Coma and other disorders of consciousness
Jouvet M.
Handbook of Clinical Neurology Vol.3. P. J. Vinken and G. W. Bruyn , eds. North-Holland Publishing Company. Amsterdam,(1969)


Physiopathological basis of coma (introductory remarks)

Nervous structures necessary for consciousness

Periodic physiological dissolution of consciousness: sleep and coma

From experimental to clinical neurophysiology

Physiopathology of nervous lesions responsible for coma

Aetiological classification of comas and of disturbances of consciousness of organic origin

Symptomatological classification of coma

Tentative anatomoclinical classification


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Nervous structures necessary for consciousness

A priori, failure to "perceive" a signal may result theoretically from the following lesions (Fig. 1):

  • a lesion of the ascending pathways specifically responsible for the conduction of stimuli from the external environment to the "integrating central structures";
  • a lesion of the efferent pathways responsible for providing external evidence that the signal has been integrated (i.e. via muscular or vegetative effectors);
  • finally, a lesion affecting the integrating central structures.

Neurophysiology has shown that the first two hypotheses do not apply in the great majority of cases. Indeed, lesions simultaneously affecting the afferent pathways on both sides are rare; besides, in animals, experimental de-afferentation of the various receptors, or even transection of the specific lateral afferent pathways in the brainstem (without damaging the central paft of the tegmentum) do not lead to a comatose state. The animal is still capable of reacting correctly to a number of conditioned reflexes (Sprague et al. 1963). Also, if a general de-efferentation may sometimes result in a clinical picture of coma, a closer examination would usually show that normal perception is preserved. This is the case in patients suffering from advanced tetanus, and are kept under artificial respiration after intense and prolonged curarization. These patients may at first sight appear comatose as they are unable to show objectively by means of movements their perception of external stimuli, and yet they are fully aware of their surroundings. We tested this by showing our curarized patients various cards (ace of hearts, king of spades) and asking them to identify the cards later in a shuffled pack of cards. When they recovered and curarization was stopped, they were perfectly capable of recognizing the cards which had previously been shown to them. These cases are exceptional as there is no clinical test that enables us to assess the state of consciousness of a curarized patient. It is possible that an electroencephalogram by showing an arousal reaction, might provide important, if not decisive information.

Even though it may appear to be of purely theoretical interest, this question is of prime importance. Some lesions of the brainstem, in particular lesions of the ventral part of the mesencephalic or pontine tegmentum, can in fact involve the extrapyramidal system, and prevent certain voluntary movements, as well as cause a motor de-efferentation. At this point, we would like to mention an observation by Lhermitte et al. (1963). A patient with a lesion of the mesencephalic reticular formation presented the clinical picture of deep coma. She had bilateral ptosis, which gave the impression that she was in a state of permanent sleep, and failed to respond even to strong stimuli. It was noticed, however, that she was still able to move her wrists slightly. Due to these movements of the wrist, it was possible to establish a code by means of which she was able to answer complicated questions in a simple manner. This fact leads to two practical points worth remembering when one is faced with patients presenting a state of "akinetic mutism". First, one should always have recourse to all possible paraclinical examinations (including polygraphy) before deciding that a patient has lost all perception. Secondly, one should always remember that a patient who is akinetic and speechless, may still understand all that is being said around him.

It would appear therefore that neither a subtotal nor a total de-efferentation can (alone) result in complete loss of perception. This is why disturbances of consciousness seem to be connected with an organic or functional lesion of the integrating central structures. These structures belong to two main groups. The first group includes the ascend ing activating reticular system, the normal functioning of which is essential for waking, but is not sufficient to insure normal perceptivity. The second group includes the thalamocortical integration system, the integrity of which is necessary for normal perceptivity.

The ascending reticular activating system (ARAS) and the arousal reaction.

