spontaneous thrombosis in giant intracranial aneurysms

Journal of Neurology, Neurosurgery, and Psychiatry 1982;45:1040-1047

Spontaneous thrombosis in giant intracranialaneurysms

IAN R WHITTLE, NICHOLAS W DORSCH, MICHAEL BESSER

From the Department ofNeurosurgery, Royal Prince Alfred Hospital, Sydney, Australia

SUMMARY Twelve patients in a series of 22 with giant intracranial aneurysms demonstratedneuroradiological features of partial or total spontaneous intra-aneurysmal thrombosis. Thepresence of this intra-aneurysmal clot significantly altered the computed tomographic appearance

of the giant aneurysm. Massive intra-aneurysmal thrombosis did not protect against subarachnoidhaemorrhage and the likelihood of rupture of a clot containing giant aneurysm was not significantlydifferent from that of a non-thrombosed giant aneurysm. Although parent artery occlusion from athrombosed giant aneurysm, and massive aneurysmal thrombosis leading to the formation of giantserpentine aneurysm were documented, these are rare epiphenomena. The risk of embolisationfrom a partially thrombosed giant aneurysm, which was documented in one case, would appear tobe greater than that from a non-thrombosed giant aneurysm. The findings in this series, and areview of literature, suggest that the presence of intra-aneurysmal clot in giant intracranialaneurysms has little prognostic significance and does not alter the management or outcome aftertreatment.

Since Morley and Barr ' defined intracranialaneurysms with a diameter of greater than 2- 5 cm asgiant, these lesions have become recognised as adiscrete neuropathological entity. Recent publi-cations on giant intracranial aneurysms have docu-mented their diagnostic neuroradiological features2"and the trends in their neurosurgical management.58An interesting feature, commonly noted in thesestudies, is the propensity for intra-aneurysmalthrombosis, either total or more commonly partial.This epiphenomenon was initially reported by Lyell9as an incidental finding at the necropsy of a man whohad died of unrelated head injuries. Subsequently,additional case reports have documented furtherrelevant clinical, neuroradiological and surgicalmanifestations of spontaneous thrombosis in giantintracranial aneurysms.'"'4 However, despite thepioneering work of Black and German'5 on intra-aneurysmal thrombogenesis there has been nosystematic study of this phenomenon in giant

Presented at 55th General Scientific Meeting of the RoyalAustralasian College of Surgeons, Christchurch, New Zealand,29 January 1982.Address for reprint requests: Dr Ian R Whittle, NeurosurgeryDepartment, Royal Prince Alfred Hospital, Missenden Road,Camperdown NSW 2050, Australia.

Received 1 July 1982Accepted 9 August 1982

intracranial aneurysms despite its frequentoccurrence. The clinical significance of thispathophysiological process has been further cloudedby contradictory statements in the literature.5

In this paper the authors examine the diagnosticfeatures and incidence of intra-aneurysmalthrombosis in 22 patients with giant intracranialaneurysms. The significance of this epiphenomenonwas assessed with particular reference to theproblems of subarachnoid haemorrhage, thrombo-embolism and parent artery occlusion from athrombosing giant intracranial aneurysm. Ourconclusions are compared to reported data, andimplications with respect to neurosurgicalmanagement are discussed.

Patients and methods

During the period 1976-81, 302 patients with a diagnosis ofintracranial aneurysm were admitted to the neurosurgicalunit at the Royal Prince Alfred Hospital. Diagnosis wasconfirmed in each case by a combination of cerebralangiography, cerebral computed tomography (CT) or post-mortem examination. Review of these studies together withclinical and operative records revealed that 22 of thepatients had aneurysms of giant dimensions (>2 5 cmdiameter). The neuroradiographic studies of these patientswere examined in detail for evidence of intra-aneurysmalthrombosis. Angiographic features suggestive of significantintra-aneurysmal thrombosis were irregularity and

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Spontaneous thrombosis in giant intracranial aneurysms

asymmetry of the aneurysmal lumen, decrease in the size ofthe aneurysmal lumen on serial angiography, and disparityin the size and shape of the aneurysm as suggested by theangiographic and CT data. The CT features suggestive ofpartial or total giant intracranial aneurysm thrombosis weremixed high density attenuation values within theaneurysmal lumen, the presence or absence of "TargetSign"2 and peripheral ring enhancement after contrastadministration, and curvilinear calcification of theaneurysmal wall. Neuroradiographic data in each case wascorrelated with the clinical course and operative or post-mortem findings. An attempt was made to evaluate thesignificance of intra-aneurysmal thrombus with respect toclinical parameters such as subarachnoid haemorrhage,parent artery occlusion, thrombo-embolism and patientmorbidity and mortality.

