Full Text Archive logoFull Text Archive — Free Classic E-books

The Origin and Nature of Emotions by George W. Crile

Part 3 out of 3

Adobe PDF icon
Download The Origin and Nature of Emotions pdf
File size: 0.3 MB
What's this? light bulb idea Many people prefer to read off-line or to print out text and read from the real printed page. Others want to carry documents around with them on their mobile phones and read while they are on the move. We have created .pdf files of all out documents to accommodate all these groups of people. We recommend that you download .pdfs onto your mobile phone when it is connected to a WiFi connection for reading off-line.

the chemical activity of the body is increased 10 per cent.
In acute infections there is aversion to food and frequently there
is vomiting. In fever, then, we have diminished intake of energy,
but an increased output of energy--hence the available potential
energy in the body is rapidly consumed. This may be an adaptation
for the purpose of breaking up the foreign protein molecules
composing the bacteria. Thus the body may be purified by a chemical
combustion so furious that frequently the host itself is destroyed.
The problems of immunity are not considered here.

As to the mechanism which produces fever, we postulate that it
is the same mechanism as that which produces muscular activity.
Muscular activity is produced by the conversion of latent energy
into motion, and fever is produced largely in the muscles by
the conversion of latent energy into heat. We should, therefore,
find similar changes in the brain, the adrenals, the thyroid,
and the liver, whatever may be the purpose of the conversion of energy--
whether for running, for fighting, for the expression of emotion,
or for combating infection.

We shall first present experimental and clinical evidence which tends
to show what part is played by the brain in the production of both
muscular and febrile action, and later we shall discuss the parts
played by the adrenals, the thyroid, and the liver. Histologic Changes
in the Brain-cells in Relation to the Maintenance of Consciousness
and to the Production of the Emotions, Muscular Activity, and Fever

We have studied the brain-cells in human cases of fever,
and in animals after prolonged insomnia; after the injection
of the toxins of gonococci, of streptococci, of staphylococci,
and of colon, tetanus, diphtheria, and typhoid bacilli; and after
the injection of foreign proteins, of indol and skatol, of leucin,
and of peptones. We have studied the brains of animals which had been
activated in varying degrees up to the point of complete exhaustion
by running, by fighting, by rage and fear, by physical injury,
and by the injection of strychnin (Figs. 2, 4, 5, and 37). We have
studied the brains of salmon at the mouth of the Columbia River
and at its headwater (Fig. 55); the brains of electric fish,
the storage batteries of which had been partially discharged,
and of those the batteries of which had been completely discharged;
the brains of woodchucks in hibernation and after fighting;
the brains of humans who had died from anemia resulting from hemorrhage,
from acidosis, from eclampsia, from cancer and from other chronic diseases
(Figs. 40 to 43, 56, 74, and 75). We have studied also the brains
of animals after the excision of the adrenals, of the pancreas,
and of the liver (Figs. 57 and 60).

In every instance the loss of vitality--that is, the loss
of the normal power to convert potential into kinetic energy--
was accompanied by physical changes in the brain-cells (Figs. 45
and 46). The converse was also true, that is, the brain-cells
of animals with normal vital power showed no histologic changes.
The changes in the brain-cells were identical whatever the cause.
The crucial question then becomes: Are these constant changes in
the brain-cells the result of work done by the brain-cells in running,
in fighting, in emotion, in fever? In other words, does the brain
perform a definite role in the conversion of latent energy into
fever or into muscular action; or are the brain-cell changes caused
by the chemical products of metabolism? Happily, this crucial
question was definitely answered by the following experiment:
The circulations of two dogs were crossed in such a manner that the
circulation of the head of one dog was anastomosed with the circulation
of the body of another dog, and vice versa. A cord encircled the neck
of each so firmly that the anastomosing circulation was blocked
(Fig. 58). If the brain-cell changes were due to metabolic products,
then when the body of dog "A" was injured, the brain of dog "A"
would be normal and the brain of dog "B" would show changes.
Our experiments showed brain-cell changes in the brain of the dog
injured and no changes in the brain of the uninjured dog.

The injection of adrenalin causes striking brain-cell changes:
first, a hyperchromatism, then a chromatolysis. Now if adrenalin
caused these changes merely as a metabolic phenomenon and not as a
"work" phenomenon, then the injection of adrenalin into the carotid
artery of a crossed circulation dog would cause no change in its
circulation and its respiration, since the brain thus injected
is in exclusive vascular connection with the body of another dog.
In our experiment the blood-pressures of both dogs were recorded
on a drum when adrenalin was injected into the common carotid.
The adrenalin caused a rise in blood-pressure, an increase
in the force of cardiac contraction, increase in respiration,
and a characteristic adrenalin rise in the blood-pressure of both dogs.
The rise was seen first in the dog whose brain alone received adrenalin
and about a minute later in the dog whose body alone received adrenalin
(Fig. 59). Histologic examinations of the brains of both dogs
showed marked hyperchromatism in the brain receiving adrenalin,
while the brain receiving no adrenalin showed no change.
Here is a clear-cut observation on the action of adrenalin
on the brain, for both the functional and the histologic
tests showed that adrenalin causes increased brain action.
The significance of this affinity of the brain for adrenalin begins
to be seen when I call attention to the following striking facts:

1. Adrenalin alone causes hyperchromatism followed by chromatolysis,
and in overdosage causes the destruction of some brain-cells.

2. When both adrenal glands are excised and no other factor
is introduced, the Nissl substance progressively disappears from
the brain-cells until death. This far-reaching point will be taken
up later (Fig. 60).

Here our purpose is to discuss the cause of the brain-cell changes.
We have seen that in crossed brain and body circulation trauma
causes changes in the cells of the brain which is disconnected
from the traumatized body by its circulation, but which is
connected with the traumatized body by the nervous system.
We have seen that adrenalin causes activation of the body connected
with its brain by the nervous system, and histologic changes in
the brain acted on directly by the adrenalin, but we found no notable
brain-cell changes in the other brain through which the products
of metabolism have circulated.

