## Neurobiological Basis of ADHD **Key Point:** Dopamine dysregulation is the most widely accepted neurobiological abnormality in ADHD, particularly affecting the prefrontal cortex (executive function) and striatum (reward and motor control). ### Dopamine Hypothesis The catecholamine hypothesis of ADHD centers on dysfunction of dopaminergic neurotransmission: 1. **Prefrontal cortex involvement**: Reduced dopamine availability impairs executive functions (working memory, impulse control, attention regulation). 2. **Striatal involvement**: Dopamine deficiency in the nucleus accumbens and caudate nucleus affects reward processing and motivation. 3. **Neuroimaging evidence**: Functional MRI and PET studies show reduced dopamine transporter density in individuals with ADHD. ### Supporting Evidence | Finding | Implication | |---------|-------------| | Stimulant medications (methylphenidate, amphetamines) increase dopamine | Confirms dopamine deficiency as core pathology | | Reduced dopamine transporter (DAT) binding | Suggests impaired dopamine reuptake and clearance | | Genetic polymorphisms in DAT1 and DRD4 genes | Heritable dopamine system dysfunction | | Structural abnormalities in prefrontal-striatal circuits | Anatomical substrate for dopamine dysregulation | **High-Yield:** The dopamine hypothesis explains why stimulants (which block dopamine reuptake) are the first-line pharmacological treatment for ADHD. This is the most frequently tested neurobiological mechanism in NEET PG psychiatry. **Clinical Pearl:** While serotonin and norepinephrine also play secondary roles, dopamine dysregulation remains the primary and most consistent finding across neurobiological studies of ADHD.
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