Assessment In Child Psychiatry
Assessment in child psychiatry is a comprehensive, developmentally informed evaluation integrating clinical interviews with the child and caregivers, behavioral observations, standardized rating scales, and collateral information to diagnose and formulate mental health problems in children and adolescents.
Assessment in child psychiatry is the systematic, developmentally informed process of gathering information about a child or adolescent's emotional, behavioural, cognitive, and social functioning in order to arrive at a diagnosis, formulation, and management plan. Unlike adult psychiatry — where you largely sit across from one patient and take a structured history — child psychiatry assessment is inherently multi-informant, multi-method, and developmentally contextualized.
The word "assessment" here is broader than just "history-taking." It encompasses:
- Clinical interviews (with the child, parents/carers, family together, and sometimes school staff)
- Behavioural observation (play, interaction patterns, developmental milestones)
- Standardised rating scales and psychometric instruments
- Collateral information (school reports, social worker notes, previous medical records)
- Physical examination and investigations (to exclude organic causes)
- Formulation — the synthesis of all gathered data into a biopsychosocial understanding
The fundamental principle: a child is not a small adult. The presentation of psychiatric illness in children is shaped by developmental stage, and the child cannot be assessed in isolation from the family system and social context. [1] [2]
2. Epidemiology and Context
- Approximately 10–20% of children and adolescents worldwide have a diagnosable mental health condition at any given time.
- In Hong Kong, community surveys have shown roughly 13–16% prevalence of psychiatric morbidity in school-age children and adolescents.
- The most common categories are:
- Anxiety disorders (commonest overall) [1]
- Behavioural disorders (ADHD, ODD/CD)
- Neurodevelopmental disorders (ASD, intellectual disability)
- Mood disorders (depression increases sharply after puberty)
- Referral pathways in Hong Kong: typically via MCHC (Maternal and Child Health Centre), paediatrician, school, or direct family referral to CAMHS (Child and Adolescent Mental Health Service) under Hospital Authority.
- Developmental context: A behaviour that is normal at age 3 (e.g., tantrums) is pathological at age 13. You must always compare symptoms to same-age, same-culture norms. [1]
- Limited self-report capacity: Young children cannot articulate internal states; you rely on behavioural observation, parent report, and projective techniques.
- Multi-system involvement: School, family, peer group — each is both a source of information and a potential aetiological/maintaining factor.
- Rapid developmental change: The child you assess at age 5 is cognitively, emotionally, and socially very different from the same child at age 10. Assessment must be repeated longitudinally.
3. General Principles of Assessment in Child Psychiatry
More flexible approach: difficult to follow a set routine when assessing children. [1] Unlike adult psychiatric interviews, which can follow a relatively standardised structure, child assessment demands improvisation. A 4-year-old will not sit still for a formal MSE; an oppositional 14-year-old may refuse to talk at all.
Who to interview: with parents, with the whole family, and with the child alone (for older children). [1] The assessment is multi-layered:
- Parents/carers first (to get the "adult version" of the problem without the child feeling anxious or defensive)
- Child alone (to get the child's own perspective and look for things they won't say in front of parents, such as abuse, bullying, or self-harm)
- Family together (to observe interactional dynamics)
- Other informants (school, social worker, GP)
Obtain collateral information: especially from school (educational, academic, behavioural). [1] [2] School reports are gold. They tell you about attention span in a structured setting, peer relationships, academic trajectory, and behavioural issues that parents may minimise or be unaware of.
Think of child psychiatric assessment as answering five key questions:
- Is there a problem? (compared to developmental norms)
- What is the problem? (characterise symptoms, get a differential)
- Why has this child developed this problem now? (predisposing, precipitating, perpetuating factors — the "3 Ps" in a biopsychosocial framework)
- What is the impact? (on the child, family, school functioning)
- What can we do about it? (management plan)
4. The Paediatric and Psychiatric History — Detailed Components
The pathway to care is the first question: "Why this child and why now?" [1] This immediately orients you — was the referral from a worried teacher who noticed social withdrawal? A frustrated parent who can't cope with aggression? A paediatrician who found no organic cause for recurrent abdominal pain?
This parallels the adult psychiatric HPI but with crucial child-specific modifications:
| Component | Details | Why It Matters |
|---|---|---|
| Presenting complaint | Whose concern is it? (parent, teacher, child?) | Children are often brought involuntarily; the "identified patient" may not see themselves as having a problem |
| Ascertain whether it's truly a symptom | Compare to other children of the same age from the same culture [1] | Tantrums at age 2 = normal. Tantrums at age 12 = pathological. Cultural norms matter (e.g., eye contact expectations vary) |
| Details of CC | Onset, nature, severity, precipitating/ameliorating factors, impact, progression, and coping [1] | Standard characterisation, but ask who noticed first and what they tried before seeking help |
| Review of comorbid problems | Systematic screening — see below | Child psychiatric conditions are highly comorbid (e.g., 70% of youth depression has comorbid anxiety) [1] |
Systematic Comorbidity Screen [1]
This is crucial. Child psychiatry conditions rarely come alone. When a child presents with one problem, you must screen for the others:
- Physical symptoms: headache, stomachache, hearing, vision, seizures, faints — both because somatic complaints may be the presenting feature of anxiety/depression in children, and because organic conditions (epilepsy, hearing loss) can mimic or cause psychiatric symptoms [1]
- ADHD symptoms: level of activity, attention span, concentration — ADHD is the great comorbidity with almost everything [1]
- ASD symptoms: relationship with peers, close friends, hobbies/interests, behaviour — ASD may present late, especially in girls who mask [1]
- ODD/CD symptoms: disobedient behaviour, response to frustration, temper tantrums, antisocial behaviour, aggression, stealing, truancy, delinquency [1]
- Mood disorder symptoms: mood, energy level, anxiety [1]
- Other behavioural disorders: eating, sleeping, elimination problems (enuresis, encopresis), sexual interest and behaviour [1]
Clinical Pearl
The comorbidity screen is your safety net. A child referred for "school refusal" may actually have separation anxiety disorder, social phobia, depression, bullying, or even early-onset psychosis. Always cast a wide net before narrowing.
4.2 Developmental History [2]
This is the single biggest difference from adult psychiatry. You need a full neurodevelopmental timeline:
| Domain | What to Ask | Relevance |
|---|---|---|
| Pregnancy | Was the pregnancy planned/wanted? Any complications (gestational DM, pre-eclampsia, infections — TORCH)? Maternal alcohol and substance abuse during pregnancy [1] | Prenatal insults → neurodevelopmental disorders. Foetal alcohol spectrum disorder (FASD) is a specific cause of intellectual disability and ADHD-like symptoms |
| Delivery | Mode (NSD vs CS), gestational age, low birth weight and prematurity [1], APGAR scores, any birth asphyxia or NICU admission? | Prematurity and birth complications are risk factors for ADHD, ASD, intellectual disability, and cerebral palsy |
| Neonatal period | Feeding difficulties, jaundice, infections, neonatal seizures? | Neonatal complications can signal early neurological compromise |
Child growth and development is a cornerstone of the assessment. [2] You must know the normal milestones to detect deviations:
| Domain | Key Milestones | Red Flags |
|---|---|---|
| Gross motor | Head control (3–4 mo), sitting (6 mo), crawling (9 mo), walking (12–15 mo), running (18–24 mo) | Persistent hypotonia, not walking by 18 months |
| Fine motor | Palmar grasp (4–5 mo), pincer grasp (9–10 mo), scribbles (15 mo), draws circle (3 yr) | Persistent fisting, inability to hold objects |
| Speech/Language | Babbling (6 mo), first words (12 mo), two-word phrases (2 yr), sentences (3 yr) | No babbling by 12 mo, no words by 18 mo, no phrases by 24 mo — screen for ASD and hearing loss |
| Social/Emotional | Social smile (6 wk), stranger anxiety (8 mo), parallel play (2 yr), cooperative play (3–4 yr), theory of mind (4–5 yr) | No social smile by 3 mo, no joint attention by 12 mo, no pretend play by 18 mo — red flags for ASD |
| Cognitive/Adaptive | Object permanence (8–9 mo), symbolic play (18 mo), toilet training (2–3 yr) | Regression of any previously acquired skill at any age is a major red flag |
Developmental Regression
Any loss of previously acquired skills must be taken extremely seriously. In a toddler, think Rett syndrome, childhood disintegrative disorder, metabolic conditions (e.g., mucopolysaccharidoses), or epileptic encephalopathy. In an older child, think early-onset psychosis, neurodegenerative disease, or severe depression.
Thomas and Chess described three temperament types:
- Easy (40%): regular, adaptable, positive mood
- Difficult (10%): irregular, slow to adapt, intense reactions, negative mood — at higher risk for behavioural disorders
- Slow-to-warm-up (15%): initially withdrawing but gradually adapting — may present as "shy" or anxious
Temperament is not the same as psychopathology, but it modifies risk. A difficult temperament + poor parenting = synergistic risk for ODD/CD. [1]
| Component | What to Ask | Why |
|---|---|---|
| Psychiatric family history | Depression, bipolar, schizophrenia, anxiety, ADHD, ASD, substance abuse, suicide in 1st/2nd degree relatives | Nearly all child psychiatric conditions have heritable components (e.g., ADHD heritability ~75%, ASD ~80%) |
| Family structure | Who lives at home? Parents married/separated/divorced? Siblings and their ages and health | Parental separation is a risk factor for emotional disorders; sibling dynamics matter (e.g., sibling rivalry disorder) |
| Parenting style [1] | Baumrind's parenting styles: authoritarian, permissive, authoritative, neglecting | Authoritative (warm + firm boundaries) is protective; authoritarian or neglecting styles are risk factors for behavioural problems |
| Marital/parental relationship | Conflict, domestic violence, parental mental health | Interparental conflict is one of the strongest risk factors for child psychopathology, independent of divorce per se |
| Socioeconomic status | Housing, income, employment, social support | Poverty and social deprivation are consistently linked to higher rates of child psychiatric problems |
| Domain | Details |
|---|---|
| Educational history | Current school, academic performance, any special educational needs (SEN) support, grade retention, school changes |
| Peer relationships | Number and quality of friendships, bullying (victim or perpetrator), social media use |
| Interests and activities | Hobbies, screen time, sports — tells you about the child's strengths and motivation |
| Adverse childhood experiences (ACEs) | Abuse (physical, sexual, emotional), neglect, domestic violence exposure, parental incarceration, parental substance use — these are dose-dependently related to psychiatric and medical morbidity |
| Trauma history | Specific traumatic events, PTSD symptoms |
| Substance use (adolescents) | Alcohol, cannabis, other drugs — increasingly relevant from age 12+ in Hong Kong |
- Chronic illnesses: epilepsy (associated with psychiatric comorbidity in ~30%), asthma (anxiety), diabetes (depression)
- Medications: especially those with psychiatric side effects (e.g., corticosteroids → mood changes, beta-agonists → anxiety, anti-epileptics → behavioural changes)
- Allergies
- Past hospitalisations and surgeries (traumatic for young children)
- Hearing and vision testing — undiagnosed hearing loss is a common mimicker of inattention and language delay
- Previous psychiatric diagnoses and treatments
- Previous contact with CAMHS, educational psychologist, clinical psychologist
- Previous psychometric testing (IQ testing, adaptive functioning assessment)
5. Conducting the Interview — Techniques and Practical Approach
Similar to history taking in adult psychiatry but with the following additions [1]:
- Obtain a complete description of main concerns/chief complaint [1]
- Obtain a complete history systematically (especially family, psychiatric, neurodevelopmental, educational, medical) [1]
- Should also indirectly evaluate the parents in terms of personality, marital relationship, and style of parenting [1] — this is subtle but critical. Watch how they talk about the child. Do they use warm language or hostile/critical expressed emotion? Do they agree with each other or contradict?
Expressed Emotion
High expressed emotion (EE) in families — characterised by criticism, hostility, and emotional over-involvement — is a well-established predictor of relapse in many psychiatric conditions (originally studied in schizophrenia, but also relevant in childhood mood and behavioural disorders). During the parent interview, you are implicitly assessing EE.
5.2 Interviewing the Child Alone [1]
This is an art. The general rules:
- Developmentally appropriate terms: simplify your terminology and avoid complex questions [1] — Instead of "Do you experience low mood?", try "Do you feel sad a lot?"
- Physical contact: be judicious, don't touch anybody for male doctors, especially cautious in patients with prior sexual abuse and physical abuse (damage rapport) [1] — Children who have been abused may interpret physical touch as threatening or, conversely, may show premature sexualising behaviour and develop inappropriate attachments if the doctor is too physically familiar. [1]
- Standardised behaviour rating scales: more objective, but diagnosis should still be based on structured interview and collateral information only (rating is for reference only) [1]
| Age Group | Technique | Rationale |
|---|---|---|
| Younger children (< 7–8 years) | Observe kid in play or ask to express feelings in painting/drawing [1] | Young children communicate primarily through play, not verbal narrative. Watch themes in their drawings (violence, isolation, family composition) |
| Older children (8–12 years) | Start by discussion on neutral topics (e.g., pets, favourite games) → then family, school, peer relationships → presenting problem [1] | Gradual warm-up builds trust. Moving from safe to sensitive topics mirrors motivational interviewing principles |
| Adolescents | Treat more like adults but maintain developmental sensitivity. Identify any sensitive issues beforehand (e.g., child abuse, sexual issues) [1]. Confidentiality is important but risky behaviour (e.g., self-harm, harming others) should be reported [1] | Adolescents value autonomy and privacy; they will shut down if they feel you will tell their parents everything. Be upfront about limits of confidentiality |
- Ask for the child's aspirations for the future — A child who says "I don't have a future" is flagging depression/suicidality
- Projective questioning on 3 wishes, or 3 goals they want to achieve from MHS — This tells you what matters to the child, not what matters to the parents
- Note that children are more suggestible than adults and may try hard to give the 'desirable answer' to questions → particularly important to not use leading questions [1]
Leading Questions
Never ask "Did your father hit you?" unless there is a specific reason. Instead, ask open questions: "What happens when your dad gets angry?" Children are highly suggestible and may provide false affirmatives to please the interviewer. This is especially critical in forensic contexts (child protection cases).
- Discuss with the family the interview arrangements beforehand — who gets interviewed first matters. Some clinicians prefer to see the adolescent first to signal that their voice matters; others see parents first to get background before seeing the adolescent. There is no fixed rule, but discuss and agree. [1]
- Confidentiality: Be explicit. "What you tell me stays between us, unless I'm worried about your safety or someone else's safety." [1]
- Screen for: substance use, self-harm, sexual activity, eating behaviour, online safety, cyberbullying
Essential to allow assessment of family interactions and dynamics. [1]
Should see the family at the first assessment or soon after it, before the interviewer has formed a close relationship with the young patient or one of the parents. [1] — Why? Because once you've allied with one family member, observing neutral family dynamics becomes impossible.
Observe for: [1]
- Family hierarchy: most dominant person? Usual spokesperson?
- Other family dynamics: Any alliances? How do they communicate with each other? How do they deal with conflict?
- Others: Who seems most worried about the problem? Any monopolising of the interview? (Ask other members to comment on his/her views)
Structural Family Assessment
In family systems theory (Minuchin), you look for:
- Enmeshment (boundaries too diffuse — everyone is in everyone else's business) vs Disengagement (boundaries too rigid — family members are emotionally disconnected)
- Triangulation (child is drawn into parental conflict as a mediator or scapegoat)
- Parentification (child takes on a parental role, e.g., caring for siblings or even parents) These patterns are both diagnostic clues and treatment targets.
The adult MSE framework (Appearance → Behaviour → Speech → Mood → Thought → Perception → Cognition → Insight) still applies, but with developmental modifications:
| MSE Domain | Child-Specific Considerations |
|---|---|
| Appearance | Hygiene, nutritional status (neglect?), clothing appropriate to weather/context, dysmorphic features (syndromic causes of ID/ASD, e.g., Down syndrome facies, FAS facies), injuries (bruises in unusual locations → consider non-accidental injury) |
| Behaviour | Activity level (hyperactive?), distractibility, impulsivity, eye contact (poor in ASD, anxiety; may also be culturally mediated), separation behaviour (clings to parent? Indifferent?), quality of play (repetitive? Symbolic?), tics, stereotypies, self-stimulatory behaviour |
| Rapport | Ease of engagement, warmth, reciprocity — children with ASD may show limited social reciprocity; anxious children may be withdrawn; oppositional children may be hostile |
| Speech & Language | Rate, volume, articulation, language level (appropriate for age?), echolalia (ASD), selective mutism (speaks at home but not at school) |
| Mood & Affect | Self-reported mood (in age-appropriate language), observed affect (congruent? Flat? Labile?), anxiety level, irritability. Note: children may show irritability more than sadness in depression |
| Thought Content | Worries, fears, obsessions, preoccupations, suicidal ideation (ask directly in older children/adolescents), self-harm thoughts |
| Thought Form | Less commonly formally assessed in younger children; relevant in adolescents with possible psychosis (loosening of associations, tangentiality) |
| Perceptions | Hallucinations (note: imaginary friends in young children are developmentally normal, not psychotic). True auditory hallucinations in a child are significant and warrant investigation for early-onset psychosis or PTSD-related dissociation |
| Cognition | Orientation (rarely impaired unless organic cause), attention/concentration (directly observed during interview), memory, estimated intellectual functioning |
| Insight | Age-dependent. A 5-year-old cannot have "insight" in the adult sense. In adolescents, assess understanding of their difficulties and motivation for help |
Imaginary Friends vs Hallucinations
Up to 65% of children aged 3–7 have imaginary friends. These are controlled by the child (the child knows the friend isn't real and can start/stop the interaction at will), serve a developmental function (practicing social skills, processing emotions), and are not distressing. Psychotic hallucinations, by contrast, are involuntary, perceived as external and real, and typically distressing or commanding. Always clarify the phenomenology carefully.
