On the Necessity for a Modification of Certain 
Physiological Doctrines regarding the Inter- 
relations of Nerve and Muscle. 
By THOMAS W. POOLE, M. D. Read before the Physiological Section of the Ninth 
International Medical Congress, held in Washington, 
September, 1887. 
ON THE NECESSITY FOE A MODIFICATION OF CERTAIN PHYSIO- 
LOGICAL DOCTRINES REGARDING THE INTER- 
RELATIONS OF NERVE AND MUSCLE. 
THOMAS W. POOLE, M. D. 
For some years past I have endeavored to bring to the notice of the profession a view of the inter-relations of 
nerve and muscle—more especially of the vaso-motor nerves and the arterial muscles—which is entirely at variance 
with what is taught in our physiological text-books. 
I should be unable to find any excuse or apology for attempting so bold a task, were it not that the proofs which 
I have to advance are drawn entirely from the authentic storehouse of physiological research. While the facts to be 
here advanced are the results of observation by the great Masters in this department of science, I hope to be able to 
show, conclusively, that the inferences or interpretations placed upon these facts are in some instances erroneous and 
ought to be modified or reversed. 
In the examples how to be cited of an erroneous interpretation of authentic experiments, the idea evidently 
dominating the physiological mind was that a stimulus from nervous energy is necessary to induce muscular contrac 
tion. As a corrollary to this idea, of course, it followed that when the motor nerve supplying a muscle was cut, or 
paralyzed from any cause, the muscle thus deprived of nerve influence was rendered incapable of displaying its con- 
tractile power. 
That such an idea was apparently justified by the behavior of the voluntary muscles is undoubtedly true; but not 
so in regard to the non-striated or involuntary muscles of organic life, which have been pronounced by physiologists 
to be paralyzed and powerless, at the very moment that the observers saw and recorded the palpable evidences of their 
more or less active contraction. In fact, so far from the current teaching of physiology being true, as regards the re- 
lations of motor nerves to involuntary muscles, the very reverse is true ; the actual fact being that muscles of the m- 
voluntary class, as a rule, contract, not when stimulated by their proper motor nerves, but when these nerves are cut, or are 
paralyzed, or dead. 
THE OESOPHAGEAL AND GASTRIC MUSCLES- 
To come now to the facts. The statement continues to be repeated in each succeeding text book on physiology, 
that section of the pneumogastric nerves (vagi) is followed by paralysis of the oesophagus and stomach. Now, on the 
theory uppermost in the minds of physiologists—referred to above—the oesophagus ought to be paralyzed here, and to 
be reduced to the condition of a mere flaccid tube. But that such is not the case is evident from the fact that after the 
operation, food and drink fed to the animal, “in a few moments are suddenly rejected by a peculiar kind of regurgi- 
tation.” (Dr. Dalton’s Phys., p. 47,3.) It needs no argument to prove that the sudden rejection of ingesta, in the 
manner stated, so far from being an evidence of paralysis, is really a proof of active contraction in the muscle. 
But it is said that sometimes the ingesta are detained in the oesophagus for a time, and, “owing to paralysis of 
this canal,” are not conveyed into the stomach. (Ib.) Dr. W. B. Carpenter, F. R. S., refers to this by stating that 
“ if the pneumogastric be divided in the rabbit, on each side, above the oesophageal plexus but below the pharyngeal 
branches, and the animal be then fed, the food is delayed in the oesophagus which becomes greatly distended.” 
(Hum. Phys., 5th Amer. Ed., p. 404.) Now the pharyngeal branches supply the upper part, and the oesophageal 
plexus, the lower extremity of this muscular tube. IJkfewk - what follows;' on”sec(tibn ‘ of the vagi between these two ! The upper part of the oesophagus, whose nerves are intact, admits the food and drink apparently in a normal manner, 
while the lower part of the tube, which has been deprived of nervous influence, contracts upon itself, and so lessens 
the calibre of the “canal” as to arrest the further passage of the superimposed ingesta, as a consequence of which the 
oesophagus “ becomes greatly distended. ” 
Whether the ingesta are thus forcibly detained or “ forcibly ejected ” would appear to depend on the point at 
Which the vagi are cut. But in either case, the result, so far from being a proof of paralysis, really bears evidence of 
activity of the muscle. And this is confirmed by the observation of Dr. M. Hall, that “ the simple contractility of 
the muscular fibre [of the oesophagus] occasions a distinct peristaltic movement along the tube after its nerves have been 
divided, causing it to discharge its contents when cut across, ” [Italics mine. ] (Dr. Carpenter’s Hum. Phys., 5th 
Amer. Ed., p. 404.) 
Dr. Burdon Sanderson expresses the idea uppermost in the physiological mind, in stating that after section of 
the vagi “the muscular fibres of the oesophagus are paralyzed, so that regurgitation of food from the stomach iB apt to 
take place.” (Hand-book for Phys, Lab., Amer. Ed., p. 318.) 
Dr. W. B. Carpenter seems to pass over this part of the subject lightly, and it is not till treating of the effects of 
section of the vagi on the gastric secretions that he plainly states that, “ the first obvious effects of this operation are 
vomiting, (in animals that are capable of it) and loathing of food.” (P. 423.) He also tells us, in another place, that 
the reopening of the cardiac orifice, on pressure from within, is one of the first of that series of reverse actions which 
constitute voniiting. (P. 404.) It is evident that the “pressure” referred to and the force necessarily required to 
eject the contents of the stomach and oesophagus could not come from “paralyzed” muscles, which the facts show to 
be really undergoing active contraction. 
That nerve force is actually in abeyance in the act of vofniting was fully recognized by Dr. Anstie, who places it 
among the effects of paralysis of the medulla oblongata in narcosis. (Stimulants and Narcotics, p. 168.) While the 
vomiting of migraine, he says, “marks the lowest point of nervous depression.” (Neuralgia, p. 39.) 
Had those eminent physiologists, Drs. Todd and Bowman, doubts of the truth of the physiological theory of the 
day, and a prescience of what the future had in store, when they wrote : “ The office of the gastric branches of the 
vagi nerves appears from Dr. Reid’s experiments to be chiefly to control the movements of the muscular coat of the 
stomach.” [Italics mine.] (Phys. Anat., p. 493.) That is precisely what the scope of this paper is designed to show 
—that in so far as the involuntary muscles* at least, are concerned, the function of nerve force is not to stimulate, 
but to restrain and control muscular activity ; which all physiologists regard as an inherent endowment of muscular 
tissue. 
THE BRONCHIAL MUSCLES. 
Dr. feurdoh Sanderson informs the readers of the “ Hand-Book,” that after section of the vagi “ the muscular 
fibres of the bronchial tubes are in a similar condition ” to those of the oesophagus and stomach. (P. 318.] Then it 
is evident that these muscular bands come under the rule or law laid down above, and contract, like other muscles of 
this class, when deprived of nervous influence. 
THE NASAL MUSCLES- 
It is a curious fact, that “owing to the great size of the velum pendulum palati, the horse is unable to breathe 
through the mouth.” (Strangeway’s Veterinary Anat., p. 209.) As a consequence, respiration is carried on in this 
animal exclusively through his nose ; and when both the facial nerves are cut, or paralyzed, “the nostrils immediately 
collapse, and the animal dies by suffocation.” (Bernard quoted by Dr. Dalton Phys., p. 458.) 
A result very similar, so far as the closure of the nostrils is concerned, has occurred in the human subject, during 
paralysis of the tacial nerve. Thus, Sir Thomas Watson, reporting the case of the girl, Jane Smith, says : “When 
she tried to snuff in air through her nose, not being able to keep the right nostril stiff and open, its sides came togeth- 
er, and no air passed up that side.” (Lectures, Prac. Physic, p. 366. 
A little reflection will show that this is necessarily due to muscular contraction. The effect produced is not to be 
accounted for by any filling up or stuffing of the nasal passage by relaxed or paralyzed muscles, because the muscles 
are on the exterior of the cartilages, and muciis membrane or fibrous t'ssue does not contract or respond to nerve 
action. The obstruction is caused by the cartilages of the nose coming together, for which the only adequate expla- 
nation is the action of the constricting muscles* which, as in other similar cases, assert their power when nervous re* 
straint is removed. SPASM OF THE GLOTTIS DUE TO NERVE PARALYSIS. 
We now come to a still more striking illustration of the truth of the proposition laid down above. The aperture 
of the glottis is closed by one set of muscles and opened or dilated by another. The constricting muscles are the 
arytenoidei and crico-arytenoidei laterales, while the dilators of the glottis are the crico-arytenoidei postici. 
Dr. Burdon Sanderson states that “the widening of the glottis is a condition of general muscular relaxation.’’ 
He further states that the closing of the glottis is equally due to a general contraction of all the muscles ; so that the 
glottis is closed, “not because the postici crico-arytenoidei muscles and the other dilating muscles* do not act with 
the rest, but because they are overpowered by the constricting muscles. (Hand-book, p. 308.) 
The situation thus depicted becomes quite remarkable and full of interest, when it is remembered that the sole 
motor nervous supply to both these sets of muscles passes through the inferior laryngeal (or recurrent) nerves, a branch 
of the pneumogastric, and that when this nerve is cut or paralyzed, the closure of the glottis takes place, as a result 
of spasm of both of the antagonizing muscles, as just stated. 
On page 318 of the Hand-book the same eminent physiologist, describing the effects of section of the vagi, says : 
“The glottis is partially closed, just as it is in death.” How the glottis is closed in death will appear from the fact, 
vouched for by Dr. Austin Flint, in the 5th edition of his “ Practice of Medicine,” when he says, the operation of 
passing a probang within the larynx, “is extremely difficult, if it be practicable, on the cadaver.” (p. 294.) 
There can be no doubt about the effect of the section referred to being of a paralyzing character, so far as the 
nerve is concerned, seeing that the simple section of the nerve during life, and the extinction of all nerve force in 
death, lead to precisely the same results as regards the closure of the glottal aperture. Dr. Burdon Sanderson adds 
that, “ in animals with divided vagi life may be prolonged by tracheotomy,” showing how complete and fatal is the 
spasm thus produced. Other evidence of similar import is not lacking. Thus, Dr Austin Flint, discussing the 
“ danger of death from suffocation ” in the “ obstructed inspiration ” occurring in nervous aphonia, says : “ The con- 
dition is analagous to that after the physiological experiment of dividing both recurrent laryngeal nerves.” (Prac. of 
Med., 5th Ed., p. 309:) The same author has “ reported a case in which the left recurrent nerve being situated be- 
tween a calcareous deposit and an aneurismal tumor, spasm of the glottis occurred so frequently and to such an extent 
as to prove fatal.” (Ib., p. 371.) 
Now since the recurrent nerve is the only motor nerve supplying these muscles, and since section or pressure on 
a nerve trunk cannot increase nerve activity—the nerve trunks being mere carriers and not producers of nerve force— 
it is evident that no other conclusion is possible than that the spasm here referred to is due to the absence of nerve 
force, and not to a stimulus from excited nerve action. And since nerve paralysis is thus shown to be directly the 
cause of spasm of the glottis, is it not necessary to infer that whatever is done by reflex action to cause spasm of the 
glottis must be of a paralyzing character to the nerve also ? Thus, what is vaguely called “ irritation,” by which is 
usually meant an excitation or exaltation of nerve power, and which consists really in a perturbation of nerve force, 
must necessarily be an influence of a paralyzing character to the nerves it traverses. Such reflex “irritations” are 
usually attributed to brain lesions, to indigestible food, and other causes of a more or less debilitating character which 
may well arrest, rather than develop, the flow of nervous activity. 
If it be true, that pain is “an expression of impeded and imperfect nerve energy, not of heightened nerve func- 
tion,” for which there is high authority (Anstie, “ Neuralgia,” pp. 12 and 163,) how much more is the perturbation 
of the nerve molecules, which constitutes “irritation,” a disturbance of normal activities which is equivalent to 
paralysis. 
RELATION OF VASO-MOTOR NERVES TO THE ARTERIAL MUSCLES. 
I propose to show here, on the very best physiological authority, that what is known as “ paralytic hypenemia ” 
is—contrary to the accepted opinion—venous and not arterial. 
1 need not delay to offer proof that the middle muscular coat of the arteries is under the control of the vasomotor 
nerves of the sympathetic, which regulate the calibre of these tubes ; or that the chief vasomotor centre is in the 
medulla oblongata, with probably lesser centres in the spinal cord. These are among the well-authenticated facts of 
recent physiology. It is in determining the action or play of this mechanism, that I have the temerity to claim that 
our physiologists have made an “ unscientific use of the imagination.” 
