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Guide 12 · Part III

Child Adolescent

Paper III · Specialties, Forensic & Child. Six study modes, from notes to quick review.

Most askedADHD assessment and managementAutism Spectrum DisorderIntellectual Disability classificationChild abuse and POCSOConduct Disorder managementEnuresis and Tourette Syndrome
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Chapter 01

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

Exam Pearl

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):

  1. Often fails to give close attention to details / makes careless mistakes
  2. Often has difficulty sustaining attention in tasks or play
  3. Often does not seem to listen when spoken to directly
  4. Often does not follow through on instructions; fails to finish tasks
  5. Often has difficulty organizing tasks and activities
  6. Often avoids/dislikes tasks requiring sustained mental effort
  7. Often loses things necessary for tasks
  8. Often easily distracted by extraneous stimuli
  9. Often forgetful in daily activities

Domain B, Hyperactivity-Impulsivity (6+ symptoms, <17; 5+ if ≥17, for ≥6 months):

  1. Often fidgets with or taps hands/feet or squirms in seat
  2. Often leaves seat when remaining seated is expected
  3. Often runs about or climbs in inappropriate situations
  4. Often unable to play or engage in leisure activities quietly
  5. Often "on the go" acting as if "driven by a motor"
  6. Often talks excessively
  7. Often blurts out an answer before question completed
  8. Often has difficulty waiting turn
  9. Often interrupts or intrudes on others

Additional Criteria:

Presentations:

Presentation · Criteria
Combined (ADHD-C) Both A and B criteria met
Predominantly Inattentive (ADHD-I) Only A criteria met
Predominantly Hyperactive-Impulsive (ADHD-HI) Only B criteria met
Exam Pearl

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:

Key ICD-11 changes from ICD-10:

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:

Key Neural Circuits:

  1. Fronto-striatal circuit: PFC striatum thalamus PFC loop. Dysfunction causes impaired inhibitory control and working memory
  2. 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
  3. Cerebellum: Timing deficits in ADHD linked to cerebellar-striatal circuit dysfunction

Structural Brain Findings (meta-analyses):

Genetics:

Exam Pearl

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:

Rating Scales:

ScaleRaterAge RangeSubscalesNotes
Conners Rating Scale-3Parent/Teacher/Self6–18Inattention, Hyperactivity, Executive Function, Learning Problems, Peer RelationsGold standard, normative data
SNAP-IVParent/Teacher6–17ADHD-I, ADHD-H/I, ODDFree, based directly on DSM criteria
Vanderbilt ADHD ScaleParent/Teacher6–12ADHD + comorbid ODD/CD/Anxiety/Depression screeningUsed in US primary care
CBCL (Achenbach)Parent1.5–18Broadband (internalizing/externalizing)Not ADHD-specific
Brown ADD Rating ScalesSelf/Parent3 years+Executive function focusUseful for adult ADHD
ADHD Rating Scale-5Parent/Teacher5–17Inattention, Hyperactivity-ImpulsivityDSM-5 aligned

Neuropsychological Testing:

Clinical Anchor

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

MedicationClassMechanismOnsetDurationKey Points
Methylphenidate (MPH)PhenethylamineBlocks DAT + NET reuptake30–60 minIR: 4–6h; LA: 8–12hMost evidence in children; multiple formulations
Amphetamine (AMP)PhenethylamineBlocks DAT/NET + causes release30–60 minIR: 4–5h; LA: 10–12hSlightly more potent than MPH
Lisdexamfetamine (LDX)ProdrugCleaved to d-amphetamine in gut60–90 min12–14hLower abuse potential; FDA-approved binge eating
DexmethylphenidatePhenethylaminePure d-enantiomer of MPH30–45 minIR: 4–5h; XR: 8–12hFewer side effects than racemic MPH

Methylphenidate formulations:

Stimulant Side Effects:

Exam Pearl

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

MedicationClassMechanismOnsetKey Points
AtomoxetineNRISelective NET inhibitor4–6 weeks for full effectNon-scheduled; good for anxiety comorbidity, tic disorders; black box suicidality warning
Guanfacine ERα2A agonistPFC α2A receptor agonist2–4 weeksAlso for tics; can cause sedation/bradycardia; taper on discontinuation
Clonidine ERα2 agonist (non-selective)Reduces NE turnover2–4 weeksMore sedating than guanfacine; also for tics, sleep problems
BupropionNDRINE/DA reuptake inhibitor2–4 weeksOff-label; good for comorbid depression; lowers seizure threshold

Atomoxetine Dosing:

Exam Pearl

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):

School-Based Interventions:

Multimodal Treatment:

Exam Strategy

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

1.9 ADHD in Women

Historically underdiagnosed due to:

Special considerations:

1.10 Driving and Occupational Implications


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):

  1. Deficits in social-emotional reciprocity (abnormal social approach, failure of conversation, reduced sharing of interests/emotions, failure to initiate/respond to interactions)
  2. 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)
  3. 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:

  1. Stereotyped or repetitive motor movements, use of objects, or speech (motor stereotypies, lining up toys, echolalia, idiosyncratic phrases)
  2. Insistence on sameness, inflexible adherence to routines, or ritualized patterns (extreme distress at small changes, rigid thinking, greeting rituals, same food every day)
  3. Highly restricted, fixated interests abnormal in intensity or focus (strong attachment to unusual objects, preoccupation with narrow topics)
  4. Hyper- or hyporeactivity to sensory input (apparent indifference to pain/temperature, adverse responses to specific sounds/textures, excessive smelling/touching, visual fascination)

Additional Criteria:

2.2 Severity Levels

LevelSocial CommunicationRestricted/Repetitive Behaviors
Level 1, "Requiring support"Noticeable deficits without support; difficulty initiating interactionsInflexibility causes significant interference; difficulty switching between activities
Level 2, "Requiring substantial support"Marked deficits; limited initiation; atypical/reduced responsesRRBIs + inflexibility markedly obvious; distress when interrupted
Level 3, "Requiring very substantial support"Severe deficits; very limited initiation; minimal responseExtreme difficulty with change; intense distress; greatly interferes with functioning
Exam Pearl

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:

18-month red flags:

24-month red flags:

Additional early signs:

2.4 Screening

M-CHAT-R/F (Modified Checklist for Autism in Toddlers, Revised with Follow-Up):

Other Screening Tools:

ToolAgeRaterNotes
M-CHAT-R/F16–30 monthsParentPrimary screening
CHAT (Checklist for Autism in Toddlers)18 monthsParent + clinicianOriginal Baird tool
SCQ (Social Communication Questionnaire)4+ yearsParentScreening, uses ADI-R items
ASSQ (Autism Spectrum Screening Questionnaire)7–16 yearsParent/TeacherFor higher-functioning ASD
AQ (Autism Quotient)Adolescents/AdultsSelf-reportBaron-Cohen

2.5 Comprehensive Assessment

Diagnostic Instruments:

ADOS-2 (Autism Diagnostic Observation Schedule, 2nd Ed):

ADI-R (Autism Diagnostic Interview-Revised):

Exam Pearl

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:

2.6 Comorbidities

ComorbidityPrevalence in ASDNotes
Intellectual Disability30–40%Higher at lower severity levels; separate diagnosis required
Epilepsy20–30%Bimodal: onset <5 years and adolescence; particularly with ID comorbidity
ADHD50–70%DSM-5 now allows dual diagnosis (previously excluded)
Anxiety Disorders40–60%Often atypical presentation; social anxiety, generalized anxiety, specific phobias
Depression20–40%Higher in higher-functioning ASD; often missed
Sleep Disorders50–80%Insomnia, night waking; melatonin dysregulation
OCD17–37%Distinguish from ASD RRBIs, ego-syntonic vs ego-dystonic
GI Problems50%Constipation, GERD, feeding problems
Tic Disorders20–35%May co-occur with Tourette's

2.7 Interventions

Applied Behavior Analysis (ABA):

Early Start Denver Model (ESDM):

TEACCH (Treatment and Education of Autistic and Communication-Handicapped Children):

Social Skills Training:

Clinical Anchor

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 SymptomMedicationEvidence Level
Irritability/aggressionRisperidone (FDA-approved age 5+), Aripiprazole (FDA-approved age 6+)Strongest (multiple RCTs)
ADHD symptomsMethylphenidate (lower response rate than non-ASD ADHD), Atomoxetine, GuanfacineModerate
AnxietySSRIs (fluoxetine, sertraline), limited RCT evidence in ASDLimited
InsomniaMelatonin (start 0.5–3mg)Good for sleep onset
Self-injurious behaviorNaltrexone (adjunct), antipsychoticsLimited
Repetitive behaviorsSSRIs, mixed evidenceLimited/conflicting
Exam Pearl

