Papilloedema, CSF pressure, and CSF in cerebral...

Journal ofNeurology, Neurosurgery, and Psychiatry, 1979, 42, 493-500

Papilloedema, CSF pressure, and CSF flowin cerebral tumours

H. VAN CREVEL

From the Department of Neurology, Erasmus University, Academisch Ziekenhuis Dijkzigt,Rotterdam, Netherlands

SUMMARY The presence or absence of papilloedema and the cisternal CSF pressure werecompared with the RIHSA cisternograms in 24 patients with supratentorial tumours. It wasfound that severe subarachnoid obstruction of CSF flow, leading to impaired CSF absorption atthe superior sagittal sinus, was the main cause of raised CSF pressure and papilloedema associ-ated with supratentorial tumours.

Some brain tumours cause papilloedema, others,often quite as large, do not. This paper attemptsto explain the main cause of that difference.

In large series of patients with cerebral tumours,papilloedema was present in 60%, and in supra-tentorial tumours in 50% of cases (Petrohelos andHenderson, 1951; Bregeat, 1956; Huber, 1956;Tonnis, 1959). The presence of papilloedema ishighly correlated with raised CSF pressure, andits absence is usually due to absence of sustainedelevation of CSF pressure (van Crevel, 1975).Therefore (with some qualifications, see Dis-cussion), to understand the presence or absence ofpersistently raised CSF pressure is to understandthe presence or absence of papilloedema in cere-bral tumours.The approach to this problem has been

dominated by the Monro-Kellie doctrine and itslater elaborations. It was postulated that brain,blood, and CSF are incompressible and containedwithin a rigid skull, and that, therefore, all space-occupying lesions must lead to raised CSFpressure once the capacity for "compensation"-for example, by expulsion of CSF into thespinal theca-is exhausted (Langfitt, 1972). Ifthis were true for tumours, a high correlationshould be found between tumour size and papil-loedema. In fact, however, this correlation islow (Bregeat, 1956) or, according to some authors,absent (Tonnis and Krenkel, 1957).

Address for reprint requests: Dr H. van Crevel, Department of Neur-ology, Academisch Ziekenhuis Dijkzigt, Rotterdam, Netherlands.Accepted 27 December 1978

It should not be surprising that the Monro-Kellie doctrine and the implied simple relation-ship between intracranial volume and CSFpressure do not fit the facts in a slow process likethe growth of a tumour. In the first place, giventime, brain is compressible-that is, it atrophies,as is obvious from the large indentations producedby meningiomas. So, if brain atrophy shouldroughly equal tumour growth, the CSF pressureneed not rise at all. Furthermore, in the Monro-Kellie concept, the CSF is regarded as a staticcomponent, whereas of course it is producedcontinually at a rate of some 500 ml/day (Davson,1967; Milhorat, 1972), and must be absorbed atthe same rate if the CSF pressure is to stay normal.Therefore, the following hypothesis could bemade. By obstructing CSF flow, a tumour, irres-pective of its size, could lead to impaired CSFabsorption at the superior sagittal sinus, and soto raised CSF pressure (Fig. 1B); but as long asthe quantity of CSF reaching the superior sagittalsinus equals its production, CSF pressure neednot necessarily rise (Fig. IC). This hypothesis isexamined in the present study for supratentorialtumours, by comparing the presence or absenceof papilloedema, and the CSF pressure, withradioiodinated human serum albumin (RIHSA)cisternograms.

Patients and methods

Twenty-four patients were studied, 12 with and12 without papilloedema (Table 1). The size ofthe tumours was measured in three dimensions

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Papilloedema, CSF pressure, and CSF flow in cerebral tumours

Fig. 1 Proposed mechanism forthe rise of CSF pressure insupratentorial tumours (see text).A =normal CSF circulation.B= total obstruction of CSF flow.C=partial obstruction of CSFflow. T=tumour.

A B C

(sagittal, vertical, and coronal) from the angio-graphy subtraction pictures and the isotope brainscans. This proved possible to approximations ofcentimetres in 20 cases.Before CAT equipment became available, we

used RIHSA cisternography for some time in thediagnosis of supratentorial tumours, as recom-

mended by Di Chiro (1973). It was done only inclinically stable adult patients. Cisternal puncturewas preferred to lumbar puncture as it causeslittle or no after-leakage of CSF, and so theintracranial dynamics are not upset. Because brainshift is more dangerous than raised CSF pressurein itself (van Crevel, 1972), signs of brainstemcompression were regarded as a contraindication,but papilloedema was not. Cisternal puncture was

performed with the patient almost supine, theshoulders raised and supported, the neck flexed,and the head resting against a special standdesigned for pneumoencephalography (Ziedses desPlantes, 1950). Apart from the puncture, thepatients experienced no discomfort, and no com-

plications occurred. The CSF pressure was

measured with the shoulder as reference point; ina large number of cases this technique has beenshown to produce values roughly equal to thoseof lumbar puncture in the lateral recumbentposition.

