tions that I know of are, the cases in which the muscles are either poisoned by some material present in them as, for example, in the paralysis of lead-palsy, the cramps of cholera; or disorganized by fatty degeneration, as we see in the heart, the muscles of disused limbs, &c. In these cases, the disease is radically and pri marily muscular. In all other cases, muscular disturbance is but the index of nervous disease. Hence the very fact that the phenomena of asthma are muscular, is all but proof positive that the nervous system is the seat of the primary derange

ment.

2. That the phenomena of asthma-the distressing sensation and the demand for extraordinary respiratory efforts-immediately depend upon a spastic contraction of the fibre-cells or organic muscle, which minute anatomy has demon

strated to exist in the bronchial tubes.

Although this is a proposition that many perhaps might think it hardly worth while to set about proving, yet I think it will be well not to assume it, partly for the reasons I have already mentioned (the general absence, namely, of precise pathological views on the subject), partly because it is a necessary stepping-stone to the succeeding propositions, and partly because I think its proof will be the best way of expressing my notions of the ultimate pathology of asthma, and my reasons for them. It will certainly be an advantage if it can be shown beyond cavil that spasmodic stricture of the bronchial tubes is the only possible cause of asthma, that it is adequate to the production of all the phenomena, that it is a form of perverted physiology that may exist pure and uncomplicated with any organic disease, and that the view that would assign it as the sole essential condition in asthma is what all pathological views should be-physiological and rational. I think perhaps the eliminative or exhaustive method of proof will be as good as any.

I will suppose a case of severe uncomplicated asthma, such as we sometimes see. Now, what have we here? We have, as the sole constituent symptom, dyspnoea -dyspnoea of a peculiar kind—sudden in its access, intense, and agonizing, following a state of perfect apparent health and ease, and relapsing as suddenly, possibly, and speedily, and perhaps without any expectoration, into ease and tranquillity again. What, then, can give rise to such phenomena as these? We know that the only way in which such an arrear in the respiratory changes as produces a sense of dyspnoea can be brought about, is by a derangement of the supply of one or both of the two fluids, the air or the blood, or by a disorganization of the functioning portion of the lung. On what recognised diseases, then, can we fall back, as supplying in such an instance the necessary conditions? On heart-disease, possibly, bronchitis and emphysema. But if we examine the heart, we find it all right, it cannot then be that. The mucous membrane of the air-passages could not assume and relinquish a condition of inflammation so suddenly; and moreover, to produce such dyspnoea, the inflammation must be intense, and could not fail to give rise to the results of inflammation, yet none such are thrown out. There is not necessarily any mucous exudation; crepitation or expectoration may both be absent. Besides, it would be impossible for bronchitis to exist to such an extent as to give rise to the amount of dyspnoea, without producing the constitutional signs of inflammation; but none such are present-the patient is not ill, he is wheezing and labouring-he passes from a state of health to a state, not of illness, but of dyspnoea, and back again from dyspnoea to health: there are no sequela, there is no convalescence. It cannot therefore be bronchitis. Emphysema we know it is not, for the dyspnoea of emphysema is constant and unvarying, and moreover, we listen to the breathing before and after the attack, and find evidence that the spongy structure of the lung is perfectly healthy. We see, then, that in none of the three ways in which dyspnoea is ordinarily produced-on the side of blood-supply, on that of air-supply, or on that of injured functioning structure,by heart-disease, emphysema, or bronchitis respectively-can the symptoms of asthma be explained. Moreover, the character of the dyspnoea is altogether peculiar; it is utterly unlike either of the three dyspnoeas that have been mentioned.

Heart-dyspnoea is intolerant of the slightest exertion, or of the recumbent position, and sitting up, or stillness, may cure in two minutes the most violent paroxysm. The breathing, too, has rather a panting and gasping than the wheezing, labouring character of asthma. Bronchitic dyspnoea is short, crepitous, and accompanied with cough; asthma, often long-drawn, dry, and without cough. In pure emphysema, the dyspnoea is abiding, varies but little, and has no wheeze.

