CLONIDINE-INDUCED AND METHOHEXITAL-INDUCED EPILEPTIFORM DISCHARGES DETECTED BY MAGNETOENCEPHALOGRAPHY (MEG) IN PATIENTS WITH LOCALIZATION-RELATED EPILEPSIES

Citation
K. Kirchberger et al., CLONIDINE-INDUCED AND METHOHEXITAL-INDUCED EPILEPTIFORM DISCHARGES DETECTED BY MAGNETOENCEPHALOGRAPHY (MEG) IN PATIENTS WITH LOCALIZATION-RELATED EPILEPSIES, Epilepsia, 39(10), 1998, pp. 1104-1112
Citations number
32
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00139580
Volume
39
Issue
10
Year of publication
1998
Pages
1104 - 1112
Database
ISI
SICI code
0013-9580(1998)39:10<1104:CAMEDD>2.0.ZU;2-A
Abstract
Purpose: During presurgical evaluation, 14 patients with medically int ractable focal epilepsies underwent magnetoencephalographic (MEG) reco rdings to localize the epileptogenic focus. To increase the number of epileptiform discharges required for MEG analysis, methohexital a shor t-acting barbiturate that is known to activate epileptiform activity, was used. Additionally, we investigated the spike provoking properties of clonidine in comparison to methohexital. Methods: After oral preme dication with clonidine, shortlasting anesthesia was provided by intra venously administered methohexital. The number and location of epilept iform MEG discharges were assessed after clonidine premedication and d uring methohexital anesthesia. Results were compared with baseline MEG recordings. Results: Methohexital increased the frequency of focal ep ileptiform discharges in eight of 13 patients (one of the 14 patients did not receive methohexital after premedication with clonidine). Addi tionally, premedication with clonidine was found to increase focal epi leptiform discharges in nine of 14 patients. When compared with baseli ne MEG recordings, recordings after treatment with both clonidine prem edication and methohexital anesthesia showed a significant increase in the total number of epileptiform signals and the number of spikes con tributing to MEG source localizations. Conclusions: This study confirm s the selective proconvulsant effects of methohexital on the epileptog enic focus as suggested previously by EEG and electrocorticogram (ECoG ) investigations. Additionally, our data establish for the first time that clonidine increases epileptiform activity in patients with seizur e disorders. These results indicate that clonidine is suited as an act ivating agent for the localization of epileptogenic foci by means of M EG. This effect of clonidine on specific epileptic activity also indic ates that clonidine should be used with caution as an antihypertensive drug in patients with seizure disorders.