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Luau is uuao

dition of two opposites, there is a corresponding doublephysical condition, also of two opposites, of the highestlevel; there is loss of function of, I will suppose, the

highest "layer," answering to the negative part of the

sleeper’s mental condition and there are increased activitiesof the uncontrolled lower layers which answer to the menta-tion of his dream. The nervous activities correlative withthe mentation of his dream are, I suppose, confined, or nearlyconfined to his highest level, the nerve currents not beingstrong enough to overcome the resistance of, or of but fewof, the elements of the middle motor centres ; there is there-fore wide irradiation of these boxed-up" currents in thehighest level. But if the dream becomes very vivid and,correspondingly, the correlative nervous activities very strong.the resistance of the motor centres of the middle (and nextthat of those of the lowest level) is overcome ; the middlemotor centres being overcome are then paths (downward) ofleast resistance; the irradiation in the highest level will bemuch less wide ; the dream ceases, or rather its mentationmerges into, or gives place to, waking mentation. I will nowtake a case of somnambulism, sleep with elaborate actions ;from this condition, the rule is, nothing is remembared onfull awakening. In this case the middle centres are over-come ; if they were not (and after them the lowest), therecould be no actions; thus the nerve currents are not con-fined to the highest level and consequently, in com-

parison with what occurs during a dream, there is lesswide irradiation in that level and consequently thedream is very faint, or possibly there is no dream.To say that there is no dream in somnambulism ishowever to say more than one can know; it is betterto say that nothing is remembered from the state of som-nambulism on awakening. Here is an old question. Is even

deepest sleep ever dreamless ? (Leibnitz, Kant, Jouffroy,and Sir W. Hamilton thought sleep was never dreamless.)I feel sure that in somnambulism there are some nervousactivities of lower layers of the highest level, determining,by sub-agency of motor centres of lower levels, the elaborateactions of the somnambulist; there may or may not be menta-tion (a dream unremembered on recovery) attending thoseactivities.

Such relations between the different levels as I have illus-trated by different states of sleep are very important withregard to epilepsy, especially a particular variety of it ; Imean cases in the minor paroxysms of which there is theso-called intellectual aura, or, as I prefer to call thisvery elaborate mental condition, the dreamy state."The patient on coming fully round from his fitand its effects remembers that mental state (else we

should get to know nothing about it) ; but when afterthe fit in which it occurs there is a stage of elaborateactions with so-called loss of consciousness, he remembersnothing from that state. I think it unlikely that the"dreamy state ceases when the patient begins to act not-withstanding that he remembers nothing from that stage ;more likely it diminishes and becomes more definite. In somecases there is a traceable community of nature between the"dreamy state and the subsequent actions : I have spokenof such cases.49 "A patient of mine had the dreamystate’ of being somewhere else’ ; after the paroxysm he,as his friends put it, I made for the door.’

" Here I believeis the explanation of so-called Procursive Epilepsy. I donot think that anything like an epileptic discharge wouldcause a man to run; the running in these cases begins, Ibelieve, when that discharge is over, but before the highestlayers of his highest centres rendered functionless by thatdischarge have become again functionable ; the running isdetermined by activities of lower layers of the highest level(with concomitant dream), with hub-agency of the middleand lowest levels.

49 Lectures on the Diagnosis of Epilepsy, Medical Times andGazette, vol. i., 1879, p. 143; at p. 225 op. cit.

Clinical LectureON

A CASE OF CHRONIC MEDIASTINITIS.Delivered at Paddington Green Children’s Hospital on

Dec. 13th, 1897,BY G. A. SUTHERLAND, M.D. EDIN.,

M.R.C.P. LOND,PHYSICIAN TO THE HOSPITAL.

GENTLEMEN,-The case which I bring before you to-dayis not a common one, but its interest lies not so much

in its rarity as in the physical signs which are extremelyinstructive. It is an advantage from some points of view tobe able to recognise a leading symptom, to label the disease,and at once to prescribe the appropriate treatment, but thisdoes not conduce to much thought or to much progress inknowledge. There are advantages, on the other hand, inconsidering a case like the one before you because the

history and the physical signs must be carefully gone intoand the diagnosis can only be reached by a process of

reasoning based on a careful study of all the symptomspresent. Further, this is not an affection much referred toin the text-books, but it is none the less important, and whenonce you have studied one case you are much more likely torecognise the next that presents itself.

