Part 70

=89.= We are now ready to consider in how far Shell-shock[13] is a distinctive disease. The physical event, shell-shock[13] we have seen at work in most of the major groups of mental disease and in some groups of nervous disease. Shell-shock, the physical event, has started up a “Shell-shock” paresis, a “Shell-shock” epilepsy, a “Shell-shock” Graves’ disease, a “Shell-shock” dementia praecox, wherein the term “Shell-shock” is merely a more specific term than the term “traumatic.” The physical event, shell-shock, has in special ways also changed the responses of the feeble-minded, the alcoholic, the cyclothymic, and the psychopathic person of whatever ill-defined sort may get into military service.

[13] I capitalize Shell-shock here (as elsewhere) to indicate the name of a supposed disease entity and leave shell-shock without an initial capital to indicate the physical event.

The physical event, shell-shock, has likewise caused focal irritative and destructive brain disease, spinal cord disease, peripheral nerve disease; and many well-recognized species of the so-called “organic” diseases of the nervous system have been produced. Shell-shock “organic” diseases have proved as difficult to tell from all sorts of Shell-shock “functional” diseases as ever have been the organic and functional analogues of these diseases in peace practice.

But, besides (_a_) sharing in the cause of mental and nervous disease (in the sense of “Shell-shock” general paresis and “Shell-shock” tabes, wherein at least one other factor, _viz._ the spirochete, is known to be at work) and (_b_) producing mental and nervous disease by killing or weakening or sensitizing neurones in the classical manner of the “focal” lesion, the physical event, Shell-shock, (_c_) appears able to bring out the subtler diseases and dispositions of mind which we term psychoneuroses, that is, hysteria, neurasthenia, psychasthenia. Just as we have for years spoken of “traumatic” psychoneuroses, so we may now speak of “Shell-shock” psychoneuroses--nor should anyone believe we cheat ourselves with the idea that the adjective “Shell-shock” has helped us more _re_ genesis than the adjective “traumatic.” “Shell-shock hysteria” and “traumatic hysteria” are on precisely the same--slippery--footing in the matter of their origin. The physics and chemistry of the psychoneuroses remain in Egyptian darkness.

The physical event, shell-shock, then, as the common man might say, affects body, brain, and mind in a great number of familiar ways; and these familiar ways remain as plain or as blind as the neuropathology and the psychopathology of today leave them. If thunderstorms and earthquakes got suddenly more frequent, we should have numbers of “lightning neuroses” and “earthquake hysterias,” neither of which would render the physics and chemistry of the psychoneuroses immediately a whit clearer.

When the common man speaks of some one as suffering from lightning stroke or earthquake, he is entitled to be met halfway by his hearer, who readily understands that the victim is suffering some sort of transient or permanent effects of the stroke or quake. In a like common sense should the term shell-shock be taken. Stroke, quake, or shock, each physical event is recognized as a factor in the situation. An event has become a factor. A condition for which the noun “shell-shock” was descriptive, in the present tense of some event, has passed into history; and the adjective “shell-shock” is now explanatory of the past cause, or one of the past causes, of a new situation. Shell-shock, the physical event, takes part in a great number of pathological events and as such lapses from noun to adjective.

But what are these pathological events, _viz._, the conditions of disease, that supervene? So far, in our consideration of psychoses incidental in the war, we have found Shell-shock _varieties_, perhaps, of mental disease; again, possibly a few Shell-shock _species_, using both these terms, variety and species, in a quasi botanical or zoölogical sense. But in either instance we do not rise, under the ordinary principles of nomenclature, beyond the adjective: Is there any evidence that shell-shock, the physical happening, has issued in a pathological event of greater dignity, namely, a _genus of disease_? Can shell-shock rise to the dignity of a proper noun, Shell-shock, so that we might think of _e.g._, a new genus of the psychoneuroses, something coördinate with hysteria, neurasthenia, psychasthenia? None, I believe, has the hardihood to propose a new genus of mental or nervous disease for Shell-shock regarded as a pathological event. _A fortiori_, it is unheard-of to think of Shell-shock, the pathological event, as representing a new _order_ of such events, coördinate with the psychoneuroses or the epilepsies, for example.

