Chapter 17 - Depression of consciousness


Some definitions are necessary because medical and lay jargon for the various levels of depression of consciousness is legion and loosely applied. The subject's behavior or absence of behavior as determined by careful observation and described in simple terms is most informative.


Coma is a pathologic state of unconsciousness from which a person cannot be aroused to make purposeful responses. As a rule light coma is present when reflex motor response (i.e., decorticate and decerebrate posturing) can be elicited by noxious stimulation. In deep coma there is no response.


Stupor is a state of pathologic reduced consciousness from which the patient can be aroused to purposeful response only with persistent external stimulation. This covers the broad range from persistent drowsiness from which the patient can be aroused by constant stimulation for periods of alert wakefulness to deep stupor from which the patient can be aroused only to the level of poorly directed defense against noxious stimuli.

Sleep is a nonpathologic depression of consciousness from which the subject can be aroused to persistent alert wakefulness with appropriate non-noxious stimuli. Sleep is an active and reversible suppression of reticular arousal.

Coma-like States

Hysterical coma or stupor is feigned or subconsciously assumed depression of consciousness differentiated clinically from true coma or stupor by a normal and alert electroencephalogram, the presence of nystagmus on caloric irrigation of the external auditory canal (see Chapter 6) and the absence of abnormal neurologic signs.

The de-efferented state, in which a person has lost most if not all motor behavior, can occur with several conditions. Diffuse neuromuscular dysfunction as with myasthenia gravis (myasthenic crisis or overmedication with cholinesterase inhibitors) and diffuse polyradiculoneuropathy (the Guillain-Barre syndrome, porphyria) can make a patient behaviorally unresponsive, although s/he may be perfectly lucid with respiratory support. The history and presentation of these disorders are such that the patient is unlikely to be considered comatose.

When the base of the pons (less often the midbrain) is transected or the lower pons is transected in its entirety by hemorrhage or infarction, a state of deefferentation occurs that renders the patient acutely unresponsive (despite being awake and aware). Such patients are unable to move except for vertical and convergent eye movement and eye-opening systems (these functions are located in the preserved tegmentum of the midbrain). The auditory system, lying laterally along the brain stem, usually is not affected by the central hemorrhage or infarction, which often arises from involvement of the paramedian vasculature. Thus the patient hears and sees. Unless the clinician asks them to look up or down, the patient may be said to be "locked in", a term aptly applied to this state by Plum and Posner. These patients' minimal ability to communicate is often unrecognized, so they are usually considered and treated as if comatose.

Table 17-1 lists examples of the more common processes leading to pathologic depression of consciousness.

Substrates of consciousness

Consciousness requires normal activity of the cerebral cortex since the hemispheres are the substrate for awareness of self and environment and embody the sentient functions that define human intellectual existence. Therefore, anything that diffusely depresses the activity of cerebral cortical neurons will produce stupor and coma. In general, this can be due to actual destruction of cortical neurons or can be due to conditions that suppress the activity of the cortex, which is generically called "encephalopathy". However, this normal activity of the cerebral cortex also requires normal activity in the reticular formation of the rostral brain stem extending from the midpons through the diencephalon (Figure 17-1), termed the reticular activating system.

The reticular formation can function normally even after destruction of the cerebral cortex (such as following diffuse cerebral anoxia from cardiac arrest). In general, the reticular formation and brain stem are more resistant to damage than is the cerebral cortex. In the case of the patient with diffuse cerebral cortical damage, the surviving reticular formation and brain stem may be capable of supporting a crude sleep-waking vegetative state. In contrast, the cerebral hemispheres cannot function in the absence of reticular activation. Bilateral loss of the reticular formation at the midbrain level (for example from ischemic or hemorrhagic transection of the upper brain stem), will terminate all sentient cerebral activity.

In this chapter we concern ourselves with processes that depress consciousness either by diffusely suppressing cerebral cortical activity or by damaging the reticular formation (or both). We will consider these two potential substrates for stupor and coma and how we approach the evaluation of such patients.

Cerebral Hemispheres

Stupor and coma can result from depression of function of both cerebral hemispheres. This depression is almost invariably the result of metabolic abnormality or toxic effect on the cortex and is termed "encephalopathy". Depending on the type and degree of metabolic insult, this may also depress the function of the reticular formation. Generally, the reticular formation is substantially more resistant to metabolic and toxic influences than the cerebral cortex.