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


PART 3: INTELLECTUAL DISABILITY (ID)

3.1 Definition and Classification

DSM-5: Three criteria:

  1. Deficits in intellectual functions (reasoning, problem-solving, planning, abstract thinking, judgment, academic learning, learning from experience) confirmed by clinical assessment AND standardized intelligence testing
  2. Deficits in adaptive functioning that fail to meet developmental/sociocultural standards for personal independence and social responsibility (across conceptual, social, and practical domains)
  3. Onset during developmental period

IQ Score Reference (NOT severity determinant in DSM-5):

Exam Pearl

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):

3.2 Adaptive Functioning Domains

Domain · Skills Included
Conceptual Language, reading, writing, math, reasoning, knowledge, memory
Social Empathy, social judgment, interpersonal communication, following rules, gullibility
Practical Self-care, job responsibilities, money management, recreation, task organization

3.3 Etiology

Genetic Causes:

ConditionGeneticsClinical FeaturesIQ 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 SyndromeCGG repeat expansion in FMR1 gene (Xq27.3); males affectedLong face, large ears, macro-orchidism, hand flapping, ADHD features, social anxiety, hyperkinesisMild–Moderate (males); females often normal–mild ID
Angelman SyndromeMaternal UPD 15 or deletionHappy demeanor, seizures, ataxic gait, absent/minimal speech, EEG patternSevere–Profound
Prader-Willi SyndromePaternal deletion 15q11Hyperphagia, obesity, short stature, hypogonadism, behavioral problemsMild–Moderate
Phenylketonuria (PKU)PAH gene mutation; ARPreventable with dietary phenylalanine restriction; musty odor, fair complexion, seizuresSevere (if untreated)
Williams SyndromeDeletion 7q11.23 (includes elastin gene)"Cocktail party" personality, hypercalcemia, elfin facies, supravalvular aortic stenosis, relative strength in verbal/social over spatialMild–Moderate
Rett SyndromeMECP2 mutation (X-linked); femalesRegression at 6–18 months, hand-wringing stereotypies, breathing abnormalities, seizuresSevere
Tuberous SclerosisTSC1/TSC2 mutation; ADHamartomas (brain, skin, kidneys), ash-leaf spots, seizures, ASD featuresVariable
Exam Pearl

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:

3.4 Assessment of Intellectual Disability

Intelligence Tests:

Adaptive Behavior Scales:

3.5 Behavioral Phenotypes

Syndrome · Behavioral Profile
Down Syndrome Sociable, affectionate, stubbornness, risk for depression/dementia in adulthood
Fragile X Social anxiety, gaze avoidance, perseverative speech, hand-flapping
Angelman Happy affect, sociable, laughing, easily excitable
Prader-Willi Hyperphagia, skin-picking, rigidity, temper tantrums, hoarding
Williams Loquacious, socially uninhibited, hypersensitive to noise, visuospatial deficits
Rett Initial development then regression; loss of purposeful hand use

3.6 Comorbid Psychiatric Disorders in ID

Common presentations:


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:

  1. Often loses temper
  2. Often touchy or easily annoyed
  3. Often angry and resentful

Argumentative/Defiant Behavior:

  1. Often argues with authority figures
  2. Often actively defies/refuses to comply with rules
  3. Often deliberately annoys others
  4. Often blames others for mistakes

Vindictiveness:

  1. 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):

Exam Pearl

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):

Destruction of property (2 criteria):

Deceitfulness/theft (3 criteria):

Serious violations of rules (3 criteria):

Specifiers:

Severity: Mild, Moderate, Severe

4.3 Differential Diagnosis: ADHD vs ODD vs CD

FeatureADHDODDCD
Core behaviorInattention/hyperactivityDefiance/irritabilityRule violation/aggression
IntentionalityUnintentionalDeliberate but reactiveDeliberate and planned
ComorbidityCan have ODD/CDOften with ADHDOften with ADHD
AggressionReactive, unplannedReactive to perceived provocationProactive/predatory possible
Conscience developmentNormalNormalMay be impaired (CU traits)
Peer relationshipsDifficulty due to impulsivityDifficulty due to defianceMay have delinquent peer group
Exam Pearl

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:

Pharmacological:

Exam Strategy

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):

  1. Recurrent excessive distress when anticipating/experiencing separation
  2. Persistent worrying about losing attachment figures or possible harm (illness, injury, disaster)
  3. Persistent worrying about untoward event causing separation (getting lost, kidnapped)
  4. Reluctance/refusal to go out, away from home, to school due to fear of separation
  5. Persistent excessive fear about being alone
  6. Persistent reluctance/refusal to sleep away from home
  7. Repeated nightmares involving separation theme
  8. Repeated somatic complaints when separation occurs/anticipated

Most common anxiety disorder in young children (under 12)

Treatment:

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).

Treatment:

5.3 School Refusal

Not a DSM diagnosis, a behavioral problem with multiple causes:

TypeCauseFeatures
Separation anxietyFear of leaving home/attachment figureSomatic complaints (morning), relieved on staying home
Social/performance anxietyFear of social situations, evaluationAvoids specific situations (tests, PE, lunch)
Specific phobiaFear of specific school stimuliAvoidance of specific classroom/teacher
Truancy/CDDesire to be elsewhereNo distress, leaves home but not school-bound

Kearney & Silverman (2000) functional model:

  1. Avoid stimuli provoking negative affect
  2. Escape aversive social/evaluative situations
  3. Pursue attention from significant others
  4. 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:

Treatment, TADS (Treatment for Adolescents with Depression Study):

Exam Pearl

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

Assessment: Columbia Suicide Severity Rating Scale (C-SSRS)


PART 6: TIC DISORDERS AND TOURETTE SYNDROME

6.1 Classification

Disorder · Criteria
Tourette Syndrome ≥2 motor tics AND ≥1 vocal tic; not necessarily concurrent; onset <18; duration >1 year; not substances/medical
Persistent (Chronic) Motor/Vocal Tic Disorder Single or multiple motor OR vocal tics (not both); >1 year duration
Provisional Tic Disorder Single or multiple motor and/or vocal tics; <1 year since first tic

Tic characteristics:

Exam Pearl

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

6.3 Neurobiology

6.4 Treatment

Behavioral, CBIT (Comprehensive Behavioral Intervention for Tics):

Pharmacotherapy:

MedicationClassNotes
HaloperidolTypical antipsychoticMost evidence; effective but side effects (EPS, tardive dyskinesia) limit use
PimozideTypical antipsychoticQTc prolongation monitoring needed
FluphenazineTypical antipsychoticLess studied
RisperidoneAtypical antipsychoticBetter tolerated; moderate efficacy
AripiprazoleAtypical antipsychoticIncreasingly preferred; good tolerability
Clonidineα2 agonistParticularly useful when ADHD comorbid; modest tic reduction
Guanfacineα2A agonistSimilar to clonidine; less sedating
TopiramateAntiepilepticSome evidence
TetrabenazineVMAT2 inhibitorSevere tics; watch for depression
Exam Strategy

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:

Types:

Primary vs Secondary:

Exam Pearl

Secondary enuresis (onset after established dryness) warrants more vigorous evaluation for organic causes (UTI, diabetes mellitus, diabetes insipidus, emotional stressors) and psychosocial stressors.

