, Huntington chorea
- Autism spectrum disorders (in children & adolescents)
- Alzheimer disease
- Depression (SGA include 5-HT2A antagonist e.g. SARI, NASA)
- Dementia

First Generation Antipsychotics (FGA)

- aka Typical or Conventional Antipsychotics
- Older, Cheaper
- Effective against Positive symptoms only

Examples
Chemical classes Drugs

Chlorpromazine (Largactil®), Thioridazine, Perphenazine (Trilafon®),

Phenothiazine
Trifluoperazine (Stelazine®), Fluphenazine# (Modecate®)

Thioxanthene Thiothixene, Flupentixol# (Fluanxol®), Zuclopenthixol# (Clopixol®)

Butyrophenone Haloperidol# (Haldol®)

Diphenylbutylpiperidine Pimozie

Substituted Benzamide Sulpiride (Dogmatil®)

# = Depot available (Flu- and -ol)

MOA
- Dopaminergic-2 receptor (D2R) antagonist → ↓ Dopamine in Mesolimbic pathway
→ Improve Positive symptoms
- Histaminergic-1 receptor (H1R) antagonist
- Adrenergic-1 or -2 receptor (α1R, α2R) antagonist
- Muscarinic receptor (mAChR) antagonist

ADR

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- More extrapyramidal side effects (EPSE)(due to ↓ Dopamine in Tuberoinfundibular pathway)
- Less metabolic side effects
- Other side effects depending on receptor blockade properties

Second Generation Antipsychotics (SGA)

- aka Atypical Antipsychotics
- Newer, expensive
- Effective against both Positive & Negative symptoms
- Efficacy comparable to FGA

MOA
- D2R antagonists → ↓ Dopamine in Mesolimbic pathway → Improve Positive symptoms
- 5-HT2AR antagonist → ↑ Dopamine in Mesocortical pathway → Improve Negative
symptoms
- Different SGAs have different additional receptors blockade properties
e.g. Amisulpride also block D3R, Olanzapine also blocks M1R & M2R, Sertindole also blocks 5-
HT2R, α1R

ADR
- Less EPSE
- More Metabolic side effects esp. Olanzapine
- Other side effects depending on receptor blockade properties

Clozapine (Clozaril®)
- The very first invented SGA but the last resort in treatment-resistant SZ
History
- First synthesised in 1959 with ability to block amphetamine- induced locomotor activity without
producing catalepsy in rodent
- It was subsequently withdrawn in 1975 after a series of deaths due to agranulocytosis in Finland
- Reintroduced in 1989 after its effectiveness in 30-60% of resistant schizophrenia was
demonstrated
- Current indications
• Failed 2 Antipsychotic with at least one being SGA with adequate duration and dosage
• Last resort for Tardive Dyskinesia
- Cognitive function improvements especially verbal fluency, immediate and delayed verbal
learning and memory, attention were noted
Common ADR
- Weight gain
- Hyper-salivation
- Sedation, Dizziness
- Exacerbation of obsessive-compulsive symptoms
- Postural hypotension, Hypertension, Hypotension
- Constipation
- Tachycardia
- Fever

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- Nocturia
Severe and life-threatening ADR
- Seizure esp. in high dose
- Liver failure
- Pancreatitis
- Intestinal obstruction
- Pericardial effusion/ Pulmonary embolism/ Myocarditis/ Cardiomyopathy
- Agranulocytosis/ Neutropenia
• 1-3% risk, dose-independent
• Peak between 4 and 18 weeks
• Require regular CBC+DC Q1week for 18w, then Q1month

Risperidone (Risperdal®)
- Not well tolerated by patients with Parkinson’s disease
- Benefits on primary negative symptoms and cognition including working memory, attention,
executive function, verbal learning and memory
- Well tolerated among elderly patients taking low dose
- Side effects include:
• Moderate weight gain
• Orthostatic/ postural hypotension
• Dose related hyperprolactinaemia and EPSE (Less than FGA but more than other SGA)
• Exacerbation of obsessive compulsive symptoms and tics
- *Risperidone is the only SGA with depot route

Olanzapine (Zyprexa®)
- Once-a-day administration with proven effectiveness for negative symptoms and possibly
cognition. Low extrapyramidal side effect profile
- Lower relapse rate than placebo and haloperidol during 1-year period study
- Side effects include:
• Dose dependent extrapyramidal side effects
• Weight gain can be significant
• Some patients develop T2DM
• Orthostatic/ postural hypotension
• Increase in liver enzymes and prolactin level
- CYP2D6 substrate (DDI with Fluoxetine, Paroxetine)

Quetiapine (Seroquel®) (Q仔)

- Highest serotonin/dopamine binding ratio hence least dopaminergic among the SGA
- Fewer extrapyramidal side effects and no effect on serum prolactin levels
- It has a flat dose-response curve with large variation of dose required
- Side effects include
• Headache
• Somnolence
• Dry mouth
• Weight gain
• Orthostatic/ postural hypotension
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• Animal studies suggest an increase risk of cataracts

Ziprasidone (Zeldox®)
- Parenteral formulation has been developed
- Favourable side effect profile with no weight gain and no prolactin elevation
- Major side effects are nasal congestion and somnolence.
- Increase QTc interval has been reported

Amisulpride
- Minimal EPSE and reduce negative symptoms in low doses
- Can increase prolactin level with associated endocrine effects

Sertindole
- Lowest potential for EPSE other than Clozapine
- Can cause prolongation of QTc interval

Iloperidone
- Potential to be made into a long acting form

Aripiprazole
- Partial agonist at D2/D3 & 5HT1A receptor with antagonist activity of 5HT2A
- No weight gain

FGA vs SGA
SGA
FGA
(excl. Clozapine)

Variable
Receptor profile Variable
5-HT2AR and D2R antagonism in common

D2R affinity High Lower

All dopaminergic
Site of action More Mesolimbic selective
pathways

EPSE Commoner Less common

Less common
HyperPRL Commoner Commoner in Amisulpride, Risperidone, Paliperidone
None in Quetiapine and Ziprasidone

Efficacy in negative Better

Lacking
symptoms (5-HT antagonism, D2 partial agonism, reduced EPSE)

Efficacy in affective Lacking except All have indications for either mania and/or depressive
symptoms Flupenthixol disorders except Amisulpride, Paliperidone, Sertindole

Increased risk esp. Olanzapine

Metabolic syndrome Variable
Aripiprazole & Ziprasidone → Weight neutral

Long QT Variable Sertindole → Significant risk

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ADR of Antipsychotics
- ADR depends on receptor antagonism profile and respective affinity
Mesocortical Pathway: Secondary negative symptoms
D2R Antagonism
Nigrostriatal Pathway: EPS/ EPSE
* more prominent in FGA due to
Tuberoinfundibular Pathway: Hyperprolactinaemia
higher affinity to D2R
Neuroleptic Malignancy Syndrome (NMS)

D2 Agonism Psychomotor activation e.g. Akathisia

H1 Antagonism Sedation, Drowsiness, Weight gain

Blurred vision, Dry mouth, Constipation, Sinus tachycardia, Urinary

mACh Antagonism
retention, Memory dysfunction

α1 Antagonism Priapism, Postural hypotension

α2 Antagonism Dizziness, Reflex Tachycardia

Other ADR Long QT, Long PR, Flat T, ST depression, HypoNa

Extrapyramidal Syndrome (EPS)/ Extrapyramidal Side Effects (EPSE)

- a/w long-term use (usu. after years, ≥6 months);
DSM-4 require ≥3 months exposure to neuroleptics to diagnose EPSE
- More likely in high-potency FGA (5% in adult) with persistence up to 68% within 25yr
- Less common in SGA (0.8% in adult)
Clinical presentation
1. Acute Dystonia
• i.e. Hyperkinesis/ Spasm, involuntary contraction
• e.g. Oculogyric crisis (fixed upward gaze 反⽩白眼), Spastic Torticollis/ Cervical Dystonia
• Dose-dependent, usu. present within days
2. Akathisia
• i.e. Motor restlessness (kathisis = sit down; akathisia = 坐唔定)
• e.g. Keep pacing, Leg fidgeting (un/䟴腳), Hand fidgeting
• Dose-dependent, usu. present within weeks
3. Parkinsonism/ Pseudo-Parkinsonism
• e.g. Rigidity, Resting tremor, Cognitive impairment
• Dose-dependent, usu. present within months
4. Tardive Dyskinesia
• Idiosyncratic, dose-independent, usu. occur after years (tardive = late onset)
• Painless, repetitive oro-facial-lingual movements (e.g. Tongue protrusion, Lip smacking,
Pouting, Lip puckering, Grimacing, Eye-blinking) or even truncal movement in severe cases
5. Rabbit Syndrome (rare); Ddx of Tardive Dyskinesia
• Only vertical oral movement resembling chewing movements of a rabbit
Management
- Central Anticholinergics e.g. Benzhexol (Artane®) - effective against Acute Dystonia,
Parkinsonism, and Rabbit Syndrome
- Benzodiazepines - effective against Acute Dystonia, Akathisia
- β-blockers e.g. Propranolol - effective against Akathisia, Parkinsonism
- Tardive Dyskinesia: Stop anticholinergics, Switch to SGA, Reduce dosage, Vitamin E,
Tetrabenazine, Switch to Clozapine as last resort (less EPSE due to less selective action)
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Hyperprolactinaemia
Clinical presentation
- Galactorrhoea (only in female with developed breast tissue)
- Tertiary Hypogonadism (Pituitary-Adrenal-Gonadal axis)
• Delay/ Absent puberty
• Growth retardation, 2° sexual characteristics regression
• Infertility, Reduced libido
• Acne, Hirsutism
• Female: Anovulation, Amenorrhoea (Pseudopregnancy)
• Male: Impotence, Erectile dysfunction, Gynaecomastia, Testicular atrophy

Neuroleptic Malignant Syndrome (NMS)

- Rare, 1 in 500 (0.01-3%), MEDICAL EMERGENCY, potentially fatal
Clinical presentation
- Insidious onset, occur after 1-3 days up to weeks since insult
- Fever or Hyperthermia, Diaphoresis/ Hyperhydrosis
- Psychological aphasia/ Mutism
- Tachycardia, High/ unstable BP
- Mydriasis
- Myolysis, High Creatinine Kinase (CK)
- Immobility
- Leadpipe rigidity
- Hyporeflexia
Management
- r/o Serotonin Syndrome (Acute, Clonus, Hyperreflexia)
- r/o Malignant Hyperthermia (due to GA/ NMB toxicity)
- Immediate drug withdrawal
- Supportive treatment
- Dantrolene (RyR antagonist)
- Dopamine agonist (Bromocriptine, Levodopa)

Metabolic Side Effects

- More common in SGA esp. Olanzapine
Clinical presentation
- Obesity
- HyperG/ IGT/ DM
- Hyperlipidaemia
- Hypercholesterolaemia
- Hyperprolactinaemia

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Assessment of ADR of Antipsychotics

Triple assessment
- History
- PE
- Investigations
• Metabolic: Lipid profile, Fasting plasma glucose, HbA1c, BMI esp. for SGA
• Clozapine: CBC+DC Q1w x 18w and then Q1month

Assessment tools
- Abnormal involuntary movement scale
- Barnes Akathisia rating scale
- Simpson-Angus Extrapyramidal side effect scale
- The Udvalg for Kliniske Undersogelser (UKU) Side effect rating scale

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Mood Disorders
Depressive Disorders
- Depression is a biological disorder, an illness, not a weakness

Spectrum of Depressive Disorders

DSM-5: Depressive disorders
- Disruptive Mood Dysregulation Disorder
• New entity in DSM-5 to address concerns about over-diagnosis and over-treatment of Bipolar
Disorder in Children
• Refers to children with persistent irritability and frequent episodes of extreme behavioural
dyscontrol up to 12yo
- Major Depressive Disorder (MDD)
• The classical condition in the group of depressive disorders
• Characterised by recurrent episodes of major depressive episodes
- Persistent Depressive Disorder (Dysthymia)
• A more chronic form of depression (>2yr in adults, >1yr in children)
• Replaced DSM-4 diagnostic categories of Chronic Major Depression and Dysthymia
- Premenstrual Dysphoric Disorder
• A depressive disorder that begins sometime following ovulation and remits within a few days
of menses with marked impact on functioning
- Substance/ Medication-induced Depressive Disorder
- Unspecified Depressive Disorder
* Common features of all of these disorders is the presence of sad, empty, or irritable mood,
accompanied by somatic and cognitive changes. What differs among them are duration, timing,
or presumed aetiology.

ICD-10: F30-F39 Mood [affective] disorders

- Manic episode
- Bipolar affective disorder
- Depressive episode
• Mild vs Moderate vs Severe vs Severe with Psychotic s/s
• w/ vs w/o Somatic syndrome
• Extra: Other depressive episodes, Depressive episode, unspecified
- Recurrent depressive disorder
- Persistent mood [affective] disorders
• Cyclothymia
• Dysthymia
- Other mood [affective] disorders
- Unspecified mood [affective] disorders

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Epidemiology of Depressive Disorders

- 359 million people worldwide (WHO, 2012)
- 1 out of 10 men, 1 out of 5 women have Depression
- Lifetime prevalence of 15% (c.f. 1% of Schizophrenia)
- Mean age of onset ~20-30yo
- Concordance rate in Monozygotic twin = 50%
- 4th leading cause of disability worldwide
- 15-30% mortality (Risk ratio: 1.2-4.0)
• Behavioural risk factors e.g. Poor drug compliance, Inactivity, Alcoholism
• Biological risk factors e.g. Altered thrombogenesis
• Subclinical diseases/ Prevalent disease e.g. Cardiovascular disease

HK
- est. 400,000 people with Depression
- Risk of women having depression = 1.43X of men
- 18.45% unemployed have depression (3X risk of employed)
- Costs $85 billion HKD yearly for lost of productivity (e.g. sick leave, un-education)

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Aetiology of Depressive Disorders

Evolution of proposed mechanisms
- Hippocrates (460-357 B.C.): Melancholia emerges when environmental influences, such as
planet alignment, cause the spleen to secrete black bile, which darkens the mood….lmao
- Burton (1621): Depressed people are often born of melancholy parents
- Kraepelin (1856-1926): Detected a genetic contribution to manic-depressive illness
- Meyer (1866-1950): Coined the term “psychobiology”; depression was due to biological and
environmental factors combined
- Bunney and Davis (1965): Biogenic amine hypothesis – depression was caused by a deficiency
in brain concentration or receptor function of NE, dopamine, and 5-HT
- Carroll and Davies (1970): Hypothalamic-pituitary-adrenal / -thyroid axes correlation to
depression
- Janowsky et al. (1972): Cholinergic activity relative to NE activity is associated with mood
disorders

Diathesis-Stress Model in Depression

- Diathesis: Genetic factors, Childhood trauma
- Stress: Chronic difficulties, Struggling to cope, Adverse life events

Cognitive Theory: Cognitive distortions in depression

Common cognitive distortions in depression
- Personalisation 過度⾃自責: Assume responsibility for things that have little/ nothing to do with
oneself
- Jumping to conclusion/ Arbitrary inference 妄下判斷: Draw a conclusion in absence of evidence
- Overgeneralisation 以偏概全: Draw a general conclusion on the basis of a single incident
- Mental filtering/ Selective abstraction 斷章取義: Focus on a detail and ignoring more important
features of a situation

Psychoanalytic Theory
- Freud: Depression is like a grief reaction to loss of an important relationship (e.g. parents)

Secondary Depression
- Head trauma
- Infection
- Stroke, HF, MI
- Metabolic disturbance e.g. HypoMg, B3 deficiency, B12 deficiency
- Hypothyroidism
- Cushing Syndrome, Adrenal insufficiency
- Hyperparathyroidism
- Vitamin deficiency
- Multiple sclerosis, neurodegeneration
- Drug intoxication or withdrawal
- Iatrogenic/ Drugs
• Cardiac & Anti-HT e.g. β-blockers
• Sedatives
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• Stimulants and Appetite suppressants
• Steroids
• Antibiotics
• Analgesics and Anti-inflammatory drugs
• Cancer drugs

Pathogenesis of Depressive Disorders

Functional and structural changes in Depression
- ↑ Activities in VMPFC → Hypersensitivity to pain, anxiety, depressive rumination, tension
- ↓ Activities in DLPFC → Psychomotor retardation, apathy, inattention and poor working memory
- ↓ Connectivity between Amygdala and Anterior cingulate cortex (ACC) → ACC fails to serve its
inhibitory role in emotional regulation
- ↓ Hippocampal volume
• Predisposing factor for depression
• Changes also accumulates in the course of the disease

Neuro-chemical/ Hormonal changes in Depression Brain-derived Neurotrophic Factor (BDNF)

- ↑ CRH, Cortisol - May be a downstream target of drugs
- Anti-depressant-like effect
- ↑ Pro-inflammatory cytokines - Protects against neuronal damage
- ↓ BDNF - Decreased level in depressed patients
- ↓ 5-HT neurotransmission - Stress → ↑ Cortisol → BDNF gene
suppressed
- ↓ NE neurotransmission - May also explain treatment time lag

Hypothalamic-Pituitary-Cortisol Hypothesis
Hypothesis
- ↑ CRH → ↑ Cortisol → ↓ Hippocampal volume, ↓ BDNF → ↓ Neurogenesis → ↓ Cognitive
and memory impairment in depression
- Antidepressants → Activate cAMP cascade → ↑ CREB Induction→ ↑ BDNF, Neurogenesis →
Stabilise and/or improve depression
Contradiction to hypothesis
- Reduced hippocampal volume not observed in some studies
- BDNF knockout mice do not have depression or anxiety
- Social-stressed animal have increased BDNF levels in contrary

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Monoamine Deficiency Hypothesis
Hypothesis
- Depletion of Noradrenaline (NE) → Loss of Alertness, Wakefulness, Energy (Locus Coeruleus)
- Depletion of Serotonin (5-HT) → Loss of Obsession, Compulsions (Raphe nuclei)
• Treatment-related targets: 5-HT1A, 2A, 2C receptor
- Depletion of Dopamine (DA) → Loss of Pleasure, Motivation, Award, Attention
Evidence supporting hypothesis
- “Manufacturer” level
• inhibition of tyrosine hydroxylase or depletion of dietary tryptophan
• increased frequency of a mutation affecting the brain-specific form of tryptophan hydroxylase
(TPH-2)
• increased specific ligand binding to MAOA
- “Customer” level
• sub-sensitive 5-HT1A receptors
• malfunctioning 5-HT1B receptors and/or decreased levels of p11
• polymorphisms of the serotonin-reuptake transporter
• inadequate response of G-proteins to neurotransmitter signals
• reduced levels of cAMP , inositol, and CREB (cAMP response-element binding protein)
Contradiction to hypothesis
- Monoamine deficiency/ dysfunction not observed in all depressed patients
- Time lag between serum monoamine conc. and clinical benefits
- Deterioration of symptoms in first week of treatment is common
- Removal of serotonin precursor (Tryptophan) does not cause depression

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Clinical presentation of Depressive Disorders

Psychological
- Depressed mood
• Often described as depressed, sad, hopeless, discouraged, or “down in the dumps”
• Nearly always present at a certain degree in depressed patients
• May be denied at first but subsequently elicited by interview (e.g. by pointing out that the
individual looks as if he/she is about to cry)
• Some may complain of feeling empty, having no feelings, or feeling anxious, the presence of
depressed mood can be inferred from facial expression and demeanour
• Mood in children and adolescents may be irritable or cranky rather than depressed
- Loss of interest or pleasure/ Anhedonia
• Nearly always present, at least to some degree
• e.g. Reported less interested in hobbies, “not caring anymore”, or not feeling enjoyment in
activities that were previously considered pleasurable, or noticed social withdrawal, or noticed
neglect of pleasurable avocations by family, or loss of libido
- Impaired ability to think, concentrate, or make even minor decisions
• In the elderly, memory difficulties may be the chief complaint and may be mistaken for
Dementia (aka Pseudo-dementia) that often fully abate after successful treatment
• However, a major depressive episode may sometimes be the initial presentation of an
irreversible Dementia (Behavioural psychological symptoms of Dementia, BPSD)
- Sense of Worthlessness or Guilt (Delusional or Near-delusional)
- Sense of Hopelessness
- Suicidality
• May range from a passive or active idea (32.5%), to plan (16.9%), to attempts (5.5%)
• Depressed patients account for 50% of completed suicide
• 1970 data: 15% committed suicide (Narrow definition, only include severe cases)
• Current data: 6.7%
• Higher risk when mood is improving, around discharge

Somatic
- Appetite change (either reduction or increase)
- Significant weight change (i.e. +/-5% within 1month)
- Sleep disturbance
• Can p/w Induction insomnia (i.e. difficulty falling sleep),
or Middle insomnia (i.e. waking up during the night and difficult returning to sleep),
or Terminal insomnia/ Early morning awakening (commonest),
or even Hypersomnia in terms of prolonged nocturnal sleep or increased daytime sleep
• Reduced REM latency (i.e. enter REM sleep earlier), Shortened NREM Stage 3-4
- Psychomotor changes include retardation (e.g. slowed speech, thinking, and body
movements; increased pauses before answering; speech that is decreased in volume, inflection,
amount, or variety of content, or muteness) or agitation (e.g. inability to sit still, pacing,
handwringing; or pulling or rubbing the skin, clothing, or other objects)
- Decreased energy, tiredness, fatigue
• Common symptoms

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• May report sustained fatigue w/o physical exertion, or require substantial effort with the
smallest tasks, or reduced efficiency of accomplishing tasks
- Constipation
- Pain (reported by 60% patients at Dx)
• Increased risk of developing chronic MSS pain, headache, chest pain up to 3yr later
• 1/3-1/2 patients presenting to pain clinic have current major depression
• Depression is a better predictor of disability than pain intensity and duration
- Impotence due to loss of libido

Social
- Not coping at work
- Social withdrawal

Cognitive
- Cognitive biases → Rumination (i.e. deep thoughts)
- Selective attention to negative events
- Negative appraisal of trivial social cues
- Selective activation of negative memories
- Internal (self) attribution of failure rather than external (situational)

Natural history of Major Depressive Disorder

- Variable onset, peak in 20-30yo
- Variable prognosis
- 40% recovery begin within 3 months, 80% begin within 1 year
- Recency of onset is a strong determinant of likelihood of recovery

Poor prognostic factors

- Psychotic features
- Prominent anxiety
- Personality disorder
- Severe symptoms

High recurrence risk factors

- Higher in severe preceding episodes
- Young
- Hx of recurrence
- Persistence of depressive symptoms during remission
Mnemonics: A SAD FACES
Anhedonia
Sleep disturbance
Appetite & weight changes
Depressed mood
Fatigue
Agitation (or Retardation)
Concentration
Esteem (worthless/ hopeless/ guilt)
Suicidality
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Diagnosis of Depressive Disorders

DSM-5 Criteria of Major Depressive Disorder
A. 5 (or more) of the following symptoms have been present during the same 2-week period
and represent a change from previous functioning; at least one is either (1) depressed mood
or (2) loss of interest or pleasure
Note: Do not include symptoms that are clearly attributable to another medical condition
1. Depressed mood, subjectively (e.g. feels sad, empty, hopeless) or observed (e.g. appears
tearful)(Note: can be irritable in children and adolescents)
2. Markedly diminished interest or pleasure in all, or almost all, activities
3. Significant weight loss when not dieting or weight gain (e.g. a change of >5% body weight
in a month), or decrease or increase in appetite
(Note: In children, consider failure to make expected weight gain)
4. Insomnia or Hypersomnia
5. Psychomotor agitation or retardation (observed by others, not just merely subjective
feelings of restlessness or being slowed down)
6. Fatigue or loss of energy
7. Feelings of worthlessness or excessive or inappropriate guilt
(which may be delusional)(not merely self-reproach or guilt about being sick)
8. Diminished ability to think or concentrate, or indecisiveness (either by subjective
account or as observed by others)
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation w/o a
specific plan, or a suicide attempt or a specific plan for committing suicide
(The criterion symptoms must be present nearly every day to be considered present)
B. The symptoms cause clinically significant distress of impairment in social, occupational, or
other important areas of functioning
C. Not due to substance use or another medical condition
Note: Criteria A–C constitute a major depressive episode. Major depressive episodes are
common in bipolar I disorder but are not required for the diagnosis of bipolar I disorder.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a natural
disaster, a serious medical illness or disability) may resemble a depressive episode. Presence of a
major depressive episode in addition to the normal response be carefully considered, based on
individual’s history and cultural norms.
D. Not better explained by another mental disorder
E. There has never been a manic episode or a hypomanic episode
Specifiers
- with anxious features e.g. keyed up, restless, decreased concentration, irrational fear, fear of
loss of control
- with mixed features
- with rapid cycling (i.e. ≥4 episodes/yr)
- with melancholic features e.g. Severe Anhedonia, Early morning awakening, Weight loss,
Profound feelings of guilt
- with atypical features e.g. Mood reactivity, Increased appetite, Weight gain, Hypersomnia,
Leaden paralysis (i.e. sense of limb heaviness), Interpersonal rejection sensitivity
- with mood-congruent psychotic features (i.e. consistent with typical depressive themes)
- with mood-incongruent psychotic features
- with catatonia
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- with peripartum onset (during pregnancy/ <4w-postpartum)
- with seasonal pattern
- in partial remission vs full remission (i.e. no significant s/s of disturbance for 2month)
- Severity
• Mild: Few symptoms in excess of those required to make diagnosis
• Moderate: Between mild and severe
• Severe: Substantial number of symptoms in excess of those required to make diagnosis,
seriously distressing intensity of symptoms, marked interference with social/ occupational
functioning

Major Depressive Manic Hypomanic

Diagnosis (DSM-5)
Episode (MDE) Episode Episode

Regardless Yes Regardless Bipolar I Disorder

Yes No Yes Bipolar II Disorder

Yes No No Major Depressive Disorder (MDD)

Persistent No No Persistent Depressive Disorder/ Dysthymia

Ddx of Major Depressive Episode/ Disorder

Ddx Differing features

Mainly sense of emptiness and loss (c.f. Depressed mood and Anhedonia)
Dysphoria drop in intensity over days to weeks (c.f. Persistent)
Occurs in waves a/w thoughts or reminders of the deceased (c.f. Persistent)
Normal bereavement May be accompanied by positive emotions and humour (c.f. None)
Preserve self-esteem (c.f. Worthlessness in MDE)
Suicidality because of the deceased and possibly “joining” the deceased
(c.f. due to worthlessness, undeserving or unable to cope with depression)

Presence of Manic or Hypomanic episodes

Bipolar I or II Disorder
(MUST r/o before giving Antidepressants; may precipitate a Manic episode)

Cyclothymic Disorder Numerous periods of hypomanic and depressive symptoms

Meet Criterion A of Schizophrenia

Schizoaffective Disorder
Delusion or Hallucination for 2 weeks w/o Depressive symptoms

Psychotic Disorders with

Predominantly Psychosis with concurrent Depressive symptoms
Depressive symptoms

Medical condition e.g. Stroke, Huntington, Parkinson, Brain trauma, Cushing, Hypothyroidism

Substance/ drug induced e.g. Steroid, Triptans, OC pills, Cocaine withdrawal

Other Ddx of MDD

- Dysthymic Disorder (Depressed mood > 2yr)
- Adjustment Disorder (Stressor identified, onset < 3 month, Resolve < 6 month)
- Mixed Anxiety Depressive Disorder (MADD)
- Borderline personality disorder

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DSM-5: Major Depressive Episode ICD-10: Depressive Episode

Mild: ≥2 Core + ≥2 Asso. symptoms
≥5 symptoms with ≥1 Core Moderate: ≥2 Core + ≥3 Asso. symptoms
Severe: ≥2 Core + ≥4 Asso. symptoms

Core symptoms

1. Depressed mood
1. Depressed mood
2. Loss of interest
2. Loss of interest or pleasure in activities
3. Decreased energy

Asso. symptoms

3. Fatigue or loss of energy

4. Significant weight loss or decrease or increase in 4. Diminished appetite

appetite

5. Insomnia or Hypersomnia 5. Disturbed sleep

6. Psychomotor agitation or retardation

7. Feelings of worthlessness or excessive or 6. Ideas of guilt and unworthiness

inappropriate guilt

8. Diminished ability to think or concentrate, or 7. Reduced concentration and attention

indecisiveness

9. Recurrent thoughts of death, recurrent suicidal 8. Ideas or acts of self-harm or suicide

ideation w/o a specific plan, or a suicide attempt or a
specific plan for committing suicide 9. Bleak and pessimistic view of the future
10. Reduced self-esteem and self-confidence

Symptom assessment: PHQ-9 (Patient health questionnaire-9)

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Edinburgh Postpartum Depression Scale (EPDS)
- A screening tool for postpartum depression
- in the past 7 days, described from “Not at all” to “All the time”
1. Have you felt happy
2. Have you been laughing
3. Look forward to things & enjoy things
4. Anxious or worried for no good reason
5. Scared or panicky for no good reason
6. Things have been getting on top of me, inability to cope well compared to before
7. So unhappy that difficulty sleeping
8. Feel sad/ miserable
9. Crying
10. Thought of self-harm and suicide

Mood assessment: Emotional Stroop Test/ Task

- Assess whether reaction time (e.g. to name the colour of a word) is interfered with by emotional
content of the word e.g. SAD
- Slower in depressed than non-depressed, compared to neutral words
- False +ve: Manic patient also show depression in Stroop task

Low-dose Dexamethasone Suppression Test (LDDST) in Depression:

Non-Suppressible high level of Cortisol (HPA Axis Theory)

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**Approach to Depression**
Depressive symptoms
Core symptoms
- Pervasive depressed mood 最近呢個⽉月⼼心情如何？幾乎每⽇日? ⼀一⽇日有冇超過⼀一半時間?
- Duration 幾時開始？ 情緒低落落時，有冇某段時間特別差？持續幾耐? (>2 weeks?)
- Recent bereavement/ stressor 有冇發⽣生咗啲唔開⼼心嘅事？
- Usual interest & hobbies 以前⼀一向有乜消遣、興趣？最鍾意做乜？咁⽽而家做乜野多？
- Loss of interest & pleasure 近來來有冇做呢啲野？點解唔做？做嘅時候有冇以前咁有樂樂樂樂趣？
Other symptoms
- Sleep disturbance 訓教訓得好唔好？⼀一⽇日訓幾耐？幾點⾄至幾點？同以前有冇分別？
- Appetite & Weight loss 胃⼝口點？同以前有冇分別？體重有冇改變? 有冇瘦左? 褲頭鬆左？
- Poor concentration & indecisiveness 有冇覺得好難集中精神？做野有冇慢左？
- Worthlessness or Guilt 有冇負⾯面嘅想法? 例例如內疚、對將來來冇希望/信⼼心、⽣生冇可戀?
- Psychomotor retardation or agitation 動作或者講野俾⼈人話慢左, 或者相反坐立不安
- Recurrent suicidality 有冇⾃自殺嘅想法甚⾄至試過⾃自殺? 呢個想法會唔會⼀一直洗腦海海入⾯面重覆?
- Distress/ Functional impairment 對你黎黎講, 會唔會好⼤大困擾? 對⽇日常⽣生活有咩影響?
- Loss of libido (if appropriate) 有冇性⽣生活？同以前有冇分別？
- Somatic symptoms of depression ⾝身體點樣？有冇頭痛、背痛、便便秘等症狀狀？

Psychiatric co-morbidities/ Concurrent symptoms

- Adjustment Disorder 最近三個⽉月, 家庭、婚姻、⼯工作/ 學業⽅方⾯面有冇困難？解唔解決到？
- Bipolar 除左唔開⼼心, 會唔會有⼀一段時間情緒⾼高漲、興奮, 或者好躁
- Anxiety 會唔會有焦慮嘅感覺, 例例如坐立不安、全⾝身嘅肌⾁肉緊繃、恐懼感之類類?
- Hallucination
• 最近有冇⼀一啲唔尋常嘅經歷、聽到聲⾳音、睇到影像?
• 唔尋常嘅經歷/ 聽到聲⾳音/ 睇到影像持續左幾耐? 有冇兩兩個禮拜, 當時⼼心情係點?
• Depressed during hallucination = Depression with psychotic features
• Not depressed during hallucination = Schizoaffective Disorder
- Delusion
• Nihilistic delusion 覺得⾃自⼰己、⾝身體、思想、⾝身邊嘅⼈人同埋呢個世界都係虛無嘅?
• Persecutory delusion 覺得⾝身邊的⼈人對你點？有冇⼈人想對付你？係啲乜野⼈人？點解佢地要咁做？
你點發現佢地要咁做？佢地想點害你？
• Delusion of guilt 覺得⾃自⼰己對唔住⼈人地、對唔住呢個世界?
• Hypochondriacal delusion 覺得⾃自⼰己⾝身體有咩病?
- Substance abuse 我循例例問下, 請問你有冇吸食藥物嘅習慣?
- Suicidal risk assessment if indicated

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**Approach to Postpartum Mood**

Edinburgh Postpartum Depression Scale (EPDS)
- A screening tool for postpartum depression
- in the past 7 days, described from “Not at all” to “All the time”
1. Have you felt happy
2. Have you been laughing
3. Look forward to things & enjoy things
4. Anxious or worried for no good reason
5. Scared or panicky for no good reason
6. Things have been getting on top of me, inability to cope well compared to before
7. So unhappy that difficulty sleeping
8. Feel sad/ miserable
9. Crying
10. Thought of self-harm and suicide Risk factors of perinatal mood problems
- Past psychiatric Hx esp. Puerperal
Important history blues, PND, Postpartum psychosis
- Current pregnancy - Obstetric complications
• Advanced maternal age? - Poor neonatal outcome
• Marriage? - FHx of Bipolar or Postpartum
• Wanted & Planned pregnancy? psychosis
• Obstetric complications? - Sleep deprivation
• Neonatal complications? - Increased environmental stress
- Personal history - Lack of partner support
• Previous episodes of Puerperal blues,
Postpartum depression, Postpartum psychosis?
• Pre-existing depression or other mental illness?
• Psychotic symptoms
- Family history
• Family support esp. from Partner/ Spouse, relation with own mother
• FHx of Bipolar, Postpartum psychosis
- Social history
• Alcohol, Substance abuse?
• Other environmental stress e.g. Financial difficulties

Risk assessment
- Suicidal risk
- Infanticidal risk: Any thoughts to harm the baby?
- Thoughts about future
• Ability to take care of baby and self (e.g. groceries)
• Ability to go back to work
• Who to look after baby

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Antidepressants
- There is no ideal antidepressant for depression
- All are a/w problems though some are better tolerated
- Choice is determined by individual clinical circumstances esp. co-morbidities and medications
- Duration of treatment
• First depressive episode: 6 months
• Recurrent Depressive Disorder: 2 years
- Antidepressant time lag: 4 weeks in average
• Improve Neuro-vegetative symptom first (within 1-2 weeks) → Have energy to attempt suicide
• Improve Emotional and Cognitive symptoms later (4 weeks)

Classes
- Monoamine Oxidase Inhibitor (MAOI)
- Tricyclic/ Tetracyclic Antidepressants (TCA)
- Selective Serotonin Receptor Inhibitors (SSRI)
- Selective Serotonin Norepinephrine Receptor Inhibitor (SNRI)
- Serotonin Antagonist and Reuptake Inhibitor (SARI)
- α2-Adrenergic Antagonist/ Norepinephrine Antagonist-Serotonin Antagonist (NASA/ NaSSA)
- Norepinephrine Reuptake Inhibitor (NRI)
- Melatonin Receptor Agonist (MRA)

Recommended approach
- 1st line in elderly: Fluoxetine
- 1st line in suicidal risk: Fluoxetine (the only antidepressant w/o black box warning of suicide risk)
- 1st line in young + low suicidal risk: Amitriptyline

Q: Why is there a treatment lag?

1. Low BDNF level, suppressed by high cortisol, takes time
to go from gene to protein
2. SSRI inhibit 5-HT reuptake in Raphe nuclei in Brainstem
→ Excess 5-HT bind to auto-receptors
→ -ve feedback on 5-HT production
→ Gradual down-regulation of auto-receptors & restored
cell firing and 5-HT release
→ SSRI can now inhibit 5-HT reuptake in synaptic cleft

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Non-Pharmacological Management of Depressive Disorder

- Electroconvulsive Therapy
- Transcranial Magnetic Stimulation
- Transcranial Direct Stimulation
- Psychotherapy e.g. Cognitive Behavioural Therapy (CBT), Interpersonal Therapy

Electroconvulsive Therapy (ECT)

Indications
- Depression
• Severe depression as by diagnostic criteria in DSM/ ICD or severe symptoms e.g. Marked
weight loss, Psychomotor retardation
• Psychotic features in depression e.g. Delusion
• Strong suicidal ideation
• Postpartum depression (risk of infanticide)
- Schizophrenia
• Catatonic Schizophrenia
- Manic/ Bipolar Disorder
• Severe Mania
• Treatment-resistance Mania
• Mixed episodes of Bipolar
Issues
- No absolute contraindication
- Major stigmatisation problem
Technique
- Pretreatment evaluation
- Use of atropine, methohexital & suxamethonium/ succinylcholine
- Done under GA
- Bilateral electrode placement e.g. Bi-temporal, Bi-frontal
- Unilateral electrode placement
Side effects
- Anterograde amnesia (Gone within days-weeks; never long-term)
- Headache
- Muscle pain
- Broken teeth
- Mortality 0.01% in the past when Psychiatrists have to anaesthetise the patient themselves;
now almost none

Transcranial Magnetic Stimulation (TMS)

- Non-invasive
- Limited side effects, No need GA
- Suitable for use in medically unwell patient who cannot tolerate antidepressants or ECT
- Hand-held, plastic-coated coil placed close to the scalp
- Available in Castle Peak Hospital but not available in QMH because of departmental poverty
(WC Chan, 2018)

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Transcranial Direct Stimulation (TCDS)
Mechanism
- Anode: Increase cortical activity and excitability
- Cathode: Reduce cortical activity and excitability
- Modulates spontaneous neuronal network activity
- Modifies responsively of the targeted brain regions to afferent input or efferent demand

Psychotherapy
- Patient selection and depression type affect outcome
Approaches
- Psychodynamic approach
- Cognitive (behavioural) approach/ Cognitive Behavioural Therapy (CBT)
• Focuses on cognitive distortions
• Addressing maladaptive patterns
• Homework is important
• Equal in efficacy and fewer side effects
• Combined drug and CBT for severe depression
- Interpersonal approach/ Interpersonal Therapy
• Medical model of depression
• Interpersonal problems have early “roots”
• Three treatment phases
• Four areas of focus:
- Unresolved grief
- Social role dispute
- Social role transitions
- Interpersonal deficits
- “Integrative” approach
- Family approach
- Group approach

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Bipolar Disorders

Spectrum of Bipolar Disorders

Presentation DSM-5 ICD-10

Manic Episode
Hypomanic episode(s) only Hypomanic Episode - Hypomania
Manic episode(s) only Manic Episode
Bipolar I Disorder
Manic + Major Depressive episodes
Bipolar Affective Disorder
Hypomanic + Major Depressive episodes Bipolar II Disorder
Persistent mood [affective]
Hypomanic + Mild Depressive episode Cyclothymic Disorder disorders
- Cyclothymia

DSM-5: F31 Bipolar and Related Disorders

- Bipolar I Disorder
- Bipolar II Disorder
- Cyclothymic Disorder
- Substance/ Medication-Induced Bipolar and Related Disorder
- Bipolar and Related Disorder Due to Another Medical Condition
- Other Specified Bipolar and Related Disorder
- Unspecified Bipolar and Related Disorder

ICD-10: F30-F39 Mood [affective] disorders

- Manic episode
- Bipolar affective disorder
- Depressive episode
- Recurrent depressive disorder
- Persistent mood [affective] disorders
- Other mood [affective] disorders
- Unspecified mood [affective] disorders

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Epidemiology of Bipolar Disorders

Bipolar I Disorder
- Lifetime prevalence: 0.3-1.6%
- M=F
- Mean age of onset of first mood episode ~18yo (15-24)
- Accurate diagnosis is often delayed by 5-10 years
- 83% cases > 4 episodes, 43% cases > 7 episodes
- 1/3 attempt suicide
- 10-20% completed suicide (Risk factors: Suicidal Hx and Prominent depressive symptoms)
- Increased risk of psychiatric and medical comorbidity
- Increased healthcare and welfare service utilisation
- 9th leading cause of disability-adjusted life years (DALY) under mental, neurological, and
substance use disorders (2010) (1st cause being Depressive disorder)

Bipolar II Disorder
- Lifetime prevalence: 3.7%
- Mean age of onset ~25yo, slightly later than Bipolar I but earlier than MDD
- 12% have initial diagnosis of MDD until a Hypomanic episode occurs
- 5-15% Bipolar II eventually develop a Manic episode and diagnosed of Bipolar I

Aetiology of Bipolar Disorders

Primary Bipolar
Genetic
- 79% heritability
- ↑ risk if 1st degree relative diagnosed with Bipolar, Depression or other psychiatric disorders
- Twin concordance rate: Monozygotic twin 75%, Dizygotic twin 5-25%
- Some overlap with genes involved in Schizophrenia and Circadian rhythm regulation
- Biochemical esp. Dopaminergic, Secondary messenger, Mitochondrial, HPA axis, Thyroid
- Neuroimaging evidence of structural and functional abnormalities
Environmental risk factors
- High socioeconomic status
- Born in high-income countries (1.4% vs 0.7%)
- Significant life events e.g. Divorced, Widowed (severe stress usu. precede 1st manic episode)
- Poor social support
- Low care and overprotective parents
- Poor attachment relationship
- Childhood abuse
- Sleep deprivation
- Circadian and social rhythm disruption

Secondary Bipolar
- Drugs: Steroids, Levodopa, Stimulants (Cocaine, Amphetamine)
- Medical illness: Frontal lobe lesion, Thyrotoxicosis, Cushing Syndrome
- Electroconvulsive Therapy (ECT)
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Clinical presentation of Bipolar Disorders

Natural history
- Episodic (relapsing and remitting), but has a predominant polarity
- Average frequency of relapse
• 0-10yr of diagnosis: 4 major episodes in first 10 years
• ≥10yr of diagnosis: Increase to 1 episode/yr
• Rapid cyclers (10-15%) is defined as ≥4 episodes/yr (commoner in Female)
• Bipolar II tends to have more frequent depressive and hypomanic episodes than Bipolar I and
MDD
- Median duration of episodes if untreated
**all manic or depressive episodes will recover spontaneously**
• Manic episodes: 4 months
• Depressive episodes: 6 months
- More residual symptoms after depressive episodes

Manic Episode
- Elated mood (Happy) or Irritable mood
- Less sleep needed than usual - usu. the first symptom
- Increased energy and overactivity
- Rapid thinking and speech
- Lack of inhibitions, impaired judgement, recklessness
- Over-confident with big ego
- Grandiose delusions
- Lack of insight

Ddx of a Manic episode

- Hypomanic Episode
- Secondary to substance abuse/ medication/ medical condition e.g. Thyrotoxicosis,
Frontotemporal lesion (esp. onset of manic symptoms in late mid-life or late-life)
- Major Depressive Disorder with Irritability and Anxious distress
- Attention Deficit and Hyperactivity disorder (ADHD)
- Personality disorder with prominent irritability

Hypomanic Episode
~Manic episode but shorter and milder, NOT severe enough to cause functional impairment

Psychiatric Comorbidities
- Anxiety Disorder (Panic Disorder, Agoraphobia, Social phobia, GAD, OCD, PTSD)
- Drug Abuse and Alcohol abuse
- Sleep Disorder
- Eating Disorder
- ADHD
- Psychotic Disorder
- Personality Disorder

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Medical Comorbidities
- Cardiovascular and metabolic disease: Obesity, DM, Hypercholesterolemia
• Partly due to increased alcohol and substance use, unhealthy diet, physical inactivity, social
isolation, unemployment, low education and socio-economic status, stress, poor sleep and
mental health, and childhood abuse
• Overlapped genetic predisposition
• Side effects of pharmacotherapy, e.g. Valproate, 2nd gen. Antipsychotics

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Diagnosis of Bipolar Disorders

DSM-5 Criteria for Manic Episode
A. A distinct period of abnormally & persistently elevated, expansive (OR irritable) mood AND
abnormally & persistently increased goal-directed activity or energy lasting at least 1 week
and present most of the day, nearly every day (or any duration if hospitalisation is necessary)
B. 3 or more of the followings (4 or more if mood is only irritable)
1. Inflated self esteem or grandiosity
2. Decreased need for sleep (e.g. feel rested after only 3 hours of sleep)
3. More talkative than usual or Pressured speech
4. Flight of ideas or Racing thoughts (subjective experience that thoughts are racing)
5. Distractibility (i.e. attention too early drawn to unimportant or irrelevant external stimuli)
6. Increased goal-directed activity (either socially, at work or school
or sexually) or psychomotor agitation
Mnemonic for Manic
7. Excessive involvement in activities that have a high potential for
episode: DIG FAST
painful consequences
Distractibility
(e.g. engaging in unrestrained buying sprees, sexual
Indiscretion
indiscretions, or foolish business investments)
Grandiosity
C. Marked impairment in functioning, observable by others, pr to
Flight of idea
necessitate hospitalisation to prevent harm to self or others, or
Agitation
there are psychotic symptoms
Sleep need decrease
D. Not due to alcohol, substance, medication, other treatment or
Talkativeness
medical condition
Specifiers
- with anxious distress
- with mixed features (i.e. Same period satisfy both criteria for MDE and Manic Episode)
- with rapid cycling (i.e. ≥ 4 episodes per yr)
- with melancholic features (near-complete absence of the capacity for pleasure)
- with atypical features (e.g. mood reactivity, weight gain, hypersomnia)
- with psychotic features
- with peripartum onset (severe anxiety and even panic attacks; risk of infanticide)
- with seasonal pattern (depression begins in fall or winter and remits in spring)

DSM-5 Criteria for Hypomanic Episode

A. A distinct period of abnormally & persistently elevated, expansive OR irritable mood AND
abnormally & persistently increased goal-directed activity or energy lasting at least 4 days
B. 3 or more of the manic symptoms present (4 or more if mood is only irritable)
C. Unequivocal change in functioning that is uncharacteristic of the individual when not
symptomatic
D. Disturbance in mood and change in functioning are observed by others
E. Episode is not severe enough to cause marked impairment in social or occupational
functioning or to necessitate hospitalisation, and no psychotic symptoms
F. Not due to alcohol, substance, medication, other treatment or medical condition
* Hypomanic episodes are common in Bipolar I Disorder but not required for diagnosis

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DSM-5 Criteria for Bipolar I Disorder
A. At least one Manic Episode
B. Not better explained by another mental disorder
Specifiers
- Severity & Current/ most recent mood episode
• Mild vs Moderate vs Severe
• Current or most recent episode Manic vs Depressed (vs Hypomanic vs Unspecified)
- with psychotic features
- Extent of remission: In partial remission vs full remission

DSM-5 Criteria for Bipolar II Disorder

A. At least one Hypomanic Episode + At least one Major Depressive episode
B. Never has a Manic episode
C. Not better explained by another mental disorder
D. Symptoms of depression or the unpredictability caused by frequent alternation between periods
of depression and hypomania causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning
Specifiers
- Current or most recent episode is: Hypomanic vs Depressed
- Course if full criteria for a mood episode are not currently met: In partial vs full remission
- Severity if full criteria for a mood episode are currently met: Mild vs Moderate vs Severe

ICD-10 Criteria for Bipolar Affective Disorder

- Current episode must fulfil criteria for Hypomania or Mania
- There must have been 1 or more other affective episode (hypomanic, manic, depressive,
mixed) in the past
OR
- Current episode must fulfil the criteria for a Depressive episode
- There must have been 1 or more hypomanic, manic or mixed affective episode in the past

Criteria for Severe Manic Episode

- Presence of psychotic symptoms
- Mixed with depressive symptoms
- (Increased activity/ Agitation →) Severe overactivity
- (Indiscretion →) Excessive spending
- (Grandiosity →) Bizarre behaviour
- (Flight of idea →) Disorganised thinking
- (Talkativeness →) Incoherent speech

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Young’s Mania Rating Scale (YMRS)
- Elevated mood (0-4)
- Increased energy or motor activity (0-4)
- Sexual interest (0-4)
- Sleep (0-4)
- Irritability (0-8)
- Speech (rate and amount)
• Language - thought disorder
• Content
- Disruptive-aggressive behaviour
- Appearance
- Insight
Interpretation
- Total score 0-60
- ≥20 Mania
- ≥12 Hypomania

Baseline laboratory investigations

- CBC, LRFT
- TFT
- FPG
- Lipid profile
- 24hr CrC if with Hx of renal disease
- Urine toxicology if relevant
- Pregnancy test if relevant (risk of infanticide)
- ECG if relevant

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**Approach to Mania**
Manic Symptoms
- 最近呢個⽉月⼼心情如何？(Prevailing mood)
• 有冇長時間都好亢奮? (Elevated, Expansile mood)
• 或者長時間覺得好煩躁/ 炆憎? (Irritable mood)
• 會唔會亢奮/ 煩躁嘅同時⼜又會覺得情緒低落落? (Mixed mood)
- 有冇停唔到咁做多左野? 例例如⼯工作、社交、讀書或者性慾多左? (Increased goal-directed activity)
- 幾時開始？持續幾多⽇日? (>1 week?)
• 呢種持續亢奮嘅情況, 以前有冇試過? 最早係幾歲開始? 平均隔幾耐會⼀一次? (Rapid cycler?)
• 之前嘅幾次有冇入黎黎醫院住? (Hospitalisation)
- 會唔會容易易分⼼心? 集中唔到? 俾其他野吸引注意⼒力力? (Distractibility)
- 有冇輕率嘅⾏行行為? 例例如出街亂駛錢？買多左野？亂咁投資? (Indiscretion)
- 好有⾃自信 (Self-esteem)/ 覺得同其他⼈人唔同? 做到啲⼈人地做唔到嘅嘢? (Delusion of Grandiosity)
• 點樣唔同, 點解咁唸, 有冇證據? (Unshakable)
• 實際⾏行行為 (e.g. Ability to fly → JFH; Rich → Buying sprees)
- 唸野快左? 好似停唔到, ⼀一樣未唸完另⼀一樣就走出黎黎? (Flight of ideas)
- 有冇覺得精⼒力力旺盛? (Increased energy)/ 或者個⼈人靜唔到落落黎黎, 做沒有意義的⾏行行為，例例如到處徘
徊、搓⼿手、拉衣服、講野⼤大聲/亂叫、說話變得有攻擊性 (Psychomotor agitation)
- 瞓唔瞓到？幾多個鐘？(Reduced need of sleep)
- 講野多左？(Talkativeness)

Other important history

- Depressive symptoms 除左亢奮, 會唔會有⼀一段時間情緒低落落、唔開⼼心
- Psychotic symptoms 最近有冇⼀一啲唔尋常嘅經歷、聽到聲⾳音、睇到影像?
- Alcohol/ Substance abuse 我循例例問下, 請問你有冇飲酒、吸食藥物嘅習慣?
- Distress/ Functional impairment 對你黎黎講, 會唔會好⼤大困擾? 對⽇日常⽣生活有咩影響?

