in various organs, will be again noticed. At present I would allude to it merely in support of the view that the clot in the middle cerebral artery was in this, as in each of the other cases, directly derived from the vegetations on the left valves of the heart. At first it appears singular that in each of these cases, as also in others I have had the opportunity of seeing, the clot should be found as nearly as possible in the same situation. But a glance at the arrangement of the arteries at the base of the brain, especially in an injected specimen, will make it clear that this point is, of all others, the one perhaps most likely to arrest a solid mass floating in the blood, transmitted to the brain by the internal carotid artery; for almost directly after its entrance into the skull, the carotid divides into its two main branches, the middle and anterior cerebral, which immediately diverge in almost opposite directions. The sudden diminution in size, resulting from the division, and the different directions at once taken by the two branches, will together tend to make the angle whence the branches diverge well calculated to arrest any solid body transmitted along the carotid: while, since of the two branches, the middle cerebral is the largest, and also maintains more nearly than the anterior the original direction of the trunk from which they both sprang, a solid body seems more likely to pass into it than into the anterior division. And such is found to be the case; for if the plug is not found sticking directly at the angle, it is found a short distance up the canal of the middle cerebral.

Once arrested at the angle, or within the canal of the middle cerebral artery, a mass of fibrin, if large enough to block up the vessel, becomes at once the cause of loss of function and subsequent atrophy to almost all that portion of the brain supplied by the obstructed vessel; for, although by the arrangement of the vessels composing the circle of Willis, ample provision is made against obstruction ensuing in any of the main arterial channels of either side previous to their arrival at the circle, there is comparatively little provision for an obstruction ensuing in any of the main branches into which this arterial circle breaks up. This remark applies especially to the middle cerebral artery, which, if plugged up at its origin, becomes at once almost useless as a blood-vessel; for nearly all its divisions, especially those for the central parts of the brain, proceed to their several destinations without receiving any anastomosing branch from the other divisions of the circle of Wilis. The truth of this will be evident on examining an injected brain and the fact at once explains, why the portions of brain supplied by the branches of an obstructed middle cerebral artery, are deprived of all nourishment, except the little they may receive from the minute inosculations provided by the ultimate divisions of other arterial branches of the circle of Willis. The anterior cerebral artery is, by means of the anterior communicating branch, in great measure guarded against the occurrence of a similar evil; and in this way may be explained the infrequency of softening of the anterior cerebral lobes compared with the more frequent occurrence of this condition in the parts supplied by the middle cerebral artery.

I trust that the details of the three cases will be considered sufficiently satisfactory to establish the two principal points' which I have been desirous of proving in this part of my communication;

Namely, first, that softening of a portion of the brain, with attendant loss of function, may result from obstruction of a main cerebral artery by the lodgment of a plug of fibrin within its canal;

And, secondly, that the foreign substance thus obstructing the vessel is probably not formed there, but is derived directly from warty growths situated on the left valves of the heart.

It has long been admitted that any disease of the cerebral arteries sufficient to impede the transit of a due quantity of blood may induce softening of the brain, from imperfect nutrition. But the diseased state of the vessels to which nearly all observations on the subject apply, have reference only to the peculiarly fatty or atheromatous condition so frequently presented by the coats of the cerebral arteries, especially in persons of advanced life.

It is probable that many cases of partial and temporary paralysis suddenly ensuing, in one or more limbs, in young persons, especially if accompanied with signs of cardiac disease, may be due to interruption of a due supply of nutriment to the brain by the temporary plugging up of a principal cerebral artery by fibrin detached from a diseased valve on the left side of the heart. Temporary loss of power in one or

more limbs is not an uncommon circumstance in young persons affected with heart-disease.

[Having now discussed the effects of large masses of fibrin washed from the valves into the current of the circulation, Dr. Kirkes proceeds to describe those produced by smaller ones. One effect of these seems to be the formation of the fibrinous-looking substances sometimes found in the spleen and other organs, and known as 'capillary phlebitis,' 'metastases,' 'fibrinous deposits,' &c.; but in all cases they result from the direct transmission of particles of fibrin from the valves of the heart, or elsewhere.]

