Hyperkinetic disorders in childhood: epidemiology, etiology, clinical features, course, and treatment

Hyperkinetic disorders in childhood: epidemiology, etiology, clinical features, course, and treatment

ICD-10's hyperkinetic disorders, the narrower forerunner of attention deficit hyperactivity disorder (ADHD) in DSM-5 and ICD-11, with its core of inattention, overactivity and impulsivity from early childhood in more than one setting. How it arises, how it is assessed, how parent training, school support and medication are used by age, how the drugs are monitored, and how often it persists into adult life.

At a glance

  1. ICD-10's hyperkinetic disorder (F90) is inattention, overactivity and impulsivity together, beginning by 7, pervasive across settings and impairing. DSM-5 and ICD-11 ADHD is broader: either inattention or hyperactivity-impulsivity, several symptoms before 12, in two or more settings.
  2. About 5 per cent of children meet DSM-5 criteria for ADHD, and about 1 to 2 per cent the stricter ICD-10 criteria; boys are diagnosed two to three times as often. About 2 to 3 per cent of adults have ADHD.
  3. ADHD is highly heritable, at about 70 to 80 per cent; prematurity, prenatal alcohol, severe deprivation and brain injury add risk. Half to four-fifths of children have another disorder as well.
  4. Diagnosis is clinical, by a specialist, with histories from parents and teachers, rating scales such as the Conners, and a search for comorbidity and for conditions that mimic it.
  5. Under 5, group parent training comes first. From 5, environmental changes at school and home, then methylphenidate first-line, then lisdexamfetamine; atomoxetine or guanfacine if stimulants fail or are not tolerated.
  6. Height, weight, heart rate and blood pressure are checked before and during treatment, and stimulants, as controlled drugs, are prescribed with diversion and misuse in mind.
  7. Overactivity fades with age, but inattention often persists: about two-thirds still have impairing symptoms as young adults, and treatment reduces accidents, injuries and crime.

Definition and overview

A hyperkinetic disorder is a persistent pattern of inattention, overactivity and impulsivity, out of keeping with the child's age and developmental level, that starts early, shows in more than one setting and impairs the child's life. It is ICD-10's narrower version of what DSM-5 and ICD-11 call attention deficit hyperactivity disorder (ADHD).

ICD-10NameWhat it means
F90.0Disturbance of activity and attentionhyperkinetic disorder without conduct disorder
F90.1Hyperkinetic conduct disorderthe criteria for both hyperkinetic disorder and conduct disorder are met; kept separate because the combination has a worse outlook
F90.8, F90.9Other and unspecified
F98.8Attention deficit disorder without hyperactivitylisted among other childhood disorders; ICD-10 has no inattentive type of hyperkinetic disorder
ICD-10 hyperkinetic disorderDSM-5 ADHD
Symptomsall three domains: at least 6 of 9 inattention, 3 of 5 overactivity and 1 of 4 impulsivity symptomsat least 6 of 9 inattention symptoms, 6 of 9 hyperactivity-impulsivity symptoms, or both (5 from the age of 17)
Presentationsone, with or without conduct disordercombined, predominantly inattentive, predominantly hyperactive-impulsive
Onsetby the age of 7several symptoms before 12
Settingspervasive, in more than one setting such as home, school and clinicseveral symptoms in two or more settings
Durationat least 6 monthsat least 6 months
Exclusionsautism, mania, depression and anxiety disordersallowed with autism; not better explained by another disorder
Children affectedabout 1 to 2 per centabout 5 per cent

ICD-11 (6A05) follows DSM-5: ADHD with predominantly inattentive, predominantly hyperactive-impulsive or combined presentations, with onset usually before 12, and it no longer excludes autism. Most European countries still code with ICD-10, so a child diagnosed with ADHD may or may not meet the stricter ICD-10 criteria. UK guidance asks for the DSM-5 or ICD-11 criteria and advises against excluding the diagnosis because of autism.

Etiology and pathophysiology

ADHD has no single cause. It is a neurodevelopmental disorder in which many genes of small effect, and some environmental risks, shift the development of brain systems for attention, inhibition and reward.

