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Callosal bisection and transcallosal secondary antiepileptogenesis Wada JAEpilepsia 2005[]; 46 Suppl 1 (ä): 2-6More than 28,000 neuroscientists and 3,000 epileptologists gathered at their respective 2001 meetings of the Society for Neuroscience and the American Epilepsy Society. Yet only six articles, one directly and five indirectly, discussed the corpus callosum (CC). Is not this in itself a remarkable finding? Are there no mysteries left? The reality is that considerable uncertainties exist regarding the rationale for callosal bisection (CCB) that causes contrasting effects (i.e., amelioration of generalized seizure, at times leading to freedom from seizure, and intensification of postoperatively fragmented seizure, at times leading to status epilepticus). Similarly, the clinical relevance of EEG mirror focus formation, an experimentally well-established transcallosal consequence of partial cortical epileptogenesis, continues to be debated. This presentation revisits these unresolved issues (a) to gain insight into the dynamic role played by the CC in medically refractory epilepsy, and (b) to promote the development of antiepileptogenic tools that are currently unavailable.|Animals[MESH]|Cerebral Cortex/*physiopathology[MESH]|Corpus Callosum/physiopathology/*surgery[MESH]|Disease Models, Animal[MESH]|Electroencephalography[MESH]|Epilepsies, Partial/physiopathology/surgery[MESH]|Epilepsy/physiopathology/*prevention & control/*surgery[MESH]|Functional Laterality/*physiology[MESH]|Humans[MESH]|Kindling, Neurologic/physiology[MESH]|Macaca mulatta[MESH]|Neural Pathways/physiopathology/surgery[MESH]|Papio papio[MESH]|Postoperative Complications/etiology/physiopathology[MESH]|Status Epilepticus/etiology/physiopathology[MESH]|Treatment Outcome[MESH] |
