• Title of article

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

  • Author/Authors

    Atsuko Matsuo، نويسنده , , Tomonori Ono، نويسنده , , Hiroshi Baba، نويسنده , , Kenji Ono، نويسنده ,

  • Issue Information
    روزنامه با شماره پیاپی سال 2003
  • Pages
    7
  • From page
    2165
  • To page
    2171
  • Abstract
    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
  • Keywords
    corpus callosum , Long-term EEGs , Quantitative analysis , Epileptiform discharges , Callosotomy
  • Journal title
    Clinical Neurophysiology
  • Serial Year
    2003
  • Journal title
    Clinical Neurophysiology
  • Record number

    522816