The Enigmatic Myelopathy: Unraveling a Diagnostic Conundrum of Cord Infarction vs Transverse Myelitis
Steven Gressett1, Logan Thomas1, Muhammad Bhatti1, Ryan Chapman1, Courtney Huval1
1University of Mississippi Medical Center
Objective:
We present a case of non-traumatic myelopathy with overlapping clinical features of cord infarction versus transverse myelitis.
Background:
Acute non-traumatic myelopathy has multiple autoimmune and vascular causes. Here, we highlight Fibrocartilaginous embolism (FCE) and MOGAD transverse myelitis. FCE is a rare cause of spinal cord infarct, often after exertion or minor trauma. MRI demonstrates diffusion restriction in the affected region, while CSF typically remains benign to mildly inflammatory. In contrast, Transverse myelitis, particularly MOGAD presents subacutely with longitudinally extensive myelitis, CSF pleocytosis, and is most often confirmed with serum MOG-IgG positivity. Management varies drastically with MOGAD associated myelitis requiring acute immunosuppression and spinal cord infarct requiring secondary prevention.
Results:
A 59-year-old African American male developed acute onset of back pain shortly after lifting heavy boxes followed by four days of progressive weakness, sensory loss, saddle anesthesia, and urinary incontinence. Exam showed bilateral lower extremity weakness and numbness (right > left, distal > proximal), hyperreflexia in the upper extremities, absent Achilles and right patellar reflexes, with mute plantars.
MRI revealed a T2 hyperintense lesion extending from T11 to the conus medullaris with central cord predominance, without enhancement. Restricted diffusion was seen at the same level. No other lesions were noted throughout the neuroaxis. CSF demonstrated pleocytosis (>400 cells, neutrophil-predominant), elevated IgG index (0.78), and negative autoimmune, infectious, and MOG/NMO antibody panels. CSF MOG is currently pending. After ruling out infectious causes, intravenous methylprednisolone was administered for seven days with mild improvement, followed by plasma exchange for five days, resulting in a more robust clinical recovery.
Conclusions:
This case illustrates overlapping features of FCE (precipitating exertion, infarction pattern) and idiopathic transverse myelitis with MOGAD features (conus lesion, CSF pleocytosis, immunotherapy responsiveness). The latter is now favored in our case. Therapeutic decisions hinge on accurate etiologic differentiation and necessitate an individualized management approach.
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