Child Psychiatry (F8-9)

Other Psychiatric Conditions In Child Psychiatry

Other psychiatric conditions in child psychiatry encompass a range of disorders including childhood-onset schizophrenia, selective mutism, reactive attachment disorder, stereotypic movement disorder, and elimination disorders (enuresis and encopresis) that do not fall under the more common categories of neurodevelopmental, anxiety, or mood disorders.

Child and adolescent psychiatry (also called "paedopsychiatry") deals with psychiatric conditions presenting before the age of 18. The phrase "Other Psychiatric Conditions in Child Psychiatry" is a catch-all for the conditions that sit outside the "big" neurodevelopmental disorders (ASD, ADHD) and externalising behaviour disorders (ODD, CD) — namely:

  1. Anxiety disorders of childhood
  2. Youth (childhood/adolescent) depression
  3. Disorders of social functioning (selective mutism, attachment disorders)
  4. Sibling rivalry disorder
  5. Post-traumatic stress disorder (PTSD) in children

The unifying principle is that many adult psychiatric conditions do occur in children but manifest differently because:

  • The developing brain has a different neurobiological substrate at each age.
  • Children lack the metacognitive vocabulary to articulate internal states → symptoms "leak out" as somatic complaints, behavioural disturbance, or irritability.
  • Developmental stage colours the content of symptoms (e.g., an infant's anxiety is about strangers; an adolescent's anxiety is about social evaluation — same circuit, different trigger).

Think of it this way: the limbic system matures early, but the prefrontal cortex (which modulates it) is still under construction until the mid-20s. So children feel the full force of anxiety and low mood but lack the cortical "brakes" to rationalise or regulate those feelings. That's why you see more behavioural expression and fewer cognitive symptoms.


2. Epidemiology

ConditionPrevalenceSex RatioPeak Onset
Anxiety disorders (all types)Commonest psychiatric disorder of childhood (~5-15% of children) [1][2]Slight F > M (especially post-puberty)Varies by subtype (see below)
Separation anxiety disorder3-5% of school-age childrenSlight F > M7-9 years
Specific phobias5-10%F > MEarly childhood
Social anxiety disorder (social phobia)1-2% in children, rises in adolescenceF > MEarly adolescence (10-13y)
GAD1-3% of childrenF > MLate adolescence
Panic disorderRare before puberty, 1-2% in adolescentsF > MLate adolescence
Youth depression< 1% pre-pubertal (M:F ≈ 1:1), rises drastically after puberty (1-year prevalence ~4%, F > M ≈ 2:1) [1]See leftAdolescence
Selective mutism0.7-0.8%Slight F > MBefore age 5
Reactive attachment disorder (RAD)Rare, < 1% (but higher in institutional care/foster care)M ≈ FEarly childhood
PTSD in childrenVariable (10-25% after significant trauma)F > M in adolescenceAny age
Sibling rivalry disorderCommon clinically but rarely formally diagnosedM ≈ FTypically after birth of a new sibling

  • Hong Kong data suggest child psychiatric disorders affect ~10-15% of children/adolescents.
  • High academic pressure culture → disproportionate rates of anxiety (especially performance anxiety, test anxiety) and youth depression.
  • Rising referral rates to child psychiatric services in Hong Kong, with anxiety and ADHD being the most common referral diagnoses.
  • Selective mutism may be under-recognised in bilingual (Cantonese–English) environments where language switching can mask symptoms.
  • Youth suicide is a significant public health concern in HK, often linked to untreated depression.

3. Anatomy and Function (Neurodevelopmental Basis)

Understanding child psychiatric conditions requires a developmental neuroanatomy perspective. The key circuits involved are:

StructureFunctionDevelopmental TimingRelevance to Child Anxiety
AmygdalaThreat detection, fear conditioning, activates autonomic "fight-or-flight"Functional from birth, relatively mature earlyEarly maturation explains why children can experience intense fear responses even in infancy
Hypothalamus (dorsomedial/perifornical)Coordinates autonomic, endocrine and behavioural stress responses via HPA axisFunctional earlyExplains somatic manifestations of anxiety (tachycardia, sweating, GI symptoms)
Prefrontal cortex (VMPFC, dorsolateral PFC)Top-down inhibitory regulation of amygdala; cognitive appraisal of threatSlow maturation — not fully mature until mid-20sChildren have a "maturity gap": strong amygdala activation with weak prefrontal braking → difficulty regulating anxiety
Anterior cingulate cortex (ACC)Error monitoring, conflict detection, regulation of emotional responseGradual maturationDysfunction → difficulty extinguishing fear (relevant to PTSD, OCD)
InsulaInteroception (awareness of bodily states like heartbeat, gut feeling)Increasingly active through childhoodOveractive insula → amplification of somatic anxiety symptoms → somatic complaints
HippocampusContextual memory, distinguishing safe vs. dangerous contextsVulnerable to cortisol; volume may decrease with chronic stressCortisol-induced hippocampal atrophy → impaired context discrimination → generalised anxiety; also → ↓5HT neurotransmission [1]

StructureFunctionRelevance to Youth Depression
Ventral striatum / Nucleus accumbensReward processing (dopamine-mediated)Hypoactivity → anhedonia
Ventromedial PFCEmotional regulation, social cognition↑ activity → depressive ruminations, ↑ pain sensitivity, anxiety [1]
Dorsolateral PFCExecutive functions, working memoryHypoactivity → psychomotor retardation, apathy, concentration problems [1]
HippocampusMemory consolidation, cortisol feedbackReduced volume in depression (both predisposing and consequence) [1]
Subgenual cortex (Brodmann area 25)Mood regulation, sadnessVolume reduction and ↓ glial cells in depression [3]

SystemNuclei of OriginProjection TargetsRole in Child Psychiatry
Serotonin (5-HT)Raphe nuclei (brainstem)Cortex, limbic system, hypothalamusMood regulation, anxiety modulation, impulse control; dysregulated in anxiety and depression [1]
Noradrenaline (NA)Locus coeruleusCortex, amygdala, hippocampusArousal, vigilance, stress response; dysregulated in anxiety [1]
Dopamine (DA)VTA, substantia nigraPrefrontal cortex, striatumReward, motivation, executive function; relevant to ADHD, depression (anhedonia)

These monoamine-releasing neurones belong to the reticular activating system (RAS), which regulates global behavioural states — sleep-wake cycle, appetite, motor activity, emotional processing, learning and memory [1]. Deficiency in these neurotransmitters accounts for the broad clinical picture of depression (sleep disturbance, appetite changes, psychomotor changes, mood symptoms, cognitive impairment).

The hypothalamic-pituitary-adrenal (HPA) axis is the master stress response system:

  1. Hypothalamus releases CRH →
  2. Anterior pituitary releases ACTH →
  3. Adrenal cortex releases cortisol →
  4. Cortisol feeds back to hypothalamus and hippocampus (negative feedback)

In children exposed to chronic stress/adversity:

  • The HPA axis becomes dysregulated (blunted or exaggerated cortisol response).
  • Chronic cortisol elevation → hippocampal atrophy → impaired negative feedback → more cortisol → vicious cycle.
  • This is the neurobiological basis for why early life adversities (abuse, neglect, parental separation) are such powerful risk factors for both anxiety and depression [1][3].

4. Aetiology and Pathophysiology

Child psychiatric conditions follow a biopsychosocial model where genetics load the gun, environment pulls the trigger, and developmental stage determines the expression.

4.2 Anxiety Disorders of Childhood

  • Weak-to-moderate genetic contribution (heritability ~30-40%) [1]
  • Familial aggregation: 5× risk in first-degree relatives [2]
  • Candidate genes: those affecting serotonin and noradrenaline systems, including serotonin transporter gene (5-HTTLPR), COMT, TMEM132D [2]
  • Shared genetic risk with depression (the genetic boundary between anxiety and depression is blurry)

  • Dysregulated 5-HT/NA systems → explains why SSRIs and SNRIs work [1]
  • Overactive behavioural inhibition system (BIS) may underlie the physiology of anxiety [1]
    • The BIS (Gray's model) is a neural system that responds to novelty, punishment cues, and non-reward by increasing arousal, inhibiting behaviour, and directing attention to threat
    • Children with an overactive BIS are temperamentally inhibited — they freeze, withdraw, and become distressed in novel situations
    • This is the neurobiological basis for behavioural inhibition as a temperamental risk factor

Behavioural Inhibition System (BIS): Think of it as the brain's "alarm system" that says "stop, something might be dangerous." In anxious children, this alarm is set too sensitively — it goes off for minor threats that other children would ignore.

  • Behavioural inhibition (a temperamental trait characterised by withdrawal and distress in novel situations) is a well-established risk factor [1]
  • Present from early infancy, relatively stable over time
  • ~40% of behaviourally inhibited children go on to develop an anxiety disorder (vs ~15% of uninhibited children)

  • Anxious attachment: creates a bidirectional escalating effect — anxious mother transmits anxiety to child through modelling, and the child's anxiety reinforces the mother's anxiety → escalating anxiety in the mother-child dyad [1]
  • Overprotective parenting: prevents child from developing mastery over feared situations → maintains anxiety
  • Parental modelling: anxious parents model avoidant coping → child learns that the world is dangerous
  • Low care and overprotective parents are risk factors shared with bipolar and mood disorders [4]

  • Anxious children show attentional bias toward threat — they notice and attend to threatening stimuli more than non-anxious children
  • They also show interpretation bias — ambiguous situations are interpreted as threatening
  • These cognitive biases are the target of CBT in childhood anxiety

  • Stressful life events, particularly those involving loss, threat, and uncertainty, can precipitate anxiety disorders
  • Childhood adversities (neglect, physical/sexual abuse, parental separation) are strong risk factors [1][3][4]

4.3 Youth Depression

  • Similar genetic basis to adult depression (~37% heritability from twin studies) [1]
  • 5-HTTLPR variant (short allele of serotonin transporter gene) is associated with early onset depression in the presence of adversities [1]
    • This is the classic gene × environment interaction: the gene alone doesn't cause depression, but it increases vulnerability when combined with stressful life events

  • Cortisol-induced atrophic changes in hippocampus → ↓5-HT neurotransmission [1]
    • Why? The hippocampus is rich in glucocorticoid receptors. Chronic stress → chronic cortisol → hippocampal neuronal damage → reduced serotonergic tone → depression
  • HPA axis dysregulation — same mechanism as described above [3]
  • Structural brain changes: volume reduction and decreased quantity of glial cells in subgenual cortex, reduced hippocampal size [3]
  • Hormonal changes: dysregulation of HPA axis, lower estradiol (in women) and testosterone (in men), decreased T3 and TSH, diminished BDNF level [3]
    • BDNF (brain-derived neurotrophic factor) supports neuronal survival and growth; low levels → impaired neuroplasticity → vulnerability to depression
  • Monoamine hypothesis: deficiency in 5-HT, NA, and DA [1]

  • Negative cognitive style — tendency toward negative interpretations of self, world, and future (Beck's cognitive triad) [1]
  • Lack of social confidence, perfectionist traits [1]
  • Cognitive distortions prominent in depression (these are targeted in CBT) [3]:
    • Selective abstraction 斷章取義: focusing on a detail and ignoring more important features
    • Overgeneralisation 以偏概全: drawing a general conclusion from a single incident
    • Personalisation 過度自責: relating external events to oneself in an unwarranted way
    • Arbitrary inference 妄下判斷: drawing a conclusion when there is no evidence or even evidence against it

  • Personally salient adverse life events can precipitate onset of juvenile depression [1]
    • Events involving loss, entrapment, and humiliation (e.g., bullying, bereavement, breakup) are especially potent [1][3]
  • Early environment: parental separation, physical and sexual abuse, non-caring or overprotective parenting styles [3]
  • Lack of supportive networks, poorly functioning relationships, and poor social integration [3]
  • Personality: sociotropy (a strong need for approval), neuroticism [3]
    • Sociotropy → "socio" = social, "tropy" = turning toward; these individuals turn toward social approval as their source of self-worth, making them vulnerable to rejection
    • Neuroticism → a personality trait characterised by emotional instability, anxiety, and negative affect; it is a shared risk factor for both anxiety and depression [1]

The dramatic increase in depression prevalence after puberty (from < 1% to ~4%) [1] is explained by:

  • Hormonal changes: rising and fluctuating estrogen and progesterone alter serotonergic transmission
  • Brain reorganisation: prefrontal pruning and limbic remodelling during adolescence creates a transient period of vulnerability
  • Psychosocial stressors: academic pressure, peer relationships, identity formation, romantic relationships
  • Gene-environment interaction: genetic vulnerability (e.g., 5-HTTLPR) may only become manifest when combined with adolescent stressors

  • Definition: consistent failure to speak in specific social situations (e.g., school) where speaking is expected, despite speaking in other situations (e.g., home)
  • "Mutism" → "mutus" (Latin) = silent; "selective" = only in certain contexts
  • Not due to lack of language knowledge or comfort with the spoken language
  • Now classified under anxiety disorders in DSM-5 (previously under disorders of social functioning in ICD-10)

Pathophysiology:

  • Conceptualised as an extreme form of social anxiety — the child is so anxious about social evaluation that speech is completely inhibited
  • The amygdala-based fear response "shuts down" the speech production areas (Broca's area, supplementary motor area) in the presence of perceived social threat
  • Often associated with behavioural inhibition temperament
  • Genetics: family aggregation with social anxiety disorder
  • Environmental: may be exacerbated by bilingual environments, immigration, traumatic experiences

4.5 Attachment Disorders

These are disorders specifically arising from pathological caregiving environments.

  • Definition: a pattern of markedly disturbed and developmentally inappropriate attachment behaviours, characterised by emotionally withdrawn behaviour toward caregivers
  • "Reactive" = occurring as a reaction (to pathological care); "attachment" = the bond between child and caregiver
  • The child rarely seeks comfort when distressed and rarely responds to comfort when offered
  • Pathophysiology: the child has not experienced consistent, responsive caregiving → fails to develop a selective attachment → the "internal working model" of relationships (Bowlby's attachment theory) is one of unreliability and unavailability → the child gives up seeking comfort
  • Associated with neglect (insufficient stimulation and affection), frequent changes of primary caregiver (e.g., institutional care)
  • HPA axis dysregulation and altered oxytocin/vasopressin signalling

  • Definition: a pattern of indiscriminate sociability — the child approaches and interacts with unfamiliar adults without normal wariness
  • Pathophysiology: normal "stranger anxiety" (which develops ~8 months) depends on having formed a selective attachment. Without selective attachment, the child never develops the discrimination between "safe" (caregiver) and "potentially unsafe" (stranger) → indiscriminate friendliness
  • Same risk factors as RAD (neglect, institutional care, multiple caregiver changes)
  • Importantly, DSED can persist even after placement in a stable, nurturing environment — it is more "sticky" than RAD

In DSM-5, attachment disorders were split into RAD (inhibited type) and DSED (disinhibited type). In ICD-10, these are "reactive attachment disorder of childhood" (F94.1) and "disinhibited attachment disorder of childhood" (F94.2).

  • Definition (ICD-10 F93.3): Abnormally intense negative feelings (jealousy, hostility, aggression) toward a sibling, arising after the birth of a younger sibling, that are persistent and clearly out of the norm [1]
  • Usually manifests as regression (bed-wetting, baby-talk), temper tantrums, aggression toward the new sibling, and attention-seeking behaviour
  • Pathophysiology: Loss of exclusive parental attention is perceived as a threat to the child's attachment security → anxiety and anger → externalised as rivalry behaviours
  • The severity depends on: child's age, temperament, quality of prior attachment, parental handling of the transition

  • PTSD can occur in children and resembles the adult counterpart [1], but with important developmental modifications
  • Children may not articulate re-experiencing symptoms verbally — instead they show:
    • Repetitive play with trauma themes (the child "acts out" the trauma)
    • Trauma-specific nightmares (which may become generalised frightening dreams)
    • Regression (loss of previously acquired skills, e.g., toilet training)
    • Behavioural re-enactment (acting out the trauma in daily behaviour)

Pathophysiology (shared with adults):

  • Traumatic event → overwhelming of normal stress response → failure of fear extinction [5]
  • Amygdala hyperactivation + hippocampal suppression → emotional memory is "burned in" without proper contextualisation → re-experiencing
  • HPA axis dysregulation → chronic hyperarousal
  • Prefrontal hypoactivity → failure of top-down emotional regulation → inability to suppress fear response

5. Classification

ICD-10DSM-5 EquivalentNotes
F93 — Emotional disorders with onset specific to childhoodClassified under Anxiety Disorders (not age-specific)DSM-5 removed the childhood-specific category; anxiety is anxiety regardless of age
F93.0 Separation anxiety disorder of childhoodSeparation anxiety disorder (can be diagnosed at any age)DSM-5 allows diagnosis in adults too
F93.1 Phobic anxiety disorder of childhoodSpecific phobia
F93.2 Social anxiety disorder of childhoodSocial anxiety disorder (social phobia)
F93.3 Sibling rivalry disorderNo DSM-5 equivalentUnique to ICD-10
F93.8 Other childhood emotional disorders—Includes identity disorder, overanxious disorder
F94 — Disorders of social functioning with onset specific to childhood
F94.0 Selective mutismSelective mutism (under Anxiety Disorders)
F94.1 Reactive attachment disorderReactive attachment disorder (under Trauma-related Disorders)
F94.2 Disinhibited attachment disorderDisinhibited social engagement disorder (under Trauma-related Disorders)

This is a critical concept — the neural substrate of anxiety is the same across ages, but the content changes with developmental stage [1]:

Developmental StageTypical Fear ContentCorresponding Disorder
Infants (0-2 years)Fear of strangers→ Social anxiety disorder of childhood
Preschool (3-5 years)Fear of separation, specific objects (animals, dark)→ Separation anxiety disorder, Phobic anxiety disorder
School age (6-12 years)Fear of school performance, injury, natural disasters→ GAD features, specific phobias
Early adolescence (12-15 years)Fear of social situations / personal adequacy→ Social phobia
Late adolescence (16-18 years)Resembles adult pattern→ GAD, panic disorder

Why does anxiety content change with age?

