Our own experience does not consistently accord with this distinction between the two herniation syndromes. We have been able only occasionally to detect an orderly sequence of neural dysfunction from the diencephalic to the medullary level but this is not necessarily a contrary view to the herniation idea, only that the model is imperfect. With lateral shift and uncal herniation, one sometimes observes smallness of the pupils, rather than ipsilateral pupillary dilatation, just as drowsiness develops. Or, infrequently, the contralateral pupil may dilate before the ipsilateral one. Nor is it clear that the dilatation of one pupil is always due to compression of the oculomotor nerve by the herniated uncus. As often in pathologic material, the third nerve is stretched and angulated over the clivus or compressed under the descended posterior cerebral artery. Involvement of the third nerve nucleus or its fibers of exit within the midbrain may be responsible for the dilatation of the opposite pupil, the usual occurrence after the pupil on the side of the mass has become fixed (Ropper, 1990).
In our serial study of 12 patients with brain swelling and lateral diencephalic–mesencephalic shifts caused by hemispheral infarcts, 4 initially had no ipsilateral pupillary enlargement; in 1 patient, the pupillary enlargement was contralateral; in 3 patients, the pupils were symmetrical when drowsiness gave way to stupor or coma (Ropper and Shafran). Cyclic Cheyne-Stokes breathing was an early sign of deterioration. In one patient, the first motor sign was an ipsilateral decerebrate rigidity rather than decorticate posturing; most of the patients had bilateral Babinski signs by the time they became stuporous. The appearance of a Babinski sign on the nonhemiparetic side has been a relatively dependable but not invariant sentinel of secondary brain tissue shift at the tentorial opening.
The important elements of secondary compression of the upper brainstem may occur in some cases entirely above the plane of the tentorium and be due to horizontal shift of structures rather than to herniation. With acute masses, a 3to 5-mm horizontal displacement of the pineal calcification is associated with drowsiness; 5 to 8 mm, with stupor; and greater than 8 or 9 mm, with coma (Ropper, 1986). Shift of the septum pellucidum less dependably predicts the level of consciousness. The degree of vertical tissue distortion differs between cases. Pleasure and colleagues described a syndrome of low cerebrospinal fluid (CSF) pressure causing a purely downward herniation and stupor that was corrected by the infusion of fluid into the spinal canal. Others, notably Reich and colleagues, have found evidence for vertical shift to be more compelling than for horizontal displacement.
In any case, the location in reference to the tentorial opening, the size of a mass, and the rapidity of its expansion all determine the degree of brain distortion and displacement of crucial structures in the diencephalon and upper midbrain. Andrews and colleagues have pointed out that frontal and occipital hemorrhages are less likely to displace deep structures and to cause coma than are clots of equivalent size in the parietal or temporal lobes. Nor is it surprising that slowly enlarging masses, such as brain tumors, can cause massive displacements of brain tissue, yet result in few clinical changes. In other words, all of the above comments must take into consideration the rate of evolution of a mass and its location and relationship to vital structures that maintain arousal.
The neural dysfunction of deep structures, particularly of the RAS, resulting from compression is probably due to ischemia but this issue has not been well studied and it is possible that mechanical distortion of neurons or glia may contribute.