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No.3261. FEBRUARY 27, 1886. THE Erasmus Wilson Lectures ON EVOLUTION IN PATHOLOGY. Delivered at the Royal College of Surgeons. BY J. BLAND SUTTON, F.R.C.S., ASSISTANT-SURGEON TO THE MIDDLESEX HOSPITAL, AND LECTURER ON COMPARATIVE ANATOMY. LECTURE III. THE ETIOLOGY OF NEOPLASMS. MR. PRESIDENT AND GENTLEMEN,—The term " tumour " has been applied to so many kinds of growth, and used so loosely, especially in clinical work, that it ceases to carry with it any definite significance. It is necessary to adopt some rigorous limitation to the term, or choose a name which shall enable us to discriminate between true tumours and the curious medley with which by the majority of writers they are confounded. A neoplasm may be defined as a new growth cliaractei-ised by histological diversity from the matrix in which it grows.. it is distinguished from inflammatory new formations by the variety of its forms, mode of origin, and the frequent inherent tendency it has to increase. This definition excludes hyperplasia of organs, infective granulomata, and the like. With regard to the histological diversity exhibited by a neoplasm, it should be mentioned that it may more or less resemble the matrix tissue, but certain features may always be detected whereby their heteroplastic nature may be demonstrated. Few subjects have exercised the ingenuity of patho- logists more than the etiology of neoplasms. It is unneces- sary to recapitulate the various theories which from time to time have found adherents. There is no exclusive theory which will explain the causation and mode of origin of all known neoplasms; indeed, the various groups require separate consideration. The most scientific method of grouping neoplasms is an embryological one, leaving the histological details to determine the varieties. This mode of classification assumes considerable importance when considering the etiology of neoplasms. In this way they i may be arranged in three groups: (1) the Mesoblastic group, including the connective-tissue growths; (2) the Epiblast and Hypoblast group, comprising adenomata, carcinomata, and papillomata ; and (3) the Teratomata-neoplasms con- taining tissues derived from the three embryonic layers. Cohnheim’s theory, which ascribes the origin of neoplasms to persistent rudiments, is of all hypotheses that which has most to recommend it, if the term " tumour" be used in its most restricted sense. Throughout this lecture the expres- sion "germinal rudiment" will be used in a more extended sense than that in which Cohnheim employed it. At the outset it will be well to ask the question, Do germinal rudi- ments, such as Cohnheim’s theory demands, exist ? and have we any evidence to show that such germs may become tumours? The origin of true cysts from functionless ducts and tubules is a fact which no one can dispute; for example, the cystic dilatation of the tubules comprising the parovarium, paradidymis, and ducts of Gartner in man and animals. If we receive without demur the origin of cystic structures from functionless tubular organs, or cyst-germs, as we may call them, why should the origin of solid neoplasms from rudiments be doubted, especially if such untransformed tracts of tissue can be demonstrated unequivocally to be heteroplastic in their nature? Of course it is far easier to demonstrate the origin of cysts from pre-existing germs than in the case of neo- plasms it is ever likely to be. Nevertheless, we are certainly able to show that in the region where particular tumours are more prone to occur, there is embryological testimony to explain why they occur there. An epithelioma on the lip is what would be expected, but a similar growth starting in the midst of a block of cartilage is incomprehensible. In the same wav a nif’e of cartilage in the midst of the shaft of a femur of a boy of five years is cartilage in the wrong place; nevertheless, such islands are to be met with by those who care to expend time and labour in searching for them. Their existence has been known for some years, and, as Virchow was the first to point out, they may in later life become the starting-point of enchondromata. I have seen very many of these cartilage islands, especially in connexion with the epiphyses and diaphyses of long bones, in rickety animals and children. Not only do these examples teach us in the most positive terms that embryonic rudiments of enchondromata exist, but they teach us something of the evolution of neoplasms. In the fact that at an early age our skull is mainly cartilage, we agree with the caitilaginous fishes, sharks, rays, and the like, whose skulls never advance in development higher than cartilage impregnated with salts of lime; and as we advance to osseous fishes and amphibians the overlying bones gradually bring about absorption of the cartilage in different places; but much exists throughout the life-time of the animal, and in the skulls of mammals, even the highest, we find traces, in the oldest, of this important matrix tissue, yet in spite of this some cavil and say embryonic rudiments cannot exist in the adult. Surely they are not in earnest. Frequent spots for the existence of these belated rudiments are the region asterion immediately posterior to the external auditory meatus, the neighbourhood of the nasal fossae, the septum nasi, the lower jaw, and the vertebras. The regions just mentioned are favourite situa- tions for enchondromata and osteomata. A true osteoma may be regarded as simply a higher development of an enchondroma. If, then, we find a cartilage island, it would be impossible to say, supposing it to develop into a neo- plasm, whether it would become a cartilaginous or an osseous neoplasm. Moles and nsevi may be regarded as tumour germs; many instances are on record where a small nasvus untreated in early life later formed an angioma of considerable dimensions, and became a source of danger. All germs or rudiments do not become tumours. Three courses are open to them: (1) they may later in life undergo transformation into normal tissue; (2) they may remain quiescent throughout a long life; (3) irritation may stimulate them into abnormal activity. As to what constitutes irritation in this sense, nothing at present is definitely known. If we admit the origin of enchondromata, osteomata, and angiomata from rudiments, need we doubt the origin of other varieties of mesoblastic tumours from similar sources? There is this important fact in their favour-they are always confined to regions of the body where the elements of which they are composed are’to be unequivocally demonstrated. Before dismissing this question attention must be given to the sarcomata. I have no doubt that many cases of round- celled sarcomata are not genuine neoplasms, but the result of the irritation of micro-organisms. It is very necessary to be particularly cautious in deciding whether a given growth composed of round cells be a sarcoma or the result of a specific irritant, and more so if there be more than one growth present. Observations on animals have made me very sceptical regarding round-celled sarcomata. Mr. Pearce Gould has recently analysed the relation, which appears to exist in very many instances, between an injury and the appearance of a sarcoma, and has collected a goodly list of cases in support of the view in a paper read before the Medical Society in 1885. So far as my observations on animals have extended, it is interesting to note that sarcomata are found with greater frequency in those parts exposed to injury. In fish, the tails and fins are the parts most affected. In frogs, the limbs are the most frequent situations; in birds, it is the neck and prominent parts of the wings. In horses, sarcomata have followed blows on the jaws; I have seen a sarcoma develop on the head of a cat after being struck with a stick ; and in the case of an ox which broke its horn, a huge sarcomatous neoplasm subsequently developed from the stump. Careful examina- tion of some of these cases seems to support the notion that after the injury the inflammatory tissue, or tissue of repair, exceeds normal limits, develops erratically, and plays the part of a tumour germ. We must proceed to consider the second group of neo- plasms, whose characteristic features are the following:- In addition to mesoblastic, they contain epithelial elements derived from either the epiblast or the hypoblast, and in their structure they more or less resemble glands. If the I
Transcript
Page 1: THE Erasmus Wilson Lectures ON EVOLUTION IN PATHOLOGY

