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Diffusion tensor anisotropy and the ...
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Mount Sinai School of Medicine of New York University.
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Diffusion tensor anisotropy and the progression of schizophrenia.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Diffusion tensor anisotropy and the progression of schizophrenia./
作者:
Schneiderman, Jason S.
面頁冊數:
117 p.
附註:
Adviser: Monte Buchsbaum.
Contained By:
Dissertation Abstracts International69-08B.
標題:
Biology, Neuroscience. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3325702
ISBN:
9780549765776
Diffusion tensor anisotropy and the progression of schizophrenia.
Schneiderman, Jason S.
Diffusion tensor anisotropy and the progression of schizophrenia.
- 117 p.
Adviser: Monte Buchsbaum.
Thesis (Ph.D.)--Mount Sinai School of Medicine of New York University, 2008.
In the first of three studies, we found continued anisotropy changes consistent with myelin development from normal adolescence into early adulthood in regions connecting multimodal association areas in the frontal and temporal regions of the cortex.
ISBN: 9780549765776Subjects--Topical Terms:
1017680
Biology, Neuroscience.
Diffusion tensor anisotropy and the progression of schizophrenia.
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In the first of three studies, we found continued anisotropy changes consistent with myelin development from normal adolescence into early adulthood in regions connecting multimodal association areas in the frontal and temporal regions of the cortex.
520
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A convergence of evidence from genetics, post-mortem histology, and neuroimaging has lead to a hypothesis of a dysfunction in oligodendroglia and myelination in the pathophysiology of schizophrenia. White matter abnormalities can be visualized with MRI using diffusion tensor imaging measurement of anisotropy, a potential correlate of the development of the myelin in the brain. We used diffusion tensor anisotropy measures to localize deviations in development in white matter in schizophrenia through the lifespan and compare these with normal changes with age.
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In our second study, we found lower anisotropy in schizophrenia, possibly representing lower levels of proper myelination. Patients deviated from the normal developmental course in the tracts involved in the connectivity of the frontal lobe. This suggested that frontal connectivity is most changed during the time interval between the onset of psychotic symptoms and adulthood. In contrast, tracts connecting the temporal lobes are in place by the first psychotic episode.
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In our third study, we examined a larger patient sample ranging in age from 18 to 78 and in duration of illness from weeks to many decades. We found lower anisotropy in schizophrenia widespread, most markedly in the frontal, temporal and cingulate regions, reflecting these regions roles in the symptomatology of schizophrenia. Patients showed a greater rate of decline in orbitofrontal and superior temporal regions than normal individuals. Lower anisotropy was found in frontal, motor, and cingulate white matter in long duration patients, suggesting the white matter pathology continues to progress in these regions. Our evidence of decreased white matter anisotropy in patients with schizophrenia and the changes from the normal developmental pattern early in the course of the disease supports the hypothesis of abnormal white matter development in schizophrenia becoming prominent in individuals at the age when these regions normally myelinate.
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