The theory of the text-books is that when the influence of the vasomotor centre is cut off from the arterial muscle 
in any way, hypersemia of the arteries results. Thus in destruction of the nervous centres by the operation of 
* There are no “other dilating muscles” than the crico-arytenoidei postici. 4 
“pithing ”—as a result of section of the spinal cord just below the medulla, and on section of the chief vasomotor 
nerve trunks, in the body or viscera, it is claimed that the corresponding arteries are more or less dilated. Dr. Bur- 
don Sanderson contents himself with stating that under these circumstances, “the arteries are relaxed,” and again, 
that they “ become permanently larger.” (Hand-book, pp. 245-256.) Other physiological teachers, such as Prof. 
Kuss, say that here the arteries are “ dilated,” while Dr. Sidney Ringer, in his excellent “ Therapeutics,” has it that 
“ the arteries remain widely dilated.” (5th Amer. Ed., p. 312.) We shall presently see how far these statements are 
justified by the facts. ' ■ 
SECTION OF THE CERVICAL SYMPATHETIC-’ 
To M. Claude Bernard and Dr. Brown-Sequard we are largely indebted for what is known on this subject, as >b- 
served by them in the famous experiment on the cervical sympathetic. Dr. Brown-Sequard enters into the details at 
great length in his “Physiology and Pathology of the Central Nervous System.” Yet nowhere in this work, in re- 
gard to this or any other section of cord or nerve, does he once assert that the arteries are dilated. In the pages 
devoted to it he refers to the contemporary experiments on this subject by Waller, Donders and his pupils, by Kuss- 
maul and Tenner, Moritz and Schiff, yet he makes no mention of an allusion to dilated arteries by any of these 
eminent observers. This is surely significant. With him it was always “ the blood-vessels ” which are “ paralyzed ” 
and “the blood-vessels” which are “dilated.” He says that “the hanging down of an animal, by holding it up by 
its hind legs, in producing a congestion of the brain, produces very nearly all the effects of this section.” (P. 143.) 
From these considerations it will be evident, first, that it was by no means apparent—was indeed a matter of 
great difficulty to determine accurately what particular “ vessels ” were enlarged, hidden as they mostly were beneath 
the skin and its subjacent tissues. Nay, it is not too much to say, that the statement that it is the arteries that are 
enlarged is purely hypothetical, and not based upon an actual demonstration of the facts. Secondly, it will be also 
evident from the statement just quoted from Dr. Brown-Sequard, that venous hypersemia, the result of the b’ood 
being forced out of the arteries by their partial contraction, “ very nearly accounts for all the effects of this section.” 
The truth of this will not only appear from what is to follow now, but from the effect of other sections to be noted. 
Notwithstanding an increased afflux of blood, and consequently a relative elevation of temperature, with heigh- 
tened sensibility, “ the intimate acts of nutrition appear to be modified in nothing. * * * Nor does it 
appear that this hypersemia, however intense or prolonged it may be, has ever the effect, save under exceptional cir- 
cumstances, of determining by itself the development of inflammatory action.” (M. Charcot, Lect. Nerv. Sys.,pp. 
90-91.) This could hardly be the case if the hypersemia were arterial. 
Among the effects of this section on muscles, as recorded by Dr. Brown Sequard, are contraction of the pupil, 
retraction of the eye-ball, partial closing of the eye-lids, contraction of “almost all the muscles of the eye,” and also 
of the muscles of the angle of the mouth and nose ; contraction of the erectile muscles of the ear, and others. Now, 
seeing that it is contraction, and not relaxation of all these muscles, which follows section of this nerve, the law of 
analogy would require that the muscles of the arteries supplied by this nerve be contracted also ; otherwise the anom- 
aly would exist of the same nerve producing contraction in a large number of muscles and relaxation in a single in- 
stance. Why should the arterial muscle be regarded as an exception among so many others, especially when all the 
facts of the case are compatible with arterial contraction and venous fullness ? 
As for the second part of the experiment, in which the hypersemia is dissipated by faradization of the distal end 
of the cut nerve, that is easily accounted for. The terminal branches of the cut sympathetic evidently influence the 
muscles of the head and face over a wide area. As is well known, the effect of faradization is to set up a succession 
of rapid contractions and relaxations in muscular tissue. The pressure thus brought to bear on the swollen veins 
would amply suffice to force their contents onwards, and thus to dissipate the venous congestion. Examples of this 
very result are not lacking. Thus when Kolliker applied one pole to the umbilical artery and vein of a fresh human 
placenta, there followed contractions by which the veins forced out their contents and changed into bloodless strings.” 
(Meyer’s Elec. Hammond, p. 88 ) 
The following quotations from Rosenthal’s “Diseases of the Nervous System,” Yol. II., Wood’s Library, have a 
peculiar fitness here : “ Kussmaul and Tenner have shown in a series of experiments, by placing a watch-glass in the 
opening of a trephined skull, without allowing the air to enter (Donder’s plan,) that compression of the carotids causes 
capillary anaemia and venous hypersemia of the brain and meninges.” (P. 64.) 
“ In Verneuill's patient, upon whom ligature of the carotid was performed for a tumor of the parotid gland, per- 
sistent contraction of the pupil developed shortly afterwards, with rise of temperature and vascular dilatation upon the temple and gums, and abundant perspiration upon the side of the face, corresponding to the operation. All these 
symptoms can be produced experimentally upon animals by dividing the cervical sympathetic.” (P. 26.) 
Here is a remarkable proof that the section referred to causes arterial contraction (and not dilatation,) seeing that 
the other effects of the section are equivalent to those produced by ligature of the carotid. 
SECTION OF THE SPLANCHNICS. 
In a “ demonstration of the vasomotor functions of the splanchnics nerves,” the chief editor of the “ Hand-book 
for the Physiological Laboratory” (Amer. Ed., p 258), informs his readers that these nerves contain vasomotor fibres 
which “ are distributed to the arteries of the abdominal viscera.” 
We approach this “demonstration” expecting to find that when these nerves are cut the predicted results will 
follow in the arteries they supply being more or less “ relaxed ” or “ dilated.” What is our disappointment to find 
in all that follows in this chapter of the “ Hand-book,” the arteries are never once alluded to ! Thus the very pith 
and point of the so-called “demonstration” is entirely ignored ! What occurs is thus stated by Dr. Burdon Sanderson: 
“After section of both nerves the vessels of all the abdominal viscera are seen to be 
dilated” What “vessels” are these? Not the arteries, because Dr. B. S. continues: “The 
portal system is filled with blood; the small vessels of the mesentery and those which ramify on the surface of 
the intestine are beautifully injected ; the vessels of the kidney are dilated, and the parenchyma is hypermmic ; all of 
which facts indicate, not merely that by the relaxation of the abdominal blood-vessels, a large proportion of the resist- 
ance to the heart is annulled, but that a quuntity of blood is, so to speak, transferred into the portal system, and thereby 
as completely discharged from the systemic circulation as if a great internal hemorrhage had taken place. ” (P. 260.) 
[Italics mine.] 
It needs no italics to give point and force to this remarkable admission. It is merely stating, with a little circum- 
locution, that the arteries are empty and the veins are f.ull ! The “beautiful injected vessels,” which the learned 
editor so much admired, are not arteries but veins, the blood in which has become “ bright red, like arterial blood,” 
as Prof. Kuss explains of venous blood in the mesentery, “because oxygenation has been effected simply by exposure 
to the air.” (Lee. Phys., p. 326.) 
The contraction and emptiness of the arteries, after section of their vasomotor nerves, is thus proved on the very 
highest authority. Where now is the justification of the assertion that after a section of this kind the arteries are 
dilated and hypersemic ? 
Whatever obscurity there might be as to the actual results of section of the cervical sympathetic, for obvious 
reasons, there can be no mistake as the results here. 
Now the law of uniformity of cause and effect, demands that what is true of the relative state of the arteries and 
veins after section of the splanchnics, must be true also after section of the cervical sympathetic;—and since the arter- 
ies are thus shown to be empty and the veins full in the former case, the same condition must be held to prevail also 
in the latter. 
It is worthy of note, in this connection, that both after section of the spinal cord, and after section of the splanch- 
nics, blood pressure falls, and in both cases may be restored by faradization of the divided cord or nerve. It is evi- 
dent from this, that the fall of blood pressure (as shown by the kymograph in the carotid) on section of the cord, is 
not to be regarded as an indication of arterial relaxation, as appears to have been done ; because blood pressure fell 
also after section of the splanchnics, where we know positively that arterial dilatation could not have taken place. 
It may be asked, how could faradization of the spinal cord or of the nerve, restores the pressure or tension in the 
arteries, if the heart and arterial system were already empty ? Dr. Burdou Sanderson supplies the answer, indirectly, 
in stating : “It is seen that after section of the cord the heart is flaccid and empty, and that its cavities fill and its 
action becomes vigorous, when the vascular contraction caused by excitation of the peripheral end [of the cut cord] 
forces the blood forward so as to fill the right auricle.” (P. 251.) Now the only blood which could be “ forced for- 
ward so as to fill the right auricle,” is venous blood from the distended portal system. Thus it will be seen that all 
the facts fit, and as it were, dovetail into each other, in establishing that nervous paralysis and contraction of the 
arterial muscle go together the result being hypersemia, not of the arteries but of the veins. 
The explanation just quoted from the Hand-book, as to the forcing forward of the venous blood, as an effect of 
the faradic current, confirms the explanation made above, as to the dissipation of the venous hypersemia by the same 
current after section of the cervical sympathetic. STATE OF THE ARTERIES IN DEATH. 
Not only are the arteries invariably as empty as their physical structure will permit them to be, when their nerves 
are cut or paralyzed in the living body, but such is also their condition in death of the body, when nerve force is ex- 
tinct. This is a fact too well known to need any special proof. It is a fact, however, which ought to be explained by 
those who hold that in a condition of nerve paralysis the arteries are “dilated” and hypereemic. 
THE OPERATION OF PITHING- 
What has just been said of the contracted and empty state of the arteries is true also after the operation of 
“ pithing ” (in which the medulla and spinal cord are destroyed); as any one can easily satisfy himself, as 1 have done, 
by actual experiment. This is inadvertently proved to be the case by Dr. Burdon Sanderson in his account of an ex- 
periment designed to prove the contrary. Two frogs are taken. One is “ pithed,” in the other the nervous centres 
are uninjured. In both the heart is carefully exposed and the single ventricle slit open, so as to show the state of the 
great vessels. The experiment is intended to prove that in the pithed frog the arteries are “relaxed” and full of 
blood. On Dr. Burdon Sanderson’s showing, the results are these : In the pithed frog, “although the heart is beating 
with perfect regularity and unaltered frequency, it is empty, and in consequence, instead of projecting from the open- 
ing in the anterior wall of the chest, it is withdrawn upwards and backwards towards the oesophagus.” The heart and 
its appendages “are alike deprived of blood ; ” but on opening “ the rest of the visceral cavity,” “ the intestinal veins 
are distended.” In these, “ the whole mass of blood has come to rest, out of reach of the influence of the heart.” (P. 
246.) How significant is this ! If the arteries were dilated, and consequently full of blood, this blood could not be 
said to be “out of reach of the influence of the heart.” But this is not all. The Hand-book continues : “In the 
frog deprived of its central nervous system only a few drops of blood escape—the quantity, that is to say, previously 
contained in the heart and in the beginning of the arterial system. In the other, bleeding is not only more abundant 
but continues for several minutes after the section.” (Pp. 246-296.) [Italics mine.] 
Is it not evident that in the case of the pithed frog, the arterial system promptly emptied itself into the now 
“ distended veins,” and had “ only a few drops of blood ” left to drain away through the open ventricle (the frogs 
being both suspended); wrhile in the case of the other frog, whose nervous system was intact, this arterial contraction 
did not take place, and the arteries continued to bleed for several minutes till drained of blood. 
The “ Hand-book for the Physiological Laboratory, ” from which I have quoted so often, occupies to-day a lead- 
ing place as an exponent of physiological science. The reader who studies the details of the experiment just quoted 
will be surprised to find, that here again, in an experiment specially designed to prove that “ all the arteries are re- 
laxed,” the condition of the arteries is completely ignored, and never once alluded to ! The arteries ought to be 
“ relaxed,” “dilated,” and even “widely dilated ” here, on the theory of the text-books, but they are empty and con- 
tracted, their final act being, as in death from other causes, “ to drive their contents into the veins.” (Kuss. Phys., 
p. 181.) 
AN EXPERIMENT OF DR BROWN-SEQUARD. 
