in which the pneumatic factor is conspicuous by its absence, although in a minor degree doubtless still operative (Fig. 24, Tracing 2).

The antagonistic action of the accelerant and retardant nerves of the heart has been disputed. Retardation can be induced when artificial acceleration is in progress. It is none the less true that the safety of an abnormally inhibited heart consists in some acceleration of cardiac pulsation; and, as was mentioned last year, in the sphere of secretory motion, there appears to be a certain compensatory independence in the secretory influence of the cranial and sympathetic nerves of the sub-maxillary gland. It is probable that the same rule applies to other forms of vital motion. William Hunter,' referring to the fact that intense and even fatal jaundice may rapidly follow emotional shock, accounts for the phenomenon by suggesting a spasm or reversed peristalsis of the bile ducts while the bile is in full flood, as the probable cause. He admits, however (p. 81), that diminished quantity and increased viscidity of bile may be a cause of its absorption. The viscidity he attributes to catarrh of the bile ducts. Can a more directly neurotic hypothesis be advanced?

The main secretory nerve of the liver is the pneumogastric, and its sympathetic endowment is from the splanchnic nerve, while vasomotor nerves for the portal vein are derived, according to Bayliss and Starling, quoted by Halliburton,2 from nerves ranging from the third to the eleventh dorsal. It appears possible, therefore, that the sequence of events may be somewhat as follows:-In sudden, severe, and mental cases, shock is followed by pneumogastric inhibition and arrest of its secretory-motor function. This entails an attempt on the part of the sympathetic to come to the rescue, which it does by producing a more potent but also a more viscid bile-the nature of such potency not being at present to the point-which, like a blundering but wellmeaning friend, stands in the way, just when the pneumogastric, having recovered from its inhibition, throws out by augmented activity too large an amount of bile for rapid escape, hence absorption and rapid toxæmia in some cases, and slow poisoning in others. I do not for a moment presume to indicate this solution as correct, but it appears to me as probable as other theories suggested, and brings the motor activities of the liver 1 Allbutt, "System of Medicine,” vol. iv. p. 68 et seq.

2 Op. cit., p. 670.

into line with those of the heart, which it is my present purpose to maintain.

Again, the striking phenomena, on the one hand, of Graves' disease, which I prefer on this occasion to call Begbie's disease, and, on the other, of myxedema, appear to suggest a parallel on similar lines. The thyroid gland is innervated by the pneumogastric and visceral nerves which reach it by way of the inferior and middle ganglia of the cervical sympathetic. Of these its most active secretory nerve is probably the pneumogastric, although I am not aware that the fact has been experimentally proved. If we regard Begbie's disease as in the first instance a cardiovascular neurosis, to employ a term expressive of our ignorance, we can conceive an increased though ineffectual effort upon the part of the pneumogastric system, that is, of motor fibres probably derived from the spinal accessory nerve and running in the pneumogastric, to restrain the cardio-vascular organs in excessive visceral motion, and although unsuccessful in that effort, so stimulated by it as to provoke increased activity in its own secretory motor fibres. This would result in an excessive secretion, among others, of the thyroid juice, the effect of which upon the circulation is to accelerate it. Thus the increased activity of that gland may add fuel to the fire which burns so lustily as vasomotor commotion under the circumstances in question. This secretory increase, as we know, is at present regarded as one of the most probable causes of excessive pulsation in Begbie's disease, the etiology of which, however, is not yet by any means clear.

It is conceivable, moreover, that a period of persistent hypersecretion may result in one of hyposecretion, the retardant influence of which may be slow in showing itself, for the following reason:-The sympathetic system, besides its general vasomotor over-action, may also induce a supplementary sympathetic juice as in the case of the submaxillary gland, and thus maintain for a time the waning accelerant influence of pneumogastric secretion. We know, however, that ultimately in a large number of cases the excessive excitement of the cardio-vascular system subsides more or less, that in some cases bradycardia succeeds tachycardia, and that in yet others myxedema takes the place of Begbie's disease. The neuro-motor activity of the gland, in short, and its associated organs, is worn out, and we may expect some day to have demonstrable pathological changes in the controlling centres, which, together with peripheral degeneration, would account

satisfactorily for the striking complex of symptoms referred to, and still unexplained. Action and supplementary action, endeavour and support, overaction and reaction, error and correction, seem to be general laws of life, and there does not seem to be any just reason why they should not apply also to the life manifest in visceral motion in its various forms.

To study the matter a little more closely, and taking cardiac action as the type, let us examine the motor effects of shock upon the heart, and in the first instance of the shock of physical pain, with which Laycock's "phenalgia" must necessarily be associated, and often is in a high degree.

As has already been remarked in a previous section, pain or excessive sensibility in any organ may influence the heart's action in association with various degrees of concomitant mental emotion, proportionately to the amount of the stimulus. The tachycardia associated with a displaced kidney may be present without much associated pain, and therefore without great mental distress. With more pain the same conditions will be emphasised. The reflex effects of nephroptosis may affect many organs besides the heart, and the severity of these secondary motor disturbances is not proportionate, as Macalister has stated, to the amount of mere displacement.1

Calculi, we have seen, may induce an extreme of agony which may terminate in collapse and death, the associated cardiovascular phenomena being those of rapid and enfeebled action of the heart and a general vaso-paresis accompanied by profuse perspiration and depression of temperature. These extreme phenomena differ from those associated with angina pectoris chiefly in the situation of referred pain and in the uninterrupted duration of the agony. With this distinction these cases might be termed cases of angina pectoris hepatica, renalis, et hæ species omnes.