Results

RadiologicalTwelve (55%) of the 22 patients with a giantintracranial aneurysm demonstrated complimentaryangiographic and CT features of significant intra-aneurysmal thrombosis (table 1). There was noparticular preference in site of the distribution of thenon-thrombosed and thrombus-containing giantintracranial aneurysms (table 2). On CT scanning the12 thrombus-containing giant intracranial aneurysmsappeared as lesions of variable shape and with mixedattenuation values that were always higher than thesurrounding brain. "Target Sign" and peripheral ringenhancement after contrast administration, wereseen in 10 (83%), and seven (58%) cases respectively.

Table 2 Locations ofthe22 giant intracranial aneurysms inthe series, and incidence ofintra-aneurysmal thrombus withlocus

Locus No Intra-aneurysmal thrombus

Present None

Cavernous carotid 3 2 1Carotid-communicating/

bifurcation/ophthalmic 4 2 2Anterior cerebral A 1 0 1Middle cerebral A 10 5 5Basilar-bifurcation 4 3 1

Total 22 12 10

Two patients (17%) did not demonstrate a "TargetSign", one because of complete aneurysmalthrombosis (Case 4), and the other (Case 6) becausethe residual aneurysmal lumen was too small for theresolution of the CT scanner. Calcification of theaneurysm wall was visualised in six (50%) cases.

Disparity in the size and shape of theangiographically demonstrated aneurysm and CTlesion occurred in all 12 cases (figs 1, 2). In five (42%)cases the angiographically demonstrated lumenappeared irregular in outline, and in seven (58%)cases the angiograms suggested the presence of smallor moderate (<2- 5 cm) sized aneurysms. One totallythrombosed aneurysm (Case 4) appeared as anavascular mass. This aneurysm was associated withipsilateral carotid artery thrombosis that extendeddown to the carotid bifurcation in the neck, and wasthe only case of parent artery occlusion in the series.

Table 1 Major angiographic and computed tomographicfindings in the 12 patients with partially and totally thrombosedgiant intracranial aneurysms

Case no Angiographic features

1 R middle cerebral artery aneurysm (MCA) dumbellshaped. 8 x 18 mm. Irregular lumen

2 (1) Fusiform giant MCA aneurysm (5 x 3 cm).Cerebrovascular ectasia

(2) Massive aneurysmal thrombosis with residualeccentric serpiginous MCA channel

3 Basilar bifurcation aneurysm 1- 6 x 1- 5 cm

4 L internal carotid artery (ICA) Occlusion. AvascularL middle fossa mass. Mural calcification

5 Saccular R carotid bifurcation aneurysm(4-5 x 3-8cm)

6 Multilobed LMCA aneurysm (3 x 8 mm)

7 Saccular R MCA aneurysm (3-0 x 2 5 cm)

8 Saccular basilar bifurcation aneurysm (1- 0 x 1 3 cm).Irregular lumen

9 Triangular basilar bifurcation aneurysm with irregularlumen (2- 0 x 1- 5 cm). Proximal vasospasm

10 Ovoid basilar bifurcation aneurysm (1-8 x 1 2 cm)

11 L cavernous carotid aneurysm with irregular lumen(15 x 1-5cm)

12 L semi-saccular MCA aneurysm (2- 8 x 1- 4 cm) withirregular lumen

Computed tomographic features

Globoid, high density middle cranial fossa lesion (4- 5 x 6- 0 cm). Targetsign. Mural enhancement and calcification

