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      Alterations of the occipital lobe in schizophrenia

      review-article
      , MBBS, , MBBS, , MBBS
      Neurosciences
      Riyadh : Armed Forces Hospital

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          Abstract

          The relationship of the occipital lobe of the brain with schizophrenia is not commonly studied; however, this topic is considered an essential subject matter among clinicians and scientists. We conducted this systematic review to elaborate the relationship in depth. We found that most schizophrenic patients show normal occipital anatomy and physiology, a minority showed dwindled values, and some demonstrated augmented function and structure. The findings are laborious to incorporate within single disease models that present the involvement of the occipital lobe in schizophrenia. Schizophrenia progresses clinically in the mid-twenties and thirties and its prognosis is inadequate. Changes in the volume, the gray matter, and the white matter in the occipital lobe are quite evident; however, the mechanism behind this involvement is not yet fully understood. Therefore, we recommend further research to explore the occipital lobe functions and volumes across the different stages of schizophrenia.

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          Most cited references71

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          The role of oscillations and synchrony in cortical networks and their putative relevance for the pathophysiology of schizophrenia.

          Neural oscillations and their synchronization may represent a versatile signal to realize flexible communication within and between cortical areas. By now, there is extensive evidence to suggest that cognitive functions depending on coordination of distributed neural responses, such as perceptual grouping, attention-dependent stimulus selection, subsystem integration, working memory, and consciousness, are associated with synchronized oscillatory activity in the theta-, alpha-, beta-, and gamma-band, suggesting a functional mechanism of neural oscillations in cortical networks. In addition to their role in normal brain functioning, there is increasing evidence that altered oscillatory activity may be associated with certain neuropsychiatric disorders, such as schizophrenia, that involve dysfunctional cognition and behavior. In the following article, we aim to summarize the evidence on the role of neural oscillations during normal brain functioning and their relationship to cognitive processes. In the second part, we review research that has examined oscillatory activity during cognitive and behavioral tasks in schizophrenia. These studies suggest that schizophrenia involves abnormal oscillations and synchrony that are related to cognitive dysfunctions and some of the symptoms of the disorder. Perspectives for future research will be discussed in relationship to methodological issues, the utility of neural oscillations as a biomarker, and the neurodevelopmental hypothesis of schizophrenia.
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            The reduced neuropil hypothesis: a circuit based model of schizophrenia.

            In recent years, quantitative studies of the neuropathology of schizophrenia have reignited interest in the cerebral cortex and focused attention on the cellular and subcellular constituents that may be altered in this disease. Findings have ranged from compromised circuitry in prefrontal areas to outright neuronal loss in temporal and cingulate cortices. Herein, we propose that a reduction in interneuronal neuropil in the prefrontal cortex is a prominent feature of cortical pathology in schizophrenia and review the growing evidence for this view from reports of altered neuronal density and immunohistochemical markers in various cortical regions. The emerging picture of neuropathology in schizophrenia is one of subtle changes in cellular architecture and brain circuity that nonetheless have a devastating impact on cortical function.
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              The neuropathology of schizophrenia. A critical review of the data and their interpretation.

              Despite a hundred years' research, the neuropathology of schizophrenia remains obscure. However, neither can the null hypothesis be sustained--that it is a 'functional' psychosis, a disorder with no structural basis. A number of abnormalities have been identified and confirmed by meta-analysis, including ventricular enlargement and decreased cerebral (cortical and hippocampal) volume. These are characteristic of schizophrenia as a whole, rather than being restricted to a subtype, and are present in first-episode, unmedicated patients. There is considerable evidence for preferential involvement of the temporal lobe and moderate evidence for an alteration in normal cerebral asymmetries. There are several candidates for the histological and molecular correlates of the macroscopic features. The probable proximal explanation for decreased cortical volume is reduced neuropil and neuronal size, rather than a loss of neurons. These morphometric changes are in turn suggestive of alterations in synaptic, dendritic and axonal organization, a view supported by immunocytochemical and ultrastructural findings. Pathology in subcortical structures is not well established, apart from dorsal thalamic nuclei, which are smaller and contain fewer neurons. Other cytoarchitectural features of schizophrenia which are often discussed, notably entorhinal cortex heterotopias and hippocampal neuronal disarray, remain to be confirmed. The phenotype of the affected neuronal and synaptic populations is uncertain. A case can be made for impairment of hippocampal and corticocortical excitatory pathways, but in general the relationship between neurochemical findings (which centre upon dopamine, 5-hydroxytryptamine, glutamate and GABA systems) and the neuropathology of schizophrenia is unclear. Gliosis is not an intrinsic feature; its absence supports, but does not prove, the prevailing hypothesis that schizophrenia is a disorder of prenatal neurodevelopment. The cognitive impairment which frequently accompanies schizophrenia is not due to Alzheimer's disease or any other recognized neurodegenerative disorder. Its basis is unknown. Functional imaging data indicate that the pathophysiology of schizophrenia reflects aberrant activity in, and integration of, the components of distributed circuits involving the prefrontal cortex, hippocampus and certain subcortical structures. It is hypothesized that the neuropathological features represent the anatomical substrate of these functional abnormalities in neural connectivity. Investigation of this proposal is a goal of current neuropathological studies, which must also seek (i) to establish which of the recent histological findings are robust and cardinal, and (ii) to define the relationship of the pathological phenotype with the clinical syndrome, its neurochemistry and its pathogenesis.
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                Author and article information

                Journal
                Neurosciences (Riyadh)
                Neurosciences (Riyadh)
                Neurosciences
                Neurosciences
                Riyadh : Armed Forces Hospital (Saudi Arabia )
                1319-6138
                July 2015
                : 20
                : 3
                : 213-224
                Affiliations
                [1] From the University of California, Davis (Tohid), UC Davis, Los Angeles, UCLA, and the Napa State Hospital (Tohid), Napa, California, United States of America, and Sindh Medical College (Faizan, M, Faizan U), Dow University of Health Sciences, Jinnah Postgraduate Medical Center, Karachi, Pakistan
                Author notes
                Address correspondence and reprint request to: Dr. Hassaan Tohid, Center for Mind and Brain, UC Davis, CA, United States of America. E-mail: hassaantohid@ 123456hotmail.com
                Article
                Neurosciences-20-213
                10.17712/nsj.2015.3.20140757
                4710336
                26166588
                85f2565b-79b6-48ec-b437-181f4334b4f3
                Copyright: © Neurosciences

                Neurosciences is an Open Access journal and articles published are distributed under the terms of the Creative Commons Attribution-NonCommercial License (CC BY-NC). Readers may copy, distribute, and display the work for non-commercial purposes with the proper citation of the original work.

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