Lack of asymmetrical transfer for linguistic stimuli in schizophrenia: an ERP study.
ABSTRACT To assess the mechanisms underlying lack of speeded information transfer asymmetry (faster right to left) for verbal information in schizophrenia.
Interhemispheric transfer times (IHTT) between the hemispheres were assessed using a lateralized lexical-decision task in males with schizophrenia (N = 12) and matched controls (N = 12). Words were presented to the left visual field (LVF), right visual field (RVF), or bilaterally (BVF) while 128-channel EEG was recorded continuously. A direct measure of IHTT in each direction was obtained by comparing the latencies of the N160 evoked potential (EP) component in the hemispheres contralateral and ipsilateral to stimulation.
Controls showed faster information transfer from the right to left hemisphere (R-to-L) for linguistic stimuli. The two groups did not differ for IHTTs L-to-R. Lack of IHTT asymmetry in the schizophrenia groups was associated with an overall concomitant decrease in the amplitude of the N160 in the right hemisphere.
Differences in IHTT asymmetry may be attributed to lack of right hemisphere activation and not callosal dysfunction as has been previously suggested.
It is suggested that a relative excess of myelinated axons in the right hemisphere speeds IHTT faster R-to-L, findings are discussed with reference to differences in right hemisphere white matter connectivity in schizophrenia.
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ABSTRACT: Cerebral lateralisation appears to be decreased in schizophrenia. Results of studies investigating this, however, are equivocal. To review quantitatively the literature on decreased lateralisation in schizophrenia. Meta-analyses were conducted on 19 studies on handedness, 10 dichotic listening studies and 39 studies investigating anatomical asymmetry in schizophrenia. The prevalence of mixed- and left-handedness ('non-right-handedness') was significantly higher in patients with schizophrenia as compared to healthy controls, and also as compared to psychiatric controls. The analysis of dichotic listening studies revealed no significant difference in lateralisation in schizophrenia. However, when analysis was restricted to studies using consonant-vowel or fused word tasks, significantly decreased lateralisation in schizophrenia emerged. Asymmetry of the planum temporale and the Sylvian fissure was significantly decreased in schizophrenia, while asymmetry of the temporal horn of the lateral ventricle was not. Strong evidence is provided for decreased cerebral lateralisation in schizophrenia.The British Journal of Psychiatry 05/2001; 178:344-51. · 6.61 Impact Factor
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ABSTRACT: Brain imaging, molecular genetic, and ultrastructural evidence indicate the existence of pathologic alterations in the cortical and subcortical white matter of schizophrenic patients. We performed a stereologic analysis of numbers, densities, and spatial distribution of oligodendrocytes in layer III and in the gyral white matter of Brodmann's area 9 in the superior frontal gyrus to assess whether these cells are affected in schizophrenia. Counts were obtained on Nissl-stained materials and on sections immunolabeled for the oligodendrocyte marker 2',3'-cyclic nucleotide-3'-phosphodiesterase (CNPase) in seven schizophrenic and seven age-matched control cases. A 28% decrease in total numbers (or densities) of cortical layer III oligodendrocytes and a 27% decrease in the white matter were detected in schizophrenic compared with control cases based on CNPase immunostaining. Nissl and CNPase immunohistochemistry yielded comparable results. The spatial distribution of oligodendrocytes in area 9 white matter exhibited a less clustered arrangement in schizophrenic cases. These results suggest a severe pathology of oligodendrocytes in schizophrenia and provide a quantitative cellular correlate of the white matter changes observed by brain imaging in vivo, showing reduced fractional anisotropy in schizophrenia. The data support recent evidence that several genes encoding myelin-related proteins consistently exhibit reduced expression in schizophrenia.Biological Psychiatry 07/2003; 53(12):1075-85. · 9.25 Impact Factor
- Biological Psychiatry - BIOL PSYCHIAT. 01/2000; 47(8).