Autistic Spectrum Disorder

• Worldwide prevalence: approximately 1–1.5% of the population ^[2]. The US CDC (2023 data) estimates ~1 in 36 children (2.8%), though this partly reflects broadened diagnostic criteria and improved surveillance.
• Hong Kong: Local studies suggest a prevalence of approximately 1 in 27 to 1 in 59 primary school children (estimates vary), with increasing referrals to the Child Assessment Service (CAS) of the Department of Health over the past two decades. HK figures are broadly consistent with international data.
• The apparent rise in prevalence over time is largely attributed to diagnostic substitution (children previously labelled as having intellectual disability or language disorders now receive ASD diagnoses), broadened criteria, increased awareness, and earlier detection — rather than a true increase in the underlying condition.

• Sex ratio: Male : Female ≈ 4–5 : 1 ^[2].
  • Why the male predominance? This is incompletely understood. The "female protective effect" hypothesis suggests that females require a greater cumulative genetic burden (more risk variants) to manifest ASD, meaning girls are relatively protected unless they carry a higher mutational load. When girls do present, they often have more severe phenotypes or co-occurring intellectual disability.
  • Additionally, diagnostic bias plays a role: girls with ASD may present with less obvious RRBs, better superficial social mimicry ("masking" or "camouflaging"), and more internalising symptoms, leading to under-recognition.
• Socioeconomic status: ASD occurs across all racial, ethnic, and socioeconomic groups ^[2]. Earlier studies showing higher prevalence in higher-SES families were artefacts of diagnostic access bias.

Comorbidity in ASD is the rule, not the exception ^[2]:

• Family history of ASD: Siblings of an individual with ASD have approximately a 3–10% recurrence risk (25× the population risk) ^[2].
• Broader autism phenotype (BAP): Family members may show subclinical traits (social awkwardness, rigidity, language quirks) without meeting full diagnostic criteria.
• Concordance rates: MZ twins ~60–90% vs DZ twins ~0–30% ^[2] — demonstrating a very strong genetic contribution but also a role for non-shared environmental factors.

• Advanced paternal age (and to a lesser extent, maternal age) — possibly related to accumulation of de novo mutations in sperm and/or alterations in genetic imprinting ^[2].
• Maternal medication exposure: Notably valproate (sodium valproate / Epilim) during pregnancy — well-established teratogen associated with ~10% risk of ASD in exposed offspring ^[2].
• Obstetric complications: Prematurity, low birth weight, perinatal hypoxia, birth defects ^[2]. These may act as "second hits" on a genetically vulnerable background.
• Prenatal infections: Rubella (historical), CMV, and possibly other TORCH infections.
• Maternal factors: Gestational diabetes, maternal immune activation during pregnancy (e.g., febrile illness), prenatal stress.

• Maternal migration (especially if migration occurred around pregnancy): Possibly related to maternal stress, reduced immunity to endemic infections, or vitamin D deficiency ^[2].
• Socioeconomic factors primarily affect access to early diagnosis and intervention rather than causation per se.

• Parenting style is NOT a cause. The outdated "refrigerator mother" theory (Bettelheim, 1960s) — blaming cold, emotionally distant mothers — is categorically wrong and harmful.

• Accelerated early brain growth: Infants who later develop ASD often show accelerated head circumference growth during the first 1–2 years of life, resulting in macrocephaly in ~20% of cases ^[2]. This is followed by a plateau or even relative decline in brain volume later.
• Why does this matter? The period of accelerated growth coincides with critical windows for synaptogenesis and synaptic pruning. Aberrant overgrowth may reflect deficient synaptic pruning — too many synapses that are poorly organised, leading to noisy, inefficient neural circuits.

The prevailing neurobiological model is one of altered connectivity ^[2]:

• Under-connectivity of long-range connections (e.g., frontal-posterior pathways) — impairs integration of information across brain regions (e.g., combining facial expression + voice tone + context to understand social meaning).
• Over-connectivity of local/short-range connections — may contribute to enhanced local processing (explaining savant abilities, attention to detail) but at the expense of holistic processing.

This maps beautifully onto the Weak Central Coherence theory (see below).

