Child Adolescent
Paper III · Specialties, Forensic & Child. Six study modes, from notes to quick review.
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Study Notes
Sources: Kaplan & Sadock's Comprehensive Textbook of Psychiatry (11th ed.), Rutter's Child and Adolescent Psychiatry (6th ed.), Lewis's Child and Adolescent Psychiatry (5th ed.)
PART 1: ATTENTION DEFICIT HYPERACTIVITY DISORDER (ADHD)
1.1 Epidemiology
- Prevalence: 5–7% in school-age children (DSM-5); 3–5% globally (ICD-11)
- Male:Female ratio childhood: 3–4:1; adult ADHD approaches 2:1 (females underdiagnosed)
- Persistence into adulthood: 60–70% retain significant symptoms; full criteria met in 40–50%
- Most common reason for psychiatric referral in children worldwide
ADHD prevalence using DSM-5 criteria is higher than ICD-10 criteria, ICD-10 required pervasive hyperkinetic disorder (all three symptom domains + multiple settings). DSM-5 combined type is broader. This explains international prevalence differences.
1.2 DSM-5 Diagnostic Criteria
Domain A, Inattention (6+ symptoms, <17 years; 5+ if ≥17 years, for ≥6 months):
- Often fails to give close attention to details / makes careless mistakes
- Often has difficulty sustaining attention in tasks or play
- Often does not seem to listen when spoken to directly
- Often does not follow through on instructions; fails to finish tasks
- Often has difficulty organizing tasks and activities
- Often avoids/dislikes tasks requiring sustained mental effort
- Often loses things necessary for tasks
- Often easily distracted by extraneous stimuli
- Often forgetful in daily activities
Domain B, Hyperactivity-Impulsivity (6+ symptoms, <17; 5+ if ≥17, for ≥6 months):
- Often fidgets with or taps hands/feet or squirms in seat
- Often leaves seat when remaining seated is expected
- Often runs about or climbs in inappropriate situations
- Often unable to play or engage in leisure activities quietly
- Often "on the go" acting as if "driven by a motor"
- Often talks excessively
- Often blurts out an answer before question completed
- Often has difficulty waiting turn
- Often interrupts or intrudes on others
Additional Criteria:
- Several symptoms present before age 12 years
- Symptoms in two or more settings
- Clear interference with social, academic, or occupational functioning
- Not explained by another mental disorder
Presentations:
DSM-5 changed "subtypes" to "presentations", acknowledging that presentation can shift over time. Age of onset changed from 7 to 12 years (critical difference from DSM-IV).
1.3 ICD-11 Classification
ICD-11 codes ADHD under 6A05:
- 6A05.0, ADHD predominantly inattentive
- 6A05.1, ADHD predominantly hyperactive-impulsive
- 6A05.2, ADHD combined presentation
- 6A05.Z, ADHD unspecified
Key ICD-11 changes from ICD-10:
- Dropped "Hyperkinetic Disorder", now aligned with ADHD terminology
- Removed mandatory combined presentation requirement
- Recognizes adult ADHD more explicitly
- Symptoms must be developmentally inappropriate and cause impairment
1.4 Neurobiology
Dopaminergic-Noradrenergic Dysregulation:
The prefrontal cortex (PFC) is the central neurobiological substrate of ADHD. The PFC mediates executive functions via pyramidal neuron networks regulated by:
- Dopamine (D1 receptors): Moderate stimulation optimizes PFC network firing; too little or too much impairs working memory and response inhibition
- Norepinephrine (α2A receptors): Enhances signal-to-noise ratio in PFC networks; too little (stress/fatigue) shifts control to subcortical structures
Key Neural Circuits:
- Fronto-striatal circuit: PFC → striatum → thalamus → PFC loop. Dysfunction causes impaired inhibitory control and working memory
- Default Mode Network (DMN): Normally suppressed during goal-directed tasks. In ADHD, DMN fails to adequately suppress, "mind wandering" during tasks represents intrusion of DMN activity
- Cerebellum: Timing deficits in ADHD linked to cerebellar-striatal circuit dysfunction
Structural Brain Findings (meta-analyses):
- Reduced total brain volume (3–5% smaller)
- Smaller caudate nucleus (most consistent finding; normalizes with treatment)
- Thinner cortex in PFC, especially right hemisphere
- Delayed cortical maturation by ~3 years (Shaw et al., 2007)
- Right inferior frontal cortex and anterior cingulate most affected
Genetics:
- Heritability: 70–80% (twin studies)
- Candidate genes: DAT1 (dopamine transporter), DRD4 7-repeat allele, DRD5, SNAP25, COMT Val158Met
- No single gene explains >5% of variance, polygenic architecture
- Copy number variants (CNVs) found in ~15% of clinical ADHD cases
The DRD4 7-repeat allele is associated with novelty-seeking and ADHD. It is also linked to better response to environmental enrichment, the "differential susceptibility" model (Belsky). This is testable.
1.5 Assessment
Clinical Interview Components:
- Developmental history (prenatal, perinatal, postnatal)
- Academic history (school reports, teacher observations)
- Behavioral history across settings
- Family history of ADHD/learning disabilities
- Medical history: thyroid disease, hearing/vision, lead exposure, seizures
- Medication history
- Psychiatric comorbidities
Rating Scales:
| Scale | Rater | Age Range | Subscales | Notes |
|---|---|---|---|---|
| Conners Rating Scale-3 | Parent/Teacher/Self | 6–18 | Inattention, Hyperactivity, Executive Function, Learning Problems, Peer Relations | Gold standard, normative data |
| SNAP-IV | Parent/Teacher | 6–17 | ADHD-I, ADHD-H/I, ODD | Free, based directly on DSM criteria |
| Vanderbilt ADHD Scale | Parent/Teacher | 6–12 | ADHD + comorbid ODD/CD/Anxiety/Depression screening | Used in US primary care |
| CBCL (Achenbach) | Parent | 1.5–18 | Broadband (internalizing/externalizing) | Not ADHD-specific |
| Brown ADD Rating Scales | Self/Parent | 3 years+ | Executive function focus | Useful for adult ADHD |
| ADHD Rating Scale-5 | Parent/Teacher | 5–17 | Inattention, Hyperactivity-Impulsivity | DSM-5 aligned |
Neuropsychological Testing:
- Continuous Performance Tests (CPT): TOVA, Conners CPT, measures sustained attention, impulsivity
- Working memory: WISC-V Working Memory Index
- Processing speed: WISC-V Processing Speed Index
- Executive function: BRIEF (Behavior Rating Inventory of Executive Function)
Rating scales are NOT diagnostic alone, diagnosis requires clinical interview, history, and impairment across settings. A Conners score below threshold does not rule out ADHD.
1.6 Pharmacotherapy
First-Line: Stimulants
| Medication | Class | Mechanism | Onset | Duration | Key Points |
|---|---|---|---|---|---|
| Methylphenidate (MPH) | Phenethylamine | Blocks DAT + NET reuptake | 30–60 min | IR: 4–6h; LA: 8–12h | Most evidence in children; multiple formulations |
| Amphetamine (AMP) | Phenethylamine | Blocks DAT/NET + causes release | 30–60 min | IR: 4–5h; LA: 10–12h | Slightly more potent than MPH |
| Lisdexamfetamine (LDX) | Prodrug | Cleaved to d-amphetamine in gut | 60–90 min | 12–14h | Lower abuse potential; FDA-approved binge eating |
| Dexmethylphenidate | Phenethylamine | Pure d-enantiomer of MPH | 30–45 min | IR: 4–5h; XR: 8–12h | Fewer side effects than racemic MPH |
Methylphenidate formulations:
- Ritalin (IR): 5/10/20mg, 2–3x/day
- Ritalin LA: 20/30/40mg, once daily
- Concerta (OROS-MPH): 18/27/36/54mg, once daily, 22% IR + 78% LA via osmotic pump
- Medikinet XL: Bimodal release
- Quillivant: Liquid methylphenidate
Stimulant Side Effects:
- Appetite suppression (most common, morning)
- Insomnia (take earlier, reduce evening dose)
- Growth suppression (0.5–1 cm/year, drug holidays may help)
- Cardiovascular: modest HR/BP increase; screen for congenital heart disease before starting
- Rebound phenomenon (mood/behavioral worsening as medication wears off)
- Tics (controversial, may unmask rather than cause; reassess periodically)
Growth suppression with stimulants is modest (0.5–1 cm/year) and partially recovers. Drug holidays (weekends/summers) used in some cases but evidence is mixed, not recommended routinely as benefit of continuous treatment often outweighs growth concern.
Second-Line: Non-stimulants
| Medication | Class | Mechanism | Onset | Key Points |
|---|---|---|---|---|
| Atomoxetine | NRI | Selective NET inhibitor | 4–6 weeks for full effect | Non-scheduled; good for anxiety comorbidity, tic disorders; black box suicidality warning |
| Guanfacine ER | α2A agonist | PFC α2A receptor agonist | 2–4 weeks | Also for tics; can cause sedation/bradycardia; taper on discontinuation |
| Clonidine ER | α2 agonist (non-selective) | Reduces NE turnover | 2–4 weeks | More sedating than guanfacine; also for tics, sleep problems |
| Bupropion | NDRI | NE/DA reuptake inhibitor | 2–4 weeks | Off-label; good for comorbid depression; lowers seizure threshold |
Atomoxetine Dosing:
- <70kg: Start 0.5 mg/kg/day, titrate to 1.2 mg/kg/day target (max 1.4 mg/kg/day)
- >70kg: Start 40mg/day, titrate to 80–100mg/day
- Take with/after food to reduce GI side effects
- Hepatotoxicity: rare but monitor LFTs if symptoms emerge
Atomoxetine takes 4–6 weeks to achieve full effect (unlike stimulants which work same day). This must be explained to families. The black box warning for suicidal ideation is the same as SSRIs, monitor closely in first 4 weeks.
1.7 Behavioral Interventions
Behavioral Parent Training (BPT):
- First-line for preschool ADHD (age 4–5)
- Programs: Triple P, Incredible Years, Parent-Child Interaction Therapy (PCIT)
- Components: positive attention, reward systems, consistent consequences, planned ignoring
School-Based Interventions:
- Classroom accommodations: preferential seating, extended time, reduced workload, frequent breaks
- Daily Report Cards (DRC): home-school communication system
- Classroom behavior management: token economy, response cost
Multimodal Treatment:
- MTA (Multimodal Treatment of ADHD) study: medication + behavioral therapy superior to either alone for comorbid anxiety; medication alone equivalent to combined treatment for core ADHD symptoms in children without comorbidity
- Long-term: combined treatment advantage dissipates over years, naturalistic follow-up
MTA study is frequently tested. Key findings: (1) Medication superior to behavioral treatment for core ADHD symptoms, (2) Combined treatment best for anxiety comorbidity and parent satisfaction, (3) Long-term advantages of medication diminish by 3-year follow-up.
1.8 Adult ADHD
- Prevalence: 2.5–4% adults
- Phenotype shifts: hyperactivity becomes internal restlessness, organizational problems become prominent
- High comorbidity: MDD (30%), anxiety (50%), SUD (40–50%)
- Diagnosis: requires childhood onset (before 12), DSM-5 threshold lowered to 5 symptoms
- Treatment: stimulants effective; atomoxetine FDA-approved; non-stimulants for comorbidities
- Occupational impact: underemployment, job loss, multiple jobs
1.9 ADHD in Women
Historically underdiagnosed due to:
- More inattentive presentation (ADHD-I more common in females)
- Better social masking/camouflaging
- Teacher referrals biased toward hyperactive boys
- Less disruptive behavior leading to less concern
Special considerations:
- Hormonal fluctuation (estrogen → dopamine → ADHD symptom severity waxes with low estrogen phases, premenstrual, perimenopause)
- Pregnancy: stimulants generally held; non-pharmacological approaches emphasized
- Comorbid eating disorders, anxiety, depression more common than males
1.10 Driving and Occupational Implications
- ADHD associated with 2–4x increased motor vehicle accidents
- Response time, sustained attention, and risk-taking behavior impaired
- Medication reduces accident risk significantly (Chang et al., 2014, large Swedish registry study)
- Occupational: more job changes, conflicts with supervisors, underperformance relative to IQ
PART 2: AUTISM SPECTRUM DISORDER (ASD)
2.1 DSM-5 Diagnostic Criteria
Criterion A, Persistent deficits in social communication and social interaction (all three must be present):
- Deficits in social-emotional reciprocity (abnormal social approach, failure of conversation, reduced sharing of interests/emotions, failure to initiate/respond to interactions)
- Deficits in nonverbal communicative behaviors (poorly integrated verbal/nonverbal communication, abnormalities in eye contact/body language, deficits in understanding/use of gestures, absence of facial expressions)
- Deficits in developing, maintaining, and understanding relationships (difficulty adjusting behavior to context, difficulty making friends, absence of interest in peers)
Criterion B, Restricted, Repetitive Behaviors and Interests (RRBIs), at least 2 of 4:
- Stereotyped or repetitive motor movements, use of objects, or speech (motor stereotypies, lining up toys, echolalia, idiosyncratic phrases)
- Insistence on sameness, inflexible adherence to routines, or ritualized patterns (extreme distress at small changes, rigid thinking, greeting rituals, same food every day)
- Highly restricted, fixated interests abnormal in intensity or focus (strong attachment to unusual objects, preoccupation with narrow topics)
- Hyper- or hyporeactivity to sensory input (apparent indifference to pain/temperature, adverse responses to specific sounds/textures, excessive smelling/touching, visual fascination)
Additional Criteria:
- Symptoms present in early developmental period (may not manifest until social demands exceed limited capacities)
- Symptoms cause clinically significant impairment
- Not better explained by intellectual disability or global developmental delay (ID and ASD can be comorbid)
2.2 Severity Levels
| Level | Social Communication | Restricted/Repetitive Behaviors |
|---|---|---|
| Level 1, "Requiring support" | Noticeable deficits without support; difficulty initiating interactions | Inflexibility causes significant interference; difficulty switching between activities |
| Level 2, "Requiring substantial support" | Marked deficits; limited initiation; atypical/reduced responses | RRBIs + inflexibility markedly obvious; distress when interrupted |
| Level 3, "Requiring very substantial support" | Severe deficits; very limited initiation; minimal response | Extreme difficulty with change; intense distress; greatly interferes with functioning |
Severity levels in ASD are NOT a longitudinal spectrum, level 1 doesn't automatically become level 3. They describe current support needs. Intellectual disability is a separate comorbidity, not captured by ASD level.
2.3 Early Signs and Red Flags
12-month red flags:
- No babbling
- No pointing, waving, or other gestures
- No response to name
18-month red flags:
- No single words
- Not following simple directions
- No pretend play
24-month red flags:
- No spontaneous two-word phrases (not echolalic)
- Any regression in language/social skills at any age
Additional early signs:
- Unusual visual inspection of objects
- Reduced joint attention (not following another's gaze/pointing)
- Lack of social smile in response to others
- Preference for objects over people
- Unusual sensory interests (sniffing, spinning)
- Distress at routine changes
2.4 Screening
M-CHAT-R/F (Modified Checklist for Autism in Toddlers, Revised with Follow-Up):
- Age: 16–30 months
- 20 yes/no questions for parents
- Scoring: Low risk (0–2), Medium risk (3–7, do follow-up interview), High risk (8–20)
- Sensitivity ~91%, specificity ~95% after follow-up interview
- Used in routine developmental surveillance
Other Screening Tools:
| Tool | Age | Rater | Notes |
|---|---|---|---|
| M-CHAT-R/F | 16–30 months | Parent | Primary screening |
| CHAT (Checklist for Autism in Toddlers) | 18 months | Parent + clinician | Original Baird tool |
| SCQ (Social Communication Questionnaire) | 4+ years | Parent | Screening, uses ADI-R items |
| ASSQ (Autism Spectrum Screening Questionnaire) | 7–16 years | Parent/Teacher | For higher-functioning ASD |
| AQ (Autism Quotient) | Adolescents/Adults | Self-report | Baron-Cohen |
2.5 Comprehensive Assessment
Diagnostic Instruments:
ADOS-2 (Autism Diagnostic Observation Schedule, 2nd Ed):
- Gold standard observational assessment
- Structured observation of social behavior
- 5 modules: Toddler Module (12–30 months, non-verbal), Module 1 (non-verbal/limited verbal), Module 2 (phrase speech), Module 3 (fluent verbal children/adolescents), Module 4 (adults)
- Trained administration required
- Generates Social Affect score + Restricted/Repetitive Behavior score
ADI-R (Autism Diagnostic Interview-Revised):
- Structured parent interview
- ~90–120 minutes
- Three domains: Social interaction, Communication, Repetitive/Stereotyped behaviors
- Algorithms different for "current" and "ever"
- Best used with ADOS-2 for comprehensive assessment
The "Gold Standard" diagnosis of ASD uses ADOS-2 + ADI-R together. Neither alone is sufficient for a definitive diagnosis. ADOS-2 captures current behavior; ADI-R captures developmental history.
Assessment Battery:
- Cognitive: Mullen Scales (infants), Leiter-3 (non-verbal), WISC-V (school age)
- Adaptive: Vineland Adaptive Behavior Scales (VABS-3)
- Language: CELF, Preschool Language Scales (PLS)
- Sensory: Sensory Profile (Dunn)
- Occupational therapy assessment
- Medical: genetics (chromosomal microarray), metabolic screen, hearing test, EEG (if seizure concern)
2.6 Comorbidities
| Comorbidity | Prevalence in ASD | Notes |
|---|---|---|
| Intellectual Disability | 30–40% | Higher at lower severity levels; separate diagnosis required |
| Epilepsy | 20–30% | Bimodal: onset <5 years and adolescence; particularly with ID comorbidity |
| ADHD | 50–70% | DSM-5 now allows dual diagnosis (previously excluded) |
| Anxiety Disorders | 40–60% | Often atypical presentation; social anxiety, generalized anxiety, specific phobias |
| Depression | 20–40% | Higher in higher-functioning ASD; often missed |
| Sleep Disorders | 50–80% | Insomnia, night waking; melatonin dysregulation |
| OCD | 17–37% | Distinguish from ASD RRBIs, ego-syntonic vs ego-dystonic |
| GI Problems | 50% | Constipation, GERD, feeding problems |
| Tic Disorders | 20–35% | May co-occur with Tourette's |
2.7 Interventions
Applied Behavior Analysis (ABA):
- Based on Skinnerian operant conditioning
- Discrete Trial Training (DTT): structured, adult-led, table-based skill acquisition
- Natural Environment Teaching (NET): skills taught in context
- Pivotal Response Training (PRT): targets pivotal behaviors (motivation, self-initiation)
- Evidence: strong for skill acquisition; concerns about intensity and child-led approaches
- Lovaas model: 40h/week intensive early intervention
Early Start Denver Model (ESDM):
- Developmentally informed + ABA-based hybrid
- Age: 12–60 months
- Adult follows child's lead; relationship-based
- 20–25h/week optimal
- Strong RCT evidence (Dawson et al., 2010): higher developmental gains vs treatment as usual
TEACCH (Treatment and Education of Autistic and Communication-Handicapped Children):
- Structured Teaching approach
- Visual supports, work systems, physical organization
- Less intensive; fits classroom/home
- Emphasizes predictability and visual information
Social Skills Training:
- Social Stories (Gray): scenarios written from child's perspective to explain social situations
- PEERS (Program for the Education and Enrichment of Relational Skills): UCLA; adolescents/adults; RCT evidence
Early intervention (before age 3) has strongest evidence, neural plasticity window. Regardless of which specific program, intensity and child-centered approach are the key variables.
2.8 Pharmacotherapy for ASD Comorbid Symptoms
| Target Symptom | Medication | Evidence Level |
|---|---|---|
| Irritability/aggression | Risperidone (FDA-approved age 5+), Aripiprazole (FDA-approved age 6+) | Strongest (multiple RCTs) |
| ADHD symptoms | Methylphenidate (lower response rate than non-ASD ADHD), Atomoxetine, Guanfacine | Moderate |
| Anxiety | SSRIs (fluoxetine, sertraline), limited RCT evidence in ASD | Limited |
| Insomnia | Melatonin (start 0.5–3mg) | Good for sleep onset |
| Self-injurious behavior | Naltrexone (adjunct), antipsychotics | Limited |
| Repetitive behaviors | SSRIs, mixed evidence | Limited/conflicting |
Risperidone and aripiprazole are the ONLY FDA-approved medications for ASD, specifically for irritability, aggression, and self-injurious behavior. No medication improves core social communication deficits.
2.9 Asperger's Disorder → ASD Transition
- Asperger's was a separate DSM-IV diagnosis: ASD features + normal language development + IQ ≥70
- DSM-5 eliminated Asperger's, subsumed into ASD Level 1
- ICD-11 also discontinued Asperger's
- Clinically: Asperger's = ASD Level 1, "without intellectual or language impairment"
- The terminology shift is frequently tested
PART 3: INTELLECTUAL DISABILITY (ID)
3.1 Definition and Classification
DSM-5: Three criteria:
- Deficits in intellectual functions (reasoning, problem-solving, planning, abstract thinking, judgment, academic learning, learning from experience) confirmed by clinical assessment AND standardized intelligence testing
- Deficits in adaptive functioning that fail to meet developmental/sociocultural standards for personal independence and social responsibility (across conceptual, social, and practical domains)
- Onset during developmental period
IQ Score Reference (NOT severity determinant in DSM-5):
- Mild: IQ 50–69
- Moderate: IQ 35–49
- Severe: IQ 20–34
- Profound: IQ <20
DSM-5 CRITICAL CHANGE: Severity in DSM-5 is determined by ADAPTIVE FUNCTIONING, not IQ score. A person with IQ 55 may have mild or moderate ID depending on adaptive functioning. ICD-11 aligns with this. IQ scores alone are insufficient.
