Child and Adolescent Psychiatry

Genetic / non-modifiable

• Polygenic heritability: ADHD and autism spectrum disorder (ASD) are among the most heritable psychiatric conditions (twin estimates roughly 70–80%); first-degree relatives of a proband carry markedly increased risk. Examiners plant "father was a poor student who never sat still."
• Single-gene and copy-number syndromes: Fragile X (FMR1 CGG expansion — the most common inherited cause of intellectual disability, often with ASD features), tuberous sclerosis, Rett syndrome (MECP2, girls, hand-wringing, acquired microcephaly), and 22q11.2 deletion, which carries one of the strongest known risks for early-onset schizophrenia.
• Male sex for ADHD, ASD, and childhood-onset conduct disorder; advanced paternal age (de novo mutations) for ASD and schizophrenia.
• Prematurity, low birth weight, and perinatal hypoxia: disrupt frontostriatal white matter maturation and are reproducible risks for ADHD.

Prenatal and toxic exposures (modifiable)

• Maternal tobacco, alcohol, and opioid use: fetal alcohol spectrum disorder produces inattention, impulsivity, and low IQ and is the leading preventable cause of intellectual disability.
• Prenatal valproate exposure: teratogenic for neurodevelopment with increased ASD and lowered IQ — a reason ACOG and neurology guidance avoid valproate in people who may become pregnant.
• Lead exposure: dose-dependent attention and behavioral impairment; the AAP supports targeted blood lead screening in high-risk children.

Psychosocial (modifiable — where conduct disorder and ODD live)

• Maltreatment, neglect, and household adversity: high adverse childhood experience burden drives amygdala hyperreactivity and HPA dysregulation, the strongest environmental predictor of conduct disorder and early substance use.
• Harsh, inconsistent, or coercive parenting and parental psychopathology (maternal depression, paternal antisocial personality/substance use): coercive-cycle reinforcement of oppositional behavior — and the target of parent management training.
• Poverty, community violence, deviant peer affiliation, school failure, and chronic sleep deprivation all lower the symptom threshold.

• The classic distractor: vaccines, thimerosal, "refrigerator mothers," dietary sugar, and screen time alone do not cause ASD; parenting style is not an etiology.

• Developmental neurobiology and prefrontal cortex maturation: The prefrontal cortex (responsible for impulse control, executive function, and emotional regulation) undergoes protracted development through the second decade of life. Myelination and synaptic pruning continue into the early 20s, creating a window of vulnerability where psychiatric symptoms may manifest as frontostriatal circuits and limbic-cortical connections develop asynchronously. This explains why impulse control deficits, emotional dysregulation, and behavioral disinhibition are prominent in childhood disorders.

• Neurotransmitter system development: Developmental changes in dopamine (reward and motivation circuits), serotonin (mood and impulse control), norepinephrine (attention and arousal), and glutamate/GABA systems create age-specific vulnerabilities. Puberty-related hormonal changes trigger significant remodeling of these systems, explaining why mood and anxiety disorders often emerge or worsen during adolescence.

• Genetic vulnerability with environmental interaction: Most childhood psychiatric disorders follow multifactorial inheritance patterns where genetic predisposition (identified through family studies and polygenic risk scores) combines with environmental stressors (trauma, neglect, parental psychopathology, socioeconomic adversity, peer rejection) to exceed a threshold for symptom emergence. Epigenetic modifications—stable changes in gene expression without DNA sequence alteration—represent a molecular mechanism by which early adversity alters stress response systems.

• Altered stress-response circuitry: Childhood adversity and trauma cause hyperactive amygdala and hypoactive prefrontal regulation, leading to enhanced threat perception, exaggerated startle responses, and poor emotional dampening. The hypothalamic-pituitary-adrenal (HPA) axis becomes dysregulated, producing abnormal cortisol patterns (typically elevated in depression/anxiety, blunted in trauma/dissociation) that persist into adulthood.

• Neurotransmitter receptor and transporter abnormalities: Reduced serotonin transporter (SERT) availability in depression, altered dopamine signaling in ADHD, and glutamate system dysfunction in autism spectrum disorder and early-onset schizophrenia represent specific pathological mechanisms. These abnormalities are often genetically determined but can be acquired through early adversity.

• Inflammatory and metabolic factors: Increasing evidence implicates elevated inflammatory cytokines (IL-6, TNF-α, CRP) in early-onset depression and psychosis, particularly when childhood adversity is present. Metabolic dysfunction and mitochondrial abnormalities may contribute to mood instability and treatment resistance.