Risk assessment
- Harm to self e.g. Self-destructive, Dangerous, Self-neglect, Suicide
- Harm to others

Ddx of Manic episode

- Manic episode (≥1week) = Bipolar I Disorder
- Severe Manic episode if psychotic, mixed-depressive, severe overactivity, excessive spending,
bizarre behaviour, disorganised thinking, incoherent speech
- Hypomanic episode (≥4 days) + Depressive episode = Bipolar II Disorder
- Substance abuse
- Organic cause e.g. Thyrotoxicosis
- Antidepressant discontinuation syndrome

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Misdiagnosis of Bipolar Disorders

Under-diagnosis
- Especially common in some early studies
- Hypomanic episode is often overlooked due to lack of functional impairment, observability and
psychotic symptoms
- Bipolar II Disorder (Hypomanic + Depressive) often misdiagnosed as Major Depressive
Disorder
- Manic episode with Psychotic symptoms sometimes misdiagnosed as Schizophrenia
- Correct diagnosis and treatment was delayed by 5-7 years in average
Problems
- Distress caused by untreated mood symptoms → Suicide, Comorbid Anxiety, Substance abuse
- Poor QOL, Greater functional impairment and increased healthcare cost
- Antidepressant monotherapy is less effective and results in manic switch and cycle acceleration

Over-diagnosis
- Due to incorrect understanding of the term “Manic” “躁”
- Among 180 outpatients who were previously diagnosed with Bipolar disorder, structured
interview could not confirm the diagnosis in 43 (33%) of them
- Only 43% of the 145 patients who reported a previous diagnosis of Bipolar disorder had the
condition confirmed by structured interview
Problems
- Unnecessary ADR of mood stabilisers
- Increase sick role and disability claims

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Management of Bipolar Disorders

Principles
1. Correct diagnosis and re-evaluate when in doubt
2. Illness acceptance and treatment adherence
3. Family psycho-education
4. REFERRAL to specialist
5. Pharmacological and psychosocial treatment
- Often requires several medications
- AVOID Antidepressants if possible otherwise at limited dose and duration
because it may trigger a manic episode
6. Special treatment in special situations: Childbearing-age women, pregnancy, child and
adolescents, elderly
7. Treatment of psychiatric and medical comorbidity

Different Treatment in different phases of Bipolar Illness

Different phases 1st line 2nd line 3rd line

Bipolar I Disorder
Monotherapy of:
- Lithium
- Valproate
- SGA (Olanzapine, Combination of:
Acute Manic Episode - Lithium Electroconvulsive
Risperidone, - Valproate
(CANMAT guideline) Therapy
Quetiapine, - SGA
Aripiprazole,
Ziprasidone)
- Carbamazepine
Monotherapy + any of:
Monotherapy of: - SSRI
Acute - Quetiapine Electroconvulsive
- Bupropion
Depressive Episode - Lithium - Venlafaxine Therapy
- Lamotrigine - Another Monotherapy
Maintenance and - Lithium, Valproate, Quetiapine, Lamotrigine, Carbamazepine, Risperidone
Prophylactic treatment - Psychosocial augmentation

Bipolar II Disorder
- Lamotrigine
- Lithium
Acute - Valproate
- Quetiapine
Depressive Episode - Lithium or Valproate + Antidepressants
- Valproate + Lithium
- SGA + Antidepressants

Combination of:
- Valproate
Maintenance and - Lithium - Lithium
Prophylactic treatment - Lamotrigine - SGA
- Antidepressants

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Maintenance and Prophylactic treatment
Indications
- Established bipolar disorder
- Episodes of mania or depression
- Severe single episode - suicidal attempts, psychotic episodes and significant functional
impairment
Options
- Bipolar I:
• Lithium or Valproate or Quetiapine
• Psychosocial augmentation: Psycho-education, CBT, Interpersonal and social rhythm therapy,
Family-focused treatment, Carer-focused treatment, Intensive case management, Less
hostile, more supportive, better drug compliance
- Bipolar II:
• 1st line: Lithium or Lamotrigine
• 2nd line: Combination of Valproate, Lithium, Atypical antipsychotics, Antidepressants
Recurrence rate
- Abrupt discontinuation of Lithium/ Antipsychotics: 60-80%
- Discontinuation during ongoing therapy: 20-50%
- Gradual discontinuation is better
Indication of discontinuation
- No strict guideline on duration, probably lifelong
- At least a few years w/o relapse (cases that have no relapse for >10years can still relapse after
discontinuation of treatment)
- Absence of sub-syndromal symptoms between mood episodes is a prerequisite

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Prognosis of Bipolar Disorders

- 2-year outcome despite treatment after first manic episode
• Syndromal recovery 98%
• Symptomatic recovery 72%
• Functional recovery 43%
• Recurrence 40%
- Patients on maintenance treatment with no relapse for many years can still relapse after
stopping the drugs

Poor prognostic factors

- Early age of onset
- Mixed episodes
- Rapid cyclers (≥4 episodes/yr)
- Repeated episodes
- Previous hospitalisations
- Residual symptoms
- Cognitive impairment
- Poor insight
- Side effects of medications
- Comorbid substance abuse or Personality disorder

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Screening of Bipolar Disorders

Mood Disorder Questionnaire (MDQ)

Hypomania Checklist (HCL-32)

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Psychotic Disorders
What is Psychosis?
- In the past, “Psychosis” is a over-generalisation of symptoms in mental disorders
- Psychosis vs Neurosis
- In a broader sense, psychosis = “out of reality”
- A syndrome characterised by the following symptoms:
• Delusions
• Hallucinations
• Disorganisation (thinking and/or behaviour)
• Lack of insight
- Psychotic disorder is a disease of the brain
- Schizophrenia is only one type of Psychotic disorders

Spectrum of Psychotic Disorder

DSM-5 ICD-10

Schizotypal (Personality) Disorder Schizotypal Disorder

Persistent Delusional Disorder

Delusional Disorder
Induced Delusional Disorder

Brief Psychotic Disorder

Acute and transient psychotic disorders (ATPD)
Schizophreniform Disorder

Schizophrenia Schizophrenia

Schizoaffective Disorder Schizoaffective Disorder

Substance/Medication-induced Psychotic disorder \

Psychotic disorder due to another medical condition \

Catatonia associated with another mental disorder \

Catatonia disorder due to another medical condition \

Unspecified catatonia \

Other specified Schizophrenia spectrum and other

Other non-organic psychotic disorders
psychotic disorder

Unspecified Schizophrenia spectrum and other

Unspecified non-organic psychosis
psychotic disorder

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Epidemiology of Psychotic Disorder

Lifetime prevalence in HK (Chang WC et al., 2017)
- Psychotic disorders overall: 2.47% (2-3%)
• 1.25% Schizophrenia
• 0.15% Delusional Disorder
• 0.38% Psychotic disorder not otherwise specified
• 0.31% Bipolar Disorder with Psychosis
• 0.33% Depressive Disorder with Psychosis
- Median incidence rate of Schizophrenia: 15.2/ 100,000 per year

Demographics
- Incidence rates varied widely across regions (7.7 to 43.0/100,000 per year), with elevated
incidence rate being associated with the following socio-environmental factors:
• Migrants of ethnic minority
e.g. from developing countries to western developed countries e.g. UK, Netherlands
compared to locally-born Caucasians
• Urbanicity/ Individuals being brought up in urban areas (c.f. rural areas)
• Lower socioeconomic classes (Social drift rather than social causation)
- Onset of Schizophrenia usu. in late adolescence & early adulthood
• Male: 18-25yo
• Female: 25-35yo
- Male to female incidence = 1.4:1

Early Intervention Paradigm

- Early-Intervention model for psychosis has been the major focus in mental health service
development in the past two decades
- Rationale:
• Early detection: shorten treatment delay/ duration of untreated psychosis (DUP)
• Phase-specific intervention: optimal treatment in the critical period (3-5years after illness
onset)
- Both overseas and local research consistently demonstrated effectiveness of EI over standard-
care on improving clinical and functional outcomes of FEP
- Hong Kong: EASY program (Early Assessment Service for Young people with psychosis)
• EASY program reduced suicide & hospitalisation rates, improved functioning and symptom
outcomes, lowered default rate
• Detection and Intervention for at-risk mental state (ARMS) for psychosis (i.e. putatively
prodrome for psychosis) (indicated prevention)

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Schizophrenia
- Different use of Chinese terms to describe Schizophrenia in different regions
• HK: 思覺失調 (coined by HA since 2001), 精神分裂 (before 2001)
• Japan: 統合失調 (widely in use by 2002)
• Taiwan: 思覺失調 (officially in use since 2014)
- Huge Socioeconomic burden
• One of the leading disabilities worldwide (Global Disease Burden 2015)
• Account for substantial direct (hospitalisation, medication) and indirect (loss of productivity,
disability allowance) cost to society
• Profound disruptions in individual’s personality development, social relationship, scholastic
and vocational trajectories

History of Schizophrenia
Wilhem Griesinger, 1861: Unitary Psychosis
- i.e. All forms of psychosis are surface variations of a single underlying disease process

Emil Kraepelin, 1896: Dementia praecox

- “Praecox” means “earlier stage”
- Schizophrenia was considered precursor state of Dementia with progressive cognitive
impairment (~ Simple subtype Schizophrenia described by Bleuler)
- Kraepelin dichotomy on Psychosis:
• Dementia praecox (i.e. Schizophrenia) vs Manic-depressive Insanity (i.e. Bipolar affective
disorder aka Bipolar II Disorder)

Eugene Bleuler, 1991: Schizophrenias

- Bleuler coined this term from Greek, meaning “Splitting of the mind or psychic functions”
- He recognised the variety of Schizophrenia and concluded the fundamental symptoms as
“Loosening of association, affect flattening, autism, ambivalence”
4 Classical subtypes described by Bleuler
- Paranoid: Prominent positive symptoms
- Hebephrenic/ Disorganised: Prominent thought disorder, incongruous affect
- Catatonic: Constellation of specific motor signs e.g. posturing, waxy flexibility, mutism
- Simple: Lack of positive symptoms, gradual function decline, prominent negative symptoms
* This classification is no longer included in DSM-5
* Catatonia is a syndrome NOT specific to Schizophrenia and currently a diagnostic specifier in
DSM-5; more commonly a/w Mood disorders and can occur in neurological conditions

Epidemiology fo Schizophrenia
- Lifetime risk ~1% (c.f. 15% of Depressive episodes)
- Median incidence rate: 15.2/100,000 per year
- Onset usu. in late adolescence & early adulthood
- Male > Female (1.4:1)

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Aetiology of Schizophrenia
- Schizophrenia is not entirely Genetic but also Environmental

Genetics
* High degree of heritability (estimated as 80% contributed by genetic cause)
Familial risk
- Both parents: 50%
- Single parent: 13%
- Monozygotic twin: 50% +ve (the other half has to come from environmental factors)
- Siblings/ Dizygotic twin: 10%
- First degree relatives: 10-15% +ve
- Second degree relative: 2-5% +ve
- No relative (i.e. general risk): 1%
Polygenic (i.e. multiple genes with small effects contributed by each gene)
- Many identified candidate genes are related to dopamine, glutamate, synaptic functions, and
immune mechanisms
• Dopamine receptor D2 (DRD2)
• Glutamate receptors (GRM3, MRIN2A, SRR)
• Calcium channels (CACNA1C, CACNA1L, CACNB2)
Monogenic (i.e. rare copy number variants (CNV) with larger effect)
- Chromosome 22q11.2 deletion syndrome
• aka DeGeorge Syndrome, Velocardiofacial syndrome (VCFS)
• 1 in 4,000 living births
• 25% (22-31%) develop SZ or Schizoaffective disorder
• i.e. 20-30X risk of Schizophrenia (1% risk in general population)
• This deletion is present in 1.1% of SZ patients
- Chromosome 15q11.2 deletion syndrome
• Odds ratio of SZ = 7
• a/w ASD, Developmental delay, Language delay
- Disrupted in Schizophrenia (DISC1) gene in large Scottish family

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Environmental
Risk factors
- Maternal malnutrition: Epigenetic defect (i.e. defect of DNA methylation)
- Advanced paternal age (>50yo) at conception
• de novo mutation or epigenetic mutation?
• Poorer family relationship?
- Birth in winter months (1.1X risk)
• Postulated in Western studies to be a/w higher latitudes +/- more influenza
• Very controversial as it is not observed in Asian countries where winter ain’t that cold
- Obstetric complications
• Foetal growth retardation
• Foetal perinatal hypoxia
• Maternal infections e.g. Influenza, Toxoplasmosis
- Substance abuse e.g. Cannabis
- Smoking
- Immigrants
- Urbanicity (urban birth and urban upbringing): Social fragmentation compared to rural areas
- Childhood and Adolescent difficulties e.g. Trauma, Parental loss (Death, Divorce, Separation),
Maltreatment (Physical, Emotional, Sexual abuse)
- Chronic Difficulties
• Chronic unremitting stress cause sustained activity of the HPA axis
• Chronically high level of Glucocorticoids → Impair brain, immune and metabolic functions
• e.g. Immigrants (2-4X risk of SZ) esp. 2nd generation Immigrants, living in areas w/ low
density of migrants - “Social Defect” proposed as explanation
- High expressed emotions (hostility, over-involvement,
critical comments)
from family members can increase risk of relapse of
Schizophrenia

Stress-Vulnerability Model
- An extension of Stress-Diathesis Model
- Describe the synergistic effect of stress and
vulnerability and the variation in stress threshold for
symptoms at different vulnerability

Distal factors:
Proximal factors:
Neurodevelopmental predisposition/
Social precipitation/ “Stress”
“Vulnerability”

Substance abuse e.g. Cannabis

Genetic factor
Smoking
Maternal malnutrition
Chronic difficulties
Advanced paternal age (>50yo) at conception - Immigrants
Winter birth
Childhood and Adolescent difficulties
Obstetric complications - Childhood trauma
- Foetal growth retardation - Parental loss (Death, Divorce, Separation)
- Foetal perinatal hypoxia - Maltreatment (Physical, Emotional, Sexual abuse)
- Maternal infections
Recent (within 1 month) adverse life events

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Pathogenesis of Schizophrenia
Dopamine Hypothesis
Increased pre-synaptic dopamine synthesis in Ventral Striatum (aka Nucleus accumbens)
→ Hyper-dopaminergic transmission → Manifestations of Psychosis
Basis of hypothesis
- It was found out that dopamine receptors antagonists reduce symptoms of schizophrenia while
dopamine receptor agonists exacerbate it.
- Untreated schizophrenia show increased Dopamine Receptor density in brain
- However, Antipsychotics are only effective in most but not all patients, and some Antipsychotics
have higher affinity to other receptors e.g. Serotonin receptor rather than D2R
Dopamine pathways
Functions Role in Schizophrenia

1. Mesolimbic hyper-dopaminergic
Motivation
VTA → Limbic System Accounts for Positive symptoms
Emotion
(Nucleus Accumbens/ Ventral e.g. Delusion, Hallucination
Reward
Striatum, and Amygdala)

VMPFC & OFPFC: Accounts for Negative symptoms

Social Cognition e.g. Affect Flattening, Avolition,
2. Mesocortical hypo-dopaminergic Anhedonia, Alogia, Asociality
VTA → PFC DLPFC:
Thinking, Planning, Accounts for Cognitive impairment
Working memory e.g. Memory loss

3. Nigrostriatal
ADR of Antipsychotics:
SNpc → Dorsal Striatum Motor Control
Extrapyramidal side effects (EPSE)
(Caudate, Putamen)

4. Tuberoinfundibular
Inhibit tonic Prolactin ADR of Antipsychotics:
Infundibular nucleus of Hypothalamus
release Hyperprolactinaemia
→ Medial eminence of APG

VTA = Ventral Tegmental Area; PFC = Prefrontal Cortex; VMPFC = Ventromedial PFC; DLPFC =
Dorsolateral PFC; SNpc = Substantia nigra Pars compacta; APG = Anterior Pituitary Gland

Dopamine receptors
- 5 Dopamine receptors; divided into D1-like & D2-like families that antagonist each other
• D1-like family (D1R, D5R): Increase intracellular cAMP
• D2-like family (D2R, D3R, D4R): Decrease intracellular cAMP
- D2R is the only one a/w psychotic symptoms
• Most concentrated in Cortex, Striatum, Limbic System, Basal Ganglia, APG, Hypothalamus
(i.e. Mesolimbic & Mesocortical pathways)
• Blockade of Mesocortical & Mesolimbic pathways → Antipsychotic effect
• Blockade of Nigrostriatal pathway → Extrapyramimdal Syndrome (EPS)/ Extrapyramidal Side
Effects (EPSE)
• Blockade of Tuberoinfundibular pathways → Hyperprolactinaemia
Other neurotransmitters
- Glutamate (NMDA hypo-function), GABA → Neurotoxicity, Hyperdopaminergia

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4 Dopaminergic pathways in brain

Glutamate Hypothesis
Basis of hypothesis
- Antagonist of NMDA could induce Schizophrenic-like psychosis
- NMDA co-agonist reduce some symptoms
- Altered level of Glutamate and Metabolite in Schizophrenic brains
- Schizophrenic genes affecting Glutamate signalling
- Anti-NMDA Ab can reduce symptoms of Schizophrenia

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Neuropathological & Neuroanatomical findings
- Although Schizophrenia was previously considered a precursor of Dementia, there is no
pathological evidence of Gliosis, Neuronal death, but reduction in synapse-rich neuropile.
This goes against the Neurodegeneration hypothesis in Alzheimer’s Disease.
- by structural MRI, Schizophrenic brains show
• Reduced whole brain volume/ grey matter volume esp. in Temporal lobe (Hippocampus,
Amygdala, Superior Temporal gyri STG, Pre-Frontal Cortex, Thalamus, Anterior Cingulate)
• Ventricular enlargement → a/w negative symptoms
• Cortex thinning, Reduced surface area
• Reduced connectivity between brain regions esp. frontal and temporal lobes
- Structural & functional connectivity alterations:
• Altered integrity of white matter tracts (via DTI)
• Altered resting-state functional connectivity (via fMRI)
- Evidence indicates a progressive structural brain changes (volume reduction) across the course
of illness, at least in a subgroup of patients
- Alterations in neurophysiological measures and in-vivo brain functions

Neurodevelopmental Hypothesis
- Motor function deficits occur before onset of illness
- Neurological soft signs
- Poor premorbid adjustment
- Low IQ / mental retardation associated with higher risk of schizophrenia
- Cognitive deficits emerge in prodromal period

Stress-Vulnerability Model for psychosis development

(Social defeat hypothesis / Stress dopamine sensitisation)
- ~ Depression
- Vulnerability: Genetic liability (polygenic) + Distal risk factors (Prenatal and Perinatal)
- Stress: Environmental triggers

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Clinical presentation of Schizophrenia

- Onset usu. in adolescence (15-25yo)
- Onset can be abrupt or insidious
- Psychotic symptoms tend to diminish over life course, ? a/w age-related decline in dopaminergic
activity
- Late-onset cases (i.e. >40yo) are over-represented by married female (unclear same entity?)

Natural history of Schizophrenia

1. Premorbid Phase in Childhood
2. Prodrome (aka At risk mental state ARMS, or Clinical high risk state CMR)
3. First-episode Psychosis (FEP)
4. Residual symptoms
5. Full recovery or Residual deficits or Deterioration

Symptomatology of Schizophrenia
1. Primary symptoms e.g. Delusion, Hallucination

2. Negative symptoms e.g. Affect flattening, Alogia, Anhedonia, Avolition, Asociality

3. Disorganisation e.g. Formal thought disorders

4. Mood/ Affective symptoms e.g. Depression, Mania, Insomnia (15-20%+ve)

5. Motor signs e.g. Catatonia

6. Cognitive impairment

Complications & Associations

- Suicide
- Non-suicidal mortality
- Hostility & aggression towards others (actually rare in Schizophrenia) typically in young males
with past history of violence, non-adherence with treatment, substance abuse, and impulsivity

Positive symptoms
- “Positive” means symptoms additional to normal individual
Types
- Hallucinations
• Auditory Hallucination esp. AVH
• Visual Hallucination
- Delusions
• Schizophrenic delusions tend to be more Un-understandable or Bizarre (Jaspers, 1913)
• e.g. Persecutory Delusion (i.e. people are trying harm patient/ patient is a victim)
• e.g. Referential Delusion (i.e. people are talking about patient/ random personal experience
have strong personal significance or will affect patient’s own destiny)
Most common positive symptoms
- Delusion of Persecution/ Persecutory Delusion
- Delusion of Reference/ Referential Delusion
- Auditory Verbal Hallucination (AVH)

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Schneiderian’s First Rank Symptoms (FRS)

A list of symptoms composed by Kurt Schneider (1959) that were of “first rank of importance”
i.e. specific to Schizophrenia and thus facilitate diagnosis
1. Third-person AVH with multiple voices conversing with each other
2. Third-person AVH in the form of running commentary
3. Thought echo/ AVH with voice repeating patient’s own thoughts aloud
4. Delusion of thought alienation including thought insertion, withdrawal & broadcasting
5. Delusion of control/ passivity/ influence (i.e. affect, actions, impulse experienced are
made or influenced by external agents)
6. Delusional perception (i.e. a true perception that triggers a delusional thought)
7. Somatic hallucination
Limitation
- However, studies showed that FRS are NOT specific to Schizophrenia and are of minimal
prognostic predictive value
- Nonetheless, FRS are still widely applied and emphasised in current classifications

Negative symptoms
- “Negative" means symptoms less to normal individual
- A core symptom of Schizophrenia
- Key determinant of functional outcome
- Predict unmet therapeutic need, usu. not responsive to First generation Antipsychotics
- Multi-dimensional construct
- Tends to be the most persistent symptoms
Common negative symptoms (5As)
- Affect flattening: Reduced affect response in terms of facial expression, gesture, spontaneous
movement, intonation, eye contact
- Alogia: Poverty of speech
- Anhedonia: Reduced capacity to experience pleasure
- Avolition: Reduced motivation with reduced goal-directed behaviour
- Asociality: Reduced social drive with social withdrawal, can be due to avolition but also limited
opportunities for social interactions

Disorganisation: Formal though disorders (FTD)

- Loosening of association/ Derailment of though and speech
• i.e. Train of thought jump from one to another unrelated/ indirectly related thought
• Speech content is fragmented and disconnected
- Circumstantial thoughts → Circumstantial speech/ Circumstantiality
• i.e. Train of though goes non-linearly but eventually reach the point
• Speech would contain many unnecessary trivial details before reaching the point
- Tangential thoughts → Tangential speech/ Tangentiality
• i.e. Train of thought goes off topic and never return to initial point
• Speech go from the point to a topic and then to another topic related to the previous one
- Clang association/ Clanging
• i.e. association of words based upon sound rather than concepts
• Rhyming w/o meaning
• e.g. “the train brain rained on me”, 「今天下雨，雨天要帶傘，傘兵很厲害，害⼈人不長命」
- Word Salad
• i.e. loss of syntax and basic structure of speech (將D字炒埋⼀一碟)
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- Neologism - i.e. make up new words

Mood/ Affective symptoms in Schizophrenia

- Mood symptoms and full mood episodes are common in Schizophrenia and may be concurrent
with active-phase symptomatology
- ~1/2 complain of depressive symptoms
- However, as distinct from a psychotic mood disorder, a diagnosis of Schizophrenia requires
presence of delusions or hallucinations in the absence of mood episodes
- Mood episodes should be present for only a minority of the total duration of illness

Catatonia/ Catatonic behaviours

- Catatonia is a constellation of specific motor signs
- Not specific to Schizophrenia
- More commonly found in Mood disorders and neurological disorders
- Rare now
Common signs
1. Stupor (i.e. no psychomotor activity; not actively relating to environment)
2. Agitation, not influenced by external stimuli
3. Grimacing
4. Echolalia (i.e. mimicking another’s speech)
5. Mutism (i.e. no, or very little, verbal response)
6. Mannerism (i.e. odd, circumstantial caricature of normal actions)
7. Stereotypy (i.e. repetitive, abnormally frequent, non-goal-directed movements)
e.g. Lips pouting/ pursing (aka Schnauzkrampf, German for lips pouting)
8. Posturing (i.e. spontaneous and active maintenance of a rigid, inappropriate, or bizarre
posture against gravity)
9. Waxy flexibility (i.e. slight, even resistance to positioning by examiner)
10. Catalepsy (i.e. passive induction of a posture held against gravity)
e.g. Psychological pillow (head held in air as there’s a pillow when asked to lie on a bench)
11. Negativism (i.e. opposition or no response to instructions or external stimuli)
12. Echopraxia (i.e. mimicking another’s movements)
13. Ambitendence (i.e. alternate between opposite movements and so on repeatedly)
• Typical example is ambitendence in shaking hand (hands go forth and back)
• NOT in DSM-5 criteria for Catatonia

Cognitive impairment
- A core feature in schizophrenia
- Key determinant of functional outcome esp. Anosognosia (commonest predictor of non-
adherence to treatment due to absence of insight)
- Indicate unmet therapeutic need, not responsive to antipsychotic treatment
- Generalised cognitive impairment encompassing multiple cognitive domains:
• Sustained attention
• Executive functions (planning, set-shifting, inhibition control)
• Working memory
• Verbal and visual memory (immediate registration and recall)
• Processing speed
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- In general, 1-2 standard deviations below normal healthy controls
- Healthy first-degree relatives of patients also demonstrates cognitive deficits (albeit less severe)
- Impairment in social cognition observed including deficits in ToM (theory of mind), emotion
recognition
- Cognitive impairments may persist when other symptoms are in remission and contribute to the
disability of the disease

Suicide in Schizophrenia
- Suicide is the single largest cause of premature death in Schizophrenia (Brown et al. 1997)
- Sometimes in response to command hallucinations to harm oneself or others
- Meta-analysis showed a ~5% risk (Palmer et al. 2005)
- 12X risk of general population (Dutta et al. 2010)
- Risk is highest in the early stage of psychotic disorders esp. in the first year after FEP
- Predictors
• Depressed mood - frequently observed in early stages
• Feelings of hopelessness
• Unemployment
• After a psychotic episode
• After hospital discharge

Mortality in Schizophrenia
- Schizophrenia reduce lifespan of a patient by an average of 10-15years
- All-cause standardised mortality ratio (SMR) = 2.6 (McGrath et al. 2006)
- On top of Suicide, premature deaths are attributed to a wide range of physical illnesses
• Lifestyle (sedentary lifestyle, lack of exercise, poor nutrition)
• Cigarette smoking, substance or alcohol abuse
• Metabolic syndrome (Obesity, DM, Hyperlipidaemia etc.) - ADR of SGA
• Inherent disease process involving accelerated ageing and medical morbidity

Prodrome in Schizophrenia
- Mild or sub-threshold forms of hallucinations
- Unusual or odd beliefs but not delusional e.g. ideas of reference, magical thinking
- Unusual perceptual experiences e.g. sensing the presence of an unseen person
- Understandable but vague speech
- Negative symptoms are common and could be severe
- The above signs are often the first sign of Schizophrenia
- Similar signs are observed in phase of residual symptoms

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Diagnosis of Schizophrenia
DSM-5 Criteria
A. 2 or more of the following characteristic symptoms, with at least one from 1-3
1. Delusions
2. Hallucinations
3. Disorganised speech e.g. Frequent derailment, Incoherence
4. Grossly disorganised or Catatonic behaviour
5. Negative symptoms i.e. diminished emotional expression or avolition
B. For a significant proportion of time, one or more major areas of functioning such as work,
interpersonal relations, or self-care are markedly below the level achieved prior to the onset
(or when the onset is in childhood or adolescence, failure to achieve expected level of
interpersonal, academic, or occupational achievement)
C. Minimal duration:
• Individual symptom: Significant portion of 1-month period or less if successfully treated
• All symptoms: At least 6 months (incl. prodromal, residual symptoms)
D. Ruled out Schizoaffective disorder, Schizophreniform disorder (i.e. symptoms last 1-6 months),
and Depressive or Bipolar disorder with psychotic features
E. Not attributable to Substance abuse or Another medical condition
F. If there is a Hx of ASD or Communication disorder of childhood onset, the additional diagnosis
of Schizophrenia is made only if prominent delusions or hallucinations, in addition to the other
required symptoms of Schizophrenia, are also present for at least 1 month
Specifiers
- No. of episodes and state of remission
• First vs Multiple episodes vs Continuous
• Acute episode vs Partial remission vs Full remission
- with catatonia

Alternative Ddx of Schizophrenia

- Medical causes e.g. Cushing, Thyroid, SLE, NMDA Encephalitis, Temporal Lobe Epilepsy
- Substance-induced Psychosis e.g. Steroid, Alcohol, Cannabis, Hallucinogens, Inhalants,
Amphetamines, Cocaine etc
- Acute and Transient Psychotic Disorder (ICD-10)/ Brief Psychotic Disorder (DSM-5),
Schizophreniform Disorder (DSM-5)
- Schizoaffective Disorder
- Delusional Disorder
- Depression with psychotic features
- Bipolar Disorder with Psychotic features
- Paranoid personality disorder
- Schizotypal personality disorder

Rule out secondary causes and alternative Ddx

- Review DHx
- CBC, LRFT, TFT, CaPO4, BG, VDRL, Cortisol, PTH, Tumour markers, Cu, Caeruloplasmin
- Urine toxicology
- ECG, EEG
- CT/ MRI Brain: Ventriculomegaly with cerebral atrophy and reduced hippocampus volume
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ICD-10 Criteria
- ≥1 of the A-D symptoms,
A. Thought echo/ insertion/ withdrawal/ broadcasting
B. Delusion of control/ passivity// delusional perception
C. Auditory hallucination voices giving running commentary/ third person voices discussing the
patient among themselves/ voices “originating” from some part of the body
D. Bizarre delusions
- OR ≥2 of E-I symptoms
E. Other hallucinations that either occur every day for weeks or that are a/w fleeting delusions
or sustained over-valued ideas
F. Thought disorganisation (loosening of association, incoherence, neologisms)
G. Catatonic symptoms (abnormal muscle tone, hyperkinesis or stupor)
H. Negative symptoms
I. Change in personal behaviour e.g. Loss of interest, Aimlessness, Idleness
- Symptoms have been clearly present for most of the time during a period of 1 month or more
- Not diagnosed in the presence of organic brain disease or during intoxication or withdrawal
- Exclusion criteria
• Schizoaffective disorder
• Mood disorders with psychotic features
ICD-10 subclassifications of Schizophrenia
- Paranoid Schizophrenia
• Prominent positive symptoms
- Disorganised Schizophrenia/ Hebephrenic Schizophrenia
• Prominent thought disorder
• Incongruous affect
• Younger onset with poorer prognosis
- Catatonic Schizophrenia
• Schizophrenia with Catatonia
• Rare nowadays
- Simple Schizophrenia
• Lack of positive symptoms, Prominent negative symptoms, gradual functional decline
• Rare nowadays
- Residual Schizophrenia - denotes the residual phase
- Undifferentiated
- Post-Schizophrenic Depression

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**Approach to Psychotic symptoms**

Delusions
Delusion of thought alienation
- 有冇諗諗吓嘢啲思想被⼈人抽走左？突然消失？(Thought Withdrawal)
- 有冇覺得⾃自⼰己嘅思想係被⼈人放入去？(Thought Insertion)
- 有冇覺得⾃自⼰己嘅思想好似電波咁散播出去？⼈人⼈人都接收到，知道你諗乜？(Thought Broadcast)
- 係唔係有⼀一把⼈人聲將你諗緊嘅嘢⼤大聲講出嚟？ (Exclude Thought Echo, which is a hallucination)

Delusion of control/ passivity

- 有冇覺得思想/ ⾏行行為/ 情緒畀⼈人控制住？(Passivity of thought/ volition/ emotion)
- 係唔係有把聲叫你去做某啲事？(Exclude Commanding AVH)

Delusion of persecution
- 覺得⾝身邊的⼈人對你點？
- 有冇⼈人想對付你？係啲乜野⼈人？點解佢地要咁做？你點發現佢地要咁做？
- 佢地想點害你？

Delusion of reference
- 覺得⾝身邊的⼈人對你點？
- 有冇⼈人成⽇日討論你？笑你？幾時開始？
- 有冇試過睇電視、報紙、聽收⾳音機，係覺得講緊你、同你有關？

Must ask for all delusions

- 你肯唔肯定？1到10分有幾肯定? (Degree of conviction, Unshakable)
- 有冇証據？ (Absence of evidence, Unshakable)
- 有冇可能有第⼆二個解釋? (Unshakable)
- 呢種情況 (Each individual symptoms) 幾時開始, 最長持續幾耐? (> 1 month?)
- 呢啲情況 (All symptoms together) 最早幾時開始? (> 6 months?)

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Hallucinations
Before asking for hallucinations
- 我問嘅問題會有少少特別, 請唔好介意
- 如果你有類類似經歷, 你會明⽩白
- Start by recalling the scenario

Auditory Hallucination
- 有聽到聲，但附近冇⼈人？
- 聲⾳音係邊到黎黎
• 聲⾳音係從外⾯面嚟, 好似耳仔聽到, 同我講野⼀一樣清楚? (AVH: External space, will-independent)
• 定係係腦海海入⾯面？你控制到? (Pseudo-hallucination: Internal space, will-dependent)
- 咩時候會出現
• 啱啱準備瞓教？(Hypnagogic)
• 啱啱瞓醒？(Hypnopompic)
- 聲⾳音係咪⼈人聲？(AH vs AVH) 你識唔識佢？(Familiarity) 有幾多⼈人？(No. of voice) 男/女？
- 講野內容同你有冇關？
- 同你講緊野還是談論緊你？(2nd vs 3rd person AVH) 4Cs of suspected
hallucination
- 有冇形容緊你嘅動作, 你做咩佢就講咩？(Running Commentary)
- Clear?
- 評論你? (Criticising) 鬧你? (Derogatory) - Constant?
- 或者將你諗緊嘅講出嚟？(Thought Echo) - Controllable?
- Conscious?
Visual Hallucination
- 有冇睇到特別嘅野？係⼈人地睇唔到，可能係唔存在嘅？
- 當時你喺邊？時間？嗰度⿊黑唔⿊黑？睇得清唔清楚？

Olfactory/ Gustatory/ Somatic/ Tactile Hallucination

- 有冇聞到特別嘅野？係⼈人地聞唔到，可能係唔存在嘅？
- 有冇味道/ 感覺同平常的唔同？
- 有冇試過覺得⽪皮膚下⾯面有蟲仔係到爬黎黎爬去? (Formication)

Negative Symptoms
- 冷淡，漠不關⼼心 (Affect flattening)
- 少左講野 (Alogia)
- 少左樂樂樂樂趣 (Anhedonia)
- 少左動⼒力力返⼯工, 返學, 做運動? (Avolition)
- 有冇出街？少左同朋友⾒見見⾯面? (Asociality)
- 呢啲情況幾時開始, 最長持續幾耐? (> 1 month?)

Formal Thought Disorder (FTD)

- More likely observed than asked
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- Can ask for subjective feeling of abnormal thinking 有冇覺得

Other important history

- Mood disturbance 最近⼼心情點樣?
- Substance abuse/ Alcohol abuse 有冇飲酒、吸食藥物嘅習慣?
- Suicidal risk assessment 有冇⾃自殺嘅念念頭/計畫?
- Insight 你認為點解會咁?
- 對你黎黎講, 會唔會好⼤大困擾? 對⽇日常⽣生活有咩影響? (Distress/ Functional impairment)

Ddx of Psychotic symptoms

- Schizophreniform Disorder (1m-6m)
- Brief Psychotic Disorder (1d-1m)
- Schizophrenia
- Schizoaffective Disorder (Meet MDD criteria and mood-exclusive psychosis for 2w)
- Depression with psychotic features
- Bipolar Disorder with psychotic features
- Delusional Disorder (X meet criterion A of Schizophrenia)
- Paranoid Personality disorder
- Schizotypal Personality disorder
- Substance abuse/ induced e.g. Steroid
- Organic cause e.g. Brain tumour, Wilson’s Disease
- Antidepressant discontinuation syndrome

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Management of Schizophrenia
- Pharmacological: Antipsychotics (D2 receptor antagonist)
- Non-pharmacological: Psychotherapy
• Cognitive Behavioural Therapy (CBT) - for residual positive psychotic symptoms (e.g. AVH),
and comorbid depressive and anxiety symptoms
• Treatment compliance therapy
• Cognitive remediation
• Occupational rehabilitation/ vocational support & training/ social skills training
• Community case-management approach
• Family intervention (Expressed-emotions, Caregiver stress & burden, Psycho-education,
Support)
• Electroconvulsive Therapy for Catatonia/ Treatment-resistant Schizophrenia

Antipsychotics
(See Antipsychotics in previous chapters)
- Antipsychotic medication is the mainstay treatment
- Duration: 4-6 weeks + 1-3 years maintenance after positive symptom remission of FEP
Outcome
- 2 generations: First (FGA), Second (FGA)
• FGA is effective in treating positive psychotic symptoms only
• SGA is effective in treating both positive & negative symptoms
- >80% patients with FEP respond to antipsychotics in their FEP
- ~80% risk of relapse at 1 year, majority due to non-adherence to antipsychotics
- Withdrawal symptoms e.g. Tardive Dyskinesia, Nausea, Vomiting, Anorexia, Anxiety, Agitation,
Restlessness, Insomnia, Psychosis (?relapse)
- Tolerance due to skipping dose
MOA
- D2 receptor antagonist; inhibiting Mesolimbic and Mesocortical dopaminergic pathways
ADR
- Due to excessive D2 blockade in Nigrostriatal & Tuberoinfundibular pathways
- Extrapyramidal symptoms (EPS)
• Acute dystonia - i.e. Hyperkinesis/ Spasm, involuntary contraction
• Akathisia - i.e. Motor restlessness
• Parkinsonism e.g. Rigidity, Resting tremor, Cognitive impairment
• Tardive dyskinesia - i.e. late onset, painless, repetitive orofacial movement e.g. Tongue
protrusion, Lip smacking
- Hyperprolactinaemia
• Galactorrhoea
• Tertiary Hypogonadism: Delay/ Absent puberty, Growth retardation, 2° sexual characteristics
regression, Infertility, Reduced libido, Acne, Hirsutism, Female: Anovulation, Amenorrhoea
(Pseudopregnancy), Male: Impotence, Erectile dysfunction, Gynaecomastia, Testicular
atrophy
- Metabolic side effects
• Obesity, HyperG/ IGT/ DM, Lipid, Cholesterol, HyperPRL
• Commoner in SGA
• Require regular metabolic monitoring
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Treatment-resistant Schizophrenia
- Occurs to ~30% Schizophrenic patients
- i.e. Persistent, prominent positive psychotic symptoms despite at least 2 trials of different
types of Antipsychotics with adequate dose and duration (6-8weeks each)
- Approach (OACS): Optimise, Augment, Change/ Combine, Switch medication
- Clozapine is indicated
• The very first SGA invented
• 30% response in Treatment-resistant Schizophrenia
• Require admission for blood tests for initiation
• Require regular CBC and ANC due to increased risk of Agranulocytosis/ Neutropenia
• Weekly blood test for 18 week and then Monthly until tail off treatment

Prognosis of Schizophrenia
Good prognostic factors Poor prognostic factors

- Late onset - Early onset

- Schizotypal personality, Poor work records
- Good premorbid personality and
Demographics - +ve FHx, PMHx
work record -
- No FHx, PMHx Comorbid substance abuse
- Male sex
- Insidious onset
- No precipitators
- Sudden onset - Prominent negative symptoms/ Simple
Symptomatology - With precipitators type
- Prominent affective symptoms - Severe cognitive impairment
- Prominent thought disorder/ Hebephrenic
type
- Early treatment - Delayed treatment/ Long DUP
Treatment - Good initial response - Poor initial response
- Good drug compliance - Poor drug compliance
- Low caregivers expressed emotions - High EE - i.e. hostile, critical, intolerant of
(EE) patient
Social support - - Lack of family support
Married, Good family support
- Employed/ Working - Unemployed, Social drift

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Brief Psychotic Disorder

- Accounts for 9% of first-onset psychosis in USA
- M:F = 1:2
- May appear in adolescence or early adulthood, Mean onset = mid 30s

Clinical presentation of Brief Psychotic Disorder

- Typically experience emotional turmoil or overwhelming confusion (aka Stressor)
- “Sudden onset” (i.e. within 2 weeks) of psychotic symptoms
- Good prognosis: Eventually has a full return to premorbid level
- Sometimes the duration of psychotic symptoms may be only a few days

Complications
- Self neglect
- Act on basis of delusions
- Suicide

Diagnosis of Brief Psychotic Disorder

- ICD-10: Acute and Transient Psychotic Disorders range between 1-3 months in duration
- Polymorphic features (Cycloid psychosis): Rapidly changing clinical pictures, Prominent
fluctuated mood state, Perplexity

DSM-5 Criteria
A. Presence of one or more of the following symptoms. At least one must be 1-3
6. Delusions
7. Hallucinations
8. Disorganised speech e.g. frequent derailment or incoherence
9. Grossly disorganised or catatonic behaviour
B. Duration of an episode of the disturbance is at least 1 day but less than 1 month, with
eventual full return to pre-morbid level of functioning
C. Not better explained by another mental disorder, and is not attributable to the physiological
effects of a substance or another medical condition
Specifiers
- with or w/o Marked stressor(s)
(i.e. symptoms occur in response to events that, singly or together, would be markedly stressful
to almost anyone in similar circumstances in the individual’s culture)
- If postpartum onset
- with catatonia
- Severity

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Schizophreniform Disorder
- Similar prevalence to Schizophrenia
- 1/3 of individuals with an initial diagnosis of Schizophreniform disorder (provisional) recover
within 6 month period and Schizophreniform disorder is their final diagnosis.
- Majority of the remaining 2/3 eventually receive a diagnosis of schizophrenia or Schizoaffective
disorder

Diagnosis of Schizophreniform
DSM-5 Criteria
A. 2 or more of the following, each present for a significant portion of time during a 1-month
period (or less if successfully treated). At least one must be 1-3
1. Delusions
2. Hallucinations
3. Disorganised speech e.g. frequent derailment or incoherence
4. Grossly disorganised or catatonic behaviour
5. Negative symptoms e.g. diminished emotional expression or avolition
B. An episode of the disorder lasts at least 1 month but less than 6 months. When the
diagnosis must be made without waiting for recovery, it should be qualified as “provisional"
C. Schizoaffective disorder and Depressive or Bipolar disorder with psychotic features have been
ruled out because depressive or manic episodes does NOT occur concurrently or only
present for a minority of the total duration
D. The disturbance is not attributable to the physiological effects of a substance or another
medical condition
Specifiers
- with or w/o good prognostic features (good if ≥2 of the following present)
• Onset of prominent psychotic symptoms within 4 weeks of the first noticeable change in usual
behaviour or functioning
• Confusion or perplexity
• Good premorbid social and occupational functioning
• Absence of blunted or flat affect
- with catatonia
- Severity
**Note the lack of criterion requiring impaired social and occupational functioning. While such
impairments may potentially be present, they are no necessary for the diagnosis**

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Schizoaffective Disorder
- Prevalence ~1/3 of Schizophrenia
- F>M, mainly due to increased incidence of depressive type among females
- usu. early adult onset

Clinical presentation of Schizoaffective Disorder

- usu. have another diagnosis before Schizoaffective disorder later when mood become apparent
- Less severe negative symptoms than Schizophrenia
- usu. no insight (aka Anosognosia) but less severe than Schizophrenia
- Classical pattern: Marked auditory hallucination and persecutory deletions for 2 months before
onset of prominent major depressive episode. The psychotic symptoms and full major
depressive episode are the present for 3 months. Then the individual recovers completely from
major depressive episode, but the psychotic symptoms persist for another month before they too
disappear

Diagnosis of Schizoaffective Disorder

DSM-5 Criteria
A. An uninterrupted period of illness during which there is a major mood episode (Depressive or
Manic or mixed, must include depressed mood)
concurrent with a criterion A of Schizophrenia
B. Delusions or hallucinations for 2 or more weeks in the absence of a major mood episode
(depressive or manic) during the lifetime duration of the illness
C. Symptoms that meet criteria for a major mood episode are present for the majority of the
total duration of the active and residual portions of the illness
D. The disturbance is not attributable to the effects of a substance e.g. a drug of abuse, a
medication, or another medical condition
Specifiers
- Type of mood episode
• Bipolar type: Manic episode is part of the presentation, +/- Major depressive episodes
• Depressive type: Major Depressive episodes are part of the presentation
- with Catatonia
- No. of episodes and state of remission
- Severity

ICD-10 Criteria
- Both affective and schizophrenic symptoms prominent within same episode, preferable
simultaneously, but at least within a few days of each other
- Manic type
• Must be a prominent elevation of mood, or a less obvious elevation of mood combined with
increased irritability or excitement
• Within same episode, at least one and preferably 2 typical schizophrenic symptoms (i.e.
Thought alienation, Delusions of control, AVH of running commentary, Bizarre delusions)
- Depressive type
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Delusional Disorders
- Prevalence 0.15% in HK (Chang WC et al., 2017)
- M=F, but Jealous delusion is commoner in male than female
- Significant familial relationship with both Schizophrenia and Schizotypal personality disorder
- Commoner in older individuals

Clinical presentation of Delusional Disorder

- Classically described as systematised, non-bizarre, single-theme delusion(s)
- Commonest theme: Persecutory
- No or non-prominent hallucination/ no perceptual symptoms
that satisfy Criterion A of Schizophrenia; e.g. last < 1month
- Minimal negative symptoms, reported of having better functioning
- Over-represented by women and adult onset
- Relatively rare

Diagnosis of Delusional Disorder

DSM-5 Criteria
A. Presence of one (or more) delusions with a duration of 1 month or longer
B. Criterion A for Schizophrenia has never been met
C. Apart from the impact of the delusion(s) or its ramification, functioning is not markedly
impaired, and behaviour is not obviously bizarre or odd
D. If manic or major depressive episodes have occurred, these have been brief relative to the
duration of the delusional periods
E. Not due to a substance or another medical condition and is not better explained by another
mental disorder
Specifiers
- Type of delusion: Erotomanic, Grandiose, Jealous, Persecutory, Somatic, Mixed, Unspecified
- if with Bizarre content: Delusions are deemed bizarre if they are clearly implausible, not
understandable, and not derived from ordinary life experiences e.g. belief that a stranger has
removed his or her internal organs and replaced them with someone else’s organs w/o leaving
any wounds or scars
- Number of episodes and state of remission
• First vs Multiple vs Continuous
• Acute episode vs Partial remission vs Full remission
- Severity

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Anxiety and related Disorders

Epidemiology of Anxiety Disorders
- Often have an early onset: Teenage or Early 20s
- Female predominance (F:M = 2:1)
- Wax-and-wane course over lifetime

Risk factors of Anxiety Disorders

- Female
- Parents who has anxious personality
- Sensitive/ Emotional character
- Hx of Child abuse (Physical/ Sexual/ Neglect)
- Vitamin B12 deficiency
- Drug side effect, Substance abuse

Pathogenesis of Anxiety Disorders

Limbic System
The “Triune” Brain Model
Human brains were proposed to be comprised of 3 layers in forebrain in contrast to other species
1. Reptilian Complex, 2. Paleomammalian Complex, and 3. Neomammalian Complex
It was later found to be more organised than it proposed
Reptilian Complex Brainstem
Survival response
Allocortex “The Lizard Brain” Cerebellum
- The phylogenetic
Paleomammalian Complex/
counterpart (older) of
Paleocortex Limbic System Process emotions
Neocortex (younger)
- Accounts for majority “The Mammal Brain”
of Cortex in less Arhicortex
intelligent species e.g.
Fish transition between
Periallocortex
Allocortex & Neocortex

Rational thoughts
Neomammalian Complex Cerebrum
Neocortex Language, Abstraction,
“The Human Brain” Basal Ganglia
Planning, Perception

Components of Limbic System

Medial Frontal Cortex (MFC), Orbitofrontal Cortex, Piriform cortex,
Cortical area
Subcallosal gyrus, Cingulate gyrus, Parahippocampal gyrus, Dentate
aka Limbic Cortex/ Lobe/ Gyrus
gyrus, Hippocampus, Subiculum, Fornix

Subcortical area
Amygdala, Septal area, Nucleus accumbens
aka Intra-Limbic Gyrus

Diencephalic area Hypothalamus, Anterior nuclei of Thalamus, Mammillary body

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Amygdala-based Neuro-circuit for Anxiety
- Close communication between Medial Prefrontal Cortex (MFC), Hippocampus, Hypothalamus,
Brainstem nuclei and Amygdala
- Amygdala: Register emotionally significant stimuli → Develop emotional memory
- Hypothalamus & Brainstem nuclei: Somatic manifestation of anxiety
- Hippocampus: Store the cues to anxiety
- MFC: Cognitive control & manifestation of anxiety

Neurochemistry of Anxiety
Dysregulation of the following 3 anxiety-manage systems
- GABA system
• Inhibitory neurotransmitters
• Suppress other neurotransmitter e.g. Serotonin, NE, Dopamine
- Norepinephrine system
• Autonomic arousal and somatic symptoms in Anxiety
- Serotonin system
• Appetite, Energy, Sleep, Mood, Libido, Cognitive function in Anxiety

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Clinical presentation of Anxiety Disorders

Normal Anxiety Pathologic Anxiety

- Adaptive, an inborn response to threat or to the - Excessive

absence of people or objects that signify safety - Impairs function
- Result in cognitive and somatic symptoms.
- A healthy amount of stress improve performance.