Psychological measures, e.g., intelligence tests, social and other developmental assessment tools are a key adjunct. [1]
| Category | Examples | When to Use |
|---|---|---|
| Intelligence/Cognitive | Wechsler Intelligence Scale for Children (WISC-V), Stanford-Binet | Suspected intellectual disability, uneven cognitive profile (e.g., in specific learning disorders) |
| Developmental | Bayley Scales of Infant Development, Griffiths Scales | Infants/toddlers with suspected developmental delay |
| ASD-specific | Autism Diagnostic Observation Schedule (ADOS-2), Autism Diagnostic Interview-Revised (ADI-R), M-CHAT (screening) | Suspected ASD |
| ADHD-specific | Conners Rating Scales, Vanderbilt ADHD Diagnostic Rating Scale | Suspected ADHD — obtains separate parent and teacher ratings |
| Behavioural/Emotional | Child Behavior Checklist (CBCL), Strengths and Difficulties Questionnaire (SDQ) | Broad screening for emotional/behavioural problems |
| Mood | Children's Depression Inventory (CDI), Screen for Child Anxiety Related Disorders (SCARED), PHQ-A | Suspected mood/anxiety disorders |
| Adaptive functioning | Vineland Adaptive Behavior Scales | Required for diagnosis of intellectual disability (must have impaired adaptive functioning AND low IQ) |
| Family/Environmental | Family Assessment Device, Parenting Stress Index | Assessment of family functioning and parenting stress |
Rating Scales Are Not Diagnoses
Diagnosis should still be based on structured interview and collateral information only (rating is for reference only). [1] A high score on the SDQ or Conners tells you there's a concern — it does not make a diagnosis. Many conditions share symptom profiles on rating scales (e.g., anxiety and ADHD both score high on inattention items).
Collateral from school: academic performance, behaviour in classroom, relationship with other classmates. [1]
Why school is so important:
- Cross-situational consistency: ADHD, by definition, must be present in ≥ 2 settings. A child who is "hyperactive" only at home but fine at school may have a behavioural/parenting issue rather than ADHD.
- Academic trajectory: A sudden drop in grades may signal depression, substance use, or psychosis. A longstanding pattern of underperformance may suggest specific learning disorder or intellectual disability.
- Peer relationships: Social difficulties reported by teachers may be the first clue to ASD (especially in girls who mask in clinical settings).
- Behavioural observations: Teachers see the child in a structured environment for 6–8 hours a day — far more observation time than any clinician gets.
Other collateral sources:
- Social worker reports (family circumstances, child protection concerns)
- Previous medical records (past assessments, investigations, diagnoses)
- Other professionals (speech therapist, occupational therapist, educational psychologist)
9. Physical Examination and Investigations
Many psychiatric presentations in children have organic underpinnings or mimics:
| Organic Condition | Psychiatric Mimic |
|---|---|
| Hearing impairment | Inattention (mimics ADHD), social withdrawal (mimics ASD), language delay |
| Epilepsy (especially absence seizures) | "Daydreaming" and inattention (mimics ADHD) |
| Thyroid dysfunction | Hypothyroidism → depression, fatigue; Hyperthyroidism → anxiety, restlessness |
| Iron deficiency anaemia | Fatigue, poor concentration, restless legs (mimics ADHD) |
| Lead poisoning | Behavioural problems, developmental regression |
| Genetic syndromes | Fragile X (ASD features, intellectual disability), 22q11 deletion (psychosis risk), Williams syndrome (hypersociability), Prader-Willi (overeating) |
| Obstructive sleep apnoea | Daytime hyperactivity, inattention, poor academic performance (mimics ADHD) |
| Brain tumour | Personality change, headache, new-onset seizures |
- Growth parameters: Height, weight, head circumference (plot on growth charts — child growth and development [2])
- Microcephaly → consider genetic/metabolic causes
- Short stature → consider Turner syndrome, growth hormone deficiency, neglect
- Obesity → consider Prader-Willi, hypothyroidism, medication effects
- Dysmorphology screen: Minor physical anomalies (facial features, hand creases, ear shape) — may suggest genetic syndrome
- Neurological examination: Tone, reflexes, coordination (cerebellar signs), cranial nerves, gait
- Signs suggestive of neurodevelopmental impairment/delay, e.g., clumsiness, language delay, abnormalities of speech [1]
- Neurological "soft signs" (mild motor coordination difficulties, mirror movements) are more common in ADHD and ASD
- Skin: Café-au-lait spots (neurofibromatosis), ash-leaf macules (tuberous sclerosis — associated with ASD and epilepsy), bruising in unusual locations (non-accidental injury)
- Hearing and vision: Basic screening; formal audiometry and ophthalmology referral if indicated
| Investigation | Indication |
|---|---|
| TFTs | Mood changes, weight changes, lethargy, hyperactivity |
| CBP, ferritin | Fatigue, pica, restless legs |
| Lead level | Developmental regression, pica, high-risk environment |
| Chromosomal microarray / karyotype | Intellectual disability, multiple congenital anomalies, ASD with dysmorphic features |
| Fragile X testing | Males with intellectual disability ± ASD features |
| Metabolic screen | Developmental regression, unexplained neurological deterioration |
| EEG | Suspected seizures, staring spells, developmental regression |
| MRI Brain | Focal neurological signs, developmental regression, microcephaly/macrocephaly |
Paediatric history taking follows a structured approach that parallels but extends adult history taking [2]:
Key components specific to paediatric history: [2]
- Birth history (antenatal, perinatal, postnatal)
- Feeding history (breast/bottle, weaning, current diet)
- Developmental history (milestones in all four domains)
- Immunisation history
- Growth history (weight, height, head circumference — plotted on centile charts)
- Schooling and education
- Family and social history (including genogram)
In paediatric history taking, always approach the child in a developmentally appropriate manner and build rapport before diving into sensitive topics. [2]
11. Ethical and Legal Considerations [3]
Consent and refusal of treatment in child psychiatry raises unique ethical challenges [3]:
- Age of consent: In Hong Kong, patients aged ≥ 18 can give independent consent. For those < 18, parental/guardian consent is generally required.
- Gillick competence / "mature minor" doctrine: A child under 16 who demonstrates sufficient understanding and intelligence to fully appreciate the nature, purpose, and consequences of a proposed treatment may be considered competent to consent. This is assessed on a case-by-case basis. [3]
- Assent: Even when parental consent is obtained, the child's assent (agreement/cooperation) should be sought in a developmentally appropriate way. This respects the child's emerging autonomy.
Why should I be locked up? Ethics in psychiatry. [3]
- In Hong Kong, the Mental Health Ordinance (Cap. 136) governs involuntary detention and treatment.
- For minors: Parental consent can authorise voluntary admission. If the child/adolescent or parents refuse treatment but the clinical team believes the patient poses a significant risk to themselves or others, involuntary procedures may be initiated.
- Ethical principles [3]:
- Autonomy: Respect the developing autonomy of the child while balancing protective obligations
- Beneficence: Acting in the child's best interest
- Non-maleficence: Avoiding harm (including harm from unnecessary detention or forced treatment)
- Justice: Fair allocation of resources and equitable treatment
Confidentiality with Adolescents
Confidentiality is important, but risky behaviour (e.g., self-harm, harming others) should be reported. [1] Be transparent about this from the start: "What you say stays between us unless I'm worried you or someone else could get hurt." This is both ethical and practical — it maintains trust while keeping the adolescent safe.
- In Hong Kong, suspected child abuse must be reported to the Social Welfare Department and handled through the Multi-disciplinary Case Conference on Protection of Child with Suspected Abuse (MDCC) framework.
- Types of abuse: physical, sexual, emotional, neglect
- During assessment, be alert for:
- Unexplained injuries, especially in unusual locations
- Inconsistent history between child and parent
- Premature sexualising behaviour (in sexual abuse) [1]
- Fearfulness around specific carers
- Excessive compliance or frozen watchfulness
12. Formulation in Child Psychiatry
The formulation is the intellectual synthesis — the "so what?" of all the data you've gathered. It follows the same structure as adult psychiatry but with developmental emphasis:
| Component | Content |
|---|---|
| Summary | Brief demographic and clinical description (age, gender, presenting complaint, duration) |
| Provisional diagnosis | Most likely diagnosis based on clinical features and diagnostic criteria |
| Differential diagnosis | Other conditions to consider |
| Aetiology | Predisposing (genetics, temperament, early adversity, developmental vulnerabilities), Precipitating (life events, school transition, family change, trauma), Perpetuating (ongoing family dysfunction, untreated comorbidity, lack of support), Protective (strengths, good peer relationships, caring family) — using a biopsychosocial framework |
| Management plan | Short-term and long-term, biological/psychological/social interventions, school liaison, family work, risk management |
| Prognosis | Based on nature of disorder, severity, protective/risk factors |
| Factor | Biological | Psychological | Social |
|---|---|---|---|
| Predisposing | Genetic loading, prenatal insults, neurodevelopmental delay | Difficult temperament, insecure attachment, low self-esteem | Poverty, parental mental illness, family dysfunction |
| Precipitating | Acute illness, medication change, head injury | Bullying, exam pressure, identity crisis | School transition, parental separation, bereavement |
| Perpetuating | Untreated medical condition, ongoing substance use | Cognitive distortions, avoidant coping, secondary gain | Ongoing family conflict, inadequate school support, peer rejection |
| Protective | Normal intelligence, good physical health | Resilient personality, good coping skills, secure attachment | Supportive family, good school, positive peer group |
13. Special Considerations for Assessment in the Hong Kong Context
- Academic pressure: Hong Kong's highly competitive education system is a significant stressor. Children may present with anxiety, somatic complaints, or school refusal related to exam stress.
- Stigma: Mental health stigma remains significant in Chinese culture. Families may present late, minimise symptoms, or prefer somatic framings ("headache" rather than "depression").
- Language: Assessment may need to be conducted in Cantonese, Mandarin, or English depending on the family background. Interpreter use introduces additional complexity.
- Domestic helpers: Many HK children are primarily cared for by domestic helpers. The attachment dynamics and caregiving consistency must be explored.
- Small living spaces: Hong Kong's tiny apartments mean families live in extremely close proximity, which can exacerbate family conflict and reduce the child's private space.
- MCHC (Maternal and Child Health Centre) → developmental screening
- Child Assessment Centre (CAC) under Department of Health → comprehensive developmental assessment for children < 12
- CAMHS (Child and Adolescent Mental Health Service) under Hospital Authority → psychiatric assessment and treatment
- School-based services: Educational psychologists, school social workers
- NGOs: e.g., Caritas, Boys' and Girls' Clubs Association, HKFYG — provide counselling and support
14. Assessment of Specific Domains During Interview [1]
During the interview, get an impression of how difficult the child is and how good the parenting is: [1]
- Overall compliance to parents' commands: [1]
- Temper: [1]
- Symptom screening: ODD symptoms first → screen CD symptoms if ODD symptoms present [1] — This reflects the developmental progression: ODD often precedes CD, and early identification of ODD is an opportunity for intervention before it escalates.
The content of childhood anxiety is influenced by developmental stage [1]:
- Infants: fear of strangers → social anxiety disorder of childhood
- Preschool: fear of separation, specific objects → separation anxiety and phobic anxiety disorders
- Early adolescence: fear of social situations/personal adequacy → social phobia
- Late adolescence: resembles adult → GAD, panic disorders
Key point: Anxiety and fears can be developmentally appropriate. Diagnose only when developmentally inappropriate (more severe and prolonged than usual) AND causes significant distress + functional impairment. [1]
Childhood depression may present differently from adults:
- Somatic complaints (unexplained abdominal pain, headache, anorexia, enuresis) [1]
- Irritable mood and anxiety features (rather than classic sadness) [1]
- Behavioural problems [1]
- Always screen for suicidality — even in young children (suicidal ideation can occur from age 6+)
- Note: ~25% of bipolar affective disorder first presented as juvenile depression in their first episode [1] — this is why longitudinal follow-up is essential
Risk assessment in children follows similar principles to adults but with specific considerations:
| Risk Domain | Child-Specific Considerations |
|---|---|
| Risk to self | Self-harm (increasingly common from age 10+), suicidal ideation, suicide attempts. Methods may include cutting, overdose, jumping. Screen for online pro-self-harm content |
| Risk to others | Aggression, violence, fire-setting, sexual harmful behaviour (in conduct disorder or after sexual abuse). Animal cruelty is a red flag for severe CD |
| Risk from others | Abuse, neglect, exploitation, bullying, online grooming — the child may be a victim as well as (or instead of) a perpetrator |
| Vulnerability | Self-neglect, wandering (in ASD/ID), exploitation by peers (in ID) |
High Yield Summary
Assessment in Child Psychiatry — Key Principles:
- Multi-informant: Always interview parents, child (alone), and family together. Obtain school collateral.
- Developmentally contextualised: Compare symptoms to same-age, same-culture norms. Use age-appropriate interview techniques.
- Developmental history is essential: Full pregnancy/birth history, milestones (gross motor, fine motor, language, social), temperament.
- Systematic comorbidity screen: ADHD, ASD, ODD/CD, mood, anxiety, eating, sleeping, elimination — child psychiatric conditions rarely come alone.
- MSE is modified for children: Observe play, activity level, eye contact, separation behaviour; imaginary friends ≠ hallucinations.
- Rating scales supplement but do not replace clinical interview.
- Physical examination and investigations are essential to exclude organic mimics (hearing loss, epilepsy, thyroid, genetic syndromes).
- Risk assessment includes risk to self, to others, FROM others (abuse/neglect), and vulnerability.
- Formulation uses the 4 P's (predisposing, precipitating, perpetuating, protective) in a biopsychosocial framework.
- Ethical considerations: Consent requires parental involvement for < 18; Gillick competence for mature minors; confidentiality limits must be stated upfront; safeguarding is paramount.
- Hong Kong context: Academic pressure, stigma, MCHC → CAC → CAMHS referral pathways, domestic helper caregiving dynamics.
Active Recall - Assessment in Child Psychiatry
[1] Senior notes: ryanho-psych.md (Chapter 12: Child Psychiatry, sections 12.1, 12.5) [2] Lecture slides: CFB (PAE01) Paediatric history taking.pdf; CFB (PAE02) Child growth and development.pdf [3] Lecture slides: GC 173. Why should I be locked up Ethics in psychiatry, Consent and Refusal in Treatment.pdf
Differential Diagnosis in Child Psychiatric Assessment
When a child or adolescent is brought for psychiatric assessment, the presenting complaint is almost never pathognomonic for a single condition. Children present with behaviours (aggression, school refusal, poor concentration) and symptoms (sadness, worry, odd behaviour) that sit at the intersection of multiple possible diagnoses. Your job during the differential diagnosis process is to systematically consider, weigh, and discriminate between these possibilities.
The outcomes of history taking include: formulate and prioritize differential diagnoses; exclude the less likely differential diagnoses; ascertain severity of the problems and their impact on child and family. [4]
- Developmental overlap: Many "symptoms" are normal at certain ages (e.g., tantrums at 2, imaginary friends at 4, mood swings in early adolescence). The question is always: is this beyond what is developmentally appropriate? [1]
- High comorbidity: Child psychiatric disorders are spectacularly comorbid. ADHD + ODD occurs in ~40–60% of cases; 70% of youth depression has comorbid anxiety; ASD frequently co-occurs with ADHD (30–50%) and intellectual disability [1]. You don't just pick one diagnosis — you often need to diagnose several.
- Limited self-report: Young children can't tell you "I have intrusive thoughts" or "I feel anhedonia." You rely on behavioural observation and informant reports, which are inherently less specific.
- Phenotypic convergence: Different underlying conditions can produce identical surface behaviours. A child who "can't sit still" might have ADHD, anxiety, mania, ASD, trauma-related hyperarousal, hyperthyroidism, or simply be in an understimulating classroom.
The Golden Rule of Child Psychiatric DDx
Always ask: "Could this presentation be explained by a different condition, a combination of conditions, or a normal developmental variant?" Never anchor on the first diagnosis that comes to mind. The referral label (e.g., "query ADHD") is a hypothesis, not a conclusion.
The approach to DDx in child psychiatry can be organised by presenting complaint — because that is what you actually encounter clinically. Below, I present the major presenting complaint clusters with their differential diagnoses, the key distinguishing features, and the pathophysiological reasoning behind each distinction.
