VASCULAR ANATOMY OF THE SPINAL CORD

The spinal cord is supplied by three main arteries: the anterior spinal artery and the two smaller posterior spinal arteries. The anterior spinal artery is located along the ventral midline of the cord and supplies the anterior two thirds (often closer to the anterior 75%) of the cord tissue. The posterior spinal arteries lie on each side of the posterior aspect of the cord and supply its posterior third (or 25%). Thus the anterior, central, and lateral regions of the cord are irrigated by the anterior spinal artery and the dorsal horns and columns receive blood from the ipsilateral posterior spinal artery. An internal watershed area can be found in the central cord between small penetrating branches from the anterior and posterior spinal arteries. Branches from the three spinal arteries encircle the surface of the cord forming a fine pial plexus with multiple anastomosis (known as the vaso corona).

The anterior spinal artery receives blood from the vertebral arteries in the cervical region and from radicular arteries in the thoracic and lumbar regions. Often two branches arising from each vertebral artery join at the upper cervical level to form the anterior spinal artery; however, many anatomical variations exist and these branches may arise from the posterior inferior cerebellar arteries or from cervical segmental branches. Just a few radicular arteries are responsible for the blood supply to the spinal arteries at the thoracolumbar level. They stem from segmental branches of the aorta (posterior intercostal and lumbar branches), which reach the intervertebral foramina and divide into the anterior and posterior radicular arteries. The largest radicular artery is the arteria radicularis magna of Adamkiewicz (or main anterior radicular artery), which most commonly arises on the left from T9 to T12 but occasionally can be positioned on the right (17% of cases) and arise anywhere from T5 to L4. Between the lower cervical and the mid- to lower thoracic levels, there are usually just two or three small radicular branches supplying this long segment of the cord. Hence the midthoracic area is traditionally considered a watershed territory at high risk for ischemia from hypoperfusion.^4,⁵ Yet most cases of documented spinal cord ischemia do not occur in this area.⁶^–⁸

Figures 9-1 and 9-2 illustrate the normal vascular anatomy of the spinal cord.

Figure 9-1 Longitudinal view of the normal vascular anatomy of the spinal cord.

Figure 9-2 Axial view of the normal vascular anatomy of the spinal cord.

Case Vignette

A 52-year-old woman with history of ovarian cancer in remission and no previous vascular disease presented with sudden onset of bilateral leg weakness. She had acute back pain initially, but it was short lasting. There was no loss of sphincter control. In the emergency department, she had flaccid paraplegia and leg areflexia. On sensory examination, she had decreased superficial pain and temperature sensation in both legs, but there was no sensory level detected in the trunk. Proprioception was normal. Computed tomography (CT) angiogram of chest and abdomen excluded aortic dissection but disclosed diffuse atherosclerotic changes throughout the descending aorta. MRI of the thoracolumbar spine revealed changes consistent with acute spinal cord ischemia from T11 to the tip of the conus medullaris (Figure 9-3). She was treated with interventions to optimize blood pressure, intravenous dexamethasone, and lumbar drainage. Over the following 48 hours, her sensation in the legs became nearly normal, but she only regained minimal motor function (some activation of hip flexors). She developed signs of neurogenic bladder and bowel. Comprehensive vascular evaluation uncovered no other mechanisms for the spinal cord ischemia other than aortic atherosclerosis. Three months later, her neurological condition remained unchanged.

Figure 9-3 Magnetic resonance imaging (MRI) scan of the thoracolumbar spine showing signs of acute spinal cord ischemia. Sagittal T2 fast spin echo sequence (upper left panel) demonstrates hyperintense signal and cord enlargement in the affected area (T11 to conus). Axial cut at the T12 level shows high signal intensity in the territory of the anterior spinal artery, more prominent in the ventral gray matter (upper right panel). Diffusion-weighted imaging (DWI) confirms the acuity of the lesion by revealing diffusion restriction (lower left panel). Post-gadolinium T1 fat-saturated sequence shows modest enhancement of the lesion on a repeat MRI scan 5 days after the onset of deficits (lower right panel).

♦ The presentation of spinal cord infarction depends on the underlying cause, the level of ischemic injury, and the extent of the infarction.

♦ Multiple risk factors and etiologies have been associated with the occurrence of spinal cord ischemia.^2,⁴ Aortic disease (atherosclerosis, dissection) and aortic surgery (repair of thoracoabdominal aortic aneurysm) are the most common causes of spinal cord ischemia.⁴^–⁹ Severe hypotension, especially that due to cardiocirculatory arrest, may also produce spinal cord ischemia,^4,^7,⁸ but this complication is infrequent. Presence of multiple vascular risk factors (hypertension, smoking, hypercholesterolemia, diabetes mellitus, previous vascular events) appears to increase the risk of spinal cord infarction.^6,⁷ Many cases remain classified as cryptogenic.^4,⁶^–⁹

♦ Anterior spinal artery infarction, exemplified by the previous vignette, is the most frequent form of spinal cord ischemia.^4,^6,^7,⁹ It typically presents with sudden flaccid paralysis (paraplegia or quadriplegia according to the level of the lesion), areflexia, loss of spinothalamic sensory modalities (pain and temperature), and autonomic deficits (such as atonic urinary bladder, paralytic ileus, and abolished sphincter tone) below the level of the lesion.⁴ Posterior column sensory modalities (vibration and proprioception) are preserved, resulting in dissociated sensory loss. Back or radicular pain may be severe at the site of infarction, but this is an inconsistent symptom. After the phase of acute spinal shock, pyramidal signs (spasticity, hyperreflexia, Babinski signs, clonus) supervene.

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