Neuroradiology
Correlation of Computed Tomographic, Angiographic, and Neuropathological Changes in Giant Cerebral Aneurysms 1 Richard S. Pinto, M.D., Irvin I. Kricheff, M.D., Alan R. Butler, M.D., and Raj Murali, M.D. Giant aneurysms involving or adjacent to the circle of Willis exhibit three CT patterns: nonthrombotic, partially thrombotic, and completely thrombotic. Partially thrombotic aneurysms have the most specific pattern, consisting of a "target" configuration on the post-contrast scan. Ring calcification of the wall or mural thrombus is frequently observed in partially or completely thrombotic aneurysms. Calcification is not seen in nonthrombotic lesions. Angiographic and neuropathological findings are correlated with the CT findings. INDEX TERMS:
Aneurysm, cerebral, 1[7].730 • Computed tomography, head, 1[0].1211 • Meninges, hemorrhage
Radiology 132:85-92, July 1979
IANT ANEURYSMS usually present clinically as intracranial masses, frequently producing dementia and multiple cranial deficits (1-10); infrequently subarachnoid hemorrhage is present (11). By convention, aneurysms have been considered "giant" if the lumen is larger than 1 em at angiography. Using computed tomographic (CT) criteria, aneurysms are considered "giant" if their image is 1 cm or greater, even though at angiography the lumen may be less than 1 cm. Partially or completely thrombosed giant aneurysms may easily be mistaken for neoplasms on the CT scan unless attention is paid to detail. The purpose of this report is to describe the CT characteristics of giant aneurysms and offer an angiographic and neuropathological correlation.
G
METHODS AND MATERIALS
Twenty-one giant aneurysms studied with CT at New York University Medical Center since the installation of a scanner with a 160 X 160 matrix were reviewed. Follow-up scans were also studied for post-therapy changes. CT studies were done before and after instillation of intravenous contrast material in all patients except for one who did not have a contrast study because of iodine sensitivity. Using a drip infusion of methylglucamine diatrizoate, 42.3 g of iodine was delivered over a period of 6-8 minutes. The pre- and post-contrast appearance was : correlated with plain skull radiographs, angiograms, surgical findings, and histopathological findings when available. The location and size of the aneurysms were reviewed and correlated with the post-contrast scan. Five surgical specimens were examined microscopically for intraluminal thrombosis, vascularity of the luminal thrombus, presence and location of calcification, and vascularity and thickening of the aneurysmal wall. RESULTS
Clinical, CT, and Angiographic Findings ( TABLE I) Fifteen patients (71 % ) had clinical findings suggesting
an intracranial mass, including dementia, focal or generalized seizures, headaches, dysphasia, diplopia, and multiple cranial nerve deficits. Six patients had subarachnoid hemorrhage. Most aneurysms were located in the cavernous carotid artery (8 patients) (TABLE II), followed by the internal carotid artery near the origin of the ophthalmic artery (3 patients), the trifurcation of the middle cerebral artery (3 patients), the internal carotid artery near the origin of the posterior communicating artery (2 patients), the vertebrobasilar region (2 patients), the posterior cerebral artery (1 patient), the anterior communicating artery (1 patient), and the bifurcation of the internal carotid artery (1 patient). If the supraclinoid segment of the internal carotid artery is considered as one site, it would be the second most frequent location (6 patients). Correlation of CT and angiographic findings revealed three distinct patterns: (a) nonthrombotic thin-walled aneurysms, (b) partially thrombotic aneurysms, and (c) completely thrombotic aneurysms. Thin-Walled, Nonthrombotic Aneurysms (10 cases): Aneurysms in this category did not differ in size on the CT scan and angiogram when both studies were scaled to actual size (Fig. 1). Nine were slightly hyperdense (CT number> normal brain tissue) on the pre-contrast scan (Fig. 1, a); the tenth (CASE 3), which was also the smallest aneurysm in this series (16 X 10mm), was isodense (CT number = normal brain tissue). None of the aneurysms was surrounded by edema. Following contrast infusion, all 10 aneurysms were uniformly and markedly enhanced (Fig. 1, b). Routine skull radiographs showed a long-standing, expanding mass in 2 patients, causing Widening of the superior orbital fissure in one (CASE 4) and erosion of the carotid sulcus in the other (CASE 14). No intracranial calcification (a sign of a giant aneurysm) was observed. Partially Thrombotic Aneurysms (7 cases): All but one of the partially thrombotic aneurysms demonstrated a ring-shaped hyperdense region of variable thickness and density on the pre-contrast scan (Fig. 2, a). Five had curvilinear peripheral calcification. Following contrast infusion, central or eccentric peripheral enhancement was
1 From the Departments of Radiology (R.S.P., U.K., ARB.) and Neurosurgery (A.M.), New York University Medical Center, New York. N.Y. Received July 25, 1978; accepted and revision requested Oct. 31; revision received Jan. 23, 1979. Presented at the Sixteenth Annual Meeting of the American Society of Neuroradiology, New Orleans, La., Feb. 26-March 3, 1978. sjh
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TABLE 1: Patient
Presenting Signs and Symptoms
1. Dementia, blindness in left eye, right temporal field cut 2. Palsy of right third nerve 3. Headaches, seizures
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FINDINGS IN 21 PATIENTS WITH GIANT ANEURYSMS
Location (Artery)
Pre-contrast
