POSTGRAD. MED. J. (I962), 38, 4I7 THE SO-CALLED GENERAL SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE Clinico-pathological Report Based on a Study of 100 Cases FATHY W. TADROS, PH.D., M.R.C.P.(Edin.), D.P.M. S. A. ZAKI, M.D., B.Sc. 0. H. SEROUR, M.CH. RASHAD SAKR, M.D., D.CH. From the Faculty of Medicine, Cairo University THERE has been much controversy regarding the pathogenesis of the so-called general symptoms of brain tumours. They are often ascribed to one or more factors which produce an increase in the intracranial pressure. It is generally accepted that these factors are: firstly, the increase in the contents of the intracranial cavity produced by the size of the tumour and the surrounding cedema; secondly, the effect on the vascular system, producing rise in the venous pressure; and, thirdly, the effect on the flow of the cerebrospinal fluid. The present work is devoted to the study of the general hydrocephalic symptoms in ioo con- secutive cases of increased intracranial pressure. An attempt at clarification of the controversies with regard to the pathogenesis of these symptoms, based on the pathological changes encountered in these cases, is made. Material and Methods The material presented comprises ioo con- secutive cases of increased intracranial pressure, 56 with infratentorial and 44 with supratentorial lesions. Of the 56 infratentorial cases, 32 were cerebellar tumours, one subarachnoid cyst between the tentorium and superior surface of the cere- bellum, five pineal region tumours, five brain-stem tumours, four cerebellopontine angle tumours, five post-meningitic hydrocephalus, two choroid plexus tumours in the fourth ventricle and two cases of gliosis of the aqueduct of Sylvius. Supra- tentorial lesions comprised nine parasagittal menin- giomas, six thalamic tumours, five temporal, one occipital, four pariet-occipital, five frontal lobe tumours, four extensive tumours in one hemi- sphere, two lateral ventricle tumours, two supra- sellar tumours, one case of corpus callosum tumour, four cases of secondary metastatic nodules irregularly dispersed in the cerebral hemispheres and one case of chronic subdural hematoma. Fifty-one cases were gliomas, of which 29 were in the cerebellum, brain stem and around the aqueduct and 22 in the cerebrum; I2 cases were meningiomas, nine parasagittal, one in the lateral sphenoid ridge, one suprasellar and one infra- tentorial in the pineal region. The rest comprised IO tuberculomas, eight cerebellar and two hemi- spherical; four pinealomas; two neurinomas; two choroid carcinomas; one cranio-pharyngioma; one cholesteatoma; four hamangioblastoma cere- belli and two chronic abscesses, one cerebellar and one temporal. In each case serial coronal sections of the brain were made and the extent of the lesion verified. The ventricles were examined with particular attention to their size and position. Paraffin sections stained with H. and E. were prepared from the lesion, parts of the affected and contra- lateral hemispheres, including the basal ganglia and diencephalon, and the brain stem. The optic nerves and chiasma from six cases showing papill- cedema and six cases of post-papilkedemic optic atrophy were examined histologically, using H. and E. and Smith Queigley stains. The clinico-pathological data relevant to our issue and discussions of the pathogenesis of the general symptoms of increased intracranial pres- sure will be presented in two separate parts, the first dealing with the factors responsible for the production of hydrocephalus in space-occupying lesions, while the second deals with the patho- genesis of the individual manifestations of the so-called general symptoms of increased intra- cranial pressure. Factors Responsible for Production of Hydro- cephalus in Space-occupying Lesions Pathology At autopsy all the cases showed the presence of tonsillar herniation, indicating a downward shift of the whole brain. Tumours in the supratentorial space showed, in addition, displacement of the cerebral hemispheres to the contralateral side and copyright. on 18 August 2019 by guest. Protected by http://pmj.bmj.com/ Postgrad Med J: first published as 10.1136/pgmj.38.441.417 on 1 July 1962. Downloaded from
Transcript
POSTGRAD. MED. J. (I962), 38, 4I7
THE SO-CALLED GENERAL SYMPTOMS OFINCREASED INTRACRANIAL PRESSURE
Clinico-pathological Report Based on a Study of 100 CasesFATHY W. TADROS, PH.D., M.R.C.P.(Edin.), D.P.M.