In the foregoing we find direct evidence that the products of
metabolism are not the principal cause of the brain-cell changes.
We shall now present evidence to show that for the most part
the brain-cell changes are "work" changes. What work? We postulate
that it is the work by which the energy stored in the brain-cells is
converted into electricity or some other form of transmissible energy
which then activates certain glands and muscles, thus converting latent
energy into beat and motion. It has chanced that certain other studies
have given an analogous and convincing proof of this postulate.
In the electric fish a part of the muscular mechanism is replaced
by a specialized structure for storing and discharging electricity.
We found "work" changes in the brain-cells of electric fish
after all their electricity had been rapidly discharged
(Fig. 61). We found further that electric fish could not discharge
their electricity when under anesthesia, and clinically we
know that under deep morphin narcosis, and under anesthesia,
the production both of heat and of muscular action is hindered.
The action of morphin in lessening fever production is probably
the result of its depressing influence on the brain-cells, because
of which a diminished amount of their potential energy is converted
into electricity and a diminished electric discharge from the brain
to the muscles should diminish heat production proportionally.
We found by experiment that under deep morphinization brain-cell
changes due to toxins could be largely prevented (Fig. 62);
in human patients deep morphinization diminishes the production
of muscular action and of fever and conserves life when it is
threatened by acute infections. The contribution of the brain-cells
to the production of heat is either the result of the direct
conversion of their stored energy into heat, or of the conversion
of their latent energy into electricity or a similar force,
which in turn causes certain glands and muscles to convert latent
energy into heat.

A further support to the postulate that the brain-cells contribute
to the production of fever by sending impulses to the muscles
is found in the effect of muscular exertion, or of other forms of
motor stimulation, in the presence of a fever-producing infection.
Under such circumstances muscular exertion causes additional fever,
and causes also added but identical changes in the brain-cells. Thyroid
extract and iodin have the same effect as muscular exertion and infection
in the production of fever and the production of brain-cell changes.
All this evidence is a strong argument in favor of the theory that
certain constituents of the brain-cells are consumed in the work
performed by the brain in the production of fever.

That the stimulation of the brain-cells without gross activity
of the skeletal muscles and without infection can produce heat
is shown as follows:

(_a_) Fever is produced when animals are subjected to fear without
any consequent exertion of the skeletal muscles.

(_b_) The temperature of the anxious friends of patients will rise
while they await the outcome of an operation (Fig. 63).

(_c_) The temperature and pulse of patients will rise as a result
of the mere anticipation of a surgical operation (Fig. 64).

(_d_) There are innumerable clinical observations as to the effect
of emotional excitation on the temperature of patients.
A rise of a degree or more is a common result of a visit from
a tactless friend. There is a traditional Sunday increase
of temperature in hospital wards. Now the visitor does not bring
and administer more infection to the patient to cause this rise,
and the rise of temperature occurs even if the patient does
not make the least muscular exertion as a result of the visit.
I once observed an average increase of one and one-eighth degrees
of temperature in a ward of fifteen children as a result of a Fourth
of July celebration.

Is the contribution of the brain to the production of heat due
to the conversion of latent energy directly into heat, or does
the brain produce heat principally by converting its latent energy
into electricity or some similar form of transmissible energy which,
through nerve connections, stimulates other organs and tissues,
which in turn convert their stores of latent energy into heat?

According to Starling, when the connection between the brain
and the muscles of an animal is severed by curare, by anesthetics,
by the division of the cord and nerves, then the heat-producing power
of the animal so modified is on a level with that of cold-blooded animals.
With cold the temperature falls, with heat it rises. Such an animal
has no more control over the conversion of latent energy into heat
than it has over the conversion of latent energy into motion.

Electric stimulation done over a period of time causes brain-cell changes,
and electric stimulation of the muscles causes a rise in temperature.

Summary of Brain-cell Studies

In our crossed circulation experiments we found that neither waste
products nor metabolic poisons could be considered the principal
cause of the brain-cell changes. We found that in the production
both of muscular action and of fever there were brain-cell changes
which showed a quantita-tive relation to the temperature changes
or to the muscular work done. We observed that under deep
morphinization the febrile response or the muscular work done was
either diminished or eliminated and that the brain-cell changes were
correspondingly diminished or eliminated. We found also that brain-cell
changes and muscular work followed electric stimulation alone.
I conclude, therefore, that the brain-cell changes are work changes.

We shall next consider other organs of the kinetic system in their
relation to muscular activity, to emotion, to consciousness,
to sleep, to hibernation, and to heat production.

The Adrenals

In our extensive study of the brain in its relation to the production
of energy and the consequent exhaustion caused by fear and rage;
by the injection of foreign proteins, of bacterial toxins,
and of strychnin; by anaphylaxis; by the injection of thyroid extract,
of adrenalin, and of morphin, we found that, with the exception
of morphin, each of these agents produced identical changes in
the brain-cells. As we believed that the adrenals were intimately
associated with the brain in its activities, we concluded that
the adrenals also must have been affected by each of these agents.
To prove this relation, we administered the above-mentioned
stimuli to animals and studied their effects upon the adrenals
by functional, histologic, and surgical methods, the functional
tests being made by Cannon's method.

Functional Study of the Adrenals.--Our method of applying
the Cannon test for adrenalin was as follows: (_a_) The blood
of the animals was tested before the application of the stimulus.
If this test was negative, then (_b_) the stimulus was applied
and the blood again tested. If this second test was negative,
a small amount of adrenalin was added. If a positive reaction
was then given, the negative result was accepted as conclusive.
(_c_) If the control test was negative, then the stimulus was given.
If the blood after stimulation gave a positive result for adrenalin,
a second test of the same animal's blood was made twenty-five minutes
or more later. If the second test was negative, then the positive
result of the first test was accepted as conclusive.

We have recorded 66 clear-cut experiments on dogs, which show that
after fear and rage, after anaphylaxis, after injections of indol
and skatol, of leucin and creatin, of the toxins of diphtheria and
colon bacilli, of streptococci and staphylococci, of foreign proteins,
and of strychnin, the Cannon test for adrenalin was positive.
The test was negative after trauma under anesthesia, and after
intravenous injections of thyroid extract, of thyroglobin,
and of the juices of various organs injected into the same animal from
which the organs were taken. Placental extract gave a positive test.
The test was sometimes positive after electric stimulation
of the splanchnic nerves. On the other hand, if the nerve supply
to the adrenals had been previously divided, or if the adrenals
had been previously excised, then the Cannon test was negative
after the administration of each of the foregoing adequate stimuli.
Blood taken directly from the adrenal vein gave a positive result,
but under deep morphinization the blood from the adrenal vein
was negative, and under deep morphinization the foregoing adequate
stimuli were negative.

In brief, the agencies that in our brain-cell studies were found to
cause hyperchromatism followed by chromatolysis gave positive results
in the Cannon test for adrenalin (Fig. 62). The one agent which was
found to protect the brain against changes in the Nissl substance--
morphin--gave a negative result in the Cannon test for adrenalin.
After excision of the adrenals, or after division of their nerve supply,
all Cannon tests for adrenalin were negative.

Histologic Study of the Adrenals.--Histologic studies of the adrenals
after the application of the adequate stimuli which gave positive
results to the Cannon test for adrenalin are now in progress,
and thus far the histologic studies corroborate the functional tests.