Right cavernous carotid
CT Scan Post-contrast
Isodense; peripheral calcification
Completely thrombostic
No enhancement
Erosion of the carotid sulcus Negative
Completely thrombostic
4. Palsy of third, fourth, and sixth nerves
Left cavernous carotid
Homogeneous enhancement
5. Subarachnoid hemorrhage 6. Frontal headaches
Hyperdense Anterior communicating Right ophthalmic Hyperdense with calcification
7. Headaches, diplopia
Left carotid bifurcation Right middle cerebral Left posterior cerebral
Hyperdense Hyperdense Centrally isodense with hyperdense ring Hyperdense
10. Diplopia, swirling noise in the right ear 11. Dysphagia, retro-orbital pain
Right cavernous carotid Left middle cerebral
12. Diplopia
Right cavernous carotid
13. Diplopia, palsy of the right third nerve 14. Palsy of the third nerve
16. Subarachnoid hemorrhage
Right cavernous carotid Right cavernous Hyperdense carotid Right posterior Hyperdense communicating Left middle Hyperdense with cerebral calcification
17. Diplopia on the left, lateral rectus paresis 18. Sabarachnoid hemorrhage 19. Dementia
Left canvernous carotid Vertebrobasilar junction Basilar
20. Subarachnoid hemorrhage
Left ophthalmic
21. Diplopia
Left ophthalmic
15. Seizures
TABLE II:
Hyperdense with calcification Isodense, with hyperdense ring and calcification Hyperdense
Hyperdense Hyperdense Centrally isodense, with peripheral calcification Eccentric peripheral hyperdense region; calcification Homogeneous, hyperdense
LOCATION OF 21 GIANT CEREBRAL ANEURYSMS
Location Cavernous carotid artery Supraclinoid carotid artery Internal carotid near the origin of the ophthalmic artery Internal carotid near the origin of the posterior communicating artery Bifurcation of the internal carotid Trifurcation of the middle cerebral artery Vertebrobasilar arteries Posterior cerebral artery Anterior communicating artery
No. of Patients
8 6 3 2
3 3 1 1
Angiogram
Calcification
Homogeneous enhancement
Hyperdense
Plain Radiograph
Homogeneous
Right cavernous Hyperdense carotid Right posterior Isodense communicating
8. Subarachnoid hemorrhage 9. Subarachnoid hemorrhage
July 1979
Homogeneous enhancement Luminal and peripheral enhancement Homogeneous enhancement Homogeneous enhancement Peripheral enhancement
Erosion of the superior orbital fissure Negative
Thin-walled aneurysm 16 %mmult 10 X 10mm Thin-walled aneurysm
Negative
Thin-walled aneurysm 10 X 10 X 10 mm Thin-walled aneurysm
Negative
Thin-walled aneurysm
Negative
Thin-walled aneurysm
Negative
Completely thrombotic aneurysm
Homogeneous enhancement Luminal and peripheral enhancement Peripheral enhancement
Negative
Thin-walled aneurysm
Calcification
Partially aneurysm thrombotic
Negative
Central enhancement Homogeneous enhancement Not done
Negative
partially thrombotic aneurysm with recanalization Partially thrombotic aneurysm Thin-walled aneurysm
Central and peripheral enhancement Homogeneous enhancement Homogeneous enhancement No enhancement
Erosion of the carotid sulcus Negative Calcification
Partially thrombotic aneurysm Partially thrombotic aneurysm
Negative
Thin-walled aneurysm
Negative
Thin-walled aneurysm
Negative
Completely thrombotic aneurysm
Eccentric peripheral Calcification enhancement
Partially thrombotic aneurysm
Homogeneous enhancement
Thin-walled aneurysm
Negative
seen in all 5 (Fig. 2, b). No edema was observed. One patient (CASE 11) exhibited a nonenhanced lucent area adjacent to the aneurysm; however, biopsy demonstrated cerebral gliosis, probably due to an old infarction. Angiography and CT differed markedly as to the size of the aneurysm (Fig. 2, c and d). Angiography demonstrated only the lumen, whereas CT revealed luminal thrombosis and the thickened wall. Angiography demonstrated a local mass in all cases but did not show a peripheral blush corresponding to the hyperdense ring seen on the postcontrast scan. One aneurysm (CASE 12) was isodense centrally and hyperdense peripherally on the pre-contrast
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Fig. 1. Nonthrombotic, thin-walled giant aneurysm. a. Pre-contrast scan demonstrates an ill-defined hyperdense areaobliterating the suprasellar cistern (arrows). b. Contrast enhancement reveals homogeneous uptake by an asymmetric lesion mostly to the left of the midline. e and d. Left internal carotid angiograms in the AP (e) and lateral (d)projections demonstrate a giantaneurysm at the bifurcation of the internal carotid artery. No intraluminal irregularity or thrombosis is observed. After correcting for magnification, the aneurysm is about thesame sizeon both the angiogram and the CTscan.
1e ,d
scan (Fig. 3, a); tollowing contrast infusion the hyperdense region was prominentiy enhanced (Fig. 3, b). Angiography (Fig. 3, c and d) revealed that th is finding represented a reformed channel through an almost completely thrombotic aneurysm. Routine skull radiographs showed discernible intracranial calcifications iri 2 of 5 patients; they were curvilinear in one patient and amorphous and nodular in the other. Completely Thrombotic Aneurysms (4 cases): These aneurysms exhibited a distinctive ring-shaped hyperdense region on the initial scan which was enhanced by contrast infusion. No central or eccentric enhancement or edema was seen (Fig . 4, a and b). Angiography demonstrated a focal mass without filling of the lumen in all 4 cases (Fig . 4, e and f). The diagnosis was made at surgery in CASE 1, autopsy in CASE 19, and demonstration of recanalization on an angiogram obtained one year earlier in CASE 9 (Fig. 4, c and d); it is unproved in CASE 2 except for typical plain radiographic changes of erosion of the carotid sulcus and absence of contrast enhancement on CT .
