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ADHD Encyclopedia
Complete Glossary of Terms & Definitions
By Dr. Ryan Sultan, Columbia University Psychiatrist & ADHD Specialist
Last Updated: February 17, 2026
About This Encyclopedia: Comprehensive ADHD encyclopedia with 75+ medical and clinical terms defined by Columbia psychiatrist Dr. Ryan Sultan, including executive function, dopamine, stimulants, comorbidity, and neurodevelopmental concepts.
📚 How to Use This Encyclopedia
This comprehensive glossary covers all ADHD-related terminology used in clinical practice, research, and patient education. Each term includes a clear definition and links to related concepts where applicable.
Quick Navigation: Use the alphabet links below to jump to terms starting with that letter, or scroll to browse all definitions.
For clinicians: Technical definitions include current diagnostic criteria and evidence-based standards.
For patients & families: Plain-language explanations help you understand your diagnosis and treatment.
— A —
ADHD (Attention-Deficit/Hyperactivity Disorder)
A neurodevelopmental disorder characterized by persistent patterns of inattention, hyperactivity, and impulsivity that interfere with functioning and development. Affects approximately 5-7% of children and 4-5% of adults worldwide. Diagnosis requires symptoms present before age 12, occurring in multiple settings, and causing significant impairment.
ADD (Attention Deficit Disorder)
Outdated term for ADHD, previously used to describe individuals with primarily inattentive symptoms without hyperactivity. No longer used in clinical practice since DSM-IV (1994); replaced by "ADHD, Predominantly Inattentive Presentation."
Amphetamine
A class of stimulant medications used to treat ADHD by increasing dopamine and norepinephrine in the brain. Includes dextroamphetamine (Dexedrine), mixed amphetamine salts (Adderall), and lisdexamfetamine (Vyvanse). Typically more potent than methylphenidate with slightly longer duration of action.
Anterior Cingulate Cortex (ACC)
Brain region involved in error detection, conflict monitoring, and emotional regulation. fMRI studies show reduced activation in individuals with ADHD during attention tasks, contributing to difficulty recognizing and correcting mistakes.
Atomoxetine (Strattera)
Non-stimulant ADHD medication that works by selectively blocking norepinephrine reuptake in the prefrontal cortex. First-line alternative for patients who cannot tolerate or do not respond to stimulants. Takes 4-6 weeks to reach full effectiveness, not a controlled substance.
— B —
Basal Ganglia
Subcortical brain structures (caudate, putamen, nucleus accumbens) involved in motor control, reward processing, and habit formation. Brain imaging studies consistently show reduced volume in ADHD, particularly in the caudate nucleus. Dopamine dysfunction in these regions contributes to motivation and impulse control deficits.
Behavioral Therapy
Non-medication treatment approach using structured interventions to modify ADHD-related behaviors. Includes parent training (teaching behavioral management strategies), classroom interventions, and organizational skills training. Most effective when combined with medication for moderate-to-severe ADHD.
— C —
CBT (Cognitive Behavioral Therapy)
Psychotherapy approach focusing on identifying and changing negative thought patterns and behaviors. For ADHD, targets executive dysfunction, time management, organization, and emotional regulation. Evidence-based treatment for adult ADHD, often combined with medication.
Comorbidity
Presence of one or more additional conditions co-occurring with ADHD. Common comorbidities include anxiety disorders (50%), depression (30%), learning disabilities (30%), oppositional defiant disorder (40% in children), and substance use disorders. Comorbidities complicate diagnosis and treatment.
Combined Presentation
ADHD subtype (per DSM-5) characterized by significant symptoms of both inattention and hyperactivity-impulsivity. Most common presentation, accounting for approximately 50-75% of ADHD diagnoses. Requires meeting criteria for both symptom domains.
— D —
Default Mode Network (DMN)
Brain network active during rest and mind-wandering, typically deactivating during focused tasks. In ADHD, the DMN fails to fully deactivate during attention-demanding tasks, causing internal distraction and difficulty maintaining focus. Measured via fMRI connectivity studies.
Differential Diagnosis
Clinical process of distinguishing ADHD from other conditions with similar symptoms. Must rule out anxiety disorders, depression, learning disabilities, sleep disorders, thyroid dysfunction, and autism spectrum disorder. Thorough evaluation includes clinical interview, rating scales, and consideration of age of onset and symptom pattern.
Dopamine
Neurotransmitter crucial for attention, motivation, reward processing, and impulse control. ADHD involves dopamine signaling dysfunction, particularly in the prefrontal cortex and striatum. The core problem is timing: dopamine neurons fire too weakly or too briefly, causing weak signal-to-noise ratio. Stimulant medications work by increasing dopamine availability.
