Authors: Lewis,
Steven L.
Steven L.
Title: Field
Guide to the Neurologic Examination, 1st Edition
Guide to the Neurologic Examination, 1st Edition
Copyright ©2004 Lippincott Williams &
Wilkins
Wilkins
> Table of Contents > Section 3 –
Neurologic Examination in Common Clinical Scenarios > Chapter 42 –
Examination of the Comatose Patient
Neurologic Examination in Common Clinical Scenarios > Chapter 42 –
Examination of the Comatose Patient
Chapter 42
Examination of the Comatose Patient
GOAL
The goal of the history and examination of the comatose patient is
to look for clues to the localization and etiology of the process causing
coma.
to look for clues to the localization and etiology of the process causing
coma.
PATHOPHYSIOLOGY OF COMA
Normal consciousness depends on the cerebral hemispheres to provide
cognition and the reticular formation of the upper brainstem (from the midpons
and above) to provide alertness. Coma, the absence of consciousness, can occur
only due to dysfunction of both cerebral hemispheres, dysfunction of the upper
brainstem, or a combination of bilateral hemisphere and upper brainstem
dysfunction.
cognition and the reticular formation of the upper brainstem (from the midpons
and above) to provide alertness. Coma, the absence of consciousness, can occur
only due to dysfunction of both cerebral hemispheres, dysfunction of the upper
brainstem, or a combination of bilateral hemisphere and upper brainstem
dysfunction.
Much of the examination of the comatose patient focuses on
assessing brainstem function. This is because most structural brainstem
processes causing coma produce easily identified abnormalities on examination,
but structural disorders of the hemispheres or diffuse metabolic disorders
generally show preservation of brainstem function on examination. Therefore, if
the brainstem is functioning normally, a structural brainstem process (such as a
brainstem stroke or brainstem compression) is unlikely to be the cause of coma;
the process causing coma would then most likely be due to structural lesions
affecting both of the hemispheres or a diffuse metabolic process.
assessing brainstem function. This is because most structural brainstem
processes causing coma produce easily identified abnormalities on examination,
but structural disorders of the hemispheres or diffuse metabolic disorders
generally show preservation of brainstem function on examination. Therefore, if
the brainstem is functioning normally, a structural brainstem process (such as a
brainstem stroke or brainstem compression) is unlikely to be the cause of coma;
the process causing coma would then most likely be due to structural lesions
affecting both of the hemispheres or a diffuse metabolic process.
TAKING THE HISTORY OF A COMATOSE PATIENT
The history needs to be obtained from witnesses, family, or friends
for any clues they may provide to the cause of the patient’s problem. If
possible, try to obtain information regarding the temporal course of development
of impaired consciousness, any recent systemic or neurologic symptoms, head
trauma, the patient’s past medical and social history, medications, and any
other potentially relevant available historical information.
for any clues they may provide to the cause of the patient’s problem. If
possible, try to obtain information regarding the temporal course of development
of impaired consciousness, any recent systemic or neurologic symptoms, head
trauma, the patient’s past medical and social history, medications, and any
other potentially relevant available historical information.
HOW TO EXAMINE THE COMATOSE PATIENT
General Examination
As part of a detailed general and neurologic examination, look in
the fundi for evidence of papilledema (see Fig. 11-2),
which would suggest increased intracranial pressure, or retinal hemorrhages (see
Fig. 11-3), which would suggest subarachnoid hemorrhage.
Look for evidence for a basilar skull fracture by looking in the ear canals for
blood, inspecting the mastoid areas for ecchymosis (Battle’s sign), or finding
ecchymosis around the eyes (raccoon eyes). Fever suggests the possibility of
meningitis, encephalitis, or sepsis. Meningismus (see Chapter
45, Examination of the Patient with Headache) is a clue to meningitis or
subarachnoid hemorrhage but may be an insensitive sign in deep
unconsciousness.
the fundi for evidence of papilledema (see Fig. 11-2),
which would suggest increased intracranial pressure, or retinal hemorrhages (see
Fig. 11-3), which would suggest subarachnoid hemorrhage.
Look for evidence for a basilar skull fracture by looking in the ear canals for
blood, inspecting the mastoid areas for ecchymosis (Battle’s sign), or finding
ecchymosis around the eyes (raccoon eyes). Fever suggests the possibility of
meningitis, encephalitis, or sepsis. Meningismus (see Chapter
45, Examination of the Patient with Headache) is a clue to meningitis or
subarachnoid hemorrhage but may be an insensitive sign in deep
unconsciousness.
