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J Neurol Neurosurg Psychiatry. Apr 2006; 77(4): 512.
PMCID: PMC2077500

Brain involvement in a Schistosoma mansoni myelopathy patient

A 65 year old Brazilian man developed a progressive paresis in lower limbs. Urinary and fecal dysfunction, pain, and tingling in lumbosacral dermatomes appeared in the following weeks. A diagnosis of inflammatory myeloradiculopathy was done at that point. The patient received pulse with methyl‐prednisolone, having improved from paraparesis. Six months later, he suffered several tonic‐clonic partial seizures. He was admitted to our hospital with symptoms of headache, nausea and vomiting, right arm and leg hemi paresis, and dysphasia. Neurological examination at admission disclosed T6 hyperesthesia level, lower limb paraparesis (Medical Research Council (MRC) grade 2/5), absent ankle tendon reflex, lower limb hypo‐palestesia, urinary and rectal sphincter dysfunction, and bilateral Babinski sign. A right faciobraquiocrural hemiparesis (MRC grade 0/5) was also observed.

S mansoni antibodies (indirect immunofluorescence assay) in serum were positive. Analysis of CSF disclosed absence of pleiocytosis (5 white cells; 85% lymphocytes); IgG index, CSF protein (0.39 g/l) and glucose (2.66 mmol/litre) levels were normal Microscopical examination of urine and stool specimens disclosed no ova or parasites. A rectal biopsy was negative. Magnetic resonance imaging of the brain showed hyper intensity areas in the left frontal‐parietal white matter; these lesions heterogeneously enhanced after the administration of gadolinium (figure 1A, BB).). Spinal cord MRI showed swelling of lower thoracic spinal cord and conus medullaris.

figure jn78014.f1
Figure 1 (A) Axial T2‐weighted MRI of the brain demonstrating hyperintense signal in the left frontal parietal white matter. (B) Contrast‐enhanced coronal T1‐weighted brain MRI revealing enhancement throughout the left ...

A stereotactic needle biopsy of the brain lesion was performed. Pathological examination of the biopsy specimen revealed multiple sclerosing granulomas scattered within the parenchyma of the brain, with deposits of helminth ova in the centre of these granulomas. Granulomas had giant cells and linfomononuclear infiltrates around S mansoni eggs (fig 1C1C).). The patient was treated with praziquantel and dexamethasone; nevertheless, no improvement of haemiparesis was observed during follow up.

Schistosomiasis (bilharziasis) is a parasitic disease caused by blood flukes of the genus Schistosoma.1 Neuroschistosomiasis, the infection of the central nervous system by S mansoni, S japonicum or S haematobium, constitutes a severe presentation of the disease.2S mansoni related neuroschistosomiasis involves the spinal cord far more frequently than the brain.3 The extraordinary collection of ova in the frontal‐parietal cortex in our patient suggests the ectopic location of a worm pair in the intracranial venous circulation, with local deposition of ova in brain parenchyma.

Our case illustrates that: (1) S mansoni encephalitis should be considered in the differential diagnosis in patients presenting with seizures and focal motor deficits from areas where schistosomiasis is endemic; and (2) brain involvement in schistosomal myeloradiculopathy can occur simultaneously.


Competing interests: none declared


1. Del Brutto O H, Carod‐Artal F J, Román G C. et alTropical Neurology. In: American Academy of Neurology, ed. Continuum. Philadelphia: Lippincot, Williams & Wilkins, 2002
2. Ross A G, Bartley P B, Sleigh A C. et al Schistosomiasis. N Engl J Med 2002. 3461212–1220.1220 [PubMed]
3. Carod Artal F J, Vargas A P, Horan T A. et al Schistosoma mansoni myelopathy: clinical and pathologic findings. Neurology 2004. 63388–391.391 [PubMed]

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