Alterations in Arousal

Alterations in level of arousal may be caused by structural, metabolic, or psychogenic (functional) disorders.

Pattern of Breathing

Respiratory patterns help to evaluate level of brain dysfunction and level of coma. Rate, rhythm, and pattern of breathing should be assessed. The breathing patterns can be categorized as hemispheric or brainstem breathing patterns (Table 17-4 and Figure 17-1).

TABLE 17-4

PATTERNS OF BREATHING

BREATHING PATTERN	DESCRIPTION	LOCATION OF INJURY
Hemispheric Breathing Patterns
Normal	After a period of hyperventilation that lowers the arterial carbon dioxide pressure (Paco2), the individual continues to breathe regularly but with a reduced depth.	Response of the nervous system to an external stressor—not associated with injury to the CNS
Posthyperventilation apnea	Respirations stop after hyperventilation has lowered the Pco2 level below normal. Rhythmic breathing returns when the Pco2 level returns to normal. (Usually an intact cerebral cortex will trigger breathing within 10 seconds regardless of Pco2.)	Associated with diffuse bilateral metabolic or structural disease of the cerebrum
Cheyne-Stokes respirations	Breathing pattern has a smooth increase (crescendo) in the rate and depth of breathing (hyperpnea), which peaks and is followed by a gradual smooth decrease (decrescendo) in the rate and depth of breathing to the point of apnea when the cycle repeats itself. The hyperpneic phase lasts longer than the apneic phase (represents an amplitude change).	Bilateral dysfunction of the deep cerebral or diencephalic structures; seen with supratentorial injury and metabolically induced coma states unrelated to neurologic dysfunction; may see also in CHF
Brainstem Breathing Patterns
Central reflex hyperpnea (central neurogenic hyperventilation)	A sustained deep rapid but regular pattern (hyperpnea) occurs, with a decreased Paco2 and a corresponding increase in pH and increased Po2.	May result from CNS damage or disease that involves the lower midbrain and upper pons; seen after increased intracranial pressure and blunt head trauma
Apneusis	A prolonged inspiratory cramp (a pause at full inspiration) occurs. A common variant of this is a brief end-inspiratory pause of 2 or 3 seconds, often alternating with an end-expiratory pause.	Indicates damage to the respiratory control mechanism located at the pontine level; most commonly associated with pontine infarction but documented with hypoglycemia, anoxia, and meningitis
Cluster breathing	A cluster of breaths has a disordered sequence with irregular pauses between breaths.	Dysfunction in the lower pontine and high medullary areas
Ataxic breathing	Completely irregular breathing occurs, with random shallow and deep breaths and irregular pauses. Often the rate is slow.	Originates from a primary dysfunction of the lower pons or upper medulla
Gasping breathing pattern (agonal gasps)	A pattern of deep “all-or-none” breaths is accompanied by a slow respiratory rate.	Indicative of a failing medullary respiratory center

CHF, Congestive heart failure; CNS, central nervous system.

With normal breathing, a neural center in the forebrain (cerebrum) produces a rhythmic breathing pattern. When consciousness decreases, lower brainstem centers regulate the breathing pattern by responding only to changes in Paco₂ levels. This irregular breathing pattern is called posthyperventilation apnea (PHVA).

Cheyne-Stokes respiration is an abnormal rhythm of breathing (periodic breathing) with alternating periods of hyperventilation and apnea (crescendo-decrescendo pattern). The pathophysiology of Cheyne-Stokes respiration involves a hyperventilatory response to carbon dioxide stimulation. In the damaged brain, higher levels of Paco₂ (hypercapnia) are required to stimulate ventilation, and the response is hyperventilation. As a result, the Paco₂ level decreases to below normal and breathing stops (PHVA) until carbon dioxide reaccumulates and stimulates hyperventilation. In cases of opiate or sedative drug overdose, the respiratory center is depressed and the rate of breathing gradually decreases until respiratory failure occurs.

Central neurogenic hyperventilation is a respiratory pattern of sustained hyperventilation caused by a lesion in the central pons. Apneustic respirations have prolonged inspiratory and expiratory phases caused by injury to the pons or upper medulla. Cluster respirations are characterized by periods or clusters of rapid respirations of near equal depth resulting from trauma or compression to the medulla or from chronic opioid abuse. Ataxic respirations are irregular respirations with prolonged periods of apnea associated with damage to the medulla (see Figure 17-1).

