RESTING AND SPONTANEOUS
EYE MOVEMENTS
A great deal of information may be gained by
carefully noting the position of the eyes and
any movements that occur without stimulation.
Table 2–3 lists some of the spontaneous eye
movements that may be observed in uncon-
scious patients. Detailed descriptions are given
in the paragraphs below. Most individuals have
a mild degree of exophoria when drowsy and
not maintaining active fixation. However, other
individuals have varying types of strabismus,
which may worsen as they become less re-
sponsive and no longer attempt to maintain
conjugate gaze. Hence, it is very difficult to
determine the meaning of dysconjugate gaze
in a stuporous or comatose patient if nothing
is known about the presence of baseline stra-
bismus.
On the other hand, certain types of dyscon-
jugate eye movements raise suspicion of brain-
stem injury that may require further exami-
nation for confirmation. For example, injury
to the oculomotor nucleus or nerve produces
exodeviation of the involved eye. Unilateral
abducens injury causes the involved eye to
deviate inward. In skew deviation,
114
in which
one eye is deviated upward and the other
downward, there typically is an injury to the
brainstem (see below).
CONJUGATE LATERAL DEVIATION
OF THE EYES
This is typically seen with destructive or irri-
tative lesions, as compressive or metabolic dis-
orders generally do not affect the supranuclear
ocular motor pathways asymmetrically. A de-
structive lesion involving the frontal eye fields
causes the eyes to deviate toward the side of
the lesion (away from the side of the associ-
ated hemiparesis). This typically lasts for a few
days after the onset of the lesion. An irritative
lesion may cause deviation of the eyes away
from the side of the lesion. These eye move-
ments represent seizure activity, and often
there is some evidence of quick, nystagmoid
jerks toward the side of eye deviation indica-
tive of continuing seizure activity. If seizure
activity abates, there may be a Todd’s paralysis
of gaze for several hours, causing lateral gaze
deviation toward the side of the affected cor-
tex (i.e., opposite to the direction caused by
the seizures). Hemorrhage into the thalamus
may also produce ‘‘wrong-way eyes,’’ which
deviate away from the side of the lesion.
115,116
Table 2–3 Spontaneous Eye Movements Occurring in Unconscious Patients
Term
Description
Significance
Ocular bobbing
Rapid, conjugate, downward movement;
slow return to primary position
Pontine strokes; other structural,
metabolic, or toxic disorders
Ocular dipping
or inverse ocular
bobbing
Slow downward movement;
rapid return to primary position
Unreliable for localization; follows
hypoxic-ischemic insult
or metabolic disorder
Reverse ocular
bobbing
Rapid upward movement;
slow return to primary position
Unreliable for localization; may
occur with metabolic disorders
Reverse ocular dipping
or converse bobbing
Slow upward movement;
rapid return to primary position
Unreliable for localization; pontine
infarction and with AIDS
Ping-pong gaze
Horizontal conjugate deviation of the
eyes, alternating every few seconds
Bilateral cerebral hemispheric
dysfunction; toxic ingestion
Periodic alternating
gaze deviation
Horizontal conjugate deviation of the
eyes, alternating every 2 minutes
Hepatic encephalopathy; disorders
causing periodic alternating
nystagmus and unconsciousness
or vegetative state
Vertical ‘‘myoclonus’’
Vertical pendular oscillations (2–3 Hz)
Pontine strokes
Monocular
movements
Small, intermittent, rapid monocular
horizontal, vertical, or torsional
movements
Pontine or midbrain destructive
lesions, perhaps with coexistent
seizures
From Leigh and Zee,
93
with permission.
Examination of the Comatose Patient
69
This may be due to interruption of descending
corticobulbar pathways for gaze control, which
pass through the thalamic internal medullary
lamina, rather than the internal capsule. Dam-
age to the lateral pons, on the other hand, may
cause loss of eye movements toward that side
(gaze palsy, Figure 2–9). The lateral gaze devi-
ation in such patients cannot be overcome by
vestibular stimulation, whereas vigorous ocu-
locephalic or caloric stimulation usually over-
comes lateral gaze deviation due to a cortical
gaze paresis.