Neuropathological Findings: Microscopic examination of five partially thrombotic giant aneurysms revealed that the intraluminal thrombus was moderately vascular and lacked calcification. The aneurysmal wall consisted of markedly thickened fibrous connective tissue with prominent blood vessels and focal areas of calcification (Fig. 5). DISCUSSION
Thin-walled aneurysms appear slightly hyperdense on pre-contrast scans and exhibit a homogeneous increase in density following contrast infusion. This is easily explained on the basis of the hyperdense blood pool which is subsequently opacified by circulating iodinated contrast material (12-14) (Fig. 1, a and b), i.e., both the hyperdensity and the subsequent enhancement can be explained on a purely intravascular basis . Partially thrombotic aneurysms are seen on the pre-contrast scan as a central or eccentric hyperdense region within an isodense zone which is in turn
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2a,b
2c,d
Fig. 2. Partially thrombotic giantaneurysm. a. Pre-contrast scan demonstrates a large. bilobate lesionin the left temporofrontal region. with peripheral calcification (arrow). The lesion hasan internal region and a hypderdense peripheral rim. Notethe lack of edema. b. Following contrast lnfusfon. the hyperdense internalregion (i) is homogeneously and markedlyenhanced. as is the periphery of the lesion (p) , while the central area remains isodense ("target" sign). c. Left internal carotid arteriogram(frontal projection) shows an irregular, multilobular middle cerebral artery (MCA) aneurysm corresponding in size and location to the enhanced central areain Figure 2. b. Theaneurysm appears smaller than it did on the CT scan, sinceonlythe intraluminal portion is filled. Theangular border and displacement of the mainbranches of the MCA(arrows) suggest a larger mass. d. The lateral projection demonstrates the temporalmasseffect produced by the thromboticportion of the aneurysm. Notethe irregularity of the luminal wall and the displacement and stretching of the main sylvian branch andtemporal opercularbranches of the MCA(arrows). The peripheralenhancement noted on the CTscan cannotbe seenon the angiogram.
surrounded by a peripheral hyperdense or calcific area. The central and peripheral zones are enhanced by contrast material, whereas the isodense zone is not (Fig. 2, a and b). While the peripheral enhancement cannot be explained angiographically (Fig. 2, c and d), the central enhancement is the result of iodine circulating within the blood pool (13) . The thickened fibrous wall that surrounds the aneurysm is formed from multipotential cells of the adjacent meninges in response to the subarachnoid mass, and hence the prominent vascularity of this layer of granulation tissue is not derived from the brain, nor is a blood-brain barrier present. We believe peripheral enhancement is the result of extravascular diffusion of contrast material into the
vascularized fibrous tissue wall and is analogous to normal contrast enhancement of the dura mater. Of the seven giant aneurysms with peripheral enhancement in our series, one was completely thrombotic (Fig . 4). In CASE 12 the enhancement did not appear to be due to a vascular aneurysmal wall (Fig. 3); rather, the angiogram demonstrated a reformed channel through the periphery of the massive thrombosed aneurysm, corresponding to the enhanced area. On CT, the hyperdense ring varied in thickness before and after contrast infusion and was incompletely enhanced. This is quite different from a fibrous aneurysmal wall, which is of constant thickness and exhibits complete enhancement The peripheral en-
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Fig. 3. Recanalization of a giant aneurysm. a. Pre-contrast scan demonstrates a mass having an isodense central zone and a calcific. slightly hyperdense peripheral zone. No edema is present. b. The post-contrast scan demonstrates a ring pattern of variable thickness, distinguishing it from the peripheral enhancement seen with thrombotic aneurysms. c. Right common carotid angiogram (frontal projection) demonstrates a peripheral channel through a giant aneurysm. The ends of the channel are tapered at its origin from the supraclino id segment of the internal carotid artery. and it terminates at the middle cerebral branches. The stretched anterior temporal artery (indicating a larger mass than the observed aneurysm) and the irregularity of the luminal channel suggest thrombosis. d. The lateral projection again demonstrates the tapered ends of the channel . explaining the variable peripheral enhancement (Fig. 3. b).
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3a,b
3c,d
hancement ot the reformed channel was more intense and had a sharper internal interface than that of the fibrous wall. Microscopic examination of partially thrombotic giant aneurysms reveals that the thickened and vascular aneurysmal wall is made up of fibrous connective tissue associated with atrophy of the lamina media and adventitia (Fig. 5). Published microscopic descriptions of ruptured aneurysms demonstrate disruption of the lamina elastica and muscularis, irregular thinning and fibrosis of the adventitia , and thickening of the lamina intima (15). The thickened fibrous wall observed in our microscopic examinations may be peculiar to giant aneurysms and related to a long-standing process: the presence of a mass over a long period of time may stimulate production of fibrous connective tissue. causing the lesion to be encapsulated. It has been hypothesized (16) that thickening of the wall is secondary to subarachnoid hemorrhage. but only 3 of our 6 patients with peripheral enhancement of a thickened fibrous wall had a definite history of bleeding. Two patients without documented hemorrhage had recurrent frontal or retro-orbital pain which may have represented sub-
arachnoid hemorrhage but most likely was the result of traction or pressure by the aneurysm on the tentorium, causing pain to be referred through the fifth nerve fibers (15). Calcification within the wall of the aneurysm (1. 15.17.18) was seen on the pre-contrast scan in 7 patients (Fig. 2, a). including 5 with partially and 2 with completely thrombotic aneurysms. None of the thin-walled aneurysms was calcified. Thus this finding may be useful in predicting thrombosis of a giant aneurysm. Pathological examination showed that calcification develops within the thickened thickened connective tissue layer of the wall , probably secondary to microscopic hemorrhage within this prominently vascular structure. If such bleeding is profuse and disruptive, it may be responsible for the occasional recanalization (CASES 9 and 12) and subarachnoid hemorrhage (CASES 7 and 15). Completely thrombotic giant aneurysms may be a diagnostic problem even after angiography, which frequently demonstrated only an avascular mass (18, 19). Of our 4 patients, only one (CASE 9) had a history of subarachnoid bleeding (Fig. 4). Angiography one year earlier demon-
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4c ,d
Fig. 4. Completely thrombotic giant cerebral aneurysm. a. Pre-contrast scan reveals a large mass with an isodense center and a ring of slight hyperdensity in the left infrathalamic region. There is no edema. The third ventricle is displaced to the right. b. Following contrast infusion, there is prominent peripheral enhancement without internal enhancement. This is different from the ring sign of malignant glioma, metastasis, or abscess. c. Frontal projection from a right brachial angiogram obtained one year earlier demonstrates filling of a posterior cerebral artery (PCA) aneurysm (arrowhead) with an irregular lumen and recanalization . There is a mass effect, seen as displacement of the anterior cerebral artery to the right . d. Early venous phase of the right brachial arteriogram (lateral projection) shows the reformed channel to better advantage(arrows).