Direct techniques are not available formeasuring CSF absorption at the superior sagittalsinus in patients. Therefore, the amount of activityalong the superior sagittal sinus on the RIHSAcisternograms 24 hours after injection was re-

garded as an index of the CSF absorption there.This was described on the anterior and lateral24 hour scans, and rated as: normal or nearlynormal, absent or nearly absent, and intermediate(+, -, and + in Table 1). After completion ofthe whole study, the rating was repeated withoutknowledge of the clinical data, with one changeas a result. Examples of the three rating gradesare shown in Fig. 2.Plasma RIHSA activity was measured 24 hours

after cisternal injection, as an index of totalCSF absorption.

Results

PAPILLOEDEMA AND CSF PRESSURE

Not unexpectedly, the correlation betweenpapilloedema and raised CSF pressure was con-firmed (Fig. 3). Six patients without papilloedemahad borderline or moderately raised CSF pressure,with a maximum of 300 mm water. Normallumbar CSF pressure may range between 40 and250 mm water (Gilland et al., 1974). All patientswith papilloedema had a CSF pressure above300 mm water.

PAPILLOEDEMA AND CSF FLOWThe main result of this study is shown in Table 2.The correlation between the presence ofpapilloedema and the reduction of RIHSAactivity along the superior sagittal sinus at 24hours is statistically significant (P<0.01, Yates-Cochran test). This supports the hypothesis thatpapilloedema in supratentorial tumours is mainlycaused by severe obstruction of CSF flow, result-ing in impaired absorption of CSF at the superiorsagittal sinus.The two patient groups are compared further

in Table 3. The age difference of more than 10years is probably not fortuitous and will be dis-cussed below. The type of tumour was notdifferent for the two groups. Tumour size couldbe measured in 20 cases only, 10 in both groups.Though the mean size in the papilloedema groupwas slightly greater, the difference is not statisti-cally significant, neither in each dimension

Table 2 Relationship between papilloedema and theamount of RIHSA activity along the superiorsagittal sinus 24 hours after injection

Normal Intermediate Absentor nearly or nearlynormal absent

Patients withpapilloedema (n= 12) 2 0 10Patients withoutpapilloedema (n= 12) 6 4 2

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Fig. 2 Rating grades of RIHSA activity along the superior sagittal sinus; anterior and right lateral 24 hrscans. A =normal or nearly normal (case 10). B=absent or nearly absent (case 6). C=intermediate (case 8).

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Fig. 3 Relationship between cisternal CSF pressureand the presence (0) or absence (0) of papilloedema.CSF pressure measurement was omitted in case 4.

Table 3 Comparison of patients with and withoutpapilloedema

Patients with Patients withoutpapilloedema papilloedema(n= 12) (n=12)

Mean age 45.6 years 56.2 yearsType of tumour Metastases (4) Metastases (4)

Gliomas (5) Gliomas (4)Meningiomas (3) Sarcoma (I)

Meningiomas (3)Mean size of tumour 49 x 41 x 39 mm 45 x 38 x 38 mm

separately nor in the three combined (P>0.20,Wilcoxon's two-sample test). As to the remainingfour tumours, the two from the group withoutpapilloedema (cases 8 and 10) were, if anything,larger than the two from the papilloedema group(cases 9 and 22) as judged from the surgical andpathological notes. The site of the tumours wassimilar in both groups; only parietal lobe tumourswere less common in the papilloedema group.

Finally, the 24 hour plasma RIHSA activityyielded values of very wide range, and will not bereported here in detail. However, the mean valuesfor the groups with and without papilloedemawere almost exactly equal.

CSF OBSTRUCTION AS THE MAIN CAUSE OFPAPILLOEDEMA IN SUPRATENTORIAL TUMOURSThe results are compatible with the hypothesis thatpapilloedema in supratentorial tumours is duemainly to obstruction of subarachnoid CSF flow,leading to impaired CSF absorption at the superiorsagittal sinus and so to raised CSF pressure. Theclassic observations of Lundberg (1960) have re-vealed that in patients with cerebral tumours, theCSF pressure, continuously recorded, is subjectto marked fluctuation. Our CSF pressure valuesrepresent single measurements made at chancemoments. Nevertheless, they correlated surpris-ingly well to the absence or presence of papil-loedema. Therefore the division into a"papilloedema" and a "no papilloedema" group,the former with higher CSF pressure than thelatter, seems justified.The idea that, in cerebral tumours, obstruction

of CSF flow causes raised CSF pressure is of coursenot new, but has usually been applied only tointraventricular obstruction, and has not beeninvestigated for subarachnoid CSF flow. This idearests on the traditional concept of the CSF beingsecreted mainly within the ventricles, and drainedmainly through the arachnoid villi and granula-tions into the superior sagittal sinus. This conceptis still regarded as essentially correct, even thoughventricular CSF production may be decreased withhigh CSF pressure (Milhorat, 1972; Pollay, 1977).

