An integrated view of pathophysiological models of schizophrenia.

摘要: Abstract Pathophysiological processes that underlie the profound neuropsychiatric disturbances in schizophrenia are poorly understood. However, clinical course of disease, and a number basic science observations, provide direction for formulating pathophysiological models could be empirically tested. For example, repeated psychostimulant administration to healthy subjects can induce psychotic symptoms, acute stimulant challenge patients precipitate psychosis. Also, NMDA antagonists positive, negative, cognitive schizophrenic-like symptoms volunteers thought disorder delusions patients. These human studies support dopamine receptor hypofunction hypotheses schizophrenia. Well-documented effects on systems basis integrate hypotheses. Furthermore, it has become apparent prominent actions antipsychotic drugs, especially those with `atypical' properties, involve antagonism behavioral, electrophysiological brain metabolic produced by antagonists. A confluence data suggests an early developmental insult, potentially involving reduced function, facilitate sensitization systems, leading formal onset late adolescence adulthood. Although clearly speculative, this conceptual model is consistent existing evidence lines future experimental investigation.