Further Investigations as to 
the Existence of a Corti- 
cal Motor Center for 
the Human Larynx. 
BY 
D. BRYSON DELAVAN, M. D., 
PROFESSOR OK LARYNGOLOGY IN THE NEW YORK 
POLYCLINIC. 
REPRINTED FROM 
tE&e Neto Yodt jfHefiical journal 
for June 22, 1SS9. Reprinted from the New York Medical Journal for June 22, 1889. 
FURTHER INVESTIGATIONS AS TO THE 
EXISTENCE OF A CORTICAL MOTOR CENTER 
FOR TIIE HUMAN LARYNX.* 
By D. BRYSON DELAVAN, M. D., 
PROFESSOR OP LARYNGOLOGY IN THE NEW YORK POLYCLINIC. 
At the Eighth International Medical Congress, held in Copen- 
hagen in 1884, the writer presented a paper in which attention was 
called to the possibility of localizing in the brain the cortical motor 
center for the human larynx. 
In support of the hypothesis that such a center existed, the his- 
tories of two cases, one of which was original, were related, and 
through them clinical evidence was for the first time brought to bear 
upon the question. 
The study of these cases seemed to suggest the possibility of the 
following conclusions: 
1. That there is a cortical center of motion for the human larynx. 
2. That this center is in the course of the third branch of the 
middle cerebral artery. 
3. That it is toward the proximal end of this vessel. 
4. That it is in the vicinity of the convolution of Broca. 
Although by no means sufficient evidence was furnished to prove 
the above, the subject was one of such unusual scientific interest 
that, with the intention of calling forth discussion and of inciting 
others to its more careful investigation, it was thought worthy of 
presentation. In this respect at least the effort has been successful, 
for since the appearance of the article several others upon the same 
topic have been published, and results of considerable value attained. 
* Read before the American Laryngological Association at its tenth annual 
meeting, September 19, 1888. 2 
THE EXISTENCE OF A CORTICAL MOTOR CENTER 
In the recent work of Gottstein (“ Kranklieiten des Kehlkopfes,” 
Leipsic, 1888) there is given such an excellent synopsis of the litera- 
ture of the subject that it appears unnecessary to reproduce it here. 
In the case reported by the writer in 1884 it was impossible 
then to verify the diagnosis. The patient having since died and an 
autopsy having been made, another instance is now added to the 
small list of those in which a full history has been obtained, and 
among which that reported by Garel (“ Rev. mens, de laryngologie,” 
May, 1886) is the only one in which, corresponding with a paralysis 
of the larynx, a cortical lesion has been found. The complete record 
of the writer’s case is as follows : 
Case I.—Male, aged sixty, retired merchant, family history excellent, 
except for rheumatic diathesis. Has always been very strong and healthy, 
of regular habits, and strictly temperate in the use of alcoholics, but an 
immoderate tobacco smoker. Since middle life has suffered much from 
rheumatism, and has rapidly accumulated fat, but gives no history of any 
other diathesis. Has also suffered from naso-pharyngeal catarrh. Is 
right-handed. In 1876 had a slight attack, attended with vertigo, par- 
tial insensibility, and numbness, but without any distinct paralysis. A 
year later was again attacked, this time with well-marked hemiplegia. 
Although complete insensibility was at no time present during the attack, 
there was intense pain in the back of the head and in the nose on the left 
side, numbness and impairment of motion of the left arm, side, and leg, 
almost total inability to swallow, and, finally, a remarkable change in the 
quality of the voice, which, from having been full, deep, and sonorous, 
was reduced to a cracked, piping, and uncertain tone, which rendered its 
use almost impossible. Articulation was also impaired, the patient for 
months afterward being obliged to pronounce each syllable separately, 
speaking slowly and with difficulty. There was at no time or to any 
degree aphasia. 
