CLINICAL REMARKS 
ON THE PROCLIVITY OF THE ABDUCTOR FIBRES OF THE RECUR- 
RENT LARYNGEAL NERVE TO BECOME AFFECTED SOONER 
THAN THE ADDUCTOR FIBRES, OR EVEN EXCLUSIVELY, IN 
CASES OF UNDOUBTED CENTRAL OR PERIPHERAL INJURY OR 
DISEASE OF THE ROOTS OR TRUNKS OF THE PNEUMOGASTRIC, 
SPINAL ACCESSORY, OR RECURRENT NERVES 
BY 
FELIX SEMON, M. D., M. R. C. P 
LONDON 
[Reprinted from the Archives of Laryngology, Vol. ii, No. 3, July, 1881] 
NEW YORK 
G. P. PUTNAM’S SONS 
27 & 29 WEST 23D STREET 
188 l CLINICAL REMARKS* 
ON THE PROCLIVITY OF THE ABDUCTOR FIBRES OF THE RECUR- 
RENT LARYNGEAL NERVE TO BECOME AFFECTED SOONER 
THAN THE ADDUCTOR FIBRES, OR EVEN EXCLUSIVELY, IN 
CASES OF UNDOUBTED CENTRAL OR PERIPHERAL INJURY OR 
DISEASE OF THE ROOTS OR TRUNKS OF THE PNEUMOGASTRIC, 
SPINAL ACCESSORY, OR RECURRENT NERVES. 
By FELIX SEMON, M. D., M. R. C. P., 
LONDON. 
THE curious and important fact, which forms the sub- 
ject of the present communication, is by no means 
entirely new or unknown. The relatively greater disposi- 
tion to implication of the abductor filaments was illustrated 
by Gerhardt1 as long ago as 1863, and by Morell Mac- 
kenzie,2 in 1868, and alluded to since by Schech,3 Pen- 
zoldt,4 Burow,5 again by Mackenzie,6 by myself,7 by Bos- 
worth,8 by Rosenbach,9 and possibly by others. 
With the only exceptions, however, so far as I know, of 
Bosworth’s argument—with which I but very partially 
* Dr. Semon’s MS. was received in December, iBBo. Its publication has 
been unavoidably so long postponed. This statement is made both as acknowl- 
edgment of the fact and as apology.—Ed. 
1 Studien u. Beobachtungen liber “ Kehlkopflahmung.” Virchow's Archiv, 
vol. xxvii, p. 88, etseq. (Cases 10, 12, 13.) 
2 “ Hoarseness and Loss of Voice.” Cases ig and 20, 
8 “ Experimentelle Untersuchungen liber die Functionen der Muskeln und 
Nerven des Kehlkopfs.” Wurzburg, 1873, p. 44. 
4 “ Ueber die Paralyse der Glottiserweiterer.” Deutsches Archiv fur Klin, 
Medizin, vol. xiii, 1874, p. 107, et seq. 
5 “ Paralyse der Muse, crico-arytsenoidei postici, etc.” Berliner Klin, 
Wochenschrift, 1879, Nro. 33. 
6 “ Diseases of the Throat and Nose,” 1880, p. 440. 
7 German edition of Mackenzie’s work. Foot-notes on pages 574, 575, 587,629. 
8 New York Med. Journal, Nov. 1880, p. 460. 
9 Bresl. drztl. Zeitschrift, I, 2, 3, 1880. 
Reprinted from the Archives of Laryngology, Vol. ii, No. 3, July, 1881. Felix Senion. 
2 
agree,I—of1—of Rosenbach’s paper (which comes to my knowl- 
edge only in a short abstract in Schmidt's Jahrbiicher, vol, 
188, 1881, p. 134, while I am correcting the proof-sheets 
of this communication), and of the remarks in the English 
and German editions of Mackenzie’s recently published 
“Diseases of the Throat and Nose,” all these allusions are 
merely incidental, and intended rather to explain, by some 
hypothesis or other, what is considered a pathological curi- 
osity, than to come to certain definite and important general 
conclusions. 
Although this does not apply to Mackenzie’s later re- 
marks in his text-book, nor to my foot-notes in the Ger- 
man edition thereof, yet the form in which they had to be 
couched in a book of this kind, naturally prevented the 
subject from receiving the more elaborate consideration 
from a clinical point of view that it certainly deserves. 
Its importance is, I hope to show, so great—especially 
with regard to the diagnosis of diseases of the brain and 
chest, in which the laryngeal affection plays the role of an 
important, sometimes pathognomonic symptom—that I 
consider it not only justifiable, but even very desirable, that 
this question should be once more and separately brought 
before those who have the opportunity of either corrobo- 
rating or correcting my statements and conclusions. 
The question at issue stands thus : 
It is well known that, with the exception of the crico- 
thyroid muscles (the tensors of the glottis), which are sup- 
plied by the superior laryngeal nerve, all the other laryn- 
geal muscles, adductors as well as abductors, receive their 
motor innervation from the recurrent laryngeal nerve.2 
But this fact, simple and natural as it seems to be to all 
of us who are accustomed to look at it as to a self-under- 
stood matter, nevertheless invites a consideration concern- 
1 I think it right to state here that the MS. of this paper was already in the 
hands of the Editor, when I became acquainted with Dr. Bosworth’s important 
paper. I have preferred to refer to some of his statements which bear upon (he 
question under consideration, by making foot-notes under the original text, in- 
stead of interrupting my own argument by a discussion of controversial points. 
3 The thyreo-epiglottici and ary-epiglottici muscles are perhaps partially sup- 
plied by the superior laryngeal nerve. (Leube, Deutsches Archiv fur Klin. 
Afedizin, vol. vi, p. 266.) Proclivity to Disease of the Abductor Fibres. 
3 
ing a very interesting, very important, and wholly unsolved 
question, viz., as to the manner in which this small nerve 
accomplishes its most complicated and intricate functions. 
Quite apart from the delicacy of the mechanism of the 
vocal apparatus, over which the recurrent nerve, in conjunc- 
tion with the superior laryngeal nerve, has to preside, the 
natural question must present itself at once to our mind; 
In what way are the diametrically opposed functions of 
opening and closing the glottis accomplished, over which, 
as far as we know at present, the recurrent nerve alone pre- 
sides? Are we to believe that the nerve is, in fact, a ho- 
mogeneous one, but that different stimuli, or stimuli com- 
ing from different centres, can set up in its root different 
forces, conducted through the same nerve-fibres, and result- 
ing at one time in a general involuntary contraction of the 
abductor muscles, and at another in the almost always 
voluntary contraction of their antagonists ? 1 Or are we to 
suppose that, though the nerve is apparently homogeneous, 
1 Bosworth states that the action of the glottis-opening muscles is, “of 
course, purely involuntary, in that it is entirely beyond the control of the will.” 
This statement seems to me somewhat too absolutely framed. Igo so far with 
him, that I believe that under normal conditions of breathing this action is quite 
as automatic as that of respiration in general ; but at the same time I do not see 
why the more energetic contractions of the abductor muscles, during deep inspira- 
tion, should not be occasionally quite as much under the control of the will as 
the act of deep inspiration itself. Why should the wider opening of the glottis 
in a voluntary deep inspiration be regarded as an exclusively involuntary and 
reflex movement, following the voluntary act of deep inspiration, and why not 
as a part of this act itself ? It must not be forgotten that the posterior crico- 
arytsenoid muscles are striped muscles. This is not the occasion on which to 
discuss this very interesting physiological question more fully, but I personally 
am much more inclined to reason as follows : 
‘ ‘ In order to understand correctly the movements taking place within the 
larynx, it should always be remembered that they are not exclusively results of 
the direct action of the muscles. Dilatation and constriction of the different 
laryngeal compartments can, up to a certain degree, be produced as well by the 
elastic membrane of the larynx returning to its former state, after certain 
muscles, which brought it into a state of tension, have ceased to act. This 
state of things much resembles that acting upon the thorax during inspiration and 
expiration.” (Luschka, “ Der Kehlkopf des Menschen,” p. 115. The italics 
are my own.) Now it seems to me that the state of the glottis, seen with the laryn- 
goscope, in a quietly-breathing, healthy person (viz., an opening of middle size, 
but larger than that seen in the dead body, with but very little dilatation in 
inspiration and equally insignificant constriction in expiration), is the result of a 
permanent automatic “ half-tension ” (Luschka, I. c., p. 132) of the abductor 
muscles, superadded to the natural tension of the elastic membrane (which ten- 
sion alone is best illustrated by the “ cadaveric position ” of the vocal cords, 
i. e., the state of the glottis seen after death), and that a further contraction of 
the glottis-openers, involving a greater dilatation of the glottis, might, in ac- 
cordance with the general laws of the mechanism of respiration, be effected 
voluntarily or involuntarily, as the case may be. Felix Seinon. 
