Are Traditional Societies Schizophrenogenic?Allen, John S.
doi: 10.1093/schbul/23.3.357pmid: 9327501
Schizophrenia is apparently less common in traditional than in nontraditional societies, and the course of illness in these cultural settings may also be more benign. Viral, political, economic, social labeling, and other explanations have been offered over the years for these differences. In contrast to those ideas that suggest the presence of a schizophrenogenic stress in urbanized, Westernized populations, I propose that traditional societies are actually schizophrenogenic compared with nontraditional societies. Assuming a multifactorial threshold model for the development of schizophrenia, traditional societies may be characterized by a lower threshold for developing schizophrenia in at-risk individuals. In the short term, this leads to a greater proportion of all clinical cases being of a less severe variety; in the long term, genes predisposing individuals to develop schizophrenia are exposed to the effects of negative selection, ultimately resulting in a relatively lower level of overt schizophrenia in these populations. The greater social demands placed on individual actors in traditional societies and the lack of variability in social network size may contribute to the (relatively) schizophrenogenic environment.
Are Traditional Societies Schizophrenogenic?Allen, John S.
doi: 10.1093/schbul/23.3.357pmid: 9327501
Schizophrenia is apparently less common in traditional than in nontraditional societies, and the course of illness in these cultural settings may also be more benign. Viral, political, economic, social labeling, and other explanations have been offered over the years for these differences. In contrast to those ideas that suggest the presence of a schizophrenogenic stress in urbanized, Westernized populations, I propose that traditional societies are actually schizophrenogenic compared with nontraditional societies. Assuming a multifactorial threshold model for the development of schizophrenia, traditional societies may be characterized by a lower threshold for developing schizophrenia in at-risk individuals. In the short term, this leads to a greater proportion of all clinical cases being of a less severe variety; in the long term, genes predisposing individuals to develop schizophrenia are exposed to the effects of negative selection, ultimately resulting in a relatively lower level of overt schizophrenia in these populations. The greater social demands placed on individual actors in traditional societies and the lack of variability in social network size may contribute to the (relatively) schizophrenogenic environment.
The Neuroanatomy of Schizophrenia: Editors' IntroductionBuchanan, Robert W.; Stevens, Janice R.; Carpenter, William T.
doi: 10.1093/schbul/23.3.365pmid: N/A
In the past 20 years there has been a marked increase in the number of studies examining the neuroanatomy of schizophrenia. This increase has been paralleled by even greater advances in our understanding of the structure and function of neurons and the brain. These advances in our knowledge of schizophrenia and the brain, in combination with the development of more sophisticated structural and functional imaging and postmortem analytic techniques, promise a more decisive study of the neuropathology of schizophrenia in the future. This issue of Schizophrenia Bulletin provides a review of the status of research on the neuroanatomy of schizophrenia, the nature of the evidence implicating specific brain regions, and which brain regions are best candidates for hypothesis-testing studies.
The Neuroanatomy of Schizophrenia: Editors IntroductionBuchanan, Robert W.; Stevens, Janice R.; Carpenter, William T.
doi: 10.1093/schbul/23.3.365pmid: N/A
In the past 20 years there has been a marked increase in the number of studies examining the neuroanatomy of schizophrenia. This increase has been paralleled by even greater advances in our understanding of the structure and function of neurons and the brain. These advances in our knowledge of schizophrenia and the brain, in combination with the development of more sophisticated structural and functional imaging and postmortem analytic techniques, promise a more decisive study of the neuropathology of schizophrenia in the future. This issue of Schizophrenia Bulletin provides a review of the status of research on the neuroanatomy of schizophrenia, the nature of the evidence implicating specific brain regions, and which brain regions are best candidates for hypothesis-testing studies.
The Neuroanatomy of Schizophrenia: Editors’ IntroductionBuchanan, Robert W.; Stevens, Janice R.; Carpenter, William T.
doi: N/Apmid: N/A
In the past 20 years there has been a marked increase in the number of studies examining the neuroanatomy of schizophrenia. This increase has been paralleled by even greater advances in our understanding of the structure and function of neurons and the brain. These advances in our knowledge of schizophrenia and the brain, in combination with the development of more sophisticated structural and functional imaging and postmortem analytic techniques, promise a more decisive study of the neuropathology of schizophrenia in the future. This issue of Schizophrenia Bulletin provides a review of the status of research on the neuroanatomy of schizophrenia, the nature of the evidence implicating specific brain regions, and which brain regions are best candidates for hypothesis-testing studies.