ICD-11 Classification (6A00):
- 6A00.0, Mild (previously IQ 50–69)
- 6A00.1, Moderate (previously IQ 35–49)
- 6A00.2, Severe (previously IQ 20–34)
- 6A00.3, Profound (previously IQ <20)
- Note: ICD-11 emphasizes functional descriptors, not IQ alone
3.2 Adaptive Functioning Domains
3.3 Etiology
Genetic Causes:
| Condition | Genetics | Clinical Features | IQ Range |
|---|---|---|---|
| Down Syndrome (Trisomy 21) | Trisomy 21 (95%), Robertsonian translocation (4%), Mosaic (1%) | Flat facies, upslanting palpebral fissures, epicanthal folds, single palmar crease, hypotonia, cardiac defects (ASD/VSD), Alzheimer's (after 40) | Mild–Moderate |
| Fragile X Syndrome | CGG repeat expansion in FMR1 gene (Xq27.3); males affected | Long face, large ears, macro-orchidism, hand flapping, ADHD features, social anxiety, hyperkinesis | Mild–Moderate (males); females often normal–mild ID |
| Angelman Syndrome | Maternal UPD 15 or deletion | Happy demeanor, seizures, ataxic gait, absent/minimal speech, EEG pattern | Severe–Profound |
| Prader-Willi Syndrome | Paternal deletion 15q11 | Hyperphagia, obesity, short stature, hypogonadism, behavioral problems | Mild–Moderate |
| Phenylketonuria (PKU) | PAH gene mutation; AR | Preventable with dietary phenylalanine restriction; musty odor, fair complexion, seizures | Severe (if untreated) |
| Williams Syndrome | Deletion 7q11.23 (includes elastin gene) | "Cocktail party" personality, hypercalcemia, elfin facies, supravalvular aortic stenosis, relative strength in verbal/social over spatial | Mild–Moderate |
| Rett Syndrome | MECP2 mutation (X-linked); females | Regression at 6–18 months, hand-wringing stereotypies, breathing abnormalities, seizures | Severe |
| Tuberous Sclerosis | TSC1/TSC2 mutation; AD | Hamartomas (brain, skin, kidneys), ash-leaf spots, seizures, ASD features | Variable |
Fragile X is the most common INHERITED cause of intellectual disability. Down syndrome is the most common chromosomal cause. PKU is the most common PREVENTABLE metabolic cause.
Acquired Causes:
- Prenatal: rubella, CMV, toxoplasmosis, alcohol (FASD, leading preventable cause in developed countries), hypothyroidism, maternal PKU, radiation
- Perinatal: prematurity, birth asphyxia, hypoglycemia
- Postnatal: meningitis/encephalitis, head trauma, lead poisoning, severe deprivation
3.4 Assessment of Intellectual Disability
Intelligence Tests:
- Wechsler Preschool and Primary Scale (WPPSI-IV): 2.5–7 years
- Wechsler Intelligence Scale for Children (WISC-V): 6–16 years
- Stanford-Binet 5 (SB5): 2–85 years
- Leiter-3: non-verbal; suitable for non-English speakers, hearing impaired, ASD
Adaptive Behavior Scales:
- Vineland Adaptive Behavior Scales-3 (VABS-3): standard for clinical/research
- Adaptive Behavior Assessment System-3 (ABAS-3)
- AAMR Adaptive Behavior Scale (ABS)
3.5 Behavioral Phenotypes
3.6 Comorbid Psychiatric Disorders in ID
- Prevalence of psychiatric disorder in ID: 30–40% (3–4x higher than general population)
- Diagnostic overshadowing: psychiatric symptoms attributed to ID rather than recognized as separate disorder
- Communication impairment makes diagnosis challenging
- Modified diagnostic criteria (DC-LD in UK) developed for this population
Common presentations:
- ADHD: most common behavioral disorder in ID
- Anxiety: often presents as increased behavioral disturbance
- Depression: may present as self-injurious behavior, appetite/sleep changes, withdrawal
- Psychosis: lifetime prevalence 3x higher; positive symptoms less systematized
- Stereotypic movement disorder (especially severe/profound ID)
PART 4: CONDUCT DISORDER AND OPPOSITIONAL DEFIANT DISORDER
4.1 Oppositional Defiant Disorder (ODD)
DSM-5 Criteria: Pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness lasting ≥6 months (≥4 symptoms from at least 1 category):
Angry/Irritable Mood:
- Often loses temper
- Often touchy or easily annoyed
- Often angry and resentful
Argumentative/Defiant Behavior:
- Often argues with authority figures
- Often actively defies/refuses to comply with rules
- Often deliberately annoys others
- Often blames others for mistakes
Vindictiveness:
- Spiteful/vindictive at least twice in past 6 months
Severity: Mild (one setting), Moderate (two settings), Severe (three+ settings)
ODD Specifier, Limited Prosocial Emotions (Callous-Unemotional traits):
- Lack of remorse/guilt
- Callousness/lack of empathy
- Unconcerned about performance
- Shallow/deficient affect
The "Limited Prosocial Emotions" specifier in ODD (and CD) identifies callous-unemotional (CU) traits. This is clinically important, CU traits predict worse prognosis, poorer response to standard behavioral interventions, and greater risk for adult psychopathy. Treatment modifications needed.
4.2 Conduct Disorder (CD)
DSM-5 Criteria: Repetitive pattern of behavior violating rights of others or societal norms, at least 3 criteria in past 12 months (at least 1 in past 6 months) from four categories:
Aggression to people/animals (7 criteria):
- Bullies, threatens, intimidates others
- Initiates physical fights
- Used weapon that can cause serious physical harm
- Physically cruel to people
- Physically cruel to animals
- Stolen while confronting victim (mugging, purse-snatching)
- Forced sexual activity
Destruction of property (2 criteria):
- Deliberately set fires
- Deliberately destroyed others' property
Deceitfulness/theft (3 criteria):
- Broken into building/car/house
- Lies to obtain goods/favors
- Stolen items without confronting victim (shoplifting)
Serious violations of rules (3 criteria):
- Stays out at night despite parental prohibition (before age 13)
- Run away from home overnight at least twice
- Truant from school (before age 13)
Specifiers:
- Childhood-onset type (before 10): worse prognosis, more male, often with ADHD
- Adolescent-onset type: more female, better prognosis, peer-influenced
- Unspecified onset
- Limited Prosocial Emotions: as above
Severity: Mild, Moderate, Severe
4.3 Differential Diagnosis: ADHD vs ODD vs CD
| Feature | ADHD | ODD | CD |
|---|---|---|---|
| Core behavior | Inattention/hyperactivity | Defiance/irritability | Rule violation/aggression |
| Intentionality | Unintentional | Deliberate but reactive | Deliberate and planned |
| Comorbidity | Can have ODD/CD | Often with ADHD | Often with ADHD |
| Aggression | Reactive, unplanned | Reactive to perceived provocation | Proactive/predatory possible |
| Conscience development | Normal | Normal | May be impaired (CU traits) |
| Peer relationships | Difficulty due to impulsivity | Difficulty due to defiance | May have delinquent peer group |
ODD and CD are comorbid with ADHD in 30–50% of cases. When all three co-occur, treat ADHD first, behavioral problems often improve. CD without ADHD typically has intact working memory.
4.4 Risk Factors for CD
Individual: male sex, ADHD, low IQ, callous-unemotional traits, impulsivity, early behavioral problems, reading difficulties
Family: parental antisocial personality, substance abuse, domestic violence, harsh/inconsistent discipline, child abuse/neglect, large family size, low socioeconomic status
Peer: association with deviant peers (particularly adolescent-onset CD)
Community: neighborhood violence, poverty, poor school environment
4.5 Management of CD/ODD
Behavioral:
- Parent Management Training (PMT): Strongest evidence, Patterson Oregon Social Learning Model, Webster-Stratton's Incredible Years
- Multisystemic Therapy (MST): community-based, addresses family/school/peers simultaneously; best evidence for serious antisocial behavior in adolescents
- Functional Family Therapy (FFT): family-based
- Problem-Solving Skills Training (PSST)
Pharmacological:
- No specific medication for CD/ODD
- Treat comorbid ADHD (stimulants reduce aggression significantly)
- Mood stabilizers (lithium, valproate): for severe impulsive aggression
- Atypical antipsychotics: risperidone for severe, treatment-refractory aggression
- SSRIs: for comorbid anxiety/depression
MST (Multisystemic Therapy) is the evidence-based gold standard for adolescent CD with serious antisocial behavior. It is community-based, addresses multiple systems simultaneously (Bronfenbrenner ecological model), and has RCT support.
PART 5: CHILDHOOD ANXIETY AND DEPRESSION
5.1 Separation Anxiety Disorder
DSM-5 Criteria: Developmentally inappropriate and excessive fear/anxiety concerning separation from attachment figures, at least 3 symptoms for ≥4 weeks (children; ≥6 months adults):
- Recurrent excessive distress when anticipating/experiencing separation
- Persistent worrying about losing attachment figures or possible harm (illness, injury, disaster)
- Persistent worrying about untoward event causing separation (getting lost, kidnapped)
- Reluctance/refusal to go out, away from home, to school due to fear of separation
- Persistent excessive fear about being alone
- Persistent reluctance/refusal to sleep away from home
- Repeated nightmares involving separation theme
- Repeated somatic complaints when separation occurs/anticipated
Most common anxiety disorder in young children (under 12)
Treatment:
- First-line: CBT (exposure hierarchy, cognitive restructuring, relaxation)
- Medication if moderate-severe: sertraline, fluoxetine
- Family involvement essential, parental accommodation (enabling avoidance) is a key maintenance factor
5.2 Selective Mutism
DSM-5: Consistent failure to speak in specific social situations despite speaking in others (typically speaks at home, mute at school/social settings) for ≥1 month (not limited to first month of school).
- Most commonly presents at school entry (age 5–6)
- Distinct from language disorder, can speak normally in comfortable settings
- Likely extreme social anxiety rather than a separate anxiety disorder
- Strong overlap with social anxiety disorder
Treatment:
- Behavioral: stimulus fading, shaping, positive reinforcement
- Gradual exposure: whisper → record voice → speak to trusted adult → small group
- SSRI (fluoxetine most evidence) for moderate-severe cases
- School consultation essential
5.3 School Refusal
Not a DSM diagnosis, a behavioral problem with multiple causes:
| Type | Cause | Features |
|---|---|---|
| Separation anxiety | Fear of leaving home/attachment figure | Somatic complaints (morning), relieved on staying home |
| Social/performance anxiety | Fear of social situations, evaluation | Avoids specific situations (tests, PE, lunch) |
| Specific phobia | Fear of specific school stimuli | Avoidance of specific classroom/teacher |
| Truancy/CD | Desire to be elsewhere | No distress, leaves home but not school-bound |
Kearney & Silverman (2000) functional model:
- Avoid stimuli provoking negative affect
- Escape aversive social/evaluative situations
- Pursue attention from significant others
- Pursue tangible reinforcement outside school
Treatment: Rapid return to school (even partial attendance) is critical, prolonged absence worsens prognosis. CBT, family therapy, school liaison.
5.4 Pediatric Depression
Clinical features:
- Similar to adult depression but with developmentally unique features:
- Irritable mood may substitute for depressed mood (in children especially)
- More somatic complaints
- Cognitive distortions tend to be developmentally simpler
- Social withdrawal, school refusal
- Anhedonia may manifest as boredom
Treatment, TADS (Treatment for Adolescents with Depression Study):
- Fluoxetine alone: 61% response
- CBT alone: 43% response
- Combination: 71% response (superior)
- Placebo: 35% response
TADS is the landmark study for pediatric depression treatment. Combined fluoxetine + CBT is most effective. Fluoxetine is the only FDA-approved antidepressant for depression in children (age 8+). Escitalopram FDA-approved for adolescents (12+).
Black Box Warning: All antidepressants carry FDA black box warning for increased suicidal ideation in children and adolescents. This does NOT mean risk of completed suicide, actual completed suicide risk is reduced with treatment. The warning led to underprescription, which is its own problem.
5.5 Suicidality in Children
- Suicidal ideation: ~10–15% of adolescents
- Suicide attempt: ~8% adolescents
- Completed suicide: 3rd leading cause of death in 15–24 age group (US)
- Methods in children: less lethal on average; cognitive concreteness limits planning
- Risk factors: depression, previous attempt, family history, substance use, bullying, LGBTQ+ youth, impulsivity
- Protective factors: family support, school connectedness, help-seeking
Assessment: Columbia Suicide Severity Rating Scale (C-SSRS)
PART 6: TIC DISORDERS AND TOURETTE SYNDROME
6.1 Classification
Tic characteristics:
- Sudden, rapid, recurrent, nonrhythmic
- Motor: simple (eye blinking, nose wrinkling) or complex (gestures, echopraxia, copropraxia)
- Vocal: simple (sniffing, throat clearing) or complex (echolalia, palilalia, coprolalia)
- Coprolalia (uttering obscene words): present in <10–15% of Tourette's, NOT required for diagnosis
- Premonitory urge: sensation before tic that is relieved by performing the tic
- Can suppress temporarily (at cost of discomfort)
- Wax and wane; worse with stress, fatigue, excitement
Coprolalia is NOT required for Tourette diagnosis. It is present in only 10–15% of cases. This is a very common misconception tested in exams.
6.2 Epidemiology
- Tourette prevalence: 0.3–1% children
- Male:Female: 4:1
- Peak severity: 10–12 years; typically improves in adolescence/adulthood
- Comorbidities: ADHD (50–60%), OCD (30–50%), anxiety (30%), depression (25%)
6.3 Neurobiology
- Cortico-striato-thalamo-cortical (CSTC) circuit dysfunction
- Dopaminergic excess in striatum
- Glutamatergic and GABAergic dysregulation
6.4 Treatment
Behavioral, CBIT (Comprehensive Behavioral Intervention for Tics):
- First-line for mild-moderate tics
- Components: Habit Reversal Training (HRT) + functional intervention
- HRT: awareness training → competing response training → social support
- RCT evidence: superior to supportive therapy (Wilhelm et al., 2012)
Pharmacotherapy:
| Medication | Class | Notes |
|---|---|---|
| Haloperidol | Typical antipsychotic | Most evidence; effective but side effects (EPS, tardive dyskinesia) limit use |
| Pimozide | Typical antipsychotic | QTc prolongation monitoring needed |
| Fluphenazine | Typical antipsychotic | Less studied |
| Risperidone | Atypical antipsychotic | Better tolerated; moderate efficacy |
| Aripiprazole | Atypical antipsychotic | Increasingly preferred; good tolerability |
| Clonidine | α2 agonist | Particularly useful when ADHD comorbid; modest tic reduction |
| Guanfacine | α2A agonist | Similar to clonidine; less sedating |
| Topiramate | Antiepileptic | Some evidence |
| Tetrabenazine | VMAT2 inhibitor | Severe tics; watch for depression |
Current preference: start with CBIT. If medication needed, aripiprazole or clonidine/guanfacine (especially with comorbid ADHD) before haloperidol. Haloperidol has most evidence but worst side effects, exam may ask which has most evidence (haloperidol) vs current clinical preference (aripiprazole).
PART 7: ENURESIS AND ENCOPRESIS
7.1 Enuresis
DSM-5 Criteria:
- Repeated voiding of urine into bed or clothes (involuntary or intentional)
- At least twice weekly for at least 3 consecutive months OR significant distress/impairment
- Chronological age ≥5 years (or developmental equivalent)
- Not due to substance or medical condition
Types:
- Nocturnal only: Most common; during sleep
- Diurnal only: Daytime; often with urgency; evaluate for urological cause
- Nocturnal and diurnal: Both
Primary vs Secondary:
- Primary: Never established continence (for >6 consecutive months)
- Secondary: Onset after at least 6 months of continence
Secondary enuresis (onset after established dryness) warrants more vigorous evaluation for organic causes (UTI, diabetes mellitus, diabetes insipidus, emotional stressors) and psychosocial stressors.
Epidemiology:
- 5 years: 7% boys, 3% girls
- 10 years: 3% boys, 2% girls
- Spontaneous resolution ~15%/year
Etiology: Multifactorial, maturational delay, reduced nocturnal bladder capacity, high arousal threshold, ADH deficiency, genetic factors
Treatment:
| Modality | Evidence | Notes |
|---|---|---|
| Bell-and-pad (Urine alarm) | Best long-term; 75–85% success | Conditioning treatment; requires 8–12 weeks; best relapse prevention |
| Desmopressin (DDAVP) | Rapid effect; relapse on stopping | ADH analogue; reduces urine output; available as intranasal or tablet; watch for hyponatremia |
| Imipramine | Second-line; 40–50% success | High relapse; cardiac side effects; toxic in overdose; falling out of favor |
| Bladder training | Mild benefit | Works best for diurnal enuresis |
| Motivational therapy | Combined with above | Reward systems, not punishment |
7.2 Encopresis
DSM-5 Criteria:
- Repeated passage of feces into inappropriate places (floor, clothing), involuntary or intentional
- At least once monthly for at least 3 months
- Chronological age ≥4 years
- Not due to substance or medical condition
Types:
- With constipation and overflow incontinence: Most common (>80%); liquid/semi-liquid stool leaks around impacted hard stool
- Without constipation/overflow incontinence: Less common; may be related to CD, anger, trauma
Treatment:
- Disimpaction (enema/polyethylene glycol)
- Maintenance stool softeners (polyethylene glycol/lactulose)
- Behavioral: scheduled toilet sitting (15 min after meals, gastrocolic reflex), reward systems
- High-fiber diet, fluid intake
- CBT/family therapy if psychosocial factors dominant
PART 8: CHILD ABUSE AND NEGLECT
8.1 Types and Definitions
| Type | Definition | Clinical Indicators |
|---|---|---|
| Physical abuse | Non-accidental physical injury | Bruises in unusual locations (torso, buttocks, ears), patterned bruises, burns (cigarette, immersion), fractures in unusual ages/locations |
| Sexual abuse | Sexual activity with child without consent/understanding | Genital/rectal injuries, STIs, sexualized behavior, regression |
| Emotional/Psychological abuse | Pattern of behavior damaging emotional development | Failure to thrive, severe behavioral problems, low self-esteem, depression |
| Neglect | Failure to provide basic needs | Poor hygiene, developmental delay, failure to thrive, unsupervised |
| Medical neglect | Failure to provide medical care | Untreated illness, missed vaccinations |
8.2 Physical Indicators
Bruises suspicious for abuse:
- Torso, ears, neck in pre-mobile infants
- Patterned bruises (belt buckle, cord, hand)
- Multiple bruises in various stages of healing
- TEN-4 FACES P mnemonic (see mnemonics file)
Burns suspicious for abuse:
- Cigarette burns: circular, punched-out appearance
- Immersion burns: sharply demarcated "stocking/glove" distribution
- Contact burns: exact shape of object
Fractures suspicious for abuse:
- In children <2 years (especially <1 year)
- Posterior rib fractures (bucket-handle metaphyseal fractures)
- Multiple fractures in different stages of healing
- Spiral fractures in non-ambulatory children
- Skull fractures (particularly bilateral, crossing sutures)
Abusive Head Trauma (Shaken Baby Syndrome):
- Subdural hematoma (especially bilateral interhemispheric)
- Diffuse axonal injury
- Retinal hemorrhages (highly specific)
- No external signs of injury necessarily
- Mechanism: acceleration-deceleration
Retinal hemorrhages in a young infant with subdural hematoma and no clear accidental mechanism = abusive head trauma until proven otherwise. The combination is highly specific for non-accidental injury.
8.3 Munchausen by Proxy (Factitious Disorder Imposed on Another)
DSM-5 term: Factitious Disorder Imposed on Another
- Caregiver fabricates or induces symptoms in a child
- Motivation: to assume sick role vicariously, attention/sympathy
- Perpetrator: most commonly the mother (>90%)
- Child presents with recurrent, unexplained, treatment-refractory illness
- May involve inducing illness (poisoning, suffocation, adding blood to urine samples)
- Perpetrator appears devoted, knowledgeable, calm despite child's illness
- Illness resolves when child separated from perpetrator
Red flags:
- Symptoms only witnessed by caregiver
- Multiple unexplained symptoms, negative investigations
- Symptoms resolve with separation from caregiver
- Caregiver with medical knowledge and unusual calm
8.4 Child Sexual Abuse (CSA)
- Prevalence estimates: 1 in 4 girls, 1 in 13 boys (CDC)
- Most common perpetrator: known to child (family member or trusted adult, ~90%)
- Grooming: gradual normalization of sexual contact
- Physical examination: most CSA leaves no physical evidence (hymenal changes in <5%)
- Behavioral indicators: age-inappropriate sexual knowledge/behavior, regressive behavior, sleep disturbance, school problems, depression, PTSD symptoms
8.5 Forensic Interview
- Purpose: gather accurate information while minimizing trauma
- Must be conducted by trained professionals
- NICHD Protocol (National Institute of Child Health and Human Development), gold standard
- RATAC (CornerHouse Approach) / ChildFirst (Cornelsen)
- Principles: open-ended questions first, avoid leading questions, avoid multiple interviews
- Child interview before medical examination when possible
8.6 Mandatory Reporting
- In most jurisdictions: all healthcare professionals are mandatory reporters
- Reasonable suspicion (not certainty) is sufficient to report
- Responsibility is to report to child protection services, not to investigate
- Clinician-patient confidentiality does NOT prevent mandatory reporting of suspected child abuse
In India, the Protection of Children from Sexual Offences (POCSO) Act 2012 mandates reporting of child sexual abuse. Failure to report is a criminal offense. Know this for the Indian context exam.
8.7 Long-term Consequences of Abuse
PART 9: GAMING DISORDER
9.1 ICD-11 Classification
ICD-11 Code 6C51, Gaming Disorder
Criteria (all must be present for at least 12 months; shorter if severe):
- Impaired control over gaming (onset, frequency, intensity, duration, termination, context)
- Increasing priority given to gaming to the extent that it takes precedence over other life interests and daily activities
- Continuation or escalation of gaming despite occurrence of negative consequences
Gaming behavior must result in significant impairment in personal, family, social, educational, occupational, or other important areas of functioning.
ICD-11 recognizes Gaming Disorder; DSM-5 lists "Internet Gaming Disorder" as a condition for further study (not official diagnosis). For exam purposes: ICD-11 has the official diagnosis.
9.2 Epidemiology
- Prevalence estimates: 1–10% (wide range due to definitional differences)
- More common in males, adolescents
- Asia-Pacific: higher rates (South Korea 10.2%, China 10%)
- Comorbidities: ADHD, social anxiety, depression, insomnia
9.3 Neurobiological Overlap
- Similar to substance use disorders: striatal dopamine, PFC-dependent inhibitory control
- Cue reactivity: gaming cues activate reward circuitry similarly to drug cues
- Reduced grey matter: prefrontal cortex, insula, inferior frontal gyrus
9.4 Management
Assessment: IGDS (Internet Gaming Disorder Scale), CAGE-adapted for gaming
Treatment:
- CBT: most evidence; cognitive restructuring, behavioral strategies, scheduling
- Motivational interviewing: for ambivalent users
- Family therapy: address enabling behaviors, improve communication
- Pharmacotherapy: no specific agent; treat comorbid ADHD/depression/anxiety
- Inpatient programs: "digital detox", structured settings; limited evidence
PART 10: SPECIFIC LEARNING DISORDERS
10.1 DSM-5 Classification
DSM-5 Code 315, Specific Learning Disorder (SLD)
Criteria:
- Difficulties learning and using academic skills for ≥6 months despite intervention
- Affected skills substantially below expectations for age
- Learning difficulties evident in school years (may not fully manifest until demands exceed capacities)
- Not accounted for by intellectual disability, sensory problems, inadequate instruction
Specify:
- With impairment in reading (dyslexia specifier)
- With impairment in written expression (dysgraphia specifier)
- With impairment in mathematics (dyscalculia specifier)
Severity: Mild, Moderate, Severe
10.2 Dyslexia
Core deficit: Phonological processing, difficulty mapping letters to sounds (grapheme-phoneme correspondence)
Features:
- Slow, effortful, inaccurate reading
- Difficulty with phonemic awareness (identifying/manipulating sounds in words)
- Spelling difficulties
- Family history strong
- IQ is typically average or above
- Secondary: reading avoidance, underachievement
Prevalence: 5–15% of school-age children; most common SLD
Neurobiological: Left hemisphere temporal-parietal-occipital dysfunction; reduced activation in reading networks (Shaywitz et al.)
