To describe a case of spinal cord infarction mimicking transverse myelitis.
Spinal cord infarctions remain an underrecognized cause of stroke, accounting for approximately 1% of all strokes in the United States. Spontaneous spinal cord infarctions in healthy, young adults represent a minority of these cases and result in significant long-term morbidity. Transverse myelitis can present similarly; etiologies include central nervous system demyelinating disorders, systemic autoimmune conditions, infections, and paraneoplastic syndromes.
Case report.
A 32-year-old male with no prior medical history presented to the emergency department with thoracic back pain followed by bilateral upper and lower extremity weakness and paresthesias. Exam revealed a T4 sensory level, distal right upper extremity weakness, and paraparesis. Initial MRI of the cervical and thoracic spine demonstrated hyperintensities of the bilateral ventral horns from C7-T1. Transverse myelitis was suspected and 1g of intravenous methylprednisolone was given daily for 5 days with clinical improvement. Cerebrospinal fluid (CSF) analysis showed no pleocytosis and normal protein, atypical for transverse myelitis. Repeat MRI 3 days later showed a non-enhancing hyperintensity involving the anterior bilateral spinal cord from C6-T1/2, without cord edema. An ischemic etiology was considered. MRI of the cervical spine with DWI demonstrated restricted diffusion within the aforementioned lesion. Spinal angiography on day 8 was non-diagnostic, yet an anterior spinal artery infarction was concluded to be probable given DWI findings. Echocardiogram was negative for a patent foramen ovale or cardiac thrombi. Hypercoagulability panel was negative. The patient made daily, incremental improvements in motor function; he was able to stand independently and walk with support upon discharge to physical rehabilitation 11 days after admission.
Spontaneous spinal cord infarction can manifest similarly to transverse myelitis. In this case, the lack of associated enhancement and cord edema, non-inflammatory CSF, and DWI findings led to the diagnosis of an anterior spinal artery infarction.