strated a reformed channel through the aneurysm; at the time of CT it showed complete thrombosis, and the left posterior cerebral artery was occluded. Two other completely thrombotic aneurysms were confirmed at surgery and postmortem examination, respectively. One case remains unproved. The CT appearance of completely thrombotic aneurysms varied. One (CASE 9) had an isodense center and a slightly hyperdense or calcific peripheral zone with no edema (Fig. 4, a). Following contrast infusion, the scan demonstrated peripheral enhancement of a fibrous wall (Fig. 4, b). A second patient (CASE 1) showed homogeneous contrast enhancement in a surgica11y proved thrombotic aneurysm. There are two possible explanations for this difference: either (a) the section included only the wall of the aneurysm, not the more central isodense thrombus, or (b) revascularization and possibly fibrous
tissue infiltration of the intraluminal thrombus caused the enhancement. Another patient (CASE 19) exhibited prominent calcification of the periphery of the aneurysm but no discernible enhancement. We assume that the calcification was the result of previous bleeding into the highly vascular wall, so that the resultant thrombosis precluded enhancement. Our fourth case (CASE 2) is unproved, but a thrombotic cavernous carotid aneurysm was suspected on the basis of a nonenhanced but slightly hyperdense lesion adjacent to the pituitary fossa, producing focal erosion of the carotid sulcus. The absence of a tumoral blush at angiography and the elevation of the cavernous carotid support this diagnosis. The lack of an enhanced fibrous tissue layer in this patient supports the supposition that arachnoidal irritation is needed for thickening of the connective tissue . The slightly increased density of the lesion on the pre-contrast scan may be the
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e. Selective left vertebral angiogram (frontal projection) obtained at the time of CT(Fig. 3, a and b)reveals occlusion of the left PCA (arrow), aneurysm, and channel. f. The lateralprojection demonstrates a focalthalamic masswith anterior bowing of the left anterior thalamoperforating artery (open arrow)andposterosuperior displacement of both themedial andlateralposterior choroidal arteries (closed arrows). There is no filling of the left PCA, aneurysm, or channel. 5a,b
Fig. 5. a. High-power photomicrograph of the periphery of a giant aneurysm demonstrates a thick layerof granulation tissue with many endothelium-lined vascular channels which do not have the tight junctions of brain vessels. This fibrous layer produces the peripheral enhancement seen in thrombotic aneurysms. (H&E X100) b. High-power photomicrograph of theperiphery of another giant aneurysm shows a thickened layer of fibrous tissue surrounding thelumen (L) and containing many small vessels. The dark purple stain around several small channels represents calcification secondary to microscopic bleeding. result of revascularization or calcification of the intraluminal thrombus or an averaging effect produced by the inclusion of bone within the CT section. Since no discernible enhancement was demonstrated, and since our limited neuropathological study failed to conclusively demonstrate calcification within the intraluminal thrombus, we feel that the latter explanation is more likely. Thus no specific pattern for a completely thrombotic aneurysm was observed in our 4 cases, although a mass with an isodense center with or without peripheral calcification, demonstrating ring enhancement, and lacking edema is highly suspicious. It is very unusual for a primary glioma to have an isodense center within a peripheral zone of enhancement (ring sign) and lack adjacent edema. CT is useful in following up patients who undergo carotid
ligation for a giant aneurysm (Fig. 6). Intraluminal thrombosis is easily assessed by comparing the pre- and postligation scans (Figs. 1 and 6). Since CT is usually performed first in neurological conditions, giant aneurysms are easily detected (12-14). However, they may be mistaken for a neoplasm. When we reviewed our pre-angiographic CT reports, a giant aneurysm was either the prime diagnosis or included in the differential diagnosis in 13 patients, 6 of whom had a clinical history of subarachnoid hemorrhage which may be assumed to influence the diagnosis. In 3 patients, curvilinear peripheral calcification prompted consideration of a giant aneurysm. Of the cases in which a giant aneurysm was not initially suggested, 6 tumors were diagnosed as a meningioma (CASES 4, 10, 14, 15, 17, and 21), one
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6a,b
Completely thrombotic giant aneurysms lack the central or eccentric zone of hyperdensity and corresponding enhancement. No discernible CT pattern was observed in our small series of patients; however, a mass with an isodense center, with or without peripheral calcification, not surrounded by a zone of edema, and with a ring-shaped zone of enhancement would suggest a completely thrombotic aneurysm . REFERENCES
Fig. 6. Same case as in Fig. 1, a and b, showing the effect of carotid ligation on a nonthrombotic giant aneurysm. a. Pre-contrast scan one week after ligation demonstrates a hyperdense midline area with an adjacent isodense zone representing intraluminal thrombosis (arrow) which was not present on the preoperative study. b. Internal enhancement (i) represents the intraluminal portion of the aneurysm. The isodense region represents partial thrombosis. There is also peripheral enhancement (p) of the fibrous wall.
