Attention Deficit Hyperactivity Disorder

ADHD is a chronic neurodevelopmental disorder of childhood onset, defined by a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development. It is one of the most heavily tested paediatric psychiatry topics in NEET PG, with favourites being the age-of-onset criterion, the three presentations, stimulant pharmacology (methylphenidate), the rebound effect, and the tic caveat.

Definition & DSM-5 classification

ADHD per DSM-5 requires a persistent pattern (≥6 months) of inattention and/or hyperactivity-impulsivity that is inconsistent with developmental level and produces impairment in ≥2 settings (e.g., home and school).

Symptom count rule:

• Children (≤16 years): ≥6 symptoms from a domain.
• Adolescents/adults (≥17 years): ≥5 symptoms suffice (threshold lowered because symptoms attenuate with age).

High-yield: The single most-tested DSM-5 change is the age-of-onset criterion — several symptoms must be present before age 12 years (DSM-IV required onset before 7 years). Remember "ADHD by 12."

The three presentations (specifiers)

Presentation	Dominant features	Typical picture
Predominantly Inattentive	Careless mistakes, poor sustained attention, forgetful, loses items, easily distracted, fails to follow through	Quiet "daydreamer," more in girls, often missed/diagnosed late
Predominantly Hyperactive-Impulsive	Fidgeting, leaving seat, running/climbing, "on the go," talks excessively, blurts answers, can't wait turn, interrupts	Younger children, more in boys
Combined	Meets criteria for both domains	Most common presentation overall

Severity is graded mild / moderate / severe based on symptom number and functional impairment.

High-yield: Combined presentation is the commonest. The previously used term "ADHD predominantly inattentive type" largely replaces the old "ADD."

ICD-11 note

ICD-11 uses the term "Attention deficit hyperactivity disorder" (harmonised with DSM-5), abandoning the older ICD-10 term "Hyperkinetic disorder," which required pervasive inattention and overactivity and impulsivity together (a narrower, more severe construct).

Epidemiology

• Worldwide childhood prevalence ≈ 5–7%; one of the commonest childhood psychiatric disorders.
• Male : female ≈ 2–4 : 1 in clinic samples (girls under-recognised as they are more often inattentive).
• Up to 50–65% persist with symptoms into adulthood; hyperactivity tends to remit while inattention persists.
• Onset of recognisable symptoms typically by age 3–4 years; diagnosis often at school entry.

Etiology & pathophysiology

ADHD is highly heritable (~70–80%) — one of the most heritable psychiatric disorders.

Genetic / neurochemical basis:

• Dysregulation of dopamine and noradrenaline in fronto-striatal and fronto-cerebellar circuits.
• Implicated genes: DRD4 (dopamine receptor), DRD5, DAT1/SLC6A3 (dopamine transporter).
• The prefrontal cortex (executive function), basal ganglia/striatum, and cerebellum show reduced volume/activity; overall a catecholamine-deficit model in the prefrontal cortex underlies poor executive control and impulse inhibition.

Environmental / risk factors:

• Maternal smoking and alcohol in pregnancy.
• Low birth weight / prematurity, perinatal hypoxia.
• Lead exposure.
• Severe early deprivation/institutional rearing.

High-yield: ADHD is a disorder of catecholamine (dopamine + noradrenaline) dysregulation in the prefrontal cortex. This explains why stimulants (which raise synaptic DA/NA) paradoxically calm hyperactive children — they enhance top-down prefrontal inhibitory control.

Clinical features

The triad is inattention, hyperactivity, and impulsivity, but presentation evolves with age:

• Preschool: excessive motor activity, temper outbursts, accident-proneness.
• School age: academic underachievement, classroom disruption, poor peer relationships, "doesn't finish tasks."
• Adolescence: overt hyperactivity fades to inner restlessness; inattention, disorganisation, risk-taking (substance use, reckless driving) dominate.
• Adults: poor time management, job instability, relationship difficulties, "always running late," procrastination.

Associated features: low frustration tolerance, mood lability, low self-esteem, and specific learning disorder comorbidity.

Diagnosis & investigations

ADHD is a clinical diagnosis — there is no laboratory or imaging test that confirms it. Diagnosis rests on:

1. History from multiple informants (parents + teachers) confirming symptoms in ≥2 settings.
2. Standardised rating scales (to quantify and track, not to "diagnose" alone).
3. Direct observation and exclusion of other causes.

Rating scales (exam favourite)

Scale	Use
Conners Rating Scale (Conners CRS / Conners 3)	Most classic NEET PG answer — parent + teacher versions, screens & grades ADHD severity
Vanderbilt ADHD Diagnostic Rating Scale	Parent/teacher, also screens comorbidities
SNAP-IV	Symptom rating tied to DSM items
Child Behaviour Checklist (CBCL)	Broad-band behavioural screen

High-yield: When the stem mentions a teacher-and-parent questionnaire to assess a hyperactive, inattentive child → answer the Conners Rating Scale.