Somatic/ Physical symptoms

- GI: Dry mouth, Swallowing difficulty, Epigastric discomfort, Excessive belching, Frequent loose
bowel motions (Diarrhoea)
- Resp.: Chest constriction/ discomfort/ pain, Breathing difficulty, Choking, Tachypnoea,
Hyperventilation
- CVS: Tachycardia, Heart-racing/ Palpitation, Syncope, Sweating
- Genito-urinary: Frequency voiding, Erectile failure, Lack of libido, Increased menstrual
discomfort
- CNS: Tinnitus, Blurred vision, Dizziness, Headache, Muscle aches and stiffness, Hand tremour
- Others: Sleep disturbance, Vivid unpleasant dreams

Cognitive/ Psychological symptoms

- Worrying thoughts
- Fearful anticipation
- Irritability
- Restlessness
- Noice sensitivity
- Poor concentration
- Subjective poor memory
- Avoidance of situations
- Obsessive behaviour
- Compulsive behaviour
* About 30% people with Anxiety disorders also have Depressive Disorder (i.e. Mixed Anxiety
and Depressive Disorder MADD)

Screening questions for Anxiety Disorders

- How ever experienced a panic attack? (Panic)
- Do you consider yourself a worrier? (GAD)
- Have you ever had anything happen that still haunts you? (PTSD)
- Do you get thoughts stuck in your head that really bother you or need to do things over and over
like washing your hands, checking things or count? (OCD)
- When you are in a situation where people can observe you do you feel nervous and worry that
they will judge you? (Specific Anxiety Disorder)

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Spectrum of Anxiety Disorders

Social Phobia Fear of embarrassment

Fear of crowds cannot

Agoraphobia
Phobic Anxiety escape
Disorders
Fear of specific items e.g.
Specific Phobia Height, Blood, Animal,
Thunder

Acute Stress Disorder

Trauma and Fear of traumatic memory
Stressor-related Post-Traumatic Stress Disorder (PTSD)
Anxiety Disorders
Adjustment Disorder (a milder form of depression)
Anxiety Generalised Anxiety Disorder (GAD) Free floating anxiety
Disorders
Panic Disorder Fear of imminent death

Fear of intrusive, obsessive

Obsessive-Compulsive Disorder (OCD)
ideas

Mixed Anxiety and Depressive Disorder

Others
Separation Anxiety Disorder (SAD)

Selective Mutism

Anxiety Disorder substance-induced/

another medical condition

Anxiety Disorder NOS

Management of Anxiety Disorders

- Pharmacological
• Antidepressants e.g. SSRI (Fluoxetine, Paroxetine), SNRI (Venlafaxine), TCA
- GAD: Paroxetine
- Panic Disorder: Fluoxetine, Imipramine
- OCD: Fluoxetine, Clomipramine
- Social Phobia: Paroxetine
- PTSD: Sertraline
• Anxiolytics e.g. Benzodiazepines, Barbiturates (obsolete due to ADR), Buspirone
• Antipsychotics
• Mood stabilisers
- Non-Pharmacological
• Psychotherapy e.g. Cognitive Behavioural Therapy (CBT), Mindfulness-based Cognitive
Therapy, Mindfulness-based Stress Therapy

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Generalised Anxiety Disorder

- M:F = 1:2
- Median age of onset = 30yo
- Monozygotic twin concordance rate: 21.5%; Dizygotic twin concordance rate: 13.5%

Clinical presentation of GAD

- Many report that they have felt anxious and nervous all of their lives
- Children and adolescents tends to worry about quality of their performance or competence at
school or in sporting evens, punctuality, or catastrophic events (e.g. earthquakes, nuclear war)
- Adults tends to worry about well-being of family or their own physical health

Comorbidities
- 2/3 of GAD patients have other psychiatric diagnosis
• Depression (i.e. Mixed Anxiety & Depressive Disorder MADD)
• Other anxiety disorders e.g. Panic Disorder, Social Anxiety
• Personality disorders e.g. Anankastic/ Obsessive-Compulsive, Paranoid, Avoidant
• Alcohol and Drug abuse

Diagnosis of GAD
DSM-5 Criteria
A. Excessive anxiety & worry, occurring more days than not for at least 6 months, about a
number of events or activities
B. The individual finds it difficult to control the worry
C. Associated with 3 or more of the following 6 symptoms
(with at least some having been present for more days than not for the past 6 months)
1. Restlessness or feeling keyed up or on edge
2. Being easily fatigued
3. Difficulty concentrating or mind going blank
4. Irritability
5. Muscle tension
6. Sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying sleep)
D. Causes clinically significant distress & functional impairment
E. Not due to the direct physiological effects of substance or general medical conditions
F. Not better explained by another mental disorder
GAD: Worry WWARTS?
- Worry excessively and
uncontrollably
- Wound up (irritable)
- Worn out (fatigue)
- Absentminded
- Restlessness
- Tensed muscles
- Sleep disturbance
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Approach to GAD

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**Approach to Anxiety**
- 有冇咩情况會令你緊張、擔⼼心、害怕?
• 冇特別嘅原因 (Generalised Anxiety Disorder)
• 去多⼈人/ 密封/ 空曠嘅地⽅方 (Agoraphobia)
• ⾯面對多⼈人嘅時候/ 尷尬嘅場⾯面/ 俾⼈人評論嘅時候 (Social phobia)
• 某啲特別嘅原因/ 場合/ 情況 (Specific phobia)
• 最近(三個⽉月)家庭、婚姻、⼯工作/ 學業⽅方⾯面嘅困擾？解唔解決到？(Adjustment Disorder)

GAD
- 最近幾個⽉月⼼心情如何? 經常緊張、擔⼼心、害怕? (Anxiety & worry)
• ⼼心情係咪經常出現? ⼀一⽇日入⾯面, 有幾多時間擔⼼心緊呢樣嘢? (Excessive)
• 可唔可以控制到? (Uncontrollable)
• 持續左幾耐? (>6 months?)
- 有冇覺得坐立不安? (Wound up/ Restlessness)
- 成⽇日都好容易易攰? (Worn out/ Easily fatigued)
- 集中唔到, 腦海海⼀一⽚片空⽩白? (Absentminded/ Difficulty concentrating or mind going blank)
- 情緒容易易煩躁? (Restlessness/ Irritability)
- 肌⾁肉緊蹦? 鬆弛唔到? (Muscle tension)
- 訓唔著教? (Sleep disturbance)

Other important history

- 對你黎黎講, 會唔會好⼤大困擾? 對⽇日常⽣生活有咩影響? (Distress/ Functional impairment)
- Depressed mood
- Alcohol, Substance
- Suicidality

Ddx of Anxiety
- Generalised Anxiety Disorder
- Panic Attacks/ Panic Disorder (if abrupt unexpected onset that last for a short time)
- Mixed Anxiety & Depressive Disorder
- Depression with anxious features
- Adjustment Disorder

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Panic Disorder

Clinical presentation of Panic Disorder

- Recurrent Panic attacks that are Unpredictable and Acute in onset
• Not consistently a/w a specific situation or object and often occurring spontaneously
• Not a/w marked exertion or with exposure to dangerous or life-threatening situations
• c.f. Phobia is consistent and predicable
- Symptoms reach peak in a few minutes and may last for 10 minutes
- Median age of onset in USG: 20-24yo

Symptoms during Panic Attacks

- Tachycardia, Palpitation
- Overheating, Sweating
- Tremour
- SOB, Choking
- Chest pain/ discomfort
- Dizziness
- Feeling of unreality or being detached from oneself
- Fears of losing control
- Fear of dying
- Nausea or Stomach pain
- Rapid change in body temperature

Complication
- Recurrent attacks → Persistent fear of having another attack → Avoid that situation → Phobia
e.g. Agoraphobia if attack was in various situations
- Self-demoralisation
- Depression

Comorbidities
- Depression
- Other anxiety disorders e.g. Agoraphobia
- Alcohol abuse
- Drug abuse

Ddx of Panic Disorder

- Physical disorders e.g. Epilepsy, Thyroid disease, Cardiac disease, Vestibular dysfunction,
Phaeochromocytoma
- Substance abuse (Intoxication or Withdrawal)
- Other anxiety disorders

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Diagnosis of Panic Disorder

DSM-5 Criteria of Panic Attack
A. An abrupt surge of intense fear or intense discomfort that reaches a peak within minutes,
and during which time 4 (or more) of the following symptoms occur:
Note: The abrupt surge can occur from a calm state or an anxious state
1. Palpitations, pounding heart, accelerated heart rate
2. Sweating
3. Trembling or shaking
4. Sensations of shortness of breath or smothering
5. Feeling of choking
6. Chest pain or discomfort
7. Nausea or abdominal distress
8. Feeling dizzy, unsteady, lightheaded, or faint
9. Chills or heat sensations
10. Paraesthesia (numbness or tingling sensations)
11. Derealisation (feelings of unreality) or depersonalisation (being detached from self)
12. Fear of losing control or “going crazy”
13. Fear of dying

DSM-5 Criteria of Panic Disorder

A. Recurrent unexpected Panic Attacks
B. At least one of the attacks has been followed by 1 month of one or both of the following
1. Persistent concerns about having additional attacks or their consequences
(e.g. losing control, having a heart attack, “going crazy”)
2. A significant maladaptive change in behaviour related to the attacks
(e.g. behaviours designed to avoid having panic attacks, such as avoidance of exercise or
unfamiliar situations)
C. Not due to direct physiological effects of a substance or a general medical condition
D. Not better accounted for by another mental disorder

ICD-10 Criteria of Panic Disorder

- Minimal duration: At least 1 month
- Characteristic feature: Symptoms developed abruptly and reached a peak within 10 minutes
- Core symptoms: A discrete period of intense fear or discomfort
- Asso. symptoms
• Palpitation
• Sweating
• Trembling or shaking
• Sensation of SOB
• Feeling of choking
• Chest pain or discomfort
• Nausea or abdominal distress
• Feeling dizzy, unsteady, lightheaded or faint
• Derealisation of depersonalisation
• Fear of losing control or going crazy
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• Fear of dying
• Paraesthesia (numbness or tingling sensation)
• Chills or hot flushes

**Approach to Panic Disorder**

Signs and symptoms of panic attack
- 你可唔可以講下嗰次⼼心⼝口痛/ 驚恐嘅事? (Intense fear or discomfort)
- 突然之間發作, 幾分鐘之內就去到頂點? (Peak within minutes)
- 有冇其他地⽅方唔舒服? e.g. Palpitation ⼼心跳好快/⼤大⼒力力/⼤大聲/噗噗跳, Sweating 流汗, Trembling/
Shaking 個⼈人震嗮, Shortness of breath 抖唔到氣, Choking sensation 喉嚨有野卡住, Chest pain/
discomfort ⼼心⼝口痛/唔舒服, Nausea/ Abdominal distress 作嘔/個肚唔舒服, Dizzy/ Unsteady/ Faint
頭暈暈, Chills/ Heat sensation 覺得凍/熱, Paraesthesia ⾝身體麻痺/針拮嘅感覺, Depersonalisation 覺
得失去⾃自我感/ ⾃自⼰己好似第三者望住⾃自⼰己, Derealisation 覺得世界唔真實, Fear of losing control 驚
會控制唔到⾃自⼰己, Fear of dying 驚死

Onset/ Precipitating factors

- 當時做緊乜嘢? 有冇⾒見見到乜嘢? (Spontaneous & Unpredictable)
- 當你驚恐發作時腦海海中唸緊咩?

Progression
- 幾時開始第⼀一次發作? (≥1 month) 持續幾耐?
- 有冇越來來越頻密? (Recurrent)
- 由第⼀一次發作開始, 有冇擔⼼心不停發作或者會有負⾯面嘅影響? (Persistent concern)
- 由第⼀一次發作開始, 有冇嘗試避免⼀一啲地⽅方、活動? (Maladaptive change in behaviour)
- 對你黎黎講, 會唔會好⼤大困擾? 對⽇日常⽣生活有咩影響? (Distress/ Functional impairment)

Comorbidities
- Depression
- OCD
- Agoraphobia

Explanation of signs and symptoms

- Hyperventilation
• 當我們受驚時, 在正常的情況下, ⾝身體會作出防衛 / 逃走
• 因此, ⾝身體需要較多的氧氣 (給肌⾁肉⽤用), 呼吸亦因此加速
- Headache, Dizziness, Tinnitus, Feeling of weakness
• 當呼吸加速時, 你會吸入較多的氧氣, 亦會呼出多⼆二氧化碳
• ⾝身體少了了⼆二氧化碳時, 會令你頭痛, 頭暈暈, 眼花, 耳鳴, ⼿手腳軟弱等
- Management of Panic attack
• Controlling breath 嘗試控制呼吸, ⽤用⼿手或者紙袋蓋住黎黎呼吸
• Antidepressant 抗抑鬱藥, CBT ⾏行行為治療
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Management of Panic Disorder

- Antidepressants
• TCA: Imipramine
- Psychotherapy
• Interpretation of body sensation
• Understand physiological response to fear
• Relaxation techniques e.g. Paper-bag breathing during attacks, Slow-breathing exercises

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Phobic Anxiety Disorders

- Psychological and somatic manifestation of anxiety
- Occur ONLY in particular circumstances
- Result in Avoidance and Anticipatory Anxiety
- 3 types: Specific Phobia, Agoraphobia, Social Phobia

**Approach to Phobia**
- 有冇咩情况會令你緊張、擔⼼心、害怕?/ 地⽅方你不敢去?
• 冇特別嘅原因 (Generalised Anxiety Disorder)
• 去多⼈人/ 密封/ 空曠嘅地⽅方 (Agoraphobia) e.g. 搭𨋢/ 排隊或者⼈人多嘅地⽅方/ 獨⾃自離開屋企
• ⾯面對多⼈人嘅時候/ 尷尬嘅場⾯面/ 俾⼈人評論嘅時候 (Social phobia)
• 某啲特別嘅原因/ 場合/ 情況 (Specific phobia)
- 緊張到點樣, 會唔會
• ⼼心跳、⼿手震、出汗
• 透唔到氣、⼼心⼝口唔舒服
• 頭暈暈、抽離現實、幾乎死的感覺
• 好熱、起嗮雞⽪皮、⼿手腳麻痺
• Social phobia: Blushing 臉紅, Urgency 急尿尿, Fear of micturition/ defaecation 驚⽤用公廁
- 會唔會主動避免呢啲令你驚嘅情況 (Avoidance)
- 會唔會未去到/經歷嗰啲情況已經會緊張、擔⼼心、害怕? (Anticipatory anxiety)
- 咁嘅情況維持左幾耐? (>6 months)
- 對你黎黎講, 會唔會好⼤大困擾? 對⽇日常⽣生活有咩影響? (Distress/ Functional impairment)
- Comorbidities: Mood, Sleep, Alcohol, Substance, Suicide

Ddx of Phobia
- Anxiety symptoms: Physical disorder, Substance abuse
- Avoidance features: Personality disorder (e.g. Autism), Psychosis, Depression

General Management of Phobic Anxiety disorders

- Antidepressants
• MAOI: Phenelzine, (RIMA/ MAOAI) Moclobemide
- Psychotherapy
• Targeting the avoidance (hierarchy list)
• Exposure techniques
- Graduated, repeated, prolonged, clear tasks
- Real-life, imaginal exposure
- Home-based, relative support
• Relaxation exercise
• Social phobia: Social skill training, Cognitive treatment for fear of negative evaluation from
others

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Agoraphobic

Clinical presentation of Agoraphobia

- Anxiety triggered by being away from home or in crowds/ situations they cannot leave easily
- Results in avoidance of crowd
- Common places of fear: Buses, Trains, MTR, Supermarket, Queue, Hairdresser’s chair, Cinema
- Need of being accompanied
- Homebound in severe cases

Diagnosis of Agoraphobia
DSM-5 Criteria
A. Marked and consistently fear or anxiety about 2 or more of the following 5 situations
1. Using public transportation
2. Being in open spaces
3. Being in enclosed places
4. Standing in line or being in a crowd
5. Being outside of the home alone
B. The individual fears or avoids these situations because of thoughts that escape might be
difficult or help might not be available in the event of developing panic-like symptoms or
other incapacitating or embarrassing symptoms.
C. The agoraphobic situations almost always provoke fear or anxiety.
D. The agoraphobic situations are actively avoided, require the presence of a companion, or
are endured with intense fear or anxiety.
E. The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic
situations and to the sociocultural context.
F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
H. If another medical condition is present, the fear, anxiety, or avoidance is clearly excessive.
I. Not better explained by another mental disorder

Symptoms of anxiety in the feared situation at some time since the onset of disorder, with at least
two symptoms present together, on at least one occasion, from the list below, one of which must
have been from
- Autonomic arousal symptoms
• Palpitations (pounding heart), accelerated heart rate
• Sweating
• Trembling or shaking
• Eye or mouth dryness
- Chest and abdomen
• Difficulty breathing
• Feeling of choking
• Chest pain or discomfort
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• Nausea or abdominal distress e.g. Churning in stomach
- Brain and mind
• Dizziness, Unsteadiness, Fainting, Light-headed
• Derealisation (objects are unreal), Depersonalisation (one’s self is distant or not really here)
• Fear of losing control, going crazy, passing out
• Fear of dying
- General
• Hot flushes or cold chills
• Numbness of tingling sensation

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Social Phobia

Clinical presentation of Social Phobia

- Median age of onset in USA is 13yo, 75% between 8-15yo
- Anxiety in situations (observed, criticised, embarrassment or humiliation)
e.g. Speak in small group, Introduced to stranger, Eat/ Write in public
- Fear of angry, rejecting face, avoid eye-contact, Blushing and trembling
- “Pathological shyness”

Comorbidities
- Depression
- Alcohol and Substance abuse
- Panic disorder with Agoraphobia

Diagnosis of Social Phobia

DSM-5 Criteria
A. Marked fear or anxiety about one or more social situations in which the individual is
exposed to possible scrutiny by others. Examples include social interactions (e.g. having a
conversation, meeting unfamiliar people), being observed (e.g. eating or drinking), and
performing in front of others (e.g. giving a speech)
Note: in children, the anxiety must occur in peer settings and not just during interactions with
adults
B. The individual fears that he or she will act in a way or show anxiety symptoms that will be
negatively evaluated. (i.e. will be humiliating or embarrassing; will lead to rejection or offend
others)
C. The social situations almost always provoke fear or anxiety.
Note: in children, the fear or anxiety may be expressed by crying, tantrums, freezing, clinging,
shrinking, or failing to speak in social situations
D. The social situations are avoided or endured with intense fear or anxiety.
E. The fear or anxiety is out of proportion to the actual threat posed by the social situations and to
the sociocultural context.
F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
H. The fear, anxiety, or avoidance is not attributable to the physiological effects of a substance or
another medical condition.
I. Not better explained by another mental disorder
J. If another medical condition (e.g. Parkinson’s Disease, Obesity, Disfigurement from burns or
injury) is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive.
Specifiers
- if performance only (i.e. fear is restricted to speaking or performing in public)

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Specific Phobia

Clinical presentation of Specific phobia

- Intense anxiety provoked in the presence or anticipation of specific situation(s) or object(s)
- Common to have multiple specific phobias (75% fear >1 situation/ objects, 3 in average)
- Sometimes develop following a traumatic event (e.g. being attacked by an animal or stuck in an
elevator), observation of others going through a traumatic event (e.g. watching someone drown),
an unexpected panic attack in the to be feared situation (e.g. an unexpected panic attack while
on the subway), or informational transmission (e.g. extensive media coverage of a plane crash)
- usu. develops in early childhood, with majority prior to 10yo
- Specific phobia in children:
• May express fear and anxiety by crying, tantrums, freezing, or clinging
• Not able to understand the concept of avoidance
• Beware that excessive fears are normal but usu. transitory and mildly impairing
- Specific phobia in the elderly:
• More natural environment specific phobias, Phobia of falling
• Tends to co-occur with medical concerns incl. CAD, COPD
• More likely to attribute the symptoms of anxiety to medical conditions
• More likely to manifest anxiety in atypical manner e.g. both anxiety and depression
• a/w Poor QoL and risk factor of Dementia

Diagnosis of Specific Phobia

DSM-5 Criteria
A. Marked fear or anxiety about a specific object or situation.
B. The phobic object or situation almost always provokes immediate fear or anxiety.
C. The phobic object or situation is actively avoided or endured with intense fear or anxiety.
D. The fear or anxiety is out of proportion to the actual danger posed by the specific object or
situation and to the sociocultural context.
E. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
F. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
G. Not better explained by another mental disorder
Specifiers
- Phobic stimulus
• Animal e.g. spiders, insects, dogs
• Natural environment e.g. Height, Storms (Astraphobia), Water (Aquaphobia)
• Blood-injection-injury e.g. Needles (Trypanophobia), Invasive medical procedures, Blood
(Haemophobia), Injections and transfusions, other medical care, Injury
• Situational e.g. Airplanes, Elevators, Enclosed places (Claustrophobia)
• Others e.g. situations that may lead to choking or vomiting, loud sounds, costume characters,
darkness (Nyctophobia)

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Post-Traumatic Stress Disorder

Spectrum of Trauma-and Stressor-related Disorders

- Include disorders in which exposure to a traumatic or stressful event is listed explicitly as a
diagnostic criterion
• Reactive Attachment Disorder
• Disinhibited Social Engagement Disorder
• Post-traumatic Stress Disorder (PTSD)
• Acute Stress Disorder
• Adjustment Disorder

Epidemiology of PTSD
- Prevalence:
• General population: 7-9%
• Trauma victims (60-80%) > Sexual Assault victims (50-80%) > Combat veterans (30%)
- Increased risk in women, younger people
- Risk increases with “dose” of trauma, lack of social support, pre-existing psychiatric disorder

Aetiology of PTSD
Exposure to actual or threatened death, serious violence, or sexual violence
- Direct experiencing of traumatic event(s)
- Witnessed in person the events as it occurred to others
- Learning that the dramatic events occurred to person close to them
- Experiencing repeated or extreme exposure to aversive details of trauma

Pathogenesis of PTSD
- Conditioned fear +/- Genetic or Familial vulnerability
→ Stress-induced release of NE, CRF, Cortisol
(Autonomic arousal immediately after trauma predicts PTSD)

Functional Neuroimaging
- Increased Amygdala activation is seen in PTSD patients compared to controls
- Hypo-activation of the medial prefrontal cortex including the orbitofrontal cortex and anterior
cingulate cortex (area implicated in affect regulation)

Co-morbidities
- Depression
- Other Anxiety disorders
- Substance use disorder, Alcoholism
- Somatisation
- Dissociative disorders (aka Conversion disorders)

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Diagnosis of PTSD
DSM-5 Criteria
A. Exposure to actual or threatened death, serious injury, or sexual violence in one (or more) of
the following ways
1. Directly experiencing the traumatic event(s)
2. Witnessing, in person, the event(s) as it occurred to others
3. Learning that the traumatic event(s) occurred to a close family member or close friend. In
cases of actual or threatened death of a family member or friend, the event(s) must have
been violent or accidental
4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s)
(e.g. first responders collecting human remains; police officers repeatedly exposed to
details of child abuse)
B. Presence of one (or more) of the following intrusive symptoms
1. Recurrent, involuntary and intrusive memories of event
2. Recurrent trauma-related nightmares
3. Dissociative reactions
4. Intense physiologic distress at cue exposure
5. Marked physiological reactivity at cue exposure
C. Persistent avoidance of stimuli
1. Avoidance of distressing memories, thoughts or feelings of the event(s)
2. Avoidance of external reminders of that arouse memories of event(s) e.g. people, places,
activities
D. Negative alterations in cognitions and mood, as evidence by 2 or more of the following
1. Inability to remember an important aspect of the traumatic event(s)
(typically due to dissociative amnesia and not to other factors such as head injury, alcohol,
or drugs)
2. Persistent distorted cognitions about cause or consequence of event that lead to blame of
self, others, or the world (e.g. “I am bad,” “No one can be trusted,” “The world is completely
dangerous,” “My whole nervous system is permanently ruined”)
3. Persistent negative emotional state (e.g. fear, horror, anger, guilt, or shame)
4. Marked diminished interest
5. Feeling detached from others
6. Persistent inability to experience positive emotions
(e.g. inability to experience happiness, satisfaction, or loving feelings)
E. Marked alterations in arousal and reactivity, as evidence by 2 or more of the following
1. Irritable behaviour and and angry outbursts
2. Reckless or self-destructive behaviour
3. Hyper-vigilance
4. Exaggerated startle response
5. Problems with concentration
6. Sleep disturbance
F. Duration of disturbance (Criteria B, C, D, E) is more than 1 month
G. Clinically significant distress or impairment in social, occupational, or other important areas of
functioning
H. Not due to a substance, or another medical condition
Specifiers
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- Presence of Dissociative symptoms
1. Derealisation: Experiences of feeling detached from, and as if one were an outside
observer of, one’s mental processes or body (e.g. feeling as though one were in a dream;
feeling a sense of unreality of self or body or of time moving slowly)
2. Depersonalisation: Unreality of surroundings (e.g. the world is unreal, dream-like, distant, or
distorted)
- if with delayed expression (do not meet criteria until > 6 months after event)

Ddx of PTSD
- Adjustment Disorder
• The stressor can be of any severity or type rather than that required by PTSD Criterion A
• This diagnosis is used when
- PTSD stressor (meet Criterion A) + non-PTSD responses (not meet Criterion B-E)
i.e. response are not to the extent of PTSD
- Non-PTSD stressor (not meet Criterion A) + PTSD responses (meet Criterion B-E)
e.g. spouse leaving, being fired
- Acute Stress Disorder
• Distinguished by duration of 3 days to 1 month following exposure to the traumatic event

**Approach to PTSD**
- Clarify the exposure that triggered anxiety
- Time of exposure (<6 months?)
- Duration of symptoms (>1 month?)
- Criterion B: Intrusive, uncontrolled symptoms
e.g. Flashbacks 腦海海中回帶, Nightmare 惡惡夢, Dissociative symptoms 現實/⾃自⼰己係虛無嘅,
Physiological distress/ reaction ⾝身體反應
- Criterion C: Avoidance of trigger
e.g. place/ similar situations/ conversations/ people
- Criterion D: Negative cognition and mood
• Dissociative amnesia 失憶
• Cognitive distortions
• Negative emotional state 害怕, 驚恐, 憤怒怒, 罪惡惡感, 羞恥
• Diminished interest 失去興趣
• Feeling detached from others 覺得同其他⼈人失去聯聯繫
• Unable to experience positive emotions 感受唔到正⾯面嘅情感
- Criterion E: Increased arousal
• Easily startled, hyper-vigilance 容易易受驚/ 驚⼸弓之⿃鳥
• Anger outbursts 憤怒怒爆發
• Insomnia, Poor concentration 失眠, 集中⼒力力下降
- 對你黎黎講, 會唔會好⼤大困擾? 對⽇日常⽣生活有咩影響? (Distress/ Functional impairment)

Other important history

- Depression
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- Anxiety
- Alcohol/ Substance abuse
- Suicidal risk

Management of PTSD
- Debriefing immediately following trauma is NOT necessarily effective
(may result in Secondary trauma by repeated traumatic memory retrieval)
- Cognitive-behavioural therapy (CBT)
- Group therapy
- Eye Movement Desensitisation and Reprocessing (EMDR)
- Medications: Antidepressants, Mood stabilisers, β-blockers, Clonidine, Prazosin, Gabapentin

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Acute Stress Disorder/ Reaction

Diagnosis of Acute Stress Disorder

DSM-5 Criteria
A. ~PTSD Criterion A
B. Presence of >3 of 5 categories of
• Intrusion
• Negative mood
• Dissociation
• Avoidance, and
• Arousal related to the trauma
C. Duration of disturbance is >3days and <1 month after trauma exposure
D. Causes significant impairment
E. Not due to a substance, another medical condition, or better explained by Brief Psychotic
Disorder

Adjustment Disorder

Diagnosis of Adjustment Disorder

DSM-5 Criteria
A. The development of emotional or behavioural symptoms in response to an identifiable
stressor(s) occurring within 3 months of the onset of the stressors(s)
B. These symptoms or behaviours are clinically significant, as evidenced by one or both of the
following
- Marked distress that is out of proportion to the severity or intensity of the stressor, taking
into account the external context and the cultural factors that might influence symptom
severity and presentation
- Significant impairment in social, occupational, or other important areas of functioning
C. Does not meet the criteria for another mental disorder and is not merely an exacerbation of a
pre-existing mental disorder
D. Do not represent normal bereavement
E. Once the stressor or its consequences have terminated, the symptoms do not persist for
more than an additional 6 months
Specifiers
- with depressed mood
- with anxiety
- with mixed anxiety and depressed mood
- with disturbance of conduct
- with mixed disturbance of emotions and conduct
- unspecified

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Obsessive-Compulsive Disorder
Some says OCD is a spectrum between Neurosis and Psychosis

Epidemiology of OCD
- 2% of general population
- Mean age of onset 19.5yo, 25% start by age 14yo, Male earlier than Females
- M:F = 1:1
- Monozygotic twin concordance rate 57%, Dizygotic twin 22%
- Comorbidities
• >70% have lifetime dx of an Anxiety disorder such as PD, SAD, GAD, phobia
• >60% have lifetime dx of a Mood disorder, MDD being the most common
• Up to 30% have a lifetime Tic disorder
• 12% of persons with Schizophrenia or Schizoaffective disorder

Aetiology of OCD
Genetics
- Serotonergic dysfunction
- Cortico-striato-thalamo-cortical loop
- Autoimmune - PANDAS (Paediatric Autoimmune Neuropsychiatric Disorder Associated with
Streptococcal infections)
- Evidenced by functional neuroimaging showing increased activity in the right caudate is found in
patients with OCD and Cognitive behaviour therapy reduces resting state glucose metabolism or
blood flow in the right caudate in treatment responders.
- Similar results have been obtained with pharmacotherapy

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Clinical presentation of OCD

- Recurrent, compulsive nature
- Maintained insight and regarded as senseless
- Presence of resistance

Over-valued Idea
- An isolated preoccupying belief, not delusional nor obsessional in nature, dominating person’s
life, affecting his actions
- Egosyntonic in nature (c.f. OCD is Egodystonic)

Obsession
DSM-5 definition
1. Recurrent and persistent thoughts, impulses or images that are intrusive and unwanted
that cause marked anxiety or distress
2. The individual attempts to ignore or suppress such thoughts, urges or images, or to
neutralise them with some other thoughts or actions (i.e. compulsion)
Common themes
- Dirt/ Contamination (→ Hand-washing/ Cleaning)
- Symmetry/ Orderliness/ Precision (→ Ordering, Counting, Repeating, Hoarding, Slowness)
- Aggression
- Sex
- Illness
- Religion

Compulsion
DSM-5 definition
1. Repetitive behaviours or mental acts that the person feels driven to perform in response to
an obsession or according to rigidly applied rules
2. The behaviours or acts are aimed at reducing distress or preventing some dreaded situation
however these acts or behaviours are not connected in a realistic way with what they are
designed to neutralise or prevent
Note: Young children may not be able to articulate the aims of these behaviours or mental acts
Common behaviours
- Checking rituals
- Hand-washing/ Cleaning
- Counting
- Slowness

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**Approach to OCD**
- 有冇⼀一啲想法/ 衝動/ 畫⾯面不停喺腦中出現? (Obsession) 例例如覺得
• 啲野好污糟 (Dirt/ Clean)
• 唔整齊 (Orderly)
• 覺得⾃自⼰己⾝身體唔舒服 (Illness)
• 破壞嘅衝動 (Aggression)
• 關於性⾏行行為 (Sex)
• 關於宗教 (Religion)
- 肯唔肯定啲想法係來來⾃自⾃自⼰己⽽而唔係其他⼈人放入去嘅? (exclude Thought insertion)
- 你對呢啲想法有乜感受？令你焦慮/ 唔舒服? (Distress & Anxiety)
- ⾃自⼰己想唔想呢個情況出現? (Unwanted, Egodystonic)
- 有冇試過唔去想佢、控唔控制到？ (Uncontrollable)
- 可唔可以唸其他嘢令⾃自⼰己分⼼心? (Cannot neutralise with other thoughts)
- 幾時開始？有冇越黎黎越多？通常乜野時候出現？(Onset, Progression, Trigger)
- 會唔會重覆做某件事，⽽而通常⼈人地只係會做⼀一兩兩次？(Compulsion) 例例如
• 清潔 (Cleaning)
• 檢查 (Checking)、點算物件數⽬目 (Counting)、收埋啲物件 (Hoarding)
• 或者做得好慢 (Slowness)
- 有冇特定嘅步驟? (Rituals) 唔跟步驟/ 俾⼈人打斷左會點?
- 如果唔做會點, 會唔會更更加焦慮/ 唔舒服, 做完會唔會舒服啲? (Temporary relief by compulsion)
- 勉勉強唔做會點? 做完⼜又點？會唔會好咗？(Compulsion reduce distress)
- 係你⾃自⼰己主動要做，定係畀⼈人控制/威脅咁做？(exclude Delusion of control or Commanding AVH)
- 當時有冇飲完酒？或者食過藥？(Alcohol/ Substance abuse)
- 浪費時間? (Time-consuming)
- 對你黎黎講, 會唔會好⼤大困擾? 對⽇日常⽣生活有咩影響? (Distress/ Functional impairment)
- 你認為點解會咁？你覺得呢啲想法/⾏行行為係正常嘅? (Insight)

Other history
- Depression
- Anxiety
- Suicidal risk

Ddx of OCD
- Obsessive-Compulsive personality disorder (Egosyntonic)
- Autism-spectrum disorder (Rigid ritualised behaviour)

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Diagnosis of OCD
- Obsession and Compulsion can be normal; excessive O&C is termed OCD

DSM-5 Criteria
A. Presence of obsessions, compulsions, or both
B. The obsessions or compulsions
- cause marked distress,
- or is time consuming (e.g. take > 1hour/day or subjective time-consuming)
- or cause clinically significant distress or impairment in social, occupation or other
important areas of functioning
C. Not due to the direct physiological effects of substance
D. Not better explained by another mental disorder
Specifiers
- Degree of insight
• Good/ fair insight - recognises that beliefs are definitely or most likely not true
• Poor insight - think they are probably true
• Absent insight - is completely convinced the OCD beliefs are true
- if Tic-related

Management of OCD
- Only 40-60% patients respond to treatment

Supportive
- Explanation/ Education
- Reassurance

Psychotherapy
- Cognitive behavioural therapy (CBT)
• Exposure and ritual prevention
• Thought stopping and distraction for rumination (resist only increase occurrence)
• Cognitive change
- “If I don’t do it perfectly, then I have done it horribly”
- “If something bad is going to happen, it is much more likely to happen to me or to someone
I love about than to others”
• Modification of responsibility beliefs
• To consider evidence for less threatening alternative explanation

Medications
- Antidepressants e.g. SSRI, SNRI, TCA (Clomipramine), MAOI
- β-blockers e.g. Propranolol
- Benzodiazepines
- Buspirone
- Pregabalin
- Psychosurgery

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Sleep-Wake Disorders
Spectrum of Sleep-Wake Disorders
- Insomnia Disorder
- Parasomnia
- Hypersomnolence Disorder
• Nacrolepsy
- Circadian rhythm sleep-wake Disorders
- Breathing-related sleep disorders
- Movement-related sleep disorder e.g. Restless Leg Syndrome
- Substance/ medication-induced
- Sleep-wake disorders NOS

**Approach to Sleep-Wake Disorders**

1. History, Sleep history
2. P/E, MSE
3. Blood test and imaging studies
4. Sleep investigation

Sleep History
Components
- Bedtime: Time of bed, Duration of sleep induction, Consumption of caffeine-containing
beverages, On-bed activity
- Wakes: Time of wake, Trigger of wake (natural, alarm clock, external stimuli), Location of wake
- Duration: Duration of sleep
- Quality: Daytime function, Occupational safety (e.g. driver, heavy-machinery controller),
Subjective feeling, Frequency of dozing (e.g. reading, in conversation), Symptoms e.g.
Headache, Fall
- Quantity: Total sleep time, Total bed time
- Sleep Efficacy (i.e. Total sleep time divided by Total bed time)
- Behaviours: Frequency of dreams, Content of dreams, Snoring, Restless leg, Sleepwalking
- Remarks e.g. use of sleep diary, actigraphy

Other important history

- Other causes of Insomnia
• Poor sleep hygiene, Inadequate opportunity for sleep
• Psychiatric illness e.g. Depression, Anxiety, PTSD, Mania, Schizophrenia
• Medical illness e.g. Chronic pain, Nocturia, Paroxysmal nocturnal dyspnoea
• Substance abuse e.g. Caffeine, Stimulants
- Functional impairment e.g. Daytime sleepiness
- Significant distress/ concern over inability to sleep, performance anxiety
- Self-medication
- Suicidal risk assessment
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Sleep Investigations
- Sleep diary
- Actigraphy
• Watch-like device to assess rest-activity/ sleep-wakefulness
- Sleep studies
• Full-night Polysomnography (PSG)
• Daytime Sleep studies e.g. Multiple latency sleep test

Physiology of Sleep
- Sleep is an universal physiological drive present in all animals in form of rest-activity cycle but
timing, amount and type of sleep can vary dramatically across species e.g. Circadian in Human
- Sleep is a/w a typical pattern of physiological and behavioural processes

Definition of Sleep:
“Reversible behavioural state of perceptual disengagement from and unresponsiveness to the
environment”

Sleep-wake regulation
**Two-process model**
- Circadian rhythm (aka Process C)
• Neuro-pathway regulated by Suprachiasmatic nucleus, Pituitary gland, and Pineal gland
• Under control by a set of clock genes
• Key neurotransmitter: Melatonin
- Sleep-wake homeostasis (aka Process S)
• Product of a complex network of brain regions and neurotransmitter pathways, which control
sleep onset and maintenance
• Key neurotransmitter: Adenosine

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Normal Sleep Architecture

- Range of healthy sleeping time: 7-9 hours
- There are 2 important physiological states of sleep
1. Non-Rapid eye movement (Non-REM/ NREM) sleep
2. Rapid-eye movement (REM) sleep
3. Awakening (should normally accounts for <5min of total sleep time)
- NREM & REM sleep alternate in cycles, each cycle takes ~90 min
- There are usu. 4-5 cycles per night of sleep

Phases of sleep
- Defined by EEG (Brain activities): Awake, Drowsy, Stage 1, Stage 2, Delta Sleep, REM Sleep
- Defined by EOG (Eye movements): REM, NREM

Non-REM Sleep REM Sleep

75% of total sleep time 20-25% of total sleep time

Time Sleep cycle start with Non-REM REM occur at ~90min after fallen asleep
Progressively shorter 10 minute at first, progressively longer

Brain Decreased mental activities Active brain activity, Dreaming

Eye No movement Rapid movement

Vitals Low HR, BP, Vascular tone, Temp Irregular HR, RR

Paralysed body (Brainstem & Motor neurons

Motor Low BMR, Movable body inhibited)
Irregular muscle movements

Repair and growth Difficult to arouse to stimuli

Feature
Builds up energy Recurrent burst of EMG, REM, Sym. activity

2-5%
N1 Transition phase Tonic REM Parasympathetic activity
Alert if awakened during this period

45-55%
N2 The longest NREM stage
Stages
Light sleep

13-28% Phasic REM Sympathetic activity

N3, Deep sleep/ Slow-wave sleep
N4 Tired if awakened during this period
Goes shorter and fewer with ageing

N1 = 5%; N2 = 50%; N3-4 = 20%; REM = 25%

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Sleep Deprivation
- Sleep deprivation studies showed that sleep is important for normal functioning
- Majority are studied via animal experiments, human experiments and epidemiological studies.
- Animal experiments showed that sleep-deprived animals became weak, uncoordinated, lost
ability to regulate body temperature, increase food intake due to increased metabolism and
eventually died
- Human experiments showed that
• Partial sleep deprivation and short sleep duration (<7hr vs 7-8hr) is a/w mental and physical
health risks e.g. Cardio-metabolic diseases
• Long sleep duration (>9hr) also has health risks

How much sleep is enough?