Shell-shock, the pathological event, we conclude, is a variety or a species, hardly a genus or an order of mental or nervous diseases. If we can keep in mind the obvious distinction between shell-shock, the physical event, and Shell-shock, the pathological event, we shall save ourselves much trouble. And if we can apply the ordinary criteria for the differentiation of the great groups (or orders) and the lesser groups (or genera) of mental and nervous disease to the given concrete case, we shall not go far wrong therapeutically in any case of so-called Shell-shock. For Shell-shock, the pathological event, becomes a humble variety or species of disease whose therapeutic indications are in larger part those of higher and comparatively well-recognized genera of disease, _e.g._, hysteria, neurasthenia, psychasthenia.

A shock is not a smash, a crush, a breach. A shock literally shakes. The shaken thing stays, for a time at least. Shaken up or down, the victim of shock is not at first thought of as done for. The spirit of the language is against the thought of shock as destruction or even as permanent irritation. Shock ought to be a “functional” rather than an “organic” thing, as medicine bandies these terms about. Shell-shock or Surgical Shock, it is all one to the logic of shock, which is thought of as a physical or chemical disturbance of mechanisms and arrangements that are, or ought to be readjustable. The one character which the late Professor Royce told me (in conversation) he could find in the term “functional” was the idea “reversible.” Shock is or ought to be, as a pathological event, reversible.

If this thought is in the backs of our minds as we think of Shell-shock, it can readily be seen why the “organic,” that is, non-reversible diseases, do not take kindly to the term Shell-shock. Shell-shock, the pathological event, prefers to be an item in the pathology of function. Can we further specify? The pathology of function, neuropsychically taken, considers such great groups as the psychoneuroses; (so far as we know) the cyclothymias; some of the symptomatic psychoses; a portion of the alcohol and drug group; some of the epilepsies; perhaps the dementia præcox group; not to mention various unresolved psychopathias. The psychoneuroses are the group most innocent of every “organic” taint: the machinery is assumed to be most normal in them and presumably the effects of disorder most reversible.

Shall we not therefore accept the psychoneuroses as the group in which to place those pathological happenings called Shell-shock? It will do no harm to make this choice if we do it humbly in the spirit of acknowledgment that we know next to nothing about the psychoneuroses. The psychoneuroses should fall on their knees to Shell-shock rather than that Shell-shock make obeisance to the psychoneuroses. For what is a psychoneurosis? It is a functional disease of the nervous system in which the mind plays an important part--it is also probably much else. But the “much else” is as likely to be found in Shell-shock as anywhere else during these particular years.

Thus, rehearsing in a broad way =the case arrangement of Section B=, we find, first, autopsied cases and cases with lumbar puncture data; then cases with prominent admixture of organic phenomena; a few cases to illustrate the victims’ own impressions of their disease; the long toe to top, or “cephalad” series (crural monoplegias and paraplegias, campto-cormias, astasia-abasias, brachial monoplegias, brachial paraplegias, deafmutism, blindness); the series to illustrate the idea of reflex or physiopathic disorders; the series of delayed Shell-shock phenomena; the series to show the picking out by Shell-shock of ante-bellum weak spots and tendencies in the organism; cases touching the hereditary question; peculiar and unique cases; examples of Shell-shock equivalents; and cases of a psychopathic rather than local hystero-traumatic trend.

=90.= At the outset of Section B (Shell-shock: Nature and Causes), we face the question of the possibly organic nature of Shell-shock. It is safe to say that the vast majority of cases of Shell-shock do not die of Shell-shock, and the collection of material from true Shell-shock cases that are killed by accident or intercurrent disease has proved a matter of great difficulty under military conditions. Of course, it is possible to answer the question _à priori_, by agreeing that any case with structural lesion of whatever sort, is by the same token not a case of Shell-shock.

