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Why Are There Seizures in Neurocysticercosis: Is It in the Genes?
Author(s) -
A. Clinton White
Publication year - 2010
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/656396
Subject(s) - neurocysticercosis , epilepsy , cysticercosis , taenia solium , medicine , helminthiasis , biology , pediatrics , pathology , psychiatry
(See the article by Verma et al, on pages 1219–1225.) " The demon slammed him to the ground and threw him into convulsions " —Luke 9:42. Neurocysticercosis is an ancient disease, yet it remains widely misunderstood [1]. Aristotle described the cystic form in the muscles of pigs, and similar descriptions were made by early Islamic scholars. In 1850, Kuchenmeister demonstrated the development of adult tapeworms in the intestines of prisoners who were fed Tae-nia solium cysticerci, and the fact that cys-ticercosis followed ingestion of T. solium eggs from tapeworms was also recognized at that time. English physicians carefully described all of the clinical manifestations of infection among British citizens returning home from India in the first half of the 20th century [2]. Neurocysticercosis was rarely diagnosed until the advent of noninvasive neuroimaging techniques of computed tomography and magnetic resonance imaging. Nevertheless, neurocys-ticercosis remains widely misunderstood in the medical community. Many physicians assume that the presence of the parasites in the central nervous system (CNS) causes symptomatic neu-rocysticercosis. Indeed, biblical descriptions of seizure note invading demons (parasites?) seizing patients and throwing them to the ground. The pathogenesis is clearly more complex than simply having organisms in the brain. Neurocysticercosis is very pleomorphic [1, 3]. Cysticerci in the brain parenchyma go through a series of stages. The mature vesicular lesions develop within a few weeks, but they are typically asymptomatic and suppress the host inflammatory response. The lesions later become inflamed, with the host response gradually clearing the parasite. This transitional phase is frequently complicated by seizures. In some cases, the le-sions will resolve completely. However, in other cases, resolution is incomplete, leaving a residual calcified lesion, which is often associated with chronic epilepsy [3]. Cysticerci in the ventricles can be asymp-tomatic or cause symptomatic obstructive hydrocephalus with headaches, altered mental status, nausea, vomiting, and uncal herniation. Cysticerci in the subarachnoid space present with a range of clinical manifestations. Cysticerci located over the brain convexity resemble those in the brain parenchyma. When cysticerci develop in the fissures, they often enlarge dramatically. The cysticerci themselves or associated inflammation may lead to mass effect. Cysticerci in the basilar cisterns are often associated with basilar arachnoiditis and vasculitis, which may present with meningitis, communicating hydrocepha-lus, or stroke. Several lines of evidence suggest a key role of host inflammation in the patho-genesis of neurocysticercosis. First, despite the fact that the cysticerci reach their mature size within …

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