Introduction
Many patients in the neurocritical care unit (NCCU) are in coma, have altered consciousness, or have a disease process that may lead to altered consciousness. Coma and other disorders of consciousness are common clinical problems that indicate a severe disturbance of brain function. Monitoring and management of patients with disturbed consciousness depend in large part on the underlying etiology. The principal means of monitoring the comatose patient are clinical neurologic examinations, the use of rating scales, neuroimaging, and electrophysiologic tests. In addition, a variety of invasive and noninvasive monitors of brain function is available and discussed in other chapters of this book. Goals of monitoring include establishing an etiologic diagnosis and excluding coma mimics, determining the location and severity of injury, assessing response to therapy, and determining prognosis. This chapter provides an overview of the anatomy of consciousness, the general clinical approach to the coma patient, and neurologic assessment, with a focus on the clinical examination, quantitative coma scales, and electrophysiologic and imaging studies that may provide insight into the prognosis of coma. In addition, other critical care scores that provide insight into extracerebral pathophysiology are briefly discussed.
Anatomy of Brain Circuits Involved in Arousal, Alertness, and Conscious Behavior
Level of arousal (alertness) depends on the coordinated activity of multiple brainstem nuclei that send projections to diencephalic targets in the thalamus and hypothalamus and diffusely to the cerebral cortex. Areas of the thalamus that receive information from arousal centers in the brainstem in turn send widespread projections to both cerebral hemispheres. Thus isolated brainstem lesions, bilateral thalamic damage, or diffuse bilateral cerebral injury can cause global impairments of consciousness and coma. An important corollary to this general rule is that unilateral lesions should not cause global reductions in consciousness unless they are large enough to produce significant mass effect on the contralateral hemisphere or there is a preexisting contralateral lesion. Because brainstem arousal centers are close to other important nuclei and tracts that control eye movements and breathing, the location of lesions causing global impairments in consciousness often can be readily determined by careful physical examination.
In the early 20th century Baron Constantin von Economo first proposed the concept that specific brainstem nuclei control arousal and alertness after his detailed clinicopathologic study of patients with encephalitis lethargica. The vast majority of these patients had profound somnolence along with parkinsonism and focal oculomotor abnormalities, and spent only a few hours awake each day. Postmortem analysis of these patients demonstrated damage to the paramedian reticular formation near the junction between the midbrain and the diencephalon. A small subset of patients who suffered from debilitating insomnia in contrast had damage to the anterior hypothalamus. Based on these results, von Economo proposed that a specific arousal-promoting center exists in the midbrain, and a separate sleep-promoting center is in the hypothalamus.
Studies by Morruzi and Magoun in the 1940s showed that selective lesions of the midbrain paramedian reticular formation in cats caused electroencephalographic slowing and behavioral unresponsiveness similar to sleep. Lesions in the midbrain that contained ascending sensory pathways caused defects in somatosensory and auditory-evoked responses but had no effect on the normal desynchronized electroencephalographic pattern seen in awake animals. These investigators coined the term ascending reticular activating system (ARAS) to describe the critical function of the paramedian reticular formation in alertness. Subsequent lesion studies in humans have confirmed the importance of the upper brainstem to promote and maintain behavioral arousal. Specifically, injury to either the paramedian midbrain or bilateral dorsolateral pontine tegmentum causes coma. Lesions of other parts of the brainstem outside of this ascending arousal system, although often debilitating, do not cause global impairments of consciousness. Multiple brainstem nuclei that form distinct cholinergic and monoaminergic projection systems are now known to constitute the ascending arousal system. Although these nuclei are not all located within the paramedian midbrain reticular formation, their output fibers in general course through this structure on their way to targets in the diencephalon and cerebral cortex.
