Fifty years of evolution of the ideas on the postconcussional Syndrome

Pierre-Marie GAGEY

Institut de Posturologie, PARIS

Tel.: 01 43 29 54 48


A) Introduction

     In the 1950's we knew that we did not know much on the postconcussional syndrome, and my boss, neurosurgeon Guillaume, clearly told us: «I do not know what the postconcussional syndrome is».

     Yet we had inherited a remarkable work, the meeting of the Société de Neurologie on April, 6 & 7, 1916, organised around the Minister of Health, to try and agree on the line to follow concerning the soldiers affected by a postconcussional syndrome. Together with Pierre Marie (1916), remarkable figures such as Babinski, Froment, Villaret, Guillain, etc., agreed on defining the clinical picture of the postconcussional syndrome only with subjective symptoms: headaches, dazzlements (# dizziness + instability +visual disorders), sleep disorders, disorders of the fixing memory, mood disorders, etc.

     That meeting broke away from the tradition of medical thought.«Skull wounds produce delirium» wrote Hippocrates in his aphorisms (Section VII, 24) and at the end of the XIXth century, the only aftereffects recognised in cranial traumatisms were the psychiatric disorders (cf. Benon, 1913, in his«historical» chapter). Now, that meeting clearly observed the objectivity to the subjective disorders for«all the subjects' descriptions are absolutely identical, and made with the same expressions». So after this meeting began the research on what the basis of that objectivity could be. The attempts at explaining it by voltaic vertigo were not to succeed, as Pierre Bonnier had predicted during that same meeting. It was not before the«sense of attitudes», the subjects' posture, but also the biomechanics of the cranial traumatism, its tissue impact, were taken into account that the objective bases of the postconcussional syndrome began to be understood.

     Those objective bases of the postconcussional syndrome, far from excluding psychiatric aspects, on the contrary allow us to understand and integrate them: everyone has his own way of reacting to his personal accidental transformations (cf. for instance Cohandon's remarkable text (1983) on that subject). And those psychiatric consequences of the postconcussional syndrome cannot be assimilated to post-traumatic neurosis (Crocq, 1969) which is due to the psychic traumatism following the accident, the clinical picture of which is very particular.


B) The objective bases of the postconcussional syndrome

1) Lesions due to the cranial traumatism

     a) Lesions due to the shock wave

     Any shock on a physical body generates the propagation of a shock wave inside that body.

     Two studies on the shock wave of the cranial traumatism have been carried out by different teams and they both draw the same conclusion: whatever the point of impact, the shape of the skull focuses the wave shock on the region normally occupied by the brainstem.

     Gurdjian & Lissner (1961) have used a container in the shape of a skull and filled with a solution of Miling yellow. The transmission of the polarised light through that solution is modified by the mechanical strains it is submitted to. That is how we observe a gradient of the strains appear, which gets tighter and tighter as the occipital hole gets closer.

 FIG. 1 - Schematic representations of the variations of the intensity of the wave observed in the median sagittal plane.

Br: Impact in the Bregma;

P.f.: plane of Frankfurt;

T.o.: occipital Foramen .

(from Amphoux & Sevin, 1975)


     Amphoux et Sevin (1975) used human skulls, dry or fresh, and measured, in various places, the intensity of the soundwave provoked by a shock. Whatever the point of impact, the wave reaches its peak in the posterior cranial fossa (figure 1).

     The results of those experiments are coherent with the publications of pathology, that all note that the brainstem is practically always injured after a cranial traumatism (cf. bibliography in Vedrenne & Chodkiewicz, 1975) and medical imaging now observes in vivo those lesions of the brainstem (Gean et al., 1995).

     As the postconcussional syndrome is not an illness leading to death, we do not have many pathological studies of subjects who died for another cause while they showed a fully characterised postconcussional syndrome. Makishima (1976) has, indeed, studied two subjects who died, the first five months and the second six years after a cranial traumatism having only induced a short fainting, but unluckily he does not state whether they still showed a postconcussional syndrome at the time of their death. Yet his study is doubly interesting, on the one hand because it reaches an histopathological level, and on the other hand because it describes, at that level, exactly the same lesions as the ones we can reproduce experimentally on animals: the injured brainstem structures are not totally destroyed, only part of the neurons look like dead cells, that is to say they are degenerated with a pycnotic nucleus.

     In the mouse submitted to a minor frontal cranial traumatism and sacrificed after a few days of survival during which the existence of postural disorders was clearly identified, Tangapregassom et al. (1983) describe exactly the same type of lesion in nuclei of the brainstem, varying from one subject to another. It looks as if the shock wave had destroyed part only of the neuronal population of brainstem nuclei.

     b) Lesions of the cervical stem

     Such an important mass as the cephalic extremity cannot be hit without implying the stem that supports it.