Because the cognitive content of anxiety depends on what the child's brain is capable of processing. An infant cannot worry about exam performance because they don't have the concept of "exams." A toddler cannot have panic about bodily sensations because they lack the interoceptive awareness and catastrophic misinterpretation that adults have. As cognitive development progresses, the themes of anxiety become more abstract and future-oriented — but the underlying amygdala-based fear response is the same.

ClassificationKey Points
ICD-10Same diagnostic criteria as adult depression (F32-F33); no separate childhood category
DSM-5Same criteria as adult MDD, BUT allows irritable mood to substitute for depressed mood in children/adolescents

Key Exam Point

In adults, the core mood symptom of depression is "depressed mood." In children and adolescents, irritability can replace depressed mood as the core symptom (DSM-5). This is why many depressed children are initially misdiagnosed as having ODD or ADHD — their irritability and behavioural problems mask the underlying depression.


6. Clinical Features — Symptoms and Signs

6.1 Anxiety Disorders of Childhood

Symptoms (subjective — what the child/parent reports):

SymptomPathophysiological Basis
Excessive worry (content varies with developmental stage)Amygdala hyperactivation with insufficient prefrontal regulation → persistent threat appraisal
Somatic complaints (headaches, abdominal pain, nausea, chest tightness)Hypothalamic-mediated autonomic activation (sympathetic → GI slowing, muscular tension; vagal → nausea); also overactive insular cortex amplifying interoceptive signals
Sleep disturbance (difficulty falling asleep, nightmares)Hyperarousal state maintained by noradrenergic system (locus coeruleus) prevents transition to sleep
IrritabilityChronic amygdala activation → reduced frustration tolerance; also reflects the child's limited emotional vocabulary — they can't say "I'm anxious" so they express it as anger
Difficulty concentratingAnxiety commandeers attentional resources → reduced availability for academic tasks
School refusalAvoidance behaviour — the school environment is associated with threat (separation, social evaluation, performance) → conditioned avoidance

Signs (objective — what you observe):

SignPathophysiological Basis
Clinginess to caregiversActivation of attachment system by perceived threat → proximity-seeking behaviour (Bowlby)
Tearfulness / distress on separationAmygdala-driven fear response when attachment figure (safety signal) is removed
Psychomotor agitation (fidgeting, restlessness)Sympathetic activation → motor tension
Autonomic signs (tachycardia, sweating, tremor)Direct sympathetic nervous system activation via hypothalamic-sympathetic pathway
Avoidance behaviours (refusal to enter feared situations)Conditioned avoidance — anxiety is negatively reinforced by escape/avoidance (operant conditioning)
Difficulties with peer relationships [1]Social withdrawal due to anxiety → reduced social practice → poor social skills → further withdrawal (vicious cycle)
Low self-esteem [1]Chronic anxiety → perceived inability to cope → negative self-evaluation

Atypical Presentations of Childhood Anxiety

Remember that childhood anxiety may present atypically [1]:

  • School refusal (not to be confused with truancy — the anxious child wants to go to school but can't)
  • Frequent somatic complaints (headache, tummy ache → often presents to paediatrics, not psychiatry)
  • Difficulties with peer relationships
  • Low self-esteem
  • Irritability and temper tantrums (the child cannot articulate their anxiety)

The key clinical skill is to ask about these presentations and think anxiety when a child has unexplained somatic symptoms or school refusal.

FeatureExplanation
Excessive fear/anxiety about separation from attachment figures [1]Overactive attachment/fear system → normal separation protest is amplified and prolonged beyond developmental appropriateness
Anxiety may present with psychosomatic complaints (abdominal pain, headache, nausea, vomiting — especially on school mornings) [1]Autonomic activation mediated by hypothalamus → real physical symptoms that the child genuinely experiences
Nightmares about separationThreat-related memories processed during sleep → manifest as separation-themed dreams
Refusal to go to schoolSchool = separation from caregiver; avoidance behaviour reduces anxiety (negative reinforcement)
Refusal to sleep aloneDarkness + separation = compounded threat → need for proximity to attachment figure
Persistent worry about harm befalling attachment figuresCatastrophic cognitions (developmental analogue of "worry" in GAD)
Physical complaints (headaches, stomach aches) when separation is anticipatedAnticipatory anxiety activates the same fear circuits as actual separation

Normal vs. pathological: Separation anxiety is normal in infants (peaks 10-18 months). It becomes a disorder when:

  • It persists beyond the expected developmental period (≥ 4 weeks in children, ≥ 6 months in adults per DSM-5)
  • Severity is out of proportion to the developmental stage
  • Causes significant distress AND functional impairment

FeatureExplanation
Intense fear of social situations/scrutinyAmygdala hyperreactivity to social-evaluative cues → excessive threat perception in social contexts
Fear of embarrassment or humiliationPrefrontal areas involved in self-monitoring are overactive → hyper-awareness of potential negative evaluation
Avoidance of social situationsConditioned avoidance
In children: may manifest as crying, freezing, tantrums, clinging, or failing to speakYounger children lack the capacity for avoidance planning → more primitive fear responses (freeze, cry)
Selective mutism (in severe cases)The anxiety is so intense that it completely inhibits speech output → Broca's area "shut down" by amygdala-mediated fear

  • Primarily seen in late adolescence [1]
  • Features: excessive, uncontrollable worry about multiple domains (school, health, family, future), muscle tension, restlessness, fatigue, irritability, poor concentration, sleep disturbance
  • Pathophysiology: tonic (persistent) overactivity of the amygdala-prefrontal circuit, with failure of prefrontal regulatory mechanisms → "the worry switch can't be turned off"

  • Rare before puberty, primarily seen in late adolescence [1]
  • Features: recurrent unexpected panic attacks (sudden surge of intense fear with physical symptoms: palpitations, chest pain, dyspnoea, dizziness, paraesthesias, derealization)
  • Panic response is mediated by amygdala → hypothalamus (dorsomedial hypothalamus/perifornical region coordinates rapid mobilisation of behavioural, autonomic, respiratory and endocrinologic responses to stress) [2]
  • Other structures involved: insula, dorsal ACC, VMPFC [2]
  • Neurotransmitters: 5-HT, NA, GABA are suggested to be related to panic response [2]
  • Neurobiological changes in panic disorder: ↓cortical 5HT1A binding, ↓cortical GABA levels [2]

6.2 Youth Depression

Symptom/SignPathophysiological Basis
Depressed mood (or irritable mood in children/adolescents)↓5-HT transmission → emotional dysregulation; ↑VMPFC activity → depressive ruminations [1]
Anhedonia (loss of interest/pleasure)↓Dopamine in mesolimbic reward pathway (VTA → nucleus accumbens)
Fatigue / loss of energyMonoamine deficiency in RAS → ↓arousal; HPA axis dysfunction → cortisol-related fatigue
Sleep disturbance (insomnia or hypersomnia)Dysregulated monoamine-RAS pathway → disrupted sleep-wake cycle; circadian rhythm disruption is common in adolescents
Appetite/weight changesHypothalamic dysregulation (5-HT and NA are involved in appetite regulation)
Poor concentration↓Dorsolateral PFC activity → executive dysfunction [1]
Psychomotor retardation/agitationRetardation: ↓DA in frontal-subcortical circuits; Agitation: sympathetic overactivation
Guilt / worthlessnessNegative cognitive schema (Beck's cognitive triad)
Suicidal ideationSevere depression + impulsivity (immature PFC) + hopelessness

In younger children, the clinical picture differs because of developmental immaturity:

FeatureWhy It Differs in Children
Somatic complaints (unexplained abdominal pain, headache, anorexia, enuresis) [1]Children lack the metacognitive vocabulary for "I feel sad" → distress is expressed somatically through autonomic pathways
Irritable mood (rather than sadness) [1]Developing prefrontal cortex cannot modulate negative affect into "sadness" → instead manifests as low frustration tolerance/irritability
Anxiety features [1]High comorbidity (70% have anxiety disorder) [1]; shared neurobiological vulnerability (5-HT, HPA axis)
Behavioural problems [1]Depression → frustration, anger → externalising behaviours; examples from notes: "one case tried to steal a bus because of frustration at home, take cannabis to lift mood due to depression" [1]
School refusalAnhedonia + fatigue + low self-esteem → avoidance of school demands
Regression (bedwetting, baby talk)Stress-induced regression to earlier developmental stage

  • 70% have comorbid anxiety disorder [1]
  • Conduct disorder (CD)
  • Substance abuse (SA)
  • Dysthymia (persistent depressive disorder)

Critical Point: Bipolar Masked as Depression

~25% of bipolar affective disorder (BAD) first presents as a juvenile depressive episode [1]. This means that when you see an adolescent with depression, you should ALWAYS screen for:

  • Family history of bipolar disorder
  • History of any hypomanic/manic symptoms
  • Rapid cycling or seasonal pattern
  • Psychotic features (more suggestive of bipolar)
  • Marked atypical features (hypersomnia, hyperphagia, leaden paralysis)

This is critical because treating bipolar depression with antidepressants alone (without a mood stabiliser) can trigger mania.

FeaturePathophysiological Basis
Consistent failure to speak in specific social situations (e.g., school) despite speaking normally at homeAmygdala-mediated social anxiety → speech production areas are inhibited in perceived threatening social contexts
Normal language development (speaks fluently at home)This is NOT a language disorder — the speech apparatus and language centres are intact
May communicate with gestures, nodding, or writingThe child finds alternative channels to bypass the speech "block"
Onset typically before age 5Coincides with entry into kindergarten/school (first major social context outside family)
Duration > 1 month (not limited to the first month of school)DSM-5 criterion to distinguish from normal adjustment
Social withdrawal, clinginessAssociated anxiety behaviours

6.4 Attachment Disorders

FeaturePathophysiological Basis
Emotionally withdrawn behaviour toward caregiversAbsent or inconsistent caregiving → child learns that seeking comfort is futile → attachment system "shuts down"
Minimal seeking of comfort when distressedNo "safe base" was established → child does not expect comfort to be available
Minimal response to comfort offeredThe child has not learned that caregiver contact reduces distress
Reduced positive affectChronic deprivation → blunted reward/attachment circuitry (oxytocin, vasopressin pathways)
Episodes of unexplained irritability or sadnessEmotional dysregulation without the soothing function of secure attachment

FeaturePathophysiological Basis
Indiscriminate social approach to unfamiliar adultsFailure to develop selective attachment → no "stranger anxiety" → everyone is treated as equivalent
No checking back with caregiver in unfamiliar settingsNo "safe base" → no need to reference caregiver for safety cues
Willingness to leave with unfamiliar adultsAbsent stranger wariness → potential safety risk
Overly familiar verbal/physical behaviour with strangersSocial approach system is activated without the normal inhibition from the attachment-mediated "discrimination" system

FeatureDevelopmental ModificationPathophysiological Basis
Re-experiencingIn young children: repetitive play with trauma themes, trauma-specific nightmares (may become generalised)Amygdala-encoded fear memory intrudes into consciousness; play = attempt to master the traumatic experience
AvoidanceMay be less obvious; shown as avoidance of trauma-related activities, places, or peopleConditioned avoidance — same as adults
Negative cognitions/moodMay manifest as regression, loss of developmental skills, withdrawn behaviourHippocampal suppression → poor contextualisation of trauma; prefrontal hypoactivity → emotional dysregulation
HyperarousalSleep disturbance, exaggerated startle, irritability/temper tantrums, concentration difficultiesChronic noradrenergic hyperactivation (locus coeruleus) → persistent "fight-or-flight" state

PTSD can occur in children and resembles the adult counterpart [1], but the developmental modifications listed above are critical for diagnosis.

Stress-Related Disorders in Children — From the Lecture

The lecture on stress-related disorders [5] emphasises that:

  • PTSD requires exposure to actual or threatened death, serious injury, or sexual violence
  • Children < 6 years have a separate set of criteria in DSM-5 (more behaviourally based, fewer symptoms required)
  • Acute stress disorder (3 days to 1 month) and adjustment disorder (within 3 months of stressor, < 6 months after stressor ends) are important differentials
  • Risk factors include: pre-existing psychiatric illness, poor social support, severity and duration of trauma, peritraumatic dissociation

FeaturePathophysiological Basis
Extreme jealousy toward sibling (persistent, clearly out of norm) [1]Perceived loss of exclusive parental attention → threat to attachment security → anger and fear
Regression (baby-like behaviour: bed-wetting, thumb-sucking, baby talk)Unconscious attempt to recapture the parental attention given to the "baby"
Aggression toward the sibling (hitting, biting, deliberate harm)Anger at the perceived "rival" for parental affection
Attention-seeking behaviour (temper tantrums, acting out)Direct bid for parental attention
Sleep disturbance, appetite changesAnxiety and distress → autonomic and behavioural disruption

Anxiety and fears CAN be developmentally appropriate [1]. A disorder is only diagnosed when:

  1. Symptoms are developmentally inappropriate (more severe and prolonged than usual)
  2. They cause significant distress
  3. They cause functional impairment (academic, social, family functioning)

Differential Diagnosis Considerations (to be expanded in next section)

  • Organic causes must always be considered: hyperthyroidism, arrhythmias, neurological disease, substance-induced anxiety (alcohol, illicit drugs, caffeine) [1]
  • For depression: thyroid dysfunction, Addison's disease, anaemia, medication-related (corticosteroids), substance use
  • Normal developmental fears vs. pathological anxiety
  • Other psychiatric disorders (ADHD, ODD, CD — all can present with irritability and concentration difficulties)

High Yield Summary

Anxiety Disorders in Children:

  • Commonest psychiatric disorder of childhood
  • Content of anxiety varies by developmental stage: strangers (infancy) → separation/specific objects (preschool) → social evaluation (early adolescence) → resembles adult (late adolescence)
  • Aetiology: dysregulated 5-HT/NA + overactive BIS + behavioural inhibition temperament + anxious attachment + cognitive biases
  • Atypical presentations: school refusal, somatic complaints, peer difficulties, low self-esteem, irritability
  • Diagnosis: only when developmentally inappropriate + distress + functional impairment
  • Management: CBT (1st line) > SSRIs (severe cases)
  • Prognosis: ~2/3 resolve in 3-5 years but ~1/3 develop other anxiety disorders

Youth Depression:

  • Rare pre-puberty (< 1%), rises dramatically post-puberty (~4%)
  • Adolescent depression ≈ adult depression
  • Childhood depression is more: somatic complaints, irritable mood, behavioural problems, anxiety
  • 70% have comorbid anxiety; ~25% of BAD first presents as juvenile depression
  • Aetiology: 5-HTTLPR × adversity, cortisol → hippocampal atrophy → ↓5-HT, cognitive distortions
  • Management: antidepressants (SSRIs) for moderate-severe + CBT; beware suicidal risk with SSRIs
  • Prognosis: episodic relapsing; majority recover < 3 months but 15% last > 18 months

Selective Mutism: Extreme social anxiety → speech inhibition in specific social contexts; normal speech at home

Attachment Disorders: RAD (inhibited — emotionally withdrawn) vs DSED (disinhibited — indiscriminate sociability); arise from pathological caregiving (neglect, institutional care)

PTSD in Children: Resembles adult PTSD but with repetitive play, trauma-specific nightmares, regression, behavioural re-enactment

Sibling Rivalry Disorder: Persistent, abnormally intense jealousy/hostility toward sibling after birth of new sibling; ICD-10 specific


Active Recall - Other Psychiatric Conditions in Child Psychiatry

[1] Senior notes: ryanho-psych.md (Section 12.5 Other Psychiatric Conditions in Child Psychiatry, Section 12.1.2 Overview of Psychiatric Disorders in Child/Adolescents) [2] Senior notes: ryanho-psych.md (Section on Panic Disorder Aetiology) [3] Lecture slides: GC 164. I am depressed Mood disorders.pdf (p12-13) [4] Lecture slides: GC 163. I am a superman Bipolar disorder.pdf (p28) [5] Lecture slides: GC 171. Stress-related disorders and obsessive-compulsive disorder.pdf

Differential Diagnosis of Other Psychiatric Conditions in Child Psychiatry

The differential diagnosis of psychiatric conditions in children is harder than in adults for one core reason: developmental immaturity changes how symptoms present. A depressed child may look like an ODD child (irritability). An anxious child may look like an ADHD child (poor concentration, restlessness). A child with ADHD may look manic (hyperactivity, talkativeness, impulsivity). The art is in recognising which circuit is driving the behaviour, and that requires careful history, developmental context, and pattern recognition.

This section systematically addresses the differential diagnosis of each major "other" child psychiatric condition, followed by a unifying algorithmic approach.


1. Differential Diagnosis of Childhood Anxiety Disorders

The senior notes explicitly state: D/dx: consider organic causes, e.g. hyperthyroidism, arrhythmias, neurological disease, substance-induced anxiety (alcohol, illicit drugs, caffeine) [1].

The lecture slides reinforce the same principle for adults that applies equally to children: DDx for anxiety symptoms — Physical disorder, substance abuse etc and DDx for avoidance features — Personality disorder, psychosis, depression [6].

These must always be considered first because anxiety symptoms (tachycardia, tremor, sweating, restlessness, poor concentration) are non-specific — they can be produced by any condition that activates the sympathetic nervous system or mimics its effects.