Cholinergic Projection Systems
The main source of arousal promoting inputs to the thalamus is from the pedunculopontine and laterodorsal tegmental nuclei in the pons. These areas send cholinergic projections through the midbrain reticular formation mainly to the intralaminar thalamic nuclei and the thalamic reticular nucleus, although they also project to the thalamic relay nuclei. The intralaminar nuclei are excited by their ascending cholinergic input and send widespread diffuse excitatory projections to the cortex. The thalamic reticular nucleus, by contrast, sends local inhibitory projections to thalamocortical relay nuclei, and its principal neurons are inhibited by acetylcholine. Thus activity in the pedunculopontine and laterodorsal tegmental nuclei—which is greatest during awakening and decreases during sleep—both activate diffuse excitatory projections from the intralaminar nuclei and disinhibit excitatory thalamocortical relay neurons by inhibiting the reticular nucleus.
A second source of cholinergic inputs arises from the basal forebrain. These neurons receive inputs from brainstem monoaminergic projection systems (discussed following) and neighboring excitatory brainstem nuclei and send widespread projections throughout the cerebral cortex. Interestingly, single axons from the basal forebrain have patchy, spatially defined projection patterns to defined subsets of cortical neurons. Thus regulated activity of different parts of the basal forebrain can have spatially restricted effects on different cortical areas.
Monoaminergic Projection Systems
Multiple monoaminergic projection systems also provide telencephalic input from the brainstem and diencephalon that influence alertness and conscious behavior. Activity of these monoaminergic projections has complex effects on cortical activity and often decreases background activity but increases the responsiveness of a cortical neuron to its best stimulus, thereby increasing signal to noise ratio. These systems therefore have critical functions in regulating attention, memory, and other higher order cognitive processes in addition to providing a more general arousal-promoting stimulus.
Dopaminergic neurons are found in the midbrain in both the substantia nigra and in the ventral tegmental area. Projections from the substantia nigra terminate in the basal ganglia and are crucial for motor control and modulation. The ventral tegmental projections course through the midbrain reticular formation and provide a mesolimbic projection to the nucleus accumbens, basal forebrain, cingulate cortex, hippocampus, and amygdala and a mesocortical projection to the prefrontal cortex. Mesolimbic dopaminergic pathways are involved in reward-mediated behavior, and overactivity of these projections is thought to be central in the pathogenesis of thought disorders such as schizophrenia. Mesocortical projections likely are involved in attention and working memory.
Noradrenergic projections to the cerebral hemispheres arise mainly from the locus ceruleus, located in the upper pons near the fourth ventricle. Locus ceruleus activity increases with awakening, and this area likely is important in behavioral state switching (i.e., from sleep to wakefulness). These noradrenergic systems, like serotonergic systems (see following text), also are pharmaceutical targets in mood disorders.
Multiple midline brainstem areas throughout the midbrain, pons, and medulla that comprise the raphe nuclei provide serotonergic input to the brain. Of these, the rostral raphe nuclei in the midbrain and pons project diffusely throughout the cortex, thalamus, and basal ganglia. Serotonin effects on these areas are complex and can be either excitatory or inhibitory. These pathways also are thought to play a major role in psychiatric diseases such as depression, anxiety, and obsessive-compulsive disorder.
A widespread histaminergic pathway arises from the tuberomamillary nucleus in the posterior hypothalamus. Histaminergic neurons are important in sleep and arousal regulation, and activity of tuberomamillary nucleus neurons is greatest during waking and rapid eye movement (REM) sleep. Histamine receptor blockers that can cross the blood-brain barrier, such as diphenhydramine, can exert a powerful sleep-promoting effect.
Interactions Between Arousal-Promoting Brain Centers
The anatomy of the pathways described previously and their aggregate importance in arousal have been recognized for decades. However, the specific ways in which these pathways interact to promote conscious behavior, attention, or memory and regulate the transitions between multiple behavioral states is only beginning to be elucidated. Other inputs, including the galanin and gamma aminobutyric acid–secreting (GABAergic) inputs from the ventrolateral preoptic (VLPO) area of the hypothalamus, orexin-containing neurons from the lateral hypothalamus, and descending cortical inputs provide modulatory control over the ARAS. Nevertheless, the concept of an ascending brainstem arousal system whose activity promotes alertness and conscious behavior remains invaluable clinically when evaluating patients with disorders of impaired consciousness.
