Coma is a life-threatening process that often requires immediate recognition, appropriate diagnosis of the cause, and proper initial management. The causes of coma can be divided into structural versus causes of diffuse neuronal dysfunction. Causes of diffuse neuronal dysfunction can be further classified into toxic and metabolic. The definitive treatment of patients with coma needs to be disease-specific.
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Beyond the Consciousness

Different areas of the nervous system jointly control the degree of consciousness:

Alertness / Vigilance: ARAS region (activating reticular ascending system in the Formatio reticularis).

Awareness: Thalamus in the diencephalon.

Self-revelation: Default Mode Network (DMN, with island involvement, singular cortex, prefrontal cortex).

Self-location / self-perception: Seat in the parietal lobe.

If the nerve cells of these centers do not communicate, or if the connecting nerve pathways are damaged, there is a misregulation of the consciousness.

Falling Into Coma

According to ancient Greek, a coma is nothing more than a “deep sleep.” Recognizable is the coma for the medical practitioner in the closed eyes, the impossibility of arousing the patient and the fact that he does not react to pain. A coma can have a pathological cause or can be artificially initiated. Any form of coma is life-threatening. In addition, there is no uniform concept of this syndrome.

The causes of “real” coma in the context of morbid disorders are manifold. All impairments of the vital functions are possible. If the causes are not obvious, one should think of injuries or diseases of the brain and consider poisoning or metabolic disorders.

Causes:  Any Cause of Diffuse Neuronal Dysfunction
Structural Toxic Metabolic
  • Intoxication
  • Anesthetics
  • Dissociative agents
  • Carbon monoxide poisoning
  • Toxic alcohols
  • Antidepressants
  • Antiepileptics
  • Asphyxia
  • Serotonin syndrome
  • Neuroleptic malignant syndrome
  • Clonidine
  • Respiratory failure
  • Dysthermia
  • Dysglycemia
  • Infection including meningitis and encephalitis
  • Hypothyroidism
  • Thiamine deficiency
  • Non-convulsive status epilepticus
  • Electrolyte disturbances

Coma mimics can present with a picture that is similar to coma however the patient will not be in “real” coma. They include:

  • Locked-in syndrome
  • Neuromuscular paralysis
  • Akinetic mutism
  • Psychogenic unresponsiveness

Although the search for causes is important, one should first and foremost take the deep unconsciousness seriously. A coma threatens the body due to the failure of important protective reflexes and the lack of regulation of the vital functions. The first steps to take when one encounters a coma patient are therefore—always—to secure and keep the airways as well as to control the circulation.

Estimating the Depth and Stages of the Coma

Consciousness is not a light switch, which can be turned on and off. Rather, it is like a dimmer, over which the brightness is infinitely adjustable. Before people fall into coma, the phases of somnolence, a marked drowsiness and the sopor usually precede the condition. In the latter, the patients are only aroused by very strong stimuli.

In order to be able to assess how deep a patient has fallen into coma, tests are available for pain reactions. The pressure on the fingernail is a common method and can suffice for a coma assessment:

Grade I: immediate and directed response.

Grade II: delayed but directed response.

Grade III: no targeted reaction.

Grade IV: no reaction.

The Glasgow Coma scale

The use of the Glasgow Coma scale, which was already developed in the 1970s, continues to be established in the clinical world.

It is easy to calculate that the point sums must lie between 3 and 15. A number below 8 points indicates a severe brain disorder that makes intubation necessary.

Points Best Eye Opening Best Verbal Best Motor

Cognition

Level 

of 

Consciousness

6 Obeys command
5 Oriented Localizes pain
4 Spontaneous Confused Withdraws to pain
3 To speech Inappropriate Decorticate posturing
2 To pain Incomprehensible Decerebrate posturing
1 None None None

Types of Coma

Artificial coma

An artificial coma is quite different. Rather, it corresponds to a long anesthesia, in which a patient is placed to protect himself. The artificial coma involves two components – sedation by narcotic agents and analgesia by painkillers. If both components are used, one speaks of analgosedation.

After severe brain damage, the artificial coma should prevent the neuronal activity and the intracranial pressure from increasing, and the nerve cells from dying. The blood pressure is lowered; the metabolism is lowered. Also, anxiety and emotional stress situations can be interrupted, which would severely impair the success of the treatment.

