Contemporary somatic treatments in schizophrenia rely largely on second-generation antipsychotic medication for amelioration of positive symptoms of hallucinations and delusions and are neutral with respect to key and highly disabling features of the illness, such as neurocognitive deficits, negative symptoms, and psychosocial impairment. Initial neurobiological conceptualizations suggested efficacy of first-generation antipsychotics based on their ability to block dopamine receptors and address a state of hyperdopaminergia in the brain that served as the presumed neurobiological basis of the disorder. Contemporary models emphasize increased dopaminergic activity in subcortical circuits as a final common pathway for the production of delusions and hallucinations that occur as a function of any number of potential neurochemical abnormalities or environmental stressors and insults. Medications focused on mitigating generalized inflammation processes and oxidative stress in the central nervous system are promising avenues of future research.
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