S. A. ZAKI, M.D., B.Sc.0. H. SEROUR, M.CH.
RASHAD SAKR, M.D., D.CH.From the Faculty of Medicine, Cairo University
THERE has been much controversy regarding thepathogenesis of the so-called general symptoms ofbrain tumours. They are often ascribed to one ormore factors which produce an increase in theintracranial pressure. It is generally accepted thatthese factors are: firstly, the increase in thecontents of the intracranial cavity produced bythe size of the tumour and the surrounding cedema;secondly, the effect on the vascular system,producing rise in the venous pressure; and,thirdly, the effect on the flow of the cerebrospinalfluid.The present work is devoted to the study of
the general hydrocephalic symptoms in ioo con-secutive cases of increased intracranial pressure.An attempt at clarification of the controversieswith regard to the pathogenesis of these symptoms,based on the pathological changes encountered inthese cases, is made.
Material and MethodsThe material presented comprises ioo con-
secutive cases of increased intracranial pressure,56 with infratentorial and 44 with supratentoriallesions. Of the 56 infratentorial cases, 32 werecerebellar tumours, one subarachnoid cyst betweenthe tentorium and superior surface of the cere-bellum, five pineal region tumours, five brain-stemtumours, four cerebellopontine angle tumours,five post-meningitic hydrocephalus, two choroidplexus tumours in the fourth ventricle and twocases of gliosis of the aqueduct of Sylvius. Supra-tentorial lesions comprised nine parasagittal menin-giomas, six thalamic tumours, five temporal, oneoccipital, four pariet-occipital, five frontal lobetumours, four extensive tumours in one hemi-sphere, two lateral ventricle tumours, two supra-sellar tumours, one case of corpus callosumtumour, four cases of secondary metastatic nodulesirregularly dispersed in the cerebral hemispheresand one case of chronic subdural hematoma.
Fifty-one cases were gliomas, of which 29 were
in the cerebellum, brain stem and around theaqueduct and 22 in the cerebrum; I2 cases weremeningiomas, nine parasagittal, one in the lateralsphenoid ridge, one suprasellar and one infra-tentorial in the pineal region. The rest comprisedIO tuberculomas, eight cerebellar and two hemi-spherical; four pinealomas; two neurinomas;two choroid carcinomas; one cranio-pharyngioma;one cholesteatoma; four hamangioblastoma cere-belli and two chronic abscesses, one cerebellar andone temporal.
In each case serial coronal sections of the brainwere made and the extent of the lesion verified.The ventricles were examined with particularattention to their size and position. Paraffinsections stained with H. and E. were preparedfrom the lesion, parts of the affected and contra-lateral hemispheres, including the basal gangliaand diencephalon, and the brain stem. The opticnerves and chiasma from six cases showing papill-cedema and six cases of post-papilkedemic opticatrophy were examined histologically, using H.and E. and Smith Queigley stains.The clinico-pathological data relevant to our
issue and discussions of the pathogenesis of thegeneral symptoms of increased intracranial pres-sure will be presented in two separate parts, thefirst dealing with the factors responsible for theproduction of hydrocephalus in space-occupyinglesions, while the second deals with the patho-genesis of the individual manifestations of theso-called general symptoms of increased intra-cranial pressure.
Factors Responsible for Production of Hydro-cephalus in Space-occupying LesionsPathologyAt autopsy all the cases showed the presence of
tonsillar herniation, indicating a downward shiftof the whole brain. Tumours in the supratentorialspace showed, in addition, displacement of thecerebral hemispheres to the contralateral side and
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uncal herniation that was more marked on the sideof the lesion.
All cases, whether the tumour was supra- orinfratentorial, central or lateral, were associatedwith internal hydrocephalus which was either com-municating or partially so. Tumours arising in ornear ventricles, as those of the third ventricle andsuprasellar, pineal, cerebellar and cerebello-pontine angle tumours, produced obstruction tothe flow of the CSF. In these cases the ventricularsystem above the level of the obstruction wasdilated and central in position. Supratentorialtumours away from the cavity of the third ventricleshowed dilatation of the third and of the twolateral ventricles only. The ventricular system wasshifted to the opposite side of the lesion. Therewas a kink at the upper end of the cerebral aque-duct near its opening in the third ventricle (Figs.i and 2). This part of the aqueduct was flattenedfrom side to side with obliteration of the flow ofCSF. This finding was noted irrespective of thesite of the tumour in the hemisphere, whetherfrontal, temporal or occipital, peripheral or central(Figs. 3, 4, 5 and 6).Naked-eye examination of the brain stem
showed the presence of multiple hemorrhageirregularly dispersed in 23 cases (Figs. 7, 8 and 9).In two of these cases there was hamorrhages inthe diencephalon as well, on the same side of thelesion (Fig. 6). Histological examination revealedthe presence of ischamic infarcts in 6i cases.The infarcts were of recent origin. Some showedearly necrosis, others presented complete break-down of tissue, while others still showed thepresence of compound granular corpuscles (Fig.Io).Himorrhages only were present in i2 cases,
infarcts in 50 and both together in ii. Thusvascular changes in the brain stem were presentin 73 cases. Out of these 73 cases, 32 were supra-tentorial, i.e. 72.7% of supratentorial cases and 44infratentorial, i.e. 73.2% of infratentorial cases. Itis evident from these percentages that vascularchanges in the brain stem occur with equalfrequency in supra- and infratentorial cases.(Edema in the tumour and surrounding brain
tissue was present in 26 cases: nine supratentorial,i.e. 20.5% of supratentorial cases, and i6 infra-tentorial, i.e. 28.5% of infratentorial cases.Cerebral cedema associated with brain tumourswas therefore absent in a large number of cases inour series. When present it was seen in thetumour as well as in the rest of the affectedhemisphere. It is noteworthy that edema waspresent only in cases that were surgically treated.The cases that were not interfered with surgicallyor subjected to lumbar puncture or ventriculo-graphy did not show cedema.