Out of 21 cases in which I have observed these deposits in the spleen, kidneys, or other parts supplied with blood directly from the left side of the heart, and in which I have noted the condition of the heart and other principal organs, I have found disease of the valves or of the interior of the left side of the heart in every instance but two; and of these two exceptional cases, one was a case of cholera, in which a doubtful mass of capillary phlebitis existed in the liver, the other a case of aneurism of the aorta,-which tends rather to prove than disprove the explanation I offer of the fibrinous masses existing in the various organs. Omitting these two cases, however, I find that of the remaining 19 it is not merely stated that the heart or the valves were diseased in each of them, but that in 14 there were fibrinous growths on the surface of the left valves or interior of the left cavities, while in the remaining 5 there is simple mention of valvular disease, without any statement as to whether the fibrinous deposits existed or not. The mere fact of so large a number of cases of so-called capillary phlebitis in internal organs being distinctly associated with the presence of fibrinous material on the valves of the heart, is sufficient to suggest a very close relation between these two morbid states; and the existence of some such close relation is rendered more probable by the absence, in all these cases, of any other condition likely to have induced a poisoned state of the blood, to the existence of which the formation of these deposits has not unfrequently been ascribed. In many of the cases cardiac dropsy is noted as the fatal disease, while in none of them does there seem to have been any proof of the existence of a so-called blood-disease, such as typhus, purpura, or the like.

That such blood-diseases have, indeed, nothing to do with the deposits in question seems proved by the fact that, out of the examination of a large number of fatal cases of fever, I have never yet met with an instance in which masses of capillary phlebitis existed in any part of the body in this disease. From their general absence in other diseases, then, as well as from their frequent occurrence in diseases of the heart, we have equally strong reason for believing in the existence of a close connection between these morbid deposits in internal organs and the presence of fibrinous growths on the inner surface of the heart or on its valves.

The close connection subsisting between endocarditis and fibrinous deposits in distant organs has, I am aware, been strongly insisted upon by Rokitansky, and has also attracted the notice of Hasse; therefore it may seem superfluous to have said so much on the subject. But I would plead a twofold excuse for so doing: first, because, so far as I know, the connection pointed out by Rokitansky has never yet been confirmed, scarcely even recognised, in this country; and secondly, because I believe, with all deference, that it may admit of an interpretation somewhat different from that which Rokitansky has given. After careful and repeated perusal of all I can find bearing on this subject in Rokitansky's great work on Pathological Anatomy, I cannot find that he in any place even hints at the explanation I have ventured to offer of the real cause of the secondary deposits in distant organs in cases of valvular disease of the heart. His observations seem to show quite plainly that he ascribes them to a poisoned state of the blood, consequent on the admixture of the products of endocarditis with this fluid, whereby it acquires an increased tendency to coagulate, which tendency cannot well be manifested in the arteries, owing to the velocity of the current, but is brought about within the capillaries on account of the slowness with which the blood there moves, and the increased facility which is thus afforded for the morbid material derived from the inflamed heart to exercise its influence on the composition of the blood.

The view, however, which I have ventured to take is, that the deposits in the various organs are the direct

fibrin detached from some pa

rrest of solid particles of too large to traverse the

minute capillary canals to which they are brought by the circulating blood. By the obstruction which their arrest occasions, they may induce coagulation of blood behind them; while, by their mere presence, they may act as local irritants, and so induce secondary processes of inflammation and suppuration, like any other foreign body. In either or both of these ways may be produced the various appearances characteristic of these singular deposits. This view-which seems supported by the other evidence I have adduced of the direct transmission of masses of fibrin from the valves of the heart has the advantage, too, of explaining some of those cases in which very similar fibrinous deposits are found in various organs, independent of any warty or other growths within the heart. For example, in a fatal case of aneurism of the abdominal aorta, to which I have already alluded, several patches of capillary phlebitis existed in one of the kidneys, though for the origin of these there seemed to be no other explanation than that afforded by the existence of fibrin abundantly deposited in laminated masses within the sac of the aortic aneurism. It is easy to conceive that portions of such fibrin might be broken up, mingled with the circulating blood, and subsequently arrested within the capillaries of the kidney or spleen.