• Serotonin (5-HT): ~30% of individuals with ASD have hyperserotonemia (elevated whole-blood serotonin) ^[2]. Serotonin is critical for brain development, mood regulation, and GI motility. This may explain both the psychiatric comorbidities and GI symptoms seen in ASD.
• Oxytocin: Reduced levels or altered receptor expression. Oxytocin is the "social bonding" neuropeptide → deficiency may contribute to impaired social motivation and attachment.
• GABA/Glutamate imbalance: Evidence of excitatory-inhibitory (E/I) imbalance in cortical circuits — possibly explaining sensory hypersensitivity and epilepsy risk.
• Dopamine: Mesolimbic pathway abnormalities may affect reward processing and social motivation ^[2].

• Mirror neurons (frontal and parietal regions) fire both when performing an action and when observing someone else perform the same action. They are thought to be the neural substrate for empathy, imitation, and understanding others' intentions.
• Evidence suggests dysfunction of the mirror neuron system in ASD ^[2], which may contribute to difficulties with imitation, empathy, and theory of mind.

ASD (299.00) is a single diagnostic entity with specifiers ^[1]:

Under Pervasive Developmental Disorders (F84) ^[2]:

Aligns with DSM-5 — single entity ASD (6A02) with dimensional specifiers for:

• Intellectual functioning (with/without disorder of intellectual development)
• Functional language level (with/without impairment of functional language)
• Loss of previously acquired skills

While ASD is primarily diagnosed through behavioural observation and history, clinical examination may reveal:

This is one of the trickiest distinctions. Why? Because both conditions cause language delay, behavioural difficulties, and social immaturity. The critical insight is proportionality ^[2]:

• A child with ID alone and a mental age of 2 years will have the social skills of a typical 2-year-old — they will seek comfort, share enjoyment (at a 2-year-old level), use pointing and gestures, and engage in simple social games (peek-a-boo). Their social behaviour matches their cognitive level.
• A child with ASD and a mental age of 2 years will have social skills below even that of a typical 2-year-old — they may not point, may not seek comfort, may not share enjoyment, and may show qualitatively unusual social behaviour (e.g., treating people as objects).

This is why DSM-5 Criterion E states: "To make comorbid diagnosis of ASD with ID, social communication should be below that expected for general developmental level" ^[2].

A child with a pure language disorder (e.g., developmental language disorder / specific language impairment) has difficulty with the mechanics of language (phonology, grammar, vocabulary) but their social intent to communicate is intact ^[2]. Watch them carefully:

• They will compensate nonverbally — pointing vigorously, pulling you by the hand, using facial expressions, making eye contact to check if you understood.
• They engage in imaginative play — feeding dolls, pretending a banana is a phone.
• They have no RRBs.

In ASD, it's the opposite: even if speech is fluent, the social use of language (pragmatics) is impaired, and nonverbal communication is also abnormal.

• ADHD: The child knows how to interact socially but can't sustain attention or can't inhibit impulsive behaviours that disrupt social interactions (blurting out, interrupting, not waiting for turns). When they are calm and focused, their social skills are intact ^[2].
• ASD: The child fundamentally doesn't know how to interact — they lack the intuitive social understanding, even in calm moments.
• Remember: these frequently co-occur (30-60%). When they co-occur, you see both the qualitative social communication deficits of ASD AND the attentional/impulsivity symptoms of ADHD.

This is a beautiful clinical distinction ^[2]:

• OCD: Repetitive behaviours (compulsions) are performed to reduce distressing, intrusive thoughts (obsessions). The person does not want to perform them — they are ego-dystonic (experienced as foreign to the self). There is subjective distress.
• ASD: Repetitive behaviours are typically ego-syntonic — the person finds them comforting, enjoyable, or neutral. There is no distressing obsessional thought driving them. The behaviours serve a self-regulatory function (e.g., hand-flapping when excited).

However, be aware that individuals with ASD can also develop comorbid OCD — in which case you see both ego-syntonic stereotypies AND ego-dystonic obsessions/compulsions.

• ASD: Neurodevelopmental — present from early childhood, continuous course (though severity may wax and wane). Social withdrawal is due to fundamental social communication deficits.
• Schizophrenia: Typically emerges in late adolescence/early adulthood with an episodic course. Social withdrawal in the prodrome or negative symptom phase may mimic ASD, but there should be evidence of positive psychotic symptoms (delusions, hallucinations, formal thought disorder) ^[2]. Premorbid development was usually (though not always) normal.
• Important DSM-5 rule: If a patient has a history of ASD, the additional diagnosis of schizophrenia requires prominent delusions or hallucinations present for at least 1 month in addition to other criteria ^[2].

