A more vigorous stimulus for ocular movements in coma is accomplished by irrigation of one ear with 10 mL of cold water (or room-temperature water if the patient is still arousable). This causes slow conjugate deviation of the eyes toward the irrigated ear, followed in a few seconds by compensatory nystagmus (fast component away from the stimulated side). This is the vestibulo-ocular (oculovestibular), or caloric test. The ears are irrigated separately several minutes apart. In comatose patients, the fast “corrective” phase of nystagmus that is mediated by the frontal lobes is lost and the eyes are tonically deflected to the side irrigated with cold water, or away from the side irrigated with warm water; this position may be held for 2 to 3 min. Brainstem lesions disrupt these oculovestibular reflexes; if one eye abducts and the other fails to adduct, one can conclude that the medial longitudinal fasciculus has been interrupted (an internuclear ophthalmoplegia on the side of adductor paralysis) or that the third nerve nucleus has been damaged. Abducens palsy is indicated by an esotropic resting position and a lack of outward deviation of one eye with the reflex maneuvers. The complete absence of ocular movement in response to oculovestibular testing indicates a severe disruption of brainstem tegmental systems in the pons and midbrain or, as already mentioned, a profound overdose of sedative, anesthetic, or anticonvulsant drugs.
A reduction in the frequency and eventual loss of spontaneous blinking, then a loss of response to touching the eyelashes, and, finally, a lack of response to corneal touch (the corneal reflex afferent limb travels in the trigeminal nerve and efferent limb, facial nerve) are among the most dependable signs of deepening coma. A marked asymmetry in corneal responses indicates either an acute lesion of the opposite hemisphere or, less often, an ipsilateral lesion in the brainstem.
Restless movements of both arms and both legs and grasping and picking movements signify that the corticospinal tracts are more or less intact. Oppositional resistance to passive movement (paratonic rigidity), complex avoidance movements, and discrete protective movements have the same meaning; especially if they are bilateral and they suggest the coma is not deep. Abduction movements (away from the midline) to escape a noxious stimulus have the same significance and differentiate a motor response from posturing, described below. Focal motor epilepsy indicates that the corticospinal pathway to the convulsing side is intact. With massive destruction of a cerebral hemisphere, as occurs in hypertensive hemorrhage or internal carotid–middle cerebral artery occlusion, seizure activity may be manifest solely in the ipsilateral limbs, the contralateral limbs being prevented from participating by the hemiplegia. Elaborate forms of semivoluntary movement may be manifest on the nonhemiparetic side in patients with extensive disease in one hemisphere; they probably represent some type of disinhibition of cortical and subcortical movement patterns. Choreic, athetotic, or hemiballistic movements indicate a disorder of the basal ganglionic and subthalamic structures, just as they do in the alert patient, but are not helpful in localizing the cause of coma.
Posturing in the Comatose Patient