Spinal Cord Infarction/Ischemic Myelopathy


Clinical Vignette

A vigorous 56-year-old state police officer was found to have an extensive thoracoabdominal aneurysm requiring heroic surgical repair with replacement of his entire descending aorta from its arch in the chest to the distal bifurcation within the abdomen. Although the primary surgical procedure appeared to be successful, when the patient awakened he was unable to move his legs or empty his bladder and he had numbness distal to T8-T10. Neurologic examination demonstrated the patient to be paraplegic but with preserved strength in his arms and upper body, loss of temperature and pain sensation, with a vague numbness from his upper abdomen to the tips of his toes, and preserved position and vibratory sensation.

Thoracic and cervical MRI performed within a few hours of his awakening was normal. This excluded a mass lesion potentially capable of being surgically treated but could not reveal an early spinal cord infarct. The patient’s clinical course was otherwise stable. When there was no improvement in his neurologic status, he was transferred to a spinal rehabilitation unit.

The clinical picture of paralysis secondary to loss of corticospinal tract function and sensory change from impaired spinothalamic function, as well as infarction of the anterior horn cells, but with very preserved posterior column function, is classic for an anterior spinal artery distribution spinal cord infarction (Fig. 45-8). Onset of anterior spinal artery syndrome, although usually sudden, may occasionally be gradual over hours or days.

Because of the significant collateral circulation, spinal cord infarction is very much less common than cerebral ischemia; thus spinal cord infarction and transient ischemic attacks involving the spinal cord rarely occur. This diagnosis must be considered in patients who present with sudden onset of nontraumatic weakness, a sensory loss with a definable level to pain and temperature with preserved posterior column function, and bladder dysfunction. Paresthesia or radicular pain can occur at

Loss of pain and temperature sensation

Position sense retained

Dissecting aortic aneurysm obstructing artery of Adamkiewicz by blocking intercostal artery

Figure 45-8 Spinal Cord Infarction.

A. Sagittal T2-weighted MR image showing slightly enlarged spinal cord with patchy increased T2 signal representing edema. B. Sagittal T1 - weighted MR image with only minimal enhancement within the spinal cord.

The infarct level. Patients may develop either a bilateral flaccid paraplegia or quadriplegia depending on the site of cord occlusion. At the cervical level, the arms are flaccid and eventually atrophic because of anterior horn involvement, although the legs become spastic. Thoracic cord infarcts lead to a spastic paraplegia. Initial areflexia changes to hyperreflexia with the presence of Babinski signs.

Spinal cord infarction is typically secondary to inadequate arterial flow through the anterior spinal artery, which supplies the anterior funiculi, anterior horns, base of the dorsal horns, and anteromedial aspects of the lateral funiculi. Thus, the corticospinal and spinothalamic tracts are affected bilaterally. The upper to midthoracic spinal cord is poorly vascularized, and these watershed zones are more susceptible to infarction. Interruption of blood supply from the aorta to the intramedullary spinal vasculature can cause infarction. In contrast, a posterior spinal artery infarction is rare because of well-developed collaterals.

Spontaneous dissecting aneurysms of the descending thoracic or upper abdominal aorta can occlude the ostia of segmental spinal arteries; atherosclerosis of the aorta and its branches, and iatrogenic ischemia from recent aortic surgery are the usual pathophysiologic mechanisms predisposing to spinal cord infarction. Aortic surgical procedures may reduce vascular supply to the radicular and spinal arteries. Procedures such as thoracotomy and nephrectomy sometimes compromise intercostal or lumbar artery flow, which give rise to radicular arteries. The presence of concomitant chest or abdominal pain, limb ischemia, or loss of peripheral pulses suggests a possible aortic dissection.

Very rarely emboli or arteritis may be responsible for an intramedullary cord infarction. Emboli to the anterior spinal artery may be derived from atheromatous, septic, fibrocartilaginous, and air (decompression illness/caisson disease) sources. Vascular angiitis with subsequent thrombosis from primary CNS vasculitis, syphilis, tuberculosis, sarcoidosis, and schistosomiasis can all cause cord infarction.

