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Acute depression in level of consciousness is a critical, life-threatening emergency that requires a
systematic approach for evaluation of etiology. The variety of causes of  are myriad.
Therefore, a reliable history should be obtained from family, witnesses, or medical personnel, and
examination should seek representative localizing neurological and general physical findings.

Clues can be ascertained from the onset of . An acute onset in a previously healthy
individual may indicate a cerebral vascular etiology (i.e., subarachnoid hemorrhage, intracerebral
hemorrhage, or hemispheric or brain stem stroke), generalized epileptic activity, traumatic brain
injury, or drug overdose. Likewise, a subacute deterioration may point to systemic illness, evolving
intracranial mass, or a degenerative infectious or paraneoplastic neurologic disorder. Moreover,
the duration of a comatose state should be documented because it may have predictive value for
prognosis in certain causes.

Frequently the etiology of acute depression in consciousness in the hospitalized patient includes
sepsis, acid-base and electrolyte disorders, or hepatic, renal, or cardiac failure. Therefore careful
physical examination is performed with attention to vital signs, spontaneous breathing pattern,
and careful auscultation of the lungs and heart (Table 67-3). Airway patency and protective
reflexes should be assessed. Emergency measures should be taken to ensure vital functions
continue despite an obscure diagnosis. Furthermore, laboratory studies should be obtained to
exclude metabolic and endocrine causes.


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During evaluation, core body temperature is an important clue. Hypothermia can be seen in drug
overdose, brain death, or acute spinal cord transection. Moreover, hyperthermia can be seen in
infection; traumatic brain injury; subarachnoid, intracerebral, or pontine hemorrhage; and
hypothalamic dysfunction.

The neurologic exam in a patient with depressed level of consciousness can be a valuable tool to
localize the etiology. The important neurologic features include (Table 67-4): (1) respiratory
pattern, (2) pupillary size and reactivity, (3) eye position and movements, (4) corneal reflexes,
and (5) motor function.

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The determination of the level of consciousness depends on analyzing arousability and content
(see Table 67-1). Initially, observe whether the patient appears asleep or wakeful with
spontaneous eye opening. In a sleeping patient, quantify how much stimulation is required to
arouse the patient. Attempts should be made to elicit a behavioral response by verbal command
alone. If no response is obtained, then physical stimulation should be used, first by shaking the
patient. Then noxious stimulation can be applied by digital pressure to the supraorbital nerves or
nailbeds of the fingers or toes. Purposeful attempts by the patient to remove the offending
stimulus indicate preservation of brain stem function and intact connections to the appropriate
cerebral hemisphere. Eye opening, either spontaneous or in response to stimulation, indicates
preserved function of the RAS in the upper brain stem and hypothalamus. Once aroused, the
patient's ability to remain wakeful and respond coherently is determined.

Lethargy (or drowsiness), stupor, and  represent different points on a continuum of
decreasing levels of consciousness. Patients in these states appear to be sleeping with eyes
closed. In contrast, patients with akinetic mutism and locked-in syndrome appear to be awake
with eyes opened.

The Glasgow
 Scale (Table 67-5) is used to assign a numerical description of consciousness.
The scale was devised to evaluate patients with head injury and is most reliable and reproducible
in trauma patients.16,17 Its application in nontraumatic conditions is less reliable, but it is still the
most widely used clinical scale to evaluate the level of consciousness. Furthermore, it provides a
reproducible tool to monitor progression.

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The cerebral cortex and forebrain are important in the control of regular respiration. Patients with
isolated brain injury uncomplicated by other critical medical illnesses may have characteristic
breathing patterns that aid in neuroanatomic localization (Fig. 67-1). However, these patterns are
not reliable in patients with multiple organ system failure who are receiving mechanical
ventilation. Nevertheless, a discussion is warranted.
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‰% Respiratory patterns in .

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Cheyne-Stokes respiration is a periodic breathing pattern in which periods of hyperpnea regularly
alternate with apnea in a smooth crescendo-decrescendo pattern. This neurogenic respiratory
alteration occurs with damage to the cortex and forebrain bilaterally, or secondary to cardiac or
respiratory failure. It is the result of the loss of frontal lobe control over respiratory patterns with
excessive dependence on blood CO2 levels to trigger brain stem respiratory centers.

Midbrain and upper pontine lesions may cause a central neurogenic hyperventilation syndrome
with persistent deep hyperventilation. It can only be diagnosed with arterial blood gas
measurements, since hyperventilation also occurs secondary to hypoxemia and acidemia.
Likewise, metabolic disorders, especially the early stages of hepatic , cause central
neurogenic hyperventilation.

Lesions of the middle or lower pons are characterized by deep prolonged inspiration followed by a
long pause referred to as ˜ 
˜  . Most patients with this respiratory pattern require
early intubation and mechanical ventilation.