In 23 cases lumbar puncture was performed andCSF pressure and chemistry were recorded. Thepressure was increased in io out of these 23 cases(41'7%). At autopsy it was confirmed that thosecases with normal pressure of CSF had completeobstruction to its flow with a non-communicatinghydrocephalus. On the other hand, the lesion inthe cases showing rise of pressure was located insuch situations as to cause only partial obstructionto the flow of CSF producing communicatinghydrocephalus (Table i). Somewhat conflicting re-sults are reported from examination of spinal fluidpressure, e.g. Ayer (1929) and Puusepp (1928) re-ported normal fluids in only a few cases of theirseries, while Greenfield and Carmichael (I925) andMandelboim (1930) found normal or even sub-normal pressures in the majority of their cases.
DiscussionConsidering the pathological findings in the I00
cases of brain tumours presented in this report,we are of the following opinion: firstly, obstructionto the flow of the CSF is the main factor in thepathogenesis of increased intracranial pressure.This is produced either by the presence of thetumour along the route of flow of the CSF, asin the majority of infratentorial and intraventriculartumours, or by displacement of the brain, as insupratentorial tumours. If we recall that thecranial cavity is divided by the tough falx cerebriand tentorium cerebelli into three compartments,two supratentorial and one infratentorial, the con-tents of either of the supratentorial compartmentsare increased when a space-occupying lesionreaches a certain size. Faced with the bony cal-varium and tough dural membranes, the swollenbrain can only escape laterally under the falx tothe contralateral side and downwards through thetentorial opening. The lateral and downward shiftof the brain would kink the junction of the thirdventricle with the aqueduct. Obstruction at thissite with consequent internal hydrocephalusresults. It is worthy of mention that hydro-cephalus arising by the mechanism just describeddepends on the size rather than the site of tumourin the various lobes, or its being deeply seated orsuperficial in position. The attempt at correlationbetween the site of the tumour and time ofappearance of hydrocephalic manifestations is thusrendered futile. The only factor determining theearly or late appearance of hydrocephalic symptomsin relation to focal manifestations, in our opinion,is the presence of the tumour in a dominant lobeor a silent area.
Secondly, we believe that the role of the in-crease in contents of the intracranial cavity causedby the size of the tumour and the surroundingcedema in the production of increased intracranial
July I962 TADROS, SEROUR, ZAKI and SAKR: Increased Intracranial Pressure 419
TABLE I
Nam SxDanssCSF CSFName Sex Diagnosis Pressure Protein
S.S. F Pineal-region meningioma .. .. .. .. .. .. N 50M.M. M 4th vent. choroid carcinoma .. .. .. .. .. .. N iooA.Az. M Pinealoma .. .. .. .. .. .. .. .. .. N 8oW.M. F Gliosis of Sylvian aqueduct .. .. .. .. .. .. N 8oKh.I. F 4th vent. choroid carcinoma .. .. .. .. .. .. N 70H.S. M Post. fossa meningioma .. .. .. .. .. .. N 65A.Sh. M Cerebellar hmmangioblastoma .. .. .. .. .. .. N 70M.D. M Pineal-region glioma .. .. .. .. .. .. N 75Y.M. M Cerebellar medulloblastoma .. .. .. .. .. .. N 40M.Sh. M Rt. cerebellar tuberculoma .. .. .. .. .. .. N 40A.T. M Upper cerebellar glioma .. .. .. .. .. .. N 40H.S. F Cerebellar glioma .. .. ..-. .. .. .. .. .. N 20I.Ch. F Cerebellar medulloblastoma .. .. .. .. .. .. N goT.F. M Lt. frontal glioma .. .. .. .. .. .. .. .. Raised I20S.A. F Meningioma, parasag. o.. .. .. .. .. .. .. ,, 9A.Sh. M Cerebello-pontine angle ncuroma .. .. .. .. .. ,, I00An.B. M Lt. cerebellar tuberculoma .. .. .. .. .. .. ,, 150A.A. M Occipital glioma .. .. .. .. .. .. .. .. ,, 40R.M. F Parasag. meningioma .. .. .. .. .. .. .. ,, 40F.A. F Parieto-occip. glioma .. .. .. .. .. .. .. ,, 20M.H. M Corp. callosum glioma 1.. .. .. .. .. .. .. ,, 20A.Az. F Rt. cerebell. abscess .. .. .. .. .. .. .. ,, I 00H.R. M Rt. lower cerebellar glioma .. .. .. .. .. .. ,. 6o
.....