No.3261.

FEBRUARY 27, 1886.

THE

Erasmus Wilson LecturesON

EVOLUTION IN PATHOLOGY.Delivered at the Royal College of Surgeons.

BY J. BLAND SUTTON, F.R.C.S.,ASSISTANT-SURGEON TO THE MIDDLESEX HOSPITAL, AND LECTURER ON

COMPARATIVE ANATOMY.

LECTURE III.THE ETIOLOGY OF NEOPLASMS.

MR. PRESIDENT AND GENTLEMEN,—The term " tumour "

has been applied to so many kinds of growth, and used soloosely, especially in clinical work, that it ceases to carrywith it any definite significance. It is necessary to adoptsome rigorous limitation to the term, or choose a namewhich shall enable us to discriminate between true tumoursand the curious medley with which by the majority ofwriters they are confounded. A neoplasm may be definedas a new growth cliaractei-ised by histological diversity fromthe matrix in which it grows.. it is distinguished frominflammatory new formations by the variety of its forms,mode of origin, and the frequent inherent tendency it has toincrease. This definition excludes hyperplasia of organs,infective granulomata, and the like. With regard to thehistological diversity exhibited by a neoplasm, it should bementioned that it may more or less resemble the matrix

tissue, but certain features may always be detected wherebytheir heteroplastic nature may be demonstrated.Few subjects have exercised the ingenuity of patho-

