Abstracts

Six cases involving transient focal lesions in the splenium of the corpus callosum (SCC) following the modification of antiepileptic drug therapy are reported. Discrete, non-contrast enhancing, well circumscribed, non-hemorrhagic lesions in the SCC are a rare finding occurring in patients with epilepsy. The etiology and pathogenesis of these lesions are currently unknown. Current hypotheses include transient interictal focal white matter edema associated with transhemispheric connection of seizure activity, antiepileptic drug toxicity, demyelination, and alteration of vasopressin concentrations in addition to vitamin deficiencies. However, a consistent relationship between these factors and its occurrence has not been observed.
We reviewed clinical material on 6 patients who were found to have focal lesions involving the SCC on MR imaging of the brain.
Six patients of Caucasian, Hispanic, and Native American ethnicities with ages ranging from 27-33 were studied. Four of the six patients were admitted to the epilepsy monitoring unit where carbamazepine, phenytoin, and lamotrigine were tapered or discontinued for seizure monitoring. One patient was admitted for neutropenia with oxcarbazepine, phenytoin, and lamotrigine discontinued and valproic acid started, the other for seizure activity related to poor medication compliance with levitiracetam. MR imaging of the brain was obtained from 1-10 days following the last seizure event in all patients. MRI of the brain demonstrated focal hypointensities on T1 and hyperintensities on T2 weighted images in the SCC. Contrast enhancement was not observed in all lesions and dissociative symptoms were not observed in all patients. Of those individuals undergoing repeat MR imaging, complete resolution of the lesions in the SCC were seen within 5 days to 1.5 months after initial identification.
Lesions involving the SCC in patients with epilepsy require no invasive diagnostic procedures or treatment. Repeat MRI brain scans demonstrated spontaneous and complete resolution of lesions within days to months following initial identification. Reasons for these changes are currently not well understood, however recent seizure activity in addition to acute changes in the antiepileptic drug regimen may be responsible for its occurrence. Determining why these lesions occur may provide a better understanding of the functional and anatomic significance of the corpus callosum in epilepsy. Additional studies assessing the occurrence of these lesions are needed.