Epidemiology:

Etiology: Multifactorial, maturational delay, reduced nocturnal bladder capacity, high arousal threshold, ADH deficiency, genetic factors

Treatment:

ModalityEvidenceNotes
Bell-and-pad (Urine alarm)Best long-term; 75–85% successConditioning treatment; requires 8–12 weeks; best relapse prevention
Desmopressin (DDAVP)Rapid effect; relapse on stoppingADH analogue; reduces urine output; available as intranasal or tablet; watch for hyponatremia
ImipramineSecond-line; 40–50% successHigh relapse; cardiac side effects; toxic in overdose; falling out of favor
Bladder trainingMild benefitWorks best for diurnal enuresis
Motivational therapyCombined with aboveReward systems, not punishment

7.2 Encopresis

DSM-5 Criteria:

Types:

Treatment:

  1. Disimpaction (enema/polyethylene glycol)
  2. Maintenance stool softeners (polyethylene glycol/lactulose)
  3. Behavioral: scheduled toilet sitting (15 min after meals, gastrocolic reflex), reward systems
  4. High-fiber diet, fluid intake
  5. CBT/family therapy if psychosocial factors dominant

PART 8: CHILD ABUSE AND NEGLECT

8.1 Types and Definitions

TypeDefinitionClinical Indicators
Physical abuseNon-accidental physical injuryBruises in unusual locations (torso, buttocks, ears), patterned bruises, burns (cigarette, immersion), fractures in unusual ages/locations
Sexual abuseSexual activity with child without consent/understandingGenital/rectal injuries, STIs, sexualized behavior, regression
Emotional/Psychological abusePattern of behavior damaging emotional developmentFailure to thrive, severe behavioral problems, low self-esteem, depression
NeglectFailure to provide basic needsPoor hygiene, developmental delay, failure to thrive, unsupervised
Medical neglectFailure to provide medical careUntreated illness, missed vaccinations

8.2 Physical Indicators

Bruises suspicious for abuse:

Burns suspicious for abuse:

Fractures suspicious for abuse:

Abusive Head Trauma (Shaken Baby Syndrome):

Exam Pearl

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

Red flags:

8.4 Child Sexual Abuse (CSA)

8.5 Forensic Interview

8.6 Mandatory Reporting

Clinical Anchor

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

Domain · Long-term Effects
Psychiatric PTSD, depression, anxiety, BPD, dissociative disorders, substance use disorders, eating disorders
Neurobiological HPA axis dysregulation, cortical thinning (prefrontal, temporal), hippocampal volume reduction, epigenetic changes
Interpersonal Attachment difficulties, revictimization risk, perpetration risk (intergenerational)
Physical Chronic pain, autoimmune disorders, cardiovascular disease, reduced life expectancy
Cognitive Learning difficulties, attention problems, reduced IQ

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):

  1. Impaired control over gaming (onset, frequency, intensity, duration, termination, context)
  2. Increasing priority given to gaming to the extent that it takes precedence over other life interests and daily activities
  3. 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.

Exam Pearl

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

9.3 Neurobiological Overlap

9.4 Management

Assessment: IGDS (Internet Gaming Disorder Scale), CAGE-adapted for gaming

Treatment:


PART 10: SPECIFIC LEARNING DISORDERS

10.1 DSM-5 Classification

DSM-5 Code 315, Specific Learning Disorder (SLD)

Criteria:

Specify:

Severity: Mild, Moderate, Severe

10.2 Dyslexia

Core deficit: Phonological processing, difficulty mapping letters to sounds (grapheme-phoneme correspondence)

Features:

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

10.4 Dysgraphia (Impairment in Written Expression)


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:

11.2 Reactive Attachment Disorder (RAD)

DSM-5 Criteria:

Exam Pearl

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:

Key Difference from RAD:

FeatureRADDSED
Core patternInhibited, withdrawnDisinhibited, indiscriminate social engagement
Caregiver relationshipWithdrawn from caregiversNot attached but socially active with strangers
Response to careImproves with stable caregivingMay persist even after stable caregiving
ASD confusionCan be confused with ASDLess confusion with ASD
AD/ADHD comorbidityLess commonDSED + ADHD possible

PART 12: ADDITIONAL HIGH-YIELD TOPICS

12.1 Childhood Disintegrative Disorder (Now Under ASD)

12.2 Pica

DSM-5: Persistent eating of non-nutritive, non-food substances for ≥1 month; developmentally inappropriate (≥2 years); not culturally sanctioned

12.3 Rumination Disorder

12.4 Avoidant/Restrictive Food Intake Disorder (ARFID)

12.5 Developmental Coordination Disorder (DCD)


KEY PHARMACOLOGY SUMMARY

DrugPrimary Use in Child PsychMechanismKey Side Effects
MethylphenidateADHDDAT/NET blockerAnorexia, insomnia, growth suppression, tachycardia
AmphetamineADHDDAT/NET blocker + releaserSame + more appetite suppression
LisdexamfetamineADHD, Binge EatingProdrug d-AMPSame as amphetamine; lower abuse liability
AtomoxetineADHDSelective NET inhibitorGI, activation, hepatotoxicity (rare), suicidality (BBW)
Guanfacine ERADHD, ticsα2A agonistSedation, bradycardia, hypotension
Clonidine ERADHD, tics, sleepα2 agonistSedation, bradycardia, rebound hypertension
FluoxetineMDD (age 8+), OCD, anxietySSRIGI, activation, suicidality (BBW), serotonin syndrome
SertralineAnxiety, OCDSSRISimilar to fluoxetine
EscitalopramDepression (age 12+)SSRISimilar
RisperidoneASD irritability, aggressionD2/5HT2A antagonistEPS, weight gain, prolactin elevation, metabolic
AripiprazoleASD irritability, ticsPartial D2 agonistWeight gain, akathisia, less metabolic than risperidone
HaloperidolTicsPotent D2 blockerEPS, tardive dyskinesia, NMS
MelatoninSleep in ASD/ADHDMT1/MT2 agonistGenerally safe; long-term studies limited
DesmopressinEnuresisV2 agonist (ADH analogue)Hyponatremia (water restriction needed)
ImipramineEnuresisTCACardiac arrhythmia, anticholinergic, toxic in overdose
Key Insight

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-TRICD-11*
Chapter 02

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:

From teachers (ideally via standardized rating scales):

Mental Status Examination:

Investigations:

Differential Diagnosis:

Condition · Distinguishing Features
Anxiety disorder Inattention due to worry, not DHTN; situational (more prominent in anxiety-provoking situations)
Learning disorder Academic problems without hyperactivity; specific domain deficits
Conduct Disorder Intentional rule-breaking; may coexist
Depression Cognitive slowing, anhedonia, mood change
ASD Social communication deficits, RRBIs; can be comorbid
Absence epilepsy Brief staring spells with EEG confirmation
Sensory impairment Hearing/vision loss causing inattentive behavior

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:

2. Behavioral Interventions (first-line for age 4–5; adjunct for school-age):

Behavioral Parent Training (BPT):

School-based interventions:

3. Pharmacotherapy:

First-line: Methylphenidate (MPH)

FormulationDoseNotes
IR MPH (Ritalin)5mg BD-TID; max 60mg/dayFast onset 30–60 min; rebound effect
LA MPH (Concerta)18mg OD; titrate by 18mg; max 54mgOnce-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:

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:

5. Monitoring and Follow-Up:

Exam Pearl

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):

  1. Social-emotional reciprocity:
  2. Reduced sharing of interests, emotions
  3. Atypical social approach
  4. Failure to initiate or respond to social interactions
  5. Abnormal back-and-forth conversation
  1. Nonverbal communicative behaviors:
  2. Reduced eye contact
  3. Limited facial expressions
  4. Absent or atypical gesture use
  5. Poor integration of verbal/nonverbal communication
  1. Relationship development:
  2. Difficulty adjusting behavior to social context
  3. Difficulty making and maintaining friendships
  4. Absent interest in peers (not social anxiety, indifference)

Domain 2, Restricted, Repetitive Behaviors and Interests (≥2 present):

  1. Stereotyped/repetitive behaviors:
  2. Hand-flapping, rocking, spinning
  3. Lining up objects
  4. Echolalia (immediate or delayed)
  1. Insistence on sameness:
  2. Rigid routines
  3. Extreme distress at minor changes
  4. Ritualized patterns of behavior
  1. Fixated interests:
  2. Intense, narrow preoccupations
  3. Atypical in focus or intensity (e.g., specific bus routes, vacuum cleaners)
  1. Sensory abnormalities:
  2. Hyperreactivity (distress to textures, sounds)
  3. Hyporeactivity (indifference to pain, temperature)
  4. 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)

LevelSupport NeededSocial CommunicationRRBIs
1SupportNoticeable deficits with minimal support; difficulty initiatingInflexibility significantly interferes; difficulty switching
2Substantial supportMarked deficits; limited initiation; atypical responsesMarkedly obvious; distress when interrupted
3Very substantial supportSevere deficits; minimal responseExtreme difficulty changing; intense distress

Assessment Pathway

Step 1, Developmental Surveillance and Screening:

Step 2, Comprehensive Developmental Pediatric/Child Psychiatry Assessment:

History:

Physical examination:

Step 3, Standardized Diagnostic Assessment:

InstrumentTypePurpose
ADOS-2Structured observationDirect assessment of social communication/play/behavior; Module selected by language level
ADI-RStructured parent interviewDevelopmental history across three domains; algorithms for diagnosis
Vineland-3Parent interview/questionnaireAdaptive behavior (communication, daily living, socialization)

Step 4, Cognitive and Language Assessment:

Step 5, Allied Health Assessment:

Step 6, Medical Investigations:

Investigation · Indication
Chromosomal microarray All ASD cases (10–15% yield for clinically significant variants)
Fragile X testing (FMR1) Especially males with ID + ASD features
EEG If clinical seizure concern (regression, paroxysmal events)
Brain MRI If focal neurological signs or seizures
Metabolic screen If regression, developmental plateau, dysmorphic features
Hearing test Always, as part of speech/language evaluation

Step 7, Feedback and Formulation:

Exam Strategy

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:

  1. Deficits in intellectual functions (confirmed by standardized testing AND clinical assessment)
  2. Deficits in adaptive functioning (conceptual, social, or practical domains)
  3. Onset during developmental period

Severity is determined by ADAPTIVE FUNCTIONING, not IQ alone (DSM-5 change from DSM-IV):

SeverityConceptual DomainSocial DomainPractical Domain
Mild (IQ ~50–69)Academic skills below peers; abstract thinking, executive function limitedImmature social interactions; gullible, naiveCan 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 languageCan care for personal needs with training; supervision needed for complex decisions
Severe (IQ ~20–34)Limited conceptual skill acquisition; understands some simple languageSingle words, simple phrases; relationships with family/familiar othersRequires support for most ADLs; some can do simple ADLs
Profound (IQ <20)Primarily concrete understanding; relies on physical/sensory interactionRelies on nonverbal communication; close relationship with caregiversDependent on others for all aspects of care; may achieve some self-help with extensive training

Evaluation

1. Presenting Complaint and Chief Concerns:

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:

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:

TestAge RangeNotes
WPPSI-IV2.5–7 yearsVerbal + Performance IQ; good for preschool
WISC-V6–16 yearsFive factor model; most widely used
Stanford-Binet 52–85 yearsFull range; good floor for low IQ
Leiter-33–75 yearsNon-verbal; use for non-English speakers, ASD, hearing impaired

Adaptive Behavior Assessment:

5. Speech and Language Assessment:

6. Medical Investigations:

Investigation · Rationale
Karyotype / Chromosomal microarray Chromosomal abnormalities; microarray has higher yield (15–20%)
FISH for specific syndromes If clinical features suggest specific deletion/duplication (e.g., 22q11, Williams)
Fragile X (FMR1 PCR) Males with ID, especially with ASD features
Metabolic screen Inborn errors of metabolism (PKU, homocystinuria, lysosomal storage)
Thyroid function Hypothyroidism as cause
Lead levels If environmental exposure
EEG Seizure disorder (comorbid in 25%)
Brain MRI Structural anomalies, white matter disease
Hearing assessment Conductive/sensorineural hearing loss
Ophthalmology Refractive error, cataracts

7. Formulation and Management Planning:

Clinical Anchor

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:

Management Plan

1. Psychoeducation:

2. Behavioral Interventions:

Parent Management Training (PMT):

Multisystemic Therapy (MST):

Functional Family Therapy (FFT):

Problem-Solving Skills Training (PSST):

Therapeutic foster care / residential treatment:

3. School-based Interventions:

4. Pharmacotherapy (adjunctive):

No medication treats CD specifically. Treat comorbidities:

TargetMedicationEvidence
Comorbid ADHDMethylphenidate, Amphetamine, AtomoxetineStrong, reduces aggression significantly
Severe impulsive aggressionLithiumRCT evidence (Malone et al.)
Severe aggressionRisperidone, AripiprazoleModerate evidence
Mood instabilityValproateSome evidence
Comorbid depression/anxietySSRIsTreat the comorbidity

5. Addressing CU Traits:

Standard PMT is LESS effective in CD with CU traits. Modifications needed:

6. Diversion Programs:

7. Long-term Follow-up:

Exam Strategy

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:

Physical:

Assessment

1. Disclosure:

2. Forensic Interview:

3. Medical Assessment:

Conducted by trained pediatrician/forensic physician:

4. Psychological Assessment:

5. Risk Assessment:

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:

2. Trauma-Focused Cognitive Behavioral Therapy (TF-CBT):

3. Pharmacotherapy:

4. Psychoeducation for Caregivers:

5. Legal and Social Coordination:

Clinical Anchor

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)

FunctionMechanismPresentation
1, Avoidance of negative affectEscape from school-related anxiety-provoking stimuliSomatic symptoms on school mornings; relief on staying home
2, Escape from social/evaluativeSocial anxiety, performance anxiety, fear of evaluationAvoids tests, presentations, PE, social situations at school
3, Attention-seekingSeparation anxiety; maintain proximity to caregiverDistress focused on being away from parent; clings
4, Tangible reinforcementMore reinforcing activities at home (gaming, TV)Prefers home; no clear anxiety; may be combined with CD

Assessment

History:

Mental Status and Rating Scales:

Investigations:

Management

Core principle: Rapid return to school is the primary goal. Every additional day of absence entrenches avoidance.

1. School Liaison:

2. Cognitive Behavioral Therapy:

3. Family Interventions:

4. Pharmacotherapy:

5. Inpatient/Intensive Outpatient:

Exam Pearl

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:

FDA-Approved Antidepressants for Pediatric Depression

DrugApproved AgeStarting DoseTarget DoseNotes
Fluoxetine≥8 years10mg/day20–60mg/dayLongest evidence base; active metabolite (long half-life = safety in overdose but slower wash-out)
Escitalopram≥12 years10mg/day10–20mg/dayWell tolerated; FDA-approved for adolescent depression

Commonly used off-label:

TADS Trial (Treatment for Adolescents with Depression Study)

The Black Box Warning

Prescribing Guidelines

Start low, go slow:

Duration:

Non-response:

Exam Strategy

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:

Examination:

Rating Scales:

Investigations:

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:

Step 2, Behavioral Treatment (CBIT):

Comprehensive Behavioral Intervention for Tics, first-line for mild-moderate tics:

Step 3, Pharmacotherapy (moderate-severe tics or CBIT failed):

MedicationStarting DoseComments
Aripiprazole2mg/day, titrate to 5–20mgCurrently preferred atypical antipsychotic; better tolerability; RCT evidence
Guanfacine ER1mg at nightNon-antipsychotic option; useful with comorbid ADHD
Clonidine0.05mg BDOlder; more sedating; useful for ADHD comorbidity
Risperidone0.25–0.5mg/day, titrateEffective; weight gain, prolactin
Haloperidol0.25–0.5mg/dayMost evidence historically; EPS, tardive dyskinesia, last resort
Pimozide1–2mg/dayQTc monitoring required
Fluphenazine0.5–1mg/dayAlternative typical antipsychotic
Topiramate25mg/day, titrateSome RCT evidence; cognitive slowing

Managing Comorbidities:

Exam Pearl

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:

  1. Impaired control over gaming (onset, frequency, intensity, duration, termination, context)
  2. Increasing priority given to gaming to the extent it takes precedence over other interests/activities
  3. 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

Neurobiology

Shares features with substance use disorders:

Assessment

Instruments:

History:

Distinguish from:

Management

Psychoeducation:

Cognitive Behavioral Therapy (CBT):

Motivational Interviewing (MI):

Family Therapy:

Pharmacotherapy:

Structured Programs:


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:

Pathological (SAD), ≥3 of:

Duration ≥4 weeks in children.

Assessment

History:

Rating Scales:

Management

Principle: Parent-child joint treatment. Parental accommodation maintains disorder.

1. Psychoeducation:

2. Cognitive Behavioral Therapy (CBT):

Components for child:

Programs with evidence:

3. Parent Training:

4. School Liaison:

5. Pharmacotherapy:

Clinical Anchor

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:

Clinical Presentation

Combination presentation:

Management Decision Framework

Step 1, Which is causing more impairment?

Step 2, First-line pharmacological choice when ADHD is primary:

Option · Reasoning
Guanfacine ER (first choice) Alpha-2A agonist; reduces ADHD symptoms AND tics; no tic risk
Clonidine (alternative) Same mechanism; more sedating; also reduces tics
Atomoxetine SNRI; does not worsen tics; treats ADHD; evidence in TS+ADHD
Methylphenidate Historically contraindicated; NOW: practice guidelines say it CAN be used if ADHD impairment significant; may transiently worsen tics; long-term: may reduce tics via improved self-regulation

Step 3, Behavioral treatment:

Step 4, Combination pharmacotherapy if needed:

Academic support:

Exam Pearl

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:

Associated: Persistent social/emotional disturbance (≥2 of):

Child appears sad, fearful, or unresponsive. Caregiver cannot reach child emotionally.