Organic CauseWhy It Mimics AnxietyHow to Distinguish
Hyperthyroidism ("hyper" = excessive; "thyroid" = thyroid gland)Excess T3/T4 → ↑metabolic rate → tachycardia, tremor, heat intolerance, restlessness, weight loss, irritability — these overlap substantially with anxiety symptomsTFTs (↑free T4, ↓TSH); look for goitre, exophthalmos, warm moist skin; symptoms are persistent and not situational
Cardiac arrhythmias (SVT, WPW)Paroxysmal tachycardia → palpitations, chest tightness, dizziness, shortness of breath → misinterpreted as panic attacksECG, Holter monitor; episodes are truly paroxysmal with sudden onset/offset; no cognitive anxiety component between episodes; no avoidance behaviour
Epilepsy (temporal lobe epilepsy particularly) [7]Auras can produce intense fear, déjà vu, depersonalisation, autonomic symptoms → mimics panicEEG; stereotyped episodes; may have post-ictal confusion; temporal relationship to seizure activity
Phaeochromocytoma [7]Episodic catecholamine release → paroxysmal hypertension, tachycardia, sweating, pallor, headache → mimics episodic panic24h urinary catecholamines/metanephrines; paroxysmal hypertension is the key clue; no situational trigger
Hypoglycaemia↓Blood glucose → sympathetic activation → tremor, sweating, palpitations, anxiety, irritabilityBlood glucose during episode; symptoms resolve with glucose administration; temporal relationship to fasting/meals
Vestibular dysfunction [7]Dizziness and unsteadiness → may trigger secondary anxiety and avoidance (especially in panic disorder)Vestibular testing; true vertigo (room spinning) rather than light-headedness; nystagmus on examination
Neurological disease (brain tumour, demyelination) [1]Depending on location, can cause anxiety, personality change, irritabilityNeuroimaging; focal neurological signs; progressive course
Asthma / respiratory diseaseDyspnoea → air hunger → panic-like symptomsWheezing on auscultation; peak flow variability; response to bronchodilators

First-principles reasoning: The sympathetic nervous system activation that underlies anxiety symptoms is a final common pathway. Any condition that increases sympathetic tone — whether endogenous (thyrotoxicosis, phaeo) or exogenous (stimulants, caffeine) — will produce the same autonomic symptoms. You cannot diagnose a psychiatric anxiety disorder until you have excluded these organic mimics.

SubstanceMechanism
Caffeine (very common in adolescents via energy drinks, coffee)Adenosine receptor antagonism → ↑arousal, ↑sympathetic activation
Stimulants (amphetamines, cocaine, methylphenidate if misused)↑DA and NA release → sympathetic activation → anxiety, agitation, paranoia
CannabisAt high doses or in predisposed individuals → acute anxiety/panic; chronic use → withdrawal anxiety
Alcohol withdrawalLoss of GABA-ergic inhibition → CNS hyperexcitability → anxiety, tremor, seizures
Intoxication: alcohol, stimulants (amphetamines, cocaine, caffeine), cannabis, inhalants, hallucinogens [2]
Withdrawal: alcohol, sedatives/hypnotics (BZDs, opiates), caffeine, cocaine, nicotine [2]
Side effects of medications: antidepressants (esp first 2 weeks), corticosteroids, sympathomimetics, T4, anticholinergics, antipsychotics (akathisia) [2]

Caffeine in Children — An Overlooked Culprit

In Hong Kong, energy drink consumption among adolescents is increasing. A single can of a popular energy drink contains ~80-160 mg of caffeine — equivalent to 1-2 strong coffees. Caffeine has a half-life of ~5 hours and can cause jitteriness, insomnia, tachycardia, and anxiety indistinguishable from an anxiety disorder. Always ask about caffeine intake in an anxious adolescent.

DifferentialWhy It Mimics AnxietyHow to Distinguish
ADHDRestlessness, poor concentration, distractibility overlap with GAD [3]ADHD: distractibility is by external stimuli, new activities, enjoyable preoccupations (not by worry). Symptoms are pervasive and trait-like (present since early childhood). No excessive worry. ↑Motor activity is present in ADHD but not typical of anxiety [3][4]
ODD / Conduct disorderIrritability overlaps with anxiety [3]ODD: irritability is characterised by negativity, hostility, defiance — directed at authority figures. Anxiety: irritability arises from chronic fear/tension and is more generalised. ODD children resist demands due to opposition; anxious children resist due to fear [4]
DepressionPoor concentration, irritability, sleep disturbance overlap with anxiety [3]Depression: usually later onset, episodic course, prominent anhedonia, ↓energy. Concentration difficulty is due to rumination/psychomotor retardation rather than hypervigilance. However, note 70% comorbidity — both can co-exist [1]
Mania / hypomaniaPoor concentration, ↑motor activity, distractibility, irritability overlap [3]Mania: episodic (not chronic), a/w ↑self-esteem, grandiosity, ↓need for sleep (different from insomnia — the child genuinely feels rested with less sleep), flight of ideas, elated or expansive mood [5]
Psychotic disorders (schizophrenia)Anxiety can be secondary to persecutory delusions or command hallucinationsFocus of anxiety is delusional content (e.g., "people are watching me"); presence of formal thought disorder, negative symptoms; bizarre/disorganised behaviour; poor reality testing
OCDAnxiety is triggered by obsessional thoughts → compulsive behaviours → may look like anxious avoidanceOCD: anxiety is linked to specific intrusive thoughts (contamination, harm, symmetry) with compulsive rituals to neutralise them. The content is often odd, irrational, or magical rather than realistic worries [8]
PTSDGeneral anxiety, hyperarousal, avoidance overlap with anxiety disordersPTSD: linked to specific traumatic event; presence of re-experiencing (flashbacks, nightmares with trauma content); avoidance is of trauma-related stimuli specifically [9]
Separation anxiety vs. School phobia vs. TruancyAll present as "not going to school"Separation anxiety: the child is anxious about separation from caregiver (not about school itself); school refusal resolves if parent stays. School phobia (social anxiety): child fears the school environment (peers, performance). Truancy: child is not anxious — they choose not to attend, often engaging in pleasurable activities instead (conduct problem)
Personality disorder [6]Avoidant PD (fear of rejection), dependent PD (fear of abandonment) can mimic anxiety disordersPD: enduring, pervasive pattern across situations from adolescence; more rigid/inflexible; distress arises from interpersonal patterns rather than situational triggers
Adjustment disorderAnxiety symptoms following a stressorStressor is identifiable but non-traumatic; symptoms develop within 3 months of stressor; does not meet full criteria for a specific anxiety disorder; resolves within 6 months after stressor ends [9][10]
Normal developmental fearsMany fears are age-appropriate (stranger anxiety, separation protest, fear of dark)Key distinction: severity and duration are proportionate to developmental stage; no functional impairment; the child can be reassured and the fear does not dominate daily life [1]

Overlap Table — A High-Yield Exam Resource

The senior notes provide this invaluable overlap table [3]. Memorise it — it shows exactly which symptoms are shared across common child psychiatric differentials:

FeatureADHDODD/CDGADDepressionMania
Restlessness✓✓
Poor concentration✓✓✓✓
↑Motor activity✓✓
Distractibility✓✓✓
Irritability✓✓✓✓

Notice: irritability is the one feature shared by ODD, GAD, depression, AND mania — but NOT by uncomplicated ADHD. If a child has irritability + poor concentration, think anxiety/depression/mania before ADHD.

Within the anxiety disorder family, the differentials are important because management differs:

ConditionFocus of AnxietyTriggerAge Pattern
Separation anxiety disorderHarm befalling attachment figures; being separatedSeparation from caregiverPeak 7-9y
Specific phobiaSpecific object or situation (animals, heights, blood)Exposure to phobic stimulusEarly childhood
Social anxiety disorderSocial evaluation, embarrassment, humiliationSocial/performance situationsEarly adolescence
GADMultiple domains (school, health, family, future)Not situation-specific; "free-floating"Late adolescence
Panic disorderRecurrent unexpected panic attacks + fear of next attackInitially unexpected; later situational avoidance may developLate adolescence (rare before puberty)
Selective mutismSpeaking in specific social situationsSpecific social contexts (school)Before age 5

Key principle from the lecture: Panic attacks tend to be expected in other anxiety disorders (e.g., triggered by social situations in social phobia, by separation in separation anxiety disorder) [7]. Only in panic disorder are there recurrent unexpected (uncued) panic attacks with persistent worry about further attacks.


2. Differential Diagnosis of Youth Depression

Organic CauseMechanismHow to Distinguish
Hypothyroidism↓T3/T4 → ↓metabolic rate → fatigue, weight gain, cold intolerance, constipation, psychomotor slowing, depressed moodTFTs; physical signs (dry skin, bradycardia, delayed relaxation of reflexes); onset usually gradual
Anaemia (iron deficiency, common in adolescent girls)↓O₂ delivery → fatigue, poor concentration, irritabilityFBC, ferritin; pallor, tachycardia; responds to iron replacement
Addison's disease (adrenal insufficiency)↓Cortisol → fatigue, weight loss, low mood, hypotensionSynacthen test; look for hyperpigmentation, postural hypotension, hyperkalaemia
Infectious mononucleosis (EBV)Post-viral fatigue → prolonged lethargy, poor concentration → mimics depressionMonospot/EBV serology; sore throat, lymphadenopathy, hepatosplenomegaly
Substance useCNS depressants (alcohol, cannabis) → low mood, anhedonia, poor motivation; stimulant withdrawal → crashDrug history, urine toxicology; temporal relationship to substance use
Medications (corticosteroids, isotretinoin, OCP)Various mechanisms affecting monoamine pathwaysTemporal relationship to medication initiation
Chronic medical illness (diabetes, epilepsy, IBD)Acts as non-specific stressor; some have direct neurobiological effectsKnown medical history; treat the primary condition
Brain tumour, neurological conditionsDepending on location (frontal lobe, hypothalamus) → apathy, personality change, mood symptomsNeuroimaging; focal neurological signs; progressive course

DifferentialWhy It Mimics DepressionHow to Distinguish
Normal sadness / bereavementSadness is a normal emotion, especially after lossNormal sadness: self-limited, fluctuating ("waves of grief"), self-esteem preserved, no pervasive anhedonia, functional recovery within expected timeframe
Adjustment disorder with depressed moodDepressive symptoms following identifiable stressorDevelops within 3 months of stressor; does not meet full criteria for MDE; resolves within 6 months after stressor ends [10]
Anxiety disorderOverlapping symptoms (insomnia, poor concentration, irritability, somatic complaints)Anxiety: core feature is excessive worry/fear; concentration difficulty due to worry (not anhedonia/psychomotor retardation). However, 70% comorbidity — both can co-exist [1]
ADHDPoor concentration, restlessness, irritabilityADHD: onset early (before 6-12 years), pervasive and persistent (trait-like, not episodic), ↑motor activity; no sustained depressed mood or anhedonia [3][4]
ODD / Conduct disorderIrritability, behavioural problemsODD/CD: hostile, defiant, deliberately annoying; irritability is directed at authority figures specifically; no pervasive sadness or anhedonia; onset and course differs
Bipolar affective disorder (BAD)~25% of BAD first presents as juvenile depression [1]Screen for: FHx of bipolar, any hypomanic/manic symptoms (↑energy, ↓need for sleep, grandiosity, pressured speech), psychotic features, atypical features (hypersomnia, hyperphagia, leaden paralysis). Discerning features: psychotic features, atypical features (e.g. hypersomnia, hyperphagia, leaden paralysis) [5]
Schizophrenia (prodromal)Negative symptoms (apathy, social withdrawal, flat affect) can resemble depressionLook for positive symptoms (hallucinations, delusions), formal thought disorder; negative symptoms tend to be more pervasive and lack the subjective distress of depression
Substance use disorderCannabis, alcohol → low mood, anhedonia, poor motivationTemporal relationship to substance use; urine toxicology; symptoms improve with abstinence
Chronic fatigue syndromeProfound fatigue, poor concentration, unrefreshing sleepFatigue is the dominant symptom; typically post-infectious onset; absence of pervasive low mood/anhedonia (though these can develop secondarily)
Eating disorderWeight loss, poor concentration, low mood, social withdrawalCore psychopathology is fear of weight gain/body image distortion; food restriction is deliberate; low mood often secondary to malnutrition

The Bipolar Trap

~25% of BAD first presents as juvenile depression [1]. This is one of the most important facts in child psychiatry exams. If you diagnose depression and start an SSRI without screening for bipolar, you risk triggering mania. Always ask:

  1. Has there ever been a period of unusually high energy, reduced need for sleep, or grandiosity?
  2. Is there a family history of bipolar disorder?
  3. Are there psychotic features (more common in bipolar depression than unipolar)?
  4. Are there atypical features (hypersomnia, hyperphagia)?

Misdiagnosis is very common → correct diagnosis and treatment is often delayed by 5-7 years on average [5].


DifferentialHow to Distinguish
Normal shyness / adjustment to new environmentDSM-5 specifies that symptoms must last > 1 month and not be limited to the first month of school. Normal shyness does not prevent all speech in social settings
Speech/language disorderIn selective mutism, the child speaks fluently at home — language competence is intact. In language disorder, the difficulty is present across all settings
Hearing impairmentHearing test is normal; the child responds to sounds and can speak at home
ASDASD: poor social reciprocity, restricted interests, and communication difficulties are present across all settings, not just specific social contexts. The child with ASD doesn't speak because of social communication impairment, not because of anxiety
Intellectual disabilityGlobal developmental delay including language; speech difficulties present across all settings
Traumatic mutismSudden onset of mutism after a traumatic event, affecting all settings (not selective). Rare
Social anxiety disorder without mutismSocial anxiety may cause significant distress in social situations but the child still manages to speak (even if quietly or briefly)

DifferentialHow to Distinguish
ASDASD: social communication difficulties are due to neurodevelopmental impairment (poor theory of mind, restricted interests, stereotypies), not due to pathological caregiving. ASD does not require a history of neglect. Restricted/repetitive behaviours are not a feature of attachment disorders
ADHDDSED children may appear impulsive and socially indiscriminate, but ADHD impulsivity is about motor/cognitive disinhibition, not about attachment indiscrimination. ADHD children still show selective attachment to caregivers
Intellectual disabilityChildren with ID may have poor social judgment but typically form selective attachments; developmental level explains social difficulties
Normal variation in temperamentSome children are naturally more sociable/outgoing — but they still show selective attachment, check back with caregivers, and show appropriate wariness with strangers
DepressionRAD can resemble depression (withdrawn, flat affect, reduced positive emotion), but RAD specifically involves attachment-related disturbance in the context of pathological caregiving, not a mood episode

D/dx of PTSD [9]:

DifferentialHow to Distinguish
Adjustment disorderStressor can be of any severity or type, but either the stressor is non-traumatic or the symptomatology does not meet criteria for PTSD [9]. Adjustment disorder is the diagnosis when symptoms follow a stressor that does not meet Criterion A (actual/threatened death, serious injury, sexual violence)
Acute stress disorderLasts for 3 days to 1 month following exposure to traumatic event [9]. Same symptom cluster but shorter duration. If symptoms persist > 1 month, reclassify as PTSD
OCDRecurrent intrusive thoughts are present, but they are unrelated to traumatic event [9]. OCD intrusions have themes of contamination, harm, symmetry — not trauma re-experiencing
Other anxiety disordersAnxiety symptoms (worries, avoidance, arousal) are not related to traumatic events [9]. The key is whether the symptoms are thematically linked to a specific trauma
Traumatic brain injury (TBI)TBI-related neurocognitive symptoms may mimic PTSD symptoms (e.g. irritability, startle response, poor concentration), but usually there are no re-experiencing and avoidance symptoms but may have persistent disorientation and confusion [9]
DepressionCan co-exist. Depression: pervasive anhedonia and low mood without the specific re-experiencing/avoidance cluster. But note that PTSD Criterion D (negative cognitions/mood) overlaps with depression
Normal stress responseTransient distress after trauma is normal. PTSD is only diagnosed when symptoms persist > 1 month and cause functional impairment
Dissociative disordersDissociative symptoms can occur in PTSD (the "dissociative subtype") but if dissociation is the dominant feature without re-experiencing, consider a dissociative disorder
Behavioural disorder (ODD/CD)In children, PTSD hyperarousal may manifest as irritability and aggression → misdiagnosed as ODD/CD. Key: look for the trauma history and the re-experiencing symptoms

This is included because ~25% of BAD first presents as juvenile depression [1], and manic episodes in adolescents need careful differentiation.

