Pupils

Sluggish light reactivity retained until all other brain stem reflexes are lost

Diffuse cellular cerebral dysfunction (toxic-metabolic encephalopathy)

Unilateral pupillary dilation, pupil unreactive to light

3rd cranial nerve compression (eg, in transtentorial herniation), usually due to an ipsilateral lesion (see Anisocoria)

Pupils fixed in midposition

Midbrain dysfunction due to structural damage (eg, infarction, hemorrhage)

Central herniation

Severe metabolic depression by medications, illicit drugs, or toxins (all other brain stem reflexes are also absent)

Constricted pupils (1 mm wide)

Massive pontine hemorrhage

Toxicity due to opioids or certain insecticides (eg, organophosphates, carbamates)

Eye movements

Early abnormal pupillary and oculomotor signs

Primary brain stem lesion

Spontaneous, conjugate roving eye movements but intact brain stem reflexes

Early toxic-metabolic encephalopathy

Gaze preference to one side

Brain stem lesion on the opposite side

Cerebral hemisphere lesion on the same side

Absent eye movements

Further testing required (eg, oculocephalic and oculovestibular reflexes)