..........
FIG. i.-Glioma in basal ganglia region. Ventricularsystem is dilated and shifted.Aqueduct in upper midbrain is compressed and
markedly displaced laterally.
pressure is over-emphasized. It must be notcdthat the growth of the tumour is associated withsimultaneous destruction of brain tissue. It is alsoknown that the brain is a collapsible organ. Thisfact is well demonstrated in seven cases of hugemeningiomas encountered among the presentseries. In these cases the cerebral hemispheres
FIG. 2.-Section of hemisphere showing ventricularependymoma, dilatation and shifting of ventricularsystem. Aqueduct appears in upper midbraincompressed laterally and shifted.
were compressed and actually flattened withoutcorresponding appreciable signs of neural de-ficiency. As to cedema surrounding the braintumour (Reichardt, 1905; Cassirer and Lewy,1920; Fortig, 1921), it was noticed that itoccurred in 26 cases only and that these cases wereinterfered with surgically or by puncture.
Thirdly, venous obstruction or rise of venouspressure as a cause of decreased absorption orincreased formation of CSF is doubtful. Theabsorption of CSF in the superior sagittal sinusis a passive process and depends only on thegradient of pressure between it and the sub-arachnoid space. The sinus is well protected in
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FIG. 3.-Occipital lobe glioma. Ventricular system aboveaqueduct is dilated and shifted to opposite side.
FIG. 4.-Temporal lobe compression by middle fossameningioma. Ventricular system dilated andshifted.
FIG. 5.-Deep frontal glioma. Ventricular system dilatedand shifted to opposite side.
FIG. 6.-Section from case of parieto-occipital gliomashowing dilatation and shifting of ventricular system.Heemorrhages in basal ganglia region on same side oftumour.
FIG. 7.-A frontal meningioma. Both lateral ventricleand third ventricle dilated. Section of pons showshlmorrhages.
FIG. 8.-Section of cerebral hemisphere showing gliomain left thalamus. Brain stem shows hTmorrhagesin the midbrain.
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FIG. 9.-Chronic abscess in right temporal lobe.Ventricular system above aqueduct is dilated andshifted to left side. Section of midbrain showssecondary hemorrhages.
S! re. ... ..:.-.-....
... ..:Yl..l...L--t..:..-..:
iwi(~~.. -|1....-.....,.J...j N .fi.w.. .. .... .. .
FIG. io.-Photomicrograph of brain stem in a case offrontal glioma showing ischamic infarct withcompound granular corpuscles. (x i8o)
the tough membranous dura and the pressure ofthe intracranial contents is not directly trans-mitted to the sinus, which is neither compressible
nor collapsible. This fact, coupled with ourfindings of normal CSF pressure in a large numberof cases which showed high degrees of hydro-cephalus, both pathologically and symptomatically,renders the decreased absorption of CSF as acause of hydrocephalus improbable. As to theincreased formation of CSF, it is known that it isan active process of secretion by the choroidplexus which depends on the arterial blood flowin that plexus.We believe that the level of pressure in the
subarachnoid space depends on the site of thetumour. Those occurring in or near the ventriclesproducing complete obstruction of the CSF withnon-communicating hydrocephalus are accom-panied by normal or low subarachnoid pressure.On the other hand, those causing partial obstruc-tion show the reverse.
Pathogenesis of the so-called General Symp-toms of Increased Intracranial PressureThe incidence of symptoms of increased intra-
cranial pressure in the ioo cases presented in thiswork is shown in Table 2.
HeadacheHeadache was the commonest symptom in all
our cases. In 95% it was the first symptom andwas preceded by vomiting in only 5%. Thesefive cases were all children suffering from sub-tentorial tumours.
