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We can therefore now say, there is no form of disturbance of this kind known which can be traced to the abolition of the action of a nerve. A part may be paralyzed without becoming inflamed; it may be anesthetic without becoming exposed to this danger. There is always required in addition some special irritation, either of a mechanical or chemical nature, and proceeding either from without or from the blood, in order to produce the peculiar liability.

In this manner therefore we have, as you see, a series of connecting links between facts eminently pathological and the most common processes of physiological life, facts of which the special import can, however, only be understood and defined, when the distinctions are made to which I called your attention at the commencement of the lecture, that is, when the different kinds of irritation are separated according to their functional, nutritive or formative nature. If they are jumbled together, as they have been by the neurists, and especially, if the formative and nutritive processes are not kept apart, then it is impossible to arrive at any simple explanation of the phenomena.

Those states of irritation which we witness in the course INFLAMMATORY IRRITATION. 315

vated into inflammation (asthenic inflammation). But in these cases the inflammation is always the consequence of some special irritation, never the direct result of the section of the nerves. Still, as in the case of the fifth pair and the pneumogastric, such section may be the cause of irritants' (foreign bodies and other agents) more readily acting upon the anaesthetic or paralyzed parts. CI. Bernard has recently declared that the section or irritation of nerves in weakened parts produces effects which cannot be elicited in healthy ones. We have therefore here to deal with a very complicated slate of things. The change in the nerve is generally succeeded by a disturbance in the function or circulation of the part, or in both, and when the part is already weakened (i. e., altered in its nutrition) this disturbance may prove a source of irritation to it, and thus the effects be produced which Bernard ascribed to other causes. In quite a similar manner we see that, even when the nervous supply is in its normal state, purely mechanical disturbances in the circulation act u|K>n weakened parts as morbid irritants.—From a MS. note by the Author.

of the severer forms of disease—the really inflammatory kinds of irritation—never in any case admit of a simple explanation. In inflammation we find side by side all the forms of irritation of which I have given you an analysis. Indeed, we very frequently see, that when the organ itself is made up of different parts, one part of the tissue undergoes functional or nutritive, another formative, changes. If we consider what happens in a muscle, a chemical or traumatic stimulus will perhaps in the first instance produce a functional irritation of the primitive fasciculi; the muscle contracts, but then nutritive disturbances declare themselves. On the other hand in the interstitial connective tissue, which binds the individual fasciculi of the muscle together, real new-formations are readily produced, commonly pus. Here we have to deal with a formative irritation, whilst the inflamed primitive fasciculus commonly produces no pus, any more than it does new muscular substance; on the contrary we most frequently see, when the irritation has attained a certain height, degenerative processes set in. In this manner the three forms of irritation may be distinguished in one part. Of course there may be in addition also an irritation of the nerves, but this has, at least if we do not take function into account, no connection of cause and effect with the processes going on in the tissue proper, but is nothing more than a collateral effect of the original disturbance. This must, in my opinion, be regarded as the most important result derived from the facts of Special Histology, and it is all the more certain, because it can be tested both by experiment, and by physiological and pathological experience.

Soon, I will shew you how in the study of inflammatory processes a clearer apprehension of their nature may hereby be obtained.

LECTURE XT.

APRIL 10, 1858.
PASSIVE PROCESSES. FATTY DEGENERATION.

Passive processes in their two chief tendencies to degeneration; Necrobiosis
(softening and disintegration) and induration.

Fatty degeneration.—Histological history of fat in the animal body; fat as a component of the t issues, as a transitory infiltration, and as nccrobiotic matter.

Adipose tissue.—Polysarcia.—Fatty tumours.—Interstitial formation of fat —Fatty degeneration of muscles.

Fatty infiltration.—Intestines; structure and functions of the villi.—Reabsorption and retention of the chyle.—Liver; intermediate interchange of matter by means of the biliary ducts. Fatty liver.

Fatty metamorphosis. — Glands; secretion of sebaceous matter and milk (colostrum).— Granule-cells and granule-globules. — Inflammatory globules.—Arteries; fatty usure and atheroma in them.—Fatty debris.

We have, gentlemen, hitherto nearly always spoken of the actions of cells and the processes which manifest themselves in them, when, in consequence of any external influence, they give signs of their vitality. There take place in the body, however, also a tolerably large number of passive processes, in which, as far at least as can be demonstrated, there is no particular activity displayed by the cells. Allow me therefore, before we proceed farther in the description of the active processes, to speak a little more in detail concerning these passive processes. For the history of the affections of cells, as they are exhibited to us in our patients, is generally composed of processes, which belong, some of them, rather to the active class, and some of them, rather to the passive one; and the

DEGENERATION. 317

obvious results are in many cases apparently so similar in both classes, that the ultimate changes which we meet with, after the continuance of the process for a certain time, may very nearly be the same. Here particularly it was for a time very difficult to define the boundaries, and a great part of the confusion which marked early microscopical efforts, was occasioned by the extraordinary difficulty there was in separating active and passive disturbances.

Passive disturbances I call those changes in cellular elements, whereby they at once either merely lose a portion of their activity, or are so completely destroyed, that a loss of substance, a diminution in the sum total of the constituents of the body is produced. Both series of passive processes, taken together, viz., those which are in the first instance marked by an essential diminution of power, and those which terminate in a complete destruction of the parts, constitute the chief part of the domain of what is called degeneration, although—a point that we must hereafter consider more closely—a great part of what must be called degeneration must be transferred to the series of active processes.

It makes of course an extremely great difference whether a vital element continues to subsist as such, or whether it entirely and completely perishes; whether at the conclusion of the process, it still exists, even though in a condition of much diminished functional power, or whether it is altogether destroyed. And here we have the important practical distinction, that in the one series of processes there is a possibility of a repair of the cells, whilst in the other direct repair is impossible, and a regeneration can only take place by means of a substitution of new cells from the neighbourhood. For when a cell has perished, it is of course impossible for any further development to originate in it.

This latter category, where the cells are destroyed during the course of the process, I proposed a few years ago to designate by a term which has been employed to express disease generally by K. H. Schultz, viz., Necrobiosis} For we have, namely, always here to deal with a gradual decay and death, a dissolution, we might almost say, a necrosis. But the idea of necrosis really does not offer any analogy to these processes, inasmuch as in necrosis we conceive the mortified part to be preserved more or less in its external form. Here on the contrary the part vanishes, so that we can no longer perceive it in its previous form. We have no necrosed fragment at the end of the process, no mortification of the ordinary kind, but a mass in which absolutely nothing of the previously existing tissues is preserved. The necrobiotic processes, which must be completely separated from necrosis, are in general attended by softening as their ultimate result. This commences with a friability of the parts; they lose their coherence, at last really liquefy, and more or less moveable, pulpy or fluid products take their place. We might therefore without more ado name this whole series of necrobiotic processes softenings, if a number of them did not run their course, without the malaria's ever becoming apparent to the naked eye. As soon, namely, as a process of this sort sets in in a compound organ, as for example, a muscle, a palpable myo-malacia is certainly produced when all the muscular elements at a given point are at once affected; but it happens far more frequently that, in the course of a muscle, only a comparatively small number of primitive fasciculi are affected, whilst the others remain almost intact. Then indeed a softening really does occur,

1 Necrobiosis is death brought on by (altered) life—a spontaneous wearing out of living parts—the destruction and annihilation consequent upon life— natural as opposed to violent death (mortification). From a MS note by tie Author.

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