Attention-Deficit/Hyperactivity Disorder (ADHD)

• Inattention symptoms: Difficulty sustaining attention, careless mistakes, forgetfulness in daily activities, easy distractibility, difficulty organizing tasks (onset before age 12, present in multiple settings)
• Hyperactivity-impulsivity symptoms: Fidgeting, inability to remain seated, excessive talking, difficulty waiting turns, impulsive decision-making, interrupting conversations
• Clinical pearl: Combined presentation is most common; predominantly inattentive type often underdiagnosed in girls (who may internalize symptoms); predominantly hyperactive-impulsive type more common in younger children and boys; symptoms must cause functional impairment (academically, socially, occupationally)

Major Depressive Disorder (MDD)

• Core mood symptoms: Persistent depressed/irritable mood (more commonly irritability than sadness in children), anhedonia, social withdrawal, sleep disturbance (insomnia or hypersomnia)
• Associated features: Fatigue, concentration difficulties, feelings of worthlessness or guilt, appetite change, psychomotor changes, suicidal ideation/attempts
• Clinical pearl: Irritability may be the primary mood presentation in prepubertal children rather than sadness; depression in adolescents increasingly presents with anhedonia rather than mood complaints; higher suicide risk in adolescents than adults

Anxiety Disorders (Generalized Anxiety, Social Anxiety, Separation Anxiety, Panic)

• Excessive worry: Age-inappropriate, difficult to control, persisting for ≥6 months; in children often focused on performance, competence, or family safety
• Physical manifestations: Restlessness, fatigue, concentration difficulties, irritability, muscle tension, sleep disturbance; panic symptoms include chest pain, shortness of breath, dizziness, derealization
• Avoidance behaviors: School refusal/avoidance, social withdrawal, reluctance to separate from parents, avoidance of feared situations
• Clinical pearl: Separation anxiety is normative until age 2-3 but pathological when persistent beyond age 5 and functionally impairing; school refusal in anxious children often misattributed to "oppositional" behavior

Oppositional Defiant Disorder (ODD)

• Angry/irritable mood: Frequent loss of temper, easily annoyed, often angry and resentful (presents as baseline irritability)
• Argumentative/defiant behavior: Argues with authority figures, actively defies rules, deliberately annoying others, blames others for mistakes
• Vindictive behavior: Deliberately causing harm, seeking revenge (present in ≤25% of cases, associated with worse prognosis)
• Clinical pearl: Irritability is the most common presentation, not overt defiance; must persist ≥6 months and cause functional impairment; distinguish from disruptive behavior due to ADHD, anxiety, or mood disorder

Conduct Disorder

• Aggression to people/animals: Bullying, physical fights, weapon use, physical cruelty, sexual coercion
• Property violation: Deliberate fire-setting, property destruction, theft
• Deceitfulness/theft: Lying, stealing, breaking into homes/cars
• Rule violation: Running away, school truancy, curfew violation
• Clinical pearl: Requires ≥3 criteria over 12 months with functional impairment; childhood-onset (before age 10) predicts worse outcomes and increased violence risk; strong association with ADHD and trauma; high risk for substance abuse and antisocial personality disorder in adulthood

Autism Spectrum Disorder (ASD)

• Social communication deficits: Reduced eye contact, difficulty initiating/maintaining conversations, impaired nonverbal communication, difficulty understanding social cues, preference for solitude
• Restricted/repetitive behaviors: Repetitive movements (stimming), insistence on sameness/routines, intense restricted interests, unusual sensory responses (covering ears, seeking textures)
• Clinical pearl: Symptoms must manifest in early childhood but may not fully appear until social demands exceed capacity; increased recognition in girls due to "camouflaging"; intellectual disability present in ~30% of cases; co-occurring ADHD, anxiety, and depression common; not associated with parenting style

Early-Onset Schizophrenia (EOS; onset before age 18)

• Positive symptoms: Delusions (often bizarre, persecutory, or referential), hallucinations (auditory most common; "command voices" telling patient to harm self/others), disorganized speech, disorganized/catatonic behavior
• Negative symptoms: Reduced emotional expression, diminished motivation, poverty of speech, anhedonia
• Cognitive decline: Marked decline in academic/social functioning, concentration difficulties, memory problems
• Clinical pearl: EOS is rare but more severe than adult-onset schizophrenia with worse premorbid adjustment; higher rates of developmental delays, neurological soft signs, and neurodevelopmental abnormalities; increased suicide risk (10-15%); male predominance with earlier onset; often preceded by prodromal phase with social withdrawal, declining grades, and magical thinking

Bipolar Disorder (Early-Onset)

• Manic/hypomanic episodes: Elevated/expansive or irritable mood, decreased need for sleep (feeling rested after 3 hours

• Diagnosis is clinical and criterion-based: every disorder here is diagnosed by DSM-5-TR criteria applied to multi-informant history (parent, teacher, child). There is no confirmatory laboratory or imaging test; labs and neuroimaging serve only to exclude mimics.

