Abstract Number ‐ 219: Spinal cord infarct in young: Fibrocartilaginous Embolism with Occlusion of Anterior Spinal Artery

Abstract

Introduction Spinal cord infarctions are rare and account for fewer than 1% of all strokes. Diagnosis is usually established by clinical symptoms of sudden onset paraplegia and sensory dysfunction along with radiographic evidence of a non‐enhancing, diffusion‐restricted T2 hyperintense lesion on spinal cord MRI. We describe an interesting case of anterior spinal artery infarct from suspected fibrocartilaginous embolus from intervertebral disc. Methods Case report. Demographics and clinical history were obtained by chart review. MRI and cerebral angiogram images were reviewed and compared to radiology reports. Results 21‐year‐old female with no prior medical history presented with sudden onset headache, bilateral arm tingling, and neck stiffness that rapidly progressed within the hour to quadriplegia with numbness below the T2 sensory level. She continued to worsen, developed respiratory failure and required intubation. MRI of the cervical cord revealed a longitudinally extensive, non‐enhancing, diffusion‐restricted lesion extending from the bilateral medial medulla to the ventral spinal cord at C5/6 vertebral level. Cerebral and spinal digital subtraction angiography was notable for non‐opacification of the cervical anterior spinal artery. She had extensive work up for dissection, vasculitis, hypercoagulable state, autoimmune conditions that were all negative. However, there was a diminished T2 signal in her C5‐6 intervertebral disc with subtle loss of intervertebral disc space concerning for disc compression, likely related to her job requiring intensive heavy lifting. It was surmised that she developed a ventral cervical cord infarct secondary to fibrocartilaginous embolization and occlusion of anterior spinal artery, from recent mechanical compression of her C5‐6 disc. Cases of spinal cord infarcts following mechanical trigger, such as heavy lifting or falls, with histopathological confirmation of fibrocartilaginous material in the vasculature postmortem are well reported. It is postulated as a mechanism of spinal cord infarct in young patients that compressive forces on the intra‐vertebral body trigger embolization of nucleus pulposus material through persistent nuclear anastomoses to the spinal circulation. Conclusions Ischemic infarct should be considered in the differential diagnosis for sudden onset of symptoms localizable to spinal cord, especially when spinal MRI shows restricted diffusion in a vascular distribution. Demonstrating non‐opacification of the anterior spinal artery on digital subtraction angiography confirms the diagnosis. In case of negative work up for spinal cord infarct, the presence of an abnormal signal in the intervertebral disc on MRI may suggest fibrocartilaginous embolism as a mechanism of infarction in young patients.