The Bedside Diagnosis of Coma

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Chapter 20 The Bedside Diagnosis of Coma

“I live first among the dead and the dying. That is the best world for a physician, but when it lasts too long it becomes overwhelming.”

-René Theophyle Yacinthe Laennec, 1810; letter to his cousin Cristophe

“Ignore death up to the last moment; then, when it can’t be ignored any longer, have yourself squirted full of morphia and shuffle off in a coma.”-Aldous Huxley, Time Must Have a Stop

“His was a great sin who first invented consciousness. Let us lose it for a few hours.”

-John, in The Diamond as Big as the Ritz, by F. Scott Fitzgerald—uttered before falling asleep

Generalities

1 How important is the bedside evaluation of coma?

–Important, since bedside exam can be used not only to localize the responsible lesion but also to provide diagnosis and prognosis. Hence, most maneuvers are valuable (in fact, essential) for all practicing physicians.

2 What is coma?

From the Greek word for deep sleep, coma is a disturbance of consciousness characterized by inability of the central nervous system (CNS) to receive, integrate, and willfully respond to environmental signals. Knowledge of anatomic pathways is thus key for a competent evaluation, but this must be combined with an understanding of the many (and often multifactorial) conditions that may disrupt consciousness.

3 What is consciousness?

Our most integrative function and one that provides the essential human characteristics. It is a state of awareness of self and the environment that is determined by two separate functions: (1) awareness per se (content of consciousness) and (2) wakefulness or arousal (level of consciousness). Each relies on different physioanatomic systems.!

4 What is the content of consciousness?

It is the sum of cognitive and affective mental functions (awareness) (i.e., the knowledge of one’s existence and the recognition of both internal and external worlds). It depends on the integrity of the limbic system (basal forebrain, amygdala, hippocampus, hypothalamus, and cingulum) and the cortex. Hence, it is a high-level function.

5 What is stupor? Obtundation?

They are gradations of awareness. Yet, since both terms lack precision, coma should be assessed by more objective measurements such as the Glasgow Coma Scale.

6 What is arousal? What does it depend on?

Arousal is a series of behavioral changes that occur whenever a person awakens from sleep or transits to a state of alertness—the most discernible being opening of the eyes. Arousal depends on the ascending reticular activating system being intact and properly connected with the diencephalus. Hence, it is a subcortical phenomenon that depends on a functioning brain stem.

7 Are the patient’s eyes open or closed in coma?

Closed, since coma is a sleep-like state. Yet they can be open in metabolic comas (hepatic or uremic) or in chronic posttraumatic encephalopathies. For example, eyes are open in the late stage of hypoxic encephalopathy, in fact roving around so much as to convince friends, family, and Washington legislators that the patient has finally emerged from coma, when, in reality, the patient has entered vigil coma (persistent vegetative state—PVS).

8 So why are comatose patients unconscious?

Because they lack both arousal (brain stem) and content of consciousness (cortex/limbic system). Conversely, PVS patients have arousal (hence, wakefulness), but still lack content of consciousness. Hence, they have awareness/arousal dissociation. In fact, Kinney has defined PVS as a “locked-out syndrome,” insofar as “the cortex is disconnected from the external world, and all awareness of it is lost.” This is usually due to three causes: (1) widespread and bilateral cortical lesions (hypoxic or ischemic), (2) diffuse damage of intracortical/subcortical connections in the white matter of the cerebral hemispheres (due to trauma or hypoxia-ischemia), and (3) bilateral necrosis of the thalamus.

9 Why can thalamic lesions cause coma?

Because they interrupt the cortex-activating fibers that pass through them. Bilateral hypothalamic lesions can cause coma, too, and also present with sleep phenomena, such as yawning, stretching, and sighing.

10 What is the neurologic basis of coma?

It is a diffuse and bilateral cortical dysfunction. This is either primary or secondary to a brain stem injury that compromises the ability of the ascending reticularis activating system to arouse the cortex.

11 What is the ascending reticular activating system (RAS)?

A core of gray matter that runs dorsally through the four layers of the brain stem. It connects caudally with the reticular intermediate grey lamina of the spinal cord and rostrally with the diencephalus (subthalamus, hypothalamus, and thalamic nuclei). Its main function is to “power” the cortex (i.e., to provide arousal).