Dopamine Transporter (DAT)
Protein that pumps dopamine from the synapse back into neurons (reuptake). People with ADHD often have higher DAT density, causing faster dopamine clearance and weaker signaling. Stimulant medications work by blocking DAT, preventing dopamine reuptake and increasing signal strength.
DRD4-7R Gene Variant
Genetic variant of the dopamine D4 receptor associated with increased ADHD risk and novelty-seeking behavior. The 7-repeat allele creates less responsive dopamine receptors, requiring stronger signals. Theorized to have been advantageous in ancestral hunter-gatherer environments.
DSM-5 (Diagnostic and Statistical Manual, 5th Edition)
Current diagnostic criteria for ADHD published by the American Psychiatric Association (2013). Requires 6+ symptoms of inattention and/or hyperactivity-impulsivity for children (5+ for adults age 17+), present before age 12, occurring in multiple settings, causing significant impairment. Replaced term "subtypes" with "presentations."
— E —
Executive Function
Umbrella term for cognitive processes that control and regulate behavior, including working memory, cognitive flexibility, planning, organization, time management, and impulse control. Mediated primarily by the prefrontal cortex. Executive dysfunction is a core feature of ADHD, causing difficulty with goal-directed behavior despite intact intelligence.
Emotional Dysregulation
Difficulty controlling emotional responses, including quick temper, frustration intolerance, and mood swings. Common in ADHD (present in 30-50% of cases) but not part of official diagnostic criteria. May overlap with rejection sensitive dysphoria (RSD). Responds to ADHD treatment and emotion regulation skills training.
— F —
fMRI (Functional Magnetic Resonance Imaging)
Brain imaging technique measuring brain activity by detecting blood flow changes. ADHD fMRI studies show reduced activation in prefrontal cortex, anterior cingulate, and parietal regions during attention tasks, plus failure to deactivate the default mode network. Not used for diagnosis but validates ADHD as a brain-based condition.
— G —
Guanfacine (Intuniv)
Non-stimulant ADHD medication that activates alpha-2A adrenergic receptors in the prefrontal cortex, strengthening "signal" and reducing "noise." FDA-approved for children and adolescents, often used as adjunct to stimulants. Improves working memory and impulse control with minimal side effects. Not a controlled substance.
— H —
Heritability
Proportion of ADHD risk attributable to genetic factors, estimated at 70-80% based on twin and family studies. One of the most heritable psychiatric conditions. If one parent has ADHD, children have 50% risk; if both parents have ADHD, risk approaches 80%. Genome-wide association studies have identified multiple risk genes affecting dopamine and norepinephrine systems.
Hunter-Gatherer Hypothesis
Evolutionary theory proposing that ADHD traits (hyperactivity, impulsivity, novelty-seeking) were advantageous in ancestral hunter-gatherer environments requiring rapid response to threats, exploration, and risk-taking. Modern sedentary, rule-based environments create "mismatch" making these same traits impairing.
Hyperactivity
One of three core ADHD symptom domains, characterized by excessive motor activity, fidgeting, inability to remain seated, and restlessness. More prominent in children; in adults often manifests as internal restlessness or feeling "driven by a motor." Required for Combined or Hyperactive-Impulsive presentations.
Hyperactive-Impulsive Presentation
ADHD subtype characterized by predominant symptoms of hyperactivity and impulsivity without significant inattention. Least common presentation, accounting for <15% of cases. More common in young children; many transition to Combined presentation as inattention symptoms emerge with academic demands.
Hyperfocus
Paradoxical ability to intensely focus on highly engaging or rewarding tasks despite general attention difficulties. Not an official symptom but commonly reported by individuals with ADHD. Reflects dysregulation of attention rather than deficit: difficulty controlling what gets focused on rather than inability to focus at all.
— I —
Impulsivity
Acting without forethought or consideration of consequences. One of three core ADHD symptom domains. Manifests as interrupting others, difficulty waiting turn, making hasty decisions, risk-taking behavior. Mediated by prefrontal cortex and improves with dopamine-enhancing medications.
Inattention
Core ADHD symptom domain characterized by difficulty sustaining attention, distractibility, forgetfulness, losing items, failure to follow through on tasks, and avoidance of sustained mental effort. More persistent across lifespan than hyperactivity. Caused by weak dopamine signaling in attention networks.
Inattentive Presentation (ADHD-I)
ADHD subtype characterized by predominant symptoms of inattention without significant hyperactivity or impulsivity. Accounts for 20-30% of cases. More common in girls/women, often diagnosed later due to less disruptive behavior. Previously called "ADD" (outdated term).
— L —
LiteSpeed Cache
Just kidding. We don't talk about that here. 😅
Lisdexamfetamine (Vyvanse)
Prodrug stimulant medication converted to dextroamphetamine in the body. Long-acting (12-14 hours), smooth onset/offset, lower abuse potential than immediate-release amphetamines due to required enzymatic conversion. FDA-approved for ADHD and binge eating disorder.
