Title : A rare presentation of transeverse myelitis – transeverse myelitis plus syndrome
Abstract:
Introduction- Transverse Myelitis is characterized by abrupt onset progressive weakness with sensory disturbances. Pathogenesis is usually implicated with direct viral invasion or vasculitis or an autoimmune response. TM Plus syndrome is association with another neuroinflammatory condition, like Multiple Sclerosis (MS), Neuromyelitis Optica Spectrum Disorder (NMOSD), or Acute Disseminated Encephalomyelitis (ADEM), presenting more severe symptoms affecting brain areas or widespread areas. We present a case report with an unusual paradigm of clinical signs and symptoms confirmed subsequently on radiological imaging and treated as Transverse myelitis Plus syndrome.
Methods- Case Report: A 7 Years old child presented with complaints of Fever for 5 Days, Weakness of lower limbs X 2 days R>L in the form of high stepping gait s/o of an asymmetrical ascending motor weakness. On examination had GCS 15/15, with Single Breath Count 18. Power affected in Right Hip flexors 1/5 and left hip flexors 3/5, with power at knee Joint > 2/5 in both sides and Ankle Joint >2/5 with absent Knee Joint Reflexes, other deep tendon reflexes were preserved. No sensory loss or bladder bowel involvement
Investigations- CSF analysis showed no albumin- cytological dissociation, with a negative Autoimmune panel. Nerve Conduction study showed F wave latency Bilaterally with absent H reflex, suggestive of Demyelinating motor polyneuropathy.
MRI BRAIN and WHOLE SPINE- Long segment Intramedullary T2 Hyperintensity in entire dorsal cord – Holocord myelitis – central cord likely Acute Transverse Myelitis with nerve root enhancement cauda equina
Result- In View of Asymmetrical nature of the disease MRI Whole Spine was done s/o Transverse Myelitis given pulse dose of Methyl prednisolone for 5 days at 30mg/kg/day then shifted to oral prednisolone at 2 mg /kg for two weeks followed by tapering.
Conclusion- Hence, Transverse Myelitis Plus Syndrome is a rare presentation which in our case had asymmetrical ascending motor weakness with no significant sensory involvement although NCS s/o demyelinating polyneuropathy.
