Attention-deficit hyperactivity disorder

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

ADHD comprises persistent inattention and/or hyperactivity–impulsivity that is inconsistent with developmental level and interferes with social, educational or family function. A symptom is meaningful only when its intensity, frequency, context and impact exceed what is expected for age. Diagnosis therefore cannot be made from normal exuberance, one difficult classroom, parental strain or a questionnaire alone.

The clinical presentation may be predominantly inattentive, predominantly hyperactive–impulsive or combined. Inattention includes losing track of instructions, disorganisation, avoidable errors, task abandonment, distractibility and forgetfulness. Hyperactivity–impulsivity includes excessive movement or talking, difficulty waiting, acting without considering risk and interrupting. The outward form changes with age: running about may become inner restlessness, while organisational demand reveals impairment in adolescence.

Aetiology is multifactorial and strongly heritable. Common genetic variants contribute most population risk, with rare variants and neurodevelopmental conditions relevant in some individuals. Prematurity, prenatal exposures and early adversity are associated with ADHD but do not establish a single cause in a child. Sugar, vaccines and ineffective parenting do not cause ADHD; parenting interventions change function and relationships rather than correcting parental blame.

Pathophysiology involves altered maturation and coordination of distributed frontostriatal, frontoparietal, cerebellar, arousal and reward networks. Dopamine and noradrenaline signalling contribute to attention allocation, working memory, inhibition and reward timing. This is not a simple chemical deficiency, and response to a stimulant neither proves nor disproves the diagnosis. Sleep, stress, task novelty and environmental structure modify how the underlying regulation difficulty is expressed.

The differential is broad. Sleep deprivation or obstructive sleep apnoea causes poor concentration and irritability; hearing, vision or language difficulty produces apparent non-listening; learning disorder causes task-specific avoidance; anxiety produces preoccupation; depression reduces drive; trauma can cause hyperarousal or dissociation; autism affects flexibility and reciprocity; absence seizures interrupt awareness; and medication, caffeine or substances can alter arousal. Several may coexist with ADHD.

Key points

ADHD is a neurodevelopmental disorder: symptoms are developmentally inappropriate, began before age 12, persist, occur in at least 2 important settings and cause clear functional impairment.
Diagnosis is specialist and clinical. Rating scales support multi-informant assessment but neither a positive nor a negative score can independently diagnose or exclude ADHD.
Always assess sleep, hearing, vision, language, learning, autism, tics, anxiety, depression, trauma, epilepsy and the classroom environment; coexistence is common.
Under age 5, first-line treatment is an ADHD-focused group parent-training programme; medicine requires a second specialist opinion and persistent severe impairment.
From age 5, provide information, parent support and school environmental modifications before medicine; offer medication when significant impairment persists after these measures have been implemented and reviewed.
First-line medicine for children aged 5 years and over is methylphenidate. Age 5 use is off-label and remains specialist initiated.
After an adequate 6-week methylphenidate trial at an effective tolerated dose, switch to lisdexamfetamine when benefit remains insufficient.
Use dexamfetamine when lisdexamfetamine works but its longer effect is not tolerated; use atomoxetine or guanfacine when stimulants are not tolerated or separate adequate trials are ineffective.
Before medication record height, weight, pulse, blood pressure, cardiovascular history and current medicines; routine ECG is unnecessary without a clinical cardiac indication or interacting cardiac-risk medicine.
Monitor growth, pulse, blood pressure, sleep, appetite, mood, tics, seizures, adherence and diversion; review the continuing need for medicine at least annually.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Polygenic neurodevelopmental liability

ADHD is strongly heritable and usually reflects the combined effect of many common variants rather than one deterministic gene.

Rare and shared genomic factors

Rare variants and neurodevelopmental syndromes contribute in a minority, and genetic influences overlap with autism, learning and other psychiatric conditions.

Prenatal and perinatal associations

Prematurity and some prenatal exposures are associated with risk, but confounding is important and an association does not identify individual causation.

