Difficulties in diagnosis of supratentorial gliomas

Journal ofNeurology, Neurosurgery, and Psychiatry, 1979, 42, 485-492

Difficulties in diagnosis of supratentorial gliomas byCAT scan

B. E. KENDALL, J. JAKUBOWSKI, P. PULLICINO, ANDL. SYMON

From the Lysholm Radiological Department and Gough Cooper Department of Neurological Surgery,The National Hospital for Nervous Diseases, London

S UMM ARY The false positive and false negative computed tomography diagnoses of gliomamade using an EMI 1010 machine on a consecutive series of patients seen over a period of twoyears are recorded. About 1.5% of gliomas were not detected on initial CAT scan, 6.5% weremisdiagnosed as benign lesions, and in 6.5% of the cases identified as glioma a non-malignantcondition was subsequently diagnosed.

Computed tomography (CAT) generally revealssome abnormality in patients with intracranialtumours at the time of clinical presentation andat an earlier stage of the disease than any otherradiological procedure (Wende et al., 1977). Thishas modified the spectrum of neurosurgical in-vestigation and has virtually replaced isotopeencephalography and invasive procedures as ascreening test. In previous studies (Claveria et al.,1977, 1978) the advantages and some of the limi-tations of CAT in the diagnosis of malignanttumours were evaluated. The experience gainedfrom these studies has been applied to routineexamination of scans carried out over the pasttwo years. Diminished use of other diagnosticmethods for confirmation of the nature of lesionsshown by CAT has occurred even though relianceon CAT may contribute to misdiagnosis in a fewcases.We considered that an analysis of the accuracy

of CAT in the diagnosis of the supratentorialgliomas examined during this period would be ofinterest, together with a critical appraisal of diag-nostic errors.

Method

The clinical and pathological records of allpatients in the National Hospital for Nervous

Address for reprint requests: Dr B. Kendall, Lysholm RadiologicalDepartment, The National Hospital, Queen Square, London WClN3BG.Accepted 27 December 1978

Diseases with a diagnosis of supratentorial gliomaduring the period of 1976 and 1977 were reviewed.All CAT scans in which a diagnosis of supraten-torial glioma had been suggested during thisperiod, were also reviewed and the data werecorrelated, giving four groups:1. CAT diagnosis correct.2. Glioma present but no abnormality detectedby CAT.3. Glioma present but incorrectly diagnosed as adifferent pathology by CAT.4. Another pathology incorrectly diagnosed asglioma by CAT.

Results

During the period of study there was a total of314 patients with proven gliomas. All of themhad CAT examination, and 274 (87.3%) werecorrectly diagnosed on the initial scan. The re-maining 40 cases (12.7%) were either consideredto be normal (five cases), misdiagnosed as anotherpathology (26 cases), or diagnosed only as a masslesion (nine cases). The wrong diagnoses includedmeningioma (eight cases), metastasis (six cases),inflammation (four cases), cerebral infarction(three cases), intracranial haemorrhage (threecases), and vascular malformation (two cases).

Detailed histological examination revealed thathigh grade astrocytomas (grade 3-4) were presentin 67.5% (27 patients) of the 40 misdiagnosedcases. The remaining 32.5% (13 patients) sufferedfrom low grade astrocytomas (six), oligodendro-glioma (five), or microglioma (two) (Table 1).

485

Protected by copyright.

on Novem

ber 5, 2021 by guest.http://jnnp.bm

j.com/

J Neurol N

eurosurg Psychiatry: first published as 10.1136/jnnp.42.6.485 on 1 June 1979. D

ownloaded from

http://jnnp.bmj.com/

B. E. Kendall, J. Jakubowski, P. Pullicino, and L. Symon

Table 1 Histology of gliomas not detected or misdiagnosed on CAT

Misdiagnosed (Total) Low grade High grade Oligodendroglioma Microglioma1-2 3-4

Unspecified mass (9) 2 5 2Meningiomas (8) - 6 2Metastases (6) - 6 -

Normal scans (5) 1 4 - _Inflammations (4) - 3 1Infarct (3) 1 1 - IIntracerebral haemorrhage (3) - 2 - 1Vascular malformation (2) 2 - - -

