Abstracts

A focal lesion in the splenium of the corpus callosum (SCC) in patients with epilepsy and/or on antiepileptic agents is a rare finding. To date approximately 16 case reports have been published documenting this finding in this specific population. This study reviews 6 additional cases for similarities and comparison to current published reports. MRI reports from September 2001 to April 2005 performed at St. Paul Radiology for patients undergoing an inpatient evaluation with the Minnesota Epilepsy Group, PA were reviewed. One male and five females (ages 18-44 yrs) were found to have a focal lesion in the SCC during an inpatient evaluation. Analysis included documentation of patient demographics, seizure type/frequency, admission medication regimen, inpatient medication adjustments, comorbid diagnoses, abnormal laboratory values, MRI results and any clinical manifestations of a lesion in the SCC. 4/6 had CPS [plusmn] secondary generalization. 2/6 had solely NES diagnosis. All were admitted on a polytherapy AED regimen that included at least 1 sodium channel blocker. 6/6 had at least one AED rapidly tapered/discontinued prior to MRI. 4/4 on CBZ had CBZ tapered/discontinued in 1 to 4 days (avg admission dose = 1450mg/day). 2/4 on CBZ had an additional AED, LEV, rapidly tapered/discontinued over 2 days (admission dose = 2000mg and 2250mg/day respectively). 1/6 had PHT (400 mg/day) and LEV (1000mg/day) discontinued over 2 days and VPA (2625mg/day) over 5 days. One patient had OXC (1500mg/day) tapered/discontinued in 3 days and ZNS (600mg/day) over 6 days. We noted no similarities in concomitant medications/comorbid diagnoses. MRI scans were performed 1 - 11 days after discontinuation of the first AED. 6/6 had a previous MRI that did not show a focal lesion in the SCC prior to hospitalization. Repeat MRI in 3 patients were completed 2-5 months after initial identification of the lesion and demonstrated complete to near complete resolution of the lesion. We did not identify any abnormal laboratory data or significant clinical manifestations of the lesion. Previous publications implicate seizure activity as contributing to development of a similar lesion in the SCC. Our finding that 2/6 patients had a NES diagnosis argues against this interpretation. All 6 patients were found to be on polytherapy AED regimens that included a sodium channel blocker. Each patient underwent a rapid taper/discontinuation of a sodium channel blocker. No other similarities were discerned among the 6 patients. Our findings support previous reports that suggest rapid serum concentration fluctuation of an AED could contribute to development of a lesion in the SCC.