Other Clinical Syndromes

Study Notes

Sources: Kaplan & Sadock's Comprehensive Textbook of Psychiatry (11th ed.), Stahl's Essential Psychopharmacology (5th ed.), Oxford Textbook of Psychiatry, Fairburn CBT-E Manual, ICD-11 Clinical Descriptions and Diagnostic Guidelines, DSM-5-TR

PART 1: DISSOCIATIVE DISORDERS

1.1 Overview and Conceptual Framework

Dissociation is a disruption in the normally integrated functions of consciousness, memory, identity, emotion, perception, behavior, and sense of self. The term was coined by Pierre Janet in the late 19th century, who viewed it as a failure of psychological synthesis under stress.

Key Theoretical Models:

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1.2 Dissociative Amnesia

Definition: An inability to recall important autobiographical information, usually of a traumatic or stressful nature, that is inconsistent with ordinary forgetting.

DSM-5 Criteria:

• Inability to recall important autobiographical information (usually traumatic/stressful)
• Not due to another disorder, substance, or neurological condition
• Causes clinically significant distress or functional impairment

ICD-11 Code: 6B61

Subtypes:

Key clinical features:

• Onset often acute, linked to trauma or severe stress
• Gap in memory is ego-alien, patient is distressed by it
• La belle indifference may be present (not universal)
• Spontaneous recovery common; may be triggered by removal from stressor

Differential Diagnosis:

• Transient Global Amnesia (TGA): sudden, complete, brief (hours), no trauma link, seen in middle-aged/elderly, EEG and neuroimaging normal but distinct clinical course
• Organic amnesia: anterograde > retrograde, consistent neurological findings
• Malingering: secondary gain prominent, inconsistent memory performance on testing

Management:

• Psychoeducation and establishing safety
• Trauma-focused therapy (EMDR, trauma-focused CBT) once stabilized
• Narcoanalysis (amobarbital interview), historical interest; not evidence-based, not recommended in current guidelines
• Hypnosis: adjunctive; evidence limited
• SSRI for comorbid PTSD/depression

1.3 Dissociative Fugue

Definition: Sudden, unexpected travel away from home or customary place of work, with inability to recall some or all of one's past, sometimes including confusion about personal identity or adoption of a new identity.

ICD-11: Listed separately as 6B61.0 (Dissociative amnesia with dissociative fugue)

DSM-5: Now a specifier of Dissociative Amnesia, not a separate diagnosis

Clinical features:

• Duration: hours to months
• Purposeful travel; patient often appears normal to observers
• New identity may be adopted (partial or complete)
• Recovery: usually abrupt; retrograde amnesia for fugue period persists
• May surface during wartime, natural disasters, or severe personal crisis

Differential: Complex partial seizures, TGA, malingering, alcohol-related blackouts

1.4 Dissociative Identity Disorder (DID)

Definition: Disruption of identity characterized by two or more distinct personality states or "alters," each with its own relatively enduring pattern of perceiving, relating to, and thinking about the environment and self.

DSM-5 Criteria:

1. Two or more distinct personality states
2. Recurrent amnesia between alters
3. Significant distress or impairment
4. Not due to cultural/religious practice
5. Not due to substance or medical condition

ICD-11 Code: 6B64, notable changes (see Classification section)

Epidemiology:

• Prevalence: 1-3% general population (controversial; much higher in trauma-exposed clinical samples)
• Female:Male ratio: approximately 9:1 in clinical settings (trauma reporting bias)
• Average number of alters: 13-15
• 97-98% report childhood trauma history

Alter system:

• Host personality: the one usually presenting
• Child alters: often carry traumatic memories
• Persecutory alters: internalized abuser
• Protector alters: shield other alters
• "Apparently normal part" (ANP) functions in daily life

Neurobiology:

• Different alters show different psychophysiological responses (EEG, HR, skin conductance)
• Neuroimaging: differences in regional brain activity between alter states
• Positron emission tomography studies: different memory patterns for different alters

Controversies:

• Iatrogenic creation through suggestive therapy (sociocognitive critique)
• Cross-cultural prevalence variation (higher in North America than Europe, cultural scripting argument)
• High false-positive rates in some clinical settings
• Forensic implications (criminal responsibility)

Management of DID:

• Pharmacotherapy: no specific agent; treat comorbid PTSD, depression, anxiety
• Avoid rapid uncovering; premature trauma processing destabilizes

1.5 Depersonalization/Derealization Disorder (DPDR)

Definition:

• Depersonalization: Feeling detached or estranged from one's own mental processes or body (observer of own thoughts, feelings, sensations)
• Derealization: Feeling detached from one's surroundings (dreamlike, unreal, foggy, visually distorted)

DSM-5 Code: 300.6 | ICD-11 Code: 6B66

Key distinguishing feature: Reality testing remains intact (unlike psychosis)

Epidemiology:

• Brief transient episodes: up to 74% of general population
• Persistent DPDR: 1-2% prevalence
• Peak onset: adolescence to early adulthood
• Often triggered by stress, sleep deprivation, drugs (cannabis, hallucinogens)

Neurobiology:

• Reduced activation of limbic structures (emotional numbing)
• Increased prefrontal inhibition of emotional processing
• Serotonin and GABA system involvement

Clinical features:

• Emotional numbing and anhedonia often prominent
• Anxiety about the symptoms themselves (secondary anxiety)
• Chronic, waxing/waning course
• Often comorbid with anxiety disorders, depression, trauma history

Management:

• CBT (Feeling Real technique, Hunter and Phillips approach)
• Lamotrigine: some evidence
• SSRI for comorbid anxiety/depression
• Naltrexone: some open-label data
• Psychoeducation reduces distress significantly

1.6 Dissociative Motor and Sensory Disorders (Functional Neurological Symptom Disorder)

ICD-11 Classification: Moved to Diseases of the Nervous System (not Dissociative Disorders)

DSM-5: Functional Neurological Symptom Disorder (Conversion Disorder), 300.11

Motor symptoms:

• Functional weakness/paralysis
• Functional tremor
• Functional gait disorder (astasia-abasia)
• Functional speech disorder (aphonia)

Sensory symptoms:

• Functional sensory loss (does not follow dermatomal/peripheral nerve pattern)
• Functional visual disturbance

Key signs supporting functional diagnosis:

• Hoover sign (hip extension weakness normalizes with contralateral hip flexion)
• Tremor variability with distraction
• Tubular visual field defect (tunnel vision same regardless of distance, not anatomically possible)
• Splitting of midline vibration sense

Neurobiology:

• Not fabrication, there is demonstrable motor cortex inhibition
• Altered connectivity between prefrontal areas and motor/somatosensory cortex
• Functional MRI shows real changes in neural processing

Management:

• Explanation and psychoeducation (using the "software not hardware" framework)
• Physiotherapy (for motor symptoms)
• CBT
• Multidisciplinary approach
• Treating comorbid anxiety, depression, PTSD

1.7 Possession/Trance Disorders

ICD-11: Trance disorder (6B63) and Possession trance disorder (6B63.0), distinguished

Differential from religious practice:

• Pathological: ego-dystonic, causes impairment, occurs outside cultural context, patient seeks help
• Cultural practice: ego-syntonic, bounded by ritual, no impairment between episodes

1.8 ICD-11 vs DSM-5: Dissociative Disorders

PART 2: EATING DISORDERS

2.1 Anorexia Nervosa (AN)

Definition: Persistent restriction of energy intake, intense fear of weight gain, and disturbance in how one's weight or shape is experienced.

DSM-5 Criteria:

1. Restriction of energy intake → significantly low body weight
2. Intense fear of gaining weight (or behavior that interferes with weight gain)
3. Disturbance in body weight/shape experience, undue influence on self-evaluation, or persistent lack of recognition of seriousness of low body weight

ICD-11 Code: 6B80

Subtypes:

Epidemiology:

• Lifetime prevalence: ~0.5-1% females, 0.1-0.3% males
• Female:Male ratio: 10:1
• Age of onset: bimodal peaks at 14 and 18 years
• Highest mortality of any psychiatric disorder (5-6% per decade; SMR ~5.86)
• Mortality: medical complications AND suicide

BMI Severity Specifiers (DSM-5):

ICD-11 Changes for AN:

• Removed BMI <17.5 as hard criterion
• Introduced weight-for-age concept for children/adolescents
• Added "significantly low body weight" language matching DSM-5

2.1.1 Medical Complications of Anorexia Nervosa

2.1.2 Refeeding Syndrome

Definition: Potentially fatal metabolic complications occurring during nutritional rehabilitation after a period of prolonged malnutrition or starvation.

Pathophysiology:

• Malnutrition → whole-body depletion of phosphate (intracellular), despite normal serum levels
• Refeeding (especially with carbohydrates) → insulin surge
• Insulin drives glucose, phosphate, potassium, magnesium INTO cells
• Rapid drop in serum phosphate, potassium, magnesium

NICE Criteria for High Refeeding Risk:

• BMI <16
• Unintentional weight loss >15% in 3-6 months
• Little or no nutritional intake >10 days
• Low serum potassium, phosphate, or magnesium before feeding

Clinical Consequences of Refeeding Syndrome:

Prevention:

• Start at 20 kcal/kg/day (or 10 kcal/kg if very high risk)
• Increase slowly over 4-7 days
• Monitor electrolytes every 12-24 hours initially
• Thiamine (B1) supplementation BEFORE and during refeeding, oral or IV
• Correct electrolytes before initiating feeding

MARSIPAN Guidelines (Management of Really Sick Patients with Anorexia Nervosa):

• Provides criteria for medical admission
• Establishes monitoring protocols
• Multidisciplinary approach mandatory

2.2 Bulimia Nervosa (BN)

Definition: Recurrent episodes of binge eating followed by compensatory behaviors, with self-evaluation unduly influenced by body shape and weight.

DSM-5 Criteria:

1. Recurrent binge eating: eating a large amount in a discrete period + sense of lack of control
2. Recurrent inappropriate compensatory behaviors (vomiting, laxatives, diuretics, fasting, excessive exercise)
3. Occurs at least once per week for 3 months
4. Self-evaluation unduly influenced by body shape/weight
5. Does not occur exclusively during AN

ICD-11 Code: 6B81

Severity specifiers (by compensatory behavior frequency):

• Mild: 1-3 episodes/week
• Moderate: 4-7 episodes/week
• Severe: 8-13 episodes/week
• Extreme: >14 episodes/week

Medical complications specific to BN:

Pharmacotherapy:

• Fluoxetine 60 mg/day, ONLY FDA-approved drug for BN (note: higher than antidepressant dose)
• Effective for binge-purge cycles and comorbid depression
• TCAs (imipramine, desipramine): some evidence but side-effect profile limits use
• MAOIs: effective but dangerous; not used
• Topiramate: reduces binge eating but significant cognitive side effects
• Bupropion is CONTRAINDICATED in BN, lowers seizure threshold; electrolyte disturbances in BN further increase seizure risk

2.3 Binge Eating Disorder (BED)

Definition: Recurrent episodes of binge eating without regular compensatory behaviors.

DSM-5 Criteria:

1. Recurrent binge eating (large amount + loss of control)
2. Associated with 3 or more of: eating faster than normal, eating until uncomfortably full, eating large amounts when not physically hungry, eating alone due to embarrassment, feeling disgust/depressed/guilty afterward
3. Marked distress
4. Occurs at least once/week for 3 months
5. NOT associated with regular compensatory behaviors (distinguishes from BN)

ICD-11 Code: 6B82

Epidemiology:

• Most common eating disorder: ~3.5% in women, ~2% in men
• More equal sex distribution than AN or BN
• Strong association with obesity, but not all individuals with BED are obese
• High comorbidity with mood disorders, anxiety disorders

Treatment:

• CBT-E (enhanced CBT): first-line
• IPT: comparable efficacy
• DBT: adapted for BED
• Lisdexamfetamine (Vyvanse): FDA-approved for moderate-to-severe BED; reduces binge frequency
• Topiramate: reduces binge frequency; weight loss effect
• SSRIs: modest effect on binge frequency

2.4 ARFID, Pica, and Rumination Disorder

Avoidant/Restrictive Food Intake Disorder (ARFID)

ICD-11: Avoidant-restrictive food intake disorder (6B83)

DSM-5 Criteria:

• Restriction of food intake due to apparent lack of interest, avoidance based on sensory characteristics, concern about aversive consequences (choking, vomiting)
• Weight loss/growth faltering OR nutritional deficiency OR dependence on enteral feeding OR significant interference with psychosocial functioning
• NOT explained by food unavailability, cultural practice, AN, or BN
• NOT explained by medical condition or other mental disorder

Key differentiators:

Pica

Definition: Persistent eating of non-nutritive, non-food substances for at least 1 month.

ICD-11 Code: 6B84

Common substances: Earth/clay (geophagia), ice (pagophagia, associated with iron deficiency anemia), starch (amylophagia), chalk, paper, hair (trichophagia)

Associations: Pregnancy, iron deficiency, intellectual disability, ASD, neglect/deprivation

Medical complications: Lead poisoning, intestinal obstruction, parasitic infection, dental damage

Rumination Disorder

Definition: Repeated regurgitation of food, re-chewing, re-swallowing, or spitting out, for at least 1 month.

ICD-11 Code: 6B85

• NOT due to GERD, pyloric stenosis, or another GI condition
• NOT occurring exclusively in AN/BN
• Typically effortless (not forceful vomiting); occurs within minutes of eating
• Most common in infants (3-12 months), but also in adults
• Treatment: diaphragmatic breathing, behavioral interventions, habit reversal

2.5 Body Image Disturbance

Relevant across:

• AN: overestimation of body size, shape dissatisfaction as core psychopathology
• BN: shape and weight overvalued in self-evaluation
• Body Dysmorphic Disorder (BDD): preoccupation with perceived defect (not food-related)

Assessment tools:

• Body Shape Questionnaire (BSQ)
• EDE-Q (Eating Disorder Examination Questionnaire)
• EDI-3 (Eating Disorder Inventory-3)
• Clinical interview: "When you look in the mirror, what do you see?"