Investigations are done only to exclude mimics: hearing/vision testing, thyroid profile if features suggest hyperthyroidism, lead levels if exposure risk, EEG only if seizures (e.g., absence seizures) are suspected. Routine neuroimaging/EEG is NOT indicated.

Diagnostic approach (flow)

Concern raised (parent/teacher) → Detailed history + symptom counting against DSM-5 → Confirm onset before 12 yrs and impairment in ≥2 settings → Apply rating scales (Conners/Vanderbilt) → Rule out medical/sensory/other psychiatric mimics → Assign presentation + severity → Plan management.

Management

A multimodal approach is standard. Treatment choice is age-dependent — this is high-yield.

Stepwise / age-based approach

1. Preschool children (4–5 years): Behavioural parent training (BPT) is first-line, not medication. Methylphenidate is added only if behavioural therapy fails and impairment is significant.
2. School-age children (≥6 years) & adolescents: Stimulant medication (methylphenidate or amphetamine) + behavioural therapy combined — the MTA study showed combined/medication arms superior for core symptoms.
3. Adults: stimulants or atomoxetine + cognitive/behavioural strategies.

High-yield: In a 4–5-year-old, the answer is parent behaviour training first, not a stimulant. Stimulants are first-line drug therapy in the ≥6-year-old.

Pharmacotherapy

A. Stimulants — first-line drugs (drugs of choice):

Drug	Mechanism
Methylphenidate	Blocks dopamine + noradrenaline reuptake transporters (DAT/NET) → ↑ synaptic DA & NA
Dexamfetamine / mixed amphetamine salts	Block reuptake and promote presynaptic release of DA & NA (reverse transporter), also weak MAO inhibition

High-yield: Methylphenidate is the drug of choice / first-line for ADHD. Mechanism = dopamine and noradrenaline reuptake inhibitor. Amphetamines additionally increase release of catecholamines — that extra "release" mechanism is the discriminator in MCQs.

Common stimulant adverse effects:

• Anorexia / appetite suppression and growth (height & weight) retardation — monitor growth; consider drug holidays.
• Insomnia (avoid late-day dosing).
• Headache, abdominal pain, irritability, tachycardia, mild rise in BP.
• Worsening or precipitation of tics.

High-yield — REBOUND EFFECT: As a short-acting stimulant dose wears off (typically late afternoon/evening), the child may show transient worsening of hyperactivity, irritability and overactivity beyond baseline. Managed by using long-acting/extended-release preparations or adjusting timing. This "rebound" is a classic single-best-answer.

High-yield — TICS / Tourette's caveat: Stimulants can unmask or worsen tics and are traditionally avoided (relative contraindication) in children with comorbid tic disorder/Tourette syndrome. In ADHD + tics, prefer a non-stimulant — atomoxetine or an alpha-2 agonist (clonidine / guanfacine). Other relative contraindications: serious cardiac disease/arrhythmia, uncontrolled hypertension, glaucoma, current psychosis, and history of substance misuse (amphetamines).

B. Non-stimulants — second-line / specific situations:

Drug	Class / mechanism	Best used when
Atomoxetine	Selective noradrenaline reuptake inhibitor (NRI)	Comorbid tics, anxiety, substance-abuse risk, or stimulant intolerance; non-controlled, no abuse potential
Clonidine / Guanfacine	Alpha-2 adrenergic agonists	Comorbid tics, aggression, sleep problems; can augment stimulants
Bupropion	NA/DA reuptake inhibitor (off-label)	Comorbid depression

High-yield: Atomoxetine is the leading non-stimulant, a selective noradrenaline reuptake inhibitor, has no abuse potential, but carries a black-box warning for suicidal ideation and takes 2–6 weeks for full effect (unlike stimulants which act within hours). It can cause hepatotoxicity (rare).

Mnemonic for stimulant cautions — "CATS GHT": Cardiac disease, Anxiety/agitation, Tics/Tourette, Substance abuse history, Glaucoma, Hypertension, Thyrotoxicosis.

Psychosocial interventions

• Behavioural parent training and classroom behaviour management (token economy, structured routine, clear consequences).
• Social skills training, organisational skills coaching for adolescents.
• Educational accommodations (extra time, preferential seating).

