A 36-year-old male from central region of Kenya presented to our institution with a 3-day history of back pain, followed by itching and numbness of the feet and ankles. On presentation, his symptoms had progressed to weakness of the lower limbs with inability to walk and he had developed urinary incontinence. He denied speech and swallowing difficulties and reported no weakness of the upper limbs. The patient reported no history of fevers, blurred vision, loss of consciousness, or seizure. He also denied a history of trauma, use of blood thinners, use of illicit drugs (including tobacco and alcohol use), a history of exposure to tuberculosis, or ingestion of raw milk. He did report swimming in a nearby pond for many years. His family history was unremarkable, and he was an only child.
On examination, he had normal vital signs and was conscious and alert. A neurological exam revealed normal cranial nerves. Visual field was also preserved. Examination of both his upper limbs was normal. He had tenderness of the lower back, power grade 4/5 on hip flexors and extensors bilaterally, grade 4/5 and 2/5 on the right and left knee extensors, respectively, and power grade 3/5 and 1/5 on the right and left knee flexors, respectively, and dorsiflexion was grade 1/5 bilaterally. A knee jerk reflex was present on his right lower extremity but reduced on the left. Ankle reflexes were absent bilaterally. Sensory level was present at L2.
His complete blood count and a comprehensive metabolic panel were within normal limits. A lumbar puncture revealed a protein count of 0.97 g/l (0.15-0.45 g/l), with a pleocytosis of 35 mm3(normal <5). A differential count showed 30% of segmented neutrophils and 70% of lymphocytes. Monocytes, eosinophils, and basophils were absent. The glucose level was normal. Cultures of the cerebrospinal fluids, including for tuberculosis, were negative. Serological test for HIV, herpes virus, and syphilis was also negative. An autoimmune screen including ANA, anti-ds DNA, and ENA was negative. A vasculitis screen and serum angiotensin-converting enzyme were also reported as normal.
His thyroid stimulating hormone, vitamin B12, and folate level were all within normal limits.
An MRI of the spine showed longitudinally extensive transverse myelitis (T2 hyper intense intramedullary signal spanning T6-L1 with enhancement) (Figures 1-3).
Based on his MRI results and clinical symptoms, neuromyelitis optica (NMO) was high on the differential diagnosis. He was initiated on high-dose steroids, methylprednisone one gram intravenously for 5 days. However, his neurological status continued to decline. Five sessions of therapeutic plasma exchange were also attempted with no improvement in his symptoms. Serum and CSF neuromyelitis antibodies and oligoclonal bands as well as serum MOG antibodies (myelin oligodendrocyte glycoprotein) were later reported as negative.
A few days into his hospitalization, his Schistosoma antibody (IgG) titer was reported at at 1 : 80. A subsequent liver ultrasound was reported as normal. He was immediately started on praziquantel at 60 mg/kg/dose and high-dose steroids with minimal improvement in his overall symptoms. He was discharged home with recommendations for home care and aggressive physical therapy.