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The Medical Herald

Incorporating the

Kansas City Medical Inder-Lancet

Under the Editorial Direction of

Chas. Wood Fassett and S. Grover Burnett

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CAUTION!-Whenever the true merit of

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This forms convincing proof that only an authoritatively sanctioned article can be relied on.

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MEDICAL

MAY, 1913

Organized at Council Bluffs, Iowa, September 27, 1888. Objects: "The objects of this society shall be to foster, advance and disseminate medical knowledge; to uphold and maintain the dignity of the profession; and to encourage social and harmonious relations within its ranks."-Constitution

MISSO

SIN

SOCIETY

VALLEY

Official Proceedings

THE MEDICAL SOCIETY OF
THE MISSOURI VALLEY

26th Annual Meeting, Omaha, Neb., September, 1913

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A STUDY OF LANDRY'S PARALYSIS.*

E. M. Hummel, M. D., New Orleans, La.

Visiting Neurologist, Charity Hospital; Lecturer on Nervous Diseases, Tulane University.

On March 22, 1912, I was consulted in the case of Mr. R., aged 46, giving the following history: There had occurred no accident of any consequence to his health in early life. Though born in the northern section of this country he had lived since early childhood in the southern part of Louisiana. Late in his teens he was involved in very unfortunate domestic trouble which occasioned him a great deal of worry and intense mental depression. In the midst of this domestic affair, after his physical health had become perceptibly

*The following papers were read before the Medical Society of the Missouri Valley at Kansas City, Mo., March 20, 1913.

affected thereby, he suddenly became paralyzed, first in his legs, but shortly thereafter in his arms and whole body. For some time he was profoundly weakened and came near dying from inability to breathe. After some three weeks, recession of these symptoms commenced, but fully six months elapsed before he was quite well again. During the attack no febrile reaction was noticeable nor was pain or any other sensory disturbance experienced. The sphincters were not disturbed. After the acute symptoms had subsided, the legs and arms were weak, flabby and wasted, and only very gradual recovery from the weakness in his extremities was the occasion of his be

ing sick so long. When 21, the subject contracted a venereal sore, but its exact natrue was not determined nor were any secondary symptoms noticed. Since then a second wife has borne him four apparently healthy children, but has also given birth to two dead ones. In the interval his health has remained good and he has been totally abstemious regarding alcohol and tobacco. He had, however, during the few months preceding his last illness had severe business losses and had worked very hard, riding and walking and subjecting himself to physical exhaustion inspecting timber lands. Exactly one week before the inception of paralytic symptoms he was attacked with a mild case of mumps. He had not quite fully recovered from the effects thereof when he began to experience weakness in the feet, ankles and knees-three days before my first consultation. The weakness in question gradually grew worse, ascending in distribution until at the time of my consultation the arms, trunks and facial muscles were perceptibly though mildly involved. He was quite unable to walk, sit or stand alone. The weakness began first in the right leg and advanced more rapidly on the whole right side of the body. At the inception of the paralysis a sort of aching was felt in the calves of the legs, but this soon passed away.

Physical examination at this time showed absence of the deep reflexes in the lower extremities, plantar reflexes could not be elicited. The cremaster and abdominal reflexes were present and apparently normal. Deep reflexes in the arms were preserved, though diminished. The patient wished. his lips moistened often and said that they felt numb. On this account he was unable to appose the lips perfectly and this rendered his speech somewhat indistinct. Patient likewise frequently insisted that his body felt as though made of wood and complained of numbness up and down the spine. Also when he was placed in packs he insisted upon having the water so hot that the nurse could not tolerate her hands in it. This gave him a sense of comfort and no vasomotor reaction was provoked in the skin. With these exceptions, however, his disability was limited to motor weakness in the voluntary muscle system-the whole condition closely resembling a profound attack of polyneuritis. On the next day the patient was perceptibly worse and was affected with a peculiar psychic disturbance in which he was restless and utterly unable to sleep, and so acutely aware of his condition and its alarming nature that the situation was very distressing. The

