Purpose: To relate the occurrence of contralateral electroencephalogram slo
wing (CES) to amobarbital distribution, we performed electroencephalogram (
EEG) monitoring and intracarotid single photon emission computed tomography
(SPECT) during an intracarotid amobarbital procedure (IAP).
Methods: IAP was performed on 22 patients with temporal lobe epilepsy. CES
was defined as the occurrence of significant EEG slowing on the contralater
al hemisphere (>50% of the ipsilateral hemisphere slowing) after amobarbita
l injection. To map the distribution of the amobarbital, we injected a mixt
ure of amobarbital and (99m)technetium-ethylcysteinate dimer (Tc-99m-ECD) i
nto the internal carotid artery and performed a brain SPECT 2 h later. In t
he SPECT images, regions of interest were determined by ipsilateral and con
tralateral anterior cerebral artery territories (iACA, cACA), ipsilateral a
nd contralateral middle cerebral artery territories (iMCA, cMCA), and ipsil
ateral and contralateral posterior cerebral artery territories (iPCA, cPCA)
, as well as ipsilateral and contralateral anterior and posterior mesial te
mporal regions (iAMT, cAMT, iPMT, cPMT). The perfusion of amobarbital was i
nterpreted visually in each region.
Results: Amobarbital was distributed in the iMCA in all the patients; in th
e iACA in 20 (90.9%) patients; in the iAMT in 14 (63.5%); and in the iPCA a
nd iPMT in only two (9.1%). CES was observed in 13 (59.1%) patients. Cross-
perfusion of amobarbital in limited areas of the cACA were observed in only
four of 13 patients. Wada retention memory scores (WRMS) showed no signifi
cant difference between the CES- (n = 9) and CES+ (n = 13) groups.
Conclusions: Amobarbital rarely perfused the iPCA territory and the iPMT re
gion and was rarely delivered to the contralateral hemisphere. The occurren
ce of CES was not related to the cross-perfusion of amobarbital. CES appear
s to be produced by a transient functional disconnection from the ipsilater
al hemisphere.