4 
it consists in reality of a bundle of strictly differentiated 
fibres, bound together simply by a common nerve-sheath, 
and actually differentiated throughout their peripheral 
course, in fact having ganglionic centres of their own ? 
This physiological question, which is no doubt not only 
of the greatest interest in itself, but, it will be seen, also of 
the highest importance for the pathological question, which 
forms the subject of this paper, has scarcely met with its 
due share of attention. It is simply taken as granted that 
the recurrent laryngeal nerve supplies the greater part of 
the motor innervation of the larynx, and here the curiosity 
of most observers has ceased.1 This is not the occasion to 
attempt to solve the question from the physiological point 
of view, but I may state at once that the pathological facts 
to be communicated later on strongly support the greater 
probability of the second hypothesis, viz.: that the fibres of 
the recurrent laryngeal nerve are differentiated in the nerve- 
centre itself, and only surrounded by a common neuri- 
lemma. 
It will be seen that even this hypothesis is by no means 
sufficient to explain all the pathological phenomena with 
which we shall have to deal in this paper; but if it be ac- 
cepted so far, we have at once a locus standi for the rejection 
of some conclusions concerning the effects of a lesion or 
disease set up in the centres or in the trunks of the spinal 
accessory, pneumogastric, or recurrent nerves, which might 
1 An incidental allusion to this question will be found in a very interesting 
annotation in The Lancet, 1878, vol. i, p. 584, and in my reply to it, ibid., p. 
630. Schech (/. c., p. 42) believesdt very probable that the abductor possesses, 
besides those fibres originating from the pneumogastric and accessory nerves, 
others, which are in some form of relation with the respiratory centre, and are 
stimulated from this source, but says that this hypothesis has not been proved 
up to the present. Merkel (“ Stimra- und Sprachorgan,” 1863, p. 154) makes 
a statement similar to that of Bosworth to be presently quoted, but more 
guarded. He says, after speaking of some other controversial points in relation 
to the nervous supply of the larynx: “It is not less doubtful, whether the 
muscles closing the glottis, on the one hand, and the glottis-openers, on the 
other, are presided over by specifically differentiated nerves (Magendie, H. Ley), 
although it seems to me personally at least very probable, that the glottis- 
openers, which are in a state of involuntary tension, must be presided over by 
nerves of a different kind and of another origin than the glottis-closers, which 
are almost entirely under the control of the will.” Bosworth says (/. c., p. 
461): “Reasoning from analogy, we are justified in the conclusion, that this 
glottis-opening function of the larynx is presided over by an independent 
ganglionic centre, situated in the brain, but which neither physiological experi- 
ment nor pathological investigation has as yet been able to locate.” Proclivity to Disease of the Abductor Fibres. 
5 
be very naturally made with regard to the anatomical rela- 
tions of the single terminal branches of the recurrent laryn- 
geal nerve. These anatomical relations are as follows ; 
The recurrent nerve is of considerable length. “ The left 
is longer than the right in consequence of its being given 
off much later than the right from the trunk of the pneumo- 
gastric nerve. It springs from the latter at a very sharp 
angle, whilst the pneumogastric passes in front of the end 
of the arch of the aorta; winds round the transverse part of 
the arch, outside of the ligamentum arteriosum; passes 
between the aorta and left bronchus to the posterior part 
of the former; leaves this between the origin of the carotis 
primitiva sinistra and the truncus anonymus, and ascends 
in front of the oesophagus in the groove formed by this part 
and the trachea.” 
“ The right recurrent nerve is given off from the trunk of 
the pneumogastric as the latter descends in front of the 
origin of the subclavia dextra. It winds round the lower 
and posterior convexity of this vessel, crosses the carotis 
dextra behind its origin, and ascends behind this vessel, 
running toward the middle line in the groove formed be- 
tween the right lateral wall of the trachea and the oesopha- 
yy i 
gus. 1 
Although during this long course several twigs are given 
off by the nerve (rami cardiaci inferiores, tracheales and 
cesophagei superiores), yet it is only when in close proximity 
to the larynx itself that those branches are sent off which 
serve as motor nerves to the individual muscles of the 
organ. These are : 
a. The posterior crico-arytcenoid nerves. As the trunk 
of the inferior laryngeal nerve is passing close along the 
posterior crico-arytsenoid muscle, it gives off two branches, 
one of which passes above, the other beneath the crico-ary- 
tsenoid articulation, under the lateral edge of the muscle. 
The former of these two branches commences to run ob- 
liquely toward the median line at the border of the lower 
and middle third, the latter at the border of the middle and 
1 This as well as the following anatomical quotations are taken from Luschka, 
1 Der Kehlkopf des Menschen,” Tubingen, 1871, pp. 164-166. 6 
Felix Semon. 
upper third of this edge, between the plate of the cricoid 
cartilage and the substance of the muscle. The first branch 
having given twigs to the lower half, the second to the 
upper half of the muscle, both combine and form a small 
trunk, which becomes visible as the 
b. Nervus arytamoideus transversus on the upper border 
of the posterior crico-arytsenoid muscle. This nerve crosses 
the upper edge of the cricoid plate close to the inner end of 
the crico-arytsenoid articulation, and distributes its final 
branches within the transverse arytaenoid muscle, which is 
thus supplied with nerves from both sides. 
c. The nervus crico-arytcenoideus lateralis is a slender 
twig, which is given off by the trunk of the recurrent 
nerve, whilst passing either across the middle of the muscle 
of the same name, or under some of its bundles. 
d. The nervi thyreo- and ary-epiglottici are given off by 
the trunk at the upper border of the crico-arytsenoid mus- 
cle. They send forth their extremely slender terminal twigs 
into the muscles of the same name. 
e. The nervus thyreo-arytcenoideus is the final branch of 
the recurrent laryngeal nerve. It descends between the 
lateral crico-arytsenoid and thyreo-arytsenoid muscles, and is 
concealed from view midway between the thyroid cartilage 
and the processus muscularis of the arytsenoid cartilage. 
In the depth of the gap left between these muscles, the 
trunk of the nerve splits up, like a brush, into thin twigs, 
which radiate from below into the substance of the muscle 
of the vocal cord proper. 
This description clearly establishes the previous state- 
ment, viz,, that the individual muscular branches are only 
given off by the trunk of the inferior laryngeal nerve when 
close to the larynx. 
Considering this anatomical fact, and another equally 
plain one, viz., that the diameter of the trunk of the nerve is 
a very small one (i mm. when close to the larynx, according 
to Luschka), it is very tempting to draw at once the conclu- 
sions alluded to above, viz.: 
i. That any lesion or disease affecting the nerve from 
its centre to the spot where it gives off the first branch for Proclivity to Disease of the Abductor Fibres. 
7 
the posterior crico-arytaenoid muscle, ,must of necessity 
affect all the laryngeal muscles (with the exception, of 
course, of the crico-thyroid muscles, and perhaps of the epi- 
glottidean muscles). 
2. That, on the other hand, any impairment of mobility 
—if not due to mechanical or myopathic influences I—of1—of a 
single one or some of the laryngeal muscles seems to point 
out clearly that the cause of this impairment must be a 
local one, due to injury or disease of the respective nerve 
tzvigs. 