Differential diagnosis of manic episode [5]:

  • Depressive disorder with irritability and anxious distress
  • Psychotic disorder or schizoaffective disorder
  • Substance/medication-induced/medical conditions
  • Attention deficit and hyperactivity disorder
  • Personality disorder with prominent irritability
DifferentialKey Distinguishing Features
ADHDADHD: chronic, trait-like (present since early childhood, not episodic); no ↑self-esteem, grandiosity, flight of ideas, ↓need for sleep [5]. Mania: episodic with clear change from baseline
Psychotic disorder / schizoaffective disorderSchizophrenia: psychotic symptoms persist outside of mood episodes; FTD more a/w loosening of association, neologism, thought blocking (cf mania: circumstantiality, tangentiality, flight of ideas); speech more hesitant/halting (cf mania: pressured, difficult to interrupt); may have catatonia or negative symptoms [5]
Borderline personality disorderNo FHx of BAD; rapid shifts of mood over hours (not days-weeks); no classic mania symptoms (↑energy, grandiosity); mood disturbances often triggered by interpersonal issues [5]
Substance-inducedTemporal relationship to substance use; symptoms resolve with abstinence; urine toxicology [5]
Organic brain lesionConsider in older patients or those with no psychiatric history; extreme social disinhibition without gross mood disorder → consider frontal lobe pathology [5]

The following mermaid diagram provides a clinical approach to the child presenting with emotional/behavioural symptoms, systematically narrowing the differential:


In clinical practice and exams, you are often presented with a child who is irritable, refusing school, with somatic complaints. The differential is wide:

Step 1: Exclude organic causes

  • History and physical examination
  • Basic investigations: CBP, R/LFT, thyroid function test [11]. Others: blood alcohol level, blood and urine toxicology screen if indicated [11]

Step 2: Identify the primary psychopathology

  • Ask about the theme of the child's distress:
    • Worry about gaining weight → eating disorder [2]
    • Worry about having serious illness → hypochondriasis [2]
    • Fear of being poisoned or killed → delusional beliefs in paranoid schizophrenia [2]
    • Ruminatory thoughts of guilt or worthlessness → depression [2]
    • A/w obsessional thoughts or resisting a compulsion → OCD [2]
    • Separation or abandonment → borderline, dependent personality disorder [2]
    • Being rejected or inadequate → avoidant personality disorder [2]

Step 3: Determine if symptoms are developmentally appropriate

  • Is the severity and duration proportionate to the child's age and developmental stage?
  • Is there functional impairment (academic, social, family)?
  • If both yes → meets criteria for psychiatric disorder [1]

Step 4: Consider comorbidity

  • Comorbidity is the rule, not the exception, in child psychiatry
  • 70% of depressed children have comorbid anxiety [1]
  • 50% of ADHD children have comorbid psychiatric conditions [3]
  • Always screen for multiple conditions

The Theme-of-Anxiety Approach

When presented with an anxious child, the single most useful question is: "What is the child worried about?" The answer tells you the diagnosis:

  • Worried about separation → Separation anxiety disorder
  • Worried about social judgment → Social anxiety disorder
  • Worried about everything → GAD
  • Worried about specific object/situation → Specific phobia
  • Worried about contamination/harm with rituals → OCD
  • Worried about trauma → PTSD
  • Worried about weight → Eating disorder
  • Worried about illness → Health anxiety / hypochondriasis
  • No cognitive worry but physical symptoms → Consider organic cause or somatoform disorder

High Yield Summary

Key Differential Diagnosis Principles in Child Psychiatry:

  1. Always exclude organic causes first: hyperthyroidism, arrhythmias, hypoglycaemia, phaeochromocytoma, epilepsy, substance use (especially caffeine in adolescents), medication side effects

  2. Symptom overlap is enormous — use the overlap table:

    • ADHD: restlessness + poor concentration + ↑motor + distractibility (NO irritability)
    • ODD: irritability is the defining feature (hostile, defiant)
    • GAD: restlessness + poor concentration + distractibility + irritability (but NO ↑motor)
    • Depression: poor concentration + irritability (but also anhedonia, ↓energy)
    • Mania: poor concentration + ↑motor + distractibility + irritability (PLUS grandiosity, ↓need for sleep, flight of ideas — these are absent in ADHD)
  3. ADHD vs Mania: ADHD is trait-like and chronic; mania is episodic. ADHD lacks grandiosity, ↓need for sleep, and flight of ideas

  4. ~25% of BAD presents as juvenile depression → always screen for hypomania/mania in any depressed adolescent. Misdiagnosis delays correct treatment by 5-7 years on average

  5. Normal developmental fear vs anxiety disorder: diagnosed only when developmentally inappropriate + significant distress + functional impairment

  6. Theme of anxiety guides the specific diagnosis: separation → SAD; social evaluation → social phobia; everything → GAD; unexpected panic → panic disorder; trauma-related → PTSD; intrusive thoughts with rituals → OCD

  7. PTSD vs Adjustment disorder: stressor severity (Criterion A traumatic vs non-traumatic) and symptom profile (full PTSD criteria vs subthreshold)


Active Recall - Differential Diagnosis of Child Psychiatric Conditions

References

[1] Senior notes: ryanho-psych.md (Section 12.5 Other Psychiatric Conditions in Child Psychiatry, Section 12.1.2 Overview) [2] Senior notes: ryanho-psych.md (Section 7.3 Approach to Anxiety, differential diagnosis) [3] Senior notes: ryanho-psych.md (Section 12.3 ADHD — overlap table and comorbidities) [4] Senior notes: ryanho-psych.md (Section 12.3 ADHD — differential diagnosis) [5] Senior notes: ryanho-psych.md (Section 7.1.2 Approach to Elated or Irritable Mood; differential diagnosis of mania) [6] Lecture slides: GC 167. I feel very nervous Anxiety disorders.pdf (p27) [7] Lecture slides: GC 167. I feel very nervous Anxiety disorders.pdf (p18) [8] Senior notes: ryanho-psych.md (Section on OCD differential diagnosis) [9] Senior notes: ryanho-psych.md (Section on PTSD differential diagnosis) [10] Senior notes: ryanho-psych.md (Section on Adjustment Disorder differential diagnosis) [11] Lecture slides: GC 164. I am depressed Mood disorders.pdf (p13)

Diagnostic Criteria, Diagnostic Algorithm, and Investigations

Before diving into specific criteria, it is essential to understand why psychiatric diagnosis in children follows a particular logic:

Diagnostic criteria in psychiatry universally consist of [12]:

  1. A cluster of symptoms — core (discriminating) symptoms + associated (characteristic) symptoms
  2. Minimal duration — to separate transient reactions from disorders
  3. Distress or functional impairment — the symptoms must actually matter to the child's life
  4. Exclusion criteria — rule out organic causes, substances, and other psychiatric disorders that better explain the picture

In child psychiatry, there is a crucial additional layer: developmental appropriateness. Many "symptoms" of psychiatric disorders are actually normal at certain ages (separation anxiety in toddlers, stranger anxiety in infants, impulsivity in preschoolers). The diagnostic threshold is crossed only when severity and duration are out of proportion to the developmental stage [1].

Think of it like fever — a temperature of 37.5°C is normal after exercise but abnormal at rest. Similarly, fear of separation is "normal" at age 2 but "abnormal" at age 12.


2. Diagnostic Criteria for Specific Conditions

FeatureICD-10 (F93.0)DSM-5
Core criterionAnxiety focused specifically on separation from attachment figures, beyond that expected for developmental levelDevelopmentally inappropriate and excessive fear/anxiety concerning separation from attachment figures, evidenced by ≥ 3 of 8 symptoms
Symptom examplesUnrealistic worry about harm to/loss of attachment figures; refusal to go to school; reluctance to sleep alone; nightmares about separation; somatic complaints on separationSame symptom list, more explicitly operationalised
DurationNot explicitly stated but implied persistent≥ 4 weeks in children/adolescents; ≥ 6 months in adults
Age criterionOnset before 6 yearsNo specific age-of-onset requirement, but developmentally inappropriate
ImpairmentCauses significant distress and functional impairmentClinically significant distress or impairment in social, academic, or other important functioning
ExclusionNot part of a more pervasive disturbance of emotions, personality, or pervasive developmental disorderNot better explained by another mental disorder (e.g., refusing to leave home due to excessive resistance to change in ASD, psychotic disorder, agoraphobia)

DSM-5 Criteria in Detail (309.21 / F93.0):

A. Developmentally inappropriate and excessive fear or anxiety concerning separation from those to whom the individual is attached, as evidenced by ≥ 3 of the following:

  1. Recurrent excessive distress when anticipating or experiencing separation from home or attachment figures
  2. Persistent and excessive worry about losing attachment figures or about possible harm to them
  3. Persistent and excessive worry about an untoward event causing separation (e.g., getting lost, being kidnapped)
  4. Persistent reluctance or refusal to go out/away from home (school, work) because of fear of separation
  5. Persistent and excessive fear of or reluctance about being alone or without attachment figures at home or other settings
  6. Persistent reluctance or refusal to sleep away from home or without being near an attachment figure
  7. Repeated nightmares involving the theme of separation
  8. Repeated complaints of physical symptoms (headaches, stomach aches, nausea, vomiting) when separation from attachment figures occurs or is anticipated

B. Duration ≥ 4 weeks in children/adolescents, ≥ 6 months in adults C. Clinically significant distress or impairment D. Not better explained by another mental disorder

Why ≥ 3 of 8? Because separation anxiety manifests across multiple domains — cognitive (worry), behavioural (avoidance/refusal), somatic (physical symptoms), and affective (distress). Requiring ≥ 3 ensures the diagnosis captures a pervasive pattern rather than an isolated symptom.

DSM-5 Criteria (300.23 / F40.10):

A. Marked fear or anxiety about ≥ 1 social situations in which the individual is exposed to possible scrutiny by others (e.g., social interactions, being observed, performing in front of others)

  • In children: the anxiety must occur in peer settings and not just during interactions with adults B. The individual fears that they will act in a way or show anxiety symptoms that will be negatively evaluated C. The social situations almost always provoke fear or anxiety
  • In children: may be expressed by crying, tantrums, freezing, clinging, shrinking, or failing to speak D. The social situations are avoided or endured with intense fear/anxiety E. The fear/anxiety is out of proportion to the actual threat posed by the social situation F. Duration ≥ 6 months G. Clinically significant distress or impairment H. Not attributable to substance or another medical condition I. Not better explained by another mental disorder J. If another medical condition (e.g., stuttering, obesity) is present, the fear/anxiety is clearly unrelated or excessive

Specify if: Performance only (fear is restricted to speaking or performing in public)

Key child-specific modification: In adults, the person must recognise the fear is excessive. In children, this requirement is dropped — children often lack the metacognitive capacity to evaluate their own fear as "excessive."

FeatureICD-10 (F41.1)DSM-5 (300.02)
CoreGeneralised, persistent anxiety not restricted to specific situations ("free-floating anxiety")Excessive anxiety and worry about a number of events or activities, occurring more days than not for ≥ 6 months
SymptomsMust have ≥ 4 symptoms from a list including autonomic arousal, chest/abdominal symptoms, mental state symptoms, general symptoms, tension, and other nonspecific symptomsThe worry is difficult to control; ≥ 3 of 6 symptoms: restlessness, fatigue, poor concentration, irritability, muscle tension, sleep disturbance. In children: only 1 of 6 required
Duration≥ several months, on most days≥ 6 months
ExclusionNot due to panic disorder, phobic disorder, OCD, or hypochondriasis (ICD-10 treats GAD as a "diagnosis of exclusion") [13]Not attributable to substance/medical condition; not better explained by another mental disorder. DSM-5 allows comorbid diagnosis

ICD-10 vs DSM-5 for GAD — A Key Exam Distinction

ICD-10 treats GAD as a diagnosis of exclusion — you cannot diagnose GAD if the patient meets criteria for panic disorder, phobic anxiety, OCD, or hypochondriasis [13]. DSM-5 emphasises excessive worry as a core feature and specifies 6 months minimum duration, making DSM-5 diagnosis of GAD possible even in the presence of other anxiety disorders [13]. In children, DSM-5 requires only 1 of 6 associated symptoms (vs 3 of 6 in adults), reflecting the fact that children's anxiety often presents with fewer somatic/cognitive elaborations.

DSM-5 Criteria (312.23 / F94.0):

A. Consistent failure to speak in specific social situations in which there is an expectation for speaking (e.g., at school), despite speaking in other situations B. The disturbance interferes with educational/occupational achievement or social communication C. Duration ≥ 1 month (not limited to the first month of school) D. The failure to speak is not attributable to a lack of knowledge of, or comfort with, the spoken language E. The disturbance is not better explained by a communication disorder and does not occur exclusively during ASD, schizophrenia, or other psychotic disorder

Why the "first month of school" exclusion? Because many children are shy and quiet when entering a new environment. This is a normal adjustment. The 1-month rule ensures we are not pathologising normal adaptation.

DSM-5 Criteria (313.89 / F94.1):

A. A consistent pattern of inhibited, emotionally withdrawn behaviour toward adult caregivers, manifested by both:

  1. The child rarely or minimally seeks comfort when distressed
  2. The child rarely or minimally responds to comfort when distressed B. A persistent social and emotional disturbance characterised by ≥ 2 of:
  3. Minimal social and emotional responsiveness to others
  4. Limited positive affect
  5. Episodes of unexplained irritability, sadness, or fearfulness even during nonthreatening interactions C. The child has experienced a pattern of extremes of insufficient care, as evidenced by ≥ 1 of:
  6. Social neglect or deprivation (persistent lack of basic emotional needs for comfort, stimulation, affection)
  7. Repeated changes of primary caregivers that limit opportunity to form stable attachments
  8. Rearing in unusual settings that limit opportunities to form selective attachments (e.g., institutions) D. The care in Criterion C is presumed to be responsible for the disturbed behaviour in Criterion A E. The child does not meet criteria for ASD F. The disturbance is evident before age 5 years G. The child has a developmental age of ≥ 9 months

Why exclude ASD? Because both RAD and ASD involve poor social responsiveness — but the mechanism is completely different. In RAD, the social circuit is intact but suppressed due to environmental deprivation. In ASD, the social circuit is neurodevelopmentally impaired. The clinical clue: RAD children show improvement when placed in a nurturing environment; ASD children do not dramatically change.

DSM-5 Criteria (313.89 / F94.2):

A. A pattern of behaviour in which the child actively approaches and interacts with unfamiliar adults, exhibiting ≥ 2 of:

  1. Reduced or absent reticence in approaching unfamiliar adults
  2. Overly familiar verbal or physical behaviour
  3. Diminished or absent checking back with adult caregiver after venturing away
  4. Willingness to go off with an unfamiliar adult with minimal or no hesitation B. Behaviours in A are not limited to impulsivity (as in ADHD) but include socially disinhibited behaviour C. History of extremes of insufficient care (same as RAD Criterion C) D. The care in C is presumed responsible for the behaviour in A E. The child has a developmental age of ≥ 9 months

Why distinguish from ADHD impulsivity? An ADHD child might impulsively approach a stranger, but this is part of general behavioural disinhibition — they are also impulsive in non-social contexts (blurting out answers, can't wait their turn). DSED children are specifically and selectively indiscriminate in their social approach — their impulsivity is social attachment-specific.

The DSM-5 criteria for PTSD in children ≥ 6 years are essentially the same as for adults [9]:

A. Exposure to actual or threatened death, serious injury, or sexual violence via direct experience, witnessing, learning about it happening to a close family member/friend, or repeated exposure to aversive details

B. Intrusion symptoms (≥ 1): recurrent intrusive memories, distressing dreams, dissociative reactions (flashbacks), psychological distress at exposure to cues, marked physiological reactions to cues

C. Avoidance (≥ 1): avoidance of distressing memories/thoughts/feelings; avoidance of external reminders

D. Negative alterations in cognitions and mood (≥ 2): inability to remember important aspects of trauma, persistent negative beliefs about self/world, persistent distorted cognitions about cause/consequences, persistent negative emotional state, diminished interest in activities, detachment, persistent inability to experience positive emotions [9]

E. Marked alterations in arousal and reactivity (≥ 2): irritable behaviour/angry outbursts, reckless/self-destructive behaviour, hypervigilance, exaggerated startle, concentration problems, sleep disturbance [9]

F. Duration > 1 month G. Clinically significant distress or functional impairment H. Not attributable to substance or medical condition [9]

This is a separate criteria set in DSM-5, tailored for young children who cannot articulate internal experiences:

  • Criterion B (Intrusion): same, but traumatic dreams may not have recognisable content (generalised frightening dreams); re-enactment may occur in play
  • Criteria C and D are combined into one cluster requiring only 1 symptom (instead of requiring both avoidance AND negative cognitions separately) — because young children have limited avoidance capacity and cannot report cognitive distortions
  • Criterion E (Arousal): same as adults
  • Duration > 1 month, functional impairment, not substance-related

Why a lower threshold for young children? Young children have limited verbal capacity and metacognitive ability. A 3-year-old cannot tell you "I have distorted cognitions about the cause of the trauma" or "I feel emotionally numb." The preschool criteria rely more on observable behaviours (play re-enactment, regression) and set a lower symptom count because the same underlying disorder expresses through fewer observable channels.

DSM-5 criteria for Major Depressive Disorder [14]:

A. ≥ 5 of the following symptoms present during the same 2-week period, representing a change from previous functioning; at least one must be (1) or (2):

  1. Depressed mood most of the day, nearly every day — in children and adolescents, can be irritable mood
  2. Markedly diminished interest or pleasure in all or almost all activities
  3. Significant weight loss/gain or decrease/increase in appetite — in children, failure to make expected weight gains
  4. Insomnia or hypersomnia
  5. Psychomotor agitation or retardation (observable, not just subjective)
  6. Fatigue or loss of energy
  7. Feelings of worthlessness or excessive/inappropriate guilt
  8. Diminished ability to think/concentrate or indecisiveness
  9. Recurrent thoughts of death, suicidal ideation, or suicide attempt

B. Symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning [14]

C. The episode is not attributable to the physiological effects of a substance or to another medical condition [14]

D. Not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other psychotic disorders [14]

E. Absence of previous manic or hypomanic episode [14]

Key DSM-5 Changes Relevant to Youth Depression

The lecture slides highlight several key changes from DSM-IV [14]:

  • Removal of the "bereavement exclusion" — depressive symptoms may be understandable in context of significant loss (bereavement, financial ruin, disaster, serious illness), but clinical judgment based on individual history and cultural norms should be exercised [14]
  • Dysthymia → Persistent Depressive Disorder (includes both chronic MDD and the previous dysthymic disorder) [14]
  • Introduction of Disruptive Mood Dysregulation Disorder (DMDD): persistent irritability and frequent episodes of extreme, out-of-control behaviour in children up to 18 years [14]. This was created to reduce overdiagnosis of paediatric bipolar disorder in irritable children
  • Introduction of Premenstrual Dysphoric Disorder (PMDD): mood symptoms during the final week before menses, improving within days of menses [14]

Why can irritable mood substitute for depressed mood in children? As discussed in the pathophysiology section, the developing prefrontal cortex cannot modulate negative affect into the articulate experience of "sadness" — instead, it manifests as low frustration tolerance and irritability. The DSM-5 explicitly accommodates this developmental reality.