In this connection I must notice in the briefest manner, an experiment of Dr. Brown-Sequard in which the 
doctrine here supported is confirmed in a remarkable manner. 
In a dog, a section was made of a lateral half of the spinal cord just below the medulla. The result was, extreme 
hypcrsemiaof the “ blood-vessels,” to use Brown-Sequard’s term, of one posterior limb, while the “blood-vessels ” of 
the other posterior limb displayed a state of spasm and ischaemia quite as extreme. “Very often the spasm persists 
for days,” wrote the observer, “ and it may be so great that the circulation is almost entirely suspended,” so that 
“ the cutting of the skin hardly gives a drop of blood.” 
The question at once arose, was the paucity of blood in one limb due to the excess of blood circulating in the 
other, or vice versa '? Was the spasm on one side, or the dilatation on the other, the primary or direct effect, through 
the spinal vasomotor nerves of the half section of the cord ? 
In order to solve this question, Dr. Brown-Sequard made “direct experiments.” Among others he ligatured the 
iliac artery feeding the dilated blood-vessels of the hypersemic limb, thus directing “almost the whole of the blood 
coming from the aorta ” into the iliac artery of the limb in which the circulation was so much diminished Notwith- 
standing this, the spasm was but partially overcome : “ the temperature rose but little ; ” and “ it was quite evident 
the small arteries near the toes did not allow the blood to pass freely.” 
Here was complete evidence, not only that there was spasm, but also that this spasm was arterial. Although the 
vasomotor mechanism of the spinal cord is as yet only very imperfectly understood, there seems no reason to doubt 7 
that this active contraction of the arterial muscle was here, as elsewhere, due to nervous paralysis, the result of the 
half section of the spinal cord. 
MORE ABOUT THE ARTERIAL MUSCLES. 
It will be obvious that the relative state of the arteries and veins in the foregoing experiments is incompatible 
with what M. Charcot calls “ the paralytic dilatation ” of the arteries, as a result of vasomotor nerve section, and 
could not occur, if after this section the arteries remained, “widely dilated,” and “permanently larger,” as asserted by 
other authorities already quoted. If this were the condition of the arteries, it is evident that they would be wholly 
incapable of contracting upon their contained blood, so as to force it forwards through the capillaries and into the 
veins ; an act depending entirely upon arterial contraction, because the force ot the heart has already expended itself, 
and the capillaries have no muscular walls ; while, that the veins are merely passive, is shown by the fact they have 
no vasomotor nerves, and their calibre is not, as in the case of the arteries, regulated by nerve influence. (Dr. M. 
Foster’s Phys., pp. 265-263.) Thus all the facts show that the arteries, so far from being “dilated” and “paralyzed” 
are undergoing active contraction. 
Some recent authorities appear to suggest the modified idea that the dilation of the arteries, instead of being 
“ permanent,” as alleged by some authorities, is a temporary effect—“ an opening of the flood gates,” so to speak, in 
order to facilitate the transmission of blood to the veins. Thus Dr. M. Foster writes : “The section of the splanch- 
nic nerves causes the mesenteric and other abdominal arteries to dilate, and these being very numerous, a large 
amount of the peripheral resistance is taken away and the blood pressure falls accordingly ; a large increase of flow 
into the portal veins takes place and the supply of blood to the face, arms and legs is proportionately diminished.” 
(Phys., 3rd Amer. Ed., pp. 240 and 220.) 
It would appear that here, as elsewhere, “ the fall of blood pressure ” is regarded as evidence of “ lessened peri- 
pheral resistance,” and a proof that the arteries are “ dilated,” the fallacy of which will presently appear. 
We read again : “When the nervous system is destroyed, dilation of the splanchnic vascular area causes all the 
blood to remain stagnant in the portal vessels ; and probably these as well as other veins are rendered unusually lax, 
so that the blood is largely retained in the venous system, and very little reaches the heart.” (Ib., p. 367.) And 
further : “ When in the frog, the brain and spinal system are destroyed, very little blood comes back to the heart, as 
compared with the normal supply, and the hpart in consequence appears almost bloodless and beats feebly . . . 
the veins become abnormally distended and a large quantity of blood becomes lodged and hidden as it were in them.” 
(Ib., p.263.) 
Here is the secret, both of the emptying of the arteries and of the fall of blood pressure. The blood comes to 
rest in the more capacious venous system, (Ib., p. 154,) “ out of reach of the influence of the heart.” Now seeing 
that the rapidity of the arterial circulation is such that only one-seventh of a second is required for blood to pass from 
the heart to the radial pulse, how long, think you, would be required to empty the arterial system of the pithed frog, 
seeing that at first little blood, and very soon no blood, finds its way back through the heart, into the arterial trunks ? 
Why, the time required would be counted by seconds rather than by minutes. There would be no time and no ne- 
cessity for the terminal arteries to dilate ; the emptying of the arteries and the fall of blood pressure being amply 
accounted for by the fact that hlood is passing out of the arterial system faster than it is being returned to it. 
A precisely similar condition to that just described as resulting from nerve destruction, occurs also in the fatal 
stage of asphyxia. Here, too, the arteries are “contracted” and empty, and the large veins are so distended that “ if 
cut into they spirt like arteries.” (Dr. Burdon Sanderson, Hand-book, etc., p. 332.) And here also, Dr. M. Foster 
tells us there is a fall of blood pressure in the midst of general arterial contraction. He says: “On account 
of the increasing slowness and feebleness of the heart, the blood pressure, in spite of the continued arterial contrac- 
tion, begins to fall ; since less and less blood is pumped into the arterial system.” (Phys., p. 445.) It will be seen 
that the parallel between the two cases is complete, and that the plain facts, as given by the highest authorities, 
do away completely with the assumption that, here, the fall of blood pressure is to be regarded as a proof of arterial 
relaxation. 
Even in the slower forms of death, when the process of emptying the arteries is more gradual, there is still no 
evidence of, and no necessity for, a dilation of the terminal arteries to give exit to the blood ; for, granting that con- 
traction of the terminal arteries would tend to hinder the outflow of blood, this effect would be counteracted by the 
stronger contraction of the larger arterial trunks above, forcing the blood through and out of the numberless terminal 
branches ending in the capillaries. 8 
The facts thus far presented refer only to the great vasomotor areas of the cervical sympathetic and splanchnics. 
It seems unnecessary to attempt to discuss the lesser and local vascular mechanisms, about which little is known, and 
that little comes to us under the segis of an erroneous theory. The greater always includes the less. What hap- 
pens when the life of the chief nervous centres is killed, either by sudden and intended destruction, or in death from 
ordinary causes, happens also in a more limited area when local or subordinate centres are killed or paralyzed. Since 
in the former case the arteries are found contracted and empty, the same rule must be held to hold good in the case of 
the individual nerve and artery. 
THE STIMULATION (?) OF ASPHYXIA. 
Is it not a strange proposition to put forward in the name of medical science, that an animal dying of asphyxia is 
actually undergoing a high degree of nervous excitation. Yet such is actually the teaching of the text-books in phy- 
siology to-day ! Dr. Burdon Sanderson treating of asphyxia says : “ One of the effects of diminishing the proportion 
of oxygen in the blood is to excite the vasomotor centre, and thus to determine general contraction of the small 
arteries. The immediate consequences of this contraction is to fill the venous system.” As the process advances 
“ the heart’s contractions become more and more ineffectual till they finally cease, leaving the arteries empty and the 
veins distended.” (Hand-book, etc., p. 333.) 
There is no mention here of arterial relaxation or dilation, to facilitate the outflow of blood. On the contrary 
“ the immediate consequences ” of “ a general contraction of the small arteries ” is “ to fill the venous sysem,” and in 
a few minutes “ the arteries are empty and the veins dilated,” the animal being dead. This is precisely the condition 
which we have seen in a former page to be the direct result of destruction of the nervous centres. It is a process 
which invariably prevails in the dying and is complete in death. Thus according to Paul Bert, quoted by Prof. Kuss, 
“ death is always owing to asphyxia.” (Phys., p. 330.) 
Why has it been assumed by physiologists that in this rapid sinking into death the nervous centres are under- 
going an unusual excitation ? Because as we have just seen, there is “ a general contraction of the small arteries,” 
and other spasms and contractions of the respiratory muscles fixing the chest and arresting respiration ; and in ac- 
cordance with the theory of the day, these spasms and contractions of the muscles, depend on active discharges of 
nerve force, stimulating the muscles to contract. How is this assumed extraordinary activity of the nerve centres to 
be accounted for in an animal actually dying ? There is a “ physiological law ” which declares that the activity of an 
organ is directly dependent upon its receiving a due supply of arterialized blood (Dr. C. B. Radcliffe); and Dr. W. B. 
Carpenter has said of venous blood, that “ it exerts a depressing influence upon the nervous centres,” from which 
they are at length “ completely paralyzed.” (Hum. Phys., p. 537.) 
One would have imagined that bad blood, deficient in oxygen and loaded with carbonic acid, would have been the 
very last thing which a physiologist would have chosen, as a pabulum from which to generate an excess of nerve force! 
and doubtless the choice was embarrassing enough. But necessity compels. The exigency of the theory is inexor- 
able. Muscular contraction without nervous stimulation is deemed impossible, and there being nothing else to fall 
back upon, it has been assumed that impure, non-arterializea blood plays the part of a stimulant to the nervous 
centres. 
Accordingly we find a recent and popular writer—Dr. J. Milner Fothergill—in his “ Antagonism of Therapeutic 
Agents,” declaring that “ the more venous the blood the greater the activity of the respiratory centre. The effect of 
venous blood is to augment the natural explosive decomposition of the nerve cells. . . . The effect of defective 
arterialization causes more rapid as well as deeper breathing ; more perfect and extensive respiration is set up until 
properly oxygenated blood is procured.” This author would almost lead one to believe that a kindness was done to 
the rabbit in having its vagi cut. He says, “ When the vagi are cut, the respiration is modified ; it becomes deeper 
and more prolonged, fuller and more complete.” (P. 88.) 
But unfortunately this view of an apparently improved respiration is wholly delusive ; for, as Dr. Burdon Sander- 
son tells us, “ notwithstanding the vigor of the respiratory movements, the blood becomes more or less venous,”—the 
itnimal is dying, and does die, “commonly before the end of the first day.” (Hand-book, p. 317.) 
Let it be kept in view that the theory of the day explicitly teaches that “ the muscles receive from the nerv >us 
system a preternatural stimulus to action ” (Dr. Pereira. Yol. 2, p. 541,) and that spasm and convulsion “are de- 
pendent upon excessive activity of the spinal centres :” (Dr. W. B. Carpenter, lb., p. 846.) and we shall see present- 
ly to what apparent absurdity this doctrine has led. In one of Kussmaul and Tenner’s experiments, the carotid 
arteries are ligatured with the effect of inducing “ immediate loss or consciousness and general and violent convul- 
sions,” which are promptly recovered from, and nervous control over the muscles restored, as soon as the ligatures are 9 
untied and blood is admitted to the brain. Dr. M. Foster’s view of this experiment is, that here “the nervous cen- 
tres being no longer furnished with fresh blood, become rapidly asphyxiated through lack of oxygen.” And yet 
strangely enough he holds that in this almost fatal condition of “ rapid asphyxiation ” the nervous centres are under- 
going stimulation ! for he adds : “ similar anaemic ” convulsions are seen after sudden and large loss of blood from the 
body at large ; the medulla being stimulated by the lack of arterial blood.” (Phys., p. 441.) Surely such a view as 
this may be gravely challenged, even when put forward on high physiological authority ! Dr. M. Foster remarks in 
another page, in his chapter on “ Death,” that “ blood is not only useless but injurious unless it be duly oxygenated.” 
(P. 833.) And again he says of venous blood that if it “ continues to be driven through a muscle the irritability of 
the muscle is lost even more rapidly than in the entire absence of blood. It would seem that venous blood is more 
injurious than none at all.” (P. 126.) Why should nerve function be augmented by what is useless and injurious, 
not only to muscle, but to every other tissue in the body ?” 
THE CHEYNE-STOKES RESPIRATION. 
What seems a lower depth of absurdity, if possible, has yet to be reached in the explanations of the Cheyne- 
Stokes respiration. 1 quote here from Dr. L. Sansom’s “ Physical Diagnosis of the Heart,” by whom Traube’s theory 
ou this subject is said to be “ the most plausible.” According to Traube, “the first thing which occurs is the estab- 
lishment of a condition of impaired irritability of the respiratory centre through mal-oxygenation ; the long respira- 
tory arrest gives time for the accumulation of carbonic acid in excess in the blood. Arrived at a certain maximum 
this begins to stimulate, slowly and imperfectly at first and afterwards in increasing degrees, the centre, so that it 
developes the respiratory efforts till they culminate in dyspnoea. Then as the centre ceases to be stimulated or be- 
comes exhausted, dyspnoea again supervenes.” (P. 37.) 
