A previously healthy, 29-year-old Saudi male presented with a 2-month history of bilateral lower limb weakness and urinary incontinence. The weakness gradually progressed with time. He also had pain in his right thigh accompanying the weakness. He had no history of other sensory symptoms, nor of a trauma or a fall. There was no history of fever or similar illness in the past and no weakness in the upper limbs accompanied his symptoms, and there was no history of headache or loss of consciousness. Though he did travel to Egypt, he had no history of contact with TB in the past, nor did he have a history of cough, loss of weight, or night sweating. Upon examination, he was vitally stable and afebrile. The patient's higher mental function and cranial examination were completely normal, upper limb motor and sensory examination was also normal, and lower limb examination showed no atrophy and normal tone. The power was 4/5 with bilateral hyperreflexia and plantar response was equivocal. He could walk independently, but with difficulty due to the pain.
The patient's erythrocyte sedimentation rate was normal. His white blood cell count was 4.9 with no eosinophilia. His hemoglobin was measured at 14.6 g/dl, the liver function test was normal as were the CT results of his abdomen and pelvis. The CSF analysis showed a white blood cell count of 157 (mainly mononuclear cells at 98% and polymorphonuclear leukocytes at 2%) and a red blood cell count of 3. His protein and glucose levels were at 0.79 (normal: 0.15-0.45) and 3.7 (normal: 2.2-3.9), respectively. The oligoclonal band in the CSF was positive in this patient, and his Schistosoma antibody titer was very high on 2 occasions: 512 and 4,096 (normal <16 titers). His results for brucellosis, HIV, leishmaniasis, amebiasis, echinococcosis, and cytomegalovirus serology were all negative; furthermore, a rectal snip biopsy was negative for ova, and no schistosomal ova were detected in the patient's urine or stool. An MRI of the patient's brain showed normal results and an MRI of the whole spine presented high signals in the conus medullaris (fig. 2).