Surgery for focal cortical dysplasia

Abstract

Three decades since its comprehensive and elegant description (Taylor et al ., 1971), focal cortical dysplasia (FCD) remains an enigmatic condition. Its true incidence is not well known, as even high-resolution MRI studies may not enable its detection. In surgical series, which are inevitably pre-selected, FCD is the most common developmental pathology identified. Undoubtedly, FCD may cause severe refractory epilepsy including epilepsia partialis continua or generalized status epilepticus that can be directly life-threatening. Despite the attention focused on FCD because of this not infrequent malign presentation, much of its biology remains obscure, from its molecular pathology to its natural history. For example, we do not know why paediatric and adult presentations may differ; we do not know if the newly comprehended cellular dynamics of the postnatal human brain, including neoneurogenesis, constitute an important component of FCD biology; and fundamentally we do not know why FCD causes epilepsy or looks so bizarre under the microscope. When antiepileptic drugs fail to bring about complete seizure freedom in FCD, surgical resection of the FCD may hold the prospect of at least some relief for some patients. Practising epileptologists will all have seen individual patients who, following focal resection of the FCD, have done well or even become seizure free, and whose quality of life has improved even if seizure freedom has not been achieved. A previous review found that in comparison with the benchmark of patients having therapeutic resective surgery for epilepsy caused by hippocampal sclerosis, post-surgical outcome for FCD is less good, with ∼45% of reported patients becoming seizure free overall (Sisodiya, 2000); nevertheless, this figure is likely to be considerably …