Tumors and Tumoral Epilepsy
Developmental tumors and adjacent cortical dysplasia: Single or dual pathology?
Version of Record online: 12 DEC 2013
Wiley Periodicals, Inc. © 2013 International League Against Epilepsy
Special Issue: Tumors and tumoral epilepsy
Volume 54, Issue Supplement s9, pages 18–24, December 2013
How to Cite
Palmini, A., Paglioli, E. and Silva, V. D. (2013), Developmental tumors and adjacent cortical dysplasia: Single or dual pathology?. Epilepsia, 54: 18–24. doi: 10.1111/epi.12438
- Issue online: 12 DEC 2013
- Version of Record online: 12 DEC 2013
- Long-term epilepsy-associated tumors;
- Cortical dysplasia;
- Dual pathology;
- Developmental tumors
Developmental tumors often lead to refractory partial seizures and constitute a well-defined, surgically remediable epilepsy syndrome. Dysplastic features are often associated with these tumors, and their significance carries both practical and conceptual relevance. If associated focal cortical dysplasia (FCD) relates to the extent of the epileptogenic tissue, then presurgical evaluation and surgical strategies should target both the tumor and the surrounding dyslaminated cortex. Furthermore, the association has been included in the recently revised classification of FCD and the epileptogenicity of this associated dysplastic tissue is crucial to validate such revision. In addition to the possibility of representing dual pathology, the association of developmental tumors and adjacent dysplasia may instead represent a single developmental lesion with distinct parts distributed along a histopathologic continuum. Moreover, the possibility that this adjacent dyslamination is of minor epileptogenic relevance should also be entertained. Surgical data show that complete resection of the solid tumors and immediately adjacent tissue harboring satellites may disrupt epileptogenic networks and lead to high rates of seizure freedom, challenging the epileptogenic relevance of more extensive adjacent dyslaminated cortex. Whether the latter is a primary or secondary abnormality and whether dyslaminated cortex in the context of a second lesion may produce seizures after complete resection of the main lesion is still to be proven.