A 5-year-old boy from South Sudan presented with complaints of sudden onset, progressive bilateral lower limb weakness for the past month, and inability to walk or stand without assistance. Before the onset of symptoms, he could walk and run without support. He has had urinary incontinence since the onset of weakness. He had experienced a few episodes of fever and cough for the past month. His prior medical history did not reveal any other clinical comorbidity. The family was from a peri-urban area of South Sudan known for its endemic intestinal and urogenital schistosomiasis, particularly with Schistosoma mansoni species.
On examination, he was noted to have grade 2 weakness of the lower limbs, right more than left. He could not stand and sit without support but could roll over in bed and had areflexia, which involved absent knee, ankle and plantar reflexes. He was also observed to have no cremasteric reflex, lax anal tone, and neurogenic bladder.
MRI of the brain with the whole spine showed an intramedullary lesion extending from D11 to L1 with irregular margins in conus medullaris and perilesional edema [Figure 1]. Differential diagnoses of astrocytoma, ependymoma, and granulomatous conditions were suspected, and he was investigated to rule out the differentials.
Urine and stool routine examinations were done to observe viable Schistosoma eggs, which were reported negative. Serum angiotensin converting enzyme (ACE) level was done to rule out Sarcoidosis, which was noted to be within normal limits. Serum neuromyelitis optica (NMO) and myelin oligodendrocyte glycoprotein (MOG) levels were done to rule out immune-mediated disorders, Brucella antibodies IgG/IgM to rule out brucellosis and immunoblot antinuclear antibody (ANA) profile to rule out antinuclear antibody-positive disease were reported negative. Systemic involvement of schistosomiasis was ruled out as well. Since there was no definitive diagnosis, a surgical biopsy was contemplated, and therefore, he underwent a laminoplasty proceed biopsy under intraoperative neuromonitoring, C-arm, and fluorescein guidance. Intraoperatively, the edematous and inflamed nerve roots were noted, along with an intramedullary conus lesion [Figure 2]. The culture of tissues showed no growth of organisms after 48 h of incubation. Gene X-pert and acid-fast bacilli were done to rule out tuberculosis, which was reported to be negative.
Histopathological examination of the spinal cord lesion showed necrotising granulomatous chronic inflammation with Schistosoma eggs and no evidence of malignancy [Figure 3]. As per the clinical, laboratory, and imaging evidence of neuroschistosomiasis, he was treated with steroids and Praziquantel 300 mg. He was initially treated with a high dose of parenteral steroid, tapered down, and converted to the oral route along with the oral anti-parasitic agent Praziquantel as recommended by the World Health Organization protocol.
Postoperatively, he was given regular intensive in-house rehabilitation and physiotherapy. Before his discharge, he became well ambulant and had gross improvement in the power of his lower extremities, the tone of the anal sphincter improved, and he was voiding well by himself. The postoperative MRI scan showed decreased conus swelling and decreased enhancement in the residual conus medullaris lesion with edema cranial to the conus medullaris completely resolved [Figure 4].