logists more than the etiology of neoplasms. It is unneces-sary to recapitulate the various theories which from timeto time have found adherents. There is no exclusive theorywhich will explain the causation and mode of origin of allknown neoplasms; indeed, the various groups requireseparate consideration. The most scientific method ofgrouping neoplasms is an embryological one, leaving thehistological details to determine the varieties. This modeof classification assumes considerable importance whenconsidering the etiology of neoplasms. In this way they imay be arranged in three groups: (1) the Mesoblastic group,including the connective-tissue growths; (2) the Epiblastand Hypoblast group, comprising adenomata, carcinomata,and papillomata ; and (3) the Teratomata-neoplasms con-taining tissues derived from the three embryonic layers.Cohnheim’s theory, which ascribes the origin of neoplasms

to persistent rudiments, is of all hypotheses that which hasmost to recommend it, if the term " tumour" be used in itsmost restricted sense. Throughout this lecture the expres-sion "germinal rudiment" will be used in a more extendedsense than that in which Cohnheim employed it. At theoutset it will be well to ask the question, Do germinal rudi-ments, such as Cohnheim’s theory demands, exist ? and havewe any evidence to show that such germs may becometumours? The origin of true cysts from functionless ductsand tubules is a fact which no one can dispute; forexample, the cystic dilatation of the tubules comprisingthe parovarium, paradidymis, and ducts of Gartner inman and animals. If we receive without demur theorigin of cystic structures from functionless tubularorgans, or cyst-germs, as we may call them, why shouldthe origin of solid neoplasms from rudiments be doubted,especially if such untransformed tracts of tissue can

be demonstrated unequivocally to be heteroplastic in theirnature? Of course it is far easier to demonstrate the originof cysts from pre-existing germs than in the case of neo-plasms it is ever likely to be. Nevertheless, we are certainlyable to show that in the region where particular tumoursare more prone to occur, there is embryological testimonyto explain why they occur there. An epithelioma on thelip is what would be expected, but a similar growth startingin the midst of a block of cartilage is incomprehensible.In the same wav a nif’e of cartilage in the midst of the

shaft of a femur of a boy of five years is cartilage in thewrong place; nevertheless, such islands are to be metwith by those who care to expend time and labour insearching for them. Their existence has been known forsome years, and, as Virchow was the first to point out,they may in later life become the starting-point ofenchondromata. I have seen very many of these cartilageislands, especially in connexion with the epiphyses anddiaphyses of long bones, in rickety animals and children.Not only do these examples teach us in the most positiveterms that embryonic rudiments of enchondromata exist,but they teach us something of the evolution of neoplasms.In the fact that at an early age our skull is mainly cartilage,we agree with the caitilaginous fishes, sharks, rays, and thelike, whose skulls never advance in development higherthan cartilage impregnated with salts of lime; and as weadvance to osseous fishes and amphibians the overlyingbones gradually bring about absorption of the cartilage indifferent places; but much exists throughout the life-time ofthe animal, and in the skulls of mammals, even the highest,we find traces, in the oldest, of this important matrixtissue, yet in spite of this some cavil and say embryonicrudiments cannot exist in the adult. Surely they are not inearnest. Frequent spots for the existence of these belatedrudiments are the region asterion immediately posterior tothe external auditory meatus, the neighbourhood of thenasal fossae, the septum nasi, the lower jaw, and thevertebras. The regions just mentioned are favourite situa-tions for enchondromata and osteomata. A true osteomamay be regarded as simply a higher development of anenchondroma. If, then, we find a cartilage island, it wouldbe impossible to say, supposing it to develop into a neo-plasm, whether it would become a cartilaginous or an

osseous neoplasm.Moles and nsevi may be regarded as tumour germs; many

instances are on record where a small nasvus untreated inearly life later formed an angioma of considerable dimensions,and became a source of danger. All germs or rudiments donot become tumours. Three courses are open to them:(1) they may later in life undergo transformation intonormal tissue; (2) they may remain quiescent throughout along life; (3) irritation may stimulate them into abnormalactivity. As to what constitutes irritation in this sense,nothing at present is definitely known. If we admit theorigin of enchondromata, osteomata, and angiomata fromrudiments, need we doubt the origin of other varieties ofmesoblastic tumours from similar sources? There is this

important fact in their favour-they are always confinedto regions of the body where the elements of which theyare composed are’to be unequivocally demonstrated.