Coma Etiology
Causes of altered mental status and coma are protean, and can be divided into primary brain disorders and systemic derangements that secondarily affect brain function ( Table 10.1 ). Primary brain disorders can be caused by structural abnormalities (e.g., cerebral infarction, tumors, subdural hematomas, intraparenchymal hemorrhages, and abscesses among others) that either directly distort the circuitry of the ascending arousal system or globally increase intracranial pressure (ICP), or by diffuse nonstructural disturbances such as seizures. Often both structural and nonstructural abnormalities may exist together in the same patient, for example, a patient with a cerebral abscess who develops seizures. Systemic disturbances cause encephalopathy through diffuse bilateral cerebral dysfunction and can include metabolic derangements, exposure to toxins, systemic infections, or diffuse encephalitis caused by primary central nervous system (CNS) infections, autoimmune processes, or paraneoplastic syndromes.
| PRIMARY BRAIN DISORDERS |
| Structural Lesions |
|
| Nonstructural Disorders |
|
| SYSTEMIC DISORDERS |
| Toxic Encephalopathies |
|
| Metabolic Encephalopathies |
|
| Infections |
|
The most common causes of coma are traumatic brain injury (TBI), hypoxic-ischemic encephalopathy (HIE), drug overdose, ischemic and hemorrhagic strokes, CNS infections, and brain herniation from space-occupying lesions. A detailed discussion of these conditions is beyond the scope of this chapter; however, a few warrant special mention because rapid diagnosis and urgent treatment are essential to limit brain injury. These include seizures, infections, acute hydrocephalus, herniation, ischemic and hemorrhagic strokes, subarachnoid hemorrhage (SAH), cerebral venous sinus thrombosis, hypertensive encephalopathy, and TBI.
Differential Diagnosis (Mimics) of Coma and the Vegetative State
Patients may become unresponsive from conditions that mimic coma or a vegetative state. Care must be taken not to consider these patients as comatose because they have no impairments of conscious behavior and often can communicate with clinical staff and other individuals if an appropriate communication system is devised. In the locked-in syndrome, destruction of the ventral pons leaves the patient quadriplegic and mute. Patients often are aware of their surroundings and may communicate only through vertical eye movements and blinking, which are spared. With more rostral pontine lesions, vertical eye movements and blinking are lost. In this state that can be likened to receiving a neuromuscular blocking agent without a sedative, the patient has no means of communication. Severe Guillain-Barré syndrome, botulism, and critical-illness neuropathy may similarly result in complete de-efferentation. Catatonia is a manifestation of severe psychiatric illness in which patients open their eyes, do not speak or follow commands, and may exhibit waxy flexibility. The remainder of the neurologic exam and the electroencephalogram (EEG) are normal. Akinetic mutism that results from bilateral medial frontal lobe injury is a profound form of abulia (lack of motivation) in which patients are unable to speak or to move, but open their eyes, occasionally track visual stimuli, and sometimes respond when prompted.
Neurologic Examination of the Comatose Patient
The initial neurologic examination of a patient with altered consciousness allows the lesion to be localized: this helps to narrow the list of etiologic possibilities. For example, integrity of brainstem function and absence of focal signs suggests a toxic or metabolic disorder. In contrast, asymmetric findings and brainstem dysfunction are more consistent with a structural etiology. The exam also is used to exclude conditions that may mimic coma. Serial examinations of the comatose patient over time are essential and provide information about treatment efficacy, progression of the primary process, and prognosis. The clinical examination of the comatose patient is discussed first, followed by some of the standardized scales that have been developed to evaluate coma ( Fig. 10.1 ).
The coma examination is focused on four elements: (1) determination of the patient’s level of arousal (wakefulness), (2) eye examination, (3) motor responses and presence of abnormal reflexes, and (4) observation of breathing patterns.
