Surgical pathology of epilepsy‐associated non‐neoplastic cerebral lesions: A brief introduction with special reference to hippocampal sclerosis and focal cortical dysplasia

Abstract

Among epilepsy-associated non-neoplastic lesions, mesial temporal lobe epilepsy with hippocampal sclerosis (mTLE-HS) and malformation of cortical development (MCD) including focal cortical dysplasia (FCD), are the two most frequent causes of drug-resistant focal epilepsies constituting about 50% of all surgical pathology of epilepsy. Several distinct histological patterns have been historically recognized in both HS and FCD, and several studies have tried to perform clinicopathological correlation; results, however, have been controversial, particularly in terms of postsurgical seizure outcome. Recently, the International League Against Epilepsy constituted a Task Forces of Neuropathology and FCD within the Commission on Diagnostic Methods, to establish an international consensus of histological classification of HS and FCD, respectively, based on agreement with the recognition of the importance of defining a histopathological classification system that reliably has some clinicopathological correlation. Such consensus classifications are likely to facilitate future clinicopathological study. Meanwhile, we reviewed neuropathology of 41 surgical cases of mTLE, and confirmed three type/patterns of HS along with no HS, based on the qualitative evaluation of the distribution and severity of neuronal loss and gliosis within hippocampal formation; i.e., HS type 1 (61%) equivalent to ‘classical’ Ammon’s horn sclerosis, HS type 2 (2%) representing CA1 sclerosis, HS type 3 (17%) equivalent to end folium sclerosis, and no HS (19%). Furthermore we performed a neuropathological comparative study on mTLE-HS and dementia associated HS (d-HS) in elderly, and confirmed that neuropathological features differ between mTLE-HS and d-HS in the distribution of hippocampal neuronal loss and gliosis, morphology of reactive astrocytes and their protein expression, and presence of concomitant neurodegenerative changes particularly Alzheimer type and TDP-43 pathologies. These differences may account, at least in part, for the difference in pathogenesis and epileptogenicity of HS in mTLE and senile dementia. However, the etiology and pathogenesis of most epileptogenic lesions are yet to be elucidated.

Unique Hard Scleral Lens Post-LASIK Ectasia Fitting

“…The CA1 subregion of the hippocampus is selectively vulnerable to HS regardless of the etiology; other subregions can also be affected. For example, the CA4 subregion is involved in a subset of TLE cases (1–3), but involvement of this subregion is relatively uncommon in FTLD and H–I (4). However, it is unclear to what extent the anatomic distribution of HS can help in the differential diagnosis of the underlying condition in autopsy neuropathology.…”

Staged anticonvulsant screening for chronic epilepsy

“…This may be due to an anticonvulsant drug discovery pipeline that relies on chemically or electrically induced seizures in otherwise normal brain tissue 4, 6. However, chronically epileptic tissue is significantly different from normal tissue,41 and may respond differently to drugs. We developed a three‐stage pipeline for discovering new anticonvulsants that relies on chronic epilepsy models at each stage.…”

Congenital and Acquired Conditions of the Mesial Temporal Lobe: A Pictorial Essay

“…Neuropathologic findings consist of different grades of neuronal loss and gliosis in Ammon's horn [4]. When there is concomitant focal cortical dysplasia the term ''dual pathology'' is used.…”