Two Cases of Laryngeal Pa- 
ralysis, with, a Consideration 
of the Points involved. 
BY 
JONATHAN WEIGHT, M.D., 
BROOKLYN. 
REPRINTED FROM 
BT6* Neto Yorft fWeWcal journal 
for September SB, 1889. Reprinted from the New York Medical Journal 
for September 28, 1889. 
TWO CASES OF LARYNGEAL PARALYSIS, 
WITH A CONSIDERATION OF THE POINTS INVOLVED. 
By JONATHAN WRIGHT, M. D., 
BROOKLYN. 
The peruser of recent medical literature, especially in 
the domain of laryngology, must often be struck with the 
divergence of views and the discrepancies of statement in 
works on laryngeal paralysis. There is an undoubted tend- 
ency toward bewilderment of mind the more one reads and 
studies the various experiments to settle the nerve supply 
and the modus operandi of the dilators and closers of the 
glottis with the complicated interrelation of the various 
contributory muscles. The laryngologist himself, if his 
experience is large, must from time to time see certain 
laryngeal paralyses whose aetiology, after the most exhaust- 
ive local and general examination, is a mystery. All other 
muscular groups are normal, and the patient may otherwise 
be in good health. Ascribing them to some pre-existing 
laryngitis or to rheumatism or gout is far from satisfactory 
without an explanation of how these very common affec- 
tions, in particular cases, can bring about such results. It 
has been the lot of the writer to see several such cases 
when the most careful local inspection and the most pains- 
taking physical examination of the chest failed to disclose 2 
TWO CASES OF LARYNGEAL PARALYSIS. 
the cause. In most of these cases (all, I think) the immo- 
bile vocal cord was in the median line. The chagrin which 
they have caused has led me to study the two cases pre- 
sented in this paper with more interest than they wTould 
have otherwise excited. They, of course, do not belong to 
the group of puzzling cases just mentioned : 
Case I. Left Lingual and L,aryngeal Paralysis; Atrophy 
of the Left Side of the Tongue.—G. K., aged twenty-nine, a 
German shoemaker, came to the throat department of the 
Roosevelt Hospital on July 20, 1887. His family history is 
good. He had typhoid fever when twelve years old; otherwise 
he has never been sick, though always delicate as a child. He 
is a moderate drinker of malt liquors. Nine years ago the pa- 
tient had gonorrhoea and a chancre. He took medicine only 
four weeks, and had no secondary symptoms nor any trouble 
attributable to syphilis until four years ago. At that time he 
began to feel quite weak, but could go on with his work. He 
states that at that time he was treated for syphilis, but since 
then has never felt entirely well. 
The weak feelings continue and he suffers often from pain 
in the back of the head and neck, which occasionally extends 
to the vertex. Last January (1887) he began feeling very much 
weaker, and noticed that he reeled to the left side when walk- 
ing in the dark, and felt dizzy. He says his arras and legs felt 
as though asleep. These symptoms have grown gradually 
worse. Five weeks ago he suddenly noticed an impediment in 
his speech. He also began to swallow with difficulty, though 
he seems undecided as to the time at which this began. He 
says that when he drinks, the fluids come out of his nose. The 
patient has a cachectic appearance. His voice is nasal in tone, 
and he articulates indistinctly. His mental faculties seem nor- 
mal. There is a slight paresis of the left side of the face, notice- 
able both in quiescence and when attempting to smile. He 
can, however, whistle fairly well. His general muscular power 
seems to be much less than one would expect from his appear- 
ance. When he closes his eyes and attempts to walk he falls to 
the left. On protruding the tongue it is seen to deviate mark- TWO CASES OF LARYNGEAL PARALYSIS. 
3 
edly to the left side. There is considerable atrophy of the left 
side of it, apparent to the eye and appreciated by the finger.* 
No loss of taste or of tactile sense can be made out. There is 
no sensory paralysis anywhere. The left palatine arch is com- 
pletely paralyzed. On laryngoscopio examination, the left vocal 
cord is seen immovably fixed in the median line. It seems loose 
and the edge rises slightly with expiration. The right vocal 
cord overrides it somewhat on phonation.f The cords are both 
congested. There is abundant muco-purulent secretion on the 
left side of the naso-pharynx and in the left nostril. There is 
no sterno-mastoid or trapezius paralysis. 
Dr. T. T. Janeway, of this city, kindly made an examination 
of the patient’s vision and of his hearing with the following 
results: 
R- V., Ts/7; with -gV |£. L. Y., with -fa |-£. 
Ophthalm.; R. L. . 
H. D. R. W. = 18". H. D. L. W. = 1". After inflation, 
H. D. R. W. = 18". H. D. L. AY. =O. 
Aerial sound conduction better in both ears than hone. 