But the dyspnoea of asthma tells a plainer tale than this; it tells us not only what it is not, but what it is. It gives the most positive evidence of narrowing of the air passages. The asthmatic's breathing is what our forefathers called "strait," what we call "tight;" he feels as if a weight were on his sternum, as if his chest were compressed, as if a cord bound him, as if it would be the greatest relief to him if some one would cut his breast open and allow it to expand; he rushes to the window to get air, he cannot tolerate people or curtains about him, his clothes are loosened, and all the muscles of respiration tug and strain their utmost to fill his chest. But he can neither get air in or out, he can neither inspire nor expire -his respiration is almost at a dead-lock; he cannot blow his nose, can hardly cough or sneeze, cannot smoke a pipe, and if his fire is failing, cannot blow it up; he has hardly air enough to produce the laryngeal vibrations of speech. The chest is distended, indeed, to its greatest possible limit, the cavity of the thorax is enlarged both in the costal and diaphragmatic directions; the costal distension is shown by the fact that a waistcoat that would ordinarily fit will not meet over his chest by two inches, while the descent of the diaphragm is shown by the increased girth of the abdomen and by the heart being drawn down to the scrobiculus, where it is seen beating plainly; such are the violent instinctive efforts of the respiratory muscles to overcome the obstruction to the access of air. But they are unavailing; the air that is without cannot get in, and that which is within is locked up. In spite of the violent muscular effort there is hardly any respiratory movement, the parietes of the chest cannot follow the action of the muscles; on listening to the chest, the respiratory murmur is inaudible, even when not drowned by the wheezing; respiration is almost nil. Where, then, can this obstruction to the introduction and exit of air be? It must be in some part of the air passages -the larynx, trachea, or bronchial tubes. In the larynx and trachea we know, from the symptoms, it is not. The fact of bronchial stricture, then, is certain.

The very intensity of the dyspnea, too, its agonizing and laborious character, implies that the seat of the mischief is in the air-passages. Dyspnoea is essentially remedial, and tends directly, both by its sensory and muscular phenomena to diminish and relieve its cause. As soon as respiration is not going on satisfactorily, the sense of dyspnoea or want of breath, at once prompts to more violent respiratory efforts, which tend to relieve it. The distressful sensation is an essential link in the chain-it gives warning of the condition to be remedied, and is the irresistible stimulus to the remedial efforts. But this sense of dyspnoea, being in its nature remedial, would be likely to be felt only in those cases in which the condition giving rise to it could be remedied by those extraordinary respiratory efforts to which it irresistibly prompts. Now, consistently with this view, I think I have noticed a very curious law with regard to dyspnoea-it is this, that it is proportionate, not to the amount of injury done to the organ, but to the amount of relief that the condition admits of by extraordinary respiratory efforts. If the parenchyma of the lung, its functioning structure, is injured, no amount of respiratory effort will better the condition, and accordingly violent dyspnoea is not induced. Thus, half the lung may be destroyed by phthisis or solidified by pneumonia, and the tranquillity of the respiration be hardly interfered with: a little hurried, perhaps, but no distress or violent effort. But if, while the lung-substance is healthy, the free access of air is prevented, violent and distressing dyspnoea is immediately induced as in croup, laryngitis, the sudden infarction of a large bronchus. For here, if the air could only be got in sufficient quantity to the healthy functioning structure, the balance of the function would be completely restored; hence it is that such cases are always characterized by those violent respiratory efforts which

have for their object the freer introduction of air, and that urgent sense of want of breath which is the constituted stimulus to these efforts. We recognise, therefore, in the very urgency of asthmatic dyspnea, evidence that the mischief is in the air-passages, and that it is of such a nature as to shut off the air-supply. But the sounds of asthma give us perhaps still more certain and circumstantial evidence as to the condition of the bronchial tubes. We know in health that respiration is noiseless, but that when the breathing becomes asthmatic it is accompanied with a shrill sibilant whistle. We know, too, that hollow tubes give no musical sound, when air rushes through them, if they are of even calibre, but if they are narrowed at certain points, if their calibre is varied, the air in them is thrown into vibrations, and they become musical instruments. The wheezing of asthma, then, is as positive evidence of bronchial contraction as if we could see the points of structure-it is physical demonstration.

