Asthma, like other neuroses, is much more frequent among the educated and refined than among the coarser and more ignorant classes of society, and those leading luxurious lives are more liable to the disease than those of simple and frugal habits. Of the various professions, those which involve much exertion of the voice furnish the largest contingent; hence it is common among public speakers, clergymen, and lawyers.
In former days the retrocession of cutaneous eruptions was supposed to play an important rôle in the production of asthma, but of late years this theory of causation has found but few advocates among intelligent physicians, the only author of any prominence who still adheres to it being Waldenburg, who has proposed to designate such cases as a. herpeticum.
PATHOLOGY.—We have elsewhere alluded to the various theories with which the older writers endeavored to explain the phenomena of asthma, and need not here refer to them again.
The first step toward a truly scientific theory of the pathology of asthma was the discovery by Reisseisen of the smooth muscular fibres of the bronchial tubes. These fibres are found not only in the large and medium-sized bronchi, but even in those of the smallest calibre, Kölliker having demonstrated them in bronchioles 0.18 millimeter in diameter. It was ascertained by Williams that by irritating the lung he could cause contraction of these fibres, and Longet subsequently proved that the same effect could be produced by galvanizing the pneumogastric nerve. Guided by these important discoveries, most modern pathologists have arrived at the conclusion that bronchial asthma is a spasmodic contraction of the middle and finer bronchi, dependent upon some derangement in the function of the pneumogastric nerve. This, the so-called spasmodic theory, is not entirely new, Willis, as we have before stated, having described as early as 1682 a variety of asthma which he believed to be the result of a "spasmodic action of the muscles and nerves of respiration," and to which he applied the term "asthma convulsivum." Although revived from time to time, it was not until some two hundred years later, and after Romberg had definitely settled the question of the essential character of the disease, that the spasmodic nature of asthma received general recognition. Bergson adopted it in his prize essay in 1840, and ten years later it found a warm supporter in the person of Hyde Salter, whose valuable contributions have added so much to our knowledge of bronchial asthma. The theory that asthma is due to spasm of the bronchial muscles met with but little opposition until 1854, when Wintrich, after a series of experiments, arrived at conclusions directly opposed to those of Williams and Longet in regard to the contractility of the muscular fibres of the bronchi, and refused to accept the spasm theory on the ground that it afforded no rational explanation of the phenomena of asthma. He believed that the various symptoms of that disease were due to tonic spasm either of the diaphragm alone or of the diaphragm and the other muscles of respiration. These experiments of Wintrich were so carefully conducted, and his standing as a specialist in respiratory diseases so high, that his theory found many supporters, and might perhaps have been generally accepted had it not been for the distinguished French physiologist, Paul Bert, who in 1870, with improved methods of scientific research, succeeded in demonstrating that Williams and Longet were after all correct in their statements as to the contractility of the bronchial muscles.
One of the most zealous advocates of the spasm theory of asthma, and at the same time its most learned expositor, is Biermer,13 whose classical lecture on that disease, which appeared a short time after the publication of Bert's experiments, is perhaps the most satisfactory work ever published on the subject. He defines bronchial asthma as a "neurosis depending upon tonic spasm of the bronchial muscles and caused by faulty innervation of the pneumogastric nerve." He claims that this theory is confirmed by clinical experience—that the suddenness with which the attack comes and disappears, and the long and forced expiration with the sibilant râles and other evidences of stenosis which accompany it, admit of no other explanation. In support of this view he calls attention to the rapidity with which the paroxysm yields to chloral, all of its symptoms disappearing within from five to ten minutes after the administration of a moderate dose of that agent. Wintrich and his supporters, besides denying the contractility of the bronchial muscles, object to the spasm theory that the distension of the thorax and descent of the diaphragm, both constant symptoms, are incompatible with spasmodic closure of the bronchial tubes, and that constriction from such cause by impeding the entrance of air into the alveolæ would be more likely to cause diminution in the size of the thorax than its enlargement, and that the diaphragm, instead of descending, would be drawn upward. Biermer acknowledges that this to a certain extent is true, and concedes that constriction of the tubes would interfere with both acts of respiration, but claims that it does not do so to the same extent in the two movements. The spasmodic constriction acts as a sphincter which is readily overcome during inspiration, but prevents the escape of air during expiration, the latter movement being slower and less complete than the former. Were the expiratory pressure exerted upon the contents of the alveolæ alone, it would readily overcome the spasmodic constriction of the bronchi, but it also compresses at the same time the bronchioles. "When the bronchi are spasmodically contracted, they are subjected during expiration to the general pressure of that movement plus the pressure of the spastic contraction of the bronchial muscles. The walls of the bronchioles being soft and compressible, the expiratory pressure, instead of overcoming the obstruction and opening them, would tend to close them all the more tightly." He calls attention to an analogous condition which obtains in capillary bronchitis, when, owing to swelling of the mucous membrane and to the accumulation of secretion in the tubes, the alveolæ are cut off. Here, too, the expiratory pressure is often sufficiently powerful to overcome the obstruction, but if under these circumstances it is too feeble, collapse of the lung ensues. When, on the other hand, the inspiration is strong enough to overcome this obstacle, air enters the alveolæ, and, being imprisoned there, causes inflation of the air-cells as in asthma. That collapse of the lung does not occur in the latter disease is due to the fact that the inspiratory act is always sufficiently powerful to overcome the spastic contraction of the bronchioles.
