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TUMOURS OF THE FRONTAL LOBEBy GEOFFREY JEFFERSON, M.S., F.R.C.S., F.R.C.P., F.R.S.

Professor of Neurology, University of Manchester

General ConsiderationsThe difficulties in diagnosing frontal tumours

have been well recognized, not only by all writerson the subject, but by all clinicians whether theyhave contributed to the written word or not. Thereasons for this are not hard to find, and centrechiefly round the fact that large though the frontallobes are they contain no structure whose destruc-tion must necessarily cause an obvious alterationin the patient, an alteration that could not havebeen produced by a lesion elsewhere. Objectionsto this statement come to mind, for it will be re-membered that the motor area and the pre-motorarea both lie within the frontal lobe. They de-marcate, however, its extreme posterior border andit is clear that unless a tumour is so far back in thefrontal lobe that it almost ceases to be a purefrontal tumour no disturbance of motion willresult. On the left side the so-called motor speech

centre, or Broca's area, comes within theanatomist's definition of the frontal lobe, so thatdifficulties in the exteriorization of speech mightwell be found with a frontal tumour far enoughback to involve these mechanisms. We must notbe unduly impressed with the importance of thegrey matter of the cortex at the posterior end ofthe left third frontal convolution. Tumours, andfor- that matter other lesions as well, more com-monly produce their effects by interference withthe white matter, by cutting deep association andprojection fibres, than by destruction of the layersof cells in the cortex. It is more probable thatdefects of speech are due to damage to these deepfibres than to loss of cells with a special functionin the cortex. This belief has led in more recentyears to speech defects being referred to damage of' the region of the insula ' (island of Reil), a brainarea that belongs as much to the temporal lobe as

Sketch of a right frontal lobectomy showing the bare floor of the anterior fossa falxand left anterior cerebral artery.

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134 POSTGRADUATE MEDICAL JOURNAL March 1950

to the frontal. Tumours have a way of trans-gressing the anatomical boundaries of tradition; atumour may be temporal as well as frontal, tem-poral as well as parietal, occipital as well as bothtemporal and parietal. When, therefore, onewishes to speak of the signs of a tumour in anyarea it is best to confine the examples to lesionswhich are entirely local. Hence frontal tumours ofclassical description will only slightly, if at all, en-croach on the motor area, nor will all of those evenon the left side lead to deficiency in speech. Isthere then within the frontal lobe no other struc-ture, is it an unbroken mass of white matter withthe usual grey matter covering it ? There lieswithin it the caudate nucleus and the front end ofthe lateral ventricle. It may be that the tremor towhich Grainger Stewart first drew attention inI906 and has since been noticed by many as apeculiarity of frontal tumours, is due to partialinvolvement of the caudate nucleus and basalganglia. The anterior horn of the lateral ventriclecould have no neurological significance, but it isimportant that the foramen of Monro lies withinthe frontal lobe and if a tumour is so situated thatit could block it, a great rise in intracranialpressure must follow. Otherwise the pressurewithin the skull tends to be low with anteriorlyplaced tumours, as Stopford first pointed outthough not for the reason that he adduced (absenceof pressure on the vein of Galen).

In this review of the neural structures of thefrontal lobe, in the search for areas whose destruc-tion might lead to outspoken signs or symptoms,no mention has been made as yet of intellectualprocesses. Are not the frontal lobes the ' organsof the mind,' the organizers of personality, thecensors of conduct, almost one might say the seatof the soul ? Is there no recognizable anatomicalcortical area which houses the mind ? Althoughthe frontal lobes are concerned in these things, andprobably more concerned than any other part ofthe brain, all the evidence points to these qualitiesbeing more diffusely spread throughout the brainthan was thought as recently as 20 years ago. Itis more possible for a patient to have a large frontallesion without alteration in his memory or per-sonality or moral sense. Sometimes of coursethese things are disturbed, but much less com-monly than would be the case if the frontal cortexwas an exceedingly highly specialized mosaicwhere the whole of our intellectual and (for wantof a better word) spiritual potentialities or achieve-ment were lodged. This fascinating subject willbe dealt with a little more fully below.