Comparing first-line drug options at a glance

Feature	Methylphenidate (stimulant)	Atomoxetine (non-stimulant)
Class / action	DA + NA reuptake inhibitor	Selective NA reuptake inhibitor
Onset of effect	Within hours (same day)	2–6 weeks for full benefit
Abuse potential	Yes (Schedule controlled)	None
Use with tics	Avoid / caution	Preferred
Key warning	Appetite/growth suppression, insomnia, rebound	Black-box suicidality, hepatotoxicity (rare)
Dosing pattern	Often divided / long-acting forms	Once-daily

Monitoring on therapy

• Height and weight plotted on growth charts at each visit (stimulant growth suppression).
• Pulse and blood pressure before and during stimulant therapy.
• Re-screen for emergent tics, mood change, sleep disturbance, and suicidal ideation (especially atomoxetine).
• Periodic reassessment of need to continue — many children can be trialled off medication during structured "drug holidays" (e.g., weekends/vacations) to allow catch-up growth and reassess baseline.

Complications & comorbidities

ADHD rarely travels alone — comorbidity is the rule:

• Oppositional Defiant Disorder (ODD) and Conduct Disorder — most common externalising comorbids.
• Specific Learning Disorder (reading/maths).
• Anxiety and depressive disorders.
• Tic disorders / Tourette syndrome.
• Substance use disorders in adolescence/adulthood (untreated ADHD increases risk; effective stimulant treatment reduces later substance risk).
• Functional consequences: academic failure, accidental injuries, low self-esteem, occupational and relationship problems, increased motor-vehicle accidents.

Key differentials

Condition	Distinguishing pointer
Age-appropriate high activity	No impairment, single setting only
Absence (petit mal) epilepsy	Brief staring spells, EEG 3-Hz spike-and-wave, sudden onset/offset (vs continuous inattention)
Oppositional Defiant Disorder	Defiance is volitional/oppositional, not from inattention
Autism Spectrum Disorder	Social-communication deficits, restricted/repetitive behaviours dominate (can co-occur — DSM-5 now allows dual diagnosis)
Anxiety / depression	Inattention is mood/worry-driven, episodic
Hearing/vision deficit	Sensory testing abnormal; "inattention" is sensory
Hyperthyroidism	Tremor, weight loss, ↑T4/↓TSH
Lead poisoning	Exposure history, anaemia, ↑blood lead
Specific Learning Disorder	Attention intact except in the affected academic domain
Intellectual disability	Global cognitive delay; attention appropriate for mental age

High-yield: A school child with brief staring spells and 3-Hz spike-and-wave on EEG = absence seizures, not ADHD. This is a classic distractor pairing.

Recently asked / exam angle

• Age-of-onset criterion: "Symptoms must be present before age ___?" → 12 years (the DSM-IV→DSM-5 change is a perennial favourite).
• Mechanism of methylphenidate → dopamine + noradrenaline reuptake inhibition.
• Rebound phenomenon of short-acting stimulants in the evening — single best answer.
• Stimulant contraindicated / to be avoided in a child with tics / Tourette → use atomoxetine instead.
• Atomoxetine class → selective noradrenaline reuptake inhibitor (non-stimulant).
• Most common presentation → Combined.
• First-line treatment in a 4–5-year-old → behavioural parent training, not a stimulant.
• Conners scale as the diagnostic rating tool when a parent/teacher questionnaire is described.
• Most common adverse effect of stimulants → appetite suppression / growth concerns and insomnia.
• MTA study association with combined-treatment superiority.
• Image/clinical-vignette style: hyperactive boy unable to wait turn, blurts answers, fails to finish homework, problems at home and school → ADHD combined.

Rapid revision

1. ADHD = chronic neurodevelopmental disorder; triad of inattention + hyperactivity + impulsivity.
2. DSM-5: several symptoms before age 12, impairment in ≥2 settings, ≥6 symptoms (≥5 if ≥17 yrs).
3. Three presentations — inattentive, hyperactive-impulsive, combined; combined is commonest.
4. Highly heritable (~70–80%); DRD4, DAT1 genes; prefrontal catecholamine deficit.
5. Risk factors: maternal smoking/alcohol, prematurity, lead, low birth weight.
6. Diagnosis is clinical; Conners Rating Scale is the classic tool; no confirmatory lab/EEG.
7. Methylphenidate = drug of choice = DA + NA reuptake inhibitor; amphetamines also release catecholamines.
8. Rebound effect = evening worsening as short-acting stimulant wears off → use long-acting forms.
9. Stimulants avoided in tics/Tourette → switch to atomoxetine (selective NRI, non-stimulant, suicidality black-box, slow onset).
10. Stimulant adverse effects: appetite/growth suppression, insomnia, ↑HR/BP, tics.
11. In 4–5-year-olds, behavioural parent training is first-line, not medication.
12. Commonest comorbids: ODD/conduct disorder; key differential = absence epilepsy (3-Hz spike-wave EEG).