It was noted that headache disappeared whenhydrocephalus was advanced. In fact, whenhydrocephalus reached the stage in which it wasaccompanied by post-papillcedemic optic atrophyheadache was never complained of.
It appears, as is generally accepted, that head-ache is the result of stretch of the arachnoidcovering with its blood vessels by the expandingbrain (Penfield, Evans, Brickner and German,1934). The cessation of the complaint of headacheis usually ascribed either to the clouding of con-sciousness accompanying the hydrocephalus in itslate stages or to the fact that the arachnoid hasreached its maximum limit of stretch.
VomitingVomiting was encountered in 57 cases: 47
subtentorial (84% of subtentorial lesions) and iosupratentorial (22.7% of supratentorial lesions).
TABLE 2
INCIDENCE OF MAJOR SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE AMONG 100 CASES OF BRAIN TUMOURS
It was more common in children (39 cases, 68.4%)than in adults (i8 cases, 3i.6%). It was noticedthat most brain tumours in children were locatedin the cerebellum, fourth ventricle and pinealregion and that vomiting in adults was associatedmore commonly with cerebellar tumours. Thesefacts conform with the observations of Puusepp(1928). In four out of the five cases of brain-stem tumours in our series vomiting was absent.In the fifth it occurred late when other symptomsof hydrocephalus developed in the terminal stage.This was also noted by Wilson (I93I).Vomiting was an early symptom in the evolution
of hydrocephalus. It often accompanied headache,especially when the latter was at its peak. Inyoung children (five cases) it appeared even earlierthan headache, i.e. it was noted before the childwas able to complain of the latter. Vomiting likeheadache showed amelioration with the advanceof hydrocephalus.On account of the close relationship of vomiting
to headache we believe that vomiting is a reflexmechanism in response to the pain afferents whichproduce headache. Its frequent occurrence withcerebellar and fourth ventricle tumours is due tothe early and severe headache accompanying thesetumours rather than to their intimate and closerelation to the vomiting centre in the medulla.This view is supported by the following facts:firstly, in tumours of the brain stem the lesion isnearer to the vomiting centre than in cerebellarand fourth ventricle tumours, yet vomiting wasrarely noticed in such cases. Secondly, medullarycentres other than the vomiting centre are the lastto be affected in cases of increased intracranialpressure. Had vomiting been due to the directeffect of the neoplasm on the cerebellum or fourthventricle, one could hardly imagine how thevomiting centre alone could be affected while therest remain intact and, in particular, the vaso-motor centre, which is closely related to thevomiting centre. One would argue that vomitingmight be due to ischemic irritation of the vomitingcentre produced by the stretch on brain-stemvessels consequent to shift of the brain. Butischamia affects all the medullary centres equallyand in absence of a proof of a selective sensitivityof vomiting centre this explanation seems im-probable.
PapillaedemaPapillcedema was present in 86 cases. This
agrees with its incidence in Paton's (I909) andVan Wegenen's (1929) series.
In the 14 cases in which fundus changes wereabsent were four brain-stem tumours, four para-sagittal meningiomas, four secondary metastases,one cerebello-pontine angle tumour and one
chronic subdural hamatoma. It is noted thatnearly half of the meningiomas in our series (fourcases out of nine) showed no fundus changes.This conforms with the findings of Bollack andHartmann (1928), who described the presence ofpapillcedema in 22 out of 59 meningiomata. It isalso observed that papillkedema was absent incases with minimal increase in the intracranialpressure as well as in those with very slowlygrowing tumours.Out of the 86 cases showing papilledema, 55
were supratentorial (79°% of the supratentorialcases) and 5' infratentorial (9I% of the infra-tentorial lesions). From this it is evident thatfundus changes are somewhat commoner in infra-than supratentorial lesions. It was interesting toobserve that papillcedema was advanced (4 D)in the majority of supratentorial compared withthe subtentorial tumours (27 out of 35 in the firstand only i6 out of 5I in the second). Far-reaching in its significance is the finding that I4cases that presented complete obstruction to theflow of CSF with non-communicating hydro-cephalus and normal or subnormal pressure ofCSF in the subarachnoid space showed veryminimal papillcedema (2 D). In some of thesecases, particularly those that proceeded rapidlyto optic atrophy, it was really difficult to judge ifthe atrophy was post-papillcedemic.Summing up, we can safely deduce that the
incidence and degree of papillcedema depends onthe amount of CSF in the basal subarachnoidspace. This is supported by the fact that in casesof idiopathic (benign) intracranial hypertensionwhich are associated with a fully communicatinghydrocephalus papillcedema was often very markedand chronic. Although fundus changes are com-moner in subtentorial tumours, yet the changesare severe and more advanced in the supratentoriallesions.