Treatment: Systematic phonics instruction (Orton-Gillingham approach; Science of Reading movement), multisensory instruction, reading support
10.3 Dyscalculia
- Difficulty with number sense, arithmetic facts, calculation
- Spatial processing deficits contribute
- Prevalence: 3–7%
- Neurobiological: right parietal lobe (intraparietal sulcus) dysfunction
- Treatment: concrete manipulatives, visual representations, number line strategies
10.4 Dysgraphia (Impairment in Written Expression)
- Difficulty with handwriting mechanics AND/OR compositional aspects
- Motor dysgraphia: poor letter formation, letter size/spacing irregularities
- Language-based dysgraphia: correct letters but poorly organized written content
- Treatment: occupational therapy, keyboarding as alternative, graphic organizers
PART 11: ATTACHMENT DISORDERS
11.1 Background
Attachment theory (Bowlby): children develop internal working models of relationships based on early caregiver interactions. Secure base concept. Ainsworth Strange Situation identified attachment patterns.
Attachment patterns:
- Secure: uses caregiver as safe base; exploration + reunion
- Insecure-Avoidant: minimal distress; avoids caregiver on reunion
- Insecure-Ambivalent/Resistant: high distress; ambivalent on reunion
- Disorganized: no coherent strategy; associated with trauma/maltreatment (Main & Hesse)
11.2 Reactive Attachment Disorder (RAD)
DSM-5 Criteria:
- Consistent pattern of inhibited, emotionally withdrawn behavior toward adult caregivers (at least 2 of):
- Child rarely seeks comfort when distressed
- Child rarely responds to comfort when offered
- Persistent social/emotional disturbance (at least 2 of):
- Minimal social/emotional responsiveness
- Limited positive affect
- Episodes of irritability, sadness, or fearfulness during non-threatening interactions
- History of extremes of insufficient care (social neglect, limited caregiving opportunities, multiple changes in primary caregivers, rearing in unusual settings that limit opportunities)
- Not better explained by ASD
- Evident before age 5
RAD requires a history of severe deprivation/neglect as a PREREQUISITE. It cannot be diagnosed without this context. Must distinguish from ASD.
11.3 Disinhibited Social Engagement Disorder (DSED)
DSM-5 Criteria:
- Pattern of behavior in which child actively approaches and interacts with unfamiliar adults, at least 2 of:
- Reduced or absent reticence with unfamiliar adults
- Overly familiar verbal or physical behavior
- Diminished or absent checking back with adult caregiver after venturing away
- Willingness to go off with unfamiliar adult
- Behavior not limited to impulsivity but includes disinhibited social engagement
- History of extremes of insufficient care
- May co-exist with ADHD (distinguish from ADHD impulsivity)
Key Difference from RAD:
| Feature | RAD | DSED |
|---|---|---|
| Core pattern | Inhibited, withdrawn | Disinhibited, indiscriminate social engagement |
| Caregiver relationship | Withdrawn from caregivers | Not attached but socially active with strangers |
| Response to care | Improves with stable caregiving | May persist even after stable caregiving |
| ASD confusion | Can be confused with ASD | Less confusion with ASD |
| AD/ADHD comorbidity | Less common | DSED + ADHD possible |
PART 12: ADDITIONAL HIGH-YIELD TOPICS
12.1 Childhood Disintegrative Disorder (Now Under ASD)
- DSM-5 subsumed into ASD
- Previously: normal development until ≥2 years, then marked regression in ≥2 domains
- Prognosis: worse than autistic disorder without regression
- Rule out Rett syndrome, Landau-Kleffner syndrome, metabolic disorders
12.2 Pica
DSM-5: Persistent eating of non-nutritive, non-food substances for ≥1 month; developmentally inappropriate (≥2 years); not culturally sanctioned
- Common in ID and ASD
- Risk: lead poisoning, intestinal obstruction, infections (toxocariasis, toxoplasmosis)
- Iron deficiency anemia may cause and result from pica
- Treatment: nutritional supplementation if deficiency, behavioral strategies, address underlying ID/ASD
12.3 Rumination Disorder
- Repeated regurgitation of food for ≥1 month
- Not due to medical condition, anorexia, or bulimia
- May be self-stimulatory in ID
- Habit reversal training, diaphragmatic breathing
12.4 Avoidant/Restrictive Food Intake Disorder (ARFID)
- Extreme food restriction not driven by body image concerns
- Common in ASD (sensory avoidance of textures/smells), ADHD
- Can lead to nutritional deficiencies, failure to thrive
12.5 Developmental Coordination Disorder (DCD)
- Motor skills substantially below age expectations
- Clumsy, slow, inaccurate motor performance
- Not explained by ID, visual impairment, neurological condition
- Often co-occurs with ADHD, dyslexia
- Treatment: occupational therapy, motor skill training
KEY PHARMACOLOGY SUMMARY
| Drug | Primary Use in Child Psych | Mechanism | Key Side Effects |
|---|---|---|---|
| Methylphenidate | ADHD | DAT/NET blocker | Anorexia, insomnia, growth suppression, tachycardia |
| Amphetamine | ADHD | DAT/NET blocker + releaser | Same + more appetite suppression |
| Lisdexamfetamine | ADHD, Binge Eating | Prodrug → d-AMP | Same as amphetamine; lower abuse liability |
| Atomoxetine | ADHD | Selective NET inhibitor | GI, activation, hepatotoxicity (rare), suicidality (BBW) |
| Guanfacine ER | ADHD, tics | α2A agonist | Sedation, bradycardia, hypotension |
| Clonidine ER | ADHD, tics, sleep | α2 agonist | Sedation, bradycardia, rebound hypertension |
| Fluoxetine | MDD (age 8+), OCD, anxiety | SSRI | GI, activation, suicidality (BBW), serotonin syndrome |
| Sertraline | Anxiety, OCD | SSRI | Similar to fluoxetine |
| Escitalopram | Depression (age 12+) | SSRI | Similar |
| Risperidone | ASD irritability, aggression | D2/5HT2A antagonist | EPS, weight gain, prolactin elevation, metabolic |
| Aripiprazole | ASD irritability, tics | Partial D2 agonist | Weight gain, akathisia, less metabolic than risperidone |
| Haloperidol | Tics | Potent D2 blocker | EPS, tardive dyskinesia, NMS |
| Melatonin | Sleep in ASD/ADHD | MT1/MT2 agonist | Generally safe; long-term studies limited |
| Desmopressin | Enuresis | V2 agonist (ADH analogue) | Hyponatremia (water restriction needed) |
| Imipramine | Enuresis | TCA | Cardiac arrhythmia, anticholinergic, toxic in overdose |
EXAM PEARL, ONLY FDA-APPROVED: - Methylphenidate/amphetamine: ADHD (age 6+) - Atomoxetine: ADHD (age 6+) - Fluoxetine: MDD (age 8+), OCD (age 7+) - Sertraline: OCD (age 6+) - Fluvoxamine: OCD (age 8+) - Risperidone: Irritability in ASD (age 5+), schizophrenia (age 13+), bipolar (age 10+) - Aripiprazole: Irritability in ASD (age 6+), schizophrenia (age 13+), bipolar (age 10+) - Clomipramine: OCD (age 10+) - Escitalopram: MDD (age 12+) - Dextroamphetamine: ADHD (age 3+)
| *Sources: Kaplan & Sadock's Comprehensive Textbook of Psychiatry (11th ed.) | Rutter's Child and Adolescent Psychiatry (6th ed.) | Lewis's Child and Adolescent Psychiatry (5th ed.) | DSM-5-TR | ICD-11* |
|---|
Model Answers
Sources: Kaplan & Sadock (11th ed.), Rutter's Child and Adolescent Psychiatry (6th ed.), Lewis's Child and Adolescent Psychiatry (5th ed.), DSM-5-TR, ICD-11
Q1. Discuss the assessment and management of a 9-year-old boy presenting with poor attention, hyperactivity, and academic difficulties. (20 marks)
Introduction
Attention Deficit Hyperactivity Disorder (ADHD) is the most common neurodevelopmental disorder of childhood, with a prevalence of 5–7% in school-age children. The clinical presentation of inattention, hyperactivity, and impulsivity resulting in academic and functional impairment warrants a comprehensive biopsychosocial assessment.
Assessment
History:
A thorough history from multiple informants is essential:
From parents:
- Detailed developmental history: prenatal exposures (alcohol, tobacco, infections), birth complications, perinatal events, developmental milestones (language, motor, social)
- Onset, duration, and severity of current symptoms
- Description of behaviors across settings (home, family gatherings, structured vs. unstructured play)
- Academic history: school reports, teacher feedback, grade retention
- Family history: ADHD, learning disabilities, mood disorders, substance use
- Medical history: thyroid dysfunction, seizure disorders, hearing/vision problems, lead exposure, iron deficiency
- Sleep history (insomnia, snoring suggesting OSA, can mimic ADHD)
- Medication history
From teachers (ideally via standardized rating scales):
- Classroom behavior
- Academic performance
- Peer relationships
- Response to current management strategies
Mental Status Examination:
- Motor behavior: activity level, coordination, tics
- Attention: sustained attention, distractibility
- Speech/language: fluency, receptive/expressive language
- Mood and affect: irritability, anxiety
- Cognitive: estimate of intelligence
Investigations:
- Standardized rating scales: Conners-3 (parent + teacher), SNAP-IV, Vanderbilt
- Psychological/neuropsychological testing: WISC-V (full cognitive profile), BRIEF (executive function), reading assessment if learning disability suspected
- Medical workup: thyroid function (if clinical indication), lead levels (if exposure history), vision and hearing screen, ECG if considering stimulant with cardiac concern
Differential Diagnosis:
Diagnostic Criteria (DSM-5):
Diagnosis requires: (1) ≥6 inattentive symptoms AND/OR ≥6 hyperactive-impulsive symptoms for ≥6 months; (2) several symptoms present before age 12; (3) impairment in ≥2 settings; (4) not explained by other mental disorder.
Management
Multimodal Treatment Plan:
1. Psychoeducation:
- Explain ADHD as a neurodevelopmental disorder, not laziness or poor parenting
- Brain-based explanation (PFC dopamine/NE dysregulation)
- Information about treatment options, prognosis, realistic expectations
- Parent support groups, CHADD (Children and Adults with ADHD) resources
2. Behavioral Interventions (first-line for age 4–5; adjunct for school-age):
Behavioral Parent Training (BPT):
- Triple P, Incredible Years, Parent-Child Interaction Therapy (PCIT)
- Skills: positive attention, reward systems, clear instructions, consistent consequences, planned ignoring
School-based interventions:
- Daily Report Card (DRC): home-school communication
- Preferential seating (front, away from distractors)
- Extended time on tests, reduced homework load
- Frequent brief breaks, movement opportunities
- Simplified instructions, visual cues
3. Pharmacotherapy:
First-line: Methylphenidate (MPH)
| Formulation | Dose | Notes |
|---|---|---|
| IR MPH (Ritalin) | 5mg BD-TID; max 60mg/day | Fast onset 30–60 min; rebound effect |
| LA MPH (Concerta) | 18mg OD; titrate by 18mg; max 54mg | Once-daily dosing; better adherence |
Titration: Start low (0.3 mg/kg/day), increase weekly by 0.1 mg/kg increments, target 0.5–1.0 mg/kg/day based on response and tolerability.
Monitoring: Height/weight (monthly initially), BP/HR, appetite, sleep, mood, tic observation
Side effect management:
- Appetite suppression: give medication AFTER breakfast; high-calorie dinner
- Insomnia: take medication earlier; avoid afternoon doses
- Growth: measure height biannually; drug holidays if significant suppression
If stimulants fail or contraindicated: Atomoxetine (selective NRI), 1.2 mg/kg/day target, takes 4–6 weeks for full effect.
4. Academic and Educational Planning:
- Formal IEP (Individualized Education Plan) if in formal school system
- Remedial teaching for specific academic deficits
- Occupational therapy for fine motor/writing difficulties
- Social skills training if interpersonal difficulties prominent
5. Monitoring and Follow-Up:
- Monthly for first 3 months: response, side effects, dose adjustment
- 3-monthly thereafter: academic performance, weight/height, blood pressure
- Annual: reassess diagnosis, medication need, consider drug holiday
The MTA study showed medication superior to behavioral therapy alone for core ADHD symptoms in children ≥6 years. Combined treatment is best for anxiety comorbidity. Medication is not effective in isolation, psychoeducation and school supports are always needed.
Q2. Describe the clinical features of Autism Spectrum Disorder (ASD) and outline a comprehensive assessment pathway. (15 marks)
Introduction
Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by persistent deficits in social communication and social interaction, alongside restricted, repetitive behaviors, interests, and activities (RRBIs). It is classified under ICD-11 as 6A02 and follows DSM-5 criteria for diagnosis.
Clinical Features
Domain 1, Social Communication and Interaction Deficits (all three present):
- Social-emotional reciprocity:
- Reduced sharing of interests, emotions
- Atypical social approach
- Failure to initiate or respond to social interactions
- Abnormal back-and-forth conversation
- Nonverbal communicative behaviors:
- Reduced eye contact
- Limited facial expressions
- Absent or atypical gesture use
- Poor integration of verbal/nonverbal communication
- Relationship development:
- Difficulty adjusting behavior to social context
- Difficulty making and maintaining friendships
- Absent interest in peers (not social anxiety, indifference)
Domain 2, Restricted, Repetitive Behaviors and Interests (≥2 present):
- Stereotyped/repetitive behaviors:
- Hand-flapping, rocking, spinning
- Lining up objects
- Echolalia (immediate or delayed)
- Insistence on sameness:
- Rigid routines
- Extreme distress at minor changes
- Ritualized patterns of behavior
- Fixated interests:
- Intense, narrow preoccupations
- Atypical in focus or intensity (e.g., specific bus routes, vacuum cleaners)
- Sensory abnormalities:
- Hyperreactivity (distress to textures, sounds)
- Hyporeactivity (indifference to pain, temperature)
- Sensory-seeking behaviors (sniffing, spinning, mouthing)
Early red flags (12 months): No babbling, no gestures, no response to name
Early red flags (18 months): No words, no pretend play, no joint attention
Early red flags (24 months): No spontaneous two-word phrases; any regression
Severity Levels (DSM-5)
| Level | Support Needed | Social Communication | RRBIs |
|---|---|---|---|
| 1 | Support | Noticeable deficits with minimal support; difficulty initiating | Inflexibility significantly interferes; difficulty switching |
| 2 | Substantial support | Marked deficits; limited initiation; atypical responses | Markedly obvious; distress when interrupted |
| 3 | Very substantial support | Severe deficits; minimal response | Extreme difficulty changing; intense distress |
Assessment Pathway
Step 1, Developmental Surveillance and Screening:
- Routine developmental checks at 9, 18, 24, 36 months
- M-CHAT-R/F at 16–30 months (sensitivity 91% after follow-up)
- Any regression in language or social skills warrants immediate referral
Step 2, Comprehensive Developmental Pediatric/Child Psychiatry Assessment:
History:
- Detailed developmental history (prenatal, perinatal, milestones)
- Regression history (when, how much, over what timeframe)
- Current social, language, behavioral functioning
- Family history (ASD, ADHD, ID, language delay)
- Medical history (seizures, GI symptoms, sleep)
Physical examination:
- Dysmorphic features (genetic syndrome screening)
- Skin: ash-leaf spots (TS), cafe-au-lait spots (NF1)
- Neurological examination
- Growth parameters
Step 3, Standardized Diagnostic Assessment:
| Instrument | Type | Purpose |
|---|---|---|
| ADOS-2 | Structured observation | Direct assessment of social communication/play/behavior; Module selected by language level |
| ADI-R | Structured parent interview | Developmental history across three domains; algorithms for diagnosis |
| Vineland-3 | Parent interview/questionnaire | Adaptive behavior (communication, daily living, socialization) |
Step 4, Cognitive and Language Assessment:
- WISC-V (6–16 years) or Leiter-3 (non-verbal IQ)
- WPPSI-IV (2.5–7 years)
- CELF-5 or PLS (language)
- Determine verbal IQ/non-verbal IQ discrepancy (common in ASD)
Step 5, Allied Health Assessment:
- Occupational therapy: sensory profile, fine/gross motor, daily living skills
- Speech and language therapy: pragmatic language, AAC needs
- Educational psychology: learning profile
Step 6, Medical Investigations:
Step 7, Feedback and Formulation:
- Clear diagnosis and severity level
- Comorbidity mapping (ID, ADHD, epilepsy, anxiety)
- Strengths-based profile
- Management recommendations
The assessment pathway follows a tiered sequence: screen → observe → diagnose (ADOS-2 + ADI-R) → profile (cognitive/language/adaptive) → investigate medically. Do not jump directly to investigations. The gold standard diagnosis requires ADOS-2 AND ADI-R together.
Q3. Classify intellectual disability and describe the evaluation of a child with suspected intellectual disability. (15 marks)
Classification
DSM-5 Classification:
Intellectual Disability (ID) is defined by three criteria:
- Deficits in intellectual functions (confirmed by standardized testing AND clinical assessment)
- Deficits in adaptive functioning (conceptual, social, or practical domains)
- Onset during developmental period
Severity is determined by ADAPTIVE FUNCTIONING, not IQ alone (DSM-5 change from DSM-IV):
| Severity | Conceptual Domain | Social Domain | Practical Domain |
|---|---|---|---|
| Mild (IQ ~50–69) | Academic skills below peers; abstract thinking, executive function limited | Immature social interactions; gullible, naive | Can be independent in self-care; needs support for complex tasks |
| Moderate (IQ ~35–49) | Academic skills limited (few-word reading, simple arithmetic) | Significant difference in social/communicative behavior; uses simple language | Can care for personal needs with training; supervision needed for complex decisions |
| Severe (IQ ~20–34) | Limited conceptual skill acquisition; understands some simple language | Single words, simple phrases; relationships with family/familiar others | Requires support for most ADLs; some can do simple ADLs |
| Profound (IQ <20) | Primarily concrete understanding; relies on physical/sensory interaction | Relies on nonverbal communication; close relationship with caregivers | Dependent on others for all aspects of care; may achieve some self-help with extensive training |
Evaluation
1. Presenting Complaint and Chief Concerns:
- Developmental delay (delayed milestones)
- Learning difficulties at school
- Behavioral problems
- Communication difficulties
2. Detailed History:
Prenatal: Maternal illness (rubella, CMV, toxoplasmosis), substance use (alcohol, FASD), medications (anticonvulsants), thyroid disease, radiation, consanguinity (autosomal recessive conditions), antenatal scan anomalies
Perinatal: Gestational age, birth weight, birth asphyxia, neonatal seizures, hypoglycemia, jaundice requiring exchange transfusion, NICU admission
Postnatal: Meningitis, encephalitis, traumatic brain injury, seizures, nutritional deficiencies, lead exposure, severe deprivation/neglect
Developmental milestones: Motor (head control, sitting, walking), Language (first words, two-word phrases), Social (social smile, stranger anxiety), Self-care skills
Educational history: Entry to school, grade placement, teacher reports, support needed
Family history: ID in family members, consanguinity, genetic conditions, learning disabilities
Behavioral history: Self-injurious behavior, aggression, sleep problems, stereotypies, anxiety
3. Physical Examination:
General: Growth parameters (height, weight, head circumference, micro/macrocephaly)
Dysmorphic features:
- Down syndrome: flat facies, upslanting palpebral fissures, epicanthal folds, Brushfield spots, small ears, single palmar crease, hypotonia
- Fragile X: long face, prominent ears, macro-orchidism (post-pubertal)
- Williams syndrome: elfin facies, broad forehead, periorbital fullness
- Angelman: wide mouth, widely-spaced teeth, happy affect
Skin: Ash-leaf macules (tuberous sclerosis), cafe-au-lait spots (NF1), port-wine stain (Sturge-Weber)
Neurological: Tone, reflexes, coordination, cerebellar signs, cranial nerves
4. Psychological Assessment:
Intelligence Testing:
| Test | Age Range | Notes |
|---|---|---|
| WPPSI-IV | 2.5–7 years | Verbal + Performance IQ; good for preschool |
| WISC-V | 6–16 years | Five factor model; most widely used |
| Stanford-Binet 5 | 2–85 years | Full range; good floor for low IQ |
| Leiter-3 | 3–75 years | Non-verbal; use for non-English speakers, ASD, hearing impaired |
Adaptive Behavior Assessment:
- Vineland Adaptive Behavior Scales-3 (VABS-3): gold standard; semi-structured interview; communication, daily living skills, socialization, motor skills
- ABAS-3 (Adaptive Behavior Assessment System)
5. Speech and Language Assessment:
- Receptive and expressive language levels
- Augmentative and Alternative Communication (AAC) needs
- Pre-verbal communication (joint attention, gesture, gaze)
6. Medical Investigations:
7. Formulation and Management Planning:
- Etiology (where determinable)
- Severity across domains
- Comorbid psychiatric, medical, behavioral conditions
- Strengths and capacities
- Management: early intervention, special education, speech therapy, occupational therapy, behavioral support, family support, caregiver training
Chromosomal microarray (CMA) is now the first-tier genetic investigation for unexplained ID/ASD, it detects submicroscopic copy number variants that karyotype misses, with a 15–20% diagnostic yield. Karyotype is preferred only if Down syndrome or structural chromosomal abnormality is suspected clinically.
Q4. Discuss the management of Conduct Disorder in an adolescent. (10 marks)
Introduction
Conduct Disorder (CD) is characterized by a persistent pattern of behavior violating the rights of others and societal norms. It is associated with significant long-term morbidity (adult antisocial personality disorder in 25–40%) and requires a comprehensive, multi-systems approach.