Aerial and bone conduction both more reduced in left than 
in right ear. Tuning-fork in median line heard better in the 
right ear. 
T. F. R., aerial, 19"; bone, 8". L., aerial, 4"; bone, 3". 
After inflation no improvement. 
Urinary Examination.—Negative. No sugar. There is no 
appreciable lung lesion. 
Treatment.—The patient was put on large doses of the iodide 
of potassium. The limit of tolerance seemed to be about half 
an ounce daily. During intermissions and along with it were 
given from time to time arsenic and the syrup of the iodide of 
iron. 
The patient was under observation for about a year. Short- 
ly after his first presentation he had three attacks of inspiratory 
* The appearance was similar to the case represented in the “ Berl. 
klin. Woch.,” No. 29, 1887, reported by Pel. 
f I give here the usual appearance. At times I was in doubt as to 
these minor appearances which are nevertheless so important. TWO CASES OF LARYNGEAL PARALYSIS. 
dyspnoea, probably each time from food or drink dropping into 
the larynx. He also had a quite severe attack from an applica- 
tion of the solution of the chloride of iron to the congested 
vocal cords with a brush. At the end of a year, when he passed 
out of observation, there was the following change in his condi- 
tion : 
The dizziness and reeling to the left ceased soon after the 
commencement of the iodide treatment. The difficulty in swal- 
lowing was also soon overcome entirely. Ilis articulation be- 
came distinct, though his voice was husky at times. The slight 
facial paresis disappeared. There was partial though not com- 
plete relief from the palate paralysis. His general muscular 
weakness was relieved so that he could resume work. There 
was no improvement in the lingual atrophy and paralysis, and 
no change in the laryngeal condition. 
A second examination was made by Dr. Janeway four 
months after the first, with these results ; 
Eyes; R. Y., 5 with f L. Y., ; with §•§■• 
Ears; H. D. R. W. 12". H. D. L. W. 
Aerial conduction better in both than bone. 
Bone conduction better in the right than the left. 
Tuning-fork gave increase in duration both of bone and 
aerial conduction, the record being R., aerial, 25"; bone, 10". 
L., aerial, 17"; bone, 9". No improvement after inflation. 
Case 11. Left Laryngeal and Sterno-mnstoid and Trapezius 
Paralysis.—M. M., aged twenty-seven, a married woman and a 
native of Ireland, came to the Dennet Dispensary April 17, 
1888. Her mother died of bronchitis (?); one sister died of 
consumption. 
The patient is an exceedingly nervous and excitable person 
of limited intelligence. When a child she had lumps in her 
neck which disappeared later. Four years ago the patient “got 
a wetting.” Since then she has not been unwell and has had 
“ the whites.” Alcoholic and specific histories are denied. 
Two years ago her voice began to be husky at times and she 
had occasional “choking fits.” There was no cough at that 
time. Six weeks ago the patient began to cough and raise a 
little blood. She had pain in her back and her leucorrhoea in- TWO CASES OF LARYNGEAL PARALYSIS. 
5 
creased. She became short of breath and began to have night- 
sweats with chilly feelings, followed in the afternoon by fever. 
Her appetite is poor. She has lost flesh and strength. 
Examination.—Her general appearance is fairly good. The 
circulation in her extremities is poor. Her voice is exceedingly 
husky. At the apex of the left lung in front there is dullness 
on percussion, crepitant and subcrepitant rales, increased vocal 
fremitus, and roughened breathing. There is great tenderness 
to pressure and percussion over this area, which extends down- 
ward to the upper border of the third rib. Posteriorly the 
signs are not so marked. There is no other pulmonary change. 
There are no cardiac or aneurysmal indications. 
Her voice is unsteady, at times clear, but usually somewhat 
husky. 
The laryngoscope shows the left vocal cord and arytenoid 
cartilage immovable in the median line. The cord itself is con- 
gested and lax, and there is general laryngeal congestion, but 
no swelling or infiltration. The right cord moves spasmodi- 
cally. There is no palate or facial paralysis. There is decided 
paresis of the upper portions of the left trapezius muscle and 
almost total paralysis of the left sterno-cleido-mastoid, but no 
restriction of the movements of the head. 
It will be noticed in this history that the symptoms refer- 
able to the laryngeal paralysis antedated those assignable to 
the lung lesion about two years. The case when last seen was 
running the ordinary course of phthisis in the first stages, with 
no change in the laryngeal symptoms. 
