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Neurocysticercosis, caused by infestation of the nervous system by the larval form of Taenia solium,continues to baffle the neurologist, because of varied clinical manifestations. A large body of the literature related to this disease is clinically oriented, enough attention has not been given to parasite related factors modulating the host response. Using immunohistochemical techniques, three features related to the biology of the Cysticercus cellulosa ewere studied. Firstly, to the question as to which part of the worm is recognised by the host immune system, the surface glycoprotein is found to be immunolabelled by the CSF from patients of neurocysticercosis. This surface protein is depleted following specific antihelmenthic therapy, thus accounting for a fall in anticysticercal antibosy level in the CSF. Secondly, the cysticercal cyst, by immunochemical and histochemical methods, is found to have “ACTH like” molecule in the body wall and has neurotransmitter and mitochondrial metabolic pathways similar to the host, facilitating the immune evasion and successful parasitisation. Finally, Cysticercus cellulosaeis found to contain a “peptide” opening the blood brain barrier at the arteriolar level when injected into mice intravenously. Similar phenomenon may be functional in the patients as well, resulting in cerebral oedema, especially following praziquintel therapy.

Neurocysticercosis is the most common parasitic disease affecting the human central nervous system, with protean clinical manifestations. During the last 17 years, 153 cases of neurocysticercosis were histopathologically diagnosed on surgically resected and autopsied material. Variable number of cysts, from a solitary one to multiple were found invading different parts of the neuraxis (118 cases). These cestode larval forms had a prediliction for locating in the cerebral grey matter (98 cases), followed by subcortical nuclear area (12), cerebral ventricles and subarachnoid cisterns (26 cases). Patients harbouring parenchymal cysts manifested predominantly with seizures and encephalitis (113 cases) whereas those with ventricular and/or cisternal cysts presented with features of chronic meningitis and hydrocephalus. The unusual clinical presentations were psychiatric symptoms with behavioural abnormalities and stroke in the young as a result of cysticercal meningitis with associated arteritis. Primary cysticercal abscess in the brain parenchyma was an interesting pathological feature noted in 3 cases. In the endemic areas, the co-existence of neurocysticercosis appears to enhance the morbidity and mortality due to Japanese encephalitis (31 cases). The surface glycoprotein of the cysticercal cyst has been identified to be the antigenic component to which the host immune system responds by forming antibody in the CSF.