A previously healthy 10-year-old Indian boy developed acute onset of weakness and numbness of both lower limbs 7 days before admission. The weakness reached nadir over a period of approximately two days. On the fourth day of the illness, he developed a difficulty in micturition leading to urinary retention while bowel passage was normal. There was a history of fever, vomiting, and headache 2 weeks before admission.
General physical examination was unremarkable. On neurological examination, the child was fully alert, there were no cranial nerve palsies or meningeal signs. Biceps, triceps, and brachioradialis reflexes were normal while knee and ankle reflexes were brisk. Muscle tone was normal, muscle power (MRC scale) for both lower limbs was 1/5. Upper limbs were unaffected. Touch, position, temperature sensations were decreased more in the left lower limb compared to the right, but a clearly defined sensory level could not be identified.
An outside cerebrospinal fluid (CSF) report showed white blood cells (WBC) 258/microL, with lymphocyte 93.4%. A repeat CSF on the following day showed a WBC of 268/microL. CSF PCR for Mycobacterium tuberculosis, Escherichia coli, Haemophilus influenzae, Listeria monocytogenes, Neisseria meningitidis, Streptococcus agalactiae, Streptococcus pneumonia, cytomegalovirus, enterovirus, HSV 1 and 2, human herpesvirus 6, human parechovirus, varicella zoster virus, and Cryptococcus neoformans/gatti were negative. Cerebrospinal fluid PCR for EBV was positive, serum IgG for EBV capsid antigen was positive while IgM was negative. Cerebrospinal fungal stain and culture, oligoclonal bands, anti-aquaporin-4, and anti-MOG tests were negative. Whole spine contrast MRI showed a mild diffuse increase in cord bulk with an intramedullary hyperintense signal on T2 weight images involving the entire length of the spinal cord and conus medullaris, indicating a longitudinally extensive transverse myelitis (Figure 1). Contrast MRI of the brain revealed leptomeningeal enhancement involving the brain and pial surface of the spinal cord (Figure 2).
The patient was treated with a high dose (1 g/day) of intravenous methylprednisolone for 5 days, after which he began to show clinical improvement. It was then continued with oral prednisone (60 mg/day) for 4 weeks and then was tapered off. Ceftriaxone, clindamycin, and azithromycin were also given. He underwent physiotherapy that was continued after discharge. A follow-up CSF examination performed on the seventh day of admission showed a reduction of WBC count to 59/microL and negative EBV PCR.
At the time of discharge, muscle power improved to grade 4/5 on both lower limbs. He started walking a few steps without support. There was no numbness in the lower limbs, bowel passage and micturition were normal. Sensations of touch, position, temperature were normal. He was discharged on oral prednisolone and physiotherapy after nine days of hospitalization (16 days after initial onset). Two weeks after discharge patient regained almost complete mobility. Three months after discharge the child was completely normal and his spine and brain MRIs showed complete resolution of lesions and disappearance of contrast enhancement.