Despite the elucidation of these causes of spinal cord infarction, a large group in any series has no identifiable cause; for example, an etiology could be established in only 7 of 27 consecutive cases in the series from Novy and colleagues. The clinical manifestations of spinal arterial occlusion will, of course, vary with the level and portions of the cord that are infarcted, but common to practically all cases of infarction in the territory of the anterior spinal artery is pain in the neck or back and the development of paralysis and loss of pain and thermal sensations below the level of the lesion, accompanied by paralysis of sphincteric function. Except in high cervical lesions, the sensory changes are dissociated, that is, pain and temperature sensations are lost (because of interruption of the spinothalamic tracts), but vibration and position sense are unimpaired (a result of sparing of posterior columns).
Rarely, infarction is preceded by spinal transient ischemic attacks as has been emphasized in cases related to cocaine use. The symptoms may develop instantaneously or, more often in our experience, over 1 or 2 h; in any case, more rapidly than in the inflammatory myelitides. Radicular pain corresponding to the upper level of the lesion is sometimes a complaint. Paralysis is usually bilateral, occasionally unilateral, and rarely complete. Also reported is a bibrachial paralysis as a fragment of the anterior spinal artery syndrome, as mentioned earlier. In cases that cause a complete transverse myelopathy, the limbs are initially flaccid and areflexic, as in spinal shock from traumatic lesions, followed after several weeks by the development of spasticity and the return of a degree of voluntary bladder control (unless sacral segments have been infarcted). Many patients regain a substantial degree of motor function, mainly in the first month but extending over a year (see Sandson and Friedman; Cheshire et al; Novy et al).
Infarction in the territory of the posterior spinal arteries is uncommon and the corresponding syndrome is not stereotyped; only 2 of 27 cases from the series by Novy and colleagues had this pattern. It may occur with surgery or trauma of the spine or rarely with vertebral artery dissections.
Some, but not all, spinal cord infarctions are detected by MRI (Fig. 42-7). After a few days, there are obvious lesions on the T2 sequences, presumably reflecting edema that extends over several levels. There may be slight enhancement after infusion of gadolinium. It is notable, however, that the MRI taken in the first hours or day is often normal, including sometimes diffusion weighted images. The reason for the delay in the appearance of the imaging findings is not known. In the chronic stages, the infarcted region collapses and has an attenuated signal on MRI.
Dissecting aneurysm of the aorta, which is characterized by intense interscapular and/or chest pain (occasionally it is painless), widening of the aorta, and signs of impaired circulation to the legs or arms and various organs, gives rise to a number of myelopathic syndromes. The neurologic picture was first described by Kalischeri in 1914 and the aortic lesion leading to dissection, according to Erdheim, was a medionecrosis. The spinal syndromes of aortic dissection according to Weisman and Adams are (1) paralysis of the sphincters and both legs with sensory loss below T6; (2) ischemic infarction of the cord confined to the gray matter, in which case there is an abrupt onset of muscle weakness or myoclonus and spasms in the legs but no pain or sensory loss; (3) obstruction of the origin of a common carotid artery with hemiplegia; and, less commonly, (4) obstruction of a brachial artery with a sensorimotor neuropathy of the limb.