Level of Consciousness
Patients who exhibit spontaneous eyes opening, verbalization attempts, moaning, tossing, reaching, leg crossing, yawning, coughing, or swallowing have a higher level of consciousness than those who do not. The examiner should next assess the patient’s response to a series of stimuli that escalate in intensity. The patient’s name should be called loudly. If there is no response, the examiner may stimulate the patient by gently shaking him or her. If this produces no response, the examiner should use a noxious stimulus, such as pressure to the supraorbital ridge, nailbeds, or sternum, or nasal tickle with a cotton wisp. Responses such as grimacing, eye opening, grunting, or verbalization should be documented. Motor responses provide information not only about sensation and limb strength but also level of consciousness. The examiner should note whether stimuli produce “purposeful,” nonstereotyped limb movements, for example, reaching toward the site of stimulation (“localization”). This implies a degree of intact cortical function. Stereotyped limb movements generally are mediated by brain and spinal reflexes and do not require cortical input. Examples include extension and internal rotation of the limbs (decerebrate posturing), upper extremity flexion (decorticate posturing), and flexion at the ankle, knee, and hip (“triple-flexion”). Several scales designed to quantitate level of consciousness are available to help reduce inter- and intraobserver variability and to facilitate accurate follow-up. These scales (Glasgow Coma Scale [GCS], Full Outline of UnResponsiveness [FOUR] score, Reaction Level Scale 85 [RLS85], and Innsbruck Coma Score are discussed later in this chapter.
The Eye Examination
In coma, the neuro-ophthalmologic examination should focus on: (1) the pupils, (2) resting eye position and eye movements, (3) retinal appearance, and (4) the corneal reflex.
Pupillary Examination
Pupillary examination is perhaps the most important part of the coma examination, because it can help localize and differentiate between structural lesions and diffuse metabolic encephalopathies that cause bilateral cerebral hemispheric dysfunction. Pupillary constriction is mediated by cholinergic parasympathetic efferents that arise from the Edinger-Westphal nucleus in the midbrain and travel within the oculomotor nerve. Pupillary dilation, in contrast, is mediated by sympathetic efferents originating in the hypothalamus that travel through the brainstem and cervical spinal cord and then synapse onto postganglionic neurons in the superior cervical ganglion. These noradrenergic neurons then course along the carotid artery into the cavernous sinus and through the superior orbital fissure before reaching the iris.
Pupillary size, shape, and reactivity to light should be assessed. In general, abnormalities of the pupillary light reflex suggest a structural abnormality. However, certain drugs also may affect the pupillary light reflex. These agents can cause pupillary abnormalities that are mistakenly attributed to structural brain lesions ( Table 10.2 ). Metabolic causes of coma typically do not affect the pupils.
| Drug Class | Examples | Effect on Pupils | Comments |
|---|---|---|---|
| Muscarinic antagonists | Atropine, scopolamine, ipratropium, tiotropium, tropicamide | Dilate pupils by blocking action of acetylcholine | Ipratropium and tiotropium can cause inadvertent pupillary dilation if accidentally gets into eye during respiratory treatment. Tropicamide eyedrops commonly used to dilate pupils for ophthalmologic evaluation. |
| Beta agonists | Epinephrine, isoproterenol, salmeterol, formoterol, albuterol | Dilate pupils by activating beta-adrenergic receptors | Albuterol, salmeterol, and formoterol can cause inadvertent pupillary dilation if accidentally gets into eye during respiratory treatment. |
| Cholinesterase inhibitors | Physostigmine, edrophonium, pyridostigmine, rivastigmine, donepezil, organophosphates | Constrict pupils by increasing acetylcholine concentration at synaptic cleft | Rivastigmine and donepezil used for treatment of dementia. Pyridostigmine used for treatment of myasthenia gravis. |
| Muscarinic agonists | Pilocarpine | Constrict pupils by activating muscarinic acetylcholine receptors | Pilocarpine eyedrops are used to distinguish pharmacologic pupil dilation from oculomotor nerve injury. |
| Serotonin-2A (5HT-2A) receptor agonists | Lysergic acid diethylamide (LSD) | Dilate pupils through unclear mechanism | Commonly used recreational hallucinogen. |
| Monoamine reuptake inhibitors | Cocaine, hydroxyamphetamine | Dilate pupils by blocking reuptake of norepinephrine at synaptic cleft | Hydroxyamphetamine eyedrops can help distinguish if constricted pupil is from preganglionic or postganglionic injury. |
| Norepinephrine release potentiators | Hydroxyamphetamine | Dilate pupils by increasing norepinephrine concentration at synaptic cleft | See above. |
| Opiate receptor agonists | Morphine, fentanyl, hydromorphone | Constrict pupils | Commonly used analgesics in hospitalized and critically ill patients |
Normal pupils are round, have equal diameters, and briskly constrict when illuminated. When unequal pupils (anisocoria) are observed, it is important to establish whether it is the larger or the smaller pupil that is abnormal. This is accomplished by examining the eyes both in the light and in the dark. When the lights are extinguished, an abnormally small pupil will fail to dilate fully and the degree of anisocoria will increase. In contrast, when the abnormal pupil is the larger one, the degree of anisocoria will be maximal under full illumination when the larger pupil fails to constrict fully.