Symptoms and Signs of Frontal LobeTumoursAs the result of the analysis of frontal lobe

tumours which have been made during the past30 years a certain uniformity of description hasemerged. Writers differ in the emphasis whichthey place on this or that symptom or sign; suchemphasis tends to be individualistic and what hashelped one observer may be thought unimportantby another, even though he agrees that the observa-tion is correct. However desirable it may be forteaching purposes to produce a syndrome, aformula, something which shall represent thephotographic likeness of a disease entity, we knowvery well that in practice the resemblance will bea family rather than an exact one. It is exceed-ingly rare for any case to show every sign whichthe closest scrutiny of a large number of cases hasproved to be a possibility. Only too often but oneor two of the theoretically possible diagnosticcritical points are all there is to work on.We will begin with a list of symptoms and signs,

and first amongst them we must place those of thatrise in intracranial pressure which is the generalrule in intracranial tumours.

x. Signs of raised intracranial pressure: head-ache, choking of the optic nerve heads, vomiting,paralysis of cranial nerves at a distance, usuallythe abducens, and (in later stages) drowsiness.

2. Signs and symptoms due to interference withthe brain mass of the frontal lobes:

(a) Epileptic fits.(b) Memory defects, personality changes, in-

continence, inertia, loss of powers of concentra-tion and of introspection, facetiousness, un-warranted good humour (Witzelsucht, euphoria).

(c) Weakness of the contralateral limbs, per-haps a ' grasp reflex.'

(d) ' Motor ' aphasia, if the lesion is left-sided in a right-handed person.

(e) Tremor of the arms, often ipsilateral.(f) Pseudo-cerebellar signs-dizziness, ataxia,

nystagmus.(g) Electro-encephalographic evidence of a

focal or general disturbance of cortical activity.3. Neighbourhood signs, due to compression of

nearby structures:(a) Anosmia, uni- or bilateral.(b) Optic atrophy, especially when it is uni-

lateral. Central scotomata. Foster Kennedy-Paton syndrome.4. X-ray evidence of:

(a) Calcification in the benign frontal gliomas.(b) Hyperostosis of the floor of the anterior

fossa or of the vault, associated with some, butnot all, meningiomas.

(c) Increased local diploic vascularity.Discussion

If all the signs mentioned above occurred alwayswe should have a very clear picture indeed, unless

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March 1950 JEFFERSON: Tumours of the Frontal Lobe 135

ANALYSIS OF THE SYMPTOMS OF 50 FRONTAL LOBE TUMOURS

20 Cases of 30 Cases ofMeningioma GliomaPer cent. Per cent.

i. Pressure signs:Headache, vomiting, visual disturbances, etc. .. .. .. .. .. 90 77

2. Symptoms and signs attributable to the frontal lobe:(a) Epileptic attacks:

Generalized .. .. .. .. .. .. .. .. .. 20 50Localized .. .. .. .. .. .. .. .. .. 0 27Minor . . .. . . . . . . . . 5 I 3

(b) Contralateral pareses .. .. .. .. .. .. .. .. 20 27(c) Other pyramidal signs .. .. .. .. .. .. .. 25 23(d) Early apathy, loss of concentration, memory defects, euphoria, personality

changes .. .. .. .. .. .. .. .. .. 30 20

(e) Grasp reflex .. .. .. .. .. .. 3(f) Aphasia .. .. .. .. .. .. .. .. .. .. 25 I0(g) Hypersomnia .. .. .. .. .. .. .. .. .. 3

3. Pseudo-cerebellar signs:(a) Ataxia .. .. .. .. .. .. .. .. .. .. 25 0

(b) Tremor o. .. .. .. .. .. .. .. .. .. I0 7

(c) Vertigo .. .. .. .. .. .. .. 25 20

(d) Nystagmus .. .. .. .. .. .. .. .. .. 5 3

4. Neighbourhood signs:(a) Anosmia .. .. .. .. .. .. .. .. .. .. 25 7

(b) Optic atrophy, and Foster Kennedy-Paton syndrome .. .. .. 25 75. X-ray evidences:

Calcification, hyperostosis .. .. .. .. .. .. .. 40 33

the cerebellar signs were also outspoken. Theremight then be a conflict in the observer's mind as towhich signs were the more reliable. It is betternot to get involved in that problem at this stage,so we will go back to the signs of raised pressure.Unless these are insistent the idea of a tumourbeing present is scarcely likely to arise. This is,alas, only too true and many a patient with afrontal tumour has been thought to be a hystericor to be at fault in some system other than thenervous. It is a good working rule to attributenervous symptoms to the nervous system. Thepractitioner is not always so ready to do so as heshould be. Headaches are often dismissed asbilious or migrainous, vomiting as due to gastricor other sub-diaphragmatic disorder, and thesymptoms otherwise generally attributed, if sexand age make that possible, to menopausal dis-turbances. Unless the patient has a fit or thedoctor an ophthalmoscope things may drag onindefinitely in this way until the tumour is in-operable. A fatality at this late stage may con-firm the doctor's impression that brain tumours arevery risky things and that most patients die ofthem. Although there must of course be a sub-stratum of truth in such an opinion, otherwise itwould not have arisen, the more conscientiouswould more properly wonder whether the picturewould not be different if tumours were diagnosedwhen they were small. They never will be recog-nized at that stage unless the practitioners to whomthe -patients first go with their complaints are

' tumour conscious' and ready to suspect a brainlesion on little evidence. The last ten years hasshown a remarkable improvement in this directionin this country, for which praise must be given tohim to whom it is due, the family doctor.

i. General pressure signs. There is nothing verynoteworthy about the headaches from which thesepatients suffer. They are often not very severe,but they are continuous and progressive. Theydo not have the paroxysmal qualities of the painproduced by some tumours in the posterior fossa.The pain may be unilateral, and then it is generallyon the same side as the tumour. It has to bedifferentiated from migraine in which the pain iscommonly unilateral, may be accompanied byfleeting visual disturbances (teichopsia) and byvomiting, but it dates back commonly over years,is well spaced in time, and periodical. It does nothave the continuously worrying character oftumour headache. Some patients with tumour,and even with very high pressure, have no head-ache at all, but thanks to the work of Pickering inEngland and of Harold Wolff and his collaboratorsin New York it appears probable that headache iscaused by distortion of brain-meningeal relation-ships. The only structures within the skull inwhich pain can be experimentally induced are thebasal dura, the great vessels and the cranialnerves; pain cannot be caused by stimulating thebrain itself. It appears therefore that a tumourcauses headache by slight rotations or drags suchas distort the relationship of the brain to the pain-

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sensitive structures mentioned. When a patienthas no headache and yet has a tumour we assumethat insufficient disturbance of intradural relation-ships has occurred.

Changes in the optic discs, papilloedema andcongestion of the nerve-heads are present in mostcases. It is undoubtedly possible for a tumour inthe anterior fossa to attain some size before anypressure signs arise. The brain does not so tightly fillits membranes and bony capsule that the slightestencroachment on the intracranial space leads toclearly recognizable cerebral embarrassment. Asmall tumour in the posterior fossa will causetrouble much earlier than one in the prefrontalregion because it will interfere with the circulationof the cerebrospinal fluid. In that case the mass offluid in the dilated ventricles must be added tothat of the tumour itself if we wish to comparetumour sizes with tumour effects. Equally a smallmeningioma springing from the sphenoidal wing,burying itself in the brain and hindering the out-flow of cerebrospinal fluid from the lateral ven-tricle will, in the end, cause more disturbance thana much larger tumour at the frontal pole. Theoutflow of cerebrospinal fluid may be interferedwith by the crebral oedema which is so commonan accompaniment of the gliomas, and whichitself adds to the bulk of the tumour proper. It isless common in meningiomas (though it can occurwith these as well) and thus it comes about that afrontal tumour springing from the meninges of theconvexity may attain a considerable size over anumber of years before its bulk is comparable witha glioma. Some of the gliomas, to be sure, arevery slow growing and it is not so rare as mightbe imagined to have a five-year, a ten-year oreven longer history with tumours of this sort.Nearly all of these are astrocytomas. And sincethis tumour tends to weave itself amongst thenormal neural structures, and even to push themon one side, disturbances of function are notnearly so obvious or so early as they are with themalignant types of glioma (especially the dreadedspongioblastoma multiforme, still, in spite ofradiotherapy, an incurable lesion). Vomiting is arare and always a late symptom, as will be deducedfrom the foregoing considerations, for it requiresfor its production involvement of centres either inthe region of the third ventricle, the hypothalamusor the posterior fossa.