These conclusions, as sketched here, cannot be rejected a 
priori as unreasonable. The anatomical facts seem to sup- 
port them strongly, and although it was known at a very 
early period in laryngological studies that the abductor and 
adductor muscles could become separately affected,3 yet the 
possibility has been emphatically denied that such a partial 
paralysis could be due to either central causes or affections 
of the main nerve trunks. Navratil,3 the champion of 
this opinion, expresses himself as follows : 
“ The question whether, under these circumstances, the 
paralysis be a central or a peripheral one, can be easily de- 
cided. Considering that there cannot be any disease-pro- 
ducing cause in the centre which would act upon the ad- 
ductors alone, without affecting simultaneously the abduc- 
tors, any central disease can be excluded with certainty. 
The same is to be said of the pneumogastric and recurrent 
nerves, and I dispute Gerhardt’s view, that any pathological 
cause could affect just that part of the recurrent nerve (the 
diameter of the entire nerve is very small) from which (?) 
the narrowing and the tension (?) are effected.4 ” 
I do not know whether this view is still defended by Nav- 
ratil, or whether he has any followers in the camp of laryn- 
1 See my paper “On Mechanical Impairments of the Functions of the 
Crico-Arytenoid Articulation,” etc. Med. Times and Gazette, 1880, vol. ii, 
Nro. 1577 and seq. 
2 Gerhardt, “ Studien u. Beobachtungen liber Kehlkopflahmung. ” Virchow's 
Archiv, vol. xxvii, p. 88. 
3 Berliner Klin. Wochenschrift, 1869, pag. 383. 
4 It would confuse my subject if I entered upon any discussion of the other 
very controversial statements made in this quotation and the lines following it 
in the original. 8 
Felix Semon. 
gologists, but I think it is still held by a great many general 
practitioners. 
Yet it is openly fallacious in consequence of the omission 
of a very simple but very important consideration, viz., 
that we must distinguish between a complete and an incom- 
plete as well as between an acute and a gradually progressive 
lesion of the nerve !1 
llt is certainly remarkable that the same omission has led Bosworth to 
make a statement, in part directly opposed to that of Navratil, but equally inad- 
missible, viz. : to argue that all cases of what he well terms “primary” par- 
alysis of the abductor muscles must be of a central nature (/. c., p. 476.). In 
his argument on this point he says (/. c., p. 475): “ The question arises, does 
the seat of the original morbid changes which produce the paralysis lie in the 
nerve-trunks? Ido not see how this view of the subject can be entertained for 
a moment. Any disease of the recurrent laryngeal nerve, which has progressed 
so far as to destroy its conductivity (the italics are my own), must destroy and 
paralyze all the muscles which it supplies.” The conclusion of this last sentence 
would be certainly quite correct and unattackable if the premise were beyond 
doubt ; but it is just here, in the presumption that the disease in question 
must be judged from those cases in which it has “ progressed so far as to 
destroy the conductivity of the recurrent laryngeal nerve,” that I think Dr. 
Bosworth’s argument is open to criticism. Must a disease affecting a nerve, 
or a pressure exercised upon a nerve, destroy, of necessity, the conductivity 
of all its fibres. \ If so, I see no explanation at all for the cases in which, 
during life, paralysis of one or of both the abductors alone was observed and 
in which, after death, compression of the trunk or trunks of the recurrent nerves 
was found. (See Cases 3, 4, 5, g, 16, 17, 20, 22 of the following literary retro- 
spect.) But the essential point in which I differ from Dr. Bosworth, is 
that I believe that in such cases it is impossible that all fibres of the nerve 
should have been destroyed. If they were, we would simply, as he himself 
justly observes, find trophic changes in all the muscles supplied by the nerve. 
But here we are in possession of positive facts : During life we find paralysis of 
the adductors alone ; after death, evidence of compression of the trunks of the 
recurrent nerves, trophic changes of the abductors only, integrity of the other 
laryngeal muscles. In other words, clinical observation as well as the results of 
the. post-mortem examination prove, that none but the abductor fibres can have suf- 
fered. In the face of such facts it seems to me that any theory which attempts 
to explain uniformly the pathology of this disease by a presumption of central 
changes having taken place in all cases entirely collapses. Nor do I think, as 
is admitted by Dr. Bosworth (/. c., p. 476), that because it is “among the pos- 
sibilities,” that a pressure may “ discriminate among the nerve-fibres,”—that he 
is justified in altogether rejecting the possibility of the original morbid changes, 
which produce the paralysis, ever lying in the nerve-trunks (see above), and this 
simply on account of the—theoretically—small probability that such a discrim- 
inating pressure should affect both recurrent nerves in a large series of cases. 
That such a contingency is rare, is proved by the small number of cases hitherto 
recorded ; but it certainly has happened repeatedly, and as no theory of central 
origin would account for these cases, I believe that a theory of a uniformly cen- 
tral origin of bilateral paralysis of the abductors is untenable, though admitting, 
at the same time, that in a large proportion of these cases the original morbid 
changes, which produce the paralysis, are no doubt to be found in the brain. 
I here take leave of Dr. Bosworth’s important paper. There are several 
more points in it which invite discussion, but I am afraid that these foot-notes, 
which are being added to my paper four months after its completion, give it 
much more of a polemical character than I could have wished. Still, I feel 
that, with regard to the importance and comparative novelty of the subject un- Proclivity to Disease of the Abductor Fibres. 
9 
If we have an acute complete lesion, such as is produced 
by, say transverse cutting of the pneumogastric or recurrent 
nerves, experiments on animals,1 as well as occasional obser- 
vations 2 on human beings, have shown beyond doubt that 
the consequences are such as would be expected theoreti- 
cally, viz., total loss of the functions of all the laryngeal 
muscles (with the exception of the crico-thyroid muscles), 
with the usual results and symptoms. So far, therefore, 
facts and theoretical conclusions quite agree with each 
other. 
Matters, however, become entirely different, if we have 
to deal with either an incomplete acute or an incomplete grad- 
ually progressive lesion. The former of these two conditions 
is certainly an extremely rare one in practice, though it 
can be easily produced by experiment; the latter, on the 
other hand, is the form which is not only practically the 
most important, but almost the only one which occurs in 
reality. 
For if we set aside for a moment the rare contingencies in 
which the nerve centres or trunks suffer from traumatic in- 
fluences, or in which the centres are suddenly disabled from 
fulfilling their functions by certain acute poisonous influ- 
ences, or by the still rarer occurrence of a hemorrhage, or 
the bursting of an abscess into the floor of the fourth ven- 
tricle,3 almost all the other causes which can be thought of 
as occurring in practice are such as belong to the category 
of slowly progressive and—at any rate at first—incomplete 
lesions. Implication of the roots of the pneumogastric and 
spinal 'accessory nerves in central diseases, such as syphilitic 
processes, progressive bulbar paralysis, disseminated cerebro- 
spinal sclerosis, locomotor ataxy with final participation of 
the medulla oblongata; tumors or aneurisms within the 
der consideration, it would be wrong to take no notice of so important a paper 
as that of Dr. Bosworth, and as, unfortunately, our opinions do not agree 
on some important points, I have considered it a duty to offer the reasons for 
my objections to some of his ideas. 
1 Schech, /. c., p. 31, and seq. 
2 Fano, “ Schmidt's Jahrbiicher,” vol. xci, p. 19 ; Kappeler, Archiv der Heil- 
kunde,\B64, p. 271 ; Mackenzie, Brit. Med. Journal, December 24, 1870, and 
“ Diseases of the Throat and Nose,” p. 433, etc. 