It will be observed that here the deficiency of oxygen and subsequently the presence of carbonic acid are 
made to play opposite and antagonistic parts !• The lack of oxygen (instead of stimulating the medulla, as supposed 
by Dr. M. Foster), first enfeebles the respiratory centre, in the medulla, and then, the same blood, still deficient in 
oxygen, but now loaded with carbonic acid, counteracts the previous depression, and tones up the weak nerve centre, so 
that, ere long, it displays extraordinary activity. But, unfortunately, this exhilarating pabulum—carbonic acid—is 
soon exhausted, and the nerve centre resumes its former feebleness till a new supply can be procured. The physiolo- 
gist is certainly quite impartial, and allows the rivals to have their “ innings” turn about. How such nonsense as this 
“ most plausible theory ” could find a place in physiological literature seems explicable only on the exigency of the 
hypothesis so long in vogue. 
Filehne’s theory in explanation of this state is more complicated, and at least equally absurd. Instead of the re- 
spiratory centre being stimulated (as Traube says), it is the vasomotor centre which is excited by the presence of 
carbonic acid. Arterial contraction follows, till “ a gradually increasing ansemia of the respiratory centre” is brought 
about. This anaemic condition excites the respiratory centre “ and inspiration becomes more and more deep,” till 
oxygen is supplied to the blood ; “the arterial spasm is thus relieved,” owing to the freshly oxygenated blood failing 
to stimulate the vasomotor centre (so as to contract the arteries), as the carbonic acid had previously done. With the 
relief of arterial spasm, and a consequent normal dilation of the arteries, “ the anaemia of the respiratory centre passes 
off, and with it the exaggerated impulse to respiration, and breathing once more becomes superficial.” (P. 137,) In 
other words, the respiratory centre functionates best when it is supplied not only with non-arterialized blood, but 
when it has too little even of that ; as soon as the anaemia passes off, and this nervous centre gets a fair supply of 
blood, it ceases to act—suspends business—till the better times of bad blood and deficient blood come round again,, 
when it is moved to activity once more ! 
There is still another explanatory theory to be noticed, which I find referred to editorially in the Canada Lancet 
for February, 1886: “ Bramwell, who follows the teaching of M Foster and others, supposes that the respiratory 
centre consists of two portions, one accelerating (or motor), and one inhibitory. He further believes that these two 
portions are acted on in opposite directions by the blood, whether arterial or venous. Thus while venous blood stim- 
ulates the discharging cells of the centre and depresses the inhibitory portion, arterial blood acts in exactly the op* 
posite direction.” 
“ At the close of the period of apnoea, the discharging portion of the centre is stimulated by the venous blood,” 
with its excess of carbonic acid, and this same blood, at the same time, is depressing the rival, or inhibitory part of the 
centre. The motor or discharging portion of the centre triumphs ; respiration becomes established and even exagger- 
ated. Unhappily the victor fails to “ hold the fort.” As soon as the blood becomes “ fully oxygenated,” the “ in- hibitory portion becomes stimulated, and gradually overpowers the discharging portion,” so that “the respirations 
grow weaker and weaker until the state of apnoea results.” Then the suspension of breathing restores the venous 
character of the blood and accumulates a store of carbonic acid, the stimulation of which reanimates the centre pre- 
viously depressed by the presence of oxygen in the blood Such appears to be the scope of this theory. 
In this, as in the previous explanations, arterial blood is made to play the part of a depressor and paralyzer of 
the respiratory process, which it is constantly tending to arrest; but while paralyzing one portion of the respiratory 
centre it is stimulating another ; and a similar double character is attributed to the action of venous blood. Thus 
during the brief time from the beginning of apnoea to the culmination ot dyspnoea—a period rarely exceeding one 
minute—the blood passing to the brain is called upon to exert four different and even diverse effects ; first as venous 
blood stimulating one part of the respiratory centre and paralyzing another portion of the same centre : reverse effects 
being produced a few seconds later by the same blood on its becoming oxygenated. 
One is really at a loss to understand how such an explanation could have been admitted to a place in physiologica 
literature. Again it is the exigencies of an erroneous theory which have led to such a complicated and unsatisfactory 
hypothesis. 
If it be asked how the state of apnsea is induced by forced vigorous respirations, if it be not due to an excess of 
oxygen introduced into the blood, and how the opposite condition, or demand for air by breathing, seems to attend 
the absence of oxygen and the presence of venous blood, I can only answer as to the last that if no better explanation 
than that venous blood is a stimulant has yet been found, some better explanation is surely to be looked for. And as 
to the state of apntea referred to, I find Dr. Austin Flint stating that “according to Hoppe-Seyler, apnoea, in the 
limited sense above mentioned, is to be attributed, not to an excess of oxygen in the blood, but to fatigue of the 
respiratory muscles.” (Prac. of Med., 5th Ed., p. 70.) 
A NEW THEORY SUGGESTED- 
Dr. Sansom regards the condition of the respiratory centre in this case as one of paresis and direct exhaustion. 
He shows that during the apnoeal period “ the arteries are strongly contracted.” The proof of this is found in the 
rise of arterial tension ; in the depression of the “great fontanelle ” of the head, and also in the arrest of the process 
by the inhalation of nitrite of amyl, which dilates the arteries. On the theory of these pages, arterial contraction is 
due to vasomotor nerve depression or paralysis ; and accordingly we find here that the vasomotor centre, as well as 
the respiratory centre, is depressed in function. It has been amply shown above, that contraction of the arteries oc- 
curs in the dying and is complete in death. It is also one of the prominent phenomena during the last stages of as- 
phyxia and is invariably attended by venous fullness. The condition present during the stage of apnoea in the Cheyne- 
Stokes respiration, with its contracted arteries and dilated veins, appears to correspond very closely to that present as 
death approaches and in the latter stages of asphyxia. The original paretic and exhausted condition of the respiratory 
and vasomotor centres is aggravated by the further depression caused by mal-oxygenation of the blood ; which, when 
venous and loaded with carbonic acid, is invariably a depressing, and never a stimulating agent to nerve function. 
Vasomotor nerve failure induces contraction of the arterioles, systemic emptiness and venous engorgement, as the 
foregoing examples abundantly prove ; and as a consequence, the great mass of the blood “ becomes lodged and hid- 
den as it were ” in the great venous trunks. At that moment death is very near, but as the heart continues to beat, 
it is fair to assume that a small quantity of blood still finds its way through the lungs, and, from its very scantiness, 
is capable of being aerated by means of the exchanges of gases still going on in the lungs, owing to the presence of 
residual air, during the temporary, partial or complete arrest of respiration. As a consequence, the quantity of blood 
reaching the nerve centres, though small, is at least partially oxygenated, and serves to revive the function of these 
centres “ imperfectly at first,” but with momentary improvement. 
The effect of this revival on the vasomotor centre, is to facilitate the dilatation of the arterioles ; in which the 
pulmonary vessels share, permitting, ere long, the inrush of venous blood from the distended vena cava and portal 
system, and its transmission onwards through the heart and lungs. 
This corresponds to the period of increase in respiratory function, in which the laborious efforts of a feeble 
mechanism have been mistaken for an “exaggerated impulse ’ from excited and overacting or “exploding” nerve 
centres. 
Meanwhile, impure blood from the venous reservoirs (finding an entrance through the now fairly dilated pulmon- 
ary vessels,) begins to fill the lungs in such a quantity (as it is drawn onwards by an inequality of pressure, towards 
10 11 
the as yet unfilled arteries), that the whole mass of blood, failing to be arterialized with sufficient rapidity, again be- 
comes unfit for the maintenance of nerve-function and the perpetuation of processes depending upon it. 
In such a case, a previously weak organ or centre is the first to suffer. The medulla oblongata is such an organ 
in this case, and its contiguous centres for respiration and circulation fail together ; bad blood and deficient blood, 
acting on centres previously paretic, or enfeebled, have done their work, and again the respiration is suspended. 
The vasomotor centre is again so functionally weakened that it loses control of the arterial muscle—the “ inherent 
contractile force,” which all physiologists assign to muscular tissue, thus freed (as in the examples enumerated above), 
induces “ the strong arterial contraction ” referred to by Dr. Sansom, which contraction of the artery is all the 
stronger the nearer nerve force is to cease in the extinction of life. 
This arterial, or systemic contraction, again empties the lungs and refills the venous reservoirs, from which the 
blood is again drawn, at first slowly and then again more rapidly, as the process repeats itself. 
Here, then, is an explanation of the Cheyne-Stokes respiration based upon sound, though as yet unacknowlged, 
physiological principles, according to which paretic and enfeebled nerve centres are helped by their appropriate pabu- 
lum—oxygenated blood—and are overwhelmed and have their function suspended by what is naturally calculated to 
poison and paralyze them, impure, venous blood, deficient in oxygen and loaded with carbonic acid. 
THE INTESTINAL AND UTERINE MUSCLES. 
In sustaining the contention that, as a rule, muscles of the involuntary class contract, not when stimulated by 
their appropriate nerves, but when deprived of nerve energy, I have not yet alluded to the involuntary muscular 
fibres of the intestines and uterus. The antagonism of nerve and muscle is not here so evident as in the cases 
already cited, but here the relations of nerve and muscle have not as yet been completely investigated. (Dr. Jj. 
Brunton.) 
Dr. M. Foster states that section of the vagi “renders difficult the passage of food along the oesoplugus,” and 
causes “ a spasmodic contraction of the cardiac orifice of the stomach ; in other words, the tonic action of the 
sphincter is increased”; (Phys., pp. 346, 347),— facts which sustain what has been already stated above as to the non-par- 
alization of the muscles concerned, after section of their nerves. The peristaltic movements of the intestine, he 
states, may occur “wholly independent of the central nervous system,” and are “at bottom automatic,” (p. 348). We have 
it on the authority of the late Dr. W. B. Carpenter, F.R.S., that “ the intestinal tube from the stomach to the rectum is 
not dependent upon the nervous centres either for its contractility or for its power of exercising it, but is enabled to 
propel its contents by its own inherent powers.” (Hum. Phys., p. 410). So also of the uterus, the contractions of 
which are not due to a reflex activity of the spinal cord, but to its own inherent power of contraction ; parturition 
having taken place after destructive injury and paralysis of the cord, and even after somatic death. (Ib., pp. 979, 
980). In these cases, also, the nerve would seem to be useless as the ally of the muscle, but would play an impor- 
tant part in controlling and regulating, by antagonizing, its contractile energy. 
I must notice, in this connection, an observation of Dr. M. Foster regarding the bladder. He says :—“ The 
escape of the fluid [from the bladder] is, however, prevented by the resistance offered by the elastic fibres of the 
urethra, which keep the urethric channel closed. Some maintain that a tonic contraction of the sphincter vesicse 
aids in. or, indeed, is the chief cause, of this retention. The continuity of the sphincter vesicse with the rest of the 
circular fibres of the bladder suggests that it probably is not a sphincter, but that its use lies in its contracting after 
the rest of the vesical fibres, and thus finishing the evacuation of the bladder. On the other hand, the fact that the 
neck of the bladder can withstand a pressure of twenty inches of water so 1 mg as the bladder is governed by an 
intact spinal cord, but a pressure of six inches only when the lumbar cord is destroyed or the ve ical nerves are 
severed, affords very strong evidence in favor of the view that the obstruction at the neck of the bladder to the exit 
of urine depends upon some tonic contraction maintained by a reflex or automatic action of the lumbar spinal cord.” 
(Phys., p. 448). 
But this experiment admits of a very different inference. We have just seen, on the authority of Dr. M. Fos- 
ter, that section of the chief motor nerves of the stomach “increases the tonic action of the sphincter’ of the 
stomach, as we had before seen it does of the entire contractile tissues of that viscus. We have a right to look for a 
similar increase of tonic contraction in the bladder, when deprived of its nervous connection with the spinal cord, or 
when the latter is paralyzed. Admit that here, as in the examples cited above, the spinal nerves exercise a restraint 
over the contractile fibres of the bladder, tending to prevent its contraction. With this restraint intact, the bladder 12 
is able to bear a pressure of twenty inches of water before the sphincter is overcome ; whereas, with nerve influence 
withdrawn by section or paralysis, and the muscular fibres of the bladder set free to contract, (as in the case of the 
oesophagus and stomach), the resistance at the outlet, though also relatively increased, is overcome by the superior 
expelling force from above, with the aid of only six inches of water pressure. 