There was distinct ptosis, with paralysis of the left side of the face 
and tongue. After continuing two or three days, the general symptoms 
began to subside, beginning with the leg, then the arm, and, last of all, 
the face, and slow but steady improvement continued for many months 
in all the above-mentioned conditions except the voice. In this there was 
little apparent change for some time, but by degrees it became more 
readily controlled and lees discordant, although the high-pitched quality 
has continued up to the present time, together with the loss of power and 
inability to force it. In 1882 a laryngoscopical examination showed the 
existence of complete abductor paralysis of the left vocal band, the posi- 
tion of which was in the median line. The larynx was remarkably easy 
of demonstration, and the diagnosis was afterward confirmed by Dr. 
Clinton Wagner. Laryngoscopic examinations made at intervals since 
1882—one on February 12, 1886, in consultation with Dr. George M. FOR THE HUMAN LARYNX. 
3 
Lefferts, and the last one in January, 1888—have demonstrated no change 
in the position of the cord. There was, however, a slight attempt at rota- 
tion on the part of the left arytenoid, due evidently to the action of the 
inter-arytmnoideus muscle. Efforts made to determine the electrical ‘‘re- 
action of degeneration” proved unsuccessful. To summarize, in a case 
of common left hemiplegia, in which pharyngeal and laryngeal paralysis 
were especially well marked, all of the symptoms disappeared in regular 
order, except those relating to one set of muscles—namely, the laryngeal 
abductors of the left side, and these continued paralyzed for a period of 
ten years. 
Death, due to valvular lesion of the heart and pulmonary oedema, 
occurred April 12, 1888. 
An autopsy was made, twenty-four hours after death, by my friend 
I)r. Frank Ferguson, of the New York Hospital. The brain was ex- 
amined sixty-two hours after death by Dr. M. Allen Starr, with the fol- 
lowing result: 
Arteries.—Left vertebral artery distended to the diameter of one 
fourth of an inch and very tortuous, being de- 
flected forward and outward so as to lie upon 
the outer side of the medulla oblongata be- 
hind the olivary body and upon the ninth, 
tenth, and eleventh nerves at their exit 
(Fig. 1). 
The right vertebral artery was less dis- 
tended and thickened but very atheromatous, 
and occupied its normal position, being, how- 
ever, constricted at its entrance to the basi- 
lar. 
The basilar artery, also much wider than 
normal and intensely atheromatous, had be- 
come elongated so that it pursued a curved 
course, with the convexity toward the right 
upon the pons. 
In both vertebral and basilar firm, calcified plates could be felt, pro- 
ducing such a rigid condition of these vessels that they could not be com- 
pressed by the fingers. At no point in their course, however, could any 
embolus or thrombus be discovered. The posterior cerebral arteries were 
also atheromatous, as were all the smaller branches of these larger trunks. 
The posterior communicating arteries were unusually small and appar- 
ently unaffected by the atheroma. Both carotids were equally atheroma- 
tous with the basilar, calcified plates being easily felt in their walls. 
The middle cerebral artery and all its branches over the island of Reil 
were extremely atheromatous, and this atheroma extended to the finer 
branches throughout the cortex, and was especially marked in some of 
the smaller arteries of the anterior perforated space. 
Fig. 1. THE EXISTENCE OF A CORTICAL MOTOR CENTER 
4 
The anterior cerebral artery of the right side was normal, as was the 
anterior communicating. On the left side it was very atheromatous. 
Eight Hemisphere.—The appearance of the pia mater was that of 
moderate congestion. It was neither oedematous nor opaque excepting 
at one point, about an eighth by a sixteenth of an inch in extent, over 
the posterior extremity of the second frontal convolution near to its 
junction with the ascending frontal convolution, and even here the pia 
was not adherent. 
Left Hemisphere.—Pia congested ; vessels atheromatous; no opacities; 
no adhesions. Cortex of the island of Reil and of the convolutions ap- 
parently normal in all respects. 
