Attention-Deficit/Hyperactivity Disorder – Comprehensive Study Notes
DSM-5 Classification & Core Criteria
- ADHD is grouped under Neurodevelopmental Disorders alongside autism, intellectual disability, etc.
- Shared attributes of neurodevelopmental disorders
- Childhood onset
- Atypical development of core skills that usually emerge gradually (motor, language, social, self-regulation)
- Persist, in some form, into adulthood
- Impair personal, social, academic, occupational functioning
- High rates of co-occurrence with each other
- DSM-5 conceptualises ADHD through three symptom clusters
- Inattention (more accurately “dysregulated attention”)
- Wanders off task, lacks persistence, easily distracted
- Disorganisation, loses things, forgetful
- Hyperactivity
- Excessive motor activity when inappropriate
- Fidgeting, tapping, running/climbing, talkativeness
- Impulsivity
- Hasty acts without forethought; seeks immediate reward
- Difficulty delaying gratification; social intrusions (blurting, interrupting)
- Diagnostic thresholds (observable behaviour only)
- ≥6 inattentive and/or ≥6 hyperactive–impulsive symptoms for ≥6 months (children ≤ 16 yrs)
- Adults (≥ 17 yrs): ≥5 symptoms in either/both clusters
- Several symptoms must have been present before age 12
- Symptoms present in ≥ 2 settings (home, school, work, social)
- Must cause clinically significant impairment
- Cannot be better explained by oppositionality, comprehension failure, hostility, or other disorders
- Presentation specifiers
- Combined (both thresholds met)
- Predominantly Inattentive
- Predominantly Hyperactive/Impulsive
- Severity specifiers (mild, moderate, severe)
- Consider total symptom load, degree of functional impairment, comorbidity
- Contextual caveat
- High-reward, novel, or 1-to-1 environments can mask symptoms
- Boring, low-structure, low-stimulation settings exacerbate them
- Lack of cross-situation symptoms ≠ absence of ADHD
Developmental Manifestation Across the Lifespan
Preschool (≤ 5 yrs)
- Short play sequences, incomplete activities, non-listening
- Little sense of danger, constant motion, scant sustained attention
- High false-positive risk: typical toddlers are naturally impulsive and active
- Subtle early markers often missed; environment still low-demand
Primary School (≈ 6–11 yrs)
- Classroom expectations expose deficits: sitting, concentrating, self-management
- Signs:
- Forgetfulness, disorganisation, distractibility
- Excessive restlessness, blurting, rule-breaking accidents
- Academic under-achievement; behavioural issues; peer problems
- Elevated teacher/parent stress
Adolescence (12–17 yrs)
- Transition to self-management (timetables, homework, multiple classrooms)
- Previously compensated children may “fall apart” academically & socially
- Manifestations:
- Missed details, scheduling failures, poor foresight & risk taking
- Car or DIY accidents; impulsive money/drug/alcohol behaviours
- Emerging self-medication reports
Adulthood (18 yrs +)
- Inattention: bills, deadlines, appointments
- Continued impulsivity/hyperactivity (restlessness, job-hopping, driving offences)
- Mood, anxiety and substance disorders common (see Comorbidity)
- Poorly managed adults often describe lifelong compensatory strategies or illicit stimulant use
Differential Diagnosis & Cultural/Gender Issues
- Girls often less hyperactive → later/under-diagnosis
- Cultural norms: some societies expect early exuberance, later academic endurance
- ESL learners: inattentive appearance may be language processing fatigue
- Lack of conventional schooling, refugee trauma, or sensory overload can mimic ADHD
- Must rule out / distinguish from:
- Oppositional Defiant Disorder (ODD) – refusal, defiance vs. dysregulated attention
- Anxiety disorders – worry-driven distraction & fidgeting via cortisol surge
- Autism Spectrum Disorder (ASD) – core social-communication deficits, RRBs, sensory processing differences
- Learning disorders, intellectual disability, trauma, sleep disorder, thyroid, etc.