Continuation of CSF production with cessationor severe impairment of CSF absorption in thesuperior sagittal sinus necessitates absorption bysubsidiary routes. Such routes-for example, thebasal sinuses and the spinal arachnoid villi-areknown to exist, though their importance undernormal circumstances is uncertain (Millen andWoollam, 1962; Davson, 1967; Kido et al., 1976).Another possibility, in cases with hydrocephalus,is ventricular reabsorption (Milhorat, 1972; Jameset al., 1975). Absorption of CSF by non-physiological routes in brain tumours has beenestablished by the isotope studies of Paraicz et al.(1972), and is confirmed by our mean plasmaRIHSA values being equal in the two groups. Ourfindings indicate that the superior sagittal sinusis only replaced by other CSF absorption routesif the CSF pressure is raised (with possibleexceptions, see below).

DEFECTS OF THE CONCEPT OF CSF OBSTRUCTIONAlthough the concept of CSF obstruction pro-posed in this paper may be valid, it is too simplisticand four cases were inconsistent with it.

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Two patients (cases 6 and 19) had no papil-loedema though RIHSA was virtually absentalong the superior sagittal sinus. The CSF pressurewas only 220 and 210 mm respectively, so thisinconsistency cannot be explained by a time lagbetween the rise of CSF pressure and the develop-ment of papilloedema. Possibly, normal CSFpressure, in spite of superior sagittal sinus in-accessibility, is the result of absorption of CSF bysubsidiary routes at normal CSF pressure, knownto exist in some conditions. For example, in"normal" pressure hydrocephalus (with totalinaccessibility of the superior sagittal sinus) sus-tained elevation of CSF pressure and papilloedemaare absent, though transient rises in CSF pressurehave been recorded (Symon et al., 1972). In ex-perimental communicating hydrocephalus theCSF pressure is increased initially, but later fallsinto the normal range (James et al., 1975). Hydro-cephalus was present in case 6; in case 19 airstudies were not done.Two other patients (cases 9 and 21) did have

papilloedema (CSF pressure 520 and 320 mmrespectively), and yet "enough" RIHSA alongthe superior sagittal sinus. In this context, itshould be remembered that CSF absorptionthrough the arachnoid villi can be functionallyimpaired, while the subarachnoid CSF channelsare anatomically patent. For example, in "benignintracranial hypertension" the CSF infusion testindicates impaired CSF absorption (Martins,1973), but RIHSA cisternography is normal(James et al., 1974). Raised CSF pressure withoutobstruction of CSF pathways is also found inother conditions-for example, raised venouspressure or high CSF protein content. Case 21had a CSF protein of 4.65 g/l; case 9 remainsunexplained.These speculations are mentioned in view of

further investigation, and to stress that RIHSAcisternography is not a direct index of CSFabsorption at the superior sagittal sinus.

FACTORS DETERMINING THE OCCURRENCE OFPAPILLOEDEMA IN CEREBRAL TUMOURSIn cerebral tumours, raised CSF pressure is neces-sary but not sufficient for the development ofpapilloedema (Table 4). Raised CSF pressure mustnot only be present for a certain period of time,but the optic nerve sheaths must also be patent,as shown experimentally (Hayreh, 1968). Uni-lateral or bilateral absence of papilloedema incerebral tumours with raised CSF pressure maythus be caused by compression of the optic nervesheath(s) by the tumour (Levatin, 1957), or bycongenital occlusion of the sheath(s) (Walsh and

Table 4 Absence of papilloedema in cerebraltumours

Rarely In most cases

CSF pressure is raised, but CSF pressure is notpapilloedema is absent persistently raised, usually(*unilaterally or bilaterally) because CSF flow to thebecause of: superior sagittal sinus isTime factor not severely obstructed.Optic nerve sheath occlusion* This depends on:Glaucoma*, myopia Age of patientOptic atrophy* Site of tumour

Size of tumourOedema, hydrocephalus

Hoyt, 1969). Further, glaucoma (Bregeat, 1956)and severe myopia (Huber, 1956) can account forunilateral or bilateral absence of papilloedema.Optic atrophy also prevents papilloedema, as iswell known from the Foster-Kennedy syndrome.In our series, one patient (case 24) had unilateralpapilloedema, which was explained by antecedentoptic atrophy in the other eye. Otherwise therewas a good correlation between raised CSFpressure and papilloedema. Absence of papil-loedema in cerebral tumours is usually due toabsence of persistently raised CSF pressure. Thefactors which determine the CSF pressure incerebral tumours will now be discussed, in relationto CSF obstruction.