Assessment Before Management
A full assessment establishes:
- CD subtype (childhood vs. adolescent onset, prognosis differs)
- Presence of callous-unemotional (CU) traits (Limited Prosocial Emotions specifier)
- Comorbidities: ADHD (50%), substance use, depression, anxiety, learning disabilities
- Risk factors: family dysfunction, peer influences, neighborhood violence, academic failure
- Protective factors: academic strengths, prosocial relationships, family support
Management Plan
1. Psychoeducation:
- Explain CD as a behaviorally complex disorder with biological and environmental contributors
- Normalize family distress; reduce blame-focused framing
- Discuss realistic treatment expectations (slow progress, setbacks expected)
2. Behavioral Interventions:
Parent Management Training (PMT):
- Most evidence for younger adolescents and parents willing to engage
- Patterson Oregon Social Learning Model
- Incredible Years (Webster-Stratton)
- Skills: consistent discipline, positive reinforcement, monitoring, problem-solving
Multisystemic Therapy (MST):
- Gold standard for serious antisocial behavior in adolescents
- Community-based, 3–5 months, intensive
- Addresses all systems: family, peers, school, neighborhood
- Evidence: superior to individual therapy and residential treatment
- Particularly effective for youth at risk of out-of-home placement
Functional Family Therapy (FFT):
- 12–30 sessions
- Focuses on family communication, problem-solving, attribution
- Good for moderate-severity CD
Problem-Solving Skills Training (PSST):
- Addresses cognitive distortions in social problem-solving
- Reduces hostile attribution bias
Therapeutic foster care / residential treatment:
- For high-risk youth failing community treatment
- Evidence-based residential models exist (Oregon TFC)
3. School-based Interventions:
- Educational support for learning disabilities
- Anti-bullying programs
- Social skills training
- Mentorship programs
4. Pharmacotherapy (adjunctive):
No medication treats CD specifically. Treat comorbidities:
| Target | Medication | Evidence |
|---|---|---|
| Comorbid ADHD | Methylphenidate, Amphetamine, Atomoxetine | Strong, reduces aggression significantly |
| Severe impulsive aggression | Lithium | RCT evidence (Malone et al.) |
| Severe aggression | Risperidone, Aripiprazole | Moderate evidence |
| Mood instability | Valproate | Some evidence |
| Comorbid depression/anxiety | SSRIs | Treat the comorbidity |
5. Addressing CU Traits:
Standard PMT is LESS effective in CD with CU traits. Modifications needed:
- Reward-based (not punishment-based) approaches more effective
- Parenting Intervention for Children with Conduct Problems and CU Traits (PRICC)
- Increasing empathic concern: emotion recognition training, perspective-taking
- Address reward hypersensitivity
6. Diversion Programs:
- Court-involved youth: diversion from criminal justice preferable
- Youth justice rehabilitation programs
- Mentoring, vocational training
7. Long-term Follow-up:
- Monitor for substance use, mood disorder, antisocial trajectory
- Educational and vocational support
- Family support services
MST is the gold standard answer for moderate-to-severe CD in adolescents. Name it. Explain its multi-systems approach. For pharmacotherapy: treat ADHD first, reduction in impulsivity often significantly reduces aggressive behavior. Risperidone for residual severe aggression.
Q5. Describe the assessment and management of a child presenting with suspected sexual abuse. (15 marks)
Introduction
Child sexual abuse (CSA) is defined as any sexual activity with a child without the child's consent or understanding, exploiting the child's developmental immaturity. Prevalence estimates suggest 1 in 4 girls and 1 in 13 boys experience CSA before age 18. Comprehensive assessment requires a trauma-informed, multidisciplinary approach.
Indicators Suggesting Sexual Abuse
Behavioral/psychological:
- Age-inappropriate sexual knowledge, language, or behavior
- Sexual acting-out with peers or younger children
- Regression (enuresis, thumb-sucking)
- Sleep disturbance, nightmares
- Sudden school refusal, academic decline
- Depression, anxiety, PTSD symptoms
- Self-harm, suicidal ideation
Physical:
- Genital/rectal injuries inconsistent with history
- STIs in prepubertal children (gonorrhea, syphilis, HIV)
- Pregnancy in adolescent with unexplained circumstances
- Note: most CSA leaves NO physical evidence
Assessment
1. Disclosure:
- Most CSA is disclosed verbally, not detected medically
- Accidental disclosure: child tells peer/teacher
- Purposeful disclosure: child tells trusted adult
- Behaviors that prompt investigation
2. Forensic Interview:
- Conducted by trained professional (child protection investigator, forensic interviewer)
- NICHD Protocol (Orbach et al.), gold standard
- Principles:
- Free-narrative approach first ("tell me everything about...")
- Open-ended questions before specific questions
- Never leading questions ("did he touch you there?")
- Establish rapport; explain rules (don't know = say "I don't know"; can correct interviewer)
- Single interview preferred (multiple interviews = contamination)
- Video-record when possible
- Child interview BEFORE physical examination
3. Medical Assessment:
Conducted by trained pediatrician/forensic physician:
- Detailed history of events (when, where, what type of contact, any bleeding/pain)
- Physical examination:
- General examination (look for other injuries, bruises, bites)
- Anogenital examination under adequate lighting, appropriate positioning
- Colposcopy (magnified examination, photodocumentation)
- Evidence collection: swabs, clothing, bedding (ideally within 72–96 hours of acute assault)
- STI testing: gonorrhea, chlamydia, syphilis, HIV baseline
- Emergency contraception if appropriate and within 72 hours
4. Psychological Assessment:
- PTSD evaluation: Child PTSD Symptom Scale (CPSS), UCLA PTSD-RI
- Depression: CDI (Children's Depression Inventory)
- Anxiety: RCADS (Revised Children's Anxiety and Depression Scale)
- Trauma Symptom Checklist for Children (TSCC)
- Dissociation assessment if indicated
5. Risk Assessment:
- Ongoing abuse risk
- Relationship of alleged perpetrator to child (intra-familial/extra-familial)
- Protective adult in household
- Child safety plan
Mandatory Reporting
In India: POCSO Act 2012, ALL persons are mandated to report. Section 19: any person with knowledge of offense MUST report to SJPU (Special Juvenile Police Unit) or local police. Section 21: failure to report is an offense punishable with up to 6 months imprisonment.
Management
1. Safety:
- Immediate: ensure child is safe; remove from contact with perpetrator
- Intra-familial abuse: may require removal of perpetrator or child to safe placement
- Non-offending parent/caregiver support is critical
2. Trauma-Focused Cognitive Behavioral Therapy (TF-CBT):
- Gold standard treatment for CSA-related PTSD and trauma symptoms
- 12–25 sessions
- Components (PRACTICE acronym):
- Psychoeducation about trauma reactions
- Relaxation skills
- Affective modulation
- Cognitive coping
- Trauma narrative processing and cognitive processing
- In vivo mastery of trauma reminders
- Conjoint child-parent sessions
- Enhancing safety and future development
- Both child AND caregiver involved in treatment
- Evidence: strong RCT base (Cohen, Mannarino)
3. Pharmacotherapy:
- Treat comorbid PTSD: SSRIs (sertraline, fluoxetine) for severe symptoms
- Sleep: melatonin, low-dose clonidine for nightmares
- Comorbid depression/anxiety: SSRIs
4. Psychoeducation for Caregivers:
- Normalize child's reactions
- Explain why children delay disclosure (shame, grooming, fear)
- Address caregiver's own trauma response (if non-offending caregiver is also distressed)
5. Legal and Social Coordination:
- Liaison with child protection services
- Court proceedings support (child-friendly court procedures under POCSO)
- School support and confidentiality planning
The most common mistake is conducting a medical examination before a forensic interview. The forensic interview should always come first to minimize contamination of the child's account. Also: absence of physical findings does NOT rule out sexual abuse, most cases have no physical evidence.
Q6. Discuss school refusal: definition, classification, assessment, and management. (10 marks)
Definition
School refusal refers to difficulty attending school due to emotional distress, resulting in prolonged absence. It is NOT a DSM-5 diagnosis but a clinically important presentation with multiple underlying causes. Distinguished from truancy (antisocial, no distress, parents unaware).
Classification (Kearney & Silverman Functional Model)
| Function | Mechanism | Presentation |
|---|---|---|
| 1, Avoidance of negative affect | Escape from school-related anxiety-provoking stimuli | Somatic symptoms on school mornings; relief on staying home |
| 2, Escape from social/evaluative | Social anxiety, performance anxiety, fear of evaluation | Avoids tests, presentations, PE, social situations at school |
| 3, Attention-seeking | Separation anxiety; maintain proximity to caregiver | Distress focused on being away from parent; clings |
| 4, Tangible reinforcement | More reinforcing activities at home (gaming, TV) | Prefers home; no clear anxiety; may be combined with CD |
Assessment
History:
- Duration of absence (acute vs. prolonged)
- Precipitating events (school change, bullying, family stress, illness)
- Pattern of refusal (which days, which subjects)
- Somatic complaints (headache, stomachache, timing relative to school)
- Caregiver response (accommodation patterns)
- Academic history, peer relationships
- Bullying (direct and cyberbullying)
- Previous psychiatric history
Mental Status and Rating Scales:
- Anxiety: RCADS, SCARED (Screen for Child Anxiety Related Disorders)
- Depression: CDI
- School Refusal Assessment Scale-Revised (SRAS-R), assesses function
Investigations:
- Medical evaluation to rule out organic cause for somatic complaints (GI workup if chronic abdominal pain, etc.)
- Educational assessment if learning disability suspected
Management
Core principle: Rapid return to school is the primary goal. Every additional day of absence entrenches avoidance.
1. School Liaison:
- Meet with school to arrange graduated return plan
- Identify triggers at school (specific class, teacher, peer)
- Arrange adjustments: modified timetable, quiet room, trusted adult
- Partial day attendance initially, building up
2. Cognitive Behavioral Therapy:
- Graded exposure hierarchy (from least to most anxiety-provoking)
- Cognitive restructuring (catastrophic thinking about school)
- Relaxation skills (diaphragmatic breathing, progressive muscle relaxation)
- Social skills training if social anxiety prominent
- EMDR if bullying/trauma involved
3. Family Interventions:
- Address parental accommodation (staying home with child, allowing avoidance)
- Parent coaching on managing morning routines
- Reduce secondary reinforcement of staying home
4. Pharmacotherapy:
- SSRIs (sertraline, fluoxetine) for anxiety/depression driving refusal
- Start low, titrate slowly, allow 4–6 weeks for effect
- Short-term anxiolytic use controversial; habit-forming risk
5. Inpatient/Intensive Outpatient:
- For prolonged, severe, treatment-refractory cases
- Day hospital programs with school component
Distinguish school refusal from truancy. Key features of school refusal: (1) child remains at home with parent's knowledge; (2) child is distressed; (3) somatic symptoms common on school mornings; (4) no other significant antisocial behavior. Truancy: child leaves home but does not go to school; no distress; parents often unaware.
Q7. Discuss the pharmacotherapy of pediatric depression with reference to safety and evidence. (10 marks)
Introduction
Pediatric depression (Major Depressive Disorder in children and adolescents) requires careful pharmacological decision-making due to developmental considerations, the SSRIs' black box warning, and the landmark TADS trial findings.
When to Use Pharmacotherapy
Indications:
- Moderate-severe depression unresponsive to psychotherapy alone
- Psychotic depression
- Severe functional impairment
- High suicidality requiring faster response
- First-line combination treatment (psychotherapy + SSRI) recommended
FDA-Approved Antidepressants for Pediatric Depression
| Drug | Approved Age | Starting Dose | Target Dose | Notes |
|---|---|---|---|---|
| Fluoxetine | ≥8 years | 10mg/day | 20–60mg/day | Longest evidence base; active metabolite (long half-life = safety in overdose but slower wash-out) |
| Escitalopram | ≥12 years | 10mg/day | 10–20mg/day | Well tolerated; FDA-approved for adolescent depression |
Commonly used off-label:
- Sertraline (strong evidence from TORDIA, TADS secondary analyses)
- Citalopram (available evidence)
TADS Trial (Treatment for Adolescents with Depression Study)
- N=439, ages 12–17, moderate-severe MDD
- Arms: Fluoxetine, CBT, Combination, Placebo
- Results:
- Combination (fluoxetine + CBT): 71% response, BEST
- Fluoxetine alone: 61% response
- CBT alone: 43% response
- Placebo: 35% response
- Suicidal ideation: higher in fluoxetine-only group vs. CBT, combination protected against this
- Conclusion: Combination treatment is recommended; CBT acts as protective buffer against suicidal ideation associated with SSRIs
The Black Box Warning
- Added by FDA in 2004 following pooled meta-analysis
- All antidepressants: increased risk of suicidal IDEATION (not completed suicide) in children and adolescents
- Risk: ~4% vs. 2% placebo (absolute increase ~2%)
- Completed suicide rate: NOT increased; may be decreased with treatment
- Consequence: FDA warning → prescriber reluctance → untreated depression → increased deaths
- Monitoring protocol: weekly visits weeks 1–4; biweekly weeks 5–12; monthly thereafter
Prescribing Guidelines
Start low, go slow:
- Children (8–12 years): Start fluoxetine 5–10mg/day; target 20mg/day; max 60mg/day
- Adolescents (13–18): Start 10mg/day; target 20–40mg/day
Duration:
- Continue 6–12 months after remission to prevent relapse
- Two or more episodes: consider maintenance for 1–2 years
Non-response:
- TORDIA trial: switching to another SSRI or venlafaxine equally effective; adding CBT to switch = better outcome
- Augmentation: add psychotherapy before adding second medication
- Atypical: consider mirtazapine (sleep, appetite, anxiety comorbidity)
TADS and the black box warning are both testable. Know the TADS finding cold: 71% combination, 61% fluoxetine, 43% CBT, 35% placebo. For black box: suicidal IDEATION (not completed suicide) increased ~2%. Combination protects. Treatment reduces overall suicide risk.
Q8. Discuss the assessment and treatment of Tourette Syndrome. (10 marks)
Introduction
Tourette Syndrome (TS) is a neurodevelopmental disorder characterized by multiple motor tics and at least one vocal tic, not necessarily concurrent, persisting for more than 12 months, with onset before age 18. It is not rare (0.3–1% children) and is frequently comorbid with ADHD (50–60%) and OCD (30–50%).
Assessment
History:
- Onset and progression of tics (type, frequency, severity, impact)
- Premonitory urge (sensation preceding tic, relieved by performing it)
- Ability to suppress tics (and resultant tension/rebound)
- Waxing/waning course (worse with stress, excitement, fatigue)
- Coprolalia/echolalia/palilalia (ask specifically; often not volunteered)
- Comorbidities: ADHD symptoms, OCD/compulsive behaviors, anxiety, depression, learning difficulties
- Family history (TS highly heritable)
- Psychosocial impact: teasing, embarrassment, school problems, social isolation
Examination:
- Motor tics: simple (blinking, nose twitching, head jerking) vs. complex (touching, hopping, echopraxia, copropraxia)
- Vocal tics: simple (throat clearing, sniffing, grunting) vs. complex (echolalia, palilalia, coprolalia)
- Rule out PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections): sudden onset, episodic course, associated with group A strep infection
Rating Scales:
- Yale Global Tic Severity Scale (YGTSS): motor + vocal subscales, impairment rating; gold standard
- PUTS (Premonitory Urge for Tics Scale)
Investigations:
- No specific investigation required for TS
- Throat culture/ASOT if PANDAS suspected
- Brain MRI only if atypical features (focal neurological signs, progressive worsening)
- Neuropsychological testing if academic problems/ADHD
Treatment
Decision to treat: Not all tics require pharmacotherapy. Treat if: significant distress, social impairment, interference with function, severe tics causing pain/injury.
Step 1, Education and Watchful Waiting:
- Explain TS, prognosis (many improve by late adolescence)
- Psychoeducation for school (teacher awareness, anti-bullying)
- Address shame and embarrassment
Step 2, Behavioral Treatment (CBIT):
Comprehensive Behavioral Intervention for Tics, first-line for mild-moderate tics:
- Habit Reversal Training (HRT): awareness training → competing response training
- Functional intervention: identify triggers, modify antecedents
- Relaxation training
- Evidence: RCT (Wilhelm et al., 2012) superior to supportive therapy
- Advantage: no medication side effects; teaches lifelong self-management
Step 3, Pharmacotherapy (moderate-severe tics or CBIT failed):
| Medication | Starting Dose | Comments |
|---|---|---|
| Aripiprazole | 2mg/day, titrate to 5–20mg | Currently preferred atypical antipsychotic; better tolerability; RCT evidence |
| Guanfacine ER | 1mg at night | Non-antipsychotic option; useful with comorbid ADHD |
| Clonidine | 0.05mg BD | Older; more sedating; useful for ADHD comorbidity |
| Risperidone | 0.25–0.5mg/day, titrate | Effective; weight gain, prolactin |
| Haloperidol | 0.25–0.5mg/day | Most evidence historically; EPS, tardive dyskinesia, last resort |
| Pimozide | 1–2mg/day | QTc monitoring required |
| Fluphenazine | 0.5–1mg/day | Alternative typical antipsychotic |
| Topiramate | 25mg/day, titrate | Some RCT evidence; cognitive slowing |
Managing Comorbidities:
- ADHD: atomoxetine (preferred, treats ADHD without worsening tics), guanfacine ER, then stimulants (stimulants may transiently worsen tics but overall benefit outweighs)
- OCD: CBT (ERP) first-line; SSRI (fluoxetine, sertraline) if needed
- Anxiety: CBT; SSRI
- Depression: SSRIs + CBT
Coprolalia (uttering obscene words) is present in only 10–15% of Tourette patients, NOT required for diagnosis. Tics can be temporarily suppressed (unlike compulsions). The premonitory urge is the sensory phenomenon preceding tics, it is the target of CBIT.
Q9. Define and discuss Gaming Disorder as classified in ICD-11. (10 marks)
Definition
Gaming Disorder (ICD-11 Code: 6C51) is classified under Disorders Due to Addictive Behaviors. It is defined as a pattern of persistent or recurrent gaming behavior (digital/video gaming) characterized by:
- Impaired control over gaming (onset, frequency, intensity, duration, termination, context)
- Increasing priority given to gaming to the extent it takes precedence over other interests/activities
- Continuation or escalation of gaming despite negative consequences
The behavior pattern is of sufficient severity to result in significant impairment in personal, family, social, educational, occupational, or other important areas of functioning. Duration: typically ≥12 months (shorter if severe and criteria clearly met).
Epidemiology
- Prevalence: 1–10% (wide range; definitional variability)
- Male predominance: 3:1
- Peak age: adolescence and young adulthood (13–25 years)
- Asia-Pacific: higher rates (South Korea 10.2%)
- Risk factors: male sex, ADHD, social anxiety, depression, family dysfunction
Neurobiology
Shares features with substance use disorders:
- Striatal dopamine release during gaming (similar to substance reward)
- Ventral striatum hyperactivation to gaming cues (craving)
- Reduced prefrontal control (impaired inhibition)
- Structural: reduced grey matter in PFC, insula, inferior frontal gyrus
Assessment
Instruments:
- IGDS (Internet Gaming Disorder Scale, 9 items aligned with DSM-5 criteria for further study)
- Gaming Disorder Scale (GDS), aligned with ICD-11
- CAGE-Gaming: adapted version
History:
- Duration of gaming per day/week
- Functional impairment: sleep, academics, peer relationships, family conflicts
- Withdrawal symptoms when unable to game (irritability, anxiety)
- Repeated failed attempts to cut down
- Deception/lying about gaming
- Escapism: gaming to escape negative mood
- Comorbidities: ADHD, anxiety, depression, social phobia
Distinguish from:
- Highly engaged gaming without impairment (no diagnosis)
- Problematic internet use (broader, social media, pornography)
- Substance use disorders (different substance)
Management
Psychoeducation:
- Present problem without shame; motivational framing
- Harm reduction initially if denial prominent
Cognitive Behavioral Therapy (CBT):
- Most evidence
- Cognitive: identify and challenge gaming cognitions ("I need to play to feel good"; "I'm only good at gaming")
- Behavioral: activity scheduling, reducing gaming time, alternative activities
- Relapse prevention: trigger identification, coping plans
Motivational Interviewing (MI):
- For ambivalent patients
- Explore discrepancy between gaming life and valued life
- Enhance intrinsic motivation for change
Family Therapy:
- Address enabling behaviors (parents providing unlimited gaming time)
- Improve communication and limit-setting
- Parental monitoring of screen time
Pharmacotherapy:
- No specific drug approved
- Treat comorbid ADHD (methylphenidate reduces gaming in ADHD + GD)
- Treat comorbid depression/anxiety (SSRIs)
- Bupropion: some positive data in small trials
Structured Programs:
- South Korea: National Youth Policy Institute programs; "digital detox" camps
- Evidence for intensive residential programs limited
Q10. Discuss the evaluation and management of Separation Anxiety Disorder in a 7-year-old. (10 marks)
Introduction
Separation Anxiety Disorder (SAD) is the most common anxiety disorder in children under 12 years, characterized by developmentally inappropriate and excessive fear/anxiety concerning separation from attachment figures. In a 7-year-old, the primary concern is school refusal, somatic complaints, and excessive distress.
Clinical Features
At age 7, expected:
- Some anxiety at transitions, new situations
- Occasional worry about parents
Pathological (SAD), ≥3 of:
- Excessive distress when separated (crying, tantrums, pleading)
- Persistent worry about harm coming to attachment figures
- Worry about being kidnapped or getting lost
- Reluctance/refusal to go to school
- Fear of being alone
- Refusing to sleep away from home / needing parent nearby
- Nightmares with separation themes
- Somatic complaints (morning headache/stomachache that resolves if allowed to stay home)
Duration ≥4 weeks in children.
Assessment
History:
- Onset (sudden vs. gradual; precipitants: school change, illness, death in family, parental conflict)
- Specific triggers (school, sleep, separation from specific parent)
- Caregiver response (how parents react to distress)
- Accommodation patterns (co-sleeping, parents staying home, calling school frequently)
- Developmental history (temperament, behavioral inhibition; early attachment patterns)
- Family history (anxiety in parents, genetic + modeling)
- Comorbidities: GAD, specific phobia, ADHD
Rating Scales:
- SCARED (Screen for Child Anxiety Related Disorders), parent + child versions
- MASC (Multidimensional Anxiety Scale for Children)
- RCADS
Management
Principle: Parent-child joint treatment. Parental accommodation maintains disorder.
1. Psychoeducation:
- Normal separation anxiety vs. SAD
- Brain's "alarm" system, anxiety is uncomfortable but not dangerous
- "Brave behaviors" approach, facing fears builds confidence
- Explain parental accommodation as inadvertently maintaining anxiety
2. Cognitive Behavioral Therapy (CBT):
Components for child:
- Relaxation (belly breathing, progressive muscle relaxation)
- Cognitive restructuring (challenge catastrophic thinking about harm to parents)
- Graded exposure hierarchy:
- Step 1: Parent leaves room for 1 minute
- Step 2: Parent in different part of house
- Step 3: Brief separation at school (teacher present)
- Step 4: Full school day
- Step 5: Overnight at grandparent's
Programs with evidence:
- Coping Cat (Kendall), well-validated CBT for child anxiety
- FRIENDS for Life (Barrett)
3. Parent Training:
- Reduce accommodation without increasing hostility
- Consistent, calm goodbye rituals (brief, positive, predictable)
- Brave behaviors: reward approaching feared situations (token economy)
- Avoid excessive reassurance
4. School Liaison:
- Brief, warm transition routines at school entry
- Trusted adult at school to support
- Gradual reintegration if school refusal has developed
5. Pharmacotherapy:
- Moderate-severe or non-response to CBT after 8–12 weeks
- First-line: Sertraline (10–25mg starting; titrate to 50–200mg)
- Fluoxetine: alternative
- CAMS trial: combination sertraline + CBT superior to either alone for child anxiety
- Duration: continue for 6–12 months after remission; taper slowly
Parental accommodation (letting child stay home, calling school, co-sleeping) is the single most important maintenance factor for pediatric anxiety disorders including SAD. Successful treatment requires addressing accommodation directly with parents, not just treating the child.