This is one of the commonest referral reasons. The child "can't concentrate," "is always on the go," "won't listen," or "is disruptive in class."
| Differential Diagnosis | Key Distinguishing Features | Pathophysiological Basis for Distinction |
|---|---|---|
| ADHD | Pervasive (present in ≥ 2 settings), onset before age 12, chronic trait-like course. Core triad: inattention, hyperactivity, impulsivity. [1] | Fronto-striatal dopamine/noradrenaline hypoactivity → deficits in executive function (working memory, inhibition, planning). The symptoms are endogenous and stable, not situation-dependent |
| ODD | Negativity, hostility, defiance — resists work because of refusal to conform, not because of inability to sustain attention. Can co-occur with ADHD. [1] | Hypothesised to involve disrupted reward processing and impaired emotion regulation circuits (amygdala–OFC). The behaviour is volitional opposition, not cognitive inability |
| Conduct Disorder (CD) | More severe antisocial behaviours: aggression, stealing, truancy, delinquency, fire-setting. Violation of societal rules and the rights of others [1] | Callous-unemotional traits linked to reduced amygdala reactivity to distress cues. Distinguished from ADHD by the intentional, antisocial nature of the acts |
| Learning disorder / Intellectual disability | Inattention is not pervasive — only during academic tasks. May appear inattentive from frustration, lack of interest, or limited cognitive ability. [1] Gifted children may also seem disruptive if under-stimulated | The "inattention" is secondary to task–ability mismatch, not a primary attentional deficit. Once the child is engaged in something within their ability range, attention is normal |
| ASD | May show inattention and social dysfunction, but these arise from poor social skills and restricted interests rather than impulsivity and poor self-control. Normal imaginary play absent; pragmatic language often impaired. [1] | Atypical connectivity in social brain networks (superior temporal sulcus, mirror neuron system, medial PFC). "Inattention" reflects lack of social motivation rather than dopaminergic executive dysfunction |
| Anxiety disorders | Can appear distracted, but distraction is due to worrying themes (e.g., "What if mum doesn't pick me up?"), not external stimuli or novelty-seeking. [1] | Amygdala hyperactivation and threat-monitoring bias consume attentional resources, producing anxiety-driven inattention that mimics ADHD |
| Depression | Diminished concentration, poor motivation, indecisiveness — but these emerge only during depressive episodes when mood is low. Later onset, episodic course. [1] | Prefrontal hypofunction in depression affects executive and attentional function, but it is state-dependent (present only during episode), unlike the trait-like pattern of ADHD |
| Bipolar affective disorder (BAD) | Distractibility, impulsivity, talkativeness overlap with ADHD, but in BAD these are episodic and accompanied by elated mood, grandiosity, decreased need for sleep. [1] [5] | Mania involves widespread monoaminergic overactivity (especially dopamine in mesolimbic circuits), producing episodic bursts of disinhibited behaviour — contrast with chronic fronto-striatal hypofunction in ADHD |
| Substance use | ADHD-like symptoms occur only in the context of substance use — episodic, temporally linked to intoxication/withdrawal [1] | Stimulants, cannabis, and alcohol all disrupt prefrontal executive function, but the effect is pharmacologically mediated and time-limited |
| Hearing impairment | "Doesn't listen," poor language, appears inattentive — but responds normally to visual cues, and inattention resolves when communication modality is changed (e.g., written instructions) | Conductive or sensorineural hearing loss prevents auditory input from reaching cortical processing centres — not an attentional deficit per se |
| Absence epilepsy | Brief "staring spells" (typically 5–15 seconds), abrupt onset/offset, may occur many times daily. Not associated with hyperactivity or impulsivity. EEG shows 3 Hz spike-and-wave | Generalised thalamocortical hypersynchrony produces transient loss of consciousness — distinct from the sustained inattention of ADHD |
| Obstructive sleep apnoea | Daytime hyperactivity and inattention secondary to poor sleep quality. Look for snoring, mouth breathing, restless sleep, tonsillar hypertrophy | Fragmented sleep → daytime sleepiness → compensatory hyperactivity (paradoxical response in children, unlike adults who become somnolent) |
ADHD vs Bipolar in Children
Misdiagnosis is very common → correct diagnosis and treatment often delayed by 5–7 years on average. [5] ~25% of BAD first presented as juvenile depression in their first episode. [1] ADHD is chronic and trait-like; BAD is episodic. ADHD does NOT feature grandiosity, decreased need for sleep, or flight of ideas. If you see episodic clusters of disinhibition with mood change, think BAD. Requires informants and collateral information (e.g., medical record) to confirm past history of mania/hypomania. [5]
The child "doesn't have friends," "is in their own world," "behaves strangely."
| Differential Diagnosis | Key Distinguishing Features | Pathophysiological Basis |
|---|---|---|
| ASD | Persistent deficits in social communication + restricted, repetitive behaviours/interests. Onset in early developmental period. Social impairment is qualitative (not just quantitative) — deficits in reciprocity, non-verbal communication, and relationship development [1] | Atypical neural connectivity in the "social brain" (fusiform gyrus, amygdala, superior temporal sulcus, medial PFC) → impaired social cognition, theory of mind, and pragmatic language |
| ID / GDD | May have poor social skills, but these are developmentally appropriate for their cognitive level. Communication efforts are proportional to cognitive ability. No restricted/repetitive behaviours. [1] | Global neurodevelopmental impairment affects all domains proportionally. Social difficulty is a consequence of overall cognitive limitation, not a selective social-communication deficit |
| Language disorder | Difficulty with verbal communication, but normal non-verbal communication, normal social reciprocity, normal desire to communicate, appropriate imaginative play. No restricted/repetitive behaviours. [1] | Impairment is specifically in language production/comprehension circuits (Broca's/Wernicke's areas), while social cognition networks remain intact |
| Hearing impairment | Distinguished by normal social reciprocity, imaginative play, normal eye contact and facial expressions indicative of intention to communicate. [1] | Peripheral sensory deficit, not a central social-cognitive deficit. The child wants to interact but can't hear |
| Social anxiety disorder | Child desires social contact but is fearful of it — avoidance is driven by anxiety, not lack of interest. Has appropriate social skills when comfortable (e.g., with family) | Amygdala hyperreactivity to social threat cues → avoidance behaviour. Preserved social cognition (they understand social rules, they're just afraid of failing at them) |
| Selective mutism | Speaks normally in some settings (typically home) but not in others (typically school). Social anxiety is usually the underlying mechanism | Extreme social anxiety produces speech inhibition in specific contexts, not a global social-communication deficit |
| Schizophrenia (prodrome) | Social impairment and atypical interests/beliefs may resemble ASD. But look for positive symptoms of psychosis (delusions, hallucinations) and deterioration from a previous level of functioning [1] | Dopaminergic dysregulation (mesolimbic excess → positive symptoms; mesocortical deficit → negative symptoms). The social withdrawal is part of the negative symptom complex and represents loss of previously normal function |
| Reactive attachment disorder (RAD) | Results from severe early neglect/deprivation. Child shows emotionally withdrawn, inhibited behaviour with caregivers. Social deficits improve with appropriate caregiving environment | Disrupted attachment formation due to inadequate early caregiving → failure to develop normal social-emotional regulatory circuits. Distinguishable from ASD by history of deprivation and potential for improvement with environmental change |
| OCD | Behavioural features may overlap (repetitive behaviours), but in OCD these are experienced as distressing (ego-dystonic), whereas in ASD they are not. Social and communication skills usually normal in OCD [1] | OCD involves cortico-striato-thalamic loop dysfunction producing intrusive thoughts and compulsive responses. The repetitive behaviours serve to reduce anxiety, not to provide sensory satisfaction |
| Tic disorder / Stereotypic movement disorder | Repetitive purposeless motor behaviour but normal social, language, and communication skills [1] | Basal ganglia dysfunction produces involuntary movements, but social brain circuits are intact |
The child won't go to school, complains of headaches/stomachaches, seems worried all the time.
| Differential Diagnosis | Key Distinguishing Features | Developmental Context |
|---|---|---|
| Separation anxiety disorder (SAD) | Excessive fear of separation from attachment figures. May present with psychosomatic complaints (stomachache before school) [1]. Content is specifically about loss/harm to attachment figure | Developmentally normal in toddlers/preschool; pathological when persistent and severe beyond age 6–7 |
| Social phobia | Fear of social evaluation and humiliation. Anxiety is focused on peer/teacher interactions, not on separation from parents | Emerges in early adolescence when social awareness and self-consciousness peak |
| Specific phobia | Fear of specific objects or situations (animals, blood, heights). Avoidance is limited to the phobic stimulus | Preschool/early childhood onset typical for animal/natural environment type |
| GAD | Excessive, uncontrollable worry about multiple domains — school, health, family, future. Unlike OCD, worries are about real-life concerns (not odd/magical beliefs) [1] | Late adolescence onset; resembles adult GAD |
| Panic disorder | Recurrent unexpected panic attacks with anticipatory anxiety about further attacks. Uncommon before puberty | Late adolescence; distinguished by the unexpected nature of the attacks (not cued by specific situations) |
| OCD | Intrusive thoughts (obsessions) that are ego-dystonic + rituals (compulsions) performed to reduce anxiety. Content may be contamination, harm, symmetry. Ruminations are odd, irrational, or magical [1] | Can present from age 6+; tic-related OCD especially in boys |
| Depression | School refusal + somatic complaints + withdrawal may be the presenting features. Look for irritable mood (may replace sadness in children), anhedonia, sleep/appetite changes [1] | In childhood: somatic complaints predominate. In adolescence: more adult-like features |
| PTSD | Anxiety symptoms are temporally linked to a traumatic event. Re-experiencing (nightmares, flashbacks), avoidance of reminders, hyperarousal [1] | Can occur at any age; look for history of trauma (abuse, accident, witnessing violence) |
| Medical conditions | Hyperthyroidism (anxiety, tremor, weight loss, tachycardia), arrhythmias (palpitations mistaken for panic), neurological disease, substance-induced anxiety (caffeine, drugs) [1] | Always exclude organic causes before concluding a primary psychiatric diagnosis |
| Adjustment disorder | Anxiety develops within 3 months of an identifiable stressor, does not meet full criteria for another specific disorder, and typically resolves within 6 months of stressor cessation [1] | Common after school transitions, family upheaval, bereavement |
| Somatic symptom disorder | Physical symptoms with excessive thoughts, feelings, or behaviours related to the symptoms. Distinguished by the disproportionate preoccupation with somatic complaints beyond what is expected [1] | May present at any age; look for alexithymia and developmental history of poor emotional awareness |
School Refusal Is Not a Diagnosis
School refusal is a behaviour, not a diagnosis. It is the final common pathway of many conditions — separation anxiety, social phobia, depression, bullying, ASD (sensory overload), specific learning disorder (academic frustration), or even truancy in CD (but truancy is about doing something more appealing, whereas anxious school refusal is about avoiding something frightening). Always ask: "What is driving this child away from school?"
| Differential Diagnosis | Key Distinguishing Features |
|---|---|
| Major Depressive Disorder | Core symptoms of low mood/anhedonia ≥ 2 weeks + additional symptoms. In children: irritable mood and somatic complaints may predominate [1] |
| Bipolar Affective Disorder | Hypomanic episodes are often overlooked. Patients with BP II are misdiagnosed as having major depressive disorder. [5] Look for episodic mood elevation, decreased sleep need, grandiosity. ~25% of BAD first presented as juvenile depression. [1] |
| Dysthymia | Chronic low-grade depressive symptoms not meeting full MDD criteria, lasting ≥ 2 years. May have "double depression" (dysthymia + superimposed MDD episodes) [1] |
| Adjustment disorder with depressed mood | Depressive symptoms temporally linked to a stressor, not meeting full MDD criteria [1] |
| Anxiety disorders | Anxiety and depression are highly comorbid in children (70% overlap). Distinguish which is primary by temporal sequence and predominant symptoms [1] |
| Substance use disorder | Substance-induced mood changes should resolve with cessation of use. Screen all adolescents |
| Medical conditions | Hypothyroidism, anaemia, chronic fatigue syndrome, epilepsy, autoimmune conditions (SLE), medications (corticosteroids, isotretinoin) |
| Bereavement / Grief | Normal grief can resemble depression but typically preserves self-esteem and is focused on the lost person. Prolonged grief disorder if symptoms persist beyond culturally normative period with functional impairment |
| Personality disorder (emerging) | BPD may present with affective instability, self-harm, identity disturbance in adolescents. Rapid mood shifts (hours/days) triggered by interpersonal issues distinguish from BAD (episodic, days-weeks, not necessarily interpersonally triggered) [1] |
Rare in pre-pubertal children, but important to consider in adolescents.
| Differential Diagnosis | Key Distinguishing Features |
|---|---|
| Early-onset schizophrenia | Onset before age 18 (very rare before 13). Positive symptoms (delusions, hallucinations) + negative symptoms (social withdrawal, flat affect, avolition) + cognitive decline. Must distinguish from normal childhood fantasy |
| Bipolar disorder with psychotic features | Manic episode with psychotic symptoms may be misdiagnosed as schizophrenia. [5] Psychotic symptoms change quickly in content and seldom outlast mood disruption in BAD [1] |
| ASD | "Odd beliefs" may actually be restricted interests expressed with unusual intensity. Social oddness reflects social-cognitive deficit, not psychosis. No hallucinations or formal thought disorder |
| PTSD with dissociative features | Flashbacks may be mistaken for hallucinations; hypervigilance may seem paranoid. Trauma history is key |
| OCD with poor insight | Obsessional beliefs may approach delusional intensity (overvalued ideas). Distinguished by preservation of other cognitive functions and absence of formal thought disorder |
| Substance-induced psychosis | Cannabis, especially high-potency forms, can induce psychotic episodes in adolescents. Should resolve with cessation |
| Organic causes | Anti-NMDA receptor encephalitis, Wilson's disease, temporal lobe epilepsy, brain tumour, metabolic disorders — always consider in first-episode psychosis |
The differential diagnosis of a manic episode includes: [5]
- Depressive disorder with irritability and anxious distress [5] — Irritable depression can mimic the irritable variant of mania. Key distinguisher: in mania, there is also ↑energy, grandiosity, ↓need for sleep; in depression, energy is typically ↓
- Psychotic disorder or schizoaffective disorder [5] — Schizophrenia is the hardest to distinguish from mania [1]. In mania, psychotic symptoms change quickly and resolve with mood normalisation
- Substance/medication-induced/medical conditions [5] — e.g., stimulant use, corticosteroids, hyperthyroidism
- Attention deficit and hyperactivity disorder [5] — ADHD is chronic/trait-like; mania is episodic. ADHD should NOT feature ↑self-esteem, grandiosity, flight of ideas, ↓need for sleep [1]
- Personality disorder with prominent irritability [5] — Especially BPD. Mood shifts are rapid (hours), interpersonally triggered, without classic manic symptoms [1]
Overdiagnosis of bipolar disorder can occur due to incorrect understanding of the term "manic" ("躁"). [5] Among 180 outpatients previously diagnosed with bipolar disorder, structured interview could not confirm the diagnosis in 43 (33%) of them. [5] In another study, only 43% of 145 patients with a previous diagnosis of bipolar disorder had the condition confirmed by structured interview (retrospective recall can be inaccurate). [5] It is important to follow diagnostic criteria in making psychiatric diagnosis. [5]
Underdiagnosis also occurs: hypomanic episodes are often overlooked, and patients with BP II are misdiagnosed as having major depressive disorder. Manic episodes with psychotic symptoms are misdiagnosed as schizophrenia. [5] Correct diagnosis and treatment was delayed by 5–7 years on average. [5]
The following flowchart guides the clinician through the DDx process when a child presents with a common symptom cluster:
Key Cross-Cutting Principles for DDx in Children
In adult psychiatry, you often aim for a single parsimonious diagnosis. In child psychiatry, you should expect comorbidity:
- ADHD + ODD: ~40–60%
- ADHD + ASD: ~30–50% [1]
- Depression + Anxiety: ~70% [1]
- ASD + Intellectual Disability: ~30–50%
- CD + Substance Use: very common in adolescents
When conditions co-occur, diagnose all that meet criteria. Don't force a single label.
The same underlying disorder presents differently depending on the child's developmental stage:
| Condition | Younger Child Presentation | Adolescent Presentation |
|---|---|---|
| Depression | Somatic complaints, irritability, behavioural problems [1] | More adult-like: sadness, anhedonia, suicidality |
| Anxiety | Separation anxiety, specific phobias, somatic complaints [1] | Social phobia, GAD, panic disorder [1] |
| Bipolar | Very rare; may present as extreme irritability, behavioural outbursts | More classic manic/depressive episodes |
| OCD | Rituals around bedtime, food, parents; poor insight | Clearer obsessions/compulsions, better verbalisation |
| Psychosis | Extremely rare; may be mistaken for developmental disorder | Prodromal symptoms, then positive/negative symptoms |
For every child psychiatric presentation, maintain a low threshold for organic workup:
| Psychiatric Presentation | Consider Organic |
|---|---|
| Inattention | Hearing loss, absence epilepsy, iron deficiency, OSA, thyroid |
| Developmental regression | Metabolic disorders, epileptic encephalopathy, Rett syndrome |
| First-episode psychosis | Anti-NMDA receptor encephalitis, Wilson's disease, TLE, substance use, brain tumour |
| New-onset mood change | Thyroid, Cushing's, medications, substance use, SLE |
| Anxiety with autonomic features | Thyrotoxicosis, phaeochromocytoma, hypoglycaemia, arrhythmia [1] |
This is an elegant clinical shortcut from the senior notes:
- Worry about gaining weight → eating disorder
- Worry about having a serious illness → hypochondriacal disorder / illness anxiety
- Fear of being poisoned or killed → delusional beliefs (paranoid schizophrenia)
- Ruminatory thoughts of guilt or worthlessness → depression
- Associated with obsessional thoughts or resisting compulsion → OCD
- Separation or abandonment → separation anxiety, borderline/dependent PD
- Being rejected or inadequate → avoidant PD, social phobia [1]
High Yield Summary
Differential Diagnosis in Child Psychiatric Assessment — Key Points:
- Always exclude organic causes first — hearing loss, epilepsy, thyroid, anaemia, genetic syndromes, sleep disorders, substance use.
- Compare to developmental norms — a behaviour is only a symptom if it exceeds what is expected for age and culture.
- Comorbidity is the rule — expect and diagnose multiple conditions when criteria are met (ADHD+ODD, depression+anxiety, ASD+ID).
- Inattentive child DDx: ADHD (pervasive, chronic) vs learning disorder (academic only) vs anxiety (worry-driven) vs depression (episodic) vs BAD (episodic with mood change) vs ASD (poor social skills, restricted interests) vs organic (hearing, epilepsy, OSA).
- Socially odd child DDx: ASD (qualitative social deficit + restricted behaviours) vs ID (proportional delay) vs language disorder (normal non-verbal communication) vs social anxiety (desires but fears interaction) vs schizophrenia prodrome (deterioration from baseline + psychotic features).
- Bipolar DDx pitfalls: Underdiagnosed (hypomania missed → labelled as MDD) AND overdiagnosed (incorrect use of "manic"/"躁"). Correct diagnosis delayed 5–7 years on average. Follow diagnostic criteria strictly; use collateral information.
- ADHD vs BAD: ADHD is chronic/trait-like; BAD is episodic. ADHD lacks grandiosity, ↓sleep need, flight of ideas.
- School refusal is a behaviour, not a diagnosis — systematically consider separation anxiety, social phobia, depression, bullying, ASD, specific learning disorder, or conduct-related truancy.
- Note the theme of anxiety to guide DDx (weight → eating disorder, illness → hypochondriasis, intrusive thoughts → OCD, separation → SAD/BPD, rejection → social phobia/avoidant PD).
Active Recall - Differential Diagnosis in Child Psychiatry
References
[1] Senior notes: ryanho-psych.md (Chapter 12: Child Psychiatry, sections 12.1, 12.2, 12.3, 12.4, 12.5; Chapter 7: Mood Disorders; Chapter 8: Anxiety Disorders) [4] Lecture slides: CFB (PAE01) Paediatric history taking.pdf (p22, Box 2.2 Outcomes of History Taking) [5] Lecture slides: GC 163. I am a superman Bipolar disorder.pdf (p10, p12, p13)
Diagnostic Criteria, Diagnostic Algorithm, and Investigation Modalities
In adult psychiatry, the patient usually tells you what's wrong and you map their self-report onto diagnostic criteria. In child psychiatry, you're trying to pin a diagnostic label on a moving target — the child's behaviour changes with context, development, and who is watching. This makes rigorous use of diagnostic criteria even more important, because without structured criteria the risk of both over-diagnosis and under-diagnosis is enormous.