Ataxic and irregular periodic breathing occurs with lesions in the dorsomedial medulla and may be
accompanied by hypersensitivity to respiratory depressants. These patterns are not compatible
with sustained life.

When assessing a comatose patient, the rate and pattern of respiration should be observed. In
addition, vomiting and hiccups should be noted because they may result from intrinsic brain stem
pathology or transmitted pressure on the brain stem. Furthermore, spontaneous yawning may
occur in comatose patients. The neurogenic networks for this complex respiratory response are
integrated in the lower brain stem.

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In one study of 346 comatose patients, the pupillary reflex was shown to be the strongest
prognostic variable for awakening when compared with evoked-potential studies.18 Pupillary size is
controlled by the autonomic nervous system and is dictated by the balance between sympathetic
and parasympathetic input to the pupillary dilators and constrictors, respectively. The
parasympathetic efferents to the pupil originate from the Edinger-Westphal nucleus in the upper
midbrain and travel with the ipsilateral third cranial nerve (oculomotor). Dysfunction within this
pathway will produce unopposed sympathetic input to the pupil and relative pupillary dilation
ipsilateral to the lesion. The sympathetic efferents to the pupil originate in the hypothalamus,
descend through the brain stem and cervical spinal cord, and exit the upper thoracic spinal cord
(T1 to T3 levels). From this point they ascend the carotid sheath and follow the vasculature to the
pupil. Any disruption of the sympathetic fibers along this loop can lead to unopposed
parasympathetic pupillary activity and subsequently an ipsilateral small (miotic) pupil.

A light stimulus to one eye produces constriction of the ipsilateral pupil (direct response) and
contralateral pupil (consensual response), through a network of connections. Table 67-
6 summarizes the pupillary changes commonly seen in  and their significance.

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Small reactive pupils may be due to a toxic-metabolic disturbance. Very small pupils (pinpoint)
that react to naloxone are characteristic of narcotic overdose. Pinpoint pupils that are poorly
reactive are characteristic of pontine dysfunction. Lesions rostral or caudal to the midbrain may
disrupt descending sympathetics and produce small pupils.

Bilateral, widely dilated, fixed pupils are due to sympathetic overactivity from an endogenous
cause (seizures or severe anoxic ischemia) or exogenous catecholamines
(dopamine or norepinephrine) or atropine-like drugs.

Since the midbrain is the one location in the brain stem where parasympathetic and sympathetic
pupillary fibers are adjacent, a midbrain lesion classically results in intermediate pupil size. Such
pupils are seen in brain death and severe midbrain injuries.
A unilaterally dilated, unreactive pupil in a comatose patient may be caused by herniation of the
ipsilateral temporal uncus through the tentorium, which compresses the ipsilateral oculomotor
nerve and its parasympathetic fibers. In this setting, the large pupil is eventually accompanied by
other evidence of cranial nerve (CN) III disruption (i.e., ipsilateral eye deviation inferolaterally). In
the setting of head trauma, this implies an ipsilateral epidural, subdural, or intracerebral
hematoma. In nontraumatic conditions, it usually occurs with large cerebral infarcts, spontaneous
intracerebral hematoma, or supratentorial brain tumors.

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The eye muscles are controlled by three sets of cranial nerves, CN III, CN IV (trochlear), and CN
VI (abducens), their nuclei being located in the upper midbrain, lower midbrain, and
pontomedullary junction, respectively. Proper eye movement control requires a network of
interconnections between these nuclei so that the eyes move conjugately. This interconnection is
referred to as the medial longitudinal fasciculus (MLF), which is also integrated with the vestibular
nuclei and allows for reflex conjugate eye movement in response to positional head changes.

Figure 67-2 displays the relevant anatomy accounting for horizontal conjugate eye movements.
Each frontal eye field controls gaze to the contralateral side by stimulating the contralateral
pontine paramedian reticular formation (PPRF) at the pontomedullary junction. Lesions of the
frontal eye fields or the PPRFs lead to conjugate eye deviation, provided that the MLF is intact.
Therefore, a lesion of the right frontal eye field or left PPRF impairs leftward gaze, and thus the
eyes conjugately deviate to the right. In short, the eyes turn toward the lesion with frontal eye
field dysfunction and away from the lesion with PPRF dysfunction. In contrast, MLF lesions are
manifested as poor adduction of the eye ipsilateral to the MLF lesion. Spontaneous "roving" eye
movements in all directions in the comatose patient demonstrate integrity of a significant portion
of the brain stem. If no spontaneous eye movements are observed, the intactness of the
interconnections responsible for eye control is in question. Since comatose patients are unable to
follow commands, maneuvers that take advantage of vestibular input to ocular control must be
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‰% Schematic representation of the neurologic pathways controlling horizontal conjugate gaze.
PPRF, pontine paramedian reticular formation; MLF, median longitudinal fasciculus; CN III, third

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cranial nerve; 1±4, sites of possible pathologic lesions (see text).

