The relation between involvement of the central nervous system in schistosomiasis mansoni and the clinical forms of the parasitosis. A review

Abstract

A review of the available literature on the involvement of the central nervous system (CNS) in schistosomiasis mansoni was undertaken to assess the schistosomal lesions in the spinal cord and brain and the clinical forms of the disease that are associated with these lesions. In almost all clinically symptomatic cases of neuroschistosomiasis mansoni (NSM), involvement of the CNS starts in the early stages of infection (non-toxaemic form), during evolution of the disease to its chronic forms, or concomitantly with the (oligo or asymptomatic) chronic intestinal and hepatointestinal forms. In-situ ova deposition following the anomalous migration of adult worms appears to be the main, if not the only, mechanism by which Schistosoma mansoni may reach the CNS in patients with the intestinal and hepatointestinal forms of the parasitosis. The mass effect produced by the heavy concentration of ova and granulomas in circumscribed areas of the spinal cord and brain explains the severe neurological symptoms observed in most of these patients. Though more frequent, CNS involvement associated with the hepatosplenic and cardiopulmonary forms is almost always asymptomatic. The random distribution of ova in the CNS of patients with these forms suggests that ova are carried there mainly as emboli via the arterial system or through retrograde venous flow. Because of the discrete inflammatory reaction elicited by the sparsely distributed ova, neurological symptoms attributable to ova deposition are not present in most NSM patients with the hepatosplenic and cardiopulmonary forms.