3 In the strict sense of the term the last two contingencies might as well 
be said to belong to the class of “ traumatic ” causes. 10 
Felix Semon. 
skull, pressing on the spinal accessory nerve; tumors of the 
neck ; aneurism of the carotids ; goitres, cancers, gummata ; 
aneurisms of the arch of the aorta, or the subclavia dextra ; 
mediastinal tumors pressing on the trunk of the pneumo- 
gastric nerve; tumors of a similar nature and position pres- 
sing on the trunk of the recurrent nerve ; and in addition to 
these, carcinoma of the oesophagus, pleuritic adhesions im- 
plicating the right recurrent nerve close to the apex of the 
right lung in phthisis, and large pericardial exudation 
(Baumler), are all processes, which may lead to lesions of the 
motor innervation of the larynx, and different as they are 
from each other in nature and in progress, yet have one 
point in common, that if they implicate these centres or 
these trunks, the implication is a comparatively slow and 
gradual one. The small size of the nerves does not alter 
this fact. Of course a smaller nerve will be more quickly 
implicated by a carcinoma, or suffer earlier from a pressure 
exercised upon it, than a large one ; but at all events there 
must be some time in which a small nerve as well as a larger 
one begins to experience the effects of the disease-producing 
cause encroaching upon its functions. 
The question now presents itself: What are the early 
symptoms in such cases ? 
Here we may consider the two hypotheses introduced at 
the commencement of this paper. 
If we believed that all the fibres of the recurrent 
nerve were identical and not differentiated, but that differ- 
ent stimuli coming from either the same or from different 
centres, could be transmitted through them, it seems to me 
that in every case in which there is an incomplete impair- 
ment affecting the roots or trunks of the spinal accessory, 
pneumogastric, or recurrent nerves, we could reasonably ex- 
pect one and the same sequence only, viz. : diminution of 
ALL the functions of ALL the laryngeal muscles suppplied with 
motor fibres by the recurrent laryngeal nerve, and this dimi- 
nution in proportion to the number and strength of the fibres 
disabled by the disease-producing cause. In other words, 
every paralysis of the recurrent nerve, unless acute and 
complete from its commencement, ought to begin with Proclivity to Disease of the Abductor Fibres. 
11 
loss of the adductive as well as of the abductive power, and 
this equal impairment should progress pari passtt with the 
disablement of the still conducting fibres, until at last, all of 
them having become devoid of conducting elements by some 
external cause or internal retrogressive metamorphosis, the 
stage of complete paralysis of the nerve with immobility of 
the corresponding vocal cord in the cadaveric position is 
attained. 
Now I must say, that although for several years past this 
question has interested me very much, and although I have 
been seeking a case in which the symptoms should develop 
in this way, I have not been able to find a single one, while 
during the same time I have seen several cases in which the 
paralysis developed under my eyes, and in which the prog- 
ress was different. Yet lam not disposed to dispute, after 
the fashion of some writers of the day, the possibility of an 
occurrence, for the sole reason that it never occurred to 
myself, and I am quite ready to believe that a paralysis of 
the recurrent nerve which finally becomes complete, can 
manifest itself during its beginning and progress by the 
symptoms sketched above. 
But what I wish most decidedly to contradict is the proba- 
bility of the hypothesis first alluded to, by which such an oc- 
currence could be explained, viz.: that the fibres of the nerve 
are all identical, and that different stimuli can be transmit- 
ted through all of them, exciting at one time the action of 
one set of muscles, at another the action of their antagonists. 
No doubt this hypothesis explains why and how in such 
a hypothetical case of gradually progressive paralysis the 
action of all the laryngeal muscles should gradually become 
weaker, and more and more insufficient; but on the other 
hand its own indefensibility becomes clear from the consid- 
erations already alluded to. 
If in reality all the fibres of the recurrent nerve were 
identical, the loss of some of them by any pathological pro- 
cess must, as I have tried to explain, zinder all circumstances 
be followed by the same consequences. The intensity of 
these consequences might vary according to the number of 
the disabled fibres, and perhaps according to the rapidity 12 
Felix Semon. 
of the pathological process ; but in all cases the differences 
could only be quantitative, never qualitative. 
In other words, if this hypothesis were correct, it would 
not admit of a single exception to the rule. A single ex- 
ception, a single good observation, proving that in a case 
of gradually progressive paralysis of the roots or the 
trunks of the accessory, pneumogastric, and recurrent nerves 
one set of laryngeal muscles was either before their antag- 
onists or even exclusively paralyzed, annihilates the 
entire hypothesis of the homogeneousness of the fila- 
ments of the recurrent nerve, for if they were really homo- 
geneous, the laryngeal muscles could never be separately 
affected by a lesion involving the trunk of the nerve itself. 
Now we have not one, nor a few, but many cases on 
record, in which clinical observation and the post-mortem 
examination have actually shown that, although the disease- 
producing cause acted upon the whole nerve-trunk, yet one 
set of laryngeal muscles only became affected, or one much 
more than the other, so that it is sufficient to refer to any of 
the text-books of laryngology or to the medical journals of 
the last decade; moreover, I have but little doubt, that 
almost every reader of this paper has observed if not pub- 
lished cases of this sort as occurring in his own practice. 
I do not think that there is any possibility of reconciling 
this positively ascertained fact with the theory of the 
homogeneousness of the recurrent nerve, and I therefore 
believe that this theory must be completely given up. 
The second hypothesis appears the more probable, and 
one a priori harmonizing much more with the complexity 
and delicacy of the vocal functions of the laryngeal muscles, 
viz. ; that the filaments of the recurrent nerve are strictly 
differentiated throughout the course of the pneumogastric 
nerve and even possess ganglionic centres of their own. 
The adoption of this hypothesis at once gives a clue to 
the explanation of the frequent clinical observations, that 
in cases of intrinsic nerve disease as well as of external mis- 
chief to the nerve, and in cases of central as well as of peri- 
pheral lesion, one set of the muscles is earlier affected 
than the other or even exclusively. If, for instance, a dis- Proclivity to Disease of the Abductor Fibres. 
13 
seminated sclerotic affection of the brain should happen 
to affect those ganglionic centres only which form the nu- 
clei of the abductor filaments of the recurrent nerve ; if a tu- 
mor of the neck should happen to press on those nerve- 
fibres only which supply the crico-arytaenoideus lateralis, 
the thyreo-arytsenoideus, and the arytsenoideus proprius 
muscles,I—it1—it would not need further explanation to prove 
that in the first instance we would see, laryngoscopically, 
the vocal cords not in the cadaveric but in the phonatory 
position, because the posterior crico-arytsenoid muscles only 
were paralysed, and that, on the other hand, in the second 
instance we would see the glottis widely open, and meet 
with complete aphonia in consequence of the inability of the 
solely paralysed adductor muscles to bring the vocal cords 
together for the purpose of phonation. In each of the two 
cases this state of things could remain stationary (viz.: if 
the pathological process occasioning the paralysis came to a 
standstill), or could lead to complete paralysis with its con- 
sequences (viz. : if the antagonistic centres or fibres, which 
were left free at the beginning, became also affected later on). 
I find myself thus far in complete accord with v. Ziemssen 
who, although not entering upon any discussion on the mo- 
dus operandi of these gradual and incomplete paralyses, ex- 
presses himself as follows:3 
“ Paralysis of individual branches of the recurrent, which 
go to the laryngeal muscles and to the mucous membrane 
of the trachea and the larynx, may arise through incomplete 
lesions of the trunk of the recurrent; for instance, when it 
is exposed to unequal pressure, or when, for any other 
cause, the nerve-filaments are affected in an unequal degree 
by degenerative changes. This generally takes place at 
the beginning of a severe lesion of a nerve, gradually lead- 
ing to complete paralysis of conduction—for instance, 
owing to aneurism or carcinoma—and we can therefore al- 
most always distinguish between an initial stage of incom- 
plete paralysis—now more pronounced in one muscle, 
1 This example has been chosen only for the sake of an illustration. It will 
be shown hereafter that, so far as I know, no such case has thus far been re- 
ported. 
3 Cyclopaedia (English edition), vol. vii, p. 948. Felix Semon. 
again in another,—and the stage of total paralysis.” Simi- 
lar views are held, I believe, by the majority of laryngolo- 
gists, whilst the question has not met with any special con- 
sideration at the hands of the medical profession at large. 