as a pituitary adenoma with suprasellar extension (CASE 7), one as a chordoma (CASE 19), and one as a glioma (CASE 11). A parasellar location, hyperdensity on the pre-contrast scan, calcification, and prominent enhancement all simulate meningioma, especially in patients with thin-walled aneurysms of the cavernous or supraclinoid carotid (CASES 4,7, 10, 14, 17, and 21). However, the lack of edema should rule out meningioma or malignant glioma. SUMMARY AND CONCLUSIONS
CT scanning is highly reliable in the detection of intracranial masses and may suggest a giant aneurysm prior to angiography. Difficulty may arise with thin-walled aneurysms, since the slight hyperdensity of the lesion on the pre-contrast scan and homogeneous enhancement by contrast material may simulate a meningioma. Proximity to the circle of Willis or major intracranial vessels and absence of edema should suggest a thin-walled aneurysm. The CT signs of partially thrombotic aneurysms are highly specific, consisting of (a) a central or eccentric zone of slight hyperdensity, representing the intraluminal component, surrounded by (b) an isodense zone, representing the thrombotic portion, and (c) a peripheral zone of increased density, representing a layer of fibrous tissue ("target" sign). Following contrast infusion, the central and peripheral zones will both be enhanced. The presence of curvilinear wall calcification and the absence of edema support the diagnosis of a partially or completely thrombotic giant aneurysm.
1. Bull J: Massive aneurysms at the base of the brain. Brain 92:535-570, 1969 2. Heiskanen 0 , Nikki P: Large intracranial aneurysms . Acta Neurol Scand 38:195-208, 1962 3. Jefferson G: Compression of the chiasma , optic nerves. and optic tracts by lntracranial aneurysms. Brain 60:444-497, Dec 1937 4. Morley TP, Barr HWK: Giant intracranial aneurysms: diagnosis, course, and management. Clin Neurosurg 16:73-94, 1969 5. Obrador S, Dierssen G, Rodriguez Hernandez J: Giant aneurysm of the posterior cerebral artery . Case report . J Neurosurg 26: 413-416,Apr1967 6. Polis Z, Brzezinski J, Choclak-Gajewicz M: Giant intracranial aneurysm. Case report. J Neurosurg 39:408-411, Sep 1973 7. Rischbieth RHC. Bull JWD: The significance of enlargement of the superior orbital (sphenoidal) fissure. Br J Radiol 31:125-135, Mar 1958 8. Sadik AR, Budzilovich GN, Shulman K: Giant aneurysm of middle cerebral artery : a case report. J Neurosurg 22: 177-181, Feb 1965 9. Sarwar M, Batnitzky S, Schechter MM, et al: Growing intracranial aneurysms. Radiology 120:603-607, Sep 1976 10. White JC, Ballantine HT Jr: Intrasellar aneurysms simulating hypophyseal tumours. J Neurosurg 18:34-50. Jan 1961 11. Sarwar M, Batnitzky S, Schechter MM: Tumorous aneurysms. Neuroradiology 12:79-97, 11 Nov 1976 12. Davis KR, New PFJ, Ojemann RG, et al: Computed tomographic evaluation of hemorrhage secondary to intracranial aneurysms. Am J RoentgenoI127:143-153, Jul1976 13. Pressman BO, Gilbert GE, Davis DO: Computerized transverse tomography of vascular lesions of the brain. Part II: Aneurysms. Am J RoentgenoI124:215-219, Jun 1975 14. Scotti G, Ethier R, Melal)yon D, et al: Computed tomography in the evaluation of intracranial aneurysms and subarachnoid hemorrhage . Radiology 123:85-90, Apr 1977 15. Pool LJ, Potts DG: Aneurysms and Arteriovenous Anomalies of the Brain. Diagnosis and Treatment. New York, Harper & Row, 1965, pp 47-48 16. Cravioto H: Personal communication 17. Bull JWD: Contribution of radiology to the study of intracranial aneurysms . Br Med J 2:1701-1708,29 Dec 1962 18. Schunk H: Spontaneous thrombosis of intracranial aneurysms. Am J RoentgenoI91:1327-1338, Jun 1964 19. Lukin RR, Chambers AA, Mclaurin R, et al: Thrombosed giant middle cerebral aneurysms. Neuroradiology 10:125-129, 19 Dec 1975
Department of Radiology Section of Neuroradiology New York University Medical Center 560 First Ave. New York, N.Y. 10016
Correlation of Computed Tomographic, Angiographic, and Neuropathological Changes in Giant Cerebral Aneurysms 1 Richard S. Pinto, M.D., Irvin I. Kricheff, M.D., Alan R. Butler, M.D., and Raj Murali, M.D. Giant aneurysms involving or adjacent to the circle of Willis exhibit three CT patterns: nonthrombotic, partially thrombotic, and completely thrombotic. Partially thrombotic aneurysms have the most specific pattern, consisting of a "target" configuration on the post-contrast scan. Ring calcification of the wall or mural thrombus is frequently observed in partially or completely thrombotic aneurysms. Calcification is not seen in nonthrombotic lesions. Angiographic and neuropathological findings are correlated with the CT findings. INDEX TERMS:
Aneurysm, cerebral, 1[7].730 • Computed tomography, head, 1[0].1211 • Meninges, hemorrhage
Radiology 132:85-92, July 1979
IANT ANEURYSMS usually present clinically as intracranial masses, frequently producing dementia and multiple cranial deficits (1-10); infrequently subarachnoid hemorrhage is present (11). By convention, aneurysms have been considered "giant" if the lumen is larger than 1 em at angiography. Using computed tomographic (CT) criteria, aneurysms are considered "giant" if their image is 1 cm or greater, even though at angiography the lumen may be less than 1 cm. Partially or completely thrombosed giant aneurysms may easily be mistaken for neoplasms on the CT scan unless attention is paid to detail. The purpose of this report is to describe the CT characteristics of giant aneurysms and offer an angiographic and neuropathological correlation.