(1) Fusiform high density LMCA lesion. Uniform contrastenhancement

(2) Mixed density lesion. Target sign and mural enhancement

Ovoid suprasellar (3- 0 x 2- 0 cm) lesion of mixed density. Target signenhancement

Globoid (6-0 x 5-0 cm) L parasellar high density lesion. Muralcalcification and enhancement. Absent target sign

Ovoid (5-0 x 3-0 cm) suprasellar mixed high density lesion. Targetsign enhancement. Contiguous. Frontal lobe oedema

Globoid (3-0 x 2- 5 cm) L middle fossa lesion of mixed high density.Mural calcification. No target sign enhancement

Globoid (4- 5 x 4- 5 cm) R middle fossa mass of mixed high density.Mural and target sign enhancement. Mural calcification

Ovoid (4-0 x 2- 8 cm) suprasellar mixed high density lesion. Mural andtarget sign enhancement

Globoid (2 5 x 2- 5 cm) suprasellar mass of mixed high density.Target sign enhancement

Saccular (3- 3 x 3- 6 cm) suprasellar mass of mixed high density. Muralcalcification and enhancement. Target sign enhancement

Globoid (2- 5 x 2 5 cm) left paraseliar mass of mixed high density.Target sign enhancement

Globoid (2- 8 x 2- 5 cm) left suprasellar mass of mixed high density.Target sign enhancement. Mural calcification

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Whittle, Dorsch, Besser

Fig 1 Carotid angiograms and enhanced CTscan ofCase 1. The anteroposterior (a) and lateral (b) carotidangiograms show a dumbell-shaped left middle cerebralartery aneurysm ofapproximate dimensions 0 8 x 1 8 cm.Although there is distortion ofthe M3 segment, and asuggestion ofa larger contiguous aneurysmal cavity, theCTscan (c) reveals the true dimensions ofthe lesion.This study also demonstrates the mural calcification andmixed attenuation values ofthe intra-aneurysmalthrombus.

There was one case (Case 2) documented with serialangiography, of almost complete spontaneous giantintracranial aneurysm thrombosis, in a previouslynon-thrombus-containing giant fusiform middlecerebral artery aneurysm. The middle cerebralartery, remained patent as a serpiginous channelthrough the avascular mass, thus resulting in theformation of a "Giant Serpentine aneurysm"10 I (fig3). CT' studies suggested a similar process hadoccurred in another patient (Case 7); however, severecontrast allergy precluded angiographic docu-mentation.

ClinicalSymptoms and signs leading to clinical presentationof the 12 patients with thrombus-containing giantintracranial aneurysms are listed in table 3.Symptomatology emanating from the intracranialmass effect of the aneurysm (viz progressive focalneurological deficit, focal epilepsy, intellectualimpairment and headache) accounted forpresentation in eight (67%) patients. However fourof these patients had no focal neurological deficit onclinical examination. Headache was the mostcommonly recorded symptom, being documented in10 (83%) patients in the weeks prior to admission.There was one case of recurrent faciobrachial paresisand dysphasia due to embolism from a largelythrombosed giant left middle cerebral arteryaneurysm (Case 2). Four (44%) of the nine patientswith partially thrombosed giant intracranialaneurysms at presentation had experienced

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Fig 2 Vertebrobasilarangiogram (subtractionfilm) and CTscan of Case 10. The anteroposterior angiographicfilm (a)shows an ovoid basilar bifurcation aneurysm ofapproximately 1 8 x 1 2 cm, with a regular lumen. The CTscan (b) again reveals the true dimensions of the lesion. Acentral " Target sign ", mural calcification and contrastenhancement ofthe aneurysm wall are also demonstrated.

subarachnoid haemorrhage and it was the presentingsyndrome in three of these cases. Subarachnoidhaemorrhage had occurred in five (42%) of the 12patients who at presentation had non-thrombosedgiant intracranial aneurysms. This difference in theincidence of haemorrhage from non-thrombosed andthrombus-containing giant intracranial aneurysms isnot significant. In those patients presenting withsubarachnoid haemorrhage the mortality was 60%for non-thrombosed and 66% for thrombus-containing giant intracranial aneurysms.