In the NCCU, the most important causes of a unilaterally dilated pupil are compressive lesions of the oculomotor nerve complex (e.g., uncal herniation or a posterior communicating artery aneurysm). A complete third nerve palsy results in ipsilateral mydriasis, inferolateral deviation of the eye, and ipsilateral ptosis. As a rule a third nerve palsy with pupil involvement means a surgical lesion (i.e., compressive), whereas when the pupil is spared the cause is medical (e.g., diabetes, meningovascular syphilis). Patients with myasthenia gravis may present with ptosis and ophthalmoparesis secondary to neuromuscular weakness that is often unilateral. Therefore, this condition also should be considered in patients who present with what appears to be a pupil-sparing third nerve palsy.
The most important cause of a unilateral small pupil is Horner syndrome, which is caused by damage to sympathetic efferents to the eye and consists of miosis and mild ipsilateral ptosis. Horner syndrome can be seen from multiple areas of brain damage, including (1) hypothalamic injury, (2) brainstem damage to descending inputs that synapse onto cervical sympathetic preganglionic neurons, (3) cervical spine injury, (4) injury to sympathetic paravertebral ganglia (e.g., with an apical lung mass), or (5) damage to sympathetic postganglionic fibers because they course along the internal carotid artery (e.g., carotid artery dissection). Depending on the lesion location, ipsilateral facial anhidrosis and other focal neurologic signs also may be present. The presence of Horner syndrome unequivocally places the lesion ipsilateral to the pupillary abnormality. Bilaterally fixed and dilated pupils are seen in the terminal stages of brain death but also with anticholinergic medications, such as atropine. Hyperadrenergic states (e.g., pain, anxiety, cocaine intoxication) produce bilaterally large and reactive pupils. Reactive pinpoint (<1 mm) pupils are observed with opiate and barbiturate intoxication, and after extensive pontine injury. Patients with long-standing diabetes mellitus may have small pupils secondary to hyperglycemia-induced damage of the sympathetic fibers that mediate pupillary dilation.
Resting Eye Position and Eye Movements
Eye position and spontaneous movements including horizontal or vertical misalignment, spontaneous roving, or rhythmic and repetitive vertical movements should be looked for and documented. The frontal lobe cortex (frontal eye fields) mediates conjugate deviation of the eyes toward the contralateral side. Lateral deviation of both eyes therefore indicates a destructive lesion in the ipsilateral frontal lobe or an excitatory focus (seizure) in the contralateral hemisphere. A destructive unilateral pontine lesion, and rarely, a thalamic lesion, causes conjugate deviation to the contralateral side. Downward deviation (or lack of upward gaze) of the eyes is caused by dysfunction of the dorsal midbrain and may be seen with hydrocephalus, tumors, strokes, and pineal region abnormalities. Dysconjugate gaze frequently is seen in sedated patients and usually represents unmasking of a latent eso- or exophoria. Roving, or slow to-and-fro eye movements, implies functional integrity of the brainstem. Ocular bobbing—fast conjugate downward gaze followed by a slow upward correction to midposition—implies extensive pontine injury. Ocular dipping—slow conjugate downward gaze followed by fast upward gaze—also localizes to the pons. With a skew deviation, a vertical misalignment of the eyes that is not caused by an isolated cranial nerve palsy, the lesion usually is in the midbrain on the side of the higher eye, or in the pontomedullary junction on side of the lower eye. In comatose patients there is a high incidence of nonconvulsive seizures, and jerking movements of the eyes may be the only evidence of seizure activity.
