Assessment of the arousal component of consciousness is an evaluation of the reticular activating system and its connection with the thalamus and the cerebral cortex. Arousal is the lowest level of consciousness, and observation centers on the patient’s ability to respond to verbal or noxious stimuli in an appropriate manner. To stimulate the patient, the nurse should begin with verbal stimuli in a normal tone. If the patient does not respond, the nurse should increase the stimuli by shouting at the patient. If the patient still does not respond, the nurse should further increase the stimuli by shaking the patient. Noxious stimuli should follow if previous attempts to arouse the patient are unsuccessful. To assess arousal, central stimulation should be used (Box 17-2).

Content of consciousness is a higher-level function, and appraisal of awareness is concerned with assessment of the patient’s orientation to person, place, and time. Assessment of content of consciousness requires the patient to give appropriate answers to a variety of questions. Changes in the patient’s answers that indicate increasing degrees of confusion and disorientation may be the first sign of neurological deterioration.1,3,4

The most widely recognized level of consciousness assessment tool is the Glasgow Coma Scale (GCS).5 This scored scale is based on evaluation of three categories: eye opening, verbal response, and best motor response (Table 17-1). The best possible score on the GCS is 15, and the lowest score is 3. A score of 8 or less on the GCS usually indicates coma. Originally, the scoring system was developed to assist in general communication concerning the severity of neurological injury. Recent testing of the GCS revealed a moderate to high agreement rating among physicians and nurses.^6,7 Several points should be kept in mind when the GCS is used for serial assessment. It provides data about level of consciousness only, and it never should be considered a complete neurological examination. It is not a sensitive tool for evaluation of an altered sensorium, nor does it account for possible aphasia. The GCS is also a poor indicator of lateralization of neurological deterioration.⁷ Lateralization involves decreasing motor response on one side or unilateral changes in pupillary reaction.

Initially, the muscles should be inspected for size and shape. The presence of atrophy is noted. Muscle tone is assessed by evaluating the opposition to passive movement. The patient is instructed to relax the extremity while the nurse performs passive range-of-motion movements and evaluates the degree of resistance. Muscle tone is appraised for signs of flaccidity (no resistance), hypotonia (little resistance), hypertonia (increased resistance), spasticity, or rigidity.8

Having the patient perform a number of movements against resistance assesses muscle strength. The strength of the movement is then graded on a 6-point scale (Box 17-3). Ask the patient to extend both arms with the palms turned upward and to hold that position with the eyes closed. If the patient has a weaker side, that arm will drift downward and pronate. The lower extremities are tested by asking the patient to push and pull the feet against resistance or to elevate the legs.^9,10

If the patient is incapable of comprehending and following a simple command, noxious stimuli are necessary to determine motor responses. The stimulus is applied to each extremity separately to allow evaluation of individual extremity function. Peripheral stimulation is used to assess motor function (see Box 17-2).^1,2 Motor responses elicited by noxious stimuli are interpreted differently from those elicited by voluntary demonstration. These responses may be classified as shown in Box 17-4.⁸

Abnormal flexion also is known as decorticate posturing (see Figure 17-1, A). In response to painful stimuli, the upper extremities exhibit flexion of the arm, wrist, and fingers with adduction of the limb. The lower extremity exhibits extension, internal rotation, and plantar flexion. Abnormal flexion occurs with lesions above the midbrain, located in the region of the thalamus or cerebral hemispheres. Abnormal extension also is known as decerebrate rigidity or posturing (see Figure 17-1, B); when the patient is stimulated, teeth clench, and the arms are stiffly extended, adducted, and hyperpronated. The legs are stiffly extended with plantar flexion of the feet. Abnormal extension occurs with lesions in the area of the brainstem. Because abnormal flexion and extension appear similar in the lower extremities, the upper extremities are used to determine the presence of these abnormal movements. It is possible for the patient to exhibit abnormal flexion on one side of the body and extension on the other (see Figure 17-1, C).^1–3 Outcome studies indicate that abnormal flexion or decorticate posturing has a less serious prognosis than does extension, or decerebrate posturing. Onset of posturing or a change from abnormal flexion to abnormal extension requires immediate physician notification.³