Overall there was no significant difference in age,sex distribution, morbidity, mortality and incidenceof definitive aneurysm surgery in the patients withnon-thrombosed and thrombus-containing giantintracranial aneurysms (table 4). Preoperativemanagement which consisted of a routine regime ofanti-fibrinolytic, anticonvulsant and steroid therapy,was not influenced by the presence of intra-aneurysmal clot.

Pathological examinationThe neuroradiographic diagnosis of significant intra-aneurysmal thrombosis was confirmed at operation insix patients (Case 1, 4-6, 10) and in one (Case 2) atnecropsy. Macroscopic and histopathologicalexamination of the aneurysmal fundi removed atoperation (Case 4-6) or necropsy (Case 2) revealedlamination and variable organisation of the thrombusin all cases (fig 4).

Discussion

Spontaneous intra-aneurysmal thrombosis is a welldocumented phenomenon that, as in our series, hasbeen noted in approximately 50% of giantintracranial aneurysms 356'' as well as being thetopic of many case reports.9-'4 This high incidence ofthrombus formation within giant intracranialaneurysms is related to a critical ratio, betweenaneurysmal volume and aneurysmal neck size, belowwhich intra-aneurysmal thrombosis occurs.'5Although other biophysical and dynamic parameterscontribute to the delicate balance betweenthrombogenesis and thrombolysis within theaneurysm (vide infra), the volume/orifice ratio wouldappear to be the major factor.'5Computed tomography has considerably

facilitated the diagnosis of partially or totallythrombosed giant intracranial aneurysms. Althoughintra-aneurysmal thrombus significantly alters the CTappearance, the pathognomonic features of theselesions have recently been well documented.2' Thisvariable appearance may, however, simulate manydifferent intracranial lesions, the differentialdiagnosis of which includes germinoma, pituitaryadenoma, meningioma, glioma, acoustic neuroma,epidermoid cyst and craniopharyngioma.2 Disparityin the size and shape of the lesion as visualised by CTand cerebral angiography is diagnostic of partial ortotal giant intracranial aneurysm thrombosis.Angiography may be non-diagnostic or frequentlymisleading with respect to the aneurysm size ifsignificant thrombosis has occurred. The clinicalcorrelation is also variable since, although 47% ofpatients with giant intracranial aneurysms maypresent with subarachnoid haemorrhage, the

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~~~~~~~~~~~. .. ........F .. e.. ..

Fig 3 Sequential carotid angiograms and CTscans of Case 2 showing the evolution ofa giant serpentineaneurysm from a previously non-thrombus-containing giantfusiform middle cerebral artery aneurysm.Carotid angiography (a) and enhanced CTscan (b), performed in December, 1980 reveal a giantfusiformleft middle cerebral artery aneurysm, and diffuse cerebrovascular ectasia. Subsequent studies performed inAugust, 1981 (c, d) following the onset ofheadaches and transient ischaemic attacks, reveal extensivethrombosis of the aneurysm, with preservation ofserpiginous middle cerebral arterial lumen.

remaining patients present with neurologicalsymptoms and signs that are either non-specific orrelated to intracranial mass effect.5" The clinicalsignificance of intra-aneurysmal thrombus formationin giant intracranial aneurysms has not previouslybeen studied, although contradictory statementshave appeared in the neurosurgical literature,particularly with regard to its efficacy in theprevention of subarachnoid haemorrhage.

Organisation of the thrombus has been claimed toprovide a skeletal lattice that protects againsthaemorrhage'3 6 and enhances enlargement of theaneurysm to giant dimensions.'8 Conversely Drake'has suggested that even massive intra-aneurysmal clotdoes not protect against haemorrhage. The results inthis small series and data extrapolated from the largerseries of Drake5 and Hosobuchi,6 would support thecontention that unless the giant intracranial

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Table 3 Clinical symptomatology and signs together with treatment and outcome ofthe twelve patients with partially ortotally thrombosed giant intracranial aneurysm

Case Age Sex Giant Thrombosis Symptom Focal signs Outcome commentsno (yr) aneurysm

1 47 F R MCA Extensive Jacksonian epilepsy Nil Aneurysm clipped. Well.(previous sub- Occasional seizuresarachnoidhaemorrhage)

