Intracranial tumours

Preface

The following pages are based on a series of Lectures, which, in the capacity of Lecturer on Clinical Medicine in the University of Durham, I delivered, now some ten years ago, to the Students of the College of Medicine, Newcastle-on-Tyne. Portions of the work were communicated in the form of three Lectures to the gentlemen attending the Edinburgh Post-Graduate Course during the autumn of last year.

The work is essentially based upon my own clinical experience, but I have not hesitated, whenever it has seemed necessary, to avail myself of the opinions of other observers. In particular, I have to acknowledge my great indebtedness to the writings of Dr. Hughlings Jackson, of whose work on this subject British Medicine will always be justly proud.

My sincere thanks are due to Mr. A. W. Hare, M.B., F.PuC.S.E., for the chapter on the Surgical Treatment of Intracranial Tumours which he has kindly written for me; also to Drs. Clouston and Carry le Johnstone for the remarkable specimens of Intracranial Aneurism which are represented on pages 165 and 168; to Dr. T. W. McDowall for the Brain represented in Pig. 113 ; and to Dr. David Drummond for the cuts of his cases of Perforating Sarcoma.

23 Drumsheugh Gardens,

Edinburgh, 1st May 1888.

Contents

CHAPTEE I.

DEFINITION INTRODUCTION — ETIOLOGY — GENERAL PATHOLOGY, OR

PATHOLOGICAL PHYSIOLOGY.

Chapter I

DEFINITION" — INTRODUCTION — ETIOLOGY — GENERAL PATHOLOGY AND PATHOLOGICAL PHYSIOLOGY.

Definition. — Under the term intracranial tumour, it is customary to include all new growths which originate within, or are contained in, the cavity of the cranium.

Localised inflammatory thickenings or deposits, more especially when syphilitic and tubercular, are, in some cases, with difficulty distinguished from the more sharply defined new growths — tumours properly so called ; indeed the distinction may be impossible, for the two conditions are often combined, and may insensibly run one into the other.

Cerebral abscesses are not included under the definition ; for, although in some cases it may be difficult or impossible to differentiate a chronic abscess from a cerebral tumour during life, the distinction is readily enough made post mortem.

Large aneurisms and parasitic cysts must be regarded as intracranial tumours.

Simple cysts, as well as cysts which develop in connection with gliomata and other forms of new growth, are usually described in connection with intracranial tumours.

Introduction. — The subject of intracranial tumours is of great interest, from a clinical, physiological, and pathological point of view.

A

2 INTRODUCTION.

The brain and its membranes are favourite situations for the formation of new growths. In no other situation in the body is such a great variety of tumours met with ; it would almost indeed seem that the delicate and soft brain tissue, richly supplied as it is with blood-vessels and lymphatics, is as fine a forcing and feeding ground for new growths as Koch's nutrient jelly is for micrococci and allied organisms. Syphilitic and tubercular tumours, gliomata, and the various forms of sarcoma, are most frequently met with ; different varieties of cancer, endotheliomata (cylinclromata), and psammomata are not uncommon ; while cholesteatomata, parasitic cysts (Echinococci and Cysticercus Celluloses), melanomata, osteomata, fibromata, lipomata, and neuromata are more rare.

New growths may occur in any part of the intracranial cavity. In some cases the tumour is single, in others multiple. The tumour may derange the functions of the great intracranial nerve centres as a whole ; or it may invade, and irritate or destroy, individual parts — limited portions of grey matter, conducting tracts, or peripheral (cranial) nerves. The symptoms are in some cases of the most diverse and complicated character ; and the diagnosis may be attended with great difficulty. But in no disease is an exact diagnosis of more importance ; for, while experience has abundantly shown that it is impossible to cure intracranial tumours (the syphilitic variety in many cases excepted) by any internal remedies with which we are at present acquainted, the results obtained by Hughes Bennett, Godlee, and Victor Horsley go far to prove that in some cases at all events intracranial tumours may be satisfactorily removed by operation. But since the removal of the new growth is in many instances altogether impossible, a correct diagnosis is obviously essential for successful interference. The exact localisation of the tumour is necessarily a point of the first importance ; while a knowledge of the pathological character of the new growth may enable us to decide whether an operation is feasible or not.

