Pathogenesis and Pathophysiology. Spinal cord infarcts are most often caused by interruption of the blood flow in one or more of the arteries that feed into the anterior spinal arterial system. A large anterior spinal artery runs in the ventral midline from the medullospinal junction rostrally to the conus medullaris and the filum terminale caudally. This anterior spinal artery system is supplied by five to 10 single radicular arteries. The cervical region is supplied by the anterior spinal artery branch of the intracranial vertebral artery and inferiorly by branches of the thyrocervical and costocervical branches of the subclavian arteries. The thoracic and lumbar spinal cord segments are fed by radicular arterial branches of the deep cervical and intercostal arteries and branches of the aorta. The lower thoracic cord is supplied by direct branches from the aorta, the largest of which is the artery of Adamkiewicz, which most often enters between T12 and L2. The sacral cord and cauda equina are supplied by branches of the hypogastric and obturator arteries. [ji This anterior system is vulnerable to interruption of flow through any one of the feeding arteries. Resulting infarcts usually affect the anterior horns and the lateral and ventral white matter columns.
In contrast to the anterior spinal artery system, there are paired posterior spinal arteries, which are fed by small posterior radicular arteries and which enter along nerve roots at every level from both sides. The posterior spinal arteries form a rete of communicating vessels that supply the posterior columns and posterior gray horns of the spinal cord. Because of the multiple feeding channels, this system is very resistant to interruption of its blood supply.
Interruption of blood flow in anterior spinal branches is probably most often due to disease within the aorta. Aortic aneurysms, surgery on the aorta, aortic dissections, and emboli from atheromatous aortic plaques can result in obstruction to flow in feeding arteries. Disc cartilage can also fragment and enter spinal arteries and veins and lead to infarction.
AV fistulas are also an important cause of spinal cord infarction. These lesions are most common in older men. Direct communications develop between radicular arteries and veins outside the dura mater. This greatly increases pressure in the venous system, and large drainage veins develop on the surface of the spinal cord. At the same time, shunting of blood decreases flow to the spinal cord from the feeding artery. In order to maintain adequate spinal perfusion, the pressure of blood in the arterial system must exceed venous pressure. The spinal-dural AV fistula often creates a situation in which intermittently venous pressure exceeds arterial pressure, and ischemia develops. At first, ischemia can be intermittent, and spinal cord TIAs can result.
Spinal infarcts can also develop in relation to infections in the meninges and parasitic invasion of the spinal arteries. Syphilis, tuberculosis, and lyme borreliosis can involve the spinal arteries. Adhesive arachnoiditis can also cause obliteration of spinal arteries and lead to cord ischemia, especially in the central portion of the spinal cord. Schistosomiasis can involve feeding spinal arteries. Hypoxic-ischemic injury to the spinal cord also develops in patients with severe systemic hypotension and shock. In these patients, brain damage usually is more severe than spinal injury and makes it difficult to identify the spinal pathology clinically.
Spinal cord hemorrhage most often results from trauma. Bleeding diathesis, especially anticoagulation, is another important cause. Aneurysms of intradural arteries and intradural AVMs and cavernous angiomas are other causes of spinal cord hemorrhages.
Epidemiology and Risk Factors. Spinal strokes are very rare in comparison to strokes that involve the brain. The rarity of spinal cord strokes and the inaccessibility of the spinal cord vascular system to imaging during life have greatly limited knowledge about the causes and pathophysiology of spinal strokes. In addition, the spinal cord and its vascular system are seldom examined in detail during postmortem examinations. The major risk factor for spinal strokes is disease of the aorta and aortic surgery. In older individuals, aortic disease and dural fistulas account for the bulk of cases. In younger persons, trauma, cartilaginous emboli, and congenital vascular malformations and bleeding diatheses account for most instances of spinal strokes.
Clinical Features and Associated Disorders. Spinal cord infarcts usually develop abruptly. Most spinal strokes are thoracic or lumbar, so that the lower extremities are selectively involved. The most common signs are motor and include both lower motor neuron and upper motor neuron abnormalities within the lower limbs. Paraplegia is usually symmetrical. There may be a pain and temperature level along the thorax. Sphincter function is most often lost. Posterior column functions (vibration and position sense) are usually spared. The findings are most often roughly symmetrical. When the lesion is asymmetrical or unilateral, sensory dissociation occurs, producing a Brown-Sequard-like pattern. In patients with spinal-dural AV fistulas, TIAs and steplike development of deficits are common.
Differential Diagnosis. Almost always, the symptoms and signs allow recognition that the lesion is spinal. Occasionally, medullary and pontine infarction can be a consideration. Tumors, abscesses, and syrinxes usually cause symptoms that develop gradually, but hemorrhage into a spinal cord tumor, most often an ependymoma, can be an important consideration. Spinal cord compression caused by cancer, epidural and subdural infections, and hematomas are other considerations.
Almost all compressive spinal cord lesions involve the vertebral column. Plain bone x-ray studies and CT, MRI, and bone scans can yield information about osseous lesions that could compress the spinal cord. MRI is the best method to visualize the spinal cord, dura mater, and overlying bony structures. MRI can show spinal hemorrhages and infarcts and can identify the presence of spinal cord compression. MRI is not very sensitive for the detection of
spinal-dural AV fistulas. Myelography may be needed to show the characteristic dilated veins that course on the surface of the spinal cord. Lumbar puncture is helpful in identifying spinal hemorrhage and infection. Spinal angiography is often necessary to characterize spinal vascular malformations and fistulas.
Management. There is little information about treatment of patients with spinal cord infarcts. Definitive treatment depends, as it does in the brain, on identification of the etiology in the individual patient. Hemorrhage, infection, and infarction can be separated by MRI and lumbar puncture. Identification of spinal-dural AV fistulas is very important because obliteration of the abnormalities can prevent further spinal cord damage. Rehabilitation and management of sphincter functions is similar to that pursued in other diseases of the spinal cord.
Prognosis and Future Perspectives. Outcome depends almost entirely on the cause of the spinal cord vascular damage. In the future, we need to develop more accurate ways to study the aortic blood supply to the spinal cord. Intravascular ultrasound is promising. Perhaps further development of MRA and venography will be helpful and obviate the need for spinal angiography, which can be hazardous. Basic research on spinal cord protection may help limit damage in patients with vascular spinal cord insults.
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