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Calcific neurocysticercosis and epileptogenesis

From the Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (Dr. Nash), Diagnostic Radiology Department, Clinical Center (Dr. Butman), and National Institute of Neurological Diseases and Stroke (Dr. Theodore), National Institutes of Health, Bethesda, MD; Department of Neurological Sciences (Dr. Del Brutto), Hospital-Clínica Kennedy, Guayaquil, Ecuador; Instituto Nacional de Neurologia y Neurocirugia (Dr. Corona), Mexico DF; UCLA (Drs. Delgado-Escueta and Duron), Los Angeles, CA; Department of Infectious Diseases & Microbiology (Dr. Evans), Imperial College London, UK; Department of International Health (Drs. Gilman, Gonzalez, and Garcia), Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD; Department of Microbiology (Drs. Gilman and Garcia), Universidad Peruana Cayetano Heredia, Lima; School of Veterinary Medicine (Dr. Gonzalez), Universidad Nacional Mayor de San Marcos, Lima; Department of Neurology & The Center for Molecular Medicine and Genetics (Dr. Loeb), Wayne State University, Detroit, MI; Universidad Nacional Autonoma de Honduras (Dr. Medina), Tegucigalpa, Honduras; Epilepsy Foundation of America (S. Pietsch-Escueta), Los Angeles, CA; Cysticercosis Unit (Drs. Pretell and Garcia), Instituto Nacional de Ciencias Neurológicas, Lima, Peru; Department of Neurology (Dr. Takayanagui), School of Medicine of Riberao Preto, Universidade de Sao Paulo, Ribeirno Preto, Brazil; and Division of Parasitic Diseases (Dr. Tsang), National Center for Infectious Diseases, Centers for Disease Control, Atlanta, GA.

Address correspondence and reprint requests to Dr. Theodore E. Nash, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; e-mail tnash{at}niaid.nih.gov

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.

Received June 20, 2003. Accepted in final form December 9, 2003.

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