Step 1 — screening and surveillance

• ADHD: the AAP (2019 ADHD guideline) directs clinicians to evaluate any child 4–18 with academic or behavioral problems and inattention/hyperactivity. Standardized scales — the Vanderbilt ADHD Diagnostic Rating Scale or Conners — must be obtained from both home and school.
• ASD: AAP recommends developmental surveillance at every visit with standardized developmental screening at 9, 18, and 30 months and autism-specific screening (M-CHAT-R/F) at 18 and 24 months. USPSTF found evidence insufficient for universal ASD screening in asymptomatic toddlers — know both positions.
• Mood/anxiety: USPSTF (2022) recommends screening for anxiety in youth ages 8–18 and depression in ages 12–18; PHQ-A and SCARED are the usual instruments.

Step 2 — criteria that carry the numbers

• ADHD: ≥6 inattentive and/or ≥6 hyperactive-impulsive symptoms (≥5 if age ≥17) for ≥6 months, onset of several symptoms before age 12, present in ≥2 settings, with functional impairment.
• ODD: ≥4 symptoms for ≥6 months. Conduct disorder: ≥3 criteria in 12 months, ≥1 in the past 6 months. Separation anxiety: ≥4 weeks in children. MDD: ≥2 weeks. GAD: ≥6 months.
• ASD: deficits in all three social-communication domains plus ≥2 restricted/repetitive behavior domains, with early-childhood onset; severity graded by support level.

Step 3 — confirmatory and exclusionary workup

• ASD gold standard: structured multidisciplinary assessment with ADOS-2 ± ADI-R, plus audiology testing in every child with language delay.
• Etiologic testing in ASD/global delay: chromosomal microarray and Fragile X testing are first-line (AAP/ACMG).
• Rule out the mimics: hearing and vision impairment, absence seizures (EEG if staring spells with unresponsiveness), obstructive sleep apnea, lead toxicity, thyroid disease, and substance use.

Immediate priorities

• Safety first: assess suicidal ideation, access to firearms and lethal medications, and abuse/neglect before anything else. Acute suicidality, psychosis with command hallucinations, or aggression endangering others warrants emergency evaluation and possible hospitalization.

ADHD (AAP 2019 guideline, age-stratified)

• Ages 4–5: parent training in behavior management (PTBM) and behavioral classroom intervention are first-line; methylphenidate only if behavior therapy fails and impairment is moderate-severe.
• Ages 6–18: FDA-approved medication plus behavioral therapy and school supports (IEP/504 plan). Stimulants — methylphenidate or amphetamine class — are first-line and have the largest effect size; they block DAT/NET, raising synaptic dopamine and norepinephrine in prefrontal-striatal circuits.
• Second-line/non-stimulants: atomoxetine (selective norepinephrine reuptake inhibitor) or extended-release alpha-2A agonists (guanfacine ER, clonidine ER), useful with tics, comorbid anxiety, insomnia, or diversion risk. These take weeks to work, unlike stimulants' same-day effect.
• Contraindicated/cautioned: concurrent MAOIs (hypertensive crisis), symptomatic cardiovascular disease or known structural heart lesion, and untreated substance misuse. Routine pre-treatment ECG is not required — a targeted cardiac history, family history of sudden death, and exam suffice.

Depression and anxiety (AACAP/GLAD-PC framing)

• Mild: CBT alone. Moderate–severe: SSRI plus CBT — fluoxetine has the best pediatric evidence for depression, and escitalopram is also FDA-approved for adolescent depression.
• Pediatric anxiety: SSRIs (sertraline, fluoxetine) have the strongest trial evidence (CAMS trial) though largely used off-label — sertraline's pediatric FDA indication is OCD; duloxetine carries the pediatric GAD indication.
• Avoid benzodiazepines (disinhibition, dependence) and avoid TCAs for pediatric depression (ineffective, cardiotoxic in overdose). All antidepressants carry a boxed warning for suicidality in patients <25 — see the child weekly early on.

Disruptive behavior and ASD

• ODD/conduct disorder: parent management training and, for adolescents, multisystemic therapy; no medication is FDA-approved — treat comorbid ADHD first.
• ASD: early intensive behavioral intervention, speech and occupational therapy. Risperidone and aripiprazole are approved only for irritability/aggression, not core social deficits.
• Early-onset schizophrenia/bipolar mania: second-generation antipsychotics; lithium for bipolar; clozapine for treatment-resistant psychosis.