In discussing the pathogenesis of papillcedemain cases of brain tumours we have to differentiatebetween the mechanisms underlying each of itstwo main components: swelling of the optic discand congested retinal veins. We believe thatswelling of the optic disc is due to stagnationof CSF in the base of the brain and hencein the sheaths of the optic nerves. Thisis due to impairment of the movement ofCSF over the hemisphere to reach thesuperior sagittal sinus. Normally the cir-culation of the CSF is maintained by thepropulsion and suction effect of the brainpulsations on the subarachnoid space (Dott, I954).In case of increased intracranial pressure suchpulsations are diminished or absent. The view ofPaton and Holmes (9i9I) that the increased sub-arachnoid CSF pressure is transmitted to the
FIG. i I.-Section of optic nerve in a case of advancedpapilledema. No interstitial cedema is detected.The subarachnoid space is widened. (x 82)
optic sheath with consequent pressure on opticveins and development of papilleedema cannotexplain the many cases of brain tumour showingpapillcedema in which normal or even subnormalpressure of CSF was present. Reichardt's (1905)and Spatz's (1930) suggestions that interstitialcedema in optic nerves, tract and chiasma is re-sponsible for papillerdema were not substantiatedin our cases. We studied the optic nerves, tractsand chiasma in I2 cases manifesting papillcedemaor post-papillcedemic optic atrophy microscopicallyfor the presence of interstitial cedema. In noneof these cases was such a finding encountered(Fig. ii). As to the pathogenesis of congestedretinal veins, we agree with the current opinionthat the rise of venous pressure associated withbrain tumours is the responsible factor.
The pathogenesis of optic atrophy followingpapilledema requires careful consideration. Itwas a complication in 43 out of 5I subtentorialtumours manifesting papillcedema (84%), while itwas only noted in IO out of 35 supratentorial cases(28.6%).
It was more common and earlier in cerebellarand fourth ventricle tumours than those of thebrain stem and supratentorial lesions.At autopsy it was noted that post-papillcedemic
optic atrophy was directly related to the degree ofdilatation of the third ventricle. It was observedthat in cases of hydrocephalus secondary to braintumours the third ventricle is enlarged at theanterior part of its floor and to a lesser extent in itstransverse diameter. Other dimensions werehardly affected. Table 3A and B, compares thedimensions of the third ventricle in I3 tumourcases and in I2 normal cases.The anterior part of the floor of the third
ventricle is the most delicate part. It constitutesboth the optic and the infundibular recesses. Thedilatation of the optic recess occurs at the expenseof compression, flattening and, later, atrophy ofthe optic chiasma and roots of the optic nerves.In some cases these were reduced to flattened thinfilaments stretched over the dilated floor of thethird ventricle, which appeared as a cyst. Inconfirmation of this hypothesis: firstly, three cases(two subtentorial and one supratentorial tumours)had their fields of vision examined before theonset of atrophy and complete blindness. In thesecases various field defects were shown indicatingcompression of various fibres of the optic chiasmand nerves with patchy limitation of conductionbefore final retrograde atrophy had set in.Secondly, in hemispherical tumours optic atrophy
TABLE 3A
MEASUREMENTS OF THIRD VENTRICLE IN I3 CASES OF SPACE OCCUPYING LESIONS
Vertical DiameterA-P Maxim.
No. Age Pathology Duration Diam. Optic Infund. Mamill. Posterior WidthYear Recess Recess Body Level
occurred late in IO cases and not at all untildeath in 25 cases. In these cases the third ventriclewas not as markedly dilated as in cases ofsubtentorial tumour. Thirdly, in cases of otitichydrocephalus and idiopathic hypertensivehydrocephalus where the hydrocephalus iscommunicating and the ventricles are not dilatedto any considerable extent the papillcedema ismore marked, and however chronic it may becomeeven for a year or more it rarely, if ever, leads topost-papillcedemic optic atrophy.The mechanism of optic atrophy in tumours
directly related to the optic nerves and chiasma isdue to direct pressure. This was seen in suprasellartumours.