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Assess the Level of Consciousness
Assess the patient’s level of consciousness within the continuum
from drowsiness to coma by looking at the response to external stimuli, as
follows:
from drowsiness to coma by looking at the response to external stimuli, as
follows:
Assess response to verbal stimuli by calling the patient’s name
loudly or asking the patient to follow a simple command, such as “open your
eyes,” “blink your eyes,” or “stick out your tongue.”
Assess response to visual stimuli first by opening the patient’s
eyes and seeing if the patient attends to you. Test the patient’s response to
visual threat by holding the patient’s eyes open and assess whether the
patient blinks when you make a quick motion with your hands in front of each
eye. To avoid inadvertently producing a corneal reflex from air pushed into
the cornea, bring your hands in from the sides when testing visual
threat.
In any potentially comatose patient, ensure that the patient does
not actually have the locked-in syndrome by holding
the patient’s eyes open and asking the patient to look down. Patients with the
locked-in syndrome are not comatose. They are awake but quadriplegic and have
paralysis of horizontal eye movements; they can communicate only by looking
down or blinking on command. This syndrome occurs due to large lesions of the
base of the pons, usually infarction.
Assess Resting Eye Position
Open the patient’s eyes and look at the resting position of the
eyes for any tonic (persistent) deviation of the eyes to one side (called a
gaze preference), as follows:
eyes for any tonic (persistent) deviation of the eyes to one side (called a
gaze preference), as follows:
A gaze preference away from the side of a hemiparesis is
consistent with a large acute cerebral hemispheric lesion. This is because the
frontal eye fields (see Chapter 14, Examination of Eye
Movements) of each hemisphere move the eyes to the contralateral side;
therefore, a large lesion of one of the hemispheres causes the eyes to deviate
toward the damaged hemisphere because of the unopposed action of the intact
frontal eye field from the opposite healthy hemisphere. In
other words, the eyes look to the side of an acute hemispheric lesion and away
from the hemiparesis.
A gaze preference toward the side of a hemiparesis is consistent
with an acute lesion in the brainstem, particularly the pons. This is because
the lateral gaze mechanisms located on each side of the pons move the eyes to
the ipsilateral side; therefore, a lesion of one side of the pons causes the
eyes to deviate away from the damaged side of the brainstem because of the
unopposed action of the intact lateral gaze center on the opposite healthy
side of the pons. In other words, the eyes look away from
the side of a pontine lesion and toward the hemiparesis.
Sustained downgaze deviation of both eyes can be seen in the
setting of processes that affect the posterior (dorsal) upper
midbrain/thalamic region, such as pineal tumors.
Observe for Any Spontaneous Eye
Movements
Movements
Open the patient’s eyes and look for any spontaneous eye movements,
as follows:
as follows:
Roving eye movements are slow conjugate horizontal movements of
the eyes from one side to the other. The presence of spontaneous roving eye
movements implies that the brainstem mechanisms in the pons and midbrain that
move each eye laterally and medially, respectively, are intact. Roving eye
movements are seen in situations in which there is bilateral hemispheric
dysfunction with relative preservation of brainstem function, such as anoxic
encephalopathies.
Ocular bobbing consists of downward jerks of both eyes, which
then slowly return upward to mid-position before jerking downward again.
Ocular bobbing is seen in patients who have lost their horizontal gaze
mechanisms due to a lesion of the base of the pons, but who have preservation
of the mechanisms that control downward vertical gaze in the midbrain. Because
ocular bobbing is seen in patients with pontine lesions, these patients should
particularly be assessed for the locked-in state.
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Assess Reflex Eye Movements
Testing of reflex horizontal eye movements is important when trying
to decide if brainstem function is intact, but you haven’t observed any
spontaneous eye movements. You don’t need to test reflex eye movements when
spontaneous horizontal roving eye movements are seen, because their presence
already tells you that the brainstem control of eye movements is intact. Test
reflex eye movements as follows:
to decide if brainstem function is intact, but you haven’t observed any
spontaneous eye movements. You don’t need to test reflex eye movements when
spontaneous horizontal roving eye movements are seen, because their presence
already tells you that the brainstem control of eye movements is intact. Test
reflex eye movements as follows:
Test for the oculocephalic (doll’s eyes) reflex by turning the
patient’s head to one side and then to the other. In a comatose patient whose
brainstem is intact, turning the head to one side should result in conjugate
deviation of both eyes to the contralateral side. In other words, turning the
head to the left should result in deviation of both eyes to the right, and
turning the head to the right should result in deviation of both eyes to the
left. This can be reported as a “positive” or “intact” doll’s eyes response,
or to be even clearer, can be reported as “turning the head resulted in
bilateral conjugate horizontal eye deviation to the opposite side.”