2 59 M L MCA Extensive Headaches, uncinate Nil Aneurysm wrapped. Progressiveseizure, intellectual deterioration. Recurrent emboli,impairment transient ischaemic attacks. Died

with pulmonary emboli3 66 F Basilar Partial Subarachnoid Subarachnoid Rebleed. Died day 10

bifurcation haemorrhage, haemorrhage,Prodromal headache grade 3(1 month)

4 26 M L cavernous Total Headache, L proptosis, Aneurysmotomy, thrombectomy.ICA ophthalmoplegia ophthalmoplegia, Well

facial dysaesthesia5 56 F R I carotid Partial 1/52 headache, Nil Aneurysmectomy. Clipping.

bifurcation intellectual Unchanged intellectimpairment

6 57 M L MCA Extensive 1/12 progressive R Brachial paresis, Aneurysmectomy and throm-brachial paresis dysphasia bectomy. Dysphasia. R hemi-

paresis. Post-op. seizure x 17 47 F R MCA Extensive Headache Nil Well. Aneurysm wrapped and glued8 63 F L carotid Extensive Subarachnoid Subarachnoid Aneurysm clipped. Herniparesis

bifurcation haemorrhage. haemorrhage. Grade resolved. Intellect improvedGrand mal 3 hemiparesis after ventriculoperitonealseizures. Headache. (right), intellectual shuntingIntellectual impair- impairment, oculo-ment motor palsy

9 45 F Basilar Partial Subarachnoid Subarachnoid Rebleed. Died day 9bifurcation haemorrhage. haemorrhage,

Prodromal grade 5headaches

10 50 F Basilar Extensive Headache. Progres- Mild L hemiparesis Aneurysm clipped. Mild residual Lbifurcation sive L hemiparesis hemiparesis

11 53 F L cavernous Extensive Ophthalmoplegia 1/52 Ophthalmoplegia ICA ligation with BTA-MCAcarotid bypass. Ophthaimoplegia

unchanged12 21 M L MCA Extensive Non-haemorrhagic R hemiplegia Currently rehabilitating. CT scan

syncope show focal capsular infarction

aneurysm is totally thrombosed, intra-aneurysmalclot does not protect against subarachnoidhaemorrhage. The incidence of subarachnoidhaemorrhage from partially thrombosed giantintracranial aneurysms in the latter two series was40% compared to an incidence of subarachnoidhaemorrhage from non-thrombosed giantintracranial aneurysms of 48% and 40%respectively.S6 In both these series, as in ours, thesedifferences are not significant.The incidence of haemorrhage from thrombus-

containing giant intracranial aneurysms may bespuriously elevated by the detection of thrombusformed after the haemorrhage. Alteredhaemodynamics at the time of haemorrhage andsubsequent cerebral vasospasm could enhance intra-aneurysmal vascular stasis. Nonetheless theneuroradiological, operative and post-mortemfindings, would suggest that in most cases laminatedthrombus antedates the haemorrhage. Peripheralring enhancement and mural calcification are

believed to be related to longstanding aneurysmalthrombosis and clot organisation.'018 Furthermore,thrombus deposition within the aneurysm is non-uniform because of flow dynamics, turbulencepatterns and the pattern of endothelial damage.Consequently, although sections of the giantintracranial aneurysm wall may be fibro-calcific,other segments may be extremely tenuous, and it isfrom these sites that rupture occurs.The significance of intra-aneurysmal thrombus in

the genesis of thrombo-emboli from a giantintracranial aneurysm is uncertain, mainly because ofthe infrequency with which, until recently, embolifrom aneurysms had been recognised as a cause oftransient cerebral ischaemia. In a review of theliterature to 1978 only twelve well documented casesfrom all intracranial aneurysms had been reported.'9Reversible ischaemic neurological deficitsattributable to emboli emanating from partiallythrombosed giant intracranial aneurysms have beendocumented on several occasions618192' and our Case

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Table 4 Comparative patientprofiles showing the incidenceofmajor neurosurgical intervention, mortality and morbidityin patients with non-thrombosed and thrombus containinggiant intracranial aneurysms