Six months ago this boy, who is now eight years old, wasbrought to the hospital because of swelling of the abdomenand exhaustion with shortness of breath on exertion. The

symptoms had commenced some months previously and themedical man who was called in found that the patient wassuffering from heart disease. There had been no oedema ofthe lower limbs, but the face was noticed to be rather puffyabout the eyes. His previous health had been good on thewhole. Three years previously he had had an attack ofleft-sided pleurisy with effusion. In infancy he had sufferedfrom rickets and bronchitis and at the age of three years hehad been troubled with a paroxysmal cough. He had neverhad scarlet fever, chorea, or "growing pains." There wasan absence of any constitutional disease in the familyhistory.Examination on admission showed that the boy was

rather thin with some puffiness about the eyes and adusky colour on the cheeks, lips, and tongue. Therewas no oedema of the extremities but the finger-and the toe-nails were somewhat blue and the superficialveins generally were dilated. A prominent feature was thelarge globular abdomen, measuring 27 in. in circumference,which was distended with free fluid so that normal intestinalresonance was present only over a small area around theumbilicus. The fluid also passed in front of the liver whichcould be felt on dipping to extend for some distance belowthe costal margin. The spleen was not enlarged, but thetense state of the abdominal wall prevented any completeexamination at this stage as to the presence of enlargedglands or other growths. The respirations were short andrapid but not accompanied by any signs of dyspnoea or bycoughing. The expansion of the chest wall was limitedand the percussion note generally was not good, there

being distinct impairment over the left base anteriorlyand posteriorly. The breathing was harsh vesicular backand front for some distance around the mid lineand rather faint in the axillae and at the bases ofthe lungs. Cardiac pulsation could not be determined bypalpation, but on percussion the area of dulness was not

apparently enlarged. At the apex the sounds were weak butregular and no murmur or other evidence of organic diseasecould be detected. The urine was of normal amount andspecific gravity and contained no albumin or sugar. Thus farwe were not able to come to any definite diagnosis. The boywas put nn a diuretic mixture and mercurial inunction wasordered for the abdomen. At the end of a fortnight the fluidin the abdomen had increased and in addition the heart wasweaker and more irregular, the breathing was more laboured,the face was more puffy and more cyanosed, and albumin waspresent in the urine. Accordingly the abdomen was tapped

B 2

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and 106 ounces of clear albuminous fluid were drawn off ;with great relief to the patient and with the disappearanceof the pressure symptoms just mentioned. Examinationnow showed the liver to be enlarged downwards, the lowerborder extending to the level of the umbilicus. Thesubstance felt firm, the margin was sharp, and it was :thought that the surface was rather irregular With thisexception nothing abnormal could be detected in the abdo-minal cavity.Now, if you examine the abdomen to-day you will find that

the condition is very much as I have just described it.During these six months the abdomen has been tappedeleven times and fluid varying in amount from seven to tenpints has been drawn off. The liver appears to be somewhatsmaller and harder than it was, but I cannot detect anymarked irregularity-certainly there are no definite nodules.The abdominal wall seems thickened as if from peritonitis,but there are no adhesions, as evidenced by the completenesswith which the fluid is evacuated on tapping. Considernext the boy’a general condition. He is sitting up in bedin his usual position and with his usual expressionof placid contentment. If you ask him he will assure youthat he has at present no pain or discomfort of aoy kind andthat he eats and sleeps well. Perhaps I should qualify thelast statement by saying as far as his duties allov him, forhe acts as his own clinical clerk and carefully records anysymptom which may arise during the day or night. His

temperature, apart trom complications to which I shall refer,has been normal. The urine at times is scanty and containsalbumin, more especially when there is great abdominaldistension, but this condition passes off after tappingand there are no tube casts or other signs of renaldisease. The state of the heart has not materiallyaltered. The sounds are still rather weak and the pulseis soft. He has had several attacks of follicular tonsillitiswith considerable pyrexia You will observe the duskyappearance of the lips, tongue, and fingers which was pre-sent on his admission and which is prartically unchanged.

accidentally discovered. The friction, which is ot an extremelycoarse grating character, is still well marked, especially after the abdomen has been tapped and the respirations havebecome fuller. It can then be traced from the mid-line infront outwards into the axillse, downwards over the hepaticregion to the costal margin, and around the bases of the lungsto the back. You will also be able to make out the definitedulness over the mediastinal region anteriorly with veryharsh bronchial breathing over a larger area than normal.Now let us consider the question of the diagnosis. On the

boy’s admission the ascites was the most prominent sign andnaturally led us to think of the three great causes of thatcondition-cardiac, renal, and hepatic. Although theheart-sounds were weak there was no evidence of dilatationor hypertrophy or valvular disease. Further, althoughenlargement of the liver with ascites may be a prominent ,