Test the oculovestibular (cold caloric) reflex if the
oculocephalic (doll’s eyes) maneuver fails to show normal horizontal eye
movements or cannot be performed. This test is most important clinically in
the assessment of possible brain death (see Brain Death section).
Oculocephalic testing does not need to be performed if normal horizontal eye
movements have already been observed spontaneously or during the doll’s eyes
maneuver, because normal brainstem control of eye movements has already been
proven. To perform cold caloric testing:
Raise the patient’s head (or the head of the bed) up to
approximately 30 degrees.
Using an otoscope, look to be sure that the external auditory
canals are patent and that the tympanic membranes are intact.
Prepare a mixture of ice water and draw the ice-cold water up
into a large syringe. Attach a large-gauge plastic intravenous catheter
(with the needle removed) to the end of the syringe.
Place the catheter within one of the ear canals (don’t go too
deep to avoid piercing the tympanic membrane). Slowly instill up to 100 mL
of the ice-cold water into the ear canal.
Observe the response of the eyes for the next 1 to 2
minutes.
After waiting at least 5 minutes, perform the same maneuver on
the other side.
In a comatose patient whose brainstem is intact, instilling ice
water into the ear canal should result in conjugate deviation of both eyes
toward the side of the irrigated ear. In other words, instilling ice water
into the left ear should result in deviation of both eyes to the left, and
instilling ice water into the right ear should result in deviation of both
eyes to the right. This can be reported as a “positive” or “intact” caloric
response, or to be even clearer, can be specifically reported as “cold caloric
irrigation of each ear resulted in bilateral conjugate horizontal eye
deviation to the side of the irrigated ear.”
The presence of intact horizontal eye movements spontaneously or
on oculocephalic or oculovestibular testing implies that the brainstem is
structurally intact, and the coma is most likely due to structural lesions
affecting both of the hemispheres or a diffuse metabolic process affecting the
hemispheres or brainstem.
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Assess Pupillary Function
Assess resting pupillary size and pupillary responses to light for
diagnostic clues, as follows:
diagnostic clues, as follows:
Bilateral pinpoint (1 mm) pupils suggest a pontine lesion, such
as infarction or hemorrhage. On close inspection, these pupils do constrict to
light.
Bilateral mid-position (4 to 6 mm) pupils that are unreactive to
light can be seen due to midbrain lesions.
A unilaterally dilated pupil, regardless of whether there are
other motor signs of third nerve dysfunction, such as lateral and downward
deviation of the eye, suggests a third nerve palsy (see Chapter
10, Examination of the Pupils, and Chapter 14,
Examination of Eye Movements). In the comatose patient, this suggests
herniation of a unilateral hemispheric mass lesion causing pressure on the
third nerve or its nucleus in the midbrain. A third nerve palsy can also be
seen from other compressive lesions, such as a posterior communicating artery
aneurysm.
Metabolic disorders generally don’t affect the pupils, except for
opiate intoxication, which leads to small pupils that react to light, and
anticholinergic drugs, such as atropine, that may cause dilated and unreactive
pupils.
Assess Motor Function
Observe the patient for spontaneous movements of the extremities
and the presence of abnormal posturing (which may be seen spontaneously or after
noxious stimuli), as follows:
and the presence of abnormal posturing (which may be seen spontaneously or after
noxious stimuli), as follows:
Diminished movement of the extremities on one side of the body
compared to the other suggests a hemiparesis. A hemiparesis can also be
suspected by observing that one of the legs is externally rotated.
Decerebrate (extensor) posturing is characterized by extension of
the arms with extension of the legs. There may also be extension of the neck.
Although posturing is not entirely specific in terms of localization, the
presence of extensor posturing generally suggests severe midbrain or pontine
dysfunction, which may be due to intrinsic brainstem lesions or compression
from a hemispheric mass. Extensor posturing can also rarely be seen in severe
metabolic encephalopathies.
