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Diagnosis of early spinal cord infarction with diffusion weighted imaging (DWI). 2012

General Spine

Daniel, K, Powell, MD, BA
Edward, Libfeld, MD, CAQ Neuroradiology, Non ASSR Member

Poster

Purpose

Spinal cord infarction is often suggested by history, as few other myelopathies present as abruptly. However, MRI is highly sensitive for early detection of infarct before symptoms have progressed. We will discuss the relevant literature in conjunction with our case. Background: The most common type of spinal infarct, "anterior spinal artery (ASA) syndrome," includes paralysis, incontinence, and pain and temperature desensitization. Proprioception and vibration sense are preserved. A single ASA supplies the anterior two-thirds of the cord and is fed by 6-10 of the 31, paired radicular arteries, fewer than the posterior circulation (fed by 10-23).1,2 Posterior spinal artery infarction produces proprioception and vibratory sensation loss. Transient weakness is mild. Unilateral involvement is common due to paired arteries.1,2 A third of cases present atypically, presumably due to partial collateralization, venous infarction, or injury. Compressive myelopathy from mass, hematoma or abscess is important to exclude, requiring decompression. Transverse myelitis and acute polyneuropathy (e.g. Guillain-Barré Syndrome) also rarely mimic infarction, however symptoms typically evolve or ascend over time.1,2 Etiologies are many: aortic aneurysm repair, being the most common (10-29% causing infarct),3 aortic dissection, hypotension, aortography, and surgical or degenerative injury to a feeding artery are others. Atherothrombotic disease is presumed responsible in 74% of cases without identified etiology.1,5 Mortality is 10-20%. Only 11-46% achieve independent gait. Chronic incontinence, spasticity, and pain are common.1,2,5,6,7,8

Methods & Materials

A 51-year old male presented with severe back pain, lower extremity paralysis and numbness. Emergent MRI revealed ovoid T2 hyperintensity and restricted diffusion in the central conus medullaris without enhancement. MRI 5 days later, now with clinical progression of gait imbalance and weakness, showed evolved conspicuity of the findings.

Results

Imaging findings are quite distinctive. Restricted diffusion is highly sensitive, seen centrally by 1 hour, rapidly evolving over the first few days, then disappearing after a week. This is significantly more sensitive than T2 changes, however, paucity of reporting precludes an estimate of sensitivity. Intramedullary T2 hyperintensity tends to increase over time but is initially slight and nonspecific and is not seen in up to 45% of cases. Similarly, no enhancement is seen initially, with possible evolution of mild late enhancement.4,5,6 In our case, marked focal restriction of diffusion in the central cord can be seen on day 5 (image 1). Corresponding T2 hyperintensity on STIR imaging was seen slightly on day 1 with increased conspicuity on day 5 (images 1 and 2), without contrast enhancement (image 3), compatible with spinal infarct. Many pathologies exhibit DWI hyperintensity, however, restricted diffusion is specific for infarction. Other such etiologies typically differ in that active demyelination is dorsolateral and multifocal, hemorrhage is heterogeneous, cellular masses expand the cord, and acute compression has a mechanical source.6 T2 hyperintensity in a vascular territory is seen in approximately 45%, and up to 73% after the first week, justifying repeat imaging.5,6 Adjacent vertebrae infarction, found in 4-35% of patients, is specific for ischemia.2

Conclusion

Many studies demonstrate the exquisite sensitivity of DWI for early spinal infarction. T2 changes are also fairly sensitive, but not nearly as specific. Sequential examinations can identify the typical evolution of findings.

References/Financial Disclosures

1. Nedeltchev K, Loher TJ, Stepper F, et al. Long-term outcome of acute spinal cord ischemia syndrome. Stroke 2004; 35:560. 2. Cheng MY, Lyu RK, Chang YJ, et al. Concomitant spinal cord and vertebral body infarction is highly associated with aortic pathology: a clinical and magnetic resonance imaging study. J Neurol 2009; 256:1418. 3. Messé SR, Bavaria JE, Mullen M, et al. Neurologic outcomes from high risk descending thoracic and thoracoabdominal aortic operations in the era of endovascular repair. Neurocrit Care 2008; 9:344. 4. Thurnher MM, Bammer R. Diffusion-weighted MR imaging (DWI) in spinal cord ischemia. Neuroradiology 2006; 48:795. 5. Küker W, Weller M, Klose U, Krapf H, Dichgans J, Nägele T. Diffusion-weighted MRI of spinal cord infarction-high resolution imaging and time course of diffusion abnormality. J Neurol. 2004 Jul;251(7):818-24. 6. Zhang J, Huan Y, Qian Y, Sun L, Ge Y. Multishot diffusion-weighted imaging features in spinal cord infarction. J Spinal Disord Tech. 2005 Jun;18(3):277-82. No financial disclosures.

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