Plum and posner’s diagnosis of stupor and coma fourth Edition series editor sid Gilman, md, frcp
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lateral prefrontal impairment. 137
It is elicited by gently stroking the palm of the patient with the examiner’s fingers. The patient may grasp the examiner’s fingers, as if grasping a branch of a tree. The pull reflex is a variant in which the examiner curls his or her fingers under the patient’s as the patient attempts to grasp. The grasp is often so strong that it is possible to pull the patient from the bed. Many elderly 72 Plum and Posner’s Diagnosis of Stupor and Coma patients with normal cognitive function will have a mild tendency to grasp the first time the reflex is attempted, but a request not to grasp the examiner quickly abolishes the response. Patients who are unable to inhibit the reflex invariably have prefrontal pathology. The grasp reflex may be asymmetric if the prefrontal in- jury is greater on one side, but probably re- quires some impairment of both hemispheres, as small, unilateral lesions rarely cause grasp- ing. 137
Grasping disappears when the lesion involves the motor cortex and causes hemi- paresis. It is of greatest value in a sleepy pa- tient who can cooperate with the exam; it dis- appears as the patient becomes more drowsy. Like paratonia, prefrontal reflexes are normally present in young infants, but disappear as the forebrain matures. 135 Motor Responses After assessing muscle tone, the examiner next tests the patient for best motor response to sensory stimulation (Figure 2–10). If the pa- tient does not respond to voice or gentle shak- ing, arousability and motor responses are tes- ted by painful stimuli. The maneuvers used to provide adequate stimuli without inducing actual tissue damage are shown in Figure 2–1. A Metabolic encephalopathy B Upper midbrain damage C Upper pontine damage Figure 2–10. Motor responses to noxious stimulation in patients with acute cerebral dysfunction. Levels of associated brain dysfunction are roughly indicated at left. Patients with forebrain or diencephalic lesions often have a hemiparesis (note lack of motor response with left arm, externally rotated left foot, and left extensor plantar response), but can gen- erally make purposeful movements with the opposite side. Lesions involving the junction of the diencephalon and the mid- brain may show decorticate posturing, including flexion of the upper extremities and extension of the lower extremities. As the lesion progresses into the midbrain, there is generally a shift to decerebrate posturing (C), in which there is extensor posturing of both upper and lower extremities. (From Saper, C. Brain stem modulation of sensation, movement, and con- sciousness. Chapter 45 in: Kandel, ER, Schwartz, JH, Jessel, TM. Principles of Neural Science. 4th ed. McGraw-Hill, New York, 2000, pp. 871–909. By permission of McGraw-Hill.) Examination of the Comatose Patient 73
Responses are graded as appropriate, inap- propriate, or no response. An appropriate re- sponse is one that attempts to escape the stim- ulus, such as pushing the stimulus away or attempting to avoid the stimulus. The motor response may be accompanied by a facial gri- mace or generalized increase in movement. It is necessary to distinguish an attempt to avoid the stimulus, which indicates intact sensory and motor connections within the spinal cord and brainstem, from a stereotyped withdrawal response, such as a triple flexion withdrawal of the lower extremity or flexion at the fingers, wrist, and elbow. The stereotyped withdrawal response is not responsive to the nature of the stimulus (e.g., if the pain is supplied over the dorsum of the toe, the foot will withdraw into, rather than away from, the stimulus) and thus is not appropriate to the stimulus that is ap- plied. These spinal level motor patterns may occur in patients with severe brain injuries or even brain death. It is also important to assess asymmetries of response. Failure to withdraw on one side may indicate either a sensory or a motor impairment, but if there is evidence of facial grimacing, an increase in blood pressure or pupillary dilation, or movement of the con- tralateral side, the defect is motor. Failure to withdraw on both sides, accompanied by facial grimacing, may indicate bilateral motor im- pairment below the level of the pons. Posturing responses include several stereo- typed postures of the trunk and extremities. Most appear only in response to noxious stim- uli or are greatly exaggerated by such stimuli. Seemingly spontaneous posturing most often represents the response to endogenous stim- uli, ranging from meningeal irritation to an oc- cult bodily injury to an overdistended bladder. The nature of the posturing ranges from flexor spasms to extensor spasms to rigidity, and may vary according to the site and severity of the brain injury and the site at which the nox- ious stimulation is applied. In addition, the two sides of the body may show different patterns of response, reflecting the distribution of in- jury to the brain. Clinical tradition has transferred the terms decorticate rigidity and decerebrate rigidity from experimental physiology to certain pat- terns of motor abnormality seen in humans. This custom is unfortunate for two reasons. First, these terms imply more than we really know about the site of the underlying neuro- logic impairment. Even in experimental ani- mals, these patterns of motor response may be produced by brain lesions of several different kinds and locations and the patterns of motor response in an individual to any one of these lesions may vary across time. In humans, both types of responses can be produced by supra- tentorial lesions, although they imply at least incipient brainstem injury. There is a tendency for lesions that cause decorticate