2. Signs and symptoms due to interference withlocal brain mechanism. (a) Tremor has already beenmentioned and is rarely an outstanding sign orcomplaint. Much more important are epilepticfits. These occur in about 50 per cent. of frontaltumours, and they are often almost, or even quite,indistinguishable from the idiopathic variety.They are commoner in glioma than in meningioma

cases. If the tumour spreads far back towards themotor area the myoclonic movements may pre-ponderate in the contralateral limbs and may rarelybe Jacksonian. Most often the convulsions comewithout warning or with an uninformative aura.The importance of this apparently idiopathiccharacteristic is that the fits may be the only sign ofa tumour for months or years. How are we todistinguish fits of this kind from the idiopathic ?Only by general inference and by auxiliary tests.The vast majority of idiopathic epilepsies beginbefore the patient is 20 years old. As age advancestrue idiopathic epilepsy becomes rarer, and it isour duty to search most carefully for a cause in allpatients in whom it starts during the third, fourth,fifth and later decades of life. The fact that thefit begins with turning of the head to the oppositeside is not diagnostic, because a great manyyouthful epileptics do that. James Collier (1929)thought that point important, but something elsethat he observed seems to the writer much moreso-the tendency of these fits to be multiple, toapproach or to attain ' status epilepticus,' if thereis a tumour in the frontal lobe. This has certainlybeen so in some of my own cases. If, therefore,a man or woman in the forties, let us say, begins tohave generalized fits and at the same time head-ache and some unaccountable falling off in workingpowers we ought certainly to suspect that a frontaltumour is present. If there is as yet no papil-loedema the best plan will be to examine thecerebro-spinal fluid for pressure and for raisedalbumen content, and to make pneumograms orelectro-encephalograms.

(b) Loss of memory for recent events, somesubtle alteration in personality, loss of applicationat work and failure to recognize that duties mustbe completed, loss of reticence and decency, arefrequently encountered in patients with frontaltumours. Complete moral breakdown so that thepatient becomes delinquent or liable to imprison-ment for his acts is in the writer's experience veryuncommon (one case only). Much more commonis it to find the patient good humoured and docile,though given at times to periods of unreasonable-ness impenetrable to persuasion or argument.Few of my frontal tumour series have realized theseriousness of their condition, few have beenworried at the prospects of an operation, which tothe lay mind is particularly dangerous, few havebeen bothered about money matters, the expenseor duration of their illness has brought no anxietiesor questionings. They have a certain amount ofinsight, for they may be brought to understandperfectly what is the matter with them, but eventhen they seem to be spared anxieties of a reallyworrying kind.There is no doubt whatever that all of the mental

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March 1950 JEFFERSON: Tumours of the Frontal Lobe 137

troubles so firmly linked in our minds until re-cently with tumours of the frontal lobes also occurwith tumours elsewhere. As the result of ex-periences in the unilateral removal of the frontallobes in man the writer has been driven to theconclusion that although the frontal lobes havemuch to do with the workings of the intellect, andof all the faculties subsidiary to it, that they are notits one and only seat. Nor can any differences bedetected whether it be the right lobe or the leftthat is excised. If a frontal lobe is removed thepatient is left quantitively with less neural tissuethan he had before to carry on his life and thought,to direct his conduct. So much is obvious. Butwhat could not have been foretold is that thedeprivation makes remarkablv little difference tohim. It is clear that thought processes are not sointensively cultivated in the frontal cortex thatremoval of a part leads to permanent loss of suchand such a faculty of the mind. It would havebeen very interesting if it were so, for a carefulcorrelation study of pathological material and ofthe observed clinical facts would have led to theestablishment of individual human faculties indifferent areas of the cortex. Some might havebeen in the right lobe, some in the left. Such anarrangement would have completely justified thephrenologists, Gall and Spurzheim, the firstlocalizers of function.The facts are, of course, quite otherwise.

