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About the Authors:
Masahiro Fujita
* E-mail: [email protected]
Affiliation: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health. Bethesda, Maryland, United States of America
Siddhartha Mahanty
Affiliation: Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America
Sami S. Zoghbi
Affiliation: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health. Bethesda, Maryland, United States of America
Maria Desiree Ferraris Araneta
Affiliation: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health. Bethesda, Maryland, United States of America
Jinsoo Hong
Affiliation: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health. Bethesda, Maryland, United States of America
Victor W. Pike
Affiliation: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health. Bethesda, Maryland, United States of America
Robert B. Innis
Affiliation: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health. Bethesda, Maryland, United States of America
Theodore E. Nash
Affiliation: Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America
Introduction
Neurocysticercosis, due to infection with the cystic larval form of the tapeworm, Taenia solium, is the cause of about 29% of epilepsy in endemic regions [1]. Degenerating viable cysts commonly resolve into calcified cysticerci, which are found in 10-20% of individuals in randomly studied endemic populations and are commonly the foci of seizures and epilepsy [2]. Perilesional edema around calcifications is a recently described manifestation of neurocysticercosis. In a prospective series of 110 persons in Lima, Peru, with only calcifications due to neurocysticercosis and a recent history of seizures and a positive serology, 50% of those with recurrent seizures demonstrated perilesional edema [3]. The pathophysiology of perilesional edema is unclear but edema secondary to the seizure itself, release of ionized calcium, intermittent release of antigen from a calcified lesion and subsequent host inflammatory response or unknown causes are commonly suggested mechanisms [2,4].
Expression of translocator protein, (TSPO), located in the mitochondrial membrane is increased in inflammatory conditions of the brain [5]. TSPO is mostly up regulated in microglia, migrating macrophages as well as astrocytes [6,7]. Positron emission tomography (PET) scanning with a number of ligands has been used...