     Indeed, Wackenheim (1972) described five original radiological signs concerning the traumatology of the cervico-occipital region. Together with Gentaz (1975), we have searched those radiological signs of cervical injury in 100 patients who were affected by a postconcussional syndrome following an apparently exclusively cephalic traumatism, and we found one such sign or another in 49 of these subjects.

     c) Lesions of the mandibular joint

     The accelerations/decelerations of the cephalic mass consecutive to a cranial traumatism are transmitted to the mandible through the intermediary of the mandibular joints. So it is possible, and sometimes confirmed (Avrahami, 1994), that those articulations are injured by a cranial traumatism, even if it is more frequent after a direct hit (Garcia, 1996; Pressman, 1992).

2) Interrogation of the postconcussional syndrome

     The list of symptoms drawn up by Pierre Marie has not evolved much since 1916.

     The notion of «Dazzlements» has gradually been forgotten, probably because it was considered that it did not make a clear difference between vertigo/instability and the symptoms of heterophory. We can regret it because the notion of«Dazzlements», closer to the patients' expressions, underlined a link between vertigo and vision/oculomotricity.

     Petit-Dutaillis and Weil (1958) provided arguments for the thirst and diuresis disorders appearing after a cranial traumatism to be ascribed to it.

     However it has been defined how to lead the interrogation. At first, it must be open and the patient must be asked one question only:«What is wrong since the accident?». After all spontaneous answers have been given, and only then, can we check if the patient is affected or not by symptoms he has not mentioned. When the subject has forgotten several symptoms, we can hardly think that he is trying to exaggerate his disorders (Filliozat et al., 1975).

 FIG. 2 - Projection on the first two axes of a factorial analysis of the interrogation data.

PC (Perte de Connaissance): length of the loss of consciousness,

SA (Symptômes Annoncés): number of symptoms spontaneously given during the open interrogation,

SD (Symptômes Découverts): number of symptoms discovered during the closed interrogation


The projection reveals a link between the length of the loss of consciousness, taken as an indication of the seriousness of the traumatism, and the number of symptoms the patients are affected by, taken as an indication of the seriousness of the postconcussional syndrome.

(from Amphoux et al, 1977)


     The interrogation had given Pierre Marie a sign of objectivity for, as he said,«all the subjects' descriptions are absolutely identical, and made with the same expressions». That interrogation gave us another sign of objectivity by allowing us to make a link between the seriousness of the traumatism, estimated by the length of the loss of consciousness, and the seriousness of the syndrome, estimated by the number of symptoms the patient shows. A survey on that subject, carried out on 10,000 workers in building sites of the parisian area, and the results of which have been submitted to a factorial analysis, clearly shows the existence of such a link (figure 2)(Amphoux et al, 1977).

3) The postural check-up

     The subjects affected by a postconcussional syndrome have problems in standing up. So the clinical examination is logically particularly thorough in the exploration of anomalies in that posture or its control.

     a) The control of the orthostatic posture

     Standing up implies two neuro-muscular activities - a tonic activity and a phasic activity. The one and the other must be examined.

     The tonus fixes the position of the skeletal pieces corresponding to the considered posture. It is easy to see clinically if the muscular tonus is symmetrical or not.

     The bursts of phasic contractions permanently struggle against the deviations of the vertical of gravity relatively to its mean balance position. It is impossible to estimate,by naked eye, the efficiency of that phasic activity. Today, stabilometry is the only way of estimating it we know.

     The subgroup of postural mechanisms controlling those tonic and phasic activities of the orthostatic posture is called the«upright postural control system».

     b) The clinical examination of the postural tonus

     The postural tonus is frankly asymmetric during postconcussional syndromes. It can be observed thanks to classical tests such as Barré's vertical or Fukuda-Unterberger's stepping test which is but a variant of Babinski-Weil's star-like gait. But that test has the advantage of introducing the measure of walk deviations, and so of allowing a statistical validation (Weber et al., 1984) - over 50° of the spin movement, we know that the subject is out of the limits of normality at 95%.

     Posturologists have gradually adapted other tonic tests to their needs:

     * Evaluation of the movements of latero-flexion rotation of the rachis according to Fryette's laws and of the movements induced by Henke's axis - called «posturo-dynamic» test (Villeneuve, 1995).

     *«Thumbs» test (Fournier, 1993).

