Acta neurol. belg., 2005, 105, 89-93 Abstract We describe clinical and magnetic resonance (MR) features in a 69-year-old, Caucasian woman presenting with an unusual meningeal onset of cerebral schisto- somiasis. Magnetic resonance work-up demonstrated supra- and infratentorial lesions with prominent brain- stem involvement contrasting with the paucisymptomatic clinical presentation. Because of a recent stay in Uganda, including swimming in Lake Victoria, a diag- nosis of neuroschistosomiasis was suggested. Serolo- gical tests and rectal biopsy confirmed the putative diagnosis. The patient was successfully treated with praziquantel at a dose of 50 mg/kg/day for 15 days. Brain MRI abnormalities improved dramatically within two months. Key words : Cerebral schistosomiasis ; Schistosomia mansoni ; parasitic cerebral disease. Introduction Schistosomiasis, also called bilharzia, is a chronic parasitic infestation caused by trematode blood flukes of the flatworm species Schistosoma (Liu, 1993). Schistosomiasis is transmitted to humans by skin contact with infested water. It is estimated that around 200 million people harbour this parasitic infestation. The main forms of human schistosomi- asis are caused by four species : i. Schistosoma mansoni, which causes intestinal schistosomiasis and is prevalent in 52 countries and territories of Africa, the Caribbean, the Eastern Mediterranean, and South America ; ii and iii. Schistosoma japon- icum and Schistosoma mekongi, which cause intestinal schistosomiasis and are prevalent in seven African countries and the Pacific region ; iv. Schistosoma haematobium, which causes urinary schistosomiasis and affects 54 countries in Africa and the Eastern Mediterranean. All, uncommonly, can infect the central nervous system. When they do so, S. japonicum usually affects the brain where- as S. haematobium and S. mansoni more often involve the spinal cord. We present a rare case of paucisymptomatic cerebral infestation by S. mansoni, predominantly involving the medulla oblongata. Case report A 69-year-old, right-handed, Caucasian woman with a long medical history of bronchiectasis due to recurrent episodes of pneumoniae between the ages of 13 and 20, was admitted on April 2004 for mild but unusual headaches and dizziness. The symptoms had started one month prior to admission by a “thun- derclap” right-sided headache early in the morning resulting in nausea and vomiting. The patient also complained of chronic bronchorrhoea, and took can- renol 50 mg daily for moderate systemic hyperten- sion. Brain CT scan at this time was unremarkable. The neurological examination on admission was normal, but the patient complained of slight, per- sistent instability and mild left sided headache. History taking revealed a 4-year stay in Uganda (from 1997 to 2001) during which the patient recalled an isolated episode of bare-foot walking along the muddy bank of Lake Victoria and a swim in the lake. Contrast-enhanced brain MR examination was abnormal, showing : i : ill-defined left temporal lesions with focal meningeal thickening and abnor- mal enhancement, together with ‘oedematous’ changes within the adjacent brain parenchyma of the temporal lobe (Fig. 1C), and ii : abnormal T2/FLAIR hypersignal intensity of the medulla oblongata and multiple parenchymal foci of strong contrast-enhancement ; iii : similar changes within the left middle cerebellar peduncle (Fig. 1A, 1B and 1D). Spinal contrast-enhanced MR was normal (not shown). The cerebrospinal fluid (CSF) was clear and contained two mononuclear cells/μL. No eosinophils were detected. The protein (44 mg/dL) and the glucose (63 mg/dL) levels were normal but the lactate concentration was slightly increased at 3.8 mM/L (N < 2.4 mM/L). Oligoclonal IgG bands were present in the CSF, with a mixed pattern (pat- tern III in Andersson et al., 1994) : some bands were also present in the serum but several were CSF specific. The white blood cell count was slightly increas- ed (11210 cells/ μL), with mild hypereosinophilia Paucisymptomatic brainstem lesions revealing CNS schistosomiasis D. ROMMEL 1 , M. RAGÉ 1 , T. DUPREZ 2 , M. P ARENT 3 and C. J. M. SINDIC 1 1 Department of Neurology ; 2 Radiology and Medical Imaging ; 3 Department of Pathology, Cliniques universitaires Saint-Luc, B-1200 Brussels, Belgium ————