ICD-116A05	ATTENTION DEFICIT HYPERACTIVITY DISORDER (ADHD) Attention deficit hyperactivity disorder
ICD-10F90.0	Disturbance of activity and attention
DSM-5-TRF90.0–F90.2	Attention-Deficit/Hyperactivity Disorder

1. Definition and nosology

Attention Deficit Hyperactivity Disorder (ADHD; ICD-11: 6A05 Attention deficit hyperactivity disorder; DSM-5-TR: F90.0–F90.2x ADHD) — a neurodevelopmental disorder characterized by a pattern of inattention, hyperactivity, and impulsivity that begins in early development (by age 12), causing functional impairment in academic, social, or occupational activities.

In ICD-11 and DSM-5-TR three presentation forms:

• 6A05.0 — predominantly inattentive type;
• 6A05.1 — predominantly hyperactive-impulsive type;
• 6A05.2 — Combined presentation.

2. History

• Still G.F. (1902) — “abnormal defect of moral control” — in the Goulstonian Lectures (Lancet) he described 43 children in total; of these, 20 (15 boys, 5 girls) showed the defect without general impairment of intellect and without physical disease.
• 1937 — Bradley C. — accidental discovery of stimulant (benzedrine) therapy in children with behavior problems.
• DSM-II (1968) — “Hyperkinetic Reaction of Childhood”.
• DSM-III (1980) — “Attention Deficit Disorder” (with or without hyperactivity) — attention deficit accepted as core.
• DSM-IV (1994) — standardization of the term “ADHD” and its 3 subtypes (inattentive, hyperactive-impulsive, combined).
• DSM-5 (2013) and ICD-11 (2019) — the term “presentation” reflects that the course may change over time; the age of onset has been raised from 7 to 12; in adults the number of symptoms required for diagnosis is reduced (5 of 9 symptoms instead of 6 in each category, for age 17 and older).

3. Epidemiology

• Spread in children: 5–7% (Polanczyk G.V. et al. Am J Psychiatry 2007 systematic review and meta-analysis, 102 studies). CDC in the US: 9.8% of children aged 3–17 years by parent-reported ever-diagnosis (NSCH 2016–2019), 11.4% in 2022; this is not a clinical assessment but a parent report of a previously made diagnosis.
• Prevalence in adults: 2.5–4% (Kessler R.C. et al. Am J Psychiatry 2006 — National Comorbidity Survey Replication).
• Sex: in childhood 2–4 times higher in boys (under-recognition in women — less hyperactivity, more inattention); difference decreases in adulthood.
• Persistence: 60–70% of childhood ADHD continues to some degree in adulthood (Faraone S.V. et al. meta-analysis, Psychol Med 2006).
• Comorbidity: Oppositional behavior disorder 40%, conduct disorder 14%, anxiety 25%, depression 15–30%, learning disorder 25–40%, tic disorders 7–20%, autism spectrum 30–50% (in ASD patients), substance use disorder risk increased 2–3 times in adolescence and adulthood.

4. Aetiology and pathogenesis

4.1 Genetic factors

• Heritability: 74% (Faraone S.V., Larsson H. Mol Psychiatry 2019 meta-analysis of twin and family studies) — one of the highest heritability neurodevelopmental disorders.
• Genetic architecture: Polygenic — hundreds of small-effect variants. GWAS (Demontis D. et al. Nat Genet 2019, n>55,000) identified 12 risk loci (FOXP2, SORCS3, DUSP6, and others).
• Dopamine system genes — DRD4, DRD5, DAT1 (SLC6A3) — candidate genes; effect size small.
• CNV — rare; common variations are fundamental.

4.2 Neurobiological mechanisms

• Dysfunction of the dopaminergic and noradrenergic systems — particularly prefrontal cortex, striatum, cerebellum circuitry; stimulants reduce symptoms by acting on these systems.
• Structural changes: A reduction in total brain volume and specific regions (caudate, putamen, prefrontal cortex) volume (Hoogman M. et al. Lancet Psychiatry 2017 ENIGMA-ADHD n>3000 — small effect sizes).
• Functional relationship: dysregulation between the default mode network and the executive control network.
• Executive function model (Barkley R.A.) — poor inhibition as core deficit; affects working memory, foreplanning, emotional regulation.
• Reward system dysfunction — Delayed reward sensitivity (Sonuga-Barke E.J. Neurosci Biobehav Rev 2003).

