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Normally, the cerebral cortex triggers another breath within 10 seconds regardless of the PaCO2

1. Periods of "apnea" are actually times when the respiratory amplitude is too low to measure, but the respiratory rhythm is unchanged;

2. Congestive heart failure prolongs the reflex are (blood leaving the lungs takes longer to reach the brain stem than is normal) and may produce this finding without any neurologic dysfunction

When present in patients with brain stem lesions or subarachnoid hemorrhage, CRH is most commonly due to the hypoxia that accompanies neurogenic pulmonary edema. True central neurogenic hyperventilation is rare.

Does not support adequate ventilation (true for all following patterns as well). Isolated lesions at these levels do not produce coma.

is primarily concerned with the maintenance of pH and PaO2 , not PaCO2 . Thus, compensation for a metabolic acidosis produces a pattern resembling central reflex hyperpnea, but the arterial blood gas analysis shows a pH below 7.35, which is indicative of a primary metabolic problem, such as diabetic ketoacidosis. The anatomical correlations of the major respiratory patterns are found in Ta.bie.,,1,:..1. , and the patterns themselves are summarized in Table 1:3 .

Motor Examination. The level of neurological dysfunction is often best defined by the motor examination. If the patient responds to noxious stimuli by any defensive maneuver, such as withdrawal from the stimulus, that patient is not truly comatose. Such a response may be seen in patients whose examinations otherwise suggest no cortical function, presumably because a noxious stimulus powerfully evokes an arousal response. Stereotyped posturing (spontaneous or induced) indicates that the cerebral cortices are no longer in command of the motor system.y The physiological levels of dysfunction are summarized in the motor component of the Glasgow Coma Scale (Table 1-4 ).

Experiments in animals led to the concepts of decorticate and decerebrate rigidity. These terms have produced endless confusion, and these states are perhaps better called by the labels used in the Glasgow Coma Scale: decorticate rigidity is abnormal flexion, and decerebrate rigidity is abnormal extension. Physiologically, these states reflect loss of higher motor control functions, either leaving the rubrospinal system in command (in flexor posturing) or ceding control to the vestibulospinal and reticulospinal systems (in extensor posturing). These postures do not mean that the higher control centers have been destroyed but indicate that they are not functioning. Patients with lateral mass lesions may demonstrate flexor posturing on one side of the body and extensor posturing on the other (usually the side contralateral to the mass; see ChapterJ 5 ).

ASSESSMENT OF AWARENESS

Although the comatose patient, by definition, does not manifest spontaneous eye opening (except in association

TABLE 1-4 -- GLASGOW COMA SCALE

Item

Response

Score

Verbal response

Oriented

5

Confused

4

Inappropriate words

3

Incomprehensible

2

None

1

Eye opening

Spontaneous

4

To speech

3

To pain

2

None

1

Motor

Obeys commands

B

Localizes pain

5

Withdraws

4

Abnormal flexion

3

Abnormal extension

2

None

1

with the vertical eye movements that may accompany a suppression-burst EEG pattern), the presence of spontaneous eye opening and even conjugate eye movements does indicate awareness; these findings are part of the vegetative state, in which the patient has arousal without awareness. Thus, testing for awareness must involve observation for the response to various stimuli and is not practically separable from testing for attention, because inattention to the stimuli chosen could be misinterpreted for unawareness (e.g., failure to respond to verbal commands on the part of a deaf patient). The patient who appears to be awake (i.e., aroused) but fails to attend to any stimuli (internal or external) is identified as lacking awareness.

ASSESSMENT OF ATTENTION

Tests of attention must include several modalities and be presented from both sides of the patient in order to avoid misinterpreting disorders of primary sensation or attention as disordered awareness. Typically, verbal, visual, and somatosensory stimuli are employed. Descriptions of the available tests for attention take up major portions of neuropsychology texts and are beyond the scope of this chapter. Only the basic principles commonly used in bedside screening of patients with impaired consciousness are discussed here.

Patients who are unable to respond to verbal commands (e.g., owing to receptive aphasia) may be able to direct themselves toward a voice or other sound (usually presented contralateral to the nondominant hemisphere). Assessing the response to visual stimuli may require passive eye opening (e.g., in patients with nondominant parietal lesions who have a transient apraxia of eyelid opening). Standardized tests of attention (e.g., the trailmaking test) are valuable in following patients over time, especially in assessing their response to therapy.

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