Environmental expression

Sleep, stress, classroom demand, trauma and support alter severity and visibility; they can be causes of mimics or modifiers without being the primary origin of ADHD.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Executive-control networks
Developmental differences in frontostriatal and frontoparietal systems affect inhibition, working memory, sustained attention and organisation over time.
2
Reward and timing
Altered reward anticipation and delay processing can favour immediate reinforcement and make long, low-feedback tasks disproportionately difficult.
3
Catecholamine modulation
Dopamine and noradrenaline regulate attention and response control, explaining treatment targets without implying a single measurable chemical deficiency.
4
Developmental and contextual change
Motor hyperactivity may lessen while planning demand rises; structure, novelty, sleep and interest change expression across situations.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Predominantly inattentive pattern

Disorganisation, distractibility, forgotten belongings, slow task completion and inconsistent output dominate, often without disruptive behaviour.

Hyperactive–impulsive pattern

Excessive movement, talking, interruption, poor waiting and rapid risk-taking are developmentally excessive and impairing across settings.

Masked or compensated pattern

High effort, parental scaffolding or a highly structured setting conceals symptoms, while lateness, exhaustion, emotional dysregulation or home collapse reveals cost.

Coexisting-needs pattern

Autism, tics, language or learning disorder, anxiety, depression, conduct difficulty, epilepsy and sleep disorder can shape presentation and treatment.

Red flags requiring action

Syncope on exertion, exertional chest pain, sudden-onset rapid regular palpitations, a murmur or a first-degree relative who died suddenly before age 40 requires cardiovascular opinion before ADHD medication.
Blood pressure persistently above the 95th centile for age and height requires paediatric hypertension assessment before or during treatment.
New hallucinations, delusions, marked mood elevation, severe agitation or suicidal thinking demands urgent mental-health review and medicine reassessment.
Developmental regression, seizures, focal neurological signs, episodic altered awareness or a major change from baseline is not explained by uncomplicated ADHD.
Severe sleepiness, loud snoring with witnessed apnoeas or profound insomnia can mimic or worsen inattention and needs a sleep-focused assessment.
Rapid weight loss, marked slowing of linear growth, persistent tachycardia or hypertension during medication requires dose review and specialist action.
Requests for early replacement prescriptions, sharing, selling or coercion around stimulants raise diversion and safeguarding risk.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Reference standard: specialist clinical diagnostic assessmentFirst stepReference standard
Why
Integrate developmental and psychiatric history, symptom criteria, onset, persistence, multi-setting impairment, observation, collateral and differential diagnosis.
Interpretation and limitations
There is no diagnostic blood test, brain scan, ECG, computerized attention test or medication trial; the whole longitudinal pattern establishes diagnosis.
02
First-line: multi-informant history and collateralFirst line
Why
Obtain concrete examples from child, caregivers and education, including strengths, impairment, age of onset, masking and environmental support.
Interpretation and limitations
Differences between settings require explanation; absence in a low-demand setting does not automatically exclude ADHD, but impairment must affect at least 2 important settings.
03
Validated symptom and impairment scales
Why
Standardise baseline parent and teacher observations and monitor change during intervention.
Interpretation and limitations
Scores support but do not replace diagnosis; interpret age, informant, culture, learning profile and context, and never use one threshold as a gatekeeper.
04
Developmental, mental-health and learning assessment
Why
Identify autism, language disorder, intellectual or specific learning difficulty, tics, anxiety, depression, trauma, conduct problems and substance risk.
Interpretation and limitations
Coexisting conditions are common and may require parallel intervention; do not force all difficulties into one diagnosis.
05
Hearing, vision, sleep and physical assessment
Why
Find sensory loss, sleep-disordered breathing, neurological disease, thyroid or other physical features suggested by history and examination.
Interpretation and limitations
Arrange formal sensory or sleep assessment when indicated; routine laboratory panels and neuroimaging are low value in an otherwise typical presentation.
06
Pre-medication baseline
Why
Record height, weight, pulse, blood pressure with correct cuff, cardiovascular history, current medicines and risk of misuse or diversion.
Interpretation and limitations
Routine ECG is not required unless history, examination, congenital heart disease, prior cardiac surgery or another medicine creating cardiac risk provides a clinical indication.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Sleep disorder

Insufficient sleep, obstructive apnoea, restless legs and delayed sleep phase cause inattention, irritability and hyperactivity; ask about snoring and schedule.