[Lastly, the principal points of the subject are thus recapitulated :]

They are, 1st, the general fact that fibrinous concretions on the valves or the interior of the heart admit of being readily detached during life, and mingled with the circulating blood: 2ndly, that if detached and transmitted in large masses, they may suddenly block up a large artery, and so cut off the supply of blood to an important part; if in smaller masses, they may be arrested in vessels of much less size, and give rise to various morbid appearances in internal organs; while, under other circumstances, the particles mingled with the blood may be extremely minute, possibly the debris of softened fibrin, yet in sufficient quantity and with sufficient power to produce a poisoned state of the circulating fluid, as manifested in the production of typhoid or phlebitic symptoms: 3rdly, that the effects produced and the organs affected will be in a great measure determined by the side of the heart from which the fibrinous masses have been detached; for, if the right valves have furnished the source of the fibrin, the lungs will bear the brunt of the secondary mischief, displaying it in coagula in the pulmonary arteries, and various forms of deposit in the pulmonary tissue; but if, as is far more commonly the case, the left valves are affected, the mischief is more widely spread, and may fall on any systemic part, but especially on those organs which, such as the brain, spleen, and kidneys, are largely and directly supplied with blood from the left side of the heart.— Edinburgh Med. and Surg. Journal, July 1, 1853, p. 119.

29.-ON THE CAUSES OF DILATATION OF THE HEART.

By DR. W. T. GAIRDNER.

[Dr. Gairdner read a most valuable paper upon this subject before the MedicoChirurgical Society of Edinburgh; dwelling also upon the connexion of the heart affection with disease of the lung. He sums up by a synopsis of the whole. He says:]

The following conclusions seem to be fairly deducible from this inquiry, as to its ultimate and most important results:

1. It is possible (judging from other cases which I have observed, I should say not improbable), that disease of the aorta and of the kidney may have an influence in determining cardiac hypertrophy. In the case of the kidney, however, this influence is exceptional; in the case of the aorta, it is only exercised in extreme cases of disease, and chiefly in the case of aneurism or dilatation of the arch.

2. There is no good reason to ascribe to disease of the liver, pancreas, spleen, or brain, any considerable influence in determining disease of the heart.

3. Chronic disease of the lung has a most important influence in determining hypertrophy and dilatation of the heart; and the very great majority of cases of cardiac disease, not caused by deformity of the valves, owe their origin to pulmonary affections.

4. Hypertrophy and dilatation of the heart, arising from pulmonary disease, affect

in the first instance the right cavities; but when the hypertrophy exceeds a fev ounces, the left cavities also become invariably involved in the disease.

5. It is possible that part of the influence of pulmonary disease on the heart may be due to obstruction of the circulation in the pulmonic capillaries (as is commonly supposed); nevertheless, it appears, that under various circumstances producing serious pulmonary obstruction, hypertrophy of the heart does not occur in a consi derable proportion of cases.

6. Tubercular disease of the lung produces hypertrophy of the heart only wher combined with pulmonary atrophy and induration. Retrograde or obsolete tubercle with contracting or obliterated cavities, concretions, cicatrices, &c., is very generally associated with secondary disease of the heart; while advancing tubercle has no appreciable influence (or rather, is frequently the cause of cardiac atrophy).

6. It is not ascertained that pneumonic consolidation, considered per se, has any tendency to produce cardiac hypertrophy; but in some cases it appears to do so when accompanied by atrophy or collapse of the lung and emphysema.

8. The great majority of the pulmonary lesions which give rise to hypertrophy and dilatation of the heart are accompanied by partial atrophy of the lung; and usually also by emphysema, which (as I have elsewhere shown) is the almost invariable consequence of such atrophy.

9. Atrophy of the lung tends, in an equal degree, to produce cardiac disease, whether it proceed from bronchitis, pneumonia, or tubercle; whether it be "simple atrophy," or accompanied by induration; whether it be seated at the base, apex, anterior or posterior parts of the lung. Generally speaking, a given amount of pulmonary atrophy may be expected to develop a degree of hypertrophy of the heart, proportionate to the dyspnoea which it entails, and the amount of contraction produced by it in the affected tissue.

