Calcific neurocysticercosis and epileptogenesis

T E Nash, Óscar H. Del Brutto, John A. Butman, Teresa Corona, Antonio V. Delgado‐Escueta(University of California, Los Angeles), Reyna M. Durón(University of California, Los Angeles), Carlton A. Evans(Imperial College London), Robert H. Gilman(Johns Hopkins University), Armando E. González(Johns Hopkins University), Jeffrey A. Loeb(Wayne State University), Marco T. Medina, Susan Pietsch-Escueta, E. Javier Pretell, Osvaldo Massaiti Takayanagui(Universidade de São Paulo), William H. Theodore, Victor C. W. Tsang, Héctor H. Garcı́a(Universidad Peruana Cayetano Heredia)
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Abstract

Neurocysticercosis is responsible for increased rates of seizures and epilepsy in endemic regions. The most common form of the disease, chronic calcific neurocysticercosis, is the end result of the host's inflammatory response to the larval cysticercus of Taenia solium. There is increasing evidence indicating that calcific cysticercosis is not clinically inactive but a cause of seizures or focal symptoms in this population. Perilesional edema is at times also present around implicated calcified foci. A better understanding of the natural history, frequency, epidemiology, and pathophysiology of calcific cysticercosis and associated disease manifestations is needed to define its importance, treatment, and prevention.


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