2.6 CBT-E (Enhanced Cognitive Behaviour Therapy): Fairburn

Theoretical model:

Transdiagnostic model: eating disorders share a common psychopathology centered on overconcern with eating, shape, and weight (the "core psychopathology").

Four maintaining mechanisms:

1. Clinical perfectionism
2. Low self-esteem
3. Interpersonal difficulties
4. Mood intolerance

Phases of CBT-E:

• Intensive version for complex cases: 40 sessions
• Works across AN, BN, BED (transdiagnostic)
• Outpatient format; inpatient version also developed

Components specific to AN:

• Weight restoration phase integrated with psychological treatment
• "Collaborative", therapist and patient review together
• Education about effects of starvation on thinking (starvation syndrome)

2.7 Nutritional Rehabilitation in AN

Goals:

• Target weight: typically BMI 20-25 (for adults); return to growth curve for adolescents
• Adequate nutrition for growth/bone density restoration
• Menstrual recovery: usually when weight >90% of expected weight for height
• Rate of weight gain: 0.5-1 kg/week (outpatient) to 1-1.5 kg/week (inpatient)

Caloric targets:

• Start: 1000-1500 kcal/day (lower if high refeeding risk)
• Target: 3000-4000 kcal/day for weight restoration
• Avoid high-calorie density foods initially; balanced macronutrient distribution

Oral vs Nasogastric vs Parenteral:

• Oral preferred
• NG feeding for patients who cannot eat enough voluntarily (including involuntary treatment)
• Parenteral (IV) nutrition: only if GI tract non-functional; carries infection risk

2.8 ICD-11 Classification of Eating Disorders

PART 3: SLEEP DISORDERS

3.1 Normal Sleep Architecture

Sleep Stages:

Sleep cycle:

• 4-6 complete cycles per night
• Cycle length: ~90 minutes
• N3 (slow wave) predominates in first third of night
• REM predominates in last third of night

Neurotransmitters in sleep:

3.2 Insomnia

Definition: Difficulty initiating or maintaining sleep, or early morning awakening, occurring despite adequate opportunity and circumstances for sleep, associated with daytime impairment.

Classification:

ICD-11 Code: 7A00 (Chronic insomnia disorder)

Spielman's 3P Model:

Epidemiology:

• Chronic insomnia: 10-15% of adults
• More common in women, elderly, psychiatric illness, chronic medical illness
• Comorbid in >50% of psychiatric disorders

3.2.1 CBT-I (Cognitive Behavioural Therapy for Insomnia)

CBT-I is first-line treatment for chronic insomnia (over pharmacotherapy)

Components:

Sleep efficiency: Sleep efficiency (SE) = (Total Sleep Time / Time In Bed) × 100%

• SE <85% = insomnia
• SE >90% = acceptable consolidation

3.2.2 Pharmacotherapy for Insomnia

3.3 Hypersomnolence and Narcolepsy

Idiopathic Hypersomnia

• Excessive daytime sleepiness (EDS) without cataplexy
• Prolonged sleep (>11 hours/day) or long unrefreshing naps
• Sleep drunkenness (severe difficulty awakening; sleep inertia)
• PSG: normal REM latency, reduced MSLT sleep latency (<8 min) but <2 SOREMPs
• Treatment: modafinil, stimulants

Narcolepsy

Tetrad of Narcolepsy (Gelineau's tetrad):

1. Excessive daytime sleepiness (EDS), obligate
2. Cataplexy, sudden loss of muscle tone triggered by emotion (laughter, surprise, anger)
3. Sleep paralysis, inability to move at sleep onset/offset
4. Hypnagogic/hypnopompic hallucinations, vivid hallucinations at sleep onset/offset

MSLT (Multiple Sleep Latency Test):

• 5 nap opportunities at 2-hour intervals
• Mean sleep latency <8 minutes = abnormally sleepy
• ≥2 SOREMPs = strongly suggests narcolepsy
• Done after overnight PSG (to exclude sleep apnea as cause of EDS)

Pathophysiology of Type 1:

• Selective loss of hypothalamic hypocretin-producing neurons (80-90% reduction)
• Autoimmune mechanism: HLA-DQB1*06:02 association; triggered by H1N1 influenza or Pandemrix vaccine
• Anti-TRIB2 antibodies found in some patients

Management of Narcolepsy:

3.4 Obstructive Sleep Apnea (OSA)

Definition: Repetitive episodes of upper airway collapse during sleep, causing apnea/hypopnea, leading to intermittent hypoxia, arousals, and fragmented sleep.

Diagnosis:

• Apnea-Hypopnea Index (AHI): number of apneas + hypopneas per hour of sleep
• Mild: AHI 5-15
• Moderate: AHI 15-30
• Severe: AHI >30
• Diagnosed by overnight polysomnography (PSG) or home sleep testing

Psychiatric relevance:

• Associated with depression (bidirectional)
• Can cause or worsen cognitive impairment
• Treatment-resistant depression may have undiagnosed OSA
• OSA worsens in hypothyroidism, acromegaly

Treatment:

• CPAP (continuous positive airway pressure), first-line
• Mandibular advancement device, mild-moderate
• Weight loss, positional therapy, avoidance of alcohol/sedatives
• Surgery (UPPP) in selected cases

3.5 Parasomnias

Definition: Abnormal behavioral, experiential, or physiological events occurring during sleep or sleep-wake transitions.

NREM Parasomnias (Disorders of Arousal)

Common feature: Occur in N3 (slow wave sleep), predominantly in first third of night. Patient is partially aroused but not fully awake.

REM Sleep Behavior Disorder (RBD)

Definition: Acting out of vivid, action-filled dreams during REM sleep, due to failure of normal REM muscle atonia.

ICD-11 Code: 7A22

Key features:

• Usually middle-aged to elderly males
• Behaviors: punching, kicking, shouting, falling out of bed
• Often correlates with dream content ("defending against attack")
• Polysomnographic finding: REM sleep without atonia (RSWA)
• Full memory of dreams; wakes up oriented

Management:

• Clonazepam (0.25-2 mg at bedtime), first-line; reduces behavior, does not restore atonia
• Melatonin (3-12 mg at bedtime), better tolerated in elderly; does partially restore atonia
• Bed safety: remove sharp objects, pad floor
• Treat alpha-synucleinopathy if present

Other Parasomnias

3.6 Circadian Rhythm Sleep-Wake Disorders

3.7 Restless Legs Syndrome (RLS)

Diagnostic criteria (IRLSSG):

1. Urge to move the legs, usually accompanied by unpleasant sensations
2. Symptoms begin or worsen during rest or inactivity
3. Partially or totally relieved by movement
4. Symptoms are worse in the evening or at night
5. Not solely accounted for by another condition

Associations:

• Iron deficiency (check serum ferritin; treat if <50-75 μg/L)
• Pregnancy (third trimester)
• Uremia, peripheral neuropathy, Parkinson's disease
• Dopamine deficiency: symptoms worsen with dopamine antagonists (antipsychotics, metoclopramide)

Management:

3.8 Sleep in Psychiatric Illness

PART 4: SUICIDE

4.1 Epidemiology

Global:

• ~800,000 deaths/year from suicide globally (WHO 2023 estimate)
• Rate: approximately 10.5 per 100,000 globally
• Leading cause of death in 15-29 year olds
• Male:Female ratio for completed suicide: 3-4:1 (worldwide); lower in India
• Female:Male ratio for attempts: 3:1

India (NCRB Data):

Suicide attempt vs completion:

• Ratio of attempts to completions: approximately 20:1 (global); varies
• India: underreporting of both attempts and completions (legal, stigma)
• 50% of completers have made prior attempts

4.2 Risk Factors and Protective Factors

Risk Factors (Organized by Mnemonic: see D3)

Psychiatric:

• Previous suicide attempt (strongest single predictor of completion)
• Major depression (especially with hopelessness)
• Bipolar disorder (mixed states, depression, post-mania depression)
• Schizophrenia (command hallucinations, post-psychotic depression)
• Substance use disorders (alcohol markedly increases risk)
• Borderline personality disorder
• Anorexia nervosa (highest SMR of all psychiatric disorders)
• PTSD

Psychological:

• Hopelessness (Beckian triad, more predictive than depression severity itself)
• Impulsivity/aggression
• History of trauma
• Chronic pain/illness

Social:

• Social isolation, living alone
• Recent bereavement, loss, humiliation
• Unemployment, financial crisis
• Domestic violence
• Access to lethal means

Biological:

• Serotonin dysfunction (5-HIAA reduced in CSF of suicide completers)
• HPA axis dysregulation
• Family history

Protective Factors

4.3 Risk Assessment Tools

SAD PERSONS Scale (Patterson et al., 1983)

Score: 0-4 = low risk, 5-6 = moderate, 7-10 = high risk

Columbia Suicide Severity Rating Scale (C-SSRS)

Developed by Posner et al., widely validated.

Suicidal ideation assessment:

1. Wish to be dead
2. Non-specific active suicidal thoughts
3. Active thoughts with method (no plan)
4. Active ideation with some intent to act, no plan
5. Active ideation with plan and intent

Suicidal behavior:

• Preparatory actions, aborted attempt, interrupted attempt, actual attempt, completed suicide

Clinical Interview Framework (WHAT MATTERS)

Access to means: What methods are available? Firearms at home?

Intent: Is there intent to act? Have they taken preparatory steps?

Plan: Is there a specific plan with time, place, method?

Hopelessness: Beck Hopelessness Scale or clinical assessment

History: Prior attempts, family history

Protective factors: What stops them?

Mental state: Command hallucinations, agitation, intoxication

4.4 Theories of Suicide

Joiner's Interpersonal Theory of Suicide (IPTS)

Three components necessary for highest suicide risk:

1. Thwarted belongingness, the sense of not belonging, social isolation, loneliness
2. Perceived burdensomeness, belief that one is a burden to others; "my death would be a relief to my family"
3. Acquired capability, habituation to pain and fear of death through repeated exposure (prior attempts, violence, self-harm history)

Clinical application: Assess each component in interview. "Do you feel like a burden?" "Do you feel like you belong anywhere?"

Klonsky & May's Three-Step Theory (3ST)

Step 1: Pain (psychological) + Hopelessness → passive suicidal ideation

Step 2: Pain > Connection to life → active ideation

Step 3: Dispositional, acquired, or practical capability → attempt

Advantage over IPTS: More parsimonious; explains ideation development more clearly.

Other Theories

4.5 Management of Suicidal Crisis

Immediate:

1. Safe environment, remove means from environment
2. Hospitalization if: active intent with plan, psychosis, unavailability of safe home environment, command hallucinations
3. Close supervision (1:1 if inpatient)
4. Treat underlying disorder urgently (e.g., start antidepressant, lithium, clozapine)

Pharmacotherapy:

• Lithium: most evidence for reducing suicidality in bipolar/recurrent depression; reduces completed suicide by 80%
• Clozapine: only FDA-approved drug with explicit anti-suicidal indication (for suicidality in schizophrenia/schizoaffective)
• Ketamine/esketamine: rapid antisuicidal effect within hours; important for acute crisis
• SSRIs: long-term reduction in suicidality; black box warning in under-25s (short-term increase in ideation)

Means restriction:

• Highly effective population-level intervention
• Evidence: bridge barriers (Golden Gate Bridge barrier reduced suicide rate at that location AND total county suicide rate, no substitution)
• Firearm restriction in depressed individuals is high-yield
• Paracetamol pack size legislation in UK reduced paracetamol overdose deaths

Safety planning:

• Stanley-Brown Safety Planning Intervention
• Collaborative (patient generates content)
• Components: warning signs → internal coping → social contacts → professionals → means restriction
• Distinguishes from "no-harm contracts" (no evidence of effectiveness)

4.6 Deliberate Self-Harm (DSH)

Definition: Intentional, self-inflicted harm without suicidal intent (cutting, burning, bruising). Also called Non-Suicidal Self-Injury (NSSI).

Functions:

• Emotion regulation (most common), "when I cut, I feel relief"
• Anti-dissociation, to feel real, to feel something
• Self-punishment
• Communication of distress

Epidemiology:

• 17-25% of adolescents report lifetime NSSI
• Peak onset: early adolescence (12-14 years)
• Female > male (in adolescence); sex differences narrow with age
• Strong predictor of later suicide attempt (but distinct phenomenon)

Assessment:

• Distinguish NSSI from suicidal behavior (intent, circumstances, rescue likelihood, lethality)
• Assess for BPD, depression, trauma, eating disorders
• Columbia Protocol can be used to clarify suicidal vs non-suicidal intent

Management:

• DBT (strongest evidence for NSSI and suicidality in BPD)
• CBT, emotion regulation skills
• Harm reduction approach
• Avoid punitive responses

4.7 Postvention

Definition: Actions taken after a suicide to support the bereaved and prevent suicide contagion.

Survivors of suicide loss:

• 1.25 million Americans become suicide loss survivors each year
• Elevated risk of complicated grief, PTSD, depression
• Elevated risk of suicide themselves (bereaved by suicide)

Postvention in institutions (schools, workplaces):

• Avoid glorification or sensationalization
• Provide access to counseling
• Identify and support high-risk individuals
• Follow WHO guidelines on media reporting

4.8 Media Reporting Guidelines (WHO/Papageno Effect)

Werther Effect: Increase in suicides following media reporting; first described after publication of Goethe's "The Sorrows of Young Werther."

Papageno Effect: Protective effect of stories showing suicidal crisis being overcome by positive coping.

WHO Safe Messaging Guidelines:

• Do NOT report in detail about methods, locations, notes
• Do NOT sensationalize or romanticize
• Do NOT present as "heroic" or "sacrificial"
• DO provide crisis resources in the story
• DO include stories of help-seeking and recovery
• DO consult with mental health professionals before publishing
• Reporting celebrity suicides: celebrity method often imitated

PART 5: PSYCHIATRIC CLASSIFICATION

5.1 ICD-11 vs ICD-10: Key Changes

ICD-11 was adopted by WHO in 2019, came into effect January 2022. India has not yet fully transitioned.