The brainstem reticular formation includes the areas of grey matter in the bulbar tegmentum, the pons and the mesencephalon, but excluding the cranial nerve nuclei, and the relay centres of the cerebellar system. It is continuous at the bulbospinal junction with the spinal reticular formation. Anteriorly, its limits are not clearly defined, and in the sub thalamic area it is continuous with the diffuse thalamic system. Thus the reticular formation appears as a complex collection of neurones which serves as a converging point for signals from the external and the internal environments, and is capable of exercising a dynamogenic effect on the electrical activity of the cortex, and on the motor and vegetative efferent system.

Since 1949, thanks largely to the work of Moruzzi, Magoun and their school (Lindsley et al . 1950; French and Magoun 1952) it has been shown that after destruction of the mesencephalic reticular formation, an animal remains immobile and "comatose". Sensory stimuli, auditory or painful, fail to clinically elicit the arousal reaction. The electrical activity recorded from the cortex is similar to a sleep-recording, and with the exception of olfactory stimuli, all forms of sensory stimulation fail to elicit a reaction. Excitation of the reticular formation in sleeping animals confirms its activating influence: when high frequency excitation is applied, the animal wakes up, opens its eyes, and there is mydriasis and increase in muscle tone, etc.; in some cases, the animal will give an impression of attention. At the same time, there is a rapid, low voltage EEG cortical activity which is characteristic of the "arousal reaction".

This work led to the discovery in the brainstem of a system of neurones which is now regarded as the basis of the waking mechanism. Further work has shown that the structures responsible for the maintenance of the waking state are situated in the posterior diencephalon and at the mesodiencephalic junction, while the cell groups responsible for cortical activation are localized in the posterior mesencephalon and the anterior part of the nucleus reticularis pontis oralis (Rossi and Zanchetti 1956).

Cortex, perceptivity and learning.

It is now established that the cortical centres are responsible for the nerve connections acquired during the history of the organism. Thus, after decortication, either widespread or limited to a specific area, all the possibilities of conditioning, achieved in animals by means of complex stimuli, are lost. This state is comparable in man to visual, auditory, somesthetic agnosia resulting from lesions either of a specific cortical area or of the nonspecific adjacent areas of integration (Ajuriaguerra and Hécaen 1960).

It is necessary at this point to sum up briefly the present data concerning the structures responsible for the facio-vocal reactions to pain. Indeed, investigation of reactions to painful stimuli should be an integral part of the examination of a comatose patient, as it serves to test some of the essential mechanisms of reactivity.

Structures responsible for responses to painful stimuli.

We know that a painful stimulus activates a complex afferent system, the organisation and integration centres of which are only now being partly elucidated. We can accept the view of Bard and Mountcastle (1948) according to which the neocortex, the cingulate cortex, the amygdaloid nucleus and the pyriform lobe correspond to zones of the inhibition of pain and anger reactions. Their influence would be transmitted as far down as the brainstem by way of a circuit similar to the amygdaloid pathway. They suggest the presence, in addition, of a direct extra-amygdaloid pathway via which the neocortex might exert a facilitatory influence on the mesencephalic centres.

The mesencephalic structures where the facial and vocal components of the pain reaction are integrated are situated in the central part of the brainstem, within the peri-aqueductal grey matter. Destruction of this area in animals results in complete loss of vocal or expressive reactions following a painful stimulus (Adametz and O'Leary 1959; Kelly et al. 1946), while excitation of this same area provokes intense vocal and facial reactions. The vegetative responses to pain (pupillary, respiratory, cardiac vasomotor) are elaborated in the inferior part of the brain stem; they result from mechanisms originating in the mesencephalic, rhombencephalic and bulbar areas. The spinal component may suffice when a limb is withdrawn from a painful stimulus applied to the skin; this is the classical flexor reflex.

And finally, although no absolute correlation exists between the disturbances of perceptivity and reactivity on the one hand, and of muscle tone on the other, in most cases a clinical correlation is found between lesions of the integrative structures and those affecting the centres controlling muscle tone.

Neurophysiological basis of abnormalities of posture.

