A neurological examination is performed to assess the etiology of unconsciousness. The goal is to determine whether there is a bihemispheric process or a reticular activating system problem, and particular attention is paid to signs of herniation ( Brock..and...lBj.§ckll199.5).

One neurological cause of pseudocoma that needs to be excluded immediately is the 'locked-in' state ( Hawkes 1974). In this condition, which is usually due to pontine infarction or hemorrhage, all cortical control except that of vertical gaze is disconnected. Often the patient is only able to look upward, but may not even be capable of opening the eyelids. If, after the eyelids are opened, the patient can follow the command to look up, he or she is not comatose but locked in, and needs studies directed towards identifying a pontine lesion.

Pupillary responses

The pupils should be examined, preferably with a bright light in a darkened room. The pupillary light reflex requires intact sympathetic and parasympathetic systems to dilate and constrict respectively. The key paradigm to remember is that damage to the midbrain affects both the reticular activating system and pupil reactivity, whereas metabolic disease produces coma but usually leaves the light reflex intact ( Plum and Posner.1982).

Specific structural lesions produce particular pupillary patterns. Hypothalamic lesions, either by direct involvement or secondary to increased pressure from above, interrupt the efferent sympathetic pathways, producing small reactive pupils. Unilateral diencephalic dysfunction may cause Horner's syndrome of unilateral pupillary constriction and ptosis, which may be a an early sign of herniation. Dorsal midbrain damage interrupts the parasympathetic efferents, and the pupils become slightly large and unreactive but may spontaneously fluctuate in size (hippus). Central midbrain lesions damage both sympathetic and parasympathetic tracts, producing fixed, often irregular, midposition pupils. This is most frequently seen in the setting of true transtentorial herniation and generally implies a poor outcome. Pontine lesions, usually hemorrhagic, interrupt the descending sympathetic fibers and irritate the parasympathetic fibers, producing pinpoint pupils. More caudal lesions affect only the sympathetic system, again causing Horner's syndrome. Finally, a unilateral fixed dilated pupil suggests third-nerve compression and herniation ( Plum and...

Small reactive pupils are the hallmark of drug intoxication, particularly by opiates, and metabolic disease, but there are a few exceptions. The light reflex is usually resistant to metabolic disease, but it may be suppressed in the setting of severe drug overdose, particularly barbiturates. Severe opiate intoxication may mimic the pinpoint pupils of pontine hemorrhage. Anticholinergics may produce large unreactive pupils associated with altered mental status, as may glutethemide intoxication. Anoxia may cause fixed dilated pupils, which become reactive if cerebral oxygen delivery is restored in time.

Eye movements

If purposeful movements, such as visual tracking movements looking toward a loud noise, are absent, check for spontaneous roving eye movements. Roving movements are often seen with metabolic encephalopathies. All these findings imply intact cortical control of the brainstem. A fixed deviation of the eyes usually means that there is a hemispheral lesion on the side towards which the eyes deviate, often associated with a contralateral hemiparesis. Isolated pontine lesions affecting the conjugate gaze centers cause paresis of gaze toward the damaged side, often associated with ipsilateral facial paresis and contralateral weakness of the arm and leg. A fixed downward gaze is seen with midbrain compression from above. Inability of one eye to move medially is seen with upper brainstem lesions to the medial longitudinal fasciculus on the side of the abnormal eye, and is called an internuclear ophthalmoplegia.

If no spontaneous movement is found, the cervico-ocular reflex should be tested (doll's eyes maneuver); an important caveat is to ensure prior to testing that there is no possibility of a cervical cord or spine lesion. The reflex is tested by rapidly turning the head from midline to one side and observing the eye movements. In the intact brainstem this produces a contralateral conjugate eye movement, the net effect of which is to keep the eyes seemingly fixed on a point in space. After a few moments the eyes should return to midposition. The head should then be turned in the opposite direction to check for symmetry of the response. Failure of the reflex in either direction implies brainstem dysfunction. The reflex also works in the vertical plane and should be tested in a similar fashion. If this maneuver fails or is untestable because of neck injury, the vestibular-ocular reflex may be assessed by caloric testing. This is done by elevating the patient's head to 30°, if possible, and rapidly instilling about 50 ml of ice water with a syringe. It is important to check first that the ear canal is clear and that the tympanic membrane is not damaged, which is a relative contraindication to the test. Cold water instilled against the tympanic membrane produces cooling of the adjacent semicircular canal, increasing the local density of the endolymph, and creating a net flow towards the cooler side. This direction of flow mimics the head turning away from the stimulated side, and therefore causes reflex slow eye movement towards the stimulus. In an intact brain, the frontal eye fields attempt to override this brainstem-driven tonic eye deviation, producing rapid saccades away from the stimulus (nystagmus), but with cortical damage the eyes will maintain a fixed deviation. Cold caloric testing is a potent stimulus to the brainstem and may produce gaze deviation even when head turning fails to do so. The key observation is that whenever conjugate gaze occurs, regardless of the stimulus, it implies an intact brainstem in the region of the reticular activating system ( P!uml.l.andl.lPosn§L.1982).