=91.= Apparently the most informatory case yet presented is that of Mott (Case 197). In this case, death came in 24 hours, and the immediate cause of death was doubtless a small hemorrhage of the spinal bulb. There was a congestion of veins in the bulb, as well as a congestion of the pia mater over all other parts of the brain. Nor was the bulbar hemorrhage unique, for there were a number of superficial punctate hemorrhages. In short, the brain was not even grossly normal, such as one might desire in a case of true Shell-shock as conceived by _à priori_ workers. Yet, according to Mott, there are microscopic changes of an intimate nature that lie nearer to the microscopic possibilities in true Shell-shock. For example, in the bulb itself there was a distinct and photographable change of nerve cells: =the vago-accessorius nucleus had cells in a state of chromatolysis=. The internal alterations of these cells, with dissolution of chromatic material, may possibly indeed have been the direct cause of death or an indicator of its direct cause. Here again, to accord full justice to Mott’s contention, we are dealing perhaps more with a phenomenon of the cause of death than with a Shell-shock phenomenon. According to Mott, the Shell-shock symptoms themselves are due to capillary anemia and to nerve cell changes such as he found in various regions. These nerve cell lesions were of the nature of chromatolysis and identical with those of the vago-accessorius nucleus. In this connection, one thinks of the ideas of Crile concerning exhaustion and its effect upon certain nerve cells and other cells, and indeed the whole conception runs back to the early years of discussion of the meaning of chromatin deposits in nerve cells, and to the work on fatigue of such cells. It may well be that Mott’s suggestion is sound, and that changes of the order of chromatolysis are what subtend some, if not most, of the phenomena of Shell-shock. On account of the myriad interconnections of neurones and the remote effects upon normal neurones of disturbances of a microchemical or microphysical nature in a few neurones, it would not do to throw out of court forthwith such a contention as that of Mott by triumphantly pointing to the miracle cures of certain Shell-shock phenomena; for it will not necessarily be the chromatolytic (or otherwise microchemically or physically altered) cells that will be directly responsible for the symptoms in question. Cells whose activity is but temporarily in abeyance (perhaps by phenomena akin to diaschisis) might be reached from an unusual source in the process of “miracle cure,” whereupon the newly opened paths of energy might conceivably remain open. Nevertheless, it cannot be denied that there are considerable stretches of speculation in the thread of this hypothesis.

=92.= Particularly important is the question, how frequently such hemorrhages as those found by Mott in Case 197 occur. Cases are given in the text which show such hemorrhages.

Rather often quoted in this relation is Case 201, a case of Sencert, in which a shell exploded one metre away from a soldier and injured him so that he died that night through the bursting of the pleura of both lungs within a thoracic cage which was quite intact. This sort of finding reminds one of cases in which the inner partitions of houses are burst by explosion when the outer walls remain intact. In particular, one thinks of the physical changes within an aneroid barometer, which have been shown to come about when something is exploded near by. If such an event may happen as the bursting of the lungs within an otherwise intact body, so also is there evidence that a similar event occurs in the nervous system. Clinical evidence of this is obtained in the hemorrhage and pleocytosis of spinal fluid obtained early in the clinical examination of certain cases. In fact, in Case 205 (one of Souques), there is a pleocytosis of the fluid as late as a month after shell-shock. When there is no pleocytosis or hemorrhage, there may be a hypertension of the fluid,--a finding sometimes attributed to Dejerine (see, for example, Case 207, of Leriche). It might be inquired whether the fall sustained by the patient as a result of the shell explosion could not be responsible for the hemorrhage, and this may indeed be the fact in certain instances. Babinski has offered in Case 209, an instance in which hematomyelia (with later partial recovery) was produced in a subject who was lying prone in the performance of machine-gun duty (the phenomena in this case were well described by the victim himself, a veterinary student who was six months a captive in Germany). Doubtless, it would not be difficult to produce a complete series of cases with and without trauma to the tissues investing the nervous system, with definite clinical or autopsy evidence of organic lesions of the nervous system, whether by mechanical impact, by the concussion (windage) of the air, or even by the effects of muscular contractions.

