Focal Cortical Dysplasia: A Review of Pathological Features, Genetics, and Surgical Outcome

Vincent Y. Wang, M.D. Ph.D.; Edward F. Chang, M.D.; Nicholas M. Barbaro, M.D.

Disclosures

Neurosurg Focus. 2006;20(1) 

In This Article

Abstract and Introduction

Abstract

Focal cortical dysplasia (FCD) is found in approximately one-half of patients with medically refractory epilepsy. These lesions may involve only mild disorganization of the cortex, but they may also contain abnormal neuronal elements such as balloon cells. Advances in neuroimaging have allowed better identification of these lesions, and thus more patients have become surgical candidates. Molecular biology techniques have been used to explore the genetics and pathophysiological characteristics of FCD. Data from surgical series have shown that surgery often results in significant reduction or cessation of seizures, especially if the entire lesion is resected.

Introduction

Focal cortical dysplasia is a significant cause of medically refractory epilepsy. Although aberrant cortical lamination had been described in epilepsy patients in the past, FCD was not extensively studied until Taylor, et al.,[50] in 1971 described a series of 10 epileptic patients with various degrees of cortical dysplasia. The characteristic balloon cells in these lesions were first described in this report. During the last 35 years, developments in imaging, electroencephalography, and electrocorticography have allowed more patients with medically refractory epilepsy to undergo resective surgery. Advances in molecular biology and physiology have led to a better understanding of the genetics and pathophysiological characteristics of FCD. We review the pathological features, pathophysiological characteristics, and genetics of FCD, as well as report on surgical outcomes in patients with FCD.

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