The same principle applies to involuntary discharges from the rectum, which Drs. Todd and Bowman say is due 
not to paralysis of the sphincter, against which the fseces are driven, but to the “active pressure of the parts above 
which are not paralyzed.” (Path. Anat., p. 180 ) The “parts above” are the intestinal muscles, which, in the last 
stages of exhausting disease, (when such discharges usually occur), have attained their freedom, just as the arterial1 
muscles do under like circumstances, owing to the general decadence of nervous energy. 
VOMITING OF PREGNANCY. 
With the evidence before us as to the contraction of the gastric muscle on severance of its nerves, vomiting in 
general may surely be regarded as due to nerve depression rather than to nervous excitation. An additional 
observation in proof of the same is to be found in the fact that injury of the vagus may produce constant vomiting, 
(Bryant’s Surgery, Amer. Ed., p. 208) ; and further, that vomiting is mentioned by Dr. C. Bastian among the symp- 
toms of hemiplegia. (Brain Disease, p. 56.) An explanation of the vomiting of pregnancy would be found if we 
might assume that a monopoly of nerve energy was being expended in the uterus, owing to the extraordinary develop- 
ment taking place in that organ, thus starving the gastric nerves, so to speak, which, no longer able to restrain the 
gastric muscle, permit the untimely and abnormal contractions of that viscus. That this occurs chiefly in the early 
months of pregnancy might be accounted for by the unusual demand rather suddenly made upon the nervous 
resources, which tend to equalize their expenditure, as the months go on, and the organism becomes accustomed to its 
new condition. 
HOW ARTERIAL SEDATIVES ACT. 
Ergot of Rye is an agent which produces in a marked degree contractions of involuntary muscular fibre every- 
where, but whose effects are especially seen in the arterioles and uterus. Must not a uniform law or rule govern the 
occurrence of such contractions ? We have seen that they occur best under a deprivation of nerve action, and are 
never so complete as in the general death of the body. How then can Ergot be regarded as a stimulant ? Who 
would ever think of administering it in cases of faintness and exhaustion as a restorative of nerve energy? Must it 
not act, like nerve section and nerve paralysis, in lessening the tone of the vascular and motor nerves, so setting free 
the contractile energy of the arterial and uterine muscles, which contract accordingly ? 
Dr. Sidney Ringer grows enthusiastic over the action of aconite in acute congestion of the tonsils, and that, too, 
in doses too small to reduce the action of the heart. Aconite undoubtedly causes contraction of the arterioles, and 
accordingly on the theory of the day it must be classed as a stimulant, as it actually has been by some authors, Dr. 
Edward Meryon, M.D, F.R.C.P., for instance, who holds that “it stimulates the dormant fibres of Remak and by 
so doing diminishes the calibre of the arterioles.” (Rational Therapeutics, p. 52.) Errors of this kind must be 
charged to the misleading guidance of an erroneous theory. Aconite is a profound paralyzer, and in small doses, by 
lowering the activity of the vaso-motor nerves, it frees the contractile power of the muscular bands of the arterioles, 
which contract accordingly, lessening or curing congestive states. 
Is not this precisely the role of the galvanic current, when brought to play upon the cervical sympathetic, say in 
exophthalmic goitre ? The thyroid gland and its appendages are being overfed by dilated arteries. Bring about 
contraction of these arterial tubes, by lowering the activity of the vaso-motor nerves in the way just indicated, and 
the congestion and hyperplasia are relieved if not cured. 
But the electric current, for therapeutic purposes, has been classed as a stimulant ! So has strychnia ; so ought 
to be prussic acid, for it, too, causes spasms and convulsions of muscle ! So is fatal hemorrhage. All stimulants, 
as well as aconite, on the theory of the day ! 
It would require a volume to elucidate these points, and I must condense what I have to say into a few para- 
•graphs. 
STRYCHNIA A PARALYZING AGENT- 
Dr. Harley has shown that strychnia probably acts by preventing the oxygenation of the blood, which Dr. C. B. 
Radcliffe vory properly holds cannot be the role of a stimulant. Dr. Ringer tells that “ after traumatic and strychnia 
tetanus the functions of the motor nerves and muscles are depressed ; the motor nerves conveying impressions imper- 13 
fectly. ” But may not this motor nerve depression be due to a reaction from previous over excitement ? Dr. Ringer 
says no ! and adds, “Strychnia directly depresses motor nerves, for large doses kill without exciting convulsions, when 
the motor nerves are found to have lost their conductivity.” (Therapeutics, 5th American Ed., p. 499) which in 
physiological language means that the nerves are paralyzed. 
Dr. W. A. Hammond has recounted an experiment performed by himself and Dr. S. Weir Mitchell which, he 
says, “ shows that the action of strychnia is to destroy the nervous excitability from the centre to the periphery.” 
(Dis. Nerv. Syst., p. 539.) 
Dr. Ringer further furnishes strong evidence that paralysis, and not over-action, is the condition of the nerve 
centres in tetanus. He instances “ certain poisons, like gelseminum and buxus sempervirens, which produce at the 
name time both weakness of natural co-ordinated reflex action, cord paralysis and tetanus.” He says “it is impos- 
sible that the tetanus should depend on stimulation of the cord, for we have seen that the tetanus was preceded by 
considerable depression of the cord and continues until the depression ends in extinction of all cord function” ; or, as 
he says again, the tetanus “ occurred in a dying cord.” (London Lancet, Feb. 17, 1887, p. 228; Braith Retros., 
July, 1887, p. 98). 
In strychnia poisoning, death occurs from asphyxia, (Fothergill, Antag. Ther. Agents, p. 55), with its contracted 
and empty arteries and engorged veins the precise condition of the vascular system produced by destruction of the 
spinal cord, as in pithing, as already shown in a previous page. Do not the foregoing facts shew that strychnia does 
not kill as a stimulant, or excitant, of the spinal cord ? Moreover, medical literature clearly shows the value of 
alcoholic stimulants in strychnia poisoning, but I cannot delay to quote it. On the other hand, chloral hydrate, 
which has some reputation in these cases, is “not by any means antagonistic” to the action of strychnia. It acts by 
simply lessening the contractile energy of the muscles, like other amesthetics, by de-oxidizing the blood, and thus 
retarding the chemical processes in the muscle, whereby its contractile force is generated. In this way the convul- 
sions are arrested, and time gained for the elimination of the poison. But dangerously large doses—seven or eight 
grammes—(about two drachms)—are required for this purpose. (Lyman’s Amesthetics, Wood’s Library, pp. 264, 
267, 275.) “ Strychnia affects paralyzed, sooner than unparalyzed muscles,’’ writes Dr. Ringer : but this is not exact. 
Strychnia does not affect the muscles at all, as Dr. R. himself shows ; and the muscles are not paralyzed in the 
cases to which he refers. What he means is that strychnia induces twitches and spasms in muscles whose nerves are 
enfeebled, sooner than in muscles whose nerves are acting normally. Why is this ? If strychnia were a stimulant, 
would it not sooner excite vigorously acting nerves than enfeebled ones? But since its effect is to cause “depres- 
sion of the motor nerves,” nerves already suffering in this way have their vital activity more easily extinguished, and their 
muscles set free, than is the case with healthy nerves. The same thing is equally true of the other paralyzer, electri- 
city. Twitches, tremors, spasms and tetanus are all but varying stages of nerve paralysis and of muscular freedom. 
ELECTRICITY A PARALYZING AGENT. 
Prof. Tyndall tells us that a mere trace of iron in the cfils of a galvanometer, of even such splendid instruments 
as those used by Prof. Du Bois Reymond in his researches on animal electricity, caused a fallacious deflection of the 
needle, to the extent of thirty degrees and more. (Heat as a Mode of Motion, p. 34.) It is therefore not to be 
wondered that erroneous conclusions were sometimes arrived at in experiments so beset with fallacies, even when 
conducted apparently with the greatest care. 
So mysterious a force, which exhibits itself alike in the lightning’s flash, in a tiny spark and in the quiver of the 
eminently sensitive protoplasm of a muscle, might well excite wonder and enthusiasm. As investigation proceeds, 
however, the exaggerated ideas as to the important part played by electrical currents in the phenomena of nerve and 
muscle, and even of life itself, which prevailed some years ago have been rapidly on the decline among students of 
electro-physiology ; but will doubtless linger long in the popular and even in the professional mind. 
But electricity is not nerve force, nor can it cause the generation of nerve force, which is impossible in a mere 
nerve trunk separated from its nervous centre. This must be obvious. If it produce effects equivalent to a loss of 
vital action such as occurs in the death or destruction of portions of the nervous system, it must be classed as a 
sedative and not as a stimulant. In the experiments about to be mentioned the currents employed are those used 
for ordinary physiological and therapeutic purposes. 
The effect of such a current applied to the inferior laryngeal nerves is to induce spasm of the muscles of the 
glottis. “ The rima is completely closed.” (Dr. B. Sanderson, Handbook, p. 308.) That is to say, it does precisely what we have seen above is done by section and paralysis of these nerves. Applied to the lotver ends of the vagi it 
causes contraction of the oesophagus and stomach and “ in most cases vomiting.” (Meyer’s Prac. Elec. Hammond, p. 
87.) Just as we have before seen, results from section of those nerves.- We have had proof that section of the spinal 
cord and of vaso-motor nerve trunks induces contraction of corresponding arterioles. Similar effect is produced by 
electrization of the same parts, the calibre of the arteries being sometimes reduced to one-sixth of their normal size. 
(Weber-Meyers, lb., page 88.) 
Dr. M. Foster tells us that section of the spinal cord at the medulla, or in the dorsal region, arrests the secre- 
tion of urine; and such a section of the cord is of course a paralyzing act. He also tells us that electrization of the 
spinal cord below the medulla also arrests the secretions of urine. Then is not this a paralyzing act also ? It is 
unnecessary to multiply examples. Shall we continue to call an agent a stimulant and refer to it as an excitant of 
nerve activity, the ordinary effects of which on nerves are equivalent to nerve section, nerve paralysis and death ! 
MILD CURRENTS PARALYZE. 
It is sometimes said that powerful currents may paralyze and even kill, but that mild or weak currents merely 
stimulate or excite. Is there any proof of this? Where in the records of electro-physiology do we find a claim for 
opposite effects from weak and strong currents? It is true that we are cautioned against the depressing effects of 
long continued applications of even mild currents. But this is not to t’.e present point. The short seance, with its 
mild currents, may and probably does afford a stimulation of increased vigor, but this is mainly due to the moderate 
exercise which it gives the muscles and their consequently improved nutrition (Drs. Beard and Rockwell); perhaps 
also in some degree to the mental impressions of the patient. The longer seances, with stronger currents, are fatigu- 
ing and exhausting in proportion as they are depressing or paralyzing. 
Is it not true that the weakest current which can affect a muscle at all, causes a momentary contraction of the 
muscle ; and that the strongest current that can be borne during life, or that can be brought to play upon a still irri- 
table nerve and muscle after death, simply produces a more vigorous effect of the same kind ; the contraction becom- 
ing continuous in spasm or tetanus ? It is never contraction on one hand and relaxation on the other, unless, indeed, 
other conditions intervene and muscular contractile energy is at an end. As a matter of fact, weak and strong cur- 
rents act precisely in the same manner, and differ only in the lesser or greater contraction of the muscle which they 
produce. The process is a uniform one, as indeed it must be, since a purely physical force cannot change its charac- 
ter, and play fast and loose in the mode of its operation. 
The treatises on this subject bear ample evidence of the paralyzing effects of electrization when even weak cur- 
rents are used, as could only be the case for therapeutic purposes. Althaus .found that the electric current produced 
an anaesthetic and paralyzing effect on the ulnar and sciatic nerves. Drs. Beard and Rockwell tell us that “in rhin- 
itis, pharyngitis and laryngitis,”—where only very mild currents are admissable,—“ they have for years been accus- 
tomed continually to make use of the benumbing effects of electrization.” (Med. and Surg. Elec., p. 123.) Even 
“ weak electrization of the upper part of the neck may arrest resjiiration,” as well as produce spasm of the glottis 
and of the muscles of inspiration. (Ib., p. 133.) Currents necessarily weak, because applied to the neck of “a 
sensitive young lady,” induced amemia of the brain, with drowsiness and other effects indicative of arterial contrac- 
tion. (lb., p. 134.) Other authors equally allude to the “ paralyzing effects of the constant current,”—(Valentine, 
Matteucci, Eckhard, Meyers.) 