FactorWhat is known
Genesheritability about 70 to 80 per cent; polygenic, overlapping with autism, depression and substance use; siblings have a risk several times higher; rare copy number variants in some
Prematurity and low birth weightthe earlier the birth, the higher the risk
Prenatal exposuresalcohol (fetal alcohol spectrum disorder) and valproate; the link with maternal smoking largely disappears in sibling studies, which points to shared genes
Early adversity and toxinssevere institutional deprivation; lead
Brain disorderstraumatic brain injury, epilepsy, genetic syndromes such as fragile X, 22q11.2 deletion and neurofibromatosis type 1

The core changes are in fronto-striatal and fronto-cerebellar circuits regulated by dopamine and noradrenaline: weaker inhibitory control and working memory, and a preference for small immediate rewards over larger delayed ones. Imaging shows a cortex that matures a few years later than usual, most clearly in prefrontal regions, and slightly smaller brain volumes on average, though no scan diagnoses ADHD. The drugs act on the same systems: stimulants raise dopamine and noradrenaline at the synapse by blocking the dopamine transporter and the noradrenaline transporter, and amphetamines also release them.

Clinical features

DomainWhat it looks like in a child
Inattentioncareless mistakes; cannot sustain attention in tasks or play; seems not to listen; does not finish tasks; disorganised; avoids sustained mental effort; loses things; easily distracted; forgetful
Overactivityfidgets and squirms; leaves their seat; runs and climbs when it is not appropriate; cannot play quietly; "driven by a motor"; talks excessively
Impulsivityblurts out answers; cannot wait their turn; interrupts and intrudes on others

The picture changes with age. Preschool children show relentless overactivity and accidents; school-age children show classroom problems, poor schoolwork and conflict with peers; adolescents feel inner restlessness rather than running about, and take risks with driving, sex and substances; adults struggle with disorganisation, lateness, forgetfulness, emotional volatility and unstable work and relationships. Girls more often have inattentive symptoms, attract less attention and are diagnosed later.

Comorbidity is the rule, with half to four-fifths having at least one other condition:

  • oppositional defiant disorder and conduct disorder;
  • specific learning disorders such as dyslexia, and developmental coordination disorder;
  • autism, tics and Tourette syndrome;
  • anxiety, depression and emotional dysregulation;
  • sleep problems;
  • in adolescence and adult life, substance misuse and, in some, antisocial personality disorder.

The consequences are real: academic underachievement and exclusion from school, injuries and road accidents, early pregnancy, unemployment, criminal convictions and a roughly doubled mortality, mostly from accidents.

ADHD from childhood to adult life
Three pale lanes, one above the other, run across the same years, from early childhood on the left to thirty on the right, with ticks for the years beneath them. In each lane a soft lavender area rises with how marked one group of symptoms is. Inattention, in the top lane, is high through childhood and falls only a little into adult life. Overactivity, in the middle lane, is highest in early childhood and falls steeply through adolescence to a low level. Impulsivity, in the bottom lane, falls too, but less. Three fine dotted lines cross all the lanes: at seven, at twelve and at twenty-five.

Point at a name or a part to light it.

ADHD begins in childhood, by 7 in ICD-10 and with several symptoms before 12 in DSM-5 and ICD-11, but it often does not end there. Overactivity fades most through adolescence, often to inner restlessness, impulsivity less and inattention least. By 25 about 15 per cent still meet the full criteria, and about 65 per cent, counting them, still have symptoms that impair them.

Simplified: the heights have no scale: each lane shows how marked one group of symptoms is, relative to itself; the course is typical, drawn by hand, not one person's; some recover fully and some keep all their symptoms; the figures at 25 come from a meta-analysis of follow-up studies and depend on how remission is defined.

5 sources
  1. World Health Organization. The ICD-10 Classification of Mental and Behavioural Disorders: Diagnostic Criteria for Research (DCR-10). WHO, 1993. F90, Hyperkinetic disorders.
  2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th edition, text revision (DSM-5-TR). APA, 2022. Attention-deficit/hyperactivity disorder.
  3. World Health Organization. Clinical Descriptions and Diagnostic Requirements for ICD-11 Mental, Behavioural and Neurodevelopmental Disorders (CDDR). WHO, 2024. Attention deficit hyperactivity disorder, 6A05.
  4. Biederman J, Mick E, Faraone SV. Age-dependent decline of symptoms of attention deficit hyperactivity disorder: impact of remission definition and symptom type. American Journal of Psychiatry, 2000;157(5):816–818.
  5. Faraone SV, Biederman J, Mick E. The age-dependent decline of attention deficit hyperactivity disorder: a meta-analysis of follow-up studies. Psychological Medicine, 2006;36(2):159–165.