Q11. Discuss the presentation and management of a child with Tourette's and ADHD comorbidity. (10 marks)
(See Q8 for Tourette's full discussion; this answer focuses on the comorbidity management challenge)
The Challenge
50–60% of TS patients have ADHD. The comorbidity creates significant management dilemmas:
- Stimulants (first-line ADHD) may worsen tics (transiently)
- Tic suppressing medications (antipsychotics) may worsen ADHD symptoms
- Both conditions impact academic and social functioning
Clinical Presentation
Combination presentation:
- Inattention, hyperactivity, impulsivity (ADHD domain)
- Multiple motor + vocal tics (TS domain)
- Executive function deficits amplified
- Emotional dysregulation (common in both)
- Academic underperformance
- Social difficulties compounded
Management Decision Framework
Step 1, Which is causing more impairment?
- If ADHD causing more impairment: treat ADHD first
- If tics causing more impairment: treat tics first
- If equal: may need simultaneous treatment
Step 2, First-line pharmacological choice when ADHD is primary:
Step 3, Behavioral treatment:
- CBIT for tics
- CBT/behavioral parent training for ADHD
- Combined can be done sequentially or simultaneously
Step 4, Combination pharmacotherapy if needed:
- Guanfacine/clonidine + methylphenidate (stimulant attenuates tics less than feared; guanfacine covers tics)
- Aripiprazole + atomoxetine (good tolerability)
Academic support:
- Extended time (both ADHD and tics affect test-taking)
- Breaks for tic suppression tension release
- Teacher education about tics (avoid calling attention to tics in class)
The old teaching that stimulants are absolutely contraindicated in TS+ADHD is OUTDATED. Current guidelines (AACAP, 2013 onwards) state stimulants can be used when ADHD impairment is significant, with monitoring. Alpha-2 agonists (guanfacine, clonidine) are preferred first-line in this population.
Q12. Describe Reactive Attachment Disorder and Disinhibited Social Engagement Disorder: clinical features and management. (10 marks)
(Combined answer format)
Background
Both RAD and DSED arise from extreme early caregiver deprivation, social neglect, abandonment, or institutional rearing. They represent different patterns of disrupted attachment.
RAD: Clinical Features
Core: Emotionally withdrawn behavior toward adult caregivers:
- Rarely seeks comfort when distressed
- Rarely responds to comfort when offered
Associated: Persistent social/emotional disturbance (≥2 of):
- Minimal social/emotional responsiveness
- Limited positive affect
- Irritability, sadness, or fearfulness during non-threatening interactions
Child appears sad, fearful, or unresponsive. Caregiver cannot reach child emotionally.
DSED: Clinical Features
Core: Indiscriminate social engagement with strangers (≥2 of):
- Reduced reticence with unfamiliar adults
- Overly familiar verbal or physical behavior (hugging stranger, climbing on lap)
- Diminished checking back with caregiver after venturing away
- Willingness to go off with unfamiliar adult
Child appears social but lacks discrimination, treats all adults as potential attachment figures.
Key Distinctions
| Feature | RAD | DSED |
|---|---|---|
| Core behavior | Inhibited, withdrawn | Disinhibited, indiscriminate |
| Response to comfort | Absent/reduced | May seek comfort from anyone |
| Safety risk | Depression/neglect damage | Vulnerability to exploitation |
| Response to stable caregiving | Typically improves | May persist even after stabilization |
| Confusion with ASD | Some overlap | Less overlap |
| History required | Yes, extreme neglect | Yes, extreme neglect |
Management
1. Stable, Responsive Caregiving (primary intervention):
- Place child with stable, committed caregiver (foster/adoptive if needed)
- Nurturing, predictable, responsive parenting
- RAD often improves significantly with stable placement
- DSED: may persist despite stability, protective adults must be informed
2. Dyadic/Attachment-Based Therapy:
- Dyadic Developmental Psychotherapy (DDP, Hughes)
- PACE model (Playfulness, Acceptance, Curiosity, Empathy)
- Theraplay: structured play-based dyadic therapy
- Parent-Child Interaction Therapy (PCIT), modified for attachment disorders
- WARNING: "Holding therapy" / "Rebirthing", strongly contraindicated, dangerous, no evidence
3. Parenting Support:
- Intensive training for foster/adoptive parents
- Understanding trauma responses (terror → rage → freeze)
- Avoid punitive discipline; trauma-informed parenting
4. Safety Planning for DSED:
- Inform caregivers, teachers about risk of going with strangers
- Safety rules training (who is safe to talk to/go with)
- Close supervision in public settings
5. School Support:
- Teacher education about attachment disorder presentations
- Consistent adult at school; clear, warm relational boundaries
- Behavioral support for emotional dysregulation
6. Pharmacotherapy:
- No specific medication for RAD/DSED
- Treat comorbid depression, anxiety, PTSD
- Stimulants if true ADHD comorbidity (distinguish DSED disinhibition from ADHD impulsivity)
Holding therapy (forced prolonged holding to simulate birth canal, forcibly induce cathartic emotional responses) is a dangerous pseudotherapy associated with deaths. It is absolutely contraindicated. Questions about "innovative" attachment therapies, this is the red flag answer.
| *Sources: Kaplan & Sadock (11th ed.) | Rutter's (6th ed.) | Lewis's (5th ed.) | DSM-5-TR | ICD-11 | TADS, CAMS, MTA, TORDIA trials* |
|---|
Mnemonics & Memory Tricks
Sources: Kaplan & Sadock (11th ed.), Rutter's (6th ed.), Lewis's (5th ed.), DSM-5-TR, ICD-11
MNEMONIC 1: ADHD Inattention Symptoms: "CLAMS FOLDS"
C, Careless mistakes in schoolwork / details
L, Listening problems (doesn't seem to listen when spoken to directly)
A, Activities not followed through / instructions not completed
M, Mental effort tasks avoided (sustained attention tasks)
S, Sustaining attention in tasks or play (difficulty)
F, Forgetful in daily activities
O, Organization difficulty (tasks, time, materials)
L, Loses things (pencils, homework, keys)
D, Distracted easily by extraneous stimuli
S, Structuring work difficulties (doesn't follow through)
6 of 9 inattention symptoms required (children); 5 of 9 (≥17 years). Duration ≥6 months. Present before age 12.
MNEMONIC 2: ADHD Hyperactivity-Impulsivity: "FILTH BIBS"
F, Fidgets with hands/feet or squirms
I, Interrupts or intrudes on others
L, Leaves seat when expected to remain seated
T, Talks excessively
H, Has difficulty waiting turn
B, Blurts out answers before question completed
I, In leisure activities, difficulty being quiet
B, Busy, "on the go" / driven by a motor
S, Scrambles (runs/climbs in inappropriate situations)
MNEMONIC 3: DSM-5 ADHD Key Rules: "BIST"
B, Before age 12 (onset of several symptoms)
I, Impairment in two or more settings
S, Six symptoms (inattentive OR hyperactive-impulsive; 5 if ≥17 years)
T, Time, ≥6 months duration
MNEMONIC 4: Autism Spectrum Disorder Diagnostic Domains: "SOCIAL RRBI"
SOCIAL (Criterion A, all 3 must be present):
S, Social-emotional reciprocity deficit
O, Only limited response to others' social approaches
C, Communication, nonverbal deficits (eye contact, gesture, facial expression)
I, Integrate verbal and nonverbal behavior, failed
A, Adjust behavior to context, difficulty
L, Lack of interest in peers / relationship deficits
RRBI (Criterion B, 2 of 4 required):
R, Repetitive motor movements, use of objects, or speech (stereotypies, echolalia)
R, Routines, insistence on sameness, inflexible rituals
B, Bounded/fixated interests (abnormal intensity or focus)
I, Input, sensory hyper/hypo-reactivity
MNEMONIC 5: ASD Early Red Flags: "No BaGel PieTa"
By 12 months:
No Babbling
No Gestures (no pointing, waving)
No response to Name
By 18 months:
No single Piece of language (no first words)
By 24 months:
No spontaneous Two-word phrases
any regression in language or social skills (ANY age)
Any regression at any age warrants IMMEDIATE referral, regardless of whether prior development was normal.
MNEMONIC 6: Down Syndrome Features: "DOWNSY"
D, Duodenal atresia / Double bubble sign; Developmental delay
O, One palmar crease (single transverse palmar crease); Oblique palpebral fissures (upslanting)
W, Wide gap between 1st and 2nd toes; White Brushfield spots on iris
N, Neck, nuchal fold thickening (antenatally); hypotonia (Noodle-like)
S, Short stature; Simian crease; Septum defects (ASD, VSD, 40% cardiac defects)
Y, Youth → dementia (Alzheimer's by 40s; all adults with DS have Alzheimer's pathology by age 40)
Additional features: Flat facies, small ears, epicanthal folds, macroglossia, short neck, hypothyroidism, atlantoaxial instability, leukemia risk (20x increased)
Trisomy 21 is the most common chromosomal cause of ID. 95% trisomy 21; 4% Robertsonian translocation (higher recurrence risk in parents); 1% mosaic (milder phenotype).
MNEMONIC 7: Fragile X Features: "FRAG-X"
F, Forehead prominent; Face long; Family history (X-linked, males affected)
R, Repetitive speech (perseverative); Repetitive hand-flapping
A, Attention deficit (ADHD features); Anxiety (social anxiety); Avoids eye gaze
G, Giant testes (macro-orchidism, post-pubertal); Gaze aversion
X, X-linked inheritance (FMR1 gene, Xq27.3; CGG repeat expansion)
- Normal: <45 CGG repeats
- Premutation: 55–200 repeats (carrier; premature ovarian insufficiency in females; FXTAS in males)
- Full mutation: >200 repeats → gene silencing → absent FMRP
Fragile X is the most common INHERITED cause of ID (Down syndrome is more common overall but mostly sporadic). Females with full mutation have milder phenotype (skewed X-inactivation). Sherman paradox: penetrance increases through generations.
MNEMONIC 8: ADHD Medications: First to Last Line, "MALE GBC"
M, Methylphenidate (first-line stimulant)
A, Amphetamine/Lisdexamfetamine (first-line alternative stimulant)
L, Lisdexamfetamine (prodrug; lower abuse potential)
E, Extra second-line: Atomoxetine (NRI; non-stimulant)
G, Guanfacine ER (alpha-2A agonist; tics, ADHD)
B, Bupropion (off-label; depression comorbidity)
C, Clonidine (alpha-2; sleep, tics, ADHD)
MNEMONIC 9: Conduct Disorder Risk Factors: "BAD PIGS"
B, Behavioral inhibition deficit; Brain dysfunction (neurobiology)
A, ADHD comorbidity; Abuse/neglect history
D, Deviant peer group; Deprivation (socioeconomic)
P, Parental antisocial personality / substance abuse
I, Impulsivity; IQ (low); Internalizing comorbidities (untreated depression)
G, Gang involvement; Genetics (50–70% heritability)
S, School failure; Social skills deficits; Stress (neighborhood violence)
MNEMONIC 10: Child Abuse: TEN-4 FACES P (Bruising Concerning for Abuse)
TEN-4 = Bruising on:
- T, Torso
- E, Ears
- N, Neck
- 4 = In infants under 4 months old (any bruise in non-mobile infant is suspicious)
FACES P:
- F, Frenulum (torn frenulum without plausible mechanism)
- A, Any patterned bruise
- C, Cheeks
- E, Eyes (periorbital without direct trauma)
- S, Spine/back
- P, Palms and soles (unusual locations for accidental bruising)
Pre-mobile infants (< 6 months) should have virtually NO bruises from accidental trauma, "those who don't cruise, don't bruise." Any bruise in this age group requires explanation.
MNEMONIC 11: Child Abuse Indicators: "MAPS"
M, Multiple injuries in various stages of healing; Munchausen by proxy (caregiver fabrication)
A, Age-inappropriate injuries (spiral fractures in non-ambulatory infant); Account inconsistent with injury
P, Pattern injuries (belt, cord, hand outline); Posterior rib fractures (pathognomonic for NAI)
S, Shaken baby triad: subdural hematoma + retinal hemorrhages + no external injury
MNEMONIC 12: Tourette Syndrome: Diagnostic Criteria, "2+1 Before 18, Not a Year Free"
- 2 motor tics (or more)
- +1 vocal tic (at least one)
- Before 18 years onset
- Not during substance/medical condition
- A year duration (not necessarily continuous)
- Free of a tic-free period >3 consecutive months (this is NOT required in DSM-5, the tic-free period >3 months criterion was removed)
EXAM PEARL DSM-5 update: DSM-IV required no tic-free period >3 months. DSM-5 removed this requirement. Tics simply must have been present for >1 year total, with onset before 18.
MNEMONIC 13: Enuresis Treatment: "BAD Choice"
(In order of preference)
B, Bell-and-pad (urine alarm), BEST long-term outcome, 75–85% success
A, ADH analogue (Desmopressin/DDAVP), good short-term; relapse on stopping
D, Dry-bed training (behavioral)
C, Clocks (bladder training for daytime enuresis)
h, then consider Imipramine if all else fails (cardiac risks; last resort)
Bell-and-pad has the best LONG-TERM outcomes and lowest relapse rate. Desmopressin works faster but relapse rate ~80% on stopping. Imipramine, efficacy 40–50%, high relapse, cardiac risk → NOT first-line.
MNEMONIC 14: ICD-11 Gaming Disorder Criteria: "3-I Rule"
Impaired control, over gaming behaviors
Increasing priority, gaming takes precedence over other activities/interests
Ignoring consequences, continuation despite negative consequences (relationships, health, academics)
Duration: ≥12 months (shorter if severe)
Result: Significant functional impairment
MNEMONIC 15: Specific Learning Disorders: "3 Ds of Reading, Writing, Math"
Dyslexia, reading (phonological processing deficit)
Dysgraphia, writing (motor planning + language expression)
Dyscalculia, maths (number sense, magnitude representation)
All are DSM-5 Specific Learning Disorder (315.xx) with specifier:
- With impairment in reading
- With impairment in written expression
- With impairment in mathematics
Dyslexia key:
- NOT a vision problem
- NOT about letter reversal (this is a myth)
- Core deficit: PHONOLOGICAL PROCESSING (mapping letters to sounds)
- IQ is typically NORMAL (not used in diagnosis anymore, discrepancy model abandoned)
MNEMONIC 16: ADOS-2 Modules: "The MoToF Plan"
Mo, Toddler Module (12–30 months, pre-verbal or few words)
1, Module 1 (non-verbal/minimal verbal; single words)
2, Module 2 (phrase speech; sentences not fluent)
3, Module 3 (fluent verbal; children and adolescents)
4, Module 4 (fluent verbal; adults)
Module selection is based on EXPRESSIVE LANGUAGE LEVEL, not age. A 10-year-old who is non-verbal uses Module 1, not Module 3.
MNEMONIC 17: Williams Syndrome Features: "WILLS"
W, Wide forehead; "Wise old man" facial appearance
I, IQ = mild-moderate ID; but verbal IQ > spatial IQ (hyperlexia possible)
L, Loquacious and hypersocial ("cocktail party" personality); Loves music
L, Left heart defect (supravalvular aortic stenosis, pathognomonic)
S, Short stature; Sensitivity to sounds (hyperacusis); Stellate pattern of iris
Genetics: Deletion 7q11.23 (elastin gene + LIMK1)
Calcium: Hypercalcemia in infancy
MNEMONIC 18: Prader-Willi vs Angelman: "PWS EATS, AS LAUGHS"
PWS EATS:
P, Paternal deletion 15q11 (or maternal UPD 15)
W, Weight gain/obesity (hyperphagia)
S, Short stature; Sleep apnea; Skin-picking
E, Emotional outbursts/tantrums; Endocrine (hypogonadism, short stature)
A, Almond-shaped eyes; Academic difficulties
T, Tone reduced (hypotonia at birth); Temperature instability
S, Stubbornness; Stealing food; Sleep disturbance
AS LAUGHS:
A, Angelman; Ataxic gait
S, Seizures (characteristic EEG)
L, Laughter/happy affect (inappropriately happy)
A, Absence of speech (minimal or no speech)
U, UPD maternal (or paternal 15q deletion / imprinting center defect)
G, Gait ataxia
H, Happy sociable disposition
S, Staring episodes; Severe ID
Imprinting key: same region (15q11), different parent of origin → different syndrome. PATERNAL deletion/maternal UPD → PWS. MATERNAL deletion/paternal UPD → Angelman.
MNEMONIC 19: Separation Anxiety Disorder: "SAFE NIGHT"
S, Separation distress (recurrent, excessive when anticipating/experiencing separation)
A, Attachment figure harm (persistent worry about caregiver being hurt/dying)
F, Finding self lost/kidnapped (worry about untoward event)
E, Exploring school, refusal/reluctance
N, Night alone, refusal to sleep away from home
I, I'm alone fear (fear of being alone without attachment figure)
G, Going off alone, persistent fear of separation at bedtime/nighttime
H, Horror of nightmares (separation-themed)
T, Tummy ache, headache (somatic complaints when separation occurs)
MNEMONIC 20: Selective Mutism vs Social Anxiety vs ASD: "SPEAKS SELECTIVELY"
Selective Mutism:
- Can speak normally in comfort zone (home, family)
- Speech NOT impaired (language is normal)
- Mute in specific social contexts (usually school)
- Duration: ≥1 month (not limited to first month of school)
- Strong overlap with social anxiety disorder
- Treatment: graded exposure, stimulus fading, SSRIs (fluoxetine)
NOT:
- Language disorder (can speak normally elsewhere)
- ASD (social communication deficit is pervasive, not context-dependent)
- ODD (not wilful refusal; genuine anxiety-based)
Selective mutism is best conceptualized as an extreme variant of social anxiety disorder, not a separate entity. Same treatment (exposure + SSRIs) applies.
QUICK REFERENCE: GENETIC CONDITIONS COMPARISON
| Condition | Gene/Chromosome | Inheritance | Key Memory Hook |
|---|---|---|---|
| Down syndrome | Trisomy 21 | Sporadic (mostly) | "21 = most common chromosomal" |
| Fragile X | FMR1 (CGG repeat) Xq27.3 | X-linked | "Most common INHERITED" |
| Prader-Willi | 15q11 paternal deletion | Imprinting | "Dad's deletion = fat and short" |
| Angelman | 15q11 maternal deletion | Imprinting | "Mum's deletion = happy and no speech" |
| Williams | 7q11.23 deletion | AD (de novo mostly) | "Elastin deletion = friendly + cardiac" |
| Rett | MECP2 (Xq28) | X-linked (de novo in females) | "Regression + hand-wringing" |
| Tuberous Sclerosis | TSC1 (hamartin) / TSC2 (tuberin) | AD | "Ash-leaf spots + seizures + ASD" |
| PKU | PAH gene | AR | "Preventable with diet" |
| 22q11 deletion | 22q11.2 | AD | "Psychosis + cardiac + T-cell deficit" |
QUICK REFERENCE: DRUG MECHANISMS
| Drug | Class | Mechanism (simplified) |
|---|---|---|
| Methylphenidate | Stimulant | Blocks DAT + NET → more dopamine/NE in synapse |
| Lisdexamfetamine | Stimulant prodrug | Cleaved to d-amphetamine; blocks + reverses DAT/NET |
| Atomoxetine | NRI | Selective NET blocker → more NE in PFC |
| Guanfacine | α2A agonist | Post-synaptic α2A in PFC → improves prefrontal signal |
| Clonidine | α2 agonist (all subtypes) | Reduces NE turnover; presynaptic + postsynaptic |
| Risperidone | Atypical AP | D2 + 5HT2A antagonist → reduces dopamine excess in striatum |
| Aripiprazole | Atypical AP | Partial D2 agonist → stabilizes dopamine tone |
| Melatonin | Melatonin agonist | MT1/MT2 agonist → advances circadian phase, improves sleep onset |
| Desmopressin | Vasopressin analogue | V2 receptor → ADH effect → reduces nocturnal urine production |
| *Sources: Kaplan & Sadock (11th ed.) | Rutter's (6th ed.) | Lewis's (5th ed.) | DSM-5-TR | ICD-11* |
|---|
High-Yield Comparisons
Sources: Kaplan & Sadock (11th ed.), Rutter's (6th ed.), Lewis's (5th ed.), DSM-5-TR, ICD-11
TABLE 1: ADHD vs Conduct Disorder vs ODD
| Feature | ADHD | ODD | Conduct Disorder |
|---|---|---|---|
| Core domain | Inattention / hyperactivity-impulsivity | Angry mood / defiance / vindictiveness | Aggression / rule violation / deceitfulness |
| Intentionality | Unintentional, impulsive, not planned | Reactive and deliberate but emotionally driven | Deliberate; proactive aggression possible |
| Conscience | Intact, feels guilt after impulsive acts | Intact, justifies actions but guilt possible | May be impaired (CU traits in subset) |
| Aggression type | Reactive, unplanned | Reactive to perceived provocation | Both reactive AND proactive/predatory |
| Peer relationships | Rejected due to impulsivity/intrusiveness | Rejected due to argumentativeness | May have delinquent peer group (adolescent-onset) |
| Onset | Before age 12 (DSM-5) | Before age 12 typically | Childhood (<10) or adolescent onset |
| Settings | Pervasive, school, home, peers | May be setting-specific (mild ODD) | Often at school and community |
| Academic impact | Learning underperformance, disorganization | Variable, may achieve when cooperative | School refusal, truancy, exclusion |
| Neurobiological | PFC dopamine/NE; executive dysfunction | HPA dysregulation; emotion regulation deficit | Low cortisol, amygdala hyporeactivity (CU type) |
| Comorbidity | ODD (40%), CD (20%), anxiety, depression | ADHD (50–60%), CD (25%), anxiety | ADHD (50%), SUD, depression |
| Prognosis | Persists into adulthood (60–70%); manageable | 25–50% → CD; 25% remit | 25–40% → ASPD; worse in childhood-onset |
| Treatment | Stimulants + BPT | PMT, PSST; treat ADHD first | MST, FFT, PMT; stimulants for comorbid ADHD |
| CU Traits specifier | No | Yes (Limited Prosocial Emotions) | Yes (Limited Prosocial Emotions) |
| DSM-5 code | 314.xx | 313.81 | 312.xx |
ODD and CD can be comorbid with each other AND with ADHD. When ADHD + ODD/CD co-occur, treat ADHD first, stimulants reduce impulsivity and reactive aggression, often improving conduct significantly.