rigidity to be more rostral and less severe than those caus- ing decerebrate rigidity. In general, there is much greater agreement among observers if they simply describe the movements that are seen rather than attempt to fit them to com- plex patterns. Flexor posturing of the upper extremities and extension of the lower extremities corre- sponds to the pattern of movement also called decorticate posturing. The fully developed response consists of a relatively slow (as op- posed to quick withdrawal) flexion of the arm, wrist, and fingers with adduction in the upper extremity and extension, internal rotation, and vigorous plantar flexion of the lower extremity. However, decorticate posturing is often frag- mentary or asymmetric, and it may consist of as little as flexion posturing of one arm. Such fragmentary patterns have the same localizing significance as the fully developed postural change, but often reflect either a less irritating or smaller central lesion. The decorticate pattern is generally pro- duced by extensive lesions involving dysfunc- tion of the forebrain down to the level of the rostral midbrain. Such patients typically have normal ocular motility. A similar pattern of motor response may be seen in patients with a variety of metabolic disorders or intoxica- tions.
138 However, the presence of decorticate posturing in cases of brain injury is ominous. For example, in the series of Jennett and Teasdale, after head trauma only 37% of co- matose patients with decorticate posturing recovered. 139
Even more ominous is the presence of ex- tensor posturing of both the upper and lower extremities, often called decerebrate postur- ing. The arms are held in adduction and ex- tension with the wrists fully pronated. Some patients assume an opisthotonic posture, with teeth clenched and arching of the spine. Tonic neck reflexes (rotation of the head causes hy- perextension of the arm on the side toward 74 Plum and Posner’s Diagnosis of Stupor and Coma which the nose is turned and flexion of the other arm; extension of the head may cause ex- tension of the arms and relaxation of the legs, while flexion of the head leads to the opposite response) can usually be elicited. As with de- corticate posturing, fragments of decerebrate posturing are sometimes seen. These tend to indicate a lesser degree of injury, but in the same anatomic distribution as the full pattern. It may also be asymmetric, indicating the asym- metry of dysfunction of the brainstem. Although decerebrate posturing usually is seen with noxious stimulation, in some patients it may occur spontaneously, often associated with waves of shivering and hyperpnea. De- cerebrate posturing in experimental animals usually results from a transecting lesion at the level between the superior and inferior colli- culi. 140
It is believed to be due to the release of vestibulospinal postural reflexes from fore- brain control. The level of brainstem dys- function that produces this response in humans may be similar, as in most cases decerebrate posturing is associated with disturbances of ocular motility. However, electrophysiologic, radiologic, or even postmortem examination sometimes reveals pathology that is largely confined to the forebrain and diencephalon. Thus, decerebrate rigidity is a clinical finding that probably represents dysfunction, although not necessarily destruction extending into the upper brainstem. Nevertheless, it represents a more severe finding than decorticate postur- ing; for example, in the Jennett and Teasdale series, only 10% of comatose patients with head injury who demonstrated decerebrate postur- ing recovered. 139
Most patients with decere- brate rigidity have either massive and bilateral forebrain lesions causing rostrocaudal deteri- oration of the brainstem as diencephalic dys- function evolves into midbrain dysfunction (see Chapter 3), or a posterior fossa lesion that compresses or damages the midbrain and ros- tral pons. However, the same pattern may oc- casionally be seen in patients with diffuse, but fully reversible, metabolic disorders, such as hepatic coma, hypoglycemia, or sedative drug ingestion. 138,141,142 Extensor posturing of the arms with flaccid or weak flexor responses in the legs is typically seen in patients with injury to the lower brainstem, at roughly the level of the vestibular nuclei. This pattern was described in the 1972 edition of this monograph, and has since been repeatedly confirmed. The physiologic basis of this motor pattern is not understood, but it may represent the transition from the extensor pos- turing seen with lower midbrain and high pon- tine injuries to the spinal shock (flaccidity) or even flexor responses seen from stimulating the isolated spinal cord. FALSE LOCALIZING SIGNS IN PATIENTS WITH METABOLIC COMA The main purpose of the foregoing review of the examination of a comatose patient is to dis- tinguish patients with structural lesions of the brain from those with metabolic lesions. Most patients with structural lesions require urgent imaging. Patients with metabolic lesions often require an extensive laboratory evaluation to de- fine the cause. When focal neurologic findings are observed, it becomes imperative to deter- mine whether there is a destructive or compres- sive process that may become life threatening or irreversibly damage the brain within a matter of minutes. On the other hand, even when there is no focal or lateralizing finding to suggest a structural lesion, it is important to know which signs point to specific metabolic causes, such as hypoglycemia or sepsis, that must be sought urgently. Therefore, the physician should be- come familiar with the few focal neurologic findings that are seen in patients with diffuse metabolic causes of coma, and understand their implications for the diagnosis of the metabolic problem.
