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convolution, and especially those in which it has beensituated in the upper part of the island of lteil.Word deafness with aphasia.-Where a destructive lesion

involves the auditory word centre aphasia is also produced,only now it is associated with word deafness. Such apat,ient’s mental condition is profoundly altered. Thus, inaddition to being speechless, speech can no longer be under-stood ; and, seeing that words a e first and principally re-vived (even in silent thought) in the auditory word centre,thought in words would be no longer possible. The powerof writing would therefore also be lost, and probably verylittle power of comprehending printed or written languagewould remain, seeing that the revival of words in the visualcentre could not be reinforced by their revival in the auditorycentre. It has already been pointed out that slighterdefects in the auditory word centre only give rise to variousdegrees of amnesia.

Commissural amnesia.-This is perhaps the most suitablename for the kind of defect we have been studying to-day,where the commissures are damaged between the auditoryand the visual word centres, and the patient is consequentlyno longer able to name and read at sight, or to write fromdictation. The precise topographical location of these com-missures remains yet to be discovered. Sometimes one-halfof this double commissure is alone damaged.Word blindness with agraphia.-A lesion in the visual

word centre gives rise to word blindness with agraphia.Though not blind in the ordinary sense, the patient may be

Diagram showing the possible situation of an apha;ia-pro- Iducing lesion, either in the losso-kinaesthetic centre (a), in .

the commissure (b), between it and the auditory centre, or inthe auditory centre itself (c), in which latter case it is asso-cia.ted with word blindness.

quite unable to understand either written or printedlanguage. He is able, however, to understand spokenlanguage, and can himself both think and speak.Agraphia.-Here the patient can speak but cannot write ;

he can read also, and there is little or no interference withthought. This defect is produced by a lesion of the cheiro-kinaesthetic centre situated in the posterior extremity ofthe second left frontal convolution. But a damage to anypart of the commissure connecting the cheiro-kinsestheticwith the visual word centre would produce exactly the samedefect, seeing that the stimulus which is to rouse the formercentre into activity must first traverse the above-mentionedcommissure. There is no paralysis of the hand except forwriting movements. (As a matter of fact, isolated agraphiaseems only to occur as a result of a lesion in the cheiro-kinaesthetic centre. The fibres of the visuo kintcsthetic com.missure, d, probably run, not as they are represented in thediagram, Fig. 1, distinctly separate from those of the audito-kinaesthetic commissure, c; they probably run in close

proximity to one another, so that a lesion along their tractdamages both at the same time, and consequently pro-duces not a simple agraphia, but a typical aphasic con-dition, in which there is loss of speech as well as of thepower of writing. This accounts for the comparative rarityof simple agraphia.)In conclusion, Dr. Bastian pointed out that the mode of

Iviewing speech defects which he had submitted to them didnot countenance the classification of these defects, whichhad been common of late years, into

11 motor and sensoryaphasias." The defects were in all cases, as he thought, insensory centres or else in the commissures between such

centres, excepting in the case of aphemia, where the lesionproducing the defect was in the course of the internuncialfibres, passing from the third frontal to the motor centresin the bulb. The fact that a paralytic disability is pro-duced does not, as the case studied had shown, in any wayprove that it is not due to a defect in a sensory centre orin a commissure between two such centres ; it is here, infact, that we have to look for the sources of volition.

LectureON

THE PATHOLOGY OF DROPSY.Delivered at King’s College Hospital,

BY NESTOR TIRARD, M.D. LOND., F.R.C.P.,PHYSICIAN TO THE EVELINA HOSPITAL FOR SICK CHILDREN ; SENIOR

ASSISTANT PHYSICIAN, KING’S COLLEGE HOSPITAL.

GENTLEMEN,—There are many diseases, and many con.ditions occurring in the course of various diseases, whichwe meet with so commonly in our hospital work that weare tempted to take for granted the explanations which areto be found in our text-books, or those which have beenfirmly fixed in our minds, almost as articles of belief, in ourstudent life. Waves of investigation from time to timedisturb some of our cherished notions ; the history of theprogress of medicine is full of instances illustrating thetruth of this; hence it appears to me to be worth whileraising the question of how far our ideas of this singlesymptom-dropsy-are founded on a firm basis.