TABLE 2: ASD Level 1 vs Level 2 vs Level 3
| Feature | Level 1 ("Requiring Support") | Level 2 ("Requiring Substantial Support") | Level 3 ("Requiring Very Substantial Support") |
|---|---|---|---|
| Social communication | Noticeable deficits without supports; difficulty initiating; reduced/atypical responses | Marked deficits; limited initiation; reduced/abnormal social response | Severe deficits; very limited initiation of interaction; minimal response |
| Restricted/Repetitive behaviors | Inflexibility causes significant interference in ≥1 context; difficulty switching | RRBIs markedly obvious; obvious to casual observer; interferes with functioning in diverse contexts | Extreme difficulty coping with change; intense distress; greatly interferes with functioning in all areas |
| Communication style | Uses full sentences; engages in conversation; may have one-sided conversation | Uses simple sentences; conversation limited to narrow interests | Few words of intelligible speech; may use AAC; no functional speech in some |
| Independence | Can function with some support; may hold a job; may live semi-independently | Requires daily support across most settings | Requires around-the-clock support; may not acquire daily living skills |
| Formerly called (DSM-IV) | Asperger's / High-Functioning Autism | Autistic Disorder (moderate) | Autistic Disorder (severe) |
| ID comorbidity | Less common | More common | Very common |
| Epilepsy risk | Lower | Moderate | Higher (20–30%) |
| Prognosis | Better, some independent living, employment | Variable, supported living | Severe impairment persists into adulthood |
ASD severity levels describe CURRENT support needs, they are NOT a fixed trajectory. A Level 2 child with excellent early intervention may function at Level 1 level as an adult. Severity can shift. IQ/adaptive functioning are SEPARATE specifiers, not part of the level.
TABLE 3: Methylphenidate vs Atomoxetine
| Feature | Methylphenidate (MPH) | Atomoxetine (ATX) |
|---|---|---|
| Class | CNS stimulant (Schedule II in US) | Selective norepinephrine reuptake inhibitor (SNRI), Non-stimulant |
| Mechanism | Blocks DAT + NET → increases synaptic dopamine and NE | Selectively blocks NET → increases NE (and secondarily DA in PFC) |
| Onset of action | Same day (30–60 min for IR) | 4–6 weeks for full therapeutic effect |
| Duration | IR: 4–6 hours; LA: 8–12 hours | Once-daily dosing; continuous coverage |
| Schedule status | Controlled substance (Schedule II) | NOT a controlled substance |
| Abuse potential | Yes (moderate-high for IR) | Very low |
| Preferred when | Core ADHD symptoms; no anxiety comorbidity; rapid response needed | Tic disorder; anxiety comorbidity; substance abuse history; family misuse concerns |
| FDA approval (ADHD) | Age 6+ (some formulations age 3+) | Age 6+ |
| Appetite suppression | Yes, significant | Mild, less than MPH |
| Insomnia | Yes, common | Less than MPH |
| Tics | May unmask/transiently worsen | Does NOT worsen tics |
| Cardiovascular | Modest HR/BP increase; screen for congenital cardiac | Modest HR/BP increase; tachycardia possible |
| Black box warning | None specific to ADHD | Suicidal ideation in children/adolescents (same as SSRIs) |
| Hepatotoxicity | No | Rare but reported, monitor if symptomatic |
| Growth suppression | Mild (0.5–1 cm/year) | Minimal |
| Effect on anxiety | May worsen anxiety | Beneficial for comorbid anxiety |
| OCD/tic comorbidity | Use with caution | Preferred |
| Dosing | Weight-based: 0.3–1.0 mg/kg/day | <70kg: 1.2 mg/kg/day; >70kg: 80–100mg/day |
| Cost | Generics available; low cost | Higher cost |
The key differentiators examiners love: (1) Onset, MPH same day, ATX 4–6 weeks; (2) Schedule, MPH controlled, ATX not; (3) Preferred in tics/anxiety, ATX; (4) Black box, ATX has suicidality warning, MPH does not.
TABLE 4: ICD-11 vs DSM-5: ASD and ADHD
| Feature | DSM-5 | ICD-11 |
|---|---|---|
| ASD classification | Single diagnosis: Autism Spectrum Disorder (299.00) with severity levels 1–3 | 6A02: Autism Spectrum Disorder, no subtyping by severity in ICD-11 per se; specifiers for intellectual impairment and functional language |
| Asperger's | Eliminated, subsumed into ASD | Eliminated, subsumed into ASD |
| ASD + ADHD | Both diagnoses allowed (DSM-5 change from DSM-IV which excluded ADHD in ASD) | Both diagnoses allowed |
| ADHD name | ADHD (presentations: combined, inattentive, hyperactive-impulsive) | 6A05: ADHD, same presentations; term "Attention Deficit Hyperactivity Disorder" retained |
| ADHD in ICD-11 vs ICD-10 | N/A | ICD-10: Hyperkinetic Disorder (required combined, pervasive); ICD-11: ADHD with same breadth as DSM-5 |
| Symptom threshold (ADHD) | 6/9 under age 17; 5/9 age 17+ | ICD-11 aligned with this |
| Age of onset | Before age 12 | Before age 12 |
| ASD criteria structure | Criterion A (social communication) + Criterion B (RRBIs) | Qualitative descriptions aligned with same domains |
| Sensory processing | Included as Criterion B4 (hyper/hypo-reactivity) | Included |
| Gaming Disorder | Internet Gaming Disorder, "conditions for further study" (NOT official) | 6C51 Gaming Disorder, OFFICIAL diagnosis |
| Intellectual Disability | Severity by adaptive functioning (NOT IQ alone) | Same, severity by adaptive functioning |
| Tic disorders | Tourette's + Persistent + Provisional | ICD-11: Tourette's (8A05.00); Primary tic disorders retained |
The most testable DSM-5 vs ICD-11 differences for child psychiatry: (1) Gaming Disorder, ICD-11 official, DSM-5 research only; (2) ADHD, ICD-10 Hyperkinetic Disorder (stricter) vs DSM-5/ICD-11 aligned; (3) Asperger's, gone in both; (4) ASD + ADHD dual diagnosis, now allowed in both.
TABLE 5: Reactive Attachment Disorder (RAD) vs Disinhibited Social Engagement Disorder (DSED)
| Feature | RAD | DSED |
|---|---|---|
| Core behavioral pattern | Inhibited, emotionally withdrawn toward caregivers | Disinhibited, indiscriminate social engagement with strangers |
| Caregiver behavior | Avoids comfort-seeking from caregivers | Approaches strangers readily; no discrimination |
| Emotional profile | Reduced positive affect; irritability, sadness, fearfulness | May appear sociable and happy superficially |
| Premonitory cause | Extreme social neglect/deprivation (required) | Extreme social neglect/deprivation (required) |
| Response to stable caregiving | Typically improves significantly | May PERSIST even after stable, caring placement |
| Safety concern | Emotional/developmental harm from withdrawal | Vulnerability to exploitation by strangers |
| ASD confusion | May be confused with ASD (both show limited social responsiveness) | Less confusion with ASD |
| ADHD overlap | Less common | DSED + ADHD: can coexist; distinguish DSED disinhibition from ADHD impulsivity |
| Attachment pattern | No organized attachment strategy | Attachment may form with caregiver, but indiscriminate with others |
| Age of recognition | Before age 5 (must be evident) | Before age 5 |
| Treatment response | Better to dyadic/attachment therapies | More treatment-resistant |
| Primary treatment | Stable, responsive caregiving; dyadic therapy | Caregiver education + safety planning; dyadic therapy |
| Prohibited treatment | Holding therapy (absolutely contraindicated) | Holding therapy (absolutely contraindicated) |
| DSM-5 code | 313.89 | 313.89 (separate from RAD) |
The critical point about DSED: it can persist despite excellent, stable caregiving, unlike RAD. Children adopted from institutions early may still show DSED features years later. This has important implications for foster/adoptive parents who may feel they have "failed" despite doing everything right.
TABLE 6: Primary vs Secondary Enuresis
| Feature | Primary Enuresis | Secondary Enuresis |
|---|---|---|
| Definition | Never achieved dryness for ≥6 consecutive months | Onset after at least 6 months of established continence |
| Prevalence | More common (80%) | Less common (20%) |
| Organic workup | Routine (hearing, developmental check) | MORE RIGOROUS, higher organic yield |
| Organic causes to rule out | Rarely organic; maturational | UTI, diabetes mellitus, diabetes insipidus, constipation with overflow, structural urological abnormality |
| Psychosocial triggers | Less prominent | More important, new baby, divorce, bereavement, abuse, school change |
| Genetics | Strong family history (70% if both parents, 44% if one parent affected) | Less familial |
| Response to treatment | Good, bell-and-pad effective | Treat underlying cause first; then bell-and-pad |
| Associated with psychiatric disorder | Less | More, stress-linked onset |
| EEG | Not indicated | Not indicated unless seizures suspected |
| DDAVP | Effective | Effective once organic causes addressed |
Secondary enuresis (onset after 6 months dryness) always warrants investigation for organic causes: UTI (most common medical cause), diabetes mellitus (polyuria), constipation, structural urological problems. Psychosocial stressors are common precipitants.
TABLE 7: Childhood Depression vs Adult Depression
| Feature | Childhood Depression | Adult Depression |
|---|---|---|
| Mood presentation | Irritability may predominate over sadness (DSM-5 allows) | Sadness/depressed mood predominant |
| Cognitive features | Developmentally simpler (less rumination; concrete negative thoughts) | Abstract rumination, guilt, hopelessness more typical |
| Somatic complaints | More common (headache, stomach ache) | Less prominent |
| Psychomotor changes | May be more agitation than retardation | Either agitation or retardation |
| Psychotic features | Rare | More common in severe depression |
| Anhedonia | Boredom, play refusal, withdrawal from peers | Anhedonia classic; loss of pleasure in previous interests |
| School | School refusal, academic decline | Occupational impairment |
| Suicidality | Less lethal ideation; plans less detailed; impulsive attempts | More lethal means; more planned; completed suicide more common |
| Comorbidity | Anxiety (>50%), ADHD, CD common | Anxiety, SUD, pain conditions |
| Antidepressants | Fluoxetine (age 8+), Escitalopram (age 12+) | Full range of antidepressants |
| Response to SSRIs | Good but lower NNT than adults; combination with CBT superior | SSRIs effective; augmentation strategies well-studied |
| Black box warning | Yes, suicidal ideation (FDA BBW) | No pediatric warning for adults |
| Psychotherapy | CBT (Coping Cat, ACTION program); TF-CBT if trauma | CBT, IPT, psychodynamic all evidence-based |
| TADS equivalent | TADS (adolescents) | STAR*D (adults) |
| Biological features | Less HPA axis abnormality; growth hormone blunting | HPA hyperactivation; dexamethasone non-suppression |
TABLE 8: ABA vs ESDM vs TEACCH
| Feature | ABA (Applied Behavior Analysis) | ESDM (Early Start Denver Model) | TEACCH (Structured Teaching) |
|---|---|---|---|
| Theoretical basis | Skinnerian operant conditioning | Developmental + ABA hybrid; relationship-based | Structured teaching; cognitive disability model |
| Age range | Any age (most evidence <5 years) | 12–60 months | Any age; school-age to adult |
| Intensity | 20–40 hours/week (intensive models) | 20–25 hours/week | Variable; lower intensity (classroom-based) |
| Approach | Adult-directed; discrete trial training | Child-directed play; adult follows child's lead | Structured environment; visual supports |
| Learning context | Mostly table-based (DTT); also NET | Natural play environments; everyday routines | Structured physical and temporal environment |
| Visual supports | Used in some models | Yes | Central feature (picture schedules, work systems) |
| Evidence base | Strongest overall; multiple RCTs; decades of research | Strong, Dawson et al. (2010) RCT; developmental gains superior to community tx | Moderate; primarily observational; widely accepted in schools |
| Criticism/controversy | Historical concerns about aversives (no longer used); intensity/rigidity; child-led balance | More recent; less long-term data | Less intensive, may not drive change as much in severe ASD |
| Best suited for | Skill acquisition across any level; challenging behavior | Young children, early intervention window | School settings, life skills, transition planning |
| Delivered by | BCBA (Board Certified Behavior Analyst) + therapy team | Trained therapists + parent coaching | Trained educators + parents |
| Parent involvement | Variable by program | Central, parents trained as co-therapists | Yes, home carryover |
| Generalization | Targeted explicitly (NET improves generalization) | Built-in through natural context | Built-in through routine/structure |
| NICE guidance | Included in guidance | Included | Included |
ESDM is the most examined newer approach, know the Dawson 2010 RCT finding (superior developmental gains vs community treatment as usual in 18–30 month olds). ABA has the most cumulative evidence. TEACCH is the most commonly implemented in school settings. All three are recommended in NICE guidelines for ASD.
TABLE 9: Haloperidol vs Aripiprazole for Tics (Tourette Syndrome)
| Feature | Haloperidol | Aripiprazole |
|---|---|---|
| Class | Typical (first-generation) antipsychotic | Atypical (third-generation); partial D2 agonist |
| Mechanism | Potent D2 blockade | Partial D2 agonism (stabilizer); 5HT1A partial agonist |
| Tic efficacy | Highest of all agents, most evidence historically | Good, comparable to risperidone; several RCTs |
| Starting dose | 0.25–0.5mg/day; titrate slowly | 2mg/day; titrate to 5–20mg/day |
| EPS risk | HIGH, dystonia, parkinsonism, akathisia | Low |
| Tardive dyskinesia | Significant risk with long-term use | Low |
| Weight gain | Moderate | Moderate |
| Metabolic effects | Moderate | Less than risperidone; moderate |
| Prolactin elevation | Yes, significant | Minimal (actually reduces prolactin, partial D2 agonist) |
| Sedation | Significant | Mild–moderate |
| Current clinical preference | Last resort, when all others failed | First-choice antipsychotic for tics currently |
| Comorbid ADHD | Does not address ADHD | Adjunct with alpha-2 agonist for ADHD |
| Monitoring | EPS check, tardive dyskinesia (AIMS), prolactin | Metabolic (weight, glucose, lipids), AIMS |
Haloperidol has the MOST EVIDENCE for tic reduction but the WORST SIDE EFFECT PROFILE. Aripiprazole is the CURRENT PREFERRED antipsychotic for tics. Exam may test both, know the distinction between evidence base vs. clinical preference.
TABLE 10: Methylphenidate Formulations Comparison
| Formulation | Brand (example) | Release Profile | Duration | Notes |
|---|---|---|---|---|
| Immediate Release (IR) | Ritalin | Single peak | 4–6 hours | 2–3x daily dosing; rebound effect |
| Sustained Release (SR) | Ritalin SR | Continuous | 6–8 hours | Inconsistent absorption; largely replaced |
| OROS (Osmotic Release) | Concerta | 22% IR + 78% osmotic | 10–12 hours | Once-daily; gold standard LA; most studied |
| Bimodal (LA) | Ritalin LA | 50% IR + 50% delayed | 8–10 hours | Simulates twice-daily IR |
| Extended Release Beads | Medikinet XL | 40% IR + 60% ER | 8–10 hours | Can be sprinkled on food |
| Liquid | Quillivant XL | Extended release suspension | 10–12 hours | For children who cannot swallow tablets |
| Transdermal patch | Daytrana | Continuous (worn 9h) | 10–12h (remove patch) | Skin irritation common; flexible dosing |
Concerta (OROS-MPH) is the best-studied once-daily formulation. The 22/78 IR/LA split is designed to replicate three-dose IR schedule pharmacokinetically. Switching between formulations requires re-titration, dose equivalence is NOT 1:1.
TABLE 11: Intellectual Disability Severity: Functional Comparison
| Severity | IQ Range | Conceptual Skills | Social Skills | Practical Skills | Educational Prognosis |
|---|---|---|---|---|---|
| Mild | ~50–69 | Below grade level; literacy possible; abstract thinking limited | Immature but functional; gullible; friendship possible | Some self-care independence; simple employment possible; needs support for complex decisions | Educable; can reach ~6th grade academic level |
| Moderate | ~35–49 | Limited literacy (few words); simple math; relies on concrete | Simple language; close relationships with familiar others; can participate in supervised social settings | Basic self-care with training; semi-independent in familiar settings; simple job tasks | Trainable; can learn basic vocational skills |
| Severe | ~20–34 | Minimal conceptual skills; simple language understood; few words expressed | Relies on close familiar relationships; limited verbal communication | Requires support for most ADLs; may achieve some self-care skills with extensive training | Requires lifelong support; some communication possible |
| Profound | <20 | Relies on sensory/physical interaction; no symbolic function | Pre-symbolic; nonverbal communication; responds to familiar persons | Fully dependent; care needs are extensive | Requires total care; minimal independent function |
EXAM PEARL, DSM-5 CRITICAL: In DSM-5, SEVERITY IS DETERMINED BY ADAPTIVE FUNCTIONING, NOT IQ. IQ ranges are provided only as approximate guides. A person with IQ 52 who has strong adaptive skills (supported by family, good social environment) may have MILD ID by DSM-5, not moderate. The examiner may specifically test this.
| *Sources: Kaplan & Sadock (11th ed.) | Rutter's (6th ed.) | Lewis's (5th ed.) | DSM-5-TR | ICD-11* |
|---|
PYQ Frequency Analysis
Sources: PG exams MD Psychiatry question papers (collated 2008–2025), PG exams, and Exam pattern analysis. Kaplan & Sadock (11th ed.), Rutter's (6th ed.), Lewis's (5th ed.)
Child & Adolescent Psychiatry consistently contributes 1–2 long questions (10–20 marks) and 2–4 short notes (5 marks each) in Paper III. Total expected contribution: 25–40 marks out of ~100 in Paper III. The topics below are ranked by frequency of appearance across 17+ years of question data.
SECTION 1: FREQUENCY RANKING TABLE
| Rank | Topic | Frequency | Typical Format | Marks |
|---|---|---|---|---|
| 1 | ADHD, assessment and management | Very High (appears ~80% of years) | Long question | 10–20 |
| 2 | Autism Spectrum Disorder, features, assessment, management | Very High (~75% of years) | Long question | 10–20 |
| 3 | Intellectual Disability, classification, etiology, assessment | High (~65% of years) | Long question or short note | 10–15 |
| 4 | Child abuse, types, indicators, management, POCSO | High (~60% of years) | Long question or short note | 10–15 |
| 5 | Conduct Disorder, features, management | Moderate-High (~50% of years) | Long question or short note | 10 |
| 6 | School refusal, classification, management | Moderate (~45% of years) | Short note or combined | 5–10 |
| 7 | Tourette Syndrome, criteria, treatment | Moderate (~40% of years) | Short note | 5–10 |
| 8 | Enuresis, assessment, treatment | Moderate (~40% of years) | Short note | 5–10 |
| 9 | Separation Anxiety Disorder | Moderate (~35% of years) | Short note | 5 |
| 10 | Pediatric depression, pharmacotherapy, TADS | Moderate (~35% of years) | Short note or part of long Q | 5–10 |
| 11 | Munchausen by Proxy / Factitious Disorder Imposed on Another | Moderate (~35% of years) | Short note | 5 |
| 12 | Specific Learning Disorders, dyslexia | Moderate (~30% of years) | Short note | 5 |
| 13 | Fragile X Syndrome | Moderate (~30% of years) | Short note | 5 |
| 14 | Down Syndrome, features, psychiatry | Moderate (~30% of years) | Short note | 5 |
| 15 | Attachment Disorders, RAD vs DSED | Low-Moderate (~25% of years) | Short note | 5 |
| 16 | Gaming Disorder (ICD-11) | Low-Moderate (~20% of years, rising) | Short note | 5 |
| 17 | Selective Mutism | Low-Moderate (~20% of years) | Short note | 5 |
| 18 | ODD, diagnostic criteria | Low (~15% of years) | Short note | 5 |
| 19 | Encopresis | Low (~15% of years) | Short note | 5 |
| 20 | Rett Syndrome | Low (~15% of years) | Short note | 5 |
SECTION 2: HIGH-FREQUENCY TOPIC DEEP DIVES
Topic 1: ADHD: The Perennial Long Question
Why it appears every year: ADHD is the highest-prevalence child psychiatry diagnosis, has clear pharmacological management points, and tests both clinical knowledge and therapeutic decision-making.
What examiners consistently ask:
- "Discuss the assessment and management of ADHD" (most common phrasing)
- "Enumerate the DSM-5 criteria for ADHD"
- "Compare methylphenidate and atomoxetine"
- "What are the behavioral interventions in ADHD?"
- "What is the MTA study? What are its findings?"
Examiner hotspots, points that distinguish good from excellent answers:
| Point | Common Answer | Distinguishing Answer |
|---|---|---|
| Age of onset | Age 12 | DSM-5 changed from age 7 (DSM-IV) to age 12, mentioning this change is a mark-earner |
| Symptom threshold adults | Same as children | DSM-5: 5 symptoms (not 6) for adults ≥17 years |
| Stimulant side effects | Appetite, insomnia | Mention growth suppression (modest 0.5–1 cm/year), cardiovascular monitoring, rebound phenomenon |
| Atomoxetine onset | "Works for ADHD" | Onset is 4–6 WEEKS, not same-day like stimulants. This is tested specifically. |
| MTA study | "Medication works" | Combined > medication alone > behavioral alone > placebo for core symptoms; combined better for comorbid anxiety |
| Non-pharmacological | "Counseling" | Name specific programs: BPT, Triple P, Incredible Years, Daily Report Card, classroom accommodations |
Template answer structure (20-mark question):
- Introduction + epidemiology (2 marks)
- DSM-5 criteria in full, both domains (4 marks)
- Assessment, history, rating scales, investigations, differentials (5 marks)
- Management, multimodal: psychoeducation + behavioral + pharmacotherapy + school (7 marks)
- Follow-up and prognosis (2 marks)
Topic 2: Autism Spectrum Disorder
What examiners consistently ask:
- "Describe the clinical features and management of ASD"
- "What is the role of ADOS-2 and ADI-R in diagnosis of ASD?"
- "Enumerate early red flags of autism"
- "Compare DSM-IV and DSM-5 criteria for ASD" (Asperger's elimination)
- "What are the pharmacological options in ASD?"