12 So what is the mechanism of coma?

By analogy with a computer, we could describe it as a state in which either the chips (cortex) or the generating power (reticular activating system) are dysfunctional. If the power (brain stem) is off, the computer will not work even though the chips (cortex) might be intact. Neurologically, this will manifest as lack of arousal.

13 Does a unilateral hemispheric lesion cause coma?

No, unless there is a preexistent contralateral process or a new secondary brain stem compression (due, for example, to herniation). The latter compromises the RAS, thus causing coma. In all other cases, coma requires extensive damage of both hemispheres.

14 Do all brain stem lesions cause coma?

No. The capacity of a brain stem lesion to induce coma depends on its speed of onset, site, and size. Hence, brain stem infarctions or hemorrhages are a common cause of coma, whereas slower lesions (like those of multiple sclerosis or tumor) rarely do so. Note that lesions below the pons do not normally result in coma. Finally, drugs and various dysmetabolic states produce coma by depressing both the cortex and the RAS.

15 So what are the causes of coma?

Diffuse or extensive processes affecting the whole brain (but primarily the cortex)

Brain stem lesions—including not only primary disorders of the brain stem (such as hemorrhages, infarction, and cancer), but also compression from mass lesions of the posterior fossa (such as cerebellar hemorrhage/infarction)

Supratentorial mass lesions causing transtentorial herniation with brain stem compression (these are often associated with other neurologic signs, such as third nerve palsy and crossed hemiparesis) (see Fig. 20-1)

In a large study of “medical comas,” 50% of all cases were cerebrovascular in nature, 20% due to hypoxic/ischemic injury, and the rest is a miscellanea of metabolic/infective encephalopathies.

Figure 20-1 Sites and causes of coma.

(From Bateman: Neurological assessment of coma. J Neurol Neurosurg Psychiatry 71[Suppl 1]:i13–i17, 2001, with permission.)

16 What is the function of the neurologic exam in comatose patients?

To localize the responsible lesion and, possibly, describe its nature. In this regard, the exam of comatose patients should categorize them as:

Coma without focal signs or meningism: The most common; due to dysmetabolic states of the entire CNS: anoxic/ischemic, toxic, drug-induced, infectious, postictal.

Coma without focal signs but with meningism: Due to subarachnoid hemorrhage, meningitis, and meningoencephalitis

Coma with focal signs: Due to intracranial hemorrhage, infarction, tumor, or abscess

17 What is the neurologic exam of a comatose patient?

A simple one. Since the cortex of coma is, by definition, dysfunctional, exam is only aimed at assessing brain stem function. This is carried out in a rostral-caudal and level-by-level fashion. If all four layers of the brain stem are working properly, then the coma is cortical (i.e., one in which the cortex is primarily dysfunctional). If one or more brain stem layer is damaged, then the coma is a brain stem coma (i.e., one in which the cortex is secondarily dysfunctional as a result of direct brain stem damage) (see Table 20-1).

Table 20-1 Clinical Assessment of Coma

General Examination

Skin (e.g., rash, anemia, cyanosis, jaundice)

Temperature (fever-infection, hypothermia-drugs, circulatory failure)

Blood pressure (e.g., septicemia, Addison’s disease)

Breath (e.g., fetor hepaticus)

Cardiovascular (e.g., arrhythmias)

Abdomen (e.g., organomegaly)

Neurologic Examination

Head, neck, and eardrum (trauma)

Meningism (subarachnoid hemorrhage, meningitis)

Funduscopy

Level of Consciousness

Glasgow Coma Scale (verbal response, eye opening, motor response)

Brain Stem Function

Pupillary responses

Spontaneous eye movements

Oculocephalic responses

Caloric responses

Corneal responses

Motor Function

Motor response

Deep tendon reflexes

Muscle tone

Plantars

Respiratory Pattern

Cheyne-Stokes: hemisphere

Central neurogenic hyperventilation: rapid/midbrain

Apneustic: rapid with pauses/lower pontine

(Adapted from Bateman DE. Neurological assessment of coma. J Neurol Neurosurg Psychiatry 71[Suppl 1]: i13–i17, 2001.)

18 What is a level-by-level exam of the brain stem?

An exam that tests each brain stem layer with at least one neurologic reflex. If the reflex is abnormal, the corresponding brain stem level is considered damaged or dysfunctional. Thus, the neurologic exam of coma relies on four reflexes, one for each of the brain stem layers.