=93.= A case of Chavigny’s (Case 198), in which there was an extremely careful autopsy, showed a strongly blood-stained cerebrospinal fluid; in fact, there was an intradural hemorrhage, though of minor degree and possibly not the cause of death; and throughout the brain substance there were slight hemorrhagic points. But there was no sign whatever of fracture of the cranial vault or base. Another case of similar meningeal hemorrhage but sharply localized, was Case 199, an instance of minor explosion in which neither skin nor muscles, bone or viscera showed any lesion; and the death, which occurred in seven days, seemed hardly explicable on the basis of hemorrhage itself. In fact, this case would require the sort of microscopic examination performed by Mott in Case 197 for a proof of the cause of death, which was thought by the reporters themselves (Roussy and Boisseau) to be within the field of histology.

=94.= Case 200 seems to bring proof that there may be areas of gross softening within the spinal cord produced by the concussion of the cord from shell-burst, although there had been no fracture of the spine itself and no penetration of splinters of shell or of bone into the spinal canal or the substance of the cord itself. The argument here is that the tissues that lie between the agent of violence and the interior of the spinal cord are affected _en bloc_ by the impact, the resultant gross or molar lesions being several millimetres or centimetres from the point reached by the impinging body or force. How complicated such a situation might be, we may recall from a case previously studied, namely, Case 103 (Lhermitte), wherein a missile struck the left side of the skull and produced lesions beneath its point of impact, but at the same time apparently caused a _contre-coup_ effect upon the opposite hemisphere. That particular case did not come to autopsy, but Lhermitte’s explanation of its queer association of aphasia with ipsilateral hemiplegia seems sound enough. In fine, what with the mechanical trauma to which many victims of shell explosion are subject, what with the findings in sundry autopsies, and what with the determination of hemorrhage in the spinal fluid early after the shock, it might be conceived that the majority of cases of Shell-shock are actually cases of mechanical injury to the brain or spinal cord in which hemorrhage or laceration and overriding of neuronic tissues would be found. Nor would such a hypothesis be _prima facie_ absurd with the evidence afforded by certain cases of Shell-shock having an admixture of reflex phenomena and other symptoms proved by the older neurologists to be beyond peradventure organic. (Compare, for example, such a case as that of Case 210, with herpes zoster and segmentary symptoms.) It should be remembered, however, that Mott in the case cited above (Case 197) sharply distinguishes between the hemorrhages (especially the bulbar hemorrhage which caused death) and the nerve cell chromatolysis which he regarded as possibly at the basis of Shell-shock symptoms. It is decidedly doubtful whether the hypothesis of microscopic or larger hemorrhages, or of local areas of destruction of neurones will suffice for the explanation of true Shell-shock. This is not to say that in the diagnosis of true Shell-shock (that is, roughly speaking, the psychoneurosis), we shall not need to concede and consider in every case the possibility of =traumatic focal brain disease=. This will always need =to be faithfully excluded= in all cases unless the initial set-up of symptoms is so suggestive of immediately curable psychoneurosis that without further ado miracle-therapy is undertaken and executed. But in virtually all the slower cases, an exclusion of organic brain and cord disease is undertaken. Admixtures of organic and focal phenomena are quite in the order of everyday occurrence.

=95.= Especially good instances of this co-existence of functional and organic symptoms are found in ear cases; and it may be suspected that when, after the war, all these data can be suitably gathered and compared, it will be from the field of otology that some of the most fruitful hypotheses will be developed. In the cases of Shell-shock deafness, mechanical peripheral factors are admixed with central factors in phenomena admitting in some ways more exact diagnosis than in other fields. We may await the correlation of these data by some worker, equally skilled in otology and neurology, with the profoundest interest. Analogous results may be hoped from a correlation of neurological and ophthalmological conceptions.