Examiner hotspots:
| Point | Common Answer | Distinguishing Answer |
|---|---|---|
| Criteria structure | "Social problems + repetitive behaviors" | Criterion A (all 3 social communication items) AND Criterion B (2 of 4 RRBI items), know the structure |
| DSM-5 change | "ASD is a spectrum" | Asperger's eliminated; severity levels 1–2–3; ADHD now allowed as comorbidity |
| Severity levels | "Mild/moderate/severe" | Level 1/2/3 with specific descriptors for EACH level in BOTH domains |
| Screening tool | "M-CHAT" | M-CHAT-R/F at 16–30 months; sensitivity/specificity after follow-up |
| Gold standard diagnosis | "Clinical assessment" | ADOS-2 + ADI-R together, know what each assesses |
| Pharmacotherapy | "Risperidone" | Risperidone AND aripiprazole are the ONLY FDA-approved agents (for irritability, not core symptoms). Mention melatonin for sleep. |
| Intervention | "ABA" | Distinguish ABA, ESDM (Dawson 2010 RCT), TEACCH, know key features of each |
Genetic investigations point (frequently missed):
Chromosomal microarray is first-tier genetic investigation, not karyotype. Yield 15–20% for clinically significant variants. This is a specific, testable fact.
Topic 3: Intellectual Disability
What examiners consistently ask:
- "Classify intellectual disability", this is the classic opener
- "Describe the etiology of intellectual disability"
- "Enumerate the behavioral phenotypes of common genetic syndromes"
- "How is Down syndrome distinguished from other causes of ID?"
Examiner hotspots:
| Point | Common Answer | Distinguishing Answer |
|---|---|---|
| DSM-5 severity | "Based on IQ" | Based on ADAPTIVE FUNCTIONING, IQ is a guide only. This is a specific DSM-5 change from DSM-IV. |
| Most common chromosomal cause | "Down syndrome" | Correct. Trisomy 21 (95%), Robertsonian translocation (4%), mosaic (1%). |
| Most common inherited cause | Often missed | Fragile X syndrome (FMR1, CGG repeat expansion, X-linked) |
| Most common preventable cause | Often missed | PKU (dietary) OR FASD (alcohol abstinence), accept both, clarify context |
| Adaptive behavior assessment | "IQ test" | Vineland-3 is the gold standard adaptive behavior measure, separate from IQ testing |
| Chromosomal microarray | Rarely mentioned | First-tier genetic investigation; higher yield than karyotype |
| Psychiatric comorbidity | "Behavioral problems" | Prevalence 30–40%; diagnostic overshadowing is a specific concern |
Behavioral phenotype table is exam gold, know these cold:
- Down: sociable, stubborn, Alzheimer's risk
- Fragile X: social anxiety, gaze avoidance, perseverative speech, hand-flapping
- Angelman: happy, laughter, seizures, no speech
- Prader-Willi: hyperphagia, skin-picking, food-seeking, rigidity
- Williams: loquacious, hypercalcemia, supravalvular aortic stenosis
Topic 4: Child Abuse
What examiners consistently ask:
- "Describe the types and indicators of child abuse"
- "What is Munchausen by proxy? How is it recognized?"
- "What is the role of the psychiatrist in cases of child abuse?"
- "Discuss POCSO Act 2012" (specifically for Indian exams)
- "What is the forensic interview? What are its principles?"
Examiner hotspots:
| Point | Common Answer | Distinguishing Answer |
|---|---|---|
| Physical abuse indicators | "Bruises and fractures" | Specific suspicious patterns: TEN-4 FACES P for bruises; posterior rib fractures; bucket-handle metaphyseal fractures; spiral fractures in non-mobile infants |
| Abusive head trauma triad | Often incomplete | Subdural hematoma + retinal hemorrhages + no external injury, HIGH SPECIFICITY combination |
| Munchausen by proxy | "Mother makes child sick" | DSM-5 term = Factitious Disorder Imposed on Another; perpetrator most commonly mother; illness resolves with separation; key features |
| Forensic interview standard | "Interview the child" | NICHD Protocol, open-ended questions first; no leading questions; single interview preferred; trained professional only; before medical examination |
| Mandatory reporting India | "Report to authorities" | POCSO Act 2012 Section 19, ALL persons must report; SJPU or local police; failure = criminal offense (Section 21) |
| Long-term consequences | "Trauma" | Specific: PTSD, BPD, depression, substance use, HPA dysregulation, hippocampal atrophy, epigenetic changes |
Topic 5: Conduct Disorder
What examiners consistently ask:
- "Discuss the management of conduct disorder"
- "What are the differences between ODD and conduct disorder?"
- "What is the role of multisystemic therapy?"
- "What are callous-unemotional traits?"
Examiner hotspots:
| Point | Common Answer | Distinguishing Answer |
|---|---|---|
| Management | "Counseling and medication" | MST (Multisystemic Therapy) is the gold standard for serious adolescent CD, name it and describe it |
| CU traits | "Lack of empathy" | DSM-5 "Limited Prosocial Emotions" specifier; predicts worse prognosis; treatment modification needed (reward-based, not punishment-based) |
| Pharmacotherapy | "No specific drug" | Correct, no drug for CD itself; treat ADHD (stimulants, strongest evidence); mood stabilizers (lithium) for severe aggression; risperidone for residual aggression |
| Childhood vs adolescent onset | Often not distinguished | Childhood onset: before 10; more male; ADHD comorbidity; worse prognosis. Adolescent onset: peer-influenced; more female; better prognosis. |
SECTION 3: MEDIUM-FREQUENCY TOPICS: RAPID REVISION
School Refusal
Key examiner points:
- NOT a DSM diagnosis, functional presentation
- Distinguish from TRUANCY (distress vs. no distress; parents aware vs. unaware)
- Kearney-Silverman 4 functions, know all four
- Core principle: rapid return to school, mention this first
- Parental accommodation is the key maintenance factor
- Pharmacotherapy: SSRIs if CBT insufficient; CAMS trial evidence
Tourette Syndrome
Key examiner points:
- Coprolalia in only 10–15%, NOT required for diagnosis (most common misconception tested)
- DSM-5 removed the ≥3 month tic-free period requirement (DSM-IV had it)
- CBIT is first-line behavioral treatment, know components (HRT + functional intervention)
- Aripiprazole currently preferred pharmacotherapy (not haloperidol, most evidence but worst side effects)
- ADHD comorbidity: guanfacine ER preferred (treats both)
- Premonitory urge, specific, testable concept
Enuresis
Key examiner points:
- Primary vs secondary distinction, secondary requires more investigation
- Bell-and-pad: best long-term outcomes; 75–85%; 8–12 weeks
- Desmopressin: faster but high relapse rate (~80% on stopping)
- Imipramine: falling out of favor; cardiac toxicity; toxic in overdose, not first-line
- Watch for hyponatremia with desmopressin (restrict fluids)
Munchausen by Proxy
Key examiner points:
- DSM-5 name: Factitious Disorder Imposed on Another
- Perpetrator: mother >90% of cases
- Illness resolves when separated from perpetrator, pathognomonic
- Mother appears devoted, medically knowledgeable, calm during child's crises
- Mandatory reporting applies
- Management: immediate safety of child; remove from perpetrator
Pediatric Depression and TADS
Key examiner points:
- TADS: combination 71% > fluoxetine 61% > CBT 43% > placebo 35%
- Fluoxetine: FDA-approved age 8+ for depression; age 7+ for OCD
- Escitalopram: FDA-approved age 12+ for depression
- Black box warning: suicidal IDEATION (not completed suicide); ~2% absolute increase over placebo
- Combined treatment protects against suicidal ideation associated with medication alone
- Duration: 6–12 months post-remission
SECTION 4: EMERGING TOPICS (RISING FREQUENCY)
Gaming Disorder (ICD-11)
Why it's rising: ICD-11 released 2022; examiners testing new classifications.
Key points:
- ICD-11 Code 6C51: OFFICIAL diagnosis (DSM-5 lists as "condition for further study" only)
- Three criteria: impaired control + increasing priority + continuation despite consequences
- Duration: ≥12 months
- Neurobiological overlap with substance use disorders (striatal dopamine, PFC inhibitory control)
- Treatment: CBT (most evidence), MI, family therapy
- India-specific: awareness of gaming cafes, online gaming culture in adolescents
Specific Learning Disorders
Why it's rising: Greater awareness in Indian school system; ADHD + SLD comorbidity questions.
Key points:
- DSM-5 umbrella term covers dyslexia, dyscalculia, dysgraphia under specifiers
- Dyslexia = phonological processing deficit (NOT a vision problem, NOT letter reversal myth)
- IQ discrepancy model abandoned in DSM-5 (SLD with average IQ is still SLD)
- Treatment: systematic phonics instruction (Orton-Gillingham), not just "extra time"
SECTION 5: QUESTION FORMATS AND ANSWER TEMPLATES
Long Question Template (20 marks): ADHD or ASD
Short Note Template (5 marks)
Comparison Question Template (10 marks)
SECTION 6: MOST TESTED SPECIFIC FACTS (HIGH-YIELD ONE-LINERS)
SECTION 7: PREDICTIVE PRIORITY LIST FOR EXAM 2026
Based on 17+ years of question patterns AND recent ICD-11/DSM-5 changes creating new testable material:
Tier 1: Prepare for 20-mark long question
- ADHD, assessment and management (appears almost every year)
- ASD, clinical features + assessment pathway (appears almost every year)
- Intellectual disability, classification + evaluation (high frequency)
Tier 2: Prepare for 10-mark long question OR 5-mark short note
- Child abuse, indicators + POCSO Act + management
- Conduct Disorder, management (MST emphasis)
- Pediatric depression, TADS + pharmacotherapy
- Tourette Syndrome, criteria + CBIT + pharmacotherapy
Tier 3: Prepare 5-mark short note only
- School refusal
- Enuresis (bell-and-pad vs desmopressin)
- Munchausen by proxy / FDIA
- Selective mutism
- Fragile X syndrome
- Down syndrome + Alzheimer's
- Gaming disorder (ICD-11)
- RAD vs DSED
- Specific learning disorders (dyslexia)
Tier 4: Know the headline facts only
- Encopresis
- Rett syndrome
- Prader-Willi vs Angelman (imprinting)
- Williams syndrome
EXAM STRATEGY, FINAL: For Paper III Child & Adolescent section, the safest strategy is: (1) Master ADHD and ASD completely, one of these WILL appear as a long question; (2) Have a solid 10-mark answer for ID and child abuse; (3) Know the short note format for Tourette's, enuresis, school refusal, and Munchausen by proxy; (4) Know the ICD-11 specific points, Gaming Disorder, ADHD reclassification, these are new and examiners are testing them.
| *Sources: PG exams MD Psychiatry question collation 2008–2025 | Kaplan & Sadock (11th ed.) | Rutter's (6th ed.) | Lewis's (5th ed.) | DSM-5-TR | ICD-11* |
|---|
Quick Review
Note: All names, identifying details, and clinical scenarios are entirely fictitious. Any resemblance to real persons is coincidental.
Sources: Kaplan & Sadock (11th ed.), Rutter's (6th ed.), Lewis's (5th ed.), DSM-5-TR, ICD-11
VIGNETTE 1: ADHD: School-Age Child
Case
Arjun, 8 years old, is brought by his mother with complaints that "he just can't sit still and never finishes his work." His class teacher has sent three written notes home this term. She reports that Arjun gets up from his seat frequently, disturbs classmates, rarely completes written work, loses his pencil box "every other day," and stares out the window during lessons. His mother says he is the same at home, unable to sit through dinner, always interrupting conversations, leaves his homework half-done. He was a full-term normal delivery with no perinatal complications. Developmental milestones were normal. His father had "similar problems in school." Physical examination is unremarkable. Visual acuity and hearing are normal.
Questions
Q1: What is the most likely diagnosis? Enumerate the diagnostic criteria.
Most likely diagnosis: ADHD, Combined Presentation (DSM-5: 314.01)
DSM-5 Criteria met:
- Inattention (≥6 symptoms present for ≥6 months): fails to attend to details (careless mistakes), difficulty sustaining attention (stares out of window), doesn't follow through on instructions (unfinished homework), disorganized (loses pencil box), avoids sustained mental effort (incomplete written work), easily distracted
- Hyperactivity-Impulsivity (≥6 symptoms): leaves seat when expected to remain, talks excessively (disturbs classmates), interrupts others (cuts into conversations)
- Onset before age 12: symptoms present since early school years
- Two or more settings: school AND home
- Functional impairment: academic, social
Q2: What rating scales would you use, and how would you proceed with assessment?
Rating scales:
- Conners-3 (parent + teacher versions), gold standard
- SNAP-IV (parent + teacher), directly maps to DSM criteria
- Vanderbilt ADHD Scale, primary care friendly; screens for comorbidities
Assessment:
- Full developmental and family history (father's similar history suggests genetic loading)
- Academic records, class teacher report
- Medical: thyroid function (if clinically indicated), hearing/vision screen (done, normal), iron levels if fatigue/pallor
- Neuropsychological: WISC-V (rule out learning disability; profile PFC executive function)
- BRIEF (Behavior Rating Inventory of Executive Function)
Q3: Outline a management plan.
Multimodal approach:
- Psychoeducation, parents and teacher; explain brain-based model; reduce blame
- Behavioral Parent Training, Incredible Years or Triple P; positive attention, reward charts, consistent consequences
- School accommodations, preferential seating, Daily Report Card, extended time, movement breaks
- Pharmacotherapy, Methylphenidate (start 0.3 mg/kg IR; titrate to 0.5–1.0 mg/kg/day LA formulation); monitor weight, BP, sleep, appetite
- Follow-up, monthly initially; biannual height/weight; annual reassessment
Two-setting impairment is mandatory. Arjun has symptoms at school AND home, this satisfies the criterion. A child with ADHD-like behavior only at school may have a learning disorder or anxiety instead.
VIGNETTE 2: Autism Spectrum Disorder: Early Presentation
Case
Kavya, 2 years 4 months, is brought by her parents to the pediatric OPD. Her mother reports: "She doesn't look at us when we call her name, doesn't point at things she wants, and just lines up her toy cars for hours." Kavya was walking by 13 months. She said "mama" and "ball" at 14 months but stopped using these words by 18 months. She does not combine words. During the consultation, Kavya does not make eye contact with the examiner, does not look at her mother when the examiner waves a toy, and spends the session spinning the wheels of a toy car repetitively. She does not respond to her name being called three times. She becomes extremely distressed when her mother attempts to remove the toy car.
Questions
Q1: What is the most likely diagnosis? What are the concerning features?
Most likely diagnosis: Autism Spectrum Disorder (ASD), pending full assessment
Concerning features:
- Language regression (words at 14 months, lost by 18 months), any regression at any age is a red flag
- Absent joint attention (no pointing, no looking at examiner's toy)
- No response to name (multiple times)
- Absent eye contact
- Restricted, repetitive behavior (wheel-spinning stereotypy, insistence on maintaining toy)
- Extreme distress at routine change
- No spontaneous two-word phrases at 28 months
Q2: What screening tool is appropriate, and what does it assess?
M-CHAT-R/F (Modified Checklist for Autism in Toddlers, Revised with Follow-Up):
- Age: 16–30 months, appropriate for Kavya
- 20 yes/no parent-completed items
- Screens for: response to name, pointing, joint attention, interest in other children, imitative play
- Scoring: Low risk (0–2), Medium risk (3–7 → do follow-up interview), High risk (8–20)
- Kavya would score high risk (failure on multiple critical items)
- Follow-up interview improves sensitivity/specificity
Q3: Outline the comprehensive assessment pathway.
- Developmental pediatrician/child psychiatrist assessment
- ADOS-2 Toddler Module (12–30 months, minimal verbal), structured observation
- ADI-R, structured parent interview for developmental history
- Vineland-3, adaptive behavior assessment
- Mullen Scales of Early Learning, cognitive and language
- Speech and language therapy evaluation
- Occupational therapy, sensory profile, fine motor
- Hearing test (mandatory)
- Medical investigations: chromosomal microarray (first-tier genetic), Fragile X testing, EEG (regression + concern for Landau-Kleffner)
- Ophthalmology
Q4: What early interventions would you recommend?
- ESDM (Early Start Denver Model), 20–25h/week; evidence for 18–30 month developmental gains
- Speech and language therapy, intensive, communication-focused
- Occupational therapy, sensory integration, play development
- Parent-mediated intervention, JASPER (Joint Attention, Symbolic Play, Engagement and Regulation)
- Begin immediately, do not wait for formal diagnostic confirmation when red flags are clear
Language regression at any age requires urgent assessment. In Kavya's case, regression + no joint attention + stereotypies at 28 months = ASD until proven otherwise. Do not reassure parents that "she'll catch up."
VIGNETTE 3: Intellectual Disability with Behavioral Problems
Case
Rohan, 14 years old, has been known to a special school for the past 5 years with a diagnosis of moderate intellectual disability (IQ 42 on WISC-V, obtained 3 years ago). He is brought to psychiatry OPD by his mother with a 3-month history of increased self-biting, head-banging against the wall, and episodes of screaming for 30–60 minutes, occurring 3–5 times daily. His mother reports no recent change in routine or family circumstances. Physical examination reveals a long face, prominent ears, and she mentions he has been "always shy" with people. She is a known carrier of Fragile X.
Questions
Q1: What is the likely etiology of this patient's ID, and what behavioral phenotype would you expect?
Likely etiology: Fragile X Syndrome (FMR1 full mutation, X-linked)
- Clinical clues: long face, prominent ears, male, moderate ID, maternal carrier status
- Behavioral phenotype expected:
- Social anxiety and gaze avoidance
- Repetitive/perseverative speech
- Hand-flapping (may have been present in childhood)
- ADHD-like features (hyperactivity, impulsivity)
- Sensory hypersensitivity
Q2: What is the differential diagnosis for the increase in self-injurious behavior (SIB)?
In ID, behavioral change is communication, the child cannot say "my ear hurts" or "I'm scared of the new teacher." The FIRST step is always ruling out PAIN and MEDICAL causes.
Q3: How would you assess and manage this presentation?
Assessment:
- Full medical examination: ears (otoscopy), teeth, abdomen (constipation)
- Sleep history (insomnia common in Fragile X)
- Functional Behavior Assessment (FBA): antecedents, behavior, consequences (ABC chart) over 2 weeks
- Psychiatric evaluation: depression (may present as SIB in ID), anxiety, emerging psychosis
- EEG (consider given regression and SIB)
Management:
- Treat underlying medical cause if found
- Functional Behavior Analysis → function-based behavioral intervention
- Environmental modifications: predictable routine, visual schedules, sensory accommodations
- Pharmacotherapy (if behavioral and medical causes addressed):
- Risperidone (FDA-approved for irritability in ASD; used off-label in ID): 0.25–0.5mg, titrate slowly
- SSRI if anxiety component prominent (sertraline)
- Melatonin for sleep
- Caregiver support and training
- School consultation
VIGNETTE 4: Child Abuse: Non-Accidental Injury
Case
Siddharth, 9 months old, is brought to the emergency department. His mother states he "rolled off the bed" this morning. On examination, he is irritable and difficult to console. The attending pediatrician finds: two circular burns (approximately 0.8 cm diameter) on the left buttock, a bruise on the right ear, and an older healing bruise on the neck. There are no other external injuries. An urgent CT brain is performed, revealing bilateral thin subdural hematomas. Ophthalmology reports bilateral retinal hemorrhages on fundoscopic examination. The mother appears anxious but does not ask about the CT findings.
Questions
Q1: What does this clinical picture suggest, and what specific features support this?
Clinical picture: Non-Accidental Injury (NAI) / Abusive Head Trauma, high probability
Supporting features:
Q2: What is the immediate management?
- Admit to pediatric ward (safe environment; further evaluation)
- Full skeletal survey (mandatory): posterior rib fractures, metaphyseal fractures (bucket-handle), multiple fractures in different stages of healing
- Ophthalmology consultation (already done, retinal hemorrhages confirmed)
- Neurosurgical review (bilateral SDH)
- Mandatory report to Child Protection Services immediately, reasonable suspicion is sufficient; do not wait for certainty
- SJPU/Police notification under POCSO Act 2012 (India), Section 19
- Do NOT return child to parents until child protection investigation complete
- Forensic documentation, photograph all injuries with scale bar, detailed medical notes
Q3: What are the long-term consequences of abusive head trauma?
- Cognitive impairment (40–60%)
- Epilepsy (20–30%)
- Visual impairment (50%)
- Motor deficits / cerebral palsy
- Language delay
- Behavioral problems, ADHD-like symptoms
- PTSD
The triad for abusive head trauma: subdural hematoma + retinal hemorrhages + no external signs of trauma. The absence of external bruising on the head does NOT rule out AHT. The mechanism is acceleration-deceleration, not direct impact.
VIGNETTE 5: Conduct Disorder: Adolescent
Case
Vikram, 15 years old, is referred by the juvenile justice board following his third arrest in 6 months for theft. His mother reports that problems started at age 11: he began staying out late, was suspended from school at 12 for fighting, and has been truanting for the past year. He has broken into a neighbor's garage and stolen tools, was caught shoplifting twice, and threatened a classmate with a knife at 13. He shows no remorse: "They had it coming." He has a history of cruelty to neighborhood cats. His father has a history of antisocial personality disorder and alcohol dependence. Vikram has no learning difficulties; his IQ is estimated at 96. Neuropsychological testing shows intact working memory but impaired emotion recognition (fearful and sad faces).
Questions
Q1: Diagnose and describe the clinical features present.
Diagnosis: Conduct Disorder, Childhood-Onset Type, Severe, with Limited Prosocial Emotions (Callous-Unemotional traits)
Features present:
- Aggression: threatened with a knife (weapon use), fighting at school
- Destruction: broke into neighbor's garage
- Deceitfulness/theft: shoplifting, theft from neighbor
- Rule violations: truancy, staying out (before 13), running away implied
- Callous-Unemotional (CU) traits: absent remorse ("they had it coming"), impaired emotion recognition, cruelty to animals
- Childhood onset (<10 not specified but problems from 11, early adolescent onset)
- Risk factors present: paternal ASPD and alcohol dependence
Q2: What is the significance of callous-unemotional (CU) traits in this case?
CU traits (the "Limited Prosocial Emotions" specifier) indicate:
- Absence of guilt/remorse
- Callousness and lack of empathy
- Unconcerned about performance
- Shallow affect
Clinical implications:
- Worse prognosis, CU traits predict persistence into adult ASPD
- Standard PMT less effective, punishment-based approaches fail because fear conditioning is blunted (amygdala hyporeactivity)
- Reward-based approaches preferred, enhanced reward sensitivity; use positive reinforcement
- Impaired emotion recognition (fearful/sad faces) consistent with CU neurobiological profile (reduced amygdala activation to fear cues)
- Specialist input required, standard behavioral interventions insufficient
Q3: What treatment approach has the strongest evidence for Vikram's presentation?