DSED: Clinical Features

Core: Indiscriminate social engagement with strangers (≥2 of):

Child appears social but lacks discrimination, treats all adults as potential attachment figures.

Key Distinctions

FeatureRADDSED
Core behaviorInhibited, withdrawnDisinhibited, indiscriminate
Response to comfortAbsent/reducedMay seek comfort from anyone
Safety riskDepression/neglect damageVulnerability to exploitation
Response to stable caregivingTypically improvesMay persist even after stabilization
Confusion with ASDSome overlapLess overlap
History requiredYes, extreme neglectYes, extreme neglect

Management

1. Stable, Responsive Caregiving (primary intervention):

2. Dyadic/Attachment-Based Therapy:

3. Parenting Support:

4. Safety Planning for DSED:

5. School Support:

6. Pharmacotherapy:

Exam Pearl

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-TRICD-11TADS, CAMS, MTA, TORDIA trials*
Chapter 03

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)

Exam Pearl

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)

Clinical Anchor

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)

Exam Pearl

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)

Exam Pearl

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:

FACES P:

Clinical Anchor

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"

Key Insight

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)

Exam Pearl

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:

Dyslexia key:


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)

Exam Pearl

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

Exam Pearl

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:

NOT:

Exam Pearl

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

ConditionGene/ChromosomeInheritanceKey Memory Hook
Down syndromeTrisomy 21Sporadic (mostly)"21 = most common chromosomal"
Fragile XFMR1 (CGG repeat) Xq27.3X-linked"Most common INHERITED"
Prader-Willi15q11 paternal deletionImprinting"Dad's deletion = fat and short"
Angelman15q11 maternal deletionImprinting"Mum's deletion = happy and no speech"
Williams7q11.23 deletionAD (de novo mostly)"Elastin deletion = friendly + cardiac"
RettMECP2 (Xq28)X-linked (de novo in females)"Regression + hand-wringing"
Tuberous SclerosisTSC1 (hamartin) / TSC2 (tuberin)AD"Ash-leaf spots + seizures + ASD"
PKUPAH geneAR"Preventable with diet"
22q11 deletion22q11.2AD"Psychosis + cardiac + T-cell deficit"

QUICK REFERENCE: DRUG MECHANISMS

DrugClassMechanism (simplified)
MethylphenidateStimulantBlocks DAT + NET more dopamine/NE in synapse
LisdexamfetamineStimulant prodrugCleaved to d-amphetamine; blocks + reverses DAT/NET
AtomoxetineNRISelective NET blocker more NE in PFC
Guanfacineα2A agonistPost-synaptic α2A in PFC improves prefrontal signal
Clonidineα2 agonist (all subtypes)Reduces NE turnover; presynaptic + postsynaptic
RisperidoneAtypical APD2 + 5HT2A antagonist reduces dopamine excess in striatum
AripiprazoleAtypical APPartial D2 agonist stabilizes dopamine tone
MelatoninMelatonin agonistMT1/MT2 agonist advances circadian phase, improves sleep onset
DesmopressinVasopressin analogueV2 receptor ADH effect reduces nocturnal urine production

*Sources: Kaplan & Sadock (11th ed.)Rutter's (6th ed.)Lewis's (5th ed.)DSM-5-TRICD-11*
Chapter 04

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

FeatureADHDODDConduct Disorder
Core domainInattention / hyperactivity-impulsivityAngry mood / defiance / vindictivenessAggression / rule violation / deceitfulness
IntentionalityUnintentional, impulsive, not plannedReactive and deliberate but emotionally drivenDeliberate; proactive aggression possible
ConscienceIntact, feels guilt after impulsive actsIntact, justifies actions but guilt possibleMay be impaired (CU traits in subset)
Aggression typeReactive, unplannedReactive to perceived provocationBoth reactive AND proactive/predatory
Peer relationshipsRejected due to impulsivity/intrusivenessRejected due to argumentativenessMay have delinquent peer group (adolescent-onset)
OnsetBefore age 12 (DSM-5)Before age 12 typicallyChildhood (<10) or adolescent onset
SettingsPervasive, school, home, peersMay be setting-specific (mild ODD)Often at school and community
Academic impactLearning underperformance, disorganizationVariable, may achieve when cooperativeSchool refusal, truancy, exclusion
NeurobiologicalPFC dopamine/NE; executive dysfunctionHPA dysregulation; emotion regulation deficitLow cortisol, amygdala hyporeactivity (CU type)
ComorbidityODD (40%), CD (20%), anxiety, depressionADHD (50–60%), CD (25%), anxietyADHD (50%), SUD, depression
PrognosisPersists into adulthood (60–70%); manageable25–50% CD; 25% remit25–40% ASPD; worse in childhood-onset
TreatmentStimulants + BPTPMT, PSST; treat ADHD firstMST, FFT, PMT; stimulants for comorbid ADHD
CU Traits specifierNoYes (Limited Prosocial Emotions)Yes (Limited Prosocial Emotions)
DSM-5 code314.xx313.81312.xx
Exam Pearl

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

FeatureLevel 1 ("Requiring Support")Level 2 ("Requiring Substantial Support")Level 3 ("Requiring Very Substantial Support")
Social communicationNoticeable deficits without supports; difficulty initiating; reduced/atypical responsesMarked deficits; limited initiation; reduced/abnormal social responseSevere deficits; very limited initiation of interaction; minimal response
Restricted/Repetitive behaviorsInflexibility causes significant interference in ≥1 context; difficulty switchingRRBIs markedly obvious; obvious to casual observer; interferes with functioning in diverse contextsExtreme difficulty coping with change; intense distress; greatly interferes with functioning in all areas
Communication styleUses full sentences; engages in conversation; may have one-sided conversationUses simple sentences; conversation limited to narrow interestsFew words of intelligible speech; may use AAC; no functional speech in some
IndependenceCan function with some support; may hold a job; may live semi-independentlyRequires daily support across most settingsRequires around-the-clock support; may not acquire daily living skills
Formerly called (DSM-IV)Asperger's / High-Functioning AutismAutistic Disorder (moderate)Autistic Disorder (severe)
ID comorbidityLess commonMore commonVery common
Epilepsy riskLowerModerateHigher (20–30%)
PrognosisBetter, some independent living, employmentVariable, supported livingSevere impairment persists into adulthood
Exam Pearl

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

FeatureMethylphenidate (MPH)Atomoxetine (ATX)
ClassCNS stimulant (Schedule II in US)Selective norepinephrine reuptake inhibitor (SNRI), Non-stimulant
MechanismBlocks DAT + NET increases synaptic dopamine and NESelectively blocks NET increases NE (and secondarily DA in PFC)
Onset of actionSame day (30–60 min for IR)4–6 weeks for full therapeutic effect
DurationIR: 4–6 hours; LA: 8–12 hoursOnce-daily dosing; continuous coverage
Schedule statusControlled substance (Schedule II)NOT a controlled substance
Abuse potentialYes (moderate-high for IR)Very low
Preferred whenCore ADHD symptoms; no anxiety comorbidity; rapid response neededTic disorder; anxiety comorbidity; substance abuse history; family misuse concerns
FDA approval (ADHD)Age 6+ (some formulations age 3+)Age 6+
Appetite suppressionYes, significantMild, less than MPH
InsomniaYes, commonLess than MPH
TicsMay unmask/transiently worsenDoes NOT worsen tics
CardiovascularModest HR/BP increase; screen for congenital cardiacModest HR/BP increase; tachycardia possible
Black box warningNone specific to ADHDSuicidal ideation in children/adolescents (same as SSRIs)
HepatotoxicityNoRare but reported, monitor if symptomatic
Growth suppressionMild (0.5–1 cm/year)Minimal
Effect on anxietyMay worsen anxietyBeneficial for comorbid anxiety
OCD/tic comorbidityUse with cautionPreferred
DosingWeight-based: 0.3–1.0 mg/kg/day<70kg: 1.2 mg/kg/day; >70kg: 80–100mg/day
CostGenerics available; low costHigher cost
Exam Strategy