Sections made in the frontal direction through the hemispheres from 
before backward, at intervals of one quarter of an inch, showed a normal 
condition of the centrum ovale, corpus callosum, and optic thalamus. 
In the left hemisphere, at the summit of the internal capsule, in its 
anterior half and in the corresponding portion of the caudate nucleus, and 
extending backward, outward, and downward through the entire middle 
Fig. 2.—Section of the medulla near the lower level of the wedge of softening, a, triangu- 
lar softened area; nuc. arc., nucleus arciformis; py., left pyramid ; xii, hypoglossal 
nerve; nuc. xii, hypoglossal nucleus; c. g., column of gelatinous substance of Ro- 
lando ; rad. x asc., ascending root of the vagus (respiratory fasciculus); corp. rest, 
corpus restiforme; rad. v asc., ascending trigeminus root; x, vagus strands ; nuc. x 
dor., sensory vagus nucleus; nuc. x vent., site of the motor vagus nucleus (nucleus 
ambiguus) destroyed hy the softening; m. 1. a., median lateral artery; a. 1. a., an- 
terior lateral artery supplying the sensory vagus nucleus in conjunction with the pos- 
terior median artery, p. m., entering the ventricular floor ; * z, analogue of the posterior 
horn and posterior column nuclei. 
* The vessels are represented schematically and are copied from the diagram in 
Ross’s “ Diseases of the Nervous System,” vol. i, p. '761. FOR THE HUMAN LARYNX. 
5 
body of the lenticular nucleus, was a cavity lined with connective tissue 
and containing a small amount of clear fluid, the remains of a very old 
area of softening. Below and a little outside of this cavity was a small 
Fig. 3.—Section of the medulla near the upper level of the softened wedge. (The floor of 
the ventricle is from a higher level than the pyramids, and the right half of the section 
is higher than the left half.) 6, Decussation of the external arciform fibers at the 
ventral margin of the rhaphe; py., partially degenerated right pyramid with some of 
the external arciform fibers running across it to the hilns of the olive ; x, vagus 
strands; rad. v asc., ascending trigeminal root; c. r., corpus restiforme ; nuc. Beil., 
direct sensory cerebellar tract of Edinger (fascicular portion of Deiter’s nucleus) ; 
rad. x asc., ascending vagus root; e, common sensory nucleus of ix and x nerves; 
8, vertical set of association fibers for the cells of the xii nucleus ; nuc. xii dor., 
dorsal group of cells of the xii nucleus; nuc. xii vent., ventral group of cells of the 
xii nucleus ; x sin., vagus filaments of the left side passing through the softened area 
a ; nuc. x vent., site of the motor vagus nucleus ; xii, hypoglossal filaments. 
space with smooth walls, in which one of the basilar branches of the 
middle cerebral artery had lain. 
In the right hemisphere, at a point in the upper portion of the internal 
capsule in its middle third opposite to the anterior extremity of the optic 
thalamus, a small area of softening was found. This involved the upper 
limit of the internal capsule for about a quarter of an inch from before 
backward, and the upper portion of the outer body of the lenticular nu- 
cleus. 
Sections through the crura, pons, medulla, and spinal cord presented 
nothing abnormal to the naked eye. 
In the right choroid plexus a fatty tumor five eighths by three eighths 
by two eighths of an inch was found in the descending horn of the lateral 
ventricle. In the right crus cerebri, in its middle third, a slight con- 
striction seemed to indicate a descending degeneration in the motor tract. 6 
THE EXISTENCE OF A CORTICAL MOTOR CENTER 
The following report of the microscopical appearances was made 
by Dr. Ira Van Giesen, in the Laboratory of the College of Physi- 
cians and Surgeons, New York : 
Sections of the lower termination of the two central convolutions and 
posterior one third of the third frontal convolution from both hemi- 
spheres show no abnormity in the number or arrangement of the nerve 
fibers or ganglioil cells. Many of the latter are heavily pigmented. A 
focus of softening about 7 mm. in diameter, in the posterior arm of the 
right internal capsule, just behind the knee, involving slightly the optic 
thalamus, has produced a partial degeneration of the right motor tract. 