4.3 Environmental risk factors

• Preterm birth and low birth weight — increases risk 2–3 times.
• Maternal use of tobacco, alcohol, and cannabis during pregnancy.
• Maternal perinatal stress and severe psychosocial deprivation.
• Lead exposure in childhood.
• Early traumatic brain injury (TBI).

4.4 Precise stance against ETIOLOGY MYTHS

• Sugar does not cause ADHD (Wolraich M.L. et al. JAMA 1995 meta-analysis).
• Screen time / video games do not cause ADHD (association exists, but no evidence of causal direction — Ferguson C.J. Perspect Psychol Sci 2015).
• Poor parenting does not create ADHD (heritability 74%); however, a highly conflictual family environment can affect symptom severity.

5. Clinical features

5.1 Inattention domain

• Failure to pay attention to details, careless mistakes.
• Difficulty sustaining attention in tasks.
• Appears not to listen when spoken to directly.
• Noncompliance with instructions, leaving tasks unfinished.
• Difficulty organizing tasks and activities.
• Persistent avoidance of tasks requiring sustained mental effort.
• Losing necessary items.
• Easily distracted by external stimuli.
• Forgetfulness in daily activities.

5.2 Hyperactivity and impulsivity domain

• Movement of limbs, twisting in seated position.
• Not remaining seated where sitting is expected.
• Running away or climbing in inappropriate places (in adults, feeling internal restlessness).
• Inability to play quietly.
• Behavior “as if driven by a motor”.
• Excessive talking.
• Blurting out an answer before the question has been completed.
• Unable to wait in queue.
• Interrupting others' conversations or activities.

5.3 Age-related differences

• Preschool age: hyperactivity dominant; attention short in play; behavioral control in social situations difficult.
• School age: Academic problems become prominent; inattention affects academic achievement.
• Adolescence: motor hyperactivity decreases, inner restlessness and impulsivity remain; risk behavior increases.
• Maturity: Internal distress, difficulty with planning, impulsivity in relationships; functional impairment in work and family life.

6. Diagnosis

6.1 Unified diagnostic criteria (DSM-5-TR · ICD-11 · NICE NG87 · AAP 2019 consensus points)

A. From inattention and/or hyperactivity-impulsivity symptoms in children (≤16 years) at least 6 symptoms in each category, adults (17+) at least 5 symptoms, must have lasted at least 6 months and be at a level not expected for age.

B. Several symptoms must have been present before age 12.

C. Symptoms in at least two settings (e.g., home + school, home + work) should be observed.

D. Functional impairment — significant impact on social, academic, occupational activity.

E. Exclusions — Does not occur in context of schizophrenia or other psychotic disorder; not fully explained by another psychiatric disorder.

6.2 Source-specific clarifications

• DSM-5-TR (F90.0–F90.2x): presentation — inattentive / hyperactive-impulsive / combined; severity — mild, moderate, severe. Age of onset raised to 12 (in DSM-IV 7).
• ICD-11 (6A05): Parallel structure; ‘co-morbid’ qualifiers (autism, language disorder, intellectual disability).
• NICE NG87 (2018, updated 2019): the diagnosis should be made by a multidisciplinary team (in children — pediatrician/psychiatrist; in adults — psychiatrist); structured interview and observation combined.
• AAP 2019 (Wolraich M.L. et al. Pediatrics 2019;144(4)): Diagnostic and treatment algorithm for ages 4–18 at the first medical assistance level 4–5 years — first-line parent training (PCIT, parent management training), second-line methylphenidate; 6–11 years — first-line stimulant + behavioral intervention; 12–18 years — first line stimulant + behavioral intervention (with adolescent consent).
• AACAP Practice Parameter (Pliszka S. JAACAP 2007): Comorbidity assessment and treatment sequencing.
• CADDRA Canadian ADHD Practice Guidelines (4th edition, 2018): Comprehensive algorithm for adult ADHD.

6.3 Diagnostic algorithm

1. Parent and teacher (for children) or patient themselves (for adults) interview — symptom history, onset age, contexts.
2. Standardized rating scales — Conners-3 (parent/teacher/patient), Vanderbilt (AAP recommendation), SNAP-IV; for adults ASRS (Adult ADHD Self-Report Scale, WHO/Kessler).
3. Clinical interview — confirmation of symptoms in two contexts, documentation of functional impairment.
4. Medical and neurological examination — excluding somatic causes (thyroid, hearing, vision, anemia).
5. Intellectual and academic assessment (WISC-V, academic tests) — to differentiate learning disorder and intellectual disability.
6. Comorbidity screening — ODD, conduct disorder, anxiety, depression, tic, autism, substance use.
7. Sleep disturbance and obstructive sleep apnea screening (especially in hyperactive-impulsive type).