Before dismissing this question attention must be given tothe sarcomata. I have no doubt that many cases of round-celled sarcomata are not genuine neoplasms, but the resultof the irritation of micro-organisms. It is very necessaryto be particularly cautious in deciding whether a givengrowth composed of round cells be a sarcoma or the resultof a specific irritant, and more so if there be more than onegrowth present. Observations on animals have made mevery sceptical regarding round-celled sarcomata. Mr.Pearce Gould has recently analysed the relation, whichappears to exist in very many instances, between an injuryand the appearance of a sarcoma, and has collected a goodlylist of cases in support of the view in a paper read beforethe Medical Society in 1885. So far as my observations onanimals have extended, it is interesting to note thatsarcomata are found with greater frequency in those partsexposed to injury. In fish, the tails and fins are the partsmost affected. In frogs, the limbs are the most frequentsituations; in birds, it is the neck and prominent parts ofthe wings. In horses, sarcomata have followed blows onthe jaws; I have seen a sarcoma develop on the head ofa cat after being struck with a stick ; and in the case of anox which broke its horn, a huge sarcomatous neoplasmsubsequently developed from the stump. Careful examina-tion of some of these cases seems to support the notion thatafter the injury the inflammatory tissue, or tissue of repair,exceeds normal limits, develops erratically, and plays thepart of a tumour germ.We must proceed to consider the second group of neo-

plasms, whose characteristic features are the following:-In addition to mesoblastic, they contain epithelial elementsderived from either the epiblast or the hypoblast, and intheir structure they more or less resemble glands. If the

I

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resemblance is close, the neoplasm is termed an adenoma,and the cells clothe the alveoli in a regular manner; but ifthe cells are merely tumbled in confusion in the alveoli, it iscalled a carcinoma. It is necessary to discriminate betweenhyperplasia of a gland and a glandular neoplasm; the dis-tinction is simple: the latter is impotent to produce thesecretion normal to the gland. Another feature connectingcarcinomata with the secreting glands is their relation tobloodvessels. The cells of which a gland is composed do notcome directly in contact with the bloodvessels, but are

separated from them by lymphatic spaces. It is well knownthat cancers are poorly supplied with blood, but containan abundance of lymphatics. Further, cancers in their modeof development mimic glands. Glands commence by a down-growth of epithelium from the hypoblast or epiblast, as thecase may be, into the deeper layers of the mesoblastic tissuesbeneath. This may be well seen in a section of a foetalthumb at the fourth month of intra-uterine life. The sweatglands appear as little flask-shaped diverticula. This maybe taken as a type of gland development generally. If, laterin life, irritation, local or otherwise, affect the tissue,abnormal epithelial growths may occur, and, rising abovethe general level, produce a wart, or dipping into the sub-epithelial tissues, as in the early stage of gland develop-ment ; but failing sufficient formative energy, either fromdecline of vigour or general constitutional debility, the newtissue never develops functionally, runs riot, and originatestissues of low vitality-carcinomata. Such in-growths mayoccur in the neighbourhood of any gland, mucous, sebaceous,mammary, and others, as diverticula from the acini; andaccording to the arrangement and variety of the cells andstroma, so we term them " epithelioma," " scirrhus,"" encephaloid," and the like. There is no valid reason whythese abnormal down-growths of epithelium should not beconsidered as tumour germs, in the same sense as the little imasses of cartilage lodged in the interior of a long bone.It may be asked why should cancer be more frequent in theold or debilitated than in the young and vigorous? Theanswer is, young trees bring forth the best fruit because inthem vigorous growth is at an acme; when this fades, thenthat which is inferior is produced. So with glands. Irrita-tion in the young produces papillomata in the old cancer.This is not only true of man, but also of animals. Wartsoccur in the young, and cancer in the old ones. Cancer is,however, very rarely met with in animals other than man.We must now consider the third group of neoplasms, which

