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Long‐Term Epilepsy‐Associated Tumors

Thom, Maria, Blümcke, Ingmar, Aronica, Eleonora·2012·Brain Pathology
DOI 10.1111/j.1750-3639.2012.00582.x
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Abstract

The term long‐term epilepsy associated tumor (LEAT) encompasses lesions identified in patients investigated for long histories (often 2 years or more) of drug‐resistant epilepsy. They are generally slowly growing, low grade, cortically based tumors, more often arising in younger age groups and in many cases exhibit neuronal in addition to glial differentiation. Gangliogliomas and dysembryoplastic neuroepithelial tumors predominate in this group. LEATs are further united by cyto‐architectural changes that may be present in the adjacent cortex which have some similarities to developmental focal cortical dysplasias (FCD); these are now grouped as FCD type IIIb in the updated International League Against Epilepsy (ILAE) classification. In the majority of cases, surgical treatments are beneficial from both perspectives of managing the seizures and the tumor. However, in a minority, seizures may recur, tumors may show regrowth or recurrence, and rarely undergo anaplastic progression. Predicting and identifying tumors likely to behave less favorably are key objectives of the neuropathologist. With immunohistochemistry and modern molecular pathology, it is becoming increasingly possible to refine diagnostic groups. Despite this, some LEATs remain difficult to classify, particularly tumors with “non‐specific” or diffuse growth patterns. Modification of LEAT classification is inevitable with the goal of unifying terminological criteria applied between centers for accurate clinico‐pathological‐molecular correlative data to emerge. Finally, establishing the epileptogenic components of LEAT, either within the lesion or perilesional cortex, will elucidate the cellular mechanisms of epileptogenesis, which in turn will guide optimal surgical management of these lesions.

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  • Gangliogliomas and focal cortical dysplasia type IIb represent a major cause of drug-resistant epilepsy.

    “GG and FCD type IIb represent a major cause of drug-resistant epilepsy [23], [25] and are characterized by a prominent activation of various inflammatory pathways, including the TIR signaling pathway [9], [40]–[43].”

    From MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response (2012) · cites this paper as [25]

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Sorted by citations

Authors
Thom, M., Blümcke, I., & Aronica, E.
Venue
Brain Pathology
Publisher
Wiley
Published
2012-04-12
Volume
22
Issue
3
Pages
350-379
ISSN
  • 1015-6305
  • 1750-3639
DOI
10.1111/j.1750-3639.2012.00582.x
Cited by
205
References
1
Language
en
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

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