Disclosures: Elaine K. Gregory, n/a: No financial relationships or conflicts of interest

Case Description: 71-year-old active male, had an acute onset of paraplegia and paresthesia. On exam, systemic blood pressure (SBP) was 220, lower extremities were pulseless, without reflexes. After Labetalol, SBP decreased to 180 with return of doppler signals, motor, and sensory function. Extensive imaging, Electromyography/Nerve Conduction Studies (EMG/NCS) and laboratory exams on blood and spinal fluid were performed.

Setting: Inpatient rehabilitation.

Patient: 71 y/o male with reversible paraplegia, paresthesia and bladder dysfunction. Assessment/

Results: 71 y/o male with reversible paraplegia, paresthesia and bladder dysfunction without clear etiology . Imaging work-up for: aortic aneurysm ; spinal cord vascular malformation; transverse myelitis or other inflammatory etiologies were negative. Lumbar Spine Magnetic Resonance Imaging (MRI) revealed moderate to severe spinal canal stenosis (L2-4), and moderate to severe bilateral foraminal stenosis (L2-L5), Investigations for inflammatory causes were negative. EMG/NCS revealed chronic right L5 radiculopathy. He received steroids, but had poor response. His neurologic symptoms slowly improved with mild strength and sensory deficits upon discharge.

Discussion: Lumbar spinal stenosis (LSS) causes significant disability in the aging population. LSS includes pathologic anatomic narrowing at; the intraspinal canal, lateral recess or neural foramen. Compression and/or ischemia at the nerve roots can produce neurologic symptoms. MRI can identify sites of compression, but findings often don’t correlate with symptoms. Transient ischemia, due to spinal stroke, severe vasoconstriction or decrease in perfusion with his existing lumbar pathology might explain the rapid onset and reversibility of his symptoms.

Conclusion: The exact pathophysiology of LSS is unknown, but compression and/or ischemia at the nerve roots is proposed. Compression can be direct (osseous) or indirect (increased intrathecal pressure, venous congestion or decreased arterial perfusion). MRI findings don’t necessarily correlate with disease or prognosis. Physiatrists should be aware of the pathophysiology of LSS and the pitfalls in its diagnosis, interpreting all information in the context of their history and physical exam findings.

Level of Evidence: Level V

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PM&R Meeting Abstracts - https://pmrjabstracts.org/abstract/compression-versus-ischemia-an-acute-onset-of-transient-paraplegia-paresthesia-and-urinary-retention-during-hypertensive-urgency/