A neural plasticity hypothesis of schizophrenia.
An extensive research effort has failed, thus far, to conclusively identify a specific disease process (or processes) underlying the behavioral symptoms of schizophrenia. The present paper will entertain the hypothesis that the structural and functional plasticity of the brain can constitute a "nonspecific" biological etiology of schizophrenia. This plasticity need not be accompanied by infectious processes or gross alterations in neurotransmitter levels, enzyme activities, etc. that are specific to schizophrenia. The monkey isolation syndrome provides a precedent for a causal relationship between brain plasticity and pathological behavior. In a speculative manner, it will be demonstrated that neural plasticity concepts can be invoked to potentially explain several aspects of schizophrenia: the various types of behavioral symptoms exhibited by schizophrenics, the regional alterations in brain structure and function seen in chronic schizophrenics, the involvement of genetic and environmental etiological factors, the pharmacological support for the dopamine hypothesis, and the delayed onset of neuroleptic antipsychotic action. Considering the explanatory potential of neural plasticity concepts, a research program which focuses on these concepts seems warranted.
D000818:Animals; D014150:Antipsychotic Agents / Q000627:therapeutic use; D001921:Brain / Q000503:physiopathology*; D002395:Catecholamines / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects; D004827:Epilepsy / Q000503:physiopathology; D000882:Haplorhini; D006801:Humans; D007696:Kindling, Neurologic / Q000187:drug effects; D009473:Neuronal Plasticity / Q000187:drug effects; D009474:Neurons / Q000502:physiology; D012559:Schizophrenia / Q000503:physiopathology*; D012565:Schizophrenic Psychology; D012683:Sensory Deprivation / Q000502:physiology; D014057:Tomography, X-Ray Computed
D014150:Antipsychotic Agents; D002395:Catecholamines