Occlusion of branches at the bifurcation (top) of the basilar artery results in a remarkable number of complex syndromes that include, in various combinations, somnolence or coma, memory defects, akinetic mutism, visual hallucinations, ptosis, disorders of ocular movement (convergence spasm, paralysis of vertical gaze, retraction nystagmus, pseudoabducens palsy, retraction of upper eyelids, skew deviation of the eyes), an agitated confusional state, and visual field defects. These have been summarized by Petit and coworkers and Castaigne and associates and categorized as paramedian thalamic, subthalamic, and midbrain syndromes, and by Caplan (1980) as parts of the “top of the basilar” syndrome as noted above. Limited, small infarctions on one side of the brainstem are usually due to occlusion of small penetrating vessels that originate in the basilar artery. Emboli coursing through the basilar artery can also occlude the mouths of several small penetrating vessels and cause larger heterogeneous infractions. A larger infarction in the territory of one circumferential vessel may be due to an embolus or result from an atherosclerotic plaque in the parent basilar artery. The clinical distinction is made by the rapidity of onset and the presence of risk factors such as atrial fibrillation for embolus or diabetes and hypertension for small vessel occlusion.
The main signs of occlusion of the superior cerebellar artery, the most rostral circumferential branch of the basilar, are ipsilateral cerebellar ataxia of the limbs (referable to middle and superior cerebellar peduncles); nausea and vomiting; slurred speech; and loss of pain and thermal sensation over the opposite side of the body (spinothalamic tract). Static tremor of the ipsilateral upper extremity, an ipsilateral Horner syndrome, and palatal myoclonus have also been reported.
With occlusion of the anterior inferior cerebellar artery (AICA), the extent of the infarct is extremely variable, as the size of this artery and the territory it supplies vary inversely with the size and territory of supply of the PICA. The principal findings are vertigo, vomiting, nystagmus, tinnitus, and sometimes unilateral deafness; facial weakness; ipsilateral cerebellar ataxia (inferior or middle cerebellar peduncle); an ipsilateral Horner syndrome and paresis of conjugate lateral gaze; and contralateral loss of pain and temperature sense of the arm, trunk, and leg (lateral spinothalamic tract) as shown in Fig. 33-15. The tinnitus, if present at all, may be overwhelming, called “screaming” by some of our patients. If the occlusion is close to the origin of the artery, the corticospinal fibers may also be involved, producing a hemiplegia; if distal, there may be cochlear and labyrinthine infarction. Cerebellar swelling did not occur with AICA territory infarction in the 20 collected by Amarenco and Hauw but it has been a more common occurrence in our material.
The most characteristic manifestation of all these basilar branch strokes is the “crossed” cranial nerve and long tract sensory or motor deficit reflecting a unilateral segmented infarction of the brainstem. These syndromes, which may involve any of cranial nerves III through XII, are listed in Table 33-5 and discussed in Chap. 44. Although the finding of bilateral neurologic signs strongly suggests brainstem involvement, the signs may also be limited to one side of the body.