Diagnosis and management

Assessment

  1. 1

    Referral

    A child with suspected ADHD is assessed by a specialist, a child psychiatrist or paediatrician with training in ADHD; in the UK a GP does not diagnose it or start medication.
  2. 2

    History

    From parents and child: onset, course, settings, development, family history, sleep, and the impact at home and school; from school: teacher reports and examples of work.
  3. 3

    Observation

    In clinic and, if possible, at school; rating scales such as the Conners rating scales, SNAP-IV or the Strengths and Difficulties Questionnaire, completed by parents and teachers.
  4. 4

    Examination

    Growth, heart rate and blood pressure, cardiovascular examination, hearing and vision, a neurological examination and a look for dysmorphic features.
  5. 5

    Diagnosis

    Made when the criteria are met with at least moderate impairment in more than one setting, and other explanations have been considered.

Rating scales support but do not make the diagnosis. Blood tests, an EEG and brain imaging are not routine, but are done when the history suggests a medical cause.

May mimic or coexist with ADHDClue
Normal energetic child, unrealistic expectationsproblems in only one setting or with one adult
Hearing or visual impairmentpoor response to instructions; found on testing
Absence epilepsybrief staring spells, sometimes many a day
Obstructive sleep apnoea and other sleep disorderssnoring, daytime tiredness
Intellectual disability or a specific learning disorderbehaviour fits the child's developmental level, or problems confined to learning
Anxiety, depression, trauma, maltreatment, attachment disorderonset after stress; worry, low mood, hypervigilance
Autismsocial communication difficulties and restricted interests, often alongside ADHD
Medication or substancesantiepileptics, antihistamines, salbutamol; cannabis or stimulants in adolescents
Hyperthyroidismweight loss, tremor, tachycardia

Treatment

Every family gets information about ADHD, support, and advice on changes at home and school: clear routines, short tasks broken into steps, immediate praise and rewards, seating near the teacher and away from distraction, movement breaks, and a written plan shared between home and school. Treatment then depends on age, as UK guidance sets out:

  1. 1

    Under 5

    An ADHD-focused group parent-training programme first. Medication only after a second specialist opinion from a service experienced with young children.
  2. 2

    5 and over

    If symptoms still cause significant impairment after the environmental changes, methylphenidate is first-line, short- or long-acting. Parent training is added if there is oppositional or conduct disorder; CBT can help adolescents who are on medication but still impaired.
  3. 3

    Second line

    After a 6-week trial of methylphenidate at an adequate dose without enough benefit, lisdexamfetamine; dexamfetamine if lisdexamfetamine helps but its long action is not tolerated.
  4. 4

    Third line

    If neither stimulant works or is tolerated, atomoxetine or guanfacine.
  5. 5

    Adults

    Lisdexamfetamine or methylphenidate first-line, atomoxetine if neither works or is tolerated, with psychological support for those who prefer not to take medication or still struggle.
DrugHow it worksKey points
Methylphenidateblocks reuptake of dopamine and noradrenalineimmediate release lasts about 4 hours, modified release 8 to 12; the most-studied drug, most effective in children; a controlled drug
Lisdexamfetaminea prodrug, cleaved in the blood to dexamfetamine, which releases dopamine and noradrenalineonce daily, lasting about 13 hours; amphetamines were the most effective drugs in adults in a network meta-analysis; less open to misuse than immediate-release stimulants; a controlled drug
Dexamfetaminereleases dopamine and noradrenalineshort-acting; more open to misuse
Atomoxetineselective noradrenaline reuptake inhibitor, not a stimulantfull effect takes weeks; nausea, poor appetite, sleepiness; warnings for suicidal thoughts and rare liver injury; useful with tics, anxiety or a risk of misuse
Guanfacinealpha-2A adrenoceptor agonist, not a stimulantprolonged release; drowsiness, low blood pressure, slow heart rate, QT prolongation; tapered, because stopping suddenly raises the blood pressure; authorised in the EU for 6 to 17 years when stimulants are unsuitable

Stimulants are the most effective treatment in the short term, helping about 70 per cent of children. Their common side effects are loss of appetite and weight, trouble getting to sleep, headache, stomach ache, irritability, anxiety and a small rise in heart rate and blood pressure. Rarer are tics, psychotic symptoms and mania. They are used with caution in heart disease, hypertension, a history of psychosis or substance misuse, and not with a monoamine oxidase inhibitor. Clonidine is used off-label, mainly with tics or sleep problems and in the UK only on the advice of a tertiary ADHD service; antipsychotics do not treat ADHD.

