Chapter 11

THE PHYSICAL MANIFESTATIONS OF STUPOR

We must now discuss the most difficult of all the aspects of the stupor problem. The subject is so involved and the evidence so inconclusive that observers will probably interpret the phenomena here reported according to their individual preconceptions. What we have to say is therefore published not so much to convince as to stimulate further work. The problem is wider than that of the mere etiology of the stupors we are considering. Their relationship to manic-depressive insanity is so intimate that we must tentatively consider this affectless reaction as belonging to that larger group. A discussion of the basic pathology of manic-depressive insanity is outside the sphere of this book. The author, therefore, thinks it advisable to state somewhat dogmatically his view, as to the etiology of these affective reactions, merely as a starting point for the argument concerning stupors specifically.

It is our view that the manic-depressive psychoses may be, and probably are, determined remotely but fundamentally by an inherent neuropsychic defect, but this physical and constitutional blemish is non-specific. The actual psychosis is determined by functional, that is, psychological factors. A predisposed individual exposed to a certain psychic stress develops a manic-depressive psychosis. Naturally any physical disease reduces the capacity for normal response to mental difficulties; hence physical illness may facilitate the production of a psychosis. But this intercurrent factor is also non-specific.

Such is our view of the etiology of manic-depressive insanity as a whole. When we approach the study of benign stupors, however, difficult problems appear. As will be discussed in a later chapter on the literature, reactions resembling benign stupors occur as a result of toxins, particularly following acute rheumatism. Recently the medical profession has been called on to treat many cases of encephalitis lethargica where similar symptoms are observed. If the resemblance amounted to identity, we would have to admit that a specific toxin may produce a specific mental reaction which we have concluded on other grounds to be psychogenic. As a matter of fact, in two particulars these reactions show relationship to organic delirium. Knauer reports that in post-rheumatic stupors illusions are frequent--an ice bag thought to be a cannon, or a child, etc.--and there are bizarre misinterpretations of the physical condition, such as lying on glass splinters, animals crawling on the body, and so on. Such illusions are, in our experience, not found in stupor, and, on the other hand, are cardinal symptoms of delirium. Further, Knauer reports that even at the height of post-rheumatic stupor, external stimuli make some impression, in that a thoughtful facial expression appears. In deep stupors, such as occurred in our series, this response is not seen. The same phenomenon of “rousing,” larval in Knauer’s cases, is often well marked in encephalitis lethargica and is, of course, a pathognomonic symptom of delirium. We might therefore think that these conditions are mixtures of two organic tendencies, namely, delirium and coma. It is not impossible that resemblances to benign stupor are due to functional elements appearing in the reduced physical state as additions to the organic symptoms. The prominence of pain might be taken as a likely cause for an instinctive reaction of withdrawal, which would account for the emotional palsy of these conditions on psychogenic grounds. [This argument can be better understood when the chapter on Psychological Explanation of Stupor has been read.] We therefore feel justified in holding that the resemblance of the symptoms of certain plainly organic reactions to those of benign stupor do not necessitate a splitting of these stupors from the manic-depressive group.

When we consider certain bodily manifestations of these typical stupors, however, fresh difficulties are encountered. Unlike depressions, elations and anxieties, certain physical symptoms appear with frequency, even regularity. This would seem to indicate the presence of physical disease. Inasmuch as the most constant of them is fever, the natural conclusion would be that we are dealing with an infection which produces a mental state called stupor. If we were not faced with an obvious relationship to manic-depressive insanity, where such symptoms are usually accidental and intercurrent, we would accept this explanation, but this quandary necessitates further analysis.

Let us first consider the fever. In 35 cases, on whom data of temperature could be found from the records extant, 28 showed fever usually running between 99° and 100°, often up to 101° or slightly over this point. When these cases were analyzed, however, it was found that 27 were typical and 8 atypical, showing pictures resembling those described in the last chapter. Of the latter only one had a rise of temperature, while of the typical group only one was afebrile. Therefore, since out of 27 typical cases 26 had the typical slight fever, we must conclude it to be a highly specific symptom. Of these 28 cases the incidence of the fever was as follows: 8 showed it only on admission; in 7 it was highest on admission but continued at a low rate throughout the rest of the psychosis; in 5 it extended without much variation throughout the psychosis; in 4 it appeared intermittently, while in 2 it was accentuated during periods when the mental symptoms were most pronounced. We see, then, that there is a distinct tendency for the fever to be associated with the onset of the disease.

When we look for other data from which we might discover causes for the fever, we find less than we would like. The records are of observations made, some of them, twenty years ago. Although the mental examinations were careful, the records of the physical symptoms either were not made or were lost in many cases. Consequently our description must be tentative and is published merely to stimulate further research as cases come to the attention of psychiatrists.