In hibernating woodchucks, the cells of the adrenal cortex were found
to be vacuolated and shrunken. In one hundred hours of insomnia,
in surgical shock, in strong fear, in exhaustion from fighting,
after peptone injections, in acute infections, the adrenals undergo
histologic changes characteristic of exhaustion (Figs. 66 to 67).

We have shown that brain and adrenal activity go hand in hand,
that is, that the adrenal secretion activates the brain, and that
the brain activates the adrenals. The fundamental question which now
arises is this: Are the brain and the adrenals interdependent?
A positive answer may be given to this question, for the evidence
of the dependence of the brain upon the adrenals is as clear as is
the evidence of the dependence of the adrenals upon the brain.
(1) After excision of the adrenals, the brain-cells undergo
continuous histologic and functional deterioration until death.
During this time the brain progressively loses its power
to respond to stimuli and there is also a progressive loss
of muscular power and a diminution of body temperature.
(2) {illust. caption = FIG. 66.In our crossed circulation experiments
we found that adrenalin alone could cause increased brain activity,
while histologically we know that adrenalin alone causes an increase
of the Nissl substance. An animal, both of whose adrenals
had been excised, showed no hyperchromatism in the brain-cells
after the injection of strychnin, toxins, foreign proteins, etc.
(3) When the adrenal nerve supply is divided (Cannon-Elliott), then
there is no increased adrenal activity in response to adequate stimuli.

From these studies we are forced to conclude not only that the brain
and adrenals are interdependent, but that the brain is actually
more dependent upon the adrenals than the adrenals upon the brain,
since the brain deteriorates progressively to death without the adrenals,
while the adrenal whose connection with the brain has been broken
by the division of its nerve supply will still produce sufficient
adrenalin to support life.

From the strong affinity of the brain-cells for adrenalin which was
manifested in our experiments we may strongly suspect that the Nissl
substance is a volatile, extremely unstable combination of certain
elements of the brain-cells and adrenalin, because the adrenals alone
do not take the Nissl stain and the brain deprived of adrenalin
also does not take Nissl stain. The consumption of the Nissl
substance in the brain-cells is lessened or prevented by morphin,
as is the output of adrenalin; and the consumption of the Nissl
substance is also lessened or prevented by nitrous oxid.
But morphin does not prevent the action of adrenalin injected
into the circulation, hence the control of morphin over energy
expenditure is exerted directly on the brain-cells. Apparently morphin
and nitrous oxid both act through this interference with oxidation
in the brain. We, therefore, conclude that within a certain range
of acidity of the blood adrenalin can unite with the brain-cells
only through the mediation of oxygen, and that the combination
of adrenalin, oxygen, and certain brain-cell constituents
causes the electric discharge that produces heat and motion.
In this interrelation of the brain and the adrenals we have what is,
perhaps, the master key to the automatic action of the body.
Through the special senses environmental stimuli reach the brain
and cause it to liberate energy, which in turn activates certain
other organs and tissues, among which are the adrenals. The increased
output of adrenalin activates the brain to still greater activity,
as a result of which again the entire sympathetic nervous system
is further activated, as is manifested by increased heart action,
more rapid respiration, raised blood-pressure, increased output
of glycogen, increased power of the muscles to metabolize glucose, etc.

If this conclusion be well founded, we should find corroborative evidence
in histologic changes in that great storehouse of potential energy,
the liver, as a result of the application of each of the adequate
stimuli which produced brain-cell and adrenal changes.

The Liver

Prolonged insomnia, prolonged physical exertion, infections, injections of
toxins and of strychnin, rage and fear, physical injury under anesthesia,
in fact, all the adequate stimuli which affected the brain and
the adrenals, produced constant and identical histologic changes
in the liver--the cells stained poorly, the cytoplasm was vacuolated,
the nuclei were crenated, the cell membranes were irregular, the most
marked changes occurring in the cells of the periphery of the lobules
(Figs. 69 and 70). In prolonged insomnia the striking changes
in the liver were repaired by one seance of sleep.

Are the histologic changes in the liver cells due to metabolism or toxic
products, or are they "work" changes incident to the conversion of latent
into kinetic energy? Are the brain, adrenals, and liver interdependent?
The following facts establish the answers to these queries:

(1) The duration of life after excision of the liver is about
the same as after adrenalectomy--approximately eighteen hours.

(2) The amount of glycogen in the liver was diminished in all the
experiments showing brain-adrenal activity; and when the histologic
changes were repaired, the normal amount of glycogen was again found.

(3) In crossed circulation experiments changes were found in the liver
of the animal whose brain received the stimulus.

From these premises we must consider that the brain, the adrenals,
and the liver are mutually dependent on one another for the conversion
of latent into kinetic energy. Each is a vital organ, each equally vital.
It may be said that excision of the brain may apparently cause death
in less time than excision of the liver or adrenals, but this statement
must be modified by our definition of death. If all the brain
of an animal be removed by decapitation, its body may live on for at
least eleven hours if its circulation be maintained by transfusion.
An animal may live for weeks or months after excision of the cerebral
hemispheres and the cerebellum, while an overtransfused animal may
live many hours, days even, after the destruction of the medulla.
It is possible even that the brain actually is a less vital organ
than either the adrenals or the liver.

In our research to discover whether any other organs should be
included with the brain, the adrenals, and the liver in this mutually
interdependent relation, we hit upon an experiment which throws
light upon this problem.

Groups of rabbits were gently kept awake for one hundred hours
by relays of students, an experiment which steadily withdrew
energy but caused not the slightest physical or emotional injury
to any of them; no drug, toxin, or other agent was given to them;
they were given sufficient food and drink. In brief, the internal
and external environments of these animals were kept otherwise normal
excepting for the gentle stimuli which insured continued wakefulness.
This protracted insomnia gradually exhausted the animals completely,
some to the point of death even. Some of the survivors were killed
immediately after the expiration of one hundred hours of wakefulness,
others after varying intervals.

Histologic studies were made of every tissue and organ in the body.
Three organs, the brain, the adrenals, and the liver, and these three only,
showed histologic changes. In these three organs the histologic changes
were marked, and were almost wholly repaired by one seance of sleep.
In each instance these histologic changes were identical with
those seen after physical exertion, emotions, toxins, etc.[*] It
would appear, then, that these three organs take the stress of life--
the brain is the "battery," the adrenals the "oxydizer," and the liver
the "gasoline tank." This clear-cut insomnia experiment corresponds
precisely with our other brain-adrenal observations.