It would seem, then, that the earlier symptoms in cases 
of incomplete, slowly progressing paralysis entirely de- 
pended upon the question, zvhich fibres have been acci- 
dentally first attacked by the pathological process occa- 
sioning the paralysis, and the natural conclusion would be 
that we sometimes should expect early lesion of the abduc- 
tors, at others of the adductors. 
This is, I believe, the general point of view accepted at 
the present time by laryngologists, and from this point of 
view it is easily understood, why those who have met with 
cases of bilateral paralysis of the abductor muscles, the cause 
of which was to be traced not to some local or myopathic, 
but to some central or nerve-trunk lesion, should have looked 
upon their cases as mere pathological curiosities, and should 
have tried to explain by more or less ingenious hypotheses, 
why in their individual case the pathological process, 
although acting upon the whole of the nerve, should have 
affected the abductor filaments only. 
Now I do not wish to augment the number of these 
hypotheses by the addition of a new one of my own, but 
simply to state distinctly and separately once more the 
following fact, previously proclaimed by Morell Mackenzie 
and myself : 
“ The occurrence of an isolated paralysis of the abductor 
filaments of the recurrent nerve in cases in which the roots 
or trunks of the spinal accessory, pneumogastric, and recur- 
rent 7ierves are injured or diseased, is not an isolated patho- 
logical curiosity. There is a distinct proclivity of the abduc- 
tor fibres to become affected, in such cases, either at an earlier 
period than the adductor fibres, or even exclusively.” 
A statement like this can only be proved in the following 
way: I must bring forward a comparatively large number 
of clinical observations and post-mortem examinations, show- 
ing that isolated paralysis of the posterior crico-arytaenoid 
muscles was the result of disease or injury to the centres Proclivity to Disease of the Abductor Fibres. 
15 
and nerve-trunks, or that at any rate the paralysis of these 
muscles was earlier, and respectively more developed than 
that of their antagonists, and this number must not be com- 
pensated for by an equal or approximatively equal number 
of observations proving the occurrence of a primary affec- 
tion of the adductor fibres under similar circumstances. 
I proceed to the first part of my proof and quote some 
cases belonging to the first category. 
Case 1 (Gerhardt1). Chronic disease of the brain of doubtful 
nature. The left vocal cord immovable in the median line. 
Case 2 (Gerhardt2). Probably encephalitic process in the left 
half of the brain. Right vocal cord immovable in the median line. 
Case 3 (Gerhardt3). Tuberculosis pulmonum. Incomplete 
paralysis of the left posterior crico-arytsenoid muscle. Post-mor- 
tem examination : left pneumogastric nerve completely imbedded 
in thickened connective tissue and bent backward by some swol- 
len lymphatic glands. The corresponding recurrent nerve inti- 
mately connected with a melanotic lymphatic gland. The left 
posterior crico-arytsenoid muscle in a state of fatty degeneration 
and atrophy. The adductors on the same side also degenerated, 
but not to such a degree as the abductor. Brain and medulla 
oblongata healthy. 
Case 4 (Mackenzie4). Paralysis and atrophy of the abductor 
of the left vocal cord., caused by pressure of a malignant tumor of 
the thyroid gland on the left recurrent nerve. Duration six years (!) 
Left vocal cord fixed in median line. Post-mortem examination : 
Cancerous tumor two inches in breadth, reaching from the arch of 
the aorta to the cricoid cartilage, which had “ completely incorpo- 
rated the left recurrent nerve just where it passes up beneath the 
upper border of the arch of the aorta. The left crico-arytsenoideus 
posticus was completely atrophied, only a few pale thin fibres 
could be seen at its lower and inner part, whilst it fellow was large 
and well nourished.” 
Case 5 (Mackenzie6). Paralysis of the abductor of the left 
vocal cord caused by aneurism of the arch of the aorta pressing on 
the left recurrent nerve. Left vocal cord fixed near the median 
1 L. c., p. 307, case x. 
2 L. c., p. 309, case xii. 
8 L. c., p. 310, case xiii., and postscript, p. 318. 
4 “ Hoarseness, Loss of Voice,” etc. Case xxix, p. 39. 
5 Ibidem. Case xx, p. 41. 16 
Felix Semon. 
line. Post-mortem examination ; Aneurism of the arch of the 
aorta. “ The left recurrent nerve was traced from its origin from 
the vagus round the arch of the aorta, as far as the sac of the 
aneurism, with which it became incorporated and could not be 
followed further.” The left posterior crico-arytsenoid muscle 
was completely atrophied, only a very few thin, pale fibres being 
apparent. 
Case 6 (Semon1). Boy, set. 15. History of fit and uncon- 
sciousness 7 years previously, after which he stammered for a con- 
siderable time. Voice has ever since remained hoarse. Left 
vocal cord immovable in the median line. After protracted elec- 
tric treatment slight improvement in mobility. 
Case 7 (Semon2). Woihan, get. 55. Aneurism of the first 
part of the arch of the aorta, of the innominate and of the carotis 
communis dextra. The abductive power of the right vocal cord, 
which stands nearly in the median line, is much diminished, and 
the paresis of the right abductor became more complete during 
the short time the case was under observation. The patient soon 
gave up attending the hospital. 
Case 8 (Semon3). Woman, set. 40, Fibrous nodulated 
struma. The abductive power of the left vocal cord much dimin- 
ished. It stands close to the median line. Injections of tinct. 
iodi into the goitre produce a considerable diminution in the size 
of the tumor, but the mobility of the left vocal cord does not 
improve, although later on the local applications, electricity, and 
subcutaneous injections of strychnia are made use of. 
Case 9 (Riegel4). Chronic pneumonia, bilateral paralysis of 
the abductors. Boy, get. 6, Duration of the laryngeal symptoms, 
from the beginning until the death of the patient, three years. 
Result of the post-mortem examination : Both recurrent nerves 
imbedded in dense connective tissue ; only the posterior crico- 
arytgenoid muscles in a state of atrophy and fatty degeneration, 
the other laryngeal muscles healthy. Microscopic examination of 
the recurrent nerves shows, above the points of adhesion, atrophy 
and fatty degeneration of the majority of the filaments ; but on 
both sides still a number of normal, well-preserved fibres is found. 
Case 10 (Penzoldt5). Tertiary syphilis. Repeated apoplectic 
attacks. Bilateral paralysis of the abductors. Woman, set. 61. 
1 Unpublished. 
4 Berlin. Klin. Wochenschrift, 1872. Nos. 20 and 21, and 1873, No. 7. 
3 Unpublished. 
3 Unpublished. 
5 “Deutsches Archiv fur Klin. Medizinßd. xiii, p. 107. Proclivity to Disease of the Abductor Fibres. 
17 
Duration of the disease, 1 months. Death. Result of post- 
mortem examination : Roots of both pneumogastric and accessory 
nerves strangely thin and in a state of gray discoloration. (Similar 
changes in other cerebral nerves.) Both posterior crico-arytcenoid 
muscles pale, brownish-red. The left pneumogastric and recurrent 
nerves somewhat slender and of a grayish color. Microscopic ex- 
amination of these nerves shows the majority of the primitive 
fibres as normal, but between them there are filaments which are 
distinctly broader than normal, and the neurilemma of which is 
in a state of distinct fatty degeneration. The interstitial connect- 
ive tissue is augmented and contains a great quantity of fat cor- 
puscles. 
Case ii (Paul Koch1). Compression of both recurrent nerves 
by enlarged bronchial glands. Bilateral paralysis of the abductors. 
Girl, set. 24. Diagnosis per exclusionem. 
Case 12 (Mackenzie2). General paralytic symptoms. Bilateral 
paralysis of the abductors. Man, set. 44. General paralysis affecting 
both extremities 16 months before admission. Bilateral paralysis 
of the posterior crico-arytsenoid muscles. No change in the laryn- 
geal muscles during the three months he was under observation. 