Respiratory Responses The range of normal respiratory responses includes the Cheyne-Stokes pattern of breath- ing, which is seen in many cognitively normal people with cardiac or respiratory disorders, particularly during sleep. 43–45 Sleep apnea must also be distinguished from pathologic breathing patterns. Patients with severe sleep apnea may stop breathing for 10 seconds or so every minute or two. Their color may become dusky during the oxygen desaturation that ac- companies each period of apnea. Kussmaul breathing, in which there are deep but slow rhythmic breaths, is seen in Examination of the Comatose Patient 75
patients with coma due to an acidotic condi- tion (e.g., diabetic ketoacidosis or intoxication with ethylene glycol). The low blood pH drives the deep respiratory efforts, which reduce the PCO 2
pensatory respiratory alkalosis. This must be distinguished from sepsis, hepatic encephalop- athy, or cardiac dysfunction, conditions that of- ten cause a primary respiratory alkalosis, with compensatory metabolic acidosis. 143–145
The nature of the primary insult is determined by whether the blood pH is low (metabolic aci- dosis with respiratory compensation) or high (primary respiratory alkalosis). Pupillary Responses A key problem with interpreting pupillary re- sponses is that either metabolic coma or di- encephalic level dysfunction may cause bilat- erally small and symmetric, reactive pupils. Thus, a patient with small pupils and little in the way of focal neurologic impairment may still have impairment that can be attributed to either a diencephalic lesion or to symmetric forebrain compression (e.g., by bilateral sub- dural hematomas). As a result, it is generally necessary to do an imaging study (see below) within the first few hours in most comatose patients, even if the cause is believed to be metabolic. Very small pupils may be indicative of pon- tine level dysfunction, often indicating an acute destructive lesion such as a hemorrhage. However, similar pinpoint but reactive pupils may be seen in opiate intoxication. Hence, in patients who present with pinpoint pupils and coma, it is necessary to administer an opiate antagonist such as naloxone to reverse poten- tial opiate overdose. (Because an opioid antag- onist can elicit severe withdrawal symptoms in a physically dependent patient, the drug should be diluted and delivered slowly, stop- ping as soon as one notes the pupils to enlarge and the patient to arouse. See Chapter 7 for details.) Unreactive pupils usually indicate structural disease of the nervous system, but pupils may become unreactive briefly after a seizure. When a patient is seen who may have had an unobserved seizure within the past 30 minutes or so, it is necessary to re-examine the patient 15 to 30 minutes later to make sure that the lack of pupillary responses persists. Signs of major motor seizure, such as tongue biting or incontinence, or a transient metabolic acidosis are helpful in alerting the examiner to the possibility of a recent seizure. In addition, be- cause the seizure usually results in the release of adrenalin, the pupils typically are large after a seizure. Very deep coma due to sedative intoxication may suppress all brainstem responses, includ- ing pupillary light reactions, and simulate brain death (see Chapter 6). For this reason, it is critical to do urinary and blood toxic and drug screening on any patient who is so deeply co- matose as to lack pupillary responses. Ocular Motor Responses Typical oculocephalic responses, as seen in a comatose patient with an intact brainstem, are not seen in awake subjects, whose voluntary eye movements supersede the brainstem ves- tibular responses. In fact, brainstem oculoce- phalic responses (as if the eyes were fixed on a point in the distance) are nearly impossible for an awake patient to simulate voluntarily, and therefore are a useful differential point in iden- tifying psychogenic unresponsiveness. On the other hand, oculocephalic responses may be- come particularly brisk in patients with hepatic coma. Certain drugs may eliminate oculocephalic and even caloric vestibulo-ocular responses. Acute administration of phenytoin quite often has this effect, which may persist for 6 to 12 hours.
