ABSTRACT OF The Morison Lectures ON THE RELATION OF THE NERVOUS SYSTEM TO DISEASE AND DISORDER IN THE VISCERA

1898 The Lancet  
DISORDERS OF VISCERAL MOTION. 'SIR JOHN TUKE AND FELLOws,-The separation of sensation from motion is relatively to the mind a distinction in what may be termed objective consciousness. We feel pain and can localise it and we can observe movement. The ;separation of sensibility from motility is a finer distinction and is largely in what we may term subjective consciousness or reasoning. Essentially the transmutation of one form of motion into another merely emphasises the common property by
more » ... a living universe is conditioned. Clinically the 'distinction is convenient and no circumstance reveals more instructively the relation of the nervous system to visceral motion than the influence one organ has upon another. The displaced or twisted kidney which induces a tachycardia, the diminished thyroid secretion which causes a cardiac stagger or a bradycardia, the retained excretion or the peripheral excitation which induces a convulsion, or the functional inactivity generally which disturbs metabolism,-all show how intimately one form of motion is related to another ; and when we emphasise motility in a given clinical condition we might rationally regard it in some instances as the motor feature of an essentially sensory and causal dis-..order. In touching upon some points illustrative of the relation of the nervous system to viscero-motor disease and dis--order I shall follow the plan already adopted in discussing sensory disorders and take as the type of disordered visceral motion abnormalities in the action of the heart, making 'reference incidentally to analogous conditions in other -organs. The motor innervation of the heart we know is accelerant and augmentor-motor, inhibitory and depressor-motor, and trophic or pneumogastric proper, all these movements having ' necessarily their sensory concomitants or equivalents. Gaskell and his successors, anatomical and physiological, have revolutionised, as we learned last year, our conceptions of the visceral nervous outflow in general, including the innervation of the heart. For whereas we formerly regarded the pneumogastric as a primary and the cervical sympathetic as .a secondary source of cardio-motor innervation, we now believe that the pneumogastric is a secondary and the cervical sympathetic a tertiary source of such innervation. Whether all the supra-thoracic vaso-motor outflow originates .as low down as the second dorsal spinal nerve appears still to be somewhat doubtful. Hill and Bayliss failed to evoke 'vaso-motor action in the intracranial circulation by electrical stimulation from this region. Without the aid of experimental physiology and merely using the microscope for .anatomical research I have met with conditions bearing on this point which will be seen on the table and are repro-. duced on the screen. It will be seen that what appear to be the sources both of the pia matral and pia vascular innervation are certain tassel-shaped bodies which are arranged centripetally to the vessels and of which I give a short account this month (November) in the Edinb2crg7t Medical Journal. . The precise locality of these vessels I have not yet had an -opportunity of determining, but they ,appear to me to be 1 Lectures I. and II. were published in THE LANCET of Dec. 17th and 24th, 1898, respectively. 2 Journal of Physiology, 1895. sufficiently characteristic in design to be capable of identification by injected specimens. Thus identified, the position of the bodies in question, whether they be the source of vaso-motor nerves or no, should also be determinable.3 In the meantime we may assume, notwithstanding Hill's and Bayliss's failure to elicit response, that the outflow of the indubitably existent vaso-motor nerves in the pia mater is from the same region as the general vaso-motor outflow, that is, below the level of the first dorsal nerve, and thus bring the vaso-motor phenomena of all the viscera including the brain, into line. Cardiac motion, like secretory and other motion, may be average or normal and plus or minus. A mid-point or equilibrium is a balance of extremes and vital equilibrium is maintained by a certain variation around a centre of equipoise. Acceleration and retardation, augmentation and depression, constantly correct one another with the sensitiveness of a species of tentacula to surrounding circumstances, these tentacles being the nerves and the properties with which they are endowed. This is well exemplified by the influence of respiration on the character and rate of the radial pulsation. (Fig. 1.) The sphygmogram I throw on FIG. 1. a, Pulse during quiet respiration. b, Pulse during forced respiration. the screen shows the small waves of forced inspiration on the ascending portion of the curve, followed by the large waves of prolonged expiration on the descending portion. These are no more the evidences of a mere pneumatic suction and propulsion than the cerebral circulation is the passive arteriovenous balance which Monro and his disciples conceived it to be. The pneumatic conditions play a part in the one as the comparative resistance to atmospheric pressure does in the other, but the character and rate of the waves in the two portions of the curve indicate a vaso-motor regulation, the peripheral incentive to which is, I believe, to be found in the increased pressure in the dextral chambers of the heart and pulmonary circuit during inspiration. For comparison with the tracing of forced respiration I show one of the pulse of the same subject taken at the same time during quiet breathing in which the pneumatic factor is conspicuous by its absence, although in a minor degree doubtless still operative. (Fig. 1 a. ) 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 submaxillary gland. It is probable that the same rule applies to other forms of vital motion. Dr. William Hunter,4 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 ppristalsis 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 ? 7 The main secretory nerve of the liver is the pneumogastric and its sympathetic endowment is from the splanchnic nerve, while vaso-motor nerves for the portal vein are derived (according to Bayliss and Starling, quoted by Haliburton5) from nerves ranging from the third to the 3 The neural nature of these structures has been disputed by a good microscopist, but I believe I am correct in maintaining the view I have expressed. 4 Allbutt's System of Medicine, vol. iv., p. 68, et seq. 5 Op. cit., p. 670. 1752 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 well-meaning 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 toxaemia 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 to be as probable as other theories suggested and brings the motor activities of the liver into line with those of the heart, which is my present purpose. Again, the striking phenomena on the one hand of Graves's disease, which I prefer on this occasion to call Begbie's disease, and on the other of myxoedema appear to suggest a parallel on similar lines. The thyroid gland is innervated by the pneumogastric and by 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 cardio-vascular neurosis, to employ a term expressive ef 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 coursing 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 vaso-motor commotion in 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 vaso-motor over-action, may also induce a supple. mentary 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 myxoedema 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. Action and supplementary action, endeavour and support, over-action 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 form. 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 phrenalgia" " 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 proportionate to the amount of the stimulus. The tachycardia associated with 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 liacalister has stated, to the amount of mere displacement. G Calculi, we have seen, may induce an extreme of agony which may terminate in collapse and death, the associated cardio-vascular phenomena being those of rapid and enfeebled action of the heart and a general vasoparesis accompanied by profuse perspiration and depression of temperature. These extreme phenomena differ from thoseassociated with angina pectoris chiefly in the situation of' referred pain and in the uninterrupted duration of the agony. With this distinction these might be termed cases of angina. pectoris hepatica, renalis, et haec 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 symptoms. The conditions usually first observed by the ear and the 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. Dr. Lauder Brunton was the first, so far as I know, to note graphically the cardiovascular movements connected with valvular angina. In the-Transactions of the Clinical Society of London (vol. iii.) he published a case 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. I throw on the screen a slide prepared from the published tracings. Dr. Brunton considered the pulse of the agony two, 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 toregard 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 of London? also describing what he terms vaso-motor 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 thepatient 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 theaortic 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 vaso-motor contraction to cause cramp or paralysis of a healthy ventricle; yet there are physicians who still doubt the efficacy of vaso-motor 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 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 Sir Richard: 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 topulsate 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 ventri-L cular cavity and comparative emptiness of the extra-cardiao 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 r contents into the larger comparatively empty vessels with more than "aortic" emphasis, but because its own intrinsic
doi:10.1016/s0140-6736(01)82967-6 fatcat:7rcohc5rufa2xh7utglvwbfvgy