Abstracts

Rationale: Although chronic calcified neurocysticercosis (CCL) has been considered a major cause of symptomatic epilepsy in developing countries like India, it can also be an incidental pathological finding in epileptic patients from endemic regions. To test the hypothesis that CCL causes intractable epilepsy we conducted a cross-sectional study investigating the etiology of intractable epilepsy. Methods: All patients who underwent video-EEG monitoring for refractory epilepsy from January 2005 to April 2009 at P Madhavan Nayar center for comprehensive epilepsy care, SCTIMST, South India were included in the study. The study examined the presence or absence of CCL in patients with refractory epilepsy based on set of previous diagnostic criteria. All patients had a comprehensive investigation including clinical and neurological examination and classification of seizure types and epilepsy syndromes. The CCL was established as a cause for refractory seizures by standard pre-surgical evaluation modalities including interictal and ictal scalp video-EEG (VEEG), CT scan and high resolution MRI, positron emission tomography (PET), single photon emission computed tomography (SPECT) and intracranial EEG monitoring in selected cases. Results: A total of 1954 (785 females; 40.15 %) VEEG recordings were done between Jan 2005 and April 2009 for evaluation of refractory seizures. The most common epileptogenic lesions were mesial temporal sclerosis (MTS; 40.94 %), gliosis (10.23 %), vascular (8.26 %), brain tumours (7.67 %), malformations of cortical development (5.11 %), and porencephalic cyst (2.55 %). Neuroimaging was normal in 24.32 % of patients. Calcifications were seen in 18 patients (0.92 %) and were significantly more common with MTS than in those without MTS (p<0.05). Of these 14 patients had focal seizures, one had primary generalized epilepsy and three patients had psychogenic seizures. In patients with dual lesions (seven with MTS and one with dysplasia), ictal recordings confirmed that CCL is an incidental finding rather than a cause for refractory seizures. Isolated CCL was seen in only five patients. During the follow up four patients (22.22 %) underwent epilepsy surgery. Of these two patients underwent standard temporal lobectomy with amygdalo-hippocampectomy for MTS and two other patients with isolated CCL underwent lesionectomy after chronic invasive monitoring. All patients had Engel’s class I outcome except one who had class II outcome at one year follow up. Conclusions: These data suggest that neurocysticercosis is an uncommon cause of intractable epilepsy, even in an endemic regions such as India, and that it may only represent a coexistent pathology. In addition further analysis of our findings reveals though CCL was more common in patients with MTS but its presence does not influence the clinical and pathologic profile of patients with hippocampal atrophy. Hence CCL is probably, in this set of patients, a coincidental pathology and does not have a role in epileptogenesis.