Figure 2–9. Ocular reflexes in unconscious patients. The left-hand side shows the responses to oculocephalic maneuvers (which should only be done after the possibility of cervical
spine injury has been eliminated). The right-hand side shows responses to caloric stimulation with cold or warm water (see text for explanation). Normal brainstem reflexes in a
patient with metabolic encephalopathy are illustrated in row (A). The patient shown in row (B) has a lesion of the right side of the pons (see Figure 2–8), causing a paralysis of gaze
to that side with either eye. Row (C) shows the result of a lesion involving the medial longitudinal fasciculus (MLF) bilaterally (bilateral internuclear ophthalmoplegia). Only
abducens responses with each eye persist. The patient in row (D) has a lesion involving both MLFs and the right abducens nucleus (one and a half syndrome). Only left eye
abduction is retained. Row (E) illustrates a patient with a midbrain infarction eliminating both the oculomotor and trochlear responses, leaving only bilateral abduction responses.
Note that the extraocular responses are identical to (C), in which there is a bilateral lesion of the MLF. However, pupillary light responses would be preserved in the latter case.
(From Saper, C. Brain stem modulation of sensation, movement, and consciousness. Chapter 45 in: Kandel, ER, Schwartz, JH, Jessel, TM. Principles of Neural Science. 4th ed.
McGraw-Hill, New York, 2000, pp. 871–909. By permission of McGraw-Hill.)
67
eyes toward the side of cold water stimulation.
Any activation of the anterior canal (which ac-
tivates the ipsilateral superior rectus and the
contralateral inferior oblique muscles) and the
posterior canal (which activates the ipsilateral
superior oblique and contralateral inferior rec-
tus muscles) by caloric stimulation cancel each
other out.
When caloric stimulation is done in an
awake patient who is trying to maintain fixation
(e.g., in the vestibular testing laboratory), cool
water (about 308C) causes a slow drift toward
the side of stimulation, with a compensatory
rapid saccade back to the midline (the direc-
tion of nystagmus is the direction of the fast
component). Warm stimulation (about 448C)
induces the opposite response. The traditional
mnemonic for remembering these movements
is ‘‘COWS’’ (cold opposite, warm same), which
refers to the direction of nystagmus in an
awake patient. This mnemonic can be con-
fusing for inexperienced examiners, as the re-
sponses seen in a comatose patient with an
intact brainstem are the opposite: cold water
induces only tonic deviation (there is no lit-
tle or no corrective nystagmus), so the eyes
deviate toward the ear that is irrigated. The
presence of typical vestibular nystagmus in a
patient who is unresponsive indicates a psy-
chogenic cause of unresponsiveness (i.e., the
patient is actually awake). The absence of a
response to caloric stimulation does not always
imply brainstem dysfunction. Bilateral vestib-
ular failure occurs with phenytoin or tricyclic
antidepressant toxicity. Aminoglycoside vestib-
ular toxicity may obliterate the vestibular re-
sponse, but oculocephalic responses may per-
sist, the neck muscles supplying the afferent
information.
112
On the other hand, because the oculomotor
pathways are spatially so close to those in-
volved in producing wakefulness, it is rare for a
patient to have acute damage to the oculo-
motor control system without a change in con-
sciousness.
Patient 2–1
A 56-year-old man with a 20-year history of poorly
controlled hypertension came to the emergency
department with a complaint of sudden onset of
severe dizziness. On examination, he was fully
awake and conversant. Pupils were 2.5 mm and
constricted to 2.0 mm with light in either eye. The
patient could not follow a moving light to either
side or up or down. Hearing was intact, as were
facial, oropharyngeal, and tongue motor and sen-
sory responses. Motor and sensory examination
was also normal, tendon reflexes were symmetric,
and toes were downgoing.
The patient was sent for computed tomography
(CT) scan, which showed a hemorrhage into the
periventricular gray matter in the floor of the fourth
ventricle at a pontine level, which tracked rostrally
into the midbrain. During the CT scan the patient
lapsed into coma. At that point, the pupils were
pinpoint and the patient was unresponsive with
flaccid limbs. He subsequently died, but autopsy
was not permitted.
Comment. The sudden onset of bilateral im-
pairment of eye movements on the background of
clear consciousness is rare, and raised the possi-
bility of a brainstem injury even without uncon-
sciousness. Although the CT scan demonstrated a
focal hemorrhage selectively destroying the ab-
ducens nuclei and medial longitudinal fasciculi,
the proximity of these structures to the ascending
arousal system was demonstrated by the loss of
consciousness over the next few minutes.
Finally, if there has been head trauma, one
or more eye muscles may become trapped
by a blowout fracture of the orbit. It is im-
portant to distinguish this cause of abnor-
mal eye movements from damage to neural
structures, either peripherally or centrally.
This is generally done by an ophthalmologist,
who applies topical anesthetics to the globe
and uses a fine, toothed forceps to tug on the
sclera to attempt to move the globe (forced
duction). Inability to move the globe through
a full range of movements may indicate a
trapped muscle and requires evaluation for
orbital fracture.
Interpretation of Abnormal
Ocular Movements
A wide range of eye movements may be seen,
both at rest and during vestibular stimulation.
Each presents clues about the nature of the
insult that is causing the impairment of con-
sciousness.
68
Plum and Posner’s Diagnosis of Stupor and Coma