Paralysis of the Lateral Adduc- tor Muscle of the Larynx, with Unique Case. BY FRANK DONALDSON, Jr., B. A., M. D., CHIEF OF CLINIC FOB THROAT AND CHEST, UNIVERSITY OF MARYLAND J SOME TIME SCHOLAR IN BIOI.OOY, JOHNS HOPKINS UNIVERSITY. REPRINTED FROM Else Ncto York fttebical Journal for February 12, 1887. Reprinted from the New York Medical Journal for February 12, 1887. PARALYSIS OF THE LATERAL ADDUCTOR MUSCLE OF THE LARYNX, WITH UNIQUE CASE * By FRANK DONALDSON, Jk., B. A., M. D., CHIEF OF CLINIC FOR THROAT AND CHEST, UNIVERSITY OF MARYLAND ; SOME TIME SCHOLAR IN BIOLOGY, JOHNS HOPKINS UNIVERSITY. Paralysis of the adductor muscles of the larynx, as is well known, is most infrequent; it is the abductor muscle or nerve which is affected in the vast majority of cases. Semon says in this connection: “ Not only have I never seen such a case, but in the whole range of laryngeal litera- ture which is known to me I have been unable to find a single case in which primary organic f disease of the brain or nerve trunks was proved by clinical observation or the result of post-mortem examination to have been the cause of isolated paralysis of the adductors.” Morell Mackenzie gives five cases in all of paralysis of one lateral adductor; in one case only was there a post-mortem made, and in this, though the muscle itself was atrophied, there was no dis- * Read before the Clinical Society of Baltimore, January 16, JSSY. f The word organic is used because it is well known that the func- tional neuroses show a strange predilection for affecting the adductor muscles. 2 PARALYSIS OF THE LATERAL ease of the nerve trunk. He has met with this form of pa- ralysis after small-pox and from syphilis. Cohen says it may result from organic cerebral disease, from phthisis, from metallic poisoning, from injury to or pressure upon the nerve, etc. However this may be, the affection is very rare, and, although in the following case I have no positive proof of disease of the brain or nerve trunks, I am satisfied that the lesion was a paralysis of the left lateral adductor. Owing to the importance of the observation, I asked my friends Dr. II. Clinton McSherry and Dr. Samuel Johnston to ex- amine the case. They did so upon separate occasions, and both confirmed my diagnosis. Briefly the case is as fol- lows : E. M., a farmer, aged fifty-three, consulted me in August, 1886, for partial loss of voice, which had come on somewhat suddenly eight months before, and which had become gradually worse. He was and had always been a strong, healthy man, accustomed to an out-door life, lie had never been ill in bis life. There was absolutely no history of either rheumatism or syphilis. Some months before I saw him he had suffered, how- ever, with a very severe pain located behind the right ear, fol- lowing which came considerable deafness in the left ear, with loss of voice. On laryngoscopic examination, the left cord was seen in extreme abduction, immobile during respiration and upon phonation; and, although the right cord was well ad- ducted beyond the middle line, there was still a considerable aperture between the vocal bands. The arytenoids were healthy, and this fact was specially noted, for it is well known that symptoms of a paralytic character are produced by de- struction or impairment of one of the crico-arytenoid joints from ossification or other morbid change; and in these cases there is generally some abnormal appearance, such as enlarge- ment or swelling about the base of the arytenoid cartilage. My experience, too, has been that in the latter class of cases there ADDUCTOR MUSCLE OF THE LARYNX. 3 is gradually more or less movement of the cord on the affected side. In the case in question there was absolutely no move- ment. Again, ankylosis of the arytenoid results from a peri- chondritis following typhoid fever, syphilis, rheumatism, or gout, and there was no such history in this patient. Finally, the attack of severe pain behind the ear, with the deafness and loss of voice which followed, pointed to a brain lesion as the cause of the trouble. Treatment was of no avail, and at last accounts there had been no change in the patient’s condition. The uniqueness of this case naturally suggests the ques- tion, Why in both central (brain) and in peripheral (nerve trunk) lesion are the abductors almost invariably affected ? Or, to put it more broadly, why, in such cases, do we find the cord fixed in the middle line (in the phonatory posi- tion) ? There are several explanations of this fact: 1. Semon holds that there is a natural “ 'proclivity'1'1 of the abductor fibers to disease, and he looks on all cases where the cord remains fixed in the middle line as examples of true paralysis of the posterior crico-arytenoid muscle. 