6.4 Differential diagnosis

7. Examination and assessment

7.1 Clinical scales

• Vanderbilt ADHD Diagnostic Rating Scale — parent and teacher, ages 6–12 — AAP 2019 recommendation.
• Conners-3 — complex CDDP and comorbidity assessment (6–18 years).
• SNAP-IV (Swanson, Nolan, Pelham) — 26 questions.
• ASRS (Adult ADHD Self-Report Scale, WHO/Kessler R.C.) — 18 questions; brief screening in adult patients.
• DIVA-5 (Diagnostic Interview for ADHD in adults) — structured interview.
• BRIEF-2 (Behavior Rating Inventory of Executive Function) — executive function.

7.2 Laboratory investigations

No specific laboratory indication for routine ADHD. Based on clinical suspicion:

• Complete blood count, ferritin (iron deficiency), thyroid function (TSH).
• Lead level — if risk factors are present.
• Toxicology screening — suspicion of substance use in adolescents.
• Before stimulant initiation — EKG only if cardiac risk history or family history (AAP, AHA 2008; routine EKG not required).

7.3 Instrumental investigations

• EEG — only if seizure suspected or atypical clinical manifestations.
• Brain MRI — only for focal neurological signs. No routine indication.
• Neurophysiological tests for diagnosis (TOVA, IVA, QbTest) lack sufficient evidence base — The clinical diagnosis and standardized scales are prioritized as the gold standard.

8. Treatment

8.1 General Principles (NICE NG87 · AAP 2019 · CADDRA 2018 Consensus)

1. Age-based approach (AAP 2019):
   • 4–5 years — first-line parent training (PCIT, Triple P, Incredible Years); second-line methylphenidate.
   • 6–11 years — first-line Stimulant + behavioral intervention.
   • 12–18 years — first line Stimulant + behavioral intervention; adolescent consent.
   • Adults — Stimulant or non-stimulant + CBT.
2. Multimodal intervention superior to monotherapy or behavioral intervention alone (MTA Cooperative Group. Arch Gen Psychiatry 1999, n=579 — combination superior to monotherapy, but pharmacotherapy stronger than behavioral intervention alone).
3. Stimulants — First-line pharmacotherapy (Cortese S. et al. Lancet Psychiatry 2018 network meta-analysis; in children methylphenidate first choice, in adults amphetamine more effective).
4. Non-stimulants — Atomoxetine, guanfacine (long-acting formulation), clonidine (long-acting formulation). Used when stimulant contraindicated or side effect present.
5. Behavioral intervention — parent training (PCIT, parent management training), school-based intervention (class modifications, behavior contract), child CBT.
6. Academic accommodations — Individualized education plan (IEP / 504 Plan US; EHCP UK); extra time, limited distractors, written vs oral response options.
7. Side effect monitoring — Height and weight, blood pressure, heart rate (3-month), sleep, appetite, mood. In stimulants, slight decrease in height growth (1–2 cm with long-term use) is expected.
8. Comorbidity treatment — Anxiety/depression (SSRI + CBT), tics (alpha-2 agonists or cautiously stimulants), substance use (lisdexamfetamine or atomoxetine — lower abuse potential), autism (atypical antipsychotic for comorbid irritability).

8.2 Stimulants (First-Line Pharmacotherapy)

8.3 Non-stimulants

8.4 Source-Specific Clarifications

• NICE NG87 (2018, updated 2019): 5+ years — environmental changes first; then behavioral or pharmacotherapy. In adults — first-line stimulant; second-line atomoxetine.
• AAP 2019 (Wolraich): Age-based algorithm described above.
• Cortese S. et al. Lancet Psychiatry 2018 (network meta-analysis): children — methylphenidate first-line; adults — amphetamine first-line (higher effect size); atomoxetine moderately effective.
• MTA Cooperative Group (Arch Gen Psychiatry 1999, follow-up Hechtman L. et al. JAACAP 2016): intensive pharmacotherapy combination demonstrated superiority in 14-month observation; but differences weaken at 36-month and 8-year follow-up — long-term effect debated.
• FDA and EMA monitoring requirements: Monitoring height and weight, baseline cardiovascular parameters.