ADHD vs. ASD Red Flags
- ASD-leaning indicators: fascination with repetitive movement, language regression, “savant-like” splinter skills
- ADHD can show apparent social/flexibility issues secondarily (impulsive behaviour, compensatory rigid routines)
Comorbidity Snapshot
- Children (RCH multidisciplinary sample, N = 132)
- ODD ≈52%, Anxiety 23%, Learning disability 15%, Language disorder 14%, Mood 5%, ASD 3.8%, ID 3.8%, Conduct 2%; None 23%
- Adults: high rates of mood, anxiety, substance use, and emotionally dysregulated personality disorders
Prevalence
- Global childhood pooled estimate: 7.2% (Thomas et al., 2015)
- Australian survey: most common childhood mental health condition > anxiety
- Adult prevalence declines with age; possible reasons
- Symptom remission in subset
- Historical under-recognition in older cohorts
Etiology: Interacting Mechanisms
Genetics
- High heritability: h2≈0.88 (clinical ADHD)
- More heritable than major depression; similar to bipolar/schizophrenia
- Multiple genes; dopaminergic pathways prominent (DRD4, DAT1, COMT, etc.)
- Single-gene syndromes (e.g.
fragile X) explain only a small minority
Teratogens / Medical
- Fetal alcohol exposure → ADHD-like profile; spectrum from effects to full FASD
Environment & Epigenetics
- Prefrontal cortex sensitive to early environment (Bock & Braun)
- Risk contexts
- Pathogenic care: neglect, institutionalisation, caregiver turnover
- Early trauma, coercive parenting, low SES, parental mental illness
- Escalating transactional processes: difficult temperament ↔ parental stress
- Always embedded within genetic backdrop (G×E)
Neurobiological & Cognitive Theories
Executive Dysfunction Theory
- ADHD symptoms stem from deficits in executive functions (EF): inhibition, working memory, planning, cognitive flexibility
- Evidence
- Group-level EF task impairments
- Reduced prefrontal & frontostriatal volumes/activity
Dopaminergic / Motivational Theory
- Baseline hypodopaminergia → low intrinsic motivation, reward seeking, delay aversion
- Stimulant efficacy & dopamine genes support model
Other Hypotheses
- Circadian rhythm disruption → mis-timed arousal & fatigue
- Alternative neurotransmitters (norepinephrine, serotonin, acetylcholine, etc.)
Pharmacological Interventions (Effect sizes in children ≈ adults > placebo)
Psychostimulants (first-line)
- Methylphenidate (Ritalin, Concerta)
- Dopamine & norepinephrine reuptake inhibitor
- Short-acting (2–3 doses/day) & long-acting formulations
- Low-dose therapeutic window; high doses → agitation, abuse potential
- Common adverse: insomnia, appetite loss
- Amphetamines (Adderall, Vyvanse)
- Increase synaptic DA/NE via release & reuptake blockade
- Similar benefits + side-effects (sleep, anxiety, headache, nausea)
- Street amphetamine self-medication reported in undiagnosed adults
Non-stimulants
- Atomoxetine (Strattera)
- Selective NE reuptake inhibitor; raises PFC dopamine indirectly
- Slightly smaller effect size; useful with comorbid anxiety
- α-2A Agonists
- Guanfacine XR (Intuniv) & Clonidine (Catapres)
- Reduce sympathetic tone; sedative, hypotensive side-effects
- Reserved for stimulant-intolerant or adjunctive use
Emerging / Off-label & Nootropics
- Modafinil/Armodafinil: wakefulness agents; mixed ADHD evidence
- Over-the-counter amino acids (tyrosine, phenylalanine, L-dopa precursors) – limited empirical support; popular in online communities
Long-term Considerations
- Stimulant effects attenuate over years → parallel skill-building essential
Psychosocial & Behavioural Interventions
School-Based
- Teacher psychoeducation about ADHD mechanisms (EF, dopamine, movement)
- Classroom adjustments
- Frequent breaks, fidget tools, movement access
- Reward systems (dojo points, token economies)
- Pre-loading instructions; stepwise directions; minimise distractions
- Seating: front, low-noise, clear sightlines
- Pomodoro-style work/break cycles
- Curriculum/material simplification; assistive tech
Parent Training & Family Work
- Psychoeducation: reframe ‘lazy’ as biologically-based dysregulation
- Evidence-based programmes (Triple P, PMT, Incredible Years)
- Non-judgemental delivery; acknowledge parental burden & possible parental ADHD
- Home routines, visual schedules, apps (e.g.
