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But they were by no means so implicitly accepted by the cotemporary pathologists of France. Broussais, true to his system, traced phthisis to varieties of inflammation, and propounded the notion that tubercles are the result of chronic inflammation of the lymphatics of the lungs. Being personally acquainted with the strong antagonistic feeling entertained by Laennec towards Broussais, I have little doubt that the former was biassed in his views, and framed them in opposition to those of his rival. Another eminent pathologist of that school, Andral, not less remarkable for his powers of observation than for his sound and impartial judgment, was also led to differ from the exclusive views of Laennec, and recognised inflammation as a primary agent in much of the pathology of pulmonary consumption; and he even sought to trace miliary tubercles to an inflammation of individual vesicles of the lung. Cruveilhier also maintained the inflammatory origin of tubercles, and thought that he had produced them artificially in living animals by injecting quicksilver into the bronchial tubes. But although it may be admitted that what is called yellow tubercle may be developed in both the modes thus indicated by Andral and Cruveilhier, yet the same cannot be said of miliary tubercles, the general uniformity of which, in size, shape, and substance, gives them a character quite distinct from that of inflammatory products.

The diffused consolidations, which Laennec called infiltrated tubercle, were soon proved to be of inflammatory origin, a result, in fact, of chronic pneumonia; and as these often form a large part of the lesions in phthisical lungs, the exclusive opinions of Laennec have long ago undergone modification.

One of the earliest critics of the peculiar views of Laennec on the origin of tubercles, was my revered teacher, the late Professor Alison, of Edinburgh, one of

VIEWS OF ALISON AND ABERCROMBIE.

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the most careful observers and soundest reasoners of his day. In a series of papers read before the MedicoChirurgical Society of Edinburgh during the years 1822, 1823, and 1824, he brought forward a number of cases and statistical facts to prove that tubercles and other lesions met with in the lungs of consumptive patients may originate in inflammation. I quote one sentence: 'I have also been led to believe that it is not merely, as Laennec states, a possibility, but a real and frequent occurrence, that inflammation, acute or chronic (to which I would add, and febrile action), however produced, becomes in certain constitutions the occasion of the development of tubercles; and the facts, which seem to me decisive on this point, I propose to lay before the Society.' (Trans. of Med.-Chir. Society of Edinburgh,' 1824, p. 408.) In the same volume, p. 682, is a remarkable communication from another eminent physician of that time, Dr. Abercrombie, On the Nature and Origin of Tubercular Diseases.' The views expressed in this short paper are so important, and have so apt a bearing on recent researches on tubercle, that I am induced to give their substance in a note.1

' After alluding to the complex character of the tubercular masses met with in the lungs, and the consequent difficulty of tracing their nature and progress, he mentions the tuberculous disease in the mesenteric and lymphatic glands as strictly analogous in its nature, and as exhibiting more simply and distinctly its states and stages. He traces the change from simple enlargement (hyperplasia) to increased firmness, and paleness, until it assumes a kind of semitransparency, and a texture approaching to that of soft cartilage. Then appear opaque white spots (caseation), which seems to be the last step in these changes, and strictly analogous to the white tubercle of the lungs. In the most advanced stage, the opaque white matter is most abundant; and this afterwards softens and degenerates into the soft cheesy matter, or ill-conditioned suppuration. From the effect of boiling water on the simply enlarged glands, he concludes that the enlargement is due to an accession of albuminous matter, first soft, but subsequently becoming concrete, and the mass becomes less vascular and less organised; and this albumen increases in proportion to the advance of the disease from simple enlargement to grey consolidation and opaque transmutation. Mesenteric or lymphatic glands, in their natural state, contain hardly any albumen,

These papers of Drs. Alison and Abercrombie appeared during the period of my study in Edinburgh; and I was the more interested in them as some of the cases described by Dr. Alison were under my care in the New Town Dispensary during the years 1823 and 1824. It was not to be wondered at, therefore, when I became a pupil of Laennec in 1825, that, much as I admired and profited by the clinical sagacity and skill of the discoverer of auscultation, I did not accept much of his pathology; and from that time to the present, in all my writings and lectures, I have consistently repudiated his opinions on pulmonary consumption and tubercle as unsatisfactory and unsound.' and are almost entirely dissolved in boiling water. When simply enlarged, about five-sixths are dissolved, the remaining sixth presenting the properties of coagulate albumen. Glands in the advanced state of semitransparent consolidation lose one-fourth by boiling, three-fourths remaining in the state of firm albuminous coagulum; and the white opaque tubercular matter loses still less by boiling, and, when small portions are detached from other structures, they seem to consist almost entirely of coagulated albumen. 'There seems, then, to be some ground for the conjecture that this deposition of albumen is the origin of tubercular disease. It is in the mesenteric and lymphatic glands that we have the best opportunity of marking its progress; but betwixt the various stages of disease in them and the various forms of tubercular disease in the lungs, there is the most close and remarkable analogy. In the bronchial glands we observe the same forms of disease, and according to Portal and other writers of the first authority, glands similar to these exist in very great numbers throughout the whole structure of the lungs, being found at every division of the bronchiæ, however minute. If this be the case, they must pervade every part of the pulmonary substance in such numbers as would readily account for the usual appearance of tubercular lungs, on the supposition that this disease is seated in this glandular structure. For even the larger glands which we find at the bifurcation of the trachea are very small bodies in their natural healthy state; while in the state of tubercular disease, they may acquire the magnitude of eggs, or even a still larger size. I do not, however, contend that tubercular disease is necessarily confined to a glandular structure. On the contrary, there seems every reason to believe that the peculiar deposition which constitutes it may take place from every tissue of the body; in some cases slowly and gradually, in others as the result of a low inflammatory action of a peculiarly unhealthy character.'

