The patient was a 24-year-old male from the southern part of Saudi Arabia. He presented with a 3-month history of acute-onset, progressive-course severe lower back pain. Prior to this, he was healthy. The lower back pain was followed by progressive lower limb weakness, urinary incontinence, and a loss of sensation below the umbilicus. The weakness was severe enough to make him wheelchair bound. The patient gave a remote history of swimming in contaminated wells (around 8 months before the onset of his symptoms). He had initially gone to another hospital where he was diagnosed with transverse myelitis and was given pulse steroid therapy. He improved initially for 2 weeks but then worsened.
The patient had no history of fever, blurred vision, loss of consciousness, or seizure; no associated history of trauma, use of blood thinners, or illicit drugs; no history of exposure to a tuberculosis (TB) patient or ingestion of raw milk; no history of traveling or sexual abuse, and no history suggestive of an autoimmune disease or malignancy.
Upon examination, the patient presented as vitally stable, conscious, and alert. He had normal higher mental function and cranial nerves, and a visual field examination showed no meningeal signs. Examination of both upper limbs was normal. On examination of his lower limbs, the legs showed normal bulk and were not atrophied; there was increased tone, power was 0/5 bilaterally, he was hyperreflexic, had clonus, and exhibited an increasing plantar response.
The initial MRI (fig. 1) showed an extensive lesion extending from T6 through T9 with edema. The workup of his acute myelopathy was completed. Cerebrospinal fluid (CSF) analysis showed high protein of 1.08 g/dl. His cell count and glucose were normal, and he was negative for infection and cytology. Autoimmune, paraneoplastic, and serological testing of HIV, cytomegalovirus, and Epstein-Barr virus were negative. His Schistosoma titer was high at a ratio of 1:64. A spinal cord biopsy was completed and confirmed the diagnosis of spinal cord schistosomiasis.
The patient had been treated earlier (before the biopsy) with a plasma exchange, an extended course of intravenous dexamethasone, and had been enrolled in an extensive rehabilitation program. The patient had received praziquantel and continued on steroids. His rehabilitation was without significant improvement. He was assessed 11 months later and was found to have improved sensory symptoms, but he remained wheelchair bound. He was able to make minimal movements with both lower limbs but not against gravity. The patient exhibited urinary incontinence, yet he had no erectile dysfunction.