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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Physiopathology of nervous lesions responsible for coma

Coma often results from diffuse cerebral lesions (e.g. of vascular, neoplastic or infectious origin) which are difficult to reproduce experimentally. By means of experimental head injuries, however, it has been possible to make a detailed study of the mechanisms by which primary or secondary lesions may lead to loss of consciousness (Denny Brown and Russel 1941; Holbourn 1943; Row botham 1949; Gurdjian and Webster 1958; Ward 1958; Foltz et al. 1953; De Morsier 1956).

Primary disorders
Mechanical displacement to the brain, such as occurs in a head injury, results in functional and anatomical lesions proportional to the severity of the shock.

Cerebral concussion is a transitory and reversible nervous reaction of sudden onset following physical trauma of brief duration and sufficient severity, and characterized by progressive recovery. It seems that the transitory traumatic paraIysis of the neurones might be due primarily to damage inflicted on the membranes (but with no detectable histological lesion). It is characterized by a brief loss of consciousness, with amnesia, and is never associated with prolonged coma.

When the head injury is severe enough, the disrupting forces may cause displacement of the whole cerebrum. The lesions will then depend on the degree of displacement, on which parts are displaced, and on the direction of the disrupting forces in relation to that of the nerve fibres. Such lesions are accompanied by histological changes ranging from loss of myelin to diffuse degeneration of white matter of the cerebrum (Fig.4) which are characteristic of traumatic encephalopathy as described by Strich (1956). In certain cases, the shock of the hemispheres hitting against the falx cerebri, or the lateral displacement of the hemispheres submit the corpus callosum to stretching forces which are responsible for contusions inside the corpus callosum at its points of insertion.

Foci of cerebral contusion are one of the anato mical characteristics of a brain after a head injury, and they have been described by a number of authors (Symonds 1949; Peters 1955; Gurdjian et al. 1955; Wertheimer and Descotes 1961). These histological changes, usually necrosis or haemorrhage, occur more frequently at certain points, suggesting that they are the result of mechanical forces, either from direct shock or by the classical contre-coup: the lesions are then found at the opposite pole from the point of impact, on the inferior aspect of the frontal lobe, at the temporal poles. In a few cases, the primary lesions may affect the brainstem directly (Jefferson 1952; French 1952; Mansuy et al. 1955).

Secondary lesions

There are two types of anoxic lesions: ischaemic anoxia in the case of prolonged shock with hypotension, and anoxic anoxia from lesions of the respiratory centres (apnoea, Cheyne-Stokes) or from upper respiratory tract involvement (the classical tracheobronchial congestion which tracheotomy has almost abolished). These lesions are now more clearly understood following the work of numerous investigators (Grenell 1946; Malamud and Haymaker 1947; Courville 1950, 1953; Scholtz 1953; Meyer and Denny-Brown 1955; Meyer 1956; Zeman and Youngue 1957; Mandel and Berry 1959).

It has been clearly established that the cerebellar cortex and cerebral cortex (more particularly the frontal cortex and hippocampus) are the most sensitive to anoxia, the next most sensitive being the pallidum, which is a common site for anoxic lesions (Scholtz 1953).

Finally, severe anoxia may lead to massive aseptic necrosis of the encephalon (Fig.5). The appearance is one of generalized necrosis primarily affecting the nerve cells and usually sparing the axons. The cerebral cortex, the cerebellum, the central grey nuclei and the brainstem are all affected. An important fact is that in the midst of this massive lesion of nervous tissue, there is no glial reaction (Bertrand et al. 1959; Mollaret et al. 1959; Trillet 1961). The picture of massive aseptic necrosis of the brain is found in the latest stages of coma, mainly in "brain death".

Cerebral oedema may also occur and cause the process known as necrosis of oedema since the works of Jakob (1913) and of Hallervorden (1939). It is characterized by foci of myelin disintegration affecting the subcortical white matter, and some times even by "slits of disintegration".

In certain cases, contusion, distortion, anoxia and oedema all combined may cause the rather rare pathological appearance of diffuse, traumatic degeneration of cerebral grey matter characterized by the disappearance of cells in the cortex, the thalamus, the putamen and the red nucleus (Denst et al. 1958).

The preceding data show the importance of anoxia (or hypoxia) in the development of certain secondary organic lesions leading to coma. By modern methods of investigation (by using, e.g. krypton-85) it has been shown that in certain comatose patients (in whom cerebral biopsy had revealed no abnormality) the blood supply and metabolism of the hemisphere could be reduced by up to 75% (Ingvar et al. 1964).

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