sign of failing power or failing compensation in the heart weshould expect a more generalised cedema and more markedcardiac changes than were present in this case. As regardsprimary kidney disease the normal condition of the urineand the absence of general dropsy and other renal symptomsled us to exclude tbis possibility. In the subsequentprogress of the case the temporary albuminuria and oliguriacould be explained by the pressure ot the ascitic fluid. Amore satisfactory diagnosis seemed to be indicated by theassociation of an enlarged liver with ascites and for a timewe regarded the case as one of hepatic cirrhosis withimpediment to the portal circulation. This, however, wasentirely a provisional diagnosis, made rather on account ofthe absence of positive signs of any other lesion. There wasno history of alcoholism, which is of course the commonestcause of cirrhosis, or of syphilis. As time went on there was nofurther evidence obtained of hepatic cirrhosis-that is to say,the spleen was not enlargiug, the appetite was good, there wereno symptoms of intestinal catarrh or congestion, and therewas no progressive ill-health. Amongst the other abdominalconditions which presented themselves in considering thepossible diagnoses was that of chronic peritonitis, which is

. not unfrequently accompanied by considerable enlargementiof the liver. Against this you will remember that the fluidwas large in amount and free in the peritoneal cavity,I whereas in peritonitis it is usually small in amount andshnt ofE by adhesions. That there is now a certain amount’ of chronic peritonitis I believe to be extremely probable, but, I regard it as the result and not the cause of the ascites. A

F diagnosis, then, either of hepatic cirrhosis or of chronics peritonitis has not been adhered to because (1) the symptoms in the abdomen were stationary-tbat is to say, both the3 ascites and the condition of the liver are practically thee same to-day as they were six months ago; (2) the abdominalr symptoms appeared passive rather than active, there beingy an absence of all pain, tenderness, or intestinal disturbance;n and (3) our attention was directed to changes in another party of the body.

Let me ask you to assume for a moment that there hasis been at some previous period inflammation of the lymphatics glands in the mediastinum and that this has led to enlarge-ment and matting together of these glands with chronic11 mflammation extending into the surrounding structures. In

the earlier stages we cannot make out these changes bydirect examination, we can only form an opinion from the

ts results of the pressure on air passages, blood-vessels, andnerves. I suggest to you here that there has been pressure

ie on the superior vena cava as manifested by the prominenta veins in the arms and neck, the puffiness of the face, and theot duskiness in the cheeks, lips, and tongue. Further, I suggesttie that there has been pressure on the inferior vena cava in theth chest as evidenced by the enlarged liver and ascites andof pressure on the pulmonary veins as evidenced by the attack&ve of pulmonary cedema, dyspnoea, and catarrh. Again, 1 ,

h. suggest that there has been pressure on the bronchi or on;er the nerves supplying the bronchi as evidenced by thelal paroxysmal cough which has been so persistent. I alsoed suggest that there has been an extension of the chronicad inflammation to the pleura as evidenced by the presence ofm coarse pleuritic friction appearing first at the sternum andno- extending outwards on both sides. Finally, I suggest that)th there has been a steady increase in the size of this mediastinalme growth as evidenced now by dulness on percussion over andLtn, around the sternum and the loud conduction through thisess mass of the sounds from the bronchi lying beneath it. Theltic assumption I have made as to a mediastinal lesion is thevn only one which seems to explain the various phenomena’his present in this case.was You are now in possession of the history of the illness

There is, however, some clubbing of the fingers and toeswhich is of more recent development. We have been agood deal occupied in observing the pulmonary conditionsand to the history of these I wish to direct your carefulattention. About a month after admission he developed acough which increased rapidly in intensity and became of soexplosive a character that, whooping-cough being suspected,he was removed to the isolation ward. During the course ofthe next seven weeks this cough persisted and at times wasof an extremely exhausting character. It was paroxysmal intype, most severe at night, and during an attack the facebecame much more swollen and cyanosed. Soon after theonset haemorrhage occurred in the lower eyelids and underboth conjunctivas so that the whites of the eyes were entirel3concealed by exTavasated blood. Vomiting followed ar

attack of coughing on a few occasions, but there was never an]whoop or epistaxis. The signs in the chest were those of bronchitis, there being numerous moist and dry catarrhal sound,distributed generally over both lungs. During this illnesthere was oedema of the chest wall and very marked dilatation of the veins in the upper part of the thorax. Carefuexamination was made as to the presence of any mediastinaaffection but no dulness on percussion or alteration in thbreath sounds could be determined. The expectoration waextremely scanty, frothy, and at times blood-stained. Yowill observe that these signs-with the exception of thabsence of any whoop-would fit in very well with

diagnosis of whooping-cough. The signs, however, are n(diagnostic of whooping-cough but are indications of tl

severity of the cough, being most frequently associated witthat affection but occurring with any spasmodic cough sufficient violence. We hesitated for some time but ha1now come to the conclusion that it was not whooping-couglSince the acute attack there have been others ot shortduration but presenting the same violent paroxysmuseless cough, which does not seem to be induc

by any intra-pulmonary condition, but which may Ie:to some pulmonary catarrh with scanty frothy sputuiAt times also there have been evidences of pulmnary cedema affecting the right or the left base or bobases. About two months ago we found that there was sot

impairment ot resonance over the upper part of the sternuwhich has gradually extended on each side and now duln4has become quite marked. Soon afterwards coarte pleurifriction was detected over the sternum and passing dowwards to the axillary regions on both sides. T.