[*] Further studies have given evidence that the elimination of the acids
resulting from energy-transformation as well as the conversion
of energy stored in the kinetic organs causes histologic changes
in the liver, the adrenals, and possibly in the brain.

With these three kinetic organs we may surely associate also the
"furnace," the muscles, in which the energy provided by the brain,
adrenals, and liver, plus oxygen, is fabricated into heat and motion.

Benedict, in his monumental work on metabolism, has demonstrated
that in the normal state, at least, variations in the heart-beat
parallel variations in metabolism. He and others have shown also that
all the energy of the body, whether evidenced by heat or by motion,
is produced in the muscles. In the muscles, then, we find the fourth
vital link in the kinetic chain. The muscles move the body,
circulate the blood, effect respiration, and govern the body temperature.
They are the passive servants of the brain-adrenal-liver syndrome.

Neither the brain, the adrenals, the liver, nor the muscles, however,
nor all of these together, have the power to change the rate of
the expenditure of energy; to make possible the increased expenditure
in adolescence, in pregnancy, in courting, and mating, in infections.
No one of these organs, nor all of them together, can act as a
pace-maker or sensitizer. The brain acts immediately in response
to the stimuli of the moment; the adrenals respond instantly
to the fickle brain and the effects of their actions are fleeting;
the liver contains fuel only and cannot activate, and the muscles
in turn act as the great furnace in which the final transformation
into available energy is made. The Thyroid

Another organ--the thyroid--has the special power of governing
the RATE OF DISCHARGE of energy; in other words, the thyroid is the
pace-maker. Unfortunately, the thyroid cannot be studied to advantage
either functionally or histologically, for there is as yet no available
test for thyroid secretion in the blood as there is for adrenalin,
and thyroid activity is not attended by striking histologic changes.
Therefore the only laboratory studies which have been satisfactory
thus far are those by which the iodin content of the thyroid
has been established. Iodin is stored in the colloid lacunae
of the thyroid and, in combination with certain proteins,
is the active agent of the thyroid.

Beebe has shown that electric stimulation of the nerve supply of
the thyroid diminishes the amount of iodin which it contains, and it
is known that in the hyperactive thyroid in Graves' disease the iodin
content is diminished. The meagerness of laboratory studies, however,
is amply compensated by the observations which the surgeon has been
able to make on a vast scale--observations which are as definite
as are the results of laboratory experiments.

The brain-cells and the adrenals are securely, concealed from
the eye of the clinician, hence the changes produced in them
by different causes escape his notice, but the thyroid has always
been closely scrutinized by him. The clinician knows that every
one of the above-mentioned causes of increased brain-cell, adrenal,
liver and muscle activity may cause an increase in the activity
of both the normal or the enlarged thyroid; and lie knows only too
well that in a given case of exophthalmic goiter the same stimuli
which excite the brain, the adrenals, the liver, and the muscles
to increased activity will also aggravate this disease.

The function of the thyroid in the kinetic chain is best evidenced,
however, by its role in the production of fever. Fever results
from the administration of thyroid extract alone in large doses.
In the hyperactivity of the thyroid in exophthalmic goiter one sees
a marked tendency to fever, in severe cases there is daily fever.
In fact, in Graves' disease we find displayed to an extraordinary
degree an exaggeration of the whole action of the kinetic mechanism.

We have stated that in acute Graves' disease there is a tendency
to the production of spontaneous fever, and that there is a magnified
diurnal variation in temperature which is due to an increased output
of energy in even the normal reaction producing consciousness. In Graves'
disease there is, therefore, a state of intensified consciousness, which is
associated with low brain thresholds to all stimuli--both to stimuli
that cause muscular action and to stimuli that cause fever. The intensity
of the kinetic discharge is seen in the constant fine tremor.
It is evident that the thresholds of the brain have been sensitized.
In this hypersensitization we find the following strong evidence as to
the identity of the various mechanisms for the production of fever.
In the state of superlative sensitization which is seen in Graves'
disease we find that the stimuli that produce muscular movement,
the stimuli that produce emotional phenomena, and the stimuli that
produce fever are as nearly as can be ascertained equally effective.
Clinical evidence regarding this point is abundant, for in
patients with Graves' disease we find that the three types
of conversion of energy resulting from emotional stimulation,
from infection stimulation, and from nociceptor stimulation
(pain), are, as nearly as can be judged, equally exaggerated.
In the acute cases of Graves' disease the explosive conversion
of latent energy into heat and motion is unexcelled by any other
known normal or pathologic phenomenon. Excessive thyroid secretion,
as in thyrotoxicosis from functioning adenomata, and excessive
thyroid feeding, cause all the phenomena of Graves' disease except
the exophthalmos and the emotional facies (Figs. 15 and 23).
The ligation of arteries, the division of its nerve supply,
or the excision of part of the gland, may reverse the foregoing picture
and restore the normal condition. The patient notes the effect
on the second day and often within a week is relatively quiescent.
On the contrary, if there is thyroid deficiency there results
the opposite state, a reptilian sluggishness.

At will, then, through diminished, normal, or excessive administration
of thyroid secretion, we may produce an adynamic, a normal,
or an excessively dynamic state. By the thyroid influence,
the brain thresholds are lowered and life becomes exquisite;
without its influence the brain becomes a globe of relatively
inert substance. Excessive doses of iodin alone cause
most of the symptoms of Graves' disease. As we have stated,
the active constituent of the thyroid is iodin in a special
protein combination which is stored in the colloidal spaces.
Hence one would not expect to find changes in the cells of the thyroid
gland as a result of increased activity unless it be prolonged.

We have thus far considered the normal roles played by the brain,
the adrenals the liver, the muscles, and the thyroid in transforming
latent into kinetic energy in the form of heat and motion as an
adaptive response to environmental stimuli.

The argument may be strengthened, however, by the discussion of
the effect of the impairment of any of these links in the kinetic
chain upon the conversion of latent into kinetic energy.

Effect Upon the Output of Energy of Impaired or Lost Function
of Each of the Several Links in the Kinetic Chain

(1) _The Brain_.--In cerebral softening we may find all the organs
of the body comparatively healthy excepting the brain.
As the brain is physically impaired it cannot normally stimulate
other organs to the conversion of latent energy into heat or
into motion, but, on the contrary, in these cases we find feeble
muscular and intellectual power. I believe also that in patients
with cerebral softening, infections such as pneumonia show a lower
temperature range than in patients whose brains are normal.

(2) _The Adrenals_.--In such destructive lesions of the adrenals
as Addison's disease one of the cardinal symptoms is a subnormal
temperature and impaired muscular power. Animals upon whom double
adrenalectomy has been performed show a striking fall in temperature,
muscular weakness,--after adrenalectomy the animal may not be able
to stand even,--and progressive chromatolysis.