Pupillary Changes

Brainstem areas that control arousal are adjacent to areas that control the pupils. Pupillary changes thus are a valuable guide to evaluating the presence and level of brainstem dysfunction (Figure 17-2).

Some drugs affect pupils and must be considered in the evaluation of pupillary responses in comatose states. Large doses of atropine, scopolamine, amphetamines, mydriatics, and cycloplegics can fully dilate and fix pupils. Sedatives (e.g., glutethimide) in sufficient amounts to produce a coma cause the pupils to become midposition or moderately dilated (4 to 5 mm in diameter), unequal, and frequently fixed to light. Opiates (heroin and morphine) and barbiturates, as well as extensive pontine damage, cause pinhole pupils (1 mm). Severe barbiturate intoxication may produce fixed pupils.

Severe ischemia and hypoxia produce bilaterally wide (5 mm) and fixed pupils usually caused by severe midbrain damage. Occasionally the pupils remain small (1 to 2.5 mm) or midposition even in the presence of profound hypoxia. Hypothermia also may cause fixed pupils.

Oculomotor Responses

Resting, spontaneous, and reflexive eye movements and oculovestibular (caloric) reflexes change at various levels of brain dysfunction (Table 17-5). Persons with metabolically induced coma, except in cases of barbiturate-hypnotic and phenytoin (Dilantin) poisoning, generally retain ocular reflexes, however, even when other signs of brainstem damage, such as central neurogenic hyperventilation, are present.

TABLE 17-5

CHANGES IN OCULOMOTOR RESPONSES

STATE	RESTING AND SPONTANEOUS EYE MOVEMENTS	REFLEXIVE EYE MOVEMENTS
Full consciousness	Eyes at rest, still (cortical gaze centers inhibit spontaneous roving eye movements)	Eyes move as the head turns Oculocephalic responses not elicited or inconsistently elicited (frontal gaze centers inhibit brainstem reflexes that fix gaze straight ahead) Oculovestibular (caloric) stimulation produces nystagmus
Cortical dysfunction or disruption of efferent pathways	Conjugate, horizontal, roving eye movements may well be present (cortical gaze centers no longer inhibit these brainstem-generated roving eye movements)	Gaze fixed straight ahead regardless of head position—positive doll’s eyes reaction (normal oculocephalic reflexes are no longer inhibited by frontal gaze centers)
Diffuse anoxic damage to cortex	“Ocular dipping”—slow, dysrhythmic downward movement followed by faster, upward movement	Nystagmus is no longer induced by caloric stimulation (normally a cold-water stimulus produces deviation of the eyes opposite the irrigated ear; a warm-water stimulus deviates the eyes to the same [ipsilateral] side)
		With an injury that depresses cortical gaze center function, the eyes (and often the entire head) deviate or appear to look toward the side of the injured hemisphere
		With an injury that irritates (stimulates) the neurons of the cortical gaze center, the eyes (and often the entire head) deviate away from the injured hemisphere (all fibers from the frontal gaze centers decussate and therefore control the function of the contralateral pontine gaze center, which moves the eyes in the ipsilateral direction)
Mesencephalon dysfunction	Roving eye movements cease and the eyes become immobile and directed ahead (roving eye movements require an intact brainstem) Eyes may turn down and inward	Oculovestibular reflexes become inconsistent and abnormal Loss of Bell phenomenon (upward deviation of eyes on stimulation) (requires intact eye movement pathways from the mesencephalon to pons)
Pontine dysfunction	Loss of spontaneous blinking (requires an intact pons) “Ocular bobbing”—brisk, conjugate, downward movement of eyes with loss of horizontal eye movements

The presence of brisk oculocephalic reflexes and roving eye movements, as well as the failure to elicit nystagmus with instillation of cold or warm water into the external ear canal, indicates a decrease in consciousness (loss of cortical influence) but an intact brainstem (Figures 17-3 and 17-4).

Destructive or compressive injury to the brainstem causes specific abnormalities of the oculocephalic and oculovestibular reflexes. For example, a skewed deviation, in which one eye diverges downward and the other looks upward, indicates brainstem dysfunction. Destructive or compressive disease processes that involve an oculomotor nucleus or nerve cause the involved eye to deviate outward, producing a resting dysconjugate lateral position of the eyes (each eye diverges laterally). Unilateral abducens paralysis (paralysis of cranial nerve VI) results in an upward deviation of the ipsilateral eye. With bilateral abducens paralysis, the eyes come together (converge). Reflexive eye movements may be suppressed by drugs, most commonly phenytoin, tricyclics, and barbiturates. Occasionally alcohol, phenothiazines, and diazepam may alter reflex eye movements.