It is important to follow diagnostic criteria in making psychiatric diagnosis. [5] Requires informants and collateral information (e.g., medical record) to confirm past history. [5] Among 180 outpatients previously diagnosed with bipolar disorder, structured interview could not confirm the diagnosis in 43 (33%) of them. [5] The lesson: clinical impression alone is insufficient. You must systematically apply criteria.
Diagnostic criteria typically consist of [1]:
- Core (discriminating) symptoms: present in the defined disorder but seldom in others
- Associated (characteristic) symptoms: frequent in the defined disorder but also seen in others
- Minimal duration of symptoms
- Distress or impairment in functioning
- Exclusion criteria
In child psychiatry, there are two additional layers:
- Developmental appropriateness — the symptoms must exceed what is normal for the child's age and culture
- Pervasiveness — for many conditions (especially ADHD), symptoms must be present across multiple settings (home, school, clinic)
A. Diagnostic Criteria for Major Child Psychiatric Conditions
Below are the diagnostic criteria for the conditions most commonly encountered (and examined) in child psychiatry. I present both ICD (ICD-10/ICD-11, the system used in Hong Kong's Hospital Authority) and DSM-5 where relevant, highlighting key differences.
| Feature | ICD-10 — Childhood Autism (F84.0) | DSM-5 — Autism Spectrum Disorder |
|---|---|---|
| Domain A: Social | Qualitative impairments in reciprocal social interaction | Persistent deficits in social communication and social interaction across multiple contexts, manifest by ALL 3 of: (1) Deficits in socio-emotional reciprocity; (2) Deficits in non-verbal communicative behaviours; (3) Deficits in developing, maintaining and understanding relationships [1] |
| Domain B: Restricted behaviours | Restricted, repetitive and stereotyped patterns of behaviour, interests and activities | Restricted, repetitive patterns of behaviour, interests or activities manifest by ≥ 2 of: (1) Stereotyped/repetitive motor movements, use of objects, or speech; (2) Insistence on sameness, inflexible routines; (3) Highly restricted, fixated interests abnormal in intensity or focus; (4) Hyper- or hyporeactivity to sensory input [1] |
| Domain C: Communication | Qualitative impairments in communication (separate domain) | Merged into Domain A (social communication) — language impairment is no longer a separate criterion in DSM-5 [1] |
| Onset | Developmental abnormalities must have been present in the first 3 years | Symptoms must be present in the early developmental period but may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies [1] |
| Functional impact | Implied | Symptoms cause clinically significant impairment in functioning [1] |
| Exclusion | — | Not better explained by ID or GDD. To make comorbid ASD + ID diagnosis, social communication should be below that expected for general developmental level [1] |
| Specifiers | Separate categories (Asperger's, PDD-NOS, etc.) | Single spectrum; specify severity level (1–3), with/without intellectual impairment, with/without language impairment [1] |
Key conceptual difference: DSM-5 collapsed the old ICD-10 triad (social + communication + restricted behaviours) into a dyad (social-communication + restricted behaviours). This reflects the recognition that social interaction and communication are inseparable constructs. DSM-5 also added sensory hyper/hyporeactivity as a criterion — something not explicit in ICD-10 but clinically very important (e.g., covering ears in loud environments, fascination with spinning objects). [1]
ASD Diagnosis in Girls
Girls with ASD frequently "mask" or "camouflage" their social difficulties by mimicking peers. They may have superficially adequate social skills that fool structured assessments. This means the DSM-5 clause — "may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies" — is especially relevant for late-diagnosed females. Always probe beyond surface presentation.
| Feature | ICD-10 — Hyperkinetic Disorder (F90) | DSM-5 — ADHD |
|---|---|---|
| Symptom domains | Requires both inattention + hyperactivity-impulsivity to be present (i.e., combined type only under ICD-10) | Three presentations: (1) Predominantly inattentive; (2) Predominantly hyperactive-impulsive; (3) Combined [1] |
| Inattention | ≥ 6 of 9 inattention symptoms | ≥ 6 of 9 (for < 17 years); ≥ 5 of 9 (for ≥ 17 years) [1] |
| Hyperactivity-Impulsivity | ≥ 3 hyperactivity + ≥ 1 impulsivity symptom | ≥ 6 of 9 hyperactive-impulsive symptoms (for < 17); ≥ 5 (for ≥ 17) [1] |
| Age of onset | Before age 6 years ("before school age") | Several symptoms present prior to age 12 years [1] — DSM-5 raised the threshold from 7 to 12, recognising that inattention-predominant ADHD may not become evident until later academic demands increase |
| Pervasiveness | Must be present across situations | Several symptoms present in ≥ 2 settings [1] |
| Functional impact | Interference with functioning | Clear evidence of interference with or quality of functioning [1] |
| Exclusion | Should not occur during a psychotic episode | Do not occur exclusively during course of psychotic disorder, not better explained by another mental disorder [1] |
DSM-5 Inattention symptoms (need ≥ 6/9) [1]:
- Fails to give close attention to details / makes careless mistakes
- Difficulty sustaining attention in tasks or play
- Does not seem to listen when spoken to directly
- Does not follow through on instructions / fails to finish work
- Difficulty organising tasks and activities
- Avoids tasks requiring sustained mental effort
- Loses things necessary for tasks
- Easily distracted by extraneous stimuli
- Forgetful in daily activities
DSM-5 Hyperactivity-Impulsivity symptoms (need ≥ 6/9) [1]:
- Often fidgets with or taps hands or feet or squirms in seat [1]
- Often leaves seat when remaining seated is expected [1]
- Often runs about or climbs in inappropriate situations [1]
- Often unable to play or engage in leisure activities quietly [1]
- Often "on the go," acting as if "driven by a motor" [1]
- Often talks excessively [1]
- Often blurts out an answer before a question has been completed [1]
- Often has difficulty waiting his or her turn [1]
- Often interrupts or intrudes on others [1]
Why the ICD–DSM difference matters: ICD-10's stricter criteria (requiring both domains + onset < 6) mean it captures a narrower, more severely affected group. DSM-5's broader definition captures the "inattentive" presentation (historically called ADD), which includes many girls and older children who would be missed by ICD-10.
ADHD Diagnosis in the Real World
Associated features include disinhibition in social relationships, recklessness in dangerous situations, impulsive flouting of social rules. [1] However, note that learning disorders and motor clumsiness occur with undue frequency and should be noted separately — they should not be part of the actual diagnosis of hyperkinetic disorder. [1] Many children referred for "ADHD" actually have a primary learning disorder with secondary frustration mimicking inattention.
| Criterion | Details |
|---|---|
| A. Pattern of angry/irritable mood, argumentative/defiant behaviour, or vindictiveness | Lasting ≥ 6 months, with ≥ 4 symptoms from: (1) Often loses temper; (2) Often touchy or easily annoyed; (3) Often angry and resentful; (4) Often argues with authority figures; (5) Often actively defies or refuses to comply with requests or rules; (6) Often deliberately annoys others; (7) Often blames others for mistakes; (8) Has been spiteful or vindictive ≥ 2× in past 6 months |
| B. Disturbance in behaviour | Associated with distress in the individual or others in their immediate social context, OR impacts negatively on social, educational, occupational functioning |
| C. Exclusion | Not exclusively during psychotic, substance use, depressive, or bipolar disorder; does not meet criteria for disruptive mood dysregulation disorder (DMDD) |
| Severity | Mild (1 setting), Moderate (2 settings), Severe (≥ 3 settings) |
Why ODD has three dimensions: Research has shown ODD symptoms cluster into three factors — (1) angry/irritable mood, (2) argumentative/defiant behaviour, (3) vindictiveness — and these predict different outcomes. The angry/irritable cluster predicts emotional disorders (depression, anxiety); the defiant/vindictive cluster predicts conduct disorder. This explains why ODD sits at the crossroads between emotional and behavioural pathology. [1]
| Criterion | Details |
|---|---|
| A. Pattern of behaviour violating rights of others or societal norms | ≥ 3 of 15 criteria in past 12 months (with ≥ 1 in past 6 months), across 4 categories: (1) Aggression to people/animals; (2) Destruction of property; (3) Deceitfulness or theft; (4) Serious violations of rules |
| B. Functional impairment | Clinically significant impairment in social, academic, or occupational functioning |
| C. Age exclusion | If ≥ 18 years, criteria for antisocial personality disorder are not met |
| Specifiers | Childhood-onset type ( ≥ 1 symptom before age 10); Adolescent-onset type (no symptoms before 10); Unspecified onset. Also: with limited prosocial emotions (callous-unemotional traits) |
Why onset type matters: Prognosis is worse for early-onset cases (antisocial behaviour in 40% early-onset cases and only 20% in adolescent-onset cases). [1] Early-onset CD is more strongly associated with neurobiological risk factors (low amygdala reactivity, executive dysfunction), while adolescent-onset CD may be more influenced by peer-group and social factors. [1]
The same ICD-10 and DSM-5 criteria for depressive episode apply in children, with important modifications in presentation:
ICD-10 Depressive Episode [1]:
- At least 2 of 3 core symptoms (Section A): (1) Depressed mood; (2) Loss of interest/enjoyment; (3) Reduced energy
- Plus associated symptoms (Section B): reduced concentration, reduced self-esteem, ideas of guilt, pessimistic thoughts, ideas of self-harm, disturbed sleep, diminished appetite
- Mild: ≥ 2A + ≥ 2B; Moderate: ≥ 2A + ≥ 3B; Severe: all 3A + ≥ 4B [1]
- Duration ≥ 2 weeks
Child-specific considerations:
- In children, irritable mood may substitute for depressed mood (DSM-5 explicitly allows this)
- Somatic complaints (headache, abdominal pain, enuresis) are often the presenting feature rather than expressed sadness [1]
- Weight gain failure (rather than weight loss) may represent appetite disturbance in growing children
Juvenile Depression and Bipolar Risk
~25% of bipolar affective disorder first presented as juvenile depression in their first episode. [1] Hypomanic episodes are often overlooked. Patients with BP II are misdiagnosed as having major depressive disorder. [5] This means: every adolescent presenting with depression must be carefully screened for any past history of elated mood, decreased sleep need, or episodic behavioural change.
Anxiety and fears can be developmentally appropriate. Diagnosis is made only when developmentally inappropriate (more severe and prolonged than usual) AND causes significant distress + functional impairment. [1]
Key criteria for Separation Anxiety Disorder (DSM-5):
- Developmentally inappropriate and excessive anxiety concerning separation from home or attachment figures
- ≥ 3 of 8 symptoms (e.g., recurrent excessive distress when separation occurs/anticipated, worry about losing/harm to attachment figures, reluctance to go out, nightmares, physical symptoms)
- Duration ≥ 4 weeks in children (6 months in adults)
- Clinically significant distress or functional impairment
The diagnostic process in child psychiatry is not a single moment; it unfolds across multiple encounters. Here is the step-by-step algorithm:
Explanation of Each Step
Step 1 — Multi-informant history: As detailed in Part 1. Parents are the primary informants. [4] Observe the interaction between parents/carers and the child. [4] Note the chronology and severity of presenting and associated symptoms, previous consultations, explore concerns of parents and carers, and identify important medical and psychosocial problems. [4]
Step 2 — Mental State Examination: Developmentally adapted MSE. Observe for: sensorium and cognition (level of awareness, language abilities, spatial abilities, motor coordination or clumsiness), thought/perception (delusions, hallucinations, thought disorders), insight. [1]
Step 3 — Developmental appropriateness: Compare to same-age, same-culture norms. This is the uniquely paediatric "filter" — many referrals will be for behaviours that are within normal developmental range. [1]
Step 4 — Standardised instruments: These quantify severity and provide cross-situational data (separate parent and teacher ratings). Standardized behaviour rating scales: more objective but diagnosis should still be based on structured interview and collateral information only (rating is for reference only). [1]
Step 5–6 — Organic exclusion: A critical step. Physical examination and targeted investigations (detailed below). [1]
Step 7 — Systematic criteria application: Map clinical findings onto ICD/DSM criteria. Don't diagnose by gestalt — use the checklist. [5]
Step 8 — Formulation: Formulation: integrated summary/understanding including diagnosis, aetiology, management, and prognosis. [1]
Step 9 — MDT discussion: In Hong Kong's CAMHS, diagnosis is typically confirmed through multidisciplinary review. Day hospital assessment by multidisciplinary team using standardised assessment. [1] This includes psychiatrist, clinical psychologist, educational psychologist, occupational therapist, speech therapist, and medical social worker.
Step 10 — Communication: Explain diagnosis, prognosis, and management plan to the family in developmentally appropriate terms. Address parental guilt, stigma, and misunderstanding.
C. Assessment Protocol by Condition
For efficiency, here is a condition-specific assessment summary showing which tools and assessments are indicated:
| Component | Details | Why |
|---|---|---|
| Clinical interview and assessment | Most important [1]. Multi-informant developmental history with focus on social-communication milestones, restricted interests, sensory behaviours | The core diagnostic act — no instrument replaces clinical judgment |
| Day hospital assessment by MDT using standardised assessment [1] | Child observed across structured and unstructured settings over 1–2 days by multiple professionals simultaneously | Captures behaviour across contexts; reduces single-setting bias |
| ADOS-2 (Autism Diagnostic Observation Schedule) | Semi-structured, standardised observation. Clinician creates social "presses" (opportunities for the child to respond socially) and scores social-communication and restricted/repetitive behaviours | Gold standard observational tool; high sensitivity and specificity when combined with clinical judgment |
| ADI-R (Autism Diagnostic Interview-Revised) | Structured parent interview covering early development and current function in social interaction, communication, and restricted behaviours | Captures developmental trajectory and behaviours not always observable in clinic |
| Education assessment [1] | Academic attainment, learning style, classroom behaviour | Identifies comorbid learning disorders and guides school placement |
| IQ test [1] | WISC-V or equivalent | Determines intellectual functioning; required to specify "with/without intellectual impairment" in DSM-5 and to differentiate ASD from isolated ID |
| OT assessment [1] | Sensory profile, fine motor skills, adaptive daily living skills | Sensory processing differences are a diagnostic criterion in DSM-5; OT assessment quantifies these and guides intervention |
| Speech therapist assessment [1] | Receptive and expressive language, pragmatic language | Language impairment is common (though not required for DSM-5 diagnosis); pragmatic language assessment is especially important for higher-functioning individuals |
| Theory of Mind tests | First-order (Sally-Anne test), second-order false belief tasks [1] | Assesses perspective-taking ability — impaired in ASD. Not diagnostic alone but informative |
| Vineland Adaptive Behavior Scales | Parent/caregiver interview measuring adaptive functioning across communication, daily living, socialisation, motor domains | Required to assess adaptive functioning level; helps determine support needs |
| Component | Details | Why |
|---|---|---|
| Clinical interview | Suspicion: detected at primary care (but not diagnosed). [1] Detailed developmental/behavioural history from parents AND teacher. Focus on onset, pervasiveness, functional impact | Core diagnostic information. Must demonstrate symptoms in ≥ 2 settings |
| Conners Rating Scales / Vanderbilt | Separate parent and teacher versions; quantify inattention, hyperactivity-impulsivity severity | Cross-situational severity quantification; rating discrepancy between home/school is clinically informative |
| SDQ (Strengths and Difficulties Questionnaire) | Brief screening tool with parent, teacher, and self-report versions | Good for initial screening; identifies hyperactivity/inattention, conduct problems, emotional symptoms, peer problems, prosocial behaviour |
| Cognitive/IQ testing | WISC-V | Rules out intellectual disability as primary explanation; identifies processing speed and working memory weaknesses (common cognitive profile in ADHD) |
| Educational assessment | Reading, writing, mathematics attainment | Rules out specific learning disorder (comorbid in ~25%) [1] |
| Continuous Performance Test (CPT) | Computerised test of sustained attention and impulsivity (e.g., TOVA, Conners CPT) | Objective measure of attention; useful adjunct but not diagnostic alone |
| Stepped approach [1] | Mild: advice, support, watchful waiting, offer group parent training. Moderate: refer to specialists at school age for behavioural therapy or medications. Severe: refer to specialists for medications as 1st choice. [1] | Stepped care ensures proportionate response and avoids over-medicalisation of mild cases |
D. Investigation Modalities — Physical Examination and Ancillary Tests
The purpose of investigations in child psychiatry is threefold:
- Exclude organic mimics of psychiatric symptoms
- Identify comorbid medical conditions that modify management
- Establish baseline before pharmacotherapy
Physical examination: only indicated if concern of presence of any genetic or medical disorders. [1] However, in practice, a baseline physical examination (including growth parameters, dysmorphology screen, and neurological examination) is prudent at first assessment.