psychic disturbance was one in which perception was very quick and keen, a sort of vigil in which all the psychic attributes seemed to be exalted. Sphincter control was still undisturbed. On the following day weakness of the diaphragm and intercostals was so pronounced that the subject was only able to speak in monosyllables and with great effort. He was unable to raise bronchial secretion. I copy the following from my notes of this day: "Weakness is en masse and not partial to either extensors or flexors. The lips are numb; and speech is barely audible on account of paralysis of vocal cords and expiratory weakness. Subject cannot make the facial movements necessary for the expression of emotion. Pupils normal, fundus of eye perfectly clear, there is imperfect control of sphincters today. Wassermann test is found negative. Urine shows few hyaline casts. Blood count gives slight excess of leucocytes but no parasites. Spinal puncture gives clear normal looking fluid which is reported by Dr. Duval as containing slight excess of lymphoid cells. Tests made with faradism give normal response. No temperature noticed. Peculiar vasomotor symptoms are present chiefly as disorder of sweat secretion, perspiration standing out in large drops though the weather is very cool and patient insists on being well covered. At other intervals he feels hot. On the day following, motor weakness was complete and patient developed air hunger from respiratory weakness and was in great distress. Oxygen and artificial respiration gave some relief, but everything considered this was the most pathetic and trying sickroom scene I have ever witnessed, as the patient was acutely aware of the fact that he was surely dying. The heart rhythm was irregular, obviously from involvement of the pneumogastric trunk and nucleus. Death ensued on the following day, eight days from the time of onset. later stages of the condition, notwithstanding the respiratory and circulatory distress, the capillary circulation in the skin remained good, and for four or five hours the skin of the cadaver remained pink and rosy as if life were still present. I think this must have been due to the fact that the sympathetic nervous system did not participate in the toxic weakness.

During the

Although Landry first described this condition in 1859 we do not know much more about it now than then. Many writers have assigned various causes for it, and I have recited the history of my case in rather lengthy detail in order to discuss several points of manifest interest.

that he had depleted his physical strength by excessive exertion and that he had recently sustained an attack of mumps. All this is in strong support of the opinion that lowered resistance is the preliminary necessity in the development of the disease, and the agency of psychic depression is again introduced. The acute infectious fevers are cited by Gowers as among the remote causes of this form of paralysis-its close resemblance to post diphtheric paralysis is especially striking. Gowers further says that syphilis might be indirectly responsible. In the case cited it seems possible that the patient might have become syphilitic between his first and last attack, but I am inclined to disregard this as a causative agent though the circumstances inject another interesting detail in this rather extraordinary case. The blood, urine and spinal fluid were carefully searched but the findings were trivial and the lymphocytosis of the spinal fluid was very mild and what would have been exsuspected in any toxic or inflammatory condi tion involving the central nervous system. A post-mortem would have been interesting but was impossible. Numbers of necropses have been held on the victims of Landry's paralysis but findings in the central nervous organ have been negative except in several cases examined by Immermann where distinct degenerative changes were found in the ganglia of the cord. Westphal has called attention to enlargement of the spleen and Baumgarten discovered organisms in the lymphatic glands. However pathology and bacteriology have both thus far failed of much assistance to us in our study of the disease.

In the first place, I would like to call attention to the fact that this man, judging from facts cited in the history, very probably suffered an attack of Landry's paralysis once before and recovered. Such an assumption is not out of keeping with observations to be found in the literature as a number of well authenticated cases have been known to recover. This fact if admitted tends also to prove that the subject possessed some individual susceptibil ity to the disease. If we analyze the circumstances of the first attack it seems rather probable that the predisposing cause was psychic depression. I do not know that such a cause for the development of Landry's paralysis has ever been claimed, but we are aware that body resistance may be reduced by such influences and in the case of Landry's paralysis it is conceded that various agencies which tend to weaken the organism figure as the necessary preliminary to the development of the disease. The manner in which the subject recovered from the first attack arouses a strong picion that his illness at that time partook of the nature of polyneuritis, but this again is in keeping with the opinion on the part of many writers, especially Cassirer and other German neurologists, who hold that Landry's paralysis is in the nature of a toxic neuritis which involves both the peripheral and spinal nervous system, usually, however, killing the subject before the complete manifestations of neuritis become obvious, such as reaction of degeneration, wasting and sensory disturbance. Eisenlohr has further in his pathological investigations found distinct signs of inflammatory changes in the peripheral