- Sleep need is determined by sleeping and waking in a free-running manner for at least 1 week
(i.e. no alarm clock, sleep as long as you need, wake up naturally)
- If you feel tired or sleepy in the daytime, you haven’t slept enough

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Insomnia Disorder
- Prevalence of Insomnia in HK
• by DSM-4 definition: 22.1% (~US)
• by DSM-5 definition: 10.8%

Aetiology of Insomnia Disorder

Primary Insomnia

Co-morbid Insomnia/ Secondary Insomnia (obsolete terminology)

- Medical disorders e.g. Pain, Night sweat, Hot flushes, Cancer, COPD, Parkinsonism etc
- Psychiatric disorders e.g. Depressive Disorders, Anxiety Disorders, Schizophrenia
- Sleep disorders e.g. Circadian rhythm Sleep-Wake disorder, OSAS, Restless Leg Syndrome/
Periodic Limb movement disorder

Classification of Insomnia Disorder

by Duration
- Acute (<1 month)
- Subacute (1-3 months)
- Chronic (>3 months)

by Aetiology
- Psychophysiological Insomnia
- Sleep state misperception
- Poor sleep hygiene

Pathogenesis of Insomnia Disorder

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Clinical presentation of Insomnia Disorder

- Onset can be anytime during life but 1st episode usu. in young adulthood
- Insomnia can be situational, persistent, or recurrent
- Sleep disturbance
• Difficulty initiating sleep (DIS)/ Induction Insomnia
- Defined as using >30min to initiate sleep
• Difficulty maintaining sleep (DMS)/ Middle Insomnia
• Early morning awakening (EMA)/ Terminal Insomnia
- Functional impairment e.g. Daytime sleepiness

Complications of Sleep deprivation and short sleep duration (<7hr vs 7-8hr)

- Obesity
- DM
- Pain
- Immune function
- Hypertension
- Cancer

Diagnosis of Insomnia Disorder

DSM-5 Criteria
A. A predominant complaint of dissatisfaction with sleep quantity or quality,
associated with one or more of the following symptoms
4. One or more difficulty initiating sleep (DIS)
5. Difficulty maintaining sleep (DMS), characterised by frequent awakening or problems
returning to sleep after awakenings
6. Early morning awakening (EMA) with inability to return to sleep
B. Cause clinically significant distress or impairment in functioning
C. Sleep difficult occurs at least 3 nights per week
D. Sleep difficult is present for at least 3 months
E. Sleep difficulty occurs despite adequate opportunity for sleep
F. Not better explained by another sleep-wake disorder
G. Not due to substance use or medical condition
H. Co-existing mental disorders and medical conditions do not adequately explain the
predominant complaint of insomnia
Specifiers
- with non-sleep disorder mental comorbidity, incl. substance use disorders
- with other medical comorbidity
- with other sleep disorder
- Frequency
• Episodic: Symptoms last 1-3 months
• Persistent: Symptoms last >3months
• Recurrent: 2 or more episodes within 1 year

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Insomnia Severity Index
- 7 questions (1a-c, 2-5), Each 0-4 scores
- Total score 28
Interpretation
- 0-7 Normal
- 8-14 Mild
- 15-21 Moderate
- 22-28 Severe

Epworth Sleepiness Scale (ESS)

to assess daytime sleepiness
(see next chapter on Hypersomnolence Disorder)

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Management of Insomnia Disorder

Goals
- Improve sleep quality and quantity
- Improve insomnia related daytime impairments

Recommended
- Z drugs e.g. Zopiclone (Imovane®), Zolpidem (Stilnox®)
- Melatonin receptor agonist (MRA) e.g. Ramelteon
- Cognitive behavioural therapy (CBT)

Sleeping drugs
- Approved and Pre-scriptable:
• Z drugs e.g. Zopiclone, Zolpidem
• Melatonin receptor agonist e.g. Ramelteon
• Low dose Doxepin
- Off-label drugs:
• Sedative antidepressants e.g. Mirtazapine (Remeron®), Trazodone, Paroxetine
• Sedative antipsychotics e.g. Quetiapine
- Drugs with health risks: Benzodiazepines e.g. Lorazepam, Clonazepam
- OTC drugs: Promethazine, Melatonin, Valerian

Psychotherapy
- CBT
• Sleep education
• Stimulus control
• Sleep restriction
• Relaxation training
• Cognitive therapy
• Self-help, individual, group, face-to-face, telephone-administered
• Nurse- or therapist-administered
- Mindfulness-based therapies
- Hypnosis
- Sleep hygiene is over-emphasised by family medicine, some studies even find patients who
suffer from insomnia have better sleep hygiene than average (self-compensate for insomnia)

TCM
- Chinese herbal formula
- Acupuncture
- Auricular therapy
- Acupressure

Other complementary and alternative medicine therapies

- Exercise, TaiChi, Qigong, Yoga
- Western herbs
- Aromatherapy

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Hypersomnolence Disorders

What is Sleepiness
- Sleepiness is a normal physiological drive for more sleep
- 2 processes interact in normal sleepiness
• Sleep need: Longer the wakefulness, greater the sleepiness
• Circadian timer: Greatest at 4-6cm, 2nd peak at 2-4pm
- Differs from feelings of tiredness, fatigue and lack of energy

Causes of Sleepiness
- Insufficient Sleep
- Sleep apnoea
- Narcolepsy
- Restless Leg Syndrome/ Periodic Limb Movement Disorder
- Sleep-Wake Circadian Disorder
- Medical/ Psychiatric/ Substance use
- Idiopathic Hypersomnolence

Problems with Sleepiness

- Motor vehicle accidents
- Work-related accidents
- Impaired neuropsychological function
- Impaired motor performance
- Reduced quality of life

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Sleepiness Assessment
Degree of sleepiness
- Mild: Infrequent episodes, occur in situations when little attention is required
- Moderate: Regular episodes, occur in situations when some degree of attention is required
- Severe: Occurs daily, occurs in situations even when sustained attention is required

Epworth Sleepiness Scale (ESS)

- 8 statements of 0-3 marks
- Assessment of severity of daytime sleepiness
Questions
- Sitting and reading
- Watching TV
- Sitting, inactive in a public place (e.g. a movie theatre or a meeting)
- As a passenger in a car for an hour without a break
- Lying down to rest in the afternoon when circumstances permit
- Sitting and talking to someone
- Sitting quietly after a lunch without alcohol
- Driving a car, while stopped for a few minutes in the traffic

Score for each option

- 0 = would never doze
- 1 = slight chance of dozing
- 2 = moderate chance of dozing
- 3 = high chance of dozing
Interpretation
- Total score = 24
- 0-10 = Normal sleepiness
- >10 = Excessive sleepiness
• 11-15 = Mild-moderate
• 16-24 = Severe (could be due to Narcolepsy)

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Multiple Sleep Latency Test (MSLT)
- An objective measure of sleepiness by asking the patient to try to sleep for 20 min at 2-hour
interval starting 2-4 hours after awakening for 4-5 times
- Mean sleep latency; Pathological if <5min
- REM latency - for diagnosis of narcolepsy (i.e. presence of at least one sleep onset REM on
four naps)

Narcolepsy
4 characteristics symptoms
- Excessive sleepiness or sleep attacks
- Cataplexy - sudden loss of bilateral muscle tone provoked by strong emotion. Consciousness
remains clear, varies in severity, head drop, facial sagging, jaw drop, slurred speech, buckling of
knees, few seconds to minutes
- Sleep paralysis - transient, generalised inability to move or to speak during transition between
REM sleep and wakefulness, lasts 1 to several minutes
- Hypnagogic hallucination - vivid perceptual experiences occurring at sleep onset, visual, tactile,
kinetic, affect is often fear or dread, being about to be attacked, being caught in a fire, flying
through the air

Types
- Type 1: Orexin/ Hypocretin-1 deficiency and Cataplexy
- Type 2: Normal Orexin/ Hypocretin level and no Cataplexy

Diagnosis
- Overnight PSG
- MSLT (Short sleep latency < 5 min; Sleep onset REM < 20min)
- HLA-DQB1*0602 allele
- CSF Hypocretin-1 level

Management
- Daytime sleepiness:
• Psycho-stimulants (e.g. Modafinil 冇得訓了了, Armodafinil 呀冇得訓了了, Methylphenidate)
• Ɣ-Hydroxybutyrate (Ɣ-OHB)
- Cataplexy: Antidepressants, Ɣ-Hydroxybutyrate (Ɣ-OHB)

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Breathing-Related Sleep Disorders

Obstructive Sleep Apnoea

Night-time presentation
- Snoring (loud and habitual, intermittent)
- Nocturnal choking, gasping, suffocation
- Witnessed apnoeas
- Restlessness/ excessive sleep movements
- Awakening, Insomnia
- Nocturia

Daytime presentation
- Excessive Daytime sleepiness
- Complaint of having un-refreshing sleep
- Morning headache
- Irritability
- Intellectual deterioration
- Poor concentration and memory
- Decreased libido
- Dry mouth

How to reverse sleepiness

- Regular and adequate sleep
- Caffeine (200 mg or 2-3 cups) not later than 4 pm
- Short naps (15 min)
- Bright light (esp. for shift work, jet lag, seasonal affective disorder)
- Nature of shift work (forward shift, regular night shift, 12-hour 2-shift)

Management
- Nasal CPAP
- Surgery
- Dental appliance

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Parasomnias
- i.e. Any abnormal behaviour occurring during sleep
- Classified according to sleep phase that parasomnia occurs: Sleep-wake transition, NREM, REM
- Important to determine the severity and frequency of parasomnia, which is highly variable

NREM Parasomnia
- History suggestive of NREM Parasomnia: First half of the night, Unable to recall behaviour
- Confirm by sleep studies in some cases
- ICD-10: Confusional Arousal, Sleepwalking, Sleep-related eating disorder (SRED), Sleep Terror
- DSM-5: Sleepwalking type and Sleep terror type only

Sleepwalking/ Somnambulism
- Incomplete transition from deep sleep to wake
- Neurodevelopmental disorder: peak age of onset at 7yo, diminish in frequency with ageing
- Onset of sleepwalking in adults with no prior childhood sleepwalking history should prompt a
search for specific aetiologies e.g. OSA, Nocturnal Seizures, or Drug-related
Precipitating factors
- Physical exertion, heavy exercise
- Fever
- Drugs: Zolpidem, β-blockers
- OSA
- Periodic Leg Movement Disorder (PLMD)
Clinical presentation
- Talking, Hand movement, Standing and walking, Urinating
- 2 special forms of sleepwalking defined in DSM-5
• Eating - Sleep-related Eating Disorder (SRED)
• Sexual behaviour - Sexsomnia/ Sleep Sex
Management
- Accident prevention
- Treat the precipitating factors, e.g. OSA
- Drug treatment: Clonazepam

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Sleep-related eating disorder (SRED)
- Classified under sleepwalking in DSM-5, but with different features to Sleepwalking
- Compulsive eating during sleepwalking, usu. in middle age
-Table
a/w4.Hx of eating
Major disorder,
differences Insomnia,
between Other
sleepwalkingandmental disorders
sleep-related eating disorder
-(SRED)
Management: SSRIs, Topiramate, Clonazepam

Sleepwalking SRED
Age at episode onset Childhood Middle age
Identified triggering factor (e.g., Uncommon (19%) Common (62%)
trauma, stress)
Nocturnal episodes nightly or almost Uncommon (10%) Common (73%)
nightly
Total loss of awareness during Common (39%) Rare (7%)
episode
Presence of dream-like mentation Common (67%) Rare (0%)
Injuries Common (52%) Rare (7%)
History of eating disorder Uncommon (14%) Common (60%)
Current insomnia Rare (5%) Common (73%)
Psychiatric disorders Uncommon (21%) Common (62%)

Sleep Terror/ Night Terrors/ Pavor Nocturnus 夜驚

- ≠ Nightmare
- Occurs in 3% adults, commonly with PTSD
Clinical presentation
- Sense of overwhelming dread with a compulsion to escape
- Repeated occurrence of precipitous awakening from sleep, usu. beginning with a panicky
scream or cry
- During an episode, the individual is difficult to awaken or comfort
- If awaken, the dream is only little or none, or fragmentary, single-images
- Typically has amnesia for the episode on awakening the next morning
- usu. only one episode on any one night
- Occasionally several episodes occur at intervals throughout the night
- Daytime sleepiness

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REM Parasomnia
REM sleep behavioural disorder (RBD)
- = REM Sleep w/o Muscle Atonia (RSWA) (i.e. PSG defined ↑ EMG tone during REM sleep)
+ Dream-enactment behaviours (DEB) (i.e. vocalisation/ motor behaviour during sleep,
correlating with dream mentation)
Risk factors
- Organic brain lesion esp. Brainstem
- Neurodegenerative disorder esp. Parkinson
- OSA
- Z-drug, Antidepressants
Clinical features
- Frequent vivid, action-packed, violent dream
- Loss of muscle atonia that results in enactment of dream content
Management
- Lifelong Clonazepam
- 50% of cases are a/w organic brain lesions, or neurodegenerative disorders, which affect Mx

Sleep Paralysis
“Ghost oppression” 俾⿁鬼壓/ ⿁鬼壓床
- = REM Sleep w/ Muscle atonia + Awakening
Risk factors
- Isolated: Sleep deprivation, Irregular sleep habits, Over-tiredness, Stress
- Recurrent: either Familial or a/w Narcolepsy
Clinical features
- Clear sensorium
- Difficulty in breathing, acute anxiety, hypnagogic imagery
Management
- TCAs and SSRIs which suppress REM sleep

Dreaming
- Dreaming is the result of mental activity during sleep. Most dreams occur in REM
- Sensory modality of dreams include visual, auditory, vestibular (motion), temperature, tactile,
olfactory, gustatory
- Function of dreaming: Organisation of memory
- Drugs that increase dreaming include: β-blockers (atenolol, propranolol), antidepressants
(SSRIs, SNRIs), antipsychotics (Risperidone), GABA agonists (gabapentin, zopiclone,
Benzodiazepines), AChEI (donepezil, rivastigmine), dopamine agonists (Levodopa)

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Movement-related Sleep Disorders

Restless Leg Syndrome (RLS)/ Periodic Limb Movement Disorder (PLMD)

- RLS ≠ PLMD
• RLS = Urge to move one’s legs which is often accompanied by an unpleasant sensation
• PLMD = Diagnosed by overnight PSG
- 80-90% of RLS will have PLMD → Insomnia & excessive daytime sleepiness
- Characterised by periodic episodes of repetitive and highly stereotyped limb movements
during sleep, causes repeated arousal
- Sequence of 4 or more leg movements separated by at least 5 sec and not more than 90 sec

Phenotypes of RLS
- Type I: Early-onset, Familial or Idiopathic RLS - more common
- Type II: Late-onset, Sporadic or Secondary RLS
• Iron deficiency anemia
• Renal failure/ Uraemia
• Neuropathy
• Others

Clinical presentation
- RLS worsens during rest and at night.
- Ferritin level - iron supplement indicated when ferritin < 75 µg/L
- RLS diagnosis is based on history
- PLMD is diagnosed by overnight polysomnography

Management
- alpha-2-delta ligands e.g. Gabapentin, Pregabalin
- Dopaminergics e.g. Levodopa, Pramipexole, Ropinirole
- Opioids e.g. Oxycodone
- Clonazepam

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Circadian Rhythm Sleep-Wake Disorder

Delayed sleep-wake phase disorder (DSWPD)

- The most common (80%) CRSWD
- Advanced, non-24 hr, and irregular
- More common in adolescents and young adults

Diagnosis
- Sleep diary
- Actigraphy
- Chronotype questionnaire
- Salivary dim light melatonin onset (DLMO)

Management
- Low dose Melatonin (0.5 mg) 5 hr before habitual sleep onset or 2-4 hr before DLMO
- Evening light restriction and 2 hr of bright light therapy (5000 lux) on awakening

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Personality Disorders
Personality
- Personality is the consistent cognitive and behavioural pattern of a person in adulthood
e.g. individuals prone to be in an anxious/ depressed state → “Neurotic” personality
- Normal variation in personality is best captured by dimensions rather than types
- Personality disorders are extremely deviant personality from the norm

Tests for personality

- Eysenck Personality Questionnaire → Extraversion, Neuroticism, Psychoticism
- The Big Five Personality Traits → Openness, Conscientiousness, Extraversion, Agreeableness,
Neuroticism

DSM-5 vs ICD-10
DSM-5 ICD-10

Paranoid Paranoid

Schizoid Schizoid

Schizotypal Schizotypal

Antisocial Dissocial

Emotionally unstable
Borderline - Impulsive type
- Borderline type
Histrionic Histrionic

Narcissistic Other - Narcissistic

Avoidant Anxious [avoidant]

Dependent Dependent

Obsessive-Compulsive Anankastic

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DSM-5 Criteria of different PD

1. Unjustified suspicion that others are exploiting, harming or deceiving
2. Unjustified doubts about loyalty or trustworthiness of friends
3. Reluctant to trust others
Paranoid
4. Reads hidden demeaning or threatening meanings into benign remarks
妄想型
or events
5. Persistently bears grudges
5 or more 6. Perceives inapparent attacks on his/her character or reputation and react
angrily quickly/ counterattack
7. Recurrent unjustified suspicion of fidelity of spouse or partner

1. Neither desires nor enjoys close relationships

2. Always chooses solitary activities
Schizoid
Cluster A 3. Little interest in having sexual experiences with another person
孤僻型
“weird, 4. Takes pleasure in few activities
odd, 5. Lack close friends or confidants
eccentric” 4 or more 6. Appears indifferent to praise or criticism of others
7. Emotional coldness, detachment, flattened affect

1. Ideas of reference
2. Odd beliefs or magical thinking
3. Unusual perceptual experiences
Schizotypal 4. Odd thinking and speech
思覺失調型 5. Suspiciousness or paranoid ideation
6. Inappropriate or constricted affect
4 or more 7. Odd, eccentric, peculiar behaviour/ appearance
8. Lack of close friends or confidants
9. Excessive social anxiety, a/w paranoid fears rather than negative
judgements about self

1. Failure to conform to social norms with respect to lawful behaviours

2. Deceitfulness
Antisocial
3. Impulsivity
反社會
4. Irritability and aggressiveness
5. Reckless disregard for safety of self or others
3 or more 6. Consistent irresponsibility
7. Lack of remorse

1. Frantic efforts to avoid real or imagined abandonment

2. Unstable and intense interpersonal relationships - alternating
between extremes of idealisation and devaluation
3. Identity disturbance: markedly and persistently unstable self-image or
sense of self
Borderline
4. Impulsivity that are potentially self-damaging
邊緣型
5. Recurrent suicidal behaviour, gestures, or threats, or self-mutilating
behaviour
5 or more 6. Affective instability
7. Chronic feeling of emptiness
Cluster B 8. Inappropriate, intense anger or difficulty controlling anger
“wild, 9. Transient, stress-related paranoid ideation or severe dissociative
symptoms
dramatic,

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dramatic, 1. Uncomfortable when not the centre of attention
emotional” 2. Inappropriate sexually seductive interaction with provocative
Histrionic behaviour
戲劇化 3. Displays rapidly shifting and shallow expression of emotions
(中⼆二病) 4. Consistently uses physical appearance to draw attention to self
5. Impressionistic and detail-lacking style of speech
5 or more 6. Self-dramatisation, theatricality, exaggerated expression of emotion
7. Suggestible
8. Consider relationships to be more intimate than they actually are

1. Grandiosity
2. Preoccupied with fantasies of unlimited success, power, brilliance,
beauty, love
Narcissistic 3. Idea of uniqueness and superiority
⾃自戀型 4. Excessive need of admiration
5. Sense of entitlement
5 or more 6. Interpersonally exploitative
7. Lacks empathy
8. Envious of others/ Believe others are envious
9. Arrogant, haughty behaviours or attitudes

1. Avoids occupational activities that involve significant interpersonal

contact because of fear of criticism, disapproval, or rejection
2. Unwilling to get involved with people unless certain of being liked
3. Restraint within intimate relationships because of fear of being
Avoidant
shamed or ridiculed
畏懼型
4. Preoccupied with being criticised or rejected in social situations
5. Inhibited in new interpersonal situations because of feelings of
4 or more inadequacy
6. Views self as socially inept, personally unappealing, or inferior to others
7. Unusually reluctant to take personal risks or to engage in any new
activities because they may prove embarrassing

1. Difficulty making everyday decisions w/o excessive amount of advice

and reassurance from others
2. Needs others to assume responsibility for most major areas of life
3. Difficulty expressing disagreement with others because of fear of loss
Dependent of support or approval
依賴型 4. Difficulty initiating projects or doing things on his or her own
Cluster C
5. Excessive effort for nurturance and support from others, to the point
“worried,
5 or more of volunteering to do things that are unpleasant
anxious,
6. Feels uncomfortable or helpless when alone
fearful”
7. Urgently seeks another relationship when a close relationship ends
8. Unrealistically preoccupied with fears or being left to take care of
himself

1. Preoccupied with details, rules, lists, order, organisation, or schedules

to the extent at the major point of the activity is lost
2. Perfectionism that interferes with task completion
3. Excessively devoted to work and productivity to the exclusion of leisure
activities and friendships
Obsessive-
4. Over-conscientious, scrupulous, inflexible about matters of morality,
Compulsive
ethics, or values
強迫型
5. Unable to discard worn-out or worthless objects even have no
sentimental value
4 or more 6. Reluctant to delegate tasks or to work with others unless they submit
to exactly his/her way of doing things
7. Adopts a miserly spending style towards both self and others; money
is viewed as something to be hoarded for future catastrophes
8. Rigidity and stubbornness

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Substance Abuse
and Addictions
Substance Abuse and Addictions 182 Alcohol Induced Neurodevelopmental Disorder 206

Foetal Alcohol Effect 206

Epidemiology of Substance Abuse 182
Foetal Alcohol Syndrome 206
Classification of Common Drugs of Abuse 183

Amphetamines 184 Alcohol and the Brain 207

Cocaine 184 Alcoholic Cerebellar Degeneration 207

Stimulant Overdose/ Sympathomimetic Toxidrome 185 Marchiafava Bignami Disease 208

Nicotine 186 Central Pontine Myelinolysis 209

Phenylcyclidine (PCP), Ketamine 186 Alcohol-induced Neurological deficit 210

Alcohol 187 Light-to-moderate drinking prevents dementia 210

Benzodiazepines & Z-drugs 187 Alcohol and the Eye 211

Opioids 189 Alcohol-Tobacco Amblyopia 211

D-Lysergic Acid Diethyl-amide (LSD) 190 Alcohol and Stroke 211

Cannabis/ Marijuana 190 Light to Moderate Drinking Prevents Stroke 211
Dependence & Addiction 191 Wine Prevents Stroke 211

Terminology 191 Vitamin B1 (Thiamine) Deficiency 212

Pathogenesis of Addiction 191 Aetiology of B1 Deficiency 212
Impact of Addiction 194 Pathogenesis of B1 Deficiency 212
Assessment of Substance Abuse 194 Clinical presentation of B1 Deficiency 212
**Approach to Substance Abuse** 195 Wernicke’s Encephalopathy 213
Diagnosis of Dependence Syndrome 196 Korsakoff’s Syndrome/ Korsakoff’s Psychosis/ Amnesic
Syndrome 214
Other Toxidromes 197
Wernicke-Korsakoff Syndrome 215
Anticholinergic Toxidrome 197
Management of B1 Deficiency 215
Serotonin Syndrome 198

Neuroleptic Malignancy Syndrome (NMS) 199

Vitamin B3 (Niacin) Deficiency 216
Aetiology of B3 Deficiency 216
Alcohol Related Disorders 200
Clinical presentation of B3 Deficiency 216
Alcohol Use Disorder 200
Vitamin B12 (Cobalamin) Deficiency 217
Pathogenesis of AUD 200
Aetiology of B12 Deficiency 217
Diagnosis of AUD 200
Clinical presentation of B12 Deficiency 217
**Approach to Alcohol Dependence** 201
Management of B12 Deficiency 217
Alcohol Intoxication 203
Alcoholic Related Dementia 218
Clinical presentation of Alcohol Intoxication 203
Clinical presentation of ARD 218
Alcoholic Blackouts 203
Diagnosis of ARD 218
Alcohol induced Hypoglycaemia 203
Alcohol and Sleep 219
Diagnosis of Alcohol Intoxication 204
Sleep in Chronic Alcoholics 219
Alcohol Withdrawal Syndrome 204
Sleep in Abstinent Alcoholics 219
Delirium Tremens 204

Hepatic Encephalopathy 205

Alcohol and Suicide 219
Pathogenesis 219
Alcohol and Foetus 206
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Alcohol Related Psychiatric Diseases 220
Alcoholic Hallucinosis 220

Alcohol Induced Delusional Disorders 220

Alcohol Induced Schizophrenia-like Psychosis 220

Alcohol Induced Mood Disorders 220

Alcohol Induced Anxiety Disorder 220

Alcohol Comorbid Psychiatric Disorders 221

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Substance Abuse and Addictions

Epidemiology of Substance Abuse
Commonest substances of abuse in all ages
1. Alcohol
2. Opioids e.g. Heroin, Morphine, Codeine, Methadone, Dipipanone, Opium
3. Cocaine
4. Amphetamines e.g. Amphetamine, Methamphetamine, MDMA
5. Sedatives, Hypnotics, Anxiolytics
6. Hallucinogens e.g. LSD, MDMA
7. Phencyclidines e.g. Ketamine, PCP
8. Inhalants e.g. Thinner
9. Cannabis/ Tetrahydrocannabinol
10. Nicotine e.g. Cigarette smoking, Cigar smoking
11. Caffeine
12. Cough medicine e.g. Tablet, Mixture

Commonest drugs of abuse in all ages

1. Heroin
2. Methamphetamine
3. Benzodiazepine
4. Cocaine
5. Ketamine
6. Cannabis

Commonest drugs of abuse in aged under 21

1. Cocaine
2. Cannabis
3. Methamphetamine
4. Ketamine

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Classification of Common Drugs of Abuse

Actions Example Street names

Amphetamine

Methamphetamine Speed, Meth, Ice, 冰, 凍嘢

Stimulants
MDMA/ Ecstasy 搖頭, Fing頭丸, 狂喜, 忘我, 糖

Cocaine Coke, 可樂樂樂樂

Benzodiazepines e.g. Diazepam, Estazolam,

Nimetazepam: 五仔
Flunitrazepam, Midazolam, Nimetazepam, Triazolam

Barbiturates
Depressants
Z-drugs/ Sleeping drug e.g. Zopiclone, Zolpidem Zopiclone: ⽩白瓜⼦子

Alcohol

Morphine, Codeine
Heroin, DXM, Buprenorphine
Opioids
Methadone, Pethidine, Tramadol, Fentanyl,
Propoxyphene

Cannabis/ Marijuana/ Hash/ Grass/ Pot ⼤大麻, 草, ⽜牛⽜牛

Cannabis resin

Synthetic cannabinoids
Hallucinogens
D-lysergic acid diethyl-amide (LSD) Acid

Gamma-Hydroxybutyrate (GHB) G⽔水, 強姦藥

Mushrooms Alice, Shrooms

Ketamine: K仔
Phencyclidine e.g. Ketamine, PCP
PCP: Angel dust

Other/ Mixed Piperazine derivatives

Cough syrup: B
Cough medications (Mainly Codeine + other)
Cough tablet: O仔

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Amphetamines
Examples
- Amphetamine
- Methamphetamine
• 2nd most common drug of abuse
• Inhalation route (Drug abusing activity is referred as “僕” 冰 - sniffing the smoke on table)
• Greater CNS potency, longer action, t1/2 6-30h
- MDMA
• Pills via Oral route
• Less sympathetic effect
• Faster & more positive psychotic symptoms e.g. euphoria (direct stimulation of release)
• Permanent damage of serotonergic neurons
• Specific complication: SIADH

MOA
- Acute phase
• Direct stimulation of dopamine release (independent of neuronal activity)
• Block dopamine reuptake at MCLP (Meso-cortico-limbic pathway)
• More potent in increasing dopamine → More psychotic symptoms than Cocaine
• Direct stimulate release of norepinephrine, epinephrine and serotonin
- Chronic phase
• Sensitisation: Augmentation of dopamine release
• Tolerance: Depletion of stored neurotransmitter
- Methamphetamine: Additional methyl group to Amphetamine, cross BBB, very long t1/2
→ More potent and longer acting than Amphetamine

Cocaine
- Route of administration: Smoking, Snorting, IV

MOA
- Potent CNS excitatory effect (inhibit reuptake of Serotonin, Noradrenaline, Dopamine)
• Acute phase
- Dopamine reuptake inhibition only (dependent of neuronal activity)
- Less potent in increasing dopamine (c.f. Amphetamines) → Less psychotic symptoms
- Mesocortical & mesolimbic pathway
- Acute reinforcing properties
- Sympathomimetic actions
• Chronic phase
- Decrease sensitivity of dopamine auto-receptors
- Change of post-synaptic receptors and second messenger system
- Intermittent intake → Sensitisation
- Continuous intake → Tolerance
- Other actions
• NaC blocker
• Vasoconstriction (Could induce AMI)
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• Enhance platelet aggregation (Could induce AMI)

Withdrawal symptoms
- Hypo-activity of dopamine system → Less sensitive reward system

Stimulant Overdose/ Sympathomimetic Toxidrome

Causes
- Sympathomimetic hyperactivity e.g. Phaeochromocytoma, HypoG, Alcohol withdrawal, Anxiety
- Sympathomimetic overdose e.g. Amphetamines (Amphetamine, Methamphetamine, MDMA),
Cocaine, Ketamine, (Cannabis?)

Clinical presentation
- Psychomotor Agitation (aka “Tweaking”)
• ~Schizophrenia
• Greatest risk of self-harm or harming others
- Tachycardia, Hypertension
- Hyperthermia, Diaphoresis/ Sweating, Wet skin
- Pupil dilation/ Mydriasis but still responsive (c.f. Anticholinergics)
- Tremour
- Ddx:
• Anticholinergic Toxidrome due to TCA/ Antipsychotic/ Antihistamine/ Carbamazepine overdose
(Big and fixed pupil, Dry skin, Confusion, Hypoactive bowel sound)
• Serotonin Syndrome due to Antidepressant overdose or concurrent TCA/ MAOI/ SSRI
(Hyperreflexia, Hypertonia, Clonus)
• Neuroleptic Malignancy Syndrome (NMS) due to overdose of FGA (Rigidity, Hyporeflexia)
• Delirium Tremens (Hallucination, Seizure)
• Opioid Withdrawal Syndrome (Needle mark)
• Cannabis Overdose (Euphoria, Conjunctival injection, Nystagmus, Ataxia, Slurred speech)

Complications
- Accidents
- CNS: ISS, ICH
- CVS: Angina, Arrhythmia
- Metabolic: Rhabdomyolysis, Hyperthermia, Dehydration, and SIADH (in MDMA)
- Pneumomediastinum, Pneumothorax due to sustained forceful inspiration

Management
- ABC
- IV Hydration
- Treat Hyperthermia by physical means
- Sedation with Benzodiazepine
- C/I β-blockers for Hypertension esp. in Cocaine due to lack of effect on α-adrenergic receptors
which would further increase heart load and cause AMI
- Consult Psychiatrist for psychosis
- Look out for AMI in Cocaine

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Nicotine
- Route of administration: Cigarette smoking

MOA
- Acute phase
• nAChR agonist
• Modest stimulation of dopamine release at MCLP (Meso-cortico-limbic pathway)
• Weak reinforcing action
• Also affect noradrenaline and serotonin
- Chronic phase: Tolerance, Withdrawal

Phenylcyclidine (PCP), Ketamine

- Route of administration: Smoking, Oral, IV

MOA
- Acute phase
• NMDA antagonist (Glutamate receptor) → ↓ GABA inhibitory effect → ↑ Dopamine release
→ Analgesia, Anaesthesia, Cognitive defects, Psychosis
• Direct stimulation of dopamine release
• Monoamine reuptake inhibitor → Hypertension, Tachycardia, Bronchodilation, Agitation
• σ-receptor → Lethargy, Coma
• AChR & GABA → Cholinergic Toxidrome → Bradycardia, Sweating, Sedation, Miosis
- Chronic phase
• Tolerance
• Withdrawal: Lack of clear symptoms in human

Ketamine Toxicity
Clinical presentation
- Psychomotor agitation → Euphoria
- Hallucination (aka K-hole: Profound distortion of bodily awareness, sense of floating/ falling)
- Paranoid ideas
- Thought disorganisation
- Aggression
- Delirium
- Impaired motor function
- Euphoria
- Sympathomimetic toxidrome: Mydriasis, Tachycardia, Hypertension
- Toxicity: LOC, Respiratory depression, Catatonia

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Alcohol
(See next chapter on Alcohol Related Disorders for details)
MOA
- No known receptor system
- Affect ion channels, Calcium and chloride
- Inhibits receptors of excitatory neurotransmitters, and augments activity at receptor level
- Acute phase
• Wide range of receptors involved
• Increase MCLP (Meso-cortico-limbic pathway) dopamine
• Reinforcing GABA activity → ↓ inhibition of other inhibitory neurons
- Chronic phase
• Tolerance
• Withdrawal: Alcohol-induced alteration in sensitivity of GABA and Glutamate → CNS
hypersensitivity

Causes of death
- Intoxication: Accidents, HypoG, Respiratory depression
- Withdrawal: Delirium Tremens (→ Seizure)

Benzodiazepines & Z-drugs

- Route of administration: Oral, IV

Common Benzos & Z-drugs

- Benzodiazepines
• Chlordiazepoxide (Librium®, Librax®) (綠⾖豆仔)
• Diazepam (Valium®) (羅⽒氏五號, 羅⽒氏⼗十號)
• Estazolam
• Flunitrazepam (Rohypnol®) (⼗十字架, R仔)
• Nimetazepam (5仔, ⿈黃⾶飛鴻)
• Midazolam (Dormicum®)(藍藍精靈)
• Triazolam (White preparation: ⽩白瓜⼦子, Blue preparation: 藍藍精靈)
- Z drugs
• Zopiclone (Imovane®)(⽩白瓜⼦子)
• Zolpidem (Stilnox®)

MOA
- Acute phase
• Bind to BZD receptor coupled with GABAA receptor → ↑ Cl channel opening → Enhance
inhibitory effect of GABA
- Chronic phase
• Tolerance: Reduction in functional activity of GABA
• Withdrawal

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Benzodiazepine Toxidrome
Clinical presentation
- Coma with usu. stable vital signs in Oral route
• Mild CNS depression
• Mild hypotension, bradycardia
• Mild Hypothermia
• Seldom cause life-threatening respiratory depression in isolated oral Benzodiazepine OD
- Vital signs can be unstable if IV route (usu. iatrogenic)
Management
- ABC
- Decontamination (usu. NOT considered)
- Antidote: Flumazenil (Anexate®)
• Limited role; Controversial in indication
• Oral overdose is usu. in chronic users - little danger if not given; at risk of withdrawal symptom
• IV overdose is usu. iatrogenic - more indicated
• Pros: Diagnostic and therapeutic in some cases, Able to take history
• Cons: Withdrawal symptoms e.g. Seizure
• C/I Regular sedative user, TCA co-ingestion

Benzodiazepine Withdrawal
Clinical presentation
- Agitation, Restlessness, Sweating, Insomnia, Seizure
- Nausea, Vomiting, Muscle pain, Headache
- Hand tremour
- Anxiety, Depression

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Opioids
Commonly abused opioids
- Natural opioids: Opium, Morphine, Codeine
- Semi-synthetic opioids: Heroin, Dextromethorphan (DXM), Buprenorphine
- Synthetic opioids: Methadone, Pethidine, Tramadol, Fentanyl, Propoxyphene

Route of administration
- Smoking
- IV

MOA
- Acute phase
• Mimic endogenous opioid peptide neurotransmitters
• Opioid receptors: μ, Δ, κ
• Inhibitory effect on the activation of neurons
• Increase activity of dopamine neurons in VTA via inhibition of GABA
- Chronic: Tolerance, Withdrawal

Opioid Toxidrome
Mental ↓ ↓
Clinical presentation
Pupil size ↓ ↓
- CNS depression, Coma
Ventilation ↓ ↓
- Pupil constriction/ Miosis (aka Pin-point pupils)
HR ↓ ↓
- Respiratory depression, Hypoventilation
BP ↓ ↓
- Bradycardia, Hypotension (late)
- Constipation
- a/w Needle marks (commonly in Groin, Cubital fossa, Hand dorsum, Popliteal fossa) and
Furuncles (due to S. aureus infection at injection sites)
Specific association
- Seizure: Tramadol, Pethidine, Propoxyphene
- Serotonin Syndrome: Tramadol, Pethidine, DXM (inhibit Serotonin reuptake or agonism)
- Long action: Methadone, Buprenorphine
Management
- ABC
- Antidote: Naloxone (Larcan®)
• Routes: IV, IM, Intranasal, IO, through ETT
• Short t1/2 (15-20min) of bolus, effect usu. last 45min → May need continuous infusion
• Complications of Naloxone
- Withdrawal syndrome: Agitation, Abdominal cramp, Vomiting
- Acute Pulmonary Oedema
- Symptom recurrence due to short t1/2

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Opioid Withdrawal Mental ↑ ↑
Clinical presentation Pupil size ↑ ↑
- Agitation, Restlessness, Sweating, Insomnia Ventilation ↑ ↑
- Sleepiness, Rhinorrhoea HR ↑ ↑
- Vomiting, Diarrhoea, Abdominal cramps BP ↑ ↑
- PIloerection, Dilated pupil/ Mydriasis
- Tachycardia, Hypertension
- Muscle and joint pain
Management
- Methadone
- Naltrexone
- Buprenorphine

D-Lysergic Acid Diethyl-amide (LSD)

- Route of administration: Oral
- Called “Party drug” because of augmentation of sensation

MOA
- Does not act on Dopamine system
- Acute phase
• Serotonin neurotransmitter system, esp. on auto-receptor
- Chronic phase
• Tolerance
• No evidence of withdrawal (flashback)

Cannabis/ Marijuana
- Route of administration: Smoking, Oral

MOA
- Acute phase
• delta-9-tetrahydrocannabinol (THC) - active ingredient
- Agonist CB1 (CNS), CB2
- Reduction of GABA, enhance release of dopamine
• Cannabidiol (CBD): Antagonist of CB1
- Chronic: Tolerance, Mild withdrawal
Munchies
Clinical presentation
Autonomic hyperactivity
- Euphoria
Racing heart
- Increased appetite/ Hyperphagia
Injection of conjunctiva
- Conjunctival injection/ Chemosis
Judgement impaired
- Tachycardia, Hyperpnoea, Hypertension or Postural hypotension
eUphoria
- Dry mouth
Anxiety
- Nystagmus, ataxia, slurred speech
Nystagmus
- Anxiety, depression in intoxication
Ataxia
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Dependence & Addiction

Terminology
“ Addiction is……an attachment to, or dependence upon, any substance, thing, person or idea so
single-minded and intense that virtually all other realities are ignored or given second place-and
consequences, even lethal ones, are disregarded” John F. Mack (2002)

Problem use/ Misuse Use for pleasure but with disregard for the personal or social danger

Strong and sometimes irresistible desire to use

Craving
Not necessarily pleasurable

Dependence Physical adaptation → Physical withdrawal symptoms

(Physical/ Psychological) Psychological withdrawal symptoms

Extreme end of dependent spectrum

Addiction
Social and personal decline, tolerance, withdrawal symptoms

Pathogenesis of Addiction
- Addiction to any substance starts with occasional use of the substance
- The use of substance was initially an impulsive act
• i.e. presence of increased sense of arousal & sense of tension before the act
• This drives the abusers into binging +/- intoxication
• a phenomenon of Positive reinforcement
- Later become a compulsive act
• i.e. presence of anxiety and stress before and relief after the act
• Abusers develop tolerance → withdrawal symptoms → start to crave the substance and
become preoccupied by the thoughts of using the substance until they finally take it
• a phenomenon of Negative reinforcement
- This would then repeat in a cycle of Principles of reinforcement
- A reinforcer increases the likelihood of a
• Binge +/- Intoxication
behaviour that precedes its presentation
• Withdrawal - Positive reinforcement:
• Craving & Preoccupation Positive outcome after the behaviour
- Negative reinforcement:
Behaviour supported by avoidance or
Reinforcement effect on substance abusers
termination of negative outcome
- All psychoactive drugs/ substances interact with one
or more neurotransmitters (esp. Dopamine) in
Primary neurotransmitters
different ways (Mimicking, Release, Block) - Glutamate (stimulatory)
- These interactions produce positive and negative - GABA (inhibitory)
reinforcement effects via acting on several brain - Adenosine
regions incl. Meso-cortico-limbic pathway (MCLP), Secondary neurotransmitters
Hippocampus, and Amygdala - Dopamine
- Serotonin, Noradrenaline, Acetylcholine
- Endogenous opiates e.g. Endorphin#
- Endogenous cannabinoids e.g.
Anandamide#
# intrinsically addictive
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Positive Reinforcement: Reward Circuit (Mesolimbic pathway)
- One of the 4 dopaminergic pathways
- Ventral Tegmental Area (VTA) → Ventral Striatum/ Nucleus accumbens, Amygdala
- Septal area/ nuclei// Basal forebrain (aka Pleasure centre) works with Nucleus accumbens
- Responsible for motivation, emotion and reward
Reward circuit activation mechanisms
- Dopamine-dependent mechanism (majority of substance)
• Substance of abuse → ↑ Dopamine release in VTA → ↑ Dopamine in NA
• Activate entire mesolimbic pathway
- Dopamine-independent mechanism (Cannabis, Opiates)
• Directly act on NA
• e.g. Cannabis (acts on CB1 receptor), Opiates (↑ 5-HT in Nucleus accumbens)
Contribution to addiction
- When the reinforcers are too powerful, the natural drives e.g. sex, work, eat, hygiene, may be
subsumed and hence ignored
- Positive reinforcement from substance abuse supports the actions of Binging & Intoxication

Negative Reinforcement: Tolerance → Withdrawal → Craving & Preoccupation

Tolerance
- Neural system is changeable - Neuroplasticity
- In substance abusers, the brain changes that same dose of substance have reduced effect
- This phenomenon is called Tolerance
- Mechanisms of tolerance
• Receptor mechanisms e.g. down-regulation of D2 receptors
• Post-receptor mechanisms

Withdrawal
- Tolerance to substance causes withdrawal symptoms due to reduced efficacy
- Symptoms activate extended Amygdala (Amygdala + ACC + PFC) → Inhibit Reward Circuit
- Major neurotransmitters: Corticotropin-releasing hormone (CRH) & NE
- Major projection: Hypothalamus, Brainstem

Craving & Preoccupation

- Amygdala: Conditioning/ Reinforcement (i.e. produce emotion that acts as negative reinforcer)
- Hippocampus: Retrieve episodic memory & process contextual information
(i.e. remember that using the substance is happy)
- PFC: Executive control → Actions to binge again; takes over (top-down control) to actively use
substance instead of controlled by physical symptoms
- Major neurotransmitter: Glutamate

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Stages/ Events Anatomy Mechanism Transmitter Consequence

Initial Positive
occasional use Mesolimbic pathway/ Dopamine reinforcement
Dopamine-dependent
Reward Circuit CB1
Binge & Dopamine-independent
(VTA, NA, Amygdala) 5-HT Tolerance
Intoxication

Down-regulation of D2R
Tolerance \ \ Withdrawal
(Neuroplasticity)

Amygdala, ACC, PFC

CRH
Withdrawal Hypothalamus ↓ Reward Circuit
NE
Brainstem

Amygdala Conditional reinforcement Negative

Craving & Hippocampus Memory reinforcement
Glutamate
Preoccupation
Execution
PFC Binge again
Top-down control

Other factors
- Personality
• Controversial role of personality in substance abuse or dependence syndrome
• ? sensation-seeking, impulsive personality traits, more extrovert personality → predisposed to
experiment with both licit and illicit drugs
• ? obsessional, dependent or anxious → more likely to get dependent and difficult to stop
- Environment
• Study found greater D2R levels in socially housed monkeys, compared to individually housed
• a/w less Cocaine use (less need for reward circuit stimulation?)
- Genetics

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Impact of Addiction
- Medical - depends on route (oral, inhaled, injection), form, substances, chronicity and self care
- Psychological
• Comorbid mental disorders e.g. Anxiety, Depression, Psychosis
• Motivational problems
• Insomnia
- Social
• Relationship
• Housing
• Vacation
• Finance
• Criminal activity

Assessment of Substance Abuse

Principles of Assessment
- Dependence/ Addiction
• Screening tools e.g. CAGE Questionnaire
• Diagnostic criteria e.g. ICD-10
- Formulation (What, Why, How)
• Understand the problems/ difficulties
• Understand the needs (only 20% are pleasure-seeking)
• Understand the person
- Facilitating the establishment of treatment plan
• Stages of changes (Prochaska & Diclemente):
Pre-contemplation, Contemplation, Preparation, Action, Maintenance, Relapse

CAGE Questionnaire Top 10 Reasons College Students Give for

- a screening survey for alcohol misuse Consuming Alcohol (Adler & Rosenberg, 1994)
- Named for the abbreviation of its 4 1) increase feelings of sociability
questions
- Have you ever felt you should CUT down 2) relieves anxiety or tension
on your drinking? 3) makes me feel elated/euphoria
- Have people ANNOYED you by criticising 4) makes me less inhibited
your drinking? 5) enables me to go along with my friends
- Have you ever felt bad or GUILTY about 6) enables me to experience different state of
your drinking?
- Have you ever had a drink first thing in the consciousness
morning to steady your nerves or to get rid 7) makes me less inhibited sexually
of a hangover (i.e. as an EYE-OPENER)? 8) enables me to stop worrying
9) alleviates depression
10) makes me less self-conscious

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**Approach to Substance Abuse**

Drug history
- Name of drug(s) 食邊(幾)種藥?
- Route(s) 點食法？(Oral, Injection, Sniffing)
• 有無溝藥？
• 有冇同⼈人共⽤用針頭?
- First use 第⼀一次食係幾時? 5 important time points
- Onset of dependence 幾時成為習慣？ - Start of use
- Start of regular use
- Reason of abuse ⼀一開始, 咩原因令你習慣食藥?
- Time when think of
- Drug use pattern
discontinuation and outcome
• Where 多數係邊到食? 屋企? 酒吧? 街外⾯面? - Relapse
• Who 同邊個⼀一齊食 - Key consequences
• How much 如果係⼀一個正常嘅⽇日⼦子, 會食幾多?
• How frequent ⼀一個星期有幾多⽇日係咁?
- Progression 有冇越來來越密?

Dependence symptoms
- Craving 有冇好想好想食？
- Difficulties in controlling 控唔控制到幾時食、幾時唔想食、食嘅份量量？
- Tolerance 有無越食越多、頻密左、變做打針、洗多左錢?
- Withdrawal symptoms 唔食會唔會唔舒服？例例如⼿手震、作嘔、流汗、情緒波動; 食返舒服啲？
- Neglect 影響左家庭、⼯工作、其他嘅樂樂樂樂趣? 越黎黎越嚴重?
- Persistence 知不知道食毒品不好, 有什什麼壞處？⽽而繼續食？

Impact (4Ls) 有冇因為飲酒引起後果, 例例如:

- Love & Relationships 影響左同其他⼈人嘅關係？
- Livelihood, Job, Finance ⼀一個⽉月⼤大約要⽤用幾多錢買藥？問家⼈人、朋友借錢買？
- Legal & Crime 有無因為吸毒犯過法/入過警署/ 坐過監？
- Liver: Health complications, hospital admission 影響健康、入醫院?
• Alcohol intoxication, Delirium tremens, Beriberi Disease, Alcoholic Cirrhosis, HCC
• IVDU → Shared needle → HepB, HepC, HIV

Abstinence and Reinstatement

- Previous abstinence and methods attempted 有冇試過戒？點戒？
- Reinstatement 維持到幾耐？
• Reasons for reinstatement 點解食返？
• Reason for successful abstinence 點解成功？
- 6 Stages of Change
• Pre-contemplation & Contemplation 有冇唸過戒? 覺得需唔需要戒? 覺得戒毒有冇好處壞處?
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• Preparation 點樣戒? 有冇計劃? 戒毒有冇咩困難? 有冇其他⼈人可以幫你?
• Action 準備幾時開始?
• Confidence/ belief in likelihood of success 有幾⼤大信⼼心?