Metabolic depression of brain function is the most common cause of stupor and coma and may manifest itself in a number of ways. The various manifestations of metabolic encephalopathy are discussed in greater detail in these case examples. Table 17-1 lists the basic categories of metabolic dysfunction associated with depression of consciousness that must be considered.

Reticular Formation

As described above, the midbrain reticular formation (reticular activating system) is necessary for maintenance of consciousness. The reticular formation can be suppressed by the same processes that are suppressing cerebral cortical function. Commonly, the reticular formation is somewhat more resistant to suppression than are the more sophisticated functions of the cerebral cortex, but will be affected if the suppression is greater. However, in addition to this kind of suppression of function, the reticular formation is also susceptible to direct damage because of the fact that it is contained in a relatively small area of the brain stem. There are several types of lesions that damage the reticular formation. The most common of these injuries include ischemia-infarction, hemorrhage, neoplasm, abscess, or direct traumatic disruption. In addition to these primary injuries, the reticular formation can also be damaged by compression. This usually results from a space-occupying lesion that forces part of the temporal lobe (usually the uncus) through the tentorial notch. Recall that the midbrain passes through this notch. This process, termed "transtentorial herniation" (or "uncal herniation") usually occurs due to neoplasms, hemorrhage (intracerebral, subdural, or epidural hematomas), abscess, or other conditions that cause brain edema.

In the case of herniation, the initial lesion is usually unilateral and many cases present with focal lateralizing signs and symptoms (e.g., hemiparesis, hemihypoesthesia, dysphasia) that precede secondary brain stem compression (which results in the depression of consciousness). Brain stem compression occurs because the vectors of force from an expanding supratentorial mass are ultimately directed toward the tentorial notch, which is the only significant exit from the otherwise closed, rigid-walled, supratentorial space. This progression of transtentorial herniation results in a rostrocaudal deterioration in function. Progressively, the diencephalon, mesencephalon, and finally the pons and medulla are compromised.


From the above discussion, you should be aware that depressed consciousness might result from either bilateral cerebral cortical depression (often with later suppression of reticular function) or from damage to the brain stem reticular activating system. The conditions that produce diffuse cortical suppression are very different from the conditions that damage the reticular activating system. Therefore, the initial evaluation of the comatose patient focuses on differentiation of patients with these two causes of coma. This permits the immediate and correct selection of further diagnostic tests and institution of appropriate therapeutic management of the patient. Table 17-2 lists the major steps taken by the physician from the time the patient enters the emergency department.

The neurologic evaluation of the comatose patient can be a relatively rapid and efficient procedure and should enable the examiner, with little difficulty, to differentiate between the two basic causes of depression of consciousness: (1) brain stem reticular formation depression, and (2) bilateral cerebral cortical depression (with or without accompanying brain stem reticular depression). Of course, it is not possible to examine all elements of the nervous system in the patient with depressed levels of consciousness. It has been found that careful observation of five categories of neurologic function in most cases is adequate for these purposes: (1) level of consciousness, (2) respiratory rate and pattern, (3) pupillary function, (4) oculomotor-vestibular function, and (5) motor function. The evaluation of these levels of functioning can help to ascertain what levels of the nervous system are and are not working and serial observation of these can detect progression of the condition.

1. Level of consciousness

This analysis permits determination of the degree of impairment of consciousness ranging from awake and alert to stuporous and comatose. It is based on observation of the degree of response to stimulation. Of course, the patient who is awake and alert responds appropriately and normally to questions and commands. The patient who is drowsy opens their eyes to verbal stimulation and responds appropriately, but drifts back to a condition with their eyes closed when not stimulated. A deeper stupor requires more vigorous stimulation in order to get the patient to open their eyes and attend to stimuli. And finally, in a deep coma, there is no response to even noxious stimulation (such as tickling the nares or squeezing the fingernail). This level should be recorded so that it can be determined whether the patient is deteriorating as time passes.

2. Respiration (see Figure 1-1).

The inspiratory and expiratory centers are located in the medullary reticular formation. These areas are under control from higher levels of the neuraxis and different patterns of respiration will occur as progressive levels of the nervous system are suppressed or damaged. These respiratory patterns have a general, although not perfectly reliable, relationship to involvement of different levels of the brain stem.

Obviously, the changes between these types of respirations can attend changes in the patient's condition and progression down the list (from Cheyne-Stokes to central neurogenic hyperventilation, for example) is a sign of a worsening state.