One looks, first, for other evidence of infection. Some of the cases were thoroughly examined with modern methods and nothing whatever found. Blood examinations were made in five cases; three of these had rather high temperature with the following blood pictures: Charles O., 103°, leucocytosis of 23,000, with 91.5% polymorphonuclears; Annie G. (Case 1), 103°, leucocytosis of 12,000 to 15,000, and 89% polymorphonuclears; Caroline DeS. (Case 2), 104°, 15,000 leucocytes, no differential made, Widal and diazo reaction negative. These three cases, then, had marked febrile reactions and leucocytosis. It is quite possible that they had infections which were not discovered. Of the other two Rosie K. (Case 11) had a temperature of 100° and 17,500 leucocytes associated with a fetid diarrhea, an unquestioned infection, while Mary C. (Case 7), with a temperature of only 100°, had no rise in number of total white cells but 41% of lymphocytes. This last might be due to an internal secretion or an involuntary nervous system anomaly. The possibility of the three high temperatures with leucocytosis being due to intercurrent infections must be considered. Charles O. had high fever only for ten days during a psychosis of several months. Annie G.’s high fever was of about the same duration. Caroline DeS. had short periods of marked pyrexia in the first and seventh months of her long psychosis. Except for these episodes, these three patients had the typical slight elevation of temperature. Three cases out of thirty-five, in which high fever and leucocytosis appeared episodically, are hardly enough to justify the view that stupors are the result of a specific infection. We must remember, too, that no focal neurological symptoms are ever observed, which makes the possibility of a central nervous system infection highly unlikely.

An alternative view might be that the slight rise of fever is somehow the result of stupor, not the cause of it. The editor consulted Professor Charles R. Stockard, of Cornell Medical College, as to this possibility. The following argument is the result of his suggestions:

What we call a normal temperature is, of course, the result of a balance maintained between heat production and heat loss. Either an increase in the former or a decrease in the latter must produce fever. It is possible that heat production may be increased in many stupors as a result of the muscular rigidity. Some cases showed higher temperature when this was more marked, but this was not sufficiently constant to justify any conclusions being drawn.

Heat loss occurs preponderantly as a result of radiation from the skin and by sweating with consequent evaporation of the secretion. These processes are functions of the skin and surface circulation. Are they disturbed in our stupors? We find considerable evidence that they are. Flushing or dermatographia occurred in six cases, cold or blue extremities in four cases, greasy skin in four, marked sweating in three, the hair fell out in two cases, while the skin was pathologically dry in one case, in fact there were few patients who showed normal skin function. Circulatory anomalies were also observed. The pulse was very rapid in eleven cases, weak or irregular in two, and slow in one case. All these symptoms are expressions of imbalance in the involuntary nervous system, further evidence of which is found in the rapid respiration of six cases and the shallow breathing of one patient. These pulse and respiration findings are the more striking in that individuals in stupor are, by the very nature of their disease, free from emotional excitement.

This imbalance could result from a poverty of circulating adrenalin which is necessary for the activation of the sympathetic nerves. A cause for low suprarenal function is to be found in the apathy of the stupor case. As Cannon and his associates have so conclusively demonstrated, any emotion which was open to investigation resulted in an increase of adrenalin output. As our emotions are constantly operating during the day--and often enough during sleep as well in connection with dreams--we must presume that emotional stimulus is a normal excitant for the production of adrenalin. It is therefore inconceivable that the blood could receive its normal supply of adrenalin with an apathy of the degree seen in stupor unless some purely hypothetically substitutive excitant were found.

We may therefore tentatively assume that the fever which marks the onset and frequently the course of these benign stupors is the result of a failure of the heat loss function, this being due to an imbalance in the involuntary nervous system that is occasioned, in turn, by insufficient circulating adrenalin, and the final cause for the poor suprarenal function is to be traced to the most consistent symptom of the stupor, namely, apathy. This hypothesis is welcome, not only because it would account adequately for the fever, but it also tends to accentuate the relationship with other forms of manic-depressive insanity, all of which are marked fundamentally by a pathological emotion. Naturally enough, one turns to the records again to see if the blood-pressure of these patients was low, as would be expected with a poor adrenalin supply. Unfortunately record was made of the blood-pressure in only two cases, in both of which the reading was 110 m.m. Two such isolated observations mean, of course, nothing whatever. It is possible that the drooling which so many stupor cases show is not merely the result of the failure of the swallowing reflex, but represents as well a compensation for anhydrosis by excessive salivary secretion.

