Abstract
Subacute progressive ascending myelopathy is a rare, poorly understood neurological complication of spinal cord injury, unrelated to mechanical compression, instability, or syrinx formation at the level of injury or above. To date, there is no known treatment for this dramatic spinal cord injury complication. We present a case of subacute progressive myelopathy after lumbar spine trauma. The therapy consisted of plasmapheresis, hyperbaric oxygen, high-dose cortisol, antibiotic, and antiviral drugs. At 1 year post injury, the patient had recovered most of his lost upper-extremity function and MRI demonstrated only discrete signal intensity alterations extending to T3/4.
Highlights
Subacute progressive ascending myelopathy (SPAM) is a rare, poorly understood neurological complication of spinal cord injury (SCI) [1,2,3,4,5,6], unrelated to mechanical compression, instability, or syrinx formation at the level of injury or above
In addition to 5 cycles of plasmapheresis, Hyperbaric oxygen (HBO) therapy, and high-dose cortisol, antiviral and antibiotic drugs were administered. 4 weeks post trauma, the extension of the characteristic signal alterations persisted at level C4 on magnetic resonance imaging (MRI) and the patient showed only minimal improvement of neurological symptoms
At 1 year post injury, he had recovered most of his lost upper-extremity function and MRI demonstrated only discrete signal intensity alterations extending to T3/4
Summary
Subacute progressive ascending myelopathy (SPAM) is a rare, poorly understood neurological complication of spinal cord injury (SCI) [1,2,3,4,5,6], unrelated to mechanical compression, instability, or syrinx formation at the level of injury or above. A T2-weighted MR image showed increased signal intensity within the center of the spinal cord from L2 to T11 as well as a hypointense lesion measuring 10x4 mm at level L1, suspect of an intramedullary hematoma. On posttrauma day 12, the paraplegic level had ascended to T6/7 and the increased T2-weighted MRI signal in the central cord region extended to T6 (Figure 1). On posttrauma day 14, MRI of the spine showed high signal on T2-weighted images extending from the conus to C6/7 (Figure 2). 4 weeks post trauma, the extension of the characteristic signal alterations persisted at level C4 on MRI and the patient showed only minimal improvement of neurological symptoms. At 1 year post injury, he had recovered most of his lost upper-extremity function and MRI demonstrated only discrete signal intensity alterations extending to T3/4. The 3-year-follow-up MRI showed regression of signal alterations to T4, pronounced myelon atryophy below T4, and bone fusion at L1/2 level (Figure 4)
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