Common comorbidities of dependence syndrome

- Mood: Depression, Anxiety
- Insomnia

Diagnosis of Dependence Syndrome

ICD-10 Criteria for Dependence Syndrome
Diagnostic if 3 or more of the following symptoms present together at some time during the
previous year
a) A strong desire or sense of compulsion to take the substance
b) Difficulties in controlling substance taking behaviour in terms of its onset, termination, or
levels of use
c) A physiological withdrawal state when substance use has ceased or been reduced
d) Evidence of tolerance e.g. increased dosage, frequency, change of route, increased
expenditure
e) Progressive neglect of alternative pleasures or interests
f) Persisting with substance use despite clear evidence of overtly harmful consequences

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Other Toxidromes
Refer to Emergency Medicine notes - Clinical Toxicology for details

Anticholinergic Toxidrome
Causes
- Drugs with Anticholinergic ADR
• Antihistamines e.g. Diphenhydramine
• Antidepressants e.g. TCA
• Antipsychotics (Typical and Atypical)
• Anticonvulsants e.g. Carbamazepine
- Anticholinergics
• Antiemetics/ Anti-vertigo e.g. Prochlorperazine, Promethazine, Dimenhydrinate
• Antiparkinsonism/ Anti-EPS e.g. Benzhexol (Artane®), Benzatropine (Cogentin®)
• Antispasmodics e.g. Scopolamine, Hyoscine (Buscopan®)
• Bronchodilators e.g. Atropine, Ipratropium (Atrovent®), Tiotropium
- Herbal Medicine/ Mushroom
• Scopolamine as major component e.g. 洋⾦金金花/曼陀羅, 賽茛菪/東莨菪
• Atropine as major component e.g. 顛茄/顛茄草, 茛菪/⿊黑茛菪/天仙⼦子, ⼭山莨菪/三分三, 矮茛菪/⾺馬尿尿泡,
天蓬⼦子, 茄參參

Clinical presentation
- Pupil dilation/ Mydriasis and Unresponsive (c.f. Mydriasis but responsive in Sympathomimetic)
- Hyperthermia
- Flushing
- Dry skin (c.f. Sweating in Sympathomimetic)
- Tachycardia
- Confusion (less prominent than Sympathomimetics)
- AROU
- Hypoactive/ Sluggish Bowel sound (c.f. Hyperactive in Sympathomimetic)
- Central (drug passed BBB): Confusion, Hallucination, Somnolence, Seizure

Management
- ABC
- Antidote: 1mg Physostigmine
• One of the carbamates
• Reversible AChE Inhibitor
• Been used since 1968
• Pass BBB also
• C/I TCA because of seizure potential

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Serotonin Syndrome
Causes
- Overdose or DDI between Serotonergic drugs
• Antidepressants esp. MAOI (e.g. Selegiline), SSRI except NRI, MRA
• Antipsychotics esp. TCA
• Opioids e.g. Pethidine, Tramadol, DXM/ Dextromethorphan (Cough syrup)
• Drugs of abuse e.g. Cocaine, MDMA, Methamphetamine
• Dopaminergics e.g. Levodopa/ L-Dopa
• Anxiolytics e.g. Buspirone Hunter Criteria: SS diagnosed if any 1 met
• Antibiotics 1. Spontaneous clonus
• Triptans e.g. Sumatriptan 2. Inducible clonus + Agitation/ Diaphoresis
3. Ocular clonus + Agitation/ Diaphoresis
• Herbal products e.g. St John’s wort
4. Inducible/ Ocular clonus + Hypertonia +
• Weight reduction agents (all banned in HK) Hyperthermia
e.g. Sibutramine 5. Tremour + Hyperreflexia

Clinical presentation of SS
- Rapid onset, occurs within 24h of insult (c.f. NMS is insidious onset)
- Cognitive: Headache, Agitation, Hypomania, Confusion, Hallucinations, Coma
- Autonomic: Shivering, Sweating, Hyperthermia, Vasoconstriction, Tachycardia, Nausea,
Diarrhoea, Mydriasis
- Motor: Myoclonus (Ankle Clonus), Hyperreflexia, Babinski’s sign, Tremour, Rigidity
**Rigidity and Clonus are always symmetrical and often much more dramatic in lower limbs**

Complications of SS
- Rhabdomyolysis, Metabolic acidosis, Renal
failure
- Seizure
- Hypotension
- DIC

Management
- r/o Neuroleptic Malignancy Syndrome,
- Remove drug/ toxin
- Treat hyperthermia by physical means
- Antidote: Cyproheptadine (Periactin®)
• Anti-Serotonin (5-HT3 antagonist)
• Anti-Histamine action: Used in allergies
- Sedatives: Benzodiazepine
Serotonin Syndrome NMS

Onset Acute Insidious

Mental Aphasia/ Mutism Agitation

Autonomic Hyperthermia, Shivering, Sweating, Hyperthermia, Sweating, Tachycardia

Tachycardia, Mydriasis Mydriasis

Motor Tremour, Clonus, Hyperreflexia Immobility, Leadpipe rigidity, Hyporeflexia

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Neuroleptic Malignancy Syndrome (NMS)

- Rare but life-threatening severe form of Dystonia due to central dopamine blockade
- MEDICAL EMERGENCY

Causes
- usu. a/w First generation Antipsychotics (FGA) although still rare of about 1 in 500 (0.01-3%)
- Idiosyncratic - can occur w/o overdose, dose-independent

Clinical presentation
- Insidious onset, occur after 1-3 days up to weeks since insult
- Psychological aphasia/ Mutism
- Fever or Hyperthermia, Diaphoresis/ Drug-induced Hyperhydrosis
- Tachycardia, High/ unstable BP
- Mydriasis
- Myolysis, High Creatinine Kinase (CK)
- Immobility
- Leadpipe rigidity
- Hyporeflexia

Management
- r/o Serotonin Syndrome
- r/o Malignant Hyperthermia
- Immediate drug withdrawal
- Supportive treatment
- IV Dantrolene (RyR antagonist)
- Dopamine agonist (Bromocriptine, Levodopa)

Ddx: Malignant Hyperthermia (MH)

- Congenital disorder of Ca regulation in skeletal muscles
- Occurs after inhaled GA (e.g. Halothane) or Depolarising NMB (Suxamethonium)
- p/w Hyperthermia, Rigidity, Increase in end-tidal CO2
- Mx: Supportive, IV Dantrolene (RyR antagonist)

NMS Malignant Hyperthermia

Cause First generation Antipsychotics Inhaled GA, Suxamethonium

Presentation Hyperthermia, Rigidity

Supportive treatment
Treatment
IV Dantrolene

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Alcohol Related Disorders

Alcohol Use Disorder

Pathogenesis of AUD
Alcohol intake
- Stimulation (↑ sensitivity) of GABA receptors (Ɣ-Aminobutyric acid)
→ Enhance inhibitory action of GABA neurotransmission (down-regulate in chronic state)
- Inhibition of NMDA receptors (N-methyl-D-aspartate)
→ Reduce excitatory action of Glutamate neurotransmission (up-regulate in chronic state)
- Indirectly alter the release of other neurotransmitters e.g. Serotonin, Dopamine, NE, Aspartate

Diagnosis of AUD
DSM-5 Criteria of Alcohol Use Disorder
A problematic pattern of alcohol use leading to clinically significant impairment or distress, as
manifested by at least two of the following, occurring within a 12-month period :
1. Alcohol is often taken in larger amounts or over a longer period than was intended
2. There is a persistent desire or unsuccessful efforts to cut down or control alcohol use
3. A great deal of time is spent in activities necessary to obtain alcohol, use alcohol or recover
from its effects
4. Craving, or a strong desire or urge to use alcohol
5. Recurrent alcohol use resulting in a failure to fulfil major role obligations at work, school, or
home
6. Continued alcohol use despite having persistent or recurrent social or interpersonal
problems caused or exacerbated by the effects of alcohol.
7. Important social, occupational, or recreational activities are given up or reduced because
of alcohol use
8. Recurrent alcohol use in situation in which it is physically hazardous
9. Alcohol use is continued despite knowledge of having a persistent or recurrent physical or
psychological problem that is likely to have been caused or exacerbated by alcohol
10. Tolerance, as defined by either of the following
a. A need for markedly increased amounts of alcohol to achieve
intoxication or desired effect
b. A markedly diminished effect with continued use of the same amount of alcohol
11. Withdrawal, as manifested by either of the following
a. The characteristic withdraw syndrome for alcohol (refer to Criteria A and B of the criteria set
for alcohol withdrawal)
b. Alcohol (or a closely related substance, such as benzodiazepine) is taken to relieve or
avoid withdrawal symptoms

Specific marker of Alcohol abuse: Carbohydrate deficient transferrin

Sensitive marker of Alcohol abuse: Phosphatidylethanol
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**Approach to Alcohol Dependence**

Alcohol history
- First drink 幾時開始飲？
- Onset of dependence 幾時開始習慣飲酒? 維持左幾耐? (>1yr?)
- Reason of abuse ⼀一開始, 咩原因令你習慣飲酒?
- Drinking pattern
• When 由訓醒教起⾝身開始, 幾時會飲?
• What type of alcohol 飲啲咩酒? e.g. Beer, Wine, Spirits
• Where 多數係邊到飲? 屋企? 餐廳? 酒吧? 街外⾯面?
• Who 同邊個⼀一齊飲
• How much 如果係⼀一個正常嘅⽇日⼦子, 會飲幾多?
• How frequent ⼀一個星期有幾多⽇日係咁?

CAGE Questionnaire
- Cut down 有冇覺得需要飲少啲？
- Annoyed by others ⾝身邊家⼈人朋友有冇覺得你飲得多/ 勸你飲少啲？
- Guilty 有冇內疚？覺得⾃自⼰己唔應該飲?
- Eye opener 乜野時間飲？朝朝起⾝身都要？

Dependence symptoms
- Craving 有冇好想好想飲？
- Difficulties in controlling 控唔控制到幾時飲、幾時唔想飲、飲嘅份量量？
- Tolerance 有冇酒量量⼤大左、頻密左、洗多左錢？
- Withdrawal symptoms 唔飲會唔會唔舒服？例例如⼿手震、作嘔、流汗、情緒波動; 飲返舒服啲？
- Neglect 影響左家庭、⼯工作、其他嘅樂樂樂樂趣? 越黎黎越嚴重?
- Persistence 知不知道飲酒不好, 有什什麼壞處？⽽而繼續飲？

Abstinence and Reinstatement

- Previous abstinence and methods attempted 有冇試過戒？點戒？
- Reinstatement 維持到幾耐？
• Reasons for reinstatement 點解飲返？
• Reason for successful abstinence 點解成功？
- 6 Stages of Change
• Pre-contemplation & Contemplation 有冇唸過戒? 覺得需唔需要戒? 覺得戒酒有冇好處壞處?
• Preparation 點樣戒? 有冇計劃? 戒酒有冇咩困難? 有冇其他⼈人可以幫你?
• Action 準備幾時開始?
• Confidence/ belief in likelihood of success 有幾⼤大信⼼心?

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Impact (4Ls) 有冇因為飲酒引起後果, 例例如:
- Love & Relationships 影響左同其他⼈人嘅關係？
- Livelihood, Job, Finance ⽤用太多錢買酒？
- Legal & Crime 犯左法？
- Liver: Health complications, hospital admission 影響健康、入醫院?
• Psychotic symptoms e.g. Visual hallucinations, Paranoid delusions, Pathological jealousy
• Co-morbidities e.g. Depression, Anxiety, Substance abuse, Insomnia, Suicide/ Self harm

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Alcohol Intoxication

Clinical presentation of Alcohol Intoxication

- Impairment correlates with level of alcohol in blood (or so reflected by Breathalyser)
- Breathalyser 0.1mg/L = Plasma level 21mg/dL (i.e. 2100X difference)
- HK legal limit of alcohol concentration:
• Breathalyser: 0.22mg/L
• Plasma level: 55mg/dL

Plasma level (mg/dL) Likely impairment

20-30 Slowed motor performance and decreased thinking ability

30-80 Increases in motor and cognitive problems

Increases in incoordination and judgement errors
80-200 Mood lability, Deterioration in cognition
100 mg/dL: Alcohol-induced HypoG

Nystagmus, Marked slurring of speech

200-300
Alcoholic blackouts

>300 Impaired vital signs and possible death

Alcoholic Blackouts
- Transient amnesia “斷⽚片" lasting for hours
- Impaired memory but no impairment in conscious level
- Inhibition of NMDA receptors in Hippocampus
- Failure of long term potentiation (LTP) (i.e. cellular learning and memory by high frequency/
intensity stimulation causing decrease in threshold for activation)

Alcohol induced Hypoglycaemia

- usu. occur when Alcohol blood level 100mg/dL
- a/w Carbohydrate intake/ Empty stomach
- MOA: Alcohol inhibit gluconeogenesis in Liver
- Presentation
• 6-36h after ingestion of >30g of Alcohol
• p/w Confusion, Aggression, Stupor, Coma, Hypothermia
• Often mistaken as alcohol intoxication
- Ix: Increase in blood & urine ketone (β-Hydroxybutyrate)
- Mx: IV Glucose (Glucagon not effective)

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Diagnosis of Alcohol Intoxication

DSM-5 Criteria of Alcohol Intoxication
A. Recent ingestion of alcohol
B. Clinically significant problematic behavioural or psychological changes e.g. inappropriate
sexual or aggressive behaviour, mood lability, impaired judgment that developed during, or
shortly after, alcohol ingestion
C. One or more of the following signs or symptoms developing during, or shortly after, alcohol use:
A. Slurred speech
B. Incoordination
C. Unsteady gait
D. Nystagmus
E. Impairment in attention or memory
F. Stupor or Coma
D. The signs or symptoms are not attributable to another medical condition and are not better
explained by another mental disorder, including intoxication with another substance

Alcohol Withdrawal Syndrome

- Occur 6-24h after last ingestion of alcohol
- Autonomic hyperactivity: Tremour, Sweating, Nausea, Vomiting, Anxiety, Agitation,
Tachycardia, Hypertension, Hyperreflexia, Insomnia, Nightmares, Sweating, Hyperthermia
- Down-regulation of GABA-R in chronic alcoholics
- Reversal of inhibition of NMDA receptor → Glutamate overactivity
- Disappears in 2-7 days
- Mx: Chlordiazepoxide (Librium®), Vitamin B, Hydration

Delirium Tremens
- Severe form of Alcohol withdrawal syndrome
- Occurs in ~24-96h of abstinence
- p/w Delirium (Confusion, Hallucination, Severe agitation) + “Tremour” (i.e. Seizure)
- 5% Mortality
- Medical emergency requiring hospitalisation

Management
- Benzodiazepine e.g. Chlordiazepoxide (Librium®) x 7 days in step-down dosage (starting from
200mg/d)
- Anticonvulsants e.g. Carbamazepine
- Aggressive IV Vitamins esp. Thiamine
- Neuroleptics for control of agitation
- Fluid & Electrolyte balance

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Hepatic Encephalopathy
West Haven Criteria depicts 4 stages of severity
Grade Consciousness & Intellect Signs EEG

Nil except
0 Normal Normal
Psychometric tests +ve
Covert
HE Euphoria, mild confusion, mental Tremour
I slowness, shortened attention span, Apraxia
slurred speech, disordered sleep Impaired handwriting

Lethargy or apathy, disorientation, Flapping tremour Slow 5 cycle per

II modest confusion, disinhibition/ Dysarthria second (cps)
inappropriate behaviour, drowsiness Hyporeflexia triphasic waves

Overt Marked confusion, incoherent speech, Flapping tremour

III HE Hypersomnolence or Semi-stupor, Hyperreflexia
Responsive to stimuli, Bizarre behaviour Babinski sign

IVa Coma; Responsive to pain Slow 2-3 cps delta

Decerebrate posture
IVb Deep Coma; Unresponsive to pain waves

Management of HE
- Lactulose
- Maintain appropriate protein intake level
- BCAA, LOLA
- Rifaximin
- Liver transplant

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Alcohol and Foetus

Alcohol Induced Neurodevelopmental Disorder

- 1% of all live births in USA
- Impaired fine motor skills e.g. Gait disturbance
- Sensorineural deafness
- Poor hand-eye coordination
- Learning difficulties
- Poor impulse control
- Impaired memory, attention, judgement
- Speech difficulty

Foetal Alcohol Effect

- 3-5/ 1,000 live births
- Occur in children with Hx of maternal alcohol abuse

Clinical presentation of FAE

- Prenatal & Postnatal growth retardation
- Neurological abnormality, developmental delay or intellectual impairment
- Craniofacial abnormalities

Foetal Alcohol Syndrome

- 1-4/1,000 live births in USA
- 30% risk in children of mother with heavy drinking
- Most common cause of preventable Intellectual disability/ mental retardation

Clinical presentation of FAS

- Microcephaly due to Corpus callosum agenesis and Cerebellar hypoplasia
- Low birth weight
- Facial dysmorphism: Short eyelid opening, Flat nasal bridge, Median Epicanthal folds, Short
nose, Flat mid face, Upturned nostrils, Absent/ Smooth philtrum, Thin upper lip, Micrognathism
- Growth retardation
- Short stature

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Alcohol and the Brain

Alcoholic Cerebellar Degeneration

- Due to Thiamine Deficiency → Cerebellar Vermis atrophy & Purkinje cell degeneration

Clinical presentation
- Exaggerated wide base gait
- Truncal instability
- Lower limb ataxia
- Postural hand tremour
- Cerebellar Dysarthria (Slurred scanning
speech)
- Nystagmus Left = Normal Cerebellum
Right = Alcoholic, showing Folia atrophy,
Diagnosis Sulci widening anterosuperior to Vermis
- MRI Brain: Vermis degeneration, Sulci widening

MRI (T1W and T2W) of a normal Cerebellum MRI of Vermis degeneration

MRI (Sagittal view, Axial view) of Vermis degeneration

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Marchiafava Bignami Disease

- Occur in severe chronic drinkers
- Classically found in Italian drinkers of crude red wine
- Causing Subacute Demyelination of Corpus callosum
- Typically 40-60yo

Clinical presentation
- Seizure
- Hypertonia (Spasticity/ Rigidity)
- Paralysis
- Coma
- Death
- Frontal Lobe syndrome: Dementia, Personality change

Diagnosis
- MRI Brain: Vacuolation and degeneration of Corpus callosum

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Central Pontine Myelinolysis

- aka Osmotic Demyelination Syndrome
- Demyelination of Pons

Aetiology of CPM
- Rapid rise in plasma osmolarity
e.g. Rapid infusion of hypertonic saline in HypoNa
• Correction of HypoNa should be <10-12 mmol/L/24h
• Chronic HypoNa should be corrected over at least 72 hours
- Cirrhosis
- Liver transplant
- Uraemia
- Haemodialysis
- Prolonged vomiting
- Diuretics

Clinical presentation of CPM

- Tetraplegia w/ Spasticity
- Personality change
- Inappropriate affect
- Delusion

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Alcohol-induced Neurological deficit

- Impairment in Visuospatial processing
- Memory impairment
- EEG abnormalities
- Reduction in Cerebral blood flow
- Reduction in Cerebral glucose metabolism

Light-to-moderate drinking prevents dementia

Rotterdam Study (Ruitenberg, 2002) published on The Lancet:
It was concluded that light to moderate drinking reduce dementia risk
1-3 drinks/d has a Hazard ratio of 0.58 (i.e. protective) in individual 55 or older

Wine Consumption and Dementia in the elderly (Orgogozo 1997) published on The Nature
Reviews Neurology:
- A study conducted in the Bordeaux Area on 3,777 community residents aged 65+
- Moderate drinkers has an Odds ratio of Dementia of 0.18 (Protective) and Odds ratio of
Alzheimer’s Disease of 0.25 (Protective)

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Alcohol and the Eye

Alcohol-Tobacco Amblyopia
- Occurs in heavy drinker and smoker
- Due to Thiamine (B1) or Cobalamin (B12) deficiency

Clinical presentation
- Loss of visual acuity
- Central Scotoma
- Loss of colour vision
- Optic atrophy

Management
- Vitamin B supplement

Alcohol and Stroke

Light to Moderate Drinking Prevents Stroke

According to some old studies (Van Sign 1993, Camargo 1996, Sacco 1999, Klatsky 2001),
Types of Stroke (%) Light/ Moderate drinking Heavy drinking

Haemorrhagic (15) \ Increase in risk

Ischaemic (85) Decrease in risk ?

Light or Moderate drinking prevent Ischaemic Stroke

Heavy drinking increases Haemorrhagic Stroke

Wine Prevents Stroke

According to Copenhagen City Heart Study (Truelsen et al 1998)
Risk of Stroke

Beer No relation

Spirits No relation

Wine Decrease in risk

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Vitamin B1 (Thiamine) Deficiency

Aetiology of B1 Deficiency
- Chronic Alcoholism
- Dietary deficiency e.g. white-rice-predominant diet
- Dialysis
- Chronic diarrhoea
- High dose diuretics
- Genetics

Pathogenesis of B1 Deficiency
Why Chronic Alcoholism causes Thiamine deficiency?
- Low body’s reserve of Thiamine (2-3 weeks)
- Impaired storage capacity
- Decreased intake of micro-nutrients in alcoholics
- Impaired absorption in GI tract esp. Active
• Alcohol inhibit Thiamine pyro-phosphokinase (TPKase), Thiamine pyro-phosphatase
(TPPase), and Thiamine mono-phosphatase (TMPase)
• TPKase convert Thiamine to Thiamine pyrophosphate
• TPPase and TMPase convert Thiamine pyrophosphate to Thiamine
- Increased excretion
- Thiamine dysfunction

Clinical presentation of B1 Deficiency

- B1 deficiency can present in a various ways
- “Beriberi disease” is a umbrella term for all presentation of B1 deficiency
• Wet Beriberi = Affect cardiovascular system
• Dry Beriberi = Affect central nervous system
• Infantile Beriberi = Affect infants of B1-deficient mother
• GI Beriberi = Affect gastrointestinal system

Wet Beriberi
- AFib
- Alcoholic Cardiomyopathy (a type of Dilated Cardiomyopathy)
- High-output HF → Tachycardia, SOB, Lower limb oedema

Dry Beriberi/ Endemic neuritis

- Peripheral sensory neuropathy e.g. numbness and tingling in extremities
- Muscle paralysis & weakness
- Gait disturbance, Pain, Nystagmus
- Wernicke’s Encephalopathy
- Korsakoff’s Syndrome/ Korsakoff’s Psychosis/ Amnesic Syndrome
- Wernicke-Korsakoff Syndrome
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Infantile Beriberi
- Anorexia
- Vomiting
- Lactic acidosis
- Cardiomegaly

Wernicke’s Encephalopathy
- MUST be due to Thiamine deficiency
• Mostly Alcoholic
• Some non-alcoholic

Risk factors
- Alcoholism + Malnutrition
- GI surgery (incl. Bariatric surgery)
- Repeated vomiting incl. Hyperemesis gravidarum
- Cancer
- Systemic illness (Renal failure on CAPD or HD, AIDS, Prolonged infection, Thyrotoxicosis)
- Dietary restriction e.g. Anorexia Nervosa, Elderly neglect

Clinical presentation
- Classical triad (10%): Confusion, Ataxia, Ophthalmoplegia
- Confusion: Attention deficit, Memory impairment, Hallucination
- Ophthalmoplegia, Lateral gaze paralysis, Nystagmus
- Truncal ataxia, Gait disturbance
- (50%) Peripheral neuropathy
- Hypothermia
- Apathy
- (rare) Coma

Diagnosis:
- WE is a clinical diagnosis which requires high index of suspicion
- No test are diagnostic
- EEG and CSF are normal or nonspecific; MRI Brain may show mammillary body atrophy
- Caine’s Criteria: 2 of the following 4 signs
• Dietary deficiency
• Oculomotor abnormalities
• Cerebellar dysfunction
• Altered conscious state or Mild memory impairment
- Often a/w HypoMg

Prognosis
- Only 20% got correctly diagnosed before death (Harper 1983)
- 20% mortality
- Majority progress to Korsakoff’s Psychosis
- Minority recover completely with no sequelae
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Korsakoff’s Syndrome/ Korsakoff’s Psychosis/ Amnesic Syndrome

Aetiology
- Thiamine Deficiency → Diencephalon & Brainstem problem
• Can be alcoholic or non-alcoholic (Puerperal sepsis, Infection, Primary vitamin deficiency)
• Can be precede by Wernicke’s or not
- Medial Temporal Lobe (MTL) lesion
**NOT Alcoholic; NO Thiamine Deficiency; NOT a/w Wernicke’s Encephalopathy
• Closed head trauma
• Penetrating missiles wounds
• Focal tumour
• Encephalitis
• Hypoxia & Carbon monoxide poisoning
• Infarction (PCA stroke)
• Surgery

Clinical presentation
- Anterograde amnesia (i.e. loss of memory after incident/ recent memory)
- Retrograde amnesia (i.e. loss of memory before incident/ old memory)
- Fixation amnesia (i.e. loss of ability to form new memory/ memory of the past few minutes)
- Confabulation (due to mental gap) - mimics psychosis with delusion and hallucination
- No change in consciousness (c.f. Confusion in Wernicke’s)
- No general impairment of other cognitive functions

Combination between Alcoholism, Thiamine Deficiency, MTL

lesion, Wernicke’s Encephalopathy, and Korsakoff’s Psychosis

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Wernicke-Korsakoff Syndrome
- i.e. combined presence of Wernicke’s Encephalopathy and alcoholic Korsakoff Syndrome

Aetiology
- Alcohol
- Non-Alcoholic causes
• Hyperemesis gravida
• Systemic malignancy
• GI surgery
• Dialysis
• Prolonged TPN
• Refeeding Syndrome
• Anorexia nervosa
• Dieting/ Starvation
• Gastrectomy
• AIDS

Pathogenesis
- Petechial haemorrhages, Neuronal loss, Gliosis, and Brown discolouration
in PVG, 3rd Ventricle, Sylvain Aqueduct, 4th Ventricle, Diencephalon, Brainstem

Management of B1 Deficiency
Thiamine replacement
- Poor oral bioavailability → High dose IV Thiamine
- Must be given before nay carbohydrate
- Correct HypoMg if any (Mg is a co-factor for normal functioning of thiamine-dependent enzymes)
- Balanced diet
- Continue oral thiamine after remission if still considered at risk

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Vitamin B3 (Niacin) Deficiency

- aka Pellagra

Aetiology of B3 Deficiency
- Alcoholism
- Dietary deficiency of Niacin or Tryptophan (B3 precursor)
e.g. Over-dependence on maize as food (rare now)

Clinical presentation of B3 Deficiency

Pellagra
- Classical 3Ds: Dementia, Dermatitis, Diarrhoea
- “Dementia” or Mental aberration can include Depression, Apathy, Confusion, Anxiety and
Delirium
- Irritability, Apathy, Depression, Inattention, Amnesia, Stupor, Coma
- Peripheral neuropathy
- Ddx of suspected Delirium Tremens that does not respond to Thiamine replacement

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Vitamin B12 (Cobalamin) Deficiency

- Level required for haematological function: 148 pmol/L (200 pg/ml)
- Level required for neurological function: ~250 pmol/L (~350 pg/ml)

Aetiology of B12 Deficiency

- Chronic Alcoholism
- Long term antacid use
- Partial Gastrectomy
- Atrophic Gastritis
- Pernicious Anaemia
- Dietary deficiency e.g. Vegan diet, Vegetarian diet
- Small bowel diseases e.g. Crohn’s, Coeliac

Clinical presentation of B12 Deficiency

- Subacute Combined Degeneration of Cord (SACD)
- Peripheral neuropathy
- Cerebellar Ataxia
- Optic atrophy
- Dementia
- Depression
- Psychosis
- Delirium

Management of B12 Deficiency

- IM Cyanocobalamin 1mg q.d. x 7 days, 1mg per week x 4 weeks, 1mg per month
- Oral Cyanocobalamin 1mg q.d.

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Alcoholic Related Dementia

- Direct neuronal toxicity of alcohol → Cerebral atrophy
- NOT due to Thiamine deficiency, Niacin deficiency, or Cobalamin deficiency
- NOT due to Marchiafava Bignami Disease (Subacute degeneration of Corpus callosum)

Clinical presentation of ARD

- Occurs at least 8 weeks after abstinence
- Cognitive impairment
- Mimic Frontal lobe dementia
- Partially reversible with sobriety

Diagnosis of ARD
Oslin’s Criteria (1998)
Compulsory
A. A clinical diagnosis of Dementia at least 60 days after last exposure to alcohol
B. Significant alcohol use
A. Defined by a minimum average of 35 standard drinks per week for men (28 for women) for
greater than a period of 5 years
B. Period of significant alcohol use must occur within 3 years of the initial onset of dementia
Supportive
1. Alcohol related hepatic, pancreatic or other end organ damage
2. Ataxia or peripheral sensory polyneuropathy
3. Beyond 60 days of abstinence, the cognitive impairment stabilises or improves
4. After 60 days of abstinence, any neuroimaging evidence of ventricular of ducal dictation
improves
5. Neuroimaging evidence of cerebellar atrophy, esp. the Vermis
Features that cast doubt on diagnosis
1. Language impairment esp. Dysnomia or Anomia
2. Focal neurologic signs or symptoms except Ataxia, Peripheral sensory polyneuropathy
3. Neuroimaging evidence of cortical of subcortical infarction, SDH, or other focal brain pathology
4. Elevated Hachinski Ischaemia Scale score
Features of no diagnostic significance
1. Neuroimaging evidence of cortical atrophy
2. Periventricular or deep white matter lesions on neuroimaging in the absence of focal infarct(s)
3. Apolipoprotein E4 allele (Alzheimer’s)

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Alcohol and Sleep

Sleep in Chronic Alcoholics

- Shortened sleep latency
- Rebound insomnia
- Repeated awakening
- Tolerance

Sleep in Abstinent Alcoholics

- Prolonged sleep latency
- Light & fragmented sleep
- Shortened overall sleep time
- Reduced amount of deep sleep
- Persist for 2 years after abstinence

Alcohol and Suicide

- 7% Alcohol abusers die of suicide
- 96% Alcoholics who die by suicide continue alcohol use up to the end of their lives
- 30% of all completed suicides involve alcoholism
- 50% of all suicide attempted have alcohol consumption at time of attempt

Pathogenesis
Why Alcohol encourages suicide?
- Psychological effect
• Increased impulsivity
• Aggressiveness
• Disinhibition
• Poor judgement
• Increase pain threshold
• Numbing of anxiety response
• Numbing of thoughts on consequences
- Psychosocial effect
• Marital breakdown
• Domestic violence
• Unemployment
• Financial difficulty
• Social isolation
• Poor physical health
• Loss of self esteem

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Alcohol Related Psychiatric Diseases

Alcoholic Hallucinosis
- Occurs in chronic heavy drinkers
- Auditory hallucinations
- No impairment in consciousness
- Distressing in content
- Some develop Schizophrenia, Some remit after stopping alcohol use
- Mx: Antipsychotics, Advice to abstain from alcohol
- Ddx: Delirium tremens (Due to withdrawal; Clouded sensorium, Visual hallucination)

Alcohol Induced Delusional Disorders

- Persistent non-bizarre delusions
- No characteristic schizophrenic symptoms
- Hallucination not prominent and not organised
- Mood episode not significant
- usu. morbid jealousy

Alcohol Induced Schizophrenia-like Psychosis

- Chronic heavy drinking
- Clear sensorium
- Schizophrenic-like syndrome
- Remission on stopping alcohol
- Recur with relapse of alcoholism

Alcohol Induced Mood Disorders

- Moderate or Heavy alcohol use
- Major depression
- Mania
- Persist for up to 4w after abstinence
- Clears up on stopping alcohol

Alcohol Induced Anxiety Disorder

- Symptoms occur while patient on heavy alcohol consumption
- Symptoms subside gradually on abstinence, but may persist to up to 6 months
- May present as GAD, Panic disorder, Phobic anxiety disorders (Social phobia), OCD, PTSD
- Must be distinguished from Alcohol Withdrawal Syndrome

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Alcohol Comorbid Psychiatric Disorders

- Refers to a group of psychiatric disorders commonly being the comorbidities of alcoholism and
related disorders
• 80% of Antisocial personality disorder are Alcoholics
- Begins early in life
- Severe antisocial behaviour before 15yo
- Impulsive, Violent, Manipulative
- Unable to learn from mistakes or benefit from punishment
- Separate genetic factors
• 60% of Bipolar I Disorder are Alcoholics
- Manic episode: Hyper-excitable, Impulsive
- Aggravation of Bipolar disorder
- High suicide rate
• 30% of Schizophrenia are Alcoholics
- Alcohol decrease feeling of isolation → temporary reduce symptoms of anxiety/ depression/
insomnia but increase psychotic symptoms and mood swings
- Disruptive behaviour, suicide, treatment non-compliance, drug abuse, Poor clinical outcome
- Drug accumulation due to liver damage
• 20% of Drug addicts are Alcoholics (Alcoholics have a 6X risk of being drug abusers)
• Also in Anxiety Disorders e.g. Social Phobia, Panic Disorder

Diagnostic criteria (proving that these are not due to Alcohol)

- Evidence of psychiatric disorders before onset of alcohol abuse or dependence
- Evidence of persistent psychiatric symptoms during extended alcohol-free periods (over 4
weeks)
- First degree biological relative has documented psychiatric disorder

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Childhood and
Adolescent Psychiatry
Introduction to Paediatric Psychiatry 223 Youth Depression 243
Classification of Paediatric Psychiatric Disorders 223 Aetiology of Youth Depression 243

Externalising Disorders 224 Clinical presentation of Youth Depression 243

Attention-Deficit/ Hyperactivity Disorder 224 Management of Youth Depression 243

Prognosis of Youth Depression 243

Aetiology of ADHD 224

Pathogenesis of ADHD 224 Feeding and Eating Disorders 244

Clinical presentation of ADHD 225 Myths about Eating Disorders 244

Diagnosis of ADHD 228 Epidemiology of Eating Disorders 244

Management of ADHD 229 Aetiology of Eating Disorders 244

Prognosis of ADHD 230 Anorexia Nervosa 245

**Counselling for ADHD** 230 Epidemiology of AN 245
Autism Spectrum Disorders 231 Aetiology of AN 245

Epidemiology of ASD 231 Pathogenesis of AN 246

Aetiology of ASD 231 Clinical presentation of AN 247

Diagnosis of ASD 232 Diagnosis of AN 249

Investigation of ASD 234 Classification of AN 250

Management of ASD 235 **Approach to AN** 252

Prognosis of ASD 235 Management of AN 253

**Counselling for ASD** 235 Prognosis of AN 255

Oppositional Defiant Disorder/ Conduct Anorexia Nervosa in Students 256

Disorder 237 Bulimia Nervosa 257
DSM-5 Spectrum of Disruptive, Impulse-control, and Epidemiology of BN 257
Conduct Disorders 237
Aetiology of BN 257
Epidemiology of ODD/CD 237
Clinical presentation of BN 257
Aetiology of ODD/CD 237
Diagnosis of BN 258
Clinical presentation of ODD/CD 237
Management of BN 258
Diagnosis of ODD/CD 238
Prognosis of BN 259
Management ODD/CD 239

Prognosis of ODD/CD 239

Internalising Disorders 240

Anxiety Disorders in Children & Adolescents
240
Aetiology of AD 240

Classification of Paediatric AD 240

Spectrum of Paediatric AD 241

Clinical presentation of Paediatric AD 241

Separation Anxiety Disorder 241

Management of Paediatric AD 242

Prognosis of Paediatric AD 242

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Introduction to Paediatric Psychiatry

- 1 in 6 youngsters suffer from psychiatric disorders
- Common disorders: Anxiety Disorders, Oppositional Defiant Disorder, Conduct Disorder, ADHD,
Depressive Disorders, Tics
- Common referrals to tertiary centres often are less common conditions e.g. Autism-spectrum
Disorders, Eating Disorders, OCD, Tourette’s Syndrome

Classification of Paediatric Psychiatric Disorders

- Externalising Disorders: ADHD, ODD, CD
- Internalising Disorders: Anxiety Disorders, Depression, Deliberate Self-Harm
- Pervasive Development Disorders

Red flags: DNA

- Deprivation
- Neglect
- Abuse

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Externalising Disorders
Attention-Deficit/ Hyperactivity Disorder
- 過度活躍症
- Prevalence 5% in children, 2.5% in adults
- M:F = 3:1 in HK; female more likely to present primarily with inattention
- Onset often before school age
- 55-65% by 7yo, 93% by 12yo, 98% by 16yo

Aetiology of ADHD
- Familial, ~25% risk in siblings
- Heritability is 0.7-0.8 (equivalent to Schizophrenia and Bipolar)
- Candidate genes focussed on Dopamine and Serotonin system
- Neuroimaging studies suggested the Frontal-Striatal circuit mediated by Dopamine and NE
transmission

Asso. comorbidities
- (40%) Oppositional Defiant Disorder (ODD) esp. in combined presentation
- Dyslexia
- Autism Spectrum Disorder (ASD)
- (25%) Anxiety Disorder
- (25%) Learning Disability
- (20%) Major Depressive Disorder (MDD)
- (20%) Conduct Disorder (CD)
- (15%) Sleep problems
- (5%) Tourette Syndrome

Pathogenesis of ADHD
- ADHD is a neuro-developmental disorder
- Consists of delays in two dimensions of neuropsychological development/ functioning:

1. Hyperactivity-Impulsivity (Executive Inhibition)

• Deficient motor inhibition → Restless, Hyperactivity
• Impaired verbal inhibition → Excessive talking, Interrupting, rapid premature responding
• Impulsive cognition → Difficulty suppressing task irrelevant thoughts, rapid decision making
• Impulsive motivation → Prefer immediate gratification, greater discounting of delayed
consequences
• Emotion dysregulation → Impulsive affect; poor “top down” emotional self-regulation

2. Inattention (i.e. lack of Executive Attention and Executive Function)

• Poor persistence towards goals, tasks, and the future (cant sustain attention/ action over time)
• Distractible (impaired resistance to responding to goal-irrelevant external and internal events)
• Deficient task re-engagement following disruptions (skips across uncompleted tasks)
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• Impaired working memory (forgetful in daily activities, cannot remember what is to be done)
• Diminished self-monitoring
What is Executive Function?
Domains Description

1. Activation Organising, prioritising & activating to work

2. Focus Focusing, sustaining focus, and shifting focus to tasks

3. Effort Regulating alertness, sustaining effort and processing speed

4. Emotion Managing frustration and modulating emotion

5. Memory Utilising working memory and accessing recall

6. Action Monitoring and self-regulating action

- Executive function is mainly accounted by Frontal Lobe

- Other domains requires input from other parts of CNS e.g. ARAS, Mesolimbic system, ACG,
Temporal lobes, Parietal lobes, Thalamus, Basal ganglia, Cerebellum, Amygdala

Clinical presentation of ADHD

- Toddler: Excessive motor activity - often the earliest observed features; difficult to distinguish
from highly variable normative behaviours before 4yo
- Primary school: Inattention - the most prominent and impairing feature; peak period of diagnosis
- Typically, symptoms vary depending on context within a given setting
- Signs of disorder may be minimal or absent when the individual is receiving frequent rewards for
appropriate behaviour, is under close supervision, is in a novel setting, is engaged in especially
interesting activities, has consistent external stimulation (e.g. via electronic screens), or is
interacting in one-on-one situations (e.g. the clinician’s office)

Inattention/ Attention-Deficit
1. Fails to give close attention to details or makes careless errors in schoolwork, or other activities
e.g. overlooks or misses details, work is inaccurate
2. Difficulty sustaining attention in tasks or play activities
e.g. has difficulty remaining focused during lectures, conversations, or lengthy reading
3. Does not seem to listen when spoken to directly
e.g. mind seems elsewhere, even in the absence of any obvious distraction
4. Does not follow through on instructions and fails to finish school work, chores or duties
e.g. starts tasks but quickly loses focus and is easily sidetracked
5. Difficulty organising tasks and activities
e.g. difficulty managing sequential tasks; difficulty keeping materials and belongings in order;
messy, disorganised work has poor time management; fails to meet deadlines
6. Avoids, dislikes or reluctant to engage in tasks that require sustained mental effort
e.g. schoolwork or homework
7. Easily distracted by extraneous stimuli
(for adolescents and adults, distracted by unrelated thoughts)
8. Forgetful in daily activities
e.g. doing chores, running errands

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9. Loses things necessary for tasks or activities
e.g. school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile
telephones
Inattention in older adolescents & adults
- Difficulty sustaining attention in preparing reports, completing forms, reviewing lengthy papers
- Paralysing procrastination
- Slow, inefficient
- Poor time management
- Disorganised

Hyperactivity
1. Fidgets with hands or feet or squirms in chair
2. Leaves seat in situations when remaining seated is expected
e.g. leaves his/her place in the classroom, in the office, or other workplace
3. Runs about or climbs in situations in which it is inappropriate
(May be limited to feeling restless in adults)
4. Unable to play or engage in leisure activities quietly
5. “on the go” (永遠都郁緊), acting as if “driven by a motor” (上咗摩打咁樣)
e.g. unable to be or uncomfortable being still for extended time, as in restaurants, meetings;
may be experienced by other as being restless or difficult to keep up with
6. Talks excessively
Other features of Hyperactivity in older adolescents & adults
- Workaholic
- Over-scheduled/ Over-whelmed
- Self-select very active job
- Constant activity leading to family tension
- Talks excessively

Impulsivity
7. Blurts out answers before a question has been complete
e.g. completes people’s sentences; cannot wait for turn in conversation
8. Difficulty awaiting turn
e.g. while waiting in line
9. Interrupts or intrudes on others
e.g. butts into conversations, games, or activities;
may start using other people’s things without asking or receiving permission;
for adolescents and adults, may intrude into or take over what others are doing
Other features of Impulsivity in older adolescents & adults
- Making important decisions w/o consideration of long-term consequences e.g. taking a job w/o
adequate information
- Low frustration tolerance e.g. Losing temper, Quitting jobs, Ending relationships, Driving too fast,
Addictive personality
- Irritability
- Mood lability

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Developmental impact of ADHD
Pre-school School-age Adolescence College-age Adult

Behavioural problems

Academic problems & failure

Occupational difficulties & failure

Difficulty with social interaction Relationship problems

Self-esteem issues

Legal issues, Smoking Substance abuse

Injury/ accidents

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Diagnosis of ADHD
- Symptoms of ADHD must be corroborated by someone who knows the patients well

DSM-5 Criteria for ADHD DISTRACTED

A. 6 or more symptoms (5 or more for ≥17yo) Difficult with
of either (A1) inattention or (A2) hyperactivity-impulsivity Instructions
not due to Oppositional behaviour, Defiance, Hostility, or Failure to Sustaining attention
understand tasks or instructions Task forgetting
to a degree that is inconsistent with developmental level Random (unorganised)
that have persisted for at least 6 months Avoidance
B. Several symptoms were present by age 12 years Careless mistakes
C. Several symptoms are present in 2 or more settings Thing missing
D. Clear evidence that symptoms interfere with, or reduce the quality Ear-in-ear-out
of social and academic/ occupational activities Distractibility
(e.g. at home, school, or work; with friends or relatives; in other
activities) FIDGET
E. Symptoms do not occur exclusively during course of Fidget
schizophrenia or another psychotic disorder and are not best Inappropriate
explained by another disorder Driven by motor
Specifiers Game noisily
- Presentation Easy leaving
• Combined presentation (most common) Talk excessively
• Predominantly inattentive presentation
• Predominantly hyperactive/ impulsive presentation CAT
- if in partial remission Convo interrupting
- Severity Answer blurting
• Mild: Number of symptoms just enough to make diagnosis, minor Turn awaiting
impairment
• Moderate: in between mild and severe
• Severe: Number of symptoms in excess to make diagnosis, several severe symptoms, or
marked impairment

Overlapping diagnostic criteria in ADHD with other conditions

Poor Increased
Restless- Distract-
concen- motor Irritability Specific features
ness ibility
tration activity

ADHD ✔ ✔ ✔ ✔

ODD ✔ Negativity, Hostility, Defiance

Inattention due to worry

GAD ✔ ✔ ✔
Rumination

Poor concentration during

Depression ✔ ✔
depressive episode only

Rare in pre-adolescents;
Mania ✔ ✔ ✔
Elevated mod, grandiosity

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Management of ADHD
- Most resolve by adolescence/ adulthood
- Medications
• Drugs effective in ADHD include
- Psycho-stimulants
- Non-stimulants: specific noradrenergic reuptake inhibitor, Imipramine, and Clonidine
- Careful titration of medication is most important
- More effective than psycho-social treatments
- Drug is part of an individualised comprehensive multimodal treatment programs
• Comorbid disturbances often require separated treatment
- Behavioural therapy: Parent Management Training (PMT)
- Special schooling

Psycho-stimulants
- e.g. Methylphenidate (Ritalin® 利利他林林®, Ritalin LA®, Concerta®/ Extended-release Ritalin®)
- Onset 15-30min after intake, Excreted via urine after 3-5 hours
ADR
- Common: Anorexia, Weight loss, Insomnia, Headache, Abdominal pain, Irritability, Mood swing
- Uncommon: Motor tics, Tachycardia

Noradrenergic reuptake inhibitor

- e.g. Atomoxetine (Strattera®)
- Very slow onset (4-6w)
ADR
- Common: Epigastric discomfort, Nausea, Vomiting, Sedation, Anorexia, Dizziness, Mood swing
- Uncommon to Atomoxetine: Deranged LFT

Behavioural therapy: Parent Management Training (PMT)

- Generally regarded as the most effective behavioural therapy
- Specific strategies e.g. Reward system, Time out, Cost system, Social reinforcement, Behaviour
modelling
- Identify problem situations and precipitating factors
- Parent-child interactions - enhance positive and limit negative interactions

Behavioural therapy in Classroom

- Similar to the approach used in home with parents
- Goal: Reduce inattention and disruptive behaviour
- Specific school accommodations:
• Ensure structure and predictable routines
• Employ cost-response token economy systems
• Use daily report cards
• Teach organisational and work/study skills
• Attention to place in class

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Prognosis of ADHD
- ADHD symptoms show an age-dependent decline in severity
(Rate of decline: Hyperactivity >> Impulsivity >> Inattention)
but many continue to have impairment extending to late adolescence and early adulthood
- Early school dropouts and under-achievers in work
- ADHD comorbid with Conduct Disorders are particularly at risk of antisocial, criminal behaviours
and substance abuse
- Increased risk of suicide attempt by early adulthood, primarily when comorbid with mood,
conduct, or substance use disorders
- In adulthood, impulsivity may remain problematic even when hyperactivity has diminished

**Counselling for ADHD**

- 患有過度活躍症嘅⼩小朋友有三⽅方⾯面嘅表現
• Inattention 集中⼒力力不⾜足 e.g. 粗⼼心⼤大意、唔可以長時間集中、同佢講嘢時會⼼心不在焉、唔跟指示
/唔完成功課/家務/職責、唔識整理理作業、唔鍾意/避開需要長時間集中嘅活動、容易易俾其他野分
⼼心、冇記性、遺失重要嘅物件
• Hyperactivity 好動 e.g. 多⼩小動作、擅⾃自離開座位、跑上跑落落、唔可以安靜咁玩、永遠都郁緊/
上咗摩打咁樣、不停講野
• Impulsivity 衝動 e.g. 插嘴、插隊、打斷活動
- Common disease (1 in every 20 children)
- Easily treated with medication: Methylphenidate (Ritalin®) 利利他林林
• Onset: 15-30分鐘後開始發揮作⽤用
• Elimination: 直到3-5⼩小時後透過排尿尿離開⼈人體
• Effect: 好似近視患者戴上眼鏡, 藥效期間會集中注意⼒力力, 思考同做事能⼒力力會提⾼高, 係呢段時間學
嘅良好習慣同技能可以保留留⼀一段較長時間
• 「藥物幫助他成為⾃自⼰己的老闆 」
- May resolve by adolescence/ adulthood
- Behavioural therapy: Parenting Management Therapy (PMT) ⽗父⺟母管理理訓練
教導⽗父⺟母正確嘅⽅方法去⿎鼓勵仔女做適當嘅事, 例例如⽤用稱讚、笑容、擁抱來來酬賞孩⼦子適當的⾔言⾏行行
- Social support: Special schooling may be necessary

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Autism Spectrum Disorders

- ⾃自閉症

Epidemiology of ASD
- ASD is reported to occur in all racial, ethnic, and socioeconomic groups
- ASD is almost 5X more common among boys (1 in 42) than among girls (1 in 189)
- USA: ~ 1 in 68 children according to estimates from CDC’s Autism and Developmental
Disabilities Monitoring (ADDM) Network (2010). ADDM Network also showed a rising trend in
prevalence of ASD.
- Studies in Asia, Europe, and North America have identified individuals with ASD with an average
prevalence of ~1%, up to 2.6% in a South Korean study
- HK: 5.49 per 10,000 in HK at a M:F ratio of 7:1 (V. Wong & S. Hui, 2007)

Aetiology of ASD
- Genetics
• Monozygotic twins: 36-95% +ve
• Dizygotic twins: 0-31% +ve
• Child to parents with one ASD child: 2-18%
• Subsequent siblings of an ASD child: 18.7% (Ozonoff, 2011)
• Siblings of an ASD child: 3-4%
• Heritability: >0.9
- Cognitive
• Theory of mind
• Executive function
• Central coherence
• Extreme male brain
- Anatomical/ Neurochemical
• Mesolimbic (Frontotemporal)
• Cerebellar
• Generalised abnormality with macrocephaly
• Serotonergic system
• Mirror neurons: imitate observed behaviour

Risk factors
- Old paternal & maternal age at conception
- Prematurity
- Low birth weight
- Older siblings with ASD (18.7%)
- Down Syndrome (7-18%)
- Fragile X Syndrome (21%)
- Tuberous Sclerosis (40%)
- Antenatal exposure e.g. Valproate

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Association
- 83% have one or more non-ASD developmental diagnoses
- 10% have one or more psychiatric diagnoses e.g. ADHD
- 10% also have having Down Syndrome, Fragile X Syndrome, Tuberous Sclerosis, or other
genetic and chromosomal disorders
- 46% have average to above-average intellectual ability (i.e. 54% are below average?)