Another symptom suggestive of involuntary nervous system or endocrine disorder is the highly frequent suppression of the menstrual function. At times this may occur as a sequel to mental shock, as it did in the case of Celia H. (Case 19), who was menstruating when, frightened by the suicidal attempt of her brother, the flow ceased abruptly. That purely psychic factors can produce marked changes in such functions has been demonstrated by Forel and other hypnotists time and again; presumably the effect is produced by way of alteration in the endocrine or involuntary nervous system influence. In such cases, however, we can trace the menstrual suppression directly to an emotional cause. On the other hand, most women in stupor fail to menstruate during the bulk of the psychosis at a time when we believe emotions to be absent or greatly reduced in their intensity. The recent work of Papanicolaou and Stockard[9] offers a simple explanation for this phenomenon. They have shown that in the guinea pig the œstrous cycle can be delayed by starvation, while in weaker animals a period may be suppressed completely. When one considers that even with the greatest care the nutrition of tube-fed patients is bound to be poor, it would be only natural to suppose that this malnutrition would cause such a disturbance in the œstrous cycle and was evidenced objectively by a failure to menstruate. Even in patients who are not tube-fed, under-nutrition is to be expected and, as a matter of fact, is usually observed. The work of Pawlow and Cannon has shown how essential psychic stimulus is for gastric digestion. Any condition of apathy would therefore tend to retard digestion and indirectly affect nutrition.

Finally, under the heading of Physical Manifestations of Stupor, we must consider epileptoid attacks, of which there was a history in two of our cases, both of which have already been described in the first chapter of this book. Anna G. (Case 1), in her second attack, was treated at another hospital, and from the account which they sent it appears that the stupor was immediately preceded by a seizure in which the whole body jerked. This is, of course, rather thin evidence of the existence of a definite convulsion, but in the case of Mary F. (Case 3) we have a fuller description. During the two days when the stupor was incubating, she had repeated seizures of the following nature. She sometimes said that prior to the attacks it became dark before her eyes and that her face felt funny or that she had a pain in the stomach which worked toward her right shoulder. The attack would begin when sitting in a chair, with the closing of her eyes, clenching her fists and pounding the side of the chair. She would then get stiff and slide on to the floor, where she would thrash her arms and legs about and move her head to and fro. The warning of the pain working from the stomach to the right shoulder is highly suggestive of an epileptic aura, although the other symptoms mentioned so far could have been considered hysterical or poorly described epileptic phenomena. The rest of the description indicates an epileptic seizure more strongly. She frothed at the mouth and once wet herself during an attack. They lasted only for a few minutes and she would breathe heavily after them. At the end of one attack she wiped the froth from her mouth with her handkerchief and gave it to her aunt, saying, “Burn that, it is poison.” This is perhaps a little less like epilepsy. It is plainly impossible for us to say with any positiveness that either these were or were not genuine convulsions, but it is nevertheless important to record them, because such phenomena are observed fairly frequently in dementia præcox cases but are practically unknown in manic-depressive insanity. This, then, would be another example of the resemblance to dementia præcox in these stupors which are unquestionably benign.[10]

We see, then, in reviewing all the physical manifestations of the benign stupors, that none occurred which cannot be explained as secondary to the mental changes, and therefore, until such time as physical symptoms are reported which cannot be so explained, we see no reason for changing our view that the benign stupor is to be regarded as one of the manic-depressive reactions.

FOOTNOTES:

[9] Papanicolaou, G. N., and Stockard, C. R., “Effect of Under-feeding on Ovulation and the Œstrous Rhythm in Guinea-pigs.” _Proceedings of the Society of Experimental Biology and Medicine_, Vol. XVII, No. 7, Apr. 21, 1920.

[10] As a matter of fact, if the views of Clark and MacCurdy[B] be accepted, some reason for these epileptic-like attacks may be imagined. According to them, epilepsy is a disease characterized by a lack of the natural instinctive interest in the environment which is expressed chronically in the deterioration, and episodically in the attacks, the most consistent feature of which is loss of consciousness. Now, in stupor we have an analogous reaction where, although consciousness is not disturbed in the sense in which it is in epilepsy, it is nevertheless considerably affected, inasmuch as contact with the environment is practically non-existent. The coincident thinking disorder is quite similar, both in epileptic dementia and the torpor following seizures and in these benign stupors. MacCurdy has suggested tentatively that the epileptic convulsion may be secondary to a very sudden loss of consciousness which removes a normal inhibition on the muscles, liberating the muscular contractions which constitute the convulsion. If this view were correct, it would not be hard to imagine that during the onset of these stupors the tendency to part company with the environment, which ordinarily comes on slowly, might occur with epileptic suddenness and hence liberate convulsive movements. This is, however, a pure speculation but not fruitless if it serves to draw attention to the analogies existing between the stupor reaction and some of the mental symptoms of epilepsy. These analogies are strong; aside from the obvious clinical differences, the stupor and epileptic reactions are dynamically unlike in that they are the product of different temperaments and precipitated by different situations.

FOOTNOTES:

[B] Clark, L. Pierce. “Is Essential Epilepsy a Life Reaction Disorder?” _Am. Jour. of the Medical Sciences_, November, 1910, Vol. CLVIII, No. 5, p. 703. This paper gives a summary of Dr. Clark’s theories.

MacCurdy, John T., “A Clinical Study of Epileptic Deterioration.” _Psychiatric Bulletin_, April, 1916.