Mental Symptoms and Disturbances of ConsciousnessWe prefer to discuss both these symptoms under
one heading because we believe that mental symp-toms of raised intracranial pressure have a specialgeneral character which is related to a certain degreeof disturbance of consciousness. This character isa form of an organic reaction type, in whichthe patient shows slow reaction, inattention,indifference, poor response, poor memoryand sometimes faulty insight into the gravityof his condition. In the intellectual spherethe finer qualities of mind are not clouded. Onthe affective side more often than not the patientsare apathetic, show lowering of spirits and loss ofinstinctive reaction much more than the labileunstable emotions. With the progress of thecase usually lethargy, drowsiness and stuporsupervene and later complete loss of consciousnesswhen the patient leads a vegetative existence.Most of our cases (70 out of IOO) showed this
progressive deterioration. They included frontal,temporal, diencephalic and ventricular as well as
subtentorial tumours. One of the series was a caseof glioma of the corpus callosum. His mentalpicture was that of lack of insight into his physicalailment and an appreciable degree of disorienta-tion. He had heaviness and ataxia of both lowerlimbs and did not mention the headaches unlessasked about them. However, he did not show anyspecific type of mental picture.
Specific types of mental picture have beendescribed with brain tumours. These are often,so to speak, positive symptoms unlike the negativegeneral character often met with. They werenoted by Oppenheim (I889) and Wilson (93I).Wilson, however, did not think of these syndromesas specific to brain tumours, as they were metwith in cases of encephalitis (Wilson, I9I8).
Sometimes, however, the person concerned ispredisposed and the specific psychiatric symptomsare coincidental.None of our series showed any specific positive
mental picture. The analysis of these symptomsshows that they all represent some degree ofdisturbance consciousness, e.g. loss of memory isuncQnsciousness of the past, disorientation is poorconsciousness of the surroundings, while apathyand poor response are a manifestation of lack ofattention, i.e. unconsciousness of the present.Though the mental symptoms accompanying
brain tumours at various sites are of the samereaction type, yet they may differ in degree and inthe extent to which they dominate the clinicalpicture. Thus they might still be of localizingvalue.
It is thought that pathologically these mentalsymptoms were associated with tumours whichinterfere with large association fibre systems, viz.corpus callosum, occipito-temporal fasciculus andoccipito-frontal fasciculus (Wilson, 193I; Burns,
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i908; Pfeifer, I928). This conception, adequateenough in explaining the occurrence of mentalsymptoms in tumours of the corpus callosum andfrontal lobe, does not explain the association ofmental symptoms with tumours of thalamus,suprasellar region, intraventricular tumours andsubtentorial tumours.The modern conception of the centroencephalic
system as the centre of consciousness agrees withpathological observations made in our series. Thissystem consists of the central grey matter of thethalamic, hypothalamus and brain stem. It repre-sents the different levels of consciousness fromabove downwards.
Pathological specimens examined showed thatthe lateral and downward shift of the brain pro-duced vascular ischbemia or haemorrhage in thissystem due to stretch and tear of the perforatingvessels supplying it. This, in our view, is the maincause of the general mental and conscious dis-turbances which accompany most tumours. Itmight also contribute to the production of mentalsymptoms in tumours of frontal lobe or corpuscallosum.
39 3 (I parietoccip., 30 6 (4cerebellar,i frontal, i in- (supratent) 2 pineal)travent (lateral
ventricle) )
The so-called false localizing signs of braintumours comprise those of long tract or cranialnerve manifestations which are not directly in-filtrated or destroyed by the tumour. One ofour cases which has a parieto-occipital tumourshowed cerebellar signs. Another case of frontalglioma and one of lateral ventricle ependymomawhich was infiltrating the cerebral hemispheremanifested intention tremors. Most of our supra-tentorial tumours manifested decerebrate rigidityin their terminal course. Four cerebellar casesshowed symptoms of affection of multiple cranialnerves.The brain stem which contains all ascending
and descending as well as cerebellar tracts is theseat of ischxmia as a result of downward displace-ment. This, in our opinion, is the main cause ofsuch symptoms. Stretching of the cranial nervesas a result of downward shifting explains theirfalse localizing involvement.
TABLE 5
No. ofCases
Showing Generalized JacksonianFits
8 4 (i diffuse frontal, 4 (3 meningioma,2 meningioma, i i parietal glioma)subtentorial cyst) . -
Generalized convulsions occurred throughoutthe course of one case of deep diffuse frontalglioma. In five cases of meningioma three hadJacksonian fits and two generalized convulsions.A case of parietal glioma presented with Jacksonianfits followed by generalized convulsions only in theearly stages of its course; one case of subtentorialsubarachnoid cyst which was invaginating theupper surface of the cerebellum and the mid-brain posteriorly had three major fits in its course.It is seen that convulsions occurred in 8% of thecases. Incidences given in the literature are asfollows: Parker (1930), I2% of 3I3 cases; Dana(I9I6), 25%; and Kroll (I929), 20%. Parker'scases occurred in 83.6% of supratentorial tumoursand in only i6.4% of infratentorial tumours.
