[Clinical and diagnostic approaches to neurocysticercosis].

ETIOLOGY: Cysticercosis is a tissue infection caused by larvae of the cestode Taenia solium. Neurocysticercosis is a central nervous system form of this infection. Taenia solium invades tissues in a form of a cyst with a thin, semitransparent wall. It can reach 1-2 cm in diameter in muscles and brain tissue and up to 3-6 cm in brain chambers. EPIDEMIOLOGY: Pigs are the most common intermediate hosts. The infection occurs when the parasite eggs or proglottids are ingested. It is most common in regions where human feces is used as a fertilizer, or regions with poor sanitary conditions. The man is infected with contaminated food or water, or by autoinoculation. PATHOGENESIS: The Taenia solium eggs are hatched in the duodenum. Embryos invade the intestinal mucosa, and reach various parts of the body, disseminated by the blood circulatory system. The most common localizations of cysticerci are skeleton, muscles and brain. While alive, these cysts produce a minimal reaction in hosts. Inflammation occurs when they die, often a few years after infection. CLINICAL FEATURES: While presence of adult worms of Taenia solium in the gastrointestinal tract causes unspecific symptoms, clinical features of neurocysticercosis depend on the number, size and localization of cysts, as well as on the degree of granulomatous response. The most common manifestations of this infection are epileptic seizures, whereas intracranial pressure increase can be the earliest sign of the disease. Hydrocephalus, meningitis and spinal cord compression syndrome are the most usual complications. PROGNOSIS: The death rate is low in neurocysticercosis with parenchymal cysts and calcification without hydrocephalus. However, fatal outcome occurs in hydrocephalic patients, cases with huge supratentorial cysts, multiple granuloma, brain edema or cerebral infarctions. DIAGNOSIS: Informations about travels to endemic regions are valuable in diagnosing neurocysticercosis. Cytobiochemical finding of the cerebrospinal fluid is often normal. However, in 50% of patients, lymphocytic or eosinophilic pleocytosis is found, low glucose (in 25%) and elevated protein (in 40% of cases). Further testing includes serologic examination of blood and cerebrospinal fluid. Finding of specific antibodies in the sera or cerebrospinal fluid confirms the diagnosis, although false positive reaction may occur in patients with other helminths, especially other cestode. The enzyme-linked immunotransfer blot assay is proven to be sensitive and specific in patients with multiple cysticerci. Computerized tomography and magnetic resonance imagining are techniques mostly used in establishing neurocysticercosis. They reveal the localization of cysticerci, identify the atrophic or edematous fields and assess the degree of ventricular dilatation.