Now, in these two cases we have several points of 
great interest because of the doubts in which they are in- 
volved : 
1. The peripheral manifestations of a central or nerve 
lesion. 
a. The median position of the affected vocal cords. 
b. The concomitant lingual paralysis and atrophy in one 
case and the paresis of the sterno-raastoid and trapezius 
muscles in the other, with other symptoms. 6 
TWO CASES OF LARYNGEAL PARALYSIS. 
2. The character and situation of the lesions, whether 
in the cerebral cortex, the medulla oblongata, or at some 
point of the nerve trunks supplying the various muscles. 
In order to make the conclusions arrived at clearer, it 
will be well to review, as briefly as possible, the literature 
of the subject bearing upon the salient points, and in the 
order named. Of course, it must be understood that noth- 
ing like completeness is intended or aimed at; that would 
be tiresome and useless. 
We need not go back to Galen or even to Albers in 
prelaryngoscopic days, but all the information of use is to 
be found in literature since 1860. 
It will be noted that the term laryngeal paralysis is ap- 
plied to these cases. This is for convenience rather than 
for exactitude of nomenclature. Until recently median 
position of the vocal cords was generally supposed to be 
due to paralysis of the crico-arytasnoidsei-postici muscles. 
As late as 1880 such an authority as Stork (1) said that 
paralysis of the postici was one of the rarest of laryn- 
geal neuroses. A year later Semon (2) showed conclu- 
sively that it was by far the most frequent of all partial 
laryngeal paralyses. Almost simultaneously with the in- 
troduction of the laryngoscope into medicine we find an 
account of a case of median paralysis of one vocal cord. 
Lewin (3) gave, in 1860, a wonderfully good description of 
“ paresis of the muscle of the right arytenoid cartilage 
which narrows the glottis and does not produce hoarse- 
ness,” in a patient suffering from constitutional syphilis. 
In the same year Tiirck (4) described a case of right hemi- 
plegia with immobility of the left vocal cord, which was 
displaced to the right of the median line. Three years 
later Gerhardt (5), who is usually credited with reporting 
the first cases, published his classical work on “ Laryngeal 
Paralysis,” with what appears to be the first account of the TWO CASES OF LARYNGEAL PARALYSIS. 
laryngoscopic appearances of a case of double “ posticus 
paralysis.” He reported eighteen cases of laryngeal pa- 
ralysis in all, and in regard to a cerebral laryngeal center 
contents himself with saying : “ Physiological data do not 
go far here. The superior roots of the accessorius, like the 
neighboring vagus, can be traced to the gray mass on the 
floor of the fourth ventricle.” Many cases were afterward 
reported, and many theories advanced to account for them. 
Baumler (6) and Johnson (7), in 1872 and 1873, and 
later McCall Anderson (8) and Whipham (9), reported cases 
of bilateral paralysis of the vocal cords, some of them in 
the median position, which were due to pressure on one 
vagus nerve alone. Johnson (10), in another and a very 
able paper, explained this phenomenon on the strength of 
the researches of Rosenthal and Waller and Prevost, which 
were repeated by Professor Rutherford at Johnson’s in- 
stance. Pressure on the trunk of the vagus may cause bi- 
lateral spasm or bilateral palsy, or spasm of one and palsy 
of the other side of the larynx, by reflex action due to the 
decussation of the nerve fibers in the medulla, since the 
vagus is made up of both afferent and efferent nerve fibers, 
while pressure on the recurrent alone can only cause paraly- 
sis of the affected side. This he believed to be the cause 
of many cases of sudden dyspnoea in thoracic aneurysm. 
Finally he says: “It is probable that the long-continued 
irritation of the trunk of the vagus may gradually, as in the 
cases of traumatic tetanus, induce such demonstrable struct- 
ural changes in the nerve center as will explain the bilateral 
palsy, which appears to be one of the results of this chronic 
nerve irritation.” We see here a foreshadowing of part of 
what Krause years later announced as the results of his in- 
vestigations. Indeed this article, as pointed out by Semon, 
has not received the attention and consideration it deserves 
in the history of laryngeal neurosis. Cohen’s (11) recent 8 
TWO CASES OF LARYNGEAL PARALYSIS. 
remarkable clinical observation of the stimulation of the 
peripheral sensitive distribution of the pneumogastric in 
the larynx, causing temporary relief to a flagging respira- 
tion, is in line with this early work of Johnson. 