Etiology. — The causation of intracranial tumours differs in no way, so far as I know, from the causation of tumours in other parts of the body.

In some cases the new growth is primary,, in others secondary; in

E TIOL OGY: EFFE CTS OF INJUR Y. 3

the latter, the primary tumour may be situated in any part of the body, but secondary deposits of new growth in the intracranial nerve centres are, I think, especially apt to follow similar diseased conditions of the pulmonary tissue. This is probably due to the fact that when the primary new growth is situated elsewhere, say in the abdomen, the liver and the lung act as filters, and protect the brain, catching as it were any minute particles of malignant growth which get into the venous circulation ; whereas, when the lungs are themselves the seat of the disease, any infective particles which get into the circulation, are carried to the left heart, and may consequently find their way, through the arterial system, to the brain as well as to the other organs. This explanation of course applies only to those cases in which the secondary deposits are carried to the brain through the blood-vessels.

It is unnecessary to say anything with regard to the hereditary and general constitutional causes which predispose to tumour formation.

Amongst the more direct causes, injury occupies an important place. There can, I think, be little doubt that blows and falls on the head do sometimes lead to the formation of gliomatous, and perhaps also of sarcomatous tumours ; syphilitic tumours, too, not infrequently appear to owe their exciting cause to a head injury ; and in two instances I have known a scrofulous tumour to follow a severe blow upon the head, the new growth developing either immediately below the seat of the injury, or at the point of contre-coup. The explanation of such cases is probably this, that the blow produces a local inflammatory lesion or contusion, which forms a suitable nidus for the development of the tubercular germs (tubercle bacillus or its spores) which are already circulating through the system.

How far mental anxiety and worry, or other conditions which depress and exhaust the cerebral nerve centres, and how far alcoholic excesses and other conditions which are attended with repeated cerebral congestions, may predispose to, or aid in, the formation of brain tumours, is altogether uncertain. Whether, too, any of the new growths which occur within the cavity of the cranium owe their origin to micro-organisms is unknown ; but I have for long thought it probable that the cause of some forms of glioma is of this nature.

4 ETIOLOGY.

Intracranial tumours are more frequent in the male than in the female ; in some cases this is doubtless due to the fact that men are more frequently affected with syphilis, and are more exposed to head injuries, and possibly because they are more addicted to alcoholic excesses than women.

For the same reason, those persons whose occupation exposes them to head injuries, and possibly to mental worry and anxiety, are perhaps somewhat more liable to be affected with intracranial tumours than other members of the community. Occupation is, however, a matter of very little consequence from an etiological point of view.

Age is of more importance, for undoubtedly some forms of tumour are more likely to appear at one age than at another. Scrofulous tumours are more common in the young ; syphilitic tumours in adults, the period of greatest frequency being probably between the ages of thirty and forty-five ; cancers of the brain, like cancers elsewhere, are more common in old people ; gliomatous tumours may occur at any age, but in my experience are more frequently seen in young persons or in adults — i.e., not in old people.

The general pathology and pathological physiology of brain tumours. — The number of symptoms which may be produced by intracranial tumours is very great, and the manner in which they may be grouped and arranged most diverse. Hence the clinical picture which individual cases present may be very different. "Now, since the exact nature of the symptoms which are present in any given individual case depends upon the effects which the new growth has upon (a) the intracranial contents, and (h) the cranial walls, it follows that the intelligent comprehension of this difficult part of the subject will be greatly facilitated if we start with clear notions as to the effects which intracranial tumours in general may produce upon the brain and other structures contained within the cavity of the cranium.

In the first place, it is essential to remember that, after the sutures have been ossified, the cavity of the cranium is, for all practical purposes, a closed cavity ; and that, when a tumour or new growth is developed in any part of it, the intracranial pressure must necessarily be increased, and the brain, and other structures contained within it, must necessarily be compressed, unless compensation is effected, and increased pressure and squeezing prevented, either by atrophy of intracranial structures, displacement of intracranial fluids, or yielding of cranial walls, i.e., separation of the sutures.