Learning, language or sensory difficulty

Task-specific avoidance or apparent non-listening may reflect inaccessible work, hearing loss, visual impairment or impaired comprehension.

Autism and intellectual disability

Executive and regulatory difficulty overlap, but social-communication, restricted-pattern and developmental-level assessment clinically distinguishes and identifies coexistence.

Anxiety, depression or trauma

Worry, low drive, hypervigilance and dissociation disturb concentration; time course, internal experience and triggers guide formulation.

Neurological or substance-related cause

Absence seizures, medication effects, caffeine, intoxicants and withdrawal can produce episodic or recent attentional change unlike longstanding ADHD.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01DiagnosisEstablish a persistent multi-setting patternFirst stepInattention, hyperactivity or impulsivity is causing concern.

1Screen immediately for acute risk, regression, seizures, sleep disorder, sensory loss, trauma and safeguarding concerns.
2Gather developmental history and concrete child, caregiver and education examples, then refer for specialist assessment when symptoms persist and impair function.
3AlternativeSpecialist confirms onset before age 12, presence in at least 2 settings, impairment and exclusion or recognition of alternative and coexisting conditions.

02Under 5 yearsUse parent training before medicineADHD symptoms impair a preschool child's family or nursery life.

1Offer an ADHD-focused group parent-training programme and practical nursery or home environmental adaptations without implying parental causation.
2If symptoms remain significantly impairing, obtain specialist ADHD input and coordinate education and family support.
3Do not offer medicine under age 5 without a second specialist opinion from a service with expertise in young children.

03Age 5 and overStart with information and environmental modificationADHD is diagnosed in a school-age child or young person.

1Discuss diagnosis, strengths, sleep, routines and treatment preference; offer parent support and implement documented school environmental modifications.
2Review whether modifications adequately reduce impairment, while addressing learning, communication, mental-health and family needs.
3Offer medicine when symptoms still cause persistent significant impairment after modifications have been implemented and reviewed.

04Medication sequenceUse evidence-based stepwise prescribingMedication is agreed after baseline assessment.

1Offer methylphenidate first and titrate to an effective tolerated dose with weekly parent and teacher feedback.
2After an adequate 6-week methylphenidate trial, switch to lisdexamfetamine if benefit is insufficient; use dexamfetamine when lisdexamfetamine works but its longer profile is not tolerated.
3Use atomoxetine or guanfacine if stimulants are not tolerated or separate adequate methylphenidate and lisdexamfetamine trials fail; seek tertiary advice after one stimulant and one non-stimulant are ineffective.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

NICE first-line stimulant when medication is indicated; immediate release helps flexible titration or short-duration coverage.

Methylphenidate immediate release

Child 6–17 years: start 5 mg orally once or twice daily, increasing by 5–10 mg at weekly intervals; maximum 60 mg daily in divided doses. Space doses by about 4 hours. Age 5 use is specialist and off-label.

Monitor appetite, growth, pulse, blood pressure, sleep, mood and tics. Avoid a late dose when it causes insomnia. It is a controlled drug: prescribe and store securely and assess misuse, diversion and school handling.

Longer school-day coverage without a midday dose; select formulation by required duration, swallowing ability and meal routine.

Methylphenidate modified release, approximately 12-hour tablet

For a suitable licensed formulation from age 6: start 18 mg orally each morning and increase by 18 mg at approximately weekly intervals; usual child maximum 54 mg daily. Follow the chosen product's SmPC.

Release profiles differ between brands. Prescribe by brand, follow product-specific food instructions and do not crush. Do not switch blindly. Monitor stimulant effects, appetite, growth, sleep and cardiovascular observations.

NICE next stimulant after an adequate 6-week methylphenidate trial gives insufficient benefit at a tolerated dose.

Lisdexamfetamine

Child 6–17 years: start 30 mg orally each morning, or 20 mg when a lower start is appropriate; increase by 10–20 mg at about weekly intervals; maximum 70 mg daily. Age 5 use is specialist and off-label.

