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lüll Calcific neurocysticercosis and epileptogenesis Nash TE; Del Brutto OH; Butman JA; Corona T; Delgado-Escueta A; Duron RM; Evans CA; Gilman RH; Gonzalez AE; Loeb JA; Medina MT; Pietsch-Escueta S; Pretell EJ; Takayanagui OM; Theodore W; Tsang VC; Garcia HHNeurology 2004[Jun]; 62 (11): 1934-8Neurocysticercosis 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.|Animals[MESH]|Brain Edema/etiology/parasitology[MESH]|Calcinosis/complications/parasitology[MESH]|Cysticercus/isolation & purification/physiology[MESH]|Epilepsies, Partial/*etiology/parasitology/physiopathology[MESH]|Food Parasitology[MESH]|Humans[MESH]|Latin America/epidemiology[MESH]|Neurocysticercosis/*complications/epidemiology/parasitology/prevention & control/transmission[MESH]|Taenia solium/physiology[MESH] |