Further, it must be remembered that the general cavity of the cranium is divided by the tentorium cerebelli into two separate parts ; and that while tumours growing above the tentorium chiefly compress the parts which are situated in the upper cranial cavity, and as a rule exert comparatively little pressure upon the cerebellum, pons Varolii, and medulla oblongata (i.e., the parts in the lower cavity), the reverse is by no means the case. Subtentorial tumours, in fact, may not only exert very great compression on the parts in their immediate neighbourhood (cerebellum, pons Varolii, and medulla oblongata), but may, and very frequently do, by producing dropsy of the ventricles, cause an enormous increase of pressure in the upper cavity, or, as we may term it, the cavity of the brain proper. Nay, further, a small tumour or cicatricial inflammatory product, which produces comparatively little direct (pressure) effects upon the parts below the tentorium (i.e., in its immediate neighbourhood), may cause great distention of the ventricles and enormous increase of the general intracranial pressure.

In a less perfect manner, the upper cranial cavity is divided by the falx into two separate cavities ; and by means of the resistance which this tough, partitioning membrane affords, the cerebral hemisphere on one side is to some extent protected from the pressure effects of a large, rapidly increasing tumour on the other.

As a matter of fact, flattening of the convolutions, obliteration of the sulci, ansemia of the surface of the brain, a dry, sticky condition of the membranes, and in many instances dropsical distention of the ventricles with oedema of the brain tissue — in other words, the post mortem evidences of increased intracranial pressure — are met with in the great majority of cases of intracranial tumour after death ; and it is, I believe, to this increased intracranial pressure and its results that the general symptoms of intracranial tumour, such as headache, vomiting, double optic neuritis, vertigo, mental dulness, lethargy, &c, are largely clue.

The exact causation of the double optic neuritis is a matter of dispute. Personally I am of opinion that increased intracranial pressure is in many cases an important, though not the sole or perhaps the most important, factor in its production. This point will afterwards be considered more in detail.

The term general is here used to indicate those symptoms which result from the presence of a tumour in any part of the cranial cavity, as distinct from the localising symptoms, which are due to the effects which the tumour produces on special parts, and which are indicative of its exact locality or seat.

As we shall afterwards see, headache, when localised — and more especially when associated with tenderness on skull percussion — vomiting and vertigo, when obstinate and severe, may have a localising value ; but in most instances these symptoms are general rather than localising symptoms, and cannot be taken as guides to the position of the new growth.

Now the degree of the increase of the intracranial pressure and the extent of the compression to which the intracranial contents are subjected, depend upon (a) the size, and (b) the rapidity of the growth of the tumour ; together with (c) the presence or absence of dropsical distention of the ventricles and the extent thereof.

In the case of tumours which grow rapidly and are of large size — which, in other words, are attended with great increase of the intracranial pressure — we should expect the general symptoms of tumour (headache, vomiting, double optic neuritis, &c.) to be well marked ; and such in fact is usually the case. Towards the later periods of cases of this description, and in many cases in which there is dropsy of the ventricles, the headache and other symptoms, which in the earlier stages may have been well-marked and characteristic, often become less prominent, or may altogether disappear, in consequence probably of the fact that, owing to the anaemia, oedema, and compression of the nervous tissue, the sensibility of the brain is diminished, the feelings and perceptions are dulled, and a condition of hebetude, mental apathy, semi-coma, or actual coma, is produced.

In those cases, on the contrary, in which the tumour is of small size or of slow growth ; in cases in which, as the tumour grows, the brain tissue atrophies ; in cases in which the fontanelles are not yet closed, and yielding of the bones of the skull readily takes place ; in

IRRITATIVE LESIONS. 7

other words, in those cases in which there is little or no increase of the intracranial pressure, the general symptoms of tumour may be altogether absent or little marked.

Another factor which probably plays an important part in the production of the " general " symptoms is the " irritation " which the tumour produces in the nervous tissues and in the cerebral membranes.

In some cases of intracranial tumour, as I shall afterwards point out, a diffused irritative change — which causes enlargement of the nervous tissues surrounding the tumour, and is chiefly characterised on microscopical examination by increased size of the connective tissue corpuscles or Deiter's cells — is found throughout the brain tissue ; but more especially in the hemisphere or part of the brain in which the tumour is situated.