19 What is the first step in evaluating coma?

To assess whether there is any response to verbal stimuli. This can be done by asking patients to open their eyes and look up, down, and from side to side. “Locked-in” patients (see question 54) will open their eyes on command, and even look up and down, but will be unable to make any other purposeful response. Once this is done, the next step in the evaluation of coma is to test the first and uppermost brain stem level: the thalamus.

20 Which reflex tests thalamic function?

The response to pain. Since the thalamus is an integrating center for all sensory inputs (with the exception of proprioceptive signals, which travel instead to the cerebellum), thalamic testing requires administration of painful stimuli, like compression of the supraorbital nerve. This will induce a facial grimace, which in cases of afferent peripheral lesions of the pain pathways will occur without limb response. Limb response also can be assessed by pressing down on the patient’s nail bed with a reflex hammer. Look for presence, symmetry, and nature of the response, since these can localize the lesion.

21 What are the proper/improper responses of a comatose patient to painful stimuli?

It depends. The proper response of a conscious, lethargic, or obtunded patient is to withdraw or push away the offending source. Thus, a proper response to compression of the ungual bed with a pencil would be to pull back or push away the examiner’s hand. An improper response would be to assume a particular posture—for example, decorticate or decerebrate.

22 What are these postures?

Valuable findings for localization. A decorticate posture is a sign of subcortical/thalamic dysfunction. It consists of upper extremities’ flexion, with extension and internal rotation of lower extremities. A decerebrate posture consists instead of extension and internal rotation of both upper and lower extremities. This is a sign of upper brain stem dysfunction, usually the consequence of midbrain or upper pontine lesions. Finally, lower brain stem damage (low pontine and medullary) will cause no response to painful stimuli, or just extension of the upper extremities with simple bending of the knees (a spinal reflex). Unilateral decerebrate or decorticate responses also may occur, usually indicating unilateral lesions. Overall, it is easy to separate decortication from decerebration by remembering that in de-cor-tication the hand points toward the heart (cor), whereas in decerebration the hand points away from the heart (see Fig. 20-2).

Figure 20-2 Motor response to pain. The symmetry or asymmetry of the motor response can assist localization. A, Left hemisphere lesion. The two figures illustrate localization of pain with the left hand and flexion or extension on the right. B, Subcortical: unilateral left-sided lesion exerting a variable contralateral effect. The figures illustrate flexion to pain with the left hand with either extension or flexion with the right and hyperextension in both lower limbs. C, Midbrain upper pontine: a bilateral upper and lower limb extension response. D, Lower pontine/medullary: a bilateral extensor upper limb posture with either flaccidity or minimal diminished flexor response in lower limbs.

(From Bateman: Neurological assessment of coma. J Neurol Neurosurg Psychiatry 71[Suppl 1]:i13–i17, with permission.)

23 What about other involuntary movements?

Patients with coma may exhibit various movement disorders (such as myoclonic jerks and tonicoclonic seizures). These are especially common in toxic-metabolic disorders (anoxic encephalopathy) and carry a worse prognosis.

24 What is the second layer in the brain stem?

The midbrain.

25 Which reflex tests the function of the midbrain?

The pupillary reflex. This is elicited by shining a penlight into the patient’s eye and then looking for a direct and consensual response (i.e., constriction of both the ipsilateral and contralateral eye). Assessment of pupillary response is very important for localizing the site of lesion in coma and for separating structural from toxic/metabolic causes, since pupillary responses are usually preserved in toxic-metabolic states.

26 What is the significance of pupillary abnormalities?

Paralysis of the pupil (i.e., inability to constrict in response to light) indicates an ipsilateral dysfunction of the midbrain (midbrain pupils = midposition or slightly widened and fixed pupils unreactive to light). Pontine pupils are instead bilateral small pupils that still react to light, even though this may only be visible under a magnifying glass. They reflect anatomic lesions in the tegmentum. Pinpoint pupils are both small and constricted but reactive; they often occur in metabolic encephalopathy and may be due to opiates. Bilaterally dilated pupils are instead encountered in patients with atropine and scopolamine toxicity (see Fig. 20-3). Note the following: (1) drugs that are frequently used in resuscitation from cardiac arrest (such as atropine or dopamine) may have misleading effects on pupillary reactions, (2) lesions above the thalamus and below the pons usually preserve pupillary reactions, and (3) finally, a third nerve lesion can be differentiated from a contralateral Horner’s by the position of the eye and the degree of ptosis.

Figure 20-3 Pupils in comatose patients.

