Attention-Deficit/Hyperactivity Disorder

Clinical picture

• Careless errors, lost belongings, and unfinished tasks; parents and teachers report the child hears instructions but does not follow through.
• Adults present with chronic lateness, disorganization, procrastination, and job or relationship instability rather than overt hyperactivity.
• Hyperactivity shifts with age from climbing and running to fidgeting, restlessness, and an internal sense of being driven by a motor.
• Impulsivity appears as interrupting, blurting answers, impatience waiting in line, and risky spending, driving, or sexual decisions.
• Emotional dysregulation, low frustration tolerance, and rejection sensitivity are common though not formal DSM-5-TR criteria.
• Function collapses under low structure; performance improves markedly with novelty, interest, urgency, or one-to-one supervision.

Criteria snapshot

• Requires six or more inattentive and/or six or more hyperactive-impulsive symptoms; five suffice from age 17 onward.
• Symptoms must persist at least 6 months at a level inconsistent with developmental stage and directly reduce social or academic function.
• Several symptoms must have been present before age 12 and be evident in two or more settings such as home, school, or work.
• Presentation is specified as predominantly inattentive, predominantly hyperactive-impulsive, or combined, with mild, moderate, or severe severity.
• Symptoms cannot be better explained by another disorder or occur exclusively during psychosis; partial remission is coded when criteria lapse.

Neurobiology

• Delayed cortical maturation, with peak thickness in prefrontal regions reached roughly 3 years later than in unaffected peers.
• Hypofunction of frontostriatal and frontoparietal circuits underlies deficits in response inhibition, working memory, and sustained attention.
• Deficient dopamine and norepinephrine signaling in prefrontal cortex and striatum explains response to stimulants and to atomoxetine.
• Heritability approaches 74%; risk is polygenic with no single gene of large effect and substantial overlap with autism and mood disorders.
• The default mode network fails to suppress during task engagement, producing intrusive attentional lapses and highly variable reaction times.
• Prenatal exposures including nicotine, alcohol, extreme prematurity, low birth weight, and lead raise risk beyond inherited loading.

Psychology

• Barkley's model frames ADHD as impaired behavioral inhibition that degrades working memory, self-directed speech, affect regulation, and planning.
• Delay aversion and steep temporal discounting drive selection of small immediate rewards over larger delayed ones in daily decisions.
• Years of correction and failure produce negative self-schemas, learned helplessness, and avoidance of tasks previously experienced as impossible.
• Executive dysfunction is a performance problem, not a knowledge problem; patients know what to do but cannot deploy it at the point of performance.
• Coercive parent-child cycles and inconsistent contingencies amplify oppositional behavior layered on top of core symptoms.

Differential & comorbidity

• Differentiate from anxiety, mood disorders, trauma, sleep apnea, learning disorders, absence seizures, and thyroid disease, all of which mimic inattention.
• Bipolar disorder shows episodic mood change with reduced need for sleep, whereas ADHD symptoms are chronic, daily, and situationally consistent.
• ODD co-occurs in roughly 40-60%, learning disorders in 20-45%, anxiety in 25-40%, and substance use disorders rise in adolescence.
• Untreated ADHD elevates risk of motor vehicle crashes, unintentional injury, unplanned pregnancy, academic failure, and suicide attempts.
• Screen for stimulant diversion and misuse in college populations, and review cardiac and family sudden-death history before starting stimulants.

Pharmacologic treatment

• Methylphenidate products (OROS 18-72 mg/day) and amphetamines (lisdexamfetamine 30-70 mg/day) are first line, each helping about 70%.
• Trying the second stimulant class after failure of the first raises overall response to roughly 85-90%; titrate every 1-2 weeks to effect.
• Monitor blood pressure, pulse, height, weight, appetite, and sleep at each visit; growth deceleration is usually modest and dose related.
• Atomoxetine 0.5-1.4 mg/kg/day is a non-stimulant first-line option for tics, anxiety, or diversion risk; allow 4-6 weeks for full effect.
• Guanfacine ER 1-4 mg/day and clonidine ER 0.1-0.4 mg/day work as monotherapy or stimulant adjuncts; watch sedation and hypotension.

Psychotherapy

• Behavioral parent training over 8-16 weekly sessions is first line for preschool-age children before any medication trial is considered.
• Classroom behavioral management using daily report cards, token systems, and antecedent structure produces moderate effects on target behavior.
• CBT for adult ADHD across 12-16 sessions targets organization, planning, and distractibility with added benefit beyond medication alone.
• Organizational skills training in school-age children improves homework completion, materials management, and time tracking at school and home.
• Cognitive training and neurofeedback improve trained tasks but show weak transfer to real-world function on blinded outcome ratings.

Adjunct options

• Standardized rating scales such as Vanderbilt, Conners-3, and ASRS-v1.1 anchor baseline severity and track medication titration.
• Section 504 plans and IEPs provide extended time, preferential seating, reduced written load, chunked assignments, and testing accommodations.
• Sleep evaluation is essential; treating obstructive sleep apnea or delayed sleep phase can substantially reduce daytime inattention.
• Aerobic exercise, consistent routines, external cueing systems, and reduced screen-based multitasking provide small adjunctive gains.
• Coordinate with school, ADHD coaching, or occupational therapy; driving safety counseling matters most for newly licensed adolescents.

Clinical pearls

• Chronic, cross-setting symptoms point to ADHD; episodic symptoms point somewhere else.
• Stimulant failure usually means wrong dose, wrong timing, or a missed comorbidity.
• Check pulse and blood pressure at every titration visit, not only at baseline.