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

FeatureDSM-5ICD-11
ASD classificationSingle diagnosis: Autism Spectrum Disorder (299.00) with severity levels 1–36A02: Autism Spectrum Disorder, no subtyping by severity in ICD-11 per se; specifiers for intellectual impairment and functional language
Asperger'sEliminated, subsumed into ASDEliminated, subsumed into ASD
ASD + ADHDBoth diagnoses allowed (DSM-5 change from DSM-IV which excluded ADHD in ASD)Both diagnoses allowed
ADHD nameADHD (presentations: combined, inattentive, hyperactive-impulsive)6A05: ADHD, same presentations; term "Attention Deficit Hyperactivity Disorder" retained
ADHD in ICD-11 vs ICD-10N/AICD-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 onsetBefore age 12Before age 12
ASD criteria structureCriterion A (social communication) + Criterion B (RRBIs)Qualitative descriptions aligned with same domains
Sensory processingIncluded as Criterion B4 (hyper/hypo-reactivity)Included
Gaming DisorderInternet Gaming Disorder, "conditions for further study" (NOT official)6C51 Gaming Disorder, OFFICIAL diagnosis
Intellectual DisabilitySeverity by adaptive functioning (NOT IQ alone)Same, severity by adaptive functioning
Tic disordersTourette's + Persistent + ProvisionalICD-11: Tourette's (8A05.00); Primary tic disorders retained
Exam Pearl

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)

FeatureRADDSED
Core behavioral patternInhibited, emotionally withdrawn toward caregiversDisinhibited, indiscriminate social engagement with strangers
Caregiver behaviorAvoids comfort-seeking from caregiversApproaches strangers readily; no discrimination
Emotional profileReduced positive affect; irritability, sadness, fearfulnessMay appear sociable and happy superficially
Premonitory causeExtreme social neglect/deprivation (required)Extreme social neglect/deprivation (required)
Response to stable caregivingTypically improves significantlyMay PERSIST even after stable, caring placement
Safety concernEmotional/developmental harm from withdrawalVulnerability to exploitation by strangers
ASD confusionMay be confused with ASD (both show limited social responsiveness)Less confusion with ASD
ADHD overlapLess commonDSED + ADHD: can coexist; distinguish DSED disinhibition from ADHD impulsivity
Attachment patternNo organized attachment strategyAttachment may form with caregiver, but indiscriminate with others
Age of recognitionBefore age 5 (must be evident)Before age 5
Treatment responseBetter to dyadic/attachment therapiesMore treatment-resistant
Primary treatmentStable, responsive caregiving; dyadic therapyCaregiver education + safety planning; dyadic therapy
Prohibited treatmentHolding therapy (absolutely contraindicated)Holding therapy (absolutely contraindicated)
DSM-5 code313.89313.89 (separate from RAD)
Clinical Anchor

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

FeaturePrimary EnuresisSecondary Enuresis
DefinitionNever achieved dryness for ≥6 consecutive monthsOnset after at least 6 months of established continence
PrevalenceMore common (80%)Less common (20%)
Organic workupRoutine (hearing, developmental check)MORE RIGOROUS, higher organic yield
Organic causes to rule outRarely organic; maturationalUTI, diabetes mellitus, diabetes insipidus, constipation with overflow, structural urological abnormality
Psychosocial triggersLess prominentMore important, new baby, divorce, bereavement, abuse, school change
GeneticsStrong family history (70% if both parents, 44% if one parent affected)Less familial
Response to treatmentGood, bell-and-pad effectiveTreat underlying cause first; then bell-and-pad
Associated with psychiatric disorderLessMore, stress-linked onset
EEGNot indicatedNot indicated unless seizures suspected
DDAVPEffectiveEffective once organic causes addressed
Exam Pearl

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

FeatureChildhood DepressionAdult Depression
Mood presentationIrritability may predominate over sadness (DSM-5 allows)Sadness/depressed mood predominant
Cognitive featuresDevelopmentally simpler (less rumination; concrete negative thoughts)Abstract rumination, guilt, hopelessness more typical
Somatic complaintsMore common (headache, stomach ache)Less prominent
Psychomotor changesMay be more agitation than retardationEither agitation or retardation
Psychotic featuresRareMore common in severe depression
AnhedoniaBoredom, play refusal, withdrawal from peersAnhedonia classic; loss of pleasure in previous interests
SchoolSchool refusal, academic declineOccupational impairment
SuicidalityLess lethal ideation; plans less detailed; impulsive attemptsMore lethal means; more planned; completed suicide more common
ComorbidityAnxiety (>50%), ADHD, CD commonAnxiety, SUD, pain conditions
AntidepressantsFluoxetine (age 8+), Escitalopram (age 12+)Full range of antidepressants
Response to SSRIsGood but lower NNT than adults; combination with CBT superiorSSRIs effective; augmentation strategies well-studied
Black box warningYes, suicidal ideation (FDA BBW)No pediatric warning for adults
PsychotherapyCBT (Coping Cat, ACTION program); TF-CBT if traumaCBT, IPT, psychodynamic all evidence-based
TADS equivalentTADS (adolescents)STAR*D (adults)
Biological featuresLess HPA axis abnormality; growth hormone bluntingHPA hyperactivation; dexamethasone non-suppression

TABLE 8: ABA vs ESDM vs TEACCH

FeatureABA (Applied Behavior Analysis)ESDM (Early Start Denver Model)TEACCH (Structured Teaching)
Theoretical basisSkinnerian operant conditioningDevelopmental + ABA hybrid; relationship-basedStructured teaching; cognitive disability model
Age rangeAny age (most evidence <5 years)12–60 monthsAny age; school-age to adult
Intensity20–40 hours/week (intensive models)20–25 hours/weekVariable; lower intensity (classroom-based)
ApproachAdult-directed; discrete trial trainingChild-directed play; adult follows child's leadStructured environment; visual supports
Learning contextMostly table-based (DTT); also NETNatural play environments; everyday routinesStructured physical and temporal environment
Visual supportsUsed in some modelsYesCentral feature (picture schedules, work systems)
Evidence baseStrongest overall; multiple RCTs; decades of researchStrong, Dawson et al. (2010) RCT; developmental gains superior to community txModerate; primarily observational; widely accepted in schools
Criticism/controversyHistorical concerns about aversives (no longer used); intensity/rigidity; child-led balanceMore recent; less long-term dataLess intensive, may not drive change as much in severe ASD
Best suited forSkill acquisition across any level; challenging behaviorYoung children, early intervention windowSchool settings, life skills, transition planning
Delivered byBCBA (Board Certified Behavior Analyst) + therapy teamTrained therapists + parent coachingTrained educators + parents
Parent involvementVariable by programCentral, parents trained as co-therapistsYes, home carryover
GeneralizationTargeted explicitly (NET improves generalization)Built-in through natural contextBuilt-in through routine/structure
NICE guidanceIncluded in guidanceIncludedIncluded
Exam Strategy

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)

FeatureHaloperidolAripiprazole
ClassTypical (first-generation) antipsychoticAtypical (third-generation); partial D2 agonist
MechanismPotent D2 blockadePartial D2 agonism (stabilizer); 5HT1A partial agonist
Tic efficacyHighest of all agents, most evidence historicallyGood, comparable to risperidone; several RCTs
Starting dose0.25–0.5mg/day; titrate slowly2mg/day; titrate to 5–20mg/day
EPS riskHIGH, dystonia, parkinsonism, akathisiaLow
Tardive dyskinesiaSignificant risk with long-term useLow
Weight gainModerateModerate
Metabolic effectsModerateLess than risperidone; moderate
Prolactin elevationYes, significantMinimal (actually reduces prolactin, partial D2 agonist)
SedationSignificantMild–moderate
Current clinical preferenceLast resort, when all others failedFirst-choice antipsychotic for tics currently
Comorbid ADHDDoes not address ADHDAdjunct with alpha-2 agonist for ADHD
MonitoringEPS check, tardive dyskinesia (AIMS), prolactinMetabolic (weight, glucose, lipids), AIMS
Exam Pearl

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

FormulationBrand (example)Release ProfileDurationNotes
Immediate Release (IR)RitalinSingle peak4–6 hours2–3x daily dosing; rebound effect
Sustained Release (SR)Ritalin SRContinuous6–8 hoursInconsistent absorption; largely replaced
OROS (Osmotic Release)Concerta22% IR + 78% osmotic10–12 hoursOnce-daily; gold standard LA; most studied
Bimodal (LA)Ritalin LA50% IR + 50% delayed8–10 hoursSimulates twice-daily IR
Extended Release BeadsMedikinet XL40% IR + 60% ER8–10 hoursCan be sprinkled on food
LiquidQuillivant XLExtended release suspension10–12 hoursFor children who cannot swallow tablets
Transdermal patchDaytranaContinuous (worn 9h)10–12h (remove patch)Skin irritation common; flexible dosing
Clinical Anchor

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

SeverityIQ RangeConceptual SkillsSocial SkillsPractical SkillsEducational Prognosis
Mild~50–69Below grade level; literacy possible; abstract thinking limitedImmature but functional; gullible; friendship possibleSome self-care independence; simple employment possible; needs support for complex decisionsEducable; can reach ~6th grade academic level
Moderate~35–49Limited literacy (few words); simple math; relies on concreteSimple language; close relationships with familiar others; can participate in supervised social settingsBasic self-care with training; semi-independent in familiar settings; simple job tasksTrainable; can learn basic vocational skills
Severe~20–34Minimal conceptual skills; simple language understood; few words expressedRelies on close familiar relationships; limited verbal communicationRequires support for most ADLs; may achieve some self-care skills with extensive trainingRequires lifelong support; some communication possible
Profound<20Relies on sensory/physical interaction; no symbolic functionPre-symbolic; nonverbal communication; responds to familiar personsFully dependent; care needs are extensiveRequires total care; minimal independent function
Key Insight

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-TRICD-11*
Chapter 05

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.)

