Postoperative changes in cerebral metabolism in temporal lobe epilepsy.
BACKGROUND
Fludeoxyglucose F 18 positron emission tomography ((18)F-FDG-PET) can detect focal metabolic abnormalities ipsilateral to the seizure focus in 80% of patients with temporal lobe epilepsy (TLE). Regions outside the epileptogenic zone can also be affected. We hypothesized that these remote regions might show altered metabolism, tending to return toward normal values, after surgery.


METHODS
Interictal preoperative and postoperative (18)F-FDG-PET metabolism were compared in patients with refractory TLE. Based on pathological findings, disease was classified in the following 3 groups: mesial temporal sclerosis, mass lesions, and no pathological diagnosis. Quantitative PET data analysis was performed using the region-of-interest template previously described. Global normalization was used to adjust for the effect of antiepileptic medication changes. Data were analyzed by Wilcoxon signed rank test and analysis of variance.


METHODS
The Clinical Epilepsy Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health.


METHODS
Twenty-two patients with refractory TLE.


RESULTS
Preoperatively, in all groups, cerebral metabolic rate for glucose was decreased ipsilateral to the resection site in inferior lateral temporal, inferior mesial temporal, and inferior frontal areas and thalamus. Postoperatively, in all groups, cerebral metabolic rate for glucose increased in ipsilateral inferior frontal area and thalamus. In the mesial temporal sclerosis group, we found a statistically significant increase in the contralateral thalamus.


CONCLUSIONS
Temporal lobe epilepsy is associated with extensive preoperative decreased metabolism in inferior lateral temporal, inferior mesial temporal, and inferior frontal areas and thalamus. Postoperatively, we found increased IF and thalamic metabolism. Seizures may have a reversible effect on brain areas connected with, but remote from, the epileptogenic cortex. Arch Neurol. 2000;57:1447-1452
Spanaki
M V
MV
Clinical Epilepsy Section, Epilepsy Research Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-1408, USA.
Kopylev
L
L
DeCarli
C
C
Gaillard
W D
WD
Liow
K
K
Fazilat
S
S
Fazilat
S
S
Reeves
P
P
Sato
S
S
Kufta
C
C
Theodore
W H
WH
D000328:Adult; D000927:Anticonvulsants / Q000627:therapeutic use; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism*; D003131:Combined Modality Therapy; D004833:Epilepsy, Temporal Lobe / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000378:metabolism / Q000601:surgery*; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000493:pharmacokinetics; D005500:Follow-Up Studies; D005947:Glucose / Q000378:metabolism; D006801:Humans; D008297:Male; D011184:Postoperative Period; D011300:Preoperative Care; D014055:Tomography, Emission-Computed; D016896:Treatment Outcome
D000927:Anticonvulsants; D019788:Fluorodeoxyglucose F18; D005947:Glucose