     * Evaluation of the resistance to the stretching of the external rotating muscles of the hips - called test «of the rotators» (Autet, 1985). That last test is only used and usable to study the variations of the tonus under the influence of various manipulations of the upright postural control system during the search for a potential therapy.

     c) Stabilometry

     If we stick to the rigorous physical definition of balance - two opposite, equal and aligned forces - we have to admit that man standing at rest never reaches his balance, but keeps trying to find that position without ever managing to hold it.

     That is what stabilometry makes very clear, by recording the successive positions of man's centre of pressure.

     Clinically, in a monopodal station, that phasic activity is shown by the dance of the tendons. In a bipodal station, it is impossible to appreciate it. Stabilometry only can do it, for it measures a series of parameters: length of the position shifts of the centre of pressure, area in which the centre of pressure stays, range of postural sway according to their frequency, etc.

     The interest of that technique of functional exploration did not escape doctors, but to make it usable in medicine, the apparatus and its conditions of use had to be normalised, the normal values of the various parameters and their confidence limits in a reference population had to be known - that has been done for ten years now (Bizzo et al., 1985; Association Française de Posturologie, 1985; Guidetti, 1989).

 FIG. 3 - Histogram of the areas of the statokinesigrams of 800 subjects suffering form a postconcussional syndrome.

Left: Gaussian curve of the distribution of the areas of the statokinesigrams in a normal population; 91: mean, 210: superior confidence limit at 95%.

Histogram of the areas of 800 patients.

Centre and right: Gaussian curves built on each of the two modes of distribution of areas among the patients.

Unity: square millimeter; situation: open eyes.

(from Gagey, 1991)


     A statistical study carried out on 800 patients suffering from a postconcussional syndromes recorded on that normalised platform shows that the parameter of the area of the statokinesigram of nearly all those patients is situated above the confidence limits at 95% (figure 3)(Gagey, 1991).

     d) Does the postural check-up prove the objectivity of the postconcussional syndrome?

     The question is unavoidable. The new idea that Pierre Marie gave us - that the postconcussional syndrome could have an objective basis - gave birth to so many controversies, some of them passionate, that we cannot avoid criticizing seriously the objectivity of the proofs given by the postural check-up.

     None of those clinical tests, when taken separately, stands up to such criticism, with the possible exception of the thumbs test. A malingerer, or simply a patient who wants to make it very clear to the doctor that he has difficulties standing up, can bend intentionally from Barré's vertical, turn around intentionally during the stepping test and even bend across during the posturo-dynamic test, even if it is more difficult. However we could not tell him how to cheat during the thumbs test because up to now we have not be explained the mechanism of that test by any fundamentalist. This is quite annoying: the apparently most objective test still has something mysterious... If we want to be extremely rigorous, we shall say that the clinical examination only provides a presumption of objectivity that each clinician or expert will appreciate according to his beliefs.

     The stabilometric parameters seem just as open to criticism at first sight. A subject who wants to insist on the fact that he is unstable can easily sway widely when he is on the platform and knows he is being observed. However a finer analysis of the distribution of the areas of the statokinesigrams of the postconcussional syndromes shows that it is bimodal (p<0.05). The limit between the two modes is situated at around 2,000 mm2 of area, which corresponds to a postural sway whose accelerations are at the threshold of perception of the semi-circular canals. The abnormal subjects of the population comprised between 210 and 2,000 mm2 of area (figure 3) therefore do not receive any canalicular information on their postural sway.

 FIG. 4 - Sinusoidal intercorrelation.

The sinusoidal aspect of the intercorrelation curve is proof that the forward-backward and right-left sway share the same period. They are no longer independent as in the normal subject (fig. 5) and therefore depend on the same, probably superior, centre. They are «overcontrolled».

     In the population situated above 2,000 mm2, whose subjects receive canalicular information on their postural sway, we see a unquestionable sign of postural overcontrol: the sinusoidal intercorrelation (figure 4) we find in malingerers and anxious subjects. Even if, in clinical practice, we cannot rely on stabilometry to find out any malingerer, we are statistically certain (p<0.001) that, mostly, the subjects belonging to the 210/2,000 mm2 population are not malingering (Guidetti, 1992).

 FIG. 5 - Normal intercorrelation.

Normally the intercorrelation line shows that the right-left and forward-backward sway do not share the same periodicity, they are independent, unlike what we observe in anxious subjects, malingerers or overmalingerers (cf. figure 4).

     Statistically, stabilometry confirms the objective lesion of the upright postural control system during postconcussional syndromes simply through the measure of the area of the statokinesigrams. Other stabilometric parameters are under study and they reasonably escape all possibility of malingering: percentage of the range of postural sway in the 0.2 Hz frequency band relatively to the other postural frequencies (Gagey & Toupet, 1997).