The duration of an artificial coma should be kept as short as possible since it can lead to side effects:

Nevertheless, the duration of an artificial coma does not tell us about the state of mind after awakening. It is, therefore, conceivable that a long time is surmounted in an artificial coma without neurological impairments.

Examination of the Comatose Patient

  • Say/ yell patient’s name (verbal stimulation).
  • Shake/ tap patient (tactile stimulation).
  • Press on patient’s nail beds (peripheral painful stimulation).
  • Sternal rub/ nasal swab (central painful stimulation).

If these tests fail to reveal a response, your patient is possibly in a coma: The brainstem exam is done to then determine if brain death is present.

Brainstem reflexes

Pupillary light reflex

  • Afferent: CN II
  • Efferent: CN III (parasympathetic)

Oculocephalic reflex (doll’s eyes)/cold

  • Afferent: CN VIII
  • Efferent: CN III, IV, VI

Corneal reflex

  • Afferent: CN V (ophthalmic division)
  • Efferent: CN VII

Gag reflex

  • Afferent: CN IX
  • Efferent: CN X

Cold caloric reflexes

  • 50 ml ice water injected into ear.
  • Cold is an inhibitory stimulus to the vestibular nerve.
  • The vestibular nerve projects to the contralateral CN VI nucleus.
  • Normal response is slow deviation of eyes toward the side of cold water, then fast return to midline (nystagmus).
  • In coma, if CN VIII/VI/III pathways are intact, the eyes tonically deviate toward the cold stimulus with no fast phase.
  • Remember: primitive brain looks to stimulus, higher brain brings eyes to midline.

By now, it might become clear to you that the Glasgow Coma Scale is somewhat limited in assessing a comatose patient. It does not take into account the brainstem reflexes and respiration abnormalities which can give important clues about the severity and even cause of coma. The Full Outline of Unresponsiveness (FOUR) score was developed to address these limitations.

Points Eye response Motor response Brainstem reflexes Respiration
4 Open spontaneously, or blink to command Can make a thumbs up, peace, or fist “responds to command” Pupil and corneal reflexes present Not intubated, regular pattern
3 Open spontaneously but does not track your fingers “does not respond to command” Localizes to pain 1 pupil wide and fixed Not intubated, Cheyne-Stokes pattern
2 Open to loud voices Flexion response to pain Pupil or corneal reflexes absent Not intubated, irregular breathing
1 Open to pain Extension response to pain Pupil and corneal reflexes absent Breathes above the ventilator rate
0 Closed with pain No response to pain Absent pupil, corneal and cough reflexes Breathes at ventilator rate / apnea

Time of Awakening

After severe brain damage, the patient may awaken from the coma, but his cerebrum cannot be activated or can no longer be activated. The vegetative control is essentially functional. But for the environment, the consciousness processes seem to be reduced to a minimum. This “waking coma” can last for months or for a whole lifetime. The so-called apallic syndrome describes this condition, in which the brain stem, the interbrain and the spinal cord maintain the life of a person, while higher mental processes are no longer present.

In his book “Time of Awakening,” the neurologist Oliver Sacks describes how he was able to wake up patients for a short time from the waking coma. After a period of apparently incomplete apathy, the patients were beginning to feel joy and ideas. This is hardly imaginable with a complete failure of the cerebrum. A real apallic syndrome is, therefore, difficult to diagnose in practice. No one can know whether the cerebrum of these patients has actually failed—or whether it simply does not communicate with the outside world.

Review Questions

The answers can be found below the references.

1. Where is the self-perception located?

  1. In the parietal lobe.
  2. In the frontal lobe.
  3. In the temporal lobe.
  4. In the occipital lobe.
  5. Cannot be located exactly.

2. You come to an accident location and find a patient who opens their eyes spontaneously, uncoordinated and confused to answer your questions but shows directed movements to a painful stimulus. How many points on the Glasgow Coma Scale does this correspond to?

  1. 3
  2. 6
  3. 8
  4. 10
  5. 13

3. What does not count to the side effects of artificial coma?

  1. Disorders of cardiovascular and respiratory nature.
  2. Headaches.
  3. Disorder of gastrointestinal regulation.
  4. Disorders of the immune system.
  5. Drug dependency.
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