differ from the preceding groups in that their elements arederived from the three germinal layers, epiblastic, hypo-blastic, and mesoblastic, or, as they were conveniently styledby Virchow, teratoid tumours. These neoplasms are alwayscongenital, and are remarkable for the variety of elementscomposing them. They may contain fibrous tissue, bone,cartilage, muscle, skin, hair, nerves, glands, or indeed anytissue. Teratomata are especially liable to occur in thosesituations where the three blastodermic layers are broughtinto direct continuity with each other during foetal life, butthe connexion is only temporary. Critically examined, weshall find the positions of these temporary unions are oftenindicated by a passage which may exist for a longer orshorter period in the embryo. As a matter of fact, we getwhat I have been in the habit of calling an obsolete canal orpassage. By this I mean canals which in the ancestors ofmammals were functional, but they reapppear for a time inexisting forms in obedience to the great law, heredity. As

examples of obsolete canals we may take: (1) the curiousrecess at the top of the pharynx, which brings the infundi-bulum of the third ventricle into relation with the buccalinvolution; (2) the neurenteric passage, which brings thecentral canal of the cord and the alimentary canalinto relation round the caudal end of the notochord;(3) the post-anal gut; (4) the branchial arches; and (5) thedevelopmental history of testis, ovary, and W olffian ductsupport the same view. Teratomata occurring in the sacralregion are not a simple group, and Braune’s observationslong ago made us acquainted with the fact that some of thecystic forms are connected with the spinal canal and lieposterior to the coccyx, whilst others lie anterior to thatstructure. Braune also pointed out that the cystic tera-tomata connected with the spinal canal are due to dilatationsof the spinal meninges-in fact, a spina bifida. Thoseanterior to the coccyx are, according to Braune, to be

regarded as an abnormal growth of Luschka’s glands, andother writers adopt this view. It is far more reasonable,however, to believe that these growths originate as abnormal

dilatations of the post-anal gut-a section of the alimentarycanal which for a certain period of embryonic life exists.posterior to the anus in man and very many if not all verte-brata. The minute structure of this variety of teratomataagrees in every particular with the histological details ofthis section of the gut. With regard to the cystic sacraltumours connected with the meninges, it is not always that.after birth the continuity of the cystic interior with the-spinal canal can be made out, as in the following case.

reported by Virchow. A negro child a few days old pre-sented a tumour on the left buttock to one side of the middleline. It was removed by a surgeon, Dr. Ludwig Wolff, inCentral Africa,who believed it to be a lipoma. After examiningthe tumour, Virchow came to the conclusion that, notwith-standing its lateral situation, it was in reality a diverticulumfrom the spinal meninges. At the opposite end of the noto-chord we detect similar conditions. There may be a hernia ofthe spinal meninges through the floor of the sella turcica, orwe may get a tumour containing skin, hair, nerves, muscle-fibre, and the like. In the neck, in association with thebranchial arches, cysts arise, or in rarer cases tumours com-.posed of complex elements. The same is equally true of’the ovary and testis. They arise in connexion with thegenital ridge, and at a certain period of their developmentare in intimate association with the peritoneal epithelium,and for a time are connected with it by a series of curiouscanals known to embryologists as the peritoneal funnels.In addition to this, the Wolman duct at its commencementlies closely associated with the epiblast. Viewed in this,light, I regard teratomata, not as a group of curiosities, butas a class of neoplasms full of interesting details. I regard.them as arising from pre-existing tubules or ducts, which iD,the normal development should become obliterated, but theymay in fcetal life dilate and become mixed with various.other tissues in their immediate neighbourhood, and as.

they lie on the borderland of mesoblastic, epiblastic,and hypoblastic elements, they become incorporated withthem, and form in many instances amorphous masses, aniconstitute one of the most powerful witnesses to Cohnheim’stheory of "tumour germs." The relation of the teratoidtumours to obsolete canals is illustrated in a very strikingmanner in the tongue. Professor His has recently given a fullaccount of the development of the tongue, and describes.in detail the formation of a canal which runs from theforamen cascum on the dorsum of the tongue downwards.to the third branchial arch, and finally ends in thevesicle from which the middle portion of the thyroid glandtakes origin. Later the canal is divided into two parts,due to the formation of the body of the hyoid bone. Theone in connexion with the tongue is known as the lingualduct, and terminates in the hollow of the hyoid bone. It

may occasionally be demonstrated in adult life, situatedbetween the genio-hyo-glossi muscles. This situation is.the favourite one for dermoid cysts. The lower portion ofthe duct, known as the thyroid duct, may sometimes be-detected in those cases where we find a middle lobe to thethyroid body. It is extremely interesting to note that the-structure and mode of development of the thyroid glandclosely resemble those congenital coccygeal tumours lyinganterior to the coccyx-e. g., (1) their assoclation with the.alimentary canal; (2) origin in a functionless tubule(3) consisting of vesicles lined with cubical epithelium andbound together by cellular tissue.Although not strictly tumours, yet possessing so much