Total (40) 6 27 5 2

Angiography was performed in 29 cases, and inthe majority (25) it showed an obvious abnor-mality. However, the correct diagnosis wasestablished by showing glioma vessels in only ninecases, and in five cases the angiographic diagnosiswas misleading (Tables 2, 3).A follow-up scan revealed the glioma in four

out of five cases with normal scans (Fig. 1) andEEG (two cases), and pneumoencephalography(one case) suggested the diagnosis occasionally.In 60% (24) of the cases the correct diagnosis wasnot established until histological examination.During the period under review glioma was diag-

nosed on 311 CAT scans. Out of this number 68.4%(213) were confirmed by histology and 19.6% (61)cases by other methods, mainly by angiography.A further 2.3% (seven) cases still remained uncon-firmed. Thirty cases (9.7%) were proved to have a

Table 2 Angiographic studies in gliomas notdetected or misdiagnosed on CAT

CAT diagnosis Number Number of Diagnosisof cases angiograms corrected by

performed angiography

Unspecified mass 9 6 2Meningiomas 8 6 1Metastases 6 4 2Normal scans 5 2 0Inflammations 4 3 1Infarcts 3 3 1Intracerebral haemorrhages 3 3 1Vascular malformations 2 2 1

Total 40 29 9

different pathology. The majority (26) of these(86%) were benign lesions: only four cases hadmetastases to the brain (Table 4).Angiography was performed on 21 (70%)

patients; 17 studies (80%) showed an obvious ab-normality, but in only five out of seven men-

ingiomas, and two out of four arteriovenous mal-formations did angiography correct the diagnosis.Five angiograms in cases of radionecrosis (two),metastasis (one), tuberculoma (one), or men-

ingioma (one) were mistakenly considered to showglioma circulation (Table 4).The initial CAT misdiagnosis was corrected by

other studies in 16 (53%) cases; in the remaining14 patients final pathology was established byhistological examination (Table 5).

Discussion

Most glial tumours are shown on CAT as masses

with attenuation values mixed within and belowthe normal range. There is usually surroundingwhite matter oedema. Enhancement is usuallyirregular and tends to be less than that occurringin meningiomas and metastases. Unenhancingregions of low attenuation suggesting cystic or

necrotic changes are present in over half of malig-nant gliomas.Homogeneous enhancement occurs in 15-20%

of gliomas. When the margins are well definedif may cause appearances on CAT indistinguishablefrom some solitary metastases or, if situated per-

Table 3 A ngiography in gliomas misdiagnosed on CAT

Angiographicfindings (Total) Histology

High grade Low grade Oligodendroglioma Microgliomaastrocytoma astrocytoma

Normal (4) 2 1 0 1Avascular mass (11) 7 1 3 0Glioma vessels (9) 8 1 0 0Other pathology suggested (5) 3 2 0 0

I otal (29) 20 5 3 1

486


on Novem


j.com/

J Neurol N


ownloaded from


Difficulties in diagnosis of supratentorial gliomas by CAT scan

Fig. 1 Glioma corpus callosum. (a) Normalscan. (b) Six months later. Minor dilatation oflateral ventricles. Thickening of septumpellucidum and abnormal enhancement in genuof corpus callosum and adjacent white matter.

Table 4 Angiography in cases misdiagnosed as glioma on CAT

Final diagnosis (Total) Angiogramns Resultsperformed

Normal Correct diagnosis Avascular mass "Glioma" circulation

Meningioma (7) 7 5 1 1Metastasis (4) 2 1 1Inflammation (3) 1 1AVM (4) 4 2 2Multiple sclerosis (1) I IRadionecrosis (2) 2 2Arachnoid cyst (1) I IContusion (1) I IInfarction (7) 2 1 1Total (30) 21 4 7 5 5

Table 5 Cases misdiagnosed as glioma on CAT

Final diagnosis (Total) Diagnostic study

Angiography Control CAT Isotope scan EEG Chest Histologyradiograph

Meningioma (7) 5 1 1Metastasis (4) 1 3Inflammation (3) 1 11Infarction (7) 2 1 4AVM (4) 2 2Multiple sclerosis (1) IRadionecrosis (2) 2Arachnoid cyst (1) 1Contusion (1) ITotal (30) 7 4 2 1 2 14

ipherally, from meningiomas (Fig. 2). Both thesetumour types most frequently cause well-circumscribed masses of increased attenuation.Metastases commonly cause more extensiveoedema than gliomas relative to their size, andmeningiomas less oedema. However, there is con-siderable overlap of all these features with eachtype of tumour (Fig. 3), and about 10% of men-ingiomas cause extensive intracerebral oedema(Fig. 4). Realisation of this fact led to nine gliomasbeing diagnosed merely as intracranial tumour onCAT with the implication that further study was

