Elsa C. Raimondi

With many expressions, an attempt has been made to define comma: "a state of loss of consciousness", "Absence of responses to any stimulus", the "Lack of any psychologically understandable response to an external stimulus or an internal need" (Plum and Posner). Some more complete than others, but all pointing to the same thing: the alteration of the state of consciousness. Therefore, from the point of view medical, coma is an alteration in the functioning of the central nervous system whose main symptom is a disturbance of consciousness of variable duration, reversible or irreversible, and which can be caused by multiple causes.

Being by definition a disorder of consciousness, the previous concept is completed by expressing that the state of consciousness corresponds to a person's complete knowledge of their self and the environment that surrounds them, and in response to which they are capable of expressing themselves in way of behaving, communicating and reacting appropriately in different circumstances and before different stimuli. On this basis, it is classic to distinguish two components of consciousness: content (psychological) and reactivity (physiological). The content corresponds to the totality of a person's knowledge and psychic processes, while reactivity is related to the capacity of consciousness to react to various stimuli. Both components are related to anatomical structures of the central nervous system: the content with the cortex of the cerebral hemispheres and the reactivity with neural systems of the brain stem. More specifically, the region linked to this last function corresponds to the protuberance, the midbrain and the diencephalon, although the group of neurons that make up this entire system extends more caudally to the highest part of the cervical cord. The whole set is known as an activating lattice system or substance. In essence, it is a motley and intricate conglomerate of irregularly arranged large and small neurons and members of a multisynaptic system that interconnect with each other, receiving input by collaterals from all somatic, sensory-sensory, and vegetative pathways, and that from their part more rostral emits diffuse activating projections to the cortex of the telencephalon;

Therefore, for the maintenance of the normal state of consciousness, the anatomical and functional integrity of the SARS and the cortical mantle of the cerebral hemispheres is essential, and for this it is essential that the neurons receive an adequate supply of the elements that are vital to them. (oxygen, glucose, ions, cofactors) and that they are able to take advantage of them.

 From this it follows that neuronal function will be affected in two circumstances:

  1. when the supply of nutrients fails or ceases as a consequence of disorders in blood flow.
  2. when the nerve cells themselves are primarily affected and suffer alterations that impede or interfere with their metabolic processes.

Through these mechanisms, it may happen that different noxas act producing:

  1. functional modifications (decrease or suspension) of the SRAA and / or the cerebral hemispheres without causing their destruction
  2. direct lesions in the activating areas of the Reticular System.
  3. direct wide and / or diffuse lesions of the cerebral hemispheres.

The clinical consequence, in any of these cases, will be that different degrees of alterations of the conscience appear.

If partial lesions occur in the cerebral hemispheres, reduced and specific disorders of the mental content may occur, as occurs, for example, in the case of aphasias and amnesias, and this does not constitute a disorder of consciousness.


There are different aspects under which it is possible to classify disorders of consciousness. This facilitates the location and understanding of the subject by the reader, who, in short, will be the one who, with this knowledge, must make decisions before the patient.

In the first instance, and according to the primary origin of the alteration, the following can be considered:

  1. Supratentorial lesions
  2. Infratentorial injuries
  3. Diffuse brain disorders:
    1. intrinsic (primary metabolic encephalopathy)
    2. extrinsic (secondary metabolic encephalopathy)
  4. others

Supratentorial lesions in principle partial and limited, can present without modifications in the level of consciousness; for example, it would be the case of hemispheric brain tumors in the early stages of their growth. As the pathological process progresses, neurological symptoms and signs will add up and the different degrees of alterations of consciousness will appear in progression as the initial injury produces the distortion and dysfunction of the infratentorial structures (brain stem). If the supratentorial lesion is large enough — for example, a hemispheric infarction — the coma may be initial since in this case the diencephalic reticular structures are also compromised.