Motor Responses

Assessment of motor responses helps to evaluate the level of brain dysfunction and determine the side of the brain that is maximally damaged. The pattern of response noted may be (1) purposeful (a defensive or withdrawal movement of limbs to noxious stimuli); (2) inappropriate, or not purposeful (generalized motor movement, posturing, grimacing, or groaning); or (3) not present (unresponsive, no motor response). Purposeful movement requires an intact corticospinal system. Nonpurposeful movement is evidence of severe dysfunction of the corticospinal system.

Motor signs indicating loss of cortical inhibition are commonly associated with decreased consciousness. These signs include contralateral or bilateral (depending on whether the process is localized or diffuse) reflex grasping, reflex sucking, snout reflex, palmomental reflex, and rigidity (paratonia) (Figure 17-5). Abnormal flexor and extensor responses, particularly in the upper extremities, are defined in Table 17-6 and illustrated in Figure 17-6.

TABLE 17-6

ABNORMAL MOTOR RESPONSES WITH DECREASED RESPONSIVENESS

MOTOR RESPONSE	DESCRIPTION OF MOTOR RESPONSES	LOCATION OF INJURY
Decorticate posturing/rigidity: upper extremity flexion, lower extremity extension (Figure 17-6)	Slowly developing flexion of the arm, wrist, and fingers with abduction in the upper extremity and extension, internal rotation, and plantar flexion of the lower extremity	Hemispheric damage above midbrain releasing medullary and pontine reticulospinal systems
Decerebrate posturing/rigidity: upper and lower extremity extensor responses (Figure 17-6)	Opisthotonos (hyperextension of the vertebral column) with clenching of the teeth; extension, abduction, and hyperpronation of the arms; and extension of the lower extremities	Associated with severe damage involving midbrain or upper pons
	In acute brain injury, shivering and hyperpnea may accompany unelicited recurrent decerebrate spasms	Acute brain injury may cause limb extension regardless of location
Extensor responses in the upper extremities accompanied by flexion in the lower extremities		Pons
Flaccid state with little or no motor response to stimuli		Lower pons and upper medulla

Data from Goetz CG: Textbook of clinical neurology, ed 3, Philadelphia, 2007, Saunders; Nadeau SE et al: Medical neuroscience, Philadelphia, 2004, Saunders.

Vomiting, yawning, and hiccups are complex reflex-like motor responses that are integrated by neural mechanisms in the lower brainstem. These responses may be produced by compression or diseases involving tissues of the medulla oblongata (e.g., infection, neoplasm, infarct, or other more benign stimuli to the vagal nerve). Most CNS disorders produce nausea and vomiting. Vomiting without nausea indicates direct involvement of the central neural mechanism (or pyloric obstruction). Vomiting often accompanies CNS injuries that (1) involve the vestibular nuclei or its immediate projections, particularly when double vision (diplopia) also is present; (2) impinge directly on the floor of the fourth ventricle; or (3) produce brainstem compression secondary to increased intracranial pressure.

Alterations in Awareness

Awareness (content of thought) encompasses all cognitive functions, including awareness of self, environment, and affective states (i.e., moods). Awareness is mediated by the core networks (selective attention and memory) under the guidance of executive attention networks (i.e., the networks that involve abstract reasoning, planning, decision making, judgment, error correction, and self-control). Each attentional function is not localized in a single brain area but is a network of interconnected brain circuits.

Selective attention (orienting) refers to the ability to select specific information to be processed from available, competing environmental and internal stimuli and to focus on those stimuli.¹¹ Frontal and parietal regions of the right hemisphere contribute to selective attention. The engage component is mediated by the pulvinar nucleus of the thalamus (Figure 17-7). The disengagement mechanism is mediated by the right parietal lobe. The move component is mediated by the superior colliculi for visual orienting. A weak orienting network results in a neglect syndrome.

Sensory inattentiveness is a form of neglect and may be visual, auditory, or tactile. The person with sensory inattentiveness is able to recognize individual sensory input from the dysfunctional side when asked to do so but ignores (i.e., neglects, extinguishes) the sensory input from the dysfunctional side when stimulated from both sides. This phenomenon is called extinction. The entire complex of denial of dysfunction, loss of recognition of one’s own body parts, and extinction is sometimes referred to as the unilateral neglect syndrome and is common after stroke.

