show that it is quite inconclusive: for example, it is alleged that the agency by which the limb is shortened and maintained in that state is not active contraction, and such being the case it must of necessity be passive contraction. But the ground on which active contraction is excluded from any share in the production of shortening, namely, the incompatibility of this state with the persistence exhibited in the action of the muscles, will have little weight when it is borne in mind, that if an irritant be applied to a healthy muscle, contraction will continue as long as the irritation remains, provided the latter be not of sufficient intensity to exhaust muscular irritability; and furthermore, in seeking to account for the phenomena to explain which the doctrine of passive contraction has been introduced, the advocates of this doctrine would appear to have entirely ignored the physical property of muscular elasticity. Yet this, as I hope to show, is in reality the property of muscle by the exercise of which, conjoined with active muscular contraction, the permanent shortening of the limb which characterizes fractures and dislocations is produced. The first and immediate effect on the muscles, of the shock which causes fracture or dislocation, is temporary incapacity for contraction, in which state of muscle, as has been shown by Weber, muscular elasticity is at its maximum, precisely as, in the experiments of Marshall Hall, suspension of volition was found to increase spinal irritability. As a consequence of the exaggerated elastic force thus developed, retraction of the muscles, and shortening of the limb to a slight extent occurs. After an interval, however, corresponding to the severity of the shock, the muscles recover their contractility, and being now susceptible of the mechanical irritation applied to them by the dislocated or fractured bone, they assume a state of active contraction, under the operation of which a still further degree of shortening of the limb takes place. But the irritation arising from the pressure of the displaced bone being, of necessity, of a persistent character, and at the same time insufficient in intensity to exhaust the irritability of the muscles, the latter continue in a state of spastic or sustained contraction, presenting a powerful obstacle to replacement, and should this be not effected, ultimately assuming dimensions corresponding to the altered length of the limb, in obedience to the law of adaptation which governs all organic structures.

As a fourth example of passive contraction, the advocates of this doctrine are in the habit of adducing the retraction of the divided portions which follows the division of a muscle previously relaxed.

But the phenomenon here relied on is obviously the result of

active contraction induced by the mechanical irritation applied to the fibres in the process of division.

I believe, therefore, that the so-called passive contraction of muscle rests upon insufficient evidence, that it is, in reality, nothing else than the "elastic tension" of Weber, as exhibited in the ordinary tension of muscles in a state of repose, and in the examples given, that the phenomena attributed to passive contraction are due, in part, to muscular elasticity, but mainly to active contraction induced by mechanical irritation.

The section of the subject of muscular physiology, which will appropriately close this paper is the posthumous manifestation of contractility known as cadaveric contraction, or rigor mortis.

Within a variable period after the occurrence of somatic death, the length of which will be, ceteris paribus, inversely proportioned to the rapidity of the process of dissolution, and the vigour of the muscular system at the moment of its consummation, the muscles assume a state of forcible contraction, under which the limbs become firmly flexed, and the entire body rigid. The length of time during which this state lasts has likewise reference to the mode of death, as well as to the period intervening between its occurrence and the first appearance of rigidity. Thus, leaving out of consideration the influence of special agents and diseases, such as poisons and tetanus, which necessarily derange the ordinary sequence of events, it may be laid down that when death occurs suddenly to a person in the enjoyment of vigorous health up to a short time antecedent to its occurrence, and the period of subsequent muscular flaccidity is prolonged, the duration of rigidity will be protracted in a corresponding ratio, and vice versa.

To the rigor mortis immediately succeeds putrefactive decomposition; indeed, the advent of putrefaction would appear rather to determine the duration of the rigor mortis than be determined by the latter; since the circumstances which favour or retard putrefaction are precisely those which abbreviate or protract the period of post mortem rigidity. Thus, in septic diseases in which there is a tendency to early and rapid decomposition, such as low forms of fever, and equinia or glanders when it attacks the human subject, the rigor mortis may be so imperfectly pronounced as to escape observation, or, in extreme cases in which disorganization of the tissues would appear to have commenced even before death, it may be altogether prevented.

As to the proximate cause of rigor mortis three different views have been held: first. It has been regarded as the last manifestation of contractility, as the effect of the revulsion which takes

place pending the final departure of the distinctive vital property of muscle.

This view would attribute the phenomenon to a vital agency, and involve a recognition of the distinction between somatic and systemic death. It would appear to derive support from the important and somewhat startling results obtained by M. Brown Séquard, who found, by his experiments on executed criminals, that irritability may be restored in the muscles of warm-blooded animals, already four hours in a state of rigor mortis, by injecting them with defibrinated arterial blood, and maintained by this means for forty-one hours, whilst the opposite limb will have passed into a state of putrefaction. From this remarkable experiment the inference may be legitimately drawn, that during the continuance of the rigor mortis, whether we regard it as a manifestation of contractility or not, the vitality of the muscles has not entirely departed, but that it is rather suspended preparatory to its total extinction, requiring for the sensible manifestation of its presence only that the conditions be supplied on which it depends. Of these conditions the most important is the circulation of arterial blood, upon which, as supplying the elements of nutrition, the muscles are directly and essentially dependent for the maintenance of their vital properties.

