Case Reports

Sharp lower back pain • left-side paraspinal tenderness • anterior thigh sensory loss • Dx?

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References

DISCUSSION

Possible etiologies for acute spinal cord infarction include spinal cord ischemia from compression of the vessels, fibrocartilaginous embolism, and arterial thrombosis or atherosclerosis, especially in patients with diabetes.5

The majority (86%) of spinal strokes are due to spontaneous occlusion of the vessels with no identifiable cause; much less frequently (9% of cases), hemorrhage is the causative factor.1 A retrospective study demonstrated that 10 of 27 patients with spinal stroke had an anterior spinal infarct. Of those 10 patients, 6 reported a mechanical triggering movement (similar to this case), indicating potential compression of the radicular arteries due to said movement.4

Fibrocartilaginous embolism (FCE) is worth considering as a possible cause, because it accounts for 5.5% of all cases of acute spinal cord infarction.3 FCE is thought to arise after a precipitating event such as minor trauma, heavy lifting, physical exertion, or Valsalva maneuver causing embolization of the fragments of nucleus pulposus to the arterial system. In a case series of 8 patients, 2 had possible FCE with precipitating events occurring within the prior 24 hours. This was also demonstrated in another case series6 in which 7 of 9 patients had precipitating events.

Although FCE can only definitively be diagnosed postmortem, the researchers6 proposed clinical criteria for its diagnosis in living patients, based on 40 postmortem and 11 suspected antemortem cases of FCE. These criteria include a rapid evolution of symptoms consistent with vascular etiology, with or without preceding minor trauma or Valsalva maneuver; MRI changes consistent with ischemic myelopathy, with or without evidence of disc herniation; and no more than 2 vascular risk factors.

Our patient had no trauma (although there was a triggering movement), no signs of disc herniation, and 2 risk factors (> 60 years and diabetes mellitus). Also, a neurologically symptom-free interval between the painful movement and the onset of neurologic manifestations in our case parallels the clinical picture of FCE.

Continue to: The role of factor V Leiden (FVL) mutation

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