Case 13 (Mackenzie3). Cerebrospinal symptoiris. Bilateral 
paralysis of the abductors. Repeated epileptic attacks, involuntary 
motions, and oozing away of the urine. Nearly complete immo- 
bility of the vocal cords in the phonatory position. Duration of 
the laryngeal symptoms not distinctly ascertained. Death. No 
post-mortein examination. 
Case 14 (Mackenzie4). Syphilitic disease of the brain. Bi- 
lateral paralysis of the abductors. Manifold evidence of central 
disturbance. Seizures, nausea, vomiting, pains, and loss of coordi- 
native muscular power in legs, loss of eyesight, vertigo. Partial 
paralysis of the posterior crico-arytsenoid muscles. Fifteen years 
previously primary venereal sore, followed by eruption. lodide 
of potash speedily improved all the symptoms. 
Case 15 (Mackenzie5). Imperfect paralysis of the right leg. 
Bilateral paralysis of the abductors. Dyspnoea for several years. 
Sudden death. No post-mortem examination allowed. 
Case 16 (Mackenzie6). Pressure oti both recurrent nerves by 
aneurisms. Bilateral paralysis of the abductors. Man, set. 51. 
1 “Anna/es des Maladies de I Oreille et du LarynxlB7B, Nos. 6 and 7. 
2 “ Diseases of the Throat and Nose,” vol. I, page 428. 
3 Ibidem, p. 429. 
5 Ibidem, p. 429. 
4 Ibidem, p. 429. 
6 Ibidem, p. 443. Felix Semon. 
Death. Result of post-mortem examination ; “ One very large 
aneurism, commencing in the ascending aorta and involving the 
innominate and right subclavian artery, pressed, at its upper and 
outer part, on the right recurrent nerve and slightly on the right 
pneumogastric nerve. The second smaller aneurism involved the 
under and posterior surface of the descending portion of the arch 
of the aorta, and slightly pressed on the left recurrent nerve.” 
Both posterior crico-arytsenoid muscles in a state of atrophy and 
fatty degeneration. The other laryngeal muscles healthy. 
Case 17 (Mackenzie1). Pressitre on both recurrent nerves by 
cancer of the oesophagus. Bilateralparalysis of the abductors. Man, 
set. 67. Death. Post-mortem examination ; Both recurrent nerves 
passed into a cancerous growth, originating from the oesophagus. 
Their exit from this mass could not be traced. The abductor 
muscles were found to be greatly reduced in size and presented 
signs of fatty degeneration. The other muscles of the larynx 
were healthy with the exception of the left thyro-arytsenoid 
muscle, which showed signs of molecular transformation. 
Case 18 (Mackenzie3). Pressure on both recurrent nerves by an 
enlarged thyroid gland. Bilateral paralysis of the abductors. Boy, 
set. 15. Duration of the laryngeal symptoms, four months. The 
treatment of the bronchocele resulted not only in a cure of this 
affection, but also in restoration of the function of the paralyzed 
abductor muscles. 
Case 19 (Mackenzie3 and Semon4). Pressure of an aneurisyn 
on both recurrents, and compression of the nerves by dense connective 
tissue. Bilateral paralysis of the abductors. Man, set. 60. Duration 
of the laryngeal symptoms, till death, six months. Post-mortem ex- 
amination : Hypertrophy of the heart, aneurismal dilatation of the 
first part of the aorta, chronic pneumonia, and enlargement of the 
bronchial glands, which were enveloped in abundant firm connec- 
tive tissue which compressed both recurrent nerves. Atrophy of 
both abductors ; the other laryngeal muscles were apparently 
healthy. 
Case 20 (Semon5). Aneurism of the arch of the aorta press- 
ing on both recurrent nerves. Incomplete but progressive paralysis 
of the abductors. Man, set. 51. Only complaint dyspnoea and pe- 
1 Ibidem, p. 4^3. 
8 Ibid., p. 444. 
3 Ibid., p. 444- 
4 “ Transactions of the Clinical Society,” vol. xi, 1878, p. 149. 
5 Alluded to in “ German edition of Mackenzie’s work,” foot-notes, pp. 
and 72°> and by Dr. W. M. Ord, in “ St. Thomas’ Hospital Reports,” vol. x, 
1880, p. 131. Proclivity to Disease of the Abductor Fibres. 
19 
culiar alteration of voice beginning three months before he came 
under observation. Incomplete bilateral paralysis of the abduc- 
tors, more marked on the left than on the right side, progressing, 
during the two months which elapsed before the death of the 
patient took place, almost daily tinder my eyes, At the time of the 
patient’s death the left vocal cord remained immovable in the 
median line, while the right still moved slightly outward. [At the 
same time the level of the left vocal cord was lower than that of 
the right, and its inner border slightly excavated.] Death from 
rupture of the aneurism into the oesophagus. Post-mortem exam- 
ination : Large, curiously formed aneurism of the upper and poste- 
rior part of the arch of the aorta, beginning at the commencement 
of the convexity formed by the vessel when passing from the 
ascending into the transverse part, and extending over two-thirds 
of the transverse part. The left recurrent nerve is firmly impli- 
cated for a considerable distance by the wall of the aneurism. It 
does not, however, to the naked eye1 seem to be atrophied in its 
parts situated above the aneurism, but, on the contrary, somewhat 
swollen and congested. The right recurrent nerve is pressed 
upon at the point where it is given off by the right pneumogastric 
nerve, and in the very beginning of its course by that part of 
the aneurism projecting to the right. The nerve is apparently 
not changed. The left posterior crico-arytsenoid muscle is so 
completely atrophied that but a few thin, pale, and yellowish fibres 
are seen at its inner insertion ; the right is also atrophied, but to a 
considerably less degree. The other laryngeal muscles are appar- 
ently normal, with the exception of the left crico-thyroid muscle, 
which is considerably discolored and atrophied. The left superior 
laryngeal nerve is intact.2 
Case 21 (Semon3). Disseminated cerebrospinal sclerosis. Bi- 
lateral paralysis of the abductors. Gait of the character of loco- 
motor ataxy ; numbness of (now) both legs ; incontinence of urine ; 
slight left facial paralysis ; slight nystagmus ; inequality of the 
pupils,—of late ; numbness of the mucous membrane of the upper 
lip. The laryngeal paralysis, which has remained unchanged ever 
since the beginning of the observation, /. e., 2 f years ago, preceded 
all the other symptoms for nearly two years ! 
1 Unfortunately no microscopical examination was made. 
2 Was, in this case, the motor innervation of this muscle derived from the re- 
current nerve instead of the superior laryngeal ? (v. Ziemssen, I. c., German 
edition, p. 445.) 
3 “ Transactions of the Clin. Soc.,” 1878, vol. xi, p. 146, 20 
Felix Semon. 
These two facts, viz., the permanence of the bilateral par- 
alysis of the abductors only, and the long interval between 
the appearance of this and any of the other symptoms, made 
me, when I first published this case, nearly three years ago, 
disinclined to believe in a causal connection between the 
laryngeal and the other symptoms.1 
But the case has ever since been before my mind, and has, 
in fact, led me to the considerations of which the present 
paper is the outcome. Having convinced myself that bi- 
lateral paralysis of the abductors only might be the result of 
a central lesion affecting the roots of the accessory and 
pneumogastric nerves (Cases 10, 12, 13, 14), and that a 
lesion affecting the roots or trunks of these nerves and of 
the recurrent nerve, might result in such an isolated paraly- 
sis, which remains stationary for a long time and does not 
necessarily lead to retrogressive changes of the other laryn- 
geal muscles, I cannot refrain longer from admitting that 
this is most probably a very unusual case of multiple cerebro- 
spinal sclerosis, in which the first and for a long time the 
only symptom was bilateral paralysis of the abductors.2 
Case 22 (L. Weber3). Bilateral paralysis of the abductors after 
typhoid fever. Tracheotomy. months later, pneumonia and 
nephritis. Death. Post-mortem examination : Besides other 
changes in different parts of the body, tracheitis and purulent 
peri-tracheitis were noticed. Both recurrent nerves were found to 
have been embedded entirely in this purulent infiltration. The nerves 
did not show any considerable changes to the naked eye, with the 
exception of appearing somewhat flattened ; microscopically, the 
only change to be detected was the diminished volume of some of 
the axe-cylinders. The abductor muscles themselves appeared 
perfectly healthy to the naked eye and under the microscope. 