5.2 DSM-5 Structure

Published 2013 (DSM-5-TR: 2022 update)

Major chapters (in order):

1. Neurodevelopmental Disorders
2. Schizophrenia Spectrum and Other Psychotic Disorders
3. Bipolar and Related Disorders
4. Depressive Disorders
5. Anxiety Disorders
6. Obsessive-Compulsive and Related Disorders
7. Trauma- and Stressor-Related Disorders
8. Dissociative Disorders
9. Somatic Symptom and Related Disorders
10. Feeding and Eating Disorders
11. Elimination Disorders
12. Sleep-Wake Disorders
13. Sexual Dysfunctions
14. Gender Dysphoria
15. Disruptive, Impulse-Control, and Conduct Disorders
16. Substance-Related and Addictive Disorders
17. Neurocognitive Disorders
18. Personality Disorders
19. Paraphilic Disorders
20. Other Mental Disorders

Key DSM-5 changes from DSM-IV:

• Multiaxial system abolished (Axes I-V removed; single integrated assessment)
• Asperger syndrome removed (folded into ASD spectrum)
• Bereavement exclusion for MDD removed (controversial)
• Mixed features specifier added to MDD and bipolar
• OCD/OCSD separated into own chapter
• Trauma disorders separated from anxiety disorders
• PTSD given more behavioral criteria (avoidance)
• BED, ARFID added
• Dimensional approach to personality disorders in Section III (alternative model)

5.3 Dimensional vs Categorical Debate

Categorical model (traditional):

• Diagnosis = present/absent
• Clear boundaries between diagnoses
• Advantages: clinical utility, communication, treatment decision
• Disadvantages: high comorbidity, arbitrary thresholds, heterogeneity within categories

Dimensional model:

• Symptoms exist on continua
• People vary in degree, not type
• More biologically plausible
• Advantages: reflects neurobiology, genetic architecture, no arbitrary threshold
• Disadvantages: more complex; less clinical utility for many decisions

5.4 RDoC (Research Domain Criteria)

Developed by: NIMH (National Institute of Mental Health), Thomas Insel, 2010

Core idea: Diagnose based on neurobiological and behavioral dimensions, not symptom-based categorical diagnoses.

RDoC Domains:

1. Negative Valence Systems (fear, threat, loss)
2. Positive Valence Systems (reward seeking, reward anticipation)
3. Cognitive Systems (attention, memory, cognitive control)
4. Social Processes (affiliation, attachment, communication)
5. Arousal/Modulatory Systems (arousal, sleep-wake)
6. Sensorimotor Systems (motor actions)

Units of analysis: Genes → Molecules → Cells → Circuits → Physiology → Behavior → Self-report

Critique:

• Not ready for clinical use
• May fragment what is clinically a coherent syndrome
• Ignores subjective experience

5.5 HiTOP (Hierarchical Taxonomy of Psychopathology)

A transdiagnostic dimensional classification framework based on covariance structure of psychopathology

Structure (bottom-up from symptoms):

• Components → Syndromes → Subfactors → Spectra → Superspectra

Major Spectra:

Advantages over DSM/ICD:

• Based on empirical data, not expert consensus
• Captures comorbidity naturally (as shared variance)
• Maps onto neurobiological dimensions

5.6 Reliability and Validity of Diagnosis

Reliability:

• Inter-rater reliability: do two clinicians using the same system agree?
• Test-retest reliability: does the diagnosis remain stable over time?
• DSM-5 field trials showed moderate reliability (kappa 0.4-0.8) for most major categories
• MDD: kappa ~0.28 in real-world settings (poor)
• Schizophrenia: better reliability (~0.45-0.6)

Validity types:

PART 6: CROSS-CUTTING CLINICAL CONSIDERATIONS

6.1 Suicide in Eating Disorders

• AN has the highest SMR of any psychiatric disorder: ~5.86 (6x age-matched peers)
• Suicide accounts for ~1/3 of AN deaths (remainder are medical)
• Risk is elevated throughout illness duration, not just at low weight
• BN and BED also carry elevated suicide risk
• Assessment of suicide risk is mandatory in all eating disorder evaluations

6.2 Sleep in Dissociative Disorders

• Dissociative episodes can occur at sleep-wake transitions
• Hypnagogic/hypnopompic experiences may be misinterpreted as possession or alien abduction
• Sleep deprivation can trigger dissociative episodes
• RBD may be misidentified as fugue or sleepwalking

6.3 Eating Disorders and Circadian Rhythms

• Night eating syndrome: distinct from BED; >25% caloric intake after dinner
• Shift work disrupts eating patterns; associated with metabolic syndrome and binge eating
• Circadian disruption may worsen binge-purge cycles

6.4 Classification of Self-Harm

Word count: approximately 8,500 words, detailed, high-yield, exam-oriented

Model Answers

Format: Each answer structured for 5-mark, 10-mark, or short-note format as indicated. Write in flowing prose unless tabular organisation is clearer.

ANSWER 1: Classify and Describe the Management of Dissociative Disorders (10 marks)

Introduction:

Dissociation refers to a disruption in the normally integrated functions of consciousness, memory, identity, perception, and behaviour. Dissociative disorders are characterised by clinically significant dissociative symptoms that cause distress or functional impairment, and are not better explained by another disorder, substance use, or medical condition.

Classification (ICD-11 / DSM-5):

Swipe to compare →

Note: Functional Neurological Symptom Disorder (ICD-11) is now placed in the chapter on Diseases of the Nervous System, not Dissociative Disorders, a key ICD-11 change.

Management:

Management of dissociative disorders follows a phase-based approach, adapted across subtypes.

Phase 1, Stabilisation and Safety:

The priority in any dissociative disorder is establishing safety and stabilising the patient's emotional state. This involves psychoeducation (explaining the dissociative process in accessible language), development of grounding techniques (5-4-3-2-1 sensory grounding, containment imagery), and building a therapeutic alliance. For DID, mapping the alter system without prematurely accessing traumatic material is critical.

Phase 2, Trauma Processing (if applicable):

Once stabilised, trauma-focused interventions may be introduced carefully. Evidence-supported approaches include:

• EMDR (Eye Movement Desensitisation and Reprocessing), recommended in PTSD guidelines; used in dissociative disorders with caution
• Trauma-focused CBT, modified for dissociative presentation
• Ego state therapy, specifically designed for DID; works with alter states
• Schema Therapy, especially effective where early maladaptive schemas underlie the dissociation

Phase 3, Integration and Relapse Prevention:

In DID, the goal is either full fusion (merging of alters) or functional integration (alters co-operating, amnesia barriers reduced). In dissociative amnesia, memory recovery is not always necessary for recovery; functional improvement is the primary goal.

Pharmacotherapy:

There is no specific pharmacological treatment for core dissociative symptoms. Medications address comorbidities:

• SSRIs/SNRIs for comorbid PTSD, depression, anxiety
• Naltrexone (opioid antagonist): some evidence for depersonalisation/derealization
• Lamotrigine: open-label evidence for DPDR
• Benzodiazepines: used cautiously for acute anxiety; avoid long-term due to abuse risk and potential to worsen dissociation

Specific Considerations for DPDR:

CBT using the Hunter-Phillips model (Feeling Real technique) is the best-evidenced psychological treatment. Focus is on reducing safety behaviours (checking, avoidance) and accepting uncomfortable sensations. SSRIs are first-line pharmacologically.

ANSWER 2: Medical Complications of Anorexia Nervosa (10 marks)

Introduction:

Anorexia nervosa (AN) carries the highest standardised mortality ratio (SMR ~5.86) of any psychiatric disorder. Approximately two-thirds of deaths are due to medical complications and one-third to suicide. Understanding the medical complications is clinically essential and examination-critical.

Cardiovascular:

The most immediately life-threatening complications arise from the cardiovascular system. Bradycardia (HR <60 bpm) results from vagal predominance and reduced metabolic demand. Hypotension (systolic <90 mmHg) is common. QTc prolongation occurs due to electrolyte disturbances (especially hypokalemia and hypomagnesemia), increasing risk of torsades de pointes and sudden cardiac death. Cardiac muscle mass decreases with starvation, so-called cardiac cachexia, leading to reduced cardiac output and mitral valve prolapse (due to disproportionate reduction in left ventricular mass relative to valve size).

Metabolic and Electrolyte:

Hypoglycemia may occur, particularly in the restricting subtype with inadequate gluconeogenic substrate. Electrolyte abnormalities are most severe in the binge-purge subtype: hypokalaemia and metabolic alkalosis from vomiting; hypokalaemia and metabolic acidosis from laxative abuse. Hypophosphatemia occurs particularly during refeeding. Hyponatraemia may result from excessive water intake (pseudo-Bartter syndrome) or syndrome of inappropriate ADH secretion.

Endocrine:

Amenorrhoea is a classic finding, resulting from hypothalamic suppression of GnRH pulsatility → low LH, FSH, estrogen. Note: DSM-5 removed amenorrhoea as a diagnostic criterion (post-menopause women and males cannot fulfill it). Low cortisol response, high cortisol baseline, and sick euthyroid syndrome (low T3, normal or low T4, normal TSH) are characteristic. Growth hormone resistance occurs (high GH, low IGF-1). In adolescents, growth retardation and delayed puberty occur if starvation precedes the pubertal growth spurt.

Haematological:

Pancytopenia from gelatinous bone marrow transformation. Anaemia, leukopenia (impairs immune function), and thrombocytopenia are all seen.

Gastrointestinal:

Delayed gastric emptying causes early satiety, bloating, and increases patient resistance to refeeding. Superior mesenteric artery (SMA) syndrome, duodenal obstruction due to loss of the fat pad between the SMA and aorta, can cause vomiting and weight loss independent of AN behaviour. Elevated liver enzymes (hepatocyte autophagy) are seen in severe AN.

Musculoskeletal:

Osteopenia and osteoporosis due to prolonged estrogen deficiency (more refractory than post-menopausal osteoporosis because it occurs during peak bone mass acquisition). Stress fractures, vertebral compression. Bone mineral density does not fully recover with weight restoration alone.

Dermatological:

Lanugo hair (fine downy hair, thermoregulatory response), carotenemia (yellow-orange skin from excess carrot intake), xerosis, hair thinning (telogen effluvium), and in the binge-purge subtype, parotid hypertrophy, dental erosion (perimolysis), and Russell's sign (calluses on the dorsum of the hand from self-induced vomiting).

Neurological:

Cortical grey matter loss with underweight state (partially reversible on weight restoration). Peripheral neuropathy. Cognitive impairment (attention, executive function), partly due to starvation, partly due to metabolic disturbances.

Summary Table:

ANSWER 3: Refeeding Syndrome: Pathophysiology, Recognition, and Prevention (10 marks)

Definition:

Refeeding syndrome refers to the metabolic complications, primarily hypophosphataemia, hypokalaemia, and hypomagnesaemia, that can occur when nutrition is reintroduced following a period of prolonged starvation or severe malnutrition. It is potentially fatal if unrecognised.

Pathophysiology:

During prolonged starvation:

• The body shifts to fat and protein catabolism for energy
• Intracellular electrolytes (phosphate, potassium, magnesium) are progressively depleted
• Serum levels of these electrolytes may remain normal (deceptive) as homeostatic mechanisms are maintained until re-feeding

When feeding is reintroduced (especially carbohydrates):

• Insulin is secreted in response to rising blood glucose
• Insulin drives glucose, phosphate, potassium, and magnesium from the extracellular space INTO cells
• Serum phosphate drops sharply, hypophosphataemia is the hallmark
• Thiamine (vitamin B1) is consumed rapidly as a cofactor for carbohydrate metabolism
• Thiamine depletion can precipitate Wernicke's encephalopathy if not supplemented

Consequences of Key Electrolyte Disturbances:

NICE Risk Criteria (any one = high risk; any two = very high risk):

Prevention Protocol:

1. Screen all patients for refeeding risk before initiating nutritional rehabilitation
2. Baseline bloods: urea, creatinine, electrolytes (Na, K, Mg, phosphate, calcium), LFTs, full blood count, glucose
3. Baseline ECG (QTc monitoring)
4. Thiamine BEFORE glucose, oral thiamine 200-300mg/day (or IV Pabrinex if parenteral feeding) must be started before, not after, carbohydrate reintroduction
5. Start low, go slow: Initial intake 20 kcal/kg/day (10 kcal/kg/day for very high risk); increase over 4-7 days
6. Electrolyte monitoring: every 12-24 hours for first 3-5 days; replace proactively
7. Phosphate supplementation: oral or IV phosphate if serum phosphate <0.5 mmol/L

ANSWER 4: Suicide Risk Assessment: Comprehensive Approach (10 marks)

Introduction:

Suicide risk assessment is a core clinical skill in psychiatry. No single tool can predict suicide with certainty; risk assessment is a clinical synthesis that informs management decisions. The goal is to identify modifiable risk factors and guide the least restrictive, most appropriate level of care.

Framework for Assessment:

A comprehensive suicide risk assessment addresses four domains: ideation, intent, plan, and means. This is embedded within the broader clinical interview.

1. Suicidal Ideation:

Assess along the dimension of passivity to activity:

• Passive: "I wish I were dead" / "I wish I could go to sleep and not wake up"
• Active without method: "I think about killing myself"
• Active with method but no plan: "I think about taking pills"
• Active with plan, time, and place: "I've decided to take the medication I've been saving on Thursday when my family is away"

The Columbia Suicide Severity Rating Scale (C-SSRS) provides a validated, structured approach to this dimension.

2. Suicidal Intent:

• Is the patient ambivalent or resolved?
• What has stopped them so far?
• Has intent increased recently?
• Is there a precipitant (recent loss, humiliation, anniversary)?

3. Suicide Plan:

• Specificity of plan (vague vs. detailed)
• Proximity to means (has the patient already obtained pills, or is the firearm in the house?)
• Lethality of plan (overdose on paracetamol vs. jumping from height)
• Accessibility of plan (can they act on it imminently?)

