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A 56-year-old hypertensive man collapses on the sidewalk. Rushed to an emergency room, he is unresponsive to verbal stimuli, including commands to look up or down. Blood pressure is 190/100 mm Hg, pulse is 92/minute and regular, and temperature is 100.4°F. Respirations are 12/minute, shallow, and regular. Pupils are pinpoint with a barely discernible reaction to light. Spontaneous horizontal eye movements are absent, but several times per minute, his eyes move conjugately and briskly downward, returning immediately to the primary position. There is no response to the oculocephalic maneuver or to ice water caloric testing. His limbs are flaccid with tendon reflexes of normal amplitude; plantar stimulation produces a bilateral flexor response of his legs (including dorsiflexion of his toes). There is no facial grimace or upper limb movement to any painful stimulus.

Computed tomography (CT) reveals a hemorrhage of his pons involving both the tegmentum and the base bilaterally. He is admitted to an intensive care unit and undergoes endotracheal intubation.

The following day, there is no spontaneous eye movement, and caloric testing again produces no response. His pupils are now 3 mm and no longer react to light. Corneal reflexes are absent, the limbs are still flaccid, and tendon reflexes are still present, but there is no longer any response to plantar stimulation or other noxious stimuli. He is not triggering the respirator, and he remains apneic after being disconnected from the respirator for a period sufficient to raise his arterial pCO2 to 65 mm Hg. Blood pressure is 130/80 mm Hg, and temperature is 101°F. Urine assay for drugs and toxins, including sedatives, is negative.

Six hours later, his examination is unchanged. Criteria for brain death having been met, ventilatory support is terminated.


This man’s initial examination revealed the three signs most characteristic of pontine hemorrhage, namely, coma, pinpoint reactive pupils, and absent horizontal eye movements. Coma was secondary to destruction of the reticular activating system, the most caudal extent of which is within the pons. Miosis was secondary to transection of descending sympathetic projections and to disinhibition of the parasympathetic Edinger-Westphal nucleus. Because sympathetic lesions do not interrupt the parasympathetically mediated light reflex, pupillary reactivity was still present (see Figure 7–3). As with miosis secondary to morphine or heroin overdose, the degree of pupillary constriction was so marked that light reactivity was difficult to detect without a magnifying glass.

Loss of horizontal eye movement was the result of damage to the pontine paramedian reticular formation (PPRF; the pontine horizontal gaze center), the sixth nerve nuclei (which mediate horizontal gaze as well as ipsilateral abduction), and their various projections (see Figure 7–4). Less well understood is ocular bobbing, consisting of conjugate downward movements of the eyes several times per minute at irregular intervals. Ocular ...

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