In some cases the membranes seem to be involved in this process of irritation, and there is distinct naked-eye evidence of thickening and chronic meningitis. In others, in which no such naked-eye appearances are to be seen, it is said that inflammatory changes in the meninges can be demonstrated by means of the microscope. I cannot say that I have been able to satisfy myself with regard to this point. In many of the cases of intracranial tumour which have come under my notice there have been no distinctive naked-eye appearances of diffused meningitis ; while in the great majority the usual post-mortem signs of increased intracranial pressure have been prominent. In the cases of this kind which I have subjected to careful microscopical examination, I have failed to find distinctive evidence of meningitis ; but I have in most cases detected enlargement of the connective tissue corpuscles, and evidences of irritative changes in the brain tissue surrounding the tumour. In some cases, I have satisfied myself that these irritative changes were wide-spread.

What share this diffuse irritative change in the neighbourhood of the tumour may take in the production of the general symptoms (headache, vomiting, double optic neuritis, &c), I am not prepared to say. That it has some influence is probable; but, so far as I can judge, it is not such an important factor as meningeal irritation and increased intracranial pressure.

In the second place, the new growth necessarily presses upon or involves special structures and parts ; and it is to the derangements which are produced in the structures, which are thus pressed upon or involved, that another great and most important group of symptoms — the localising symptoms, as they are termed — is due.

The exact nature of the localising symptoms depends upon the following points : —

(1.) The function of the particular part of the cerebrum, cerebellum, pons, medulla, intracranial nerves, blood-vessels, membranes, bones, &c, which is pressed upon or involved.

This point is self-evident, and needs no amplification. It is quite obvious that in a case in which the tumour is situated in the neighbourhood of the fissure of Eolando, and in which the motor centres are pressed upon or involved, the symptoms will be quite different from a case in which the tumour involves the prefrontal or occipital lobes ; and that the exact character of the paralyses or spasms, which are present in the former case, will depend upon the exact portion of the motor area which happens to be affected.

(2.) The manner in which the part which is pressed upon or involved by the tumour is affected — whether irritated or destroyed — and, more especially in the case of destroying lesions, the extent of the changes which are induced in it.

Speaking generally, it may be stated that the effect of all lesions on the nervous tissues is to produce one or other of two results, viz., either diminution or abolition of function on the one hand, or increase of function on the other. It must, however, be remembered that the increased function, which results from pathological causes, is seldom a simple increase ; as a rule, the function is not only increased, but is also perverted iii character. Paralysis, anaesthesia, and dementia are good examples of diminished or abolished function ; convulsions, neuralgia, and mania of increased and perverted function.

In some cases in which the symptoms are indicative of increased function, the primary lesion is probably, as Dr. Hughlings Jackson has suggested, a " destroying " one, i.e., a lesion which produces diminution or destruction of function. It would appear, for example, that in some cases of mania the highest and most specialised parts of the cerebral nerve apparatus are put hors cle combat, with the result

IRRITATIVE AND DESTRUCTIVE IESIONS. 9

that the lower cerebral centres are not restrained as they are in health, the net result being symptoms of a maniacal character. In cases of this description, Dr. Hughlings Jackson supposes that the increased function is apparent only, and that the increase is in reality due to the fact that the function of the highest (controlling) centres is destroyed, diminished, or temporarily suspended by the lesion.

Now, whether a tumour which is pressing upon or involving a portion of brain tissue will produce diminution or exaltation of function, would appear to be due to (a) the rapidity with which it is growing ; (b) its pathological nature ; and (c) the composition, so to speak, of the nerve tissue with which it is in contact, i.e., whether grey or white matter. Whether the pressure is continuous or intermittent is doubtless also a factor of importance. Other things being equal, a rapidly growing tumour is more likely to produce irritation of nerve tissue, and particularly of grey nerve tissue, than a slow growing one ; while a tumour of slow development is much more likely to produce a simple atrophy of the tissue on which it presses.

Further, as we shall afterwards see, irritation of grey matter of necessity gives rise to symptoms — granting of course that the irritation is sufficiently great to excite discharge, and that the way out for the nerve force is not obstructed — while destruction of grey matter is frequently compensated and unattended by any external manifestations. Again, as we have already seen, a rapidly growing tumour is more likely to produce increased intracranial pressure and diffuse irritative changes than a slow growing one. For all these reasons, then, a tumour of rapid development is more frequently attended by symptoms both general and localising than a tumour of slow growth.