• ASD: The child does not intuitively understand social cues. They may not be anxious about social situations — they simply don't grasp the social rules.
• Social Anxiety Disorder: The child understands social cues too well (hyper-mentalising) — they are acutely aware of the possibility of negative judgement and this paralyses them. Their social cognition is intact; their social performance is impaired by anxiety.

In practice, this distinction can be blurred because many individuals with ASD develop secondary social anxiety (they've learned through painful experience that social situations go badly for them). But the primary deficit differs.

Still referenced in some Hong Kong clinical settings ^[2]:

Qualitative impairments in ALL 3 domains ^[2]:

1. Reciprocal social interaction
2. Communications
3. Restricted, repetitive and stereotyped patterns of behaviour, interests, and activities

Temporal requirement: Developmental abnormalities must have been present in the first 3 years of life ^[2]. (This is stricter than DSM-5's "early developmental period.")

Additional features (non-specific): May also have other non-specific problems including fears/phobias, sleeping and eating disturbances, temper tantrums, and aggression ^[2].

The syndrome can be diagnosed in all age groups ^[2].

Key differences from DSM-5: ICD-10 requires 3 domains (separating social interaction from communication); DSM-5 collapses these into 2 domains (social communication + RRBs). ICD-10 specifies onset before age 3; DSM-5 says "early developmental period" without a strict age cutoff. ICD-10 keeps separate diagnoses (Asperger, atypical autism, etc.); DSM-5 unifies them.

Aligns closely with DSM-5:

• Two core domains: (1) persistent deficits in social communication and social interaction; (2) restricted, repetitive, and inflexible patterns of behaviour, interests, or activities
• Specifiers for intellectual functioning and language level
• Specifier for loss of previously acquired skills

ASD diagnosis in Hong Kong (and internationally) follows a multi-stage process: surveillance/screening → referral → comprehensive diagnostic assessment → post-diagnostic evaluation ^[2].

The key principle: ASD is a clinical diagnosis made by expert clinical judgement — not by any single screening tool or investigation. Standardised instruments support but do not replace clinical assessment.

In Hong Kong, the typical pathway is:

1. Concern raised — by parents, MCHC (Maternal and Child Health Centre) nurses, kindergarten teachers, or primary care doctors.
2. Referral to Child Assessment Service (CAS) — under the Department of Health. This is the primary diagnostic service for developmental concerns in children < 12 years in HK.
3. Multidisciplinary assessment at CAS — by a team including developmental paediatrician, clinical psychologist, speech therapist, occupational therapist, social worker.
4. For older children/adolescents/adults — referral to Child and Adolescent Psychiatry (HA) or adult psychiatry services.

Remember: there is no diagnostic biomarker for ASD. Medical investigations are performed to:

1. Identify treatable comorbid conditions (hearing loss, epilepsy, metabolic disorders)
2. Identify aetiological factors (genetic syndromes)
3. Exclude medical mimics

The diagnostic assessment integrates multiple sources of information:

The diagnosis is ultimately a pattern recognition exercise by an experienced clinician who synthesises all available data against the DSM-5/ICD criteria. There is no single score on any instrument that "confirms" ASD — and equally, a "negative" ADOS-2 does not rule it out if the clinical picture is otherwise compelling.

Why atypical antipsychotics for irritability? Irritability and aggression in ASD are thought to involve dysregulation of dopaminergic and serotonergic circuits (particularly mesolimbic and orbitofrontal pathways). Blocking D2 receptors dampens the excessive dopaminergic drive behind aggression, while 5-HT2A blockade further modulates mood and impulse control. Aripiprazole's partial agonism makes it a "gentler" modulator.

Important prescribing principles:

• Always try behavioural interventions first — medication is for when behavioural approaches alone are insufficient.
• "Start low, go slow": Begin at the lowest dose and titrate gradually.
• Regular review: Attempt dose reduction or discontinuation periodically to assess ongoing need.
• Monitor metabolic parameters: Weight, height, BMI, fasting glucose, fasting lipids at baseline, 3 months, then at least 6-monthly.