nerves.

The singular way in which the motor paths are overwhelmed while sensation remains only slightly disturbed is not so remarkable when we recall that this is the case in all toxic affections of the nervous system-the sensory structures seeming to be more resistive, probably because of the fact that the sensory tract is of greater organic importance and is constructed of a greater number of neurones from periphery to cerebrum, while the long neurones of the motor tract succumb more quickly. It is doubtful, however, that sensation is totally undisturbed as was suggested in our case by the fact that the subject frequently felt subjective disorder of sensation and that he tolerated great degrees of heat with comfort.

Relative to the final attack we note the very interesting fact that the subject was again under the influence of mental worry

While it must be admitted that no specific organism it likely to be proven the cause of Landry's paralysis it seems that some condition of toxicity springing out of unwonted virulence of some one of the bacterial flora native to the body and operating under the auspices of lowered resistance will be settled upon as the cause of this insidious creeping death for such might we characterize it in its clinical expression.

DISCUSSION.

DR. A. L. SKOOG, Kansas City: Landry's paralysis, as typically outlined in 1859, includes a group of symptoms which restrict the disease so as to make a narrow one. There have been quite a number of cases reported that are analogous to Landry's paralysis, included under that title which undoubtedly should not have been placed there, and this has been demonstrated at autopsies. Some cases of Landry's paralysis have been included which have come under the class of ascending myelitis and cord compression. Landry's paralysis, as described by Landry in

1859, as has been told you by Dr. Hummel, represented a disease entity, as he called it, which was very severe, sudden in its onset and rapid in its course, many of the cases occuring and terminating in five or six days. The mortality rate was likewise very high. I do not believe the essayist mentioned the mortality rate in Landry's paralysis, but it ranges from 75 to 100 per cent. This is rather interesting in the light of another fact, that is that Landry's paralysis is prone to occur in adult life. Children are much less frequently attacked by it than adults. This necessarily brings our attention to another disease, acute poliomyelitis. We know that acute poliomyelitis occurs at almost any age, but the largest number of cases also appear in children from 2 to 6 years of age. Then as we ascend in age the death rate becomes higher. Thus in the neighborhood of puberty the death rate may be approximately 50 per cent. Past 25 the death rate is possibly in the neighborhood of 80 or 90 per cent.

I would not say positively that the case reported is one of Landry's paralysis. I consider this disease as only one type of acute poliomyelitis; in the last few years, and especially through the work of Medin and others quite a number of types of acute poliomyelitis have been described. For instance, we have the frank spinal type, the neuritic type, the bulbar type, the ascending type, the cerebellar, the cerebral, and several other types. Landry's paralysis would include a group coming under the ascending type of acute poliomyelitis. However, there is a group of acute poliomyelitis cases which may be described as the neuritic type, and in some of these cases, beginning as neuritic types, the paralysis may ascend and be called neuritic plus the ascending myelitis type. Psychic depression and also physical exhaustion have been named as predisposing causes. This is quite possibly the case in many instances. We know that with mental and physical fatigue infectious processes are more likely to be engrafted upon the individual. I think that has been shown in some animal experiments with bacteria. Those who have done laboratory work, especially in the past few years with acute poliomyelitis, thoroughly believe it is due to some infectious process. Very recently Flexner and Noguchi have reported an organism as the cause of acute poliomyelitis which they think has been isolated and cultivated. It is yet too early to say they are correct, but I am inclined to believe they

are.