First, then, to consider the condition itself, and theviews at present held as to its causation. Summarisingthe opinion expressed by Dr. Lauder Brunton in the Prac-titioner, dropsy may be regarded as consisting essentiallyof an overfull condition of the lymph spaces-cavities whichare normally kept moist by the transudation of fluidfrom the capillaries, and from which the fluid is in turnwithdrawn by the combined action of the lymphatics andthe veins. Dr. Brunton lays special stress upon the fact ofremoval by both lymphatics and veins, and he emphasisesthis idea by stating that when the chief vein of any district

is ligatured the lymph flowing thence through lymphatics

is increased in quantity. He admits that this may be partlydue to the fact that the quantity poured out from thecapillaries is increased in consequence of the ligature ofthe vein ; but he considers that it is probably due in greatmeasure to the lymph, which would have been poured out inany case, passing away by the lymphatics when it can nolonger be taken up by the veins. Further, it has beenproved that complete arrest of flow through the veins is nota sufficient cause for dropsy, provided that the flow throughthe lymphatics is unaffected. Turning, then, to the causeof the flow of lymph, it is stated to be due to the differenceof pressure between the two ends of the lymphatic vessels.11 It is increased by the pressure being raised in thetissues and lowered in the vena cava, and it is retardedby opposite conditions." Dr. Brunton further sumruarisesthe conditions which will interfere with the flow of lymph,as (a) want of muscular action, (b) want of inspiratoryaction of the thorax, (c) diminution of the diastolic suctionof the heart, (d) p08itive pressure in the veins. For mypresent purposes I would direct your attention particularlyto the third condition enumerated. It distinctly impliesthat the overcharged condition of the veins is due to de-ficient force of suction exerted by the heart. Further, Dr.Lauder Brunton enumerates with greater precision the con-ditions which interfere with the flow of blood in the veins,as (a) want of muscular action throughout the body,(b) want of movement in the thorax, (c) feeble action of theheart, no matter whether we look upon the systole or dia-stole as being the active power in sucking the blood onwardsthrough the veins, (d) pressure upon the veins from without,

and (e) plugging within.

Briefly stated, then, in any case of dropsy we have to lookfor some cause or causes which will produce more rapideffusion from the capillaries, and some cause or causeswhich will impede the reabsorption by veins and lymphatics.Confining our attention for the present to cardiac dropsy,

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wb find that the most commonly accepted theory is that of actual demonstration, yet it is fully in accordance with"backward venous engorgement." According to this theory clinical experience, both as derived from consideration ofill forms of heart disease tend to impede the flow of blood the ordinary history of a case of cardiac dropsy, and alsofrom the heart; hence whether the case be one of aortic or from the results of the employment of various remedialmitral disease, obstructive or regurgitant, the left auricle is agents. Briefly, then, the theory is that one very importantlikely to become surcharged with blood, then the pulmonary element in the production of cardiac dropsy is to be foundcirculation is impeded, the right side of the heart becomes in deficient propelling force imparted to the blood at itsdistended, and eventually the engorgement acts backwards passage into the aorta. In other words, I believe thatfrom the heart along the whole of the venous system, attention has been too much directed to the backward con-making itself felt by enlargement and disordered function dition, without taking sufficient note of the diminution inef various viscera, and also by dropsical effusion into the arterial pressure which must necessarily occur at an advancedvarious lymph spaces. stage of the disease. In all cases of heart disease associated