Pupil diameter should be documented in millimeters with the use of a pupil gauge to reduce the subjectivity of description. Most people have pupils of equal size, between 2 and 5 mm. A discrepancy up to 1 mm between the two pupils is normal; it is called anisocoria and occurs in 16% to 17% of the human population.11 Change or inequality in pupil size, especially in patients who previously have not shown this discrepancy, is a significant neurological sign. It may indicate impending danger of herniation and should be reported immediately. With the location of the oculomotor nerve (CN III) at the notch of the tentorium, pupil size and reactivity play a key role in the physical assessment of intracranial pressure (ICP) changes and herniation syndromes. In addition to CN III compression, changes in pupil size occur for other reasons. Large pupils can result from the instillation of cycloplegic agents, such as atropine or scopolamine, or can indicate extreme stress. Extremely small pupils can indicate opioid overdose, lower brainstem compression, or bilateral damage to the pons.^11,12

Pupil shape is included in the assessment of pupils. Although the pupil is normally round, an irregularly shaped or oval pupil may be observed in patients who have undergone eye surgery. Initial stages of CN III compression from elevated ICP can cause the pupil to have an oval shape.^1,11

The pupillary light reflex depends on optic nerve (CN II) and oculomotor nerve (CN III) function (Figure 17-2).^3,11 The technique for evaluation of the pupillary light response involves use of a narrow-beamed bright light shined into the pupil from the outer canthus of the eye. If the light is shined directly onto the pupil, glare or reflection of the light may prevent the assessor’s proper visualization. Pupillary reaction to light is identified as brisk, sluggish, or nonreactive or fixed.¹ Each pupil should be evaluated for direct light response and for consensual response. The consensual pupillary response is constriction in response to a light shined into the opposite eye. This reflex occurs as a result of the crossing of nerve fibers at the optic chiasm.¹ Evaluation of consensual response is necessary to rule out optic nerve dysfunction as a cause for lack of a direct light reflex. Because the optic nerve is the afferent pathway for the light reflex, shining a light into a blind eye produces neither a direct light response in that eye nor a consensual response in the opposite eye. A consensual response in the blind eye produced by shining a light into the opposite eye demonstrates an intact oculomotor nerve. Oculomotor compression associated with transtentorial herniation affects the direct light response and the consensual response in the affected pupil.^1,2,11,12

In the conscious patient, the function of the three cranial nerves of the eye and their MLF innervation can be assessed by asking the patient to follow a finger through the full range of eye motion. If the eyes move together into all six fields, extraocular movements are intact (Figure 17-3).¹

In the unconscious patient, assessment of ocular function and innervation of the MLF is performed by eliciting the doll’s eyes reflex. If the patient is unconscious as a result of trauma, the nurse must ascertain the absence of cervical injury before performing this examination. To assess the oculocephalic reflex, the nurse holds the patient’s eyelids open and briskly turns the head to one side while observing the eye movements and then briskly turns the head to the other side and observes. If the eyes deviate to the opposite direction in which the head is turned, the doll’s eyes reflex is present, and the oculocephalic reflex arc is intact (Figure 17-4, A). If the oculocephalic reflex arc is not intact, the reflex is absent. This lack of response, in which the eyes remain midline and move with the head, indicates significant brainstem injury (Figure 17-4, C). The reflex may also be absent in severe metabolic coma. An abnormal oculocephalic reflex is present when the eyes rove or move in opposite directions from each other (Figure 17-4, B). Abnormal oculocephalic reflex indicates some degree of brainstem injury.^1–3

The oculovestibular reflex is performed by a physician, often as one of the final clinical assessments of brainstem function. After confirmation that the tympanic membrane is intact, the head is raised to a 30-degree angle, and 20 to 100 mL of ice water is injected into the external auditory canal. The normal eye movement response is a conjugate, slow, tonic nystagmus deviating toward the irrigated ear and lasting 30 to 120 seconds. This response indicates brainstem integrity. Rapid nystagmus returns the eyes back to the midline only in a conscious patient with cortical functioning (Figure 17-5).¹ An abnormal response is disconjugate eye movement, which indicates a brainstem lesion, or no response, which indicates little or no brainstem function. The oculovestibular reflex may be temporarily absent in reversible metabolic encephalopathy.³ This test is an extremely noxious stimulation and may produce a decorticate or decerebrate posturing response in a comatose patient. In the conscious patient, this procedure may produce nausea, vomiting, or dizziness.^1,12