13 A. Biermer, "Ueber Bronchial Asthma," Sammlung klinischer Vorträge, No. 12, Leipzig, 1870.
The air entering the lung during inspiration is pent up by the spastic constriction of the bronchi, which, acting as a valve, admits of its passage in one direction, but impedes its escape during expiration, and thus causes inflation of the air-cells and insufficient aëration. Owing to the distension of the alveolæ the thorax is expanded and the diaphragm forced downward. A tetanic spasm of the diaphragm lasting for hours, such as that which Wintrich describes, and with which he endeavors to explain the descent of that muscle as well as the other symptoms of asthma, is not only improbable, but is contrary to clinical experience. If the diaphragm were thus spasmodically contracted, it would remain fixed in one position, but Biermer has demonstrated that there is more or less rhythmic movement of that muscle even during the paroxysm; but if no movement of the diaphragm were observed, it would still be no proof of tonic spasm of that muscle, as its immobility might be due to other causes. According to Biermer, the inflation of the lungs and their insufficient ventilation afford a satisfactory explanation of the most important symptoms of asthma, as Breuer14 has shown, in his paper on the automatic regulation of respiration through the pneumogastric nerve, that various embarrassments of respiration must be corrected by some suitable modification of the act itself; hence when, as in asthma, the lung is unable to empty itself, the expiratory act must be strengthened and prolonged to overcome the obstruction occasioned by the spasmodic constriction of the bronchial tubes; whereas incomplete filling of the lung would necessitate increased inspiratory effort. According to Biermer, "expiratory dyspnoea is as characteristic of obstruction of the finer tubes," be it from spasm, as in asthma, or from stoppage with viscid mucus or from swelling of their lining membrane, as in bronchitis, as the same condition during inspiration is of narrowing of the larger air-passages—an important point in differential diagnosis to which we shall again have occasion to refer. He is unable to explain the relationship between bronchial spasm and catarrhal hyperæmia of the air-passages, but believes that it may be accounted for as follows: "Either the bronchial fluxion causes the spasm—that is, that there exists between them a causal connection—or the hyperæmia and the spasm are the joint effect of the exciting (centripetal) nerves; in other words, both are due to reflex action."15
14 "Die Selbsterneurung der Athmen durch den N. vagus," Sitzungsbericht der K. K. Akademie der Wissenschaften zu Wien, Bd. lviii. Abtheilung ii., Nov., 1868.
15 In presenting Biermer's theory the writer has drawn freely upon that author's well-known lecture on "Bronchial Asthma," as published in Volkmann's Sammlung klinischer Vorträge, loc. cit.
Another explanation of the phenomena of asthma is that proposed by Lebert,16 who, although he concedes that bronchial spasm is an all-important factor, denies that it of itself is sufficient to account for the sudden and enormous inflation of the lungs observed in that disease. He doubts the possibility of a valvular closure of the bronchi, as claimed by Biermer, but believes that the bronchial spasm, which he regards as primary, causes secondary spasmodic contractions of the diaphragm and of the inspiratory muscles of the neck and chest. The spasm of the diaphragm he believes to be tonic in its character, but not continuous, thus meeting Biermer's objection to the Wintrich theory, that tonic spasm of that muscle lasting longer than a few minutes would inevitably cause fatal asphyxia.