G
METHODS AND MATERIALS
Twenty-one giant aneurysms studied with CT at New York University Medical Center since the installation of a scanner with a 160 X 160 matrix were reviewed. Follow-up scans were also studied for post-therapy changes. CT studies were done before and after instillation of intravenous contrast material in all patients except for one who did not have a contrast study because of iodine sensitivity. Using a drip infusion of methylglucamine diatrizoate, 42.3 g of iodine was delivered over a period of 6-8 minutes. The pre- and post-contrast appearance was : correlated with plain skull radiographs, angiograms, surgical findings, and histopathological findings when available. The location and size of the aneurysms were reviewed and correlated with the post-contrast scan. Five surgical specimens were examined microscopically for intraluminal thrombosis, vascularity of the luminal thrombus, presence and location of calcification, and vascularity and thickening of the aneurysmal wall. RESULTS
Clinical, CT, and Angiographic Findings ( TABLE I) Fifteen patients (71 % ) had clinical findings suggesting
an intracranial mass, including dementia, focal or generalized seizures, headaches, dysphasia, diplopia, and multiple cranial nerve deficits. Six patients had subarachnoid hemorrhage. Most aneurysms were located in the cavernous carotid artery (8 patients) (TABLE II), followed by the internal carotid artery near the origin of the ophthalmic artery (3 patients), the trifurcation of the middle cerebral artery (3 patients), the internal carotid artery near the origin of the posterior communicating artery (2 patients), the vertebrobasilar region (2 patients), the posterior cerebral artery (1 patient), the anterior communicating artery (1 patient), and the bifurcation of the internal carotid artery (1 patient). If the supraclinoid segment of the internal carotid artery is considered as one site, it would be the second most frequent location (6 patients). Correlation of CT and angiographic findings revealed three distinct patterns: (a) nonthrombotic thin-walled aneurysms, (b) partially thrombotic aneurysms, and (c) completely thrombotic aneurysms. Thin-Walled, Nonthrombotic Aneurysms (10 cases): Aneurysms in this category did not differ in size on the CT scan and angiogram when both studies were scaled to actual size (Fig. 1). Nine were slightly hyperdense (CT number> normal brain tissue) on the pre-contrast scan (Fig. 1, a); the tenth (CASE 3), which was also the smallest aneurysm in this series (16 X 10mm), was isodense (CT number = normal brain tissue). None of the aneurysms was surrounded by edema. Following contrast infusion, all 10 aneurysms were uniformly and markedly enhanced (Fig. 1, b). Routine skull radiographs showed a long-standing, expanding mass in 2 patients, causing Widening of the superior orbital fissure in one (CASE 4) and erosion of the carotid sulcus in the other (CASE 14). No intracranial calcification (a sign of a giant aneurysm) was observed. Partially Thrombotic Aneurysms (7 cases): All but one of the partially thrombotic aneurysms demonstrated a ring-shaped hyperdense region of variable thickness and density on the pre-contrast scan (Fig. 2, a). Five had curvilinear peripheral calcification. Following contrast infusion, central or eccentric peripheral enhancement was
1 From the Departments of Radiology (R.S.P., U.K., ARB.) and Neurosurgery (A.M.), New York University Medical Center, New York. N.Y. Received July 25, 1978; accepted and revision requested Oct. 31; revision received Jan. 23, 1979. Presented at the Sixteenth Annual Meeting of the American Society of Neuroradiology, New Orleans, La., Feb. 26-March 3, 1978. sjh
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TABLE 1: Patient
Presenting Signs and Symptoms
1. Dementia, blindness in left eye, right temporal field cut 2. Palsy of right third nerve 3. Headaches, seizures
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FINDINGS IN 21 PATIENTS WITH GIANT ANEURYSMS
Location (Artery)
Pre-contrast
Right cavernous carotid
CT Scan Post-contrast
Isodense; peripheral calcification
Completely thrombostic
No enhancement
Erosion of the carotid sulcus Negative
Completely thrombostic
4. Palsy of third, fourth, and sixth nerves
Left cavernous carotid
Homogeneous enhancement
5. Subarachnoid hemorrhage 6. Frontal headaches
Hyperdense Anterior communicating Right ophthalmic Hyperdense with calcification
7. Headaches, diplopia
Left carotid bifurcation Right middle cerebral Left posterior cerebral
Hyperdense Hyperdense Centrally isodense with hyperdense ring Hyperdense
10. Diplopia, swirling noise in the right ear 11. Dysphagia, retro-orbital pain
Right cavernous carotid Left middle cerebral
12. Diplopia
Right cavernous carotid
13. Diplopia, palsy of the right third nerve 14. Palsy of the third nerve