If spontaneous eye movements are absent, then an oculocephalic response (“doll’s eyes”) should be sought by turning the head horizontally and vertically. This maneuver should not be performed on trauma patients with known or suspected cervical spine instability. Normally the eyes move opposite to the direction of head turning. Testing the oculocephalic response may uncover a vertical gaze paresis, a skew deviation, or a sixth nerve palsy that was not otherwise obvious.
If an oculocephalic response cannot be elicited, then an oculovestibular (“cold-caloric”) response is sought. First, the tympanic membrane should be visualized to ensure that is intact and unobstructed. The head of the bed should be set at 30 degrees to align the patient’s horizontal semicircular canals parallel to the floor. Then, using an angiocatheter or a butterfly catheter without the needle, 30 to 60 cc of ice-cold water are instilled into the external auditory canal against the tympanic membrane. This inhibits the ipislateral vestibular system and normally causes the eyes first to move slowly toward the ipsilateral ear and then to jerk quickly toward the contralateral ear. The initial slow response is mediated by the unopposed contralateral vestibular system in the brainstem, and the frontal eye fields mediate the subsequent corrective nystagmus. With bilateral cortical dysfunction and an intact brainstem, slow tonic deviation of the eyes toward the ipislateral ear is observed and is not followed by contralateral nystagmus. In early metabolic coma, the oculocephalic and oculovestibular responses are preserved. Absent response indicates diffuse brainstem dysfunction and is seen in primary brainstem injury, late transtentorial herniation, barbiturate intoxication, and brain death.
Retinal Examination
A funduscopic examination should be considered to look for signs of intracranial hypertension. However, successful funduscopy often requires that the pupil be dilated; if doing this pharmacologically may confuse overall patient assessment, retinal examination may be deferred. Papilledema is swelling of the optic nerve head from increased ICP. It is almost always bilateral and may be accompanied by retinal hemorrhages, exudates, and cotton wool spots, and ultimately by enlargement of the optic cup. Papilledema develops over hours to days. Its absence therefore does not imply normal ICP, especially in the acute setting. Spontaneous pulsatility of the retinal veins implies normal ICP. Terson syndrome is vitreous, subhyaloid, or retinal hemorrhage associated with SAH. Papilledema itself can be associated with visual loss, and in general when seen, even in a patient with normal consciousness, should prompt immediate investigation as to its etiology so treatment can be started in a timely manner.
The Corneal Reflex
The cornea of each eye is gently touched with a drop of saline or a cotton wisp while observing for eyelid closure to test the corneal reflex. Failure of unilateral eyelid closure suggests facial nerve dysfunction on that side. Failure of bilateral eyelid closure with stimulation of one cornea, but not the other, implies trigeminal nerve dysfunction on the stimulated side. Failure of bilateral eyelid closure on stimulation of either cornea usually implies pontine dysfunction.