Rosenbach (12), in 1880, called attention to the greater 
frequency of abductor paralysis, and Semon still further 
emphasized the point, showing that adductor paralysis from 
a central or nerve lesion was almost unknown.* Since then 
their respective claims to priority on this point have been 
urged with a persistence and an industry worthy of a bet- 
ter cause and of a more important subject. Various ex- 
planations of this preponderance have been advanced. Ro- 
senbach said that “in the inspiratory closing of the glottis 
following a paralysis of the dilators there is not primarily 
a spasm of their antagonists, but a rhythmical perverse in- 
nervation in one direction only—namely, toward the ad- 
ductors.” This sentence has been widely quoted, probably 
on account of the obscurity of its meaning. It is needless 
to say that it has no experimental proof to stand on, and, 
if I understand it rightly, can necessarily have none, but 
must always remain a theory. Semon supposed the adductor 
and abductor filaments existed separately in the recurrent 
nerve, and advanced three hypotheses to account for the 
median position of the cords. 
1. The abductor nerve fibers may be peripheral, and 
hence more exposed to external injury. 
2. There may be a specific vulnerability of the abductor 
filaments, or when adductor fibers are partially disabled the 
other adductor fibers are able to carry all the adductor 
stimulus. 
* It should be remembered that in complete one-sided paralysis of 
the larynx the vocal cord is in the cadaveric position of Ziemssen, or 
half way between adduction and abduction. TWO CASES OF LARYNGEAL PARALYSIS. 
9 
3. Possibly the nerve fibers receive an increment of 
nerve force from the superior laryngeal. 
McKenzie (13) and Riegel (14) were inclined to accept 
the first supposition, the former suggesting that the nerve 
fibers were peripheral, the latter that they were together at 
one side. Seraon himself leaned to the probability of the 
second hypothesis. It certainly seems to me that claiming 
a “ specific vulnerability ” is begging the question and is 
as unintelligible as Rosenbach’s “perverse innervation.” It 
leaves the problem, Why are the abductor filaments singled 
out for injury? unanswered. 
The third hypothesis has received some support from 
the investigations of Mandelstamm (15) and Exner (16), and 
in Lennox Browne (17) it has a prominent though not an 
unreserved supporter. Many years ago WTeir Mitchell, as 
quoted by Johnson, showed that the movements of the glot- 
tis in the turtle are due to two sets of muscles, the openers 
and the closers. The superior laryngeal nerve supplies both, 
while the inferior supplies only the openers. The superior 
laryngeal nerves were found to decussate at the base of the 
brain like the optic chiasm. The superior and inferior laryn- 
geal nerves were separate throughout their course. If all 
nerves were cut but one superior laryngeal, the larynx move- 
ments would still obtain. Schech (18) and Schmidt (19) sepa- 
rately, in 1873, did much to formulate the arrangement of 
laryngeal innervation and muscular movement given by the 
text-books and accepted up to a recent date. According to 
the investigations of Exner and Mandelstamm, the thyreo- 
arytenoid muscle in its internal division receives its inner- 
vation almost exclusively from the superior laryngeal through 
a branch from its pharyngeal division, which they call the 
middle laryngeal. This muscle is a straightener and tensor 
of the vocal cord, and is supplied by both nerves on each 
side equally. The crico-thyreoid muscle is also supplied by 10 
TWO CASES OF LARYNGEAL PARALYSIS. 
the superior laryngeal nerve of both sides equally, while the 
recurrent probably furnishes some fibers also.* 
“ The interarytenoid muscle apparently is supplied 
equally on the two sides by both the inferior and superior 
laryngeal nerves. It is probable that the other muscles, in- 
cluding the posticus, receive their principal nerve supply 
from the inferior laryngeal, though some of it from the su- 
perior laryngeal. Often the fibers of the superior laryngeal 
reach over to the other side posteriorly.” Some arrange- 
ment of this kind was suspected twenty years ago by Turck 
(loc. cit., p. 440). It has been urged that this arrangement 
does not in itself explain those cases where there is a bilat- 
eral median position with a central lesion, or a lesion in the 
vagus above the superior laryngeal. Neither does it explain 
the cases of Baumler and Johnson, nor why section of the 
recurrent causes total paralysis. 
This brings us to a consideration of the theory of a 
spasmodic action of all the laryngeal muscles, or at least 
the principal ones. 
Although Jeleneffy states [loc. cit.) that he announced 
in 1872 that the condition was due to spasm from irritation 
and not to paralysis, and although the same was hinted at 
by Johnson, as we have seen, the credit of demonstrating 
and emphasizing the fact by experiments on animals be- 
longs to Krause (21). The conclusion he arrived at as a 
result of his very careful experiments was, in a few words, 
as follows: The irritation of pressure or disease, either along 
* I have now a case under observation in which there was appar- 
ently a paralysis of the thyreo-arytenoid muscles with a paresis of the 
crico-thyreoid and interarytenoid muscles on both sides. Besides the 
elliptical opening in the glottis on adduction, the cords had the peculiar 
rounded outline described by Stork. This latter soon disappeared, but 
the laxness of the cords still obtains. This condition supervened on 
the pharyngeal inflammation caused by swallowing carbolic acid. The 
patient is gradually recovering her voice. TWO CASES OF LARYNGEAL PARALYSIS. 