Disease-related

• Suicide and self-harm — emergency: risk is highest in adolescent depression, bipolar disorder, and early-onset schizophrenia; signals include a new plan, giving away possessions, or abrupt calm after agitation. Screen at every visit; suicide is a leading cause of adolescent death.
• Academic failure and school dropout: untreated ADHD and anxiety-driven school refusal produce grade retention and loss of peer scaffolding — often the presenting "complaint."
• Substance use disorder: conduct disorder and untreated ADHD are among the strongest childhood predictors. Stimulant treatment of ADHD does not increase — and may reduce — later substance use risk; the common exam distractor that stimulants "cause addiction" is wrong. Misuse and diversion of immediate-release formulations in adolescents remain a real concern, favoring long-acting preparations or a non-stimulant.
• Progression of externalizing disorders: ODD → conduct disorder → antisocial personality disorder (only diagnosable at ≥18). Childhood-onset conduct disorder with callous-unemotional traits has the worst trajectory.
• Injury, legal involvement, teen pregnancy, and unintentional trauma from impulsivity.

Treatment-related

• Stimulants: appetite suppression with growth velocity deceleration — plot height and weight at every visit; insomnia; modest rises in heart rate and blood pressure; emergence or worsening of tics; rarely new hallucinations (stop the drug).
• Atomoxetine: boxed warning for suicidal ideation; rare hepatotoxicity — jaundice or dark urine mandates stopping.
• Alpha-2 agonists: sedation, hypotension, and rebound hypertension with abrupt discontinuation.
• SSRIs: behavioral activation/disinhibition (mistaken for mania), boxed-warning suicidality in youth, and serotonin syndrome — emergency — with clonus, hyperreflexia, hyperthermia, and agitation when combined with other serotonergic agents.
• Second-generation antipsychotics: children are especially prone to weight gain and metabolic syndrome (risperidone, olanzapine); hyperprolactinemia causing gynecomastia and galactorrhea; extrapyramidal symptoms including acute dystonia (treat with anticholinergic); tardive dyskinesia; and neuroleptic malignant syndrome — emergency — with rigidity, hyperthermia, autonomic instability, and elevated creatine kinase.
• Lithium: emergency toxicity with tremor, ataxia, and confusion, especially during dehydration or NSAID use; chronic hypothyroidism and nephrogenic diabetes insipidus.
• Clozapine: agranulocytosis and myocarditis requiring mandated monitoring.

• ADHD needs several symptoms before age 12 in ≥2 settings. Symptoms confined to a single setting do not meet DSM-5-TR criteria and should prompt evaluation for a learning disorder, anxiety, or environmental/classroom factors — though discrepant parent–teacher ratings are common and warrant further collateral rather than immediate exclusion of ADHD. Best next step in a suspected case: obtain standardized rating scales from parent AND teacher (Vanderbilt), not a brain MRI or EEG.
• Age drives ADHD first-line therapy (AAP 2019): ages 4–5 → parent training in behavior management first; ages 6–18 → stimulant plus behavioral/school intervention. Choosing medication first in a preschooler is the classic wrong answer.
• Falling off the growth curve on a stimulant is the monitoring finding examiners want; plot height and weight at each visit. Insomnia and appetite suppression are expected, not reasons to abandon the class outright.
• Comorbid tics or a diversion-prone teen → shift to a non-stimulant: atomoxetine or extended-release guanfacine/clonidine.
• Depressed adolescent, moderate-severe → fluoxetine plus CBT beats either alone; every antidepressant carries the boxed suicidality warning in patients <25, so the correct answer includes close follow-up, not withholding treatment. Benzodiazepines are the distractor for pediatric anxiety.
• Separation anxiety with school refusal: the answer is return the child to school promptly with CBT (± SSRI if severe), not home tutoring, which reinforces avoidance. Distinguish from truancy — the anxious child stays home with the parent; the conduct-disordered child is out with peers.
• ASD: risperidone and aripiprazole treat irritability/aggression only — no drug improves core social communication; early intensive behavioral intervention is the answer. Order chromosomal microarray and Fragile X testing. Vaccines do not cause autism — the perennial distractor.
• ODD vs conduct disorder: ODD violates rules and authority; conduct disorder violates the basic rights of others (aggression, animal cruelty, fire-setting, theft). Antisocial personality disorder cannot be diagnosed until age 18.