Involvement of the central nervous system in Schistosoma mansoni and S. haematobium infection. A review

• Published in: Brain (London, England : 1878) Vol. 108 ( Pt 4); p. 1023
• Main Authors: Scrimgeour, E M, Gajdusek, D C
• Format: Journal Article
• Language: English
• Published: England 01.12.1985
• Subjects: Adrenal Cortex Hormones - therapeutic use; Brain Diseases - diagnosis; Brain Diseases - drug therapy; Brain Diseases - microbiology; Brain Diseases - pathology; Humans; Schistosomiasis haematobia - diagnosis; Schistosomiasis haematobia - drug therapy; Schistosomiasis haematobia - parasitology; Schistosomiasis haematobia - pathology; Schistosomiasis mansoni - diagnosis; Schistosomiasis mansoni - drug therapy; Schistosomiasis mansoni - parasitology; Schistosomiasis mansoni - pathology; Spinal Cord Diseases - diagnosis; Spinal Cord Diseases - drug therapy; Spinal Cord Diseases - microbiology; Spinal Cord Diseases - pathology
• ISSN: 0006-8950
• DOI: 10.1093/brain/108.4.1023

A review of reports of confirmed cases of involvement of the CNS in Schistosoma mansoni (SM) and S. haematobium (SH) infection was undertaken. Deposition of ova in the brain has been reported in 17 studies of SM infection and 4 studies of SH infection. In uncomplicated schistosomiasis, SH ova are more likely than SM ova to be deposited in the brain and may be carried there by the vertebral venous plexus. The deposition of SM ova in the brain and meninges is more frequent in hepatosplenic schistosomiasis, especially with cor pulmonale, and the route to the brain may be through pulmonary arteriovenous shunts. Asymptomatic deposition of ova is common but epilepsy may occur. The formation of large granulomas and cerebral haemorrhage are rare complications. Adult SM and SH have been observed in cerebral vessels. Fifty-two case reports of SM myelopathy and 12 reports of SH myelopathy were studied. The mean age of SM patients was 27.7 years and 83% were males, whereas the mean age of SH patients was 19.7 years and 92% were males. The time between exposure to SM infection and the onset of spinal cord dysfunction ranged from 38 days to 6 years. Paraplegia developed over 24 hours in 28% and between a few days to one week in 26% of cases. Comparative figures for SH myelopathy were not available. Myelopathy was caused by an intramedullary granuloma of the conus medullaris in 78% of SM subjects and 75% of SH subjects. Areflexic flaccid paraplegia with sphincter dysfunction and disturbance of sensation was the usual presentation. Most patients had no other clinical evidence of schistosomiasis. Asymptomatic ova deposition in the spinal cord may be commoner in advanced SH infection; myelopathy is rare in hepatosplenic schistosomiasis. Adult SM only have been observed in spinal meningeal veins. Since 1965, the mortality rate for patients with confirmed schistosomal myelopathy has fallen from 72% to 11.5%. Recovery was achieved by 54% of cases in one week to four months (mean: 6 weeks). Corticosteroid therapy did not appear to improve the prognosis. There are no clinical features specific for schistosomiasis of the CNS. Laboratory investigations, including serological tests, are of limited diagnostic value. In myelopathy, eosinophilia of the CSF is inconstant but myelography is a valuable diagnostic aid.