Motor Responses and Abnormal Reflexes
The symmetry of motor responses and reflexes, and the presence of abnormal movement often permits discrimination between structural and systemic etiologies of altered mental status. First, the patient should be observed for any abnormal or spontaneous movements. Asterixis implies a metabolic disturbance such as uremia or hepatic encephalopathy. Twitching or jerking of the face or limbs, even if subtle, raises the suspicion for seizures. Asymmetry of resting limb position may be a sign of weakness. For example, a paretic leg may lie externally rotated. Next, the patient is stimulated and the examiner should observe for asymmetry in the patient’s face (grimace) and limb motor responses. A less vigorous response on one side of the body indicates a contralateral structural lesion that involves the motor pathways above the level of the caudal medulla. In general, weakness associated with a pyramidal (upper motor neuron) lesion is found in the extensor muscle groups of the arms and the flexor muscle groups of the legs. Hence a patient with a hemiparesis may lie with the arm flexed and the leg extended. Tone, on the other hand, is increased in the muscle groups that remain strong. Testing handgrip strength is not reliable because this function often is affected late in the development of spastic hemiparesis. In addition a handgrip may represent an abnormal reflex associated with frontal lobe disease. Another important reflex is the plantar response. An up-going toe is abnormal and is called a Babinski reflex (i.e., there is no such thing as a negative Babinski). This reflex can be difficult to elicit and is best obtained by stroking the lateral border of the sole and then across the ball of the foot. The toes must not be touched. It is the first movement of the big toe that is important. For example, an individual with very sensitive feet may first flex the big toe and then extend all the toes and withdraw the leg—this is a normal response. An up-going toe is associated with an upper motor neuron lesion. The presence of an abnormal plantar reflex can be cross-checked with the abdominal reflex obtained by gently stroking the abdominal wall and looking for abdominal wall muscle contraction. Absence of an abdominal reflex implies an upper motor neuron lesion above T9. The reflex can be difficult to assess in a patient who is obese or has had multiple abdominal surgeries.
Paraparesis and quadraparesis raise the possibility of spinal cord injury, especially in the setting of trauma. In these patients, in whom spinal cord injury or compression is a consideration, how they respond to sensory stimuli needs to be factored into what motor responses occur. Subtle findings such as sweat patterns may help indicate a sensory level in a comatose patient with a spinal cord abnormality. By looking at plantar and abdominal reflexes, the level of injury can be differentiated further. Priapism (reflex erection) results from loss of sympathetic tone with injury to the spinal cord. The bulbocavernosus reflex is contraction of the anal sphincter when the penile shaft is pinched or a Foley catheter is pulled. Its absence is associated with a spinal cord injury. The American Spinal Injury Association (ASIA) Muscle Grading Scale can be used to classify patients with spinal cord injury ( Table 10.3 ). This is different from the ASIA Impairment Scale that defines the severity of the injury ( Table 10.4 ).
| Grade | Clinical Description |
|---|---|
| 0 | Total paralysis |
| 1 | Palpable or visible contraction |
| 2 | Active movement, full range of motion, gravity eliminated |
| 3 | Active movement, full range of motion, against gravity |
| 4 | Active movement, full range of motion, against gravity and provides some resistance |
| 5 | Active movement, full range of motion, against gravity and provides normal resistance |
| 5* | Muscle able to exert, in examiner’s judgment, sufficient resistance to be considered normal if identifiable inhibiting factors were not present |
|
Breathing Patterns
Several different breathing patterns that depend on the type of injury and location of the pathology may be observed in coma. However, in clinical practice breathing patterns often are obscured by the use of sedatives, paralytics, and mechanical ventilation. Apneustic respirations are characterized by a prolonged end-inspiratory pause. This pattern may be seen after focal injury to the dorsal lower half of the pons (e.g., stroke), but also may be observed with meningitis, hypoxia, and hypoglycemia. Sustained hyperventilation can be seen in metabolic encephalopathies such as hepatic coma, sepsis, and diabetic ketoacidosis, but also can be seen as a consequence of focal injury to the upper pons—usually either from secondary neurogenic pulmonary edema caused by intrinsic brainstem injury or because of a tumor that creates a local cerebrospinal fluid (CSF) acidosis, which stimulates brain chemoreceptors to trigger hyperventilation. Cluster breathing consists of several rapid, shallow breaths followed by a prolonged pause, and localizes to the upper medulla. Ataxic respirations, or Biot’s breathing, is a chaotic pattern in which the length and depth of the inspiratory and expiratory phases are irregularly irregular. It may occur after injury to the respiratory centers in the lower medulla. Apnea may be seen in a variety of neurologic and non-neurologic disorders and by itself is of little localizing value. Kussmaul respirations are rapid, deep breaths that usually signal metabolic acidosis, but also may be observed with pontomesencephalic lesions. Cheyne-Stokes respiration refers to alternating spells of apnea and crescendo-decrescendo hyperpnea. It has limited value in lesion localization and is seen with diffuse cerebral injury, hypoxia, hypocapnea, and congestive heart failure. Agonal gasps reflect bilateral lower medullary injury and occur in the terminal stages of brain injury.