An isolated (pure) selective attention deficit (orientation), which manifests as a neglect syndrome, rarely, if ever, occurs clinically because typically other deficits also are present. A neglect syndrome may appear temporarily as a result of seizure activity or a postictal state. Temporary or permanent deficits may occur with contusions or subdural hematomas, encephalitis, and ischemic stroke. Progressive neglect deficits may be found with gliomas or metastatic tumor and in Alzheimer and Pick diseases.

Memory is the recording, retention, and retrieval of knowledge. Two types of memory exist: declarative and nondeclarative (Figure 17-10). Declarative memory involves the learning and remembrance of episodic memories (personal history, events, and experiences) and semantic memories (facts and information). Declarative memory is mediated by domain-specific cortical areas of the association areas. This includes: (1) areas of the temporal, parietal, and occipital lobes (Figure 17-8), where long-term memories are thought to be stored; and (2) domain-independent areas of the medial temporal lobe (i.e., hippocampus), the diencephalon (thalamic structures and hypothalamus), and the basal forebrain (located ventral to the striatum and produces acetylcholine) (Figure 17-9), where it is thought distinct domain-specific features of an experience are related or bound.¹²

Nondeclarative memory (nonconscious), also called reflexive, procedural, or implicit memory, is the memory for actions, behaviors (habits), skills, and outcomes.¹³ It is not a language memory but a motor memory. Nondeclarative memory involves the construction of the motor pattern for the motor performance so that the action, behavior, or skill becomes increasingly more automatic. The striatum of the basal ganglia supports this learning across trials (stimulus-response learning), as well as probabilistic classification learning, which supports outcome prediction.¹⁴ All skills and habits are stored in this memory network. Cerebellar memory was originally thought to be related to only motor learning but it is now believed to involve nonmotor functions of cognition, emotion, and memory.¹⁵ Emotional memory is mediated by the amygdala (located on the inner surface of the temporal lobe) (see Figure 17-9). The amygdala attaches positive (e.g., pleasure) or negative (e.g., fear) dispositions to stimuli in the absence of conscious recollection of the circumstances of the emotional experience. Additionally, the amygdala modulates the event memory during and after the event (memory-enhancing effect).¹⁶ The reflex pathways mediate nonassociative learning (e.g., habituation [decreased response to a stimulus] and sensitization [increased response to a stimulus]) (see Figure 17-10).

Dysmnesia is a disorder of the domain-independent declarative memory network. Dysmnesia is defined as the loss of past memories (retrograde amnesia) coupled with an inability to form new memories (anterograde amnesia) despite intact attentional networks. The hippocampus and other temporal lobe structures are often involved. Isolated (pure) domain-independent dysmnesia is caused by only a limited number of conditions, such as transient global dysmnesia (episodic global dysmnesia), amnestic stroke, and Korsakoff psychosis (amnestic or dysmnesic syndrome), as well as after temporal lobectomy. Many disorders may temporarily or permanently produce domain-independent dysmnesia that accompanies other deficits of the cognitive systems.^16a A temporary domain-independent dysmnesia is found during complex partial seizures that persist for a time in the postictal state, in postconcussive states, and in mild posttraumatic brain injury states. A permanent domain-independent dysmnesia may be seen in several disorders including subarachnoid hemorrhage or moderate or severe posttraumatic brain injury states; carbon dioxide poisoning and other hypoxic or anoxic states; Wernicke encephalopathy, viral encephalitis, and granulomatous meningitides; tumors; and Alzheimer and Pick diseases.

A pure auditory or visual domain–specific declarative memory deficit manifests as an isolated agnosia (see Table 17-9). An isolated (pure) domain-specific declarative memory deficit of tactile sensations rarely occurs clinically because selective attention would likely be affected as well. A temporary auditory, visual, or tactile pattern recognition (remote memory) deficit may appear as a result of seizure activity or a postictal state. A temporary or permanent deficit can occur with temporal, occipital, or parietal lobe contusion; with subdural hematoma or ischemic stroke; and in encephalitis. A progressive domain-specific declarative memory deficit may occur in temporal, occipital, or parietal gliomas; in metastatic tumors; and in Alzheimer and Pick diseases.

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