The Neuroanatomies of SchizophreniaBuchanan, Robert W.; Carpenter, William T.
doi: 10.1093/schbul/23.3.367pmid: 9327503
Schizophrenia is a brain disease whose pathophysiology has escaped detection despite intensive investigation. The failure to delineate the neuroanatomy of schizophrenia is related in part to both the subtle nature of the neuropathological abnormalities and to the failure to address adequately the pathophysiological heterogeneity of schizophrenia. The symptoms of schizophrenia aggregate into relatively independent symptom complexes, which suggests that there may be a distinct neural substrate for each complex. If this is true, then the neuroanatomy of schizophrenia is better addressed as the separate neuroanatomies of symptom complexes. However, the use of symptom complexes to guide future neuroanatomical investigations raises crucial methodological issues, including the differentiation of primary versus secondary symptoms, trait versus state characteristics, and continuous versus categorical variables. Decisive hypothesis testing requires that these issues be addressed in study design.
The Neuroanatomies of SchizophreniaBuchanan, Robert W.; Carpenter, William T.
doi: N/Apmid: N/A
Schizophrenia is a brain disease whose pathophysiology has escaped detection despite intensive investigation. The failure to delineate the neuroanatomy of schizophrenia is related in part to both the subtle nature of the neuropathological abnormalities and to the failure to address adequately the pathophysiological heterogeneity of schizophrenia. The symptoms of schizophrenia aggregate into relatively independent symptom complexes, which suggests that there may be a distinct neural substrate for each complex. If this is true, then the neuroanatomy of schizophrenia is better addressed as the separate neuroanatomies of symptom complexes. However, the use of symptom complexes to guide future neuroanatomical investigations raises crucial methodological issues, including the differentiation of primary versus secondary symptoms, trait versus state characteristics, and continuous versus categorical variables. Decisive hypothesis testing requires that these issues be addressed in study design.
The Neuroanatomies of SchizophreniaBuchanan, Robert W.; Carpenter, William T.
doi: 10.1093/schbul/23.3.367pmid: 9327503
Schizophrenia is a brain disease whose pathophysiology has escaped detection despite intensive investigation. The failure to delineate the neuroanatomy of schizophrenia is related in part to both the subtle nature of the neuropathological abnormalities and to the failure to address adequately the pathophysiological heterogeneity of schizophrenia. The symptoms of schizophrenia aggregate into relatively independent symptom complexes, which suggests that there may be a distinct neural substrate for each complex. If this is true, then the neuroanatomy of schizophrenia is better addressed as the separate neuroanatomies of symptom complexes. However, the use of symptom complexes to guide future neuroanatomical investigations raises crucial methodological issues, including the differentiation of primary versus secondary symptoms, trait versus state characteristics, and continuous versus categorical variables. Decisive hypothesis testing requires that these issues be addressed in study design.
Anatomy of Schizophrenia RevisitedStevens, Janice R.
doi: 10.1093/schbul/23.3.373pmid: 9327504
The search for an anatomy of schizophrenia has engendered an enormous, almost indigestible mass of data. In no studies do all patients show the same deviations from control samples. No morphological or microscopic abnormality has been found that is either necessary or sufficient for the diagnosis. In contrast to epilepsy, in which a proliferation of excitatory pathways or inadequate inhibitory factors are paramount, schizophrenia may represent a genetically and age-determined elaboration of one or more inhibitory networks in response to specific physiological events (e.g., the increased neuronal activity in limbic and hypothalamic structures during the physiological events of puberty) or to brain injury or defect. Current diagnostic classifications, including the positive-negative categories, have not led to separation of the disorder into etiologically or pathologically similar subgroups. Analysis of morphological and other biological pathology by a different nosological principle, such as trajectory of the illness, and separate correlation of anatomical and other biological outliers with clinical and demographic factors may be more successful strategies than pooling and averaging results from a mixture of patients diagnosed with schizophrenia.