Occipitoparietal epilepsy, hippocampal atrophy, and congenital developmental abnormalities

Purpose: Diagnostic uncertainty may arise in patients with occipitoparietal epilepsy when there is neuroimaging evidence of a posterior quadrant lesio n and coexistent hippocampal abnormalities ("dual pathology"). It is not kn own whether hippocampal atrophy (HA) in these patients results from seizure propagation to temporolimbic structures or whether it is part of the patho logical process underlying the occipitoparietal epilepsy. Clarification of this issue may have a significant bearing on the management of these patien ts. Methods: we studied 20 patients with occipitoparietal epilepsy and neuroima ging or pathologic evidence of a congenital developmental abnormality. Norm alized hippocampal volumes were obtained in all patients. The medical recor ds and video-EEG recordings were analyzed to correlate the MRI findings wit h clinical data, seizure semiology, and EEG findings. Results: HA was found in seven patients (35%). Neuroimaging abnormalities c oncordant with the side of HA were seen in all cases. There was clinical or EEG evidence of temporal spread in 12 patients. There was no correlation b etween the presence of HA and temporal lobe spread. The only clinical facto r associated with HA in this series was a younger age of seizure onset. Conclusions: HA in patients with occipitoparietal epilepsy due to congenita l developmental abnormalities is most likely to be a marker of a more wides pread process related to a common pathogenesis during prenatal or perinatal development. HA in these patients is unlikely to be the result of secondar y spread from an extrahippocampal focus. Surgical treatment should be tailo red toward the primary epileptogenic zone rather the site of seizure spread .