146 Occasionally, patients who have in- gested an overdose of various tricyclic antide- pressants may also have absence of vestibulo- ocular responses. 147
Patients in very deep metabolic coma, particularly with sedative drugs, may also eventually lose oculovestibular responses. Ophthalmoplegia is also seen in combination with areflexia and ataxia in the Miller Fisher variant of Guillain-Barre´ syndrome. While such patients usually do not have impairment of consciousness, the Miller Fisher syndrome occasionally occurs in patients who also have autoimmune brainstem encephalitis (Bicker- staff’s encephalitis), with impairment of con- sciousness, and GQ1b autoantibodies. 148
In such cases, the relationship of the loss of eye movements to the impairment of conscious- 76 Plum and Posner’s Diagnosis of Stupor and Coma ness may be confusing, and the prognosis may be much better than would be indicated by the lack of these brainstem reflexes, particularly if the patient receives early plasmapheresis or intravenous immune globulin. If breathing is also affected by the Guillain-Barre´ syndrome, the picture may even simulate brain death. 149
This condition must be considered among the reversible causes of coma that require ex- clusion before brain death is declared (see Chapter 8). Isolated unilateral or bilateral abducens palsy may be seen in some patients with in- creased intracranial pressure, even due to non- focal causes such as pseudotumor cerebri. 150 It
spontaneous leak, or after lumbar puncture. 151
In rare cases the trochlear nerve may also be involved. 152 Motor Responses Patients with metabolic coma may have para- tonia and/or extensor plantar responses. How- ever, spastic rigidity should not be present. Rarely, patients with metabolic causes of coma, particularly hypoglycemia, 153
will present with asymmetric motor responses or even hemi- plegia (see Chapter 5). Some have suggested that the focal signs represent the unmasking of subclinical neurologic impairment. It is true that most metabolic causes of coma may ex- acerbate a pre-existing neurologic focal find- ing, but the presence and even the distribution of focal findings in patients with hypoglycemia may vary from one episode to the next, so that the evidence for a structural cause is not con- vincing. Furthermore, focal signs caused by hypoglycemia are more common in children than adults, again suggesting the absence of an underlying structural lesion. Similarly, focal deficits are observed with hypertensive en- cephalopathy, but in this case imaging usually identifies brain edema consistent with these focal neurologic deficits. Cortical blindness is the most common of these deficits; edema of the occipital white matter is seen on mag- netic resonance images, the so-called posterior leukoencephalopathy syndrome. 154
A number of severe metabolic causes of coma, especially hepatic coma, may also cause either decere- brate or decorticate posturing. In general, al- though it is important to be alert to the pos- sibility of false localizing signs in patients with metabolic causes of coma, unless a structural lesion can be ruled out, it is still usually nec- essary to proceed as if the coma has a structural cause, until proven otherwise. MAJOR LABORATORY DIAGNOSTIC AIDS The neurologic examination, as described above, is the cornerstone for the diagnosis of stupor and coma. It can be done at the bedside within a matter of a few minutes, and it pro- vides critical diagnostic clues to determine the tempo of the further evaluation. If focal find- ings are seen, it may be necessary to institute treatment even before the remainder of the di- agnostic testing can be completed. The same may be true for some types of metabolic coma, such as meningitis or hypoglycemia. On the other hand, if the evidence from a nonfocal examination points toward a diffuse metabolic encephalopathy, the examiner usually has time to employ additional diagnostic tools. Blood and Urine Testing Because of the propensity for some metabolic comas to cause focal neurologic signs, it is important to perform basic blood and urine testing on virtually every patient who presents with coma. It is important to draw blood for glucose and electrolytes, and to do toxic and drug screening almost immediately. The blood should not be drawn in a limb with a running intravenous line, as this may alter the glucose Yüklə 9,02 Mb. Dostları ilə paylaş:
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