Journal
EPILEPSIA
Volume 53, Issue -, Pages 98-104Publisher
WILEY
DOI: 10.1111/j.1528-1167.2012.03619.x
Keywords
Malformations of cortical development; Seizures; EEG; MRI; FDG-PET; Single photon emission computed tomography (SPECT); MEG-MSI
Categories
Funding
- NIH [R01 NS38992]
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Cortical dysplasia is the most common etiology in children and the third most frequent finding in adults undergoing epilepsy neurosurgery. The new International League Against Epilepsy (ILAE) classification grades isolated cortical dysplasia into mild type I (cortical dyslamination), severe type II (dyslamination plus dysmorphic neurons and balloon cells), and dysplasia associated with other epileptogenic lesions (type III). Multilobar type II lesions present at an earlier age and with more severe epilepsy compared with focal type I abnormalities, often in the temporal lobe, and these findings are reflected in types and age of operations for cortical dysplasia. Presurgical evaluation of patients with epilepsy from cortical dysplasia can be challenging. Interictal and ictal scalp electroencephalography (EEG) accurately localizes cortical dysplasia with 5066% accuracy. Structural magnetic resonance imaging (MRI) is negative in roughly 30% of cases, most often linked with mild type I cases. FDG-PET can be 8090% accurate, but is not 100% sensitive. Chronic intracranial electrodes are used in about 50% of cases with cortical dysplasia, but often do not capture restricted ictal-onset zones. About 60% of patients with cortical dysplasia are seizure free after epilepsy neurosurgery, with much higher rates of becoming seizure free with complete (80%) compared with incomplete (20%) resections. The most common reason for incomplete resection is the risk of an unacceptable neurologic deficit. Future challenges include better tools in identifying subtle forms of type I cortical dysplasia, and development of adjunctive treatments from basic research for those undergoing incomplete resections.
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