The syndrome of basilar artery occlusion (Fig. 33-2), as delineated by Kubik and Adams, reflects the involvement of a large number of bilateral structures: corticospinal and corticobulbar tracts; cerebellum, middle and superior cerebellar peduncles; medial and lateral lemnisci; spinothalamic tracts; medial longitudinal fasciculi; pontine nuclei; vestibular and cochlear nuclei; descending hypothalamospinal sympathetic fibers; and the third through eighth cranial nerves (the nuclei and their segments within the brainstem). Thus the complete syndrome comprises bilateral long tract signs (sensory and motor) with variable cerebellar, cranial nerve, and other segmental abnormalities of the brainstem.
Another important syndrome, the result of occlusion of the distal end of the basilar artery, usually from embolus, consists of coma from infarction of the high midbrain reticular activating system. This “top of the basilar” artery occlusion is characterized by transient loss of consciousness, oculomotor disturbances (roving eye movements or eyes looking downward and inward with inability to reflexly elicit upward movements), hemianopia, bilateral ptosis, and pupillary enlargement with preserved reaction to light. Spontaneous recanalization of the vessel may occur, but in a delayed fashion, after the infarct has been established. MRI demonstrates one of several characteristic patterns of central midbrain, bilateral posterior thalamic, typically in the shape of a butterfly, and more variably, unior bilateral posterior cerebral artery territory infarction as discussed below.
Yet another configuration, the result of occlusion of the midbasilar artery, gives rise to the locked-in syndrome, in which the patient is mute and quadriplegic but conscious, reflecting interruption of descending motor pathways in the base of the pons but sparing of the reticular activating system (“locked-in” syndrome; see Chap. 16). Horizontal eye movements are obliterated but vertical ones and some ability to elevate the eyelids are spared. The pupils become extremely small but retain some reaction to light. Midbasilar disease may also cause coma if the posterior communicating arteries are inadequate to perfuse the distal basilar artery territory.
In the presence of the full syndrome of basilar occlusion with coma, quadriplegia, and ophthalmoplegia, it is usually not difficult to make the correct diagnosis. The aim should be, however, to recognize basilar insufficiency long before the stage of total deficit has been reached. The early manifestations (in the form of TIAs) occur in many combinations, described in detail further on.