Infratentorial lesions can be located on the brain stem; In these cases, more or less small and strategically placed injuries (SARS) will lead to comas from the beginning. In the case of cerebellar lesions, the compression and / or dysfunction that they produce in the brainstem may also lead to changes in the level of consciousness.

When diffuse brain disorders occur, the disorders lie either primarily in the same neurons, and here the use of nutrients fails, or the fault lies in those same nutritional elements that reach the neurons in insufficient or altered quantities.

It is then appropriate to introduce the etiological factors that will complete the previous anatomical classification, and which are listed in Table 50-1.

Table 50-1. Etiology of disorders of consciousness.

  1. Supratentorial lesions
    1. Hematomas: intraparenchymal, subdural, epidural
    2. Cerebral infarctions
    3. Brain tumors
    4. Brain abscess
    5. Brain cysts
  2. Infratentorial injuries
    1. Brain stem hemorrhage
    2. Brain stem infarction
    3. Brain stem tumors
    4. Cerebellum hemorrhages and infarcts
    5. Cerebellar abscesses and tumors
  3. Diffuse brain disorders
    1. Intrinsic:
      1. Senile, Pick, Alzheimer's dementias
      2. Jacob-Creutzfeldt disease
      3. Lipidosis
      4. Leukoencephalopathies
    2. Extrinsic (secondary metabolic encephalopathies):
      1. Hypoxia
      2. Hypoglycemia
      3. Hydro-electrolyte abnormalities
      4. Co-factor deficiencies
      5. Endogenous toxins
      6. Exogenous toxins
    3. Others:
      1. Subarachnoid hemorrhages
      2. Meningitis and encephalitis
      3. Brain injuries

The afore—mentioned etiologies are not all those that can produce a coma, but the most frequent or representative ones and those that should be kept in mind when evaluating the patient.

According to the degree or intensity of loss of alertness, these changes can be classified or described in four categories:

  1. Haze. It is a state in which the patient is drowsy; if stimulated, he wakes up and appears distracted; he cannot think clearly even when he is able to respond to short and simple commands; memory is faulty and may be slightly disoriented. When the clouding is greater, the patient presents a state of confusion, with difficulty understanding and obeying orders, disorientation in time and space, and marked drowsiness. In clouding pictures, when the stimuli cease, the patient falls back into the previous state.
  1. Stupor. In this case, the patient only responds to repeated and vigorous stimuli. It is disoriented in time and space and can present psychomotor excitement.

  2. Semicoma. In this situation the patient only responds with some defensive movement, reflex, before the painful stimuli. It still maintains reflex function, and a decrease in muscle tone begins to be noticed.

  3. Comma. In this state there is a lack of response to stimuli. The patient maintains some vegetative functions while he loses reflex functions as the coma progresses.

These different states of loss of consciousness can appear as successive stages and progressing towards deepening, but at the same time, any of those moments, the situation can be reversed and this will be in accordance with the etiological factor that gave rise to it and with the possibilities of an effective treatment.

Clinical features

Once the state of the patient's vital functions (cardiocirculatory and respiratory) has been evaluated, the particular case will be considered the interrogation of family members or companions that may provide the first clue in the investigation of the coma patient. The mediate and immediate antecedents that they can provide have first-rate value, but it should not be forgotten that other etiologies may have sometimes been added. Inspection of the patient is important because it reports on injuries to the skull, about the position of the body, the color and hydration of the skin, the type of breathing.

At the time of proceeding with the neurological examination, the existence of signs of focus should be investigated in the first instance, since they indicate the presence of a primary localized brain injury, generally supratentorial. Therefore, hemiplegias, asymmetries in muscle tone and osteotendinous reflexes, conjugated deviation of head and eyes, unilateral Babinski sign will have to be looked for.

Next, an accurate and careful examination of different parameters should be made, which will provide valuable information on the level, severity and prognosis of the case.

They are: 1) the breathing pattern; 2) the size and reactivity of the pupils; 3) eye movements and oculovestibular responses, and 4) motor responses.

