Ischemic infarction of the spinal cord usually involves the territory of the anterior spinal artery, that is, a variable vertical extent of the ventral two-thirds of the spinal cord. Infarctions in this territory are relatively uncommon as already mentioned, representing 1.2 percent of all strokes (Sandson and Friedman). The resulting clinical abnormalities are generally referred to as the anterior spinal artery syndrome, described by Spiller in 1909. Atherosclerosis and thrombotic occlusion of the anterior spinal artery is quite uncommon, as noted, and infarction in the territory of this artery is more often secondary to disease of the extravertebral collateral artery or to disease of the aorta, either advanced atherosclerosis, a dissecting aneurysm, or intraoperative surgical occlusion—which compromises the important segmental spinal arteries at their origins. An ischemic myelopathy has been reported in cocaine users, preceded sometimes by episodes of cord dysfunction resembling transient ischemic attacks. Cardiac and aortic surgery, which requires clamping of the aorta for more than 30 min, and aortic arteriography may also be complicated by infarction in the territory of the anterior spinal artery; more often in these circumstances damage to central neuronal elements is greater than that to anterior and lateral funiculi, as described below.
Rarely, polyarteritis nodosa may cause occlusion of a spinal medullary artery. Systemic cholesterol embolism arising from a severely atheromatous aorta may have the same effect. This latter type of embolism is prone to occur after surgical procedures, angioplasty, or cardiopulmonary resuscitation. For unexplained reasons, the spinal cord infarction sometimes follows one of the aforementioned procedures by up to 3 weeks, as emphasized in Dahlberg’s series of cases (Dahlberg et al). In almost all such patients, other evidence of widespread embolism can be expected. Infarction may also result from systemic hypotension, the most vulnerable part being of the thoracic segments of the cord. One of our patients had cord infarction during a bout of diabetic coma.
Among the most curious causes of cervical cord infarction is dissection of the extracranial vertebral arteries, either unilateral or bilateral. The resultant ischemia in the territories of the anterior spinal arteries causes anterior and central cervical cord ischemia. In two cases of this nature that have been brought to our attention, there were an asymmetric brachial diplegia and a suspended sensory loss, preceded by intense radicular and neck pain. The patients reported by Weidauer and colleagues are representative, and there are numerous other case reports although the cause of the vertebral artery dissections has not always been clear. A few patients have vertigo at the onset, directing attention to the vertebral artery damage. We have also encountered instances of myelomalacia in adolescents and young adults in whom no aortic or spinal arterial disease could be demonstrated. Possibly, some of these were because of embolization of disc material (nucleus pulposus) into the local vasculature (see further on).
A quite different progressive ischemic necrosis of the cord can occur in the neighborhood of an arteriovenous malformation or dural fistula and is considered later in this chapter (see also the section on Foix-Alajouanine Myelopathy, described earlier).