16. Subarachnoid hemorrhage
Right cavernous carotid Right cavernous Hyperdense carotid Right posterior Hyperdense communicating Left middle Hyperdense with cerebral calcification
17. Diplopia on the left, lateral rectus paresis 18. Sabarachnoid hemorrhage 19. Dementia
Left canvernous carotid Vertebrobasilar junction Basilar
20. Subarachnoid hemorrhage
Left ophthalmic
21. Diplopia
Left ophthalmic
15. Seizures
TABLE II:
Hyperdense with calcification Isodense, with hyperdense ring and calcification Hyperdense
Hyperdense Hyperdense Centrally isodense, with peripheral calcification Eccentric peripheral hyperdense region; calcification Homogeneous, hyperdense
LOCATION OF 21 GIANT CEREBRAL ANEURYSMS
Location Cavernous carotid artery Supraclinoid carotid artery Internal carotid near the origin of the ophthalmic artery Internal carotid near the origin of the posterior communicating artery Bifurcation of the internal carotid Trifurcation of the middle cerebral artery Vertebrobasilar arteries Posterior cerebral artery Anterior communicating artery
No. of Patients
8 6 3 2
3 3 1 1
Angiogram
Calcification
Homogeneous enhancement
Hyperdense
Plain Radiograph
Homogeneous
Right cavernous Hyperdense carotid Right posterior Isodense communicating
8. Subarachnoid hemorrhage 9. Subarachnoid hemorrhage
July 1979
Homogeneous enhancement Luminal and peripheral enhancement Homogeneous enhancement Homogeneous enhancement Peripheral enhancement
Erosion of the superior orbital fissure Negative
Thin-walled aneurysm 16 %mmult 10 X 10mm Thin-walled aneurysm
Negative
Thin-walled aneurysm 10 X 10 X 10 mm Thin-walled aneurysm
Negative
Thin-walled aneurysm
Negative
Thin-walled aneurysm
Negative
Completely thrombotic aneurysm
Homogeneous enhancement Luminal and peripheral enhancement Peripheral enhancement
Negative
Thin-walled aneurysm
Calcification
Partially aneurysm thrombotic
Negative
Central enhancement Homogeneous enhancement Not done
Negative
partially thrombotic aneurysm with recanalization Partially thrombotic aneurysm Thin-walled aneurysm
Central and peripheral enhancement Homogeneous enhancement Homogeneous enhancement No enhancement
Erosion of the carotid sulcus Negative Calcification
Partially thrombotic aneurysm Partially thrombotic aneurysm
Negative
Thin-walled aneurysm
Negative
Thin-walled aneurysm
Negative
Completely thrombotic aneurysm
Eccentric peripheral Calcification enhancement
Partially thrombotic aneurysm
Homogeneous enhancement
Thin-walled aneurysm
Negative
seen in all 5 (Fig. 2, b). No edema was observed. One patient (CASE 11) exhibited a nonenhanced lucent area adjacent to the aneurysm; however, biopsy demonstrated cerebral gliosis, probably due to an old infarction. Angiography and CT differed markedly as to the size of the aneurysm (Fig. 2, c and d). Angiography demonstrated only the lumen, whereas CT revealed luminal thrombosis and the thickened wall. Angiography demonstrated a local mass in all cases but did not show a peripheral blush corresponding to the hyperdense ring seen on the postcontrast scan. One aneurysm (CASE 12) was isodense centrally and hyperdense peripherally on the pre-contrast
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Fig. 1. Nonthrombotic, thin-walled giant aneurysm. a. Pre-contrast scan demonstrates an ill-defined hyperdense areaobliterating the suprasellar cistern (arrows). b. Contrast enhancement reveals homogeneous uptake by an asymmetric lesion mostly to the left of the midline. e and d. Left internal carotid angiograms in the AP (e) and lateral (d)projections demonstrate a giantaneurysm at the bifurcation of the internal carotid artery. No intraluminal irregularity or thrombosis is observed. After correcting for magnification, the aneurysm is about thesame sizeon both the angiogram and the CTscan.
1e ,d
scan (Fig. 3, a); tollowing contrast infusion the hyperdense region was prominentiy enhanced (Fig. 3, b). Angiography (Fig. 3, c and d) revealed that th is finding represented a reformed channel through an almost completely thrombotic aneurysm. Routine skull radiographs showed discernible intracranial calcifications iri 2 of 5 patients; they were curvilinear in one patient and amorphous and nodular in the other. Completely Thrombotic Aneurysms (4 cases): These aneurysms exhibited a distinctive ring-shaped hyperdense region on the initial scan which was enhanced by contrast infusion. No central or eccentric enhancement or edema was seen (Fig . 4, a and b). Angiography demonstrated a focal mass without filling of the lumen in all 4 cases (Fig . 4, e and f). The diagnosis was made at surgery in CASE 1, autopsy in CASE 19, and demonstration of recanalization on an angiogram obtained one year earlier in CASE 9 (Fig. 4, c and d); it is unproved in CASE 2 except for typical plain radiographic changes of erosion of the carotid sulcus and absence of contrast enhancement on CT .
