Developmental tumors and adjacent cortical dysplasia: Single or dual pathology?

Authors

  • André Palmini,

    Corresponding author
    1. Porto Alegre Epilepsy Surgery Program, Services of Neurology and Neurosurgery, Hospital São Lucas, Porto Alegre, Brazil
    2. Department ofInternal Medicine, Faculty of Medicine, Pontificia Universidade Catolica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil
    • Address correspondence to André Palmini, Service of Neurology, Hospital São Lucas, PUCRS, Avenida Ipiranga 6690, Porto Alegre, RS, Brazil – CEP: 90610-000. E-mail: apalmini@uol.com.br

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  • Eliseu Paglioli,

    1. Porto Alegre Epilepsy Surgery Program, Services of Neurology and Neurosurgery, Hospital São Lucas, Porto Alegre, Brazil
    2. Department ofSurgery, Faculty of Medicine, Pontificia Universidade Catolica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil
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  • Vinicius Duval Silva

    1. Department ofPathology, Faculty of Medicine, São Lucas Hospital, Catholic University of Rio Grande do Sul (PUCRS), Porto Alegre, Brazil
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Summary

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.

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