Abstracts

Rationale: Neurocysticercosis (NCC) infection is a leading cause of seizures in developing nations and is now recognized as an emerging cause of seizures in the U.S. Indeed, one recent study suggests that NCC accounts for up to 10% of patients presenting to emergency departments with seizures in the southwestern U.S.(Ong et al 2002). There are several potential mechanisms relating NCC and drug-resistant epilepsy (DRE), however, and a number of authors have reported an association between NCC and mesial temporal sclerosis (MTS) (Singla et al 2007). We report a series of patients with DRE referred for presurgical evaluation who demonstrate evidence of both remote NCC and MTS. Methods: Patients with DRE cared for in our tertiary care epilepsy clinic at LAC USC in addition to surrounding Los Angeles Department of Health Services facilities are routinely referred for presurgical evaluation at Rancho Los Amigos National Rehabilitation Center. All patients undergo inpatient video-EEG monitoring (VEM), high-resolution MRI, CT or PET-CT, and neuropsychological evaluation as part of a standard presurgical evaluation. Results: Approximately 5%(13/200) of patients referred for medically intractable epilepsy over two years demonstrated evidence of remote NCC and MTS. All patients with dual pathology had emigrated from countries with endemic NCC. In 12/13 cases of dual pathology, punctuate calcifications consistent with remote NCC were present in the hemisphere ipsilateral to MTS, frequently below the Sylvian fissure or at the temporal-occipital junction. In two cases, punctuate calcifications were associated with extensive areas of abnormal T2/FLAIR signal abnormality in addition to MTS. In almost all cases, ictal onset as determined by video-EEG monitoring was localized over the anterior temporal region coincident with MTS. One patient demonstrated a punctate calcification deep within the left temporal lobe associated with a superficial area of encephalomalacia with contralateral ictal onset. Ictal onset did not localize to extratemporal calcifications in any patient with dual pathology. Six patients have undergone standard anterior temporal lobe resection with limited amygdala-hippocampectomy. One patient experienced a single post-operative complex partial seizure, but subsequently achieved seizure-freedom (1 year at present). All remaining patients remain seizure-free since surgery and all are maintained on anti-convulsant medications. Conclusions: 1.NCC is rarely a cause of DRE and any patient who presents with DRE should be considered for standard presurgical evaluation including MRI and VEM. 2.Although the precise causal relationship between NCC and DRE is unclear at the present time, close proximity of punctate calcifications and MTS suggests that the latter may represent a sequelae of repetitive focal seizures, interictal discharges and/or focal inflammation. 3.The presence of dual pathology (MTS and NCC) does not preclude resective surgery, and many patients enjoy post-operative seizure freedom following standard temporal lobectomy.