(3) _The Liver_.--When the function of the liver is impaired
by tumors, cirrhosis, or degeneration of the liver itself,
then the entire energy of the body is correspondingly diminished.
This diminution of energy is evidenced by muscular and mental weakness,
by diminished response and by gradual loss of efficiency which finally
reaches the state of asthenia.

(4) _The Muscles_.--It has been observed clinically that if the muscles
are impaired by long disuse, or by a disease such as myasthenia gravis,
then the range of production of both heat and motion is below normal.
This is in agreement with the experimental findings that anesthetics,
curare, or any break in the muscle-brain connection causes diminished
muscular and heat production.

(5) _The Thyroid_.--In myxedema one of the cardinal symptoms
is a persistently subnormal temperature and, though prone
to infection, subjects of myxedema show but feeble febrile response
and readily succumb. This clinical observation is strikingly
confirmed by laboratory observations; normal rabbits subjected
to fear showed a rise in temperature of from one to three degrees,
while two rabbits whose thyroids had been previously removed and who
had then been subjected to fright showed much less febrile response.
Myxedema subjects show a loss of physical and mental energy
which is proportional to the lack of thyroid. Deficiency in any
of the organs of the kinetic chain causes alike loss of heat,
loss of muscular and emotional action, of mental power, and of the power
of combating infections--the negative evidence thus strongly supports
the positive. By accumulating all the evidence we believe we
are justified in associating the brain, the adrenals, the thyroid,
the muscles, and the liver as vital links in the kinetic chain.
Other organs play a role undoubtedly, though a minor one.

Studies in Hydrogen Ion Concentration in Activation of the Kinetic System

Having established the identity of some, at least, of the organs
which constitute the kinetic chain, we endeavored to secure still
further evidence regarding the energy-transforming function of these
organs by making studies of the H-ion concentration of the blood,
as one would expect, _prima facie_, that the normal reaction would
be altered by kinetic activation.[*]

[*] The H-ion observations were made in my laboratory by Dr. M. L. Menten.

H-ion concentration tests were made after the application
of the adequate stimuli by which the function of the kinetic
organs had been determined, and we studied also the effect upon
the acidity of the blood of strychnin convulsions after destruction
of the medulla; of deep narcotization with morphin before anesthesia;
of deep narcotization with morphin after the H-ion concentration
had already been increased by fear, by anger, by exertion,
by injury under anesthesia, or by anesthesia alone.

The complete data of these experiments will be later reported in
a monograph; here it is sufficient to state that anger, fear, injury,
muscular exertion, inhalation anesthesia, strychnin, alcohol, in fact,
all the stimuli which we had already found to produce histologic
changes in the brain, the adrenals, and the liver-excepting
bacterial toxins--caused increased H-ion concentration.
Of striking significance is the fact that morphin alone caused
no change in the H-ion concentration, while if administered before
the application of a stimulus which by itself produced increased
H-ion concentration, the action of that stimulus was neutralized
or postponed. If, however, morphin was administered after increased
acidity had been produced by any stimulus, or by inhalation anesthesia,
then the time required for the restoration of the normal alkalinity
was much prolonged, and in some instances the power of acid
neutralization was permanently lost.

After excision of the liver, the normal H-ion concentration
was maintained for periods varying from one to several hours,
after which the concentration (acidity) began to increase as
the vitality of the animal began to decline, the concentration
(acidity) increasing rapidly until death. After excision of
the adrenals the blood remained normal for from four to six hours,
when the H-ion concentration increased rather suddenly,
the increase being synchronous with the incidence of the phenomena
which immediately preceded death.

In none of these cases was it determined whether the increased
H-ion concentration was due to other causes of death or whether
death was due to the increased acidity.

It is also significant that after the application of each of
the adequate stimuli which increased the H-ion concentration
of the blood in other parts of the body the blood from the adrenal
vein showed a slight diminution in acidity, as, in most instances,
did the blood from the hepatic vein also.

In fact, the H-ion concentration of the blood in the adrenal vein
was less than in the blood of any other part of the circulation.

Kinetic Diseases

If our conclusions are sound, then in the kinetic system we find
an explanation of many diseases, and having found the explanation,
we may find new methods of combating them.

When the kinetic system is driven at an overwhelming rate of speed,--
as by severe physical injury, by intense emotional excitation,
by perforation of the intestines, by the pointing of an abscess
into new territory, by the sudden onset of an infectious disease,
by an overdose of strychnin, by a Marathon race, by a grilling fight,
by foreign proteins, by anaphylaxis,--the result of these acute
overwhelming activations of the kinetic system is clinically
designated shock, and according to the cause is called traumatic shock,
toxic shock, anaphylactic shock, drug shock, etc.

The essential pathology of shock is identical whatever the cause.
If, however, instead of an intense overwhelming activation,
the kinetic system is continuously or intermittently overstimulated
through a considerable period of time, as long as each of the links
in the kinetic chain takes the strain equally the result will be
excessive energy conversion, excessive work done; but usually,
under stress, some one link in the chain is unable to take the strain
and then the evenly balanced work of the several organs of the kinetic
system is disturbed. If the brain cannot endure the strain,
then neurasthenia, nerve exhaustion, or even insanity follows.
If the thyroid cannot endure the strain, it undergoes hyperplasia,
which in turn may result in a colloid goiter or in exophthalmic goiter.
If the adrenals cannot endure the strain, cardiovascular disease
may develop. If the liver cannot take the strain, then death from
acute acidosis may follow, or if the neutralizing effect of the liver
is only partially lost, then the acidity may cause Bright's disease.
Overactivation of the kinetic system may cause glycosuria and diabetes.

Identical physical and functional changes in the organs of
the kinetic system may result from intense continued stimulation
from any of the following causes: Excessive physical labor,
athletic exercise, worry or anxiety, intestinal autointoxication,
chronic infections, such as oral sepsis, tonsillitis, and adenoids;
chronic appendicitis, chronic cholecystitis, colitis, and skin infections;
the excessive intake of protein food (foreign protein reaction);
emotional strain, pregnancy, stress of business or professional life--
all of which are known to be activators of the kinetic system.

