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Calcified Neurocysticercosis: Understanding Dead (Not Necessarily Inactive) Parasites
Christina M. Coyle
christina.coyle@einsteinmed.edu
Christina M. Coyle
Department of Infectious Diseases, Albert Einstein College of Medicine, Bronx, New York;
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Javier A. Bustos
Javier A. Bustos
Center for Global Health, Universidad Peruana Cayetano Heredia, Lima, Perú;
Center for Global Health, School of Health Sciences, Universidad Peruana de Ciencias Aplicadas (UPC), Lima, Perú;
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Center for Global Health, School of Health Sciences, Universidad Peruana de Ciencias Aplicadas (UPC), Lima, Perú;
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Oscar H. Del Brutto
Oscar H. Del Brutto
School of Medicine and Research Center, Universidad EspÃritu Santo – Ecuador, Samborondón, Ecuador;
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Hector H. Garcia
Hector H. Garcia
Center for Global Health, Universidad Peruana Cayetano Heredia, Lima, Perú;
Cysticercosis Unit, Instituto Nacional de Ciencias Neurologicas, Lima, Perú;
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Cysticercosis Unit, Instituto Nacional de Ciencias Neurologicas, Lima, Perú;
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Theodore E. Nash
Theodore E. Nash
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland;
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Vedantam Rajshekhar
Vedantam Rajshekhar
Department of Neurological Sciences, Christian Medical College Ranipet Campus, Vellore, India
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Neurocysticercosis (NCC) is the most common helminthic infection of the human central nervous system (CNS), and a major cause of acquired epilepsy in most of the world. Although outcomes of NCC have been improved by advanced diagnostic tests, antiparasitic drugs, and appropriate anti-inflammatory treatment, little attention has been paid to calcified NCC. Calcification is a common outcome in NCC and carries increased risk for seizures and hippocampal atrophy/sclerosis. The pathophysiological mechanisms leading to calcification instead of complete resolution are basically unknown. Understanding the causes and mechanisms of calcification can lead to improved therapies aimed at reducing the likelihood of residual calcification or the underlying pathological mechanisms, after the resolution of parasitic lesions in the human CNS.
Author Notes
Financial support: H. H. Garcia and J. A. Bustos are supported by
Current contact information: Christina M. Coyle, Department of Infectious Diseases, Albert Einstein College of Medicine, Bronx, NY, E-mail: christina.coyle@einsteinmed.edu. Javier A. Bustos, Center for Global Health, Universidad Peruana Cayetano Heredia, Lima, Perú, and Center for Global Health, School of Health Sciences, Universidad Peruana de Ciencias Aplicadas (UPC), Lima, Perú, E-mail: javier.bustos.p@upch.pe. Oscar H. Del Brutto, School of Medicine and Research Center, Universidad EspÃritu Santo – Ecuador, Samborondón, Ecuador, E-mail: oscardelbrutto@hotmail.com. Hector H. Garcia, Center for Global Health, Universidad Peruana Cayetano Heredia, Lima, Perú, and Cysticercosis Unit, Instituto Nacional de Ciencias Neurologicas, Lima, Peru, E-mail: hgarcia@jhsph.edu. Theodore E. Nash, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Asheville, NC, E-mail: tnash@niaid.nih.gov. Vedantam Rajshekhar Department of Neurological Sciences, Christian Medical College Ranipet Campus, Vellore, India, E-mail: rajshekhar@cmcvellore.ac.in.
| Past two years | Past Year | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 2458 | 2458 | 506 |
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