=96.= Suffice it to say that the differentiation of organic and functional phenomena has long been possible on the basis of what we know concerning various reflexes (_e.g._, the Babinski reflex and its congeners); and the net result of this work is that the majority of Shell-shock cases,--that is, cases in which the physical factor shell-shock has entered,--are probably not cases in which a coarse organic disease could be proved to exist, or assumed with any color of likelihood to exist. Even limiting ourselves to cases in which the physical factor shell-shock or some sort of impact with or without an external wound occurred, we shall find cases enough of a truly functional nature, as indicated by their reflexes, to render it quite impossible to assert that they are in the classical sense “organic” cases. Putting these cases with the physical shell-shock factors together with the other large series of cases in which precisely similar symptoms occur without the presence of the physical shell-shock factor, we shall find ourselves convinced that classical Shell-shock phenomena are by and large what is called functional. We shall arrive at the hypothesis that they are cases of hysteria or other form of psychoneurosis, entitled to the diagnosis of traumatic hysteria (or hysterotraumatism, in the sense of Charcot), or not, according to whether the physical factor shell-shock was in evidence. What now underlies the concept functional, as we use it in Charcot’s sense of hysterotraumatism, or in the more modern phrase traumatic hysteria? Do we perhaps mean some microchemical or microphysical change of a reversible nature, similar to that described by Mott, _e.g._, in Case 197? It is not possible to answer this question at this time.

=97.= But if we give up the hypothesis of organic disease of the nervous system (that is, the hypothesis of coarse lesions, small or large, conceived to be the direct effect of mechanical impact), can we incriminate any other factor? Chemical factors from the gas of bursting shells may be thought of; yet in abundant cases there is no evidence that these have been in play. They and a variety of other special causes may be found working in a few instances but have nothing to do with the moot question.

=98.= Upon giving up the organic hypothesis, the modern functionalist is very apt to run directly into the embrace of hysteria. If a thing is not physical, it must be psychical in its genesis, so runs the argument. What, after all, is a neurosis? We mean ordinarily by neurosis, something functional rather than structural. We often mean something psychical rather than peripheral. Accordingly, as we have seen, many writers rush to the hypothesis that Shell-shock effects, except in a few unusual instances of organic disease, are functional; and not only are they functional but psychic, and maintained by some of the so-called “mechanisms” which abound in modern speculative writing.

=99.= Case 253, a case of Tinel, may serve to illustrate this point. Tinel’s patient was not subject to shell-shock at all, but was wounded in the arm. Three weeks later, he was able to flex his forearm only by means of the supinator longus. It was found that the biceps was soft and flaccid, though the electrical reactions of the biceps were normal. Now, since flexion of the forearm is normally produced by a synergic contraction of the biceps and supinator longus, the situation in Tinel’s case was striking in that the functions of the biceps and supinator longus had been separated out by a process which could not be hysterica. The hypothesis is that in hysteria it has always been found impossible to split the synergic action of these two muscles. What has happened? In Tinel’s picturesque phrase, the biceps muscle has been =stupefied= by a process which involved no destruction of a nerve trunk or any important nerve elements. This process of stupefaction passed away with a few weeks’ massage and rhythmic faradism. But what is this process of stupefaction, as Tinel calls it? No definite answer can be given. But is not the process analogous to what may happen in a variety of cases of shell explosion in which, for one reason or another, sundry neurones are, as it were, stupefied, stunned, anesthetized, or thrown out of gear by some internal physico-chemical readjustment of unknown nature? Perhaps that readjustment, though in Tinel’s case it probably took place within the tissues of the arm itself, is analogous to the chromatolytic process in nerve-cell bodies suspected by Mott to be at the bottom of certain Shell-shock symptoms as in Case 197.