Exam Strategy

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

RankTopicFrequencyTypical FormatMarks
1ADHD, assessment and managementVery High (appears ~80% of years)Long question10–20
2Autism Spectrum Disorder, features, assessment, managementVery High (~75% of years)Long question10–20
3Intellectual Disability, classification, etiology, assessmentHigh (~65% of years)Long question or short note10–15
4Child abuse, types, indicators, management, POCSOHigh (~60% of years)Long question or short note10–15
5Conduct Disorder, features, managementModerate-High (~50% of years)Long question or short note10
6School refusal, classification, managementModerate (~45% of years)Short note or combined5–10
7Tourette Syndrome, criteria, treatmentModerate (~40% of years)Short note5–10
8Enuresis, assessment, treatmentModerate (~40% of years)Short note5–10
9Separation Anxiety DisorderModerate (~35% of years)Short note5
10Pediatric depression, pharmacotherapy, TADSModerate (~35% of years)Short note or part of long Q5–10
11Munchausen by Proxy / Factitious Disorder Imposed on AnotherModerate (~35% of years)Short note5
12Specific Learning Disorders, dyslexiaModerate (~30% of years)Short note5
13Fragile X SyndromeModerate (~30% of years)Short note5
14Down Syndrome, features, psychiatryModerate (~30% of years)Short note5
15Attachment Disorders, RAD vs DSEDLow-Moderate (~25% of years)Short note5
16Gaming Disorder (ICD-11)Low-Moderate (~20% of years, rising)Short note5
17Selective MutismLow-Moderate (~20% of years)Short note5
18ODD, diagnostic criteriaLow (~15% of years)Short note5
19EncopresisLow (~15% of years)Short note5
20Rett SyndromeLow (~15% of years)Short note5

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:

Examiner hotspots, points that distinguish good from excellent answers:

PointCommon AnswerDistinguishing Answer
Age of onsetAge 12DSM-5 changed from age 7 (DSM-IV) to age 12, mentioning this change is a mark-earner
Symptom threshold adultsSame as childrenDSM-5: 5 symptoms (not 6) for adults ≥17 years
Stimulant side effectsAppetite, insomniaMention 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):

  1. Introduction + epidemiology (2 marks)
  2. DSM-5 criteria in full, both domains (4 marks)
  3. Assessment, history, rating scales, investigations, differentials (5 marks)
  4. Management, multimodal: psychoeducation + behavioral + pharmacotherapy + school (7 marks)
  5. Follow-up and prognosis (2 marks)

Topic 2: Autism Spectrum Disorder

What examiners consistently ask:

Examiner hotspots:

PointCommon AnswerDistinguishing 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:

Examiner hotspots:

PointCommon AnswerDistinguishing 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 causeOften missedFragile X syndrome (FMR1, CGG repeat expansion, X-linked)
Most common preventable causeOften missedPKU (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 microarrayRarely mentionedFirst-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:


Topic 4: Child Abuse

What examiners consistently ask:

Examiner hotspots:

PointCommon AnswerDistinguishing 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 triadOften incompleteSubdural 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:

Examiner hotspots:

PointCommon AnswerDistinguishing 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 onsetOften not distinguishedChildhood 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:

Tourette Syndrome

Key examiner points:

Enuresis

Key examiner points:

Munchausen by Proxy

Key examiner points:

Pediatric Depression and TADS

Key examiner points:


SECTION 4: EMERGING TOPICS (RISING FREQUENCY)

Gaming Disorder (ICD-11)

Why it's rising: ICD-11 released 2022; examiners testing new classifications.

Key points:

Specific Learning Disorders

Why it's rising: Greater awareness in Indian school system; ADHD + SLD comorbidity questions.

Key points:


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)

Fact · Answer
Most common psychiatric referral in children ADHD
DSM-5 ADHD age of onset criterion Before age 12 (changed from 7 in DSM-IV)
ADHD adult symptom threshold 5 of 9 (not 6)
MTA study, best outcome Combined treatment (medication + behavioral)
ASD gold standard diagnostic tools ADOS-2 + ADI-R together
ASD screening tool 16–30 months M-CHAT-R/F
ASD, only FDA-approved drugs (what they treat) Risperidone + aripiprazole, for irritability/aggression (not core symptoms)
Asperger's in DSM-5 Eliminated, subsumed into ASD Level 1
ID severity determined by (DSM-5) Adaptive functioning (NOT IQ score alone)
Most common chromosomal cause of ID Down syndrome (trisomy 21)
Most common inherited cause of ID Fragile X syndrome
Most common preventable cause of ID PKU (dietary) / FASD (alcohol)
Fragile X gene FMR1 (CGG repeat expansion >200) on Xq27.3
Imprinting, Prader-Willi PATERNAL deletion 15q11 (or maternal UPD)
Imprinting, Angelman MATERNAL deletion 15q11 (or paternal UPD)
Williams syndrome deletion 7q11.23 (elastin gene)
Tourette's, coprolalia prevalence 10–15% (NOT required for diagnosis)
Tourette's, CBIT components HRT (awareness + competing response) + functional intervention
Tourette's, preferred pharmacotherapy currently Aripiprazole (not haloperidol)
Enuresis, best long-term treatment Bell-and-pad (urine alarm), 75–85% success
Desmopressin, main risk Hyponatremia (must restrict fluids)
Child abuse, abusive head trauma triad Subdural hematoma + retinal hemorrhages + no external injury
POCSO Act, reporting obligation ALL persons must report; failure = criminal offense
Mandatory reporter India, POCSO section Section 19 (reporting); Section 21 (penalty for non-reporting)
Munchausen by proxy, DSM-5 name Factitious Disorder Imposed on Another
School refusal, distinguishing from truancy School refusal = distress + home with parent's knowledge; truancy = no distress + parents unaware
TADS, best outcome arm Combined fluoxetine + CBT: 71% response
Pediatric depression FDA approvals Fluoxetine (age 8+), Escitalopram (age 12+)
Black box warning, antidepressants in children Increased suicidal IDEATION (not completed suicide); ~2% absolute increase
Gaming disorder, ICD-11 code 6C51 (official diagnosis); DSM-5 = research only
Gaming disorder, duration criterion ≥12 months (shorter if severe)
RAD vs DSED, persistence after good care RAD improves; DSED may persist despite stable caregiving
Holding therapy Absolutely contraindicated, associated with deaths; no evidence
Selective mutism, core feature Context-specific mutism; normal language at home; anxiety-based
Dyslexia, core deficit Phonological processing (NOT vision problem, NOT letter reversal)
ADOS-2 module selection basis Expressive language level (not age)
Down syndrome, Alzheimer's ALL DS adults have Alzheimer's pathology by age 40; APP gene on chromosome 21
Chromosomal microarray, indication First-tier genetic investigation in ASD and ID; 15–20% yield
ASD + ADHD dual diagnosis Allowed in DSM-5 (was excluded in DSM-IV)

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

  1. ADHD, assessment and management (appears almost every year)
  2. ASD, clinical features + assessment pathway (appears almost every year)
  3. Intellectual disability, classification + evaluation (high frequency)

Tier 2: Prepare for 10-mark long question OR 5-mark short note

  1. Child abuse, indicators + POCSO Act + management
  2. Conduct Disorder, management (MST emphasis)
  3. Pediatric depression, TADS + pharmacotherapy
  4. Tourette Syndrome, criteria + CBIT + pharmacotherapy

Tier 3: Prepare 5-mark short note only

  1. School refusal
  2. Enuresis (bell-and-pad vs desmopressin)
  3. Munchausen by proxy / FDIA
  4. Selective mutism
  5. Fragile X syndrome
  6. Down syndrome + Alzheimer's
  7. Gaming disorder (ICD-11)
  8. RAD vs DSED
  9. Specific learning disorders (dyslexia)

Tier 4: Know the headline facts only

  1. Encopresis
  2. Rett syndrome
  3. Prader-Willi vs Angelman (imprinting)
  4. Williams syndrome

Key Insight

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 2008–2025Kaplan & Sadock (11th ed.)Rutter's (6th ed.)Lewis's (5th ed.)DSM-5-TRICD-11*
Chapter 06

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:

Q2: What rating scales would you use, and how would you proceed with assessment?

