NCC is the most common parasitic infection of the CNS. Cysticercosis is caused by infestation of the larva from Taenia solium, which, in humans, has a special affinity for the CNS. In some underdeveloped regions, NCC accounts for 33% of all intracranial mass lesions. There are several pathological forms of NCC, including racemose meningobasal disease, parenchy-mal lesions, intraventricular disease and mixed forms. Pathologically, NCC may result in meningoencephalitis, granulomatous meningitis, focal granulomas, space-occupying cysts, hydrocephalus and ependymitis [26,27].

The clinical presentation of NCC depends on multiple factors, including the size, number and location of cysts, as well as the toxicity of the parasite. Meningobasal disease occurs in 25% of patients with NCC and produces a syndrome typical of chronic granulomatous meningitis. Active growth of multiple small vesicles representing encysted larvae, which have a particular affinity for the basal cisterns, produces adherent or free-floating grape-like clusters that cause an intense basal arachnoiditis. This often results in secondary hydrocephalus and various cranial nerve palsies.

Parenchymal NCC occurs in 30-60% of patients. Viable parenchymal cysts produce little tissue reaction and are often asymptomatic. However, death of the parasite contained within the cyst produces an intense inflammatory response in adjacent brain and it is during this stage that patients frequently become symptomatic, with seizures and/or focal neurological findings. Large cysts may occasionally produce focal neurological findings, although the mass effect from even very large cysts is rarely life-threatening.

Intraventricular NCC affects 15-20% of patients. Larvae are believed to gain access to the ventricular system though the choroid plexus. Intraventricular cysts may be free-floating or pedunculated and, if sufficiently large or strategically positioned, can obstruct CSF flow, leading to obstructive hydrocephalus.

Diagnosis of NCC is based on serological testing and imaging. Peripheral eosinophilia may be seen, but is often inconsistent and unreliable. CSF may demonstrate findings of chronic meningitis, but can be entirely normal. However, the finding of more than 20% eosinophils is highly suggestive of parasitic infection. Antibody titers of greater than 1:64 in the serum or 1:8 in the CSF are significant. Serum titers of more than 1:64 are more sensitive for NCC, while elevated CSF titers have greater specificity. A new enzyme-linked immu-

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