11 
the nerve trunks or in the nerve centers themselves, causes 
a spasm of all the laryngeal muscles, and the adductor 
muscles—resembling the flexor muscles of the extremities, to 
which they have been repeatedly compared—having the 
greater power, cause the vocal cord of the affected side to 
assume the median or adducted position. This position 
may be permanent or it may continue a shorter or longer 
time, and then, from the progress of the disease and a de- 
struction of the nervous elements, change to one of com- 
plete paralysis, when the cords assume the cadaveric posi- 
tion. Of course this is a very crude statement of Krause’s 
very elaborate article, to which reference must be made for 
the full force of the argument. It may be said here that 
complete adductor paralysis from a nerve or central lesion 
is almost or quite unknown, though some good observers 
have confessed their inability to invariably distinguish be- 
tween the cadaveric position and complete abduction. Ad- 
ductor paralysis, usually bilateral, is the rule in the hys- 
terical form, which is never permanent.* 
That Krause’s conclusions have been subjected to many 
and very weighty criticisms can not be denied. His oppo- 
nents, until lately, if not still, are in the majority, but Jele- 
neffy’s work, unless refuted by future investigations, must 
eventually establish the reality of Krause’s conclusions, at 
least in the main. The former states—and his demonstra- 
tions are singularly convincing, at least to the writer—that 
not only is the crico-arytenoideus posticus an antagonist to 
* I have seen one case in which what was without doubt hysterical 
closure of the glottis was so persistent and caused such extreme inspir- 
atory dyspnoea that tracheotomy with artificial respiration for half an 
hour were necessary to save the patient’s life. Lately, after the lapse 
of six years, I have seen the patient, who wore the tube for many 
months. She still has occasional attacks of typical hysterical aphonia 
with an increase in other hysterical manifestations, but she has had no 
return of the nearly fatal dyspnoea. 12 
TWO CASES OF LARYNGEAL PARALYSIS. 
the lateralis in its adducting power, but beyond a certain 
point is in some of its libers a synergist. It also tends to 
fix the arytenoid cartilage on the cricoid, and prevents the 
vocal process from being depressed by the contraction of 
the lower fibers of the lateralis. By its counteraction it 
helps the thyreo-arytenoid and the crico-thyreoid muscles to 
stretch and straighten the vocal bands. It assists the inter- 
ary tenoidens also to approximate the arytenoid cartilages. 
The original article* must be consulted for an explanation 
of this somewhat complicated and yet, according to Jelen- 
effy’s demonstration, very obvious function of the posticus, 
Krause does not deny the possibility of the occurrence of 
posticus paralysis, but a little reflection will convince those 
who have seen many cases of the permanent median posi- 
tion of the cords that it must be a rare one if the above 
view of the action of the posticus is a correct one. Dr. 
Solis-Cohen (loc. cit.) seems to have adopted Krause’s views 
at least as explaining the cases where there is lesion of the 
recurrents. 
In 1885 Hooper (22) noticed in the dog that there was 
forcible abduction of the vocal cord from galvanic stimula- 
tion of the corresponding recurrent nerve when the animal 
was very profoundly anaesthetized, and adduction at other 
times. Krause noticed something of the same phenomenon. 
The former, therefore, said that the abductors belong to 
oi'ganic life, and denied their proclivity to paralysis, Don- 
aldson (23) in the following year said it was only on weak 
stimulation that the cords were abducted, and that the ab- 
duction was not due to the etherization ; but lie also denied 
the greater proclivity of the abductors to paralysis. Semon 
and Horsley (24), while denying strenuously the validity 
of Krause’s views, confirmed the statements of Hooper in 
* See for resum,!} “ N. Y, Med, Journal,” Aug, 31, 1889, TWO CASES OF LARYNGEAL PARALYSIS. 
regard to deep etherization, as well as those of Donaldson 
in regard to weak stimulation of the recurrents, but showed 
that, in repeating Hooper’s experiments, Donaldson did not 
carry the narcosis far enough. 
These authors also stated that in excision of the larynx 
in the living animal the postici muscles lose their contracti- 
bility before the other muscles, but Jeleneffy (loc. cit.) has 
shown that this is due to their smaller size and their more 
exposed condition. While the writer is inclined to accept 
Krause’s views in the main, there are some points which 
are not explained and some which seem to controvert them. 