(From Plum F, Posner JB: The Diagnosis of Stupor and Coma, 3rd ed. Philadelphia, FA Davis, 1980, with permission.)

27 What is anisocoria?

From the Greek aniso, unequal, and kore, pupil, this is a pupillary asymmetry that is often congenital and physiologic. It is common, being present in up to 20% of the population.

28 How can one distinguish physiologic from pathologic anisocoria?

The pupils of physiologic anisocoria have different size (often by <1 mm) but are still reactive to light. Presence of anisocoria may depend on ambient light or time of exam

29 What is the third level in the brain stem?

The pons.

30 Which reflex tests the function of the pons?

The doll’s eye reflex.

31 What is the doll’s eye reflex?

A very confusing term, first introduced in the heyday of physical diagnosis, when Victorian dolls were more popular, and everyone knew how their eyes behaved. Still, the neurologic description (oculocephalic reflex) is preferable, since it conveys an anatomic sense of the pathway. To test this reflex, observe the patient’s eyes during passive rotation of the skull. Yet, if you suspect cervical trauma do not rotate the patient’s head. Instead, do cold water caloric testing (oculovestibular reflex), a safer way to test the integrity of vestibular and oculomotor systems. To do so, examine the tympanic membrane (to ensure that there is no perforation or impacted cerumen); then, with the patient’s head 30 degrees higher than the horizontal line, irrigate the auditory canal with up to 120 mL of ice cold water. In the unconscious patient with intact brain stem function, this will cause the eyes to slowly and tonically deviate toward the irrigated ear.

32 What is the pathway of the oculocephalic reflex?

The stimulus is either mechanical (rotation of the patient’s head along the horizontal plane) or thermic (injection of a syringe full of liquid in the external ear canal).

The receptors are in the inner ear (semicircular canals and utriculus).

Once these receptors are activated, the afferent signal is carried to the central nervous system via the eighth cranial nerve. This enters the brain stem at the cerebellar–pontine angle.

The impulse is then taken to the ocular muscles by the efferent pathway (third and sixth cranial nerves), eliciting eye movement across the horizontal plane. Since the third nerve resides in the midbrain and the sixth in the upper pons, the electrical impulse will need a “connecting wire” to travel from the lower pons to the upper pons and midbrain. This wire is the medial longitudinal fasciculus (MLF).

Hence, when testing the integrity of the oculocephalic reflex, we test the integrity of the MLF. This is important not for the MLF per se, but because the MLF is totally imbedded in the reticular activating system (RAS), a crucial structure for arousal. Hence, the MLF acts like the canary that was used to identify gas leakage in coal mines. Dysfunction of the MLF indicates dysfunction of the surrounding RAS. Hence, loss of the oculocephalic reflex indicates a lesion in the pontine RAS, thus suggesting a brain stem coma.

33 What is a normal oculocephalic response?

It depends on whether the patient is awake or comatose and whether the coma is due to a primary (cortical) dysfunction or one secondary to pontine insults. In comatose patients with preserved brain stem function, passive rotation of the head will generate a conjugated movement of the eyes toward the opposite side. That is, the eyes do not stay fixed in the midline (as if they were painted), but they move. In cases of brain stem damage (with lost reflex), the eyes do not move. Instead, they remain in their initial position—fixed like in a cadaver. In awake patients, the cortex responds to head rotation by suppressing eye movement, thus inhibiting the oculocephalic reflex (it does so to allow the eyes to see where the head is pointing).

34 Does any other reflex test the function of the pons?

The corneal reflex. This elicits blinking of both eyes in response to a corneal sensory stimulus (like touching it with a cotton whisk). This triggers sensory input across the trigeminal (fifth) nerve, which enters the brain stem at multiple levels, including the pons and medulla. The efferent pathway is then carried out to the orbicularis muscle, along the seventh nerve, eventually eliciting a blinking of the eye. Hence, the corneal reflex consists of a long loop that relies on several connecting wires, such as the MLF, all imbedded in the RAS. Like the oculocephalic, the corneal reflex assesses the function and integrity of the RAS.

35 What is the fourth and lowermost layer of the brain stem?

The medulla.

36 Which reflex tests medullary function?

The one testing the integrity of the most primitive of all function—the cardiorespiratory. Since the medulla houses the major cardiac and respiratory centers, dysfunction of these structures will manifest with cardiorespiratory instability, such as major irregularities of heart rate and rhythm, unstable blood pressure, and apnea.