Jacksonian fits are of highly localizing value(Collier, 1904; Muskens, I928; Beduschi, I928),while generalized convulsions are not.
It is generally accepted on both physiologicaland electro-encephalographic evidence that con-vulsions are a manifestation of discharge from thediencephalon and the brain-stem reticular forma-tion. Even Jacksonian convulsions are proved tobe due to a localized diencephalic discharge inresponse to afferents from a cortical area. Thestimulus here would not be of sufficient strengthto evoke the whole diencephalon.
Being of such an origin, convulsions of the non-Jacksonian type would be considered of non-specific localizing value. Hence we find corticallesions producing generalized convulsions similarto those of central or even subtentorial localization.
Summary(i) The general symptoms of increased intra-
cranial pressure in ioo cases are described and theirpathogenesis discussed.
(2) The report is divided into two parts. Thefirst deals with the factors responsible for pro-duction of hydrocephalus in space-occupyinglesions. We are of the opinion that obstructionto the flow of the CSF is the main factor in thepathogenesis of increased intracranial pressure.
(3) The second part deals with the pathogenesisand frequency of each individual general symptom
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of increased intracranial pressure. The analysisof the pathological findings in our cases hassuggested that:
(a) Headache is due to stretch of the arachnoidcovering with its blood vessels by theexpanding brain.
(b) Vomiting is a reflex mechanism in responseto the pain afferents which produce head-ache.
(c) Papillcedema is the result of stagnation ofCSF in the basal subarachnoid space andsheaths of optic nerves.
(d) Post-papilledemic optic atrophy is caused by
dilatation of the anterior part of the floorof third ventricle with consequent com-pression of optic chiasma and tracts.
(e) Mental changes are in most cases non-specific and non-localizing and are due toimpairment of the centre of consciousnessin the centroencephalic system.
(f) False localizing signs are mainly due todownward displacement of brain and stretch-ing of blood vessels with consequent isch-xmia of brain stem.
(g) A unitary conception of the generalized andJacksonian fits is discussed.
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Rev. neurol., I, 949.BuRNs, G. (I908): 'Die Geschwulste d. Nerven-Systems'. Berlin: Springer.CASSIRER, R., and LEWY, F. H. (I920): Quoted by S. A. Kinnier Wilson in ' Neurology ': Part II, E. A., London, I947;
Intracranial Tumours: Effect on Cerebral Vascular System, p. 1220.COLLIER, J. S. (1904): The False Localizing Signs in Intracranial Tumours, Brain, 27, 490.DANA, C. L. (I9I6): 'Textbook of Nervous Diseases'. Bristol: Wright.DOTT, N. (1954): Special communication.F6RTIG, H. (I92I): Dtsch. Z. Nervenheilk, 67, 175. Quoted by S. A. Kinnier Wilson in 'Neurology': Vol. 3, Butter-
worth & Co., London, 1955; Intracranial Tumours: Effect on Cerebral Vascular System, p. I8oi.GREENFIELD, J. G., and CARMICHAEL, E. A. (I925): 'The Cerebrospinal Fluid in Chemical Diagnosis'. London:
Macmillan.KROLL, M. (1929): ' Die Neuropath Syndrome, zugleich differentialdiagnostik der Nervenkrankheiten'. Berlin:
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Tumours: General Symptomatology, p. 1225.PARKER, H. L. (1930): Epileptiform Convulsions: Incidence of Attacks in Cases of Intracranial Tumours, Arch. Neurol.
Psychiat. (Chicago), 23, 1032.PATON, L. (I909): Quoted by S. A. Kinnier Wilson in' Neurology ', Part II, E. A., London, 1947: Intracranial Tumours:
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PENFIELD, W. G., EVANS, J., BRICKNER, R. M., and GERMAN, W. I. (1934): Various Procedures in Conscious Patientsduring Craniotomies, Ass. Res. nerv. Dis. Proc., 13, 593.
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Tumours: Effects on Cerebral Vascular System', p. 1220.SPATZ, H. (I930): Ueber Encephalitis und Encephalitiden, Z. ges. Neurol. Psychiat., 54, 3 i6.VAN WAGENEN, W. P. (1929): Intracranial Tumours Symptomatology, Amer. J. med. Sci., I76, 346.WILSON, S. A. K. (I9I8): Epidemic Encephalitis, Lancet, ii, 9I.
(I93 I): Mental Symptoms Associated with Brain Tumours, Brit. med. J., i, 3"I.
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