In view of what we know of acute poliomyelitis, that it can be transmitted to monkeys, it would be of considerable interest to have a few cases with frank symptoms of the Landry's type of paralysis and attempt to inoculate animals. It is interesting here again to review the history of acute poliomyelitis with reference to its infectivity. Before the work of very recent years, since Landsteiner and Popper first produced the disease in monkeys a number of organisms were described by different men, especially diplococci. Buzzard and several others have described organisms in relation to Landry's paralysis. Buzzard had one case of Landry's paralysis which corresponded with the original Landry type in which an autopsy was performed and a diplococcus isolated. I am inclined to believe that the diplococci that have been isolated and found postmortem were contaminations due to errors in technic..

An interesting point has been mentioned here regarding the almost uniform absence of sensory symptoms in poliomyelitis. Sensory symptoms, especially paralytic, are absent in acute poliomyelitis. Why does this occur? I am inclined

to believe that it is due to phylogenesis. The motor neuron represents a latter developmental period. Enlargement of the lymphatic glands has been referred to by Dr. Hummel, and we see this plasia of the lymphatic gland in acute poliomyelitis which has been found in a number of cases at autopsy.

I recall

DR. C. C. GODDARD, Leavenworth: the case of a prison physician, a man who was perfectly well, apparently, say this evening. A dog came up to him, he reached out his hand to take hold of the ear of the animal, and found that he could not hold the ear. He tried several times to do so, but failed. He then tried with the other hand, and he was able to hold the dog's ear all right. After a short time he began thinking about this and begun trying to pick up various objects, but he could not hold on to them. He could move and flex his fingers. He went to his room, and the next morning his arm was dead to the world. Very soon the other arm became involved. That morning he thought he was bound to get up. He threw himself out of bed, tried to stand on his feet, and fell to the floor. I was called in consultation for what was thought to be a peculiar case of cerebral hemorrhage or of apoplexy. My diagnosis was Landry's paralysis, or acute ascending paralysis. I said to him, "My friend if you have got anything to do, you had better do it, as you will live but a week." He went on. He could move his feet in bed that day, but from that time on he became completely paralyzed in sensation and motion over the whole body. It started in the left arm, which is unusual, as it generally starts in the feet. His mind was perfectly clear; his pupils were all right at the time he went to bed. He told me that he had a mother in Illinois and asked whether he could get her before he died. I told him he would have to send for her at once. His mother got there the night before he died. He had no pain. He couldn't pass his urine after the second day without the aid of a catheter. He could swallow up to the fourth or fifth day, then paralysis of deglutition set in, and the most horrible thing I ever witnessed was to hear this apparently dead man talking intelligently. He had no trouble with his brain, gradually his pulse became weaker and weaker; he gave a sighing respiration, and was dead. If you have a case of paralysis with these symptoms, look out for Landry's paralysis.

DR. S. GROVER BURNETT, Kansas City: We have had some valuable lessons in this disease and still we are at sea. We know it is a disease as described by the essayist that involves paralytically the muscles of the leg, the trunk, the arms, the respiratory muscles, and the throat, and then the story is usually ended. The patient does not die of toxemia, he dies for the want of air. He dies because he has become paralyzed so far as respiratory function is concerned. It is a question whether there has not been some error in the grouping of the clinical manifestations, or whether we have not the same foundation for two diseases. For instance, we have Landry's paralysis and we have poliomyelitis; we have the bulbar and pontine form; the encephalic form, the polyneuritic, the meningitic, and the abortive form. These have all been described under Lan-. dry's paralysis, but can we neutralize it by asking ourselves the question, is there an end toxin that may attack the central nervous system in different parts? That is a question to be considered in the investigation. Differentially we must remember that Landry's paralysis occurs in men from twenty to forty years of age; while poliomyelitis occurs in babies, small children. We get very few cases

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