necessary to determine the type. The meningiomasdiagnosed as glioma were either intraventricular(one), irregular cavitating masses (Fig. 5), or rela-tively small and associated with extensive oedemaso that the tumour itself was either not identified(two) or else its extracerebral attachment was notappreciated (two) (Fig. 4).About 20% of recent infarcts have obvious mass

effect (Constant et al., 1977). They are usuallydiffuse low attenuation lesions involving grey andwhite matter and without the defined perifocalwhite matter oedema typically found with tu-

487


on Novem


j.com/

J Neurol N


ownloaded from


B. E. Kendall, J. Jakubowski, P. Pullicino, and L. Symo.n

Fig. 2 Astrocytoma grade 3-4. (a) Plain scan.(b) After intravenous contrast medium. Anisodense mass adjacent to the falx enhanceshomogeneously. There is considerable oedemain the white matter. Diagnosed as falxmeningioma.

Fig. 3 (a) Metastasis from carcinoma ofbronchus. Enhanced scan. There is a lowattenuation mass in the right posterior temporaland low parietal regions which contains a welldemarcated cyst medially. There is increasedenhancement in its lateral part. There isconsiderable mass effect but only a smallamount of white matter oedema. Diagnosed asglioma. (b) Glioma grade 3-4. After intravenouscontrast medium. There is a well-definedenhanced mass in the left occipital region withquite extensive oedema in the white matteranterior to it. Diagnosed as metastasis.

Fig. 4 Left frontal convexity meningioma.Plain scan. There is extensive low attenuationin the left frontal white matter extending across

the corpus callosum into the right frontal lobe.The meningioma itself was not identified beforeor after intravenous contrast medium.Diagnosed as glioma.

mours. Enhancement may occur in any part ofthe lesion which has not been completely deprivedof its blood supply and when this is irregular theappearances may simulate a glioma (Fig. 6). Incontrast, if mass effect and oedema accompanyinga glioma are slight, infarction may be simulated.Recent intracerebral haematoma is evident on

CAT as a well-demarcated, high attenuation mass.There is usually only a narrow well-defined sur-rounding rim of low attenuation. Enhancement,which may occur about one-16 weeks after thebleed, is confined to the margin of the lesion.Earlier and more extensive enhancenment shouldsuggest an underlying tumour or angiomatousmalformation, and could possibly have led to thecorrect diagnosis in one of our cases. The othertwo were indistinguishable from spontaneoushaemorrhages. Absorbing haematomas which areisodense or of lower attenuation than brainusually have little or no mass effect, but ring en-hancement may suggest an intracerebral tumour.The history is usually of a sudden episode withimprovement and should lead to consideration ofthe diagnosis.

488


on Novem


j.com/

J Neurol N


ownloaded from



The enlarged vessels of an angiomatous malfor-mation (AVM) show typically as round, oval, orserpiginous aggregations of increased attenuation,depending on their orientation to the CAT section,often with intervening low attenuation from gliosisand microcyst formation. There is frequentlylocal atrophy, and calcification may be present inthe walls of blood vessels or damaged brain. En-hancement is usual within the malformation or itsconnecting vessels though it may be absent insome cases in which the lesion is thrombosed (Fig.7). Mass effect is present in less than 20% ofangiomas without a history of recent haemorrhage(Kendall and Claveria, 1976), and it is not usuallymarked, though it was moderatc in two of ourcases misdiagnosed as glioma. The AVM did notoutline at angiography in two cases, including onein which enhancement was considerable and ex-tensive on CAT; both were totally thrombosed,the enhancement being caused by alteration of theblood-brain barrier (Kramer and Wing, 1977).Both of the gliomas diagnosed as AVMs on CAThad a history of recent intracranial haemorrhage.They were markedly enhancing (Fig. 8) and par-

Fig. 5 Meningioma. (a) Plain scan. (b) Aftercontrast medium. Mixed high and lowattenuation mass with partial enhancement.Diagnosed as cystic glioma.

Fig. 6 Infarct. (a) Plain scan. (b) Aftercontrast medium. Low attenuation mass rightfrontal lobe with patchy enhancement.Diagnosed as glioma.

h)

Fig. 7 Thrombosed angiomatousmalformation. Plain scan. High attenuationlesion posteriorly in right temporal lobe. It didnot enhance. Diagnosed as low grade glioma.

tially calcified with relatively less mass effect thanexpected from the size of the lesions. In one ofthem angiographic evidence of large tumourvessels with arteriovenous shunting corrected thediagnosis.