When Rernak (25) reported his case of lingual and sterno- 
mastoid paralysis with immobility of the right vocal cord, 
from injury to the nerves at the base of the skull, Fraen- 
kel (26) seemed to think that this settled the question, rea- 
soning that because there was paralysis of other muscles, 
there could not be spasm of the laryngeal group, but the 
posticus must be paralyzed. Without at all detracting from 
the force of this objection, which is open to much more 
serious criticism, it might be said that the history of laryn- 
geal paralyses abounds in such examples, and the case of 
Remak is not unique. Case IT, recorded here, is such an 
example. Fraenkel (2V) himself has elsewhere advanced an 
objection that appeared much more vital to the spasm the- 
ory. It can not be denied that even in the cases where the 
lesion is central, and hence including the bulbar origin of 
the superior laryngeal nerve fibers, the vocal cord, although 
in the median position, is often, if not usually, lax during 
respiration, and occasionally is made tense only during 
phonation. It was difficult to see how this could occur dur- 
ing spasm of all the laryngeal muscles. 
Jelcneffy’s article explains how it is that after atrophy 
due to the continued spasm we obtain a condition which is 
practically a paralysis of the posticus and thus allows a lax- 14 
TWO OASES OF LARYNGEAL PARALYSIS. 
ness of the cord to occur from the non-fixation of the aryte- 
noid cartilage and the lack of counteraction to the crico- 
thyreoideus and thyreo-aryta3noideus internes muscles. 
Nevertheless, the objections to the spasm theory are less 
numerous and Aveighty than those of paralysis of the posti- 
cus alone, since it is supplied by the same nerve as most of 
the other muscles. This supposition is unsupported by 
experimental proof, and many well-established facts seem 
utterly irreconcilable with it. But argument is of little 
use. Clinical observation can only serve to keep alive the 
interest in the subject. Physiological experiment and 
anatomical research, repeated and varied, are the only 
methods by which the problem will be solved. 
The concomitant lingual paralysis and atrophy in Case 
lis of only contributory interest to us. Although Fairlie 
Clarke (28), in reporting a case in 1871, declared that he was 
unable to find any case of lingual atrophy reported in litera- 
ture, there is at least one by Dupuytren as long ago as 1832 
referred to by Leudet (29), while Lande(3o) in 1870 re- 
ported five cases. Since then, and indeed before, many 
cases have been reported by the French writers. 
The other symptoms need only be referred to in speak- 
ing of the location of the lesions. In Case II the shoulder 
paralysis would indicate, as in Remak’s case, that we have 
to do with a lesion of the vagus and accessory immediately 
after their exit from the skull. This is still further sug- 
gested by the history of glandular enlargement in the neck 
and by the fact that the phthisis of the left pulmonary apex 
began two years after the laryngeal affection. Moreover, 
the “choking fits ” or “laryngeal crises” to which the pa- 
tient had been subject, and the spasmodic action of the 
right vocal cord, point to an irritation of the vagus, as in 
the cases of Baumler and others mentioned. It is reasona- 
ble to suppose that there was pressure exerted by some en- TWO CASES OF LARYNGEAL PARALYSIS. 
15 
larged cervical gland, although none could be distinguished 
upon examination. 
In Case I, the lesion being evidently an intracranial one, 
we have two possible locations—a cortical and a bulbar. 
The question of a cortical laryngeal center has been the 
subject of some interesting pathological and physiological 
investigations. Lewin (31), in 1874, examined a case with 
left hemiplegia and made out immobility of tbe left vocal 
cord in the middle line. There was no autopsy. So scanty 
are the data upon which to base a reliable localization of a 
laryngeal center in the cerebral cortex from pathological 
evidence, that the laryngoscopic appearance of every case 
of hemiplegia should be recorded for future reference on 
autopsy. Seguin’s(32) cases which were reported in 1877 
tended to show that the lower part of the third frontal con- 
volution of the left side, especially in right-handed people, 
was the seat not only of speech, but of laryngeal move- 
ments, This, however, was far from conclusive, as no la- 
ryngoscopic examination was made. Indeed, until very re- 
cently, either the laryngoscopic or the post-mortem appear- 
ance of these supposed cortical lesions has been lacking in 
each case. Indeed, the case of Grarel (33), so far as I know, 
is the only one in which, with a cortical lesion found at au- 
topsy, there had been in life a laryngeal neurosis noted. 
There was in his case right hemiplegia with aphasia, and 
the left vocal cord was paralyzed, thus resembling the case 
reported by Tiirck many years ago and referred to above. 
Here, however, an autopsy was subsequently obtained, and, 
besides the ordinary haemorrhagic lesion on the left side of 
the brain, there was a localized area of softening in the in- 
ferior part of the third frontal convolution on the right 
side. The report is meager in details and no account is 
given of the microscopic condition of the medulla. Dr. 
