Clinical correlations: MRI and EEG.

Main structural correlates of epileptogenesis include hippocampal sclerosis, cortical dysgenesis, foreign tissue lesions, gliosis, and dual pathology (a combination of any two). These structural abnormalities are now increasingly defined with MRI, enabling systematic EEG correlative analyses. Hippocampal atrophy (HA) and increased T2 signal in medial temporal structures predict the presence of mesial temporal sclerosis with a high degree of sensitivity and specificity. In 50 patients with clinical evidence of temporal lobe epilepsy and isolated HA, ictal scalp EEG was concordant to the atrophic temporal lobe in 33, nonlateralizing in 12, obscured in 3, and bilateral in 2, but it was discordant in none. Earlier reports of higher levels of discordance may be ascribed to the presence of dual pathology or to differing MRI and EEG criteria for localization. In a more inclusive group of 101 patients with unilateral HA, ictal scalp EEG was obtained in 99. It was unlocalized in 53, localized elsewhere in 9, and localized to the atrophic temporal lobe in 38. Of those, 51 patients had intracranial EEG: 12 were unlocalized, 29 were localized to the atrophic hippocampus, and 9 were localized elsewhere. There is thus a rare but definite subgroup of patients with unilateral HA who have EEG localization elsewhere than the atrophy. The successful cure of seizures in half these patients after removal of the EEG focus confirms the importance of this observation and emphasizes the search for more dual pathology that has remained undetected on MRI. About 10% of the patients with HA have significant atrophy bilaterally, and several series have confirmed that surgical success is predicted by removal of the EEG identified seizure onset area, not the more or less atrophic hippocampus. In patients with other kinds of dual pathology, including HA and foreign tissue lesions or cortical dysgenesis, EEG is also paramount in predicting the site of epileptogenesis for surgical intervention. EEG correlates of cortical dysgenesis are heterogeneous, but EEG has potential to provide accurate localization of the site of epileptogenesis in foreign tissue lesions also. In a study of 59 lesional patients, a small number of patients with low grade astrocytomas and oligodendrogliomas consistently localized by EEG to an area elsewhere than the lesion, and failed seizure control when the lesion was removed. Although MRI can demonstrate the structural correlate of the epilepsy in many situations, rare patients, particularly with certain tumors, cortical dysgenesis, and dual pathology, require EEG for accurate localization.