2. Krause, on the other hand, maintains that, “ in analo- gy with neurotic manifestations in other portions of the body, organic irritation of the recurrent laryngeal nerve produces spasm of all the muscles supplied by its fibers, both those which preside over the patency of the glottis for the respiratory purposes, and those which preside over the approximation of its edges for purposes of phonation, cough, or expulsion of foreign material; but that, inasmuch as the number and mass of muscles and nerve fibers predominate in the domain for closure, the equilibrium maintained by the respiratory center under normal conditions is overpow- ered, and the spasm therefore manifests itself in the closing phase only, despite the co-existent spasm of the dilator mus- cle. The opinion held, then, is that the phenomenon of 4 PARALYSIS OF TIIE LATERAL permanent fixation is due to the overpowering contracture or final spasm of the contracting muscles of the larynx, and not to a paralysis of the dilating one. The atrophy of the dilating muscle is attributed to its mechanical, not to its paralytic immobility.” Such are the two chief theories with regard to this ques- tion of laryngeal paralysis. I do not propose in this paper to give a list of authorities who agree with the one or the other, but desire here to define my own position in the matter, and to offer an explanation of the phenomena of this so-called abductor paralysis. In a paper read before the American Laryngological Association in 1886, I stated that my experiments gave no confirmation of Semon’s as- sertion. On further consideration, I find this statement too broad. Whereas I was at first inclined to deny Semon’s statement (on scientific grounds), I now go almost as far as he does—i. e., I am fully convinced that the abductor fibers are much more irritable and have much less power of re- sistance than the adductor fibers, and that they die sooner ; though I can not say that I have as yet any experimental (histological) proof that they degenerate more rapidly, after chemical, mechanical, or electrical stimulation, than the ad- ductor fibers. In the experiments related in that paper I also found that the abductor muscles responded to a much weaker stimulus than the adductors did, and that this result inva- riably followed—whether the dog was slightly, deeply, or thoroughly narcotized, whether the animal was eupnceic or apnoeic—when the medulla had been destroyed and after local death had taken place. This important fact (that the adductor muscle does respond to a slighter stimulus) has been confirmed by Semon and Horsley. In a paper “ On an Apparently Peripheral and Differential Action of Ether upon the Laryngeal Muscles,” in the “British Medi- ADDUCTOR MUSCLE OF THE LARYNX. 5 cal Journal” for August 28, 1886, page 405, they say: “ With weak stimuli, other things being equal, abduction of the vocal hands generally occurs, as has been recently shown by F. Donaldson, Jr. We have repeated in a few instances Dr. Donaldson’s experiments, and have, on the whole, obtained similar results.” My observation has, I understand, also been confirmed by a distinguished American physiologist, provided the animal is slightly under ether. Again, I found (and this, too, has been confirmed by Semon and Horsley) that, when after death the recurrent laryngeal nerve was stimulated, abduction disappeared long before adduction, which would certainly show that the ab- ductors die or become exhausted first. In view of the foregoing facts, I am forced to agree with Semon that those cases where the vocal band is found fixed in phonatory position are true paralysis of the abductor muscle, and not spasm of the adductor muscles. Moreover, the constant implication of the abductor muscle may be explained on the ground of the greater irritability of the abductor muscle or nerve fibers. For in cases of unilateral or bilateral lesion of the cords from an aneurysm or tumor the constant pressure exerted by either upon the nerve acts as a mechanical stimulus to it, and the more irritable abductors are, therefore, the first to show the result of this constant stimulation in their loss of function. Another factor in the fixation of the vocal band in the phonatory position in the majority of cases (as shown by Dr. Gowers) may be the mechanical advantage at which the chief adductor acts, as compared with the chief abductor, which gives greater power to the former, since it passes nearly at right angles (while the abductor passes at a very acute angle) to their identical insertion into the muscular process at the outer angle at the base of the arytenoid car- 6 PARALYSIS OF LATERAL ADDUCTOR MUSCLE. tilage. Any loss of power would, therefore, affect the ab- ductor muscle most. Finally, it is but right to confess that my experiments tend to confirm Semon’s conclusion. I hope in a later paper to develop further this theory of a greater irritability of the abductor muscle, which I think goes a great way toward explaining its so frequent pa- ralysis. REASONS WHY Physicians should Subscrite - FOR - The NewYork Medical Journal, Edited by FRANK P. FOSTER, M. 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