From these considerations I hold that there is no evidence whatever that weak and strong currents produce oppo 
site effects, or that one may paralyze and the other stimulate. 
DIRECT AND INVERSE CURRENTS. 
A great deal has been written about the different effects of direct and inverse currents. Dr. J. Russell Reynolds, 
in reply to the question, “ What current should I use to relieve pain and spasm, the direct or inverse ?” answers 
“ All I have to say is that so far as I have seen it does not make the smallest difference. Theoretically it makes a 
very great difference, but practically it makes none.” (Clinical Uses, etc., p. 18.) Now, I think that the evidence 
showing that both these currents are paralyzing is indisputable. Take the direct current first. A nerve-muscle 
preparation is prepared. To the middle of the nerve trunk a salt solution or the poles of an induction battery are 
applied, and in either case the effect is so regulated as just to fail to cause a contraction of the muscle. If, now, the 
poles of a galvanic battery are applied to the distant end of the nerve-trunk, the P. pole furthest from the muscle, 
so as to produce a direct current, throwing the lower end into catelectrotonus, the muscle will contract at once. 
14 Hence the direct current is said to increase the irritability of the nerve. But electricity is not nerve force, and 
nerve force cannot be generated in a mere nerve trunk. The true change in the nerve is not one of increased 
strength or vigor ; it is simply that the feebly paralyzing action of the salt solution or of the induction battery has 
been supplemented or re-inforced by the additional paralyzing wave of the direct current, and nerve force is for the 
moment annulled. What is just asserted is nothing new. Thus, “ According to Volta, both directions of the cur- 
rent are depressing in their effects.” (M. Meyer, p. 57). Prof. Matteucci found that “ the direct current” not only 
“ diminished the excitability of nerves,” but produced in them “a temporary paralysis.” (Braith. Epit., Vol. II, 
p. G61). Dr. W. B. Carpenter wrote “The direct current weakens and at last destroys the excitability of a nerve.” 
(Hum. Phys., p. 351). So much for the direct current. 
The inverse current produces in the nerve trunk, between the electrodes and the muscle, a condition of analec 
trotonus, which is admittedly one of “ diminished irritability,” which term is in itself an acknowledgement of low- 
ered vital activity, which can only be accounted for as a degree of paralysis, and is induced by weak as well as rela- 
tively strong currents. Dr. C. B. Radcliffe states of M. Eckhard : — “ This very able physiologist has ascertained that 
so long as the inverse galvanic current is closed it is impossible to produce contraction of the muscle by pinching, 
pricking or otherwise acting on this part of the nerve .... which is consequently in a state of suspended 
irritability. (Epilepsy, etc., p. 75). This is a state of paralysis, because “a nerve that is deprived of its irrita- 
bility can neither receive impressions nor transmit them.” (Ib., p. 78). 
Drs. Beard and Rockwell say that “in regard to the differential action of the ascending and descending cur- 
rents there has been an almost infinite amount of shallow observation and impulsive writing.” These writers 
offer ample evidence that the effects in question are due, not to current direction, but to the physical effects of the poles, 
at one of which acids accumulate and alkalies at the other. 
TWO EXPERIMENTS- 
Here are two experiments which show that the combined effects of strychnia and electrization are equivalent to 
the destruction of the spinal cord. In a rabbit undergoing the convulsions of strychnia poisoning the spasms will be 
at once arrested on breaking up the spinal cord by a wire thrust into the spinal canal. If instead of destroying the 
spinal cord in this manner it be subjected to electrization the spasms will be averted, or arrested if already present 
The rabbit dies, but without the characteristic spasms. (Matteucci, Periera, Radcliffe.) Is a powerful electric cur- 
rent needed here ? Not at all. Quite a moderate current will suffice ; because the strychnia poison is causing gen- 
eral contraction of the arterioles (Fothergill), filling the veins and deoxygenizing the blood. Asphyxia is also 
setting in from the same cause, joined with fixation of the chest by spasm of its muscles, whose motor nerves are 
being paralyzed (Ringer.) Electrization produces parallel effects and intensifies the fatal processes already in opera- 
tion. A weak current suffices to complete the arterial emptiness, the venous engorgement and the non-oxydization 
of the blood. The spasms cease probably because such blood as is now present is inimical to the life of the muscle, 
and destroys its contractile energy more rapidly than no blood at all. (Foster, Phys., pp. 126, 833.) 
If the theory of the day were true the rabbit ought not to have died ! With the stimulating and vitalizing action 
of an electric current, added to the previous exhileration of strychnia stimulation the rabbit should have lived and 
flourished, in the interests of the theory, which alas! as usual, is found to be out of harmony with the facts. 
Why does Dr. J Russell Reynolds say that “it would be very unwise to use any form of electricity during the 
period of shock?” (Lect. on Clin. Uses, p. 84.) Why do eminent authorities discourage its employment in cases of 
suspended animat on, as in apparent death from drowning? (Dr. Ringer, Ther., p. 792.) Why does Dr. B. W. 
Richardson, F.R S., of London, write: “ I feel it too unreasonable to recommend galvanic action as a means of 
resuscitation in threatened death from chloroform” .... fearing least under the semblance of restoring lite 
he should clench death ! (Med. Times and Gazette, 1861; Braithwaite, Jan., 1873, p. 256.) These are precisely the 
conditions under which a “stimulant, tonic and vitalizer ” should be eagerly sought for and diligently employed ! It 
is evident that electrization is none of these, and therefore it is forbidden “ in any form.” 
I think I am justified in claiming for the foregoing facts that they prove, as fully as any doctrine in physiology 
can be proved, that electrization as ordinarily employed is a paralyzing process. 
BENEFICIAL EFFECTS OF ELECTRICITY. 
Electricity is no doubt a valuable therapeutic agent, and, like other paralyzing agents, does good in appropriate 
cases. But its beneficial effects may all be accounted for in strict accordance with its role as a paralyzer of nerve 
activity. Thus, it eases pain in a perturbed nerve by temporarily paralyzing it. It lowers the activity of the 
15 vaso-motor nerves, and by thus setting free the contractile energy of the muscle it reduces the calibre of the 
arterioles, lessening or curing congestion, and consequently starving the hypertrophic growths. In other cases, by 
a momentary arrest of nerve action in the motor trunks, it induces prompt spasmodic contractions in the 
thus exercising them, and by attracting blood and pabulum to wasted muscles or tissues in the same way, it improves 
their nutrition. In chronic indurations and hyperplastic growths the purely chemical effects of the opposite poles, 
or electrodes, so modifies the nutritive activities of the tissues as to prove beneficial in restoring a more normal con- 
dition. Thus the curative effects of electrical treatment are all accounted for in strict accordance with its role as a 
paralyzing agent. To proclaim it, therefore, as “ nature’s own tonic,” or to laud it as a “ vitalizer ” or extol it as 
the ally of nerve force, may be pardonable in the instrument makers, but is to be condemned on the part of scien- 
tific medicine. 
HOW THERAPEUTICS HAS SUFFERED. 
It has sometimes been remarked that the department of therapeutics lags behind other branches of the medical 
art. Perhaps it will be pardoned if I venture to suggest that therapeutics has suffered greatly from the adoption of 
the dictum that electricity is a stimulus to nerve function How much of a huge and hypothetical inhibitory system 
has found, perhaps, its chief support in this very error. When electricity stopped the heart, some mechanism had 
to be found for the arrest of its action by a stimulus. On what must the excitation expend itself ? Noton the proper 
motor ganglia of the heart, which a stimulus would drive faster. To meet the exigency of the theory it was neces- 
sary to imagine a purely hypothetical system of inhibitory nerves, the excitation of which, by antagonizing the proper 
motor ganglia of the heart, would bring it to a stand-still. It is worthy of notice that in this experiment “the most 
marked effects are produced when the electrodes are placed on the boundary line between the sinus venosus and the 
auricles ! (Dr. M. Foster, Phys., p. 232). Now, this is the precise location of the chief motor ganglion of the heart 
in the frog,—the animal in which this observation has been made, so that the assumed stimulus has to pass over the 
proper motor ganglion in order to reach the supposed inhibitory ganglia, farther away in the septum dividing the 
auricles! It needs explanation why, under these circumstances, the “stimulus” should ignore the motor ganglion 
jn order to excite its rivals, which are further out of reach of the current. 
The theory of the day, on this subject, or rather the “ temporary hypothesis,” as Dr. M. Foster calls it, neces- 
sitates that the action of drugs be wrought out amid the struggle for supremacy between two rival nerve factions or 
camps, as it were, with results which are far from encouraging. For instance, a recent physiological work on the 
“ Action of Diledicines,” informs us in the opening paragraph regarding belladonna, that “It paralyzes the motor 
nerves in frogs, at the same time that it excites the spinal cord ; after they recover from the motor nerve paralysis 
the tetanic symptoms of spinal stimulation appear !” 
Would it not be well to try how far the results might be simplified on the view that, under the circumstances 
the heart’s action ceased from paralysis of its motor ganglia ;—thus dispensing for a time with this part of an inhibi- 
tory incubus, which threatens to become unmanageable through its very complexity? 
THE VOLUNTARY MUSCLES. 
The foregoing considerations have reference especially to the relations of nerves to involuntary muscles. Why it 
is that muscles of the voluntary or striated class do not also pass promptly into a state of spasm or contraction when 
their motor nerve trunks are cut, or when the body is dead, I am unable to explain; unless it be admitted that here 
the motor nerve trunks are more than mere carriers of nerve force—are in fact, with the nuclei and nerve plates at 
their endings, miniature magazines of nerve energy, which continue for a time to restrain the muscle after section of 
the nerve trunk or after somatic death. 
POST MORTEM MUSCULAR CONTRACTION. 
If such an hypothesis were admitted it would serve to explain certain phenomena for which an explanation is 
necessary, such as the remarkable contractions of muscles which are known to occur in certain cases after death. 
There can be no doubt that the activity of both nerve and muscle survives for a time the death of the organism. The 
life of the nerve which is more intimately dependent upon vital conditions succumbs before that of the less vital and 
more enduring contractile power of the muscle. (Foster, Phys., p. 121). And as one fasciculus or one muscle or 
one group of muscles attains its freedom the contraction which follows gives rise to the movements referred to, 
RIGOR MORTIS. 
Isa muscle contracted or shortened when it passes into rigor mortis ( All observers agree that such is the case, 
and Dr. M. Foster tells us that the shortening and contraction “may be considerable.” (Phys., p. 94). Is this con- traction and shortening the last act of the muscle in dying, or does it occur after the actual death of the muscle—that 
is, in a dead muscle ? Let us consider the latter view first, since it appears to be the one in favor by our physiolog- 
ical teachers at the present time. 
If the muscle be dead, not only is its nerve force extinct, because nerves die first, and consequently there can 
be no stimulus from nerve energy to cause the muscle to contract, and further the chemical changes in the muscle 
which generate its contractile force must also have ceased t" operate, so that its contractile power is at an end. In 
the assumed absence of contractile energy it has become customary to attribute the death stiffening to coagulation of 
the muscle plasma in the muscle This would account for the rigidity of the muscle, but would fail to account for 
the contraction and shortening admittedly present. Muscle plasma, in the living muscle, bears the same relation to 
the myosin of dead muscle that certain albuminous substances in the circulating blood do to fibrin, after blood is 
drawn off in a vessel. According to Dr. Lionel Beale, fibrin is “non-living matter, and is the.product of the death of 
albuminoid bioplasm.” (Disease Germs, pp. 136, 137). If this be true of fibrin, it may fairly be assumed to be true 
also of myosin, which closely resembles the former. Coagulated plasma, or myosin, is dead, and if the muscle also 
be dead, and its inherent contractile power at an end, in what manner does dead myosin acting on a dead muscle pro' 
uuce so perfect a counterfeit of muscular contraction, that one of the keenest observers of the day pronounced it, 
“The most steady and persistent contraction which muscle can possibly exhibit,” (Anstie, Stim. and Narc., p. 70) ; 
so perfect a counterfeit, indeed, that our eminent English physiologist, the late Dr. Carpenter, employed the micro- 
scopical appearances of muscle during rigor mortis as the chief basis for his description of the changes taking place 
in ordinary muscular contraction, as he himself has told us. (Hum. Phys., 5th Amer. Ed., pp. 307, 308). 
Again, the reaction of a living muscle in repose is neutral, or alkaline, but after exercise, or tetanus, the reaction 
becomes acid, an effect in some way depending upon the chemical processes in the muscle associated with its contrac- 
tion. In rigor mortis the reaction becomes “most distinctly acid” also. But if the muscle be already dead and 
these chemical changes at an end, what is the source of the acidity ? To the presence of this acid, the coagulation of 
the myosin and the rigidity of the muscle are of late attributed. But since the acidity is the result, or effect, of 
muscular contraction in the living muscle, how can it be the cause or starting point of the contraction and stiffening 
in the dead muscle ? 