Dr. George Johnson, in a paper in THE LANCET of with dropsy, I believe that the latter occurs when the con-June 20th, 1868, on " Some Results of a Retrograde secutive hypertrophy is no longer of sufficient compensatingEngorgement of the Bloodveesels," remarks that it is "an power-when, in fact, the heart no longer sends forth aundoubted fact that an obstructive valvular disease on the sufficient quantity of blood with an initial force adequateleft side of the heart may affect the most remote parts of to drive it round the circle until it can come under the suctionthe circulatory system. Thus the impediment resulting force which facilitates its return to the heart. The cardiacfrom a defective mitral valve may extend backwards through contractions continue, but whether owing to regurgitationthe pulmonary capillaries to the systemic veins and or to obstruction at either the mitral or aortic valves, thecapillaries, causing anasarca of the feet &c.; it may initial velocity imparted to the blood as it enters theextend through the capillaries within the liver to the portal arteries falls considerably below that of health, and, -as a-vein, and its capillary origin, causing ascites; and through consequence, although the force may be sufficient to propelthe intertubular renal capillaries to the Malpighian capil- the blood through the arterial system, it is dissipated aslaries, causing albuminuria. It is manifest that neither the blood flows through the capillaries, and but little forceextreme distance from the seat of obstruction nor the is left to carry it on its return journey through the veins.intervention of two successive sets of capillaries will prevent The natural result is fulness of the veins of the extremities,that retrograde passive engorgement of vessels which results more particularly shown in the lower extremities, where thefrom a block in the course of the circulating current." action of gravity adds to the difficulty of return. This fulnessThis theory, if we accept Dr. Lauder Brunton’s experi- necessarily implies partial stasis, and the blood being thusments, is obviously an incomplete explanation. As thus more subject to physical laws, there is first an alteration instated, it leaves out of account all mention of reabsorption the nutrition of the vessels, and then passive transudation.by lymphatics, and even without this it is not wholly satis- Thus, the theory of deficient initial force will readilytying. Surely if dropsy were produced merely by retrograde account for all the conditions left unexplained upon theengorgement, it should in most cases be preceded by a theory of backward engorgement-viz., for altered charactersuccession of events following the same definite order; in of vessels, for increased transudation of fluid, and forother words, we should expect very marked affection of the impaired reabsorption by the veins. All that remains tovessels of the lungs before those of the liver and spleen complete the picture is to mention that all these conditionsbecome involved; these parts in turn should show signs of may be present in many cases of heart disease, and yeteagorgemeat before the kidneys, and the renal engorgement dropsy will not result until the fourth factor, impeded flowin turn shoiildprecedesignsofdropayinthelowerextremities. through the lymphatics, is brought about by retrogradeAlthough, as ordinarily set forth in text-books, this back- engorgement. This last fact was insisted upon by the lateva.rd engorgement theory makes no direct reference to the Dr. Todd, in his admirable Clinical Lectures (p. 487), wherepart played by the lymphatics in every case of dropsy, it he says, " In all cases what seems to be necessary to theT.’ill be seen upon consideration that it does not negative production of dropsy is dilatation of the right side of thethe idea of impaired absorption by the lymphatics. If we heart." Further he remarks, "Dilatation may exist withoutrevert to the conditions of absorption as stated by Dr. Lauder regurgitation being manifest in the external veins; at leastBrunton, we see that increased pressure in the vena cava I think that the regurgitation need not exist to such ainvolves diminished flow of fluid through the lymphatics. degree as to cause pulsation. I am now attending a case inIncreased pressure in the vena cava is necessarily present private practice in which there are dropsy and undoubtedwhen the condition of circulation through the heart and dilatation of the right side of the heart, but no venous

luaga leads to venous engorgement, and it is quite con- pulsation whatever; and I constantly witness manyc.31vable that this should in turn impede the rapidity with similar." You see, then, that although Dr. Todd fully71hie:h fluid returns from the lymphatics to the vena cava. believed in the retrograde engorgement theory, he admittedThe theory oi backward engorgement, then, does account that it was only the final element in the causation of dropsy.

r,3,.7 one of the factors, which, according to generally received The theory of deficient initial force is entirely in accord-ve’.vs, must exist before symptoms of dropsy can be de- ance with clinical experience. Everyone must have fre-veloped. It does not satisfactorily, to my mind, account quently observed the marvellous results from rest in bed infor the failure of the veins to take their share of the cases of cardiac dropsy. Under these conditions the heartwork of reabsorption, nor for the transudation of fluid. has less resistance to encounter, and very little of its force isla fact, the diinculties of the theory are extreme when expended in the endeavour to overcome the action ofv’e consider that if the transudation is due to backward gravity. The explanation ordinarily adopted is that by theengorge tnent) starting from the vena cava, and extend- recumbent posture the return of blood is facilitated. Uponleg atong the vessels until it makes itself felt in the the retrograde engorgement theory it is not very easy toextremities it would seem legitimate to assert that no see how rest would affect the question. But assumingpressure can thus be thrown back without a certain degree deficient propelling force as an important factor in the pro-d overful ness of call the veins. In fact, if the theory were duction of dropsy, rest in bed is at once seen to lead to asorrest, we should expect to find, post mortem, that the conservation of energy by which each cardiac contractionaperies contained an abundance of blood, owing to the im- becomes more efficient, the forward force is increased, andof its being driven onwards by the last contrac- the degree of fulness of the right side of the heart is thuslions of the ventricle, since the veins are already assumed speedily diminished. Hence, provided that the muscular’:o be obstructively overfilled. This is not the case. The wall of the heart retains sufficient vital force, the conditionsveins certainty are commonly distended with dark blood, which have led to the dropsy are soon reversed. On thebut the arteries are as nearly empty after death from heart other hand, in extreme cases, with complications of pul-disease and dropsy as when the death results from any monary, hepatic, digestive, and renal mischief, the bene-<)ther cpuse. The theory, indeed, appears to assume too ficial effect of rest is less likely to be noted ; in these retro-large a quantity of blood in the body, and too great a degree grade engorgement undoubtedly plays an important part;of past mortem venous relaxation. Feeling, then, that the but, as above stated, it is not, I believe, the sole factor inbackward engorgement theory is only in part true, and that the production of dropsy.the element of truth probably affected the lymphatics Further, with regard to the therapeutic measures whichJ3.ther thin the veins, I have endeavoured to formulate a are ordinarily adopted, the whole theory of the treatment oftheory which should not be open to these objections. heart disease with cardiac tonics and cardiac stimulants