From the foregoing statements we are able to understand
the muscular weakness following fever; we can understand why
the senile have neither muscular power nor strong febrile reaction;
why long-continued infections produce pathologic changes in the organs
constituting the kinetic chain; why the same pathologic changes
result from various forms of activation of the kinetic system.
In this hypothesis we find a reason why cardiovascular disease may
be caused by chronic infection, by auto-intoxication, by overwork,
or by emotional excitation. We now see that the reason why we find
so much difficulty in differentiating the numerous acute infections
from each other is because they play upon the same kinetic chain.
Our postulate harmonizes the pathologic democracy of the kinetic organs,
for it explains not only why, in many diseases, the pathologic
changes in these organs are identical, but why the same changes
are seen as the result of emotional strain and overwork.
We can thus understand how either emotional strain or acute or chronic
infection may cause either exophthalmic goiter or cardiovascular disease;
how chronic intestinal stasis with the resultant absorption of
toxins may cause cardiovascular disease, neurasthenia, or goiter.
Here is found an explanation of the phenomena of shock, whether the
shock be the result of toxins, of infection, of foreign proteins,
of anaphylaxis, of psychic stimuli, or of a surgical operation
with its combination of both psychic and traumatic elements.

This conception of the kinetic system has stood a crucial test by making
possible the shockless operation. It has offered a plausible explanation
of the cause and the treatment of Graves' disease. Will the kinetic
theory stand also the clinical test of controlling that protean
disease bred in the midst of the stress of our present-day life?
Present-day life, in which one must ever have one hand on the sword and
the other on the throttle, is a constant stimulus of the kinetic system.
The force of these kinetic stimuli may be lessened at the cerebral
link by intelligent control--a protective control is empirically
attained by many of the most successful men. The force of the kinetic
stimuli may be broken at the thyroid link by dividing the nerve supply,
reducing the blood supply, or by partial excision; or if the adrenals
feel the strain, the stimulating force may be broken by dividing
their nerve supply, reducing the blood supply, or by partial excision.
No theory is worth more than its yield in practice, but already we
have the shockless operation, the surgical treatment of Graves'
disease, and the control of shock and of the acute infections
by overwhelming morphinization (Figs. 62, 72, and 73).


To become adapted to their environment animals are transformers of energy.
This adaptation to environment is made by means of a system of organs
evolved for the purpose of converting potential energy into heat
and motion. The principal organs and tissues of this system are
the brain, the adrenals, the thyroid, the muscles, and the liver.
Each is a vital link, each plays its particular role, and one cannot
compensate for the other. A change in any link of the kinetic
chain modifies proportionately the entire kinetic system which is
no stronger than its weakest link.

In this conception we find a possible explanation of many diseases
one which may point the way to new and more effective therapeutic
measures than those now at our command.


[*] Paper delivered before the Virginia Medical Association,
Washington, D. C., October 29, 1914.

Alkalis and bases compose the greater part of the food of man
and animals, the blood in both man and animals under normal conditions
being slightly alkaline or rather potentially alkaline; that is,
although in circulating blood the concentration of the OH-ions--
upon which the degree of alkalinity depends--is but little more
than in distilled water, yet blood has the power of neutralizing
a considerable amount of acid (Starling, Wells). At the time of death,
whatever its cause, the concentration of H-ions in the blood increases,--
the concentration of H-ions being a measure of acidity,--that is,
the potential or actual alkalinity decreases and the blood becomes
actually neutral or acid.

To determine what conditions tend to diminish the normal alkalinity
of the blood, many observations were made for me in my laboratory
by Dr. M. L. Menten to determine by electric measurements
the H-ion concentration of the blood under certain pathologic
and physiologic conditions.

As a result of these researches we are able to state that the H-ion
concentration of the blood--its acidity--is increased by excessive
muscular activity; excessive emotional excitation; surgical shock;
in the late stages of infection; by asphyxia; by strychnin convulsions;
by inhalation anesthetics; after excision of the pancreas, and in the late
stages of life after excision of the liver and excision of the adrenals.
Morphin and decapitation cause no change in the H-ion concentration.
Ether, nitrous oxid, and alcohol produce an increased acidity
of the blood which is proportional to the depth of anesthesia.

Many of the cases studied were near death, as would be expected,
since it is well known that a certain degree of acidity is
incompatible with life.

Since alkalis and bases preponderate in ingested food;
since alkalinity of the blood is diminished by bodily activity;
and since at the point of death the blood is always acid, we may
infer that some mechanism or mechanisms of the body were evolved
for the purpose of changing bases into acids that thus energy
might be liberated.

These observations lead naturally to the question, May not
acidity of itself be the actual final cause of death?
We believe that it may be so from the facts that--(1)
The intravenous injection of certain acids causes death quickly,
but that convulsions do not occur, since the voluntary muscles
lose their power of contraction; and (2) the intravenous injection
of acids causes extensive histologic changes in the brain,
the adrenals, and the liver which resemble the changes invariably
caused by activation of the kinetic system (Figs. 74 and 75). In view
of these facts may we not find that anesthesia and many instances
of unconsciousness are merely phenomena of acidity?

As has been stated already, we have found that the H-ion concentration
of the blood--its acidity--is increased by alcohol, by ether,
and by nitrous oxid. In addition our tests have shown that under
ether the increase of the H-ion concentration--acidity--is more
gradual than under nitrous oxid, an observation which accords well
with the fact that nitrous oxid more quickly induces anesthesia
than does ether.

Further striking testimony in favor of the hypothesis that
the production of acidity by inhalation anesthetics is the method
by which anesthesia itself is produced is found in the fact
that although lethal doses of acid cause muscular paralysis,
yet this paralysis may be mitigated by adrenalin--which is alkaline.
This observation may explain in part the remarkable success of
the method of resuscitation devised by me, in which animals "killed"
by anesthetics and asphyxia are revived by the use of adrenalin.

In animals under inhalation anesthesia Williams found that no
nerve-current could be detected by the Einthoven string galvanometer,
a fact which might be explained by postulating that nerve-currents
can flow from the brain to the muscles and glands only when there
is a difference of potential. Any variation from the normal
alkalinity of the body must change the difference in potential.
Since the nerve-currents in animals under anesthesia are not demonstrable
by any apparatus at our command, and since anesthesia produces acidity,
then we may infer that acidity reduces the difference in potential.
As long as there is life, a galvanometer of sufficient delicacy
would perforce detect, a nerve-current until the acidity increased
to such a point as to reduce the difference in potential to zero--
the point of death. If at this point a suitable alkali--
adrenalin solution--can be introduced quickly enough, the vital difference
in potential may be restored and the life processes will be renewed.
Bearing especially on this point is the fact that if adrenalin
in sufficient quantities be administered simultaneously with an acid,
it will not only prevent the fall in blood-pressure usually
caused by the acid, but will also prevent the histologic changes
in the brain, adrenals, and liver which are usually caused by
the intravenous injection of acids.