Function is diffusely sown in the brain, thoughno one would deny that it is heavily concentratedin certain parts. The greatest mental defects arecaused by bilateral frontal lesions or by tumours ofthe corpus callosum, which by cutting corn-missural fibres impair the activities of both lobes.Mesially placed frontal tumours are very apt toinvade the corpus callosum. Severe symptoms willalways, therefore, suggest callosal involvement.Mental power, in Foster Kennedy's (I91 i) words,depends on the exquisite integration of the entirebrain. Disturbances of commissural fibres andtracts leads to an upset in this integration far morethan does cortical damage, which is in humanpathology rarely diffuse. It is worth making thegeneralization that the kind of mental alterationwhich brain tumours bring are dementias, thedetailed patterns of which depend on the previouseducation and personality of the sufferers. Butgenerally they take the form of loss of previousabilities. Schizophrenic characters do not occur-and would not except in those who are alreadyschizophrenes. Noisiness and restlessness aremost seen in folk who are noisy and restless bynature and this is true of head injuries as well.

Remarkable disturbances of personality some-times follow left temporal lesions, neoplastic orotherwise. High intracranial pressure, wherever

the lesion, interfering as it does with the actionsof the brain as a whole, is capable of causing greatchanges in alertness and in thought, and examplescould be brought forward of a clear frontal lobesyndrome when the tumour was later proved tobe elsewhere. We must therefore be wary ofaccepting mental peculiarities as incontrovertibleevidence of a frontal lesion. If these changes arepresent in a person with no signs of high pressurethat would be better evidence.

Incontinence. In the highly compressed, drowsyor stuporous patient incontinence is commonwherever the lesion is. Normally few individualspast infancy micturate at the first feeling of desireto do so, they have acquired inhibition. Thedrowsy patient reverts to childhood's state andmay wet the bed like the sleepy child. But for anadult to do so whilst awake is always a positivesign, usually of a frontal lesion-it is as positive apiece of evidence as papilloedema or a positiveBabinski. Some patients are greatly disturbed bysuch events but explain that the bladder emptiesbefore they can prevent it, as if their powers ofinhibition have vanished. We believe that thecortical inhibitory pathways to the bladder arechiefly subfrontal, linking the frontal lobes tocentres in the hypothalamus. Incontinence is acommon happening after the deep bifrontaltransactions of complete leucotomy, rare afterlimited dorsal frontal cuts. But although thereis probably an anatomical basis in fibre-tract dis-connections in frontal tumours, the thoughtfulmay be interested to pursue their own reflectionson the subject of inhibition of micturition and theeffects that sleepiness alone might exercise upon it.But it cannot too often be repeated that incon-tinence during wakefulness is a sign with localizingvalue. In the highly compressed, drowsy orstuporous patient this calls for no special comment.But it is another matter if it occurs when thepatient is conscious. It is then strongly suggestiveof a frontal lesion. In the analvtical table of 50frontal tumours it will be observed that mental andmemory defects occur as an early sign in less thanone-third of the patients. As a late sign there arefew patients who do not show some alteration forthey must all eventually become drowsy and in-continent. These alterations are due to highpressure and are very similar whatever part of thebrain the tumour affects.

(c, d) Better still would be the additionalpresence of an aphasia, a difficulty in saying whatthe patient wishes though he declares that he isperfectly clear headed. This can only occur whenthe tumour is on the left side (with the usualreservation of right handedness) and far back.Similarly slight pyramidal signs, absent abdominalreflexes, may suggest the side of the tumour if not

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its site. Sachs has stressed particularly weaknessof the face on the opposite side; this certainlyoccurs but it is as frequent with temporal tumours.None the less Sachs' studies of frontal tumours areimportant; he regards fits, mental changes, andnystagmus as most important signs. A grasp re-flex may be present, that reflex action by whichthe patient will always clench hold of anythingwhich so touches his palm. It has been admirablydescribed by Adie and Macdonald Critchley(1927). Weakness of the leg is rare in frontaltumour patients, because the motor area slantsforward offering the face area most readily to thetumour.

(e) The cerebellar signs shown by some frontaltumours will best be dealt with in the differentialdiagnosis.