37 What is an apnea test?

It is the inability of the patient to take a spontaneous breath after maximal carbon dioxide stimulation (60 mmHg). It indicates major medullary dysfunction. To carry it out, you need to disconnect the patient from the ventilator, while administering 100% O₂ via cannula. Measure arterial PO₂, PCO₂, and pH after approximately 8 minutes, and reconnect the ventilator. The test is positive if respiratory movements are absent and arterial PCO₂ is 60 mmHg (or 20 mmHg increased over a baseline normal PCO₂).

38 What is the implication of a global absence of brain stem function?

It indicates death (see question 53). Given its implications, a repeat neurologic exam is usually required at a 12-hour interval. Also, toxic-metabolic states need to be excluded.

39 What is a toxic-metabolic coma?

id=”p0400″/>A wastebasket term indicating a global CNS dysfunction that is possibly reversible, since it is due to exogenous or endogenous toxins. Although toxins can impair both the cortex and brain stem, they usually affect the cortex more, since this is less resilient. Hence, coma patients with an intact brain stem should be considered toxic-metabolic until proven otherwise.

40 Can a localized process cause coma?

Only if affecting the brain stem (directly or indirectly [i.e., herniation]). Otherwise, a localized cortical process (like a stroke) causes lethargy or stupor, but not coma.

41 What are the causes of a toxic-metabolic coma?

They are exogenous or endogenous toxins, affecting the cortex bilaterally and diffusely.

Exogenous toxins are poisons. Hence, a toxic screen should always be carried out.

Endogenous toxins are also poisons that accumulate when there is dysfunction of major detoxifying parenchyma (hepatic, renal, or hypercapnic encephalopathy).

Endocrinopathies: These include hypothyroidism (myxedema coma) and global dysfunction of the hypophysis (panhypopituitarism) or adrenals (Addisonian crisis). In addition, defects in glucose metabolism, either in excess (diabetic ketoacidosis or hyperosmolar nonketotic coma) or in deficiency (hypoglycemic encephalopathy), also may cause coma. Finally, electrolyte disturbances (hyponatremia and hypernatremia, hypercalcemia, and hypermagnesemia), can do it, too.

Subarachnoid toxins: Direct, generalized poisoning of the cerebral cortex by toxins spreading along the subarachnoid space is another cause of toxic-metabolic coma. The most common culprit is blood (subarachnoid hemorrhage) or pus (purulent meningitis). Both can be detected by lumbar puncture. Hence, this should be part of the standard work-up of all comatose patients, especially those with meningeal signs.

A generalized electrical disturbance (such as a seizure) also may lead to coma. This can occur during or after the crisis (postictal coma). Since subclinical seizures may lack classic tonicoclonic contractions (i.e., patients can be immobile or just exhibit a fine fluttering of the eyelids), all coma patients should undergo electroencephalographic (EEG) testing.

Finally, a common cause of metabolic coma is hypoxic encephalopathy (HE), a term that is probably incorrect, since the bilateral cortical dysfunction of these patients might be due more to reperfusion injury than true hypoxia. HE affects primarily the cortex, while the brain stem remains mostly intact. Thus, after going through the initial state of coma (i.e., sleep-like), HE patients eventually emerge into persistent vegetative state, insofar as their brain stem sends impulses to the cortex (arousal) but the cortex is unable to process them. Hence, the original term of “apallic syndrome” (i.e., one characterized by destruction of the pallium, the telencephalon-covering gray matter).

42 How common is coma due to cardiac arrest?

Very common. Cardiovascular disease is the leading killer in the United States, accounting for one half of all yearly deaths. Of these, a quarter million will not even make it to the hospital (which is the equivalent of all World War II U.S. deaths in just 1 year); 500,000 will instead suffer arrest (and attempted resuscitation) during hospitalization. Survival rates for both groups are dismal: 2–33% for prehospital arrests and 0–29% for inpatient; 80% of all survivors are comatose after resuscitation, making cardiac arrest the third most common cause of coma after trauma and overdose. Rates of meaningful neurologic recovery also are poor, ranging from 10–30%. Given this premise, physical examination provides a universal and valuable tool to gather prognostic information in these patients. It is easy to perform, always available, and quite accurate.

43 In addition to cardiac arrest, what are the other causes of PSV?

The Multi-Society Task Force on PVS has classified its causes in three main groups: (1) acute injuries (most common being indeed hypoxic-ischemic or traumatic); (2) degenerative and metabolic disorders, including dementia; and (3) developmental malformations (with the most important being anencephaly). Still, the most common cause of PVS remains hypoxic-ischemic encephalopathy and head trauma.