10. The well-known concurrence of emphysema with hypertrophy of the heart is in all probability due to their common origin in atrophic lesions of the lung; the law of production of the one affection being also that of the other. It is reasonable, therefore, to suspect that pulmonary emphysema and cardiac hypertrophy may be found to be, to some extent, alternating as well as collateral affections, in cases where atrophy of the lung gives rise to the conditions necessary for the production of either.

11. It is rendered by this inqniry extremely probable, that dilatation and hypertrophy of the heart are never otherwise than secondary affections; and that they are dependent, in the very great majority of cases, 1st, on valvular deformity and other obstacles to the circulation in the heart or great vessels (dilatation from within); 2nd, on the expansion of the thorax under abnormal conditions (dilatation from without). The consequence of either of these forms of dilatation, or even of the tendency to either of them, may be hypertrophy of the muscular substance, due to the effort of the organ to act effectively under an increased resistance to its contraction. In the case of dilatation from within, an increased power is required to overcome an obstruction in the circulating system itself; in the case of dilatation from without, hypertrophy takes place, because the expansion of the thorax in inspiration tends constantly to overload the heart, and this tendency can only be resisted by increased muscular force. The increase of dilatation without corresponding hypertrophy (the aneurisme passif of Corvisart) is always the signal of disaster; because it indicates that the balance of the circulating forces is finally destroyed.Brit. and For. Med.-Chir. Rev., July, 1853, p. 224.

30.-Upon Fluids which Stop Hemorrhage. By SEDILLOT.-Eau de Pagliari, consisting of tinct. benzoes, 3 viii.; alum, fb. i.; water b. x. This preparation, which has a pale straw colour, and is transparent, possesses an extraordinary power of coagulating blood.

Eau de Rabel, consisting of acid. sulphur., 100 parts; alcohol, 300 parts. The acid should be poured upon the alcohol slowly.

Baume de Compingt has not yet been analysed, but appears to contain an empy

reumatic oil.

Eau de Hepp is a modification of the Eau de Pagliari.-Med. Times and Gazelle, Sept. 10, 1853, p. 274.

DISEASES OF THE ORGANS OF RESPIRATION.

31.-HINTS ON AUSCULTATION, WITH A VIEW TO THE SIMPLIFI OCATION OF TERMS AND ARRANGEMENT.

By DR. THEOPHILUS THOMPSON, F.R.S., &c.

[The advantages of auscultation in the examination of diseases of the chest have not always been realized, perhaps, especially from our being apt to regard the phenomena observed as intricate and complicated. Dr. Thompson observes:]

The soft silky sound, heard on listening to the chest of a healthy individual in the act of breathing, cannot be mistaken. Every practitioner must have had frequent occasion to observe this silky murmur superseded by bubbling sounds, when, in consequence of affections of a catarrhal character, the air in its entrance and its exit passes through the secretions with which the air passages are occupied : the sound being necessarily modified according as this secretion is confined to bronchi of considerable calibre, or diffused through the smaller tubes, or the aërating tissue of the lungs. When the smooth expansion of this tissue is prevented by causes extrinsic to the cells, and the air in expiration does not pass through secretion, the sound produced has not a bubbling character, and may be confined to the period of inspiration. In this way, varieties of crackling and crepitation sounds originate.

When, in consequence of thickening of the investing membranes, or the presence of any partial obstacle, the calibre of the bronchi is altered, vibratory sounds are induced, which may be grave or acute, according to the diameter of the passages affected.

The simple view thus presented sufficiently represents the principal circumstances, which require to be considered in the practical application of auscultation to those diseases of the chest, in which difficulties are most frequently experienced and errors most readily committed.

[In the subsequent tabular arrangement, Dr. Thompson only includes the sounds of practical importance. Several others, as modifications of voice, cardiac sounds, &c., are generally easily distinguished and sufficiently expressive.]

It is undesirable to give similarity of name and juxtaposition in arrangement, to sounds characteristic respectively, some of inflamed lungs, others of consumption, and I would venture to propose, as simple, distinct, and suited for clinical purposes, the division into bubbles, clicking, crepitation, crackling, and vibration, as in the preceding table.