Abstract Body: Introduction: Fibrocartilaginous embolism (FCE) is a rare etiology of spinal cord infarction that occurs when nucleus pulposus material from intervertebral discs spontaneously embolizes into a spinal artery. Younger patients are at higher risk because arterial vascularization of the nucleus pulposus is present from early life through adolescence after which it regresses.
Methods: Case report
Results: An 11yo F presented with sudden onset back pain and lower extremity sensory disturbances following an ATV ride that quickly evolved into an ascending paralysis with associated urinary retention. Exam showed 4/5 strength in proximal UEs, 2/5 grip strength on the right, and 0/5 strength in LEs with associated areflexia and decreased sensation to light touch and pinprick but preserved vibratory sense. CSF studies were unremarkable with no albuminocytologic dissociation or lymphocytic pleocytosis. EMG/NCS revealed absent F-waves consistent with possible early demyelinating polyradiculopathy. She was started on IVIG given concern for AIDP. Extensive work-up including TSH, ESR, CRP, B1, B12, heavy metals, C. jejuni Ag, stool cx, blood cx, ANCA vasculitis panel, RMSF and Arbovirus Abs, and AchR and MuSK Abs was unremarkable. MRI revealed diffusion restriction in the cervicothoracic cord without enhancement (Fig 1). She had no improvement of her symptoms after completing 5 days of IVIG. She also developed long-tract signs including +Babinski on the left and LE spasticity. Repeat imaging 4 days from prior revealed adjacent vertebral body with area of T2 hyperintensity concerning for bony infarct (Fig 2). Given her rapid onset of symptoms, lack of improvement after treatment with IVIG, and development of long-tract signs, she was given a diagnosis of spinal cord infarction. FCE was deemed the etiology given the presence of adjacent bony infarct suggesting embolic phenomenon and the lack of evidence of CNS inflammation, infection, or other etiology. Repeat EMG/NCS showed evidence of severe reduction in the amplitudes of the compound motor action potentials which can be seen in compromise of the motor neuron population due to spinal cord infarction (Fig 3). She was discharged to inpatient rehab.
Conclusion: This report alerts clinicians to FCE as a rare etiology of ischemic myelopathy that should be considered in patients who present with sudden, painful onset followed by “stroke-in-evolution” pattern of progression that may resemble the ascending paralysis seen in AIDP.