First, let me state the theory, and then I shall hope to lends support to the theory of dropsy I have enunciated,show you that, although, like all theories, it is incapable of since the primary object is always to steady the contrac-

1167

tions of the heart aad to increase their force. It is true that 1

when the strength of the cardiac contractions is increased,the degree of retrograde engorgement is diminished ; but it

I

is none the less true that increased force applied to the bloodas it enters the aorta means also increased force as it passesfrom the capillaries to the veins, and hence results indiminished transudation and increased reabsorption.The theory is not opposed by the beneficial influence of

purgatives, diuretics, and diaphoretics ; these merely favourreabsorption by altering the specific gravity of the blood-or, perhaps it might be more correct to say, by altering fora short time the total quantity of fluid in the vascularsystem, this alteration being, in favourable cases, speedilyequalised by reabsorption of fluid from the tissues. Doubt-less during the time of reduced pressure the heart isenabled to work more efficiently, and hence to relieve back-ward engorgement and to flush the venous system morethoroughly. Whether the theory of diminished force willalso serve to explain the ocurrence of dropsy in cases ofchronic kidney disease I should at present hesitate to say.It would appear, however, that, whether we believe inthe hypertrophy of the smaller arteries and their stopcockaction as held by Dr. George Johnson, or in the arterio-capillary fibrosis of the late Sir William Gull and Dr.Sutton, there is in the character of the smaller arteriessufficient cause for impaired flow of blood through thecapillaries, for altered nutrition of their walls, and fordiminished cardiac impulse communicated to the blood inthe veins-i.e., for three of the conditions necessary fordropsy.

Finally, let me briefly summarise what has been said. fCardiac dropsy is the accumulation of effused fluid in thelymph spaces ; it results from (a) an increased transudationdue to alteration in the nutrition of the vessels ; (b) fromimpaired reabsorption through lymphatics and throughveins. Through the former owing to the impeded flow oflymph resulting from distension of the right side of theheart and backward engorgement ; through the latterowing to the blood in the venous radicles receivinginsufficient propelling force from the heart, and thus beingmore entirely dependent upon the suction force for itsreturn-this last, in turn, being diminished owing to thestate of the right side of the heart.

NOTES ON THE FUNCTIONS OF THENERVOUS SYSTEM.

BY W. R. GOWERS, M.D., F.R.S.,CONSULTING PHYSICIAN TO UNIVERSITY COLLEGE HOSPITAL; PHYSICIAN

TO THE NATIONAL HOSPITAL FOR THE PARALYSED AND EPILEPTIC.

IV.&mdash;MCSCULAR ADAPTATION AND HYPNOTIC CATALEPSY

I MAY recapitulate briefly the inferences of the last, not, Ifear, very intelligible &deg; Note." The widening of contractingmuscular fibres stretches laterally the connective tissue; alltraction on the muscle acts on this tissue longitudinally.The afferent fibres end in this tissue ; impulses are certainlygenerated in them by both forms of tension. Normallythere is a perfect proportion between the two, which is notdisturbed by the contraction of the muscle, because theincreased tension due to this is caused by and borne bythe muscular fibres. The effect of all increased longitudinaltension produced by a tendency to movement of the part, isto lessen the activity of the motor cells and permit the muscleto yield to the movement. We traced the evidence of this inthe case of the contracting opponents of the muscles thatcause a movement. The same law affords so perfect anexplanation of the adaptation to position and of allrelated phenomena that we cannot avoid the conclusionthat it holds good to an equal extent of the musclesin which no voluntary contraction is taking place. Inthe state of "rest," as in the state of activity, the varia-tions in longitudinal tension will induce such variations inthe state of the motor cells as are necessary to cause themuscular fibres to assume the degree of shortening or elonga-tion that corresponds to the distance between the attach-ments. The action of passive movement will cause a