Varied clinical presentation — the lecture emphasises [14]:

  • In some younger people, the first obvious sign may be loss of interest in friends, decline in school performance, self-injury or bulimia or drug use in a previously stable adolescent
  • In some older people, symptoms may mimic dementia — deterioration of cognitive functioning and self-care
  • In some tragic cases, symptoms may be masked to others until the person is found dead by suicide

ICD-10 Criteria:

  • Some degree of emotional disturbance usually following the birth of an immediately younger sibling
  • If marked in degree and associated with abnormalities in social interactions, should be coded
  • The sibling rivalry disorder may be characterized by marked jealousy, rivalry, hostility toward the sibling
  • May manifest as behavioural regression, temper tantrums, dysphoria, sleep disturbance, attention-seeking
  • Must be persistent and clearly out of norm [1]
  • No DSM-5 equivalent (not included as a separate diagnostic entity)

Since adjustment disorder is an important differential in child psychiatry:

DSM-5 Criteria: A. Development of emotional or behavioural symptoms in response to an identifiable stressor, occurring within 3 months of the onset of the stressor B. Symptoms are clinically significant as evidenced by either:

  1. Marked distress out of proportion to the severity of the stressor
  2. Significant impairment in social, occupational, or other functioning C. Does not meet criteria for another mental disorder and is not merely an exacerbation of a pre-existing disorder D. Symptoms do not represent normal bereavement E. Once the stressor has terminated, symptoms do not persist for more than an additional 6 months

Specify subtypes: with depressed mood, with anxiety, with mixed anxiety and depressed mood, with disturbance of conduct, with mixed disturbance of emotions and conduct, unspecified


3. Standardised Assessment Instruments

Psychiatric diagnosis in children is clinical — based on thorough history (from child, parents, teachers), mental state examination, and developmental assessment. Standardised instruments are adjuncts, not substitutes.

Objective measures are useful in clinical practice and research but not diagnostic. They should not be used as a substitute for a clinical diagnosis made from a thorough interview [14].

ConditionInstrumentDetailsRole
Anxiety (general)Screen for Child Anxiety Related Disorders (SCARED)41-item child and parent-report; cut-off ≥ 25 suggests anxiety disorderScreening + severity monitoring
Anxiety (general)Spence Children's Anxiety Scale (SCAS)44 items, maps onto DSM anxiety subtypesScreening, subtype identification
Anxiety (general)Revised Children's Manifest Anxiety Scale (RCMAS)"What I Think and Feel" — 37 itemsScreening
DepressionPatient Health Questionnaire-9 (PHQ-9) [14]9 items mapped to DSM-5 MDD criteria; adolescent-modified version (PHQ-A) availableScreening + severity (5 mild, 10 moderate, 15 moderately severe, 20 severe)
DepressionChildren's Depression Inventory (CDI)27-item self-report for ages 7-17Screening + severity
DepressionBeck Depression Inventory (BDI) [14]21 items; validated in adolescents ≥ 13 yearsScreening + severity
DepressionHamilton Rating Scale for Depression (HAM-D) [14]Clinician-rated; 17-item version most commonSeverity + treatment response monitoring
DepressionMontgomery-Asberg Depression Rating Scale (MADRS) [14]10 items, clinician-rated; more sensitive to change than HAM-DTreatment response monitoring
DepressionCenter for Epidemiologic Studies-Depression Scale (CES-D) [14]20-item self-report; validated in adolescentsScreening
PTSDUCLA PTSD Reaction IndexChild and parent-report; maps to DSM-5 criteriaScreening + severity
PTSDChild PTSD Symptom Scale (CPSS)24 items mapped to DSM-5 criteriaScreening + severity
GeneralStrengths and Difficulties Questionnaire (SDQ)25 items; parent/teacher/self; 5 subscales (emotional, conduct, hyperactivity, peer, prosocial)Broad screening in primary care and schools
GeneralChild Behavior Checklist (CBCL)Parent-report; 118 items; internalising + externalising scalesComprehensive dimensional assessment
AttachmentStrange Situation Procedure (Ainsworth)Observation-based; classifies attachment as secure, avoidant, ambivalent, disorganisedResearch; guides attachment disorder assessment

The SDQ — Hong Kong Relevance

The Strengths and Difficulties Questionnaire (SDQ) is widely used in Hong Kong schools as a universal screening tool. It is brief (25 items), free, available in Chinese, and completed by parents and teachers. The "emotional symptoms" subscale is particularly useful for flagging children who may have anxiety or depression. A high total difficulties score (≥ 17 parent, ≥ 16 teacher) warrants further assessment.

InterviewDetails
Kiddie Schedule for Affective Disorders and Schizophrenia (K-SADS)Semi-structured; gold standard for DSM diagnosis in research; covers mood, anxiety, psychotic, behavioural, substance disorders; clinician-administered to child and parent
Development and Well-Being Assessment (DAWBA)Computer-based; generates ICD-10/DSM-5 diagnoses; parent, teacher, and self-report versions
Diagnostic Interview for Social and Communication Disorders (DISCO)Specifically for ASD and related conditions; useful when differentiating ASD from attachment disorders or selective mutism

4. Investigation Modalities

Investigations in child psychiatry serve two purposes:

  1. Exclude organic causes that mimic psychiatric conditions
  2. Identify comorbid medical conditions that may affect management

The key principle is: History, including medical and medication history; Mental state examination; Physical examination and investigation to rule out medical conditions that may cause depressive symptoms [14].

InvestigationRationaleKey Findings and Interpretation
CBP (Complete Blood Picture) [14]Exclude anaemia (fatigue, poor concentration → mimics depression/anxiety); infection (delirium → mimics psychosis)↓Hb → anaemia → fatigue, irritability. ↑WCC → infection. MCV may suggest B12/folate deficiency or chronic disease
Renal function tests (RFT) [14]Baseline before medications (especially lithium if BAD suspected); exclude uraemic encephalopathy↑Creatinine/urea → renal impairment → confusion, irritability
Liver function tests (LFT) [14]Baseline before medications (many psychotropics hepatically metabolised); exclude hepatic encephalopathy↑AST/ALT → liver dysfunction → consider substance abuse, medication effect, Wilson's disease
Thyroid function tests (TFTs) [1][14]Critical: hyperthyroidism mimics anxiety (tremor, tachycardia, agitation); hypothyroidism mimics depression (fatigue, weight gain, psychomotor slowing, cognitive impairment)↑Free T4 + ↓TSH → hyperthyroidism → treat endocrine cause. ↓Free T4 + ↑TSH → hypothyroidism → treat with levothyroxine

InvestigationWhen to OrderKey Findings and Interpretation
Blood glucose (fasting or random)Episodes of anxiety with autonomic symptoms; irritability; poor concentration; episodes triggered by fasting↓Glucose → hypoglycaemia → treat cause (insulinoma, medication, poor nutrition). Symptoms resolve with glucose correction
Blood alcohol level [14]Adolescent with behavioural changes, school decline, or intoxication featuresElevated → alcohol use/abuse → address substance use
Blood and urine toxicology screen [14]Adolescent with acute behavioural/mood changes; suspected substance use; psychotic presentationPositive → substance-induced psychiatric symptoms. Specific drugs detected guide management
ECGPalpitations, chest pain, syncope (to exclude arrhythmia mimicking panic); baseline before starting QTc-prolonging medications (e.g., citalopram, tricyclics)Prolonged QTc → risk of torsades de pointes; arrhythmia detected → cardiology referral. Normal ECG reassures against cardiac cause of "panic"
24-hour urinary catecholamines / metanephrinesEpisodic hypertension with anxiety symptoms → suspicion of phaeochromocytomaElevated → phaeochromocytoma → CT/MRI adrenals
EEG [14]Episodic behavioural changes, déjà vu, dissociative-like episodes → suspicion of temporal lobe epilepsy; stereotyped paroxysmal eventsEpileptiform discharges → epilepsy (especially temporal lobe) → treat with AEDs, not anxiolytics
CT or MRI brain [14]New-onset psychotic symptoms in a child; personality/behavioural change without clear psychosocial precipitant; focal neurological signs; suspicion of organic brain syndrome or hypopituitarism [14]SOL, demyelination, structural abnormality → treat organic cause. Pituitary abnormality → endocrine workup
HIV test [14]Risk factors present; behavioural changes in context of possible HIV; should be considered if indicated by historyPositive → HIV-associated neurocognitive disorder → antiretrovirals + psychiatric management
Cosyntropin (ACTH) stimulation test [14]Suspected Addison's disease (fatigue, weight loss, hyperpigmentation, low mood, hypotension)Inadequate cortisol rise → adrenal insufficiency → glucocorticoid replacement
Ferritin / iron studiesFatigue, irritability, poor concentration (especially in adolescent girls with heavy menstruation)↓Ferritin → iron deficiency (may precede anaemia) → iron supplementation
Vitamin D, B12, folateNon-specific fatigue, mood symptoms, cognitive difficultiesDeficiency → supplementation; B12 deficiency can cause neuropsychiatric symptoms
Coeliac screen (tTG-IgA)Unexplained somatic complaints, abdominal symptoms, failure to thrive with mood symptomsPositive → coeliac disease → gluten-free diet may resolve both GI and neuropsychiatric symptoms
Genetic testing (karyotype, microarray, fragile X)Intellectual disability + psychiatric symptoms; features suggestive of genetic syndrome; family history of genetic conditionsSpecific genetic diagnosis → guides prognosis, genetic counselling, and may alter management

The 'BASIC + TFT' Rule

For any child psychiatric presentation, the minimum investigation set is:

  • Blood count (CBP)
  • Assess renal/liver function (RFT, LFT)
  • Sugar (glucose)
  • Investigate thyroid (TFTs)
  • Consider toxicology if adolescent

This covers the vast majority of organic mimics. Additional investigations should be guided by history and examination.

ConditionSpecific Assessment Components
Anxiety disordersMulti-informant history (child, parent, teacher); developmental history; family psychiatric history; school observation; SCARED/SCAS questionnaire; physical examination for organic mimics
Youth depressionSafety assessment (suicidality, self-harm — mandatory); PHQ-9/CDI for severity; developmental and substance use history; medication review; family psychiatric history (especially bipolar)
Selective mutismConfirm the child speaks normally at home (audio/video recording may help); speech and language assessment to exclude communication disorder; hearing test; observation in different settings
Attachment disordersDetailed caregiving history (neglect, institutional care, caregiver changes); developmental assessment; observation of child-caregiver interaction (Strange Situation or equivalent); rule out ASD
PTSDDetailed trauma history (with developmentally appropriate interview); safety assessment; UCLA PTSD Index or CPSS; screen for comorbidities (depression, substance use)

The following algorithm integrates history-taking, examination, investigations, and diagnostic criteria into a stepwise clinical approach:


After completing the assessment, the findings are synthesised into a diagnostic formulation — this is not just a label but a holistic understanding:

ComponentContent
Presenting complaintChief complaint in the words of child and parent
Diagnosis (ICD-10/DSM-5)Primary diagnosis + comorbidities
Predisposing factorsGenetics, temperament, early adversity, attachment style
Precipitating factorsRecent life events, stressors, developmental transitions
Perpetuating factorsOngoing stressors, family dysfunction, maladaptive coping, avoidance behaviour (which maintains anxiety through negative reinforcement)
Protective factorsSupportive family, good peer relationships, above-average intelligence, engagement with school
Developmental contextCurrent developmental stage, cognitive level, any developmental delays
Risk assessmentSuicidality, self-harm, risk to others, safeguarding concerns

Why is the formulation important? Because a diagnosis tells you what the child has, but the formulation tells you why and what to do about it. Two children may both have separation anxiety disorder, but if one has it because of an anxious mother and the other because of recent parental divorce, the management approach is entirely different.


High Yield Summary

Diagnostic Criteria — Key Points:

  • Separation Anxiety Disorder: ≥ 3/8 symptoms, ≥ 4 weeks (children), developmentally inappropriate
  • Social Anxiety Disorder: In children, anxiety must occur in peer settings; child need not recognise fear as excessive; expressed as crying/freezing/tantrums/failure to speak
  • GAD: DSM-5 requires only 1/6 associated symptoms in children (vs 3/6 in adults); ICD-10 treats GAD as diagnosis of exclusion, DSM-5 allows comorbid diagnosis
  • Selective Mutism: Speaks normally at home but not in specific social situations; ≥ 1 month; exclude first month of school, communication disorder, ASD
  • RAD: Emotionally withdrawn + history of pathological caregiving + developmental age ≥ 9 months + exclude ASD
  • DSED: Indiscriminate sociability + history of pathological caregiving; distinguish from ADHD impulsivity
  • Youth MDD: Same as adult but irritable mood can substitute for depressed mood in children; ≥ 5/9 symptoms for ≥ 2 weeks
  • PTSD in children < 6: Separate criteria with combined avoidance/negative cognitions cluster and lower symptom threshold
  • DSM-5 introduced DMDD to reduce overdiagnosis of paediatric bipolar in irritable children

Investigations:

  • Baseline: CBP, RFT, LFT, TFTs, glucose ("BASIC + TFT")
  • Targeted: toxicology, ECG, EEG, neuroimaging — guided by clinical suspicion
  • Standardised instruments (PHQ-9, SCARED, SDQ, CDI) are adjuncts, not diagnostic substitutes
  • Diagnosis is clinical, based on thorough multi-informant interview, MSE, physical examination, and developmental assessment

Active Recall - Diagnostic Criteria, Algorithm and Investigations

References

[1] Senior notes: ryanho-psych.md (Section 12.5 Other Psychiatric Conditions in Child Psychiatry) [9] Senior notes: ryanho-psych.md (Section on PTSD diagnostic criteria and differential diagnosis) [12] Senior notes: ryanho-psych.md (Section on hierarchy of diagnosis and diagnostic criteria structure) [13] Senior notes: ryanho-psych.md (Section on GAD diagnostic criteria, including footnote on ICD-10 vs DSM-5) [14] Lecture slides: GC 164. I am depressed Mood disorders.pdf (p6, p9, p14)

Management Algorithm and Treatment Modalities

Before discussing specific treatments, the overarching framework must be understood:

Why is management in child psychiatry different from adults?

  1. The developing brain responds differently to psychotropics: Receptor density, neurotransmitter systems, and hepatic metabolism all change with age. Children are not small adults pharmacologically — they often metabolise drugs faster (higher hepatic blood flow relative to body mass) but their brains are more sensitive to certain effects (e.g., behavioural activation from SSRIs).

  2. Psychotherapy is first-line for most conditions: The immature but plastic brain is highly amenable to learning-based interventions. Environmental modification (changing the child's world) is often more effective than pharmacological modification (changing the child's brain chemistry).

  3. The family is the patient: Unlike adult psychiatry where the individual is the unit of treatment, in child psychiatry the family system is the therapeutic target. A child's symptoms often reflect family dysfunction, and treatment must address the system, not just the child.

  4. Multimodal treatment is the norm: Most children benefit from a combination of psychoeducation, psychological therapy, environmental modification, educational support, and (when indicated) pharmacotherapy.

  5. The hierarchy of management — think of it as concentric rings:

    • Innermost ring: Psychoeducation (always)
    • Second ring: Environmental and educational support
    • Third ring: Psychological therapy (CBT, behavioural therapy, family therapy)
    • Outermost ring: Pharmacotherapy (reserved for moderate-severe cases or treatment resistance)


3. Non-Pharmacological Treatment Modalities

ComponentRationalePractical Content
For the childUnderstanding reduces fear; fear of the unknown amplifies anxietyAge-appropriate explanation of what anxiety/depression is; normalising the experience; teaching that physical symptoms have a brain-based explanation
For parentsParents are co-therapists; their response to the child's symptoms can maintain or extinguish themEducation about the condition, its course, and prognosis; teaching parents not to accommodate avoidance (accommodation reinforces anxiety); modelling calm responses
For schoolSchool is where symptoms most commonly manifestInforming teachers about the child's condition; requesting reasonable accommodations; coordinating return-to-school plans for school refusers

Why does accommodation reinforce anxiety? If a parent allows the child to stay home every time they feel anxious about school, the child learns: "Anxiety → avoidance → relief." This is negative reinforcement (the behaviour of avoidance is strengthened by removal of the aversive stimulus). Psychoeducation teaches parents to support the child through the anxiety rather than helping them escape it.

CBT is the main psychological treatment for anxiety disorders [1][15][16].

Why CBT works in children (first-principles reasoning):

CBT targets the cognitive-behavioural cycle that maintains psychiatric symptoms:

  1. Cognitive component: Identifies and challenges distorted thinking patterns (e.g., catastrophising: "If mum doesn't pick me up, something terrible will happen"; overgeneralisation: "I failed one test, so I'll fail everything")
  2. Behavioural component: Gradually exposes the child to feared situations (exposure therapy) to break the avoidance-reinforcement cycle

The developing brain is highly plastic — children can learn new cognitive patterns more readily than adults. CBT essentially "retrains" the prefrontal cortex to regulate the amygdala more effectively.

Specific CBT techniques used in child psychiatry:

TechniqueMechanismIndication
Psychoeducation (within CBT)Understanding the anxiety cycle (trigger → thought → feeling → behaviour)All anxiety disorders, depression
Cognitive restructuringIdentifying automatic negative thoughts, evaluating evidence for/against, generating balanced alternativesGAD, social anxiety, depression
Graded exposure / systematic desensitisationConstructing a "fear hierarchy" and gradually exposing the child to feared stimuli, starting from least to most anxiety-provoking. With repeated exposure without catastrophic outcome, the amygdala's fear response habituates (fear extinction learning)Specific phobias, separation anxiety, social anxiety, selective mutism, PTSD
Behavioural experimentsTesting catastrophic predictions in real life (e.g., "Let's see what happens if you go to school without mum — will something bad really happen?")All anxiety disorders
Relaxation training [1]Progressive muscle relaxation, diaphragmatic breathing → activates parasympathetic nervous system → counteracts sympathetic arousalAll anxiety disorders, as an adjunct
Social skills trainingModelling, role-playing, and practising social interactionsSocial anxiety, selective mutism
Activity scheduling / behavioural activationScheduling pleasant and mastery activities to counteract withdrawal and anhedoniaDepression (the behavioural component of CBT for depression)
Problem-solving skills trainingTeaching step-by-step approach to interpersonal problems [15]Conduct disorders, depression, adjustment

Exposure Therapy — The Most Important Single Technique

Exposure therapy is the single most effective component of CBT for anxiety disorders. The principle is simple but counterintuitive for families: you must approach what you fear to overcome it. Avoidance maintains anxiety; exposure extinguishes it.

