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Human nervous system infection by the parasite Taenia solium, known as neurocysticercosis (NCC) is widespread in several resource-poor countries in South-Central America, South and Southeast Asia and parts of Africa (1). In addition, the infection, whilst having once been eliminated from economically developed countries like the United States largely due to improvements in meat hygiene and surveillance has re-emerged in these countries owing to increasing frequencies of travel to, and immigration from endemic regions. The World Health Organization has declared NCC as one of six foremost potentially eradicable diseases on a global level (2).
Seizures are the most common manifestation of NCC and occur in up to 80% of large series of clinical cases. A recent, multi-center survey performed at several geographically diverse but fairly characteristic locations within the United States showed that 2.1%, a considerable proportion of patients presenting to the hospital emergency departments had evidence of NCC upon their imaging studies (3). Several early studies suggested that NCC as the main cause of late-onset epilepsy in developing countries that were endemic for NCC (4). Caution, however needs to be exercised in the interpretation of these early studies, in as much as, they did not distinguish between acute symptomatic, provoked seizures and remote symptomatic, unprovoked seizures (5). An attempt should be made to categorize all seizures in the context of NCC in accordance with epidemiological and syndromic classifications of the International League Against Epilepsy. Essentially, such an attempt would entail performing imaging studies in
close temporal association with seizures. Imaging findings of inflamed cyst/s suggest that seizures are provoked while those of calcified non-inflamed lesions indicate that seizures are unprovoked. It is not known as to what proportion of seizures are provoked and unprovoked respectively upon presentation and on subsequent follow-up. Furthermore, the etiological significance of single or sometimes multiple calcified lesions, which show up frequently on imaging studies of persons with epilepsy in NCC-endemic regions, is not clear. Such lesions are sequelae of previously active NCC and may not infrequently be noted on imaging studies of otherwise symptomatic individuals or those with other neurological conditions apart from seizures. Besides, epilepsy in a proportion of individuals with such lesions has been shown to be due to other causes such as mesial temporal sclerosis.
From the prognostic point of view, there are two main clinical disease patterns with distinct geographic predilections. The first is with a limited cyst load, usually a single cysticercus granuloma, described mainly from India (6). The lesion manifests as single or few seizures and spontaneously resolves in 3-6 months. The prognosis for seizure control is excellent; anti-epileptic drugs (AEDs) are usually administered till such time that the inflammatory granuloma resolves. The other is multilesional NCC, described typically from South and Central America but is also found in other geographic locations. Prognosis for seizure control is less favorable than in the case of single cysticercus granuloma and individuals with multilesional NCC usually require long-term AED treatment.
Treatment considerations revolve around the duration of AED treatment and the role of anthelminthic treatment in modifying seizure outcome in NCC. Oligolesional forms, especially the single cysticercus granuloma found in India requires short term AED treatment usually in months. Calcified and / or multiple lesion NCC forms usually require longer durations of AED treatment and prognosis in such forms is similar to any other type of remote symptomatic epilepsy. The impact of anthelmninthic treatment on seizure outcome remains controversial. A recent study demonstrated slight and insignificant improvement in numbers of seizures following anthelminthic treatment in comparison to placebo (7).
Many issues pertaining to the epileptology of NCC are yet poorly understood and as a consequence, management decisions remain empirical rather than guided by scientific evidence. Some of these, as hitherto outlined, form a promising agenda for future clinical and epidemiological research.
Gagandeep Singh
Department of Neurology
Dayanand Medical College
Ludhiana 141 001
India
References
- Bittencourt, P.R.M., Adamolekun, B., Bharucha, N., et al. Epilepsy in the tropics: II. Clinical presentations, pathophysiology, immunologic diagnosis, economics and therapy. Epilepsia 1996;37:1121-1127.
- Roman G, Sotelo J, Del Brutto O et al. A proposal to declare neurocysticercosis an internationally reportable disease. Bull World Health Organ 2002;78:399-406.
- Ong, S., Talan, D., Moran, G., et al. Neurocysticercosis in radiographically imaged seizure patients in U.S. emergency departments. Emerging Infectious Diseases 2002;8:608-613.
- Medina, M.T., Rosas, E., Rubio Donnadieu, F., et al. Neurocysticercosis as the main cause of late-onset epilepsy in Mexico. Archives of Internal Medicine 1990;150:325-332.
- Carpio, A., Escobar, A., Hauser, W.A. Cysticercosis and epilepsy: a critical review. Epilepsia 1998;39:1025-1040.
- Rajshekhar V. Solitary cerebral cysticercus granuloma. Epilepsia 2003;44s:25-28. View Article: Text | PDF
- Garcia HH, Pretell EJ, Gilman RH et al. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med 2004;350:249-258.
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