The left side of a segment of the medulla corresponding to the upper 
three quarters of the olivary bodies contains a wedge shaped mass of soft- 
ening (3 by 4 by 5 mm. in diameter) situated in the path of the intra- 
medullary root strands of the vagus nerve. Near its lower level (Fig. 2) 
the softened mass is triangular in transection. The apex of the triangle 
(corresponding to the thin edge of the wedge) points toward the dorsal 
vagus nucleus and is mm. distant from it. The base (5 mm.) extends 
from the ascending root of the trigeminus to the olive and is about mm. 
distant from the lateral surface of the medulla. The ventral angle passes 
through the convolutions of the olive into its hilum. The dorsal angle 
involves a small portion of the ascending root of the trigeminus. 
The wedge of softening gradually tapers at the expense of its base as 
it passes upward, so that in a section at the entrance of the uppermost 
vagus root bundles (Fig. 3) the ventral angle has retreated from the olive. 
The dorsal angle lies against the ascending trigeminal root, and the apex, 
pointing toward the sensory vagus nucleus, is 2 mm. from it. Thus the 
upper portion of the focus of softening has in section an oval outline in- 
stead of the triangular outline which it presents below. 
The softened mass is not of recent origin, because it is composed 
largely of hyperplastic neuroglia. Many of the vagus root strands, the 
internal arcuate fibers, and some of the vertical fibers of the formatio 
reticularis, pass through the softened region undamaged. A few of the 
thickened anterior and median lateral arteries * running parallel to the 
intramedullary vagus strands also pass through the softened mass. The 
ventral vagus nucleus—nucleus ambiguus of Clarke—and the recurrent 
vagus root strands are present on the right side, but are absent on the 
left side. 
Many of the extra-medullary root fasciculi of the left vagus are de- 
generated. In some places the normal nerve fibers occupy less than one 
half of the volume of the fascicle (Fig. 4). The right vagus root and the 
hypoglossal roots of both sides are normal. The spinal accessory nuclei 
and the first and second cervical segments of the spinal cord are normal. 
The softening was probably produced by an obliterating endarteritis 
* For a description of the blood-vessels of the medulla, Ross’s “ Diseases of the 
Nervous System,” vol. i, p. 761, may be consulted. FOR THE HUMAN LARYNX. 
7 
of the median or anterior lateral arteries (see Fig. 2), which are branches 
of the diseased left vertebral. No area of secondary degeneration was 
found in the left ascending trigeminus root above the softened region. 
Fig. 4.—Transections of left vagus root-bundles, showing the degenerated areas. 
The focus of softening in the medulla, occurring simultaneously with 
the lesion in the internal capsule of the opposite side, was probably more 
instrumental in the production of the permanent laryngeal paralysis, by 
the complete destruction of the ventral or motor vagus nucleus, than by 
interference with the root strands. This I infer from -the fact that so 
many of the root strands pass through the old softened focus intact. 
The degenerated areas in the extra-medullary root bundles of the left 
vagus represent the paths of the motor fibers in them. The left glosso- 
pharyngeal filaments, although not directly involved by the lesion, seem 
to have been in such close proximity to the small upper pointed extremity 
of the softening that a temporary impairment of their functions ensued 
when the softening occurred. The trunk of the vagus was not preserved 
for examination. The results of the microscopical examination prove that 
the laryngeal symptoms were not due to a cortical lesion. The case is 
interesting in confirming clinically the motor character of the ventral 
vagus nucleus. 
Thus it would appear that the theory maintained by Gottstein— 
namely, that paralysis of the larynx of central origin is due to bulbar 
lesion and not to disease of the cortex—receives from this case direct 
confirmation, and that the localization of the cortical motor center 8 
THE EXISTENCE OF A CORTICAL MOTOR CENTER 
for the human larynx still remains, so far as the above is concerned, 
an uncertainty. 