An oculocephalic reflex (doll's eye maneuver) is performed by rapidly rotating the head from side
to side and observing the patient's eye positional changes (Fig. 67-3). The normal response in the
comatose patient with intact brain stem is for the eyes to remain fixed on the same point in space.
Thus when the head is turned rightward, the eyes move to the left. When the head is turned
leftward, the eyes move conjugately to the right. If a comatose patient does not have normal
doll's eyes, a disruption of brain stem ocular and vestibular connections may be present. Of
course, in the setting of trauma, the head should not be rotated due to the possibility of cervical
spine injury. In this situation or when doll's eye maneuvers are inconclusive, cold water calorics
are helpful.
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‰% Eye positions in the doll's eye maneuver and with cold caloric testing in . MLF, median

longitudinal fasciculus; PPRF, pontine paramedian reticular formation.

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Oculovestibular reflexes (cold water caloric testing) depend on vestibular system stimulation by
altering endolymphatic flow in the semicircular canals. The change in endolymphatic flow is
achieved by instilling ice-cold water in the external auditory canal, thereby cooling the mastoid
process, and in turn the semicircular canal. Prior to performing this test, the external auditory
canal should be examined to confirm intactness of the tympanic membrane and remove any
impacted cerumen. The head should then be elevated 30 degrees. A functional apparatus for
instilling the water is a butterfly catheter (with the needle removed) connected to a syringe
containing approximately 100 mL of cold water.

The responses to cold water in patients with various lesions are summarized in Fig. 67-3. In
normal wakeful patients the response is horizontal nystagmus, with the slow phase toward and the
fast phase away from the stimulated side and with minimal eye movement from the midline. With
diminishing consciousness in patients without structural brain stem damage, the fast phase of the
nystagmus disappears, and the eyes tend to deviate conjugately toward the stimulated side.
Structural brain stem disease eliminates the caloric response, as does inner ear disease, deep
drug , and anticonvulsant drug overdose. In order to ensure proper interpretation of cold
water caloric testing, the opposite side should not be stimulated until 5 minutes after the initial

The corneal reflex is an important protective mechanism for the cornea. it is a blinking reflex
triggered when the cornea is presented with a noxious stimulus. The afferent limb is via the
trigeminal nerve (CN V), and the efferent limb is via the facial nerve (CN VII). Although corneal
reflexes assess brain stem function, they have limited localizing value.

The corticospinal tract predominantly originates from the frontal cortex and descends ipsilaterally
through the corona radiata, the posterior limb of the internal capsule, and the cerebral peduncle of
the midbrain and consolidates in the pyramids, the ventral swellings of the medulla. The pyramidal
fibers decussate to the contralateral side at the junction of the medulla and spinal cord to form the
lateral corticospinal tract.

Observation is the key to the motor examination in the comatose patient. The patient is observed
for spontaneous movements or maintenance of particular postures. Lesions involving the
corticospinal tract generally lead to diminished contralateral spontaneous activity. Upper midbrain
or more rostral lesions may lead to decorticate posturing characterized by flexion of the
contralateral arm at the elbow and hyperextension of the leg. Central midbrain and high pontine
lesions, with a relatively intact brain stem inferiorly, may lead to decerebrate posturing
characterized by contralateral arm and leg extension. Such posturing may also be caused by
structural lesions or metabolic insults and it is often mistaken for seizure activity. The patient
should be observed for the presence of tremor, myoclonus, or asterixis, because these may be
associated with toxic-metabolic encephalopathies.

After observing for spontaneous movements and posturing, motor tone should be assessed by
passive flexion and extension of the extremities. Tone may be increased or decreased, depending
on the location of the motor system involvement. Afterward, noxious stimuli should then be
applied to each limb and the supraorbital regions. Purposeful movement upon noxious stimulation
suggests intactness of motor tracts to that limb, whereas decorticate or decerebrate posturing in
response to noxious stimuli has the localizing significance mentioned above.
Acute corticospinal tract lesions may cause hyporeflexia because hyperreflexia may not occur for
days to weeks after the injury. However, a Babinski sign, which is characterized by extension of
the great toe and fanning of the other toes upon lateral plantar stimulation, may be present
acutely with corticospinal tract lesions. Complete bilateral paralysis without any response to
noxious stimuli usually indicates a grave prognosis. However, spinal cord injury and
neuromuscular transmission blockade must be excluded because they may produce a similar state
of complete paralysis.