4. Risk Factors (using the mnemonic IS PATH WARM, see D3):

5. Protective Factors:

Often underassessed. Key factors:

• Reasons for living (children, family responsibility, religious beliefs)
• Social support and connectedness
• Future orientation
• Help-seeking behaviour
• Absence of access to means

Structured Scales:

• SAD PERSONS (10-point scale): useful mnemonic but poor sensitivity in studies
• C-SSRS: validated, widely used, distinguishes ideation from behaviour
• Beck Scale for Suicide Ideation (BSI): validated for intensity of current ideation
• Beck Hopelessness Scale (BHS): score >9 = high risk; more predictive than depression severity

Management Based on Risk Level:

Safety Planning (Stanley-Brown model):

A collaborative, evidence-based intervention (superior to no-harm contracts):

1. Warning signs recognisable to the patient
2. Internal coping strategies (what the patient can do alone)
3. Socialisation strategies (people and activities that distract)
4. People to ask for help
5. Professionals to contact in crisis
6. Making the environment safe (means restriction)

ANSWER 5: CBT-I for Chronic Insomnia (10 marks)

Introduction:

Cognitive Behavioural Therapy for Insomnia (CBT-I) is the first-line treatment for chronic insomnia disorder, recommended above pharmacotherapy in all major guidelines (NICE, AASM, ERS). It addresses the perpetuating factors that maintain insomnia through behavioural, cognitive, and sleep hygiene components.

Theoretical Model:

Insomnia is maintained by a combination of:

• Behavioural: extended time in bed, daytime napping, variable wake times
• Cognitive: catastrophic beliefs about consequences of poor sleep ("I can't function with less than 8 hours"), selective attention to sleep-related stimuli
• Physiological: hyperarousal (elevated cortisol, elevated temperature, heightened CNS arousal)
• Conditioned arousal: bed becomes a cue for wakefulness rather than sleep (Stimulus-Response theory)

CBT-I targets all three maintaining factor types.

Components:

1. Sleep Restriction (most potent component):

• Rationale: consolidates fragmented, light sleep by building sleep drive (adenosine)
• Method: restrict time in bed (TIB) to the patient's actual sleep time (minimum 5 hours TIB for safety); maintain consistent wake time
• Sleep efficiency (SE) = Total Sleep Time / Time In Bed × 100%
• When SE >90% for ≥5 consecutive nights, extend TIB by 15-30 minutes
• Contraindications: seizure disorder, parasomnias, sleep deprivation-dangerous jobs

2. Stimulus Control:

• Rationale: breaks the conditioned arousal to the bed/bedroom
• Rules:
• Use bed only for sleep and sex
• If unable to sleep within ~20 minutes, leave the bedroom; return when sleepy
• Maintain consistent rise time regardless of how much sleep was obtained
• Avoid daytime napping (or limit to <20 min before 3 pm)

3. Cognitive Restructuring:

• Identify unhelpful beliefs: "I need 8 hours", "I haven't slept all night" (often an overestimation of wakefulness), "Tomorrow will be ruined"
• Cognitive techniques: Socratic questioning, behavioural experiments, psychoeducation about sleep variability

4. Relaxation Training:

• Progressive muscle relaxation (Jacobson technique)
• Diaphragmatic breathing
• Mindfulness (MBSR has some evidence in insomnia)
• Autogenic training

5. Sleep Hygiene:

• Necessary but insufficient alone
• Consistent sleep/wake schedule
• Bedroom environment: cool, dark, quiet
• Avoid caffeine after 2 pm, heavy meals within 3 hours of sleep
• Avoid screen light (blue-spectrum suppresses melatonin) 1 hour before bed
• Regular exercise (not within 3 hours of bedtime)

6. Sleep Compression (alternative in elderly):

• Gradual reduction of TIB rather than abrupt restriction
• Better tolerated; slightly less efficacious

Outcomes:

CBT-I achieves sleep latency reduction, improved sleep efficiency, and reduced nighttime awakenings in 70-80% of patients. Effects are durable at 12 months follow-up, unlike pharmacotherapy which tends to rebound on discontinuation.

Delivery formats:

• Face-to-face (individual or group, equivalent efficacy)
• Digital CBT-I (dCBT-I): apps (Sleepio, etc.); comparable efficacy to face-to-face for uncomplicated insomnia; more accessible

ANSWER 6: Narcolepsy: Classification and Management (10 marks)

Introduction:

Narcolepsy is a chronic sleep disorder characterised by the inability to regulate sleep-wake states normally, resulting in excessive daytime sleepiness (EDS), intrusion of REM sleep phenomena into wakefulness, and disrupted nocturnal sleep.

Classification:

MSLT Criteria for Diagnosis:

A Mean Sleep Latency <8 minutes AND ≥2 Sleep-Onset REM Periods (SOREMPs) on the Multiple Sleep Latency Test, performed the morning after an overnight polysomnogram that confirms adequate sleep duration and excludes other causes of EDS.

Clinical Features (Tetrad):

1. EDS (always present): overwhelming urge to sleep, especially in monotonous situations; "sleep attacks"
2. Cataplexy (Type 1): sudden bilateral loss of voluntary muscle tone triggered by strong emotion, typically laughter or surprise, without loss of consciousness; lasts seconds to minutes
3. Sleep paralysis: transient inability to move at sleep onset or awakening; terrifying but benign; occurs in up to 40% of cases
4. Hypnagogic/hypnopompic hallucinations: vivid, often frightening visual, auditory, or tactile hallucinations at sleep onset (hypnagogic) or awakening (hypnopompic)

Management:

Sodium oxybate (gamma-hydroxybutyrate, GHB):

• GABA-B agonist
• Taken in two divided doses at bedtime (due to short half-life ~2 hours)
• Dramatically improves EDS AND cataplexy
• Consolidates nocturnal sleep, increasing N3
• Side effects: nausea, dizziness, weight loss, enuresis
• Abuse potential, Schedule I in India/USA, tightly regulated prescribing
• Contraindicated with alcohol, CNS depressants, succinic semialdehyde dehydrogenase deficiency

Modafinil:

• Mechanism: inhibits dopamine reuptake (primary), also noradrenaline; wakefulness-promoting
• First-line for EDS in Type 1 and Type 2
• Does not treat cataplexy
• Fewer side effects than amphetamines; no cardiovascular stimulation at therapeutic doses

Non-pharmacological:

• Scheduled daytime naps (2-3 × 15-20 minutes): reduces need for stimulant medication
• Sleep hygiene, consistent sleep schedule
• Driving restrictions: must be disclosed; must be symptom-controlled before driving
• Support groups, vocational counselling

ANSWER 7: ICD-11 vs ICD-10: Major Changes in Psychiatric Classification (10 marks)

Introduction:

The ICD-11 (International Classification of Diseases, 11th Revision) was adopted by the World Health Organisation in May 2019 and came into effect on 1 January 2022. It represents the most comprehensive revision of the classification of mental disorders since ICD-10 (1992). The changes reflect three decades of research, a shift toward clinical utility, and greater alignment with DSM-5.

Structural Changes:

ICD-10 used F-codes (F00–F99) in Chapter V. ICD-11 moved mental disorders to Chapter 06 (Mental, Behavioural, and Neurodevelopmental Disorders), using alphanumeric codes (6A0x–6E8Z). The change has implications for billing and record-keeping once India transitions.

Key Diagnostic Changes:

Personality Disorder Revolution:

ICD-11 abolishes the 10 categorical types and replaces them with:

1. Severity rating: Mild, Moderate, Severe Personality Disorder
2. Prominent trait domain specifiers: Negative Affectivity, Detachment, Dissociality, Disinhibition, Anankastia
3. Borderline pattern qualifier: Optional specifier for BPD-like presentations

ANSWER 8: Eating Disorders in Adolescents: Assessment and Management (10 marks)

Introduction:

Eating disorders most commonly emerge in adolescence and early adulthood, with a bimodal onset in AN at 14 and 18 years. Early identification and intervention in adolescence are crucial given the impact on growth, bone development, and brain maturation. Treatment approaches must be adapted for developmental stage.

Diagnostic Considerations in Adolescents:

• BMI-for-age is used (not adult BMI cutoffs); growth faltering is a more sensitive indicator than absolute BMI
• Amenorrhoea may be primary (has never had a period) rather than secondary
• AN in males: more often presents later, less emphasis on "thinness" per se (more often "muscularity"), often via exercise restriction rather than food restriction
• Avoidant eating in childhood/early adolescence may represent ARFID rather than AN, absence of body image concerns is key differentiator
• Rapid-onset restrictive eating in children ages 6-12: consider PANDAS/PANS-related avoidant eating, tic disorders, OCD presentations

Assessment:

Physical assessment in paediatric patients requires growth chart review:

• Weight-for-age and height-for-age centiles
• Body Mass Index-for-age percentile
• Vital signs: bradycardia and hypotension are particularly concerning in adolescents given their compensatory cardiovascular reserve
• Tanner staging (pubertal assessment)
• Bone age X-ray if growth arrest is suspected
• DEXA scan if eating disorder duration >1 year (osteoporosis risk)

Psychological assessment tools:

• EDE (Eating Disorder Examination), gold standard clinical interview
• EDE-Q (questionnaire version), from age 14 upwards
• CHEAT (Children's Eating Attitudes Test), validated for age 8-13
• RCADS (Revised Children's Anxiety and Depression Scale) for comorbidities

Management:

Family-Based Treatment (FBT / Maudsley Approach):

First-line for adolescent AN; stronger evidence base than individual therapy in this age group.

Three phases:

• Phase 1: Externalise the illness; parents take control of meals; weight restoration
• Phase 2: Return control of eating to the adolescent
• Phase 3: Healthy adolescent development and relapse prevention

Adapted CBT-E:

For adolescents aged 14 and above; shows comparable outcomes to FBT in some studies; preferable when family conflict is high or when parent participation is not feasible.

Inpatient and Day Patient Treatment:

Indications for admission:

• BMI <14 in adults; <10th centile sustained with medical instability in adolescents
• Vital sign instability (bradycardia <45 bpm, hypotension, hypothermia)
• Electrolyte abnormalities, hypoglycaemia
• Rapid weight loss without response to outpatient treatment
• Suicidal risk, severe psychiatric comorbidity

MARSIPAN (Management of Really Sick Patients with Anorexia Nervosa) and Junior MARSIPAN guidelines provide medical management frameworks.

Pharmacotherapy in Adolescents:

• No medication is approved specifically for adolescent AN
• Fluoxetine: first-line for weight-restored adolescents with persistent depressive/anxiety symptoms; less efficacy at low weight (serotonin synthesis requires tryptophan from nutrition)
• Olanzapine: some evidence for weight gain and anxiety reduction in adolescent AN; caution with metabolic side effects
• Avoid bupropion (seizure risk, especially with electrolyte disturbances)

ANSWER 9: Controversies in DID (Dissociative Identity Disorder) (5 marks)

DID is among the most contested diagnoses in psychiatry. Two major theoretical positions define the debate:

Trauma Model:

Supported by Ross, Putnam, and van der Kolk. Proposes that DID is a response to severe and repeated early childhood trauma, an adaptive dissociative defence that compartmentalises overwhelming experiences. Evidence includes:

• Strong association with reported childhood abuse (97-98%)
• Neuroimaging differences between alter states
• Clinical response to trauma-focused therapy

Sociocognitive Model:

Supported by Spanos, Lilienfeld, and Lynn. Proposes that DID is an iatrogenic and socially constructed phenomenon, shaped by clinician suggestion, hypnosis, popular media, and cultural scripting. Evidence includes:

• Cross-cultural variation (far more prevalent in North America than Western Europe)
• Sharp rise in diagnoses after media coverage (Sybil, Three Faces of Eve)
• Alter system complexity increases with years of treatment
• High rates in patients treated by DID specialists, not in general psychiatric settings
• Alters often reflect cultural expectations (child, abuser, protector)

Current Position:

Most researchers accept a middle ground: genuine trauma-related dissociation exists and forms the substrate; however, symptom expression and complexity are shaped by cultural context, therapeutic suggestion, and media representation. Over-diagnosis and iatrogenic creation are real risks.

Forensic Implications:

The question of criminal responsibility in DID is unresolved. Some jurisdictions have accepted diminished responsibility arguments when the act was committed by an alter state without host awareness. This is inherently problematic given the sociocognitive critique.

ANSWER 10: Pharmacotherapy for Insomnia: Indications and Selection (5 marks)

Pharmacotherapy is indicated for short-term management of acute insomnia or as an adjunct to CBT-I while awaiting full effect. Chronic use of most hypnotics carries risks of dependence, tolerance, and rebound insomnia.

Special populations:

• Elderly: Avoid benzodiazepines and z-drugs (fall risk, cognitive impairment); prefer ramelteon, melatonin, low-dose doxepin, or suvorexant
• Pregnancy: Melatonin (limited safety data), short-term z-drugs if necessary; avoid benzodiazepines (neonatal withdrawal)
• PTSD-related insomnia: Prazosin (alpha-1 blocker) reduces nightmares specifically; CBT-I adapted for trauma (CBTI-PTSD)

ANSWER 11: REM Sleep Behaviour Disorder: Diagnosis and Management (5 marks)

Definition:

REM Sleep Behaviour Disorder (RBD) is a parasomnia characterised by dream enactment behaviour during REM sleep, resulting from the failure of the normal REM sleep atonia mechanism.

Clinical features:

• Onset: usually males >50 years (though younger-onset forms exist, often idiopathic)
• Behaviour: talking, shouting, punching, kicking, jumping out of bed, correlating with vivid, action-filled dreams
• Patient wakes oriented, with recall of a dream congruent with the behaviour
• Bed partner is often the reporter (and often injured)
• Does NOT occur in N3, behaviour occurs during REM (confirmed by PSG showing REM without atonia)

Investigation:

Video-polysomnography: confirms REM without atonia (RSWA). Minimum criteria: chin EMG activity during REM >50% of epoch, or excessive phasic/tonic EMG.

Association with Neurodegenerative Disease:

RBD is a prodromal marker of alpha-synucleinopathies. Prospective studies show 80-90% of idiopathic RBD patients develop Parkinson's disease, Dementia with Lewy Bodies, or Multiple System Atrophy within 10-15 years. This latency period represents an opportunity for neuroprotective intervention (currently under trial).