The second view held as to the cause of rigor mortis, though not so extensively, is that of Brücke, who regards it as the result of coagulation of the fibrin of the muscles, and therefore as identical with the coagulation of the blood, and of purely physical origin.

The third opinion on this subject is rather implied than expressed in the doctrine of Weber, to the effect that muscular contractility and elasticity are the complement of one another. Therefore, when contractility is abolished, as it is shortly after death, the physical property of elasticity is developed to the uttermost, giving rise to the phenomenon of shortening and rigidity. This paper has already far exceeded the limits assigned to it at the outset, else I should take occasion to discuss the relative merits of the opinions just stated as to the causation of rigor mortis. It may, however, suffice to say, that whilst I believe the two last-mentioned views have little to recommend them besides their novelty and ingenuity, the first is that which accords best with ascertained facts, and although not so complete as fully to satisfy the mind of a scientific inquirer, may be taken as representing the sum of our present knowledge on the subject.

7 The statement that "Rigor mortis results from the liberation of latent force consequent on the decomposition of muscle" is only a different mode of expressing this view.

Recherches experimentales sur les propriétés physiologiques et les usages du sang rouge et du sang noir, Journal de la Physiologie, tome Premier, 1858.

ART. IX. On the Question of Morbid Types and Species. By ROBERT D. LYONS.

[Continued from p. 232.]

MONGST the most constant, remarkable, and important of

A the elements of diseased states occurring in the category of

pathological epigeneses, in the doctrines of a day not yet past, is the fluid known as Pus. It has been regarded as an independent epigenesis, or growth upon the system in disease, of an element having no prototype in the physiological elements of the body: it has been classed likewise under the head of "neubildungen", and has been defined as hetero-morphous, in respect of its being without analogue in the formations existing in the healthy organism. The "pus bonum et laudabile" formed a very independent entity in the pathology of the older writers. Chemical and microscopical research amongst the newer schools followed in the line of investigation of special entities, as already mentioned; and characters of the most specific and definite kind were assigned to this fluid. Though a product of disease, its composition, and the physical conformation of its formative elements were supposed to observe ordinarily a normal type of development, though exceptions were frequent, and the paradox of a normal abnormity was balanced by an abnormal abnormity. Its minute microscopic elements, the well-known pus-corpuscles of spherical form, with their tripartite nucleus and their familiar reaction to liquor potassæ, acetic acid, borax, and other reagents, are described by all pathologists. The opinion was, and it may almost be said, is yet, general, that pus is a new formation peculiar to disease, and that as a histological formation it has no resemblance to physiological types.

Under the terms Neubildungen,-literally, new formations, otherwise designated Pathological Epigeneses, it is usual to include various anatomical elements of disease. The views entertained as to the essential nature of the morbid elements, may perhaps be best indicated by an abstract from the writings of so recent and authoritative an observer as Vogel. In his treatise on pathological anatomy, this distinguished author, in defining the Pathological Epigeneses, observes :-"In the primary formation of a body, and subsequently in its nutrition, new formations (elementary particles and tissues) arise, interpolated as it were between those already existing. A somewhat similar process is of frequent occurrence in pathological formations; indeed, so frequent are these morbid epigeneses, that the greater number of the changes which pathological anatomy can demonstrate after

death may be arranged under this head. At the same time they are so various, and the relations of their formation, development, and termination in individual cases, are so different (two or more epigeneses being frequently associated and combined), that a satisfactory description of these conditions, including a clear arrangement and separation of the individual elementary phenomena, is a task of the greatest difficulty". He then goes on to work out, as he states it, the general laws followed by pathological formations in their development. But he admits that these laws are very analogous to those which govern the development and formation of tissues in the normal state. "Indeed", he says, "in many cases no definite line can be drawn between normal and abnormal formations". Here it would seem as if some portion of the truth had forced itself upon a mind still fettered by scholastic notions of morbid entities or diseased types. In defining the Pathological Epigeneses, Vogel divides them into two groups, distinguished by a morphologic difference, and also by a gennetic difference.

It is unnecessary to follow out in detail the views of Vogel. Suffice it to say, that he regards the formation of the first class of products as identical with the process by which crystals are formed from a mother liquid. In reference to the second class of pathological elements, his views are but little modified from those of Schwann.

Virchow, the most recent and able pathological inquirer of our day, rejects the theory of Schleiden and Schwann. He regards it as impossible that cells can originate in an amorphous blastema, and further considers as impossible the successive formation of a nucleolus, nucleus, and cell-wall. He likewise disbelieves in the origin of cells from an aggregation of molecules or granules. Finally, Virchow is of opinion that, in the vegetable as well as in the animal kingdom, there is no generatio equivoca, and that, in pathological as well as in physiological states, a cell, wherever found, arises only from a preexisting cell, whether by endogenous growth, or by fissure and cleavage of an already existing cell. It will be at once seen in what respect the views

Ac

of Virchow differ from those of Schleiden and Schwann. cording to the views of these latter authors, so long accepted, a homogeneous matter, usually known under the name of blastema or plastic exudation, was supposed to be thrown out on inflamed surfaces. It was believed that the most minute microscopic examination must fail to detect any elements having specific form in this exudation when first thrown out. The changes subsequently assumed to take place consisted in the development, firstly, of minute molecules and granules; secondly, the