Diagnosis of ASD
DSM-5 is currently criticised for blending all autistic disorders into a single spectrum causing over-
diagnosis and over-treatment. Consensus will be reached when the ICD-11 comes out.

DSM-4: Autistic Disorder

- 3 aspects of symptoms
- Diagnostic if ≥6 symptoms met with ≥2 from social and ≥1 from the other two respectively
Impaired nonverbal social interaction
Poor peer relationship
Social
Lack of spontaneous sharing
Deficits in socio-emotional reciprocity

Speech delay/ Delayed language development

(defined as inability to say single word by 2yo and communicable phrase by 3yo)
Speech Impaired conversation e.g. initiating, sustaining conversation
Idiosyncratic/ Odd language
Lack of spontaneous imaginative play

Preoccupation with restricted interest

Rigid adherence to rituals
Behavioural
Preoccupation with parts of objects
Motor mannerism
- Any patients who do not match the diagnostic criteria exactly are Atypical Autism
5 entities described by DSM-4
- Autism
- Asperger Syndrome (i.e. Autism w/o Speech delay, a/w above average intelligence)
- Rett Syndrome
- Childhood disintegrative disorder (CDD)
- PDD-NOS (Pervasive Developmental Disorder - Not Otherwise Specified)

DSM-5: Autism Spectrum Disorder

- Persistent deficits in social communication and social interaction across multiple
contexts, as manifested by the following, currently or by history
• Deficits in social-emotional reciprocity
e.g. abnormal social approach, failure of normal back-and-forth conversation, reduced sharing
of interests, emotions, or affect, failure to initiate or respond to social interactions
• Deficits in non-verbal communicative behaviours used for social interaction
e.g. poorly integrated verbal and nonverbal communication, abnormalities in eye contact and
body language, deficits in understanding and use of gestures, lack of facial expressions and
nonverbal communication

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• Deficits in developing, maintaining, and understanding relationships
e.g. adjusting behaviour to suit various social contexts, sharing imaginative play, making
friends, absence of interest in peers
- Restrictive, repetitive patterns of behaviour, interests, or activities, as manifested by at least
two of the following, currently or by history
• Stereotyped or repetitive motor movements, use of objects, or speech
e.g. simple motor stereotypes, lining up toys, flipping objects, echolalia, idiosyncratic phrases
• Insistence on sameness, inflexible adherence to routines, or ritualised patterns of verbal or
nonverbal behaviour
e.g. extreme distress at small changes, difficulties with transitions, rigid thinking patterns,
greeting rituals, need to take same route or eat same food every day
• Highly restricted, fixated interests that are abnormal in intensity or focus
e.g. strong attachment to or preoccupation with unusual objects, excessively circumscribed or
perseverative interests
• Hyper- or Hypo-reactivity to sensory input or unusual interest in sensory aspects of the
environment
e.g. apparent indifference to pain/ temperature, adverse response to specific sounds or
textures, excessive smelling or touching of objects, visual fascination with lights or movement
- Symptoms must be present in early developmental period (but may not become fully manifest
until social demands exceed limited capacities, or masked by learned strategies in later life)
- Symptoms cause clinically significant impairment in social, occupational, or other important
areas of current functioning
- Not explained by: Intellectual disability, GDD
- Patients with well-established DSM-4 diagnosis of Autistic disorder, Asperger Syndrome or
pervasive developmental disorder NOS should be given the diagnosis of ASD
- Individuals who have marked deficits in social communication, but whose symptoms do not
otherwise meet ASD criteria should be evaluated for social (pragmatic) communication disorder
Specifiers
- a/w known medical or genetic condition or environmental factor
- a/w another neurodevelopmental, mental, or behavioural disorder
- Current severity for Criterion A and Criterion B:
• Requiring very substantial support
• Requiring substantial support
• Requiring support
- With or w/o accompanying intellectual impairment
- With or w/o accompanying language impairment
- With or w/o Catatonia

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Investigation of ASD
Framework of assessment of an ASD child
- Most important: Clinical interview/ assessment
- Day hospital assessment by multidisciplinary team
- Standardised Assessment / Questionnaire / Rating Scale
• Childhood Autism Rating Scale (CARS)
• Autism Diagnostic Interview – Revised (ADI-R)
• Autism Diagnostic Observation Schedule (ADOS)
• Diagnostic Interview for Social and Communicative Disorders (DISCO)
• Aberrant Behaviour Checklist (ABC)
• Social Responsiveness Scale (SRS)
• Childhood Behaviour Checklist (CBCL)
• Teacher Report Form (TRF)
• Australian Scale for Asperger’s Syndrome (ASAS)
• Autism Spectrum Quotient (AQ)
• Social Stories Questionnaire
• Theory of Mind tests
• Eyes test
- Others: Educational Assessment, IQ Test, OT assessment, ST assessment

First Order Theory of Mind Test

- aka Sally Anne Test
- Assess “Mind reading” ability; lack of this ability is proposed to be the major cause of poor
social interaction and language communication in ASD patients (Baron-Cohen, Leslie & Frith,
1985)
Steps
- “This is Sally. Sally has a basket. This is Anne. Anne has a box. Sally has a marble. She puts the
marble into her basket. Sally goes out for a walk. Anne takes the marble out of the basket, and
puts it into the box. Now Sally comes back. She wants to play with her marble. Where will Sally
look for her marble?”
Interpretation
- Normal children >4yo will say “Sally will look into her basket” quickly
• i.e. able to put themselves in Sally’s shoe
- ASD children will say “Sally will look into the box”
• i.e. unable to differentiate between concept of “Self” and “Others” and unable to put
themselves in others’ shoes, and unable to predict others’ behaviour

Second Order Theory of Mind Test

- aka Mary and John Test
- Assess ability to “Read the mind of a mind-reader”
Steps
- “This is Mary and John, they are school friends in the park. Here comes the ice cream van. John
wants to buy an ice cream but he left his money at home. Ice cream man says ‘don’t worry, I’ll be
in the park all day, you’ve got time to go home’. John runs home to get his money. The ice cream
man changes his mind & tells Mary ‘I can’t stay here, I’m off to the church’. Mary goes home and
the ice cream man sets off to the church. But on the way the ice cream man meets John & says
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‘I’m off to the church now instead’. In the afternoon, Mary goes to John’s house & knocks on the
door. John’s mum answers the door & says ‘oh, John has gone out to buy an ice cream’…
(Perner & Wimmer)”
- Where does Mary think John has gone to buy an ice cream?
Interpretation
- Normal children will say “The park”
- ASD will say “The church”

Third Order Theory of Mind Test

Management of ASD
- Treatments aim at fostering acquisition of social, communicative, and cognitive skills at
developmentally appropriate level and are achieved by a combination of intensive structured
training, behavioural modification techniques, and appropriate education
- Psycho-education, counselling and training of parent as co-therapist, and practical help for
families
- There are no medications that can cure ASD or even treat the main symptoms. But there
are medications that can help some people with related symptoms.
- Target symptoms approach
• For example, medication might help manage high energy levels, inability to focus, depression,
or seizures.
• Antipsychotics (Risperidone and Aripiprazole; endorsed by FDA) and may be beneficial for
control of aggression, irritability,
• Possibly SSRIs may be beneficial for control of obsession

Prognosis of ASD
- Continuous course
- Prognostic markers: IQ score & Language development at 5yo
- 1/3 achieves some level of independence, but only a few manage to live fully independently
- 1/5 develops seizure at adolescence

**Counselling for ASD**

- Prevalence: 每⼀一萬個香港兒童有5名兒童確診為⾃自閉症, 男仔受影響嘅機率遠⾼高於女仔
- ⾃自閉症有3⽅方⾯面嘅表現
• Social 社交 e.g. ⾝身體語⾔言、朋輩關係、主動分享、情感回應
• Speech 語⾔言 e.g. 遲講嘢、唔識同⼈人溝通、奇怪嘅字、戲劇性遊戲
• Behavioural ⾏行行為 e.g. 局限嘅興趣、刻板及重覆動作、執著物件嘅某⼀一部分
- What is autism
• 發展過程嘅嚴重障礙
• 長期性
• 每個患者有唔同程度嘅障礙
- Pathophysiology
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• ⽣生理理同神經系統異異常
• 遺傳係⼀一個重⼤大因素
• 冇關環境、飲食、疫苗
- Prognosis
• 學習模式與⼀一般⼈人唔同
• 缺乏吸收同處理理基本資訊嘅能⼒力力
• 拖延發展語⾔言、遊戲、社交技能
•

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Oppositional Defiant Disorder/ Conduct Disorder

DSM-5 Spectrum of Disruptive, Impulse-control, and Conduct Disorders

- Intermittent Explosive Disorder
- Oppositional Defiant Disorder (ODD)
- Conduct Disorder (CD)
- Antisocial Personality Disorder
- Kleptomania (Stealing)
- Pyromania (Fire setting)
- Impulse control disorder NOS

Epidemiology of ODD/CD
- ODD: 5% of school-age children
- CD: 3-4% of school-age children
- M:F ratio = 3:1

Aetiology of ODD/CD
- Multiple risk factors in different domains (including biological factors and socio-cognitive styles in
the child, familial and environmental adversities, multiple stressors) identified.
- Risk factors are inter-related and cumulative that undermine effective parenting

Clinical presentation of ODD/CD

ODD
- Characterised by persistent and recurrent pattern of negativistic, disobedient, and hostile
behaviour towards authority figures
- Temper tantrums
- Argumentative, non-compliance, deliberate provocation
- Blames others for his mistakes
- Easily annoyed
- Resentful
- Vindictive behaviours
- ODD is a developmental precursor of CD

CD
- Repetitive and persistent pattern of norm-violating behaviours
- Various forms of aggression, destructive behaviours, theft or deceitful behaviours and
serious violations of rules e.g. stay out, run away, truant
- CD is a developmental precursor of Antisocial Personality Disorder

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Diagnosis of ODD/CD
DSM-5 Criteria of Oppositional Defiant Disorder
- A pattern of angry/irritable mood, argumentative/ deficient behaviour, or vindictiveness lasting at
least 6 months as evidenced by at least four symptoms from any of the following categories,
and exhibited during interaction with at least one individual who is not a sibling
• Angry/ irritable mood
1. Often loses temper
2. Is often touchy or easily annoyed
3. Is often angry and resentful
• Argumentative/ defiant behaviour
4. Often argues with authority figures or, for children and adolescents, with adults
5. Often actively defies or refuses to comply with requests from authority figures or with
rules
6. Often deliberately annoys others
7. Often blames others for his or her mistakes or misbehaviour
• Vindictiveness
8. Has been spiteful or vindictive at least twice within the past 6 months
* Symptomatic behaviour is defined as
* <5yo: Occur on most days for a period of at least 6 months
* >5yo: Occur at least once per week for at least 6 months
- Behavioural disturbance is asso. with distress in the individual or others in his or her immediate
social context (e.g. family, peer group, work colleagues), or it impacts negatively on social,
educational, occupational, or other important areas of functioning
- Do not occur exclusively during the course of a psychotic, substance use, depressive, or bipolar
disorder
- Exclusion criteria: Disruptive mood dysregulation disorder

DSM-5 Criteria of Conduct Disorder

- A repetitive and persistent pattern of behaviour in which the basic rights of others or major
age-appropriate societal norms or rules are violated, as manifested by the presence of at
least three of the following 15 criteria in the past 12 months from any of the categories below,
with at least one criterion present in the past 6 months:
• Aggression to people and animals
1. Often bullies, threatens, or intimidate others
2. Often initiates physical fights
3. Has used a weapon that can cause serious physical harm to others e.g. a bat, brick,
broke bottle, knife, gun
4. Has been physically cruel to people
5. Has been physically cruel to animals
6. Has stolen while confronting a victim e.g. mugging, purse snatching, extortion, armed
robbery
7. Has forced someone into sexual activity
• Destruction of property
8. Has deliberately engaged in fire setting with the intention of causing serious damage
9. Has deliberately destroyed others’ property (other than by fire setting)

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• Deceitfulness or Theft
10. Has broken into someone else’s house, building, or car
11. Often lives to obtain goods or favours or to avoid obligations (i.e. “cons others)
12. Has stolen items of non-trivial value without confronting a victim e.g. shoplifting, but
without breaking and entering; forgery
• Serious violation of rules
13. Often stays out at night despite parental prohibitions, beginning before age 13yo
14. Has run away from home overnight at least twice while living in the parental or parental
surrogate home, or once without returning for a lengthy period
15. Is often truant from school beginning before age 13yo
- Clinically significant impairment in social, academic, or occupational functioning
- Exclusion criteria: Individual >18yo and meet criteria for Antisocial Personality Disorder

Management ODD/CD
Types of Mx Programme Efficacy

Teach specific techniques to alter

Parent Management Training parent-child interaction based on 50% normalised, wide impact,
(PMT) social learning theory and long-term efficacy
behavioural modification

Using structural activities to teach

Cognitive problem-solving skills Improve but not normalised, short
children step-by-step approach to
training term efficacy
solve interpersonal problems

Amalgamation of individual, family

Promising in severely impaired
Multi-systemic therapy and extra-family techniques target
youths
on risk factors

Prognosis of ODD/CD
- Conduct problem is a stable behavioural trait especially those with early onset problems.
Associating with substance use, poor academic performance, risk-taking, suicidal behaviours,
and interpersonal problems in adolescence

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Internalising Disorders
Anxiety Disorders in Children & Adolescents
- Anxiety disorders are the commonest psychiatric disorders in youth population.
- Developmental influence on the nature of anxiety. Anxiety and fears can be developmentally
appropriate.
- Similar categories of anxiety disorders in adults could be found in children

Aetiology of AD
- Weak to moderate genetic contraction
- Anxious attachment: Bidirectional effect of escalating anxiety in mother-child dyad
- Dysregulation Serotonin and Norepinephrine systems: Overactive behavioural inhibition system
which may underlie the physiology of anxiety
- Inhibit temperament commonly reported

Classification of Paediatric AD
Late Childhood/
Early Childhood All ages
Early Adolescence

Separation Anxiety Disorder OCD

GAD
Specific Phobias Social Phobia
PTSD
Selective Mutism Panic Disorder

Age Principal sources of fear Principal Anxiety Disorders

Intense sensor stimuli

Early Infancy (0-6mo) Loss of support
Loud noises

Strangers
Late Infancy (6-12mo)
Separation

Imaginary creatures
Separation Anxiety
Toddler years (2-4yo) Potential burglars
Selective Mutism
The dark

Natural disasters
Animal Phobia
Early childhood (5-7yo) Injury, Animals
Blood Phobia
Media based fear

Poor academic and athletic Test Anxiety

Middle childhood (8-11yo)
performance School Phobia

Social Phobia
Adolescence (12-18yo) Peer rejection Agoraphobia
Panic Disorder

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Spectrum of Paediatric AD
- Generalised Anxiety Disorder
- Phobic disorders – agoraphobia, social phobia, specific phobia
- Panic disorders
- Post-traumatic stress disorders
- Adjustment disorders/acute stress reaction
- Anxiety disorder due to a general medical condition
- Substance induced anxiety disorder
- Emotional disorders with onset specific to childhood
• Separation anxiety disorder (SAD)
• Phobic anxiety disorder
• Social anxiety disorder
• Sibling rivalry disorder

Clinical presentation of Paediatric AD

- Anxiety disorder = irrational worry or fear causing significant distress + functional impairment
- Childhood anxiety could be conceptualised into 3 components: behavioural, cognitive, and
physiological

Presentation
- School refusal
- Frequent somatic complaints
- Difficulties with peer relationship
- Low self-esteem

Alternative ddx
- Thyrotoxicosis
- Arrhythmias
- Neurological diseases
- Substance induced anxiety (Alcohol, Illicit drugs, Caffeine)

Separation Anxiety Disorder

- SAD is a type of anxiety disorder with onset specific to childhood
- Characterised by recurrent excessive distress on separation from home or major attachment
figures, worry about losing or harms befalling loved ones, anticipatory distress on separation,
great difficulties at bedtime, going to school and being alone, repeated nightmares about
separation, and may present with psychosomatic complaints

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Management of Paediatric AD
- 1st line: Psychotherapy e.g. CBT, Relaxation training, Psycho-education
- Educational support to children equally effective
- There are few data to support the use of anxiolytics
- Severe cases may require SSRIs, imipramine or anxiolytics

Prognosis of Paediatric AD
- Nearly 2/3 of anxiety disorders in children is expected to disappear in 3 to 5 years’ time
- However, about 1/3 of them will have other categories of anxiety disorders at follow up

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Youth Depression

Aetiology of Youth Depression

- Stress induced atrophic changes in hippocampus may interrupt serotonin neuro-transmission
- Genes (like serotonin receptor or promoter) may interact with adverse environments leading to
depression
- A negative cognitive style and lack of social confidence, perfectionistic traits were often
associated with depression
- Personally salient adverse life event can precipitate the onset of juvenile depression

Clinical presentation of Youth Depression

- Depressive symptoms are common, but only 2-3% of the population have major depressive
disorder
- The prevalence of major depression increased after puberty
- While many of the clinical features of adult depression could be found in adolescent cases,
childhood depression tended to have more somatic complaints, irritable mood, behavioural
problems, and anxiety features
- About 70% of depressed youths had anxiety disorders, conduct disorder, substance misuse,
and/or dysthymia

Management of Youth Depression

- 1st line: SSRI
- Recent meta-analysis suggested about 2% depressed youth taking SSRIs may become
suicidal
- CBT is effective for mild to moderate severity cases and is probably less effective than SSRI in
relieving severe depression

Prognosis of Youth Depression

- Youth major depression runs an episodic relapsing course
- Majority of cases recovered within the first 3 months, but 15% last longer than 18 months
- About 25% of Bipolar II disorder first presented as a juvenile depression in their first episode

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Feeding and Eating Disorders

* Feeding and Eating Disorders are not specific to paediatric population, but many patients
admitted to paediatric psychiatric ward are because of these conditions

Myths about Eating Disorders

- Anorexia and Bulimia were viewed as “disorders of choice”
- Devalued seriousness of disorders
- Undermined treatment and recovery
- Provided NO guidance for families: “If she would only eat!”
- Concept of “genes” that influence risk for eating disorders viewed as absurd

Under-reporting of Eating disorders in men

Epidemiology of Eating Disorders - Due to stigma towards eating disorders, fear
- Disordered eating in HK (Tam, Ng, Yu, Young, 2007) of being labelled feminine, stigma of having
• Male: 3.9% psychiatric illness atypical of one’s gender
- Body dissatisfaction: Distinguish between
• Female: 6.5%
- Mortality muscularity and weight concern

• Highest mortality rate among all mental illnesses

• 30-year followup study by Swedish Research Counsel: Standard Mortality Ratio (SMR)
- Eating Disorder: 23.14
265 out of 6,000 died
- MDD: 20.35
- 32% Suicide (Violent or Non-violent)
- Sedative abuse: 20.34
- 19% Anorexia (i.e. starve to death)
- Mixed drug abuse: 19.23
- 11% Cancer - Bipolar: 15.05
- Average age at death: 34yo - Opioid abuse: 14.00
• Standard Mortality Ratio: 23.14 - Dysthymia: 12.12
- OCD: 11.54
- Panic Disorder: 10.00
Aetiology of Eating Disorders - Schizophrenia: 8.45
Genetics
- FHx +ve
• 12X risk for AN
• 4X risk for BN
- Heritability: 0.5-0.8
• MZ twin: 55% +ve
• DZ twin: 24% +ve
- Inherited: Temperamental traits, Comorbid anxiety, depression, OC tendencies

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Anorexia Nervosa
- 厭食症

Epidemiology of AN
- Incidence
• 4-5/100,000
• F:M = 10:1
• 3rd most common illness in teenage girls
- Prevalence
• 250/100,000 females (0.5-1% of female of 13-35yo)
• 22/100,000 males
• School and college women prevalence: 1%
• Models and ballet dancers prevalence: 4-6%
• May be culture bound (less in non-industrialised countries and African Americans)

Aetiology of AN
Predisposing factors
- Biological/ Genetics
• FHx of eating disorders (12X risk) or chemical dependence
• Mood disorder (Anxiety or Depression)
• Traits/ Temperament
• Increased BMI prior to onset
• Early onset puberty
• Cognitive lags
- Environmental
• Go fast, highly competitive academic or social environment
• Dieting culture
• High risk sports/ industry
• FHx of severe dieting/ exercise
• Enmeshed or disengaged family

Precipitating factors
**Almost always on internal or external experience of feeling out of control
- Abrupt weight gain (onset usu. between 11-14yo during which an average girl would gain 40
pounds with a disproportionate fat ratio)
- Major life transitions
- Traumatic events
- Family difficulty
- Onset of comorbid illness e.g. anxiety, depression
- Weight loss through dieting and/or increased exercise

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Model of Anorexia Nervosa
Familial risk factors Societal risk factors Personal risk factors

- FHx of Depression or - Social pressure on women - Poor problem-solving skills

Alcoholism - Emphasis on thinness - Low self-esteem
- Family conflict or trauma - Role confusion - Low mood
parental deprivation - Mixed message for women - Depression
- Sexual abuse - High anxiety
- Physical abuse - Nervousness
- Emotional abuse - Perfectionism
- Self-criticism
- Impulsivity
- Fears about sexuality
- Relationship problems
- Weight loss from physical
illness

Pathogenesis of AN
- Disrupted Dopamine pathways and Serotonin pathways
- Starvation → Brain malnutrition (require 500kcal/d) → Impair function esp. Cortical regulation
• ↓ Neuroplasticity, learning ability
• ↓ Executive function (Rumination, Attention stuck)
• ↓ Emotional regulation (Avoidance, Excess)
• ↓ Social cognition (Isolation)
• ↓ Global connection (Fragmented, overly detailed speech)

Anorexia Nervosa Bulimia Nervosa

- Harm avoidant - Harm avoidant

- Neurotic - Neurotic
- Obsessive - Obsessive
- Anxious - Anxious
- Perfectionistic - Perfectionistic
- Reward dependent - Impulsive, Affect dysregulation
- Low novelty seeking - Higher novelty seeking
- Extremely low self esteem - Low self-esteem

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Clinical presentation of AN
- Onset usu. teenage/ young adulthood, within a few years of the menarche
- Characterised by
• Persistent restriction of energy intake that leads to an abnormally low body weight/ BMI
• Fat phobia: Intense fear of gaining weight or becoming fat
• Distorted perception and/or importance of body weight and shape

Natural history of AN
- Secrecy and lying about dieting
1. Beginning of AN - Continued weight loss
- Hunger
- Total preoccupation with food and weight
2. AN takes over - Extreme fear of weight gain, Harder to lose weight
- Loss of hunger
HypoG, Dizziness, Tiredness, Lack of energy
Energy deficiency
Muscle loss

Low basal metabolic rate

Low Oestrogen, Amenorrhoea or irregular menses
Low FH, LSH
Endocrine, Metabolic
Low T4, Cold intolerance
High Cortisol (the only raised hormone)
Osteoporosis

Low kidney filtration

Fluid & Electrolyte Electrolyte imbalance
Water retention, Peripheral oedema

Gastroparesis
GI Intestinal hypo-motility
Deranged LFT

3. Manifestation & Bradycardia

complications of CVS Arrhythmia, Long QT
prolonged starvation Hypotension (due to Hypothermia)

Decreased brain mass

Depressed/ Anxious/ Irritable mood
Poor concentration
Decreased IQ
CNS
Poor sleep
Increased Obsession
Ritualised behaviour
Headache

Dry pasty skin

Dermatological Brittle nails
Hair thinning, Lanugo hair

Haematological Pancytopenia

Visual disturbance
Eye
Vitreous haemorrhage

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Signs
- Body weight, height, BMI
- BP, HR, Temp.
- Peripheral oedema
- Russell’s sign (i.e. Callosities over finger knuckles, usu. index and ring finger corresponding to
incisors, due to repeated self-induced vomiting by inducing gag reflex)
- Lanugo hair (i.e. compensatory mechanism of body to fight against cold environment due to low
basal metabolic rate)
- Eroded dental enamel, eroded teeth
- Pallor, Jaundice
- Cachexia/ Muscle wasting
- Proximal muscle weakness (Squat test/ Sit up test)
- Parotidomegaly
- Acrocyanosis
- Senile purpura

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Diagnosis of AN
- Significant overlapping between diagnostic criteria
of AN and BN

DSM-5 Criteria
- Minimal duration: 3 months
Symptoms
- Restriction of energy intake relative to
requirements leading to a significantly low BW in
the context of age, sex, developmental trajectory and physical health
- Intense fear of gaining weight or of becoming fat or persistent behaviour that interferes with
weight gain
- Disturbance in the way in which one’s body weight or shape is experienced, undue
influence of body weight or shape on self-evaluation, or persistent lack of recognition of the
seriousness of the current low BW

ICD-10 Criteria Normal Asian BMI:

- BW is ≥15% below expected (either lost or never achieved), 18.5-22.9 kg/m2
or BMI ≤17.5
or failure to make expected weight gain during period the growth in pre-pubertal onset
- Self-induced weight loss by
• Avoidance of "fattening foods”
• Vomiting
• Purging
• Excessive exercise
• Use of appetite suppressants and/or diuretics
- Body-image distortion in the form of a specific psychopathology whereby a dread of fatness
persists as an intrusive, over-valued idea and the patient imposes a low weight threshold on
himself or herself.
- Widespread endocrine disorder involving hypothalamic-pituitary-gonadal axis
• Women: Amenorrhoea (except on HRT e.g. OC pill)
• Men: ↓ Libido, Potency
• +/- ↑ GH, Cortisol
• +/- Abnormal Thyroid hormone metabolism, Abnormal Insulin secretion
- Puberty is delayed/ arrested in prepubertal onset AN

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Classification of AN
Subtypes described in DSM-5
- Restricting type
• i.e. does not eat
• Weight loss is accomplished through dieting, fasting, or excessive exercise
- Binge-eating/ Purging type
• Recurrence episodes of binge eating
• Purging behaviour e.g. self-induced vomiting, misuse of laxatives, diuretics, or enemas

Severity described in DSM-5

BMI Severity

17-17.5 Mild

16-17 Moderate

15-16 Severe

<15 Extreme

Maudsley BMI Table

BMI Severity Other features

20-25 Normal weight range

17.5-20 Underweight Irregular or absent menstruation, Ovulation failure

15-17.5 Anorexia Nervosa Amenorrhoea, Loss of substance from all body organs and structure

13.5-15 Severe AN All organ systems compromised: Bone, Heart, Muscle, Brain

12-13.5 Critical AN Inpatient treatment recommended. Failing organs (Muscle, BM, Heart)

<12 Life-threatening AN

Alarming signs
System Test/ Ix Concern Alert

BMI <14 <12

Weight loss per week >0.5kg/w >1.0kg/w

Nutrition (clinical)
Skin breakdown <0.1cm >0.2cm

Purpuric rash -ve +ve

sBP <90mmHg <80mmHg

dBP <70mmHg <60mmHg

Circulation
Postural BP drop >10mmHg >20mmHg

HR <50 bpm <40 bpm

Unable to get up w/o using Unable to get up w/o using

Squat Test
arms for balance arms as leverage
Musculoskeletal

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Musculoskeletal
Unable to sit up w/o using
Sit up Test Unable to sit up at all
arms as leverage

Temperature <35°C or 98°F <34.5°C or <97°F

White cell count <4 <2

Neutrophil count <1.5 <1

Bone marrow Hb <11 <9

Acute Hb drop -ve +ve

Platelet count <130 <110

Serum K <3.5 <3.0

Serum Na <135 <130

Salt/ Water
Serum Mg 0.5-0.7 <0.5
balance
Serum PO4 0.5-0.8 <0.5

Serum Urea >7 >10

Bilirubin >20 >40

ALP >110 >200

Liver AST >40 >80

ALT >45 >90

GGT >45 >90

Serum Albumin <35 <32

Nutrition
Serum CK >170 >250
(laboratory)
BG <3.5 <2.5

HR <50 <40

ECG QTc >450ms

Arrhythmia

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**Approach to AN** Core features of AN in DSM-5

Framework 1. ↓ Eating
1. Eating pattern & habits 2. Low BW
2. Methods to lose weight 3. Fear of gaining weight
3. Body weight 4. Body image distortion
4. Body image
5. Psychiatric comorbidities Core features of AN in ICD-10
6. Medical complications 1. Low BMI
7. Social impact e.g. School, Peers, Work, Family 2. Intentional weight loss
8. BN symptoms e.g. Craving, Compulsive eating, Lose 3. Body image distortion
control 4. Endocrinopathy

Eating pattern & habits

- Types of food, pre-occupation with food
- How many meals a day, how much each meal
- Hide or lie about food to others? Family conflict?

Methods to lose weight

- Restriction
- Vomiting/ Purging
- Excessive exercise
- Use of drugs

Body weight
- Before & Now
- Rate of change
- Intentional or Unintentional

Body image
- Ideal weight/ threshold 理理想體重
- Current perceived body weight + Self esteem ⽬目前對⾃自⼰己體重嘅睇法, 有冇⾃自信
- Fear of fatness 怕唔怕肥
- Repeated mirror checking + weighing 不停量量體重
- Sense of control? 覺得控制到⾃自⼰己體重?

Psychiatric comorbidities
e.g. Depression, Anxiety, OCD, Alcohol/ Substance abuse, Self harm, Suicide

Medical complications
- Malnutrition-related: Amenorrhoea, Cold intolerance, Lethargy, Weakness, Constipation,
Syncope, Osteoporosis, Bone fractures, Hair loss, Lanugo hair
- Vomiting-related: Dental carries, Parotidomegaly, Haemoptysis, Russell’s sign

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Management of AN
Principles of management
- Engage patient with ambivalent, empathic approach
- Risk assessment
• Relates to need for admission/ specialist intervention
• Medical risk
• Binging/ purging behaviours
• Suicidal risk
• Physical exam, BMI and other parameters
• Laboratory tests
- Psychological assessment
• Risk factors
• Precipitating factors
• Perpetuating factors
- Give diagnosis and feedback to patient
- Engage patient in treatment
- Multidisciplinary approach
• Nurse: Psycho-education, Meal supervision, Monitoring of physical parameters and other
comorbid symptoms
• Dieticians: Dietary advice, set up meal plan, coach preparation of meals at home, chart food
diary, food exchange
• Clinical psychologists: Psychotherapy
• Occupational therapists: Social skill training, Emotional control, Work-Leisure balance
establishment
• HK Red Cross hospital school teachers
• Medical social worker: Liaise with school and family for support and supervision arrangement

Treatment plan and setting

- Depend on initial assessment
BMI ≤14, or K <2.5, Arrhythmia, HypoG (<4), HR Refeeding
In-patient
<40 bpm or Long QT Weight restoration

Meal supervisions
BMI 14-16 and no physical complication Day patient
Multi-disciplinary assessment

BMI >16 and no physical complication Out-patient

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Weight Restoration
Steps
1. Set target weight/ BMI
- BMI target: 19-20
- Weight gain rate: 0.5-1kg/w
- Help patient to overcome the anxiety over increase calorie intake and BW
2. Normalise eating
- Regular weighting
- Homework: Food diary keeping and problem solving
- Behavioural regimes
• Toke economy and nurse supervision (supported meals and snacks) during and after
meals for controlled weight gain (supervised by multidisciplinary team approach and
group work)
• Supported eating: repeated exposure to food/eating to overcome anxiety over eating
• Rebuild normal hungry and satiety feeling and control over eating
• Target: normal social eating with right amount and variety
3. Education and Psychotherapy
- Individual Cognitive and insight orientated psychotherapy:
- CBT, IPT, CAT (Cognitive Analytical Therapy), ACT , CRT
- Family Therapy (Maudsley Model) - 3 phases
- Family support, in young patients
- Self help and support groups
- Online support
- School liaison and support
• Guideline of going back to school on certain BMI
• Must have meal supervision
• Physical health monitoring

Meal Supervision
- Supported eating
- Getting the risk portion
- Finish all the meal
- Charting food diary
- Rest for 30min afterwards
- Observe for rituals or safety behaviour and compensatory behaviour

Medical Treatment
- Medication only plays a limited role in AN
- Antidepressants
• Addition to inpatient refeeding does not improve outcome
• Fluoxetine does not reduce relapse rates
- FGA:
• Chlorpromazine promotes appetite
• Addition to inpatient refeeding does not improve outcome
- SGA:
• Olanzapine improves weight gain, reduces AN rumination, OC symptoms
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Family Therapy
- Based on Maudsley Model
- Family therapy session will be provided to discover the strengths of the family. Reorganise the
family hierarchy and support system
- Assist to finding ways to overcome the illness
Outline
- Phase I: Refeeding the patient empowered to parents
- Phase II: Eating autonomously by patient, negotiations for a new patter of relationships
- Phase II: Adolescent issues and termination

Eating Disorder carers support group

- Based on Maudsley family therapy
- The group creates a family team which battles together against a personified enemy - the eating
disorder. Family is the resource to aid in the recovery

Eating Disorder day camp

- Based on Ivan Eisler Multi-Family-Based treatment for Anorexia Nervosa
- The adolescent and family members will be invited to oversee the adolescents’ recovery at home
by providing psycho-education, skills training, and practice

Prognosis of AN
- Adolescents: Excellent outcomes with family-based treatment
• 60% well at 1yr
• 90% well at 5yr
- Adults (50% worse prognosis than Adolescents)
• Different psychotherapies (mainly individual) are better than non-specialist or dietary
treatment alone
• No clear front-runner
• 30% well at 1yr
• 40-50% well at 5yr

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Anorexia Nervosa in Students

- It is Important for teachers to recognise a student with s/s of AN

Possible clues
- Weight loss
- Lack of weight gain relative to the rest of class
- Social withdrawal and depressed mood
- Not going out to playground → Cling to radiations to keep warm or wear numerous layers of
clothes to fight off the cold
- Avoid company of others: in order to run around/ other form of exercise
- Skip school meals or eat only fruits and vegetables

What the school should do

- Pick one teacher to take the key role in managing the student
• Ideally someone who gets on best with sufferer
• Form teacher or Student guidance teacher (SGT)(輔導) or School social worker (SSW)
- Exercise
• usu. stopped in AN patients
• Encourage exercise incl. activities in timetable and extra-curricular activities
- Meal supervision
• Carefully thought out plan of action, kept under review
• Increase meal options available to student, change according to progress
- Eating as normal with other students
- Recruiting a friend to be a minder to sit with her, make sure that meals gets eaten
- Eating with a member of staff**
- Eating in a separate room**
- Eating at staff table**
- Eating away from main dinning area but with a minder/ friends
- **beware of further social alienation
• Snacks e.g. milky drinks, sandwiches are ideal
• Encourage regular small meals throughout the day
- Homework
• Perfectionist traits is common in AN. Tends to take far longer to complete
• Should set suitable time limit for study
- Examination
• AN affects concentration, cognitive function
• Letter to exam authority if needed
• Break +/- exam for hot drinks, snacks
• Troubled by cold because sitting still for long period → Provide blanket, hot water bottle as
remedial
- Career advice
• AN usu. do well academically because of innate ability + perfectionist traits → Strive harder
• Strive well in structured environment of school
• Worse with unstructured course with no guidelines/ feedback e.g. English, History, with few
lectures and little practical work

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Bulimia Nervosa
- 暴暴食症

Epidemiology of BN
- 11.4/100,000 per year incidence
- Affects 4% female adolescents
- 2-5% of female aged 13-35
- Incidence of primary care Bulimia Nervosa has increased 3 times between 1989-1993
- F:M = 10:1
- 30% have previous Anorexia Nervosa
- 1/3 previously obese
- Peak age of onset: 18 yo in average

Aetiology of BN
- Probably multifactorial
• Risk factors for psychiatric disorder
• Risk factors for dieting
• Pre-morbid negative self evaluation
• Parental problems (low contact, high expectations)
- Similar to Anorexia Nervosa
- Serotonin dysfunction and dopamine abnormalities
- Phenomenon of “counter regulation”
- Genetic: MZ:DZ = 22:9

Clinical presentation of BN
- Self referral
- Shame and secrecy about binges
- Body image disparagement is common
- Purging behaviours that relieve anxiety

Medical complications
- Fluid & electrolyte disturbance (due to vomiting)
- Parotidomegaly
- Dental caries
- ~ AN e.g. Amenorrhoea, Irregular menses
- Chronic laxative abuse → Dependence on laxatives for bowel opening, Rectal prolapse

Psychiatric comorbidities
- Depression
- Anxiety Disorder incl. OCD
- Substance abuse
- Personality disorder: Impulsivity, Borderline

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Diagnosis of BN
DSM-5 Criteria
- Recurrent episodes of binge eating
- Recurrent inappropriate compensatory behaviour to prevent weight gain
• Self induced vomiting
• Misuse of laxatives, diuretics or other medications
• Fasting
• Excessive exercise
- The binge eating and inappropriate behaviour both occur, on average, ≥1/ week for 3 months
- Self evaluation is unduly influenced by body shape and weight
- The disturbance does not occur exclusively during episodes of anorexia nervosa
**Subtypes (Purging vs Non-purging) are no longer described in DSM-5

ICD-10 Criteria
- Persistent preoccupation with eating OR
Craving for food OR
Episodes of over eating
(>2 times a week for 3 months)
- Attempts to counteract the “fattening” effects of food by one or more of the following:
• Self induced vomiting
• Alternate periods of starvation
• Purgative abuse Core features of BN in DSM
• Diuretic / stimulant misuse 1. Binge eating
- Morbid fear of fatness
2. Compensation
3. Body image distortion
Severity by no. of binge-eating episodes
- Mild: 1-3 per week
Core features of BN in ICD
- Moderate: 4-7 per week
- Eating/ Craving
- Severe: 8-13 per week
- Compensation
- Extreme: ≥14 per week
- Fear of fatness

Management of BN
- Mainly outpatient
- Psychotherapy
• Education
• Nutrition counselling
• CBT
• Self help e.g. getting better bite by bite - Treasure and Schmidt
• Online programmes
• CAT
• Motivational enhancement
• Family therapy

Medical therapy
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- Antidepressants (SSRIs)
• Address the impulse to binge
• Fluoxetine (60mg) is the most studied and has FDA indication for treatment of BN (the only
FDA-approved medication for treating ANY eating disorder)
• Other SSRI studies did not use higher than average doses
• Generally recommended as 1st line treatment of BN with therapy (unlike treatment of AN)

Prognosis of BN
- Relapsing and remitting
- Poorer outcome associated with
• Co-morbidity
• Mixed anorexia/ bulimia nervosa
• Severe symptoms
• Poor social support
- Long term prognosis better than for anorexia nervosa
- Lower suicide risk

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Psychogeriatrics
Dementia 261 Diagnosis of Delirium 289

Prognosis of Delirium 290

Spectrum of Dementia 261
Management of Delirium 290
Epidemiology of Dementia 262
Prevention of Delirium 291
Diseases causing Dementia 263

Clinical presentation of Dementia 265 Psychogeriatric Assessments 292

Diagnosis of Dementia 267 Functional Assessment/ Activities of Daily
**Approach to Dementia** 268 Living 292
Investigation of Dementia 270 Barthel Index of ADL 292

Management of Dementia 274 Katz Index of ADL 293

Alzheimer’s Disease 275 Lawton Instrumental ADL 294

Five-item Instrumental ADL 295

Epidemiology of Alzheimer 275
Functional Independence Measure (FIM) 295
Aetiology of Alzheimer 275
Advanced ADL 295
Pathogenesis of Alzheimer 276

Clinical presentation of Alzheimer 277 Depression Scales 296

Diagnosis of Alzheimer 278 Geriatric Depression Scale (GDS) 296

Management of Alzheimer 279 Hamilton Rating Scale for Depression (HAM-D) 296

Vascular Dementia 280 Selcare (D) 296

Lung Self-rating Depression Scale 296

Spectrum of VD 280

Aetiology of VD 280 Cognitive Assessment 297

Clinical presentation of VD 281 Abbreviated Mental Test (AMT) 297

Diagnosis of VD 281 Folstein Mini-Mental State Examination (MMSE) 298

Management of VD 281 Clock Drawing Test 300

Dementia with Lewy Body 282 Montreal Cognitive Assessment (MoCA) 301

5-Minute MoCA 302

Spectrum of Parkinsonian Dementias 282

Clinical presentation of DLB 282

Diagnosis of DLB 283

Management of DLB 283

Other Parkinsonian Syndromes with Dementia 284

Frontotemporal Dementia 285

Normal Pressure Hydrocephalus 285
Aetiology of NPH 285

Clinical presentation of NPH 285

Diagnosis of NPH 286

Management of NPH 286

Huntington Dementia 286

Other Cognitive Impairment 287
Delirium/ Acute Confusional State 287
Epidemiology of Delirium 287
Aetiology of Delirium 287

Pathogenesis of Delirium 288

Clinical presentation of Delirium 288

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Dementia
Spectrum of Dementia
Dementia
Chinese translation
- HK: 老⼈人癡呆症 (Obsolete term), 認知障礙症 (correspond to Neurocognitive Disorder)
- Mainland China: 腦退化
- Taiwan: 失智症
Definition
A syndrome that may be caused by a number of different brain disorders involving mental decline
severe enough to disrupt daily life that affects more than one of the following core brain functions:
- Recent memory (the ability to learn and recall information)
- Language (the ability to write or speak, or to understand written or spoken words)
- Visuospatial function (the ability to understand and use symbols, maps, etc. and the ability to
correctly judge where objects are)
- Executive function (the ability to plan, reason, solve problems and focus on a task)

Major Neurocognitive Disorder

- Described in DSM-5 with broader definition than Dementia
- Significant cognitive decline + interfere with B-ADL and I-ADL

Mild Neurocognitive Disorder

- Described in DSM-5
- Modest cognitive decline + does not interfere B-ADL nor I-ADL
- Named "Mild” instead of “Minor” because the authors want to remind people of the continuum:
10-15% of Mild NCD progress into Major NCD every year

Mild Cognitive Impairment (MCI)

- MCI is a very commonly used term but NOT described in ICD-10 or DSM-5
- Debatable concept, no consensus on diagnostic criteria
- Equals Amnesic Disorder? Mild NCD?
Definition
A condition in which someone has minor problems with cognition - his/her mental abilities such
as memory or thinking. In MCI these difficulties are worse than would normally be expected for a
healthy person of their age. However, the symptoms are NOT severe enough to interfere
significantly with daily life (B-ADL, I-ADL), and so are not defined as dementia.
- May be a transitional stage before Dementia (BUT NOT all MCI will progress to Dementia)
- 6-25% Annual rate of progression to Dementia (compared to normal individual 1-2%)
- Treatable conditions requiring monitoring

Pre-Clinical diseases
- i.e. presence of structural/ biochemical changes w/o clinical manifestation

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Epidemiology of Dementia
Prevalence
- There are >35 million people with Dementia worldwide, 50% are ≥85yo
- HK
• Prevalence of Dementia 9.1%
• Milder forms of cognitive impairment: 3-23%
- The age-specific prevalence in higher with age
• 60-64yo: 1.3%
• 65-69yo: 2.2%
• 70-74yo: 3.8%
• 75-79yo: 6.5%
• 80-84yo: 11.6%
• 85-89yo: 20.1%
• ≥90yo: 41.5%

