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.