diminished action of the motor cells, precisely proportionedto the degree of traction and the consequent recession of theattachments, and the fibres will elongate in proportion to

the extending force, while the muscles whose attachmentsare approximated will present a corresponding shortening.To understand this effect it is only necessary to remember(1) that a diminution in the longitudinal tension must havethe effect of increasing the action of the cells, and (2) thatthe elongation of a muscular fibre is the result of an activityof its protoplasm no less than the shortening ; apparentlythe shortening occurs only under the influence of the motornerve impulses, while elongation is the result of a tendency.,inherent in the protoplasm, which the nerve impulses oppose.We are bound to assume the spontaneity of the elongatingaction because all facts that have ever been observed con-nect nerve impulses with contraction only. These con-siderations seem to furnish an explanation of the mechanismof the "paradoxical contraction." The sudden diminutionin tension causes-or rather permits-such an increase inthe spontaneous activity of the cells as causes an excessivecontraction.

I would digress for a moment to mention that it seems tome of paramount importance to keep clearly before themind the distinction beween the relations that are to betraced and those that are possible. The great bane ofmedical hypotheses is to take as of equal value assumptionsbased on partial facts-partial, but certain-and assume

I tions based on no facts. The one is legitimate hypothesis,the other pure speculation. To reject the former on thestrength of the latter is a process that deserves the name ef

i suicidal science. It is a purely destructive process, whichl has only to be consistently extended to produce a sufficiently

instructive result. In the absence of contrary evidence, we. are bound to assume as true of the whole that which we3 know to be true of a part. To assert that this may not bei true of the whole, and therefore may not be true of the1 particular instance with regard to which we have as yet noa evidence, is a proceeding that perhaps involves the use off reason, but certainly is not reasoning. " One is as good ase another" is a kind of assertion that h::l.’1 a great etfect onr those who do not take the trouble to ask, " Is it really?"g ry To return to the muscles. If it is true that contractiong is the sole consequence of motor innervation and that everys " negative variation " in the motor impulses is attended bye elongation, the dependence of physiological tone on the

nerve centres follows of necessity, and would be certainwithout the aid of experiment. The explanation ofphenomena other than those by which a theory was framed.constitutes additional proof of its truth.

In considering both the action of the cerebellum and themechanism of automatic coordination, we saw that theinfluence of the afferent impulses on the motor cells of thespinal cord is repeated through the cerebellum on the motorcells of the cortex ; that the functional state of theseapparently underlies our perceptions of posture ; and wecan now perceive better the origin of these perceptions. Themechanism by which the muscles are enabled to adapt them-selves to passive changes in them-the varying stimulationof the afferent nerves-is the same as that by which (throughthe cerebellum) our perceptions of posture are produced.This was considered in the first" Note," while in thelast we saw that the afferent impulses and their effeetgentail corresponding changes in the activity of the motorcells of the spinal cord and of the motor cells of the cortex,which act upon those of the cord.Here we may perceive an explanation of the phenomena

of catalepsy, which, if not complete, at least enables us tosee its mechanism in clear outline. It has been alreadymentioned that in the flexibilitas cerea of catalepsy we canperceive only an excessive degree of the normal adaptationto posture that we have just discussed. In this adaptationthere is a synchronous, similar, and related process in thecortex of the brain and in the cells of the cord. Hypnotismconsists in such a change in the functional state of thebrain as cuts off the lower cortical mechanisms from the in-fluence of higher ones, leaving sensory and motor centresconnected with each other, sometimes with, sometimeswithout some of the lower centres that subserve mentalprocesses. In the hypnotic catalepsy, apparently, the inbibi-

I tory action includes all the structures that subserve psychicalprocesses, and the lower motor centres are in functional

, connexion only with the lower sensory centres. The- higher controls the lower, and, uncontrolled, the lowerL passes into a state of increased action. This law seemsl to obtain throughout the central nervous system. Thes spontaneous activity of the motor cortex, unrestrained,) is instantly manifested by the universal increase in the