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Much as Laennec has done in elucidating the history of phthisis pulmonalis, his opinions on tubercles and other diseased products have always

ORIGINAL VIEWS OF DR. WILLIAMS.

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Adopting, with some modifications, the general opinions of Alison and Andral, I was led by observation and reflection to conclude that the lesions constituting pulmonary consumption originate in either some form of inflammation, or a perverted nutrition, of the textures of the lungs, all tending to further degradation or degeneration, and consequent decay and destruction, of the affected parts. appeared to me artificial and unsatisfactory. Tubercles, according to this author an accidental tissue, are produced-or, according to some of his expressions, spring up-in a healthy tissue without any aid of the vessels of the part, are changed from a greyish semitransparent to an opaque yellowish white colour, and pass from a state of cartilaginous hardness, through intermediate gradations, into that of imperfect liquidity: and all this by a mechanism perfectly unknown, and in a manner entirely unexplained. It is too, in my opinion, without sufficient reason that he identifies the granulations of Bayle with the yellow tubercle-bodies quite different in their physical character-only because the one is generally in time converted into the other. As well might cartilage be called bone, or inflamed cellular tissue a stage of pus.'-Rational Exposition of the Physical Signs of the Diseases of the Lungs and Pleura, p. 154. By Charles J. B. Williams, M.D. (1828.)

I introduce this quotation to disprove assertions recently made by several writers, German and English, that the views of Laennec on tubercle have been generally adopted, and only called in question by Dr. T. Addison in this country, and more fully by German pathologists during the last ten years. My views on this subject were not unknown in Germany, for the little work above quoted was translated into German more than thirty years ago, and passed through several editions, having been used, as I have been told, as a text-book at some of the medical schools in that country.

Another early writer in this country, Dr. W. Stokes, also long ago anticipated the Germans in their opposition to the opinions of Laennec, and advanced views on the inflammatory origin of phthisis, in many points similar to those held in this volume. The titles by which Dr. Stokes designates the varieties of phthisis will sufficiently show this:—

1. Acute inflammatory tuberculisation of the lung without suppuration. 2. Acute suppurative tuberculisation. 3. Chronic progressive tubercle, with signs of local and general irritation; pulmonary ulceration. 4. Chronic progressive ulceration succeeding to an unresolved pneumonia. 5. Tuberculous ulceration succeeding to chronic bronchitis. 6. Tubercle consequent on the absorption of an empyema.'-On the Diagnosis and Treatment of Diseases of the Chest, 1837, p. 414. Allowing for difference in nomenclature, rendered necessary by advances in pathological science, several of these varieties correspond with those described in this work.

In scrofulous constitutions, whether hereditary or acquired, these results might follow any form of inflammation, acute or chronic, membranous or parenchymatous, the products of the inflammation being yellow tuberculous (caseous), tending to softening and irregular suppuration or ulceration, and infecting the system through the blood, breaking out in the form of miliary tubercles in other parts, with or without inflammation. But consumption may arise also in those previously healthy, from various chronic inflammations of the lungs, either following acute attacks imperfectly cured, or arising from the long operation of exciting causes, such as the habitual inhalation of irritating dust of stone, metal, &c., or prolonged exposure to cold and damp.

The prevalent idea to which my study of consumptive diseases led me, as expressed in my first little work in 1828, and in several subsequent editions, was that the consolidations of the lung characteristic of phthisis, instead of being, as Laennec maintained, accidental productions' or heterologous growths' (like cancer), are really merely degraded modifications of the common nutrition of the tissues of the lung, often, but not always, produced by inflammation; and that their disposition to further change and decay is owing to their defective vitality and organisation. The cause of this degradation is to be referred to the low or chronic type of the inflammation producing them, or to a depraved state of the blood from which they are formed.

Thus, in a previously healthy subject, consumptive disease can arise only from inflammation of a low type, or rendered chronic by inefficient treatment, or by the prolonged or repeated operation of its exciting cause. The result is cacoplastic consolidation, of low organisation, red or grey, which tends to undergo the further degradation into opaque and still more disorganised matter (caseous or yellow tuberculous).

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