A lateral and slight downward deviation of one eye suggests the presence of third-nerve palsy on that side, and a medial deviation, of sixth-nerve palsy. There is persistent conjugate deviation of the eyes to one side—away from the side of the paralysis with a large cerebral lesion (looking toward the lesion) and toward the side of the paralysis with a unilateral pontine lesion (looking away from the lesion). “Wrong-way eyes” a paradoxical conjugate deviation to the side opposite a large hemispherical lesion may occur with thalamic and upper brainstem lesions. During a focal seizure the eyes turn or jerk toward the convulsing side (opposite to the irritative focus). The globes turn down and inward (looking at the nose) with hematomas or ischemic lesions of the thalamus and upper midbrain (a variant of Parinaud syndrome). Retraction and convergence nystagmus and “ocular bobbing,” described in Chap. 13, occur with lesions in the tegmentum of the mid-brain and pons, respectively. “Ocular dipping,” in which the eyes move down slowly and return rapidly to the meridian, is observed with coma caused by anoxia and drug intoxications; horizontal eye movements are preserved with ocular dipping but obliterated in cases of ocular bobbing as a result of destruction of pontine gaze centers. Coma-producing structural lesions of the brainstem abolish most if not all conjugate ocular movements, whereas metabolic disorders generally do not (except for instances of deep hepatic coma and antiepileptic drug overdose).
Vestibulo-ocular reflexes (doll’s-eye movements) are elicited by turning or tilting the head and observing the movement of the globes by holding open the lids. The response in coma of metabolic origin or that caused by bihemispheric structural lesions consists of conjugate movement of the eyes in the opposite direction. Elicitation of these ocular reflexes in a comatose patient provides three invaluable pieces of information: (1) evidence of unimpeded function of the midbrain and pontine tegmental structures that integrate biocular eye movements; (2) the intactness of the oculomotor nerves (III, IV, and VI) on both sides, but also (3) loss of the cortical inhibition that normally holds these movements in check. In other words, the presence of unimpaired reflex eye movements implies that coma is not caused by compression or destruction of the upper midbrain. In reference to the last of these, coma from bihemispheral damage or metabolic suppression, the eyes appear to rock easily from side to side and vertically as the head is moved in the opposite direction. In fact, the eyes are stationary with respect to the three dimensions of space but give the impression of moving because the head is in motion. It is as if the globes are under gyroscopic control, and in fact they are through their connections to the vestibular apparatus. In an awake patient, for example, one who is feigning coma, the eyes move with the head as it is turned because the parietal lobes inhibit the oculocephalic reflexes in order to allow for visual tracking of objects. Also, in brain death the destruction of brainstem pathways and oculomotor nuclei cause the yes to move with the head as it is turned. Similarly, sedative or antiepileptic intoxication profound enough to cause coma may often the brainstem mechanisms for oculocephalic reactions and, in extreme cases, even the vestibular-ocular (caloric) responses as noted below.
Asymmetry of the elicited eye movements is a sign of focal brainstem disease. In instances of coma caused by a large mass in one cerebral hemisphere that secondarily compresses the upper brainstem, the oculocephalic reflexes are usually present, but the movement of the eye on the side of the mass may be impeded in adduction as a result of a compressive third-nerve paresis.