Before and during medication

Before starting, the specialist records the history (fainting or breathlessness on exertion, palpitations, chest pain, a family history of sudden cardiac death under 40), height and weight on a growth chart, heart rate and blood pressure on a centile chart, and examines the heart. An ECG is not routine, but is done, and a cardiologist's opinion sought, when the history or examination suggests heart disease, or with drugs that affect the QT interval.

WhatWhenIf it goes wrong
Heightevery 6 months in children and young peopleif growth falters, consider a smaller dose, breaks from treatment, or another drug
Weightevery 3 months in children aged 10 and under; at 3 and 6 months, then every 6 months, in older childrenfood before the dose and later in the evening, dietitian advice, dose change
Heart rate and blood pressurebefore and after each dose change, and every 6 monthsa sustained resting heart rate over 120, an arrhythmia or a systolic pressure above the 95th centile on two occasions: reduce the dose and refer
Sleep, mood, tics, psychotic symptoms, seizuresat each reviewadjust or change the drug
The need for medicationat least once a yeara planned trial off treatment where appropriate

Shared care with the GP is common once the dose is stable, with the specialist reviewing at least yearly.

Diversion and misuse

Stimulants are controlled drugs. They are diverted to others, often fellow students, for studying, weight loss or recreation, and immediate-release tablets can be crushed and snorted or injected. The risk is highest in adolescents and young adults and in those with a history of substance misuse. It is reduced by choosing lisdexamfetamine or a long-acting methylphenidate, or a non-stimulant such as atomoxetine; by small supplies and a parent holding the medication for younger children; by talking about it openly; and by noticing early or "lost" prescriptions. Untreated ADHD itself raises the risk of substance misuse, and treatment does not.

Epidemiology

of children meet DSM-5 criteria for ADHD
about 5per cent
meet the stricter ICD-10 criteria for hyperkinetic disorder
1–2per cent
of adults have ADHD
2–3per cent

Prevalence is similar across countries and continents when the same methods are used; apparent differences come from the criteria and the method. Boys are diagnosed two to three times as often as girls in the community and more often still in clinics, where inattentive girls are under-recognised; in adults the ratio is closer to equal. Diagnoses and prescriptions have risen steeply in the UK and much of Europe in the last decade, above all in adults and girls, with long waiting lists for assessment. ADHD is over-represented in prisons and among people with substance misuse.

Prognosis

Overactivity and impulsivity decline through adolescence, but inattention often persists. In follow-up studies, about 15 per cent of children with ADHD still meet the full criteria at 25, and about two-thirds still have impairing symptoms. A worse course is associated with comorbid conduct disorder, as in ICD-10's hyperkinetic conduct disorder, low IQ, family adversity and parental mental illness.

Treatment changes the outlook. In Swedish registers, periods on ADHD medication were associated with about a third fewer criminal convictions in men and two-fifths fewer in women, and with fewer injuries, road accidents and episodes of substance misuse; mortality in ADHD, roughly double the general population's, is mostly from accidents. Stimulants slow growth a little: in one long follow-up, children who kept taking them through childhood were about 2.5 cm shorter as young adults than those who took little, so height is monitored and breaks from treatment are considered when growth falters. Adults with ADHD benefit from treatment as children do, and transition from children's to adult services is planned rather than letting treatment lapse at 18.

Check yourselfAnswer, then say how sure you were: a lucky guess still counts as a weak point.

1A 9-year-old girl has been dreamy, disorganised and easily distracted at home and at school since she was 6, and her schoolwork is suffering. She is not overactive or impulsive. She meets the DSM-5 criteria for ADHD, predominantly inattentive presentation. Does she have an ICD-10 hyperkinetic disorder?

2A 4-year-old boy has severe, pervasive overactivity and impulsivity at home and at nursery, and a specialist confirms ADHD. What is the first-line treatment?

3A 9-year-old with ADHD still has marked impairment at school despite classroom adjustments. He has taken methylphenidate for 6 weeks at an adequate dose, with little benefit and no serious side effects. What does UK guidance suggest next?

4A 12-year-old on lisdexamfetamine has a resting heart rate of 126 beats per minute and a systolic blood pressure above the 95th centile for his age, height and sex on two separate visits. What should be done?

5A 19-year-old university student with ADHD, who used cannabis and cocaine in the past, says friends keep asking him for his immediate-release methylphenidate before exams. Which change best reduces the risk of diversion and misuse?

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Dopamine

Methylphenidate, the first-line drug for ADHD, blocks the reuptake of dopamine and noradrenaline.