The first effect of sudden visceral pain, whether cardiac or general, on the movement of the heart is to arrest its action, and probably, could we at the moment of the onset of pain auscultate that organ, we should detect an inhibition. This, however, like peripheral spasm, which is usually regarded as the cause of angina pectoris, is so early a phenomenon that it must very rarely be indubitably observed, and when observed and present it is not necessarily the essential cause of the general complex of 1Allbutt, "System of Medicine,” vol. iv. p. 344.

symptoms. The conditions usually first observed by the ear and hand are the phenomena of depression which follow inhibition, associated in many cases, shortly afterwards, with those of a rescuing augmentation and acceleration of the heart's beat.

Lauder Brunton, whose many-sided scientific activity has recently been recognised by his and our Alma Mater, and with whose name one of the most beneficent agents in the treatment of angina pectoris is indissolubly associated, was the first, so far as I know, to note graphically the cardio-vascular movements connected with valvular angina. He published a case1 of aortic valvular disease with sphygmograms, in which he showed the quick small pulse of the agony and the larger and slower pulse of the interval free from pain. Brunton considered the pulse of the agony to indicate peripheral spasm, and was at a loss to reconcile its rate with its assumed condition. Since Brunton's original observations, however, opinion has modified a good deal on this point, and there are those who feel more disposed to regard the peripheral signs usually observed as those of empty collapse rather than of active spasm-of profound collapse— in other words, such as might be caused by other visceral and even somatic pain of a certain degree of severity.

Sir Richard Douglas Powell, however, in his recent Lumleian Lectures before the Royal College of Physicians, London,2 also describing what he terms vasomotor angina in the case of a young man suffering from aortic regurgitation, spoke as follows: "It was curious to note the absolute extinction of all the aortic characters in the pulse, which became contracted to a small hard pulsating thread; whilst, as the patient sat forward, leaning against a chair in great pain, the bed shook with the violence of the cardiac beats, and his neck and subclavian vessels could be seen pulsating with responsive violence. A dose of trinitrine quickly brought back the aortic features of the pulse and dissolved the painful scene. One could not observe the labouring beat of the heart, the strongly pulsating large vessels contrasted with the almost effaced small vessels, without appreciating the power of vasomotor contraction to cause cramp or paralysis of a healthy ventricle; yet there are physicians who still doubt the efficacy of vasomotor spasm in the mechanism of angina."

I presume it is because of the humane desire not to disturb unnecessarily the patient in the throes of cardiac agony, that we

1 Trans. Clin. Soc. London, vol. iii.

2 Lancet, London, March 26, 1898.

find more frequent record of the condition of the radial pulse in these cases, than of the heart itself. If, however, the heart of such a patient be examined, it will be found that the extinction of "aortic character," which Powell noted in the radial pulse, is also very distinctly appreciable at the aortic orifice itself. The usually very considerably hypertrophied left ventricle will be found to pulsate with increased frequency, the bruits significant of the valvular defect being almost or quite hushed, and increased tension in the pulmonary circuit indicated by a well-marked accentuation of the second sound at the pulmonary arterial orifice. There is repletion of the ventricular cavity, and comparative emptiness of the extra-cardiac systemic arteries. The full and hypertrophied heart labours violently to rid itself of the residual, stimulating, and dilative burden of blood, not because it cannot jerk some of its contents into the larger comparatively empty vessels with more than "aortic" emphasis, but because its own intrinsic and momentary failure has cast upon it a paralysing weight which must be rapidly reduced if the organ is not to come to a standstill. The small peripheral pulse which is associated with such valvular angina during the period of cardiac failure, is not on this showing one of spastic narrowing, but of empty collapse. The following sphygmograms (Figs. 25–28), which I published to illustrate a paper on the blood pressure in angina pectoris,1 may render my meaning clearer. The first shows the attack at its height, with a lowering of the predicrotic wave and a flat drag in the diastolic interval, meaning, as I think, that the collapsed and comparatively empty artery has failed to reach the lever of the instrument. In the next the cardiac force is increasing, its action becoming slower, and, although blood still fails to reach the periphery in normal abundance, there is a rise in the position of the predicrotic wave and an indication of dicrotism; pain is still present under these circumstances, but the patient is easier. The next sphygmogram represents the refilled and retarded pulse and the cessation of pain. The fourth and last tracing shows the typical aortic regurgitant pulse of the patient during a period of temporarily re-established compensation. The tracings also show the influence of respiration upon the circulation. Dyspnoea, at its acme in the first, shows the rising curve of preponderant inspiration, the line falling to the expiratory and equable type as the attack subsides. With these tracings, those given on p. 94 may be compared.

1 Edin. Hosp. Rep., 1895, vol. iii.