Now, in what ways may the bronchial tubes be narrowed? In four, I think, as shown in the accompanying diagram: by a plug of tenacious mucus, partly closing the passage, Fig. 1, a; by congestive or inflammatory thickening of the mucous membrane, Fig. 2, b; by plastic exudation thrown out in the sub-mucous areolar tissue in severe bronchitis, and undergoing subsequent slow contraction (as we see in œsophageal and urethral stricture), Fig. 3, c; and by contraction of the circularly-disposed organic muscle which exists in the bronchial wall, Fig. 4, d. This last is spasmodic stricture; the other three are not; the first is no stricture of the tube at all; and the second and third are inflammatory stricture; the second recent, vascular, and mucous; the third old, fibrous, and submucous. In all these ways the column of air in a bronchial tube may be constricted, and the tube converted into a musical instrument-the seat of a sound that will be rhonchus or sibilus, of high or low pitch, according as the tube is large or small. Now, which is the cause of the sound in the cause before us-the sibilus of asthma? The sibilus depending on a plug of tenacious mucus sticking to the side of the tube is generally (always ultimately) relieved by coughing; the sibilus of asthma is never affected by coughing. Vascular tumidity of the mucous membrane can never be dissociated from the symptoms of existing bronchitis, and the sibilus arising from it is not of transient appearance and disappearance; the sibilus of

8

54

Diagram showing the four ways in which the bronchial tubes may be narrowed. 1. Bronchial catarrh. 2. Recent bronchitis. 8. Old bronchitis. 4. Asthma.

asthma, however, may come one minute, and the next be gone, and is ever changing; moreover, the signs of bronchitis are absent. The sibilus arising from the contraction of plastic exudation thrown around the tube is unvarying and irremediable -a permanent condition, and must have been preceded by some recognised attack

of severe bronchitis; the wheeze of asthma, on the other hand, ceases with the paroxysm, and there need not have been bronchitis in any part of the previous history of the case. We have thus got rid of three of the possible causes of sibilus--we have seen that in the case before us (asthmatic wheezing) it cannot be produced by mucous plugging, by vascular tumidity of the mucous membrane, or by the slow contraction of old plastic exudation thrown around the tube. Muscular spasm alone remains. And should we have in this a condition consistent with all the phenomena, and sufficient for their production? Perfectly. The supposition of spasmodic stricture of the air-tubes would explain the sudden access and departure of the dyspnoea, for it is a state that may be instantaneously induced, and may instantaneously vanish; it is consistent with perfect health in all other respects, with the absence of all organic disease or vascular disturbance in the lungs (except that which results from it), with the kind and characters of the sounds generated, with the particular type of the dyspnoea, with the effects of remedies, and with all those circumstances that point to the nervous nature of the disease, such as its causes, the effect of emotion, its periodicity, &c.; for only by the production of muscular contraction of their walls can nervous stimuli affect the condition of the bronchial tubes; everything, therefore, that points to the nervous nature of the disease, points to spasmodic bronchial stricture as its proximate pathological condition.

Thus we see by evidence as certain as sight, that in asthma bronchial spasm must and does exist, and that no other conceivable supposition will explain the phenomena. And we see this independently of that anatomical and physiological support that dissection and experiment supply, and that has hitherto been the chief evidence adduced.

But we find in the muscular furniture of the bronchial walls and the nervous furniture of the whole bronchial system, a valuable confirmation of the correctness of these views, both negatively and positively; for while their absence would be a sad stumbling-block in the way of our inferences from other evidence, their presence supplies exactly the required machinery. Nay, more, it is the most positive proof that could possibly be, that muscular contraction of the bronchial tubes does take place. For, what is the purpose of circularly-disposed muscle, if not to vary the calibre of the tube it invests? The muscular coat of the bronchiæ consists of circularly-disposed bands of fibre-cells, forming a continuous layer immediately beneath the mucous surface; these fibre-cells may be seen in tubes of great minuteness-as small as one-tenth or one-twelfth of a line in diameter. The nervous system of the lungs is derived from the vagus and the sympathetic and the anterior and posterior pulmonary plexus, and is from these origins furnished with wide-spread and varied connexions. It is the wide-spread nervous connexions that can alone explain some of the phenomena of asthma to which I shall have presently to refer. The nervous system of the lungs, thus derived, consists of ramifying plexuses, supported by the bronchial tubes as upon a scaffolding, and conducted by them to every part of the lungs. These plexuses form a sort of network, investing the bronchial tubes even to their finest ramifications, and are furnished with microscopical ganglia.