3. Pupils.

Pupil size and reactivity are mediated through variations in the equilibrium between sympathetic dilation and parasympathetic constriction (see Chapter 4).

4. Oculomotor-vestibular function (see Chapter 6).

One of the most important determinations that can be made in the comatose patient is whether there is normal oculomotor-vestibular function. This is because the reflexes involved traverse the brain stem adjacent to the reticular activating system. Additionally, in the patient with an awake and alert cerebral cortex, there are competing reflexes that produce a distinctive pattern of eye movements. Therefore, this single assessment can determine whether the brain stem reticular formation is intact and how alert the cerebral cortex is.

5. Motor function (see Chapter 8).

Rostral-caudal deterioration

Expanding masses are a model for discussion of the effects of damage to the various levels of the nervous system. Masses include tumors, abscesses or hemorrhage but also can include edema, whatever the initial cause of the injury. Expanding masses result in rostral-caudal deterioration of neural function which can be observed in patients in whom the process cannot be stopped. In this model, cortical function is affected first, followed by dysfunction of the diencephalon, then midbrain (often due to herniation of the uncus of the medial temporal lobe), then pons and medulla. Figure 17-2 depicts an expanding right intracerebral hemorrhage and its effect on the rostral brain stem. The sequential effects of such a lesion on functions in the 5 categories (consciousness, respirations, pupils, oculomotor/vestibular function and motor response) are listed in Table 17-3.

The first effect of such an expanding lesion would be due to its local effects on sensory and motor function (i.e., left hemiparesis, left hemisensory defect, left visual field deficit). However, when expansion of the mass results in bilateral pressure on the upper brain stem (i.e., diencephalon), characteristic changes in these 5 variables will begin to occur. The progression of deterioration usually occurs in sequence, although steps can be skipped, particularly in rapidly evolving lesions. For example, consciousness will progress from stupor to coma; respirations will progress from eupnea through Cheyne-Stokes respirations, central neurogenic hyperventilation, ataxic breathing and, finally apnea; pupils will progress from normal reactive, through small reactive, to midposition/fixed; the vestibulo-ocular response will go from normal nystagmus through loss of the fast component, to dyconjugate response and then loss of the tonic phase of the reflex (usually with loss of the corneal reflex); and the motor response will go from normal mobility, through paratonia, to localizing noxious stimuli to withdrawal responses, then decorticate posturing and decerebrate responses before losing all motor response other than simple spinal reflexes. The chart usually allows you to determine the level of preserved function (Table 17-3).

It is a useful didactic exercise to understand these levels of function. However, for practical purposes, the determination of progressive levels of rostrocaudal deterioration has prognostic but little therapeutic value when the process has extended beyond the midbrain. When loss of midbrain function is complete in acute deterioration, secondary hemorrhages (Duret hemorrhages) develop into the midbrain and pontine tegmentum in most patients, signaling the permanent cessation of reticular activating system function. These are presumed to occur secondary to traction and tearing of the paramedian vessels penetrating from the major basal arteries (basilar and posterior cerebral arteries). Therefore it is extremely important to recognize rostrocaudal deterioration early in order to institute therapy to prevent progression.

Metabolic encephalopathy

The cerebral cortex is more susceptible to toxic, metabolic or drug-related suppression of activity than is the brain stem. Therefore, metabolic suppression of neural functions initially tends to spare brain stem reflexes and, until very late in the process, spares primitive brain stem functions (oculovestibular, respiratory and pupillary functions) until late. The pupils are usually the last reflex to be detected with metabolic suppression, although a magnifying lens (or otoscope) and a very bright light may be necessary to detect the pupillary response. These case examples will elaborate on the various presentations of metabolic encephalopathy.

We would like to draw your attention to a single important reference for further reading on the subject of stupor and coma. The information in this chapter is considered a primer based largely on the classic text: Diagnosis of Stupor and Coma by Fred Plum and Jerome Posner. Clarity and comprehensive coverage make their book required reading and reference for all physicians who deal with patients who have depressed levels of consciousness.

