Seizures are the most common clinical manifestation of cerebral cysticercosis and occur in the presence of viable, dying, and calcified or noncalcified dead cysts. How calcified cysts provoke seizures is not known but recent observations demonstrated edema around some calcified lesions at the time of seizure activity and disappearance during periods when seizures were not occurring. Edema associated with foci in idiopathic epilepsy is highly unusual so that this observation suggests that the mechanism(s) associated with calcified cysts is unique. Documenting and understanding this phenomenon is important for a number of reasons. First, although by definition these lesions are inactive, e.g., not living larvae and do not require anti-parasitic treatment, they are frequently mistaken for active lesions and patients undergo unnecessary treatment. Second, a likely reason for perilesional edema is intermittent antigen release and subsequent host immune response resulting in inflammation and edema. If proven, then the treatment for this would not only involve suppression of seizure activity with anti- seizure medication, but also the use of anti-inflammatory medications such as corticosteroids. The present study will systematically assess the presence of edema associated with calcified lesions at the time of seizure activity and attempt to determine why some calcified lesions in the same patient are foci of seizures while others are clinically silent. There are three related but separate questions. 1) What is the most sensitive MRI technique that can detect edema around calcified or inactive lesions? It is essential to determine the most sensitive methods initially because the use of insensitive techniques will lead to inaccurate assessments of which lesions are prone to lead to seizure activity and how many patients are affected. 2) How common is perilesional edema around calcified or inactive lesions associated with seizure activity? 3) What factors determine which lesions are prone to cause seizure activity? We have reported from long-term longitudinal studies in a handful of patients that only some of many lesions seem to be associated with seizure activity and edema. - Cysticercosis, Taenia solium, seizures - Human Subjects

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Intramural Research (Z01)
Project #
1Z01AI000846-01
Application #
6227847
Study Section
Special Emphasis Panel (LPD)
Project Start
Project End
Budget Start
Budget End
Support Year
1
Fiscal Year
1999
Total Cost
Indirect Cost
City
State
Country
United States
Zip Code
Carabin, H; Krecek, R C; Cowan, L D et al. (2006) Estimation of the cost of Taenia solium cysticercosis in Eastern Cape Province, South Africa. Trop Med Int Health 11:906-16
Nash, T E; Singh, G; White, A C et al. (2006) Treatment of neurocysticercosis: current status and future research needs. Neurology 67:1120-7
Garcia, Hector H; Del Brutto, Oscar H; Nash, Theodore E et al. (2005) New concepts in the diagnosis and management of neurocysticercosis (Taenia solium). Am J Trop Med Hyg 72:3-9
Nash, T E; Del Brutto, O H; Butman, J A et al. (2004) Calcific neurocysticercosis and epileptogenesis. Neurology 62:1934-8
Nash, Theodore E (2003) Human case management and treatment of cysticercosis. Acta Trop 87:61-9
Keiser, Paul B; Nash, Theodore E (2003) Prolonged perilesional edema after treatment of parenchymal neurocysticercosis: methotrexate as a corticosteroid-sparing agent. Clin Infect Dis 36:e122-6
Nash, T E; Pretell, J; Garcia, H H (2001) Calcified cysticerci provoke perilesional edema and seizures. Clin Infect Dis 33:1649-53
Del Brutto, O H; Rajshekhar, V; White Jr, A C et al. (2001) Proposed diagnostic criteria for neurocysticercosis. Neurology 57:177-83