interest from the point of view of evolution, a few wordsmust be said concerning congenital cervical cysts. Theseformations, as Mr. Thomas Smith has so well pointed out,.all lie beneath the deep cervical fascia; they may be uni-lateral or involve the lateral and anterior regions of theneck, follow the deep fascia, and extend into the axilla, or,in rare cases, for a little distance into the mediastinum.Cases of this nature have been described and figured byMessrs. Birkett, Hutchinson, Smith, and Treves. In that thecyst extends at times into the axilla is of interest, for this.circumstance first induced me to attempt the following ex-planation. In some of the lower animals, especially thechimpanzee and howling monkeys, a very large subfascialair sac connected with the larynx extends from the hyoidbone to the manubrium sterni, and laterally under the pos-terior triangles even into the axilla. The cysts in the humansubject agree in anatomical details with the cervical sacs ofthe monkeys in such a striking manner that I am of opinionwe have in these cysts repetitions of simian characters.

In conclusion, it seems impossible to escape from the

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.conviction that anyone ambitious of becoming a scientificpathologist must first be a sound human anatomist; hemust also acquire a tolerable knowledge of comparativeanatomy and keep well abreast of the teachings of em-bryology. Having acquired a competent knowledge inthese subjects, he will then, in spite of himself, become afirm believer in the fundamental principles of the grand.doctrine of "evolution."

Clinical LectureON

C A T A R A C T.delivered at the Eye Infirmary, Newcastle-on-Tyne.

BY C. S. JEAFFRESON, F.R.C.S. ED.,SURGEON TO THE INFIRMARY.

GENTLEMEN,—Thu evening I purpose discussing thequestion of " Cataract and the operations for its relief." Ineed not say that the theme is one which is second to nonein importance within the whole range of surgery, whetherwe look at it from its own intrinsic interest, or whether weconsider the brilliant results which operative interferencebrings about in those who are the subject of this disease.An amputation or the resection of a joint may save orprolong life, but at best it leaves a deformed and mutilated’organism, and this result is only attained at great risk tolife and after great and prolonged physical suffering. A

successful and well-executed cataract operation is prac-tically painless. In a few days the wound is healed and thepatient finds himself restored to all the blessings and joyswhich sight alone can afford him. Indeed, for many sight is- only second to life itself, and there are not a few who wouldnot care to live without it. There is something magical inthis transition from darkness to light, and if the patient- experiences pleasure and gratification which at times he,can scarcely find words to express, the surgeon, as theindirect author of his pleasure, shares it equally with him.I know no feeling more gratifying and which inspires onewith more legitimate conscious pride than that whichoccurs to us when, on taking the first peep at a case ofcataract, we see a clear cornea and a dark untroubled pupil.The outline of objects first dawns upon the patient, graduallythe image becomes more distinct, and when he realises thathe sees once more his face illumines and he gives way to hisjoyful excitement. Equally bitter, on the other hand, is thefeeling should disappointment meet us at each step of ourexamination, and no ray of light penetrates to cheer thehopeful and confiding sufferer; and doubly bitter will thosefeelings be if our inner consciousness remind us that perhapsthe want of more care or more knowledge, or something leftundone, has led to the untoward result. In operations, as inall other events in life, nothing tends more to eventualsuccess than early disappointments, and if we take properlessons from our failures our proportion of successes willsteadily increase. If there is one thing more than anotherwhich characterises the surgery of the present day and hasbrought it to its pitch of perfection, it is the amount ofpersonal care and attention the surgeon gives to each indi-vidual case, and if it is necessary in general surgery it is doubly- so in ophthalmic surgery. A surgeon’s success is generallyin exact proportion to this element in the treatment, andyou will all find-I am here speaking to the younger mem-bers present-that it is far more satisfactory, and in the- end answers better in every way, to do a moderate amount ofwork thoroughly well than to do a large amount indifferently.I can only in this lecture attempt to give you a rough sketchof the matter in hand, for its full discussion would takemany lectures; but to make matters clear I must refer brieflyto the anatomy of the parts concerned....... o.