Delavan (34), in a recent paper published in this Journal, 16 
TWO CASES OF LARYNGEAL PARALYSIS. 
sums up the general testimony on this point in cerebral 
localization : 
“1. Unilateral irritation of a given cortical center ex- 
cites the corresponding bulbar center and causes bilateral 
movement. 
“ 2. Unilateral destruction of a given cortical center 
gives no result, as the influence of the opposite cortical cen- 
ter is sufficient to excite the corresponding bulbar center, 
and thus to cause bilateral movement. 
“3. Bilateral destruction of a given cortical center 
causes paralysis.” 
Now, from this standpoint we must conclude that there 
was a corresponding lesion of the same spot on the oppo- 
site side. If so, why was there not bilateral paralysis ? A 
lesion on the left side of the medulla, which, without a 
microscopic examination, might have been overlooked, 
would be what we should expect. Garel, however, had a 
physiological basis on which to stand, and this possibly 
may have caused him to be a little hasty in his conclusions. 
Krause (35), in 1884, announced his experiments on the 
brains of dogs. He demonstrated that in these animals 
there was a center for the laryngeal adductors in the gyrus 
prajfrontalis, the third frontal or Broca’s convolution, near 
its anterior and descending end. In the neighborhood were 
also areas for the muscles of deglutition and of the neck. 
The channel of communication from this region to the 
medulla is probably through the corpus mamillarc. 
These statements have been confirmed by Semon and 
Horsley (quoted by Delavan, loc. cit.). The electrical 
stimulation of this cortical area causes different laryngeal 
muscular actions in different animals—adduction in the 
monkey and dog, abduction in the cat. Dr. Delavan in the 
same year (1884) read a paper (36) before the Internation- 
al Congress, at Copenhagen, on a cortical localization of a TWO CASES OF LARYNGEAL PARALYSIS. 
17 
laryngeal center, based on a case very much resembling 
Case I of this paper. This case on autopsy, however, 
showed the causative lesion to be in the medulla. Gott- 
stein, in the last edition of his work on the throat (p. 302), 
in referring to the case, pointed out what afterward proved 
to be the correct situation of the lesion. 
There are a sufficient number of carefully reported cases, 
as well as physiological data, on which to base a diagnosis 
of and locate a lesion in the medulla oblongata. Hugh- 
lings Jackson (37), in reporting some such cases in 1864, 
which were also seen by Mackenzie (loc. cit.), asks the ques- 
tion which now confronts us, “ Where is the disease which 
suddenly produces together paralysis of the tongue, palate, 
and vocal cord, all on one side ? ” 
His answer was more unsatisfactory than ours should be to- 
day, for since then a great deal has been done to supplement 
the work of Claude Bernard, Lockhart Clarke, and others. 
Beginning at the widest part of the floor of the fourth 
ventricle, where the posterior border of the pons Yarolii 
crosses it, we find an irregular mass of gray matter extend- 
ing backward and downward to the posterior end of this 
lozenge-shaped space, where it becomes continuous with the 
gray matter of the spinal cord. Here, from before backward, 
the root fibers of the facial, acusticus, glosso-pharyngeal, 
pneumogastric, and the upper roots of the spinal accessory 
have their origin. This is not only a motor, but a sensitive 
tract. The latter, known as the sensitive or ventral nucleus 
of the vagus, is deeper and a little higher than the dorsal or 
motor nucleus, though they are continuous with one another. 
The nucleus of the hypoglossus nerve is nearer the median 
furrow and parallel with the tract of the other. A careful 
comparison of Case I, with the symptoms noted and the 
lesions found in the cases of Senator (38) and Eisenlohr (39) 
and Delavan [loc. cit.), as well as with others, helps us to a 18 
TWO CASES OF LARYNGEAL PARALYSIS. 
diagnosis and location by pathological evidence. It is proba- 
ble that the lesion was most extended toward the lower and 
in the superficial parts of the mass on the floor of the fourth 
ventricle, where it would involve the nucleus of the hypoglos- 
sus and the motor nucleus of the vagus, leaving the sensi- 
tive tract uninvaded, since there was no sensory paralysis 
of any kind noted. It must have extended upward along 
the median furrow on the left side, involving the nucleus of 
the acusticus and slightly the facial to account for the 
facial paresis, the marked diminution of hearing on the left 
side, and the palate paralysis. The deafness, the difficulty 
of swallowing, and the tendency to fall to the left we saw 
improve under treatment. The lingual and laryngeal pa- 
ralysis remained unchanged, as it usually does. To account 
for the giddiness, we have either to imagine that it was due 
to the involvement of the acusticus or to some interference 
with the blood-supply of the cerebellum. When we come 
to consider the cause and the nature of the lesion, it is 
probable, in view of the specific history and the result of 
treatment, that the patient had areas of softening and con- 
gestion due to disease of the coats of the left vertebral 
artery or its branches, the posterior spinal and the inferior 
cerebellar. The iodide of potassium relieved the areas 
where actual tissue necrosis had not taken place, and pro- 
duced some amelioration of the symptoms, while further 
improvement could not be expected. It is a singular fact, 
noticed by Elsberg (40), that, although other muscular 
groups may recover with varying rapidity and completeness 
from paralysis, the power of the laryngeal muscles rarely 
returns. This may be due to the rapidity with which they 
atrophy on account of their small size. 