(1-f) (bn

(a)

489


on Novem


j.com/

J Neurol N


ownloaded from



Fig. 8 Astrocytoma grade 2. (a) Plain scan.(b) After contrast medium. Mixed attenuationmass, left temporal lobe, with markedenhancement. Diagnosed as angiomatousmalformation.

Most cerebral abscesses are diagnosed clinically.CAT is confirmatory by showing an enhancingcapsule of almost even thickness enclosing lowattenuation pus and surrounded by intracerebraloedema. Cavities in necrotic gliomas usually butnot always have walls of irregular thickness; some-times solid tumour is also evident elsewhere. How-ever, either lesion may occasionally have featuresmore commonly found in the other (Fig. 9). Twosolitary tuberculomas with oedema causing mass

effect were mistaken for gliomas (Fig. 10), andtwo locally calcified gliomas were thought to betuberculous (Fig. 11) partly because the patientswere immigrants with pulmonary tuberculosis. Itis interesting that in only one of these gliomaswas the diagnosis corrected by angiography and,in the one inflammatory lesion (tuberculoma) inwhich angiography was performed, there was amistaken confirmation of tumour on the basis ofdoubtfully abnormal vessels.

Fig. 9 (a) Glioma grade 3-4. After contrastmedium. Low attenuation mass left parietallobe with even ring enhancement. Diagnosedas abscess. (b) Pyogenic abscess. After contrastmedium. Low attenuation mass with isodenseenhancing slightly irregular ring within it.

A Diagnosed as glioma.

Fig. 10 Tuberculoma. (a) Plain scan. (b) A ftercontrast medium. Mass of mixed attenuation inthe left frontoparietal operculum withconsiderable mass effect which shows marked

:P but irregular enhancement after intravenouscontrast medium. Diagnosed as glioma.

490

.j:.' .it - -i, .-.", "" #Z. A 0:49

-,lA ..PIW

7. "j:Ii


on Novem


j.com/

J Neurol N


ownloaded from



Fig. 11 Glioma grade 3-4. (a) Plain scan.(b) After contrast medium. Mixed attenuationmass left parietal lobe which contains a littlecalcification and shows irregular enhancement.There is some surrounding oedema. The patientwas an immigrant from India with pulmonarytuberculosis; diagnosed as tuberculoma.

Radionecrosis may reasonably be assumed whena central non-enhancing low attenuation regionappears or increases within a treated mass. Whena new low attenuation mass showing homogeneousor mixed enhancement appears in a therapy field,it may be due to tumour or a granuloma causedby deep X-ray treatment (Fig. 12). Angiographyshowed small irregular vessels around such lesionswhich led to inaccurate confirmation of tumour inour two cases. In appropriate conditions such

masses are best treated by excision, and histologyappears to be the only reliable method of diagnosis.Acute plaques of multiple sclerosis may cause

enhancing low attenuation lesions with little masseffect (Fig. 13). The large plaques are usuallyin the central white matter often adjacent to thelateral ventricles. This distribution, and the ten-dency to be associated with asymptomatic lesionselsewhere and with cerebral atrophy, usually sug-gest the correct diagnosis (Radue and Kendall,

Fig. 12 Radiation granuloma. (a) Plain scan.(b) After contrast medium. There is lowattenuation in both frontal lobes more extensiveon the left with increased attenuation at theleft frontal pole. An enhancing mass is shownat the periphery of the left anterior frontalregion after intravenous contrast medium. Thepatient had had a previous resection of a rightfrontal glioma followed by radiotherapy.Diagnosed as recurrent glioma.

Fig. 13 Multiple sclerosis. (a) Plain scan.(b) After contrast medium. Focal lowattenuation in left parietal lobe with densecentral enhancement after intravenous contrastmedium. Diagnosed as glioma. Scan returnedto normal within one year after which timedisseminated lesions were evident clinically,and the patient was confirmed to have multiplesclerosis.