[Since the presentation of this paper, the attention of the writer has 
been attracted to a case singularly parallel with the one herein described, 
reported by 0. Eisenlohe, of Hamburg (“ Archiv fiir Psychiatric,” Berlin, 
vol. xix, 1888, p. 314), in an elaborate article entitled “Zur Pathologic 
der centralen Kehlkopflahmungen.” The patient was a laborer, aged 
thirty-three, in whom, attended with severe dysphagia and aphonia, 
there was found complete left recurrent paralysis, with loss of both 
motion and sensation. There was also paralysis of the left side of the 
velum palati. The post-mortem examination showed a condition of acute 
bulbar myelitis and thrombosis of the medulla, the location of which was 
apparently identical with that of the lesion described above by Dr. Van 
Giesen.] 
On the other hand, collateral evidence to prove its existence con- 
tinues to accumulate. Following the excellent experiments of Her- 
man Krause upon the dog, Victor Horsley and Felix Semon, of 
London, have investigated the question in a series of carefully con- 
ducted experiments upon the monkey, with most interesting results. 
Through the kindness of Mr. Horsley the writer is permitted to 
publish the following resume of facts as to “the representation of 
the vocal cord movements in the cerebral cortex ” : 
1. “In the monkey there is a small area at the lower and anterior 
portion of the foot of the ascending frontal gyrus, excitation of which 
produces complete adduction of the vocal cords (bilateral action). 
We never, in this animal, observed anything but adduction. 
2. “ Around this area there is also represented adduction of the 
vocal cords, but only feebly and in association with other movements 
—i. e., deglutition, etc. 
3. “ Unilateral extirpation of the whole region produced no ap- 
preciable paralysis of the glottis closers or openers. 
4. “ Krause’s statements respecting the position of the center in 
the dog were confirmed by us. 
5. “ In the cat we found that, when the cortex was excited, 
adduction was observed very rarely, but abduction almost invari- 
ably.” 
The foregoing conclusions are extremely interesting, not only by 
reason of the additional proof which they give as to the actual exist- 
ence of a cortical motor center for the larynx, but because of their 
support of, and correspondence with, the recently accepted theories 
of cortical motor activity for voluntary movement, namely : FOR THE HUMAN LARYNX. 
9 
1. That unilateral irritation of a given cortical center excites the 
corresponding bulbar center and causes bilateral movement. 
2. That unilateral destruction of a given cortical center gives no 
result, as the influence of the opposite cortical center is sufficient to 
excite the corresponding bulbar center and thus to cause bilateral 
movement. 
3. That bilateral destruction of a given cortical center causes 
paralysis. 
These very discoveries, however, increase rather than diminish 
the difficulties in the way of solving the problem ; for, admitting the 
foregoing, it is difficult to understand how any unilateral lesion of the 
cortex could cause a corresponding unilateral paralysis of the larynx. 
The hypothesis, therefore, upon which all the hitherto reported clin- 
ical observations relating to this subject have been made would seem 
to be wrong. In other words, paralysis of the larynx of central origin 
must, as a rule, depend upon bulbar lesion and not upon cortical 
injury. 
In short, combining with the arguments of Gottstein, founded 
upon clinical and pathological evidence, the strong testimony of Mr. 
Horsley’s physiological experiments, it can not be denied that, with 
the methods hitherto employed in the human subject, the results 
have been unsatisfactory, and to a certain extent misleading, and that 
the question is not likely to be settled until more successful means for 
its solution have been discovered. That in the human brain such a 
center does exist is made more certain with every succeeding group 
of experiments made upon the lower animals, and, well established in 
the dog and the monkey, it can be but a matter of time for it to be 
unquestionably located in man. REASONS WHY 
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