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)
TABLE OF CONTENTS

Introduction

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

FIGURES

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From experimental to clinical neurophysiology

If the nervous structures responsible for waking and for the various types of sleep in animals (and especially the cat) are fairly well-known, anatomoclinical observations and neurophysiological clinical investigations seem to indicate that in man the equivalent structures may present a different organization .

In 1960, Jefferson drew a map of the areas of the brain which he believed, from his neurosurgical experience, to be necessary for the preservation of consciousness (critical point). The mapped region extends from the pons, through the mesencephalon and diencephalon, as far as the telencephalon. It appears however that the localization of structures responsible for maintaining the waking state must be based on the lowest lesion that will produce a prolonged loss of consciousness, for coma produced by a higher lesion can be due to the interruption of ascending neurones originating from the more caudal activating centres.

Rossi and colleagues (1964, 1965), after study ing their own personal observations, as well as those they found in the literature, have localized with more precision the regions of the brainstem which are vItal. in maintenance of a waking state: bulbar lesions and lesions of the caudal part of the pons cause no loss of consciousness (Fig.3) even if decerebrate rigidity is present (Halsey and Downie 1966), while lesions of the upper part of the pons and especially of the lower end of the mesencephalon are almost always associated with coma. In these cases, however, the EEG tracing may be normal even though no reactions appear on the tracing (dissociation between EEG and behaviour) (Chatrian et al. 1964; Loeb and Poggio 1953; Kaada et al. 1961).

Finally, lesions of the cephalic end of the brainstem and of the posterior part of the diencephalon always result in a picture of deep coma, both clinically and electroence phalographically (slow, non-reactive EEG). It appears therefore that the most caudal lesion of the brainstem capable of producing coma is one situated at the junction of the mesencephalon and diencephalon .

Alema et al. (1966) have also used a functional method to identify and localize the structures responsible for maintaining the waking state (and therefore normal consciousness). In man, injection of Amytal into the vertebral artery causes in activation of the lower brainstem and takes the form of bilateral palsy of the 12th, 7th, 6th, 5th, 4th and 3rd cranial nerves, as well as loss of autonomic functions of the 3rd (mydriasis and absence of light reflex); the sensory part of the 5th nerve is also affected. But in spite of this functional inactivation of the lower brainstem, the subjects show no loss of perception and continue to react normally to auditory and visual stimuli (Fig.3).

So, the combined results of anatomoclinical studies and of injection of barbiturates into the vertebral artery indicate that, in man,the neurones responsible for maintaining the waking state (and thus indirectly responsible for normal perceptivity) are situated at the junction of the mesencephalon and diencephalon.

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