How frequent is the association of neurocysticercosis and mesial temporal lobe epilepsy with hippocampal sclerosis?


To the Editors:

In an interesting article, Chandra et al. (2010) quoted us to support the view that the association of neurocysticercosis (NCC) and mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) is rare. This is not our view. Instead, we believe that this association is rather frequent. NCC is endemic in the developing world, being a major cause of epilepsy worldwide (Garcia et al., 2005). Despite the fact that the epidemiology of the association of MTLE-HS with NCC is unknown, there are some clues regarding the real occurrence of this association. The prevalence of NCC plus MTLE-HS might be high in some world regions (Bianchin et al., 2005). In a cross-sectional study of 512 patients with refractory epilepsy, 281 (54.8%) of them had MTLE-HS and 104 (37.0% of the total of patients with MTLE-HS) presented MTLE-HS plus NCC. In comparison, the prevalence of NCC in patients with other epileptogenic lesions (cortical dysplasia, brain tumors, or gliosis) was only 15%, a significant difference (Velasco et al., 2006). Given the epidemiology of both diseases, if this association also occurs in other populations, then the prevalence of MTLE-HS plus NCC worldwide would be substantial.

So far we believe that there are three possibilities for the association of NCC and MTLE-HS. First, there are patients who have NCC and MTLE-HS because of coincidence (Leite et al., 2000). Second, both diseases might share common predisposing factors, including socioeconomic-related factors (Velasco et al., 2006). Third, NCC might work as an initial precipitating injury leading to typical MTLE-HS, similarly to other infections (Wichert-Ana et al., 2004; Velasco et al.; 2006; Bianchin et al., 2006a). When associated with MTLE-HS, NCC is more common in women than in men, causes more bilateral temporal lobe interictal discharges, and patients tend to have a lower frequency of “classical” initial precipitating injury history (Bianchin et al., 2006b). In addition, NCC in MTLE-HS is anatomically related to the side of the hippocampal sclerosis (Bianchin et al., 2008). Despite these differences, when present, NCC has no major impact on MTLE-HS surgical prognosis (Bianchin et al., 2005), a finding that further supports the role of NCC as an initial precipitating injury. Based on these observations, we suggested that the mechanisms involved in hippocampal damage may be inflammation, repeated seizures involving specific neural networks, NCC-induced status epilepticus, gender-related factors, and possibly other molecular mechanisms (Wichert-Ana et al., 2004; Bianchin et al., 2006a; Velasco et al., 2006; Bianchin et al., 2010). In our view, each of these factors might act separately or together to cause hippocampal damage and MTLE-HS.

Because NCC and MTLE-HS are common diseases, it would not be a surprise if their association were highly prevalent worldwide. Moreover, some data support the view that NCC might directly cause MTLE-HS, favoring this association. Considering its prevalence, NCC could well be a major cause of MTLE-HS. Consequently, it is not possible to state that the association of NCC and MTLE-HS is rare. Further studies are necessary to evaluate the epidemiology of this association and to clarify its mechanisms.


We have no conflict of interest. We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.