NEUROCYSTICERCOSIS

Cysticercosis is an infection caused by Taenia solium larvae (cysticer ci). When the cysticercus is lodged in the central nervous system (CNS ), the disease is known as neurocysticercosis (NCC). NCC is the most f requent and most widely disseminated human neuroparasitosis. It is end emic in many parts of the world, particularly Latin America, Africa, a nd Asia, and still relatively frequent in Portugal, Spain and Eastern European countries. It is also endemic in developed countries with hig h rates of immigration from endemic areas. Man may act as an intermedi ate host after ingestion of mature, viable T. solium eggs via the feca l-oral route. The development of lesions in the brain and leptomeninge s, and the consequent onset of symptoms associated with NCC are mainly due to the host immune-inflammatory response. As long as the cysticer cus remains viable, there is relative host immune tolerance. It is onl y when the parasite dies that massive antigen exposure occurs, with in tensification of the immune response/inflammatory reaction and the app earance or worsening of symptoms. NCC can be asymptomatic or cause wid ely varied clinical manifestations, such as seizures, increased intrac ranial pressure, ischemic cerebrovascular disease, dementia, and signs of compression of the spinal roots/cord. The combination of two or mo re symptoms is common. Such clinical polymorphism is determined by 1) the number of lesions (single or multiple cysticerci); 2) the location of CNS lesions (subarachnoid, intracerebral, intraventricular, intram edullary); 3) the type of cysticercus (Cysticercus cellulosae, Cystice rcus racemosus); 4) the stage of development and involution of the par asite (vesicular or viable, necrotic, fibrocalcified nodule); and 5) t he intensity of the host immune-inflammatory response (no inflammatory reaction, leptomeningitis, encephalitis, granular ependymitis, arteri tis).