Schizophrenia: A Possible Etiology?

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Schizophrenia: A Possible Etiology? As for me, you must know I shouldn’t precisely have chosen madness if there had been any choice. What consoles me is that I am beginning to consider madness as an illness like any other, and that I accept it as such. -in a letter to his brother Theo According to the National Institute of Mental Health, nearly 20% of the US population may suffer from a diagnosable mental illness in any given six month period (1991). Obviously the issue of mental health warrants close scrutiny, as such illness can translate into lost work days and lost dollars. From a health care perspective, many of those suffering can be relieved of their symptoms and return to normal life, so to speak. Schizophrenia,…show more content…
Too strong of a signal or one given at an inappropriate time could strengthen inaccurate connections, ones that frequently don’t receive as much attention. Thus, hyperactive CA1 neurons through DA could reinforce fantasies and trivia and cause the delusions and hallucinations of paranoid schizophrenia. (Of course, the premorbid patterns would have an effect.) (Krieckhaus, Donhoe, Morgan, 1992). When does the system go awry in schizophrenia? Unlike Parkinsonism or Huntington’s, both chronic and progressive diseases, increasing evidence points to a defective neurodevelopmental process. Brain imaging techniques have exposed a variety of structural abnormalities in persons suffering from schizophrenia, and Weinberger’s monozygotic twin studies suggest that the structural differences seen in the affected twin were likely the result of developmental defects and not genetics (Kandel). Brains of schizophrenics have shown enlarged lateral ventricles (Nasralleh, 1993) that are associated with prominent prodromal symptoms (Wright, Gill, and Murray, 1993; Randel). They also have exhibited enlarged third ventricles (Nasralleh, 1993; Wright, Gill, and Murray, 1993; Kandel), present at the onset of illness and associated with both obstetric complications (see below) and prodromal symptoms (Nasralleh, 1993). Also demonstrated were hypoplasia of medial/limbic temporal structures, especially the hippocampus, and again present at the onset
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