ADHD
"attention deficit hyperactivity disorder"[MeSH Terms] AND management
ADHD brain neurobiology dopamine prefrontal cortex diagram

This medical infographic illustrates the neurobiological basis of Attention-Deficit/Hyperactivity Disorder (ADHD) by mapping cognitive deficits to specific neuroanatomical structures and neurotransmitter systems. The central visual is a translucent sagittal-view diagram of the human brain. Labeled 'ADHD' and 'Deficits,' the diagram connects executive function impairments—including inhibition, planning, attention, organization, problem-solving, and motor control—to a highlight of the prefrontal-striatal-cerebellar circuitry. Key anatomical regions identified as involved in the pathophysiology include the Prefrontal Cortex, Basal Ganglia, Cerebellum, Anterior Cingulate, and Locus Coeruleus. At the base of the diagram, the catecholamine and monoamine pathways are represented through labels for Noradrenaline, Serotonin, and Dopamine, indicating their role in modulating these cognitive processes. This educational visualization demonstrates the multi-regional and neurochemical complexity of ADHD, emphasizing how structural and biochemical alterations manifest as clinical deficits in executive functioning. It is designed for clinical neurobiology education and diagnostic conceptualization.

This grayscale anatomical diagram illustrates the mesolimbic dopamine system, often referred to as the reward or addiction circuit, within a human brain. The illustration utilizes a midsagittal view to map key functional regions. Specific structures are highlighted with circles and alphanumeric labels: the Prefrontal Cortex (PFC) at the anterior frontal lobe, the Nucleus Accumbens (NA) in the ventral striatum, the Amygdala (A) and Hippocampus (H) within the medial temporal region, and the Ventral Tegmental Area (VTA) in the midbrain. The diagram emphasizes the spatial relationships and connectivity between these cortical and subcortical structures, which collectively form the final common pathway for the neurobiology of addiction. The cerebellum is visible posteriorly with its characteristic arbor vitae pattern, and the brainstem and corpus callosum provide central anatomical landmarks. This visual is designed for medical education regarding the psychiatric and neurological mechanisms of substance use disorders and reward processing.

A three-panel anatomical diagram illustrating the neuroanatomy and neurotransmitter pathways implicated in Attention Deficit Hyperactivity Disorder (ADHD) using medial views of a hemisected human brain. Panel A labels key anatomical structures: the prefrontal cortex, orbitofrontal cortex, anterior cingulate cortex, corpus callosum, striatum (including nucleus accumbens, caudate nucleus, and putamen), thalamus, temporal lobe, amygdala, and cerebellum. Panel B details the dopamine system, mapping projections from the ventral tegmental area (VTA) to the prefrontal cortex and nucleus accumbens, and from the substantia nigra to the striatum. Panel C illustrates the norepinephrine system, showing projections originating in the locus coeruleus of the brainstem and extending to the cortex, thalamus, cerebellum, and spinal cord. This set of illustrations serves as a pathophysiological model for understanding how altered volumes and functional connectivity in these catecholaminergic circuits contribute to ADHD symptoms.

| Population | Prevalence |
|---|---|
| Children & adolescents (worldwide) | 6-9% |
| US children aged 2-17 (NSCH data) | 9.4% |
| Adults (persistence from childhood) | ~50% |
| Sex ratio | Boys diagnosed more frequently and earlier than girls |
Note: ICD-11 supports first-time diagnosis in adults, provided symptoms were present in childhood. - Maudsley Prescribing Guidelines, 15th ed.

| Condition | Key Distinguishing Feature |
|---|---|
| Conduct disorder | Deliberate rule violations, aggression |
| Oppositional defiant disorder | Defiance toward authority, anger |
| Anxiety disorder | Worry-driven inattention, not impulsivity |
| Depression | Low mood, anhedonia, cognitive slowing |
| Learning disorder | Domain-specific deficit without core ADHD symptoms |
| Trauma/ACEs | ADHD-like symptoms with clear trauma history |
| Drug | Class | Notes |
|---|---|---|
| Atomoxetine | Selective NE reuptake inhibitor (SNRI) | Non-controlled; good for abuse concern; monitor for liver dysfunction and suicidal thinking |
| Guanfacine ER | Alpha-2A adrenergic agonist | RCT evidence as monotherapy; 2023 meta-analysis showed ~60% response (vs 30% placebo); well tolerated in adults |
| Clonidine ER | Alpha-2 adrenergic agonist | Supported by multiple RCTs in children/adolescents |
| Viloxazine | NE reuptake inhibitor | Effective per limited data; less evidence than atomoxetine |
| Bupropion | DA/NE reuptake inhibitor | Off-label; limited comparative evidence |
Atomoxetine is preferred when stimulants are not tolerated, are contraindicated, or two separate 6-week trials fail. - Maudsley Prescribing Guidelines