Demographics
- Majority of cases are at advanced age: 50% cases are ≥90yo, 20-30% cases are 80-90yo
- More in lower socioeconomic status

Commonest causes of Dementia

1. 65% (50-80%) Alzheimer Disease (AD)
2. 20-30% Vascular Dementia (VD)
3. 10-25% Dementia with Lewy Body (DLB)
4. 10-15% Frontotemporal Dementia (FTD), Corticobasal Degeneration (CBD), Progressive
Supranuclear Palsy (PSP)
5. Mixed (AD + Vascular Dementia)

Mnemonics: DEMENTIA + Vascular

- Degenerative
- Endocrine
- Mass lesion
- Nutritional
- Traumatic
- Infective
- Autoimmune
- Vascular

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Diseases causing Dementia

- Alzheimer Disease
Degenerative/ Primary - Dementia w/ Lewy bodies (DLB)
- Frontotemporal Dementia (FTD)/ Picks Disease
- Single or Multiple stroke
Vascular dementia - Cortical/ Subcortical/ Lacunar
- usu. mixed w/ neurodegenerative disorders e.g. Alzheimer
- Parkinson Disease Dementia (PDD)
- Huntington Dementia
- Multiple System Atrophy (MSA)
Other - Progressive Supranuclear Palsy (PSP)
- Corticobasal Degeneration (CBD)
- Spinocerebellar Degeneration
- Syphilis (Neurosyphilis)
- AIDS
Infective/ Transmissible - Progressive multifocal leukoencephalopathy
diseases - Sub-acute sclerosing pan-encephalitis
- Creutzfeldt-Jakob Disease (CJD)
- Tumour: Glioma, Meningioma, Metastatic
- Normal Pressure Hydrocephalus (NPH)
Intracranial lesions - Chronic SDH
- Head trauma/ Chronic Traumatic Encephalopathy (CTE)
- Chronic alcoholism
- Post-irradiation
- Heavy metal poisoning
- Metabolic Encephalopathy
Encephalopathy
• Vitamin B1 or B12 deficiency
• Hypothyroidism, Thyrotoxicosis
• Chronic liver disease
• CKD
• Wilson’s Disease
• Cerebra-tendinous xanthomatosis
- Systemic vasculitis with cerebral involvement e.g. Behcet’s, PAN, ANCA,
Cryoglobulin
- Autoimmune encephalitis e.g. SLE, Sjogren, Behcet’s
Inflammatory - Multiple Sclerosis
- Paraneoplastic limbic encephalitis e.g. SCLC, Hodgkin’s Lymphoma,
Breast, Testicular Germ cell
- Autoimmune limbic encephalitis e.g. Anti-NMDA-R
- Mitochondrial disease e.g. MELAS, MERRF, NARP Syndromes
- Leukodystrophy
- Down Syndrome (early onset AD)
Congenital - Fabry Disease (XLR inheritance)
- Krabbe’s Disease
- Neimann Pick
- Neuronal Ceroid Lipofuscinosis

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Risk factors
- Hx of Traumatic brain injury
- Obesity
- Hypertension
- Smoking
- DM
- Hx of Depression
- Sleep disturbance
- Hyperlipidaemia

Protective factors
- Higher education level
- Physical activity
- Mediterranean diet
- Cognitive training
- Moderate alcohol consumption
- Social engagement

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Clinical presentation of Dementia

- 2 major classes of impairment: Cognitive & Psychiatric

Cognitive features
6 neurocognitive domains listed in DSM-5
Description Warning signs
- Increased difficulty in environments with multiple stimuli
Sustained/ Divided/ (TV, Radio, Conversation)
Complex Selective attention e.g. cannot watch TV w/o being interrupted
attention Information processing - Difficulty holding new information in mind (recalling
speed phone numbers or addresses just given or reporting what
was just said)
- Unable to perform both familiar and complex tasks
Planning, Decision making, and projects (at work and at home) e.g. I-ADL like
working memory, grocery shopping
Executive -
responding to feedback, Need to rely on others to plan I-ADL or make decisions
ability -
error correction, overriding Have problems with abstract thinking
habits and mental flexibility - Displays loss of initiative thinking
- Poor/ decreased judgement
- Repeats self in conversation, often with the same
Learning and Immediate memory conversation
memory Recent memory (free recall, - Cannot keep track of short list of items when
**the most shopping or list of plans for the day
cued recall and recognition
dominant s/s in - Requires frequent reminders to orient task at hand
memory)
early stage
Long term memory - Confusion about time and place, then people 時地⼈人
dementia**
- Repetitive behaviour
- Difficulties with expressive or receptive language
Expressive language - Often uses general terms e.g. pronouns like “that thing”
(naming, fluency, grammar
Language and nonspecific nouns “you know what I mean”
and syntax) - Severe impairment may not recall names of closer
Receptive language
friends and family
- Significant difficulties with previously familiar activities
Visual perception e.g. using tools, driving a motor vehicle, walking stairs,
Perceptual
Visuo-constructional picking up telephone, handwriting, using a fork/
motor
-praxia/ -gnosis spoon
- Significant difficulties navigating in familiar environments

Recognition of emotions - Changes in behaviour

Social
and behavioural regulation, • e.g. shows insensitivity to social standards
cognition
social appropriateness in • e.g. make decisions w/o regard to safety
terms of dress, grooming, • e.g. becomes socially withdrawn or isolated
and topics of conversation - usu. little insight into these changes

Progression
- Alzheimer: Progressive deterioration PCELLS
- Perceptual motor
- Vascular: Stepwise deterioration after each stroke - Complex attention
- Frontotemporal: Variable within a day - Executive ability
- Language
- Learning and memory
- Social cognition

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Behavioural psychological symptoms of Dementia (BPSD)
- occur in >80% of Demented patients
- Assessed by Neuropsychiatric Inventory (NPI)
Aggression/ Agitation (13%)
Anxiety (35%)
Mood & Affect
Affective symptoms (40%) (Euphoria or Depression)
Late Universal Apathy

Hallucinations (20%)
Perception
Delusions (60%)

Personality Disinhibition, Irritability, Verbal outburst (33%)

Motor behaviour abnormality

Behaviour
Night-time behavioural disturbance
- a/w Caregiver stress & Institutionalisation

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Diagnosis of Dementia
DSM-5 Criteria for Major Neurocognitive Disorder
A. Evidence of significant cognitive decline from a previous level of performance
in one or more cognitive domains (described above) based on
1. Concern of the individual, a knowledgeable informant, or the clinicians that there has been
a significant decline in cognitive function; and
2. A substantial impairment in cognitive performance, preferably documented by standardised
neuropsychological testing or, in its absence, another quantified clinical assessment
B. The cognitive deficits interfere with independence in everyday activities
C. The cognitive deficits do not occur exclusively in the context of a delirium
D. The cognitive deficits are not better explained by another mental disorder e.g. major depressive
disorder, schizophrenia

NIA-AA Criteria
- For all cause dementia
- Interfere with ability to functional work/ usual activities
- A decline from previous levels of functioning
- Not explained by delirium/ major psychiatric disorder
- Cognitive impairment dx by history + informant) and objective assessment
- A minimum 2 of the following
• ↓ ability to acquire and remember new information
• ↓ reasoning and handling of complex tasks, for judgement
• ↓ visuospatial abilities
• ↓ language function
• ↓ changes in personality, behaviour, comportment

Cognitive assessment tools

- Abbreviated Mental Test (AMT)
- Folstein Mini-Mental State Examination (MMSE)
- Montreal Cognitive Assessment (MoCA) HK Version (HK-MoCA) vs Cantonese MoCA
- Clock drawing test

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**Approach to Dementia** ABC of Dementia

- Common chief complaint: Poor memory - ADL
- BPSD
Framework
- Cognitive impairment
1. Memory assessment
- Sensory memory 3Rs of memory
- Short-term memory/ Working memory - Registration
- Long-term memory - Retaining
2. Dementia assessment - Retrieval
- Other cognitive domains
- BPSD
- ADL
3. Comorbidities
4. MMSE
5. Summary

Short-term/ Working memory assessment

- Serial 7s/ Immediate memory
• “100減7, 再減7, ⼀一路路減落落去, 直⾄至我叫你停為⽌止“
• Also assessing attention and concentration
• Normal: At least 5 subtractions
- Digit Span Test/ Immediate memory
• i.e. Read a sequence of random (single-digit) numbers and ask patient to recall immediately,
and repeat in forward and backward manner
• Gradual lengthening of sequence, with different initial number, starting with 5 digit length
• e.g. “4 2 7 3 1” (AMT)
• Normal span: At least 5 digits (7 +/-2)
- Delayed recall
• e.g. simple address immediately repeated to ensure registration, to be asked 5 min later
• e.g. “上海海街42號” (AMT)
• e.g. “蘋果、報紙、火⾞車車” (MMSE)
• e.g. “⾯面孔、絲絨、教堂、雛菊、紅⾊色” (HK-MoCA)

Long-term memory assessment

- Recent memory
• i.e. Memory lasting only for a few days
• e.g. news within the last 1-2 days, what patient had for breakfast/ last night’s dinner
• e.g. 琴晚新聞講咩? 今⽇日早餐食咩?
- Remote memory
• e.g. personal events in childhood clarified with informant, well known past events e.g. wars,
names of governors; note also the sequence of events
• e.g. 香港邊⼀一年年回歸中國? 回歸後第⼀一任特⾸首係邊個? 依家嘅特⾸首係邊個?

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Cognitive assessment
- Perceptual-motor
• Apraxia: 有⼀一啲以前做到依家做唔到嘅嘢? e.g. 揸⾞車車、打電話、⽤用筷⼦子匙羹
• Agnosia: 有冇唔認得屋企⼈人/ 唔認得熟悉嘅嘢 e.g. 電話, 筆, 電視機
- Complex attention e.g. 睇電視會唔會好容易易俾其他嘢打斷?
- Executive function (~I-ADL) e.g. 落落街市買餸煮飯有冇問題?
- Learning and memory e.g. 有冇成⽇日唔⾒見見鎖匙?
- Language
• Wernicke’s/ Expressive Dysphasia 講野唔清楚, 非常難明⽩白?
• Echolalia 不停重複⼈人地講嘅嘢?
• Palilalia 不停重複某啲字/⾳音/句句⼦子?
• Mutism
- Social cognition (usu. no insight) 唔理理⾝身邊⼈人嘅感受, 抽離社交圈⼦子

BPSD assessment
- Mood & Affect: Depressed 抑鬱? Euphoria 亢奮? Anxious 焦慮? Suicidal ⾃自殺傾向?
- Psychotic: Hallucination 幻聽, 幻覺, Delusion 妄想 e.g. Delusion of theft 以為俾⼈人偷左嘢,
Persecutory delusion 被害妄想、Morbid jealousy 忌妒妄想、Nihilistic delusion 虛無妄想
- Personality 性情⼤大變: Irritability, Violence, Aggression, Emotional lability, Verbal outburst
- Behaviour
• 重複性無⽬目的的動作: Withdrawal, Apathy, Self-neglect, Poor hygiene
• 不適當嘅性⾏行行為
• 睡眠週期混亂 (⽇日夜顛倒)
- Sundown Syndrome ⽇日落落症候群: 下午⾄至晚上出現的精神混亂及激躁⾏行行為

Activities of Daily Living (ADL)

- Basic ADL (B-ADL) e.g. Dressing 著衫, Eating 食飯, Bathing 沖涼, Toileting 去廁所
- Instrumental ADL (I-ADL) e.g. Finance 管理理錢銀, Transportation 出⾨門搭⾞車車, Meal prep 煮飯/買飯,
Communication (Phone) 打電話, Shopping 買餸, Medications 食藥

Features of non-Alzheimer
- VD: Vascular history 中風
- DLB: Parkinsonism ⼿手震、⼿手腳僵硬、⾏行行路路唔穩, Fluctuating cognition, Visual hallucination ⾒見見到
雀仔⾶飛過
- FTD: Hyperphagia 胃⼝口⼤大做, Fixation on certain kinds of food, Pica 異異食癖
- NPH: Gait disturbance ⾏行行路路唔穩, Urinary incontinence ⼩小便便失禁
- FHx of Dementia
- Early decline in social and personal conduct, apathy, and speech impairment
e.g. Stuttering, Word-finding, Forgetting meanings of words, Echolalia

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Investigation of Dementia
- Review DHx
- Depression assessment for Depressive Pseudo-dementia

Dementia Depressive Pseudo-dementia

- Insidious onset, Slow progression, Long duration - Precise onset, Rapid progression, Short duration
- Constant cognitive decline - Depressed mood
- Mood variation - Fluctuating cognitive impairment
- Conceal disability e.g. Amnesia - Highlighting his/her disability e.g. Amnesia
- Memory loss in recent events > remote events - Memory loss in both recent and remote memory
- Try to answer questions - Short answers/ Negativism
- Social skills retained - Loss of social skills often early and prominent

Blood tests
- CBC, LRFT
- Vitamin B12 & Folate level
- TFT for Hypothyroidism
- VDRL for Neurosyphilis

Basic Neuroimaging
Indications
- Doubtful clinical diagnosis e.g. AD vs Lewy body Dementia
- Organic disease suspected e.g. recent onset of signs and symptoms, Hx of head trauma
- Results of neuroimaging affects clinical management
Options
- Non-contrast CT Brain
• Can exclude most of the organic causes e.g. small vessel disease, hydrocephalus, Stroke,
SDH, Brian tumour
• Coronal and Sagittal films both required to adequately assess pattern of atrophy e.g. coronal
for hippocampus, sagittal for brainstem
- Non-contrast MRI Brain
• Better than CT brain in terms of lesion characterisation e.g. for diagnosis of Alzheimer’s
Region of atrophy & significance
Region of atrophy Significance & Ddx

Global Atrophy, White matter lesions Vascular Dementia, Nonspecific age-related atrophy

Frontal lobe FTD, Nonspecific Atrophy

Symmetrical: AD
Temporal lobe
Asymmetrical: FTD, PPA, CBD

Symmetrical: AD
Hippocampus
Less prominent in FTD

Parietal lobe AD, Nonspecific age-related atrophy, Less prominent in FTD

usu. not prominent unless in moderate or severe stage of Dementia,

Occipital lobe
if occurs in early stage, DLB is suspected

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Brainstem PSP, MSA

Cerebellum Alcoholism, MSA-C

Periventricular region SVD vs NPH

Corpus callosum
PPA, CBD
(N: 5mm thick at posterior genus)

Basal ganglia More than 5 infarcts in SVD

FTLD (Frontotemporal Lobar Degeneration), FTD (Frontotemporal Dementia), AD (Alzheimer’s Disease), PPA (Primary
Progressive Aphasia), CBD (Corticobasal Degeneration), DLA (Dementia with Lewy Bodies), PSP (Progressive
Supranuclear Palsy), MSA (Multiple System Atrophy), MSA-C (MSA with Cerebellar features), SVD (Small vessel
disease), NPH (Normal Pressure Hydrocephalus)
Specific Dementia syndromes
**Symmetrical**
Temporal atrophy in all stages
Hippocampal atrophy in Early AD
Alzheimer’s Disease
+/- Frontal, Parietal atrophy
(AD)
Asymmetrical is likely to be Atypical AD e.g. Posterior Cortical Atrophy,
Frontal AD → Perfusion SPECT

**Asymmetrical** (important clue to differ from AD)

Frontotemporal Dementia
Temporal lobe atrophy
(FTD)
Hippocampal atrophy in Moderate-Late FTD

**Asymmetrical; usu. dominant hemisphere (i.e. left) for speech**

Spread of atrophy from peri-Sylvian fissure, upward to peri-Central
sulcus in later stages (PPA, CBD, FTD as 3-in-1 syndrome)
Primary Progressive Aphasia usu. a/w Corpus callosum atrophy
(PPA) Further sub-typing may require perfusion/ metabolism brain scan
(HMPAO or ECD SPECT and 18-FDG PET)
MR Tractography showing respective fascicular atrophy in subtypes (for
research purpose)

**Asymmetrical; Cortical atrophy contralateral to the side of limb

dyspraxia**
Spread of atrophy from peri-Central sulcus, downward to peri-Sylvian
Corticobasal degeneration
fissure in later stages
(CBD)
a/w Corpus callosum atrophy
Brainstem involvement usu. in late stage
Perfusion SPECT shows characteristic corticobasal hypoperfusion

**Asymmetrical**
Earlier Brainstem involvement than in CBD and PPA, most prominent at
Pons with widening of pre-pontine space and slender anterior border of
Pons
Progressive Supranuclear Palsy +/- Frontal atrophy
(PSP) +/- Corpus callosum atrophy
Non-prominent cerebellar atrophy
MRI sagittal view shows “Hummingbird” sign in Midbrain atrophy
Definitive Dx may require SPECT or PET showing disproportional
brainstem hypo-activity

Progressive atrophy of brainstem and cerebellum, esp. prominent at

Midbrain
Multiple System Atrophy
MRI shows characteristic “Hot cross bun” sign in Midbrain atrophy
(MSA)
Supratentorial atrophy not compatibly progressive as brainstem atrophy
on serial scans

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Atrophy pattern usu. not characteristic on imaging, can be similar to AD
or age-related Cerebral atrophy
Dementia with Lewy Bodies MR Spectroscopy shows markedly depressed MAA but normal
(DLB) myoinositol level
Definitive Dx may require perfusion SPECT or 18-FDG PET with
predominant parieto-occipital hyperactivity

usu. caused by small vessel disease (SVD) with diffuse confluent

periventricular hypo-densities or hyper intensities on T2WI and FLAIR
MRI
Vascular Dementia Lacunar or Sizeable infarcts are common
(VD) May a/w global cerebral atrophy
Ventriculomegaly proportional to cerebral atrophy
Cerebral Amyloid Angiopathy shown on Susceptibility weighted imaging
(SWI)

Ventriculomegaly disproportional to cerebral atrophy

Dominant periventricular hypo-densities particularly around the horns of
lateral ventricles
Normal Pressure Hydrocephalus More suspicious if infarct is absent
(NPH) Need to have compatible clinical signs and symptoms before Indium-
DTPA cisternography is requested for characteristic ventricular reflux
activity at4 hour and disproportionally higher activity in ventricles than in
cerebral sulci at 24-48 delay scan on SPECT-CT

usu. no obvious pattern of atrophy in early stage

Depression with usu. normal MR Spectroscopy with borderline low NAA while
Pseudo-Dementia unremarkable myoinositol level
usu. nonspecific perfusion abnormality on brain SPECT

Pattern of atrophy
Temporal lobe AD AD: Symmetrical, Early Hippocampal atrophy
Hippocampus FTD FTD: Asymmetrical, Late Hippocampal atrophy

Peri-Sylvian fissure
PPA PPA: From Peri-Sylvian fissure to Peri-Central sulcus
Peri-Central sulcus
CBD CBD: From Peri-Central sulcus to Peri-Sylvian fissure
Corpus callosum
PSP PSP: Brainstem (Pons), Frontal lobe, Corpus callosum
Brainstem
MSA MSA: Brainstem (Midbrain), Cerebellum

DLB DLB: MR Spectroscopy show markedly depressed MAA

Nonspecific
Pseudo-Dementia Pseudo-Dementia: Normal MR Spectroscopy

Vascular Dementia VD: Proportional to Cerebral atrophy, Infarcts

Ventriculomegaly
NPH NPH: Disproportional to Cerebral atrophy, no infarct

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Advanced Neuroimaging
Options
- MR Spectroscopy (MRS)
• To differentiate between Pseudo-Dementia from Dementia
• To differentiate between age-related cerebral
- MR Tractography
• Dedicated processing of diffusion tensor imaging (DTI) to draw the fibre tracts
• For research purposes in sub-classification of PPA
- Brain Perfusion SPECT
• Use either HMPAO or ECD as brain perfusion agent
• Radiation dose similar to a bone scan which is acceptable in elderly (>60yo)
• Talairach analysis is preferred with a 3D brain perfusion map display
• Supplementary to conventional imaging if diagnosis in doubt after CT or MRI Brain
- PET-CT
• 18-FDG PET
- Better resolution than SPECT esp. at Brainstem and Basal ganglia
- Radiation dose to brain is high, not considered in young patients
- Concomitant CT brain performed
• Amyloid PET - i.e. Pittsburgh Compound B PET (PIB-PET)
- Patter of amyloid deposition is more specific than amount of amyloid loading
- Only able to confirm or exclude AD, sometimes DLB, but not others
• Tau PET
- Cisternography
• Intrathecal injection of Indium-DTPA, requires in-patient care for post-injection period and
delay scanning
• Indicated for clinically compatible NPH
• Equivocal result may need CSF tapping or infusion test to exclude NPH
- Dopaminergic imaging
• DaTscan and CIT scan and Dopa PET scan are the most commonly used
• Useful in differentiating AD (normal) from DLB (decrease uptake) when clinically difficult to
• Therapeutic implication for dopamine therapy in Parkinson Disease, Atypical Parkinsonism or
DLB
• Not helpful in differentiating between Parkinson Disease and atypical Parkinsonism

Biomarkers
- Alzheimer Disease
• CSF Aβ-42
• CSF tau protein
- Vascular Dementia: Still in development

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Management of Dementia
Alzheimer Disease
AChEI e.g. Rivastigmine
Mixed Vascular and AD
NMDA Antagonist e.g. Memantine
Dementia with Lewy Bodies

AChEI and NMDA Antagonist NOT recommended

Frontotemporal Dementia
SSRI may help with behavioural problems

Vascular Dementia AChEI and NMDA Antagonist NOT recommended

AChEI, Vitamin E are NOT effective in reducing risk of AD and reducing

Mild Cognitive Impairment
symptoms of MCI

Other treatments of no/ unproven benefit

- HRT for postmenopausal AD: NOT effective and even harmful
- Folate, Vitamin B12 supplement: NOT effective
- Statins: NOT effective in preventing Dementia
- Souvenaid: Possible but variable effects on cognition, no effect on global outcomes, not
recommended until further evidence available
- rTMS, tDCS: Some but unsustained benefit on cognition, not recommended until further
evidence available
- Ɣ secretase inhibitors e.g. Tarenflurbil: NOT effective in AD
- Amyloid β1-42 vaccination: Some preliminary evidence of effect in AD but does not affect clinical
course and causes cerebral inflammation

Prevention
- No current evidence to support any drug intervention to prevent Dementia e.g. Jingle Ko Bi 柏果
樹精華, Coconut oil
- Some evidence (B) shows antihypertensives may be helpful, further studies required
- Vascular risk factors should be recognised and managed

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Alzheimer’s Disease

Epidemiology of Alzheimer
- Prevalence: 24 million worldwide
- 4th leading cause of death
- Age-dependent prevalence
• 65-74yo: 3%
• 75-84yo: 19%
• >85yo: 47%
- Prevalence in HK: 3.5-4.3% (Yr 1998)
- HK: COMMONEST cause (65%, 50-80%) of Dementia esp. among elderly
- Alzheimer patients usu. die within 8-10yr since diagnosis

Aetiology of Alzheimer
Risk factors
- Advanced age
- Down Syndrome (a/w early onset Alzheimer)
- FHx of Dementia (esp. early onset) and Alzheimer
* However, only 5-10% of Alzheimer are familial; mostly sporadic
- Severe head injury
- Genetics (ApoE, CLU, CR1 polymorphisms)
- Cardiovascular diseases e.g. HT, DM, Dyslipidaemia

Genetic factors
Early onset Familial Alzheimer (i.e. ≤65yo)
- AD inheritance
- APP, Presenilin (PSEN1, PSEN2) mutation → Sufficient causes of Alzheimer
- Explain nearly all large early-onset Alzheimer families
- But ~50% early-onset Alzheimer cannot be explained genetically

Late onset Familial Alzheimer (i.e. >65yo)

- AD inheritance + age-dependence + high prevalence
- Concordance rate of MZ (40-50%) >> DZ (10-20%)

Apolipoprotein E (ApoE)
- a/w Amyloid-β clearance & neuronal repair
- Normal role is transporting plasma lipids within tissues
ApoE2 Cys-Cys Protective allele for Alzheimer Risk allele for Cardiovascular disease

ApoE3 Cys-Arg Normal allele for Alzheimer and CVD

Risk allele for Alzheimer

ApoE4 Arg-Arg - 1 Risk allele → 3X risk of Alzheimer Protective for CVD
- 2 Risk allele → 8X risk of Alzheimer

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Pathogenesis of Alzheimer
Tau hypothesis
- Tau (Tubulin-associated unit), aka MAPT (Microtubule-associated protein tau)
- Normally, tau protein binds and stabilise microtubules that are responsible for axonal transport
- Tau protein hyper-phosphorylation → “Paired helical filaments” (PHF)
→ Accumulate intracellularly → Neurofibrillary tangles (NFT)
- Loss of intracellular tau protein → Impaired axonal transport → Neuronal death
- However, evidence shows high level of Tau do not always correlate to clinical manifestation

Amyloid hypothesis
- Amyloid precursor protein (APP) is a transmembrane protein
- APP mutations increase amount of toxic Amyloid-β peptide
- APP lysed by α-secretase → C83 → lysed by Ɣ-secretase → Amyloid-α
- APP lysed by β-secretase → C99 → lysed by Ɣ-secretase → Amyloid-β40/ Amyloid-β42
(PSEN1 & PSEN2 encode subunits of Ɣ-secretase)
- Amyloid-β42 is a non-soluble, sticky peptide
→ Accumulate extracellularly
→ Gather other protein (incl. ApoE) into senile plaques
→ Neuronal death (unknown mechanism)
- A-β40/A-β42 could be degraded by neprilysin, IDE & ApoE

Clinical manifestation
- Atrophy in AD usu. starts from Temporal lobe, then to Hippocampus → Memory deficit
- Cholinergic deficit
• Loss of cholinergic biosynthetic machinery
• Loss of Septal area/ Basal forebrain cholinergic neurons (that projects to Hippocampus)
• Cholinergic deficit also contributes to memory and attention impairment

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Clinical presentation of Alzheimer

Clinical course of Alzheimer Disease
- Preclinical stage/ Subjective Cognitive Decline (SCD):
Asymptomatic brain changes
- Mild NCD: Prodromal Alzheimer Disease
- Major NCD: Alzheimer Dementia

Cognitive Features
Memory
- Anterograde episodic amnesia (loss of new memory)
- Delayed recall
- Sparing of Working memory
- Test: Word list learning
- Paired associates may help

Attention & Execution

- Poor concentration
- Problems with complex tasks
- Selective attention
- Test: Wisconsin Card Sorting Test (WCST)

Language & Knowledge

- Impaired semantics (i.e. word meanings)
- Category fluency
- Difficulty in word definitions
- Difficulty in finding words esp. proper names
- Later Phonological & Syntactic deficits

Visuospatial & Perceptual abilities

- Impaired drawing esp. 3D
- Apraxia esp. conceptual

Early Alzheimer signs: Amnesia, Spatial disorientation, Circumlocution

Advanced Alzheimer: Sloppily dressed, Slow, Apathetic, Confused, Disoriented, Stooped posture
Terminal Alzheimer: Bedridden, Stiff, Unresponsive, Nearly mute, Incontinence

Neuropsychiatric Features
- Universal Apathy
- (5-22%) Depression
- (50%) Anxiety
- Delusion (rare in early)
• Phantom lodger (i.e. believe in living other house)
• Morbid Jealousy (i.e. Delusion of partner/ spouse being unfaithful) - high risk of harm
- Theft of items and paranoia (i.e. unwarranted jealousy)
- Agitation, Disruptive behaviour (common in late)

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Diagnosis of Alzheimer
Diagnostic Criteria
- Deficits in 2 or more areas of cognition
- MMSE score < 24 + Neuropsychological test
- Progressive worsening of Cognitive function
- New criterion in 2018: CSF Amyloid-β and phosphorylated tau level

NINCDS-ADRDA Classification
- “Possible”: Dementia but not typical Alzheimer
- “Probably”: Dementia by various testing, absence of other brain disease
- “Definite”: Proven Alzheimer histopathology
- Supported by clinical progression, FHx, BPSD, ADL, EEG, CT Brain

Memory assessment: Alzheimer Disease Assessment Scale-Cog (ADAS-Cog)

Investigations
- CBC, LRFT, BG, TSH, B12, Folate, VDRL
- ECG, CXR, EEG
- Neuropsychological tests
- Structural imaging
• CT Brain can only r/o Stroke, Large tumours etc, NOT a superior option
• MRI Brain is better than CT Brain
• Symmetrical cerebral atrophy (gyri shrinkage + sulci expansion)
- Temporal lobe incl. Temporal pole, Inferior Temporal pole, Entorhinal complex
- Hippocampus
- Superior Frontal association area
- Parietal cortex
- Functional imaging
• 18-FDG PET, SPECT → Functional assessment of Brain regions
• Pittsburgh Compound B (PIB)-PET → Amyloid deposition (aka Amyloid PET)
- Biological markers
• ↓ CSF Amyloid-β (due to extracellular deposition in CNS)
• ↑ CSF phosphorylated tau level (due to neuronal death and released intracellular content)
• High accuracy
• Seldom done in HK clinical setting due to invasiveness
- Genetic studies for PSEN1, PSEN2 mutation
- Autopsy: Amyloid plaques, Neurofibrillary tangles (tangled microtubules asso. w/ tau)

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Management of Alzheimer
Pharmacological Non-pharmacological

Mild-Moderate: AChEI Cognitive stimulation

Cognition decline Severe: NMDA Antagonist Cognitive training
Vitamin E Cognitive rehabilitation (rare in HK)

(at lowest dose and shortest period possible)

AChEI
NMDA Antagonist Behavioural modification
BPSD
Antipsychotics Environmental modification
Antidepressants
Other neuroleptics

Acetylcholine Esterase Inhibitors (AChEI)

e.g. Rivastigmine (Exelon®), Galantamine, Donepezil
- 1st for mild to moderate Dementia in Alzheimer
- Rivastigmine and Donepezil for severe Dementia in Alzheimer
- Routes: Oral, Transdermal patch
MOA
- Inhibit AChE and Pseudocholinesterase (PChE) → ↑ ACh available for CNS functions
ADR
- Bradycardia
- Anorexia
- Dilutional HypoNa
- Other cholinergic symptoms e.g. dry mouth, constipation

N-methyl-D-aspartate receptor (NMDA-R) Antagonist

e.g. Memantine
- 1st line for moderate to severe Dementia in Alzheimer
- Neuro-protective and disease-modifying agent in theory
MOA
- Inhibit Glutamate (an inhibitory neurotransmitter)

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Vascular Dementia

Spectrum of VD
Vascular Dementia
- Dementia caused primarily by cerebrovascular diseases/ impaired cerebral blood flow
- Require correlation between clinical feature and location/ severity of CVD on imaging
- Pure VD is uncommon (10%)
- Mixed is more common (30-40%)

Vascular Cognitive Impairment (VCI)

- Umbrella term encompassing MCI to frank Dementia caused by or a/w CVD risk factors

Mixed Dementia
- Overlapping of Alzheimer neuropathology and vascular neurodegeneration

Aetiology of VD
- Ischaemic Stroke (ISS)
• Cardioembolism
• Large vessel diseases
• Small vessel diseases e.g. Atherosclerotic/ Amyloid Angiopathy
- Haemorrhagic Stroke
• Intracerebral Haemorrhage (ICH)
• Subarachnoid Haemorrhage (SAH)
- Hypoperfusion e.g. Hippocampal Sclerosis/ Laminal cortical sclerosis

Risk factors
Risk factors of Stroke Risk factors of Dementia in Post-Stroke patients

- Advanced age - Presence of Pre-Stroke risk factors

- HT - Multiple Stroke - Cumulative disruption of brain function w/o
- DM threshold of infarct volume
- Lipid - Stroke location:
- Smoking • Medial Frontal lobes: ACA territory
- High BMI • Language areas
- Sedentary lifestyle • Medial Temporal lobe
- Hx of IHD • Thalamus
- AFib - Stroke complications: Confusion, Seizure
- Low brain reserve
• General atrophy
• Medial temporal lobe atrophy
• Leukoaraiosis

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Clinical presentation of VD
- Variable presentation due to different location and size of stroke
• Cognitive:
- Prominent impairment of executive ability (c.f. Memory in Alzheimer)
- +/- Cortical signs e.g. Aphasia, Apraxia
- +/- Sparing of episodic memory c.f. isolated anterior thalamic infarction
- +/- Better verbal learning + recall compared to Alzheimer
• Psychiatric: Delusions, Hallucinations
• Mood: Depression, Apathy, Pseudo-bulbar effect (pathological laughing, crying)
• Motor:
- Slowing of gait: Lower body Parkinsonism
- Sparing of UL, No resting tremour
- Narrow base gait (c.f. Apraxic, wide base gait e.g. in NPH)
- VD is characterised by its “Stepwise” progression in cognitive decline
• In typical Post-Stroke Dementia, each decline is closely linked to an episode of clinically
diagnosed stroke
• In atypical cases (Non-Stroke VD), each decline occur stepwise also w/o any clinically
recognisable stroke (i.e. lack of typical clinical s/s of Stroke)(aka Silent VD) but with imaging
evidence of CVD. This group of patients usu. have poorer cognitive performance and higher
risk of dementia

Diagnosis of VD
Hachinski Score
- Points given to items present
- 2 points given for: Abrupt onset, Fluctuating course, Hx of Stroke, Focal neurological symptoms,
Focal neurological signs
- 1 point given for: Stepwise deterioration, Nocturnal confusion, Preservation of personality,
Depression, Somatic complaints, Pseudo-bulbar affect (emotional incontinence), a/w HT, a/w
Atherosclerosis
- Hachinski score >7 is predictive of likelihood of VD or VCI
- Criticised for little difference from a risk factor score for Stroke

CSF Analysis

Neuroimaging
- CT or MRI Brain
- Amyloid PET
- 18-FDG PET - VD: Patchy/ heterogenous hypo-metabolism

Management of VD
- Vascular risk factors modification can prevent and reverse dementia
- Inconclusive evidence on AChEI and Memantine for pure VD, reasonable to use due to high
prevalence of Mixed Dementia

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Dementia with Lewy Body

- 3rd common cause of Dementia (10-25%)
- Previously thought to be a subtype of Alzheimer Disease

Spectrum of Parkinsonian Dementias

- Dementia with Lewy Body (DLB): Dementia + Parkinsonism concomitantly (or earlier)
- Parkinson Disease with Dementia (PDD): Dementia in well-established Parkinson (>1yr)
- Progressive Supranuclear Palsy (PSP)
- Multiple Systemic Atrophy (MSA)
- Corticobasal Degeneration (CBD)

Clinical presentation of DLB

- Dementia
• Predominantly impairment in attention, executive function, visuo-perceptual ability
e.g. Difficulty driving, getting lost in familiar places, impaired work performance
• Early impaired figure copying (e.g. overlapping pentagons), Clock drawing, Serial seven
- Cognitive fluctuations
• Daytime drowsiness or nap >2hr
• Prolonged staring spells
• Disorganised speech
- Vivid visual hallucination
• Important feature to r/o Alzheimer (uncommon in early Alzheimer)
• From well-formed images (people) to abstract visions (shapes, colours)
- Parkinsonism
• TRAP features
• usu. more bilateral, symmetrical and milder than Parkinson Disease proper
- REM sleep disorder
• Yelling/ hitting, Violent movement during dreams +/- causing injury to bed partner
• Most cases respond to Melatonin or Clonazepam
- Neuroleptic response
• Excessive response/ sensitivity to FGA and SGA
• Severe/ irreversible parkinsonism and impaired consciousness
• +/- features suggestive of NMS
- Repeated falls w/o provocation, related to parkinsonism, cognitive fluctuation, postural
hypotension
- Autonomic dysfunction: Postural hypotension
- Sleeping disorders: Hypersomnia or Insomnia
- Non-visual Hallucinations (Auditory, Olfactory)
- Delusions
- Mood disturbances: Apathy, Anxiety, Depression

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Diagnosis of DLB
- Structural imaging: Atrophy pattern usu. not characteristic on imaging, can be similar to AD or
age-related cerebral atrophy
- MR Spectroscopy shows markedly depressed MAA but normal myoinositol level
- Functional imaging for definitive diagnosis
• Perfusion SPCET
• 18-FDG PET
• Show predominant parieto-occipital hyperactivity

Dementia with Lewy Bodies Consortium: Diagnostic Criteria of DLB

- Diagnostic if ≥2 core features OR 1 core + 1 suggestive feature
Core features
- Fluctuating cognition
- Recurrent visual hallucinations
- Parkinsonism
Suggestive features
- REM sleep disorder
- Severe neuroleptic sensitivity
- Low dopamine activity in basal ganglia on dopamine transporter SPECT or PET

PDD DLB

Late onset Earlier onset

Onset
>1 year after Parkinsonism onset <1 year after Parkinsonism onset

Visuospatial and visual memory more

Less prominent than DLB
Cognitive function severely affected
NOT fluctuating
Fluctuating

Visual hallucination Uncommon Common

Parkinsonism Prominent Mild

Management of DLB
Non-pharmacological
- preferred over pharmacological due to poor response
- Behavioural Treatment
- Physical Treatment
- Education

Pharmacological
- AChEI trial +/- Antipsychotics
- Parkinsonism: Levodopa
- REM sleep disorder: Melatonin + injury prevention +/- Clonazepam if refractory
- Postural hypotension: Fludrocortisone +/- Midodrine

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Other Parkinsonian Syndromes with Dementia

Pathology Presentation Imaging

Autonomic dysfunction
- Postural hypotension
Shy-Drager Syndrome - AROU
- Sexual dysfunction

MSA Corticospinal tract deficits

Striatonigral Degeneration/ MSA-P
Parkinsonism

Cerebellar ataxia
- Gait disturbance Hot Cross Bun sign
Olivopontocerebellar Atrophy/ MSA-C
- Dysarthria on MRI

Vertical (Inferior gaze) palsy

- Loss of downward gaze
- Slow downward saccadic movement
Hummingbird sign in
PSP Midbrain on MRI Brain
Postural instability: Frequent falls
sagittal view
Behavioural changes: Disinhibition, Apathy/ Dysphoria, Anxiety,
Impulsive (3 clap test, PSP may clap more than 3)

Asymmetric parkinsonism +
Atrophy of Cortex contralateral to side cognitive impairment Corticobasal
of limb dyspraxia (Cortico-) Ideo-motor apraxia/ Alien limb hypoperfusion on
CBD
Atrophy of Peri-Central sulcus and phenomenon Brain perfusion
Peri-Sylvian fissure (Basal) Aphasia SPECT
Absence of tremor

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Frontotemporal Dementia
- aka Picks Disease
- FHx: C9ORF72 gene, Taupathy
- Behaviour variant (bvFTLD): Social cognitive decline, Apathy, Disinhibition
- Primary Progressive Aphasia/ Aphasia type: Language decline
- Memory decline is late

Normal Pressure Hydrocephalus

- usu. >65yo

Aetiology of NPH
- Alteration in brain compliance → Brain atrophy

Idiopathic/ Primary NPH

Risk factors
- Stroke: Chronic peri-ventricular ischaemia → Increased compliance of ventricular system
- Arachnoid thickening/ scarring → Decreased CSF absorption
- Increased cerebrovascular pressure → Reduced venous absorption of CSF
- Other neurodegenerative disorders

Secondary NPH
- SAH
- Chronic meningitis
- Paget’s Disease of skull base
3Ws: Wobbly, Weird, Wet

Clinical presentation of NPH

- Hakim’s triad: Gait disturbance, Dementia, Urinary incontinence
- Gait disturbance
• The most prominent feature, one of the diagnostic requirements
• Apraxic gait: Glued gait, Small step on wide base
• Difficulty in turning: Susceptible to falls while turning
• Similar to parkinsonian gait, apart from the wide base gait
- Cognitive decline/ Dementia
• Develops after gait disturbance
• Cortical/ Subcortical features of cognitive impairment
• Psychomotor slowing/ impaired executive function
• Decreased attention/ concentration
• Apathy
- Urinary urgency (early) → urge incontinence (late)
- Long tract signs: Spastic paralysis of LL +/- Hyperreflexia, Babinski sign
- NO signs of raised ICP e.g. headache, nausea, vomiting, visual loss/ papilloedema
- NO cortical signs e.g. aphasia, apraxia
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Diagnosis of NPH
- Difficult and need to distinguish from Alzheimer Disease
- “Diagnostic” test: Clinical improvement upon drainage of CSF (~30ml)
- MMSE
- CT/ MRI brain: To assess ventricular and sulcal size
• Disproportional Ventriculomegaly
- Evans ratio > 0.31 (diameter of frontal horn/ max. cranial width)
- Absence of obstructive hydrocephalus (e.g. lesion at 3rd or 4th ventricles)
- Absence/ minimal sulcal enlargement (marker of normal cortex atrophy)
- c.f. Normal ageing: Ventriculomegaly + Proportional sulcal enlargement
• Periventricular white matter change: High signal around ventricles
• Aqueduct flow void: Reduced signal in aqueduct of Sylvius

Management of NPH
CSF Shunting
Options
- Ventriculo-peritoneal Shunt (VP Shunt)
- Ventriculo-atrial Shunt (VAP Shunt)
Non-Indications
- Predicted good functional improvement
• Early and reversible stage of neurological deficit
• Duration <2yr
• Dominant gait dysfunction
Complications
- Over-drainage/ Over-shunting
• p/w sustained / postural headaches
• Severe over-shunting: SDH (tearing veins)
- Shunt influx (from Peritoneum or Atrium)
• Raised ICP +/- infection: Headache, Malaise, N/V, Fever
• Mx: Abx +/- Shunt removal
- Seizures
- ICH from catheter placement
- Shunt failure / blocked shunt

Huntington Dementia
- Trinucleotide CAG repeat expansion in Huntingtin (HT) gene in Chromosome 4p
- Strong FHx with Anticipation phenomenon
- Movement (early manifestation): Choreiform movement of hands, face, shoulder
- Frontal lobe dementia (later manifestation): Relative preservation of memory

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Other Cognitive Impairment

Delirium/ Acute Confusional State
- 譫妄症

Epidemiology of Delirium
- Incidence rise during hospitalisation
• 5-53% of elderly patient in post-op period
• 70-87% of elderly patient in ICU
- Overall prevalence only 1-2%; increase with age - 14% in >85yo population

Aetiology of Delirium
Risk factors
Advanced age (≥65yo)
Demographic factors
Male sex

Dementia (present in 2/3 cases)

Cognitive impairment Hx of Delirium
Depression
Poor GC Functional impairment e.g. Dependence, Immobility, Inactivity, Hx of Fall

Sensory impairment e.g. Visual, Auditory

Intake impairment e.g. Dehydration, Malnutrition

Hx of AMI, DKA
CKD, Chronic Liver diseases
PMHx esp. severe/
Neurological diseases e.g. Stroke (esp. non-dominant lobe), ICH, Meningitis,
end-stage/ terminal
Encephalitis
stage and multiple
Fracture, Trauma
HIV infection

Polypharmacy
Psychoactive drugs e.g. Sedative Hypnotics, Narcotics, Anticholinergics
Drugs & Substances Drug withdrawal
Alcoholism
Alcohol withdrawal (Delirium Tremens)

Current Infection/ Sepsis

Iatrogenic complications
Hypoxia
Shock
Current illness Fever or Hypothermia
Anaemia
Hypoalbuminaemia
Metabolic derangements e.g. Electrolyte imbalance, HypoG, Acid-base
imbalance

Post-operation Orthopaedic surgery, Cardiac surgery, Prolonged cardiopulmonary bypass

ICU admission, Use of physical restraints, Urinary catheter insertion, Multiple
Environmental
procedures, Pain, Emotional stress, Sleep deprivation

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Pathogenesis of Delirium
- Poorly understood
- Generalised disruption of higher cortical functions w/o dysfunction in PFC, Subcortical,
Thalamus, BG, Frontal lobe, Temporal lobe, Parietal lobe, Fusiform cortex, Lingual gyri
- Supporting role of
• Cholinergic deficiency
• Dopaminergic excess
• Cytokines - breakdown BBB & alter neurotransmission
• Chronic hypercortisolism

Clinical presentation of Delirium

Definition of confusion:
a mental & behavioural state of reduced comprehension, coherence and capacity to reason

Clinical features
- Acute onset; usu. over a period of hours or days
- Can last for months or even years (aka Persistent Delirium)
- Fluctuating course
• Come-and-go with characteristic lucid intervals (i.e. Confused → Lucid → Confused)
• Severity can varies over 24hr period
- Inattention
• Difficulty focusing, sustaining, and shifting attention
• Difficulty maintaining conversation or following commands
- Disorganised thinking
• Manifested by diagnosed/ incoherent speech
• Rambling or irrelevant conversation or an unclear or illogical flow of ideas
- Altered level of consciousness: Clouding, Reduced clarity of awareness of environment
- Cognitive deficits: Typical global or multiple deficits in cognition incl. disorientation, amnesia and
language impairment
- Perceptual disturbance: Illusions or hallucination in ~30% patients
- Psychomotor disturbance
• Hyperactive: Agitation and vigilance
• Hypoactive: Lethargy, markedly decreased level of motor activity
• Mixed
- Altered sleep-wake cycle, daytime drowsiness. night time insomnia, fragmented sleep, complete
sleep cycle reversal
- Intermittent and labile emotion: Fear, Paranoia, Anxiety, Depression, Irritability, Apathy, Anger

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Diagnosis of Delirium
1. Determine acuity of change in mental status
2. Brief but formal cognitive test e.g. MMSE, MoCA
3. Search for underlying cause and precipitating factors of Delirium
- DHx
- Alcohol intake
- CBC for anaemia & infection
- LRFT for CKD or Chronic liver disease
- Electrolyte profile for electrolyte imbalance
- aBG for acid-base imbalance, respiratory failure
- FPG, Urine Ketone for DKA
- Septic workup for sepsis
- ECG for AMI
- CT Brain

Confusion Assessment Method (CAM)

- 1st line for diagnosis of Delirium

DSM-4 Criteria for Delirium

≥2 of the following
1. Perceptual disturbance (misinterpretation, illusions, or hallucination)
2. Incoherent speech at times
3. Disturbance of sleep-wake cycle
4. Increased or decrease psychomotor activity

DSM-5 Criteria for Delirium

A. Disturbance in attention (i.e. reduced ability to direct focus, sustain, and shift attention) and
awareness (reduced orientation to the environment)
B. Disturbance develop over a short period of time (usu. hours to days), represents a change
from baseline attention and awareness, and tends to fluctuate in severity during the course of a
day
C. An additional disturbance in cognition (e.g. memory deficit, disorientation, language,
visuospatial ability, or perception)
D. Not better explained by another pre-existing, established or evolving neurocognitive disorder
and do not occur in the context of a severely reduced level of arousal, such as coma
E. There is evidence from the history, physical examination, or laboratory findings that the
disturbance is a direct physiological consequence of another medical condition, substance
intoxication or withdrawal, or exposure to a toxin, or is due to multiple aetiologies

