Of the various indicators of brainstem function, the most useful are pupillary size and reactivity, ocular movements, vestibulo-ocular reflexes and, to a lesser extent, the pattern of breathing. These functions, like consciousness itself, are dependent on the integrity of structures in the midbrain and rostral pons.
These are of great diagnostic importance in the comatose patient. A unilaterally enlarged (“Huthcinson”) pupil is an early indicator of stretching or compression of the third nerve and reflects the presence of an overlying ipsilateral hemispheral mass as described earlier in the section on herniations. A loss of light reaction usually precedes enlargement of the pupil. As a transitional phenomenon, the pupil may become oval or pear-shaped or appear to be off center (corectopia) because of a differential loss of innervation of a portion of the pupillary sphincter. The light-unreactive pupil continues to enlarge to a size of 6 to 9 mm diameter and is soon joined by a slight outward deviation of the eye. In unusual instances, the pupil contralateral to the mass may enlarge first; this has reportedly been the case in 10 percent of subdural hematomas but has been far less frequent in our experience. As midbrain displacement continues, both pupils dilate and become unreactive to light, probably as a result of compression of the oculomotor nuclei in the rostral midbrain (Ropper, 1990). The last step in the evolution of brainstem compression tends to be a slight reduction in pupillary size on both sides, to 5 mm or smaller. Normal pupillary size, shape, and light reflexes indicate integrity of midbrain structures and direct attention to a cause of coma other than a mass.
Pontine tegmental lesions cause extremely miotic pupils (<1 mm in diameter) with barely perceptible reaction to strong light; this is characteristic of the early phase of pontine hemorrhage. The ipsilateral pupillary dilatation from pinching the side of the neck (the ciliospinal reflex) is usually lost in brainstem lesions. The Horner syndrome (miosis, ptosis, and reduced facial sweating) may be observed ipsilateral to a lesion of the brainstem or hypothalamus or as a sign of dissection of the internal carotid artery.
With coma caused by drug intoxications and intrinsic metabolic disorders, pupillary reactions are usually spared, but there are notable exceptions. Serum concentrations of opiates that are high enough to cause coma have as a consistent sign pinpoint pupils, with constriction to light that may be so slight that it is detectable only with a magnifying glass. High-dose barbiturates may act similarly, but the pupillary diameter tends to be 1 mm or more. Systemic poisoning with atropine or with drugs that have atropinic qualities, especially the tricyclic antidepressants, but also, through another mechanism the selective serotonin reuptake inhibitors is characterized by dilatation and relative unresponsiveness to light of the pupils. Hippus, or fluctuating pupillary size, is a characteristic but not invariant sign of metabolic encephalopathy.
Movements of Eyes and Eyelids and Corneal Responses
These are altered in a variety of ways in coma. In stupor or light coma of metabolic origin, the eyes rove conjugately from side to side in seemingly random fashion, sometimes resting briefly in an eccentric position. These movements disappear as coma deepens, and the eyes then remain motionless and slightly exotropic. In bihemispheral coma, the eyes may rove smoothly from side-to-side (windshield wiper” eyes).