44 What is the Glasgow Coma Scale (GCS)?

It is an important tool for evaluating coma, first introduced by Teasdale and Jennett in 1974. Prior to it, coma assessment was exclusively based on presence/absence of various brain stem reflexes (previously discussed). The GCS has instead provided a standardized way of classifying the condition, and as such has become an international standard. It consists of an ordinal scale calculated from the sum of three components: motor response, verbal response, and eye opening. Scores range from 3–15 (Table 20-2). Although originally described for traumatic coma, the GCS is equally applicable to nontraumatic coma. Still, even though it does predict poor neurologic outcome, it is not as predictive as the individual motor and brain stem reflex components (see questions 45 and 46). Moreover, assessing motor response requires that you apply central pain because peripheral stimulation may cause misleading spinal reflexes that do not represent a true motor response. Hence, to give a proper painful stimulus you need to pinch the skin of the supraorbital region or the sternum (using, for example, your knuckles to apply a firm twisting pressure).

Table 20-2 Glasgow Coma Scale

45 What are the crucial maneuvers in the evaluation of hypoxic coma?

In addition to calculating the GCS, various brain stem reflexes may provide diagnostic and prognostic information. These include the very same ones reviewed before: the pupillary reflex (which involves cranial nerves II and III), and the corneal reflex (which involves cranial nerves V and VII); but also the gag and cough reflexes (which test cranial nerves IX and X). To elicit a gag reflex, apply a tongue depressor to the posterior pharynx: the normal response is a symmetric rise in the soft palate. If the patient is intubated, you can assess instead the cough (or carinal) reflex. This is elicited by applying deep suction through the endotracheal tube to the carina. The normal response is a gasp followed by several rapid coughs. Vestibular signs also are quite important, and include the aforementioned oculocephalic (or “doll’s eye”) reflex.

46 What signs best predict lack of recovery after cardiac arrest?

In a meta-analysis of almost 2000 patients, Booth et al. found that the signs with the highest likelihood ratios (LRs) at 24 hours were absent corneal reflexes (LR, 12.9), absent pupillary reflexes (LR, 10.2), absent motor response (LR, 4.9), and absent withdrawal to pain (LR, 4.7). At 72 hours, absent motor response predicted death or poor neurologic outcome (LR, 9.2). No sign had likelihood ratios that strongly predicted good neurologic outcome. Hence, lack of pupillary and corneal reflexes at 24 hours and no motor response at 72 strongly argue against recovery.

47 Do seizures or myoclonus have significance in coma after cardiac arrest?

Yes, and both are ominous. Overall, 25–50% of comatose survivors of arrest exhibit either seizures or myoclonus, usually early in the postresuscitation stage. Seizures may be focal or generalized. Myoclonus refers instead to isolated and sudden muscular contractions, which may also be focal or generalized (the latter involving axial and limb musculature). Remember to discontinue medications that may interfere with the neurologic exam, such as paralyzing agents or sedatives—so ubiquitous in today’s intensive care units.

48 How precise is the clinical exam of coma?

Quite precise. Five studies have assessed its precision in evaluating comatose patients. Interobserver agreement was good, with little significant change between experienced nurses, residents, and practicing physicians. Overall, the precision of the examination (including GCS and brain stem reflexes) was moderate to substantial.

49 What is the bottom line for the neurologic exam of coma?

It is a valuable tool, with moderate to substantial precision and good prognostic value.

From the Greek a (lack of) and sterixis (fixed position), this is the bilateral flapping tremor of metabolic encephalopathy, particularly impending hepatic coma (see Chapter 15, question 79). It was first described in 1949 by Foley and Adams. Foley, a notorious wit, coined the term while drinking at a Greek bar across from Boston City Hospital. He then used it semiseriously in a paper, not expecting much of it. To his amazement, the word became the official academic term for flapping tremor due to the inability of maintaining a voluntary muscular contraction (asterixis requires patient cooperation and thus cannot be elicited in stupor or coma). It consists of involuntary jerking movements, in a typical sequence of flexions and extensions. Since it reflects a lapse of posture, it involves antigravitary muscles, such as those of wrist, metacarpophalangeal, and hip joints, but also toes, eyelids, and even tongue. Still, it is typically assessed in the hands.