Spinal cord ischaemia and infarction

Spinal cord ischaemia and infarction may result from embolism or occlusion of the anterior spinal artery due to atheroma, aortic disease, or a drop in perfusion pressure, and may complicate aortography. Posterior spinal artery occlusion due to intrathecal phenol injection has also been described. The motor neurons and central grey matter are generally more vulnerable to ischaemia than white matter.

Occlusion of the anterior spinal artery

Occlusion of the anterior spinal artery in the cervical region was shown by Spiller (1909) to produce infarction of the anterior and lateral columns of the cord from the fourth cervical to the third thoracic segments.

Clinically the onset is abrupt, often with pain in the neck and back and paraesthesia in the upper limbs, followed by flaccid paralysis of both arms with loss of pain and temperature sensation below a variable level in the cervical region but with preservation of light touch, vibration, and joint-position sense. Initially, there is also flaccid paralysis of both lower limbs (spinal shock) but, if the patient survives, spastic weakness of the lower limbs develops with increased reflexes and extensor plantar responses. In severe cases, paralysis remains complete and prognosis is poor, but when infarction is less extensive the lower limbs may show a variable degree of recovery.

Anterior spinal artery occlusion

Anterior spinal artery occlusion in the thoracic region is often a complication of dissecting aneurysm of the aorta, but may result from embolism as a result of disintegration of an atheromatous plaque in the aorta or from a drop in perfusion pressure, from transient cardiac arrest, or as a rare complication of spinal angiography. Other rare causes include surgical correction of aortic coarctation, inadvertent injection of contrast into the thyocervical trunk during cerebral angiography, fibrocartilaginous emboli from intervertebral disc degeneration entering bone marrow, atrial myxoma, sickle-cell anaemia, and non-compressive Paget's disease giving a spinal artery steal phenomenon reversible with calcitonin (Herzberg and Bayliss 1980). The central grey matter seems especially vulnerable to the effects of ischaemia.

Fibrocartilaginous embolism

Fibrocartilaginous embolism usually presents in healthy children or adults with abrupt pain in the neck or back followed by rapid development of a severe transverse myelopathy or a syndrome of anterior spinal artery occlusion. There is often a history of physical exertion or sometimes injury, e.g. a blow to the back during sports, within a day or so of the neurological event. Post-mortem has revealed occlusion of multiple small arteries and veins within the cord by fibrocartilage, infarction of the cord, and herniation of the nucleus pulposus of an intervertebral disc into an adjacent vertebral body. It is thought that pressure forces the disc material into vessels within the bone marrow of the vertebra with subsequent embolization to the spinal cord (Tosi et al. 1996).

Dissecting aneurysm

When dissecting aneurysm is the cause of spinal cord infarction, and occasionally in other cases, there is severe pain in the back followed by total and permanent flaccid paralysis of the lower limbs, sphincter paralysis, and loss of pain and temperature up to a sensory level at about the umbilicus (corresponding to the Th10 segment of the cord), but with preservation of some light touch sensation, and of vibration and joint-position sense.

Venous infarction may be seen as the consequence of an underlying spinal arteriovenous malformation. Infarction of the upper cervical cord, presumed to be due to spasm of spinal arteries, has been reported as a sequel of minor spinal trauma in childhood.

Other rarer causes

Other rarer causes of spinal cord embolism or infarction include:

  • collagen vascular disorders (e.g. systemic lupus erythematosus, polyarteritis nodosa),
  • bacterial endocarditis,
  • air embolism due to decompression (Caisson disease).

The latter disorder usually manifests in underwater divers; with decompression, nitrogen bubbles can form in spinal vessels, especially in the upper thoracic cord. Symptoms may be mild and transient or may be devastating with a complete transverse myelopathy. The patients should be immediately treated with recompression in a hyperbaric chamber; when the acute deficit is severe, prognosis is variable.


The diagnosis of spinal cord infarction is made largely from the clinical features but should always be supported by spinal MRI, in order to rule out alternative pathology, and in many, but not all instances, to demonstrate the area of infarction. The latter is seen as a high-signal region within the cord on T2-weighted images, sometimes with swelling, extending over a variable number of segments. In patients with anterior spinal artery occlusion, the lesion is seen predominantly in the antero-lateral cord; signal change is sometimes seen in adjacent vertebra as a result of ischaemia.


Management of spinal cord infarction includes searching for sources of embolization. If there is evidence for a coagulation disorder, or for venous infarction secondary to thrombosis within an arteriovenous malformation, anticoagulation may be indicated.