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Attention deficit hyperactivity disorder

SNOMED: 92841000087107748 wordsUpdated 03/03/2026
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Exam Tips

  • Core diagnostic triad for OSCE answers: onset before 12 years, symptoms in >=2 settings, and clear functional impairment for >=6 months.
  • In adults use lower symptom threshold (>=5 rather than >=6) and emphasize occupational/executive dysfunction.
  • Always mention collateral history (parent/school/work) and comorbidity screening as essential for diagnosis.
  • Differentiate ADHD from anxiety/depression by temporal pattern: ADHD is chronic from childhood, while concentration problems in mood/anxiety are usually episodic with affective symptoms.
  • Before prescribing stimulants, state cardiovascular history/exam and baseline BP, pulse, height/weight monitoring, plus misuse/diversion risk assessment.

Definition

Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder defined by persistent inattention and/or hyperactivity-impulsivity that causes functional impairment. Symptoms must begin before age 12 years, persist for at least 6 months, and be present in at least two settings (for example home and school/work), with the pattern not better explained by another mental disorder or psychosis.

Pathophysiology

ADHD is biologically heterogeneous and strongly heritable, with dysregulation of catecholaminergic signalling (mainly dopamine and noradrenaline) in frontostriatal and frontocerebellar networks that mediate attention, inhibition, reward processing, and executive function. Structural and functional imaging studies in textbooks commonly describe delayed cortical maturation and altered connectivity in prefrontal-striatal circuits (see standard psychiatry text figures on frontostriatal circuitry). Genetic vulnerability interacts with environmental exposures (for example prematurity, low birth weight, prenatal smoking/alcohol, psychosocial adversity), producing variable phenotypes (inattentive, hyperactive-impulsive, combined).

Risk Factors

  • Family history/genetic loading (high heritability in twin studies)
  • Male sex (diagnosed more often, though girls may be under-recognized)
  • Low birth weight and prematurity
  • Maternal smoking during pregnancy
  • Prenatal alcohol exposure
  • Epilepsy or acquired brain injury
  • Lead exposure
  • Iron deficiency
  • Psychosocial adversity and lower socioeconomic status
  • Adverse maternal mental health

Clinical Features

Symptoms

  • Poor sustained attention, careless mistakes, distractibility
  • Disorganization, poor task completion, avoidance of sustained mental effort
  • Forgetfulness and losing items needed for tasks
  • Restlessness, feeling unable to stay seated, excessive talking
  • Impulsivity: blurting out answers, interrupting others, difficulty waiting turn
  • Functional impairment in school/work, relationships, self-care, and daily organization

Signs

  • Observed fidgeting/squirming, frequent seat-leaving, motor overactivity
  • Appears not to listen despite normal hearing during consultation/classroom reports
  • Interruptive, intrusive interaction style
  • Evidence from collateral history of symptoms across multiple settings
  • Academic or occupational underperformance relative to ability

Investigations

Comprehensive clinical assessment (specialist-led; DSM-5/ICD-aligned):Symptom thresholds met (>=6 symptoms in children, >=5 in adults for inattention and/or hyperactivity-impulsivity), onset before 12 years, >=2 settings, significant impairment
Collateral history (parents/carers/school/work reports; rating scales):Cross-situational and persistent pattern of impairment, helping distinguish ADHD from situational or single-context problems
Mental health and neurodevelopmental comorbidity screen:Identify coexisting anxiety, depression, ASD, ODD/conduct disorder, tic disorder, substance misuse, learning disorders
Physical baseline before medication (height, weight, pulse, BP, cardiovascular history/exam):Provides safety baseline for stimulant/non-stimulant treatment and ongoing growth/cardiometabolic monitoring
ECG/cardiology review if indicated:Performed when there is personal/family cardiac risk, syncope, congenital heart disease, or concerning examination findings
Sensory/developmental assessment when clinically suggested:May reveal alternative contributors (hearing/visual impairment, learning disorder, seizures, fetal alcohol spectrum features)

Management

Lifestyle Modifications

  • Psychoeducation for patient and family; explain chronic course and strengths-based support
  • Structured routines, sleep optimization, task chunking, reduced distractions, school/work reasonable adjustments
  • Parent-training/behavioural programmes for children with mild-moderate impairment
  • Liaison with school/college/employer and safeguarding/risk assessment (driving risk, substance use, self-harm risk)

Pharmacological Treatment

First-line stimulants (specialist initiation and titration)

  • Methylphenidate immediate-release: usually start 5 mg once or twice daily, increase by 5-10 mg weekly; commonly up to 60 mg/day in divided doses
  • Lisdexamfetamine: start 30 mg each morning, increase by 20 mg at about weekly intervals; max 70 mg/day

Monitor pulse, BP, weight/appetite, sleep, mood and tics at baseline and during titration. Avoid/seek specialist advice in significant cardiovascular disease, hyperthyroidism, glaucoma, pheochromocytoma, or recent MAOI use; caution with misuse/diversion risk and potential growth suppression in children.

If inadequate response/intolerance to first stimulant

  • Dexamfetamine (after lisdexamfetamine response but poor tolerability): specialist individualized dosing
  • Atomoxetine: adults typically 40 mg daily for at least 7 days then 80 mg daily; max 100 mg/day

Atomoxetine can worsen suicidal ideation (especially younger people), may increase BP/HR, and rarely causes severe liver injury; monitor mental state and liver symptoms. Slower onset than stimulants.

Non-stimulant alpha-2 agonist option (children/adolescents in selected cases)

  • Guanfacine prolonged-release: start 1 mg once daily, increase by up to 1 mg/week (typical range 1-4 mg/day; specialist may use higher in adolescents)

Can cause sedation, hypotension, and bradycardia; taper gradually to avoid rebound hypertension. Useful when stimulants are unsuitable or with specific comorbidity profiles.

Complications

  • Educational underachievement and school exclusion
  • Low self-esteem, family conflict, and peer relationship difficulties
  • Increased risk-taking, accidental injury, and unsafe driving
  • Substance misuse disorders
  • Comorbid psychiatric illness (anxiety, depression, ODD/conduct disorder, possible bipolar presentations)
  • Persistence into adulthood with occupational and social impairment

Prognosis

Long-term follow-up suggests only a minority retain full diagnostic criteria by adulthood, but many continue to have residual symptoms with functional impairment. Inattentive symptoms tend to persist more than overt hyperactivity. Outcome is strongly influenced by recognition and treatment of comorbidities, psychosocial support, and continuity of care through transition to adult services.

Sources & References

💊BNF Drug References(5)

NICE Guidelines(1)

📖Textbook References(13)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1082)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 23, 24)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1081, 1082)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1041, 1042)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1695)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1081)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1082)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1080, 1081)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1307)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1046)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 24)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1080, 1081)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1045, 1046)[context]

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