The entire lateral medullary syndrome, one of the most striking in neurology, is usually caused by infarction, with only a small number of cases being the result of hemorrhage, demyelination, or tumor. Although it has traditionally been attributed to occlusion of the PICA, as mentioned earlier, careful studies have shown that most cases are due to vertebral artery occlusion by atherothrombosis; in the remainder, either the posterior inferior cerebellar artery or one of the lateral medullary arteries is occluded by atherothrombosis. Embolism to the PICA is a less-frequent cause. The inferior cerebellum may be affected in isolation if the embolus travels distal to the medullary branches of the PICA, causing vomiting, vertigo, and ataxia with occipitonuchal headache but without Horner syndrome, hiccoughs, palatal paralysis, and other features of medullary infarction.
In recent years, we have had experience with patients who initially have considerable recovery from lateral medullary infarction in the first days and weeks but experience sudden death from respiratory or cardiac arrest, even in the absence of cerebellar swelling or basilar artery thrombosis. Cases of this nature have been reviewed by Norrving and Cronqvist. The related and important issue of cerebellar swelling after vertebral artery or PICA occlusion and the need for surgical decompression is discussed later in the chapter.
The branches of the basilar artery may be instructively grouped as follows: (1) paramedian, 7 to 10 pairs, supplying a wedge of pons on either side of the midline; (2) short circumferential, 5 to 7 pairs in number, supplying the lateral two-thirds of the pons and the middle and superior cerebellar peduncles; (3) long circumferential, 2 on each side (the superior and anterior inferior cerebellar arteries), which run laterally around the pons to reach the cerebellar hemispheres (see Figs. 33-2, 33-12, and 33-14 through 33-16); and (4) several paramedian (interpeduncular) branches at the bifurcation of the basilar artery and origins of the posterior cerebral arteries supplying the high midbrain and medial subthalamic regions. These interpeduncular and other short proximal branches of the posterior cerebral artery were described earlier in the chapter.
Basilar artery occlusion, typically because of local thrombosis that is superimposed on a preexisting atherosclerotic plaque, can arise in several ways: (1) occlusion of the basilar artery itself, usually in the lower or middle third at the site of an atherosclerotic plaque; (2) occlusion of both vertebral arteries as mentioned earlier, which produces the equivalent of basilar artery occlusion if the circle of Willis is inadequate; and (3) occlusion of a single vertebral artery when it is the only one of adequate size. When there is embolism, the clot usually lodges at the terminal bifurcation of the basilar (“top-of-the-basilar syndrome” as detailed by Caplan 1980) or in one of the posterior cerebral arteries, as the clot, if small enough to pass through the vertebral artery, easily traverses the length of the basilar artery, which is of greater diameter than either vertebral artery. Also, atherothrombosis may involve a branch of the basilar artery rather than the trunk (basilar branch occlusion).