In man, disturbances of posture, which are char acterised by the rigidity of decortication and de cerebration, depend largely on the multisynaptic systems of the brainstem. And, as we know, the systems responsible for the waking reaction are closely associated with the supraspinal centres controlling muscle tone. For that reason, we would like to summarize some of the neurophysiological experimental data concerning the regulation of muscle tone (Granit 1957; Jung and Hassler 1960; Rushworth 1960). Muscle tone depends on the simultaneous control of the facilitatory and inhibitory supraspinal systems, which act on the stretch reflex.
The inhibitory influences, independent of the pyramidal system, follow a corticobulboreticular system which originates in the suppressive areas of the cortex, or a multi-relay system at the level of the striate nuclei, or again they may depend on the anterior lobe of the cerebellum. Of the supra spinal control systems, the bulbar inhibitory reticular system is one of the most dominant. Its influence reaches down to the spinal motoneurones by way of the reticulospinal tract.

The facilitatory influences, which act on the spinal level, come from the vestibulospinal tracts (probably unimportant in man), the middle lobe of the cerebellum, the pyramidal tract, and especially from the facilitatory reticular formation which is situated in the mesencephalic tegmentum, and lies very close to the inhibitory reticular formation at tne pons.

Spasticity appears whenever a lesion affects the inhibitory centres and leaves the facilitatory system to act unopposed on the spinal stretch reflexes. According to this classical conception, in the presence of a cortical lesion, the inhibitory reticular formation, though not organically damaged, undergoes a sort of "isolation dystrophy" which prevents its inhibitory action on muscle tone, and this results in spasticity. It has been shown in fact (Jouvet et al. 1961) that in the cat and in man, the reticular formation continues to have a periodic inhibitory influence in certain stages of sleep (paradoxical sleep). Thus rigidity resulting from suprapontine lesions may still be under a periodic inhibitory influence during sleep.

Thus, according to the various types of experimental lesions studied in animals, we may consider the following schematic pictures:

Total decortication in the cat (in direct opposition to what happens in man) is accompanied by minimal changes in muscle tone. On the other hand, perceptivity is completely absent: the "blinking" reflex is lost, although the light reflex persists, and the animal is unable to move to wards his food. One orientation reaction remains: startling, turning the ears and rotating the head towards a noise. Finally, the ability to learn is lost, and no conditioned reflex can be demon strated. Reactivity however remains normal: the arousal reaction is present, and the animal can be aroused from its sleep by an acoustic stimulus. Finally, the facio-vocal reactions to pain are exaggerated and result in an expression akin to that of "sham rage".

Destruction of the ascending reticular actitvating system. Here, even though the cortex is intact, perception is completely abolished, while reactivity is severely impaired. The animals also show signs of severe muscle tone disturbances (resulting in more typical cases, in a clinical picture of decerebrate rigidity in extension). The eyes are closed; the pupils are constricted; auditory and painful stimuli fail to provoke an arousal or an orientation reaction. Finally, cortical activity consists entirely of slow waves and remains unchanged by all sensory stimuli with the exception of olfactory stimuli.

In addition to these two generalized syndromes, there are those due to more localized lesions. One of these is experimental akinetic mutism resulting from lesions of the median structures situated in the peri-ependymal grey matter and the medial thalamic nuclei. The disturbances of perceptivity are more apparent than real, and appear to be due to damage to the motor effector mechanisms. The animal is still able to blink when threatened, but its immobility makes motor conditioning difficult to achieve. The waking reaction is normal, but facio-vocal reactions to pain are completely absent. There is also a generalized disturbance of muscle tone which in the more typical cases may result in catatonia.

Finally, a more generalized lesion (most com monly seen after prolonged anoxia) affecting the cortex, the mesencephalic reticular formation, the pontine reticular formation and other more caudal structures will lead to a state of brain death or even to the picture of "isolated heart-lung preparation", on condition that artificial respiration is applied. This clinical state is the ultimate stage of coma: it is characterized by complete absence of perceptivity and of reactivity, and by total cerebral electrical silence.

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