As pointed out above, large, destructive or space- consuming lesions of the cerebrum, such as hemorrhage, tumor, abscess, or infarction with brain swelling, usually impair consciousness indirectly by lateral and downward displacement of the subthalamic–upper brainstem structures and herniation of the medial part of the temporal lobe (uncus, hippocampus) into the opening in the tentorium. One consequence of purely lateral displacement of the midbrain, perhaps in contrast to the conventional notion of compression by herniation, is that the upper midbrain is pushed against the opposite edge of the tentorium (the Kernohan notch or, more properly, the Kernohan-Woltman phenomenon). This configuration causes weakness and a Babinski sign ipsilateral to the hemispheral lesion and later, extensor posturing on that side. The posterior cerebral artery and rarely the cisternal segment of the ipsilateral oculomotor nerve may also be compressed at the edge of the tentorium, leading to infarction of the occipital lobe in the former, and ophthalmoparesis with pupillary enlargement in the latter.
It follows from the foregoing discussion that unilateral destructive lesions of the hemispheres, such as infarcts or hemorrhages, do not usually cause coma unless they create some degree of mass effect, which secondarily compresses the upper brainstem. There are exceptions in which patients with massive strokes affecting the territory of the internal carotid artery are drowsy and inattentive from the onset, even before brain swelling occurs. More often they are simply apathetic with a tendency to keep their eyes closed, a state that may be misinterpreted as stupor.
The term herniation refers to the dislocation of a portion of the cerebral or cerebellar hemisphere from its normal position to an adjacent compartment that is bounded by dural folds, a phenomenon that is evident both at the autopsy table and by imaging of the brain. Thus, herniations are termed transfalcine (across the falx) or transtentorial (through the tentorial aperture) or are named by the structure that is displaced—cerebellar, uncal, etc. Figure 16-1 and Table 16-2 describe these displacements of brain tissue between dural compartments. Plum and Posner, following from observations by McNealy and Plum, divided the transtentorial brainstem displacements into two groups: one a central herniation syndrome with downward displacement and midline compression of the upper brainstem, and the other a unilateral insertion of the medial temporal lobe, including the uncal gyrus, into the tentorial opening and subsequent compression of the midbrain from the sides.
According to these authors, the central syndrome takes the form of a rostral–caudal deterioration of brainstem function: there is first apathy and drowsiness and, often, periodic Cheyne-Stokes pattern of respiration; following this, the pupils become small and react very little to light; “doll’s-head” (“doll’s-eyes,” oculocephalic) eye movements are still elicitable, as are deviations of the eyes in response to cold-water caloric testing. Bilateral Babinski signs can be detected early; later, grasp reflexes and decorticate postures appear. These signs give way to a downward gradient of brainstem signs: coma; medium-sized fixed pupils that are referable to midbrain damage; bilateral decerebrate postures; loss of vestibulo-ocular (caloric, oculovestibular) responses all of which are the result of pontine damage; irregular breathing patterns that implicate medullary destruction; and death.
The uncal syndrome, the result of herniation of the medial temporal lobe into the tentorial opening, differs in that drowsiness in the early stages is accompanied or preceded by unilateral pupillary dilatation, most often on the side of the mass, as a result of compression of the third nerve by the advancing uncal gyrus.