pleurisy was unaccompanied by any pain or pyrexia and a

89

and the physical signs which have led us to form a diagnosisof chronic mediastinitis. I do not ask you to accept thatconclusion but to examine and form your own opinion, for inthis affection there are no certain signs by means of whichwe can reach a positive diagnosis. The signs in one casewill differ from those in another, there heing constant varia-tion according to the incidence of pressure, the direction inwhich the inflammation spreads, and the size of the new

growth. Besides chronic inflammation we have to keep inview the possibility of mediastinal tumour, simple or

malignant, although the history of the case rather excludesthe latter. It is seldom possible to make a definite diagnosisbetween a mediastinal tumour and chronic mediastinitis

during the life of the patient. We have assumed that thestarting point of the disease was in the glands because thatis the most common site of origin. In other cases the affec-tion may begin in the pericardium-when it is known asmediastino-pericarditis-or in the pleura or in the lungThe condition becomes one of general inflammatory thicken-ing of the mediastinal tissues, which in time becomesfibrous or semi cartilaginous. The disease runs a chroniccourse but a progressive one, and death may ensue frompressure on a vital structure or from some complication,pneumonia, &c.The treatment is general and symptomatic. In this case

the ascites has frequently had to be relieved by Southey’s tubes. Whenever there is actual discomfort from abdominaldistension the fluid is removed and the benefit is alwaysmarked. In the early stages the boy had much more

energetic treatment and purgatives, diuretics, cardiac stimu-lants, and mercurial inunction were employed without pro-ducing the slightest effect as regards the ascites. Similarly-and this is an important point in connexi n with the

diagnosis-the paroxysmal cough was not at all affected bylocal treatment and only very slightly by full doses ofnervine sedatives, while the pleurisy is so irresponsive totreatment that we now leave it alone. He is at presentpassing a quiet, restful existence on a full nourishing dietwith plenty of cod-liver oil and iron.

ABSTRACT OF THE

Morison LecturesON THE

RELATION OF THE NERVOUS SYSTEM TODISEASE AND DISORDER IN THE

VISCERA.Delivered before the Royal College of Physicians of

Edinburgh on Nov. 1st, 3rd, and 5th, 1897,

BY ALEXANDER MORISON, M.D.,F.R.C.P. EDIN.,

PHYSICIAN TO OUT-PATIENTS, GREAT NORTHERN CENTRAL HOSPITALAND THE CHILDREN’S HOSPITAL, PADDINGTON-GREEN.

LECTURE 11.1

Delivered on Nov. 3rd, 1897.

MR. PRESIDENT AND GENTLEMEN,-When we strike themain stream of innervation at the apex of the visceral deltaof secretory, mobile, and excretory nerve distribution our

task in tracing the current is considerably simplified. Here

also, however, the threefold state referred to in the conditionsof the ultimate distribution is taken by the triple conditionsand their associated questions of medullated and non-

medullated fibres and of the ganglion cells regarded asanatomical entities and conglomerate structures.The relation of nerve fibres to gangtion cells, and clusters

of cells is of anatomical and physiological interest. Theganglion cell may occur isolated on a nerve or smallstrand of nerve tissue (Fig. 7) or embedded as it werein the heart of a considerable trunk (Fig. 8) A groupof cells may also form a fusiform or irregular enlargementon the course of a nerve larger than the nerve itself, one

1 Lecture I. appeared in THE LANCET of Jan. 1st, 1898.

end-the afferent end-being as it were lost in the enlarge-ment and a fresh trunk issuing from the other or efferent,end-afferent and efferent in this sense being used relativelyto the ganglion and not to the central nervous system,

FIG. 7.

Ganglion cells and clusters on nerve strands from the hepato-duodenal region of a mouse. a, t ongeries of cells at ajunction. b, Issuing strands, c, Smaller collections of cells.

from which both, naturally, are efferent (Figs. 9. 10 and 11).Or again a cell or group of cells may lie outside a nervetrunk and have connexions with it on one hand, whileon the other it distributes fibres in different, but always

Showing the innervation of a bronchus from the lung of akitten a, Trunk with collection ot ganglion cells in it.b, b, Branches. c, Lumen of bronchus.

centrifugal, directions (Fig. 12.). The ganglion cell may alsoapparently occupy a somewhat peculiar poirion in this wise.The cell or cells may be placed at a considerable distancefrom the nerve trunk and send axis cylinder processes into