The dopamine hypothesis of schizophrenia posits that psychotic symptoms arise from dysregulated dopaminergic neurotransmission across four major CNS pathways. The mesolimbic pathway projects from the ventral tegmental area (VTA) to the nucleus accumbens and limbic structures; hyperactivity in this pathway is responsible for positive symptoms (hallucinations, delusions, disorganized thought). The mesocortical pathway projects from the VTA to the prefrontal cortex; hypoactivity in this pathway produces negative symptoms (flat affect, avolition, anhedonia, social withdrawal) and cognitive deficits (impaired working memory, executive function). The nigrostriatal pathway connects the substantia nigra to the caudate-putamen (dorsal striatum) and regulates voluntary movement; D2 blockade here produces extrapyramidal symptoms (EPS)—acute dystonia, akathisia, drug-induced parkinsonism, and tardive dyskinesia. The tuberoinfundibular pathway connects the hypothalamus to the anterior pituitary; dopamine tonically inhibits prolactin release, so D2 blockade causes hyperprolactinemia. First-generation antipsychotics (FGAs) non-selectively block D2 receptors across all four pathways, treating positive symptoms (mesolimbic) but causing EPS (nigrostriatal) and hyperprolactinemia (tuberoinfundibular) without improving negative symptoms (mesocortical). Second-generation antipsychotics (SGAs) achieve 'limbic selectivity' through combined D2 and 5-HT2A receptor antagonism—5-HT2A blockade disinhibits dopamine release preferentially in the nigrostriatal and...