Spinal Cord Arterial Ischemia


Spinal cord ischemia is caused by deficient spinal arterial blood flow secondary to occlusion of intercostal/lumbar arteries or to involvement of the intrinsic arteries of the cord. It is also referred to as ischemic myelomalacia of the spinal cord.

Epidemiology

The precise epidemiology of spinal cord arterial ischemia is unknown. In our experience, men and women are affected equally and age range is highly variable: 0.5 to 82 years, mean age 48 years. Based on the approximately 40 cases we have seen over the past years, we estimate the incidence to be close to 1 in 100,000 people per year. Approximately two thirds of spinal cord arterial infarctions involve the thoracolumbar enlargement and the conus medullaris ( Fig. 9-1 ). The cervical region is less commonly affected.

FIGURE 9-1, A 53-year-old man presented with acute tetraparesis. A , T2W MR image 5 hours after symptom onset demonstrates no cord abnormality. Follow-up 3 days later in sagittal ( B ) and axial ( C ) planes demonstrates an extensive infarction in the territory of the anterior spinal artery.

Pathophysiology

Conditions that commonly cause cerebral infarction cause spinal cord infarction far less often.

Atherosclerosis rarely affects the spinal arteries. Simple occlusion of a spinal artery rarely causes spinal infarction because of the multiple anastomoses present among the spinal arteries. Watershed ischemia is similarly less common.

The traditional hypothesis of a watershed zone ischemic vulnerability near T4 is not supported by the relatively low incidence of spinal cord infarctions at that level in clinical and imaging analyses ( Fig. 9-2 ). Thus, the concept of a vulnerable watershed zone at T4 seems no longer to be valid in acute spinal cord ischemia.

FIGURE 9-2, This 55-year-old man experienced acute onset of severe stabbing back pain followed by subacute onset of paraplegia. A , Eight hours after onset of the symptoms sagittal T2W MR image shows a subtle pencil-shaped hyperintensity of the spinal cord. B , Diffusion-weighted sagittal MR image shows a large area of diffusion restriction indicating spinal cord ischemia.

Instead, a wide variety of less usual diseases cause arterial infarction of the cord, including aortic dissection, surgery for aortoiliac occlusive disease, thromboembolism to the spinal arteries, coagulopathy, vasculitis, radiation-induced vasculopathy, toxic effects of contrast media, epidural anesthesia, periradicular nerve root therapy with corticosteroids, decompression illness (caisson disease, “the bends”), shock or cardiac arrest, lumbar artery compression, spinal tumors, and vascular malformations. Embolism of intervertebral disc cartilage may be a specific cause of arterial infarction of the spinal cord, because postmortem studies have shown cartilaginous material within the lumina of spinal arteries when spinal ischemia is associated with spinal trauma and increased axial loading. It is postulated that acute vertical herniations of disc material into the vertebral bodies increase intraosseous pressure and cause retrograde embolism of cartilaginous tissue into the arteries supplying the spinal cord.

Compression of a lumbar artery by the crus of the diaphragm is another, exceptionally rare, cause of spinal cord ischemia. The first right and left lumbar arteries and the second right lumbar artery course through an osteotendinous canal between the vertebral body and the crus of the diaphragm. lf the artery of Adamkiewicz (great radiculomedullary artery of the lumbar enlargement) arises at these levels, the arterial supply of the spinal cord could be compromised by prolonged hyperlordosis, which kinks and compresses the lumbar arteries as they cross through the diaphragmatic crus ( Fig. 9-3 ).

FIGURE 9-3, Evolution of signal changes after spinal cord ischemia with an associated vertebral body infarction. A to C , At 1 hour after the onset of acute stabbing back pain and paraplegia, T2W and STIR images are essentially normal. D , Follow-up 3 days later with STIR MRI shows increased signal within the ischemic conus medullaris and the associated vertebral body infarction, indicating that the infarctions arose by occlusion of a segmental artery.

Clinical Presentation

Acute arterial ischemia of the spinal cord commonly presents as pain and acute onset of transverse cord symptoms. The specific neurologic deficits depend on the level and extent of cord damage. Symptoms may include nerve root deficits and sphincter disturbances. Because the arterial supply to the spinal cord is highly variable and because the anastomotic network is so extensive, true clinical spinal cord syndromes, such as the anterior spinal artery syndrome, are not often seen ( Fig. 9-4 ).

FIGURE 9-4, This 62-year-old patient experienced acute onset of a conus medullaris syndrome. MRI was performed 4 hours ( A , C ) and then 7 days ( B , D , E , F ) after symptom onset. A , B , and E are T2W sequences. C , D , and F are contrast-enhanced T1W sequences. The initial MR images are normal. Appearance of hyperintensity and contrast enhancement at 7 days confirms that the patient suffered acute ischemia of the conus medullaris.

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