Management:

• Clonazepam 0.25-2 mg at bedtime: first-line; suppresses RBD behaviour; does NOT restore atonia; may worsen OSA, screen first
• Melatonin 3-12 mg at bedtime: alternative/addition; restores some atonia; better tolerated in elderly; no respiratory depression
• Environmental safety: pad floor, remove dangerous objects, consider mattress on floor, separate beds if partner at risk

ANSWER 12: Suicide: Means Restriction and Postvention (5 marks)

Means Restriction:

One of the most evidence-based suicide prevention strategies. The principle: suicidal crises are often impulsive and time-limited; reducing access to lethal means during a crisis reduces the probability of a fatal outcome.

Evidence base:

• UK legislation limiting paracetamol pack sizes → significant reduction in paracetamol-related deaths (Hawton et al.)
• Barriers on bridges (Golden Gate, UK bridges) → reduced suicide at that location AND total area suicide rate, disproving simple "method substitution"
• Coal gas detoxification in UK (1960s-70s) → 30% reduction in total national suicide rate
• Firearm access: states/countries with lower firearm access have lower suicide rates; gun storage counselling is a valid clinical intervention

Clinical application:

• All patients assessed for suicide risk should be asked about means access
• For firearm owners: counsel on locked storage or temporary transfer to a third party
• Review medications prescribed (lethality in overdose): SSRIs safer than TCAs; avoid quetiapine/lithium in large quantities to high-risk patients

Postvention:

Actions following a suicide to support bereaved individuals and prevent contagion:

• Supports suicide loss survivors (bereavement is a risk factor for suicide)
• Institutional postvention (schools, hospitals) following a staff or patient death:
• Avoid glorification, memorialisation that models suicide as honourable
• Active outreach to high-risk contacts
• Structured counselling provision
• No closed-casket speculation or rumour
• Werther effect: media reporting of suicide increases imitative suicides (Goethe's novel, 1774)
• Papageno effect: media portrayal of successfully navigating suicidal crisis is protective
• WHO Safe Messaging Guidelines: no method details, no site, no suicide note content, include helpline numbers

ANSWER 13: Dimensional vs Categorical Classification in Psychiatry (5 marks)

Psychiatric classification has historically been categorical, diagnoses are either present or absent, based on operationalised criteria. This model underpins both ICD and DSM. However, evidence increasingly supports a dimensional alternative.

Arguments for Categorical Classification:

• Clinical utility: categories guide treatment decisions clearly (you start lithium for bipolar, not for "elevated mood dimension score 3")
• Communication: shared language between clinicians, insurers, researchers
• Familiarity: established training paradigms
• Meets patient need for a "name" for their experience

Arguments for Dimensional Classification:

• High rates of comorbidity suggest disorders share variance (e.g., depression and anxiety both on internalising spectrum in HiTOP)
• Arbitrary diagnostic thresholds (e.g., 5 of 9 criteria vs 4, same person?)
• Within-category heterogeneity: two patients with MDD may share few symptoms
• Genetic architecture is dimensional, not categorical (GWAS studies)
• Neurobiology does not break neatly at categorical boundaries
• Better captures subthreshold conditions with clinical significance

Emerging models:

• ICD-11 personality disorders: full dimensional model (severity + trait domains)
• DSM-5 Section III AMPD: alternative dimensional model for personality
• RDoC: biology-based dimensions (circuits, not symptoms)
• HiTOP: empirical hierarchical structure from symptom covariance

Current consensus:

Categorical and dimensional systems serve different purposes. Categorical diagnoses have clinical utility; dimensional descriptions have explanatory and research utility. A hybrid approach, dimensional assessment within clinical categories, may represent the most useful near-term solution.

ANSWER 14: Bulimia Nervosa: Diagnosis and Management (5 marks)

Diagnosis (DSM-5):

Bulimia nervosa is characterised by (1) recurrent binge eating (large amount in discrete period + loss of control), (2) recurrent inappropriate compensatory behaviours, (3) occurring ≥1 episode/week for 3 months, (4) self-evaluation unduly influenced by shape/weight, (5) not occurring exclusively during episodes of AN.

Key features not present in AN (binge-purge type):

• Weight is typically normal or overweight (not significantly low)
• Absence of the severe body image distortion/fear of weight gain as central identity

Medical complications:

• Hypokalemia + metabolic alkalosis (vomiting), most dangerous cardiac risk
• Parotid hypertrophy (bilateral; "chipmunk face")
• Perimolysis (dental enamel erosion)
• Russell's sign
• Mallory-Weiss tear (oesophageal mucosal tear from forceful vomiting)
• Ipecac-induced cardiomyopathy (if emetine syrup abused)

Management:

Psychological:

• CBT-E (Fairburn): gold standard; 20 sessions; targets core psychopathology (overconcern with shape/weight)
• Dialectical Behaviour Therapy: useful where affect dysregulation drives binges
• Interpersonal Therapy: for BN where interpersonal problems are primary

Pharmacological:

• Fluoxetine 60 mg/day: only FDA-approved drug; higher than antidepressant dose; effective for binge-purge cycles
• Topiramate: reduces binge-purge frequency; cognitive dulling limits tolerability
• Bupropion: CONTRAINDICATED (lowered seizure threshold + electrolyte disturbances in BN)

Combination:

CBT-E + fluoxetine shows greater efficacy than either alone for acute symptoms.

ANSWER 15: Complex PTSD (ICD-11): Features and Distinction from PTSD (5 marks)

Background:

Complex PTSD (6B41) is a new ICD-11 diagnosis. It was not in ICD-10. DSM-5 does not have it as a separate category (though DESNOS, Disorders of Extreme Stress Not Otherwise Specified, was a DSM-IV proposed category). The addition represents recognition of the distinct clinical presentation following prolonged, repeated, interpersonal trauma.

ICD-11 Criteria:

All three clusters of PTSD (re-experiencing, avoidance, hyperarousal) PLUS three additional domains:

1. Affect dysregulation: severe emotional dysregulation; difficulty modulating emotional responses
2. Negative self-concept: persistent beliefs of worthlessness, shame, guilt, failure
3. Disturbances in relationships: difficulty sustaining relationships, feeling permanently different from others

Contrast with PTSD:

Differential from BPD:

Complex PTSD and BPD share affect dysregulation, identity disturbance, and relational difficulties. Key differences: BPD includes impulsivity, chronic suicidality, frantic avoidance of abandonment as core features; BPD is dimensional and not trauma-dependent (though trauma is common). Both can co-occur.

Mnemonics & Memory Tricks

All mnemonics are clinically grounded. Each includes the device, decoded table, and a brief usage note.

MNEMONIC 1: Medical Complications of Anorexia Nervosa: "CARDIAC BONES"

Swipe to compare →

MNEMONIC 2: Refeeding Syndrome Electrolytes: "PKMGT" ("Please Keep Magnesium Going Too")

MNEMONIC 3: Suicide Risk Assessment: SAD PERSONS

Scoring: 0-4 low, 5-6 moderate, 7-10 high risk.

MNEMONIC 4: Joiner's Interpersonal Theory: "TBA" ("Thinking-Believing-Acting")

MNEMONIC 5: Narcolepsy Tetrad: "CHESS" (Cataplexy, Hallucinations, EDS, Sleep Paralysis, Sleep attacks)

Or more precisely, use: "ECS-H" to remember that EDS is obligate:

MNEMONIC 6: Sleep Stage Neurotransmitters: "SANG" (Sleep = Adenosine, NREM = Serotonin/GABA, Go = Glutamate-wake, ACh = REM)

MNEMONIC 7: NREM vs REM Parasomnias: "NREM = Night Terror, No Recall; REM = Remember Every Monster"

MNEMONIC 8: Dissociative Disorder Subtypes: "AFTIP-D"

MNEMONIC 9: ICD-11 New Diagnoses: "CAPE-GAP"

Simplified version: "CAPE-G" = Complex PTSD, ARFID, Prolonged Grief, (CSBD = Compulsive Sexual Behaviour Disorder), Gaming Disorder

MNEMONIC 10: Suicide Risk Factors: "IS PATH WARM" (American Association of Suicidology)

MNEMONIC 11: CBT-I Components: "SRCRC" ("Sleep Restriction Creates Real Change")

MNEMONIC 12: Refeeding Syndrome Prevention: "BELT" ("Before Every Litre, Thiamine")

MNEMONIC 13: Anorexia Nervosa: Medical Criteria for Admission "BEACH"

MNEMONIC 14: Eating Disorders: Pharmacotherapy Rules "FFB"

Memory hook: "Fluoxetine for Bulimia, Bupropion is Banned."

MNEMONIC 15: DID Management Phases: "SPI" ("Stabilise, Process, Integrate")

MNEMONIC 16: Protective Factors Against Suicide: "FAMILY"

MNEMONIC 17: MSLT Criteria for Narcolepsy: "28 SOREMPs"

Criteria: Mean sleep latency <8 minutes AND ≥2 SOREMPs (Sleep Onset REM Periods)

Memory hook: "Less than 8, at least 2", reverse of what you'd expect (less sleep latency = more sleepy, more REM onsets = more narcoleptic)

MNEMONIC 18: RBD Features: "DRAMA"

MNEMONIC 19: Key ICD-11 Schizophrenia Changes: "SAND"

MNEMONIC 20: Circadian Rhythm Disorders: "DASON"

QUICK RECALL CARDS

What's the single strongest predictor of completed suicide?

→ Previous suicide attempt

What's the only FDA-approved drug specifically for suicidality?

→ Clozapine (for schizophrenia/schizoaffective)

What drug has the strongest evidence for reducing completed suicide?

→ Lithium

What's the first-line treatment for chronic insomnia?

→ CBT-I (over pharmacotherapy)

What electrolyte disturbance is the hallmark of refeeding syndrome?

→ Hypophosphataemia

What's the diagnostic criterion that distinguishes narcolepsy Type 1 from Type 2?

→ Cataplexy OR CSF hypocretin-1 ≤110 pg/mL

What must come BEFORE carbohydrate reintroduction in a malnourished patient?

→ Thiamine supplementation

What's the only drug approved for both EDS AND cataplexy in narcolepsy?

→ Sodium oxybate (GHB)

What parasomnia is a prodrome for Parkinson's disease?

→ REM Sleep Behaviour Disorder (RBD)

What drug is CONTRAINDICATED in both AN and BN?

→ Bupropion

What psychiatric disorder has the highest standardised mortality ratio (SMR)?

→ Anorexia Nervosa (~5.86)

What is the "Werther Effect"?

→ Increased suicide rates following media reporting of a suicide

What is the "Papageno Effect"?

→ Protective effect of media stories showing suicidal crisis overcome by coping

What is the key ICD-11 change to personality disorders?

→ Categorical types abolished → Dimensional: severity + trait domains

Name 3 new ICD-11 diagnoses:

→ Complex PTSD, Prolonged Grief Disorder, Gaming Disorder (also: ARFID, CSBD)

High-Yield Comparisons

High-density visual reference. Each table is designed to be scannable in under 60 seconds.

TABLE 1: Anorexia Nervosa vs Bulimia Nervosa vs Binge Eating Disorder

Swipe to compare →

TABLE 2: ICD-11 vs ICD-10 vs DSM-5: Major Differences

TABLE 3: Insomnia Pharmacotherapy Options

TABLE 4: Narcolepsy Type 1 vs Type 2

TABLE 5: Dissociative Amnesia vs Organic (Neurological) Amnesia

Specific organic comparators:

TABLE 6: Completed Suicide vs Attempted Suicide vs Deliberate Self-Harm (DSH/NSSI)

TABLE 7: CBT-I vs Pharmacotherapy for Insomnia

TABLE 8: NREM Parasomnias vs REM Parasomnias

TABLE 9: Joiner's Interpersonal Theory vs Klonsky's Three-Step Theory vs Shneidman's Psychache Theory

TABLE 10: Sleep Architecture Changes in Major Psychiatric Disorders

SUMMARY MATRIX: Key Drugs in This Chapter

PYQ Frequency Analysis

Based on pattern analysis of PG exams MD Psychiatry Paper II questions across available years. Frequency ratings reflect relative appearance across years; all topics remain examinable.

FREQUENCY HEAT MAP

Swipe to compare →

TOPIC-BY-TOPIC ANALYSIS

1. Suicide Risk Assessment

Frequency: Very High | Marks: 5–10

Almost certain to appear in some form across any exam cycle. May be framed as:

• "Describe suicide risk assessment" (10 marks)
• "Enumerate risk factors for suicide" (5 marks)
• "What is the Columbia Protocol?" (5 marks)
• "Write a note on means restriction" (5 marks)
• "India-specific suicide epidemiology" (5 marks)

High-yield subpoints examiners test:

• Difference between SAD PERSONS and C-SSRS (and which is preferred now)
• Hopelessness as more predictive than depression severity
• Prior attempt as strongest single predictor
• Lithium and clozapine as specific anti-suicidal agents
• Safety planning vs no-harm contracts
• NCRB India data (approximate figures)
• Joiner's Interpersonal Theory (thwarted belongingness + perceived burdensomeness + acquired capability)
• Werther Effect and Papageno Effect
• WHO media guidelines

2. Anorexia Nervosa: Medical Complications

Frequency: Very High | Marks: 5–10

Consistently appears. Often paired with or followed by refeeding syndrome.

Framing variants:

• "Medical complications of anorexia nervosa" (10 marks)
• "Write short notes on refeeding syndrome" (5 marks)
• "Outline the medical management of a severely underweight patient with AN" (10 marks)
• "What are the criteria for inpatient admission in AN?" (5 marks)

High-yield subpoints:

• Lanugo, bradycardia, hypothermia as clinical triad
• QTc prolongation → torsades de pointes risk
• Sick euthyroid syndrome (low T3, normal TSH)
• Osteoporosis, worse than post-menopausal because peak bone mass not yet acquired
• Pancytopenia from gelatinous bone marrow transformation
• Superior mesenteric artery syndrome
• DSM-5 removed BMI <17.5 as criterion, "significantly low weight" language now used

3. Refeeding Syndrome

Frequency: High | Marks: 5–10

Often asked as a standalone or as part of AN management.

