Case of the Week
Section Editors: Matylda Machnowska1 and Anvita Pauranik2
1University of Toronto, Toronto, Ontario, Canada
2BC Children's Hospital, University of British Columbia, Vancouver, British Columbia, Canada
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August 22, 2024
Spinal Cord Infarct with Vertebral Body Infarct
- Background:
- Spinal cord ischemia occurs much less frequently compared with brain ischemia and only accounts for 6% of acute myelopathies. The most common proposed mechanism for cord ischemia is embolism or plaque rupture, which may be spontaneous or iatrogenic (eg, aortic surgery). A rare cause of ischemia is fibrocartilaginous embolism that involves embolization of material from the nucleus pulposus into a spinal artery or vein in a retrograde direction.
- Clinical Presentation:
- This is variable and depends on the vascular territory involved.
- Onset of symptoms is typically abrupt with peak symptomatology at 12 to 72 hours.
- Anterior spinal territory infarcts are typically associated with loss of motor function and pain/temperature sensation below the level of the lesion with initial flaccidity and later spasticity on physical exam.
- The typical presentation for posterior spinal artery territory ischemia includes loss of proprioception and vibratory sensation below the affected level.
- Key Diagnostic Features:
- Abnormal T2/STIR signal and restricted diffusion involving the cord may be present with possible mild expansion in subacute phase.
- Infarction of the adjacent vertebral body presenting as T2/STIR hyperintensity or loss of enhancement has been suggested as a confirmatory sign of cord ischemia, because the segmental branches of the aorta supply both the vertebral bodies as well as the spinal cord through the anterior and posterior spinal arteries.
- Pathologic processes other than a vascular event are unlikely to acutely affect the vertebral bone marrow and cord at the same level while sparing the intervening meningeal spaces.
- Differential Diagnosis:
- Inflammatory myelopathy, infectious myelopathy, or spinal tumor would not be expected to alter the adjacent vertebral body signal without an obvious extramedullary component.
- Compressive myelopathy is another consideration, but is improbable given the lack of significant degenerative changes at the same level.
- Cord contusion may have a similar appearance but is unlikely without a history of trauma.
- Treatment:
- On the 3-month follow-up, our patient continued to experience right gluteal and lower leg numbness. Motor function remained unaffected. The mainstay of treatment is occupational therapy and rehabilitation. There is potential benefit of anticoagulation or antiplatelets to address underlying suspected etiology of infarct.
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