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?

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:

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.)

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