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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, to 5 to 7 mm Normal pupillary size, shape, and light re exes indicate integrity of midbrain structures and a cause of coma other than a mass lesion 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 re ex, page 242) is also lost in brainstem lesions.

These episodes, referred to as psychogenic seizures, are nonepileptic in nature i.e., they are not caused by an abnormal neuronal discharge. They are mentioned here because they are quite common and frequently mistaken for epileptic seizures and treated with anticonvulsant drugs, to which they are characteristically unresponsive. Such seizures are most often a symptom of hysteria in the female (Briquet disease) or of compensation neurosis and malingering in males and females, in which case the terms sham seizures and pseudoseizures are appropriate. Of course, patients with true epileptic seizures sometimes exhibit hysterical seizures as well, and distinguishing the two may be dif cult. Usually, however, the motor display in the course of a nonepileptic seizure is suf cient to identify it as such: completely asynchronous thrashing of the limbs and repeated side-to-side movements of the head; striking out at a person who is trying to restrain the patient; hand-biting, kicking, trembling, and quivering; pelvic thrusting and opisthotonic arching postures; and screaming or talking during the ictus. In general, pseudoseizures tend to occur in the presence of other people, to be precipitated by emotional factors, and to be prolonged for many minutes or hours; with few exceptions, tongue-biting, incontinence, hurtful falls, or postictal confusion are lacking. No single one of these features is determinative, however. Prolonged fugue states in our practice usually have proved to be manifestations of hysteria or a psychopathy even in a known epileptic. The serum creatine kinase and prolactin levels are normal after hysterical seizures; this may be helpful in distinguishing them from genuine convulsions. Where doubt remains, a recording of the ictal or postictal EEG or the combined video and EEG recording of an attack will settle the issue. This subject is discussed further in Chap. 56.

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A 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 due to drug intoxications and metabolic disorders, pupillary reactions are usually spared, but there are notable exceptions Opiates cause pinpoint pupils with a constriction to light that is so slight that it can be seen only with a magnifying glass Highdose barbiturates may act similarly, but the pupillary diameter tends to be 1 mm or more Poisoning with atropine or with drugs that have atropinic qualities, especially the tricyclic antidepressants, is characterized by wide dilation and xity of pupils; these features are partially reversed by intravenous physostigmine Hippus, or uctuating pupillary size, is said by some observers to be characteristic of the metabolic encephalopathies.

chunks, some of which are doubtless asteroids that were captured by Saturn long after the planet and its main moon system were formed. Only five of Saturn s moons exceed 1,000 km (620 mi) in diameter. These are Titan, Rhea, Iapetus, Dione, and Tethys.

Movements of Eyes and Eyelids and Corneal Responses These may be altered in a variety of ways In light coma of metabolic origin, the eyes rove conjugately from side to side in random fashion, sometimes resting brie y in an eccentric position These movements disappear as coma deepens, and the eyes then remain motionless in slightly exotropic positions A lateral and slight downward deviation of one eye suggests the presence of a third nerve palsy, and a medial deviation, a sixth nerve palsy There may be a 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 conjugate deviation may sometimes occur with thalamic and upper brainstem lesions (page 226).

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