Giant aneurysm status

No thrombus Partial/totalthrombosis

1 No 10 122 Female: male ratio 8: 2 8: 43 Age (mean + SD) yr 50 13 50 104 Operation on aneurysm

(clipping, wrapping, glueing,aneurysmectomy, etc.) 7 8

5 Death 4 36 MorbidityNo focal neurological deficit 3 3Isolated ophthalmoplegia 2 3Intellectual impairment 2 2Epilepsy 1 0Hemiplegia/dysphasia 0 2

2 is the first report of embolisation from a giantserpentine aneurysm. In one series 59% of thethrombus-containing giant intracranial aneurysmswere associated with distal thrombo-embolism,'8 inanother it was 5%,6 and in the present series thefigure is 8%. Paroxysmal ischaemic episodes have,however, been described from non-thrombus-containing giant intracranial aneurysms"" and inthese cases it has been postulated that the cerebraldysfunction may be attributable to compressiveeffects of the aneurysm, ipsilateral carotid arteryplaques, vasoconstrictor agents (Thromboxane A2,Prostaglandin G2) activated by turbulence and stasiswithin the giant intracranial aneurysm, as well asplatelet emboli. Platelet deposition is a dynamic

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process that has recently been documented withradioisotopic technique to occur in giant intracranialaneurysm without radiographically detectable throm-bus or clinical symptomatology.'8 Overall, it wouldappear that the risk of embolisation is greater from athrombus-containing giant intracranial aneurysinalthough the relative incidence of this epi-phenomenon awaits documentation.The probability of parent artery occlusion by

propagation of thrombus from a giant intracranialaneurysm would appear to be extremely low. Thereare two reported cases of parent artery occlusionassociated with total spontaneous giant intracranialaneurysm thrombus3 12 one of which is Case 4 of thepresent series, and one report of partial parent arteryocclusion by a partially thrombosed giant intracranialaneurysm." The rarity of this epiphenomenondespite gross distortion of the parent arterial lumen orits incorporation into the aneurysmal fundus isrelated to local aneurysmal and arterial haemo-dynamics. Black and German'5 demonstrated thatintra-aneurysmal blood velocity is inversely related toaneurysmal volume, and that flow into the aneurysmis related to aneurysm neck size. Thus as an aneurysmthromboses the conditions propitious for furtherthrombosis diminish, and this equilibrium is partlydetermined by the haemodynamic capabilities of theparent artery. Conversely the dynamics of the jetstream of blood from the parent artery are altered bydistortion of the arterial lumen by the aneurysm. Theimportance of the Coanda Effect has been describedin aneurysmal surgery,23 and recently it has beenpostulated as a major factor in the formation of theeccentric serpiginous vascular channels seen in giantserpentine aneurysm. 10 The giant serpentine

Fig 4 Photomicrograph ofa segment ofthe wallofa giantaneurysm with underlyingorganised thrombus (Case 4).The tunica adventitia oftheaneurysmal wall can be seenin the top right. The underlyingmural tissue consists ofahypercellularfibrous stroma,with interspersed capillaries, thatmerges with the organisedthrombus. Vascular sinuses andcapillaries are prominent withinthe clot. (H&E x 100)

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aneurysm formed in Case 2 in this series would appearto substantiate this hypothesis, and this case alsodemonstrates that although massive aneurysmalthrombosis may occur, the parent arterial lumen maybe maintained.

Recent reports on the current trends in theneurosurgical management of giant intracranialaneurysm do not differentiate between partiallythrombosed and non-thrombosed aneurysms.5" Onemay therefore infer that no difference in the clinicalpresentation, surgical approach, and morbidity andmortality between the two groups has been noted.This would appear to be complemented by the resultsfor these parameters in this series. Thus althoughpartially thrombosed giant intracranial aneurysmmay present a diagnostic challenge the subsequentbehaviour of these aneurysms, and the principles intheir surgical management do not differ significantlyfrom non-thrombosed giant intracranial aneurysms.Totally thrombosed giant intracranial aneurysm,however, pose a different threat to the patient, andthe management of these rare aneurysms is welldocumented. 12-14

The authors thank Mr GK Vanderfield, Mr JNSegelov and Mr IH Johnston, neurosurgeons, RoyalPrince Alfred Hospital, for permission to includetheir patients, and Dr TS Lamond and Dr MSchroeder, neuroradiologists, Royal Prince AlfredHospital, for their radiological studies.