3. Neighbourhood signs. The olfactory tractsare so closely applied to the under surface of thefrontal lobes that their compression by sub-frontal tumours is well imaginable. Completeanosmia, on one or both sides, is rare unless theolfactory bulbs are disorganized, as happenschiefly when there is an olfactory groove men-ingioma. Elsberg has introduced more delicatetests for estimating depression of the sense ofsmell short of complete loss. Special, even thoughsimple apparatus, is necessary and outside hospitalit will suffice if the clinician tests the sense ofsmell with whatever easily identifiable odours hecan find to hand. These tests must be remem-bered, for especially if the loss is unilateral, thepatient may be unaware and does not mention it.When it is bilateral (in the absence of nasal disease)it is always important, always organic, though itcan be a false localizing sign (Cushing, I9I6).

Unilateral optic atrophy caused by the pressureof a frontal tumour bearing heavily on the nerveof the same side is an extremely important sign.It was first given diagnostic significance by LesliePaton, and worked up with illustrative cases in animportant paper by Foster Kennedy, whosename is usually attached to the syndrome ofatrophy of the optic nerve on the side of thetumour, papilloedema in the uncompressed nerveof the opposite side. Of recent years the signifi-cance of unilateral optic atrophy has more andmore impressed itself on ophthalmologists andneurologists. It is an organic sign of the firstorder, and never more so than when the oppositedisc is oedematous. Its presence means exactlywhat the facts indicate. (The present writer haspublished a study of compression of the opticchiasma by gliomas and discussed this syndromefully, Doyne Lecture, Trans. Ophth. Soc., 45,I945.) The optic atrophy can be as well pro-duced by a temporal tumour as-by a frontal (seeFig. I24 in W. R. Henderson's essay on the

anterior basal meningiomas, 1938). Also onemust beware of being deceived by an atrophyconsecutive to severe choking of the discs whichhas become more complete on one side than theother.

4. No special comment is required by the X-rayevidences except to say that a number of thebenign gliomas calcify and that the patterns of thesecalcifications need an expert eye to recognize.They may be very faint and easily overlooked.Of recent years angiography has proved of greatuse in the final diagnosis of brain tumours, itsadvantage being that it will often enough giveevidence not only whether a tumour is presentand where it is, but will also indicate its nature.It is particularly successful with the meningiomasbecause their self-contained fine capillary shadowmakes a well-defined mass in the X-ray film.Equally -it may demonstrate an unsuspectedangioma or the wild vascular pattern of a malignantglioma.

Differential DiagnosisWe will assume that the fits and mental changes

from which our hypothetical patient could sufferhave been proved non-syphilitic by a negativeWassermann reaction. The chief differentiationnecessary will be between either temporal orcerebellar tumours. Temporal tumours equallyproduce raised pressure (only more early becausethey tend to compress the third ventricle), facialweakness and fits. There are two points peculiarto temporal lobe tumours-uncinate fits andhomonymous visual field defects. If neither ofthese is present, differential diagnosis can only bearrived at by mechanical means.The possibility of cerebellar signs in frontal

tumours has already been mentioned once or twice.This possibility of confusion is brought about bythe important pathways which leave the frontallobes and run to the pontine nuclei, there to berelayed to the cerebellum and labyrinthineapparatus. But it can be said at once that a full-fledged cerebellar picture is never given byfrontal tumours. The symptoms and signs aresuggestive and no more. Why then should diffi-culties ever arise? The reason is that cerebellartumours themselves frequently give rise to symp-toms and signs which are scarcely more obtrusiveor classical. The clinical picture which GordonHolmes (1922) has made so well known is best seenin injuries or vascular insults of the cerebellum. Itcan, of course, occur in patients with tumours, too,but not so often as might be thought. Evennystagmus itself may, if rarely, be minimal orabsent in cerebellar lesions. It is quite certainthat the coarse, unmistakable nystagmus of somecerebellar tumnours never occurs with frontal.

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Before having recourse to angiography orventriculography the cortical potentials should bestudied electronically. Sometimes extremely ac-curate localization can be given by these means byalterations of potentials, phase reversals and soforth as Grey Walter, Denis Williams and GeorgeDawson have shown. Electro-encephalographyhas become an essential exploration of organiccerebral lesions. Further information can beobtained by angiography or ventriculography.