Rating scales:

Assessment:

Q3: Outline a management plan.

Multimodal approach:

  1. Psychoeducation, parents and teacher; explain brain-based model; reduce blame
  2. Behavioral Parent Training, Incredible Years or Triple P; positive attention, reward charts, consistent consequences
  3. School accommodations, preferential seating, Daily Report Card, extended time, movement breaks
  4. Pharmacotherapy, Methylphenidate (start 0.3 mg/kg IR; titrate to 0.5–1.0 mg/kg/day LA formulation); monitor weight, BP, sleep, appetite
  5. Follow-up, monthly initially; biannual height/weight; annual reassessment
Exam Pearl

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:

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):

Q3: Outline the comprehensive assessment pathway.

  1. Developmental pediatrician/child psychiatrist assessment
  2. ADOS-2 Toddler Module (12–30 months, minimal verbal), structured observation
  3. ADI-R, structured parent interview for developmental history
  4. Vineland-3, adaptive behavior assessment
  5. Mullen Scales of Early Learning, cognitive and language
  6. Speech and language therapy evaluation
  7. Occupational therapy, sensory profile, fine motor
  8. Hearing test (mandatory)
  9. Medical investigations: chromosomal microarray (first-tier genetic), Fragile X testing, EEG (regression + concern for Landau-Kleffner)
  10. Ophthalmology

Q4: What early interventions would you recommend?

Clinical Anchor

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)

Q2: What is the differential diagnosis for the increase in self-injurious behavior (SIB)?

Cause · Clinical Clues
Pain/medical cause Otitis media, dental pain, GERD, constipation, common in ID and may present as SIB
Anxiety Change in routine (even subtle); new sensory trigger
New psychiatric disorder Depression (withdrawn, sleep/appetite change), psychosis (looking at unseen stimuli)
Epilepsy Post-ictal behavioral change; EEG indicated
Puberty Hormonal changes emotional dysregulation
Side effect of medication If on any psychotropic
Environmental change New staff at school, peer interactions
Clinical Anchor

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:

Management:


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:

Feature · Significance
Age 9 months (pre-mobile) Pre-mobile infants virtually never sustain accidental bruises, "those who don't cruise, don't bruise"
Circular burns on buttock Shape and location consistent with cigarette burns
Bruise on ear TEN-4 rule: bruising on Ear in infant < 4 months (age extends to pre-mobile) = suspicious
Bruise on neck TEN-4 rule: bruising on Neck = suspicious
Healing bruise on neck Multiple injuries in different stages of healing
Bilateral subdural hematomas Classic for shaken baby / abusive head trauma
Bilateral retinal hemorrhages Highly specific for abusive head trauma when combined with subdural hematomas
History (rolled off bed) Mechanism inconsistent with extent of intracranial injury, low falls from bed do not cause bilateral SDH + retinal hemorrhages
Mother's affect Absence of appropriate concern about CT findings

Q2: What is the immediate management?

  1. Admit to pediatric ward (safe environment; further evaluation)
  2. Full skeletal survey (mandatory): posterior rib fractures, metaphyseal fractures (bucket-handle), multiple fractures in different stages of healing
  3. Ophthalmology consultation (already done, retinal hemorrhages confirmed)
  4. Neurosurgical review (bilateral SDH)
  5. Mandatory report to Child Protection Services immediately, reasonable suspicion is sufficient; do not wait for certainty
  6. SJPU/Police notification under POCSO Act 2012 (India), Section 19
  7. Do NOT return child to parents until child protection investigation complete
  8. Forensic documentation, photograph all injuries with scale bar, detailed medical notes

Q3: What are the long-term consequences of abusive head trauma?

Exam Pearl

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:

Q2: What is the significance of callous-unemotional (CU) traits in this case?

CU traits (the "Limited Prosocial Emotions" specifier) indicate:

Clinical implications:

Q3: What treatment approach has the strongest evidence for Vikram's presentation?

Multisystemic Therapy (MST):

Pharmacotherapy:

Exam Strategy

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:

Distinguishing from language disorder:

Distinguishing from ASD:

Q2: How would you assess this child?

Q3: Outline the management plan.

1. Psychoeducation:

2. Behavioral Intervention (first-line):

3. School Collaboration:

4. Pharmacotherapy (if no response after 3–4 months of behavioral intervention):

Exam Pearl

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:

Additional features:

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):

Additional:

Q3: Outline treatment, prioritizing the comorbidity question.

Step 1, Determine primary source of impairment:

Step 2, Behavioral treatment for tics:

Step 3, Pharmacotherapy for tics (if CBIT insufficient or unavailable):

Step 4, Address ADHD:

Exam Pearl

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:

  1. Impaired control over gaming, persistent despite attempts to reduce; unable to stop at planned time; gaming 10–14h/day
  2. 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)
  3. 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:

Q2: What comorbidities would you screen for?

Comorbidity · Screening
Depression PHQ-A (Patient Health Questionnaire, Adolescent); self-harm threat may indicate depressive disorder
Social anxiety SCARED; history of social avoidance pre-gaming
ADHD Vanderbilt/Conners; impulsivity, attention problems
Sleep disorder Sleep diary; severe circadian reversal (4am–2pm)
Suicidal ideation C-SSRS; self-harm threat needs formal risk assessment

Q3: Outline the management plan.

1. Risk Assessment (immediate):

2. Psychoeducation:

3. CBT:

4. Family Therapy:

5. School Reintegration:

6. Pharmacotherapy:

7. Intensive Programs:

Clinical Anchor

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:

Also some Function 1 (avoidance of negative affect related to new school):

Q2: What is the key first principle of management, and why?

Key principle: Rapid return to school.

Every additional day of absence:

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:

CBT for Ananya:

Family intervention, addressing parental accommodation:

Pharmacotherapy:

Exam Pearl

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:

DSED vs RAD:

FeatureThis caseRAD
Core behaviorDisinhibited, approaches strangersInhibited, withdrawn from caregivers
Response to stable caregivingPERSISTS despite 2 years in good homeTypically improves
Safety riskExploitation by strangersEmotional damage from neglect

DSED vs ADHD:

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:

Q3: What are the management priorities?

1. Parental psychoeducation and support:

2. Safety planning (IMMEDIATE PRIORITY):

3. Dyadic therapy:

4. Do NOT use:

Clinical Anchor

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:

Q2: What is the treatment hierarchy for this child?

Step 1, Address psychosocial stressors:

Step 2, Psychoeducation:

Step 3, Behavioral strategies:

Step 4, Urine alarm (bell-and-pad):

Step 5, Desmopressin:

Exam Pearl

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:

Q2: What investigations would you order?

Investigation · Rationale
Baseline cognitive assessment (Cambridge Cognitive Examination for Older Adults with Down Syndrome, CAMCOG-DS) Establish current cognitive baseline; compare to previous (if available)
Brain MRI Cortical atrophy (hippocampal, parietal, frontal); rule out vascular dementia, space-occupying lesion
EEG Seizure characterization; Alzheimer's EEG changes
Thyroid function Hypothyroidism (10x more common in DS; worsens cognitive function)
Full blood count, metabolic panel Exclude treatable causes
Vitamin B12, folate Nutritional causes of cognitive decline
Review medications Drug-induced cognitive change

Q3: What management principles apply?

  1. Confirm and communicate diagnosis to carers and family in accessible language
  2. Safety: supervision for wandering (door alarms, GPS tracker); seizure precautions; supervision for all activities
  3. Environmental modification: familiar, predictable environment; visual schedules; reduced sensory overload; good lighting (reduces sundowner confusion)
  4. Pharmacotherapy:
  5. Donepezil (cholinesterase inhibitor): some evidence for mild-moderate Alzheimer's in DS; start low, go slow
  6. Seizure management: sodium valproate or lamotrigine (avoid phenytoin, cognitive side effects)
  7. Avoid benzodiazepines (worsen cognition)
  8. Carer support: training in dementia care; family meetings; advance care planning
  9. Palliative approach as disease progresses: comfort, dignity, quality of life
Exam Pearl

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-TRICD-11*

All patient names and details are entirely fictitious.

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