Contraindications / Cautions:

• Known hypersensitivity
• Caution in patients with diabetes or metabolic syndrome (worsened by weight gain)
• Caution with QTc-prolonging medications (risperidone can prolong QTc)
• Avoid in neuroleptic malignant syndrome history

Comorbid ADHD occurs in 30-60% of individuals with ASD ^[2]. Treatment follows standard ADHD guidelines but with additional caution:

Contraindications for methylphenidate: Uncontrolled hypertension, structural cardiac disease, pheochromocytoma, hyperthyroidism, concurrent MAOI use, severe anxiety (stimulants may worsen), psychosis, tic disorders (relative).

Why SSRIs for repetitive behaviours? Serotonergic abnormalities are well-documented in ASD (hyperserotonemia). The repetitive behaviours in ASD share neurobiological overlap with OCD (cortico-striatal-thalamo-cortical circuit dysfunction). SSRIs modulate this circuit via serotonergic enhancement. However, the evidence for SSRIs reducing core RRBs in ASD is mixed — they are more consistently helpful for comorbid anxiety/OCD/depression ^[2].

Contraindications for SSRIs: Concurrent MAOI use (serotonin syndrome risk), known hypersensitivity, caution in bipolar disorder (can precipitate mania).

Sleep problems affect 50-80% of children with ASD and significantly impact daytime behaviour, learning, and family QoL.

• Occurs in ~20-30% of individuals with ASD (higher with co-occurring ID).
• Managed with standard antiepileptic drugs (AEDs) appropriate for seizure type.
• Avoid valproate in females of childbearing age (teratogenicity — and notably, prenatal valproate exposure is itself a risk factor for ASD).
• Common choices: levetiracetam, lamotrigine (may also stabilise mood), carbamazepine/oxcarbazepine.

• The most common psychiatric comorbidity in ASD ^[2].
• Types: Specific phobias, social anxiety disorder, generalised anxiety disorder, separation anxiety, selective mutism, OCD.
• Why anxiety is so common in ASD from first principles:
  • Individuals with ASD live in a social world they cannot intuitively decode. Imagine navigating a foreign country where you don't speak the language, can't read body language, and every interaction could go wrong unpredictably — that is the daily reality for many people with ASD. This chronic unpredictability breeds anxiety.
  • Executive dysfunction (cognitive inflexibility) means they cannot easily adapt when things change → any deviation from routine is experienced as threatening.
  • Sensory hypersensitivity means the physical environment itself can feel hostile (loud, bright, overwhelming).
  • Impaired interoception (difficulty reading one's own bodily signals) means they may not recognise anxiety building until it reaches a crisis point (meltdown/shutdown).
  • Especially in the adolescent stage ^[2] — as social demands increase and awareness of being "different" grows, anxiety intensifies.
• Clinical presentation: May present atypically — as increased RRBs, insistence on sameness, avoidance, aggression, meltdowns, or withdrawal rather than verbalising "I feel anxious."
• Management: Modified CBT (if cognitive/verbal ability sufficient), environmental modifications, SSRIs if severe ^[2].

• Behavioural problems, e.g., hyperactivity ^[2] and inattention are extremely common.
• Prior to DSM-5, dual diagnosis of ASD and ADHD was not permitted; now it is recognised as a genuine comorbidity.
• Why ADHD co-occurs so frequently: Shared genetic architecture (overlapping risk loci), shared neurobiological substrate (prefrontal dysfunction, dopaminergic dysregulation), and executive function deficits are core to both conditions.
• Impact: ADHD symptoms compound the social difficulties of ASD — the child not only doesn't understand social cues but also can't sustain attention to learn them. Impulsivity leads to additional social rejection.
• Management: Methylphenidate (lower response rate in ASD+ADHD, ~50%), atomoxetine, guanfacine ^[2].

• Mood problems: anxiety, depression (especially in the adolescent stage) ^[2].
• Why depression emerges, especially in adolescence from first principles:
  • Increased self-awareness in adolescence → the individual with ASD becomes painfully aware of their social differences and struggles.
  • Repeated social failure and rejection → learned helplessness.
  • Social isolation → absence of protective social buffering.
  • The chronic stress and effort of "masking" (maintaining a socially acceptable facade) is exhausting and demoralising ^[2]. ASD adults use compensation strategies and coping mechanisms to mask their difficulties in public but suffer from the stress and effort ^[2].
  • Biological vulnerability: serotonergic system abnormalities predispose to mood disorders.
• Clinical presentation: May present atypically — irritability, increased RRBs, withdrawal, loss of previously acquired skills, changes in sleep/appetite, self-harm. Verbally limited individuals may not be able to articulate low mood.
• Management: SSRIs (start low, go slow), modified CBT, addressing psychosocial stressors (bullying, isolation).