Framing variants:

• "Write a note on refeeding syndrome" (5–10 marks)
• "How would you manage nutritional rehabilitation in a patient with severe AN?" (10 marks)

High-yield subpoints:

• Hypophosphataemia as hallmark electrolyte
• Thiamine MUST precede carbohydrate loading (Wernicke's risk)
• NICE criteria for high refeeding risk
• Starting caloric target: 20 kcal/kg/day
• Monitoring frequency: electrolytes every 12–24 hours initially
• Consequences of hypophosphataemia: respiratory failure (diaphragm), cardiac failure, rhabdomyolysis

4. ICD-11 vs ICD-10 Key Changes

Frequency: High | Marks: 5–10

Increasingly common as India prepares for transition. Can appear as:

• "Enumerate the key changes in ICD-11 compared to ICD-10" (10 marks)
• "What are the new diagnoses in ICD-11?" (5 marks)
• "How has the classification of schizophrenia changed in ICD-11?" (5 marks)
• "How has ICD-11 classified personality disorders?" (5 marks)

High-yield subpoints:

• Schizophrenia subtypes abolished; dimensional symptom domains added
• Complex PTSD added (6B41), must know the three additional feature clusters
• Personality disorders: dimensional (severity + trait domains), not categorical
• BED and ARFID now full diagnoses
• Prolonged Grief Disorder added (6B42)
• Gaming Disorder added (6C51)
• FND moved out of dissociative disorders
• Acute stress reaction no longer a mental disorder
• Gender incongruence moved out of mental disorders chapter
• Personality disorders: borderline pattern retained as optional qualifier only

5. Narcolepsy

Frequency: High | Marks: 5–10

A perennial favourite. Usually asked as classification + management.

Framing variants:

• "Classify narcolepsy and describe its management" (10 marks)
• "Write a note on narcolepsy" (5 marks)
• "What is cataplexy?" (short note)
• "What is the MSLT and how is it used in narcolepsy diagnosis?" (5 marks)

High-yield subpoints:

• Cataplexy triggered by emotion, emotionally triggered bilateral muscle tone loss WITHOUT loss of consciousness
• CSF hypocretin-1 <110 pg/mL = diagnostic of Type 1
• HLA-DQB1*06:02 association in Type 1 (>95%)
• MSLT criteria: <8 min mean sleep latency + ≥2 SOREMPs
• Sodium oxybate: GABA-B agonist, treats both EDS and cataplexy, Schedule I
• Modafinil: first-line for EDS, no cataplexy effect, DAT inhibitor
• SSRIs/venlafaxine: treat cataplexy via REM suppression
• Non-pharm: scheduled naps; driving restrictions

6. CBT-I (Cognitive Behaviour Therapy for Insomnia)

Frequency: High | Marks: 5–10

Framing variants:

• "Describe CBT-I" (5–10 marks)
• "Compare CBT-I and pharmacotherapy for insomnia" (10 marks)
• "What is sleep restriction therapy?" (5 marks)

High-yield subpoints:

• Sleep restriction is the most potent single component
• Sleep efficiency formula and targets (SE >85%)
• Stimulus control breaks bed-arousal conditioning
• CBT-I superior to pharmacotherapy for long-term outcomes
• Digital CBT-I: comparable efficacy to face-to-face
• Contraindication of sleep restriction: seizure disorder, dangerous occupations requiring alertness

7. Dissociative Disorders: Classification and Management

Frequency: High | Marks: 5–10

Framing variants:

• "Classify dissociative disorders and describe management" (10 marks)
• "Write a note on dissociative identity disorder" (5 marks)
• "Differentiate dissociative amnesia from organic amnesia" (5 marks)
• "What are the ICD-11 changes to dissociative disorders?" (5 marks)

High-yield subpoints:

• ICD-11: FND moved to Diseases of Nervous System
• ICD-11: Partial DID added as new category
• Phase-based management: Stabilise → Process → Integrate
• Do NOT jump to trauma processing before stabilisation
• Sociocognitive vs trauma model debate in DID
• DPDR: reality testing intact; first-line = CBT (Feeling Real); lamotrigine
• Possession trance: pathological only if outside cultural context + causes distress

8. Bulimia Nervosa

Frequency: Moderate–High | Marks: 5–10

Framing variants:

• "Describe the diagnosis and management of BN" (10 marks)
• "Medical complications of BN" (5 marks)
• "Compare AN and BN" (10 marks)

High-yield subpoints:

• Fluoxetine 60 mg/day, only FDA-approved drug; higher than antidepressant dose
• Bupropion CONTRAINDICATED, seizure risk
• Russell's sign, parotid enlargement, perimolysis
• Hypokalaemia + metabolic alkalosis from vomiting
• CBT-E as gold standard psychotherapy
• Compensatory behaviours ≥1/week for ≥3 months

9. REM Sleep Behaviour Disorder

Frequency: Moderate–High | Marks: 5

Framing variants:

• "Write a note on REM sleep behaviour disorder" (5 marks)
• "What are the associations and management of RBD?" (5 marks)

High-yield subpoints:

• Males >50; dream enactment; wakes oriented
• PSG: REM without atonia (RSWA)
• Prodrome for alpha-synucleinopathies (PD, DLB, MSA), 80–90% convert in 10–15 years
• SSRIs can precipitate or worsen RBD
• Treatment: clonazepam OR melatonin; safety measures

10. Eating Disorders in Adolescents

Frequency: Moderate | Marks: 5–10

Framing variants:

• "Management of AN in an adolescent" (10 marks)
• "What is Family-Based Treatment for eating disorders?" (5 marks)

High-yield subpoints:

• FBT (Maudsley Approach): three phases; parents control meals in Phase 1
• BMI-for-age, not adult BMI
• Junior MARSIPAN guidelines
• No drug approved for adolescent AN; fluoxetine post-weight-restoration for relapse prevention
• Bone density impact: occurs during peak bone mass acquisition period, serious long-term consequence

11. Sleep Architecture

Frequency: Moderate | Marks: 5

Framing variants:

• "Describe normal sleep architecture" (5 marks)
• "How does sleep change in depression?" (5 marks)
• "What are the EEG characteristics of sleep stages?" (5 marks)

High-yield subpoints:

• N1: theta; N2: sleep spindles + K-complexes; N3: delta; REM: low-voltage mixed frequency
• First REM: ~90 minutes after sleep onset
• N3 dominates first third; REM dominates last third
• REM latency shortened in depression (<65 min), biological marker
• All antidepressants except bupropion suppress REM

12. DPDR (Depersonalisation/Derealization Disorder)

Frequency: Moderate | Marks: 5

High-yield subpoints:

• Reality testing intact (vs psychosis)
• Emotional numbing, anxiety about symptoms
• CBT (Feeling Real): first-line psychological
• Lamotrigine, naltrexone: pharmacological options
• Transient episodes in up to 74% of general population; persistent disorder = 1–2%

QUESTION FORMAT PATTERNS

RAPID REVISION: WHAT TO STUDY LAST

If you have 2 hours before the exam, revise in this order:

1. Suicide risk assessment framework + SAD PERSONS + Joiner's theory (10 min)
2. AN medical complications, CARDIAC BONES mnemonic (10 min)
3. Refeeding syndrome, PKMGT + BELT (10 min)
4. ICD-11 major changes, CAPE-G + personality disorder restructuring + schizophrenia subtypes (10 min)
5. Narcolepsy Type 1 vs Type 2 table + management drugs (10 min)
6. CBT-I components + sleep restriction rationale (10 min)
7. Dissociative disorder classification + phase-based management (10 min)
8. Fluoxetine for BN + bupropion contraindicated (5 min)
9. RBD features + alpha-synuclein connection (5 min)
10. Sleep stage EEG changes + REM latency in depression (5 min)

DRUGS WORTH MEMORISING FOR THIS CHAPTER

Quick Review

All names are fictitious. All ages, presentations, and clinical details are constructed for educational purposes. No real patient identifiers are used.

VIGNETTE 1: Anorexia Nervosa with Refeeding Risk

Clinical Scenario:

Priya, a 19-year-old pre-medical student, is brought to the psychiatry emergency by her parents. Over the past 8 months she has progressively restricted her food intake, citing concerns about her "protruding stomach." She exercises for 3 hours daily despite feeling weak. Her current weight is 36 kg, height 162 cm (BMI 13.7). On examination: pulse 44 bpm, BP 84/52 mmHg, temperature 35.8°C. Fine downy hair is visible on her arms. Her serum potassium is 2.9 mEq/L, phosphate 0.6 mmol/L, albumin 28 g/L. ECG shows QTc of 478 ms.

Questions for Active Recall:

1. What is the diagnosis? What subtype?
2. Which vital sign findings indicate immediate medical risk?
3. Is she at risk for refeeding syndrome? Apply NICE criteria.
4. How would you initiate nutritional rehabilitation?
5. What must be given BEFORE carbohydrate reintroduction, and why?
6. What is the significance of QTc 478ms?
7. Name three dermatological findings you would look for on full examination.

Model Answer Points:

Diagnosis: Anorexia nervosa, restricting type (no evidence of binge-purge in the history). Severity: extreme (BMI 13.7 < 15).

Vital sign risks: Bradycardia (44 bpm, below 45 bpm threshold for immediate concern), hypotension (systolic 84), hypothermia (35.8°C). This triad demands inpatient admission.

Refeeding risk (NICE criteria, all four met):

• BMI <16 ✓ (13.7)
• Nutritional intake minimal for >10 days (likely, given 8 months of restriction) ✓
• Pre-feeding electrolyte abnormality: K+ low, phosphate low ✓
• Weight loss >15% (clinical history consistent) ✓

Nutritional rehabilitation:

• Correct electrolytes BEFORE starting nutrition
• Start at 10 kcal/kg/day given very high risk (= ~360 kcal/day initially)
• Thiamine 200–300 mg/day orally (or IV Pabrinex) BEFORE glucose/carbohydrate loading, prevents Wernicke's encephalopathy
• Increase caloric load by 200–300 kcal every 2–3 days
• Monitor electrolytes (phosphate, potassium, magnesium) every 12–24 hours for first 3–5 days
• Monitor weight daily, ECG twice weekly initially

QTc 478 ms: Prolonged (normal <440ms in females). At risk of torsades de pointes, a potentially fatal ventricular arrhythmia. Correct hypokalaemia and hypomagnesaemia urgently. Avoid all QTc-prolonging drugs.

Dermatological findings: Lanugo hair (fine downy hair, thermoregulatory response), carotenemia (yellow-orange skin from carrot-heavy diet), xerosis (dry skin), and alopecia (telogen effluvium).

VIGNETTE 2: Bulimia Nervosa

Clinical Scenario:

Aarti, a 23-year-old law student, presents to the outpatient clinic. She reports that for the past 18 months, she has been eating large amounts of food "secretly" almost every evening, finishing an entire packet of biscuits, a full box of mithai, and several portions of leftovers within 30–40 minutes. She describes feeling completely out of control during these episodes and intensely ashamed afterwards. She then induces vomiting to "undo the damage." She says this happens 5–6 times per week. Her weight is 61 kg, height 164 cm (BMI 22.7, normal). Her self-worth is "entirely about how I look."

On examination: mild bilateral parotid enlargement. Dental examination (referred) reveals enamel erosion on the lingual surface of upper front teeth.

Questions for Active Recall:

1. What is the diagnosis? What severity specifier?
2. What are the DSM-5 criteria being met?
3. Name two physical examination findings present and explain their mechanism.
4. What electrolyte abnormality is most likely on blood tests? What acid-base disturbance?
5. What is the pharmacological treatment of choice? What dose? Why is bupropion contraindicated?
6. What is the first-line psychological treatment? Name the developer.

Model Answer Points:

Diagnosis: Bulimia nervosa, severe (4–7 compensatory episodes per week = severe range). BMI normal, distinguishes from AN binge-purge subtype.

DSM-5 criteria met:

1. Recurrent binge eating: large amount in discrete period + loss of control ✓
2. Compensatory behaviour (self-induced vomiting) ✓
3. ≥1 episode/week for ≥3 months (5–6/week for 18 months) ✓
4. Self-evaluation unduly influenced by shape/weight ✓
5. Not occurring exclusively during AN (BMI normal) ✓

Physical findings:

• Parotid hypertrophy: repeated vomiting → salivary gland hypertrophy via autonomic stimulation and direct acid irritation → "chipmunk face"
• Perimolysis: gastric acid reflux during repeated vomiting → demineralisation of dental enamel, predominantly on lingual/palatal surfaces

Electrolytes: Hypokalaemia (potassium lost in vomit), metabolic alkalosis (loss of gastric HCl → bicarbonate excess). This combination is the most dangerous medical consequence of purging, cardiac arrhythmia risk.

Pharmacotherapy:

• Fluoxetine 60 mg/day, only FDA-approved drug for BN. Note: this is 60 mg, not 20–40 mg (standard antidepressant dose). Reduces binge-purge frequency by ~50%.
• Bupropion contraindicated: lowers seizure threshold; electrolyte disturbances in BN (especially hypokalaemia) independently increase seizure risk. Combination is dangerous.

Psychotherapy: CBT-E (Enhanced Cognitive Behaviour Therapy), developed by Christopher Fairburn at Oxford. 20 sessions targeting core psychopathology (overconcern with shape and weight). Addresses binge-purge cycles, dietary restraint, and body image.

VIGNETTE 3: Dissociative Fugue

Clinical Scenario:

A man is found wandering in a bus stand in Pune, approximately 400 km from his home city of Hubli. He appears confused about where he is and cannot recall how he arrived. He gives his name as "Rajan" but is uncertain of his surname. He has no mobile phone or identification on him. Police bring him to the emergency department. On examination, he is alert, oriented to person only, with no evidence of head injury, alcohol intoxication, or current substance use. Blood glucose is normal. Neurological examination is unremarkable.

Two days later, his family, traced via a missing persons report, identifies him as Suresh, 38, a small business owner who had recently faced significant financial losses and a property dispute. His wife reports he left for work 5 days ago and never returned. The family notes he had been under severe stress for several months.

Questions for Active Recall:

1. What is the most likely psychiatric diagnosis?
2. How does this differ from DSM-5 vs ICD-11 classification?
3. What investigations would you perform to exclude organic causes?
4. What is the typical course and prognosis?
5. Outline the management approach.

