title: Is a cortical spike discharge "transferred" to the contralateral cortex via the corpus callosum?: An intraoperative observation of electrocorticogram and callosal compound action potentials.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Neurosurgery, Nagasaki University School of Medicine, Nagasaki, Japan. tomo@epilepsy.med.nagasaki-u.ac.jp
authors.forename: Tomonori
authors.initials: T
authors.lastname: Ono
authors.forename: Atsuko
authors.initials: A
authors.lastname: Matsuo
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Baba
authors.forename: Kenji
authors.initials: K
authors.lastname: Ono
mesh_terms: D000293:Adolescent; D000328:Adult; D002540:Cerebral Cortex / Q000503:physiopathology* / Q000601:surgery; D002648:Child; D002675:Child, Preschool; D003337:Corpus Callosum / Q000502:physiology* / Q000601:surgery; D004292:Dominance, Cerebral / Q000502:physiology*; D004569:Electroencephalography; D004831:Epilepsies, Myoclonic / Q000175:diagnosis / Q000503:physiopathology* / Q000601:surgery; D004828:Epilepsies, Partial / Q000175:diagnosis / Q000503:physiopathology* / Q000601:surgery; D004829:Epilepsy, Generalized / Q000175:diagnosis / Q000503:physiopathology* / Q000601:surgery; D005071:Evoked Potentials / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D016343:Monitoring, Intraoperative; D009435:Synaptic Transmission / Q000502:physiology*