Decorticate (flexor) posturing is characterized by flexion of the
arms with extension of the legs. The presence of flexor posturing generally
suggests higher (e.g., hemispheric) dysfunction than extensor
posturing.
If necessary, assess the patient’s motor response to noxious
stimuli, such as pressing on the nail bed. This may result in reflex motor
patterns consistent with decorticate or decerebrate posturing, which may not
have been otherwise evident spontaneously, or it may result in a more
voluntary type of withdrawal. Although it may be difficult to distinguish
voluntary withdrawal from a purely reflex response, abduction of the shoulder
or hip is likely to be a higher level response.
Assess Breathing Patterns
Most comatose patients are likely to be mechanically ventilated
when you examine them, so the interpretation of breathing patterns is usually
not a significant
part of the diagnostic process. There are
some patterns you should be aware of, however, including the following:
when you examine them, so the interpretation of breathing patterns is usually
not a significant
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part of the diagnostic process. There are
some patterns you should be aware of, however, including the following:
Cheyne-Stokes respirations are
characterized by increasing and decreasing amplitudes of respiration with
intervening apneic periods. Cheyne-Stokes respirations are typically seen due
to bilateral hemispheric or bilateral thalamic dysfunction, including
dysfunction from hypoxia and other metabolic disorders.
Central neurogenic hyperventilation is an uncommon respiratory
pattern diagnosed by the presence of sustained hyperventilation in the absence
of hypoxia or other metabolic causes of hyperventilation. Central neurogenic
hyperventilation has been associated with midbrain or pontine
lesions.
Brain Death
The details of the clinical assessment of brain death are beyond
the scope of this text, but some points are summarized here. Brain death is the
irreversible absence of all function of the brain due to a catastrophic process
involving the entirety of both cerebral hemispheres and the brainstem. In
addition to confirming complete unresponsiveness, much of the clinical
assessment of brain death focuses on confirming the absence of all brainstem
function, including the following findings on bedside testing of brainstem
function:
the scope of this text, but some points are summarized here. Brain death is the
irreversible absence of all function of the brain due to a catastrophic process
involving the entirety of both cerebral hemispheres and the brainstem. In
addition to confirming complete unresponsiveness, much of the clinical
assessment of brain death focuses on confirming the absence of all brainstem
function, including the following findings on bedside testing of brainstem
function:
Absent pupillary responses to light.
Absent eye movements, including absent eye movements to
oculovestibular (caloric) testing bilaterally.
Absent corneal reflexes. To test corneal reflexes, lightly touch
the cornea of one of the patient’s eyes with a cotton swab. The normal
response in the patient with an intact brainstem is to blink both eyes; the
absence of any blink to this maneuver is abnormal. Repeat by touching the
other cornea with the cotton swab.
Absent gag reflex and absent cough to tracheal
suctioning.
No motor responses, including absent spontaneous movements and
the absence of any kind of posturing (decerebrate or decorticate) to noxious
stimuli. Muscle stretch reflexes and Babinski signs, however, may be present,
because these are spinal cord reflexes.
The absence of breathing and respiratory drive. This requires
performing an apnea test* to confirm the absence of any respiratory
drive to hypercarbia at least 20 mm Hg above the baseline PCO2
level.
ADDITIONAL COMMENTS
There is often confusion about the purpose of caloric testing in
coma (some think it is a test for nystagmus). In clinical neurology, caloric
testing is performed only in coma, with the specific intention of looking for
evidence of brainstem function by observing for (normal) conjugate eye deviation
toward the ear that has been infused with cold water. Nystagmus is not an
expected finding when caloric testing is performed in coma. On the other hand,
if caloric testing were performed on a patient who was awake (which we don’t
intend to do), nystagmus would occur, with the fast phase away from the
irrigated ear; this nystagmus would represent an attempt by the brain to
compensate for the slow deviation of the eyes toward the irrigated
ear.
coma (some think it is a test for nystagmus). In clinical neurology, caloric
testing is performed only in coma, with the specific intention of looking for
evidence of brainstem function by observing for (normal) conjugate eye deviation
toward the ear that has been infused with cold water. Nystagmus is not an
expected finding when caloric testing is performed in coma. On the other hand,
if caloric testing were performed on a patient who was awake (which we don’t
intend to do), nystagmus would occur, with the fast phase away from the
irrigated ear; this nystagmus would represent an attempt by the brain to
compensate for the slow deviation of the eyes toward the irrigated
ear.