• Distinguish from core ASD RRBs: OCD obsessions/compulsions are ego-dystonic (distressing), whereas ASD RRBs are typically ego-syntonic (comforting). However, true OCD can develop on top of ASD.
• Why OCD co-occurs: Shared cortico-striatal-thalamo-cortical (CSTC) circuit dysfunction; serotonergic abnormalities common to both.
• Management: SSRIs, modified exposure and response prevention (ERP) CBT.

• Lifetime risk of psychosis is modestly increased in ASD (estimated ~5-10%, vs ~1% population base rate).
• Atypical beliefs or unusual perceptual experiences in ASD can be misdiagnosed as psychosis (diagnostic overshadowing).
• True comorbid schizophrenia requires prominent delusions/hallucinations for ≥ 1 month (DSM-5 Criterion F for schizophrenia) ^[2].

• ARFID (Avoidant/Restrictive Food Intake Disorder) is particularly common — driven by sensory sensitivities (texture, taste, smell, appearance), insistence on sameness (eating only specific foods), and anxiety around novel foods.
• Anorexia nervosa: emerging evidence that ASD is over-represented in anorexia, possibly related to cognitive rigidity, weak central coherence (focus on caloric detail), and difficulty with interoception.

• Shared neurobiological substrate (basal ganglia / cortico-striatal circuits).

• Behavioural problems, e.g., self-injurious behaviour ^[2]: Head-banging, biting self, scratching, hitting self. More common in ASD with co-occurring intellectual disability.
• Why SIB occurs from first principles:
  • Communication frustration: A non-verbal child who cannot express pain, hunger, discomfort, or distress may resort to SIB as the only available "communication."
  • Sensory function: SIB can provide intense sensory input that modulates an under-stimulated sensory system (hyposensitivity to pain).
  • Escape/avoidance: SIB may function to escape demands or unwanted sensory experiences.
  • Automatic reinforcement: Endogenous opioid release from self-injury may create a self-reinforcing cycle.
• Management: Functional behavioural assessment (identify the function) → teach replacement behaviour → environmental modification. Risperidone/aripiprazole for severe cases ^[2].

• Disruptive or challenging behaviour ^[2]: Aggression towards others, property destruction, tantrums.
• Why: Similar functional analysis to SIB — communication of unmet needs, sensory overload, demand avoidance, disruption of routines, anxiety, pain/medical issues.
• Critical point: Always consider whether a medical cause is driving the behavioural change. Individuals with ASD who cannot verbalise pain may present with sudden behavioural deterioration when they have dental pain, ear infection, constipation, GERD, fractures, etc. The behaviour IS the communication.

• Soiling/enuresis ^[2]: Delayed toilet training is common due to difficulties with interoception (not recognising bladder/bowel signals), communication (can't tell a caregiver they need the toilet), insistence on sameness (rigid toileting routines), and sensory issues (aversion to the toilet environment).

• Sleep disorders ^[2]: Affect 50-80% of individuals with ASD.
• Types: Sleep onset insomnia (most common), frequent night waking, early morning waking, irregular sleep-wake patterns.
• Why sleep is disrupted from first principles:
  • Melatonin synthesis abnormalities: Reduced activity of ASMT (acetylserotonin O-methyltransferase), the enzyme converting N-acetylserotonin to melatonin → lower endogenous melatonin → impaired circadian entrainment.
  • Serotonergic abnormalities: Serotonin is the precursor to melatonin — if the serotonergic system is dysregulated, melatonin production is affected.
  • Sensory hypersensitivity: Difficulty "switching off" in a sensory environment (room too bright, sounds too loud, bedding uncomfortable).
  • Anxiety and hyperarousal: The same anxiety that permeates daytime persists at night.
  • Co-occurring ADHD: Hyperactivity/restlessness interferes with sleep onset.
• Impact: Poor sleep worsens daytime behaviour, attention, learning, mood, and family stress. It is one of the most important modifiable factors in ASD.
• Management: Sleep hygiene → melatonin (first-line pharmacotherapy) → treat comorbidities (anxiety, ADHD).