Changes in respiratory patterns assist in identifying the level of brainstem dysfunction or injury. Evaluation of the respiratory pattern must include assessment of the effectiveness of gas exchange in maintaining adequate oxygen and carbon dioxide levels (Table 17-2). Hypoventilation is not uncommon in the patient with an altered level of consciousness. Alterations in oxygenation or carbon dioxide levels can result in further neurological dysfunction. ICP increases with hypoxemia or hypercapnia.^1–3

Evaluation of the respiratory function in a patient with a neurological deficit must include assessment of airway maintenance and secretion control. Cough, gag, and swallow reflexes responsible for protection of the airway may be absent or diminished.13

A common manifestation of intracranial injury is systemic hypertension. Cerebral autoregulation, responsible for the control of cerebral blood flow (CBF), frequently is lost with any type of intracranial injury. After cerebral injury, the body often is in a hyperdynamic state (increased heart rate, blood pressure, and cardiac output) as part of a compensatory response. With the loss of autoregulation as blood pressure increases, CBF and cerebral blood volume increase, and ICP therefore increases. Control of systemic hypertension is necessary to stop this cycle, but caution must be exercised. The mean arterial pressure must be maintained at a level sufficient to produce adequate CBF in the presence of elevated ICP. Attention must also be paid to the pulse pressure because widening of this value may occur in the late stages of intracranial hypertension.13

The medulla and the vagus nerve provide parasympathetic control to the heart. When stimulated, this lower brainstem system produces bradycardia. Sympathetic stimulation increases the rate and contractility.14 Various intracranial pathologies and abrupt ICP changes can produce bradycardia, premature ventricular contractions (PVCs), QT changes, and myocardial damage.^14,15

Cushing’s triad is a set of three clinical manifestations (bradycardia, systolic hypertension, and widening pulse pressure) related to pressure on the medullary area of the brainstem. These signs often occur in response to intracranial hypertension or a herniation syndrome. The appearance of Cushing’s triad is a late finding that may be absent in patients with neurological deterioration. Attention should be paid to alteration in each component of the triad and intervention initiated accordingly.3

The four sites for monitoring ICP are the intraventricular space, the subarachnoid space, the epidural space, and the parenchyma (Figure 17-7). Each site has advantages and disadvantages for monitoring ICP (Table 17-5). The type of monitor chosen depends on the suspected pathological condition and physician’s preferences.^16,17 Nursing considerations for each type of device are discussed in Table 17-5.

The ICP pulse waveform is observed on a continuous, real-time pressure display, and it corresponds to each heartbeat. The waveform arises primarily from pulsations of the major intracranial arteries but also receives retrograde venous pulsations.16,17

Normal Intracranial Pressure Waveform

The normal ICP wave has three or more defined peaks (Figure 17-8). The first peak (P1) is called the percussion wave. Originating from the pulsations of the choroid plexus, it has a sharp peak and is fairly consistent in its amplitude. The second peak (P2) is called the tidal wave. The tidal wave varies more in shape and amplitude, ending on the dicrotic notch. The P2 portion of the pulse waveform has been most directly linked to the state of decreased compliance. When the P2 component is equal to or higher than P1, decreased compliance occurs (Figure 17-9). Immediately after the dicrotic notch is the third wave (P3), which is called the dicrotic wave. After the dicrotic wave, the pressure usually tapers down to the diastolic position, unless retrograde venous pulsations add a few more peaks.^16–19

A, B, and C pressure waves are not true waveforms (Figure 17-10). Rather, they are the graphically displayed trend data of ICP over time. These waves reflect spontaneous alterations in ICP associated with respiration, systemic blood pressure, and deteriorating neurological status.

