Dados do Trabalho

Título

Cerebellar Schistosomiasis: An unusual presentation

Resumo

Case Report

A previously healthy 23 year-old man from a known endemic area for schistosomiasis was admitted at the Neurology Emergency Department. Two months before admission, he developed severe daily headache, which was refractory to common analgesics. Moreover, he complained about weight loss. One month later, he presented with a newly onset cerebellar ataxia, more pronounced on the right side.
Initial Magnetic resonance imaging (MRI) revealed high T2 signal areas with a slight expansive effect in the right aspect of the medulla; right cerebellar hemisphere and pons, and meningeal enhancement.
Cerebrospinal fluid (CSF) analysis showed normal opening pressure, slight pleocytosis (16 cells) 75% lymphocytes, protein 35mg/dL. CSF Serologies for tuberculosis, cryptococcosis, Syphilis, HIV and cultures were negative. Computed tomography of the chest and abdomen showed only nonspecific alterations. MRI Spectroscopy suggested a pattern compatible with inflammatory disease in detriment of a tumor lesion.
An inflammatory disease hypothesis was made and the patient was discharged with oral corticosteroids. However, some weeks later, he developed a right peripheral facial palsy and he was readmitted to the hospital. A new MRI showed progression; Enhancement of right VII and VIII cranial nerves and a recent ischemic event on the left lateral aspect of the pons. Finally, a cerebellar biopsy was performed and revelead a Schistosomal granulomatous cerebellitis.
The patient was treated with Praziquantel and high dose glucocorticoids with partial improvement.

Discussion
Schistosoma mansoni is endemic to many Brazilian states. Its eggs may be found throughout the Central nervous system (CNS). They have been reported into the brain, cerebellum, leptomeninges and choroid plexus. However, the most common presentation is the schistosomal myeloradiculopathy. CNS lesions may cause cerebral small vessels endarteritis with fibrinoid necrosis, or immunological reactions secondary to toxin release from the granuloma, leading to astrocytic proliferation, neuronal necrosis and demyelination.

Conclusion
This case shows the challenge of an atypical presentation of neuroschistosomiasis, which could have been easily misdiagnosed as a noninfectious inflammatory or neoplastic disease. A high index of suspicion is necessary, mainly in those patients coming from endemic areas, and histological diagnosis remains crucial.

Palavras Chave

schistosomiasis; infectious diseases; focal lesions; cerebellar lesions