Now, gentlemen, as in the physiological state the lens andits capsule are absolutely transparent, so any opacity in oneor the other is a pathological condition, and constituteswhat we call a cataract-an objectionable name, we mustallow, but one sanctioned by time, and which we must becontent to adhere to. As there are necessarily many

varieties of cataract, so there have sprung up many classifica-tions ; none of them are very complete, and some are notvery scientific, and it is not till we have enumerated themall that you will appreciate the difficulties in the matter.In the first place, anatomical position has been taken as abasis, and we speak of lenticular and capsular cataract

according as the opacity is situated in the lens or itscapsule. Lenticular cataracts are cortical or nuclearaccording as the peripheral or central parts are affected; or,again, lamellar when only an intermediate layer betweenthe nucleus and the cortex is opaque. Capsular cataracts, aswe shall see by and bye, have no real existence, and dependupon changes in the layer of cells immediately below thecapsule; these changes may take place in the anterior orposterior capsule, although in the posterior they are due todifferent causes. When close to the poles, they are calledanterior and posterior polar cataracts; when the lens andcapsule are both affected, we speak of capsulo-lenticularcataracts. When age forms a basis for classification, wespeak of infantile, juvenile, and senile cataracts; whenconsistency, we speak of hard, soft, and cretaceous cataracts.Again, when we classify them in accordance with the con-ditions which have led to their development, we speak oftraumatic, diabetic, senile, and secondary cataracts. By farthe majority of cataracts which come under the notice of thesurgeon are lenticular, and occur in elderly persons; and thereare two ways in which they usually commence : the e sclerosisor condensation or opacification which attends and is theessence of the disease commences either in the centre of thelens, when it is called nuclear, or attacks the peripheralparts of the cortex, when it is called cortical; although inthe more advanced stages it is not always easy to sayto which of these categories the cataract has chiefly belonged.At the commencement there is generally but little difficultyin deciding. The nuclear cataract occurring in the centre ofthe lens gives rise to ill-defined nebulous opacity, which some-times produces more disturbance of vision than a superficialexamination would lead us to expect. The cortical appearas star-like radii in the periphery; from their situation atthe commencement they interfere comparatively little withvision, and even when advanced, in comparison with thenuclear, do not seem to impede the light so much. In myexperience nuclear cataract occurs later in life than thecortical variety, which is certainly the more common of thetwo, and may be found in most of those cases in which thecataract, though undoubtedly senile, occurs at a compara-tively early stage. Cortical and nuclear cataracts, gentle-men, form the majority of the cases which occur in oldpersons, or the so-called senile cataracts, but there are otherforms of opacity affecting the lens substance. We havecertain forms of cataract which may be called milky cata-racts, in which the cortex does not follow the usual form ofstillate degeneration, but breaks down somewhat rapidlyand equably in all its parts; it may and does not in-

frequently pass into a fluid state, in which case the nucleusfloats free in it, and we have what is termed a Morgagniancataract. This usually occurs at a less advanced period oflife than senile cataract, and is sometimes a monocularaffection. Again, we have another form of lenticularcataract which is called the laminar or lamellar, whichconsists of an opacification of certain layers of the lens,leaving its nucleus and peripheral parts transparent. Thisis always a congenital form of cataract, though by nomeans the only one. Capsular cataracts may occur inconnexion with cortical or lenticular cataract as a senilechange, but it is not usually till a late stage that theintra-capsular cells become affected. Sometimes, how-ever, the opacity commences in this situation, usually inpersons of middle age, and who are the subjects of inheritedcataractous tendencies. At the close of the lecture I hopeto show you a case of this kind, in which numerouspunctated opacities occupy the anterior surface of the lenswithin the capsule. One of the most common forms of cap-sular cataract is what is called the pyramidal or anteriorpolar cataract, because it occurs at the anterior pole of thelens. It is usually the result of purulent ophthalmia inearly life, which, having led to a small central ulcer of thecornea and consequent loss of aqueous fluid, has caused thelens to project against and touch the posterior surface of thecornea, where it contracts adhesions blocking up the base ofthe ulcer. This allows the aqueous humour again to accu-mulate, leading to a detachment of the lens, which resumesonce more its proper position, but leaving at the spot whereit was in contact with the cornea a patch of inflammatory


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