Treatment methods

1. Parent-Child Interaction Therapy (PCIT) — Eyberg (Eyberg S.) — For children aged 4–7 years; two phases – Child-Directed Interaction (CDI) and Parent-Directed Interaction (PDI). Development of parental behavior management skills with real-time therapist coaching (in-vivo coaching). pcit.org.
2. “Incredible Years” program — Webster-Stratton (Webster-Stratton C.) — Parent, teacher, and child programs; group format 14–22 sessions; ASTPS model (Authoritative Stimulating Trustworthy Parenting Style).
3. Triple P — Positive Parenting Program — Sanders (Sanders M.) — The 5-tier system developed in Australia is universal, selective, targeted, and individual. Effective in numerous RCTs.
4. Parent Management Training — Barkley (Barkley) — 8–12 sessions behavior principles-based parent training – token system, time-out, continuous training.
5. CBT for adult ADHD (Safren CBT for Adult ADHD) — Safren (Safren S.A.) — CBT modules for adult ADHD — task organization, planning, distraction management, cognitive restructuring. Evidence: Safren S.A. et al. JAMA 2010 RCT.
6. Vanderbilt ADHD Diagnostic Rating Scale — Recommended by AAP 2019; parent and teacher forms, comorbidity subscales.
7. Adult ADHD Self-Report Scale (ASRS) — Kessler (Kessler R.C.), WHO — 18 questions; short 6-item screening section. Clinical and population screening in adult patients.
8. Diagnostic Interview for ADHD in Adults (DIVA-5 — Diagnostic Interview for ADHD in Adults) — Structured interview for adult ADHD — according to DSM-5 criteria.
9. Conners-3 — 6–18 years comprehensive assessment – ADHD symptoms, executive function, behavioral disorder, learning.
10. Behavior Rating Inventory of Executive Function (BRIEF-2 — Behavior Rating Inventory of Executive Function) — Parent and teacher assessment of executive function — inhibition, working memory, emotional regulation.
11. EEG Neurofeedback — In ADHD, neurofeedback training targeting specific brainwave patterns (theta/beta ratio). Evidence: Holtmann M. et al. Dev Med Child Neurol 2011 meta-analysis — small effect size; effect debated among field specialists. NICE NG87 — not first-line, adjunct status.

9. Prognosis

Good prognostic factors

• Early identification and intervention.
• High IQ — compensatory strategies.
• Stable and supportive family environment.
• Active treatment of comorbid disorders.
• Good response to stimulant and behavioral intervention.
• Maintaining adherence in adolescence and adulthood.

Poor prognostic factors

• Comorbid conduct disorder, oppositional defiant disorder.
• Low socioeconomic support.
• Development of substance use in adolescence.
• Severity of executive function deficit.
• Late identification.
• Intervention with unproven methods.

Follow-up targets

• Symptom and functional outcome monitoring (3–6 months).
• Stimulants: height, weight, blood pressure, pulse (3-month).
• Comorbid anxiety, depression, substance use screening.
• Academic and vocational achievement support.
• Intervention for risk behavior in adolescence (driving training, sexual health, substance).
• Adaptation in adulthood related to career, relationships, financial planning — CBT adapted to DDP.

10. Myths and misconceptions

10.1 Aetiology myths

Myth 1: “ADHD is a fabricated diagnosis; children are just lively”

Why it is widespread: Anxiety about normal child energy being misperceived as pathological; some cases of diagnostic inflation are noted.

Clinical and biological rationale: ADHD has persistent and measurable neurobiological features — heritability 74% (Faraone & Larsson 2019), brain structural (Hoogman ENIGMA-ADHD 2017) and functional differences; effect of stimulants on specific mechanism (dopamine-norepinephrine) is pharmacological evidence. Underdiagnosis (especially in women) is a more widespread problem than overdiagnosis.

Evidence: APA, AAP, WHO, NIMH — ADHD is a biologically based disorder; parent-reported US prevalence is 9.8% at ages 3–17 (2016–2019) and 11.4% (2022), international population studies meta-analysis 5–7% (Polanczyk 2007).

Real clinical step: accurate diagnosis with structured criteria; functional impairment required (not simple behavioral variation).

Myth 2: “Sugar causes ADHD or worsens symptoms”

Why it is widespread: the intuition that sugar increases child energy; ‘Feingold diet’ popularized in the 1970s.