• Seizures (25%): usually develop by adolescence ^[2].
• Bimodal onset: First peak in early childhood (< 5 years), second peak in adolescence.
• Risk factors for epilepsy in ASD: Co-occurring intellectual disability (strongest predictor), female sex, known genetic syndrome (tuberous sclerosis, Fragile X, Angelman), regression.
• Why epilepsy co-occurs from first principles: The same neurodevelopmental abnormalities that produce ASD — aberrant neuronal migration, synaptic dysfunction, excitatory/inhibitory (E/I) imbalance (GABA/glutamate), cortical malformations — also lower seizure threshold. Tuberous sclerosis (cortical tubers = epileptogenic foci) is a paradigmatic example.
• Types: Any seizure type can occur; complex partial seizures and generalised tonic-clonic seizures are most common. Subtle seizure types (absence, myoclonic) may go unrecognised.
• Management: Standard AEDs per seizure type. Avoid valproate in females of childbearing age (teratogenic; and notably, prenatal valproate exposure itself increases ASD risk — a cruel irony).

• Catatonia-like features, e.g., freezing mid-action, slowing ^[2].
• Prevalence: ~12-17% of adolescents/young adults with ASD, more common in those with ID.
• Features: Motor immobility (stupor, posturing, catalepsy), mutism, negativism, mannerisms, echolalia/echopraxia, withdrawal.
• Why catatonia occurs in ASD: Poorly understood, but possibly related to basal ganglia/frontal dysfunction, GABA-ergic abnormalities, and extreme anxiety/shutdown responses.
• Importance: Often misattributed to "just ASD" and therefore undertreated. Must be actively recognised because it responds to treatment (benzodiazepines, ECT in refractory cases).

• Motor deficits, e.g., abnormal gaits, clumsiness, toe-walking, other abnormal motor signs ^[2].
• Dyspraxia (motor planning difficulties), hypotonia, poor balance, fine motor difficulties.
• Impact: Affects handwriting, self-care skills, sports participation, and peer acceptance.

• Why: Core social communication deficits → difficulty making and maintaining friendships. Difficulty making and maintaining peer friendships ^[2]. Many individuals with ASD want social connection but lack the skills to achieve it, leading to profound loneliness.
• Impact: Social isolation is a risk factor for depression, anxiety, and suicidality. Reduced social network means fewer protective factors in times of crisis.

• Individuals with ASD are 4× more likely to be bullied than neurotypical peers.
• Why: Social naivety (can't recognise bullying, manipulation, or sarcasm), difficulty reporting (communication deficits), "different" behaviour that attracts negative attention, reduced peer protection (fewer friends to intervene).
• Impact: Compounds social anxiety, depression, school refusal, self-harm.

• Despite having average or above-average intellectual ability, many individuals with ASD underperform academically due to executive dysfunction, sensory overload in the classroom, social/behavioural difficulties, and inadequate educational support.

• Only a minority can live and work independently in adulthood ^[2].
• Adults with ASD face significant barriers to employment: social communication difficulties in interviews and workplace dynamics, sensory challenges in work environments, executive dysfunction affecting organisation and time management, stigma and discrimination.
• Unemployment rates for adults with ASD are estimated at 50-80%, even among those with university degrees.

• Difficulty understanding social rules of romantic relationships, consent, appropriate behaviour.
• Vulnerability to exploitation (especially in those with ID or social naivety).
• Sensory issues affecting physical intimacy.

• Adults with ASD (especially those without ID, sometimes called "high-functioning") have significantly elevated rates of suicidal ideation (~66%), suicide attempts (~35%), and completed suicide.
• Why: Chronic social isolation, camouflaging exhaustion ^[2], depression, unemployment, relationship failure, and a sense of being fundamentally "different" without hope of change.
• Critical implication: Always screen for suicidality in adolescents and adults with ASD, especially during transitions (school to university, university to employment) and periods of loss.

• A minority of individuals with ASD come into contact with the criminal justice system, sometimes due to misunderstanding social rules (e.g., stalking behaviour driven by social naivety rather than malice), rigid rule-following (reporting minor infractions of others), or intense interests that inadvertently cross legal boundaries.
• Vulnerability when in the justice system: difficulty understanding their rights, suggestibility during interview, sensory distress in custody.