| Investigation | Key Findings and Interpretation | Why |
|---|---|---|
| Height, weight, BMI (plotted on growth chart) | Baseline growth parameters | Stimulants (methylphenidate, lisdexamfetamine) suppress appetite → can reduce growth velocity. Antipsychotics (risperidone, olanzapine) cause weight gain. You need a baseline to monitor change |
| Blood pressure, heart rate | Hypertension, tachycardia, bradycardia | Stimulants ↑ sympathetic tone → ↑BP/HR. Must exclude pre-existing cardiovascular disease |
| ECG | Long QT interval, arrhythmias | ECG: long QT (lithium, TCA) [1]. Required before starting TCAs, some antipsychotics, atomoxetine (especially with family history of sudden cardiac death or congenital long QT syndrome) |
| Investigation | When to Order | Key Findings and Interpretation |
|---|---|---|
| CBP (Complete Blood Picture) | Fatigue, pallor, pica, suspected nutritional deficiency, pre-medication baseline | ↓Hb (anaemia) — iron deficiency anaemia causes fatigue, poor concentration, restless legs that mimic ADHD. ↑MCV (macrocytosis) — suggests B12/folate deficiency or maternal alcohol exposure. ↑WBC — infection as cause of behavioural change [1] |
| Ferritin | Restless legs, pica, suspected iron deficiency | Ferritin < 20 µg/L in children is associated with restless legs syndrome and worsening of ADHD symptoms. Iron is a cofactor for tyrosine hydroxylase (the rate-limiting enzyme in dopamine synthesis) — low iron → low dopamine → worse inattention |
| Thyroid function tests (TFTs) | Mood changes, weight changes, lethargy, hyperactivity, pre-lithium baseline | Hypothyroidism: fatigue, weight gain, poor concentration, depressed mood — mimics depression. Hyperthyroidism: anxiety, restlessness, tremor, weight loss — mimics anxiety disorder or mania. Lithium-induced hypothyroidism: must monitor [1] |
| Renal function tests (RFT) | Pre-medication baseline (especially lithium), suspected dehydration | U/Cr (renal dosing) [1]. Lithium is renally cleared; renal impairment → lithium toxicity. Check baseline before and regularly during lithium therapy |
| Liver function tests (LFT) | Pre-medication baseline (valproate, carbamazepine), suspected eating disorder, suspected substance use | Alb (malnutrition) — low in severe eating disorders, neglect. ↑GGT — suggests alcohol use in adolescents. Valproate is hepatotoxic — baseline LFTs required [1] |
| Blood glucose / HbA1c | Pre-antipsychotic baseline, obesity, suspected metabolic syndrome | Atypical antipsychotics (especially olanzapine, clozapine) increase risk of type 2 diabetes and metabolic syndrome. Baseline glucose/HbA1c essential before starting these medications |
| Lipid profile | Pre-antipsychotic baseline | Same rationale — antipsychotics (especially olanzapine) cause dyslipidaemia |
| Prolactin | Before and during antipsychotic treatment (especially risperidone) | Risperidone strongly blocks D2 receptors in tuberoinfundibular pathway → hyperprolactinaemia → gynaecomastia, galactorrhoea, menstrual irregularity in adolescents |
| Urine toxicology screen | Suspected substance use, behavioural change in adolescents | Urine/serum toxicology (substance abuse) [1]. Cannabis, amphetamines, opioids, benzodiazepines. Substance-induced mood/psychotic symptoms should resolve with cessation |
| B12 and folate | Developmental regression, macrocytic anaemia, suspected nutritional deficiency | B12/folate deficiency [1] — can cause cognitive impairment, mood changes, neuropathy. Relevant in severe eating disorders and neglect |
| Calcium | Mood changes, psychosis, fatigue | Ca (mood changes/psychosis) [1]. Hypercalcaemia → depression, confusion, psychosis. Hypocalcaemia → anxiety, irritability, seizures |
| ESR/CRP | Suspected autoimmune or inflammatory condition (SLE, anti-NMDA receptor encephalitis) | ESR/CRP [1] — elevated in inflammatory/autoimmune conditions that can present with psychiatric symptoms |
| Investigation | When to Order | Key Findings and Interpretation |
|---|---|---|
| EEG | Suspected seizures (staring spells, developmental regression, unusual episodic behaviours) | EEG for epilepsy [1]. Absence seizures: 3 Hz spike-and-wave. Temporal lobe epilepsy: temporal spikes/sharp waves (can cause behavioural changes, psychotic symptoms). Epileptic encephalopathies (e.g., Lennox-Gastaut): generalised slow spike-wave |
| CT / MRI Brain | First-episode psychosis, developmental regression, focal neurological signs, head injury, micro/macrocephaly | CT/MRI: head injury, neurological conditions [1]. Look for: structural lesions (tumour, demyelination), white matter abnormalities, cortical malformations, hydrocephalus. MRI preferred (no radiation, better resolution) |
| Audiometry | Suspected hearing impairment, language delay, apparent inattention | Conductive hearing loss (e.g., chronic otitis media with effusion — very common in young children) or sensorineural hearing loss can fully explain "inattention" and "language delay." This is a cheap, non-invasive test that should have a low threshold for ordering |
| Visual assessment | Suspected visual impairment, school difficulties | Poor vision → poor reading → school failure → frustration → behavioural problems. Squinting, sitting close to screen/board |
| Chromosomal microarray / Karyotype | ID with dysmorphic features, ASD with ID, suspected genetic syndrome | Detects copy number variants (CNVs) — deletions/duplications associated with neurodevelopmental conditions (e.g., 22q11.2 deletion → DiGeorge/velocardiofacial syndrome → high schizophrenia risk; 15q11-13 duplication → ASD) |
| Fragile X testing (FMR1 gene) | Males with unexplained ID ± ASD features, family history of ID | Fragile X syndrome is the commonest inherited cause of ID. CGG trinucleotide repeat expansion in FMR1 gene → loss of FMRP protein → abnormal synaptic plasticity. Clinical features: long face, large ears, macroorchidism (post-pubertal), intellectual disability, social anxiety, gaze avoidance |
| Metabolic screen | Developmental regression, unexplained neurological deterioration, consanguinity | Amino acids, organic acids, lactate, ammonia, very-long-chain fatty acids. Identifies inborn errors of metabolism (phenylketonuria, urea cycle disorders, mitochondrial disorders, lysosomal storage diseases) |
| Anti-NMDA receptor antibodies | First-episode psychosis (especially in adolescent girls), seizures + psychiatric symptoms, movement disorder + psychosis | Anti-NMDA receptor encephalitis: autoimmune condition presenting with psychiatric symptoms (psychosis, behavioural change), seizures, movement disorders, and autonomic instability. Often associated with ovarian teratoma. Treatable with immunotherapy — must not be missed |
Don't Miss Anti-NMDA Receptor Encephalitis
In any adolescent (especially female) presenting with first-episode psychosis plus seizures, movement disorder, or rapid cognitive decline, always test for anti-NMDA receptor antibodies. This condition is treatable (immunotherapy, tumour removal) but fatal if missed. It was the condition behind the memoir "Brain on Fire" by Susannah Cahalan. The psychiatric symptoms precede the neurological ones, so psychiatrists are often the first to see these patients.
| Tool | What It Measures | How to Interpret |
|---|---|---|
| WISC-V (Wechsler Intelligence Scale for Children, 5th edition) | Full-Scale IQ (FSIQ) plus five index scores: Verbal Comprehension, Visual-Spatial, Fluid Reasoning, Working Memory, Processing Speed | FSIQ < 70 with impaired adaptive function = intellectual disability. Discrepancy between indices is informative: e.g., low Working Memory + low Processing Speed with normal Verbal Comprehension → classic ADHD cognitive profile. High Verbal but low Performance → consider non-verbal learning disability |
| Vineland Adaptive Behavior Scales (3rd ed.) | Adaptive functioning across Communication, Daily Living Skills, Socialisation, Motor Skills | Required alongside IQ testing to diagnose intellectual disability (ID = low IQ + impaired adaptive functioning). A child with IQ 65 but good adaptive skills may not meet ID criteria |
| ADOS-2 (Autism Diagnostic Observation Schedule) | Observed social-communication and restricted/repetitive behaviours during semi-structured interaction | Provides calibrated severity score (CSS) 1–10. CSS ≥ 4 suggests ASD; ≥ 6 suggests moderate-to-severe. Must be interpreted alongside clinical history — not diagnostic in isolation |
| ADI-R (Autism Diagnostic Interview-Revised) | Parent-reported developmental history and current symptoms in ASD domains | Algorithm scores compared to diagnostic cut-offs for (1) social interaction, (2) communication, (3) restricted behaviours. Meeting cut-off on all three domains + early onset = ASD positive |
| Conners 4 | ADHD symptoms (inattention, hyperactivity-impulsivity) + comorbid domains (learning, aggression, social problems) | T-scores ≥ 65 = elevated (1.5 SD above mean). Parent AND teacher ratings must be obtained — discrepancy between raters is itself diagnostically informative (if only one rater elevated, consider environment-specific factors) |
| SDQ (Strengths and Difficulties Questionnaire) | Five domains: emotional, conduct, hyperactivity, peer problems, prosocial behaviour | Total score > 17 (parent/teacher) = abnormal. Profile pattern guides diagnostic direction: e.g., high hyperactivity + high conduct = consider ADHD + ODD |
| CDI (Children's Depression Inventory) | Self-reported depressive symptoms in children 7–17 years | Total score ≥ 20 suggests significant depressive symptoms. Subscales: negative mood, interpersonal problems, ineffectiveness, anhedonia, negative self-esteem |
| SCARED (Screen for Child Anxiety Related Disorders) | Self- and parent-reported anxiety across GAD, separation anxiety, social phobia, school avoidance, panic/somatic | Total score ≥ 25 suggests clinically significant anxiety. Subscale profile helps differentiate specific anxiety disorders |
Reliability of diagnosis is limited by information variance (inadequate interview technique or patient inconsistencies) and criterion variance (inadequate use of diagnostic criteria). The former can be improved by use of structured interviewing schedules. [1]
| Structured Interview | Population | What It Does |
|---|---|---|
| K-SADS-PL (Kiddie Schedule for Affective Disorders and Schizophrenia, Present and Lifetime) | Children and adolescents 6–18 years | Semi-structured interview administered to parent and child separately; screens for all major Axis I disorders. Generates DSM diagnoses. Gold standard research tool also used clinically |
| DISC (Diagnostic Interview Schedule for Children) | Children 9–17 years (and parents of 6–17 year olds) | Highly structured interview (can be administered by trained lay interviewers); generates DSM and ICD diagnoses |
| DAWBA (Development and Well-Being Assessment) | Children 5–17 years | Combines structured questions with open-ended descriptions reviewed by a clinician. Computer-generated probability of diagnosis |
| ADI-R | Parents of children suspected of ASD | ASD-specific structured interview (detailed above) |
This practical sequence was outlined in the senior notes and represents how a CAMHS assessment actually flows in Hong Kong practice:
- Observation, brief introduction, and rule-setting [1]
- Play alone to warm up; observe how the child plays and interacts with parents and clinician [1]
- Look for any symptom manifestations [1]
- 3-step task: Chinese and English writing, drawing about family or school, short-term memory [1] — This informally screens for learning difficulties (handwriting quality, language level), family dynamics (family drawing is a projective tool), and working memory (relevant to ADHD)
- Copying task for dyslexia [1] — Shape copying tests visual-motor integration; mirror writing or letter reversals persist abnormally in dyslexia
- Interview child alone: look for any separation anxiety [1]
- Talk about family — ask who they like the most, describe family members [1] — If descriptions are purely physical (e.g., "daddy is fat") rather than relational, this may indicate problems with attachment or emotional connection [1]
- Discuss school, peer relationships, classroom behaviour, studies [1]
- Discuss why the child has come this time and patient's own understanding [1] — This is the child's "insight" and affects motivation for intervention and treatment concordance
- Aspirations and projective questioning on 3 wishes [1]
- Theory of Mind tests: first-order, second-order [1] — Used when ASD is in the differential
High Yield Summary
Diagnostic Criteria, Algorithm, and Investigations in Child Psychiatry:
- Always use diagnostic criteria systematically — clinical impression alone leads to overdiagnosis and underdiagnosis. Up to 33% of BAD diagnoses could not be confirmed by structured interview.
- ASD: DSM-5 dyad = social-communication deficits (all 3 needed) + restricted/repetitive behaviours (≥ 2 of 4). Onset in early developmental period. Not better explained by ID alone.
- ADHD: ≥ 6/9 inattention and/or ≥ 6/9 hyperactivity-impulsivity symptoms. Present before age 12 (DSM-5) or 6 (ICD-10). Pervasive (≥ 2 settings). ICD-10 is stricter (requires both domains); DSM-5 allows inattentive-only and hyperactive-only presentations.
- Diagnostic algorithm: Multi-informant history → MSE → Developmental appropriateness filter → Standardised rating scales → Organic exclusion → Systematic criteria application → Formulation → MDT discussion.
- Assessment is MDT-based: Clinical interview (most important) + day hospital MDT assessment + IQ testing + educational assessment + OT + speech therapy + standardised instruments.
- Rating scales supplement but do not replace clinical interview.
- Key investigations to exclude organic mimics: Audiometry (hearing loss), EEG (epilepsy), TFTs (thyroid), CBP/ferritin (anaemia), MRI (structural lesions), genetic testing (fragile X, chromosomal microarray), anti-NMDA antibodies (in first-episode psychosis).
- Pre-medication baselines: Height/weight/BMI, BP/HR, ECG (if TCA/antipsychotic), CBP, RFT, LFT, TFTs, glucose, lipids, prolactin (if antipsychotic).
- ADOS-2 + ADI-R = gold standard ASD assessment tools. Conners/Vanderbilt with parent + teacher forms = key ADHD tools. K-SADS-PL = gold standard general child psychiatric diagnostic interview.
- Child-specific criteria modifications: Irritable mood can substitute for depressed mood in depression; ODD has three-factor structure predicting different outcomes; CD onset type (childhood vs adolescent) predicts prognosis.
Active Recall - Diagnostic Criteria, Algorithm, and Investigations
References
[1] Senior notes: ryanho-psych.md (Chapter 12: Child Psychiatry sections 12.1–12.4; Chapter 2: Psychiatric Assessment sections 2.2.3–2.2.4; Chapter 1: Classification) [4] Lecture slides: CFB (PAE01) Paediatric history taking.pdf (p14–16, p22) [5] Lecture slides: GC 163. I am a superman Bipolar disorder.pdf (p10, p12, p13)
Management Algorithm and Treatment Modalities
Management of psychiatric conditions in children is fundamentally different from adult psychiatry in several ways:
- The child cannot be treated in isolation from their system. The family, school, and peer group are both part of the problem and part of the solution. Every management plan must involve parents/carers and school.
- Development is ongoing. Treatment must account for the child's developmental stage and the fact that the brain is still maturing — this affects both drug pharmacology (children metabolise differently) and psychological intervention choice.
- Psychosocial interventions are generally first-line. Unlike adult psychiatry where pharmacotherapy is often the cornerstone, in child psychiatry behavioural therapy is the mainstay for many conditions, especially in younger children [1]. Medications are added when psychosocial approaches are insufficient.
- Beware of polypharmacy and difference in sensitivity to medications in children [1]. The developing brain responds differently to psychotropics. Side-effect profiles can be more pronounced (e.g., metabolic effects of antipsychotics, growth suppression with stimulants).
- Multimodal approach: The best outcomes come from individualised comprehensive multimodal treatment programmes combining biological, psychological, and social interventions [1].
Condition-Specific Management
1. ADHD Management
Approach to management: individualised comprehensive multimodal treatment programme [1]:
- Pre-school: usually behaviour therapy as mainstay [1] — Why? Because preschool children metabolise stimulants poorly, have higher risk of side effects, and respond well to environmental modification. The developing prefrontal cortex at this age is more amenable to behavioural shaping.
- School age: usually a combination of medications + psychosocial therapy [1]
- Management of comorbidities, e.g., ASD, ODD/CD, mood disorder, anxiety disorders [1]
Stepped approach [1]:
Medications: very effective (most effective among all psychotropics) → more effective than psychosocial treatment [1]
This is a key point to internalise. ADHD medications have effect sizes of ~0.7–1.0 — among the highest in all of psychiatry. The Multimodal Treatment of ADHD (MTA) study showed that medication alone was superior to behavioural therapy alone for core ADHD symptoms, though combined treatment was best for comorbid problems and functional outcomes.
| Medication | Class | Mechanism of Action | Formulations | Effect Size | Key Side Effects | Contraindications/Cautions |
|---|---|---|---|---|---|---|
| Methylphenidate | Stimulant | Blocks dopamine and noradrenaline reuptake transporters (DAT, NET) in prefrontal cortex and striatum → ↑synaptic dopamine and NA in fronto-striatal circuits → improves executive function, sustained attention, and impulse control | Short-acting (Ritalin): 4h duration; Long-acting (Concerta, Ritalin LA): 8–12h duration | 1.0 [1] | Decreased appetite, insomnia, epigastric discomfort, nausea/vomiting, sedation, dizziness, mood swing [1]. Uncommon: motor tics, tachycardia, deranged liver function [1]. Growth suppression with chronic use | Psychosis, severe anxiety, glaucoma, phaeochromocytoma, concurrent MAOI use. Caution in tic disorders (though evidence suggests stimulants are safe and do not worsen tics in most cases), seizure disorders, cardiovascular disease |
| Lisdexamfetamine (Vyvanse) | Stimulant (prodrug) | Prodrug of dexamphetamine — lisdexamfetamine is pharmacologically inactive until cleaved by red blood cell enzymes to release active d-amphetamine. This prodrug mechanism provides smoother pharmacokinetics and lower abuse potential | Long-acting only: 12–14h duration | 1.0 [1] | Similar to methylphenidate. More potent appetite suppression | Same as methylphenidate. Lower abuse potential due to prodrug design |
| Dexamphetamine | Stimulant | Directly releases dopamine and NA from presynaptic terminals AND blocks reuptake → more potent monoamine elevation than methylphenidate | Short-acting | 1.0 [1] | Similar but milder side effect profile [1] | Same as methylphenidate. Higher abuse potential than lisdexamfetamine |
| Atomoxetine (Strattera) | Non-stimulant | Selective noradrenaline reuptake inhibitor (NRI). Blocks NET in prefrontal cortex → ↑NA and (indirectly) ↑dopamine in PFC (because PFC lacks DAT, so dopamine clearance depends on NET). Does not significantly affect dopamine in striatum/nucleus accumbens → no abuse potential | Once daily dosing; takes 4–6 weeks for full effect | 0.7 [1] | Nausea, decreased appetite, fatigue, mood changes. Black box warning for suicidal ideation (rare). Hepatotoxicity (rare but serious) | Concurrent MAOI use, severe cardiovascular disease, narrow-angle glaucoma. Requires ECG if cardiac risk factors |
Why stimulants are first-line: The pathophysiology of ADHD involves hypoactivity of dopamine and noradrenaline in fronto-subcortical circuits [1]. Stimulants directly correct this deficit by increasing monoamine availability in exactly these circuits. The paradox — why do "stimulants" calm hyperactive children? — is explained by the fact that the prefrontal cortex is under-stimulated in ADHD, and stimulants bring it to an optimal activation level, thereby enabling top-down inhibitory control over subcortical motor and reward circuits.
