Cerebral Cortex Advance Access originally published online on April 14, 2004
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Cerebral Cortex August 2004; 14:892-902
© Oxford University Press 2004
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Positive and Negative Network Correlations in Temporal Lobe Epilepsy
1 Department of Neurology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA, 2 Department of Neurobiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA, 3 Departments of Medical Informatics and Radiology, Erasmus MC, University Medical Center Rotterdam, 3000 DR Rotterdam, The Netherlands, 4 Department of Radiology, University of California, San Francisco, 505 Parnassus Avenue, Box 0628, San Francisco, CA 94143-0628, USA, 5 Department of Pediatrics, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA, 6 Department of Diagnostic Radiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA
Temporal lobe seizures are accompanied by complex behavioral phenomena including loss of consciousness, dystonic movements and neuroendocrine changes. These phenomena may arise from extended neural networks beyond the temporal lobe. To investigate this, we imaged cerebral blood flow (CBF) changes during human temporal lobe seizures with single photon emission computed tomography (SPECT) while performing continuous video/EEG monitoring. We found that temporal lobe seizures associated with loss of consciousness produced CBF increases in the temporal lobe, followed by increases in bilateral midline subcortical structures. These changes were accompanied by marked bilateral CBF decreases in the frontal and parietal association cortex. In contrast, temporal lobe seizures in which consciousness was spared were not accompanied by these widespread CBF changes. The CBF decreases in frontal and parietal association cortex were strongly correlated with increases in midline structures such as the mediodorsal thalamus. These results suggest that impaired consciousness in temporal lobe seizures may result from focal abnormal activity in temporal and subcortical networks linked to widespread impaired function of the association cortex.
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