  1. Breathing pattern . Breathing is a reflex act in which influences born at different and staggered brain levels intervene and mediate. For this reason, conditions capable of producing comas will also induce respiratory modifications, so the fact of knowing which type they correspond to constitutes considerable data. However, in its evaluation it should be borne in mind that the neurogenic type of respiration can be influenced and modified by concomitant metabolic and pulmonary alterations.

    Cheyne-Stokes breathing. It is a type of periodic respiration in which inspirations and expirations occur gradually increasing until reaching a maximum and then decreasing, followed by apnea of ​​shorter duration than the hyperpnea phase. This rhythm appears frequently in case of lesions of the cerebral hemispheres and implies a bilateral dysfunction of its most deep and caudal parts or of the diencephalon. It is also seen in hypertensive encephalopathy, and in any other cause that alters the functions of those brain regions.

    Central neurogenic hyperventilation. It consists of a deep, regular, rapid and persistent hyperpnea that appears in patients who have injured the brainstem in their rostral portions (lower midbrain and middle and upper third of the pons).

    Apneustic breathing. It is given by the presence of a prolonged inspiration followed by a pause of 2-3 seconds and alternating with prolonged exhalations and pauses after them. The injuries that cause this type of respiration are located at the medial and inferior protuberance and in relation to dorsolateral structures. Sometimes it can also be observed in severe hypoglycemia, anoxias or meningitis.

    ataxic respiration. In these cases the respiratory pattern is irregular, with alternation and disorderly variation of the inspiratory and expiratory phases in terms of depth and frequency. It corresponds to lesions that, located in the dorsomedial reticular formation of the bulb, interrupt or damage the connections between the inspiratory and expiratory centers. In general, those responsible for this type of breathing are expansive and hemorrhagic or traumatic processes of the posterior fossa.
  1. Pupillary size and reactivity . The sympathetic and parasympathetic pathways regulate the size and reaction of the pupils; When any of them is affected at different levels of the brain, it can give rise to signs of diagnostic and prognostic value. The fundamental thing to retain is the following:
    1. hemispheric lesions do not affect them;
    2. mesencephalic lesions in the tectum give rise to pupils of 5-6 mm in diameter with no photomotor reflex,
    3. anisocoria, with a dilated pupil and no photomotor reflex, indicates a compromise of the III unilateral cranial nerve and may be caused by the presence of a herniated hippocampus uncus that compresses it;
    4. protuberant lesions give rise to pinpoint pupils; the photomotor reflex is present but to see it it is necessary to use a magnifying glass;
    5. When the cause of the coma is metabolic, the pupils are 2-3 mm and present a normal photomotor reflex.
  1. Eye movements and oculovestibular responses. In the brain there is a center of gaze in the frontal lobes and another in the occipital lobes, and at the level of the brain stem, another center whose delimitation is imprecise and that would be in relation to or forming part of the VI para cranial. By affecting the corresponding centers or their connections, brain injuries that produce coma can cause the conjugate deviation of the eyes towards the side of the injury; while pathologies that destroy or unilaterally compress the protuberance level can produce a conjugate ocular deviation towards the opposite side of the lesion.

    Eye movements that are induced by passively moving the patient's head or irrigating the ears with cold water (oculovestibular response) provide more information; thus, if when moving the head horizontally, the eyes deviate in a conjugated way towards the opposite side to the cephalic movement, the response is “in the eyes of the wrist” and indicates the existence of hemispheric alterations; if the eyes are fixed (“frozen eyes”), the serious injury is located in the brain stem,