Prescribing considerations:
- Start low, go slow: Begin with lowest dose, titrate up based on response and tolerability
- Drug holidays: Some clinicians offer "medication holidays" during school vacations to assess if the child still needs medication and to allow catch-up growth. This is controversial but common practice
- Monitoring on treatment: Height, weight, BP, HR at each visit. ECG if cardiovascular concerns. Reassess need for medication annually
Stimulants and Growth
Stimulants can suppress appetite → reduced caloric intake → slower growth velocity. Over 2–3 years, this amounts to approximately 1–3 cm reduction in expected height. Growth tends to normalise after medication cessation or in adulthood, but monitoring growth charts at every visit is essential. If growth suppression is significant, consider drug holidays, switch to atomoxetine, or adjust dosing.
| Intervention | Description | Rationale and Efficacy |
|---|---|---|
| Parent Management Training (PMT) | Regarded as the most effective behavioural therapy [1]. Aims: identify problem situations and precipitating factors; offer strategies to enhance positive and limit negative parent-child interactions [1] | Based on social learning theory — children's behaviour is shaped by consequences. Teaching parents to systematically reinforce desirable behaviour and extinguish undesirable behaviour changes the contingency environment |
| Specific PMT strategies [1] | Reward system: offer reward for desirable behaviour → positive reinforcement [1]. Time-out: isolated time-out area for bad behaviour [1]. Response cost system: withdrawing rewards/privileges for unwanted behaviour [1]. Behaviour modelling [1] | Each strategy targets a specific operant learning mechanism: positive reinforcement (rewards), negative punishment (response cost), extinction (time-out removes attention that maintains behaviour) |
| Behavioural treatment in classroom [1] | Goal: ↓inattention and disruptive behaviour [1]. ADHD is a type of special education need (SEN) to be provided under inclusion education policy [1] | The classroom is where ADHD causes the most functional impairment. Without school accommodations, even well-medicated children may struggle |
| Specific school accommodations [1] | Ensure structured and predictable routines [1]. Employ cost-response token economy systems, e.g., star charts [1]. Use of daily report cards [1]. Teach organisation and work/study skills [1] | Structure compensates for the child's executive function deficits. Token economies externalise motivation (the child can "see" the reward approaching) |
| Other interventions [1] | Social skills training, cognitive training, cognitive-behavioural training [1] | Address secondary impairments (peer rejection, poor self-esteem) that medications alone don't fix |
There is no cure for ASD. Management is about optimising function, supporting development, and managing comorbidities.
| Modality | Details | Rationale |
|---|---|---|
| Early intensive behavioural intervention | Applied Behaviour Analysis (ABA), Early Start Denver Model (ESDM). 20–40 hours/week of structured intervention in preschool years | The younger developing brain has maximal neuroplasticity. Early intervention can significantly improve language, cognitive, and adaptive outcomes. Best evidence base for outcomes in ASD |
| Speech and language therapy | Targets receptive/expressive language, pragmatic language skills, use of augmentative and alternative communication (AAC) systems (e.g., PECS — Picture Exchange Communication System) for non-verbal children | Language impairment is common (though not required for DSM-5 diagnosis). Communication skills are the strongest predictor of long-term outcome |
| Occupational therapy | Sensory integration therapy, fine motor skills, activities of daily living training | Sensory hyper/hyporeactivity (a DSM-5 criterion) causes significant distress and functional impairment. OT helps the child develop coping strategies |
| Social skills training | Structured group programmes teaching social rules, perspective-taking, conversation skills | ASD children lack intuitive social understanding; they can learn rules explicitly (like learning a foreign language) even if it doesn't come naturally |
| Educational placement | Mainstream with support (SEN support in HK), special school, or specialist ASD unit depending on severity and intellectual level | Education is the largest "intervention" by hours. The right placement is crucial |
| Psychotropics for problem behaviour and psychiatric comorbidities [1] | Beware of polypharmacy and difference in sensitivity to medications [1]. Risperidone/aripiprazole for irritability and aggression; methylphenidate for comorbid ADHD; SSRIs for comorbid anxiety/OCD; melatonin for sleep | No medication treats core ASD symptoms. Medications target specific comorbid symptoms only |
| Behavioural therapy for maladaptive and otherwise difficult behaviour [1] | Functional behavioural analysis → identify triggers and reinforcers of challenging behaviour → develop alternative strategies | Challenging behaviour (aggression, self-injury, meltdowns) often serves a communicative function ("I'm overwhelmed" or "I want to escape"). Understanding the function allows targeted intervention |
| Family support | Parent training, respite care, sibling support, connection with NGOs and parent groups | Caring for a child with ASD is enormously stressful. Parental wellbeing directly affects the child's outcomes |
ASD Medications — What They Don't Do
No medication improves the core social-communication deficits or restricted/repetitive behaviours of ASD. Risperidone and aripiprazole are FDA-approved for irritability associated with ASD (which includes aggression, self-injury, and tantrums), not for ASD itself. Always use behavioural strategies first and add medication only when behaviours are severe enough to impair function or safety despite environmental and behavioural interventions.
Approach to management: psychosocial treatment as mainstay [1]
| Modality | Details | Efficacy/Evidence |
|---|---|---|
| Parent Management Training (PMT) [1] | Mainstay of treatment for ODD/CD [1]. Based on social learning theory (operant learning theory) and behavioural modification [1]. Manage contingencies around child social behaviour: promote desired behaviour by attention and rewards ('catch your child being good'); extinguish unwanted behaviour by selective ignoring, punishments (by withdrawal of privileges) [1] | Most robust evidence base for ODD. NNT ~3 for significant improvement. Works best in younger children (pre-adolescent) and when parents are engaged |
| Multisystemic Therapy (MST) | Intensive, home-based, family- and community-focused intervention. Therapist works with all systems (family, school, peer group, neighbourhood) | Best evidence for adolescent CD, especially severe cases with risk of out-of-home placement. Reduces reoffending, out-of-home placement, and substance use |
| Functional Family Therapy (FFT) | Structured family therapy targeting communication patterns, family beliefs, and problem-solving | Effective for CD in adolescents; reduces recidivism |
| Cognitive Problem-Solving Skills Training (CPSST) | Teaches the child to recognise and manage anger, consider consequences, generate alternative solutions | Targets the cognitive deficits (poor perspective-taking, hostile attribution bias) that underlie aggressive behaviour |
| School-based interventions | Behavioural programmes, consistent consequences, positive behaviour support plans | Essential because school is a major arena for disruptive behaviour |
| Pharmacotherapy | No medication is first-line for ODD/CD. Consider: risperidone for severe aggression unresponsive to behavioural approaches; methylphenidate for comorbid ADHD (treating ADHD often substantially improves ODD symptoms); SSRIs for comorbid depression/anxiety | Medications are adjunctive only. They treat comorbidity and severe aggression, not the core disorder |
Psychological treatment is first-line [1]:
| Modality | Details | Rationale |
|---|---|---|
| CBT [1] | First-line for all childhood anxiety disorders [1]. Age-adapted: uses games, stories, role-play for younger children. Core components: psychoeducation, relaxation training, cognitive restructuring, graded exposure, relapse prevention | CBT targets the maintaining mechanisms of anxiety: catastrophic cognitions (cognitive distortions), avoidance (which prevents disconfirmation of feared outcomes), and physiological hyperarousal |
| Relaxation training [1] | Progressive muscle relaxation, diaphragmatic breathing, visualisation | Directly reduces sympathetic arousal (the physiological substrate of anxiety) |
| Psychoeducation [1] | For child and parents: explain the nature of anxiety, the fight-or-flight response, the role of avoidance in maintaining fear | Understanding "anxiety is not dangerous" is itself therapeutic. Parents who understand anxiety are less likely to accommodate avoidance |
| Educational support [1] | School accommodations for anxiety-related functional impairment (e.g., graded return to school for school refusal) | School refusal requires a coordinated plan between CAMHS, school, and family |
| Pharmacological treatment (for severe cases) [1] | SSRIs [1] — first-line medication when medication is needed. Fluoxetine has best evidence in children. Imipramine [1] (TCA — used less now due to side effects and overdose risk). Anxiolytics (generally avoided) [1] — benzodiazepines are avoided in children due to dependence risk, paradoxical disinhibition, and cognitive side effects | SSRIs increase serotonin availability in the amygdala-prefrontal circuit → reduce anxiety signalling. The effect takes 2–4 weeks. Start low, go slow in children |
Approach parallels adult depression management but with important modifications [1]:
| Severity | Management |
|---|---|
| Mild | Watchful waiting + psychosocial intervention [1] [6]. Active monitoring for 2–4 weeks. Self-help strategies, exercise, sleep hygiene, stress management. Guided self-help CBT |
| Moderate–Severe | Antidepressant treatment + psychotherapy [1] [6]. Fluoxetine is the only SSRI with robust evidence for efficacy in child/adolescent depression (TADS trial). CBT and interpersonal therapy (IPT) are effective psychological treatments [6] |
| Refractory | Augmentation, combination, switch, or ECT [1] [6]. Options parallel adult approach but with more caution |
Pharmacotherapy specifics:
| Medication | Evidence/Notes | Cautions |
|---|---|---|
| Fluoxetine | Only SSRI with consistent evidence of efficacy in paediatric depression (NICE, AACAP guidelines). NNT ~10. Approved by FDA for children ≥ 8 years | Beware of suicidal risk with SSRIs [1] — FDA black box warning: SSRIs may increase suicidal ideation (NOT completed suicide) in the first 1–2 weeks of treatment, especially in under-25s. Mechanism: SSRIs restore energy and motivation before mood improves → "activating" a still-depressed patient. Close monitoring required in the first 4 weeks |
| Sertraline | Second-line; some evidence of efficacy | Same black box warning |
| Other SSRIs (paroxetine, citalopram) | Limited or negative evidence in paediatric depression specifically. Paroxetine had negative trials in adolescents (Trial 329 controversy) | Not recommended as first-line |
| TCAs (imipramine, amitriptyline) | Generally NOT effective in paediatric depression (despite efficacy in adults). More dangerous in overdose (cardiac toxicity). Require ECG monitoring [1] | Avoid in paediatric depression. May still be used for enuresis (imipramine), anxiety (clomipramine for OCD) |
| Avoid antidepressants if possible in bipolar; if used, limit dose and duration [5] | Risk of switching to mania/hypomania, especially with TCAs and venlafaxine | Always screen for bipolarity before prescribing antidepressants |
Psychosocial treatments [6]:
- Cognitive behavioural therapy: monitor, evaluate, and modify negative dysfunctional thoughts and distorted perceptions and beliefs. Use cognitive techniques (e.g., list pros and cons, examine evidence). Increase activity scheduling [6]
- Interpersonal therapy: problems are understood in interpersonal context, e.g., facilitate grieving process, encourage role transition, explore interpersonal disputes, improve interpersonal skills [6]
- As many as 85% of patients receiving both antidepressants and psychotherapy achieve remission [6]
SSRIs and Suicidality in Children
The FDA black box warning on SSRIs and suicidality in under-25s is one of the most examined safety signals in psychiatry. The risk is a small increase in suicidal ideation (from ~2% to ~4%), NOT completed suicide. The mechanism is likely that SSRIs restore energy and motivation before they lift mood, creating a window where a still-hopeless patient now has the drive to act. Close monitoring (weekly for first 4 weeks, then fortnightly for next 4 weeks) mitigates this risk. The benefits of treating moderate-to-severe depression far outweigh this small risk. The real danger is not treating depression.
6. Bipolar Disorder in Children/Adolescents [5]
Outline of management [5]:
Indication for prophylactic treatment [5]:
- Established bipolar disorder [5]
- Recurrent episodes of mania or depression [5]
- Severe single episode with suicidal attempts, psychotic episodes, and significant functional impairment (to prevent future relapse) [5]
- Recurrence rate reduces by 50% for maintenance vs discontinuation [5]
- Gradual discontinuation better than abrupt discontinuation [5]
General guidelines for prophylaxis for bipolar I [5]:
- Monotherapy: Lithium or Valproate or Quetiapine [5]
- Psychosocial (augmentation): Psychoeducation, CBT, interpersonal and social rhythm therapy, family or carer-focused treatment, peer support, intensive case management [5]
- Less hostile, more supportive, better drug compliance [5]
Key summary points [5]:
- Lithium is still an important drug, given that it is the only mood stabiliser to reduce suicide [5]
- Atypical antipsychotics look promising as mood stabilisers but limited by metabolic side effects [5]
- Lamotrigine is a promising agent for treatment of bipolar depression due to its tolerability and wide therapeutic margin [5]
- Avoid antidepressants if possible; if used, limit dose and duration [5]
- Psychosocial intervention is important for prevention of relapses and overall management of bipolar disorder [5]
Special considerations for children and adolescents [5]:
- Treatment in special situations: childbearing-age women, pregnancy, child and adolescents, elderly [5] — In children/adolescents, medication evidence is extrapolated largely from adult trials. Lithium is approved for adolescents ≥ 12 in most jurisdictions. Valproate should be avoided in girls of childbearing age (teratogenic — neural tube defects). Atypical antipsychotics (especially aripiprazole, quetiapine) have emerging evidence in paediatric bipolar.
Because lithium is the gold standard prophylactic agent and has unique monitoring requirements:
| Aspect | Details |
|---|---|
| Pre-treatment | RFT (eGFR), TFT ± ECG (if CVS risk factors) + reliable contraception [1] |
| Initiation | Usually 350–500 mg/d, titrate up 300–600 mg/d every 1–5 days until therapeutic level reached (usually 900–1800 mg/d) [1] |
| Drug level monitoring | Narrow therapeutic interval. Check Q6 months if stable; before and 7 days after any dose change. Timing: 12h after last dose (trough level). Target: 0.4 mmol/L minimum; 0.6–1.0 mmol/L for prophylaxis; > 0.8 mmol/L for acute mania [1] |
| On-treatment monitoring | Plasma Li, eGFR, TFT Q6 months ± plasma Ca yearly [1] |
| Discontinuation | Lithium should not be started unless clear intention to continue ≥ 3 years. Gradually reduce dose over ≥ 1 month [1] — Abrupt discontinuation causes rebound mania |
| Key side effects | Tremor, polyuria/polydipsia (nephrogenic DI), weight gain, hypothyroidism, renal impairment (chronic interstitial nephritis), teratogenicity (Ebstein anomaly — 1st trimester), acne. Toxicity: coarse tremor, vomiting, diarrhoea, ataxia, confusion, seizures, coma |
| Modality | What It Is | Key Indications in Children | How It Works |
|---|---|---|---|
| Cognitive Behavioural Therapy (CBT) | Structured, time-limited therapy that targets the relationship between thoughts, feelings, and behaviours | Depression, anxiety, OCD, PTSD, bulimia, behavioural problems [6] | Monitor, evaluate, and modify negative dysfunctional thoughts and distorted perceptions and beliefs. Use cognitive techniques (e.g., list pros and cons, examine evidence). Increase activity scheduling [6]. In children: adapted with games, stories, worksheets |
| Interpersonal Therapy (IPT) | Focuses on interpersonal relationships as the context for psychiatric symptoms | Adolescent depression [6] | Problems are understood in interpersonal context, e.g., facilitate grieving process, encourage role transition, explore interpersonal disputes, improve interpersonal skills [6] |
| Parent Management Training (PMT) | Teaches parents operant conditioning techniques to modify child behaviour | ADHD (especially pre-school), ODD/CD [1] | Based on social learning theory: positive reinforcement of desired behaviour + extinction/negative punishment of undesired behaviour. Changes the reinforcement environment systematically |
| Family Therapy | Works with the whole family system to change dysfunctional interaction patterns | ASD (family support), CD, eating disorders, depression with family conflict [6] | Systems theory: the child's symptom serves a function within the family system. Changing communication patterns, boundaries, and hierarchies can resolve the symptom |
| Play Therapy | Uses play as the medium of therapeutic communication | Young children (< 7–8) with anxiety, trauma, attachment difficulties | Young children communicate through play. The therapist uses the child's play to understand and process emotional conflicts |
| Social Skills Training | Structured group teaching of social rules, conversation skills, emotion recognition | ASD, ADHD (secondary social impairment) | Explicitly teaches what neurotypical children learn implicitly. Uses role-play, video modelling, social stories |
| Dialectical Behaviour Therapy (DBT) | Skills-based therapy combining CBT with mindfulness and distress tolerance | Adolescent self-harm, emerging BPD | Targets emotion dysregulation — teaches four skill modules: mindfulness, distress tolerance, emotion regulation, interpersonal effectiveness |
| Condition | First-Line | Second-Line | Key Pharmacology | Key Psychosocial |
|---|---|---|---|---|
| ADHD (mild) | Psychoeducation + PMT + school accommodations [1] | Behavioural therapy | None at this stage | PMT, classroom strategies |
| ADHD (moderate–severe) | Medications + psychosocial [1] | Atomoxetine if stimulants fail/contraindicated | Methylphenidate (1st), lisdexamfetamine, atomoxetine | PMT, school accommodations, social skills |
| ASD | Early intensive behavioural intervention + SLT + OT | Specific symptom-targeted medication | Risperidone/aripiprazole for irritability; MPH for ADHD; SSRIs for anxiety | ABA/ESDM, parent training, school placement |
| ODD/CD | PMT (mainstay) [1] | MST, FFT, CPSST | Risperidone for severe aggression; MPH for comorbid ADHD | PMT, school-based programmes |
| Anxiety | CBT (1st line) [1] | SSRIs for severe cases | Fluoxetine/sertraline | CBT, relaxation, psychoeducation |
| Depression (mild) | Watchful waiting + psychosocial [1] [6] | CBT / IPT | None initially | CBT, IPT, activity scheduling |
| Depression (moderate–severe) | Fluoxetine + CBT/IPT [1] [6] | Sertraline; augmentation | Fluoxetine (1st line, only robust evidence) | CBT, IPT |
| Bipolar (mania) | Monotherapy: Li/valproate/atypical AP [5] | Combination: Li/VPA + atypical AP [5] | Lithium (reduces suicide), aripiprazole, quetiapine | Psychoeducation, CBT, family therapy |
| Bipolar (depression) | Li / Lamotrigine / Quetiapine [5] | Add SSRI (limit dose and duration) [5] | Lamotrigine (good tolerability) | IPT, social rhythm therapy |
| Bipolar (prophylaxis) | Li / VPA / Quetiapine [5] | Psychosocial augmentation [5] | Lithium — only mood stabiliser to reduce suicide [5] | Psychoeducation, CBT, IPSRT, family therapy [5] |
Special Considerations
Indications for ECT [1]:
- Emergency (life-threatening: severe depression with food refusal, persistent suicidal intent) [1]
- Catatonia [1]
- Treatment-refractory conditions [1]
ECT is rarely used in children but can be life-saving in adolescents with treatment-resistant depression, psychotic depression, or catatonia. Mechanism of action: unknown, but hypothesised to involve ↑neurotrophic signalling (e.g., ↑BDNF) → induces neurogenesis; ↑monoamine neurotransmitter release; transient ↑BBB permeability; changes in brain connectivity [1].