The pathological nature of the tumour is also of great importance in determining whether irritation or destruction will result in the nerve tissue which is implicated.

Those tumours which are surrounded by a capsule, which do not infiltrate the tissues with which they come in contact, and which have little or no tendency to produce meningitis (such as fibrous, fatty, and cystic tumours, some sarcomata, &c), are much less likely to produce irritation than those new growths (such as gliomatous, syphilitic, tubercular, cancerous tumours, and some varieties of sarcoma) which produce the opposite effects — i.e., which do infiltrate io GENERAL PATHOLOGY.

the structures with which they come in contact, or which have a strong tendency to produce cerebritis or meningitis.

Encapsuled tumours are as a rule of slow growth, but infiltrating tumours, though they usually develop rapidly, do not always do so. I have, with Dr. Leslie, reported a case of infiltrating glioma in which the duration was certainly five years ; and another case of the same kind, in which the duration was perhaps even longer. x

But whether symptoms will result from the irritative or destructive changes which a tumour produces in the nerve tissue on which it presses, or through which it infiltrates, depends to a large extent upon the fact whether that nerve tissue is composed of grey or white matter. For it is important to remember, on the one hand, that discharge of nervous energy is much more readily produced by irritatation of nerve cells than of nerve tubes ; tumours which are situated on the surface of the brain (such as tubercular and syphilitic deposits), and which involve and irritate the grey matter, are therefore much more likely to be attended with " irritative symptoms " (spasms, flashes of light, &c), than tumours which involve and irritate nerve tubes, say in the centrum ovale, internal capsule, or peripheral nerves.

On the other hand, destruction of grey matter is much more easily compensated than destruction of conducting fibres or nerve tubes. Destruction of a part of the motor cortex, indeed of a very large part, as the specimen represented in Figs. 1, 2, 3, and 4 shows, may be quite unattended with symptoms (i.e., paralysis), but a limited destruction of the conducting fibres, say of the internal capsule, is, as far as we know, almost certain to be followed by paralysis.

Whether permanent paralysis will result from destruction of motor-conducting fibres is also largely dependent upon the degree of specialisation, so to speak, of the movements w7ith which those fibres are concerned. Destruction of the fibres which innervate the muscles of the thumb and fingers will produce more lasting and permanent paralysis than destruction of the fibres which supply the muscles of the upper arm and shoulder. For the same reason, as will be afterwards more fully explained, compensation is more readily effected in the lower than in the upper extremity, for the movements of the leg are

1 Edinburyh Medical Journal, January 1887, pp. 591 and G23.

DESTRUCTION OF MOTOR CENTRES. n

more automatic (less highly specialised and less independent of those of the opposite leg) than the movements of the arms.

The effects of " destroying " and " discharging " lesions, and the important subject of " compensation," will be afterwards considered more in detail.

In considering the local alterations which the tumour produces in

T

Fig. 1. — Diagrammatic outline of the right hemisphere of the brain in the case of M. D., showing the exact position of the lesion (the dark area to which the letter T points).

The letter F points to the frontal and 0 to the occipital end of the brain ; R to the fissure of Rolando, and S to the fissure of Sylvius ; I7 to the tumour.

The patient, a girl, aged twenty, was admitted to the Newcastle-on- Tyne Infirmary under my care on February 5th, 1877, suffering from headache, vomiting, and giddiness. There was well-marked double optic neuritis, but absolutely no paralysis. Under iodide of potassium great improvement took place, and the patient felt so well that she had made arrangements to leave the hospital. The very night before she was to go home, she was seized with an epileptiform convulsion, in which she died.

At the post-mortem examination the very large tumour, represented in Figs. 2, 3, and 4, was found ; it had produced very extensive destruction of the motor centres, and yet there was never the slightest trace of paralysis.

The case is reported in full in the Edinburgh Medical Journal for February 1879, p. 693.

the parts with which it is in direct contact, it is necessary to remember that the symptoms which result are not always directly due to the derangement of function in the part which is immediately implicated, but that they may be the result of indirect and secondary alterations in some other and distant part of the nervous tissue.