Dr. Lauder Brunton finds that muscle plasma “ coagulates too quickly in the muscles of warm-blooded animals 
to allow of its preparation from them.” Now, rigor mortis does not usually set in f> r several hours after death,—Dr. 
Brown-Sequard found it to be ten hours in four rabbits,—and its onset may even be artificially delayed. The state- 
ment, therefore, is only explicable on the supposition that coagulation of the muscle plasma and rigor mortis do not 
occur together—that is, as cause and effect. It would seem to be implied that the muscle plasma coagulates too early 
to be the cause of rigor mortis. Dr. Brunton further shews that the muscle plasma may coagulate without producing 
rigor mortis. In an experiment, detailed on page 363 of the Hand-book, it is shewn that, if half a fresh muscle be 
immersed for a few minutes in water at a temperature of 104° Fah.. the reaction will be acid, as Dr. Brunton says,— 
“ from development of rigor mortis.” The other half of the muscle is to be placed for a similar time in boiling 
water ; and here the reaction “ will be alkaline.” Dr. B. adds,—“ Before rigor mortis had time to set in the albumen 
of the muscle was coagulated. This coagulation set free a quantity of alkali, hence its reaction.” Dr. Brunton’s 
exposition of this experiment, if correct, would be fatal to the myosin hypothesis, since if the coagulation of the 
muscle plasma be attended by an alkaline reaction while in rigor mortis, the reaction is strongly acid, the former 
could not be the cause of the latter, and they must be regarded as separate and distinct processes. 
The foregoing difficulties certainly seem to create distrust in the myosin hypothesis ; and we now turn from it, 
with its dead muscle and inert myosin, to the other aspect of the case, under which the complete cessation of nerve 
activity and the final contraction of the muscle marks the onset of rigidity. “The rigidity, the loss of suppleness 
and the diminished translucency,” observable in the muscle in this state, are reasonably accounted for by the conden- 
sation of tissue which is here permanent, as the contraction is continuous. That -a certain relaxation subsequently 
occurs, during which meat or game, which is at first tough, becomes more tender and toothy, is attributed by M. 
Rosenthal to the action of the acid referred to, which relaxes the connective tissue which holds the fibres together, 
so that the latter separate more readily. (Muscles, etc., p. 87-8). This is but the beginning of the chemical change 
which ends muscular contractility in the ruin of putrefaction. The following remarkable series of conditions are 
common both to muscular contraction and to rigor mortis. In both the reaction becomes acid. In both carbonic 
acid is set free in the muscle. In both the temperature rises,—often markedly so in rigor mortis). In both the 
muscle is contracted and shortened ; in some cases, as in death from cholera, “rigor mortis may be said to be simply 
17 18 
a continuation of the cramps and contractions occurring during life.” (Wood’s Prac., Vol. I, p. 717). In both, 
glycogen is converted into sugar. Do not all these coincidences in appearances and effects point strongly to a similar- 
ity of processes in muscular contraction and cadaveric rigidity ? Of course the parallel is not complete in every par- 
ticular. It is said that the muscular sound emitted during ordinary muscular contraction is absent. This sound is attri- 
buted to vibration of the muscle substance. Might it not be due in part to the altered circulation in the ordinary 
muscle during contraction, for it is well known that the blood channels, under certain circumstances, give out a musi- 
cal note ? In rigor mortis, of course, the circulation of the blood ceases, as does also the removal of waste products.. 
That the muscle substance continues to vibrate in rigor mortis is evident, because chemical changes are still taking 
place there, as is shewn by what is said above, and especially by “a marked accession of heat” ; (Foster, p. 542) ; 
and “heat is only another form of motion,” (Rosenthal, p. 42). So that, after all, it would seem as if the atoms of 
the muscle continue to vibrate, even though no sound is audible. 
That indefatigable observer, Dr. Brown-Sequard, some time ago, related to the Biological Society of Paris, 
“ some experiments he had made, by a special instrument, to determine the movements of single muscles in the 
body after death. He found that there was a very considerable degree ot contraction and relaxation, as much, for 
example, as two and a half millimetres in a muscle measuring only six millimetres in length. He thought that the 
results of his experiments disproved the theory of coagulation in the muscular tissue as the cause of cadaveric rigid- 
ity. (N Y. Med. Rec., Jan. 9, 1886). 
I am not necessitated to prove that rigor mortis is due to post-mortem contraction of the muscles; but in the 
absence of any other satisfactory explanation of this state, I am entitled to refer to it in support of my thesis ; and 
l would ask those who dissent from this view, and who, in consistence with their theory, must hold that nerve stimu- 
lus is necessary to contraction, to account for the presence of nerve force under the conditions referred to. 
SPASMS IN VOLUNTARY MUSCLES. 
It would, perhaps, be no difficult task to shew that even voluntary or striated muscles pass into a state of partial 
spasm or contraction during life, much oftener than might at first sight appear, under a form of “irritation,” which 
may very properly be regarded as consisting in a lowering of nerve activity. 
“ Irritation” is not increased nerve action. A splinter under the nail is attended by a loss of tactile sensibility. 
A mote in the eye irritates, but it obscures vision. Why should indigestible food oppressing the digestive functions 
of a child be regarded as a source of increased nervous “discharges” ? Such sources of irritation ought to be consid- 
ered as depressing rather than exciting nerve action ; a view of the case for which authorities have been already 
quoted, and others are to follow. 
Dr. Anstie wrote, “ convulsive action of the muscles, as everyone knowrs, are very common complications of 
neuralgia,” and the same acute observer held that “ pain is not a true hypersesthesia ; on the contrary, pain involves 
a lowering of nerve function.” (Neural., p. 12). 
Dr. Hilton, in his work on “Rest and Pain,” points out that the irritation of peritonitis induces contraction of 
the abdominal muscles. In the same way, pleuritis renders the chest walls fixed by spasmodic contraction of its 
muscles; while the muscles of an inflamed joint, he says, “are invariably contracted, and continually tend to 
increased flexion of the limb, not because such a position is easiest for the patient, which is not always the case, but 
owing to a reflex perturbation transferred to the muscles of the adjoining surface.” (P. 96). That peripheral irri- 
tations do produce nerve paralysis must be admitted on the authority of Dr. Brown-Sequard. (Lect. Cent. Nerv. 
Syst., pp 160, 170), and others. 
What is the “ irritation” in these cases but a mild form of nerve paresis, just as “ the irregular muscular action” 
which shows itself in tremor, fibrillary contractions, or in spasm, denotes the failure of the ordinary nervous restraint 
•over the corresponding muscles. 
Why should “ morbid conditions of the medulla oblongata ’ avowedly depending on “defective nutrition” be 
supposed to give rise to “ explosive and atactic manifestations of nerve force,” (Anstie, Neural., p. 156), when they 
are much more naturally explained as depending upon nerve failure ? The weak point in the theory of the text- 
books, is that nerve force is required to be displaying the full activity of robust health, and even more, in exaggerated 
“ discharges ” and “ explosions” at the very time there is the most undoubted evidence of nerve failure and exhaus- 
tion. Why, in cases of “early and late rigidity” of muscles, should a clot in the brain be held to be an exciting 
irritant, seeing that the brain tissue is wholly insensitive, and may be cut, pricked or seared with a red-hot iron with- 19 
out eliciting any signs of pain ? It is difficult to express here the multitude of facts which show the very frequent 
association of paralysis and spasm in disease of the brain and spinal cord. The paralysis is of the nerve and the 
spasm of the muscle —conditions very embarrassing to the theory of the day, but consistent and harmonious states in 
the theory of these pages. Is there not much significance in the statement of Seguin, that “a lesion of the lateral 
columns of the spinal cord produces paralysis with contracture” of muscles. Why ? Because, as Dr. Brown- 
Sequard has shewn, “ the motor fibres run on the exterior of the cord in its antero-lateral columns.” (Erichsen, 
Concus. Spine, pp. 29, 30). Motor nerve disease and destruction induces contraction of the muscle, which later on 
becomes atrophied, partly, no doubt, from inaction. 
It is on record, too, that while injury of the vagus nerve induces contractions of the gastric muscle, injuries of 
the spinal accessary nerve are attended by spasms of the trapezius or sterno-mastoid muscles. (Bryant’s Surgery, p. 
208). Other examples of a similar kind are not lacking. 
One might imagine that Dr. B. W. Richardson, F.R.S., intended to endorse the theory of these pages when he 
wrote as follows regarding the convulsions of the drowning. He says :—“ The convulsive movements that are seen 
are unconscious movements ; they are the same as those which mark the period of stupor, in death by hanging, by 
noxious vapors, by concussion ; and they are simply the results of action of muscles from which the controlling power 
of the nervous centres has been removed.” (Braithwaite, July, 1871, p. 255). [Italics mine]. Dr. Henry M. Lyman, 
A.M., M.D., would appear also to have had a commendable distrust, if not an entire disbelief, in the theory of the 
text-books, when, in referring to “a temporary increase of muscular movement directly caused by the abolition of 
some special source of nervous impulse,” he says Witness the tremendous liberation of muscular movement which 
follows a paralysis of the influence of the brain, by the sudden decapitation of a fowl, for example.” (Anaesthetics, 
Wood’s Lib., p. 26). [Italics mine]. 
One of Dr. Ferrier’s experiments is so much in point here, that, at the risk of being tedious, I cannot forbear 
a brief reference to it. The right brain of a monkey had been exposed and subjected to faradization. Next day 
the animal “ was found perfectly well. ” “Towaidsthe close of the day following, on which there were signs of 
inflammatory irritation and suppuration, it began to suffer from choreic spasms,” which rapidly assumed an epilepti- 
form character. Next day hemiplegia became established with the usual symptoms of “ paralysis of the left arm and 
partial paralysis of the left leg. ” “ On the day following paralysis of motion was complete over the whole of the 
left side, and continued so till death, nine days after.” Dr. Ferrier says, “In this we have a clear case of vital 
irritation producing precisely the same effects as the electric current, and then destruction by inflammatory softening 
resulting in complete paralysis, etc.” (Functions of Brain, pp. 200, 202). 
On Dr. Ferrier’s view, the stage of apparent inflammatory action was accompanied by increased production and 
discharge of nerve energy, as seen in the choreic and epileptiform spasms. But “Recent studies show chat the 
inflammatory process is a destructive and depressive one, so far as the tissues are concerned ; that it does not irritate 
and kindle into increased activity the protoplasm of the cells, but rather the reverse.” (Editorial, N. Y. Medical 
Record, Jany. 30, 1886, p. 128). So that it is now definitely understood that the inflammatory process in brain 
tissue does the reverse of Dr. Ferrier’s view, and paralyzes rather than excites nerve energy. 
Observe here, that the spasms of the muscles, on Dr. F.’s own shewing, began to occur contemporaneously with 
the “ signs of inflammatory irritation and suppuration,” and as this term “irritation,” (on so good an authority as 
the able editor of the N. Y. Medical Record), must now be interpreted to mean depression and lowering of cell 
activity, it follows that the spasms referred to occurred from the absence or failure of nerve energy, and not from its 
undue excitation. Observe, too, that Dr. Ferrier held that this “vital irritation,” as he saw it, but which we now 
know is depression or paralysis, produced “ precisely the same effects as the electric current.” Another evidence of 
the paralyzing character of electricity ! 
THE EPILEPTIC PAROXYSM. 
With the experiments on the cervical sympathetic and splanchnic nerves before us, how can we say that the 
anaemia, or rather ischaemia, of the brain, which ushers in the epileptic seizure, is due to “ excessive action of the 
spinal centres,” compelling the spasm or contraction of the arterial muscles on which this ischaemia depends? 
Have we not had proof that the arterioles contract best when their vaso-motor nerves are cut, or are paralyzed, or 
dead ; and if so, are we not bound to hold that not excess but failure of nerve power is the proximate cause of the 
epileptic paroxysm ? And is not the question of such excess or failure of nerve force a most practical one in deter- 
mining the treatment ? 20 
How far is our comparative failure to cure this terrible disease due to our approaching it under the aegis of an 
erroneous theory—that nerve force here needed to be depressed rather than exalted ? It is well for mankind that in 
this, as in some other instances, our practice has sometimes been directly at variance with the theory of the day. 
