QUANTIFICATION OF OPIATE RECEPTORS IN 2 PATIENTS WITH MESIOBASAL TEMPORAL-LOBE EPILEPSY, BEFORE AND AFTER SELECTIVE AMYGDALO-HIPPOCAMPECTOMY, USING POSITRON EMISSION TOMOGRAPHY

Citation
Pa. Bartenstein et al., QUANTIFICATION OF OPIATE RECEPTORS IN 2 PATIENTS WITH MESIOBASAL TEMPORAL-LOBE EPILEPSY, BEFORE AND AFTER SELECTIVE AMYGDALO-HIPPOCAMPECTOMY, USING POSITRON EMISSION TOMOGRAPHY, Epilepsy research, 18(2), 1994, pp. 119-125
Citations number
17
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
09201211
Volume
18
Issue
2
Year of publication
1994
Pages
119 - 125
Database
ISI
SICI code
0920-1211(1994)18:2<119:QOORI2>2.0.ZU;2-L
Abstract
Using PET, reduced glucose metabolism (rCMRglu) and increased binding of the mu opiate receptor ligand C-11-carfentanil have been demonstrat ed in lateral temporal cortex overlying mesial temporal epileptic foci . Binding of the non-specific opiate receptor ligand C-11-diprenorphin e (DPN) to lateral temporal cortex has not shown consistent asymmetrie s. We measured rCMRglu with F-18-FDG and binding of C-11-diprenorphine in two patients with temporal lobe epilepsy (TLE) before and 5 months after selective amygdalo-hippocampectomy (both patients were seizure- free post-operatively). Pre-operatively, in both patients rCMRglu was decreased in mesial temporal lobe (MTL) (asymmetry index AI = -9.1 and 9.0) ipsilateral to the EEG focus. A more marked reduction was seen i n ipsilateral lateral temporal cortex (LTC) (AI = -32.0 and 18.9). DPN binding was reduced in MTL and LTC (AI MTL = -9.3 and 16.2; AI LTC = -8.0 and 5.5) ipsilateral to the focus, but was within 2 SD of the nor mal range. Post-operatively, the reduction of rCMRglu in LTC was accen tuated in one patient and decreased in the other (AI = -23.1 and 45.7) while there was a further reduction of DPN binding in LTC in both pat ients (AI = -27.8 and 9.8). These preliminary results in only two pati ents are compatible with downregulation of opiate receptors in LTC aft er removal of the epileptic focus or post-operative neuronal dysfuncti on.