1 See The Lancet, vol. i, 1878, p. 630. 
2 Whilst correcting the proof sheets of this paper, I find that Dr. Hering, of 
Warsaw, related at the International Congress of Laryngology, held last year at 
Milan, a case of paralysis of the posterior crico-arytssnoid muscles, “ followed 
nine months afterward by symptoms of labio-glosso-pharyngeal paralysis of bul- 
bar origin, which there was every reason to believe was due to syphilis.” 
(These Archives, vol. i, 1880, p. 388.) The shortness of the communication 
does not, of course, permit of any definite conclusions being drawn ; but even 
from this short report the case appears to belong to the category under consid- 
eration, and to be very similar to the one just referred to. 
a Berl. Kli7t. Wochenschrift, Nro. 29, 1880, p. 412. Proclivity to Disease of the Abductor Fibres. 
21 
We have here then a considerable number of clinical 
observations, many of them authenticated by the discovery 
on the post-mortem table of anatomical changes correspond- 
ing to the symptoms observed during life, and proving that 
pathological processes, implicating the nerve-centres or 
the nerve-trunks themselves, are frequently manifested by 
actual changes in the abductor fibres and muscles, either 
exclusively or better developed than in the antagonistic 
muscles. I need not say that the above list by no means 
claims to be complete. It seemed to me that it was only 
necessary to show that isolated paralysis of the abductors 
in consequence of causes affecting centres or trunks was 
not an accidental curiosity, but occurred comparatively 
often. lam sure that it would have been easy to augment 
considerably the above list,—especially as far as unilateral 
paralysis of a posterior crico-arytaenoid muscle from cen- 
tral or nerve-trunk lesions was concerned,I—had1—had I made an 
extensive search through the literature of laryngeal paral- 
ysis. But I considered this the less necessary, because the 
number of 22 cases becomes important and considerable, 
if compared with the number of cases in which a central or 
trunk lesion of the nerves under consideration was found 
to have led to isolated paralysis of the adductors. 
For it must not be forgotten that I have thus far only ful- 
filled one part of my task : I have shown that in many cases 
disease of the centres or pressure upon the trunks can lead 
to isolated paralysis of the abductors. The question now is: 
Is the number of these cases covered by a similar number, 
in which, under the same circumstances, the adductors only 
became affected ? 
The answer to this question is simple and will, no doubt, 
be surprising to many readers of my paper; 
Not only have I never seen such a case, but in the whole 
range of laryngeal literature, which is known to me, I have 
been unable to find a SINGLE case, in which primary organic 3 
1 I remember in my own hospital practice, several, at least three more 
cases of aneurism of the aorta with phonatory position of the left cord, of which 
I have no notes at hand. 
2 I purposely say “ organic ” disease of the brain, or nerve-trunks, because it 
is a most remarkable fact, that the so-called “ functional” neuroses show, on the 22 
Felix Semon. 
disease of the brain or of the nerve-trunks was proved by 
clinical observation or the result of the post-mortem exami- 
nation to have been the cause of isolated paralysis of the ad- 
ductors!1 
I must say that I was not a little astonished, when I 
reached this result. The laryngeal literature, however, is 
already so large that it is not impossible that a few cases of 
this sort might have been described of which I have no 
knowledge;3 but even if this were so, I think that I have 
proved the proclivity of the abductor fibres of the recurrent 
nerve to become affected sooner than the adductor fibres, 
or even exclusively, in cases of undoubted central or pe- 
ripheral injury or disease of the roots or trunks of the 
pneumogastric, spinal accessory, or recurrent nerves. 
The next question—if the fact has been established— 
would naturally be as to the cause of this curious pro- 
clivity. To this question it is very difficult, at the present, 
to give an answer satisfactorily explaining all the condi- 
tions under which an isolated paralysis of the abductor 
muscles can take place. 
If the theory of the uniformly central origin of this paral- 
ysis, as supported by Bosworth, were correct, the presump- 
tion of the existence of an independent ganglionic centre for 
the abductors (as suggested by Mackenzie, myself, Bosworth, 
and others) would be sufficient to explain its cause. Any 
degenerative change, or, in a few cases, sudden functional 
disturbance taking place in the brain, under different influ- 
ences, if limited to these ganglia, would clearly lead to iso- 
other hand, quite as strange a predilection for ajfecting the ADductors only, as the 
“ organic ” lesions for the Adductors ! Although there are a few cases of hysteri- 
cal paralysis of the «Muctors on record (Frankel, Guttmann, Biermer, Burow, 
Schreiber, Mackenzie-Semon), yet the immense majority of cases of “hysterical 
paralysis,” hitherto recorded, concern the adductors (and tensors) only. 
1 To avoid all possible mistakes, I beg to state distinctly that I speak of such 
cases only in which isolated paralysis of the adductors could be traced to a 
“primary" lesion of the roots or trunks of the accessory, pneumogastric, and 
recurrent nerves! Such cases are not known to me. But I have no doubt that 
cases have occurred (or could be imagined), in which an originally local affection 
(such as a carcinoma) affected, in consequence of its anatomical situation, at an 
early period, the adductor fibres and muscles only, and, implicating in its later 
stages the entire recurrent nerve, led to paralysis of all the laryngeal muscles. 
8 I earnestly hope that this paper will serve in eliciting contributions corrob- 
orating or rectifying, as the case may be, my statements, from those who have 
had and have the opportunity of seeing cases in point. Proclivity to Disease of the Abductor Fibres. 
23 
lated paralysis and atrophic changes of the abductors. 
Of course there would still remain the question why the 
centres for the abductors are so often the seat of such de- 
generative processes, in preference to the common centre or 
to the probably-connected centres of the adductors (if it be 
supposed that each of those, as well, has a ganglionic centre 
of its own). 
Several answers might be given to this question, contribu- 
ting to, if not affording, a solution. 
In the first place, the very fact just mentioned, viz. : the 
mutual cooperation and probably existing anatomical connec- 
tion of the adductor centres, offers an explanation why they 
should be longer and more effectually protected against dis- 
ease-producing influences, to which the unsupported and 
isolated centres of the abductors would earlier succumb. 
(See also Penzoldt, /. c., p. 120.) Even if one or some of 
these adductor centres were diseased, it would by no means 
be improbable that the remaining healthy ones would act 
vicariously for them. That this suggestion is not a purely 
theoretical one, but that the mechanism of adduction of the 
vocal cords is actually endowed with a sort of compensatory 
tendency, is shown by the fact that, in paralysis of an entire 
recurrent nerve, with consequent immobility of the affected 
cord, in the cadaveric position, the contraction of the adduc- 
tors on the healthy side, in very many cases, is so excessive, 
when phonation is attempted, that the healthy vocal cord 
crosses the median line to join its diseased fellow. 
Another explanation might perhaps be found in the fact 
that the activity of the abductors, although, I believe, not 
entirely beyond the control of the will, is certainly much 
more automatic than that of the antagonists, and that, 
hence, perhaps, its power of resistance against disease-pro- 
ducing causes is less. 
Finally, attention is to be drawn to the very remark- 
able fact, that this proclivity of the abductor centres to suc- 
cumb to central causes of disease is quite analogous to the 
similar proclivity of the extensor muscles of the extremities 
to become sooner affected than the flexors, or even exclu- 
sively, in diseases of central origin, e.g., in lead paralysis. 
(See also Rosenbach, /. c.) 24 
Felix Semon. 
But as I have shown that the theory of a uniformly 
central origin of the disease is untenable in the face of the 
authenticated cases of paralysis and degeneration of the 
muscles in consequence of disease of, or pressure upon, the 
nerve-trunks, even the existence of an independent centre 
would not account for the origin of this latter class of 
cases. 
What, then, is the explanation of these cases ? 