Literature. 
1. Stork, “Klinik der Krankheiten des Kehlkopfes,” 1880, 
p, 880. TWO CASES OF LARYNGEAL PARALYSIS. 
19 
2. Semon, “ Archives of Laryngology,” July, 1881, et alidem. 
3. Lewin, ref. Schmidt’s “ Jahrb.,” 1860, No. 108, p. 99. 
4. Tiirck, ref. “ Klinik der Krankheiten des Kehlkopfes,” 
1866, p. 444. 
5. Gerhardt, Virchow’s “ Archiv,” xxv, p. 68, 1863. 
6. Banmler, “Trans, of the London Path. Soc.,” 1872, xxiii, 
p. 66. 
7. Johnson, “Trans, of the London Path. Soc.,” 1873, xxiv, 
p. 42. 
8. McCall Anderson, “Edinb. Med. Journal,” July, 1881, p. 
11. 
9. Whipham, “Trans, of the London Path. Soc.,” 1882, 
xxxiii, p. 82. 
10. Johnson, “ Trans, of the Med.-chir. Soc.,” 1875, vol. 
Iviii, p. 29. 
11. Cohen, “ N. Y. Med. Journal,” August 10, 1889. 
12. Rosenbach, ref. Schmidt’s “Jahrb.,” No. 188, p. 134. 
13. Mackenzie, “Diseases of the Throat,” vol. i, ed. 1880. 
14. Riegel, Volkmann’s “Vortrage,” No. 95. 
15. Mandelstamm, ref. “Monatsch. f. Ohrenheilk,,” Decem- 
ber, 1884, p. 234. 
16. Exner, ref. “ Centralbl. f. Laryng.,” Feb. 1, 1885, p. 
261. 
17. Lennox Browne, “Diseases of the Throat,” 1887. 
18. Schech, resume, “Berl. klin. Woch.,” No. 20, 1873, p. 
234. 
19. Schmidt, “Berl, klin. Woch.,” No. 3, 1873. 
20. Jeleneffy, “Berl. klin. Woch.,” No. 26, 34 et seq., 1888. 
21. Krause, Virchow’s “Archiv,” 1884, No. 98, p. 294. 
22. Hooper, “N. Y. Medical Journal,” July 4, 1885. 
23. Donaldson, “Am. Jour, of the Med. Sciences,” July, 
1886. 
24. Semon and Horsley, “ British Med, Journal,” August 
28, 1886. 
25. Remak, “ Berl. klin. Woch.,” No. 7, 1888. 
26. Fraenkel, “ Berl. klin. Woch.,” No, 8, 1888. 
27. Fraenkel, “Centralbl. fur Laryng.,” 1885-’B6, p. 189. 
28. Fairlie Clarke, “ Brit. Med. Jour.,” July 8, 1871. 20 
TWO OASES OF LARYNGEAL PARALYSIS. 
29. Leudet, “Aim. des mal. de I’oreille,” December, 1887. 
30. Lande, “Arch, gen. de m6d.,” vol. i, 1870, p. 315. 
31. Lewin, “ Berl. klin. Woch.,” 1874, No. 1, p. 10. 
32. Seguin, N. Y. “ Med. Record,” July 21, 1877, p. 463. 
33. Gfarel, “ Revue de laryng.,” May, 1886, p. 248, 
34. Delavan, “N. Y. Medical Journal,” June 22, 1889. 
35. Krause, “ Archiv f. Physiologic,” 1884, Heft 2. 
36. Delavan, N. Y. “Medical Record,” February 14, 1885. 
37. Hughlings Jackson, “ London Hospital Reports,” vol. i, 
1864, p. 361. 
38. Senator, “Archiv f. Psychiatric,” xi, 1881. 
39. Eisenlobr, “ Archiv f. Psychiatric,” xix, 1888. 
40. Elsberg, “Pbila. Med. Times,” July 30, 1881. REASONS WHY 
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