Eye deviation from hemispheral lesions can usually be overcome by these maneuvers, whereas with pontine lesions the eyes will not cross midline. Total lack of response can be seen with severe brainstem dysfunction, drug ingestion (particularly barbiturates, narcotics, and phenytoin), neuromuscular blockade, or bilateral vestibular lesions (PIum,..l§ndlE0§n®Ll982.).

Motor responses

The patient is observed for spontaneous movement or, if none is present, response to stimulus. The type of motor response and its symmetry provide important clues to assessing the location and severity of focal deficits. Any asymmetry of the motor patterns suggests a contralateral focal cerebral lesion. Comatose patients may show purposeful movements, such as reaching for their endotracheal tube or localizing painful stimuli, which require an intact sensory system, an efferent motor system, and cortical processing. Patients who cannot localize pain may withdraw from focal stimuli, again requiring functioning afferent and efferent tracts.

Abnormal motor responses include decorticate and decerebrate posturing. Decorticate posturing consists of flexion of the arms and extension of the legs, while in decerebrate posturing both the arms and the legs extend. The important principle of localization is that both forms of abnormal posture can occur with hemispheral as well as brainstem lesions. Prognostically, decerebrate posturing is worse than decorticate posturing. Any comatose patient who develops either form of abnormal posturing needs intervention for acute worsening.

Extension of the arms with weak flexion of the legs or absent leg movement implies severe structural damage of the pontine tegmentum. This finding indicates severe brainstem dysfunction and carries a grave prognosis (Turazziand Blicolo . .. .1977). Total loss of tone does not necessarily mean upper brainstem damage and can be associated with spinal cord or medullary transection (spinal shock), peripheral nerve injury or disease, or neuromuscular blockade.

Finally, care must be taken not to confuse reflex activity with other responses. In particular, triple flexion of the lower extremity is a reflex signaling upper motor neuron dysfunction. It may look like spontaneous movement of the leg away from painful stimuli, but it is a reflex; the important finding is that the reflex response is very rapid and stereotyped.


Respiration is controlled by brainstem structures with mediation by cortical influences, and specific respiratory patterns have localizing value ( Brockand BJ.§£k..19.9.5.).

Unfortunately, these patterns are often not noticed in patients receiving mechanical ventilatory support. The most common abnormal respiratory pattern is Cheyne-Stokes respiration, in which there is a sequential waxing and waning of tidal volume, including periods of apnea. It can be seen in non-comatose patients with congestive heart failure, hypoxia, or occasionally during normal sleep, and is associated with bihemispheric dysfunction in unconscious patients. Respiratory centers in the brainstem increase or decrease the respiratory rate in response to elevated or lowered PaCO2 levels respectively. However, there is frontal lobe control such that, even with very low PaCO2 levels, respiration does not stop but only slows, with a reduced tidal volume, until the PaCO2 normalizes. When bihemispheric dysfunction is present on a structural or metabolic basis, the modulating influence of the cortex is lost and Cheyne-Stokes respiration is seen.

Damage to the upper brainstem reticular formation is reported to cause sustained hyperventilation, called central neurogenic hyperventilation or central reflex hyperpnea. Tachypnea is often seen in comatose patients, but other causes, particularly hypoxia, neurogenic pulmonary edema, or metabolic disarray, are more likely. Diagnosis of true central neurogenic hyperventilation requires an increased PaO2 and a decreased PaCO2, without other metabolic changes or drug intoxication.

Apneustic, cluster, and ataxic breathing are patterns associated with lesions of the mid-lower pons, upper medulla, and caudal medulla respectively, and all provide inadequate ventilation so that mechanical support is needed. With apneusis, a patient has a prolonged inspiratory pause, or respiration may consist of cycles of quick inhalation-pause-exhalation-pause. Cluster breathing consists of several rapid shallow breaths followed by a pause, while ataxic breathing is irregular brief respirations of small random tidal volume. Finally, apnea is of poor localizing value and may be seen secondary to cardiac arrest, multifocal brain lesions, drug overdose, spinal cord transection, or primary pulmonary process.

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