Differential Diagnosis

Any condition that leads to a rapid onset of a partial transverse spinal cord lesion must be considered, including trauma, metastatic cancer, dural arteriovenous malformations, acute transverse myelitis, MS, and intramedullary tumors. Usually these lesions do not spare posterior column function, and thus position sense is affected in contrast to its presence with anterior spinal artery lesions. Spinal claudication alternatively presents as exercise-induced painless lower extremity weakness.

MRI can exclude these other lesions. Infarction appears isointense on T1 and eventually hyperintense on T2. When MRI is not available or contraindicated, a CT/myelogram can exclude cord compression, but provides less information regarding the spinal cord per se. Spinal fluid evaluation can help detect infection, demyelinating disease, and subarachnoid hemorrhage. In the acute setting, the potential concomitant diagnosis of a dissecting aortic aneurysm must be considered and appropriate body imaging pursued. If negative, studies to search for a cardiac source of embolism, vasculitis, hypercoagulable states, and aortic atherosclerosis are indicated.


With the exception of an aortic dissection where surgery may be indicated to preserve life, treatment is supportive. Aneurysmal repair will not affect spinal cord damage. Underlying etio-logic factors must be corrected, if possible, when discovered.


This depends on the level of anterior spinal artery occlusion, which determines whether the patient is paraplegic or quadriplegic. Once the infarction occurs recovery is rare, although it is possible. Less commonly, the arterial occlusion is farther from the cord, so the chance for collateral arterial supply is greater. Slow, gradual occlusion is offset by collateral development. Anatomic variations are also important; damage to a particular intercostal artery can be of variable importance. Hypoxia and low perfusion pressure aggravate damage caused by ischemia.


A rare spinal stroke, the posterior spinal artery syndrome presents with ataxia, loss of position, vibration, and fine tactile sensation and bladder and bowel disturbance. Well-developed arterial collaterals on the posterior cord account for the extreme rarity of this type of myelopathy.

Leg numbness. These new symptoms were totally different from the mild tingling and burning that had been chronically present for the past 10 years. He began to require a cane to maintain his equilibrium when walking. Although he initially tolerated the newer symptoms, he began to be concerned that he could not walk safely without relying on a walker. He sought further medical opinion. He previously had a myocardial infarction.

Neurologic examination demonstrated a broad-based, spastic gait, brisk muscle stretch reflexes, and bilateral Babinski signs. Pinprick and temperature sensation were reduced in a stocking-glove distribution in his legs. There was a question of a bilateral cord level to pin sensation at C-7. Position sense was absent at the toes, and vibratory sense lost at the ankles.

MRI revealed spinal stenosis and cord edema at C5-C6. He had severe spinal stenosis with multilevel spondylosis, disc protrusion, and end-plate osteophytes. After a 3-month period of observation, his gait difficulties increased. A cervical posterior laminectomy was performed. Subsequently, after a period of rehabilitation hospitalization, he gradually regained the ability to walk independently.

One needs to always carefully evaluate the patient with a chronic primary sensory polyneuropathy who begins to develop disproportionately increased gait difficulty. Cervical spinal stenosis is a common chronic disorder. As occurred in this instance, one may define a quite remediable condition.

Spondylosis, a normal aging process, is the most common cause of a cervical myelopathy (Figs. 45-9 and 45-10; Box 45-2). This results from disc degeneration followed by reactive osteophyte formation, fibrocartilaginous bars, spondylotic transverse bars, articular facet hypertrophy, and thickening of the liga-mentum flavum causing spinal canal narrowing. Subsequently, gradual spinal cord compression may occur; it is particularly likely in patients having congenitally narrowed spinal canals. In its simplest form, a chronically herniated central nucleus pulpo-sus in patients with congenital stenosis can produce a cervical myelopathy. Although many senior individuals have radiographic signs of cervical spondylosis, most are asymptomatic.

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