Evidence: Wolraich M.L. et al. JAMA 1995 systematic review and meta-analysis — sugar has no effect on child behavior and cognitive performance. Wolraich M.L. NEJM 1994 RCT — controlled deprivation study.

Real clinical step: A general healthy diet, but with sugar restriction, is not recommended as a DDH intervention.

Myth 3: “Bad parenting causes DMDD”

Evidence: heritability 74% (Faraone & Larsson Mol Psychiatry 2019); parental experience not etiology. However, high-conflict environment may influence symptom severity. Parental training (PCIT, Triple P) effective because it strengthens behavioral management skills — not blaming, but supportive purpose.

Myth 4: “Screen time / video games cause ADHD”

Evidence: Association exists, but causal direction debated — children with ADHD engage more in screen activity (reverse causality); Ferguson C.J. Perspect Psychol Sci 2015 review — causative effect of video games on ADHD not proven. AAP — screen time limits recommended for general health, not as a ‘cause’ of ADHD.

10.2 Harmful “treatment” methods and misconceptions

Myth 5: “Stimulants cause addiction like drugs and lead to future substance abuse”

Why it is widespread: methylphenidate and amphetamines being listed on the controlled substances schedule (Schedule II in the US); the widespread prevalence of the “narcotic” fear.

Clinical and biological rationale: At therapeutic oral dose, stimulant gradually reaches brain concentration (1–2 hours) — euphoric effect minimal. With intravenous or intranasal use (routes of misuse), different pharmacokinetics occur.

Evidence: Wilens T.E. et al. Pediatrics 2003 meta-analysis, n=2565 — substance use in adulthood among adolescents with ADHD treated with stimulants diminishes, does not increase (risk reduction ~50%). Lisdexamfetamine and osmotic-release methylphenidate (Concerta) — low abuse potential (prodrug structure, OROS technology).

Real clinical step: When comorbid substance use exists — lisdexamfetamine or atomoxetine preferred; safety education for the patient and the family.

Myth 6: “Stimulants stunt a child's height and brain development”

Evidence: MTA Cooperative Group follow-up (Swanson J.M. et al. JAACAP 2017) — adult height 1–2 cm lower in children treated with stimulants (relative to expected young adult height); this is considered small and clinically insignificant. Brain development — no evidence of harm related to stimulants (Schweren L.J.S. et al. Neuropsychopharmacology 2015 review).

Myth 7: Cannabis cures ADHD

Evidence: NIDA, NICE — cannabis not approved for ADHD treatment; increases psychosis risk (Marconi 2016), leads to cognitive impairment, reduces motivation. Subjective ‘calming’ effect masks functional impairment.

10.3 Ineffective or scientifically unfounded methods

Myth 8: Feingold diet or avoidance of food colorings/additives cures ADHD

Evidence: Pelsser L.M. et al. Lancet 2011 (INCA study) — a restrictive elimination diet may influence behavior in some children (~30%), but systematic reviews (Sonuga-Barke E.J. et al. Am J Psychiatry 2013 meta-analysis) — the effect size of eliminating food additives is small, showing a superior effect only on family-rated assessment, and weakens when a blind control is applied. AAP, NICE — not a first-line approach; there is a risk of nutritional deficiency with complex diets.

Myth 9: “Omega-3 supplements are the primary treatment for ADHD”

Evidence: Cooper R.E. et al. J Psychopharmacol 2015 and Bloch M.H., Qawasmi A. JAACAP 2011 meta-analyses — small effect size (g≈0.3); significantly weaker than stimulants (g≈1.0). May serve as adjunct; not primary treatment.

Myth 10: “EEG Neurofeedback replaces stimulants”

Evidence: Holtmann M. et al. Dev Med Child Neurol 2011 and Cortese S. et al. JAACAP 2016 meta-analysis — neurofeedback effect significantly decreases when rated by proband and teacher; effect size is small in “blinded” assessment. NICE NG87 — not first-line. Stimulant effect is far superior.

Myth 11: “Forcing exercise resolves the child's ADHD”

Evidence: Physical activity may help mildly reduce symptoms in ADHD (adjunct); but does not replace core intervention. AAP recommends structured physical activity, but not as sole treatment.

Myth 12: “Craniosacral therapy, chiropractic, homeopathy cure ADHD”

Evidence: Cochrane and systematic reviews — the effect of these complementary interventions for ADHD has not been proven.

Myth 13: “Light therapy, MUS tinted lenses cure ADHD”

Evidence: No evidence base. AAP, AAO position — not evidenced.

11. Sources

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