References

Morley TP, Barr HWK. Giant intracranial aneurysms:diagnosis, course and management. Clin Neurosurg1969;16:73-94.

2 Schubiger 0, Valavanis A, Hayek J. Computedtomography in cerebral aneurysms with specialemphasis on giant intracranial aneurysms. J ComputAssist Tomogr 1980;4:24-32.

3O'Neill M, Hope T, Thomson G. Giant intracranialaneurysms: diagnosis with special reference tocomputerised tomography. Clin Radiology 1980;31:27-39.

4Golding R, Peatfield RC, Shawdon HH, et al. Computertomographic features of giant intracranial aneurysms.Clin Radiology 1980;31:41-8.

Drake CG. Giant intracranial aneurysms: experiencewith surgical treatment in 174 cases. Clin Neurosurg1979;26: 12-95.

6 Hosobuchi Y. Direct surgical treatment of giantintracranial aneurysms. J Neurosurg 1979;51:743-56.

7 Sundt TM, Piepgras DG. Surgical approach to giantintracranial aneurysms. Operative experience with 80cases. J Neurosurg 1979;56:731-42.

8 Onuma T, Suzuki JL. Surgical treatment of giantintracranial aneurysms. J Neurosurg 1979;51:33-6.

Lyell A. Large aneurysm of the circle of Willis with cureby spontaneous thrombosis. Br Med J 1936;2:282.

'0 Fodstad H, Liliequist B, Wirell S, et al. Giant serpentineintracranial aneurysm after carotid ligation. Casereport. J Neurosurg 1978;49:903-9.

Segal HD, McLaurin RL. Giant serpentine aneurysm:report of two cases. J Neurosurg 1977;46: 115-20.

12 Whittle IR, Williams DB, Halmagyi GM, Besser M.Spontaneous thrombosis of giant aneurysm andipsilateral carotid artery. J Neurosurg 1982;56:287-9.

3 Sadik AR, Budzilovich GN, Shulman K. Giant aneurysmof the middle cerebral artery: case report. J Neurosurg1965;22: 177-81.

4 Thauvoy C, Vandresse JH, Stroobandt et al.Accroisement progressif et thrombose d'un aneurysmede la communicante anterieure. Elude clinique,radiologique et histologique. Neurochirurgie 1978;24:423-7.

'5 Black SPW, German WJ. Observations on therelationship between volume and size of the orifice ofexperimental aneurysms. J Neurosurg 1960;17:984-90.

16 Jain KK. Surgery for intracranial aneurysm: a review.Canad J Surg 1965;8: 172-87.

7 Bull JWD. Massive aneurysms at the base of the brain.Brain 1969;92:535-70.

18 Sutherland GR, King ME, Peerless SJ, et al. Plateletinteraction with giant intracranial aneurysm. JNeurosurg 1982;56:53-61.

'9 Sakaki T, Kinugawa K, Tanigake T, et al. Embolism fromintracranial aneurysms. J Neurosurg 1980;53:300-4.

20 Auld AW, Shafey A. Transient ischaemic attachs notproduced by extracranial disease. South Med J1976;69:722-4.

21 Mehdorn HM, Chater NL, Townshend JJ, et al. Giantaneurysms and cerebral ischaemia. Surg Neurol1980;13:49-57.

22 Antunes JL, Correll JW. Cerebral emboli fromintracranial aneurysms. Surg Neurol 1976;6:7-10.

23 Robinson JL, Roberts A. Operative treatment ofaneurysms and the Coanda effect. J Neurol NeurosurgPsychiatry 1972;35:804-9.

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doi: 10.1136/jnnp.45.11.1040 1982 45: 1040-1047J Neurol Neurosurg Psychiatry

I R Whittle, N W Dorsch and M Besser intracranial aneurysms.Spontaneous thrombosis in giant

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spontaneous thrombosis in giant intracranial aneurysms

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