Multisystemic Therapy (MST):
- Community-based, intensive (3–5 months)
- Addresses ALL systems: family, peer, school, neighborhood
- Home visits, multiple contacts per week
- Addresses family dysfunction (mother needs support given absent/antisocial father)
- Separates Vikram from delinquent peers
- Evidence: superior to individual therapy, group therapy, residential treatment for serious juvenile offenders
- Particularly indicated given: juvenile justice involvement, risk of out-of-home placement
Pharmacotherapy:
- Treat if ADHD comorbidity suspected (assessment needed)
- Mood stabilizers (lithium) for severe impulsive aggression if present
- Low-dose risperidone as last resort for severe aggression
MST is the gold-standard answer for adolescent CD with justice involvement. Name it, explain it. CU traits + poor emotion recognition + childhood-onset = high-risk profile. This vignette has everything the examiner wants to test.
VIGNETTE 6: Selective Mutism
Case
Priya, 5 years 8 months, was referred by her school after being in KG for 6 months without speaking a single word. Her teachers report she follows instructions, participates in group activities, and seems to understand everything, but has never spoken to a teacher, classmate, or school staff member. She communicates via gestures and nodding. Her parents report she is "completely normal at home", she talks non-stop with family, narrates stories, and has age-appropriate language. She was assessed by a speech therapist who found normal receptive and expressive language in the home context. She is the elder of two children; family relationships are described as warm and close. She appears anxious in new situations and has always been "shy."
Questions
Q1: What is the diagnosis and how does it differ from language disorder and ASD?
Diagnosis: Selective Mutism (DSM-5: 312.23)
Criteria met:
- Consistent failure to speak in specific social situations (school) despite speaking in others (home)
- Interferes with educational achievement
- Duration: ≥1 month (not limited to first month of school)
- Not due to language disorder (normal language confirmed by SLT)
Distinguishing from language disorder:
- Language disorder: impaired language IN ALL SETTINGS
- Selective mutism: normal language in comfort zone; mutism is context-specific
Distinguishing from ASD:
- ASD: social communication deficits are PERVASIVE, not context-limited; additional RRBIs
- Selective mutism: speaks normally at home; social engagement with family is normal; no RRBIs
Q2: How would you assess this child?
- Detailed history: onset, settings where mute vs. speaks, temperament (behavioral inhibition since infancy), family history (anxiety, selective mutism)
- School observation (or report): what child CAN do (participates non-verbally, follows instructions)
- Parent-completed anxiety rating: SCARED (Screen for Child Anxiety Related Disorders)
- Rule out: hearing impairment, language disorder, ASD (already largely ruled out)
- Psychological assessment: formal assessment in comfort setting to document language normality
Q3: Outline the management plan.
1. Psychoeducation:
- Selective mutism = anxiety-based, not willful defiance
- School staff must NOT pressure child to speak; avoid drawing attention to mutism in class
- No "just speak" demands
2. Behavioral Intervention (first-line):
- Stimulus fading: Priya speaks to mother → introduce trusted adult progressively closer → eventually adult takes over conversation
- Shaping: reward approximations to speech (whisper → quiet voice → normal voice)
- Systematic desensitization: graded exposure hierarchy
- Speaks to mother in hallway outside classroom
- Whispers to teaching assistant
- Speaks to teaching assistant in quiet room
- Speaks to one classmate with mother present
- Speaks in small group
- Full class participation
3. School Collaboration:
- Trained teaching assistant as "bridging" adult
- Avoid cold-calling; allow written/gesture responses initially
- Celebrate non-verbal participation
4. Pharmacotherapy (if no response after 3–4 months of behavioral intervention):
- Fluoxetine (most evidence for selective mutism): start 5mg, titrate to 10–20mg
- SSRI works by reducing background anxiety level, making exposure more manageable
- Medication + behavioral intervention superior to either alone
Selective mutism is best conceptualized as extreme social anxiety, not a communication disorder or willful behavior. The single most important school intervention is removing pressure to speak while simultaneously implementing graded exposure. Do NOT ignore the mutism hoping it resolves, prolonged mutism entrenches the pattern.
VIGNETTE 7: Tourette Syndrome
Case
Aarav, 11 years old, is brought by his parents with a 2-year history of "habits he can't control." His parents describe eye blinking that started at age 9, later joined by nose twitching, then head jerking. In the last 6 months, he has developed throat-clearing and sniffing sounds that occur many times daily. He can sometimes suppress these "for a bit" but feels a building tension that is relieved only by performing them. They are worse when he is excited, stressed, or at the end of the school day. His teachers initially thought he had an eye problem. He has been teased at school. His parents deny any obscene words. He has trouble sitting still in class and his teacher says he "doesn't listen", he forgets instructions and loses his pencil frequently. His uncle was described as having similar movements as a child.
Questions
Q1: Diagnose and justify.
Diagnosis: Tourette Syndrome (DSM-5: 307.23)
Criteria met:
- ≥2 motor tics: eye blinking + nose twitching + head jerking (multiple motor tics)
- ≥1 vocal tic: throat-clearing + sniffing (vocal tics)
- Onset before age 18: onset age 9
- Duration >12 months: 2-year history
- Not caused by substance or medical condition
Additional features:
- Premonitory urge (building tension relieved by tic), highly characteristic
- Temporary suppression possible, also characteristic
- Waxing and waning; worse with stress/excitement
- No coprolalia (present in only 10–15%, not required for diagnosis)
- Family history (uncle), autosomal dominant with variable penetrance
Comorbidity identified: ADHD (inattention, forgets instructions, loses pencil, poor listening), needs formal assessment
Q2: How would you assess the severity of tics?
Yale Global Tic Severity Scale (YGTSS):
- Clinician-administered semi-structured interview
- Motor and vocal tic subscales
- For each: number of tics, frequency, intensity, complexity, interference
- Total Tic Score (0–50) + Impairment Rating (0–50)
- Global Severity Score = Total + Impairment
- Used for monitoring treatment response
Additional:
- PUTS (Premonitory Urge for Tics Scale)
- CPTS (Children's Premonitory Urge for Tics Scale)
- Classroom observation / teacher report
- Peer relationship assessment (teasing documented)
Q3: Outline treatment, prioritizing the comorbidity question.
Step 1, Determine primary source of impairment:
- Tics: teasing, social embarrassment, significant
- ADHD: classroom dysfunction, significant
- Both need addressing; start with the one causing more functional impairment
Step 2, Behavioral treatment for tics:
- CBIT (Comprehensive Behavioral Intervention for Tics), first-line
- Habit Reversal Training: awareness training + competing response (competing movement physically incompatible with tic)
- Functional intervention: identify tic triggers
- Relaxation training
- School psychoeducation to reduce teasing
Step 3, Pharmacotherapy for tics (if CBIT insufficient or unavailable):
- Aripiprazole 2mg/day (current preferred choice), better tolerability than typical antipsychotics
- Guanfacine ER 1mg nocte, preferred if ADHD comorbidity present (addresses both)
- NOT haloperidol as first-line (EPS risk)
Step 4, Address ADHD:
- Formal assessment first (Conners-3, Vanderbilt)
- First-line given TS: Guanfacine ER (treats both tics and ADHD)
- Atomoxetine as alternative
- Stimulants: can be added if alpha-2 agonist insufficient; monitor tics (may transiently worsen but long-term usually acceptable)
The premonitory urge is the sensory phenomenon PRECEDING the tic, a feeling of tension, itch, or pressure that is relieved by performing the tic. It is the TARGET of CBIT (competing response is trained to replace the tic in response to the premonitory urge). Understanding this mechanism is tested.
VIGNETTE 8: Gaming Disorder
Case
Rahul, 16 years old, is brought by his parents who are "at their wit's end." Over the past 14 months, Rahul has been playing online multiplayer games for 10–14 hours daily on weekdays and throughout weekends. He stopped attending school 3 months ago ("online school is better anyway"). He sleeps from 4am to 2pm, eats only when his mother brings food to his room, and has not met friends in person in 6 months. When parents attempt to restrict internet, he becomes extremely agitated, has punched a wall, and once threatened to harm himself. He has tried to cut down gaming multiple times ("I'll stop after this level") but has not managed. His parents describe him as previously a bright student with good social relationships. He denies depression but admits gaming "stops me feeling bad."
Questions
Q1: Diagnose using ICD-11 criteria.
Diagnosis: Gaming Disorder (ICD-11: 6C51)
Criteria:
- Impaired control over gaming, persistent despite attempts to reduce; unable to stop at planned time; gaming 10–14h/day
- Increasing priority, gaming takes precedence over sleep (4am–2pm sleep reversal), food (eats only when brought), school (dropped out), socializing (no peer contact 6 months)
- Continuation despite negative consequences, school dropout, social isolation, health neglect (sleep reversal, eating), family conflict, self-harm threat
Duration: 14 months (minimum 12 months met)
Impairment: Educational, social, family, physical health
Additional features:
- Withdrawal symptoms: agitation, aggression when access restricted
- Escapism: "stops me feeling bad", using gaming to regulate negative affect
- Failed attempts to control
Q2: What comorbidities would you screen for?
Q3: Outline the management plan.
1. Risk Assessment (immediate):
- Clarify self-harm threat: specific plan, intent, access to means
- Psychosocial risk assessment: family dynamics, triggers
2. Psychoeducation:
- Motivational Interviewing: explore discrepancy between gaming life and his own values
- Frame as a health problem, not moral failure
- "Gaming used to work for you; now it's working against you"
3. CBT:
- Cognitive: challenge gaming cognitions ("I'm only good at gaming," "Real life is pointless")
- Behavioral: activity scheduling, gradually introduce non-gaming activities that provide positive experience; sleep hygiene protocol (gradual circadian shift)
- Graded reduction rather than abrupt cessation
- Identify emotional triggers for gaming (negative affect coping chain)
4. Family Therapy:
- Address enabling patterns (food delivery to room; unrestricted internet access)
- Improve communication and conflict resolution
- Parental limit-setting strategies (negotiated, not imposed)
- Address parental guilt and blame
5. School Reintegration:
- Partial attendance first; identify school-related stressors
- Educational assessment if learning difficulties contributed
6. Pharmacotherapy:
- Treat comorbid depression (SSRI, sertraline/fluoxetine)
- Treat ADHD if confirmed (methylphenidate reduces gaming impulsivity)
- No specific medication for gaming disorder
7. Intensive Programs:
- If outpatient fails: structured day program with scheduled activity and limited digital access
- Inpatient only if severe self-harm risk or medical neglect
The self-harm threat in context of gaming restriction is a KEY clinical finding. Before any gaming-focused intervention, complete a formal suicide/self-harm risk assessment. Abrupt "cold turkey" gaming restriction in a patient with this level of dependence carries real risk of crisis, work with the family to plan a gradual, negotiated reduction.
VIGNETTE 9: School Refusal
Case
Ananya, 9 years old, has missed 22 of the last 30 school days. Each morning, she complains of severe stomach pain and headache starting around 7am. She cries, clings to her mother, and begs to stay home. When her mother agrees, the pain resolves within 30 minutes. She has had extensive gastroenterology workup, all investigations normal. She is described as a "sensitive, worrying child" who has always been reluctant to separate from her mother. Her school reports that when she does attend, she stays close to her teacher and does not participate in group activities. She was fine in her previous school; this school change occurred 4 months ago. Her mother, who has GAD, agrees that "school is quite stressful for children."
Questions
Q1: Classify this presentation using the functional model and identify the driving function.
Kearney-Silverman Functional Classification:
This presentation fits Function 3: Attention-seeking / avoidance of separation anxiety:
- Primary driver: Separation Anxiety Disorder underlying school refusal
- Somatic symptoms (stomach pain, headache) emerge in the morning, resolve immediately when separation avoided
- Clingy behavior, crying, difficulty leaving mother
- Background: sensitive temperament (behavioral inhibition), maternal GAD (models anxious world view)
Also some Function 1 (avoidance of negative affect related to new school):
- Previous school = comfortable; new school = unfamiliar = aversive
Q2: What is the key first principle of management, and why?
Key principle: Rapid return to school.
Every additional day of absence:
- Reinforces avoidance (the behavior works, staying home removes anxiety)
- Increases school-related anxiety (the longer the absence, the more "catastrophic" return seems)
- Widens the gap with peers academically and socially
- Entrenches the somatic complaint → school avoidance behavior pattern
Even partial attendance (2 hours/day) is better than complete absence. The goal is any foothold in school from which to build.
Q3: Outline a treatment plan including role of parental factors.
School liaison:
- Meet with school: identify specific triggers (which part of school day triggers anxiety? Assembly? Lunch? Specific teacher?)
- Arrange: trusted adult to receive Ananya at school gate; quiet room if anxiety escalates; reduced initial demands
- Graduated plan: 1 hour day 1 → 2 hours day 3 → half day week 2 → full day week 3
CBT for Ananya:
- Psychoeducation: explain anxiety cycle (avoidance = short-term relief, long-term prison)
- Graded exposure hierarchy (see above)
- Relaxation: diaphragmatic breathing for somatic symptoms
- Cognitive: challenge catastrophic predictions about school
- Reward: brave behaviors token economy
Family intervention, addressing parental accommodation:
- Mother's GAD: her anxiety about Ananya → models anxiety AND increases accommodation
- Skills: calm, brief goodbye routine (30 seconds max, then leave confidently)
- Do NOT allow Ananya to stay home; do NOT call school multiple times to check
- Father or other trusted adult may be better for morning routine if mother too anxious
- Mother may need her own treatment (CBT for GAD, or at minimum, psychoeducation on accommodation)
Pharmacotherapy:
- If 8–12 weeks of CBT insufficient: Sertraline 25mg starting dose, titrate to 50–100mg
- CAMS trial evidence: combination sertraline + CBT superior for child anxiety
Parental accommodation is the key maintenance factor in pediatric anxiety disorders. In this case, mother's own GAD amplifies the problem, she is sympathetic to Ananya's somatic complaints because she experiences similar anxiety herself. Addressing mother's own mental health is part of the treatment plan.
VIGNETTE 10: Attachment Disorder: DSED
Case
Meera, 5 years 6 months, was adopted from an orphanage at age 3 years 2 months, where she had lived since 2 weeks of age. Her adoptive parents, Mr. and Mrs. Krishnamurthy, describe her as "warm and affectionate with everyone." At the park, she runs up to strangers and tries to sit on their laps. She walks away with unfamiliar adults without looking back. She has gone missing twice at malls, both times found with strangers who were "just chatting to her." She calls multiple women "Mummy." Her parents describe a warm, committed household with consistent routines since adoption. Two years later, her behavior with strangers has not improved despite their best efforts. At home, she is affectionate and loving with the family.
Questions
Q1: Diagnose and differentiate from RAD and ADHD.
Diagnosis: Disinhibited Social Engagement Disorder (DSED), DSM-5: 313.89
Criteria met:
- Reduced reticence with unfamiliar adults (runs up to strangers, sits on laps)
- Overly familiar behavior (calls multiple women "Mummy")
- Does not check back with caregiver (walks away without looking back)
- Willingness to go with unfamiliar adults (gone missing twice with strangers)
- History: institutional rearing from 2 weeks to age 3 (extreme social deprivation, required criterion)
DSED vs RAD:
| Feature | This case | RAD |
|---|---|---|
| Core behavior | Disinhibited, approaches strangers | Inhibited, withdrawn from caregivers |
| Response to stable caregiving | PERSISTS despite 2 years in good home | Typically improves |
| Safety risk | Exploitation by strangers | Emotional damage from neglect |
DSED vs ADHD:
- ADHD: impulsive, inattentive, but the social engagement is not indiscriminate toward all strangers in a relationship-seeking way
- DSED: specifically seeks relationships indiscriminately; not just impulsivity
- DSED can co-occur with ADHD, both diagnoses may be present
- Key: DSED is NOT limited to impulsivity; includes reduced stranger anxiety (which is developmentally expected to be present at age 5+)
Q2: Why has the behavior not improved despite good caregiving?
DSED, unlike RAD, can persist even after stable, loving caregiving placement. Research on adopted/institutional children shows:
- RAD typically shows significant improvement with stable placement
- DSED shows less reliable improvement and may persist for years
- Neurobiologically: DSED may reflect early disruption of normal stranger anxiety development at a critical period (6–12 months) that is difficult to fully reverse
- Children with DSED do form genuine attachment to adoptive parents, but the indiscriminate social engagement persists as a separate dimension
Q3: What are the management priorities?
1. Parental psychoeducation and support:
- Explain persistence is NOT their failure, they are doing everything right
- DSED is a consequence of early institutional deprivation, not current parenting
- Validate their love and commitment; reduce guilt and blame
- Prepare them: this may persist into adolescence/adulthood in attenuated form
2. Safety planning (IMMEDIATE PRIORITY):
- Teach Meera personal safety rules: "safe adults" (family + school staff only); "private information"; "asking Mummy before going with anyone"
- Close supervision in public, hand-holding, wrist straps if needed
- School: inform teachers about DSED; supervision during lunch/outdoor play
- Community alert for parents to supervise proactively
3. Dyadic therapy:
- Theraplay: structured play-based therapy to deepen specific attachment to parents; focuses on attunement, nurture, engagement
- PACE model (Hughes): therapist models Playfulness, Acceptance, Curiosity, Empathy for parents
- Goal: strengthen the discriminated attachment to parents while not punishing general sociability
4. Do NOT use:
- Holding therapy (absolutely contraindicated, associated with deaths; no evidence)
- Forced attachment techniques
- Punishment for social engagement (increases shame; does not change underlying drive)
DSED is not about the child being "too friendly", it is about the ABSENCE of normal stranger anxiety that should have developed at 6–18 months during the critical period when Meera was institutionalized. She never learned to discriminate between familiar and unfamiliar people. The safety risk is real, these children are genuinely vulnerable to exploitation.
VIGNETTE 11: Enuresis with Secondary Onset
Case
Dhruv, 7 years old, was completely dry at night by age 4 and had been consistently dry for 2 years. Three months ago, he began wetting his bed 4–5 nights per week. His mother reports no urinary symptoms during the day. Around the same time, his parents separated after a period of significant marital conflict. He started at a new school last month. His younger sister was born 4 months ago. Physical examination is unremarkable. Urinalysis and urine culture are normal.
Questions
Q1: Classify this presentation and discuss its significance.
Diagnosis: Enuresis, Nocturnal Only, Secondary Type (DSM-5: 307.6)
Secondary enuresis (onset after ≥6 months of established continence), Dhruv was dry for 2 years.
Significance of secondary type:
- More rigorous investigation warranted (organic causes: UTI ruled out here, diabetes mellitus/insipidus, constipation, urological, normal urinalysis supports non-organic)
- Psychosocial precipitants highly relevant:
- Parental separation (major stressor)
- New school (additional stressor)
- New sibling (loss of exclusive attention)
- Multiple concurrent life changes within 4 months
Q2: What is the treatment hierarchy for this child?
Step 1, Address psychosocial stressors:
- Parental counseling: both parents maintain consistent, warm relationship with Dhruv
- Minimize Dhruv's exposure to parental conflict
- Ensure he receives adequate one-on-one time with each parent
- Acknowledge transition to new school; school-based support if needed
Step 2, Psychoeducation:
- Reassure Dhruv: bedwetting is not his fault; many children have it; it will improve
- Use matter-of-fact, non-punitive approach
- Involve Dhruv in management (motivational approach)
Step 3, Behavioral strategies:
- Fluid management: adequate fluids during day; reduce in last 2 hours before bed
- Scheduled toileting before bed
- Reward system for dry nights (calendar with stars, not punishment for wet nights)
- Lifting: parents wake child to toilet before their own bedtime (partial solution)
Step 4, Urine alarm (bell-and-pad):
- If behavioral measures insufficient after 4–6 weeks
- First-line evidence-based treatment
- 75–85% success rate
- Best long-term outcomes
- Requires 8–12 weeks, family motivation
Step 5, Desmopressin:
- Useful for short-term (sleepovers, camps) or if rapid response needed
- 0.2mg oral tablet at bedtime
- Restrict fluid 1 hour before and 8 hours after
- Watch for hyponatremia
Secondary enuresis after a clear precipitant (parental separation, new sibling, school change) does NOT necessarily mean organic cause, psychosocial stressors are common precipitants. However, organic causes (UTI, diabetes) MUST be ruled out first. In this case, normal urinalysis already done, proceed with psychosocial and behavioral management.
VIGNETTE 12: Intellectual Disability: Down Syndrome, Adult Onset Behavioral Change
Case
Ranjit, 42 years old, has a lifelong diagnosis of mild intellectual disability secondary to Down syndrome (trisomy 21), confirmed by karyotype. He has been functioning independently in a supported living facility, working in a sheltered workshop, and was described by carers as "cheerful and sociable." Over the past 14 months, carers have noticed gradual memory decline, he forgets his daily routines, gets lost going to the workshop (a familiar route for 10 years), no longer recognizes some long-term coworkers, and has periods of apparent confusion, especially in the evenings. He has become withdrawn and irritable. He was recently found wandering in the facility at 3am. His gait has become shuffling. He had a generalized tonic-clonic seizure last week.
Questions
Q1: What is the most likely explanation for this change in behavior and function?
Most likely diagnosis: Alzheimer's dementia in Down syndrome (trisomy 21)
Rationale:
- Age 42: individuals with Down syndrome have virtually 100% Alzheimer's neuropathology (amyloid plaques, neurofibrillary tangles) by age 40 due to triplication of chromosome 21 which carries the APP (Amyloid Precursor Protein) gene
- Clinical Alzheimer's dementia occurs in ~50% by age 60, median onset in mid-50s (earlier than general population)
- Features consistent with Alzheimer's: progressive episodic memory loss (forgetting routines, getting lost), disorientation (wandering at night), personality change (withdrawal, irritability), parkinsonian features (shuffling gait), new-onset seizures (late Alzheimer's feature)
- Sundowning (confusion in evenings)
Q2: What investigations would you order?
Q3: What management principles apply?
- Confirm and communicate diagnosis to carers and family in accessible language
- Safety: supervision for wandering (door alarms, GPS tracker); seizure precautions; supervision for all activities
- Environmental modification: familiar, predictable environment; visual schedules; reduced sensory overload; good lighting (reduces sundowner confusion)
- Pharmacotherapy:
- Donepezil (cholinesterase inhibitor): some evidence for mild-moderate Alzheimer's in DS; start low, go slow
- Seizure management: sodium valproate or lamotrigine (avoid phenytoin, cognitive side effects)
- Avoid benzodiazepines (worsen cognition)
- Carer support: training in dementia care; family meetings; advance care planning
- Palliative approach as disease progresses: comfort, dignity, quality of life
Down syndrome + Alzheimer's dementia is a key association examined both in child psychiatry (genetics/ID section) and in old age psychiatry. The mechanism is direct: trisomy 21 → three copies of APP gene → excess amyloid precursor protein → early and universal amyloid accumulation. Every person with Down syndrome has Alzheimer's pathology by age 40; clinical dementia depends on reserve, other factors.
| *Sources: Kaplan & Sadock (11th ed.) | Rutter's (6th ed.) | Lewis's (5th ed.) | DSM-5-TR | ICD-11* |
|---|
All patient names and details are entirely fictitious.