This hypothesis regarding the cause of anesthesia and unconsciousness
explains and harmonizes many facts. It explains how asphyxia,
overwhelming emotion, and excessive muscular exertion, by causing acidity,
may produce unconsciousness. It explains the acidosis which results
from starvation, from uremia, from diabetes, from Bright's disease,
and supplies a reason for the use of intravenous infusions of sodium
bicarbonate to overcome the coma of diabetes and uremia (Fig. 76).
It may explain the quick death from chloroform and nitrous oxid;
and may perhaps show why unconsciousness is so commonly the immediate
precursor of death.

One of the most noticeable immediate effects of the administration
of an inhalation anesthetic is a marked increase in the rapidity
and force of the respiration. The respiratory center has evidently
been evolved to act with an increase of vigor which is proportional--
within certain limits--to the increase in the H-ion concentration,
whereas the centers governing the voluntary muscles are inhibited.
In this antithetic reaction of the higher cortical centers and the lower
centers in the medulla to acidity we find a remarkable adaptation
which prevents the animal from killing itself by the further increase
in acidity which would be produced by muscular activity. That is,
as the acidity produced by muscular action increases and threatens life,
the respiratory action, by which carbon dioxid is eliminated and
oxygen supplied, is increased, while the driving power of the brain,
which produces acidity, is diminished or even inhibited entirely;
that is, the state of unconsciousness or anesthesia is reached.
We conclude first that, without this life-saving regulation,
animals under stress would inevitably commit suicide; and, second,
that it is probable that the remarkable phenomenon of anesthesia--
the coincident existence of unconsciousness and life--is due to this
antithetic action of the cortex and the medulla.

In the human, as in the animal, the degree of acidity parallels
the depth of inhalation anesthesia.

Within a few seconds after beginning nitrous oxid anesthesia the acidity
of the blood is increased. This rapid acidulation is synchronous
with almost instantaneous unconsciousness and increased respiration.
If the oxygen in the inhaled mixture be increased, a decrease in
acidity is again synchronous with lighter anesthesia and a decrease
in the respiratory rate.

If these premises be sound, we are justified in asserting that the state
of anesthesia is due to an induced acidity of the blood. If the acidity
is slight, then the anesthesia is slight and the force of the nerve
impulses is lessened, but the patient is still conscious of them.
As the acidity increases associative memory is lost, and the patient
is said to be unconscious: the centers governing the voluntary muscles
are not inhibited, however, and cutting the skin causes movements.
If the acidity is further increased, there is loss of muscular tone
and even the strong contact ceptor stimuli of a surgical operation
do not cause any muscular response, and, finally, the acidity may be
increased to the point at which the respiratory and circulatory centers
can no longer respond by increased effort, and anesthetic death--
that is, ACID death--follows.

Certain clinical phenomena are clarified by this theory and serve
to substantiate it. For example, it is well known that inhalation
anesthesia precipitates the impending acidosis which results
from starvation, from extreme Graves' disease, from great exhaustion,
from surgical shock, and from hemorrhage, and which is present
when death from any cause is imminent.

We see, therefore, that anesthesia is made possible, first, by the fact
that inhalation anesthetics cause acidity, and, second, by the antithetic
adaptation of the higher centers in the brain and of the centers
governing respiration and circulation.

In deep contrast to the action of inhalation anesthetics is that
of narcotics. Deep narcotization with morphin and scopolamin is
induced slowly; the respiratory and pulse-rate are progressively lessened--
and there is no acidity.

By our researches we have established in what consists the generic
difference between inhalation anesthetics and narcotics.
In our experiments no increase in the H-ion concentration was produced
by morphin or by scopolamin, no matter how deep the narcotization.
In animals already narcotized by morphin the production of acid by any
of the acid-producing stimuli was delayed or prevented. On the other hand,
in animals in which an acidity had already been produced by ether,
by shock, by anger, or by fear, the later administration of morphin
delayed or inhibited entirely the neutralization of the acidity.
In other words, morphin interferes with the normal mechanism by
which acidity is neutralized possibly because its inhibiting action
on the respiratory center is sufficient to overcome the stimulating
action of acidity on that center, for, as we have stated,
the neutralization of acidity is in large measure accomplished
by the increased respiration induced by the acidity itself.


Acidity inhibits the functions of the cerebral cortex,
but stimulates those of the medulla. This antithetic reaction
to the stimulus of increased H-ion concentration is an adaptation
to prevent animals from committing suicide by over-activity,
for the mechanism for the initiation and control of the
transformation of energy is in the higher centers of the brain,
while an essential part of the mechanism for the neutralization
of acidity--the centers governing circulation and respiration--
is in the medulla. This explains many clinical phenomena--
why excessive acidity causes paralysis, why there is great thirst
after inhalation anesthesia, after excessive muscular activity,
excessive emotion--after all those activities which we have found
to be acid-producing, for water, like air, neutralizes acids.
The excessive use of alcohol, anesthetics, excessive work,
intense emotion, all produce lesions of the kidney and of the liver.
The explanation is found in the fact that all these stimuli
increase the acidity of the blood. and that, if long continued,
the neutralizing mechanism must be broken down and so the end-products
of metabolism are insufficiently prepared for elimination.

In view of these considerations we may well conclude that the maintenance
of the normal potential alkalinity of the blood is to be estimated
as the keystone of the foundation of life itself.


ABDOMEN, diseases of, phylogenetic association and, 44 Acidity,
227 Adaptive energy, 176 variation in rate of energy discharge,
177 Adrenalin, Cannon's test for, 134, 196 injection of,
changes in brain-cells from, 186 Adrenals, 196 brain and,
relation of, 1.98 diseases of, effect of, on output of energy,
216 functional study of, 196 histologic study of, 198 Alcohol,
changes in brain-cells from, 116 Alkalescence, 227 Anemia, pain of,
77 Anesthesia, 2, 227 anoci-association and, differentiation, 34 effect
of trauma under, upon brain that remains awake, 3 inhalation,
cause of exhaustion of brain-cells as result of trauma under,
8 theory of, 227 Anger, 63, 70 Anoci-association, 34 anesthesia
and, differentiation, 34 Graves' disease and, 36 prevention
of shock by application of principle of, 36 Aristotle, 127 Asher,
:37 Associational centers, dulled, 47 Austin, 2, 55, 173

BASS, 159 Beebe, 213 Benedict, 212 Biologic consideration of
adaptive variation in amounts of energy stored in various animals,
176 Brain, adrenals and, relation of, 198 diseases of, effect of,
on output of energy, 216 effect of trauma under anesthesia oil,
3 functions, physical state of brain-cells and, relation between,
111 influence of fear on, 64 Brain-cells, cause of exhaustion
of as result of trauma under inhalation anesthesia, 8 changes in,
from alcohol, 116 from drugs, 113 from fatigue, 112 from fear,
112 from hemorrhage, 113 from injection of adrenalin, 186 from iodoform,
116 from strychnin, 113 in Graves' disease, 116 in infections,
116 in insanity, 120 in insomnia, 119 histologic changes in,
in relation to maintenance of consciousness and to production
of emotions, muscular activity, and fever, 182 physical state,
brain functions and, relation between, 111

