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brown, until the cholestearine is converted into a brownish drop. Sulphuric acid alone produces a fatty-looking substance which is neither cholestearine, nor any special combination of cholestearine and sulphuric acid, but a product of the decomposition of the former. Sulphuric acid alone also produces very beautiful phenomena of colour with cholestearine.

If now, gentlemen, we trace the development of the atheromatous condition a little farther back, we come—anteriorly to the period when the pultaceous matter is found in the seat of the atheroma—across a stage, where nothing more is found than fatty degeneration in its ordinary form of granule-cells, and we distinctly convince ourselves, that the process in this stage absolutely differs in no respect from that which in the case of the heart and kidney we have just declared to constitute the stage of fatty metamorphosis. At this period, immediately before the formation of the depot, the state of matters, as seen with a high power, is about as follows. On making a section we see the fatty cells which are interspersed through the tissue becoming larger towards the middle and lying more closely together, but

Fig. 118.


Fig. 118. Vertical section from a sclerotic plate in the aorta (internal coat, inner surface) in process of fatty degeneration; i, the innermost part of the coat with round nuclei, isolated, and in groups of several (divided), h. The layer of enlarging cells; networks are seen with spindle-shaped cells which enclose sections of cells resembling those of cartilage, p. Proliferating layer; division of the nuclei and cells. a, a'. The layer which is becoming atheromatous; a, the commencement of the process, a, the advanced stage of fatty degeneration. 300 diameters.

generally bearing the form of cells; but, as we proceed from within outwards they become smaller and less numerous. All these cells are filled with small, fatty granules which strongly reflect the light. Hereby is produced what looks to the eye in a section like a whitish spot. Between these fatty corpuscles runs a meshed basis-substance, the really fibrous stroma of the internal coat, which we plainly see continued towards the exterior into the normal internal coat. This fact, that we are able to acquire the direct conviction that the fibrous layer which lies over the depot, is continued into the fibrous layer of the neighbouring normal portions of the internal coat, is one of especial value in the interpretation of these processes. In this manner the view which was for a considerable time defended by Rokitansky also, that the affection consists in a deposit upon the internal coat, is refuted. In a vertical section it is distinctly seen that the most external layers run in a curve over the whole swelling and return into the internal coat, and the old writers were quite right when they said—speaking of a stage in which the formation of the atheromatous depot had already made considerable progress—that the internal coat over the whole of the depot could be stripped off in a piece. On the other hand, however, we can convince ourselves, that the inferior layers of the internal coat run directly into the depot, and that their continuity has been broken by their degeneration, so that we have not to deal either with an interjacent deposit, (between the internal and middle coat) as the old writers supposed, but the whole of what we have before us is degenerated internal coat.

In some, particularly violent cases the softening manifests itself even in the arteries not as the consequence of a really fatty process, but as a direct product of inflammation. Whilst at the circumference a fatty softening takes place, in the centre of the seat of change a yellowish cloudy appearance is seen to arise, whereupon the substance almost immediately


softens and disintegrates, and a mass of coarse, crumbling fragments is found (Fig. 116, e, e) which fills the centre of the atheromatous depot.

In the last place, it is a question where the seat of the fatty degeneration really is. Here too again (as in the cornea) it may be imagined that the fat is deposited in spaces intervening between the lamellae; and even now there are still a small number of histologists who will not admit, that connective tissue contains only cells, and no empty spaces. But if a section through one of these (atheromatous) patches be examined from below upwards, it is seen that the same structure which presents itself in the fatty parts, shews itself also in the merely horny or half-cartilaginous layers. Bands of fibres, in the intersections of which small lenticular cavities appear, are found there as they are also in the normal condition of the internal coat; but in the cavities and in the bands of fibres lie cellular elements (Fig. 118). The enlargement which the part undergoes in consequence of the process and which we call sclerosis, depends upon this; the cellular elements of the coat increase in size and a multiplication of their nuclei takes place, so that spaces are not unfrequently found in which whole heaps of nuclei are lying. This is the mode in which the process sets in. In many cases division occurs in the cells, and a great number of young cells are met with. These afterwards become the seat of the fatty degeneration (Fig. 118, a, d), and then really perish. Thus we have here an active process, which really produces new tissues, but then hurries on to destruction in consequence of its own development. But one who knows that the fatty degeneration is here only a termination, and that the process is really a formative one, inasmuch as it begins with a proliferation—he can readily imagine the possibility of another termination, namely ossification. For here we have really to do with an ossification, and not merely, as has recently been maintained, with a mere calcification; the plates, which pervade the inner wall of the vessel are real plates of bone. Since they form out of the same sclerotic substance from which in other cases the fatty mass arises, and since a real tissue can only arise out of a pre-existing one, it follows of course that, when the process terminates in fatty metamorphosis, we cannot assume this to consist in a simple dissemination of fatty particles which has taken place in whatever interspaces we like to fix upon.

The essential difference which exists in a large vessel, as for example, the aorta, between this process [atheroma] and simple fatty degeneration is therefore this, that in the latter a very slight swelling arises on the surface of the internal coat, a swelling, which at once disappears if the superficial layers be removed by a horizontal section, and beneath which there still remains a portion of the coat unaltered. In the other case, on the contrary, we have in the extreme stage a depot which lies deep beneath the comparatively normal surface, afterwards bursts, discharges its contents and forms the atheromatous ulcer. This commences as a small hole in the internal coat, through which the thick, viscous contents of the atheromatous depot are squeezed out on to the surface in the form of a plug; gradually more and more of these contents is evacuated and carried away by the stream of blood, until at last there remains a larger or smaller ulcer which may extend as far as the middle coat, and indeed not unfrequently involves it. We have therefore always to deal with serious disease of the vessel leading to just as destructive results, as we see in the course of other violent inflammatory processes. You need only apply these observations to the history of endocarditis, and you will have a correct notion of all that goes on there also.

In the valves of the heart also we find simple fatty degeneration taking place both at the surface and deep beneath it.

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The process generally pursues its course so latently that no disturbance is perceptible during life, nor are we able, in the present state of our knowledge, to name any very obvious anatomical change as being the subsequent result of it. On the other hand, what we call endocarditis, what can be demonstrated to arise in the course of rheumatism, and may indubitably appear as a sort of equivalent to the rheumatism of the peripheral parts, begins with a swelling of the diseased spot itself. There is, namely, no exudation, but the cellular elements take up a greater quantity of material, and the spot becomes uneven and rugged. Then we see, when the process runs its course somewhat slowly,

Fig. 119.


either that an excrescence, a condyloma arises, or that the swelling assumes a more mammillated form, and afterwards becomes the seat of a calcification which may produce real bone. If the process runs a more acute course, the result is either fatty degeneration or softening. The latter gives rise to the ulcerative forms, in which the valves crumble to pieces, drop off, and embolical deposits are produced in remote parts (Fig. 73, p. 208).l

Fig. 119. Condylomatous excrescences of the mitral valve; simple, granular swellings (granulations) and larger prominences (vegetations), some villous, others branched and putting forth secondary buds; in all elastic fibres running upwards. 70 diameters.

1 This theory of the detachment of fragments from t he valves of the heart, and of the consequent secondary occlusions (cmbolia) was propounded by me,

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