    When an ear is irrigated with cold water in a healthy subject, nystagmus occurs with the slow phase directed toward the irrigated ear and the rapid phase moving away from it. The coma state suppresses the fast phase; therefore, the instillation of water will produce:
    1. conjugate deviation of the eyes towards the irrigated side (slow phase of nystagmus); occurs in supratentorial injuries or alterations;
    2. unconjugated response, which appears with lesions of the brain stem;
    3. absence of response, produced by lesions in the protuberance in the region of the nuclei of the VI cranial nerve.
  1. Motor responses. In patients in a coma, different situations can occur:
    1. Adequate responses to the painful stimulus:
      1. presenting motor responses with limbs on both sides (untouched or partially affected corticospinal tract);
      2. who has a unilateral absence of response (pyramidal pathway affected on one side at the supra or infratentoriai level);
      3. showing a bilateral absence of response (pyramidal pathway on both sides, eg, brainstem; deep coma).
    2. Inadequate responses to the painful stimulus:
      1. Decortication stiffness: the stimulus produces flexion of one or both upper limbs and uni or bilateral extension of the lower ones, which occurs in hemispheric, supratentorial lesions;
      2. Decerebrate rigidity: in this case the extension of upper and lower limbs takes place, unilaterally or bilaterally, which corresponds to infratentorial lesions.

The evaluation of the patient in a coma should be frequent in order to verify the progression or improvement of his condition and establish a prognosis. To do this, and based on the parameters described above, scales have been created in which a certain score is assigned for a given response. The Glasgow scale, proposed by Jennett and Teasdale in 1974 for traumatic comas, uses three response items:

  1. Open eyes:
    1. Does not respond
    2. Faced with a painful stimulus
    3. At an order
    4. Spontaneously
  2. Motor response:
    1. Does not respond
    2. Respond with extension posture
    3. Respond with flexed posture
    4. Remove the stimulated limb
    5. Locate the stimulus
    6. Obey orders
  3. Verbal response:
    1. Does not respond
    2. Incomprehensible sounds
    3. Inappropriate words
    4. Confusing conversation
    5. Oriented

For medical comas, Plum and Carorma add exams that investigate trunk functions to the previous scale.

As a general rule, it can be expressed that:

  1. in most cases, a prognosis cannot be guessed before 24 hours have elapsed, much less if they are children or young people;
  2. Only in the case of a patient who, after 24 hours, have no occuovestibular or motor responses, can an unfavorable evolution be foretold.

Complementary exams

Based on the presumptive diagnosis or diagnoses, the corresponding blood and cerebrospinal fluid analyzes will be requested, which may be supplemented, as appropriate, with direct skull radiographs, electroencephalogram, electrocardiogram, computed axial tomography and / or cerebral angiography. . All of them should be aimed at clarifying diagnoses and will be discarded if it is presumed that they will not provide data that aids in therapy or that may add damage and endanger the life of the patient, for example, a lumbar puncture in infratentorial injuries.

In conclusion, before the arrival of a patient in a coma, the following sequence will be followed:

  1. Check vital signs (pulse and blood pressure, airway patency).
  2. Determine the degree of loss of consciousness.
  3. Look for signs of focus.
  4. Determine the level of injury (topographic).
  5. Determine the probable etiology
  6. Indicate routine analysis according to the previous point.
  7. Perform supportive treatment.
  8. Perform etiological treatment.

Finally, it is worth mentioning certain states that can cause confusion or be misinterpreted by doctors and relatives of a patient in a coma.

These are the so-called by Jennett and Plum "persistent chronic vegetative states", an expression that is applied to patients who, after suffering serious brain injuries, remain for prolonged periods with no other functions than the vegetative ones. These patients, after a few weeks of coma, may appear with their eyes open and may even appear to follow an object with their eyes, however, there is no evidence of superior brain functions and most of them present decortication or decerebrate postures. In these patients there are sleep-wake cycles, but otherwise, their elevated functions are not verified and they never recover. These pictures correspond to the so-called "akinetic mutism" of Caims or "coma vigil" of the French,

Different is the so-called "captivity syndrome", which corresponds to a state in which the patient has quadriplegia plus bilateral paralysis of the lower cranial nerves, with or without alteration of consciousness. These patients, if conscious, can only communicate with others through vertical movements of the eyes. The injuries that originate them can be, for example, bilaterally in the foot of the pons.