Monitor appetite, growth, pulse, blood pressure, sleep, mood and diversion. Avoid monoamine oxidase inhibitors and obtain specialist cardiovascular or mental-health advice when the baseline profile requires it.

Non-stimulant when stimulants are not tolerated or separate adequate methylphenidate and lisdexamfetamine trials are ineffective.

Atomoxetine

Up to 70 kg: start 0.5 mg/kg/day orally for at least 7 days, then about 1.2 mg/kg/day. Above 70 kg: start 40 mg/day for at least 7 days, then 80 mg/day; maximum 100 mg/day. Once-daily or divided dosing follows tolerability.

Benefit develops over weeks. Monitor pulse, blood pressure, appetite, mood and suicidal thinking. Stop and assess possible hepatic injury such as jaundice or dark urine. CYP2D6 inhibitors can increase exposure.

Non-stimulant specialist option after stimulant intolerance or inadequate separate stimulant trials, selected for the child's clinical profile.

Guanfacine prolonged release

Age 6–17 years: start 1 mg orally once daily and increase by no more than 1 mg weekly. Use the current BNFC or SmPC weight- and age-banded maximum. Taper by no more than 1 mg every 3–7 days.

Sedation, dizziness, bradycardia, hypotension and syncope occur. Check pulse and blood pressure during titration; abrupt withdrawal can cause rebound hypertension. Swallow whole, avoid high-fat meals and grapefruit juice, and review CYP3A4 modifiers.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Educational and occupational restriction

Unsupported executive difficulty increases missed learning, exclusion and reduced attainment despite intact ability and limits future opportunity.

Accident and exploitation risk

Impulsivity, poor hazard anticipation, substance use and unsafe driving increase injury and safeguarding vulnerability over time.

Mental-health morbidity

Repeated failure, criticism and coexisting conditions increase anxiety, depression, self-harm, conduct problems, substance misuse and low self-esteem.

Relationship and participation strain

Conflict, peer rejection, sleep disruption and caregiver stress worsen function when needs are misunderstood or support is fragmented.

Treatment-related harm

Appetite and growth effects, insomnia, cardiovascular change, psychiatric symptoms, diversion and rebound hypertension require active prevention and monitoring.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

During titration record symptoms, functional impairment and adverse effects at every dose change using parent and teacher feedback; review regularly, commonly weekly, until optimised.
Measure height every 6 months in children and young people and plot height and weight on an age-appropriate growth chart.
Measure weight every 3 months in children aged 10 years and under. In those over 10, check at 3 and 6 months after starting and every 6 months thereafter, or more often if concern arises.
Check pulse and blood pressure before and after each dose change and every 6 months, comparing paediatric blood pressure with an age- and height-appropriate centile.
Monitor sleep with a diary, new or worsening tics, seizures, emotional change, psychotic or manic symptoms, adherence, safe storage and diversion.
Review treatment at least annually with the child and family, covering benefit throughout the day, adverse effects, education and relationships, preference, missed doses and whether a supervised dose reduction or discontinuation is appropriate.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

A calm clinic does not exclude ADHD

Novel one-to-one attention can temporarily support regulation; longitudinal examples and functional demands are more informative.

Rating scales measure reports

They improve structure and monitoring but are affected by context and cannot replace specialist diagnostic reasoning.

Response is not a diagnostic test

Stimulants can improve attention in people without ADHD, while an ineffective trial may reflect dose, formulation or a different priority need.

Formulation is part of treatment

Duration, food effects and release profile alter coverage and adverse effects; methylphenidate brands are not automatically interchangeable.

11Common pitfallsFrequent interpretation and management errors.

01
Do not diagnose ADHD from a questionnaire, classroom observation or stimulant response alone.
02
Do not use medication under age 5 without the required second specialist opinion.
03
Do not obtain a routine ECG when history and examination provide no indication.
04
Do not start medicine before baseline height, weight, pulse, blood pressure and cardiovascular review.
05
Do not switch modified-release methylphenidate brands without checking their release and food profiles.
06
Do not overlook growth, psychiatric adverse effects, safe storage or diversion during follow-up.