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Surgical pathology of epilepsy‐associated non‐neoplastic cerebral lesions: A brief introduction with special reference to hippocampal sclerosis and focal cortical dysplasia
Author(s) -
Miyata Hajime,
Hori Tomokatsu,
Vinters Harry V.
Publication year - 2013
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/neup.12028
Subject(s) - hippocampal sclerosis , cortical dysplasia , neuropathology , epilepsy , pathology , gliosis , medicine , hippocampal formation , temporal lobe , disease , psychiatry
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 correlations. However, results have been controversial, particularly in terms of post‐surgical seizure outcome. Recently, the I nternational L eague A gainst E pilepsy constituted a T ask F orces of N europathology and FCD within the C ommission on D iagnostic M ethods, 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 studies. Meanwhile, we reviewed the 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, that is, HS type 1 (61%) equivalent to “classical” A mmon'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 the 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 A lzheimer 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.