Operations on Frontal TumoursIn general the attack on a frontal tumour follows

the lines generally adopted in neurosurgery. It isassumed that the aim is the removal of the tumour.This can sometimes be effected by enucleation, inother cases the extent and position of the tumourmake the sacrifice of the lobe unavoidable. Thelobe may have to be excised to give access to atumour beneath it. The steps of the operation areas follows. An incision is made in the mid-linebackwards from a point just above the glabella toone inside the hair line. The cosmetic result issuperior if the incision is very accurately placed inthe mid-line. Having reached the higher point theincision curves over the scalp to fall verticallytowards the ear which it should reach. The scalpflap should be first marked out with iodine andthen with a scratch. Novocaine-adrenalin solution(i per cent.) is then injected along the proposedline of section. The whole scalp flap is dissecteddownwards and forwards, free from the bone.Great care must be taken by finger compression tokeep the blood-loss during the cutting of the scalpflap down to a few cubic centimetres. Suitablepoints are now chosen for making drill holes,avoiding the frontal air sinus. The bone dustobtained in making the holes is saved for replace-ment at the close of the operation. The holes aremost safely made by brace and perforator and burrworked by hand. After separation of the duramater from the bone the holes are connected withthe Gigli saw. The base of the bone flap in thetemporal fossa may be narrowed with de Vilbissforceps; it is then broken down, hinged on thetemporal muscle. The bleeding from the exposeddura is usually negligible, and is well controllablewith wet cotton or lintine. If bleeding is severeeither there is a meningioma beneath the dura witha wide attachment to it, or the anaesthetic iswrong or the airway imperfect. It is a greathandicap to good surgery to have a high intra-cranial pressure, hence the need for early diagnosis.The patient's chances of recovery are greatly en-dangered if the brain tends to bulge irresistiblythrough a dural incision. If the pressure cannotbe lowered by puncture of an intracerebral cyst or

of the ventricle it will be wiser to break off theoperation before more harm is done and try againunder local anaesthesia alone later. Supposingthat the dura can be safely opened this is nextdone, cutting it below, in front and behind. Thecortex is now inspected for evidence of tumour,which may be very clear. If not it will be foundby puncture. The recognition of the presence of atumour, of its extent and especially of its natureneeds considerable culture. It is on this vitalpoint that the general surgeon was so constantlydefeated. If excision of the frontal lobe is decidedupon the cortical veins entering the superiorlongitudinal sinus are first coagulated so that thefalx is clear. This necessitates a bone incisionexactly on the mid-line. A half- or one-inch over-hang will greatly hamper the securing of theseveins. When clearly seen they are easily dia-thermized and divided. The line of cortical in-cision is-next planned on the surface of the brain,the veins to be cut coagulated and the arteriesoccluded with silver clips. The line of this sectionwill commence below, as a rule, at the junction ofthe anterior and middle fossae. The incision intothe brain is best made with a narrow bluntdissector, which allows the recognition of deepvessels. The anterior horn of the lateral ventriclemay be cut across if the tumour has not pushed ittoo far back. This does not matter. The onlydifficulty may be the clipping of the anteriorcerebral artery on the mesial surface deep in.After the orbital surface of the brain has beencut through, the whole lobe is lifted out. Allbleeding points are secured, the large cavity filledwith Ringer's solution and the dura closed. Asmall drain can be left in between bone and durafor 24 hours, but it is certain that daily aspirationsof fluid will have to be made during the next weekor ten days. The dead space eventually settlesdown, it may permanently communicate with theventricle.Lobectomy gives the patient the best chance of

long survival and obeys the surgical maxim ofblock removal of non-enucleable tumours. Innone of the writer's cases has there been anyimportant mental, moral or-other disability as theresult of it.The prognosis depends on the nature of the

tumour. It is excellent in the meningiomas andangiomas, hopeless in the malignant gliomas andintermediate in the more benign gliomas (astro-cytomas). The writer has had several patientswith astrocytomas who have survived five yearsand a few who lived usefully for over ten yearsafter frontal lobectomy. The great advantage ofthe operation is that it leaves so large an ' internaldecompression' that given a very slowly growingtumour the space serves them well.

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140 PENNYBACKER: Pituitary, Pineal and Third Ventricle Tumours March I950'

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