B

491


on Novem


j.com/

J Neurol N


ownloaded from



1978). In one unconfirmed case diagnosed asglioma there was an extensive low attenuationenhancing lesion, with only slight mass effectcentrally in both hemispheres and in the corpuscallosum. There was a previous history of opticneuritis but the presenting lesion has not pro-gressed or tended to resolve. The diagnosis is subjudice but may well be a demyelinating disease. Afurther course towards resolution is most helpfulin elucidation of the nature of multiple sclerosis,infarction, haemorrhage, and contusion, whenmore active therapy is not mandatory.Although angiography may be diagnostic, in

many of these unusual cases it has failed to eluci-date the specific nature of the lesion. Tumourvessels were shown in only nine of the 29 gliomas:in five of the seven meningiomas and two of thefour AVMs the diagnosis was established. Vesselssuggesting malignancy were also shown in onemetastasis, but they were recorded in four benignlesions (one meningioma, one tuberculoma, andtwo granulomas after radiotherapy). Thus angio-grams performed in 50 cases were diagnosticallyhelpful in 16 (32%), misleading in four (8%), andnon-contributory in 60%.Although the series presented is relatively small

it shows that over the last two years, despite beingaware of the difficulties of CAT diagnosis from theanalysis of our earlier material, about 1.5% ofgliomas were not detected on initial CAT, 6.5%were misdiagnosed as benign lesions, and 6.5%of lesions diagnosed as gliomas were benign.The misdiagnosis of a glioma for another path-

ology is not particularly important since in mostcases it does not influence significantly the naturalcourse of the disease. Sometimes it is even bene-ficial when simple observation of the clinical andCAT course delays potentially damaging surgery.Occasionally emergency biopsy is precipitatedwhen brain abscess is suspected. Misdiagnosis ismore significant when a benign pathology is mis-taken for a glioma. Thus three meningiomas in thisseries were discharged without surgery to out-patient follow-up though happily the tumours wereremoved successfully at a later date. In onepatient, operation on an abscess was delayed, andone with infarction had an unnecessary resection.Computed tomography, despite its advantages,

by no means invariably provides final and reliable

diagnosis. It is, therefore, important that nopatient with a CAT diagnosis of glioma in whichthe appearances are also consistent with, thoughless typical of a benign, surgically treatable lesionshould be disqualified from surgery on clinicaland CAT findings alone. In such cases positiveconfirmatory evidence may be obtained fromangiograms or other studies but, if necessary, anopen biopsy should be made.

Figure 13 is reproduced by permission of theJournal of Neurology, Neurosurgery, andPsychiatry where it was originally published inAugust 1978.

References

Claveria, L. E., Kendall, B. E., and du Boulay, G. H.(1977). Computerised axial tomography in supra-tentorial gliomas and metastasis. In The FirstEuropean Seminar on Computed Axial Tomographyin Clinical Practice, pp. 83-93. Edited by G. H.du Boulay and I. F. Moseley. Springer Verlag: Berlin.

Claveria, L. E., du Boulay, G. H., and Kendall, B. E.(1978). The diagnostic limitations of computerisedaxial tomography in hemispheric tumours. In TheDiagnostic Limitation of Computerised Axial Tom-ography, pp. 2-16. Edited by J. Bones. SpringerVerlag: Berlin.

Constant, P., Renou, A. M., Caille, J. M., andVernhiet, J. (1977). CAT studies in cerebral is-chaemia. In The First European Seminar on Com-puted Axial Tomography in Clinical Practice, pp.227-236. Edited by G. H. du Boulay and I. F.Moseley. Springer Verlag: Berlin.

Kendall, B. E., and Claveria, L. E. (1976). Use ofcomputed axial tomography for the diagnosis andmanagement of intracranial angiomas. Neuro-radiology, 12, 141-160.

Kramer, R. A., and Wing, S. D. (1977). Computedtomography of angiography occult cerebral vascularmalformations. Radiology, 123, 649-652.

Radue, E. W., and Kendall, B. E. (1978). Iodide andxenon enhancement of computed tomography inmultiple sclerosis. Neuroradiology, 15, 153-158.

Wende, S., Aulich, A., Schindler, E., Grumme, T.,Meese, W., Lange, S. Kasner E., Steinhoff, H., andLanksch, W. (1977). A German multicentre studyof intracranial tumours. In Computerised AxialTomography in Clinical Practice, pp. 111-117.Edited by G. H. du Boulay and I. F. Moseley.Springer Verlag: Berlin.

492


on Novem


j.com/

J Neurol N


ownloaded from


Documents

Difficulties in diagnosis of supratentorial gliomas