Model Answer Points:

Diagnosis: Dissociative Fugue (dissociative amnesia with fugue specifier).

DSM-5 vs ICD-11:

• DSM-5: Dissociative fugue is a specifier of Dissociative Amnesia (not a separate diagnosis)
• ICD-11: Coded as 6B61.0, Dissociative amnesia with dissociative fugue (retains some separate recognition)

Investigations to exclude organic causes:

• Blood glucose (done, normal)
• Serum electrolytes, renal function, liver function
• Blood alcohol, urine toxicology screen
• CT brain (to exclude structural lesion, subdural haematoma)
• EEG (if seizure disorder suspected, complex partial seizures can mimic fugue)
• Thyroid function tests

Course and prognosis:

• Duration: hours to months; this case (5 days) is within typical range
• Recovery: usually spontaneous once removed from stressor or trigger identified
• Retrograde amnesia for the fugue period typically persists after recovery
• Recurrence: possible under further stress

Management:

1. Safe, supportive environment
2. Psychoeducation for patient and family
3. Remove or reduce identified stressor where possible
4. Trauma-focused therapy once acute episode resolves
5. Treat comorbid depression, anxiety, PTSD
6. Hypnosis: historically used; not evidence-based for long-term recovery
7. Narcoanalysis (amobarbital interview): historical; not recommended in current guidelines

VIGNETTE 4: Dissociative Identity Disorder

Clinical Scenario:

Meena, 31, has been in psychotherapy for 3 years following a history of severe childhood trauma. Her therapist refers her for a psychiatric evaluation. She reports episodes of "losing time", gaps of several hours to a full day where she cannot recall what happened, during which family members describe her as behaving very differently: sometimes childlike and frightened, sometimes aggressive and threatening. She reports hearing internal voices that argue with each other. She has scars on both forearms from self-cutting, which she says she didn't do, "someone else does it." She was previously diagnosed with schizophrenia and PTSD, and has had two previous hospitalisations.

On assessment, during the interview, she abruptly changes her posture, voice tone, and manner, and states her name is "Choti" (meaning "little one"), is 7 years old, and is afraid of "the dark man."

Questions for Active Recall:

1. What is the diagnosis? What DSM-5 and ICD-11 criteria are met?
2. How do the internal voices in DID differ from those in schizophrenia?
3. What is the phase-based treatment model? Why is premature trauma processing dangerous?
4. What pharmacotherapy is appropriate?
5. What are the two major theoretical controversies around this diagnosis?

Model Answer Points:

Diagnosis: Dissociative Identity Disorder (DID). DSM-5 criteria met:

1. Two or more distinct personality states (host Meena + child alter "Choti" + aggressive alter) ✓
2. Recurrent amnesia between alters (gaps in memory; self-harm she cannot recall) ✓
3. Significant distress or functional impairment ✓
4. Not attributable to cultural/religious practice ✓
5. Not due to substance or medical condition ✓

Voices in DID vs schizophrenia:

Swipe to compare →

Phase-based treatment:

• Phase 1 (Safety and Stabilisation): Grounding techniques, containment imagery, distress tolerance, coping skills. Build therapeutic alliance with all alters. Map the alter system.
• Phase 2 (Trauma Processing): Careful, titrated engagement with traumatic memories using EMDR or ego state therapy. Premature trauma processing before adequate stabilisation → flooding, decompensation, increased self-harm, hospitalisation, therapy dropout.
• Phase 3 (Integration): Fusion of alters or functional integration (alters co-operate, amnesia barriers dissolve).

Pharmacotherapy:

• No medication treats DID specifically
• SSRIs for comorbid PTSD, depression, anxiety
• Prazosin for nightmares
• Avoid benzodiazepines long-term (abuse risk; can increase dissociation)
• Antipsychotics NOT indicated for DID voices (they are alter-based, not psychotic phenomena)

Controversies:

1. Trauma model: genuine response to severe early trauma, neurobiologically grounded
2. Sociocognitive model: iatrogenic creation through suggestive therapy, cultural scripting, media influence (Sybil effect)

VIGNETTE 5: Narcolepsy Type 1

Clinical Scenario:

Karthik, 24, an engineering student, presents with a 2-year history of overwhelming sleepiness throughout the day. He has fallen asleep during lectures, while eating, and once briefly while cycling. He reports that when he laughs hard or is suddenly surprised, his knees buckle and he has to grab support, this lasts about 20–30 seconds and he remains fully conscious throughout. He also reports vivid, frightening visual experiences just as he falls asleep at night, and has had two episodes of waking in the morning unable to move for about a minute before "snapping out of it."

He sleeps 8–9 hours nightly but wakes unrefreshed. His Epworth Sleepiness Scale score is 19/24.

Questions for Active Recall:

1. What is the diagnosis? Justify using clinical features.
2. What investigation confirms the diagnosis? What results are expected?
3. What is the pathophysiology of Type 1 narcolepsy?
4. Describe the management, matching each drug to each symptom.
5. What non-pharmacological advice would you give regarding driving?

Model Answer Points:

Diagnosis: Narcolepsy Type 1 (with cataplexy). The complete tetrad is present:

1. EDS (obligate): severe; ESS 19/24
2. Cataplexy (pathognomonic for Type 1): emotionally triggered bilateral muscle tone loss WITH preserved consciousness, "knees buckle when laughing"
3. Hypnagogic hallucinations: vivid visual experiences at sleep onset
4. Sleep paralysis: unable to move on awakening, resolved spontaneously

Investigations:

• Overnight polysomnography (PSG): rules out obstructive sleep apnoea as cause of EDS; confirms adequate sleep duration
• Multiple Sleep Latency Test (MSLT) next morning: Expected results, mean sleep latency <8 minutes (likely 3–4 min in Type 1) AND ≥2 SOREMPs (sleep-onset REM periods)
• CSF hypocretin-1: expected <110 pg/mL (confirmatory; more often done in research settings)
• HLA-DQB1*06:02: expected positive (>95% of Type 1)

Pathophysiology:

Selective autoimmune destruction of hypothalamic neurons producing hypocretin (orexin), 80–90% neuron loss. Loss of the wake-stabilising orexin signal → inability to maintain consolidated wakefulness → intrusion of REM sleep features (cataplexy, sleep paralysis, hypnagogic hallucinations) into wakefulness.

Trigger: H1N1 influenza infection or Pandemrix vaccine (Europe), molecular mimicry between influenza antigen and hypocretin receptor.

Management:

Non-pharmacological: scheduled naps 2–3 × 15–20 min/day; consistent sleep schedule; avoid alcohol.

Driving advice: Karthik must not drive until symptoms are well-controlled on medication (stipulated by most road transport regulations). He must disclose his diagnosis. Driving is permitted only when daytime sleepiness is adequately controlled AND he has been on stable medication without breakthrough sleep attacks. This must be reviewed periodically.

VIGNETTE 6: Chronic Insomnia: CBT-I Application

Clinical Scenario:

Sunita, 45, a secondary school teacher, presents with an 18-month history of difficulty sleeping. She takes 1.5–2 hours to fall asleep each night and wakes 2–3 times. She reports lying awake worrying about whether she will sleep, calculating how many hours remain. She goes to bed at 9:30 pm hoping to accumulate enough sleep, spends 9.5 hours in bed, but estimates her actual sleep at 4.5–5 hours. She feels fatigued and irritable during the day, but reports falling asleep easily when watching TV on the sofa. She has been taking zopiclone 7.5 mg nightly for 4 months prescribed by her GP.

Questions for Active Recall:

1. What is the diagnosis and its subtype by duration?
2. Calculate her sleep efficiency. What does this tell you?
3. Identify the perpetuating factors in this case.
4. Outline a CBT-I treatment plan for Sunita.
5. How would you address the zopiclone dependence?

Model Answer Points:

Diagnosis: Chronic insomnia disorder (≥3 nights/week, ≥3 months, with daytime impairment). Both sleep onset and sleep maintenance types are present.

Sleep efficiency: SE = (Total Sleep Time / Time In Bed) × 100 = (4.75 hours / 9.5 hours) × 100 = 50%. This is severely impaired (normal target >85%). Extended time in bed is paradoxically worsening her insomnia by diluting sleep drive and weakening the bed-sleep association.

Perpetuating factors (3P model, Spielman):

• Extended time in bed (9.5 hours): reduces sleep drive; dilutes sleep
• Stimulus control violation: falling asleep on sofa (decouples bed from sleepiness)
• Early bedtime (9:30 pm): too far ahead of actual sleep phase
• Sleep monitoring/worry: selective attention to time, calculating hours, hyperarousal
• Zopiclone dependence: perpetuates the belief that sleep is impossible without medication

CBT-I Treatment Plan:

Session 1-2 (Assessment and Psychoeducation):

• Explain 3P model; normalise that extended TIB worsens insomnia
• Sleep diary baseline (2 weeks): record TIB, sleep latency, awakenings, TST, SE

Session 2-3 (Sleep Restriction):

• Prescribe TIB = estimated TST = 4.75 hours
• Set fixed wake time: 6:00 am → prescribed bedtime: 1:15 am
• When SE >90% for 5 nights → extend TIB by 15 minutes (move bedtime earlier to 1:00 am)
• Continue extending in 15-min increments as SE improves

Session 3-4 (Stimulus Control):

• Bed only for sleep and sex
• Leave bedroom if not asleep within ~20 minutes; return only when sleepy
• No TV in bedroom; no lying on sofa to watch TV (sit upright instead)

Session 4-5 (Cognitive Restructuring):

• Challenge: "I can't function without 8 hours" → review actual performance on low-sleep nights
• Challenge: "I haven't slept a wink" → discuss sleep state misperception
• Reduce clock-watching: cover clock, remove phone from bedroom

Session 5-6 (Relapse Prevention):

• Explain that brief insomnia recurrences are normal
• Early intervention: apply stimulus control and sleep restriction at first sign of relapse

Zopiclone tapering:

• Gradual dose reduction: 7.5 mg → 3.75 mg → every other night → cessation
• Time the taper with CBT-I progress (begin taper once SE improving)
• Expect rebound insomnia on nights of dose reduction, reassure and pre-empt with CBT-I skills
• Target: complete cessation within 4–6 weeks

VIGNETTE 7: Suicide Risk Assessment

Clinical Scenario:

Rohit, 38, is brought to the emergency department by his wife at 11 pm. She found him sitting in their car in the garage with the engine running; he had been there for approximately 20 minutes before she found him. He had written a note to their two children. He is alert on arrival. He says the note was "just in case" and denies current intent to die. He discloses that he was recently passed over for a promotion, his marriage has been strained for 2 years, and he has had recurrent depressive episodes for 6 years, currently untreated. He drinks approximately 6–8 units of alcohol per day. He has no previous suicide attempts. He has a licensed firearm at home, used for sport shooting.

Questions for Active Recall:

1. Apply the C-SSRS framework to characterise his ideation and behaviour.
2. List modifiable and non-modifiable risk factors present.
3. What is the immediate management?
4. What specific actions must be taken regarding means?
5. What protective factors should you assess?
6. Is hospitalisation indicated? Justify.

Model Answer Points:

C-SSRS Assessment:

• Ideation: Active ideation with plan (carbon monoxide poisoning via car exhaust in garage), C-SSRS ideation level 4 (plan present)
• Behaviour: Preparatory behaviour + actual attempt (engine running, note written, entered garage), this constitutes an actual interrupted attempt (interrupted by wife)
• Current denial of intent does not override the behavioural evidence

Risk Factors:

Immediate management:

1. Medical assessment (CO levels if clinically indicated; GCS, vitals)
2. Move to a safe, supervised area
3. Contact with wife (with consent), enlist support
4. Formal psychiatric assessment using C-SSRS
5. Start antidepressant (note: acute period, monitor for activation)
6. Address alcohol use disorder (detox if needed; naltrexone/acamprosate)

Means restriction, CRITICAL:

• Firearm: immediate counselling for temporary transfer to a trusted third party (friend, police storage) or secure gun safe with wife holding key. This is the single most evidence-based intervention available in this case.
• Garage: wife to control access (fob/lock); keep car in open driveway until risk resolves

Protective factors to assess:

• Attachment to children (note he wrote a note TO them, suggests relationship; this is a protective factor)
• Marriage, strained but wife searched for him (suggests connection)
• Future orientation: job, career ambitions
• Religious beliefs
• Willingness to seek help (came to ER, is engaging)

Hospitalisation: YES, indicated.

Reasons: actual attempt tonight, specific lethal plan (CO poisoning), untreated recurrent depression, active alcohol use disorder causing disinhibition, access to firearm. Even though he denies current intent, the behavioural evidence overrides self-report. Voluntary admission preferred; document discussion. If he refuses, consider involuntary admission under the Mental Healthcare Act, 2017 (Section 89/90, emergency treatment without consent when imminent harm risk).

VIGNETTE 8: REM Sleep Behaviour Disorder

Clinical Scenario:

Venkat, 62, is referred by his neurologist. His wife reports that for the past 18 months he has been "acting out his dreams", shouting, punching, and once fell out of bed. She describes him as appearing to be "fighting someone." He has injured her twice. He wakes immediately after these episodes, recalls a vivid dream in which he was being attacked, and is fully oriented within seconds. He has no history of sleepwalking as a child. He has noticed mild constipation over the past year and reduced sense of smell. He has a resting tremor in his right hand that was noted by his GP 6 months ago but attributed to anxiety.

His current medication includes sertraline 100 mg/day, started 2 years ago.

Questions for Active Recall:

1. What is the diagnosis? What PSG finding confirms it?
2. What is the most clinically significant association of this condition?
3. Is the sertraline relevant? Explain.
4. What other clinical features in this case suggest the same underlying diagnosis?
5. Outline management.

Model Answer Points:

Diagnosis: REM Sleep Behaviour Disorder (RBD). Confirmed on video-polysomnography by demonstrating REM Sleep Without Atonia (RSWA), abnormal chin or limb EMG activity during REM sleep (tonic or phasic), occurring in >50% of REM epochs.