The point is one of practical importance, for symptoms produced in this way may be localised and limited in extent, and may give an erroneous idea of the position of the tumour.

Symptoms of this kind — pscudo-localising symptoms, as they may perhaps be termed — are, I believe, chiefly produced in one or other of the following ways.

Fig. 2. — The outer surface of the right hemisphere of the brain in the case of M. D. (large sarcoma growing from the dura mater, which had produced extensive atrophy of the motor centres, but was unattended with paralysis), showing the tumour in situ. (Copied from a photograph and somewhat reduced in size.)

The letter A points to the outer surface of the dura mater over the centre of the tumour.

DESTRUCTION OF MOTOR CENTRES.

(1.) By alterations of the blood vascular supply to distant centres and parts. — A syphilitic gumma at the base of the brain, for example,

Fid. 3. — The outer surface of the right hemisphere of the brain in the case of M. D., showing the brain after the tumour was removed. (Copied from a photograph, and somewhat reduced in size.)

The letter B points to the extensive depression on the surface of the brain, into which the tumour fitted.

i4 GENERAL PATHOLOGY.

which involves and destroys the third nerve, may at the same time surround and obstruct the middle cerebral artery, and produce exsfifiBt* li 5

Tig. 4. — Transverse vertical section through the right hemisphere of the brain in the case of M. D., showing the tumour in section, and the depression in the brain tissue produced by it. (Copied from a photograph, and somewhat reduced in size.)

The letter A points to the tumour ; B is placed on the inner (left) side of the right hemisphere, which has been separated from the opposite (left) hemisphere by a section made from before, backwards in the middle line.

tensive softening of the motor convolutions ; the resulting paralysis — hemiplegia on the opposite, and paralysis of the muscles supplied by the third nerve on the same side — is suggestive of a chronic lesion of the crus cerebri. Other illustrative examples might be given, but this point is so obvious that further details are unnecessary. Possibly the vascular supply of a distant part of the brain tissue may be altered, and the nutrition and function of that centre affected, by the pressure of a tumour upon the vaso-motor nerves distributed to the blood-vessels.

(2.) By indirect {reflex) irritation or inhibition of distant centres. — In cases of this description the tumour produces alterations, structural and functional, in the centre with which it is immediately

PSEUDO-LOCALISING SYMPTOMS. 15

in contact (centre A), with the result that a distant centre (B) is either irritated or inhibited. The symptoms which are produced in this manner show that the function of the' distant centre (B) is deranged; hence the observer may conclude that the tumour is situated in the immediate neighbourhood of that centre.

That the function of a part of the brain which is itself free from disease may be deranged (excited or inhibited) in consequence of* disease in some other and distant part, seems certain. It is probable that in some cases of mental derangement the symptoms are produced in this way ; and the phenomena of certain cases of aphasia seem to show that lesions on the sensory side of the speech mechanism (sensory speech centres) almost of necessity produce derangements in the motor (speech) centres. Possibly, too, the nervous derangements (paralyses, spasms, &c.) which are met with in some cases of hysteria may be best explained in this manner; but that such coarse phenomena as localised spasms and localised paralyses are frequently or usually produced in this way, as Brown- Sequard in particular would have us suppose, seems to me altogether improbable. The risk of erroneous diagnosis (localisation) from this cause has, in my opinion, been exaggerated. When, in short, in a case of intracranial tumour the symptoms clearly point to derangement of function in a localised and limited portion of brain tissue, the physician will, I think, be wise to give the fact its full localising value. In the majority of cases of this description the symptoms are directly due to deranged function in the nerve tissue which is in the immediate neighbourhood of the tumour, or of some nodule of new growth in the case of a multiple lesion. Irritation is chiefly produced in the nervous tissue which surrounds the tumour. The irritative phenomena, therefore, do not so directly point to the exact position of the new growth as the symptoms due to destruction. In those cases in which no such direct relationship exists, a sufficiently carefully conducted post-mortem examination (naked eye and microscopic) may be expected to show distinct pathological changes in the part whose function was deranged, and, in some instances at all events, to demonstrate the manner in which this apparently independent lesion had indirectly resulted from the presence of the new growth — i.e., to show, for example, that the tumour had involved the vessels i6