Measuring CBF in the clinical setting is difficult, but at the bedside, an estimated pressure of cerebral perfusion can be derived. Cerebral perfusion pressure (CPP) is the blood pressure gradient across the brain, and it is calculated as the difference between the incoming mean arterial pressure (MAP) and the opposing ICP on the arteries (see Appendix B).

The CPP in the average adult is approximately 80 to 100 mm Hg, with a range of 60 to 150 mm Hg. The CPP must be maintained near 80 mm Hg to provide adequate blood supply to the brain. If the CPP drops below this point, ischemia may develop. A sustained CPP of 30 mm Hg or less usually results in neuronal hypoxia and cell death. When the mean systemic arterial pressure equals the ICP, CBF may cease.^1–3

The measurements of CBF and CPP do not address the brain’s metabolic need for oxygen. Active neurons require greater amounts of oxygen than those that are inactive. The determination that CBF matches the brain’s metabolic needs is expressed as cerebral metabolic rate (CMRO₂), the normal value of which is 3.4 mL per 100 g of brain tissue per minute. Neuronal demand for oxygen is governed by the metabolic rate. For technical reasons, this value is not easily attained, although it can be calculated. It is the product of the measured CBF and calculated arteriojugular oxygen difference (AJDO₂) (see Appendix B).²⁰

CBF can be measured using a variety of complex techniques (e.g., PET, SPECT). Most recently, continuous bedside monitoring of regional cerebrocortical blood flow has become available.⁸ Arteriojugular oxygen difference is the amount of oxygen extracted by the brain, and it is reflected in the difference between the arterial oxygen content and the jugular venous oxygen content. The normal value is 5.0 to 7.5 vol%.²⁰

One method of measuring CBF allows continuous measurement of oxygenation within the jugular venous system through the use of the jugular bulb monitor. Jugular venous oxygen saturation (SjvO₂) can be used to reflect cerebral oxygen supply-and-demand balance. Any disorder that increases CMRO₂ or decreases oxygen delivery may decrease SjvO₂, and conversely, any disorder that that decreases CMRO₂ or increases oxygen delivery may increase SjvO₂.20,21

To measure SjvO₂ a fiberoptic catheter is placed retrograde through the internal jugular vein into the jugular bulb and attached to a bedside monitor. The normal value is 60% to 80%. Patients with values less than 50% and 55% are hypoxemic or oligemic (low CBF compared with metabolic rate). Oligemia occurs as a result of decreased blood flow due to hypotension, vasospasm, or intracranial hypertension or as a result of increased brain metabolic requirements due to fever or seizures.^20,21 SjvO₂ values below 45% are indicative of severe cerebral hypoxia.²⁰ Patients with values above 75% to 80% are considered hyperemic (high CBF compared with metabolic need). SjvO₂ also increases if the brain is so severely injured the neurons are unable to extract oxygen.^20,21

SjvO₂ monitoring has several limitations. SjvO₂ is a global measure of cerebral oxygenation, and a normal SjvO₂ value does not rule out localized areas of cerebral ischemia.^20,21 Readings are affected by the movement of the patient’s head.²¹ Up to 50% of low SjvO₂ readings are false, which may be caused by technical issues with the catheter, particularly catheter migration.²² For accurate reading, the tip of the catheter must be within 1 cm of the jugular bulb.²¹

Over the past few years, a new device has become available to measure the partial pressure of oxygen within brain tissue (PbtO₂). The device consists of a monitoring probe on the end of a catheter, which is inserted into the brain parenchyma and attached to a bedside monitor. The probe may be inserted into the damaged portion of the brain to measure regional oxygenation or inserted into the undamaged portion of the brain to measure global oxygenation. One risk associated with insertion of the catheter is bleeding with hematoma formation.23 Although there is no consensus on normal values because they vary from device to device, it has been concluded that the probability of death increases with prolonged periods of PbtO₂ less than 15 mm Hg and any episode of PbtO₂ less than 6 mm Hg.²³

In the head-injured patient, the goal of treatment is to maintain the PbtO₂ greater than 20 mm Hg. Factors that decrease PbtO₂ include tissue hypoxia, hypocapnia, hypovolemia, decreased blood pressure, low hemoglobin levels, intracranial hypertension, and hyperthermia.²⁴ Treatment is directed at the underlying cause.