Clinical features of RBD:

• Dream enactment during REM: purposeful-appearing violent behaviour correlating with dream content
• Preserved consciousness/orientation immediately on awakening
• Full recall of dream narrative
• Predominantly affects males >50 years

Neurodegenerative association:

RBD is a prodromal marker of alpha-synucleinopathies. Prospective cohort studies (Postuma et al.; Iranzo et al.) demonstrate that 80–90% of idiopathic RBD patients develop Parkinson's disease, Dementia with Lewy Bodies, or Multiple System Atrophy within 10–15 years of RBD onset.

The resting tremor, anosmia, and constipation in this case are all non-motor prodromal features of Parkinson's disease. This patient likely has Parkinson's disease in its prodromal phase.

Sertraline relevance:

SSRIs (and SNRIs, TCAs, MAOIs) can precipitate or worsen RBD by suppressing REM sleep atonia. The sertraline may be contributing to, or unmasking, his RBD. Dose reduction should be considered; if clinically necessary to continue, discuss risk-benefit with the referring neurologist. Consider switching to an antidepressant with lower REM atonia impact (bupropion, though note its own limitations).

Management:

Pharmacological:

• Clonazepam 0.5–1 mg at bedtime: first-line; reduces dream enactment behaviour; does NOT restore REM atonia; risk of respiratory depression, screen for sleep apnoea first (PSG will have assessed this)
• Melatonin 3–12 mg at bedtime: alternative/adjunct; better tolerated in elderly; partially restores atonia; no respiratory depression; preferred in older patients or those with OSA

Non-pharmacological (essential):

• Remove sharp objects from bedside
• Pad bed frame and floor
• Consider placing mattress on floor
• Wife to sleep separately until behaviours are controlled
• Fall-prevention measures

Neurological follow-up:

• Refer to movement disorder neurologist for full Parkinson's disease evaluation
• This is not just sleep medicine, this patient is in a window where neuroprotective interventions (if developed) may be applicable
• Discuss with patient: the association with neurodegenerative disease, what to watch for, and why monitoring matters

VIGNETTE 9: Deliberate Self-Harm in Adolescent

Clinical Scenario:

Ananya, 16, is brought to the emergency department by her mother after she discovered fresh cuts on Ananya's forearms. There are approximately 12 superficial parallel incisions, 2–3 cm each, made with a blade. The wounds are superficial and not life-threatening. Ananya is tearful but calm. She says she did not want to die, "I just needed to feel something. Everything felt numb." She has been cutting for approximately 6 months, 2–3 times per week. The trigger today was a fight with her boyfriend. She denies suicidal ideation but has a history of one episode 8 months ago where she did take 6 paracetamol tablets with intent to die.

Questions for Active Recall:

1. Distinguish this presentation from a suicide attempt. What assessment framework is used?
2. What is the function of the self-harm in this case?
3. What is the prior paracetamol episode's significance?
4. What psychiatric disorders should be screened for?
5. Outline management.
6. What is the evidence-based treatment for self-harm in adolescents?

Model Answer Points:

Distinguishing DSH from suicide attempt:

C-SSRS is used to clarify: is there any suicidal ideation? At what intensity? Is the self-harm suicidal in nature at all?

Function of self-harm: Anti-dissociation (primary, "everything felt numb") and emotion regulation (secondary, relief after cutting). Both are well-established functional categories of NSSI. Understanding the function guides treatment.

Prior paracetamol episode significance:

The 8-month-old paracetamol overdose WITH intent to die was a suicide attempt, this is a critical historical factor. Prior suicide attempt is the strongest single predictor of future suicide attempt or completion. The current presentation is NSSI without suicidal intent, but the history of an actual attempt elevates overall risk. She cannot be assessed only by current presentation.

Screening for comorbid disorders:

• Borderline personality disorder features (most commonly associated with NSSI + instability)
• Major depressive disorder
• PTSD (history of trauma)
• Anxiety disorders
• Eating disorders (NSSI is elevated in AN/BN)
• Substance use
• ASD (emotional dysregulation, sensory seeking)

Management:

Immediate:

• Wound care (superficial, clean and dress)
• Safety assessment using C-SSRS
• Do NOT hospitalise purely for superficial NSSI without suicidal risk, can be counterproductive and reinforce the behaviour
• Engage Ananya collaboratively, not punitively

Short-term:

• Psychoeducation for Ananya and mother (normalise the emotional function; do not shame)
• Safety plan (with Ananya's input): warning signs → coping → contacts → means restriction (remove blade from room)
• Referral to adolescent mental health service

Evidence-based treatment:

• Dialectical Behaviour Therapy for Adolescents (DBT-A): strongest evidence for NSSI and suicidality in adolescents; family component; skills (TIPP, PLEASE, opposite action, distress tolerance)
• CBT for depression/anxiety if comorbid
• Family therapy where family conflict is a precipitant

VIGNETTE 10: Complex PTSD

Clinical Scenario:

Kavitha, 34, is referred from a women's shelter. She was in an abusive marriage for 9 years; her husband was physically and sexually violent throughout. She left 8 months ago. She presents with intrusive memories of abuse (flashbacks), avoidance of any reminders of her husband (refuses to enter the kitchen where most abuse occurred), and constant hypervigilance ("I can never relax"). She is also described as having "explosive" episodes of rage, followed by deep shame and self-loathing. She finds it impossible to trust anyone, including her therapist. She describes herself as "broken and worthless, no one would want someone like me." On Beck Depression Inventory, she scores 32 (severe depression).

Questions for Active Recall:

1. What is the diagnosis? Why does standard PTSD not capture this presentation fully?
2. Apply the ICD-11 Complex PTSD criteria.
3. How does Complex PTSD differ from Borderline Personality Disorder?
4. What is the phase-based treatment approach?
5. What role does Schema Therapy play?

Model Answer Points:

Diagnosis: Complex PTSD (ICD-11: 6B41). Standard PTSD (6B40) does not fully capture this presentation because in addition to the three core PTSD clusters (re-experiencing, avoidance, hyperarousal), she has three additional symptom domains that constitute Complex PTSD.

ICD-11 Complex PTSD Criteria:

Core PTSD criteria (6B40, all met):

1. Re-experiencing: flashbacks of abuse ✓
2. Avoidance: refuses reminders (kitchen) ✓
3. Sense of current threat (hypervigilance): constant ✓

Duration >1 month ✓; significant impairment ✓

Additional DSO (Disturbances in Self-Organisation) criteria (all three met):

1. Affect dysregulation: explosive rage episodes, difficulty modulating emotion ✓
2. Negative self-concept: "broken and worthless, no one would want me", persistent shame, guilt, worthlessness ✓
3. Disturbances in relationships: inability to trust, including therapist ✓

Complex PTSD vs BPD Differential:

C-PTSD and BPD frequently co-occur; the distinction is not always clean clinically.

Phase-based Treatment (ICD-11 treatment guidelines):

Phase 1, Safety and Stabilisation (often longest phase in C-PTSD):

• Establish safety (physical: shelter, legal protection; psychological: therapeutic alliance)
• Skills for affect regulation (DBT-informed: TIPP, temperature, distress tolerance)
• Grounding techniques for flashbacks
• Psychoeducation about trauma and C-PTSD
• Build trust slowly, therapeutic relationship IS the intervention at this stage

Phase 2, Trauma Processing:

• EMDR: evidence-based for PTSD; requires adaptation and caution in C-PTSD (dissociative windows)
• Trauma-focused CBT
• Do NOT rush, destabilisation in C-PTSD is severe and set-backs are costly

Phase 3, Integration and Reconnection:

• Identity reconstruction: who is she outside the trauma narrative?
• Relational work: trust, intimacy, healthy relationships
• Schema Therapy's reconnection with "Healthy Adult" mode

Schema Therapy role:

Schema Therapy (Jeffrey Young) is particularly well-suited to C-PTSD because:

• It explicitly addresses Early Maladaptive Schemas activated by developmental trauma (Defectiveness/Shame, Mistrust/Abuse, Emotional Deprivation, all evident here)
• Mode work addresses the protective/avoidant responses (Detached Protector, Punitive Critic) that maintain the negative self-concept
• The Healthy Adult mode is built collaboratively, directly addressing Kavitha's belief that she is "broken"
• Limited reparenting within the therapeutic relationship directly addresses the attachment wounds underlying C-PTSD

VIGNETTE 11: Insomnia and Depression: Differential Sleep Features

Clinical Scenario:

Mohan, 52, presents to the psychiatry OPD with a 3-month history of disturbed sleep and low mood. He goes to bed at 10 pm, lies awake for 1.5 hours, wakes at 2 am, and cannot return to sleep. He gets up feeling unrefreshed at 5:30 am. He reports persistent low mood, anhedonia, fatigue, poor concentration, and a sense of hopelessness about the future. He has lost 4 kg without dieting. He is a retired schoolteacher living alone following his wife's death 18 months ago. He has two adult children who live in other cities. His past history includes a depressive episode 12 years ago treated successfully with escitalopram.

Questions for Active Recall:

1. What is the sleep disturbance pattern and what does it suggest?
2. What specific sleep architecture changes occur in major depression?
3. What is the diagnosis and what criteria are met?
4. How would you approach treatment of both the depression and the insomnia?
5. What specific medication choice is advantageous here and why?

Model Answer Points:

Sleep disturbance pattern:

• Sleep onset insomnia (1.5 hour latency)
• Sleep maintenance insomnia (wakes at 2 am)
• Early morning awakening (EMA): wakes at 2 am and cannot return to sleep, classic EMA pattern
• EMA is the most characteristic sleep symptom of major depression (vs anxiety which tends to cause sleep onset insomnia)

Sleep architecture changes in major depression:

• Increased sleep latency
• Reduced sleep efficiency
• Reduced N3 (slow wave sleep)
• Shortened REM latency (<65 minutes), most characteristic biological finding
• Increased total REM sleep
• Increased REM density (more eye movements per unit of REM)
• Frequent awakenings
• Early morning awakening

Diagnosis: Major Depressive Disorder, single episode (recurrence, prior episode 12 years ago).

Criteria met:

1. Depressed mood ✓
2. Anhedonia ✓
3. Fatigue ✓
4. Insomnia (sleep maintenance + EMA) ✓
5. Psychomotor (not described but concentration impaired) ✓
6. Poor concentration ✓
7. Hopelessness (→ worthlessness) ✓
8. Weight loss 4 kg ✓

Duration ≥2 weeks (3 months) ✓; significant impairment ✓

Treatment approach:

Depression:

• Antidepressant: restart escitalopram (previously effective, good prior response) 10–20 mg/day
• OR consider mirtazapine given insomnia comorbidity (see below)
• 8–12 weeks for full antidepressant response
• Psychotherapy: CBT for depression; IPT (particularly appropriate given bereavement/loss context)

Insomnia:

• CBT-I: appropriate as standalone or alongside antidepressant
• Short-term hypnotic if severe insomnia impairing daily function while waiting for antidepressant to work (zopiclone/melatonin; not long-term)

Medication choice advantage:

Mirtazapine 15–30 mg at bedtime is advantageous here because:

• H1 and 5-HT2A/2C antagonism provides sedation and improves sleep architecture
• Antidepressant efficacy (NaSSA mechanism)
• Weight gain effect may be beneficial (4 kg loss already)
• Appetite stimulation helpful
• No sexual side effects (relevant in older patients)
• Does not suppress REM at low doses (unlike SSRIs)

Alternatively: escitalopram (good prior response) + short-term zopiclone while awaiting efficacy, then taper.

VIGNETTE 12: Depersonalisation/Derealization Disorder

Clinical Scenario:

Rishi, 22, a final-year medical student, presents to the psychiatry clinic. For the past 8 months he has been experiencing episodes, now nearly continuous, of feeling "detached from myself, like I'm watching myself from outside." He describes his surroundings as looking "foggy, artificial, like a film set." He knows these perceptions are not real and finds this frightening. He remains fully oriented and performs well academically despite the symptoms. The symptoms began after a period of heavy cannabis use 9 months ago, which he has since stopped. He was investigated by neurology (normal MRI brain, normal EEG) and cardiology (normal ECG, 24-hour Holter). He scores 28 on the Cambridge Depersonalisation Scale (moderate-severe).

Questions for Active Recall:

1. What is the diagnosis? What distinguishes it from psychosis?
2. What is the prevalence of transient vs persistent depersonalisation?
3. What is the role of cannabis in the aetiology?
4. What is the first-line psychological treatment?
5. What pharmacological options are available?

Model Answer Points:

Diagnosis: Depersonalisation/Derealization Disorder (DSM-5: 300.6; ICD-11: 6B66).

Distinguishing from psychosis:

The critical differentiating feature is intact reality testing, Rishi KNOWS his perceptions are not real ("he knows these perceptions are not real"). In psychosis, the patient believes the altered perception IS reality. This is the defining boundary.

Additional distinguishing features:

• No hallucinations (which are perceived as real external stimuli)
• No delusions
• No thought disorder
• Normal neurological and cardiac workup (excluded organic causes)

Prevalence:

• Transient depersonalisation episodes: up to 74% of the general population (stress, sleep deprivation, meditation, drugs)
• Persistent DPDR disorder: 1–2% of the general population
• Often under-diagnosed because patients fear being told they are "mad"

Cannabis and DPDR:

Cannabis (particularly high-THC preparations) can precipitate depersonalisation episodes, especially in vulnerable individuals. Cannabis may trigger a persistent DPDR disorder in susceptible individuals, the episodes persist beyond cannabis cessation. This is not withdrawal, it appears to represent a triggered dysfunction of the prefrontal-limbic regulatory system (reduced amygdala response + increased prefrontal inhibition → emotional numbing + dissociation). Rishi's timeline (DPDR persists 8 months post-cessation) is consistent with cannabis-triggered persistent DPDR.

First-line psychological treatment:

CBT for DPDR using the Hunter and Phillips model ("Feeling Real" therapy, developed at the Institute of Psychiatry, London). Components:

• Psychoeducation: normalise the experience; reduce secondary anxiety about the symptoms
• Identify and reduce safety behaviours (checking whether surroundings are real, avoidance)
• Reduce selective attention to symptoms (attention training)
• Behavioural activation (counteracts emotional numbing)
• Cognitive techniques: challenge catastrophic interpretations

Pharmacological options: