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239) The 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 anticonvulsant drug overdose) Oculocephalic re exes (doll s-eye movements), are elicited by briskly turning or tilting the head The response in coma of metabolic origin or that due to bihemispheral structural lesions consists of conjugate movement of the eyes in the opposite direction Elicitation of these re exes in a comatose patient provides two pieces of information: (1) evidence of unimpeded function of the oculomotor nerves and of the midbrain and pontine tegmental structures that integrate ocular movements and (2) loss of the cortical inhibition that normally holds these movements in check The presence of unimpaired re ex eye movements implies that coma is not due to compression or destruction of the upper midbrain Instead, there must be widespread cerebral dysfunction, such as occurs with cerebral anoxia or metabolic-toxic suppression of cortical activity It must be conceded, however, that sedative or anticonvulsant intoxication serious enough to cause coma may obliterate the brainstem mechanisms for oculocephalic reactions and, in extreme cases, even the oculovestibular responses as noted below Asymmetry in elicited eye movements remains a dependable sign of focal brainstem disease In instances of coma due to a large mass in one cerebral hemisphere that secondarily compresses the upper brainstem, the oculocephalic re exes 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 third nerve paresis Irrigation of each ear with 10 mL of cold water (or roomtemperature water if the patient is not comatose) normally 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 oculovestibular or caloric test (page 259) The ears are irrigated separately several minutes apart In comatose patients, the fast corrective phase of nystagmus is lost and the eyes are tonically de ected 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 With brainstem lesions, these vestibulo-ocular re exes are lost or disrupted If only one eye abducts and the other fails to adduct, one can conclude that the medial longitudinal fasciculus has been interrupted (on the side of adductor paralysis) The opposite, abducens palsy, is indicated by an esotropic resting position and a lack of outward deviation of one eye with the re ex maneuvers The complete absence of ocular movement in response to oculovestibular testing indicates a severe disruption of brainstem tegmental pathways in the pons or midbrain or, as mentioned, a profound overdose of sedative or anesthetic drugs Reduction in frequency and eventual loss of spontaneous blinking, then loss of blink in response to touching the eyelashes, and nally a lack of response to corneal touch (afferent limb trigeminal nerve; efferent limb both facial nerves) 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 Spontaneous Limb Movements Restless movements of both arms and both legs and grasping and picking movements signify that the corticospinal tracts are more or less intact Variable oppositional resistance to passive movement (paratonic rigidity), complex avoidance movements, and discrete protective movements have the same meaning; if these movements are bilateral, the coma is usually not profound The occurrence of focal motor epilepsy.

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