In Hong Kong, ECT in minors requires careful ethical consideration, parental consent, and typically specialist MDT approval.
Physical activity is listed as a treatment modality for depression [6]. This is not trivial — exercise increases BDNF, enhances monoaminergic transmission, reduces cortisol, and provides structured social interaction. For children and adolescents, regular physical activity should be part of every management plan.
| Service | Role |
|---|---|
| CAMHS (Hospital Authority) | Specialist psychiatric assessment and treatment. Provides medication, individual/group therapy, day hospital programmes |
| Child Assessment Centre (Dept of Health) | Comprehensive developmental assessment for < 12 years; coordinates MDT input |
| School-based services | Educational psychologists (psychoeducational assessment), school social workers (family support, crisis intervention), SEN coordinators (classroom accommodations under inclusion education policy) |
| NGOs | Parent training groups, social skills groups, after-school programmes, respite care, helplines |
| EASY programme | Early Assessment Service for Young people with psychosis [1] — for first-episode psychosis in 15–64 year olds. Duration: first 3 years. Involves: intensive follow-up with more allied health support and assignment of case managers. Efficacy: ↓suicide and hospitalisation rates, improved functioning and symptom outcome [1] |
High Yield Summary
Management in Child Psychiatry — Key Principles:
- Psychosocial interventions are generally first-line — especially PMT for ADHD/ODD/CD, CBT for anxiety/depression, and early intensive behavioural intervention for ASD.
- ADHD medications are the most effective psychotropics — effect sizes ~0.7–1.0. Methylphenidate is first-line stimulant. Stepped approach: mild → PMT only; moderate → medications + psychosocial; severe → medications as first choice.
- PMT is the mainstay for ODD/CD — based on social learning theory. "Catch your child being good" + systematic reinforcement/extinction.
- ASD has no cure — management is MDT-based. No medication treats core symptoms; risperidone/aripiprazole for irritability only. Beware polypharmacy.
- Fluoxetine is the only SSRI with robust evidence for paediatric depression. Black box warning for suicidal ideation → close monitoring in first 4 weeks. Benefits outweigh risks in moderate–severe depression.
- Bipolar management: Mania → lithium/valproate/atypical AP. Depression → lithium/lamotrigine/quetiapine. Prophylaxis → lithium (only drug to reduce suicide). Avoid antidepressants if possible.
- Lithium monitoring: Pre-treatment (RFT, TFT, ECG); on-treatment (Li levels, RFT, TFT Q6 months). Narrow therapeutic index. Trough level 12h post-dose.
- ECT is rarely used in children but is indicated for emergency, catatonia, and treatment-refractory cases.
- Always manage comorbidities — treat the ADHD in a child with ODD; treat the anxiety in a child with depression.
- Always involve the family and school — no child psychiatric intervention works in isolation.
Active Recall - Management in Child Psychiatry
References
[1] Senior notes: ryanho-psych.md (Chapter 12: Child Psychiatry sections 12.1–12.5; Chapter 3: Treatment in Psychiatry sections 3.1–3.3; Chapter 7: Mood Disorders section on management) [5] Lecture slides: GC 163. I am a superman Bipolar disorder.pdf (p36, p37, p40, p41, p44, p46, p47, p64, p65) [6] Lecture slides: GC 164. I am depressed Mood disorders.pdf (p16, p18)
Complications and Prognosis of Child Psychiatric Conditions
In medicine, we usually think of "complications" as things that go wrong because of a disease — like a diabetic foot ulcer from diabetes. In child psychiatry, the concept is broader. Complications arise from three sources:
- The disorder itself — untreated or inadequately treated conditions lead to cascading developmental, academic, social, and psychological harm.
- Comorbidity — child psychiatric conditions breed other conditions. ADHD leads to ODD, which leads to CD, which leads to substance abuse. Depression breeds anxiety. ASD breeds depression. This "comorbidity cascade" is arguably the biggest complication of all.
- Treatment — medications and even psychosocial interventions have side effects and unintended consequences (iatrogenic complications).
The fundamental principle: the developing brain does not wait. Every month that a child's condition goes untreated, they fall further behind their peers in academic, social, and emotional development. These deficits compound over time. A 7-year-old with untreated ADHD who misses a year of foundational literacy skills doesn't just lose one year — they lose the scaffolding upon which all subsequent learning is built. This is why early identification and intervention matter so much.
A. Complications by Condition
1. ADHD — Complications and Course
Course: generally show age-dependent ↓severity (hyperactivity > impulsiveness > inattention), but a substantial proportion persist into adulthood or experience functional impairment [1]:
- ~50% retain full diagnostic criteria in adolescence [1]
- ~40–60% experience problems in adulthood [1]
This age-dependent decline in severity follows a predictable pattern. Hyperactivity declines first because it is the most "visible" and most responsive to developmental maturation of motor circuits. Impulsivity declines next as the prefrontal cortex continues maturing (PFC maturation extends into the mid-20s). Inattention is the most persistent because it reflects the deepest deficit in executive function and working memory circuits — these higher-order cognitive processes are the last to fully mature.
Poor prognostic factors: learning difficulties, antisocial behaviour, severe overactivity [1] In particular, when comorbid with CD, particularly at risk of antisocial, criminal behaviours and substance abuse [1]
| Domain | Childhood Complications | Adolescent Complications | Adult Complications | Pathophysiological Basis |
|---|---|---|---|---|
| Academic | Underperformance despite normal IQ, grade retention, special education needs, school exclusion | School dropout, failure to graduate, inability to pursue higher education | Occupational failure [1], underemployment relative to intellectual ability | Inattention → inability to sustain effort on academic tasks → cumulative knowledge gaps. Working memory deficits → difficulty following multi-step instructions |
| Social | Peer rejection (impulsive/intrusive behaviour is aversive to peers), fewer close friendships, bullying (both as victim and perpetrator) | Social isolation, risky peer group affiliation | Relationship problems [1], higher divorce rates, interpersonal conflict | Impulsivity → social norm violation → peer exclusion. Inattention → missing social cues → misinterpreting others' intentions |
| Behavioural | ODD comorbidity (~40%), CD comorbidity (~20%) [1] | Antisocial behaviour, criminal behaviours [1], truancy, delinquency | Antisocial personality disorder (in those with childhood-onset CD) | Executive dysfunction + impulsivity → poor self-regulation → escalating oppositionality. The developmental cascade: ADHD → ODD → CD → antisocial PD |
| Substance use | — | Early initiation of tobacco, alcohol, cannabis. Substance abuse (~15%) [1] | Substance abuse [1], higher rates of nicotine dependence | Impulsivity → novelty-seeking → experimentation. Dopaminergic reward circuit dysfunction → self-medication hypothesis (substances temporarily normalise reward signalling). Paradoxically, treated ADHD reduces later substance abuse risk |
| Emotional | Low self-esteem ("I'm stupid," "I'm naughty"), frustration, demoralisation | Depression (~20%), anxiety (~25%) [1] | Self-esteem issues [1], depression, anxiety | Repeated failure experiences → learned helplessness → negative self-schema. The discrepancy between ability and performance is particularly frustrating |
| Physical safety | Injuries [1] — higher rates of A&E visits, accidental injuries | Road traffic accidents (impulsive driving), sports injuries | Injuries/accidents [1], higher rates of motor vehicle collisions | Impulsivity + inattention → failure to anticipate danger → risk-taking without awareness of consequences |
| Economic | — | — | Higher healthcare costs, lower lifetime earnings, higher welfare dependency | Cumulative effect of academic underachievement + occupational instability + relationship breakdown |
The ADHD → Substance Abuse Paradox
Parents often worry that giving their child a "controlled substance" (methylphenidate, amphetamine) will lead to addiction. The evidence shows the opposite: treating ADHD with stimulants reduces the risk of later substance abuse by approximately 50% (meta-analysis by Wilens et al.). Why? Because untreated ADHD drives self-medication with tobacco, cannabis, and alcohol. The stimulant medication normalises dopaminergic reward signalling, removing the drive to self-medicate.
| Domain | Childhood Manifestation | Adult Manifestation |
|---|---|---|
| Inattention | Difficulty sustaining attention, doesn't listen, no follow-through, cannot organise, loses important items, easily distractible, forgetful [1] | Difficulty sustaining attention in meetings, reading, or paperwork. Paralysing procrastination. Slowness, inefficiency. Poor time management. Disorganisation [1] |
| Hyperactivity | Squirms/fidgets, can't stay seated, runs/climbs excessively, can't play quietly, "on the go," talks excessively [1] | Workaholic, overscheduled and overwhelmed, self-select very active jobs [1] |
| Impulsivity | Blurts out answers, can't wait turn, interrupts | Impulsive financial decisions, relationship instability, road rage, job-hopping |
2. ASD — Complications and Course
Subsequent course: tendency for core symptoms to improve over time [1]
- Symptoms are typically most marked in early childhood and early school years [1]
- Later developmental gains result in learning and compensation, therefore remediating core symptoms to some extent [1]
Prognosis: only minority can live and work independently in adulthood [1]
- Those who do tend to have superior language and intellectual abilities (good prognostic factors) and are able to find a niche that matches their special interests/skills [1]
- ASD adults use compensation strategies and coping mechanisms to mask their difficulties in public but suffer from the stress and effort of maintaining a socially acceptable facade [1]
| Domain | Complication | Pathophysiological / Developmental Basis |
|---|---|---|
| Psychiatric comorbidity | Behavioural problems: self-injurious behaviour, hyperactivity, disruptive or challenging behaviour, soiling/enuresis, sleep disorders, ADHD (30–50%) [1]. Mood problems: anxiety, depression (especially in adolescent stage) [1] | ASD + normal/high intelligence = awareness of being "different" → social isolation → depression. Sensory overload → challenging behaviour as escape mechanism. Comorbid ADHD reflects shared neurodevelopmental vulnerability (overlapping genetic risk) |
| Seizures | Seizures (25%): usually develop by adolescence [1] | Underlying cortical hyperexcitability — the same abnormal neural connectivity that produces ASD symptoms also lowers seizure threshold. Higher risk in those with comorbid intellectual disability |
| Motor | Motor deficits: abnormal gaits, clumsiness, toe-walking, other abnormal motor signs [1]. Catatonia-like features: freezing mid-action, slowing [1] | Cerebellar and basal ganglia involvement in ASD (beyond just "social brain" networks). Catatonia risk increases in adolescence and is an underrecognised complication |
| Language | Persistent language impairment in ~50% (ranging from non-verbal to functional but pragmatically impaired) [1] | Variable depending on severity and intellectual level. Variable impairment: non-existent, only physical gestures, single words, sentences, normal speech but impairment when used in context [1] |
| Academic | Learning difficulties, inability to cope with mainstream school demands | Executive function deficits, sensory overload in classroom, inflexibility with changes in routine |
| Social | Social isolation, victimisation/bullying, exploitation by peers, difficulty maintaining employment | Core social-communication deficits persist even when compensated. Suffer from the stress and effort of maintaining a socially acceptable facade [1] — this is now called "autistic burnout" |
| Masking/Camouflaging burnout | Exhaustion, depression, suicidality — especially in late-diagnosed women and high-functioning individuals | The cognitive effort of constantly monitoring and imitating social behaviour depletes executive resources, leading to psychological collapse |
Autistic Burnout
This is an increasingly recognised phenomenon. Adults with ASD who have "camouflaged" successfully for years may suddenly decompensate — losing previously acquired coping skills, becoming unable to work, developing severe depression. It is driven by the chronic stress of masking. Clinically, it can be mistaken for a new-onset psychotic episode or severe depressive episode. Always enquire about developmental history in any adult presenting with sudden functional decline.
3. ODD/CD — Complications and Course
ODD [1]:
- Onset: usually appear during preschool years [1]
- Often precedes development of CD, especially those with defiant, argumentative, and vindictive behaviour [1]
- ↑risk of adjustment problems in adult, e.g., antisocial behaviour, impulse-control problems, substance abuse, anxiety, depression [1]
CD [1]:
- Onset: emerge mid-childhood to mid-adolescence [1]
- Variable course, with progressively severe conduct problems in some individuals (e.g., theft → rape, robbery) [1]
- Some will show antisocial personality disorder, e.g., violent offending, heavy drug usage, teenage pregnancy, inability to graduate [1]
- Prognosis is worse for early-onset cases (antisocial behaviour in 40% early-onset cases and only 20% in adolescent-onset cases) [1]
This is one of the best-documented developmental trajectories in child psychiatry:
Early childhood Middle childhood Adolescence Adulthood
ODD ────────────> CD ────────> Substance abuse ────> Antisocial PD
(defiance, (violation of (self-medication, (criminal behaviour,
tantrums) rights/norms) peer influence) inability to sustain
relationships/work)Why does this cascade happen?
- ODD → child is difficult, oppositional, hostile → peer rejection + parental exhaustion → inadequate supervision
- Inadequate supervision + peer rejection → child drifts toward deviant peer group (the only peers who accept them)
- Deviant peer group reinforces antisocial behaviour → escalation to CD-level behaviours (theft, aggression)
- CD behaviours → school exclusion, criminal justice involvement → further alienation from prosocial systems
- Without intervention, the pattern crystallises into antisocial personality disorder (by definition, diagnosed only after age 18)
Factors that predict poor outcome in children with conduct disorder [1]:
| In the Young Person | In the Family | In the Wider Environment |
|---|---|---|
| Early onset, severe antisocial behaviours, callous-unemotional traits, comorbid ADHD | Parental criminality, parental substance abuse, poor supervision, family conflict, low warmth | Economically deprived areas, disorganised neighbourhoods, schools with high delinquency rates [1] |
| Complication | Details | Mechanism |
|---|---|---|
| Substance abuse | Early tobacco, alcohol, cannabis. Progression to harder drugs. Heavy drug usage [1] | Self-medication for comorbid depression/ADHD + deviant peer influence + impulsivity |
| Criminal behaviour | Violent offending [1], property crime, juvenile detention | Violation of others' rights is the core feature of CD; without intervention it escalates |
| Educational failure | School exclusion, inability to graduate [1] | Behaviour prevents learning; school exclusion removes structure and supervision |
| Teenage pregnancy | Teenage pregnancy [1] | Impulsivity + poor decision-making + early sexual activity |
| Injuries | Self-inflicted (reckless behaviour), inflicted on others, involvement in violence | Reckless/impulsive behaviour in dangerous situations |
| Adult mental health | Antisocial PD, depression, substance use disorders, anxiety | The developmental cascade described above; chronic adversity breeds further psychopathology |
4. Childhood Anxiety Disorders — Complications and Course
Prognosis: nearly 2/3 expected to disappear in 3–5 years [1] — this sounds reassuring, but: ~1/3 of them will have other categories of anxiety disorders at follow-up [1]
This phenomenon is called homotypic and heterotypic continuity:
- Homotypic continuity: the same disorder persists (e.g., separation anxiety at 6 → separation anxiety at 10)
- Heterotypic continuity: the specific disorder changes but the broad category persists (e.g., separation anxiety at 6 → social phobia at 14 → GAD at 20)
The underlying trait of anxiety proneness (behavioural inhibition, amygdala hyperreactivity) doesn't go away — it just expresses itself through different content as the child's cognitive and social world expands.
