EYELIDS AND CORNEAL RESPONSES
Begin by noting the position of the eyes and
eyelids at rest and observing for spontaneous
eye movements. The eyelids at rest in coma, as
in sleep, are maintained in a closed position by
tonic contraction of the orbicularis oculi mus-
cles. (Patients with long-term impairment of
consciousness who enter a persistent vegeta-
tive state have alternating cycles of eyes open-
ing and closing; see Chapter 9.) Next, gently
raise and then release the eyelids, noting their
tone. The eyelids of a comatose patient close
smoothly and gradually, a movement that can-
not be duplicated by an awake individual sim-
ulating unconsciousness. Absence of tone or
failure to close either eyelid can indicate facial
motor weakness. Blepharospasm, or strong re-
sistance to eyelid opening and then rapid clo-
sure, is usually voluntary, suggesting that the
patient is not truly comatose. However, lethar-
gic patients with either metabolic or structural
lesions may resist eye opening, as do some pa-
tients with a nondominant parietal lobe infarct.
In awake patients, ptosis may result from ei-
ther brainstem or hemispheric injury. In pa-
tients with unilateral forebrain infarcts, the
ptosis is often ipsilateral to hemiparesis.
106
In
cases of brainstem injury, the ptosis may be
part of a Horner’s syndrome (i.e., accompanied
by pupilloconstriction), due to injury to the lat-
eral tegmentum, or it may be due to an injury
to the oculomotor complex or nerve, in which
case it is typically accompanied by pupillodila-
tion. Tonically retracted eyelids (Collier’s sign)
may be found in patients with dorsal midbrain
or, occasionally, pontine damage.
Spontaneous blinking usually is lost in coma
as a function of the depressed level of con-
sciousness and concomitant eye closure. How-
ever, in persistent vegetative state, it may re-
turn during cycles of eye opening (Chapter 9).
Blinking in response to a loud sound or a
bright light implies that the afferent sensory
pathways are intact to the brainstem, but does
not necessarily mean that they are active at a
forebrain level. Even patients with complete
destruction of the visual cortex may recover
reflex blink responses to light,
107
but not to
threat.
108
A unilateral impairment of the speed
or depth of the eyelid excursion during blink-
ing occurs in patients with ipsilateral facial
paresis.
The corneal reflex can be performed by ap-
proaching the eye from the side with a wisp
of cotton that is then gently applied to the
sclera and pulled across it to touch the corneal
surface.
109
Eliciting the corneal reflex in coma
may require more vigorous stimulation than in
an awake subject, but it is important not to
touch the cornea with any material that might
scratch its delicate surface. Corneal trauma
can be completely avoided by testing the cor-
neal reflex with sterile saline. Two to three
drops of sterile saline are dropped on the
cornea from a height of 4 to 6 inches.
109
Reflex
closure of both eyelids and elevation of both
eyes (Bell’s phenomenon) indicates that the
reflex pathways, from the trigeminal nerve and
spinal trigeminal nucleus through the lateral
brainstem tegmentum to the oculomotor and
facial nuclei, remain intact. However, some
patients who wear contact lenses may have per-
manent suppression of the corneal reflex. In
other patients with an acute lesion of the des-
cending corticofacial pathways, the blink reflex
may be suppressed, but Bell’s phenomenon
should still occur. A structural lesion at the
midbrain level may result in loss of Bell’s phe-
nomenon, but an intact blink response. A le-
sion at the midpontine level may not only im-
pair Bell’s phenomenon, but also cause the
jaw to deviate to the opposite side (corneal-
mandibular reflex), a phenomenon that may
also occur with eye blink.
110
EXAMINATION OF OCULAR
MOTILITY
Hold the eyelids gently in an open position
to observe eye position and movements in a
comatose patient. A small flashlight or bright
ophthalmoscope held about 50 cm from the
face and shined toward the eyes of the patient
should reflect off the same point in the cornea
of each eye if the gaze is conjugate. Most pa-
tients with impaired consciousness demon-
strate a slight exophoria. If it is possible to ob-
tain a history, ask about eye movements, as a
congenital strabismus may be misinterpreted
as dysconjugate eye movements due to a brain-
stem lesion. Observe for a few moments for
spontaneous eye movements. Slowly roving eye
movements are typical of metabolic encepha-
lopathy, and if conjugate, they imply an intact
ocular motor system.