CONJUGATE VERTICAL DEVIATION
OF THE EYES
Pressure on the tectal plate, such as occurs with
a pineal mass or sometimes with a thalamic hem-
orrhage, may cause conjugate downward devi-
ation of the eyes.
117,118
Oculogyric crises may
cause conjugate upward deviation. The classical
cause of oculogyric crises was postencephalitic
parkinsonism.
119
Few of these patients still
survive, but a similar condition is frequently
seen with dystonic crises in patients exposed to
neuroleptics
120
and occasionally in patients with
acute bilateral injury of the basal ganglia.
NONCONJUGATE EYE DEVIATION
Whereas nonconjugate eye position may be
due to an old baseline strabismus, failure of
one eye to follow its mate during spontaneous
or evoked eye movements is typically highly
informative. Absence of abduction of a single
eye suggests injury to the abducens nerve ei-
ther within the brainstem or along its course to
the orbit. However, either increased intracra-
nial pressure or decreased pressure, as occurs
with cerebral spinal fluid leaks,
121
can cause
either a unilateral or bilateral abducens palsy,
so the presence of an isolated abducens palsy
may be misleading. Isolated loss of adduction
of the eye contralateral to the head movement
implies an injury to the medial longitudinal
fasciculus (i.e., near the midline tegmentum)
on that side between the abducens and ocu-
lomotor nuclei (Figure 2–9). Bilateral lesions of
the medial longitudinal fasciculus impair ad-
duction of both eyes as well as vertical oculo-
cephalic and vestibulo-ocular eye movements,
a condition that is distinguished from bilateral
oculomotor nucleus or nerve injury in the co-
matose patient by preservation of the pupil-
lary light responses. (Voluntary vergence and
vertical eye movements remain intact, but re-
quire wakeful cooperation.)
Combined loss of adduction and vertical
movements in one eye indicates an oculomotor
nerve impairment. Typically, there may also be
severe ptosis on that side (so that if the patient
is awake, he or she may not be aware of dip-
lopia). In rare cases with a lesion of the ocu-
lomotor nucleus, the weakness of the superior
rectus will be on the side opposite the other
third nerve muscles (as these fibers are crossed)
and ptosis will be bilateral (but not very severe).
Occasionally, oculomotor palsy may spare the
pupillary fibers. This occurs most often when
the paresis is due to ischemia of the oculomotor
nerve (the smaller pupilloconstrictor fibers are
more resistant to ischemia), such as in diabetic
occlusion of the vasa nervorum. Such patients
are also typically awake and alert, whereas third
nerve paresis due to brainstem injury or com-
pression of the oculomotor nerve by uncal her-
niation results in impairment of consciousness
and early pupillodilation.
Trochlear nerve impairment causes a hy-
peropia of the involved eye, often with some
exodeviation. If awake, the patient typically
attempts to compensate by tilting the head
toward that shoulder. Because the trochlear
nerve is crossed, a trochlear palsy in a coma-
tose patient suggests damage to the trochlear
nucleus on the opposite side of the brainstem.
SKEW DEVIATION
Skew deviation refers to vertical dysconjugate
gaze, with one eye displaced downward com-
pared to the other. In some cases, the eye that
is elevated may alternate from side to side de-
pending on whether the patient is looking to
the left or the right.
95,122
Skew deviation is due
either to a lesion in the lateral rostral medulla
or lower pons, vestibular system, or vestibulo-
cerebellum on the side of the inferior eye, or in
the MLF on the side of the superior eye.
123–125
ROVING EYE MOVEMENTS
These are slow, random deviations of eye po-
sition that are similar to the eye movements
seen in normal individuals during light sleep.
As in sleeping individuals who typically have
some degree of exophoria, the eye positions
may not be quite conjugate, but the ocular
70
Plum and Posner’s Diagnosis of Stupor and Coma