Callosal role in generation of epileptiform discharges: quantitative analysis of EEGs recorded in patients undergoing corpus callosotomy.

OBJECTIVE: Corpus callosotomy tends to decrease seizure frequency and severity rather than transforming the seizure pattern from a generalized form into a lateralized or a partial one. The finding implies that bisection of the corpus callosum (CC) disrupts the epileptogenicity itself. In order to gain further insight into the possible role played by the CC in intractable generalized epilepsy, quantitative analyses of long-term EEGs were performed. METHODS: Analyses were made of epileptiform discharges contained in the pre- and postoperative long-term EEGs in 7 patients who had an anterior callosotomy for intractable epilepsy. The duration, number, and amplitude of all epileptiform burst activities were measured and statistically analyzed. RESULTS: After callosotomy, the total number of epileptiform burst activities, mean duration, and the total number of spike discharges decreased significantly. The two hemispheres could be divided into dominant and non-dominant ones as to the quantity of the residual epileptiform discharges. CONCLUSIONS: Corpus callosotomy unevenly reduced preoperative epileptiform discharges in both hemispheres, suggesting a facilitatory role played by the callosal neurons that enables the asymmetrical epileptogenic susceptible state of the two hemispheres to develop bisynchronous and bisymmetrical epileptiform discharges. SIGNIFICANCE: Corpus callosotomy decreased the quantity of the epileptiform discharges, suggesting the transhemispheric facilitation of seizure mechanisms.

Is a cortical spike discharge "transferred" to the contralateral cortex via the corpus callosum?: An intraoperative observation of electrocorticogram and callosal compound action potentials.

PURPOSE: By means of the intraoperative electrophysiologic observation, we reevaluated the "transfer" theory that a transcallosal volley invoked by a cortical spike discharge in one hemisphere directly causes its contralateral counterpart via the corpus callosum (CC). METHODS: Twenty-six patients who underwent corpus callosotomy were the subjects of this study. Intraoperatively, electrocorticograms from both hemispheres were simultaneously monitored with callosal compound action potentials (CCAPs) from the CC. Analysis was conducted on (a) the interhemispheric delay of bilaterally synchronous spike-and-wave discharges (BSSWs), and (b) the chronological relation between BSSWs and CCAPs. RESULTS: The side of prior spike discharges was never fixed but was occasionally reversed. Interhemispheric delays between the BSSWs were not constant, regardless of direction, and fluctuated in all patients. Most of the interhemispheric delays were distributed within 20 ms with a mode of 0 ms. The waveform of the CCAP was characterized by slow-rising negative potential change that attained its peak after a cortical spike discharge. These findings were identical in all the patients regardless of whether the BSSWs were changed or unchanged after callosotomy. CONCLUSIONS: If the "transfer" role of the CC is true, interhemispheric delays between BSSWs must be longer than interhemispheric axonal conduction time (about 20 ms), and a preceding cortical spike discharge must produce a CCAP and then a contralateral one in order of time. However, this hypothesis was not confirmed in the present study. We propose the interhemispheric recruitment of the epileptogenic state as a different role of the CC on epileptogenesis.