64
Plum and Posner’s Diagnosis of Stupor and Coma
The vestibulo-ocular responses are then
tested by rotating the patient’s head (oculoce-
phalic reflexes).
99
In patients who may have
suffered trauma, it is important first to rule out
the possibility of a fracture or dislocation of the
cervical spine; until this is done, it may be nec-
essary to skip ahead to caloric testing (see be-
low). The head is rotated first in a lateral di-
rection to either side while holding the eyelids
open. This can be done by grasping the head
on either side with both hands and using the
thumbs to reach across to the eyelids and hold
them open. The head movements should be
brisk, and when the head position is held at
each extreme for a few seconds, the eyes should
gradually come back to midposition. Moving
the head back to the opposite side then pro-
duces a maximal stimulus. The eye movements
should be smooth and conjugate. The head is
then rotated in a vertical plane (as in head
nodding) and the eyes are observed for vertical
conjugate movement. During downward head
movement, the eyelids may also open (the
doll’s head phenomenon).
111
The normal response generated by the ves-
tibular input to the ocular motor system is
for the eyes to rotate counter to the direction
of the examiner’s movement (i.e., turning the
head to the right should cause the eyes to de-
viate to the left). In an awake patient, the vol-
untary control of gaze overcomes this reflex
response. However, in patients with impaired
consciousness, the oculocephalic reflex should
predominate. This response is often colloqui-
ally called the doll’s eye response,
111
and nor-
mal responses in both horizontal and vertical
directions imply intact brainstem pathways
from the vestibular nuclei through the lower
pontine tegmentum and thence the upper
pontine and midbrain paramedian tegmentum
(i.e., along the course of the MLF; see below).
There may also be a small contribution from
proprioceptive afferents from the neck,
112
which also travel through the medial longitu-
dinal fasciculus. Because these pathways over-
lap extensively with the ascending arousal sys-
tem (see Figure 2–8), it is quite unusual for
patients with structural causes of coma to have
a normal oculocephalic examination. In con-
trast, patients with metabolic encephalop-
athy, particularly due to hepatic failure, may
have exaggerated or very brisk oculocephalic
responses.
Eye movements in patients who are deeply
comatose may respond sluggishly or not at all to
oculocephalic stimulation. In such cases, more
intense vestibular stimulation may be obtained
by testing caloric vestibulo-ocular responses.
With appropriate equipment, vestibulo-ocular
monitoring can be done using galvanic stimu-
lation and video-oculography.
113
However, at
the bedside, caloric stimuli and visual inspec-
tion are generally used (see Figure 2–9). The
ear canal is first examined and, if necessary,
cerumen is removed to allow clear visualiza-
tion that the tympanic membrane is intact. The
head of the bed is then raised to about 30
degrees to bring the horizontal semicircular
canal into a vertical position so that the re-
sponse is maximal. If the patient is merely
sleepy, the canal may be irrigated with cool
water (158C to 208C); this usually induces a
brisk response and may occasionally cause
nausea and vomiting. Fortunately, in practice,
it is rarely necessary to use caloric stimulation
in such patients. If the patient is deeply co-
matose, a maximal stimulus is obtained by us-
ing ice water. A large (50 mL) syringe is used,
attached to a plastic IV catheter, which is gently
advanced until it is near the tympanic mem-
brane. An emesis basin can be placed below the
ear, seated on an absorbent pad, to catch the
effluent. The ice water is infused at a rate of
about 10 mL/minute for 5 minutes, or until a
response is obtained. After a response is ob-
tained, it is necessary to wait at least 5 minutes
for the response to dissipate before testing the
opposite ear. To test vertical eye movements,
both external auditory canals are irrigated si-
multaneously with cold water (causing the eyes
to deviate downward) or warm water (causing
upward deviation).
The cold water induces a downward con-
vection current, away from the ampulla, in the
endolymph within the horizontal semicircular
canal. The effect of the current upon the hair
cells in the ampulla is to reduce tonic dis-
charge of the vestibular neurons. Because the
vestibular neurons associated with the hori-
zontal canal fire fastest when the head is turn-
ing toward that side (and thus push the eyes
to the opposite side), the result of cold water
stimulation is to produce a stimulus as if the
head were turning to the opposite side, thus
activating the ipsilateral lateral rectus and con-
tralateral medial rectus muscles to drive the
Examination of the Comatose Patient
65