Stroke and Other Vascular Syndromes of the Spinal Cord

Longitudinal Arteries

There are three longitudinal arteries, the anterior spinal artery and the two posterior spinal arteries. The single anterior spinal artery forms rostrally from the union of the two anterior spinal branches of each vertebral artery at the level of the foramen magnum. From here it descends up to the tip of the conus medullaris. The caliber of the artery is largest in the region of the lower thoracic and upper lumbar enlargement and smallest in the midthoracic region. The anterior spinal artery is reinforced by successive feeder arterial branches, which enter the artery in a caudal direction and supply the spinal cord below the point of entry. At the conus medullaris and along the filum terminale, the anterior spinal artery communicates through anastomotic branches with the posterior spinal arteries.

The two posterior spinal arteries originate directly from the vertebral arteries (see Figs. 31.1–31.3 ). Each vessel descends on the posterior surface of the spinal cord along the posterolateral sulcus. Throughout its course, each posterior spinal artery gives off branches that penetrate the cord to supply the posterior columns, dorsal gray matter, and superficial dorsal aspect of the lateral columns.

Radicular Tributary Arteries

Thirty-one pairs of radicular arteries penetrate the spinal canal through the intervertebral foramina. Usually the 62 radicular branches contribute to the vascularization of the spinal cord and define three major spinal arterial territories—cervicothoracic, midthoracic, and thoracolumbar. These radicular tributaries may be further subdivided according to their origin. The first group consists of those derived from the subclavian artery; the second group is supplied directly from the aorta. At the level of the second thoracic spinal cord segment the arterial supply changes from the subclavian artery to supply directly from the aorta.

The cervicothoracic territory consists of the cervical spinal cord, its brachial plexus enlargement, and the first two or three thoracic segments. This territory is richly supplied by the anterior spinal artery arising from the intracranial vertebral arteries, the midcervical radicular branches of the vertebral artery, and the branches of the costocervical trunk. In the midthoracic territory, the radicular arteries supplying the middle and lower thoracic cord are less prominent. This territory is usually supplied by a radicular branch arising at about the T7 level; it comprises the fourth to eighth segments of the thoracic cord.

The lower thoracic and upper lumbar segments, which contain the lumbar enlargement and lumbosacral plexus, receives its blood supply from the artery of Adamkiewicz (also called the arteria radicularis magna), which variably arises from T8 to T12 and exhibits notable differences in size between individuals. ^, The artery of Adamkiewicz may be fed by collateral segmental arteries in the setting of chronic occlusive disease, which may have implications for the development for spinal cord infarction in the setting of aortic surgery. During aortic surgery reimplanting the artery of Adamkiewicz is commonly performed to optimize spinal cord perfusion with variable results. Occlusion of the artery of Adamkiewicz during surgery has been associated with a higher risk of spinal cord ischemia. On the other hand the rich collateral network is likely equally important to spinal cord perfusion, even compromise of the artery of Adamkiewicz, and is likely to include flow in a caudal to cephalad direction via collaterals from the internal iliac arteries. These collaterals, as well as the artery of Adamkiewicz, may be further visualized by computed tomography or magnetic resonance angiography.

Intrinsic (Feeder) Arteries

When the radicular arteries reach the surface of the spinal cord, they form two distinct systems of intrinsic blood supply (see Fig. 31.3 ). The first is the posterolateral and peripheral plexus formed by the two posterior spinal arteries, which are interconnected by anastomotic channels. This plexus, a centripetal vascular territory, is formed by radial arteries directed inward as branches from the coronal arterial plexus surrounding the spinal cord. It supplies from one-third to one-half of the outer rim of the cord, including the lateral and ventral spinothalamic tracts. These radial arteries are longer in the posterior white columns than in the anterior and lateral columns. The second arterial system to the spinal cord is a centrifugal system formed by the sulcal arteries, which arise from the anterior spinal artery and pass backward in the anterior medial sulcus. These arteries enter the gray commissure and, turning left or right, supply the gray matter and adjacent white matter. The corticospinal tract is nourished by both arterial systems.

Both arterial systems are interconnected by a capillary anastomosis in the spinal cord. The number of sulcal arteries supplying each segment of the spinal cord varies with the region of the cord. They are most numerous in the thoracolumbar segment and least numerous in the upper thoracic segment.

Venous System

The intrinsic venous system can be classified into two groups based on the pattern of drainage in the anterior and posterior directions. The anterior median group (central veins) collects blood from both halves of the medial aspects of the anterior horns, anterior gray commissure, and white matter of the anterior funiculus. The central veins also drain adjacent levels above and below through intersegmental anastomoses. They commonly anastomose with other veins within the fissure. Finally, the central veins empty into the anterior median spinal vein. The second group consists of radial veins that arise from capillaries near the periphery of the gray matter or from the white matter. They are radially oriented and directed outward toward the surface of the spinal cord, where they join the superficial plexus of veins surrounding the cord and form a venous vasa corona or corona plexus. These veins are more numerous in the white matter of the posterior and lateral funiculi, but they are also found in the anterior funiculus. The radial veins are more prominent at certain cervical and thoracic levels; they drain laterally from the gray matter of the lateral horns as well as posteriorly from the dorsal nucleus of Clark.

The extrinsic venous system is conspicuous on the posterior aspect of the spinal cord and is especially prominent in the lumbosacral region. There is a rich anastomosis between the large venous trunks. The median posterior spinal vein descends in the region of the posterior median septum. This vessel drains blood from the posterior white columns and the end of the posterior horns.

The anterior spinal vein accompanies the anterior spinal artery and receives the sulcal veins. Both the anterior spinal veins and the median posterior spinal vein empty into the radicular veins, which accompany the anterior or posterior spinal roots. These radicular veins drain into the paravertebral and intervertebral plexuses, and then into the azygous and pelvic venous systems.

Pathology of Spinal Cord Infarction

Occlusion of any vessels supplying the spinal cord stemming from a wide range of etiologies may lead to infarction in the cord, while systemic or local hypoperfusion may lead to ischemia in the spinal cord “watershed” territory. The final pathologic processes appear to be similar regardless of the etiology ( Fig. 31.5 ).

The cellular events in spinal cord infarction are similar to those seen in cerebral infarction. Depending on the intensity of tissue damage, the infarct can be complete or incomplete. In complete infarction, all cellular elements die rapidly. In incomplete infarction blood vessels and, to a lesser extent, astrocytes are unaffected, while neurons undergo delayed cell death that is likely mediated through apoptosis. An initial ischemic and inflammatory cascade is triggered, including N -methyl- D -aspartate-mediated excitotoxic neuronal injury. Microglial cell activation through activation of toll-like receptor 4 mechanisms has been noted in animal models of spinal cord ischemia similar to cerebral ischemic injury models. Subsequent cell death, delayed up to 2 days after the initial ischemic injury, occurs due to apoptotic cell death via activation of caspases; this delay after the initial injury may in turn be mediated after the failure of initial endogenous neuroprotective mechanisms. Post-ischemia activation of inflammatory and apoptosis pathways may further worsen injury to the cord and could be an explanation of delayed-onset paraplegia that can be observed after surgery on the aorta. ^, The presence of heat-shock proteins, which can be observed in a range of ischemic injuries, has been noted in CSF samples of patients undergoing aortic surgery with subsequent spinal cord stroke. The presence of edema association with spinal cord infarction is mediated in part by varying expression of aquaphorin-4. The pathologic changes observed at autopsy in the spinal cord mirror those seen with cerebral infarction.