Thus we find Dr. Anstie assuring us that “our best anti-spasmodics are stimulants”; and that “alcohol is one of 
the best remedies possible in the convulsions of teething in children.” (Stiin. and Narcot., pp. 123, 129). 
no “morbid" nerve force. 
Spasms and convulsions frequently take place in the very act of dying, and under circumstances in which nerve 
force ought to be regarded as at a low ebb ; as, for example, in uraemic blood poisoning. It is customary in some 
quarters to attribute these or other spasms to “a morbid irritability” or “ a morbid nerve force” ; as if the central 
nervous ganglia were capable of producing two kinds of nerve force, one normal and the other “ morbid,” and the 
spurious variety of attaining extraordinary power just in proportion to the complete failure of nerve force proper. 
A little reflection, I think, will show that this is untenable. Nerve force may be increased or diminished : its con- 
dition may be one of excess or of failure, but that it may present a duplicate of itself, and its alter ego produce 
effects, for which nerve force proper is inadequate, and yet is responsible, is surely yielding too much to the exigency 
of an erroneous theory. 
Medical literature presents numerous examples of this appeal to a “ morbid nerve action,” and it is rather sur- 
prising to find such a writer as the late Dr. Anstie referring to “the explosive disturbances of nerve force which 
give rise to the convulsions of tetanus” as “something quite different in kind” from healthy nerve action. 
(Neural., p. 8). Now, if a nerve centre be thrown into action otherwise than by the exercise of its normal activity, 
then it is no longer the nerve centre which is acting, but a power extraneous to itself ; a modern Archaeus for which 
scientific medicine ought to have no place. And if tetanus be really due to an explosive activity of the nervous 
centres which are discharging nerve force with unwonted activity, surely to administer stimulants in such a case 
ought to be injurious, if not fatal! And yet we find that Dr. W. A. Hammond of New York has produced statistics 
in which “stimulants” stand at the very head of the list of curative agents in tetanus. (Dis. Nerv. Syst., 4th Ed., 
p. 541). Here again the theory of the day is surely out of joint with the clinical facts. 
CHLOROFORM and relaxation of an/esthesia. 
I have been asked how the rigidity, at first, and subsequently the relaxation, of the muscles during anaesthesia 
are to be accounted for on this theory. The answer is easy. The rigidity is due to the partial paralysis of motor 
nerve influence, setting the contractile power of the muscle free to act This occurs at a comparatively early stage of 
the process. The relaxation which attends complete anesthesia is due to the loss of contractile power on the part of 
the muscle, owing to the absence of oxygen in sufficient quantity in the blood ; for chloroform tends to prevent the 
oxygenation of the blood, (Ringer’s Ther., p. 286), and renders it venous in character. In this way the chemical 
processes on which the generation of contractile force in the muscle depends are retarded. (Lyman’s Anaesthetics, p. 
28; Bryant’s Surgery, Amer. Ed., p. 318). Dr. M. Foster states that “blood is not only useless, but injurious, 
unless it be duly oxygenated.” And again, “if venous blood be driven through a muscle the irritability of the 
muscle is lost even more rapidly than in the entire absence of blood.” (Phys., pp. 883, 126). This, I think, will be 
accepted as a satisfactory explanation, in strict accord with physiological facts. The relaxation, however, is not so 
great but that faradization of the muscle will induce a further degree of contraction ; showing that the contractile 
energy of the muscle, though weakened, is not lost. That the contractile power of the muscle is thus lowered offers 
a bar to the prolonged or complete administration of chloroform during parturition, for obvious reasons. 
The mode in which anaesthetics induce arterial contraction, as explained by Dr. Henry M. Lyman, may be 
quoted as follows :—“ Chloroform acting through the blood upon the nervous apparatus in the walls of the vessels, 
tends to paralyze the sensory endings of the nervous fibrils. This means a diminution of the normal impulses, which 
should continually reach the central intraparietal ganglia,” in consequence of which “the motor cells no longer 
experience the inhibitory influence which they should receive from the periphery of their territory, and a liberation 
of a motor impulse excites muscular contraction, and we have vascular spasm,” etc., as the result, (Anaesthesia, etc., 
page 27). This, of course, is purely hypothetical. The motor nerve fibrils in the muscular bands are ignored alto- 
gether, while a purely imaginary “ inhibitory” system is invoked to meet the exigency of the occasion. How much 
better to hold that the motor nerve fibrils also are more or less paralyzed, and the arterial muscle directly set free to 
contract; thus dispensing with the inhibitory apparatus altogether 21 
THE NERVE-MUSCLE PREPARATION. 
It is impossible here to enter on a critical analysis of the experiments on nerve and muscle, which a careful exami- 
nation will show to be wholly consistent with the views here advocated. When in a nerve-muscle preparation, the 
muscle is made to contract by applying to the nerve trunk the shock of electricity, the corrosion of a chemical agent 
as a quick stroke, what is there to show that the effect on the nerve is not to cause a temporary cessation of nerve 
influence, rather than the production of a stimulus ? There is really nothing, and the character of the impulse is 
merely a matter of inference. Even in what is called the rheoscopic frog, where contraction in one muscle imparts 
an influence whereby another muscle is made to contract, the molecular or electrical wave may as well be paralyzing 
as stimulating. 
THIS THEORY NOT NEW. 
In hastening to conclude, let me state that, whether this theory of the antagonism of nerve and muscle be true 
or false, I am not entitled to the praise—or blame—of originating it It was broached so long ago as 1832 by Dr. 
West, an English physician, and is said to have met with some countenance from Sir Charles Bell. Dr. C. B. Rad- 
cliffe, F.R.S., in his work on “Epilepsy, Paralysis and Pain,” has warmly adopted the views of Dr. West, and offers 
some strong evidence in support of the proposition, that “ there is reason to befieve that ordinary muscular contrac- 
tion is associated with a deprivation of nervous influence, and not with a contrary state of things.” (P. 95). 1 have 
here endeavored to support the same thesis, but with evidence drawn from other sources. 
OBJECTIONS TO THI.S THEORY. 
1. It has been objected to this theory that “ a muscle can contract when irritation is directly applied without 
the intervention of nerves.” Now, I am not in the least disposed, or obliged, to dispute this assertion, for reasons 
which will appear later on. My thesis has much to gain, and nothing to lose, by the fullest admission of the inde- 
pendent irritability of muscular tissue. But it is exceedingly difficult, if not at present impossible, to say when a 
still irritable muscle has been deprived of “ the intervention of its nerves.” Certainly such is not the case in the 
experiments edited by Dr. M. Foster, in the Hand-book heretofore referred to, where the experimenter, in order to 
produce the ideo-muscular contraction, is to choose “a muscle which has been much exhausted by treatment or by long 
removal from the body,” and to “ wait till neither muscle nor nerve give any ordinary contraction with an electric 
stimulus.” It cannot be held to be proven that in such a nerve-muscle there is not still remaining a force in the 
weakened nerve sufficient to control the equally weakened muscle. 
CURARE AND THE MOTOR NERVE ENDINGS. 
2. It has also been objected that, while the motor nerve endings are paralyzed by curare, the muscle does not 
contract, as it ought to do if this theory were correct. To this I have to reply, that if the muscles are not found 
contracted it is partly due to the insufficiency of the poisoning of the motor nerves, and partly to the fact that curare 
diminishes the contractile energy of the muscle. (Rosenthal, Muscles, etc., p. 254). Nicotine and conine act pre- 
cisely like curare, (lb., p. 253), and in the final action of these thiee poisons, motor nerve paralysis and spasm, 
or convulsion of the muscles, occupy a prominent place. (Ringer). The special results vary, of course, in different 
animals. Nicotia sometimes acts like an anaesthetic ; (Stille and Maiscfi, p. 372) ; and the same is doubtless true of 
the others. Now, anaesthetics induce muscular relaxation by deoxydizing the blood ; and nicotine is known to disor- 
ganize the red corpuscles which are the oxygen carriers It is doubtless in this way that, under the slow action of 
these poisons, muscular relaxation is brought about. If death be rapidly produced by curare, convulsions occur. 
(Stille and Maisch). Here the motor nerves are paralyzed before time has been afforded for the poison to lower the 
irritability of the muscle, which passes into tonic or clonic spasms according to its freedom, thus behaving as it 
“ ought” to do. Is not this a sufficient answer to the objection ? 
But more remains to be said. The experiments with curare are not so conclusive as to be beyond the reach of 
criticism. They were intended to prove the independent irritability of muscle, which is now generally an accepted 
fact among physiologists. M. Rosenthal asserts that these experiments (and those of Kuhne upon the sartorious 
muscle), do not prove this ; which is equivalent to stating that it is not proved that curare paralyzes the motor nerve 
endings. 
More direct evidence upon this point is that of Dr. Onimus, who, not long ago, “ read a paper before the Acad- 
emy of Medicine, Paris, upon electro-muscular contractility and the action of curare. Contrary to the opinion of 
M. Claude Bernard, Dr. Onimus believed that curare does not act on all parts of the motor nerves, but only on their 
trunks the nerve centres and terminal filaments being unaffected.” (N.Y. Med. Record, 1880, p. 73). In view of these authoritative opinions, (and doubtless of others to which I have not access), it is evident that 
this objection falls to the ground and loses the weight which otherwise might attach to it. 
But suppose it were established beyond doubt that the influence of the nerve were completely eliminated from 
the muscle in any case, and that the contractile protoplasmic masses of the muscle were left wholly to themselves, 
and their life being not yet extinct, that they gave token of that still flickering life when comparatively rudely 
assailed by a shock of electricity or a corrosive or injurious agent,—what then? Such signs of irritability, elicited 
under such circumstances, would not militate against my thesis ; for such would be the behaviour to be expected from 
still living protoplasm, wherever found, and would in no way disprove the contention that in the association of nerve 
and muscle in the organism the role of the nerve is to restrain or control the protoplasmic energy of the muscle so 
long as their mutual relations continue. For, after all, “the contraction ot muscular tissue is, in fact, a limited and 
definite amoeboid movement, in which intensity and rapidity are gained at the expense of variety.” (Dr. M. Foster. 
Phys., p. 63). 
Indeed, I think the rational view of the situation just depicted, turns the argument the other way ; and tends 
to show that in the joint role of nerve and muscle the function of the nerve is not to goad or stimulate the muscle to 
contract. To suppose this is to assign to nerve energy the relative value of the fifth wheel in the coach. Such 
enduring power of contractility as the muscle here exhibits evidently needs no supplementary aid from the nerve. 
What it really does need, however, is restraint, control and co-ordination for the purposes of the organization of 
which it is a part. 
OTHER OBJECTIONS. 
A further objection has been suggested, on the ground that on a nervous impulse reaching a muscle, an electric 
current is generated during the period immediately preceding the contraction of the muscle ; but this is an objection 
which is only of any force on the assumption that electricity is a stimulant. There is nothing in the action taking 
place here to show that the electric current is a stimulant rather than a paralyzer. There is simply a “freeing of 
the forces in the muscle,” just as the spark of electricity frees the forces bound up in gunpowder, and so fires the 
train. (Rosenthal, p. 250). 
As for the additional plea that nerve force and muscle force are too much alike for us to consider one a paralyzing 
and the other a contracting agent : that is merely begging the question Nothing whatever is known regarding the 
nature of these forces ; and the intimate structures of nerve and muscle are so widely different as to justify the 
idea that the product, so to speak, of each, is equally diverse. 
This theory has been objected to as a proposed addition to the inhibitory system of the text-books. This is a 
mistake. If the views here, enunciated were adopted, the huge incubus of the present inhibitory hypothesis could be 
in great part swept away, to the great advantage both of physiology and therapeutics. 
If it be claimed that on the cutting of the spinal cord or of a nerve trunk, the “ irritation” set up at the point 
of cutting, or the generation of electrical currents as the result of chemical change in the transverse section, act as 
a stimulus, and that contraction of the corresponding muscle is thus produced, such a claim must be regarded as 
untenable for the following reason The acts just referred to cannot be stimulating acts, because they are attended 
by precisely similar effects as are produced in the muscle by death from any cause, in which condition, it is needless 
to say, nervous activity is not increased. The proof of this has already been sufficiently vouched for, and need not 
be repeated here. 
Of course, I do not pretend that all difficulties vanish in the light of the theory here advocated. There are very 
serious, if not insurmountable, difficulties in the theory of the text-books ; as the facts of the foregoing pages fully 
shew. What I claim is, that the view here presented rests on a rational basis, and, though presented very inade- 
quately, and under many disadvantages, has the merit of fnrnishing a key to many obscure phenomena in the organ- 
ism, and is entitled to the fair and candid consideration of the members of our profession. 
Lindsay, Ont., Canada, 
August, 1887.