Surgical and postmortem pathology studies: contribution for the investigation of temporal lobe epilepsy

Abstract

Pathology studies in epilepsy patients bring useful information for comprehending the physiopathology of various forms of epilepsy, as well as aspects related to response to treatment and long-term prognosis. These studies are usually restricted to surgical specimens obtained from patients with refractory focal epilepsies. Therefore, most of them pertain to temporal lobe epilepsy (TLE) with mesial temporal sclerosis (MTS) and malformations of cortical development (MCD), thus providing information of a selected group of patients and restricted regions of the brain. Postmortem whole brain studies are rarely performed in epilepsy patients, however they may provide extensive information on brain pathology, allowing the analysis of areas beyond the putative epileptogenic zone. In this article, we reviewed pathology studies performed in epilepsy patients with emphasis on neuropathological findings in TLE with MTS and MCD. Furthermore, we reviewed data from postmortem studies and discussed the importance of performing these studies in epilepsy populations.

Blast TBI Models, Neuropathology, and Implications for Seizure Risk

“…Blood–brain barrier (BBB) opening can lead to astrocyte activation through albumin-mediated transforming growth factor β (TGFβ)-dependent signaling (54–56). Other neuropathological findings in surgical specimens from patients with TLE described granule cell dispersion and temporal lobe sclerosis (47). Other, less frequently affected regions of the brain include selective neurons of the thalamus, basal forebrain, cerebellum, and brain stem (57, 58).…”

“…Patients with TLE are usually classified in either the mesial TLE group or in the lateral or neocortex TLE group. Mesial structures of the temporal lobe with epileptogenic potential are the hippocampus and occasionally the amygdala and the entorhinal cortex (47, 48). Interestingly, histology analyses of hippocampal tissues from TBI patients with blunt head trauma or acceleration injury show similar cellular and structural changes compared to the pathology from non-trauma patients with TLE.…”

Hippocampal granule cell dispersion: a non-specific finding in pediatric patients with no history of seizures

“…Chronic epilepsy is often associated with several pathological hippocampal abnormalities [44]. These include sclerosis, characterized by neuronal loss in both dentate gyrus and Ammon's horn, gliosis, mossy fiber sprouting; as well as granule cell dispersion (GCD), which is observed in the presence or absence of sclerosis [9,10,15,30,55,56]. These studies were mostly performed in surgical resections or autopsied brain samples obtained from patients suffering from febrile seizures and temporal lobe epilepsy (TLE); it is unclear whether the putative hippocampal abnormalities are the cause or effect of epilepsy [14,25].…”

“…A variety of diagnostic criteria for GCD has been suggested, varying from complex morphometric analyses [24,37] to subjective assessment of dentate gyrus histology [1,8,9,35,36]. Some reports have suggested abnormal neuronal migration, loss of hilar cells and genetic defects to be responsible for GCD, all influenced by seizure occurrence [10,30,54]. However, a substantial cohort of controls, with no history of seizures, was seldom included in the clinical studies; many lacked even 1 control specimen.…”

A Macaque Model of Mesial Temporal Lobe Epilepsy Induced by Unilateral Intrahippocampal Injection of Kainic Acid

“…mTLE is characterized by unilateral hippocampal sclerosis without consistent and reproducible alteration of other brain structures [2]–[4]. Hippocampal sclerosis includes extensive neuron loss in CA1 and CA3 sectors and in the hilus of dentate gyrus (DG) [5], [6]. Furthermore, clinicopathologic features of mTLE can be reproduced in experimental animals to some extent.…”