| Complication | Mechanism |
|---|---|
| School refusal / academic underperformance | Avoidance of anxiety-provoking school environment → missed education → cumulative knowledge gaps |
| Social isolation | Avoidance of peer interactions → failure to develop social skills → loneliness → depression |
| Somatic symptom burden | Chronic anxiety → persistent autonomic activation → frequent somatic complaints (headache, abdominal pain) → overinvestigation → medical system burden + illness role reinforcement |
| Adult anxiety and depression | Childhood anxiety is the strongest predictor of adult anxiety disorders. Also increases risk of adult depression (shared genetic vulnerability via 5-HTTLPR, shared neural circuits) |
| Substance abuse | Adolescents with untreated anxiety may self-medicate with alcohol or cannabis (anxiolytic effect). This is especially common in social anxiety |
| Functional impairment without diagnosis | "Quiet" anxious children may be overlooked because they are not disruptive. They suffer silently with poor self-esteem, avoidance, and underperformance without ever being referred |
Prognosis: episodic relapsing course, with majority recovering < 3 months but 15% lasting > 18 months [1]
Key Complications
| Complication | Details | Mechanism |
|---|---|---|
| Suicide | Leading cause of death in adolescents with depression. Risk amplified by comorbid substance use, impulsivity (comorbid ADHD/CD), access to means, social isolation | Hopelessness + cognitive constriction ("no way out") + impulsivity in adolescents. Beware of suicidal risk in SSRIs [1] — risk highest in first 2 weeks of treatment |
| Self-harm | Cutting, overdose, burning — increasingly common from age 10+. May or may not be associated with suicidal intent | Emotional dysregulation → self-harm as affect regulation strategy ("physical pain replaces emotional pain") |
| Substance abuse | 70% has anxiety disorder, CD, substance abuse, dysthymia as comorbidities [1]. Behavioural problems, e.g., one case tried to steal a bus because of frustration at home, take cannabis to lift mood due to depression [1] | Self-medication hypothesis: cannabis and alcohol temporarily relieve depressive symptoms but worsen them long-term (alcohol is a CNS depressant; cannabis disrupts dopaminergic reward signalling) |
| Academic decline | Poor concentration, amotivation, absenteeism → falling grades | Prefrontal hypofunction → executive dysfunction + anhedonia → inability to engage with learning |
| Recurrence | ~60% will have a recurrence within 5 years. Risk of adult recurrent depressive disorder | Each depressive episode may cause neuroplastic changes (hippocampal atrophy, HPA axis sensitisation) that lower the threshold for subsequent episodes ("kindling" hypothesis) |
| Bipolar conversion | ~25% of BAD first presented as a juvenile depression in their first episode [1] | Shared genetic vulnerability. Early depression may be the first expression of an underlying bipolar diathesis. Antidepressant treatment without mood stabiliser cover may precipitate a manic switch |
| Social and interpersonal harm | Withdrawal from friends and family, loss of social skills during critical developmental window, damaged relationships | Depression → social withdrawal → peer rejection → further depression (self-perpetuating cycle) |
B. Complications of Treatment (Iatrogenic)
These are equally important because they are preventable:
| Medication | Key Complications | Mechanism | Monitoring |
|---|---|---|---|
| Stimulants (methylphenidate, amphetamines) | Appetite suppression → growth retardation (~1–3 cm over 2–3 years), insomnia, tics (uncommon, usually do not worsen existing tics), cardiovascular effects (↑HR, ↑BP), mood lability, rare psychotic symptoms at high doses | Sympathomimetic effects (NA/DA agonism) → appetite centre suppression, sleep-wake disruption, sympathetic activation | Height/weight/BMI at every visit, BP/HR, tic monitoring, appetite diary |
| Atomoxetine | Hepatotoxicity (rare but serious — stop if jaundice), suicidal ideation (FDA warning), nausea, mood changes | Selective NRI → mechanism of suicidal ideation unclear (similar to SSRI concern — restoring motivation before mood) | LFTs at baseline, monitor for mood/suicidal ideation, especially in first 4 weeks |
| SSRIs (fluoxetine, sertraline) | Suicidal ideation in first 2 weeks (FDA black box in < 25), activation syndrome (agitation, insomnia, restlessness), GI upset, sexual dysfunction (in adolescents), serotonin syndrome (if combined with other serotonergic agents), emotional blunting | ↑5HT → initial anxiogenic effect before therapeutic benefit (explains early activation). Serotonin syndrome: excess 5HT at all receptor subtypes → hyperthermia, clonus, agitation | Weekly review for first 4 weeks, then fortnightly for next 4 weeks |
| Antipsychotics (risperidone, aripiprazole) | Beware of polypharmacy and difference in sensitivity to medications [1]. Metabolic syndrome (weight gain, dyslipidaemia, hyperglycaemia — especially olanzapine, quetiapine), hyperprolactinaemia (risperidone → gynaecomastia, galactorrhoea, menstrual irregularity), sedation, extrapyramidal symptoms | D2 blockade in tuberoinfundibular pathway → ↑prolactin. H1/5HT2C blockade → appetite stimulation → weight gain. D2 blockade in nigrostriatal pathway → EPS | Weight, fasting glucose, lipids, prolactin at baseline and Q3–6 months. Watch for EPS at every visit |
| Mood stabilisers (lithium, valproate) | Lithium: tremor, polyuria/polydipsia (nephrogenic DI), hypothyroidism, renal impairment, teratogenicity (Ebstein anomaly). Valproate: hepatotoxicity, pancreatitis, teratogenicity (NTD — avoid in girls of childbearing age), weight gain, PCOS | Lithium: concentrating defect in collecting duct (antagonises ADH/V2R); interferes with thyroid hormone synthesis. Valproate: mitochondrial toxicity in hepatocytes; inhibition of folate metabolism (NTD risk) | Lithium: levels Q6mo, RFT, TFT, Ca. Valproate: LFTs, CBP (thrombocytopaenia), drug levels |
| Melatonin | Generally safe. Rare: headache, daytime drowsiness | Exogenous melatonin supplements endogenous circadian signalling | Minimal monitoring needed |
| Intervention | Potential Complications | How to Mitigate |
|---|---|---|
| Labelling effect | Being given a psychiatric diagnosis (ADHD, ASD, CD) can become a self-fulfilling prophecy. Teachers and parents may lower expectations. The child may internalise "I am broken" | Frame diagnosis as explanation, not excuse. Emphasise strengths. Psychoeducation that addresses stigma |
| Parental guilt/blame | Parents may feel responsible for their child's condition, especially in conditions where parenting is implicated (ODD/CD) or where family dynamics are explored (family therapy) | Explicitly state that psychiatric conditions are not caused by "bad parenting" alone. Validate parental struggle. PMT is about teaching skills, not assigning blame |
| Therapeutic dependency | Prolonged therapy without clear goals can create dependency on the therapist and delay development of autonomous coping | Time-limited therapy protocols (e.g., 12-session CBT) with explicit goals, built-in review points, and planned termination |
| Social skills group — negative modelling | Grouping conduct-disordered children together can paradoxically reinforce antisocial behaviour (deviant peer training effect) | Carefully curate group composition. Avoid grouping severe CD adolescents together. Mix with prosocial peers when possible |
This is rarely discussed but clinically important:
| Complication | Explanation | How to Mitigate |
|---|---|---|
| Assessment trauma | Repeated assessments by multiple professionals can be re-traumatising for children with abuse histories. Being asked to recount traumatic experiences multiple times worsens PTSD symptoms | Coordinate between agencies. Use single-assessment models where possible. Read previous records before re-asking |
| False reassurance from negative assessment | If assessment fails to identify a genuine condition (e.g., ASD in a masking girl), the family may be falsely reassured and not re-present until much later when complications have accumulated | Always document uncertainty. Advise re-referral if concerns persist. "Not meeting criteria today does not mean there is no problem" |
| Delay in assessment | Long waiting lists (a significant issue in Hong Kong's public CAMHS) mean children wait months to years for assessment. During this time, complications accumulate | Interim support from school and primary care while waiting. Prioritise high-risk cases. Use screening tools to stratify urgency |
| Labelling before assessment is complete | A premature diagnosis can lead to inappropriate treatment (e.g., stimulants for a child with anxiety-driven inattention, not ADHD) | Complete the full assessment before diagnosing. Standardized behaviour rating scales: more objective but diagnosis should still be based on structured interview and collateral information only (rating is for reference only) [1] |
Common comorbidities: 70% has anxiety disorder, CD, substance abuse, dysthymia (in youth depression) [1] Comorbidities: very common (50%), especially in severe cases (↑comorbidities for ↑number of ADHD symptoms) [1]
| Primary Condition | Common Comorbidity | Complication of Comorbidity | Why They Co-occur |
|---|---|---|---|
| ADHD | ODD (~40%), CD (~20%), learning disorder (~25%), anxiety (~25%), mood disorder (~20%), substance abuse (~15%) [1] | Each comorbidity independently worsens prognosis and compounds the other. ADHD + CD = worst trajectory (antisocial PD, crime, substance abuse) | Shared genetic vulnerability (dopamine/serotonin systems), shared environmental risk factors (adversity), cascade effects (ADHD causes frustration → ODD) |
| ASD | ADHD (30–50%) [1], ID (30–50%), anxiety, depression, seizures (25%) [1], sleep disorders | Comorbid ID = much worse functional prognosis. Comorbid ADHD = more behavioural challenges. Comorbid epilepsy = medication interactions, sudden unexpected death in epilepsy (SUDEP) | Shared neurodevelopmental mechanisms. Cortical hyperexcitability underlies both ASD features and seizures |
| Depression | Anxiety (70%), CD, substance abuse, dysthymia [1] | Suicidality risk highest when depression + SA + impulsivity. "Double depression" (MDD + dysthymia) = chronic and difficult to treat | Shared genetic/neurobiological vulnerability (5-HTTLPR, HPA axis dysregulation). Anxiety may develop first and then "evolve" into depression |
| ODD | ADHD, depression, anxiety [1] | The angry/irritable dimension of ODD predicts emotional disorders; the defiant/vindictive dimension predicts CD. Comorbid ADHD = higher risk of progression to CD | ODD straddles emotional and behavioural pathology. The comorbidity pattern predicts the developmental trajectory |
Child psychiatric conditions don't just affect the child — they affect the entire system:
| Level | Complication |
|---|---|
| Family | Parental stress, burnout, marital discord, sibling neglect (parental attention monopolised by the affected child), financial burden (therapy costs, lost work days), parental mental health deterioration |
| School | Teacher stress, classroom disruption affecting other students, resource allocation to SEN support |
| Healthcare system | Overuse of A&E for behavioural crises, repeated investigations for somatic complaints in somatising children, polypharmacy costs |
| Society | Juvenile delinquency, criminal justice costs, welfare dependency, lost productivity, intergenerational transmission of adversity (children of parents with untreated psychiatric conditions are at higher risk themselves) |
High Yield Summary
Complications of Child Psychiatric Conditions — Key Points:
-
ADHD: Age-dependent ↓ severity (hyperactivity > impulsivity > inattention), but ~50% retain criteria in adolescence and 40–60% have problems in adulthood. Key complications: academic failure, peer rejection, substance abuse, injuries, ODD/CD cascade, adult occupational failure and relationship problems. Treating ADHD with stimulants reduces later substance abuse risk.
-
ASD: Core symptoms tend to improve but only a minority achieve independent adult living. Key complications: seizures (25%), psychiatric comorbidity (anxiety, depression, ADHD), autistic burnout from chronic masking, challenging behaviour, and exploitation.
-
ODD/CD: Developmental cascade — ODD → CD → antisocial PD. Prognosis worse for early-onset (40% antisocial behaviour vs 20% in adolescent-onset). Complications include substance abuse, criminal behaviour, teenage pregnancy, educational failure.
-
Childhood anxiety: 2/3 improve in 3–5 years, but 1/3 develop other anxiety disorders (heterotypic continuity). Untreated anxiety leads to academic underperformance, social isolation, adult anxiety/depression, and substance abuse.
-
Youth depression: Episodic relapsing course. Key complications: suicide (leading cause of adolescent death), self-harm, substance abuse, recurrence, social harm. 25% may convert to bipolar disorder.
-
Iatrogenic complications: Stimulant growth suppression, SSRI suicidality risk in first 2 weeks, antipsychotic metabolic syndrome and hyperprolactinaemia, lithium toxicity, valproate teratogenicity. Also: labelling effects, parental guilt, assessment delays.
-
Comorbidity is itself a complication: Each comorbid condition worsens prognosis multiplicatively. Always screen for and treat comorbidities.
Active Recall - Complications in Child Psychiatry
References
[1] Senior notes: ryanho-psych.md (Chapter 12: Child Psychiatry sections 12.1–12.5; Chapter 11: Intellectual Disability)
High Yield Summary
Assessment in Child Psychiatry — Key Principles:
- Multi-informant: Always interview parents, child (alone), and family together. Obtain school collateral.
- Developmentally contextualised: Compare symptoms to same-age, same-culture norms. Use age-appropriate interview techniques.
- Developmental history is essential: Full pregnancy/birth history, milestones (gross motor, fine motor, language, social), temperament.
- Systematic comorbidity screen: ADHD, ASD, ODD/CD, mood, anxiety, eating, sleeping, elimination — child psychiatric conditions rarely come alone.
- MSE is modified for children: Observe play, activity level, eye contact, separation behaviour; imaginary friends ≠ hallucinations.
- Rating scales supplement but do not replace clinical interview.
- Physical examination and investigations are essential to exclude organic mimics (hearing loss, epilepsy, thyroid, genetic syndromes).
- Risk assessment includes risk to self, to others, FROM others (abuse/neglect), and vulnerability.
- Formulation uses the 4 P's (predisposing, precipitating, perpetuating, protective) in a biopsychosocial framework.
- Ethical considerations: Consent requires parental involvement for < 18; Gillick competence for mature minors; confidentiality limits must be stated upfront; safeguarding is paramount.
- Hong Kong context: Academic pressure, stigma, MCHC → CAC → CAMHS referral pathways, domestic helper caregiving dynamics.
High Yield Summary
Differential Diagnosis in Child Psychiatric Assessment — Key Points:
- Always exclude organic causes first — hearing loss, epilepsy, thyroid, anaemia, genetic syndromes, sleep disorders, substance use.
- Compare to developmental norms — a behaviour is only a symptom if it exceeds what is expected for age and culture.
- Comorbidity is the rule — expect and diagnose multiple conditions when criteria are met (ADHD+ODD, depression+anxiety, ASD+ID).
- Inattentive child DDx: ADHD (pervasive, chronic) vs learning disorder (academic only) vs anxiety (worry-driven) vs depression (episodic) vs BAD (episodic with mood change) vs ASD (poor social skills, restricted interests) vs organic (hearing, epilepsy, OSA).
- Socially odd child DDx: ASD (qualitative social deficit + restricted behaviours) vs ID (proportional delay) vs language disorder (normal non-verbal communication) vs social anxiety (desires but fears interaction) vs schizophrenia prodrome (deterioration from baseline + psychotic features).
- Bipolar DDx pitfalls: Underdiagnosed (hypomania missed → labelled as MDD) AND overdiagnosed (incorrect use of "manic"/"躁"). Correct diagnosis delayed 5–7 years on average. Follow diagnostic criteria strictly; use collateral information.
- ADHD vs BAD: ADHD is chronic/trait-like; BAD is episodic. ADHD lacks grandiosity, ↓sleep need, flight of ideas.
- School refusal is a behaviour, not a diagnosis — systematically consider separation anxiety, social phobia, depression, bullying, ASD, specific learning disorder, or conduct-related truancy.
- Note the theme of anxiety to guide DDx (weight → eating disorder, illness → hypochondriasis, intrusive thoughts → OCD, separation → SAD/BPD, rejection → social phobia/avoidant PD).
High Yield Summary
Diagnostic Criteria, Algorithm, and Investigations in Child Psychiatry:
- Always use diagnostic criteria systematically — clinical impression alone leads to overdiagnosis and underdiagnosis. Up to 33% of BAD diagnoses could not be confirmed by structured interview.
- ASD: DSM-5 dyad = social-communication deficits (all 3 needed) + restricted/repetitive behaviours (≥ 2 of 4). Onset in early developmental period. Not better explained by ID alone.
- ADHD: ≥ 6/9 inattention and/or ≥ 6/9 hyperactivity-impulsivity symptoms. Present before age 12 (DSM-5) or 6 (ICD-10). Pervasive (≥ 2 settings). ICD-10 is stricter (requires both domains); DSM-5 allows inattentive-only and hyperactive-only presentations.
- Diagnostic algorithm: Multi-informant history → MSE → Developmental appropriateness filter → Standardised rating scales → Organic exclusion → Systematic criteria application → Formulation → MDT discussion.
- Assessment is MDT-based: Clinical interview (most important) + day hospital MDT assessment + IQ testing + educational assessment + OT + speech therapy + standardised instruments.
- Rating scales supplement but do not replace clinical interview.
- Key investigations to exclude organic mimics: Audiometry (hearing loss), EEG (epilepsy), TFTs (thyroid), CBP/ferritin (anaemia), MRI (structural lesions), genetic testing (fragile X, chromosomal microarray), anti-NMDA antibodies (in first-episode psychosis).
- Pre-medication baselines: Height/weight/BMI, BP/HR, ECG (if TCA/antipsychotic), CBP, RFT, LFT, TFTs, glucose, lipids, prolactin (if antipsychotic).
- ADOS-2 + ADI-R = gold standard ASD assessment tools. Conners/Vanderbilt with parent + teacher forms = key ADHD tools. K-SADS-PL = gold standard general child psychiatric diagnostic interview.
- Child-specific criteria modifications: Irritable mood can substitute for depressed mood in depression; ODD has three-factor structure predicting different outcomes; CD onset type (childhood vs adolescent) predicts prognosis.
High Yield Summary
Management in Child Psychiatry — Key Principles:
- Psychosocial interventions are generally first-line — especially PMT for ADHD/ODD/CD, CBT for anxiety/depression, and early intensive behavioural intervention for ASD.
- ADHD medications are the most effective psychotropics — effect sizes ~0.7–1.0. Methylphenidate is first-line stimulant. Stepped approach: mild → PMT only; moderate → medications + psychosocial; severe → medications as first choice.
- PMT is the mainstay for ODD/CD — based on social learning theory. "Catch your child being good" + systematic reinforcement/extinction.
- ASD has no cure — management is MDT-based. No medication treats core symptoms; risperidone/aripiprazole for irritability only. Beware polypharmacy.
- Fluoxetine is the only SSRI with robust evidence for paediatric depression. Black box warning for suicidal ideation → close monitoring in first 4 weeks. Benefits outweigh risks in moderate–severe depression.
- Bipolar management: Mania → lithium/valproate/atypical AP. Depression → lithium/lamotrigine/quetiapine. Prophylaxis → lithium (only drug to reduce suicide). Avoid antidepressants if possible.
- Lithium monitoring: Pre-treatment (RFT, TFT, ECG); on-treatment (Li levels, RFT, TFT Q6 months). Narrow therapeutic index. Trough level 12h post-dose.
- ECT is rarely used in children but is indicated for emergency, catatonia, and treatment-refractory cases.
- Always manage comorbidities — treat the ADHD in a child with ODD; treat the anxiety in a child with depression.
- Always involve the family and school — no child psychiatric intervention works in isolation.
High Yield Summary
Complications of Child Psychiatric Conditions — Key Points:
-
ADHD: Age-dependent ↓ severity (hyperactivity > impulsivity > inattention), but ~50% retain criteria in adolescence and 40–60% have problems in adulthood. Key complications: academic failure, peer rejection, substance abuse, injuries, ODD/CD cascade, adult occupational failure and relationship problems. Treating ADHD with stimulants reduces later substance abuse risk.
-
ASD: Core symptoms tend to improve but only a minority achieve independent adult living. Key complications: seizures (25%), psychiatric comorbidity (anxiety, depression, ADHD), autistic burnout from chronic masking, challenging behaviour, and exploitation.
-
ODD/CD: Developmental cascade — ODD → CD → antisocial PD. Prognosis worse for early-onset (40% antisocial behaviour vs 20% in adolescent-onset). Complications include substance abuse, criminal behaviour, teenage pregnancy, educational failure.
-
Childhood anxiety: 2/3 improve in 3–5 years, but 1/3 develop other anxiety disorders (heterotypic continuity). Untreated anxiety leads to academic underperformance, social isolation, adult anxiety/depression, and substance abuse.
-
Youth depression: Episodic relapsing course. Key complications: suicide (leading cause of adolescent death), self-harm, substance abuse, recurrence, social harm. 25% may convert to bipolar disorder.
-
Iatrogenic complications: Stimulant growth suppression, SSRI suicidality risk in first 2 weeks, antipsychotic metabolic syndrome and hyperprolactinaemia, lithium toxicity, valproate teratogenicity. Also: labelling effects, parental guilt, assessment delays.
-
Comorbidity is itself a complication: Each comorbid condition worsens prognosis multiplicatively. Always screen for and treat comorbidities.
Sleep Disorders
Sleep disorders are a group of conditions that impair the ability to initiate, maintain, or regulate sleep or wakefulness, resulting in disrupted sleep patterns and daytime functional impairment.
Attention-deficit Hyperactivity Disorder
Attention-deficit hyperactivity disorder is a neurodevelopmental disorder characterized by persistent patterns of inattention, hyperactivity, and impulsivity that impair functioning across multiple settings.