There would be no difficulty, certainly, in explaining the 
phonatory position of the vocal cord or cords, in cases of 
undoubted nerve-trunk lesion, if this phenomenon were 
limited to a comparatively short and early period of the 
primary disease, in cases of on the nerves. Before 
any pressure disables any fibres of a nerve, it acts in the 
manner of a mechanical irritation. Schech’s beautiful ex- 
periments on animals have proved1 the following fact: 
“ If the recurrent nerve or the pneumogastric nerve is 
irritated, the result is; a position of the vocal cords in the 
median line (phonatory position) in consequence of the 
preponderance of the adductor muscles.” In other words, 
we have the same phenomenon as if the adductors alone 
were irritated. 
But this explanation holds good only for the earliest 
stages of a pathological process encroaching upon the 
nerve-trunks. Why does the phonatory position of the vocal 
cords continue in the later stages? Why do we see during 
life, or find at the post-mortem table, evidence of retrogres- 
sive changes in the posterior crico-arytaenoid muscles only, in 
cases of long duration (Cases 3, 4, 6, 9, 15, 21) and of un- 
doubted grave implication of the nerve-trunks (Cases 3, 4, 
5, 9, 10, 16, 17, 19, 20, 22)? 
Under all circumstances, we must, in order to understand 
these cases, keep one indispensable premise before our minds, 
although we may, in the present state of our knowledge, not 
always be in the position of actually proving it, viz.; that in 
all these cases it is impossible that the conductivity of all 
fibres of the nerve-trunk should have been destroyed, how- 
ever complete and long-existing the complication of the 
XL. c., p. 33. Proclivity to Disease of the Abductor Fibres. 
25 
nerve-trunk, in the morbid process, seemed to be! Riegel’s 
case of involvement of both recurrent nerves, in dense con- 
nective tissue (No. 9 of the retrospect), is an excellent 
proof that, if the microscopic examination of the com- 
pressed nerves is made with sufficient care, it will be found, 
doubtless in all such cases, that a number of normal, well- 
preserved fibres still exist. And yet in his case the duration 
of the laryngeal disease was three years ! It is thus conclu- 
sively shown that neither intensity of the morbid process nor 
long duration of the disease involve, of necessity, total de- 
struction of the nerve-trunk, and we can fairly draw the 
inverse conclusion that, if we see, during life, isolated paral- 
ysis of the abductors, or find them, after death, in a state of 
atrophy and fatty degeneration, in cases of undoubted affec- 
tion of the nerve-trunks themselves, the very limitation of 
the morbid changes to this one set of muscles, proves that 
the conductivity of the nerve cannot have been destroyed in 
its entirety. (See Cases 4 and 17 of the retrospect.) 
Again, if this explanation be correct, we find ourselves 
confronted by the same question which we considered after 
the explanation of the cases of central origin, viz.: What is 
the cause of this curious proclivity of the abductor filaments 
to become affected sooner than the? adductor fibres, or even 
exclusively, in cases of affection of the whole nerve-trunk} 
Several hypotheses might be made and have been made 
to explain this peculiar proclivity, viz.: 
1. That the anatomical distribution of the fibres of the 
recurrent nerve may be a concentrical one, and that the ab- 
ductor fibres may be situated in the periphery of the nerve, 
i. e., most exposed to all external injuries. 
2. That there may be a specific vulnerability of the 
abductor filaments, or—what would amount practically to 
the same thing—that even in cases of partial disablement 
of the adductor filaments, the remaining healthy adductor 
fibres might conduct all the nerve-force emanating from the 
adductor centres, to the adductor ftiuscles. 
3. That possibly the adductors receive an increment of 
nerve-force from the superior laryngeal nerve. 
However, all these hypotheses are open to certain ob. 26 
Felix Semon. 
jections, and none of them seems to me to offer a really sat- 
isfactory and plausible explanation. But at the same time 
I do not believe that an expla7iation is the thing we want at 
present. 
In the face of the comparative novelty of the subject 
and of all the difficulties connected with this question, I 
would rather believe that the time has not yet come when 
we can venture to give an explanation, but that, before all, 
by numerous further contributions, the fact should receive 
further corroborative evidence, that: There is a proclivity 
of the KQductor fibres of the recurrent nerve to succumb to 
pathological influences affecting the roots and trunks of the 
motor ?ierves of the larynx. 
Quite apart from the great intrinsic anatomical and phys- 
iological interest of the question, its affirmative reply 
would entitle us to lay down the following practical rule: 
Immobility of one or of both the vocal cords in the 
phonatory position—if not occasioned by mechanical impair- 
ments, or myopathic affection—invites to a consideration 
of all the possibilities which may produce paralysis of the 
entire recurrent nerve ; immobility in the position of deep 
inspiration—if not occasioned by mechanical impairments, 
or myopathic affection—is much more likely to be due to 
either a functional or a local neurosis, i. e., an affection 
produced by local disease of the adductor twigs of the re- 
current nerve. ARCHIVES OF LARYNGOLOGY 
EDITED BY 
LOUIS ELSBERG, M. D., 
NEWYORK, 
IN CONJUNCTION WITH 
J. SOLIS COHEN. M. U.. 
PHILADELPHIA, 
FREDERICK J. KNIGHT. M. D. 
BOSTON, 
GEORGE M. LEFFERTS, M. D., 
NEWYORK, 
Piid Dr. J. Bdeckel, Strassburg ; Prof. Burow, Konigsberg; Dr. Foulis, Glasgow; Prof. Ger- 
iiardt, Wurzburg; Dr. Heinze, Leipzig; Dr. Koch, Luxembourg; Prof. Krishaber, Paris; 
Prof. Labus, Milan; Dr. Massei, Naples; Dr. Morell Mackenzie, London; Prof. Oertel, 
Munich ; Dr. Smyly, Dublin ; Prof. Voltolini, Breslau, and Prof. Zawerthal. Rome. 
It is believed that the time has come for the publication of a journal devoted 
to the specialty of Laryngology. So much has been achieved in this department 
of Medicine during the last twenty years, that in the regard of both the profes- 
sion and the lay public it has acquired recognition and a certain amount of inde- 
pendence. In the further advance in every right direction the Archives are in- 
tended to give important aid. None of the existing medical journals can occupy 
its place ; it competes with none. and supplements all. It is to be a bond of 
union between the specialists themselves, and also between them and the general 
profession. Such a means of communication and interchange of ideas, constitu- 
ting at the same time a depository of contributions of permanent merit and a 
mirror of the progress of the specialty as reflected in a comprehensive digest of 
periodical and other literature in every part of the world, cannot fail to be 
of value from a scientific as well as a practical point of view. 
The scope of the Archives embraces Human and Comparative Morphology and 
Physiology of the Throat, and Pathology and Therapeutics of Throat Diseases, 
in the widest signification of these terms. 
All contributions are original. The contents are arranged in three departments, 
which are 
I. New Contributions to Literature, viz., 
a. Leading articles, comprising Monographs and accounts of cases with re- 
marks. 
b. Clinical Notes, being a briefer record of interesting cases. 
c. Society Transactions, i.e., Reports of the proceedings of Laryngologial 
Societies, or of matters relating to Laryngology occurring in other societies and 
not previously published. 
11. Report of Contemporary Literature, viz., 
a. Reviews and Notices of Books and Pamphlets. 
b. Digest of the Literature of every part of the world. 
111. Miscellany, viz., 
News Items Editorial Announcements and Answers to Correspondents,—the 
latter being planned particularly for communication between specialists and gen- 
eral practioners. 
The Archives of Laryngology is handsomely printed in large octavo form, 
each number containing 96 pages, and the articles are fully illustrated wherever 
their subjects render this desirable. 
It is issued quarterly, at the price per number of $l.OO, and the subscription 
per year of $3 00 
G. P. PUTNAM’S SONS, 182 Fifth Avenue, New York. 
London. N. TRUEBNER & CO., 59 Ludgate Hill, 
Paris. J. R. BAILT.IERE, 19 Hautefeuille.