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pubmed-article:11988229pubmed:abstractTextIf corpus callosum (CC) mediates the activation of the secondary somatosensory area (SII) ipsilateral to the side of stimulation, then the peak latencies of the contra- and ipsilateral SII activity as well as the amplitude of the ipsilateral SII activity should correlate with the size of CC. Innocuous electrical stimuli of five different intensities were applied to the ventral surface of the right index finger in 15 right-handed men. EEG was recorded using 82 closely spaced electrodes. The size of CC and of seven callosal regions was measured from the mid-sagittal slice of a high-resolution anatomical MRI. The activation in the contralateral and ipsilateral SII was evaluated using spatio-temporal source analysis. At the strongest stimulus intensity, the size of the intermediate part of the callosal truncus correlated negatively with the interpeak latency of the sources in ipsi- and contralateral SII (r = -0.83, P < 0.01). Stepwise regression analysis showed that the large size of the intermediate truncus of CC was paralleled by a latency reduction of peak activity of the ipsilateral SII, whereas both contra- and ipsilateral peak latencies were positively correlated. The peak amplitude of the ipsilateral SII source correlated positively with the size of the intermediate truncus of CC, and with the peak amplitudes of sources in the primary somatosensory cortex (SI) and in the mesial frontal cortex. The results suggest that in right-handed neurologically normal men, the size of the intermediate callosal truncus contributes to the timing and amplitude of ipsilateral SII source activity.lld:pubmed
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pubmed-article:11988229pubmed:authorpubmed-author:SchergMichael...lld:pubmed
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pubmed-article:11988229pubmed:pagination47-57lld:pubmed
pubmed-article:11988229pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:11988229pubmed:year2002lld:pubmed
pubmed-article:11988229pubmed:articleTitleSource activity in the human secondary somatosensory cortex depends on the size of corpus callosum.lld:pubmed
pubmed-article:11988229pubmed:affiliationDepartment of Normal, Pathological and Clinical Physiology, Third Faculty of Medicine, Charles University Prague, Ke Karlovu 4, 120 00 2, Prague, Czech Republic. stancak@lf3.cuni.czlld:pubmed
pubmed-article:11988229pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11988229pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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