But besides this anatomical evidence, we have the positive proof of direct experiment; for Volkman, C. J. B. Williams, and others, to whose accounts I must refer the reader, have clearly shown that the bronchial tubes undergo contraction, in some cases even to complete occlusion, from the application of various stimuli, both to the tubes themselves and to the trunks of the pneumogastric nerves. This completes the chain of evidence.

3. That the phenomena of asthma are those of excito-motory or reflex action. Whenever the peripheral application of a stimulus results in muscular motion, we say that the phenomena are reflex. And so they are, universally. As far as our present knowledge goes, we believe that a stimulant applied to a sentient surface or organ must first be transmitted to a nervous centre by incident, and thence reflected by motor filaments, before it can affect the muscular tissue and stimulate

it to contraction. The nervous centre may be a ganglion of microscopical minuteness, and the filaments emanating from it to their peripheral distribution may be of extreme shortness; but still, however near the seat of movement may be to the seat of stimulation (and this may be completely concident), such a centripetal and centrifugal course, and such an intervention of a centre, are essential. We see a very good example of this kind of reflex nervous action in the peristaltic movement of the intestines. In this case the stimulus travels along à perceptive filament to one of the ganglia of the abdominal portion of the sympathetic; there it comes into relation with a motor filament, and is by it transmitted to the muscular wall of the intestine. Of just such a nature is the contraction of bronchial tubes in obedience to sources of irritation applied to their internal surface: the filaments distributed to the mucous surface receive the impression, along them it travels to some of the scattered ganglia of the pulmonary plexuses, and thence returns by motor filaments to the bronchial muscles to which they are distributed. This is the normal function of the bronchial nervous system; it is for the production of bronchial contraction, in obedience to stimulus thus applied, that it is especially organized. It is by this reflected path that the surface-stimulation arrives at and contracts the muscular wall. It is in this way that the bronchi know when and where to contract; that a plug of mucus produces a circumscribed strait through which cough drives it with greater force; that exudation occupying the capillary bronchial tubes is expelled by their peristaltic contraction; that offending material that has found ingress through the glottis is shut off by bronchial stricture from reaching the ultimate lung-structure supposing, that is, such actions really take place.* In asthma from the effluvium of hay, and of certain animals, as cats and rabbits; asthma from inhaling the emanations from ipecacuan powder; asthma from breathing ammoniacal or carburetted fumes; asthma produced by certain airs; asthma complicating bronchitis,-in all these the bronchial spasm is of this natural, physiological character; the seat of the application of the stimulus, and its reflected path, being the same as that by which ordinary stimuli arrive at, and produce contraction of, the bronchial muscle.

But one of the peculiarities of asthma is that it may be induced by stimuli applied to remote parts; in these cases the nervous circuit is much longer, and the phenomena of reflexion clearer and more conspicuous. Take, for example, that most common of all the varieties of asthma, what we may call peptic asthma, in which the induction or prevention of attacks is entirely controlled by the state of the digestive organs, in which an error in diet-the eating some particular thing, eating too largely or late in the day-is sure to bring on an attack; while a certain dietetic abstention is as certain to be attended with immunity from the disHere the reflex character of the phenomena is clear, and the nervous circuit by which the reflexion is completed conspicuous and evident. I think there are three degrees of remoteness of the application of stimulus producing asthma, and thus three groups into which we may divide these clearly reflex cases.

ease.

1st. Those that I have just mentioned, in which the source of irritation is alimentary, and generally gastric. Here the nerve irritated is the gastric portion of the pneumogastric, by which the stimulus is conducted to the medulla oblongata; this is probably the seat of the central reflexion, and transmits the stimulus immediately to the lungs by the pulmonary filaments of the same nerve, the bronchial muscles contracting in obedience to this reflected stimulation, just as they would have done if it had been primarily pulmonary. Here we have only one nerve concerned the pneumogastric, but two portions of it, one of which plays an afferent and the other an efferent part, while the portion of the centre involved is confined to the origin of the nerve-to the seat of implantation of these respective gastric and pulmonary filaments.

2nd. Those cases in which the irritation is more remote, but is still confined to the organic system of nerves-e. g., asthma produced by a loaded rectum.

* For a further discussion of this point I must refer the reader to the concluding paragraphs of this paper.