Standardized Coma Rating Scales
Coma scales are important because it can be difficult to otherwise define levels of consciousness. States of consciousness fall along a spectrum, with coma at one end and normal consciousness at the other. Patients who are in coma do not respond to external stimuli in a “purposeful” manner but may demonstrate reflexive behavior. Their eyes are closed and sleep-wake cycles are absent. Coma is usually prolonged and lasts for at least hours to days, but rarely is permanent. Instead coma progresses to death or to a higher level of consciousness including the vegetative or minimally conscious state (see Chapter 8 , Chapter 13 ). Deterioration of normal consciousness is often designated by terms such as “confusion” or “delirium,” “stupor,” and “coma.” These labels are imprecise and have been defined inconsistently from study to study, and even occasionally within a given study. Several attempts have been made to codify criteria for coma, vegetative state, minimally conscious state, or delirium. These attempts, although laudable, have not yet led to universal adoption of standard terminology. For practical purposes for the intensive care unit (ICU) physician, it is advisable to simply describe the clinical exam and use a validated coma scale.
Several quantitative coma scales have been developed to measure the degree of coma and extent of neurologic injury in patients. Standardized scales provide an objective measure of coma that facilitates communication between physicians and ancillary medical staff, a means of comparing patients with varying coma etiologies, and a simple mechanism to track clinical changes over time. Scales describing sedation and agitation (e.g., Ramsay Sedation Scale), Richmond Agitation Sedation Scale, Vancouver Interaction and Calmness Scale, Riker Sedation-Agitation Scale, and the American Association of Critical-Care Nurses’ Sedation Assessment Scale for Critically Ill Patients also are used in critical care and are reviewed in Chapter 11 . (See also www.mc.vanderbilt.edu/icudelirium/docs/CAM_ICU_training.pdf for training in delirium assessment.)
Glasgow Coma Scale
The GCS ( Table 10.5 ) is the most widely used standardized scale to assess the degree of coma and neurologic injury in patients and has been incorporated into several models that predict outcome in a variety of neurologic insults. It was initially developed for triage in patients with head trauma but it has since been shown to correlate with survival and neurologic outcome in TBI, nontraumatic coma, intracerebral hemorrhage, SAH, dementia, and meningitis. To calculate the GCS a patient is given a numeric score in three categories (eye response, motor response, and verbal response) and then these numbers are added together to get the full score (see Table 10.5 ). The score can range from 3 to 15; a GCS of 13 or higher signifies mild brain injury, 9 to 12 signifies moderate brain injury and 8 or less signifies severe brain injury and is frequently used to define coma. The GCS is simple to calculate and provides a rapid estimate of the degree of neurologic injury. It has been widely adopted by emergency medical personnel to evaluate patients both in the field and in the emergency department (ED) to triage and guide initial therapy. The GCS has been incorporated into other validated scoring systems that assess the severity of critical illness such as the Acute Physiology and Chronic Healthy Evaluation (APACHE II) score and the Simplified Acute Physiology Score (SAPS II) score or of SAH (e.g., the World Federation of Neurosurgical Societies score; see following text) and independently predicts mortality in the general critical care patient. In addition, the GCS is used to classify patients with acute brain injury and select them for various clinical trials. Websites such as those based on the Corticosteroid Randomisation after Significant Head Injury (CRASH) study ( www.crash.lshtm.ac.uk/Risk%20calculator/index.html ) or the International Mission for Prognosis and Analysis of Clinical Trials in TBI (IMPACT) project ( www.tbi-impact.org/ ) use the GCS to help provide online prognostic predictor models after brain injury.
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