Dementia vs. encephalopathy

We have already discussed dementia (Chapter 2 and Chapter 16), which results from bilateral degeneration of the cerebral hemispheres. Of course, this causes varying degrees of loss of cognitive and emotional function. However, if this is very severe, there may be so much loss of cortical function as to produce depressed consciousness. However, more often, depressed consciousness in a patient with dementia is due to the presence of one or more metabolic dysfunctions. Patients with dementia are very susceptible to conditions such as may result from hypoxia (often due to pneumonitis), sepsis or renal failure from chronic urinary tract infection, or simply malnutrition, all of which depress further the functions of the cerebral hemispheres.



Define the following terms:

stupor, coma, delerium, encephalopathy, reticular activating system, decorticate posture, decerebrate posture, "locked-in", Cheyne-Stokes respirations, central neurogenic hyperventilation, ataxic respiration, vestibulo-ocular reflex, diencephalic pupils.
Stupor is a nonsleep depression of consciousness where normal reactions to the environment are blunted.
Coma is a nonsleep loss of consciousness where normal reactions to the environment are lost.
Delerium is a nonsleep depression of consciousness where normal reactions to the environment are blunted and replaced by agitated responses.
Encephalopathy is diffuse suppression of normal cerebral cortical function that often results in stupor or coma.
The reticular activating system is the reticular system connecting the rostral pontine and midbrain through the thalamus to the cerebral cortex.
Decorticate posture is a posture in which the lower limbs are extended and the upper limbs flexed in response to noxious stimuli.
Decerebrate posture is a posture in which the lower and upper limbs are extended in response to noxious stimuli.
"Locked-in" refers to damage to the base of the pons with preservation of consciousness and vertical eye movements, but loss of all other voluntary movements.
Cheyne-Stokes respiration is a pattern of breathing characterized by waxing and waning amplitude of respiration with preserved respriatory frequency.
Central neurogenic hyperventilation typically occurs with pontine lesions, with increased depth of respiration.
Ataxic respiration is a pattern of respiration with irregular depth and frequency of respirations with pauses.
The vestibulo-ocular reflex is the reflex that keeps eyes directed on a target during head movements. It can be elicited by head movments or caloric tests.
Diencephalic pupils refer to bilaterally small pupils with lesions of the thalamus.

17-1. What are the two potential causes of coma?

Answer 17-1. Coma may result from diffuse dysfunction of cerebral hemispheres or from damage to reticular activating system in brain stem (especially midbrain).

17-2. What are the causes of diffuse cerebral cortical suppression?

Answer 17-2. This may be due to direct cerebral effects of sedative drugs, systemic electrolyte disturbances, various severe metabolic upsets, trauma, diffuse ischemic damage,may be observed in the period after seizure (postictal). In these cases of toxic or metabolic encephalopathy, brainstem function is usually preserved until last - may see Cheyne-Stokes respirations.

17-3. What physical findings would indicate that coma was due to diffuse cerebral cortical dysfunction rather that to brain stem damage?

Answer 17-3. With diffuse cerebral cortical dysfunction you would expect to find normal dysinhibited oculovestibulor reflex eye movement to caloric testing. Motor findings and responses would be the same on both sides of the body (symmetrical). It is critical to be sure that there is no structural damage to the reticular formation. This is accomplished by determining whether eye movements are affected (extraocular nuclei are close to reticular formation).

17-4. What are key physical exam findings in patients with coma?

Answer 17-4. The vestibuloocular reflexes (oculocephalic testing or caloric testing) is critical to this assessment. Pupillary reactions may also be important.

17-5. What is transtentorial herniation?

Answer 17-5. Transtentorial herniation occurs with lateralized, supratentorial masses with displacement of the brain away from the expanding lesion. This produces stupor and coma by damaging the midbrain and reticular activating system. The uncus of the temporal lobe is usually the structure that herniates.

17-6. What are common symptoms of transtentorial herniation?

Answer 17-6. The third cranial nerve is often involved early in transtentorial herniation (with pupillary constrictor fibers usually damaged first). This is usually ipsilateral to the side of expanding lesion. The corticospinal tract is often involved next with contralateral weakness. Occasionally, with large shifts of the brain stem, this may be reversed (false localizing sign: Kernohan's notch).

17-7. What is the "locked-in" syndrome?

Answer 17-7. Locked-in syndrome usually results from damage at the level of the pons. Consciousness is preserved.

17-8. How can you recognize "locked-in" syndrome?

Answer 17-8. In the "locked-in" syndrome, vertical gaze and convergence is usually preserved. Eye opening may be preserved (eye closure is passive only). Other voluntary motions (including horizontal gaze included) are abolished.
Jump to: