Pathological findings underlying focal temporal lobe hypometabolism in partial epilepsy

Abstract

Histopathological studies were carried out on temporal lobe tissue from 25 patients with partial complex seizures who were studied by interictal positron computed tomography (PCT) with 18F-fluorodeoxyglucose and subsequently underwent anterior temporal lobe resection. Abnormalities were identified on x-ray computed tomographic scans in 7 patients, but none indicated the site of a pathologically confirmed structural lesion. Hypometabolic zones were observed on PCT scans of 22 patients and corresponded to focal pathological abnormalities in 19 (15 mesial temporal sclerosis, 2 small neoplasms, 1 angioma, 1 heterotopia). In 1 patient with a focally abnormal PCT scan and no pathological changes, the lesion may have been located posterior to the resection. In the remaining 2 patients, the hypometabolic zones later disappeared and may have represented a transient response induced by depth electrode implantation. Three patients with normal PCT scans had no pathological abnormalities in their resected tissue. The degree of relative hypometabolism measured by PCT correlated well with the severity of the pathological lesion, but the size of the hypometabolic zone was generally much larger than the area of pathological involvement. This discrepancy could not be considered an artifact of technique and must represent either structural abnormalities below the resolution of routine histopathological studies (e.g., loss of synapses) or functional inactivation of neuronal elements associated with the epileptogenic lesion.

Staggered spondaic word test in epileptic patients

“…Histopathological studies have revealed hypometabolic areas at the focus of epileptic crises, 12,13 with synapse and neuronal activity losses in the presence of disorders arising from epilepsy. According to several authors, [14][15][16][17][18][19][20] dendritic and neuronal losses are always present in epileptic patients.…”

Cerebrospinal fluid GABA and seizure control with vigabatrin.

“…We administered the drug twice a day, which suggests that new GABA-T synthesis does not exceed the number of enzyme molecules eliminated by GVG during the intervals between drug administration. The histopathological findings from the brains of drug-resistant epileptics show that in partial epilepsy gliosis increases, especially in the limbic structures (Engel et al, 1982). GABA-T is localized in neurons but also in glial cells (McGeer & McGeer, 1981).…”

Lasting Secondary Antiepileptogenesis Induced by Cingulate Kindling

“…Propagation to the ipsilateral PC, MC, and the AM required a mean of 5.6 (range, 3-8), 20.3 (range, [19][20][21][22], and 17.5 (range, 16-20) stimulations, respectively. Propagation to the AM became bilateral in three animals (AC3990, AC#992, AC#997), with a mean of 64 (range, 13-77) stimulations.…”