Papilloedema and raised CSF pressure are lessfrequent in old age (Moersch et al., 1941; Kloss,1952). This is usually explained by pre-existentbrain atrophy, more space being available for thetumour. In the concept of CSF obstruction, moresubarachnoid space would mean a smaller chanceof CSF block. Whatever its explanation, theinfluence of age was confirmed in our series(Table 3).There was no significant difference in tumour

type between our two groups (Table 3). In largeseries, no consistent relationship between tumourtype and incidence of papilloedema has beenestablished either: Bregeat (1956) saw papill-oedema more often in malignant, Huber (1956) inbenign tumours, and the results of Tonnis (1959)were equivocal. Apparently, rapid growth of atumour does not lead more often to CSF blocksthan slow growth.

It would be surprising if the size of braintumours had no influence at all on the incidenceof papilloedema, but the correlation is low. Inour two groups there was no statistically signifi-cant difference (Table 3); but the amount of brainshift (also dependent upon infiltrative versus ex-panding growth, oedema, and hydrocephalus)could not be measured, as no CAT scan was yet

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available. However, in view of our findings thetotal extra volume would be effective by obstruc-tion of CSF flow rather than by "space-occupation" in itself. Papilloedema may evenincrease (and the CSF pressure may remain high)after removal of a tumour (Paton, 1905; Bynkeand osterlin, 1960). Again, this may be due topostoperative CSF blocks, as we could demon-strate by postoperative RIHSA cisternography inone patient (case 12).The site of a tumour relative to the CSF path-

ways must be important with regard to papil-loedema. In large series, papilloedema was morefrequent in frontal and temporal than in parietallobe tumours (Br6geat, 1956; Huber, 1956; Tbnnisand Krenkel, 1957), and in our small series this isalso apparent (Table 1). This may be due to thegreater distance of parietal lobe tumours from the"strategic" CSF flow point-that is, the basalcisterns leading to the Sylvian fissures and theinterhemispheric fissure. The high frequency ofpapilloedema in infratentorial, especially cere-bellar, tumours is well known, but not self-evident.In current textbooks, it is usually attributed to theconcomitant obstructive hydrocephalus (forexample, Merritt, 1973). Again, it is conceivablethat this hydrocephalus causes increased CSFpressure by blocking the upward passage of CSF inthe subarachnoid spaces at the tentorial hiatus, andnot by simple "space-occupation." This was sug-gested long ago by Cairns (1939), and demonstratedfor hydrocephalus without tumour by RIHSAcisternography before and after a shunt byMilhorat (1972). However, posterior fossatumours may sometimes produce papilloedema butno hydrocephalus, and vice versa. This meritsfurther investigation.

PAPILLOEDEMA AS A CLINICAL SIGNIn patients with brain tumours, papilloedemasignifies that the CSF pressure has been raised forsome time, usually because the CSF flow to thesuperior sagittal sinus is severely obstructed.Papilloedema gives no indication of the type oftumour, and very little of its size. Moreover, therelationship between the CSF pressure and theclinical state of the patient is erratic, as shown bycontinuous CSF pressure recording (Jennett andJohnston, 1972).Absence of papilloedema, if not caused by

ophthalmological factors or time lag, merelymeans that the CSF pressure is not raised per-sistently, usually because CSF flow to the superiorsagittal sinus is not severely obstructed. That, initself, does not exclude extensive brain shifts oreven brain herniation (Lundberg, 1960).

As Miller and Adams (1972) have stressed, it isof vital importance not to equate raised CSFpressure with brain shift. Papilloedema is areliable sign of raised CSF pressure, but neitherpapilloedema nor its absence are a clue to thepresence, extent, or absence of brain shifts.

I am indebted to the late Professor J. W. G. terBraak who awakened my interest in CSF pressure.Dr P. Crezee, neuroradiologist, performed thecisternal injections, Mr R. van Strik gavestatistical advice, Dr J. van Gijn and Dr L. deVries made helpful comments, and Mrs C.Thooft-Schlemper prepared the manuscript.

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