The neuroscience: during exposure, the amygdala initially fires (fear response). But with repeated exposure without the feared outcome occurring, the ventromedial prefrontal cortex learns a new "safety" association that inhibits the amygdala. This is called fear extinction — it doesn't erase the original fear memory but creates a competing safety memory that suppresses it.

This is why exposure must be:

  1. Gradual (starting with manageable anxiety, not overwhelming)
  2. Repeated (one exposure isn't enough — the extinction memory needs consolidation)
  3. Prolonged (the child must stay in the situation long enough for anxiety to naturally decrease — this is called habituation)
  4. Without safety behaviours (if the child has mum on the phone the whole time, they attribute their safety to mum, not to the situation being safe)

Trauma-focused CBT is considered first-line treatment for PTSD [9][16].

ComponentDescriptionMechanism
PsychoeducationEducating child and family about normal stress reactions and their cognitive underpinnings [9]Normalisation reduces shame and fear; understanding the "why" of symptoms is itself therapeutic
Cognitive restructuringAddressing maladaptive or unrealistic appraisals by the patient towards the trauma, their response to the event, and fears of potential future harm [9]Corrects distorted cognitions (e.g., "It was my fault," "The world is completely dangerous")
Trauma narrativeThe child constructs a coherent narrative of the traumatic event with the therapist's guidanceVerbal processing of the trauma allows the hippocampus to properly "contextualise" the fear memory — moving it from a raw, fragmented emotional memory to a coherent autobiographical memory
Exposure therapyAssisting the patient in confronting feared memories and situations; allows emotional processing of emotional response following exposure to related cues [9]Fear extinction (same principle as for anxiety disorders)
Parent componentTraining parents to respond supportively; managing their own distressParents' emotional reactions directly influence the child's recovery
Safety planningAddressing ongoing safety concerns, developing coping strategiesPractical and essential; no therapy works if the child is still in danger

EMDR (Eye Movement Desensitisation and Reprocessing) is also effective for PTSD [9]:

  • Involves: patient imagines a scene from the trauma, focuses on accompanying cognition and arousal, while the therapist moves two fingers across the patient's visual field and instructs the patient to track the fingers [9]
  • Sequence repeated until anxiety decreases, with patient instructed to generate a more adaptive thought [9]
  • Most studies show it is efficacious in PTSD, superior to other less-specific psychotherapy [9]
  • Mechanism debated — may work through dual-attention (the eye movements tax working memory, reducing the vividness and emotionality of the trauma memory during reprocessing)

Critical Incident Stress Debriefing — A Common Mistake

Critical incident stress debriefing (CISD) — going through traumatic events together with the victim — although widely used, has NOT been shown to be helpful in reducing psychological distress [9]. In fact, some evidence suggests it may be harmful by re-traumatising individuals. Do not recommend routine debriefing for all trauma-exposed children. Instead, use psychological first aid (practical support, safety, connection) and monitor for development of ASD/PTSD symptoms.

ModalityMechanismIndication
Family therapyAddresses dysfunctional family dynamics that maintain the child's symptoms; reduces expressed emotion (criticism, hostility, overinvolvement)Separation anxiety (anxious parent-child dyad), family conflict contributing to depression, attachment disorders, conduct disorders
Parent management training (PMT) [15]Based on social learning theory (operant conditioning) — teaches parents to: promote desirable behaviour through attention and rewards ("catch your child being good"), extinguish unwanted behaviour through selective ignoring, withdrawal of privileges, time-out [15]ODD/CD (mainstay), ADHD (adjunct), anxiety disorders (teaching parents not to accommodate avoidance)
Family or carer-focused treatment [17]Psychoeducation, communication training, problem-solving skillsBipolar disorder, psychotic disorders, severe depression
Psychoeducation for families [17][18]Education about the illness, its course, treatment, relapse signsAll child psychiatric conditions

InterventionRationale
Educational support [1]Children with psychiatric conditions often underperform academically — not because of lack of ability but because symptoms interfere with learning. Accommodations (extra time, reduced workload, exam arrangements) reduce stress and improve functioning
Special educational needs (SEN) accommodationsMany child psychiatric conditions (ADHD, ASD, severe anxiety) qualify as SEN under Hong Kong's inclusion education policy [15]. Schools must provide appropriate support
Gradual return-to-school programmeFor school-refusing children, abrupt forced return is counterproductive (too much exposure too fast → overwhelm → worsening). A graded plan (visiting school briefly → attending part-time → full-time) follows exposure therapy principles
Peer support and social skills groupsFor socially anxious or isolated children; provides structured social practice in a safe environment

ModalityMechanismIndication
Mindfulness-based therapy [16]Training attention to present-moment experience without judgment; reduces rumination and anticipatory anxiety; strengthens prefrontal regulatory control over amygdalaAnxiety, depression, relapse prevention
Interpersonal therapy (IPT)Focuses on current interpersonal problems (grief, role transitions, interpersonal disputes, skill deficits) [15]Adolescent depression
Play therapyFor younger children who cannot engage in verbal CBT; uses play as the medium for emotional expression and processingPre-school anxiety, trauma, attachment difficulties
Supportive psychotherapy / counsellingEmpathic listening, validation, problem-solving supportAdjustment disorders, mild presentations, as adjunct [10]

4. Pharmacological Treatment Modalities

  1. Pharmacotherapy is rarely first-line — it is reserved for moderate-severe cases, cases with significant functional impairment, or when psychotherapy alone has failed [1]
  2. "Start low, go slow" — but children may ultimately need weight-adjusted doses similar to or higher than adult doses due to faster hepatic metabolism
  3. Informed consent — from parents AND age-appropriate assent from the child
  4. Close monitoring — especially in the first weeks, for suicidality (SSRIs) and side effects
  5. Time-limited trials — reassess the need for medication periodically; many childhood conditions are self-limiting

"SSRI" → Selective Serotonin Reuptake Inhibitor → selectively blocks the serotonin transporter (SERT) at the presynaptic terminal → ↑synaptic 5-HT availability → downstream receptor changes → therapeutic effect [15].

PropertyDetails
MechanismBlocks SERT → ↑5-HT in synaptic cleft → desensitisation of 5-HT1A autoreceptors over 2-4 weeks → enhanced 5-HT neurotransmission → anxiolytic and antidepressant effects
Why 2-4 week delay?Acute SERT blockade paradoxically activates 5-HT1A autoreceptors → initially DECREASES 5-HT firing. Only after autoreceptor desensitisation does 5-HT transmission actually increase. This explains the delayed therapeutic effect and the initial worsening of anxiety
First-line forChildhood anxiety disorders (moderate-severe) [1], youth depression (moderate-severe) [1], PTSD (as adjunct to TF-CBT) [9], OCD

Specific SSRI Agents:

AgentFDA/NICE Approval in YouthNotes
Fluoxetine ("fluox" = flow/fluid — conceptually "gets serotonin flowing")Only SSRI FDA-approved for depression in children ≥ 8 years and adolescents; also approved for OCD ≥ 7 yearsLongest half-life (1-3 days active; norfluoxetine metabolite 4-16 days) → least withdrawal symptoms; best evidence base in youth depression
SertralineFDA-approved for OCD in children ≥ 6 years; strong evidence for anxiety disorders in childrenOften preferred for anxiety; shorter half-life than fluoxetine
FluvoxamineFDA-approved for OCD in children ≥ 8 yearsPotent CYP1A2 inhibitor — drug interaction considerations
EscitalopramFDA-approved for depression in adolescents ≥ 12 yearsS-enantiomer of citalopram; cleaner pharmacology
CitalopramNot FDA-approved in youth; used off-labelQTc prolongation risk at higher doses → ECG monitoring

The SSRI Suicidality Warning — Critical Exam Topic

In 2004, the FDA issued a Black Box Warning for all antidepressants used in children and adolescents (extended to age 24 in 2007): SSRIs may increase suicidal thinking and behaviour in the first few weeks of treatment, especially in youth.

Why does this happen?

  • Activation before mood improvement: SSRIs can increase energy and reduce psychomotor retardation before improving mood. A severely depressed adolescent who was too lethargic to act on suicidal thoughts may now have the energy to do so, while still feeling hopeless
  • Akathisia/agitation: Some patients experience restlessness and inner agitation (akathisia-like effect) which can be distressing and increase suicidal risk
  • Paradoxical anxiety: The initial increase in synaptic 5-HT (before autoreceptor desensitisation) can worsen anxiety transiently

Clinical implication: Monitor closely in the first 4 weeks — weekly visits initially, assess for suicidality at every contact, involve parents in monitoring. The benefits of SSRIs in moderate-severe depression and anxiety outweigh the risks when properly monitored — undertreated depression itself carries a high suicide risk.

The senior notes state: antidepressants for moderate/severe depression → beware of suicidal risk in SSRIs [1].

Side Effects of SSRIs in Children:

Side EffectMechanismManagement
GI symptoms (nausea, diarrhoea, abdominal pain)5-HT3 receptor stimulation in GI tract (most 5-HT in the body is in the gut)Usually transient (1-2 weeks); take with food; dose titration
Headache5-HT-mediated vasodilationUsually transient; analgesics if needed
Sleep disturbance (insomnia or sedation)5-HT2 receptor effects (varies by agent)Give in morning if activating; at night if sedating
Behavioural activation (agitation, restlessness, disinhibition)More common in younger children; mechanism unclear but may relate to dopaminergic effects or anxiety worseningDose reduction; slow titration; consider switching
Serotonin syndrome (rare but dangerous)Excess serotonergic activity (especially with drug combinations) → autonomic instability, myoclonus, altered consciousnessAvoid combining with other serotonergic agents (MAOIs, tramadol, triptans); stop offending agent; supportive care
Emotional bluntingExcessive serotonergic dampening of emotional rangeDose reduction; consider switching
Discontinuation syndromeAbrupt cessation → rapid ↓synaptic 5-HT → dizziness, "brain zaps," irritability, flu-like symptomsTaper gradually (except fluoxetine which self-tapers due to long half-life)

AgentClassIndication in ChildrenMechanismCautions/Contraindications
Imipramine [1]Tricyclic antidepressant (TCA)Separation anxiety disorder; enuresis; treatment-resistant anxiety/depressionBlocks SERT + NRT → ↑5-HT and NA. Also blocks muscarinic, histaminergic, and α-adrenergic receptors (explains side effects)Cardiotoxicity (QTc prolongation, arrhythmias → ECG before and during treatment); anticholinergic effects (dry mouth, constipation, urinary retention); sedation; lethal in overdose (narrow therapeutic index); not first-line due to safety concerns
Anxiolytics (benzodiazepines) [1]GABA-A receptor positive allosteric modulatorGenerally avoided in children [1]; very short-term use only for acute severe anxietyEnhances GABA-mediated chloride influx → CNS depression → anxiolytic, sedative, muscle relaxantDependence and tolerance develop rapidly; paradoxical disinhibition in children (opposite of intended effect — child becomes more agitated); sedation impairs learning; cognitive impairment; respiratory depression in overdose
Serotonergic antidepressants [16]SSRIs/SNRIsOCD treatmentHigher doses often needed for OCD than for depression/anxiety (why? OCD may involve deeper serotonergic dysfunction requiring more robust SERT blockade)As above for SSRIs; SNRIs add NA-related side effects (↑BP, tachycardia)
Adjunctive antipsychotics [16]Second-generation antipsychotics (SGAs)OCD (augmentation) [16]; severe aggression in ASD; treatment-resistant depression (augmentation)D2 receptor antagonism + 5-HT2A antagonism → modulates dopaminergic and serotonergic circuitsMetabolic syndrome (weight gain, dyslipidaemia, insulin resistance); prolactinaemia; extrapyramidal symptoms; sedation; QTc prolongation. Monitor: weight, fasting glucose, lipids, prolactin
PrazosinAlpha-1 adrenergic blockerPTSD-related nightmares and sleep disturbance [9]Blocks noradrenergic hyperactivation → ↓nightmare frequency, ↓hyperarousalHypotension (especially first dose); dizziness; titrate slowly; monitor BP
MelatoninEndogenous hormoneSleep-onset insomnia (common in anxiety, ADHD, ASD)Activates MT1/MT2 receptors in SCN → resets circadian clock, promotes sleep onsetVery well tolerated; minimal side effects; not habit-forming

Condition1st-Line Pharmacotherapy2nd-Line / AugmentationKey Monitoring Points
Childhood anxiety disordersSSRI (fluoxetine or sertraline) for moderate-severe cases [1]Imipramine [1]; SNRI (venlafaxine, duloxetine); anxiolytics generally avoided [1]Suicidality in first weeks; efficacy at 4-6 weeks
Youth depressionSSRI (fluoxetine preferred — best evidence) for moderate-severe [1]Switch SSRI; SNRI; augment with lithium, quetiapine, or aripiprazole for treatment-resistant cases [15]Suicidality monitoring — weekly initially; ECG if using TCA; growth/weight
PTSDSSRI (as adjunct to TF-CBT) [9]SGA augmentation [9]; prazosin for nightmares [9]; BZDs for hyperarousal (short-term only) [9]Suicidality; ongoing safety; comorbid substance use
OCDSerotonergic antidepressants (SSRI at higher doses) [16]Adjunctive antipsychotics (e.g., risperidone, aripiprazole) [16]; clomipramine40-60% treatment response [16]; monitor metabolic parameters if using SGA
Selective mutismSSRI (fluoxetine or sertraline) for severe cases unresponsive to behavioural intervention—Most children respond to behavioural approach alone
Attachment disorders (RAD/DSED)No pharmacotherapy for core symptoms — these are relational disorders requiring relational treatmentTreat comorbidities (e.g., anxiety, ADHD) pharmacologically if presentThe treatment is stable, nurturing caregiving environment — no pill can substitute for attachment

Attachment Disorders — Pills Don't Fix Relationships

There is no medication that treats the core symptoms of RAD or DSED. These disorders arise from pathological caregiving, not from neurotransmitter imbalance. The treatment is providing a consistent, responsive, nurturing caregiver — ideally through foster care placement, adoption, or therapeutic parenting programmes. Medications may be used for comorbid conditions (anxiety, ADHD, behavioural dysregulation) but never as standalone treatment for attachment difficulties.


5. Condition-Specific Management Algorithms

Why combine SSRI + CBT for severe anxiety? The landmark CAMS (Child/Adolescent Anxiety Multimodal Study) trial showed that combination treatment (sertraline + CBT) was superior to either alone, with ~81% response rate vs ~60% for CBT alone or ~55% for sertraline alone. The SSRI lowers the baseline anxiety level, making the child more able to engage in exposure-based CBT.

Approach (adapted from NICE guidelines) [15]:

Prophylaxis [15]:

  • First episode → continue antidepressants for ≥ 6-9 months at dose that induces remission
  • ≥ 2 episodes with significant functional impairment → continue antidepressants for ≥ 2 years

Fluoxetine — The Preferred SSRI in Youth Depression

Among all SSRIs, fluoxetine has the strongest evidence base for efficacy in youth depression (the TADS — Treatment for Adolescents with Depression Study — demonstrated superiority of fluoxetine + CBT over all other arms). It is the only SSRI FDA-approved for depression in children ≥ 8 years. Other SSRIs have shown more equivocal results in youth depression trials (some studies suggest no benefit over placebo for paroxetine, citalopram in youth), though they may work for anxiety.

Treatment [9][16]:

PhaseInterventionDetails
Acute phase (within first month — ASD)Trauma-focused CBT as first-line [9]Psychoeducation, cognitive restructuring, exposure therapy. Pharmacotherapy generally not considered helpful for acute stress disorder [9]
Established PTSD (> 1 month)Trauma-focused CBT — 1st line [9]12-16 sessions; includes trauma narrative, in-vivo exposure, cognitive processing
EMDR — alternative 1st line [9]Particularly useful if child cannot engage verbally in CBT
SSRI — as adjunct/2nd line [9]Sertraline or fluoxetine; addresses comorbid depression, hyperarousal; usually as augmentation or 2nd-line to psychotherapy [9]
Adjunctive/symptomaticPrazosin for nightmares/sleep [9]α1-blocker; titrate slowly; monitor BP
SGAs (e.g., risperidone) [9]For severe aggression, dissociation, treatment-resistant symptoms; as monotherapy or augmentation
BZDs [9]Short-term only for severe hyperarousal; caution re dependence
ComorbiditiesTreat comorbid conditions [9]Alcohol/substance use disorders, sleep disorders, psychosis [9]

Treatment [16]:

  • 40-60% treatment response overall [16]
  • 1st-line: Behaviour therapy (exposure and response prevention, ERP) + serotonergic antidepressants (SSRI, usually at higher doses than for depression) [16]
  • Augmentation: adjunctive antipsychotics (e.g., risperidone, aripiprazole) for partial responders [16]
  • Refractory: psychosurgery (rarely) [16] — e.g., anterior cingulotomy or deep brain stimulation; reserved for the most severe, treatment-resistant cases with significant disability

Why higher SSRI doses for OCD? OCD is thought to involve a deeper serotonergic dysfunction in the cortico-striato-thalamo-cortical (CSTC) circuit. The higher dose may be needed to achieve sufficient SERT blockade in these specific circuits to interrupt the obsessional loop.