C) Link between the lesions due to the cranial traumatism and clinic


     Who could be surprised that a shock on the skull does not have the amazing privilege of not provoking lesions?

     But that such lesions exist and are visible not only post-mortem during the necropsy but also in vivo thanks to medical imaging, is not enough to consider them automatically as the cause of the clinical disorders.

1) Cervical lesions

     It is admitted that sprains, cervical subdislocations can lead to the appearance of a cervical nystagmus (Collard et al., 1967) and consequently disturb the position information that is needed by the upright postural control system in order to stabilise the body of man standing up (Scheibel, 1988), but the appearance of a cervical nystagmus can be induced by a simple mobility restriction of the cervical rachis (Norré et al., 1976), the relation of which to a traumatism is not obvious.

2) Trunkular lesions

     Trunkular lesions can lead to the appearance of disorders of postural control, of sleep and vigilance disorders, of oculomotor imbalances - that is coherent with what we know on the physiology of that region.

     The problem rather lies in the type of lesions observed on rare occurences in man, but systematically in experiment animals. Inside a trunkular formation, can the destruction only of a very small part of the neurons by the shock wave lead to the appearance of symptoms as important as those of the postconcussional syndrome?

     About ten years ago, we would have find it hard to answer that question. But today we know that the reduction of the number of neurons in a nervous structure, leads to the diminution of the complexity of the network dynamics (Sackellares et al., 1997) linked, by other studies (Nandrino et al., 1994), to the appearance of clinical disorders.

     In the functioning of nonlinear dynamic systems - like the upright postural control system (Martinerie & Gagey, 1992; Gagey et al., 1998) - we know that small causes can have disproportionate effects.

3) Lesions of the mandibular joint

     Many publications insist on the links existing between occlusion and posture (Clauzade & Daraillans, 1989; Nahmani et al., 1990; Hartmann & Cucchi, 1993) - whereas the reasons remain obscure, the facts are easy to observe clinically or by stabilometry (Bonnier, 1997), they can be reproduced. So much so that, if a malocclusion can be linked to a cranial traumatism, it is normal to check if it has an impact on the subject's postural tonus.

D) Treatment of the postconcussional Syndrome

     «Standing up is one of man's distinguishing features, along with language and thought. Standing on one's feet means having one's hands free to act and the joy of controlling one's body that bursts out in the practice of sports of balance. The orthostatic posture is symbolically deeply linked to the image man has of himself.

     Not being able to stand up means impotence, dependence, shame, the opposite of man standing up and proud to.

     With a cranial traumatised subject, it is therefore necessary - adapting oneself to each subject, for the width of that break can be partly unconscious - appreciate the importance of his narcissistic wound and evaluate its emotional impacts.»

     That remarkable text of Ferrey (1995) allows us to understand the importance of the psychosomatic approach to postconcussional syndromes. To be sure, all must be done so that they do not develop foreseeable psychiatric complications.

     If postural treatments (Gagey & Weber, 1995) better, if only for a limited time, the tonic disorders, they will make the psychiatrist's task much easier. On the contrary, the achievements, even relative, of a psychotherapy will have an impact on postural disorders as the influence of the autonomous nervous system on the postural system is far from negligible.

     The treatment of postconcussional syndromes is not glorious in any way!... The lesions due to the traumatism cannot be erased as if by magic and therapists have to accept the fact that patients often come back to say they do not feel better. But as years go by, the syndrome eventually ends up quieting down and gives the therapist the feeling that he has been useful after all, not because he has cured the syndrome, but because the patient regularly came back to see him.

E) Conclusion

     All therapists are right who, like Hippocrates, consider that psychiatric disorders have a foremost importance in the evolution of the postconcussional syndrome. But the root of the illness is not a psychiatric one, the root is the disorder of the upright postural control system. And, as a consequence, not being able to stand up represents so serious a wound to the subject that the most unfortunate psychiatric consequences may be feared.

     We understand the experts' hesitations, as they do not have any formal criterium to check that the patient is not exaggerating his disorders for his own profit. But when we are not sure, can we take the risk of worsening the evolution of the postconcussional syndrome by adding the experience of an injustice to that of postural disorders?

     Therapists would like, on the contrary, that during their first meeting, the expert and the patient, assumed to be honest, amicably set a compensation rate to submit that would satisfy both of them. Such an attitude would be inspired by the therapeutic concern of not worsening the evolution of the postconcussional syndrome by a decision considered to be unfair, and everybody would benefit from it as neither the postconcussional syndrome nor its compensation are definitive.

     And we indulge into thinking that the doctors' judicious intervention can influence favorably the future of the postconcussional syndrome.



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