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