StepIntervention
1st-lineBehavioural intervention: graded exposure to speaking situations (start with whispering → single words → phrases → sentences → spontaneous speech, moving from comfortable settings to challenging ones); "stimulus fading" (gradually introducing new people into situations where the child already speaks)
Family componentPsychoeducation; reducing parental accommodation (speaking for the child); coaching parents and teachers on how to gently increase verbal demands
School componentTeacher training; seating arrangements (near trusted peers); avoiding putting child on the spot; reinforcing any verbal communication
2nd-lineSSRI (fluoxetine or sertraline) for severe/persistent cases unresponsive to behavioural intervention alone

InterventionDetails
Primary treatmentProvision of stable, responsive caregiving environment — this is the treatment, full stop. For children in institutional care: placement in foster family or adoption. For children with caregivers: therapeutic parenting programmes, attachment-based family therapy
SupportivePsychoeducation for caregivers about attachment theory and the child's specific needs; managing expectations (recovery takes time, especially for DSED)
Comorbidity treatmentPharmacotherapy/CBT for comorbid anxiety, ADHD, depression as needed
What NOT to doDo NOT use "holding therapy" or "rebirthing therapy" — these are unproven and potentially harmful. Do not expect rapid results — attachment formation takes months to years

The lecture slides provide a high-level framework applicable across conditions [16]:

General treatment approaches:

  • Pharmacotherapy: Antidepressants, Anxiolytics, Antipsychotics, Mood stabilizers
  • Psychotherapy: Cognitive Behaviour Therapy (CBT), Mindfulness-based Therapy

Key summary points from the lecture [16]:

  • Anxiety, obsessive-compulsive and trauma and stressor-related disorders are common
  • There are significant comorbid psychiatric conditions associated with anxiety disorders
  • Screening questions can help identify or rule out diagnoses
  • There are many effective treatments including psychotherapy and psychopharmacology
  • There is a huge amount of suffering associated with these disorders

Management of bipolar disorder (relevant when BAD presents as juvenile depression) [17][18]:

  • Early diagnosis and maintenance treatment
  • Watch out for side effects and the need of alternative treatments
  • Deal with stigma and poor drug compliance
  • Provide psychoeducation (individual and family)
  • Pay attention to stress coping, interpersonal relationship, lifestyle regularity and other risk factors of relapse
  • Recognise and treat comorbidities, e.g. anxiety disorder, sleep problem, suicidal risk, substance abuse

ConditionPrognosis
Childhood anxiety disordersNearly 2/3 expected to disappear within 3-5 years, but ~1/3 of them will have other categories of anxiety disorders at follow-up [1]. This means anxiety often transforms rather than truly resolves — a child with separation anxiety may later develop social anxiety or GAD
Youth depressionEpisodic relapsing course — majority recover within < 3 months but 15% lasting > 18 months [1]. High recurrence rate (50-70% will have another episode within 5 years). ~25% of BAD first presents as juvenile depression [1]
PTSDVariable; many children recover with appropriate treatment within 6-12 months. Chronicity is more likely with more severe trauma, ongoing adversity, and lack of social support
OCD40-60% treatment response [16]; better prognosis with later onset, precipitating event, good adjustment, episodic symptoms
Selective mutismMany improve with appropriate intervention; may persist into adolescence if untreated; associated with ongoing social anxiety even after mutism resolves
Attachment disordersRAD generally improves with stable caregiving; DSED is more "sticky" and may persist even after placement in nurturing environment

High Yield Summary

Management Principles:

  • Psychoeducation is universal — for child, parents, and school
  • CBT is 1st-line for anxiety, depression, PTSD, OCD in children
  • Pharmacotherapy reserved for moderate-severe or treatment-resistant cases
  • SSRI is 1st-line pharmacotherapy for anxiety, depression, PTSD, OCD — fluoxetine is preferred for depression (only SSRI FDA-approved for youth depression)
  • SSRI suicidality risk: Black Box Warning; monitor weekly for first 4 weeks; benefits outweigh risks when properly monitored
  • Imipramine: 2nd-line for anxiety; cardiotoxicity risk requires ECG monitoring
  • Benzodiazepines generally avoided in children (dependence, paradoxical disinhibition, cognitive impairment)
  • Attachment disorders: no pill fixes attachment — treatment is stable nurturing caregiving
  • PTSD: TF-CBT or EMDR 1st-line; SSRI as adjunct; critical incident debriefing is NOT helpful
  • OCD: higher SSRI doses needed; 40-60% response; augment with SGA if partial response
  • Duration: continue SSRI ≥ 6-9 months after remission; ≥ 2 years if recurrent episodes

Prognosis:

  • Childhood anxiety: 2/3 resolve in 3-5 years but 1/3 develop other anxiety disorders
  • Youth depression: episodic relapsing; 25% may be bipolar
  • OCD: 40-60% treatment response

Active Recall - Management of Child Psychiatric Conditions

References

[1] Senior notes: ryanho-psych.md (Section 12.5 Other Psychiatric Conditions in Child Psychiatry) [9] Senior notes: ryanho-psych.md (Section on PTSD treatment — acute stress disorder and PTSD) [10] Senior notes: ryanho-psych.md (Section on Adjustment Disorder management) [15] Senior notes: ryanho-psych.md (Sections on Treatment in Psychiatry — antidepressants, psychotherapy, depression management, ADHD non-pharmacological interventions, parent management training) [16] Lecture slides: GC 171. Stress-related disorders and obsessive-compulsive disorder (Post-traumatic stress disorder adjustment disorder, acute stress disorder)_rev.pdf (p17, p41, p43) [17] Lecture slides: GC 163. I am a superman Bipolar disorder.pdf (p36, p47) [18] Lecture slides: GC 163. I am a superman Bipolar disorder.pdf (p64)

Complications of Other Psychiatric Conditions in Child Psychiatry

Child psychiatric conditions are not benign, self-limiting illnesses. The developing brain is uniquely vulnerable to the effects of chronic psychiatric illness because:

  1. Critical developmental windows: The brain undergoes massive restructuring during childhood and adolescence — synaptic pruning, myelination, prefrontal maturation. A psychiatric condition that disrupts this process during a critical window can have permanent effects on brain architecture and function, even after the condition itself resolves.

  2. Cascade effects: A child who is too anxious to attend school misses education → falls behind → loses peer relationships → develops low self-esteem → becomes depressed → withdraws further. Each complication begets the next in a vicious cycle that compounds over time.

  3. The developmental trajectory is altered: Unlike an adult who develops depression and returns to their prior level of functioning after treatment, a child who spends 2 years depressed has missed 2 years of social, academic, and emotional development that they can never fully recapture.

Think of it as building a house: if you skip the foundation (childhood development), everything built on top is unstable. Treating the psychiatric condition is like going back to fix the foundation — possible, but much harder once the upper floors are already built.


2. Complications of Childhood Anxiety Disorders

ComplicationMechanismEvidence
Persistence and transformation of anxietyNearly 2/3 of childhood anxiety disorders are expected to disappear within 3-5 years, but ~1/3 of them will have other categories of anxiety disorders at follow-up [1]. This is called heterotypic continuity — the phenotype changes (separation anxiety → social anxiety → GAD) but the underlying anxious diathesis persistsThe amygdala-prefrontal dysregulation and serotonergic vulnerability do not resolve simply because the content of the fear changes. The overactive behavioural inhibition system [1] is a trait, not a state
Development of adult anxiety disordersChildhood anxiety is the single strongest predictor of adult anxiety disorders. Separation anxiety → panic disorder with agoraphobia. Social anxiety → persistent social phobia. GAD → adult GADEarly fear conditioning creates neural pathways that, if not extinguished, become entrenched with repetition (long-term potentiation in amygdala circuits)
Depression (the most important complication)Anxiety and depression share neurobiological substrates (5-HT dysregulation, HPA axis dysfunction, hippocampal vulnerability). Chronic anxiety → learned helplessness → anhedonia → depression. The 70% comorbidity rate between youth depression and anxiety [1] illustrates this overlapChronic cortisol elevation from sustained anxiety → hippocampal atrophy → ↓5-HT neurotransmission → depressed mood. Additionally, avoidance behaviour → social isolation → loss of positive reinforcement → depression
Substance use disordersAdolescents with untreated anxiety may "self-medicate" with alcohol, cannabis, or benzodiazepines obtained illicitly. The anxiolytic effect of these substances provides immediate (but short-lived) negative reinforcement → substance use is maintainedGABA-ergic substances (alcohol, BZDs) reduce amygdala activation → temporary anxiety relief → reinforcement of use. Cannabis acts on endocannabinoid system to reduce anxiety acutely but chronic use can worsen it
OCDChildhood anxiety can evolve into OCD — the same underlying serotonergic dysfunction and cortico-striato-thalamic circuit abnormality manifests differently with maturationSome children with excessive worry and checking behaviours (GAD-like) develop frank obsessions and compulsions as cognitive sophistication increases

ComplicationMechanism
School refusal and academic failureAvoidance behaviour (the hallmark of anxiety) extends to school → missed education → academic underperformance → reduced future opportunities. In Hong Kong's competitive academic environment, this can have particularly severe consequences
Social isolation and peer relationship difficulties [1]Social withdrawal due to anxiety → reduced social practice → poor social skills development → peer rejection → further withdrawal (vicious cycle). Social skills are learned through practice — an anxious child who avoids peers misses this learning
Low self-esteem [1]Chronic anxiety → perceived inability to cope with situations that peers manage easily → "I am weak/different/broken" → negative self-concept that persists into adulthood
Impaired autonomy and independenceSeparation anxiety or generalised overprotection → child does not develop age-appropriate independence (sleeping alone, managing social situations, navigating the world) → delayed developmental milestones of autonomy → dependence in adulthood
Family dysfunctionThe child's anxiety creates stress for the entire family system. Parents may become overprotective (maintaining anxiety through accommodation), conflicted about management approaches, or burned out. Siblings may feel neglected

ComplicationMechanism
Chronic somatic symptomsPersistent autonomic activation → real physical symptoms (headaches, abdominal pain, muscle tension, fatigue) that become chronic and may lead to extensive medical investigations, unnecessary procedures, and iatrogenic harm
Sleep disturbanceNoradrenergic hyperarousal → difficulty initiating/maintaining sleep → chronic sleep deprivation → impaired concentration, mood, immune function, and growth hormone release
Functional gastrointestinal disorders (irritable bowel syndrome)The gut-brain axis: chronic anxiety → vagal and sympathetic dysregulation → altered gut motility, visceral hypersensitivity → IBS-like symptoms that may persist independently

ComplicationMechanismEvidence
Persistent social anxietySelective mutism is an extreme expression of social anxiety. Even when mutism resolves, the underlying social anxiety often persists → a/w later development of phobia, social anxiety [19]The anxiety circuit was never properly extinguished — the child stopped being mute but the amygdala-based threat response to social situations continues
DepressionChronic social isolation → loss of positive social reinforcement → anhedonia → depression. ↑Risk for depression in unresolved cases [19]Learned helplessness: repeated failure to communicate → perceived lack of control → depressive cognitions
Substance misuse↑Risk of substance misuse in unresolved cases [19]Same self-medication mechanism as for anxiety disorders — substances reduce social inhibition temporarily
Academic underachievementCannot participate in class discussions, oral assessments, group work → academic performance does not reflect true ability → educational disadvantageThe child's intelligence is intact but cannot be expressed through the school's verbal-dependent assessment system
Poor prognosis without treatmentPrognosis often poor, with 58% remission rate at 13 years [19] — meaning ~42% of children with selective mutism still have significant difficulties into adolescenceWithout intervention to break the avoidance cycle, the fear becomes more deeply entrenched over time (the longer you avoid, the harder it is to face the fear)

Selective Mutism — Not Just Shyness

The 58% remission rate at 13 years [19] means that nearly half of children with selective mutism carry significant difficulties into adolescence and adulthood. This is not a trivial condition. Untreated, it leads to social anxiety, depression, substance misuse, and profound social and academic handicap. Early behavioural intervention (graded exposure) is critical.


4. Complications of Youth Depression

ComplicationMechanismKey Facts
RecurrenceYouth depression has an episodic relapsing course — majority recovering < 3 months but 15% lasting > 18 months [1]. The relapse rate is 50-70% within 5 years. Each episode increases the risk of the next (kindling hypothesis: each episode sensitises the neural circuits, lowering the threshold for subsequent episodes)Kindling: initial episodes require a clear precipitant; later episodes can occur spontaneously as the circuits become "autonomously active"
Bipolar disorder~25% of BAD first presented as a juvenile depression in their 1st episode [1]. This is perhaps the most important complication to recognise — what looks like unipolar depression in adolescence may be the first expression of a lifelong bipolar illnessThe same genetic vulnerability (shared genes between MDD and BAD) and neurobiological substrate (dopaminergic/serotonergic dysregulation) can manifest as depression first and mania later, often precipitated by antidepressant treatment
Anxiety disorders70% has comorbid anxiety disorder [1]. The comorbidity is so high that some researchers consider childhood anxiety-depression to be a unified internalising spectrum rather than separate conditionsShared 5-HT dysfunction, shared HPA axis dysregulation, overlapping neural circuits (amygdala-prefrontal, hippocampal)
Conduct disorderCommon comorbidity [1]. Depression → frustration → irritability → externalising behaviour. The "behavioural problems" of childhood depression (e.g., "one case tried to steal a bus because of frustration at home" [1]) represent depression masked by conduct disturbancePrefrontal hypofunction in depression → poor impulse control → externalising. Also: low self-esteem + anhedonia → risk-taking behaviour as a form of stimulation
Substance abuseCommon comorbidity (SA) [1]. Adolescents with depression may use substances to self-medicate ("take cannabis to lift mood due to depression" [1]). This creates a vicious cycle: cannabis initially elevates mood → tolerance develops → withdrawal worsens depression → increased useCannabis: acute THC → dopamine release in mesolimbic pathway → transient euphoria. Chronic use → downregulation of CB1 receptors → ↓endocannabinoid tone → anhedonia, amotivation, worsening depression
DysthymiaCommon comorbidity [1]. Some children develop chronic low-grade depression superimposed on episodic MDD ("double depression")Persistent subthreshold depressive symptoms may reflect the trait component (neuroticism, negative cognitive style) rather than episodic illness

AspectDetails
Suicidal ideationPresent in a significant proportion of depressed adolescents. Must be actively screened at every clinical encounter
Suicide attemptsAdolescent depression is one of the strongest risk factors for suicide attempts. Risk is especially high in the first weeks of antidepressant treatment (SSRI activation effect) and during the transition from severe psychomotor retardation to improving energy (before mood improves)
Completed suicideYouth suicide is a leading cause of death in adolescents worldwide and in Hong Kong. Boys complete suicide more often (more lethal methods); girls attempt more often
Self-harm (deliberate self-harm / non-suicidal self-injury)Common in depressed adolescents; functions as emotional regulation (cutting → endorphin release → temporary relief from emotional pain) or communication of distress
Risk factors for suicide in youth depressionMale sex, previous attempt, comorbid substance use, comorbid conduct disorder, access to lethal means, family history of suicide, social isolation, impulsivity, psychotic features, hopelessness

Suicide Risk in Youth Depression — Non-Negotiable Assessment

Every depressed adolescent must be assessed for suicidality at every encounter. The senior notes emphasise: antidepressants for moderate/severe depression → beware of suicidal risk in SSRIs [1]. However, the risk of untreated depression (suicide) is far greater than the risk of treated depression with SSRIs. The message is not "don't treat" but "treat AND monitor closely."

ComplicationMechanism
Academic failurePoor concentration, psychomotor retardation, absenteeism, ↓motivation → declining school performance → lost educational opportunities → reduced socioeconomic prospects
Social developmental delayWithdrawal from peers during critical social development → missed social learning → persistent social skill deficits even after mood recovery
Impaired identity formationAdolescence is the period of identity consolidation (Erikson's "identity vs role confusion"). Depression during this period → negative self-concept becomes integrated into identity → "I am a depressed person" rather than "I have depression"
Family strainParental guilt, helplessness, conflict about management; sibling neglect; marital strain
Chronic physical complaintsSomatisation of depression (especially in younger children) → repeated medical consultations, investigations, missed diagnoses

ComplicationMechanismSpecific to RAD/DSED
Persistent social difficultiesThe "internal working model" of relationships (Bowlby) formed in early childhood serves as a template for all subsequent relationships. A child who learns that caregivers are unreliable/unavailable (RAD) or interchangeable (DSED) carries this template into adulthoodRAD: difficulty forming close relationships; emotional unavailability. DSED: indiscriminate relationships; inability to maintain deep bonds
Personality disorder (especially borderline, avoidant)Insecure attachment → unstable self-image, fear of abandonment, difficulty regulating emotions → predisposition to personality disorders. The attachment-personality disorder link is one of the strongest in developmental psychopathologyRAD → avoidant PD (emotional distance). DSED → borderline traits (unstable relationships, impulsivity)
Depression and anxietyLack of secure base → chronic insecurity → vulnerability to internalising disordersThe child never developed the internal resilience that comes from secure attachment — they face every stressor without an emotional "buffer"
Behavioural problems and conduct disorderLack of attachment → lack of internalised moral framework (moral development depends on identification with caregivers) → reduced empathy → antisocial behaviourParticularly in DSED: indiscriminate sociability + poor judgment → vulnerability to exploitation, risk-taking
Revictimisation and exploitationDSED children willingly go with strangers → at risk of abduction, sexual exploitation, traffickingThe very symptom that defines the disorder (indiscriminate sociability) creates a safety risk
Cognitive and academic delaysEarly deprivation → insufficient cognitive stimulation → delayed language, executive function, academic skillsStudies of institutionalised children show dose-dependent effects: longer deprivation → greater cognitive impairment
Growth and physical healthPsychosocial short stature (growth hormone suppression due to chronic stress); poor nutrition in neglected children; increased cortisol → immune suppression → increased infectionsThe HPA axis dysregulation from early deprivation has systemic effects beyond the brain

ComplicationMechanism
Chronic PTSDWithout treatment, acute PTSD can become chronic. The fear memory becomes deeply consolidated in the amygdala, and avoidance prevents fear extinction. Neural circuits remodel around the trauma — it becomes part of the brain's "baseline state"
Complex PTSDWhen trauma is repeated (e.g., ongoing abuse) rather than single-event, additional features develop: disturbances in self-organisation (affect dysregulation, negative self-concept, relational difficulties). This is particularly relevant in children with attachment disorders + trauma
Comorbid depressionChronic hyperarousal → exhaustion of stress systems → "burnout" → anhedonia, withdrawal. Also: negative cognitions about self and world (PTSD Criterion D) are essentially depressive cognitions
Substance useSelf-medication of hyperarousal and re-experiencing symptoms. Alcohol dampens amygdala activation; cannabis reduces nightmare frequency → both are negatively reinforcing
Behavioural problemsHyperarousal → irritability → aggression. Re-enactment of trauma (especially in younger children) may be misinterpreted as conduct disorder. Sexual abuse survivors may display sexualised behaviour
Developmental regressionYoung children may lose previously acquired skills (toileting, language) under the stress of trauma. This represents a return to earlier developmental states when the current demands exceed the child's coping capacity
Academic and social impairmentPoor concentration (hyperarousal), avoidance of school (if trauma-related), social withdrawal (negative cognitions, numbing) → missed education, lost friendships
Somatic complaintsChronic autonomic dysregulation → headaches, GI symptoms, chronic pain, fatigue. The body "keeps the score" — somatic manifestations of unprocessed trauma
Dissociative disordersParticularly after severe or repeated trauma: dissociation serves as a psychological "escape" when physical escape is impossible. Can become a habitual coping mechanism → depersonalisation/derealisation disorder, dissociative identity disorder (rare)

ComplicationMechanism
Persistent behavioural regressionIf the regression (bed-wetting, baby talk) is reinforced by parental attention, it can become a habitual pattern that persists beyond the initial adjustment period
Aggression toward siblingIf not managed, may escalate and become a persistent pattern of bullying/aggression within the family
Adjustment disorder or anxietyIf the perceived loss of parental attention is severe and prolonged, may evolve into a formal anxiety or adjustment disorder
Family dysfunctionParental guilt, frustration, and conflict about how to manage the rivalry can strain the marital relationship and family cohesion

These are complications arising from the treatments themselves — an important exam topic.

