Abstracts

Rationale: Chronic calcified neurocysticercosis (cNCC) is endemic in Brazil. In spite of this we have been observing that cNCC is significantly more common in patients with mesial temporal lobe epilepsy associated with hippocampal sclerosis (MTLE-HS). This observation might suggest a possible cause-effect relationship between these two diseases. Here we advance one step further on these matters by investigating possible anatomical connections between cNCC and MTLE-HS. Methods: We review clinical, electrophysiological, and neuroimaging data of 355 consecutive patients with unilateral MTLE-HS submitted to anterior and mesial temporal lobectomy. In patients with a single calcification, we studied anatomical relations of the calcification with hippocampal sclerosis. The side of hippocampal sclerosis was correlated with the brain hemisphere where the single calcified lesion was located, using chi-squared test. Results: Neuroimaging findings of cNCC were observed in 133 (37.46%) patients. NCC was significantly more common in women (66.4%) than in men (33.6%) (p< 0.001),Considering only this 133 patients, 57 of them presented a single lesion (42.85%). In these patients with a single calcification, the lesion was located in the left hemisphere in 34 (59.64%) patients and in the right hemisphere in 23 (40.36%) patients. The chance of observing a single calcification ipsilateral to the hippocampal sclerosis was about 2.1 times grater for left hippocampal sclerosis and 2.8 times grater for right hippocampal sclerosis. This distribution was not by chance (O.R.=5.92; CI 95%=1.83-19.20; p=0.002). Conclusions: Our finding suggests that NCC might be anatomically related with hippocampal sclerosis. We speculate that one possible mechanism is that the cysticercus, by provoking repetitive seizures or status epilepticus, could lead to the development of MTLE-HS even if the cysticercus is located outside limbic circuits. Another possible mechanism is that the cysticerci might lead to variable inflammatory responses and perhaps to hippocampal damage in patients with some still unknown genetic predisposition, similar to that reported in other forms of meningoencephalitis. Because women are prone to develop more severe forms of cNCC and more intense inflammatory reactions than men, our observation that significantly more women than men have MTLE-HS and cNCC accords with the idea of inflammation-dependent hippocampal damage caused by neurocysticercosis. Thus, not only acute seizures or status epilepticus provoked by the cysticerci, but also inflammation-mediated hippocampal damage could lead to hippocampal sclerosis and subsequent MTLE-HS. Of course, both mechanisms could contribute to the disorder in the same patient. If this is the case, then neurocysticercosis would act as an initial precipitating injury (IPI) in many patients with MTLE-HS. This conclusion is important because it adds further evidences that NCC might contribute or even causes refractory MTLE-HS in endemic regions. Work supported by CNPq AND FAPESP.