CANNON, 57, 64, 68, 73, 133, 138, 196, 202 Cannon's test
for adrenalin, 134, 196 Cells, brain-, cause of exhaustion of,
as result of trauma under inhalation anesthesia, 8 changes in,
from alcohol, 116 from drugs, 113 from fatigue, 112 from fear,
112 from hemorrhage, 113 from injection of adrenalin, 186 from iodoform,
116 from strychnin, 113 in Graves' disease, 116 in infections,
116 in insanity, 120 in insomnia, 119 histologic changes in, in relation
to maintenance of consciousness and to production of emotions,
muscular activity, and fever, 182 physical state, brain functions and,
relation between, Ill Chemical noci-association in infections,
48 Cold pain, 83 sweat, 27 Contact pain, special, 78 Crying,
90 in exophthalmic goiter, 106

DARWIN, 12, 26, 30, 91, 127, 153 on phenomena of fear, 26 Disease,
mechanistic theory of, 157 Distance receptors, discharge of energy
through stimulation of, 25 Dog, spinal, 4 Dolley, 2, 10 Drugs,
changes in brain-cells from, 113

ELIOT, 1 Elliott, 202 Energy, adaptive, 176 Energy, discharge, rate of,
adaptive variation in, 177 nervous, cause of discharge of,
12 as result of trauma under inhalation anesthesia, 12 discharge of,
role of summation in, 30 through representation of injury,
25 through stimulation of distance receptors, 25 psychic discharge,
25 output of, effect of diseases of adrenals on, 216 of brain on,
216 of liver on, 216 of muscles on, 216 of thyroid on, 217 rate
of out put, influences that cause variation in, 177 Environment,
128, 130 Evacuation pain, 77 Exophthalmic goiter, 66 crying in,
106 fear and, resemblance between, 68 laughing in, 106

FATIGUE, changes in brain-cells from, 112 Fear, 26, 52, 55 changes
in brain-cells from, 112 Darwin on phenomena of, 26 Graves'
disease and, resemblance between, 68 influence of, on brain,
61 phenomena of, 56 Fly-trap, Venus', 151 Frankel, 68 Frazier,
82 Functional study of adrenals, 196

GOITER, exophthalmic, 66 crying in, 106 Goiter, exophthalmic, fear and,
resemblance between, 68 laughter in, 106 Graves' disease, 66
anoci-association and, 36 changes in brain-cells in, 116 crying in,
106 fear and, resemblance between, 68 laughter in, 106

HARVEY, 1,57 Headache, 80 Heat pain, 77 production in infections,
purpose and mechanism, 180 Hemorrhage, changes in brain-cells from,
113 Hippocrates, 127 Histologic changes in liver, 205 study of adrenals,
198 Hitchings, 173 Hodge, 10 Hornaday, 26 Hydrogen ion concentration
in activation of kinetic system, 217 Hyperthyroidism, 42

INFECTIONS, changes in brain-Cells in, 116 chemical noci-association in,
48 heat production in, purpose and mechanism, 180 pain of,
79 Inhalation anesthesia, cause of exhaustion of brain-cells as result
of trauma under, 8 trauma under, cause of discharge of nervous energy
as result of, 12 Insanity, changes in brain-cells in, 120 Insomnia,
changes in brain-cells in, 119 effect of, 205

Iodoform, changes in brain-cells from, 116

KINETIC diseases, 219 reaction, 93 system, 173

LABOR pains, 79 Laughter, 90 causes of, 91 in exophthalmic goiter,
106 Law, Sherrington's, 24 Light pain, 77 Liver, diseases of, effect of,
on output of energy, 216 histologic changes in, 205 Livingstone,
148 Lower, 42

MALARIA, 159 McKenzie, 162 Mechanistic theory of disease, 157 view
of psychology, 127 Medical problems, phylogenetic association
in relation to, 1 Menten, 2, 55, 173, 218, 227 Muscles, diseases of,
effect of, on output of energy, 216

NAGGING, 46 Nausea pains, 78 Nervous energy, cause of discharge of,
12 as result of trauma under inhalation anesthesia, 12 discharge of,
role of summation in, 30 through representation of injury,
25 through stimulation of distance receptors, 25 psychic discharge,
25 Neurasthenia, sexual, 43 Neuroses, postoperative, 46 traumatic,
46 Noci-association, chemical, in infections, 48 Nociceptors,
14 diseases and injuries of regions not endowed with, 47

PAIN, 77, 107, 144, 158 cold, 83 contact, special, 78 evacuation,
77 heat, 77 labor, 78 light, 77 nausea, 78 of anemia, 77 of infection,
79 pleasure, 78 post-operative, 89 site of, 83 traumatic, 89 Personality,
47 Phylogenetic association, diseases of abdomen and, 44 in relation
to certain medical problems, 1 to emotions, 55 Pleasure pains,
78 Postoperative neuroses, 46 pain, 89 Propagation of species,
152 Psychic discharge of energy, 25 Psychology, mechanistic view, 127

REACTION, kinetic, 93 Receptors, distance, discharge of energy
through stimulation of, 25 sexual, 53 ticklish, 19

SELF-PRESERVATION, 152 Sexual neurasthenia, 43 Sexual receptors,
53 Sherrington, 12, 13, 14, 24, 25, 48, 52, 132, 136, 158 Sherrington's
law, 24 Shock, prevention of, by application of principle of
anoci-association, 36 Sloan, 2, 14, .55, 173 Spinal dog, 4 Starling,
195, 227 Strychnin, changes in brain-cells from, 113 Summation,
role of, in discharge of nervous energy, 30 Sweat, cold, 27

TEST, Cannon's, for adrenalin, 134, 196 Thyroid gland, 213 diseases of,
effect of, on output of energy, 217 Ticklish receptors,
19 Trauma, cause of exhaustion of brain-cells as result of,
under inhalation anesthesia, 8 effect of, under anesthesia,
upon brain that remains awake, 3 under inhalation anesthesia,
cause of discharge of nervous energy as result of, 12 Traumatic neuroses,
46 pain, 89

VAUGHAN, 180 Venus' fly-trap, 149, 151

WEEPING, 90 Welch, 1 Wells, 227 Williams, 231 Worry, 74

Book of the day:
Facebook Google Reddit Twitter Pinterest