TreatmentComplicationMechanismPrevention
SSRIsSuicidal ideation/behaviour (first 2-4 weeks) [1]Activation before mood improvement; akathisia; paradoxical anxiety worseningWeekly monitoring first 4 weeks; safety planning with family; start low/go slow
SSRIsSerotonin syndromeExcessive serotonergic activity, especially with drug combinations (MAOIs, tramadol, triptans, lithium)Avoid serotonergic polypharmacy; educate patient/family
SSRIsEmotional bluntingExcessive dampening of emotional range (both positive and negative emotions)Dose reduction; consider switching
SSRIsDiscontinuation syndromeAbrupt cessation → rapid ↓synaptic 5-HT → dizziness, "brain zaps," irritabilityTaper gradually (except fluoxetine which self-tapers)
SSRIsBehavioural activation (in young children)Agitation, disinhibition, impulsivity — more common in younger childrenStart at very low doses; close monitoring; may require discontinuation
TCAs (imipramine)Cardiotoxicity (QTc prolongation, arrhythmias)Blockade of cardiac sodium and potassium channels → conduction delay → potentially fatal arrhythmiasECG before and during treatment; avoid in cardiac disease; lethal in overdose (narrow therapeutic index)
BenzodiazepinesDependence and toleranceGABA-A receptor downregulation with chronic exposureShort-term use only; generally avoided in children [1]
BenzodiazepinesParadoxical disinhibitionParticularly in children — the expected sedation/anxiolysis is replaced by agitation and behavioural disinhibitionAvoid in children; if occurs, discontinue
BenzodiazepinesCognitive impairmentGABA-mediated CNS depression → impaired learning, memory, concentrationAvoid long-term use; impacts academic performance
Antipsychotics (SGAs)Metabolic syndrome (weight gain, dyslipidaemia, insulin resistance, type 2 diabetes)5-HT2C and H1 receptor blockade → increased appetite; insulin receptor effects → metabolic dysregulationMonitor weight, fasting glucose, lipids regularly; lifestyle advice
Antipsychotics (SGAs)HyperprolactinaemiaD2 receptor blockade in tuberoinfundibular pathway → ↑prolactin → galactorrhoea, amenorrhoea, gynaecomastia, sexual dysfunction, reduced bone density (long-term)Monitor prolactin; use prolactin-sparing agents (aripiprazole, quetiapine) if possible
Antipsychotics (SGAs)Extrapyramidal symptoms (acute dystonia, akathisia, parkinsonism, tardive dyskinesia)D2 receptor blockade in nigrostriatal pathwayUse lowest effective dose; prefer SGAs over FGAs; monitor for movement disorders
OverinvestigationIatrogenic harm from unnecessary proceduresSomatic presentations of anxiety/depression → repeated medical investigations → false positives → invasive procedures → physical and psychological harmJudicious investigation; recognise somatic presentations early
Labelling effectStigma, self-fulfilling prophecyA psychiatric label can change how the child is perceived by others (teachers, peers) and by themselves → reduced expectations → self-fulfilling prophecy of disabilityFrame diagnoses positively; emphasise treatability; avoid diagnostic labelling without treatment plan

Childhood ConditionCommon Adult Outcomes (Without Adequate Treatment)
Childhood anxietyAdult anxiety disorders (GAD, panic, social phobia, agoraphobia); adult depression; substance use disorders; reduced educational attainment; occupational underperformance; relationship difficulties
Youth depressionRecurrent major depression; bipolar disorder (25% of cases); substance abuse; suicide; reduced educational and occupational attainment; relationship instability; chronic physical health problems (cardiovascular disease via HPA/inflammatory pathway)
Selective mutismPersistent social anxiety disorder; depression; substance misuse; occupational and social handicap
Attachment disordersPersonality disorders (borderline, avoidant); relationship instability; intergenerational transmission of insecure attachment (the child who was neglected becomes the parent who struggles to attach); depression; substance abuse
Childhood PTSDComplex PTSD; personality disorders; substance abuse; dissociative disorders; relationship violence (as victim or perpetrator); chronic physical health problems; suicidality
ODD/CD (comorbid)↑Risk of adjustment problems in adult — antisocial behaviour, impulse-control problems, substance abuse, anxiety, depression [20]
ADHD (comorbid)~40-60% experience problems in adulthood [21]: occupational failure, self-esteem issues, relationship problems, substance abuse, injuries/accidents

Intergenerational Transmission

Perhaps the most sobering long-term complication is intergenerational transmission. A child with untreated attachment disorder grows into an adult with insecure attachment patterns → becomes a parent who struggles to provide consistent, responsive caregiving → their child develops attachment difficulties → the cycle continues. Similarly, a depressed mother's parenting style (withdrawal, irritability, inconsistency) increases the child's risk of depression. Breaking these cycles is one of the most powerful things we can do in child psychiatry.


DomainAnxiety DisordersYouth DepressionSelective MutismAttachment DisordersPTSD
PsychiatricOther anxiety disorders, depression, substance use, OCDRecurrence, bipolar, anxiety, CD, substance abuse, dysthymiaSocial anxiety, depression, substance misusePersonality disorders, depression, anxietyChronic/complex PTSD, depression, substance use, dissociation
Suicide/Self-harmLow direct risk (but increased if comorbid depression)HIGH RISK — leading cause of death in adolescentsLow direct riskModerate (especially with comorbid depression)Moderate-high (especially with comorbid depression)
AcademicSchool refusal, underperformanceDeclining grades, absenteeismCannot participate in oral assessmentCognitive delays from deprivationPoor concentration, avoidance
SocialPeer difficulties, isolation, low self-esteemWithdrawal, lost friendshipsInability to communicate in social settingsIndiscriminate/absent relationshipsWithdrawal, aggression misinterpreted
PhysicalSomatic symptoms, sleep disturbance, functional GISomatic complaints, sleep, appetite changesMinimal direct physicalGrowth failure, immune compromiseSomatic complaints, autonomic dysregulation
FamilyParental burnout, accommodation cycleParental guilt, marital strainFamily frustrationIntergenerational transmissionFamily trauma response, protective behaviour
Long-term adultAdult anxiety/depression, substance useRecurrent depression, bipolar, suicide, chronic diseaseSocial anxiety, occupational handicapPersonality disorders, cycle of neglectComplex PTSD, personality disorders

High Yield Summary

Key Complications to Remember:

  1. Childhood anxiety: 2/3 resolve in 3-5 years, but 1/3 transform into other anxiety disorders (heterotypic continuity). Major risk of subsequent depression and substance use

  2. Selective mutism: Poor prognosis without treatment — only 58% remission by age 13. Associated with later social anxiety, depression, and substance misuse

  3. Youth depression: Episodic relapsing course; 50-70% relapse in 5 years. 25% are actually bipolar. 70% have comorbid anxiety. Suicide is the most dangerous complication — screen at every visit

  4. SSRI suicidality risk: Increased risk in first 2-4 weeks; mechanism = activation before mood improvement. Monitor weekly initially. Risk of untreated depression > risk of treated depression

  5. Attachment disorders: Lead to personality disorders, intergenerational transmission of insecure attachment, and exploitation risk (DSED)

  6. PTSD: Can become chronic or complex; comorbid depression and substance use are common; children may present with behavioural problems rather than classic re-experiencing

  7. Iatrogenic: SSRI suicidality, TCA cardiotoxicity, BZD dependence/paradoxical disinhibition, SGA metabolic syndrome, overinvestigation of somatic presentations

  8. Intergenerational transmission: Untreated child psychiatric conditions → impaired adult functioning → poor parenting → child psychiatric conditions in the next generation. This is the strongest argument for early, effective intervention.


Active Recall - Complications of Child Psychiatric Conditions

References

[1] Senior notes: ryanho-psych.md (Section 12.5 Other Psychiatric Conditions in Child Psychiatry) [19] Senior notes: ryanho-psych.md (Section on Selective Mutism — prognosis and complications) [20] Senior notes: ryanho-psych.md (Section 12.4 ODD/CD — course and prognosis) [21] Senior notes: ryanho-psych.md (Section 12.3 ADHD — course and prognosis, adult manifestations)

High Yield Summary

Anxiety Disorders in Children:

  • Commonest psychiatric disorder of childhood
  • Content of anxiety varies by developmental stage: strangers (infancy) → separation/specific objects (preschool) → social evaluation (early adolescence) → resembles adult (late adolescence)
  • Aetiology: dysregulated 5-HT/NA + overactive BIS + behavioural inhibition temperament + anxious attachment + cognitive biases
  • Atypical presentations: school refusal, somatic complaints, peer difficulties, low self-esteem, irritability
  • Diagnosis: only when developmentally inappropriate + distress + functional impairment
  • Management: CBT (1st line) > SSRIs (severe cases)
  • Prognosis: ~2/3 resolve in 3-5 years but ~1/3 develop other anxiety disorders

Youth Depression:

  • Rare pre-puberty (< 1%), rises dramatically post-puberty (~4%)
  • Adolescent depression ≈ adult depression
  • Childhood depression is more: somatic complaints, irritable mood, behavioural problems, anxiety
  • 70% have comorbid anxiety; ~25% of BAD first presents as juvenile depression
  • Aetiology: 5-HTTLPR × adversity, cortisol → hippocampal atrophy → ↓5-HT, cognitive distortions
  • Management: antidepressants (SSRIs) for moderate-severe + CBT; beware suicidal risk with SSRIs
  • Prognosis: episodic relapsing; majority recover < 3 months but 15% last > 18 months

Selective Mutism: Extreme social anxiety → speech inhibition in specific social contexts; normal speech at home

Attachment Disorders: RAD (inhibited — emotionally withdrawn) vs DSED (disinhibited — indiscriminate sociability); arise from pathological caregiving (neglect, institutional care)

PTSD in Children: Resembles adult PTSD but with repetitive play, trauma-specific nightmares, regression, behavioural re-enactment

Sibling Rivalry Disorder: Persistent, abnormally intense jealousy/hostility toward sibling after birth of new sibling; ICD-10 specific

High Yield Summary

Key Differential Diagnosis Principles in Child Psychiatry:

  1. Always exclude organic causes first: hyperthyroidism, arrhythmias, hypoglycaemia, phaeochromocytoma, epilepsy, substance use (especially caffeine in adolescents), medication side effects

  2. Symptom overlap is enormous — use the overlap table:

    • ADHD: restlessness + poor concentration + ↑motor + distractibility (NO irritability)
    • ODD: irritability is the defining feature (hostile, defiant)
    • GAD: restlessness + poor concentration + distractibility + irritability (but NO ↑motor)
    • Depression: poor concentration + irritability (but also anhedonia, ↓energy)
    • Mania: poor concentration + ↑motor + distractibility + irritability (PLUS grandiosity, ↓need for sleep, flight of ideas — these are absent in ADHD)
  3. ADHD vs Mania: ADHD is trait-like and chronic; mania is episodic. ADHD lacks grandiosity, ↓need for sleep, and flight of ideas

  4. ~25% of BAD presents as juvenile depression → always screen for hypomania/mania in any depressed adolescent. Misdiagnosis delays correct treatment by 5-7 years on average

  5. Normal developmental fear vs anxiety disorder: diagnosed only when developmentally inappropriate + significant distress + functional impairment

  6. Theme of anxiety guides the specific diagnosis: separation → SAD; social evaluation → social phobia; everything → GAD; unexpected panic → panic disorder; trauma-related → PTSD; intrusive thoughts with rituals → OCD

  7. PTSD vs Adjustment disorder: stressor severity (Criterion A traumatic vs non-traumatic) and symptom profile (full PTSD criteria vs subthreshold)

High Yield Summary

Diagnostic Criteria — Key Points:

  • Separation Anxiety Disorder: ≥ 3/8 symptoms, ≥ 4 weeks (children), developmentally inappropriate
  • Social Anxiety Disorder: In children, anxiety must occur in peer settings; child need not recognise fear as excessive; expressed as crying/freezing/tantrums/failure to speak
  • GAD: DSM-5 requires only 1/6 associated symptoms in children (vs 3/6 in adults); ICD-10 treats GAD as diagnosis of exclusion, DSM-5 allows comorbid diagnosis
  • Selective Mutism: Speaks normally at home but not in specific social situations; ≥ 1 month; exclude first month of school, communication disorder, ASD
  • RAD: Emotionally withdrawn + history of pathological caregiving + developmental age ≥ 9 months + exclude ASD
  • DSED: Indiscriminate sociability + history of pathological caregiving; distinguish from ADHD impulsivity
  • Youth MDD: Same as adult but irritable mood can substitute for depressed mood in children; ≥ 5/9 symptoms for ≥ 2 weeks
  • PTSD in children < 6: Separate criteria with combined avoidance/negative cognitions cluster and lower symptom threshold
  • DSM-5 introduced DMDD to reduce overdiagnosis of paediatric bipolar in irritable children

Investigations:

  • Baseline: CBP, RFT, LFT, TFTs, glucose ("BASIC + TFT")
  • Targeted: toxicology, ECG, EEG, neuroimaging — guided by clinical suspicion
  • Standardised instruments (PHQ-9, SCARED, SDQ, CDI) are adjuncts, not diagnostic substitutes
  • Diagnosis is clinical, based on thorough multi-informant interview, MSE, physical examination, and developmental assessment

High Yield Summary

Management Principles:

  • Psychoeducation is universal — for child, parents, and school
  • CBT is 1st-line for anxiety, depression, PTSD, OCD in children
  • Pharmacotherapy reserved for moderate-severe or treatment-resistant cases
  • SSRI is 1st-line pharmacotherapy for anxiety, depression, PTSD, OCD — fluoxetine is preferred for depression (only SSRI FDA-approved for youth depression)
  • SSRI suicidality risk: Black Box Warning; monitor weekly for first 4 weeks; benefits outweigh risks when properly monitored
  • Imipramine: 2nd-line for anxiety; cardiotoxicity risk requires ECG monitoring
  • Benzodiazepines generally avoided in children (dependence, paradoxical disinhibition, cognitive impairment)
  • Attachment disorders: no pill fixes attachment — treatment is stable nurturing caregiving
  • PTSD: TF-CBT or EMDR 1st-line; SSRI as adjunct; critical incident debriefing is NOT helpful
  • OCD: higher SSRI doses needed; 40-60% response; augment with SGA if partial response
  • Duration: continue SSRI ≥ 6-9 months after remission; ≥ 2 years if recurrent episodes

Prognosis:

  • Childhood anxiety: 2/3 resolve in 3-5 years but 1/3 develop other anxiety disorders
  • Youth depression: episodic relapsing; 25% may be bipolar
  • OCD: 40-60% treatment response

High Yield Summary

Key Complications to Remember:

  1. Childhood anxiety: 2/3 resolve in 3-5 years, but 1/3 transform into other anxiety disorders (heterotypic continuity). Major risk of subsequent depression and substance use

  2. Selective mutism: Poor prognosis without treatment — only 58% remission by age 13. Associated with later social anxiety, depression, and substance misuse

  3. Youth depression: Episodic relapsing course; 50-70% relapse in 5 years. 25% are actually bipolar. 70% have comorbid anxiety. Suicide is the most dangerous complication — screen at every visit

  4. SSRI suicidality risk: Increased risk in first 2-4 weeks; mechanism = activation before mood improvement. Monitor weekly initially. Risk of untreated depression > risk of treated depression

  5. Attachment disorders: Lead to personality disorders, intergenerational transmission of insecure attachment, and exploitation risk (DSED)

  6. PTSD: Can become chronic or complex; comorbid depression and substance use are common; children may present with behavioural problems rather than classic re-experiencing

  7. Iatrogenic: SSRI suicidality, TCA cardiotoxicity, BZD dependence/paradoxical disinhibition, SGA metabolic syndrome, overinvestigation of somatic presentations

  8. Intergenerational transmission: Untreated child psychiatric conditions → impaired adult functioning → poor parenting → child psychiatric conditions in the next generation. This is the strongest argument for early, effective intervention.

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