— M —
Methylphenidate (Ritalin, Concerta, Focalin)
Stimulant medication that blocks dopamine and norepinephrine reuptake, primarily in the prefrontal cortex. First-line ADHD treatment since 1960s. Available in immediate-release (4 hours), extended-release (8-12 hours), and long-acting formulations. Generally better tolerated than amphetamines with slightly shorter duration.
Mismatch Theory
Concept that ADHD traits evolved for ancestral environments but are mismatched to modern sedentary, structured societies. Proposes that hyperactivity, impulsivity, and distractibility were adaptive for hunter-gatherers but impairing in classrooms and offices requiring sustained attention and behavioral inhibition.
— N —
Neurodevelopmental Disorder
Category of conditions arising from atypical brain development during childhood, characterized by deficits in personal, social, academic, or occupational functioning. Includes ADHD, autism spectrum disorder, learning disabilities, and intellectual disability. ADHD symptoms must be present before age 12 to meet neurodevelopmental criteria.
Non-Stimulant Medication
ADHD medications that don't contain amphetamine or methylphenidate. Includes atomoxetine (Strattera), guanfacine (Intuniv), and clonidine (Kapvay). First-line alternatives for patients with substance abuse history, tics, anxiety, or stimulant intolerance. Generally less effective than stimulants but useful as adjuncts or alternatives.
Norepinephrine
Neurotransmitter involved in alertness, attention, and arousal. Works alongside dopamine in ADHD pathophysiology, particularly in prefrontal cortex function. Atomoxetine and tricyclic antidepressants increase norepinephrine to treat ADHD. Stimulants also increase norepinephrine alongside dopamine.
— O —
Off-Label Prescribing
Use of FDA-approved medications for indications not specifically approved by the FDA. Common in psychiatry. Example: quetiapine for ADHD-related insomnia (approved for schizophrenia/bipolar, not ADHD). Requires careful risk-benefit analysis and informed consent.
— P —
Predominantly Inattentive Presentation
Prefrontal Cortex
Brain region at the front of the frontal lobe responsible for executive functions: planning, organization, working memory, impulse control, and attention regulation. Most "dopamine-dependent" brain region. Structural MRI shows 3-5% smaller volume in ADHD; functional MRI shows reduced activation during attention tasks. Delayed maturation explains why some children "outgrow" ADHD.
— R —
Rejection Sensitive Dysphoria (RSD)
Extreme emotional sensitivity to perceived rejection or criticism. Not an official diagnosis but commonly described by adults with ADHD. May result from chronic experiences of underachievement and negative feedback. Can respond to ADHD medication or alpha agonists (guanfacine).
Response Inhibition
Ability to suppress inappropriate or unwanted behaviors. Core executive function deficit in ADHD, measured by tasks like Go/No-Go and Stop Signal. Mediated by prefrontal cortex and improves with stimulant medication. Impaired response inhibition manifests as impulsivity and difficulty waiting.
— S —
SCT (Sluggish Cognitive Tempo)
Proposed attention disorder characterized by excessive daydreaming, mental fogginess, hypoactivity, and slowed thinking. Distinct from ADHD-Inattentive type. Not currently recognized as separate diagnosis in DSM-5. Some research suggests it may overlap with but differ from ADHD.
Stimulant Medication
First-line pharmacological treatment for ADHD. Includes methylphenidate and amphetamine compounds. Work by blocking dopamine and norepinephrine reuptake, increasing neurotransmitter availability in prefrontal cortex. 70-80% response rate. Controlled substances (Schedule II) due to abuse potential, though therapeutic use does not cause addiction.
Striatum
Brain region (part of basal ganglia) involved in reward processing, motivation, and habit formation. Includes caudate, putamen, and nucleus accumbens. Reduced volume and dopamine dysfunction in ADHD contribute to motivation deficits and reward sensitivity. Target of dopamine-enhancing medications.
— T —
Time Blindness
Difficulty accurately perceiving or estimating time passage. Common ADHD experience causing chronic lateness, poor time management, underestimating task duration. Related to working memory and executive dysfunction. Not an official symptom but widely reported.
Titration
Process of gradually adjusting medication dose to find optimal balance between effectiveness and side effects. Standard practice for ADHD medications. Typically start at low dose and increase every few days until target dose reached or side effects emerge. Individual response varies widely.
— W —
Working Memory
Ability to hold and manipulate information in mind temporarily (e.g., remembering instructions, mental math). Core executive function deficit in ADHD, mediated by dopamine in prefrontal cortex. Impaired working memory causes difficulty following multi-step directions and losing train of thought.
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Compiled by Dr. Ryan Sultan, Assistant Professor of Clinical Psychiatry at Columbia University and ADHD specialist with NIH-funded research and 411+ citations.
Last updated: February 17, 2026
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