Often under-diagnosed due to

- Fluctuating course
- Overlapping with dementia
- Lack of formal cognitive assessment
- Under-appreciation of its clinical consequences
- Failure to consider the Dx of Delirium as important
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- Hypoactive form of Delirium

EEG
- Diffuse slowing of cortical background activity (NOT correlate with underlying causes)
- Limited role
- 17% False -ve, 22% False +ve
- Most useful for detecting occult seizures & differentiate Delirium from Psychiatric disorders

Neuroimaging
- Low clinical yield
- Only performed when
• New focal neurological signs
• Hx/ Signs of head trauma
• Fever of suspected encephalitis or meningitis
• No other identifiable causes
• Nil/ incomplete Hx
• Neurological examination cannot be completed

Prognosis of Delirium
- Often is a sign of life-threatening conditions in 10-30% of elderly patients presenting to AED
- Mortality rate among hospitalised delirium patient = 22-86%
- 1-yr mortality rate a/w Delirium = 35-40%

Management of Delirium
1. Search & treat underlying causes
2. Supportive care
- ABC, Hydration & Nutrition
- Positioning & mobilisation to prevent pressure sores & DVT
- Avoid physical restraints
- Non-pharmacological means for Sx of delirium
- Calm comfortable environment
- Orienting influences (calendars, clock, familiar objects from home)
- Regular orienting communication with staff
- Limiting room & staff changes
- Coordinate schedules for drugs, vital signs assessment & procedures
- Uninterrupted sleep (low levels of noise & lighting)
- Encourage normal sleep-wake cycle
3. Prevent complications
4. Treat behavioural symptoms

Medical Treatment
- Reserved for patients whose symptoms of delirium threaten self or others’ safety or result in
interruption of essential therapy e.g. Mechanical ventilation
- Antipsychotic: Haloperidol
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- Atypical Antipsychotics: Risperidone, Olanzapine, Quetiapine
- Benzodiazepine: Lorazepam
- Antidepressant: Trazodone

Prevention of Delirium
Yale Delirium Prevention Trial
1. Orientation & therapeutic activities for cognitive impairment
2. Early mobilisation
3. Non-pharmacological approaches (minimise psychoactive drug use)
4. Interventions to prevent sleep deprivation
5. Communication methods & adaptive equipment for vision & hearing impairment
6. Early intervention for volume depletion

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Psychogeriatric Assessments
Functional Assessment/ Activities of Daily Living
- There are different pattern & rate of drop in functional level
- e.g. Stroke: Rapid decline → Gradual resolve
- e.g. Dementia: Rapid progressive decline
- e.g. Normal Ageing: Slow progressive decline

Barthel Index of ADL

(Mahoney and Barthel, 1965)
- 10 Items
- Each item given up to 1-3 points (some use 5, 10, 15 points)

Interpretation
- Total score = 20; higher the more independent; lower the more dependent
- ≤50 = Severe
- 51-75 = Moderate

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- >75 = Mild to no impairment

Katz Index of ADL

(Katz and Akpom, 1976)

Interpretation
- Total score = 6; higher the more independent; lower the more dependent

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Lawton Instrumental ADL

(Lawton & Brody, 1969)

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Five-item Instrumental ADL

(Fillenbaum et al J Am Geriatric Society 1985)
- 5 items
- 1 score given if able to perform w/o help
- 0 score given if only able to perform w/ some help
- No score given if not answered

Questions
- Can you get to places out of walking distance?
- Can you go shopping for groceries or clothes?
- Can you prepare your own meals?
- Can you do your housework?
- Can you handle your own money

Functional Independence Measure (FIM)

- Used in TWH Stroke unit and FYKH GDH, MMRC Rehab cases
- Adopted from I-ADL
- 6 functional categories
- 18 items in total
- Total score = 126

Advanced ADL
(Reuben and Solomon)
- Also incl. Recreational, Occupational, or
Community service function

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Depression Scales

Geriatric Depression Scale (GDS)

- Original version consisted of 30 questions
- Shorter version w/ 15 questions available
- Offer valid assessment of presence of depression even among mild to moderate depression
- Test-retest reliability is satisfactory
- GDS30 cut-off = 11
- GDS15 cut-off = 5
- GDS4 - need further validation

GDS15
Questions
- Have you dropped many of your activities and interests?
- Do you feel that your life is empty?
- Do you often get bored?
- Are you in good spirits most of the time?
- Are you afraid that something bed is going to happen to you?
- Do you feel happy most of the time?
- Do you often feel helpless?
- Do you prefer to stay at home rather than going out and do new things?
- Do you feel you have more problems with memory than most?
- Do you think it is wonderful to be alive now?
- Do you feel pretty worthless the way you are now?
- Do you feel full of energy?
- Do you feel that your situation is hopeless?
- Do you think most people are better off than you are?
- Are you basically satisfied with your life?
Interpretation
- Score > 8 indicate probable Depression for Chinese version

Hamilton Rating Scale for Depression (HAM-D)

Selcare (D)

Lung Self-rating Depression Scale

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Cognitive Assessment

Abbreviated Mental Test (AMT)

- 10-question test
- Screening tool for cognitive impairment in geriatrics patients

Area of assessment
- Short term memory (Recall test)
- Long term memory (Age, DOB, Date of festivals, Name of HKCE)
- Attention (count 20 to 1)
- Orientation to Time, Year, Location, Relationship

Questions
1. What is your age (+/- 5 years)
2. What is the current time (to the nearest hour, or am, pm, midnight)
3. Please remember this address “上海海街42號” and recall at the end
4. What is the year now (+/- 1 year)
5. What is the name of this place
6. Recognition of two persons (Doctors, Nurse, Relative)
7. What is your date of birth (day and month)
8. Date of Mid-Autumn festival in Lunar calendar
9. Name of the present HKSAR chief executive
10.Count backward from 20 to 1
11.Recall the address at the end

Interpretation
- Normal: 8-10
- Moderate impairment: 4-7
- Severe impairment: 0-3
- Simple cut-off = 6 (Sn 96%; Sp 94%)

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Folstein Mini-Mental State Examination (MMSE)

Areas of assessment
- Orientation
- Attention
- Short term memory
- Language
- Motor
- Visuospatial functioning

Details
- Orientation to date
• Year: Beware of use of Lunar calendar in local elderly
• Season: Beware of understanding of “season” in different persons e.g. Spring is after 立春
• Month:
• Day of month: Beware of lunar calendar, +/- 1 day also acceptable
• Day of week: Must be accurate
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- Orientation to location
• Kowloon vs NT vs HK: Must be correct
• Hospital name: Must be correct
• Floor no.: Beware of old fashioned naming of floor e.g. ⼆二樓 (1/F)
• Ward no.
- 3-item memory
• Practically do 3 trials only
• Order of words has to be correct
• Beware of memorisation of the 3 items by patients after repeated testing by nurses/ GP/ OT
- Serial 7s
• Beware of memorisation of the numbers by patients after repeated testing by nurses/ GP/ OT
• Resort to reverse digit span if unable to perform serial 7s (but actually more difficult)
- Language assessment
• 姨丈買⿂魚腸 is too short to be mistaken
• However, original English version consists of 5 words

Cons of MMSE
- Paper-pencil test
- Age and educational background dependent
- Lack of specific instructions
- COPYRIGHT ISSUE (1 USD per sheet) → Thus Hospital authority switched to MoCA
- Too much emphasis on orientation
- NOT included test on executive function/ frontal lobe function
- Ceiling effect (low sensitivity for mild problems, might not be able to pick up cognitive
impairment in high-functioning individuals e.g. previous doctors)

Interpretation
- Total score = 30
<9 10-18 19-24 24-30
Severe Moderate Mild Normal
- Normal HK primary school year 1 graduates can already score full marks
- Cut-off = 24 (Sn 90%; Sp 60%)

Cantonese Version of MMSE (C-MMSE)

Interpretation
- 18/19: Illiterate
- 19/20: Cut-off (Sn 97.5%, Sp 97.3%)(Obsolete)
- 21/21: 1-2 of schooling
- 22/23: >2yr of schooling

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Clock Drawing Test

Steps
- Give patient blank sheet of paper
- Patient is told to draw a clock incl. the clock face, all 12 numbers in correct position
- Draw clock hands to show time of 11:10

Scoring
- Drawing a closed circle: 1 point
- Number being in special order: 1 point
- Drawing 12 numbers: 1 point
- Positioning numbers correctly: 1 point
- Place clock hands at designated time: 1 point

Interpretation
- Normal = 4-5 out of 5 points
- Parkinson = Micrographia & shaky handwriting
- Alzheimer has variable presentation

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Montreal Cognitive Assessment (MoCA)

- There are two versions of MoCA in HK: Cantonese MoCA vs HK-MoCA
- Only HK-MoCA has norm data for local HK Chinese (adjusted for age and education level)

Areas of assessment
- Visuospatial/ Executive
- Naming
- Memory recall
- Attention
- Language
- Abstraction
- Delayed recall
- Orientation

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Details
- Cube drawing: Require some degree of parallel lines
- Naming
• Lion can be acceptably recognised as “Tiger”
• 犀⽜牛 can be named Pig or Cow
• Camel can be named Horse or Single-hump Camel
- Animal naming is preferred over Fruits/ Transportation in Cantonese due to lack of association
between names of animals unlike the other two
- Abstract thinking has to be abstract

Cons
- MoCA was not originally designed for stroke

Interpretation
- Easy cut-offs
• ≥22 = Normal
• ≥23 = Normal if educated <6yr
- HK-MoCA cut-offs
• 18/19 = Dementia
• 21/22 = MCI
- Percentile cut-offs
• Score adjusted for age and education level
• >16th percentile = Normal
• ≤16th percentile = Mild NCD
• ≤7th percentile = MCI
• ≤2nd percentile = Major NCD/ Dementia

5-Minute MoCA
- Used as a quick screening tool of Dementia

Areas of assessment
- Naming
- Attention
- Language
- Memory
- Orientation

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Psychiatric
Diagnostic Interview
What is a psychiatric diagnostic interview 304 Tempo/ Speed 323

Psychiatric History Taking 305 Continuity of thoughts/ Stream of thoughts 323

Socio-demographics 305 Form of thoughts 324

Chief Complaints 305 Process of thoughts 324

History of Present Illness 305 Cognition and Sensorium 325

Past Psychiatric Hx 306 Alertness/ Consciousness 325

Past Medical Hx 306 Orientation 326

Family Hx 306 Memory 326

Personal Hx 306 Attention and Concentration 327

Premorbid Personality 307 Abstract thinking 328

Potential problematic situations 308 Concrete thinking 328

Mental State Examination & General information and intelligence 328

Psychopathology 309 Judgement 328

What is MSE 309 Insight 329

Outline of MSE 309 Components of Insight 329

Appearance and Behaviour 310 **Assessment of Insight** 329

Appearance 310 Clinical significance of Insight 330

Behaviour 311

Speech 312
Rate 312

Amount 312

Tone/ Volume 312

Articulation 312

Spontaneity 312

Flow 313

Coherence/ Relevance/ Association 313

Content 313

Emotion: Mood and Affect 315

Mood 315

Affect 316

Perceptions 317
Perceptual disturbances 317

Hallucination 318

Sensory Distortion 319

Reality Distortion 320

Thoughts 321
Content of thoughts 321

Delusions 321

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What is a psychiatric diagnostic interview

Pre-interview preparation
• Safety
• Privacy
• Diagnostic criteria (ICD vs DSM)

A. ICE in Psychiatry (≠ Family Medicine)

• Introduce yourself
• Communicate clearly
Sympathy 同情 = Experience how it feels
• Empathy Empathy 同理理 = Understand & Imagine how it feels,
or “standing in someone’s shoes”
B. History + P/E
• Socio-demographics Reasons to demonstrate empathy
• Chief complaint(s) - Builds rapport
- Facilitate history taking by connecting questions
• HPI - Improves diagnostic accuracy
• Past Psychiatric Hx - Improve adherence
• Forensic Hx if present - Improve outcome
• PMHx
• FHx
• Personal Hx
• Premorbid personality

C. Diagnosis + Ix

D. Management

E. Response assessment

F. If suboptimal response → Review Diagnosis + Ix

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Psychiatric History Taking

Socio-demographics
- Background information is of utmost importance and give you clues of what the person is like
- Age, Sex
- Marital status, Education, Occupation
- Accommodation/ Place of abode
- Receipt of social welfare allowance, disability allowance

Chief Complaints
- Described using patient’s own words rather than using medical jargons
e.g. “Hearing multiple voices scolding him for a month” instead of “Auditory verbal hallucination”
- Chief complaint may not necessarily be the symptom that clinical staff emphasise for diagnostic
ascertainment (e.g. Insomnia vs AH)

History of Present Illness

- Core part of interview - usu. indicate diagnosis

1. Symptom evolution
- Identify types; Clarify nature (descriptive psychopathology or phenomenology)
- Focus on raw experiences rather than interpretations
- Focus on sequence, timing, causality of events, underlying plots
- Onset
- Development of symptoms
- Progression: Deteriorate or Static or Fluctuating, Any pattern?
- Aggravating/ Alleviating factors
- Precipitating factors (i.e. what initiate the symptom)
- Perpetuating factors (i.e. what maintain the symptom)
2. Impacts of symptom
- Distress (Emotion, Thinking pattern etc)
- Dysfunction
• Self-care/ Independent living
• Role functioning e.g. Student, Housewife, Work
• Social relationships
- Immediate social network e.g. close family members, partners
- Extended social network e.g. friends, colleagues
3. Evaluation of risk behaviours/ idea in the past and present
- Deliberate self-harm (DSH)
- Suicide attempt
- Violence towards others
- Abnormal behaviours against self or others
- Forensic issues
- Risks a/w levels of
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•
Hopelessness
•
Helplessness
•
Worthlessness
•
Guilt
4. Ddx/ Provisional Dx in mind
- Facilitate further clarification during assessment of HPI to narrow down the Ddx list
- e.g. Current substance-abuse/ dependence
- e.g. Depressive mood as CC

Past Psychiatric Hx
- Previous psychiatric FU, hospitalisations
- Previous psychiatric diagnoses
- Hx of psychiatric Tx (Medications, ECT, Psychotherapies) and treatment response
- Previous records of staying in HWH (Halfway house), SWS (Shelter workshops service), SES
(Supported employment service)
- Previous/ Current record of rehabilitation treatments/ community services
- Treatment adherence record
- Brief summary of in-between episodes intervals (indicate the functioning and symptom control
during remissions state)
- Hx of self-harm/ suicide attempt
- Hx of Substance abuse/ Alcohol misuse
- Hx of Violence/ Forensic record esp. in relation to psychiatric illness

Past Medical Hx
- Any medical diseases that may have similar neuropsychiatric manifestations
• Implications for Ddx or r/o medical causes
• e.g. Hypothyroidism and Depressive disorders
- Any medical diseases, concurrent medical treatment, drug allergy
• Implications for choice of psychotropics

Family Hx
- Some psychiatric disorders have high degree of inheritance
e.g. Schizophrenia, Bipolar disorder, Pre-Senile dementia etc
- Other conditions to be aware of:
• Intelligence impairment
• Learning disability
• Neuropsychiatric diseases e.g. Huntington’s Disease
- Also ask for FHx of Suicide, Relationships w/ Family members

Personal Hx
- Birth Hx:
• Any obstetric complications?
• Normal spontaneous delivery?
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• Pre-term?
- Developmental milestones
• esp. Speech and Motor
• IO assessment
• Psychological assessment for suspected Autism-spectrum disorders or ADHD or LD etc
- Childhood upbringing
• Parental separation, Childhood abuse
- Schooling and higher education
• Academic development
• Interpersonal relationship with peers
• School adaptation
• Delinquency
• Forensic Hx
- Occupational Hx:
• Nature
• Duration of jobs
• Able to sustain stable employment or frequent job changes
• Whether nature of job matches his or her academic ability/ qualification
• Reasons for unemployment
- Sexual/ Marital relationships
• Marital discord
• Sexual deviance
• Childcare issue
• Divorce or Separation
- Social circumstances
• More detailed enquire for current social circumstances
• Financial status
• Stress

Premorbid Personality
- i.e. a fixed pattern of thinking, behaving
- usu. develop only until late adolescence or adulthood

Areas of assessment
- Character/ Temperament/ Trait 以前朋友點樣形容你嘅性格?
- Social life/ Relationship 以前同朋友、同事關係點?
- Prevailing mood 以前⼼心情點?
- Leisure activities/ hobbies 以前有咩嗜好?
- Reaction to stress 以前點樣⾯面對壓⼒力力?
- Religions belief 有冇宗教信仰?

EASI approach to personality

Emotionality: Prevailing mood (Stable/ Sensitive/ Nervous)
Activity: Hobbies
Sociability: Do you prefer being alone or with
307others?
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Basic dimensions of personality

- Introversion
- Neuroticism
- Psychoticism

Common Personality disorders (PD)

- Borderline
- Antisocial
- Schizotypal
- Dependent
- Obsessive-Compulsive
- Schizoid
- Narcissistic

Potential problematic situations

Patient factors
- Hostile → Calm patient down, review later +/- colleague help
- Lacks insight → Be diplomatic e.g. I know you don’t feel unwell, but your family has some
concerns. Can we discuss those?
- Mute → Try to communicate with pen and paper, see if can obey simple commands, proceed to
physical examination
- Restless → Keep it brief; get info from interview informant if available

Informant factors
- Unclear/ unreliable → If info is discrepant, document it and remain neutral/ objective

Interviewer factors
- Time constraint → Prioritise questions relevant to Dx/ Tx, Short-circuit the history (e.g. What help
do you think you need?)
- Risk assessment → Rmb to assess and document risk

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Mental State Examination &

Psychopathology
What is MSE
- Cross sectional (i.e. at the time of interview)
- Continuous (i.e. can be done throughout interview)
- Dynamic (c.f. history is stable)
- Doable even if patient is mute/ incoherent/ uncooperative
- Combination of
• Observation (appearance, behaviour, movement, facial expressions)
• Specific questions
• Testing (Cognitive tests, Questionnaires)
- Consider MSE findings along w/ Hx, P/E, Ix, Collateral info

Outline of MSE
- Appearance/ Behaviour/ Attitude e.g. Posture, poise, dress, grooming (incl. hairs, nails), body
build
- Speech e.g. Rate, Amount, Flow, Tone/ Volume, Articulation, Spontaneity
- Emotion: Mood and Affect
- Perception Mnemonic: ASEPTIC
- Thoughts e.g. Tempo, Content. Continuity, Form/ Process Appearance and behaviour
- Insight Speech
- Cognition and sensorium Emotion (Mood and Affect)
• Orientation to time, place, person Perception
• Attention and concentration Thoughts
• Memory Insight
• Concrete thinking Cognition and sensorium
• Judgement

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Appearance and Behaviour

Appearance
Aspects of appearance
- Posture & Poise
- Dressing
- Facial appearance
- Body build

Posture & Poise

- e.g. Stooped/ hunched, downcast gaze → Depression
- e.g. Sits on edge of seat, upright → Anxiety
- Kempt? if unkempt → Alcohol, Drug, Depression, Dementia, Schizophrenia

Dressing
- Appropriate? if inappropriate e.g. long coat in summer → Dementia, Schizophrenia
- Colourful?
• If brightly dressed → Mania
• if dull → Depression

Facial appearance
- Odd looking?
• e.g. Corrugated forehead → Depression
• e.g. Pupil dilation, raised eyebrows, Wide eyed, Sweaty forehead → Anxiety
• e.g. Wooden/ Mask-like face, Saliva drooling → Parkinson
- Eye contact? e.g. Good, Fleeting, Avoided, Poor, None

Body build
- Weight loss? → Anorexia nervosa, Depression, Anorexia secondary to diseases, Physical
illnesses
- Overweight? → Hypothyroidism, Cushing, Steroid, SE, Pregnancy
- Skin lesions e.g. Tattoos, Scars, Needle marks

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Behaviour
Psychomotor activity
- Restless → Mania, Schizophrenia, Akathisia, Agitated depression, Intoxication, Delirium,
Dementia
- Hyperactive → ADHD, Learning disorder, ASD in small kids
- Retardation → Depression
- Tics → Tourette
- Catatonia
• Stupor (i.e. no psychomotor activity; not actively relating to environment)
• Agitation, not influenced by external stimuli
• Grimacing
• Echolalia (i.e. mimicking another’s speech)
• Mutism (i.e. no, or very little, verbal response)
• Mannerism (i.e. odd, circumstantial caricature of normal, goal-directed actions)
• Stereotypy (i.e. repetitive, abnormally frequent, non-goal-directed movements)
e.g. Lips pouting/ pursing (aka Schnauzkrampf, German for lips pouting)
• Posturing (i.e. spontaneous and active maintenance of a rigid, inappropriate, or bizarre
posture against gravity for a long time)
e.g. Psychological pillow when patient is asked to lie supine on a flat bench
• Waxy flexibility (i.e. limbs can be positioned by examiner at slight resistance and remain for
long periods)
• Catalepsy (i.e. passive induction of a posture held against gravity)
e.g. Psychological pillow (head held in air as there’s a pillow when asked to lie on a bench)
• Negativism (i.e. opposition or no response to instructions or external stimuli)
• Echopraxia (i.e. mimicking another’s movements even when asked not to do so)
• Ambitendence (i.e. alternate between opposite movements and so on repeatedly)
- Typical example is ambitendence in shaking hand (hands go forth and back)
- NOT in DSM-5 criteria for Catatonia

Movements
- Involuntary e.g. Tic, Twitches, Dyskinesia
- Voluntary e.g. Gestures, Mannerisms, Stereotypy, Echopraxia

Social behaviour
- Disinhibition
• Ddx: Mania, Frontal lobe dementia
- Suspicious behaviours
• e.g. looking around
• Ddx: Schizophrenia
- Attitude/ Rapport e.g. Cooperative, Attentive, Frank, Seductive, Defensive, Perplexed, Apathetic,
Hostile, Evasive, Guarded etc
- Negativism - i.e. person does the opposite of what is asked and actively resist efforts to
persuade them to comply

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Speech
- Speech is a manifestation of many underlying psychopathologies esp. thoughts

Aspects of speech assessment

- Rate
- Amount
- Tone/ Volume
- Articulation
- Spontaneity
- Flow (i.e. fluidity of speaking)
- Coherence/ Relevance (i.e. continuity of content)
- Content

Rate
- Fast → Mania with pressure of speech, anxiety
- Slow → Depression, Dementia, Intellectual disability, Shyness

Amount
- Increased (Pressure of speech) → Mania
- Decreased (Poverty of speech) → Depression, Schizophrenia (negative symptoms, thought
disorder), Dementia

Tone/ Volume
- Monotonous
- Dramatic
- Loud
- Soft

Articulation
- Dysarthria?
- Slurred speech?
- Accents?

Spontaneity
- Spontaneous
- Hesitant, needs prompting

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Flow
- Manifestation of Continuity of thoughts/ Stream of thoughts

Common findings
- Continuous speech
- Interrupted speech
• A result of disrupted thoughts
• Ddx: Distractibility (e.g. ADHD), Thought block

Coherence/ Relevance/ Association

- Manifestation of Form of thoughts

Common findings
- Coherent & Relevant (C/R)
- Incoherent & Irrelevant (IC/IR)
• Loosening of association/ Derailment
- i.e. suddenly slip and leave the track, return to the point but slip again
- Ddx: Schizophrenia
• Circumstantial speech/ Circumstantiality
- i.e. Unnecessary trivial details before reaching the point
- A result of circumstantial thoughts
- Ddx: Mania, Obsessive PD, Epileptic PD
• Tangential speech/ Tangentiality
- i.e. Going off topic and cannot reach the point; each sentence is understandable
• Clang association/ Clanging
- i.e. association of words based upon sound rather than concepts
- Rhyming w/o meaning
- e.g. “the train brain rained on me”, 「今天下雨，雨天要帶傘，傘兵很厲害，害⼈人不長命」
• Word Salad
- i.e. loss of syntax and basic structure of speech (將D字炒埋⼀一碟)
• Verbal perseveration
- i.e. cannot switch topic
- A result of thought perseveration
- Ddx: Organic brain disease

Content
Common findings
- Neologism
• i.e. make up new words in which the derivation is non-understandable
or use existing/ ordinary words in a very strange way
• Technical neologism = Making up a technical term for a novel experience
• Ddx: Schizophrenia (de novo or suggested by AVH voices)
- Paraphasia
• Ddx: Normal aphasia
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- Poverty of content of speech
- Echolalia
• i.e. unsolicited repetition of vocalisations made by another person
• Ddx: ASD, Catatonia
- Coprolalia
• i.e. involuntary swearing or the involuntary utterance of obscene words or socially
inappropriate and derogatory remarks
- Logoclonia
• i.e. tendency to repeat words or syllables
• Common in Parkinson Disease

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Emotion: Mood and Affect

Mood
i.e. Pervasive and sustained emotion that colours the individual’s perception of the world
- Subjective
- Note depth, intensity, duration, fluctuations and congruity with affect

Types of mood
- Elated
• Ddx: Manic or Hypomanic episode
- Euthymic (i.e. normal)
- Dysthymic (i.e. mildly depressed)
- Depressed
• Ddx: Depressive episode, BPSD of Dementia
- Anxious
• Psychological manifestation: Apprehension, worries
• Somatic manifestation: Muscle tension, Increased RR
• Autonomic manifestation: Palpitation, Diaphoresis, Dry mouth
• Behavioural changes e.g. avoidance of phobic origin
• Evidence of trigger e.g. presence of phobic object, reminders of traumatic events
• Free-floating anxiety; Ddx: GAD, MADD
• Specific anxiety; Ddx: Phobia
• Other Ddx: Panic attack, PTSD
- Irritable

Variation of mood
- i.e. describing the range of variation in mood
- Increased variation = Emotional lability/ Labile mood
- Extreme variation = Emotional incontinence
- Reduced variation = Affect flattening (Negative symptom of Schizophrenia)
- Lack of emotional sensitivity = Blunted affect (Negative symptom of Schizophrenia)
- Stable

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Affect
i.e. Present emotional responsiveness
- Inferred from facial expression, range of expressive behaviour
- Described by observer

Types of affect
- Emotional lability = Excessive or inappropriate emotional response
- Affect flattening/ Constricted affect/ Restricted affect
• i.e. reduced variation of mood
• Ddx: Schizophrenia (negative symptoms)
- Apathy
• i.e. complete absence of variation of mood (severe affect flattening)
• Ddx: Schizophrenia (negative symptoms)
- Blunted affect
• i.e. lack of sophistication and sensitivity in emotional expression
• Reflected in facial expression, gesture, spontaneous movement, intonation, eye contact
• Ddx: Schizophrenia
- Incongruous affect
• Congruity = whether mood is in keeping with the person’s circumstances & thoughts
• e.g. Giggling when talking about father’s death
• Ddx: Schizophrenia
- Emotional indifference/ La Belle indifference
• i.e. a relative lack of concern about the nature or implications of the symptoms
• Ddx: Somatoform Disorder (aka Conversion Disorder, Hysteria)

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Perceptions

Perceptual disturbances
Types of perceptual disturbances
- Delusion - NOT a perception, but a false belief
- Pseudo-Hallucination - Delusion mimicking Hallucination
- Hallucinations - i.e. Perception w/o stimulus
- Illusions - i.e. Misperception of stimulus [Pareidolic illusion]
• e.g. Pareidolic illusion/ Pareidolia You see green bell
• e.g. Completion/ Completeness illusion pepper but it’s
- Sensory distortion actually a face
• e.g. heightened intensity (Hyperacusis)
• e.g. changed quality (Micropsia; smaller than the real size)

Circumstances
- Hypnagogic/ Hypnogogic - i.e. right before falling asleep
- Hypnopompic - i.e. right before waking up
- Others e.g. Illusions in dim lighting
[Completeness illusion]
- Triggered by sensory stimulus
You see two triangles
• Sensory stimulus from one sensory modality trigger hallucination in out of incomplete lines
other sensory modalities = Reflex Hallucination
• Sensory stimulus from one sensory modality trigger hallucination in
the same sensory modalities = Functional Hallucination

Location of experience
- Outer objective space (Hallucination)
- Inner subjective space (Delusion and Pseudo-hallucination)
- Outside limits of sensory field (Extracampine hallucination)

Quality of experience
- Vividness (Hallucination is more vivid than Pseudo-hallucination and Delusion)
- Loudness
- Controllability Modalities of perception
- Gender/ Familiarity - Auditory: Verbal vs Non-Verbal
- Visual
Setting of experience - Gustatory
- Where? - Olfactory
- Presence of others? - Tactile
- Somatic
Degree of alertness
- Less alert in Hypnagogic and Hypnopompic hallucination
- Under influence of other medication?

Forms of experience

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- Simple/ Elementary e.g. phone ring, knocks
- 2nd person (use 2nd person pronoun) e.g. “You are totally useless”
- 3rd person (use 3rd person pronoun) e.g. “He is totally useless”
- Running commentary e.g. “He is getting up now…”
- Command/ Imperative hallucination (instructions to subject)
- Thought echo

Hallucination
- Hallucinations are perception-like experiences that occur w/o an external stimulus
- They are vivid and clear, with the full force and impact of normal perceptions, and not under
voluntary control
- May occur in any sensory modality, but auditory hallucinations are the commonest in
Schizophrenia and related disorders
- Hallucination MUST occur in the context of a clear sensorium
- Hallucination when falling asleep (Hypnagogic) or waking up (Hypnopompic) are NORMAL
- Hallucination may also be a normal part of religious experience in certain cultural contexts

Common modalities of hallucination

- Auditory (AH) - Verbal (AVH) vs Non-Verbal
- Visual (VH) - may suggest organic causes e.g. Dementia with Lewy Body
- Gustatory
- Olfactory
- Tactile/ Somatic/ Sensory
• e.g. Lilliputian hallucinations/ Alice in Wonderland Syndrome: Somatic size distortion
• e.g. Formication (i.e. sensation of insects crawling under skin)

Ddx of Hallucination
- Normal
• After sensory deprivation (blindness, deafness)
• Bereavement (grief reaction e.g. hearing voices of deceased parent)
- Schizophrenia
- Neurological disease
• Temporal Lobe Epilepsy (classically p/w rubber burning smell)
• Charles Bonnet Syndrome (VH a/w disease of visual pathway)
• Lewy Body Dementia (hallmark is VH)
- Hallucinogen use
- Brain tumour
AVH and the Brain
- Migraine - Internal monitoring: SMA, DLPFC
- Language areas: Broca, Wernicke,
2nd-stage Auditory areas, Bilateral
Auditory Verbal Hallucination
temporal, inferior parietal lobule
- The most commonly seen form of Hallucination - Limbic system: Anterior cingulate
Characterisation cortex, Insula, Hippocampus, Para-
- Beliefs of origin of voices hippocampus

• Number of voices
• Where: Origin of voices from body
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• How: 2nd or 3rd person (“You” vs “He/ She”)
• Who: Gender, Age, Familiarity
- Complexity
• Simple/ Elementary - Brief phrases or names
• Complex - Lengthy, structured sentences
- Content & Meaning
• Unintelligible phrases/ words
• Thought echo (voice repeating patient’s own thoughts aloud)
• Running commentary - i.e. describing what the patient was doing
• Discussing among multiple voices or conversing with each other
• Commands - i.e. asking patient to do something, may ask patient to harm self/ others
• Derogatory - i.e. scolding patient
- Vividness
- Onset, Duration & Frequency
• When’s last time
• Hypnagogic? Hypnopompic?
• How many times last week

Delusion Pseudo-hallucination Hallucination

Figurative Concrete reality

Subjective character Objective character

Internal space External space

腦入⾯面聽到 耳仔聽到

Not clearly delineated Clearly delineated

模糊的描述 清楚的描述

Less vivid, Neutral tone Vivid, Full, Fresh

唔清晰、冇語調 清晰、⽣生動

Dissipate Constant
會慢慢消失 持續

Dependent of will Independent of will

控制到 控制唔到

Sensory Distortion
Common findings
- Macropsia - i.e. objects seem larger than actually is
- Micropsia - i.e. objects seem smaller than actually is
- Pelopsia - i.e. objects seem closer than actually is
- Teleopsia - i.e. objects seem further than actually is

Alice in Wonderland Syndrome/ Lilliputian Hallucination/ Todd’s Syndrome

- aka Dysmetropsia
- usu. refer to visual sensory distortion e.g. Micropsia, Macropsia, Pelopsia, Teleopsia
- Sometimes have somatic distortion
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- Ddx: Migraine (most common), Brain tumour, Hallucinogen use, Alcohol withdrawal,
Depersonalisation/ Derealisation Disorder, Mononucleosis (EBV)

Reality Distortion
- Described as “As if” unreal feelings
- Ddx: Ketamine abuse, Dissociative Disorder, PTSD, Borderline PD
- Onset is a/w Intense emotions, seizures, dissociation, anxiety, extreme fatigue

Common findings
- Dissociation/ Dissociative symptoms 解離經驗
• i.e. disruption in the usually integrated functions of consciousness, memory, identity,
perception and movement
• e.g. dissociative amnesia, dissociative fugue, dissociative stupor, dissociative motor disorders
- Depersonalisation ⾃自我感喪失
• i.e. a change of self-awareness such that the person feels unreal, detached from his own
experience and unable to feel emotion
• “as if oneself is unreal”
- Derealisation 現實感喪失
• i.e. a similar change in relation to the environment such that objects appear unreal, people
appear as lifeless, two-dimensional cardboard figures
• “as if world is unreal”
- Nihilistic Delusion is NOT a distortion of reality

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Thoughts
Aspects of thoughts
- Content of thoughts
- Tempo of thoughts
- Continuity/ Stream of thoughts
- Form of thoughts
- Process of thoughts

Content of thoughts
- “Contents” are “symbols with individualised meaning” that are held by “Form of thoughts”

Common content of thoughts

- Delusions - i.e. false, unshakable belief that is not explained by culture and religion
- Preoccupations and worries
- Delusion-like ideas - i.e. false, unshakable belief with content meaningfully connected with
originating experience; may have psychological meaning in terms of life experiences, wishes,
hopes, anxieties; maybe related to psychological stress or trauma
- Obsessions - i.e. recurrent, persistent, egodystonic thoughts, impulses, doubts or images that
enter the mind despite efforts to exclude them
- Over-valued ideas - i.e. isolated, pre-occupying, egosyntonic belief, not delusional nor
obsessional in nature
- Negative thoughts e.g. guilt, uselessness, hopelessness
- Phobias
- Aggressive ideas
- Suicidal thoughts
- Homicidal thoughts

Delusions
- 妄想
- i.e. False, Unshakable belief, not shared with people from the same culture and religious
background (c.f. Hallucination and Illusions are perceived)

Characterisation of Delusion
- Content/ theme
- Origin of belief
- Explained by educational/ cultural/ religious background?
- Possible alternative explanation?
- Extent of conviction - i.e. how certain the patient believe in the delusion
- Acting on delusions (50% +ve esp. in Paranoid delusion & Delusion of catastrophe) e.g.
aggression to self, others, defensiveness
- Response to contrary evidence e.g. Safety behaviour (96% +ve); a/w distress from delusions &
acting on delusions; aim to avoid contrary evidence
- Pervasiveness

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- Mood-congruent
- Bizarreness
- Impact on patient

Common themes of delusion

- Persecutory Delusion
• i.e. people are trying harm patient/ patient is a victim
• The commonest theme of delusion
• Ddx: Schizophrenia
- Referential Delusion
• i.e. people are talking about patient/ random personal experience have strong personal
significance or will affect patient’s own destiny
• Ddx: Schizophrenia
- Grandiose Delusion
• i.e. believe falsely that he or she has exceptional abilities, wealth, or fame
• Ddx: Mania
- Thought Alienation
• Thought Insertion (i.e. Foreign thoughts being inserted in one’s mind)
• Thought Withdrawal (i.e. Own thoughts being withdrawn from one’s mind)
• Thought Broadcasting (i.e. Own thoughts being known by everyone else)
• Ddx: Schizophrenia (FRS)
- Delusion of Influence/ Passivity/ Control
• i.e. believe that movement of him/herself is being controlled or made by others
• In forms of
- Affect/ Emotion (Passivity of emotion)
- Idea/ Thought (Passivity of thought) and
- Impulse/ Action (Passivity of volition)
• Ddx: Schizophrenia (FRS)
- Erotomanic Delusion/ Delusion of Love
• i.e. believe in that someone is in love with him/her
• usu. are the famous people at the patient’s period
- Delusion of Jealousy
• e.g. Morbid Jealousy - i.e. spouse/ partner being unfaithful
• Ddx: Alcohol induced delusion, Dementia, Delusional Disorder
- Delusion of Poverty
- Delusion of Guilt
• Ddx: Schizophrenia, Depression
- Nihilistic Delusion/ Cotard Syndrome
• i.e. believe in that him/her is going to die
- Dysmorphophobic delusion - i.e. believe in having false bodily shape or form
- Hypochondriacal delusion
- Delusions of Misidentification
• Capgras Delusion/ Syndrome
- i.e. think that emotionally-related persons are replaced by identical imposer
- Ddx: Schizophrenia, Depression
• Fregoli Delusion/ Syndrome

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- i.e. think that different people are all in fact a single person who changes appearance or
is in disguise
* Delusions are deemed Bizarre if they are clearly implausible and not understandable to same-
culture peers and do not derived from ordinary life experience
* Example of bizarre delusion: An outside force has remove his/her organ and replaced with
someone else’s organs w/o leaving any wounds or scars
* Example of non-bizarre delusion: One is under surveillance by the police, despite a lack of
convincing evidence

Origins of delusion
- Primary delusion/ Delusion proper: Not occurring in response to another psychopathology
• Delusional intuition - i.e. autochthonous; out of the blue; Wahneinfall
• Delusional perception - i.e. false belief/ significance attached to a real perception
• Delusional atmosphere (mood)
• Delusional memory (retrospective delusion)
- Secondary delusion: Understandable in present circumstances e.g. pervasive depression
mood state or AH-triggered off abnormal belief
- Induced delusion/ Shared delusion/ Suggestion-phenomenon/ Folie á deux:
Delusion dissemination through group consciousness and feeling; larger the no. of people
involved, stronger the conviction

Tempo/ Speed
- Fast = Flight of ideas/ Racing thoughts
• i.e. Thoughts follow each other rapidly in mind
• Manifest as Pressure of speech/ Pressured speech and Clang associations
• Connections between successive thoughts appear to be random
- Determined by chance relationships, external stimulus
• Ddx: Mania, usu. manifest under pressure
- Slow = Slow thoughts
• Manifest as Poverty of speech/ Slow speech
• Ddx: Dementia, Drug-induced, Intellectual disability, Organic causes

Continuity of thoughts/ Stream of thoughts

- Whether thoughts appear continuous or disrupted

Common findings
- Continuous thoughts
- Disrupted thoughts
• Manifest as interrupted speech
• Ddx: Distractibility (e.g. ADHD), Thought block

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Form of thoughts
- Form of thought = Sub-symbolic functional architecture of thoughts
(c.f. content = symbolic reflections of words)
- Refers to the way in which the individual puts together ideas and associations

Common formal thought disorders/ disorders of thought form

- Loosening of association/ Derailment
• Manifest as Loosening of association of speech content
- Clang association/ Clanging
• i.e. association of words based upon sound rather than concepts
• Rhyming w/o meaning
• e.g. “the train brain rained on me”, 「今天下雨，雨天要帶傘，傘兵很厲害，害⼈人不長命」
- Circumstantial thoughts/ Circumstantiality
• Manifest as Circumstantial speech
- Tangential thoughts/ Tangentiality
• Manifest as Tangential speech
- Illogicality
- Thought perseveration
• i.e. cannot switch topic
• Manifest as Verbal perseveration
• Ddx: Organic brain disease
- Concrete thinking - i.e. unable to think abstractly
- Word salad
- Neologism - i.e. make up new words

Process of thoughts
- Dialogue techniques
- Empathy
- Dialogue styles
- Structure of interview

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Cognition and Sensorium

Domains of cognition
- Alertness/ Level of consciousness
- State of consciousness
- Orientation to time, space, person PCELLS of Cognition (DSM-5)
- Memory Perceptive motor
- Attention & Concentration Complex attention
- Capacity to read and write Executive ability
- Visuospatial ability Language
- Abstract thinking Learning and memory
- Concrete thinking Social cognition
- General information and intelligence
- Judgement

Alertness/ Consciousness
“Altered status of consciousness is a umbrella term that includes any abnormal consciousness”

Common findings
- Normal/ Alert and Consciousness
- Arousal problem
• Sleeping - i.e. poorly aroused
• Lethargy - i.e. poorly aroused with mild unresponsiveness
• Stupor
- i.e. Alert but unresponsive
- Ddx: Organic causes, Depression
• Clouding of consciousness
- i.e. decreased contact with environment, often accompanied by disorientation
- Ddx: Delirium
• Coma
- i.e. Cannot be aroused, complete unresponsiveness
• Pseudo-Comas e.g. Persistent Vegetative State (PVS), Akinetic Mutism, Abulia, Inattention,
Locked-in Syndrome, Catatonia
- Awareness problem
• Cognitive decline e.g. Dementia
• Delusion
• Confusion
• Inattention

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Orientation
Distortions of Recognition
- Identifying paramnesia
• Jamais vu
- i.e. failure to recognise events that have been encountered before
• Deja vu
- i.e. the feeling of having already experienced the current situation
- Spurious familiarity
- Ddx: Normal individual, Temporal Lobe Epilepsy
- Delusions of Misidentification
• Capgras Delusion/ Syndrome
- i.e. think that emotionally-related persons are replaced by identical imposer
- Ddx: Schizophrenia, Depression
• Fregoli Delusion/ Syndrome
- i.e. think that different people are all in fact a single person who changes appearance or
is in disguise

Memory
Types of memory
- Immediate memory
• e.g. Serial 7s
- Normally should be able to subtract for 5 times
- “100減7, 再減7, ⼀一路路減落落去, 直⾄至我叫你停為⽌止“
- Also require attention and concentration
• e.g. forward and backward digit span recalled immediately
- Normally should be able to do at least 5 digits
- “4 2 7 3 1” (AMT version)
- Short term memory
• e.g. simple address immediately repeated to ensure registration, to be asked 5 min later
• “上海海街42號” (AMT version)
• “蘋果、報紙、火⾞車車” (MMSE version)
• “⾯面孔、絲絨、教堂、雛菊、紅⾊色” (HK-MoCA version)
- Recent memory
• e.g. news within the last 1-2d, what patient had for breakfast/ last night’s dinner
• 琴晚新聞講咩? 今⽇日早餐食咩?
- Remote memory
• e.g. personal events in childhood clarified with informant, well known past events e.g. wars,
names of governors; note also the sequence of events
• 依家嘅特⾸首係邊個?

3Rs of memory
- Registration
- Retaining

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- Retrieval

Amnesia
Types of Amnesia
- Retrograde Amnesia
• i.e. Loss of memory before incident/ Loss of past memory
• Ribot’s law of Retrograde Amnesia: There is a time gradient in retrograde amnesia; the more
recent memory are lost before loss of remote events
- Anterograde Amnesia
• i.e. Loss of memory after incident/ Loss of recent memory
- Transient Global Amnesia
• i.e. Temporary loss of both past and recent memory

Confabulation
- i.e. False description of past event
- Content can be influenced by examiner, and highly suggestible
- A phenomenon where memory is constructed based on inadequate data to fill the memory gaps
- usu. lack of insight and critical faculty
- Ddx:
• Dementia
• Delirium
• Amnesic syndromes e.g. Korsakoff Syndrome
• Other organic conditions e.g. Stroke, Epilepsy

Attention and Concentration

Definitions
- Attention = Ability to put focus on a specific issue
- Concentration = Ability to sustain attention

Assessment tools
- Serial 7s (used in MMSE)
• Ask patient to subtract 7s from 100 (5 times in MMSE to give a total score of 5)
• Note the time taken, number of errors
• Also require immediate memory
- Serial threes
- Reverse order of calendar months
- Reverse order of days of the week
- Spell WORLD backwards for english speakers

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Abstract thinking
- i.e. ability to deal with concepts
- e.g. Look for figurative similarities (not concrete)
• Apple and Oranges - they are both fruits; X accept “they are both round”
• Truth and Beauty - they are both virtues; X accept “they are both words”
- e.g. Ask for meaning of “A rolling stone gathers no moss (滾⽯石不⽣生苔，轉業不聚財)”, “Killing a
bird with two stones (⼀一⽯石⼆二⿃鳥)”

Concrete thinking
- i.e. interpreting superficially w/o understanding of what the words literally mean

General information and intelligence

- Take into account education level
- Suggestive history - slow learner, poor scholastic achievement
- Simple daily problems e.g. how much change does he get if he gave a $20 note to pay for 3
oranges at $2.4 each

Judgement Frontal lobe is of particular

- i.e. ability to know the morally correct thing to do interest in cognition and
sensorium. Other aspects of
- e.g. 如果依家火燭, 你會點樣做?
frontal lobe function are as follow
- Verbal fluency
- Stroop task
- Limitation and utilisation
behaviour
- Apathy
- Social coarseness

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Insight
i.e. the individual’s degree of awareness and understanding of his illness
- Complex, have different levels

Components of Insight
1. Insight to symptom
- Whether symptoms are present
- Whether symptoms are abnormal
2. Insight to illness
- Awareness of whether illness is physical or mental ⾝身體上嘅定⼼心理理上
- Correct labelling of illness 你知唔知係咩病
3. Insight to treatment
- Whether treatment (incl. admission) is needed 需唔需要接受治療
- Consequences of the illness and the asso. behaviour 有咩後果

**Assessment of Insight**
Insight to Symptoms
- 知唔知⾃自⼰己點解入來來醫院？
- 覺唔覺⾃自⼰己近來來有乜轉變？
- 有無⾝身邊家⼈人朋友同你傾過？覺得你有轉變、唔係咁正常？
- 你⾃自⼰己覺唔覺？點睇佢地既諗法？

Insight to Illness
- 知唔知乜野係精神病？
- 知唔知⾃自⼰己有無精神病？
- 了了唔了了解⾃自⼰己個情況？
- 知唔知⾃自⼰己點解會有呢啲唔妥？係咪有病？係乜野病？

Insight to Treatment
- 認唔認為⾃自⼰己要接受治療？
- 知唔知有乜野可以幫到呢個病？有無跟住做？做得⾜足唔⾜足？(Compliance)
- 啲藥有無副作⽤用？食左唔舒服？點解要食藥？(Drug compliance)
- 覺得將來來點？有無信⼼心控制到個病？有乜野打算？洗唔洗繼續覆診? (Future Insight)

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Clinical significance of Insight

- Compliance: Better the insight is, more compliant the patient is likely to be

Causes of poor insight

- Poor educational level
- Cultural & environmental (incl. familial) influences
- Mental illnesses
• Mood disorders
- Depressive disorders
- Anxiety disorders
• Substance abuse
• Somatoform disorders
- Somatic Symptom Disorder
- Illness Anxiety Disorder
- Body Dysmorphic Disorder
- Factitious disorders e.g. Munchausen’s Syndrome
• Mental retardation
• or any severe mental illnesses
- Medical diseases
• Delirium
• Dementia
• Brain tumour (affecting cognition)

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