Trello, Habitica, Time-Timer)
Individual Skills & Therapies
- ADHD / Executive Function Coaching: routines, planning, externalising structure, reduce cognitive load
- Mindfulness: attentional control practice; adult utility > child
- CBT: targets comorbid anxiety, depression, self-esteem; adapt for shorter attention & high movement needs
- Exercise: regular moderate-vigorous activity lowers symptom severity
- Occupational Therapy / Sensory Integration
- Identify hypo- vs. hyper-sensitivities (noise, touch, proprioception)
- Provide sensory diets, weighted items, movement circuits
Technology-Focused
- Neurofeedback
- Train θ/β ratio (↓ daydream waves, ↑ alertness waves)
- Small adult evidence; motivation-intensive; scarce paediatric data
- Computerised Cognitive Training
- Game-like sustained attention tasks with adaptive difficulty
- Mixed transfer to real-world functioning; costly licences
Assessment Protocol
- Clinical Interviews
- Parent(s): prenatal, birth, developmental milestones, medical, temperament, family mental health, trauma, environment
- Child/adolescent (developmentally adjusted): self-perception & difficulties
- Teacher input essential
- Rating Scales / Questionnaires
- Connors-3: Inattention, Hyperactivity/Impulsivity, EF, Learning, Peer/Family
- BASC-3: broad internalising, externalising, adaptive, EF
- PLUS: SNAP-IV, ADHD-RS-5, Vanderbilt, BRIEF-2, SDQ
- Direct Observation
- Standardised testing session (clinic)
- Classroom (primary years), playground, home videos
- Performance Tests / Differential Screens
- Cognitive/IQ + academic (WISC-V, WIAT-IV) to rule out LD/ID
- Language, motor, sensory, sleep, medical investigations
Associated Clinical Features
- Sensory irregularities (hyper or hypo across modalities) – correlated with sleep problems
- Sleep: delayed sleep onset, nocturnal restlessness, daytime fatigue
- Hyper-focus capability: prolonged, intense immersion in high-interest tasks
Special Topic: Evolutionary Mismatch Theory
- Once-adaptive traits (rapid orienting to novel stimuli, high mobility) favoured survival in ancestral environments with:
- Sparse sensory input
- Need for vigilance (predation, foraging)
- Modern environments: information overload, sedentary schooling/work → same genes become maladaptive → symptomatic ADHD
- Discuss in tutorials: implications for stigma, intervention design, and societal expectations
Key Numerical References
- Diagnostic age criterion: symptoms pre-12 yrs
- Symptom threshold (child): 6+6 or 6 in one domain
- Adult threshold: ≥5 symptoms
- Heritability h2=0.88; Childhood prevalence 7.2%
- RCH comorbidity: only 23% ADHD-only; ODD 52%
Practical Implications for Future Clinicians
- ADHD is heterogeneous; tailor assessments & interventions accordingly
- Combine medication with psychosocial supports; teach lifelong self-management
- Screen systematically for comorbidities; treat most impairing condition first
- Provide culturally & developmentally informed interpretations; avoid pathologising normal variability
- Frame interventions positively: enhance strengths (creativity, hyper-focus), minimise deficits (organisation, impulsivity)