Neuropathological Findings: Microscopic examination of five partially thrombotic giant aneurysms revealed that the intraluminal thrombus was moderately vascular and lacked calcification. The aneurysmal wall consisted of markedly thickened fibrous connective tissue with prominent blood vessels and focal areas of calcification (Fig. 5). DISCUSSION
Thin-walled aneurysms appear slightly hyperdense on pre-contrast scans and exhibit a homogeneous increase in density following contrast infusion. This is easily explained on the basis of the hyperdense blood pool which is subsequently opacified by circulating iodinated contrast material (12-14) (Fig. 1, a and b), i.e., both the hyperdensity and the subsequent enhancement can be explained on a purely intravascular basis . Partially thrombotic aneurysms are seen on the pre-contrast scan as a central or eccentric hyperdense region within an isodense zone which is in turn
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2a,b
2c,d
Fig. 2. Partially thrombotic giantaneurysm. a. Pre-contrast scan demonstrates a large. bilobate lesionin the left temporofrontal region. with peripheral calcification (arrow). The lesion hasan internal region and a hypderdense peripheral rim. Notethe lack of edema. b. Following contrast lnfusfon. the hyperdense internalregion (i) is homogeneously and markedlyenhanced. as is the periphery of the lesion (p) , while the central area remains isodense ("target" sign). c. Left internal carotid arteriogram(frontal projection) shows an irregular, multilobular middle cerebral artery (MCA) aneurysm corresponding in size and location to the enhanced central areain Figure 2. b. Theaneurysm appears smaller than it did on the CT scan, sinceonlythe intraluminal portion is filled. Theangular border and displacement of the mainbranches of the MCA(arrows) suggest a larger mass. d. The lateral projection demonstrates the temporalmasseffect produced by the thromboticportion of the aneurysm. Notethe irregularity of the luminal wall and the displacement and stretching of the main sylvian branch andtemporal opercularbranches of the MCA(arrows). The peripheralenhancement noted on the CTscan cannotbe seenon the angiogram.
surrounded by a peripheral hyperdense or calcific area. The central and peripheral zones are enhanced by contrast material, whereas the isodense zone is not (Fig. 2, a and b). While the peripheral enhancement cannot be explained angiographically (Fig. 2, c and d), the central enhancement is the result of iodine circulating within the blood pool (13) . The thickened fibrous wall that surrounds the aneurysm is formed from multipotential cells of the adjacent meninges in response to the subarachnoid mass, and hence the prominent vascularity of this layer of granulation tissue is not derived from the brain, nor is a blood-brain barrier present. We believe peripheral enhancement is the result of extravascular diffusion of contrast material into the
vascularized fibrous tissue wall and is analogous to normal contrast enhancement of the dura mater. Of the seven giant aneurysms with peripheral enhancement in our series, one was completely thrombotic (Fig . 4). In CASE 12 the enhancement did not appear to be due to a vascular aneurysmal wall (Fig. 3); rather, the angiogram demonstrated a reformed channel through the periphery of the massive thrombosed aneurysm, corresponding to the enhanced area. On CT, the hyperdense ring varied in thickness before and after contrast infusion and was incompletely enhanced. This is quite different from a fibrous aneurysmal wall, which is of constant thickness and exhibits complete enhancement The peripheral en-
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Fig. 3. Recanalization of a giant aneurysm. a. Pre-contrast scan demonstrates a mass having an isodense central zone and a calcific. slightly hyperdense peripheral zone. No edema is present. b. The post-contrast scan demonstrates a ring pattern of variable thickness, distinguishing it from the peripheral enhancement seen with thrombotic aneurysms. c. Right common carotid angiogram (frontal projection) demonstrates a peripheral channel through a giant aneurysm. The ends of the channel are tapered at its origin from the supraclino id segment of the internal carotid artery. and it terminates at the middle cerebral branches. The stretched anterior temporal artery (indicating a larger mass than the observed aneurysm) and the irregularity of the luminal channel suggest thrombosis. d. The lateral projection again demonstrates the tapered ends of the channel . explaining the variable peripheral enhancement (Fig. 3. b).
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hancement ot the reformed channel was more intense and had a sharper internal interface than that of the fibrous wall. Microscopic examination of partially thrombotic giant aneurysms reveals that the thickened and vascular aneurysmal wall is made up of fibrous connective tissue associated with atrophy of the lamina media and adventitia (Fig. 5). Published microscopic descriptions of ruptured aneurysms demonstrate disruption of the lamina elastica and muscularis, irregular thinning and fibrosis of the adventitia , and thickening of the lamina intima (15). The thickened fibrous wall observed in our microscopic examinations may be peculiar to giant aneurysms and related to a long-standing process: the presence of a mass over a long period of time may stimulate production of fibrous connective tissue. causing the lesion to be encapsulated. It has been hypothesized (16) that thickening of the wall is secondary to subarachnoid hemorrhage. but only 3 of our 6 patients with peripheral enhancement of a thickened fibrous wall had a definite history of bleeding. Two patients without documented hemorrhage had recurrent frontal or retro-orbital pain which may have represented sub-
arachnoid hemorrhage but most likely was the result of traction or pressure by the aneurysm on the tentorium, causing pain to be referred through the fifth nerve fibers (15). Calcification within the wall of the aneurysm (1. 15.17.18) was seen on the pre-contrast scan in 7 patients (Fig. 2, a). including 5 with partially and 2 with completely thrombotic aneurysms. None of the thin-walled aneurysms was calcified. Thus this finding may be useful in predicting thrombosis of a giant aneurysm. Pathological examination showed that calcification develops within the thickened thickened connective tissue layer of the wall , probably secondary to microscopic hemorrhage within this prominently vascular structure. If such bleeding is profuse and disruptive, it may be responsible for the occasional recanalization (CASES 9 and 12) and subarachnoid hemorrhage (CASES 7 and 15). Completely thrombotic giant aneurysms may be a diagnostic problem even after angiography, which frequently demonstrated only an avascular mass (18, 19). Of our 4 patients, only one (CASE 9) had a history of subarachnoid bleeding (Fig. 4). Angiography one year earlier demon-
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Fig. 4. Completely thrombotic giant cerebral aneurysm. a. Pre-contrast scan reveals a large mass with an isodense center and a ring of slight hyperdensity in the left infrathalamic region. There is no edema. The third ventricle is displaced to the right. b. Following contrast infusion, there is prominent peripheral enhancement without internal enhancement. This is different from the ring sign of malignant glioma, metastasis, or abscess. c. Frontal projection from a right brachial angiogram obtained one year earlier demonstrates filling of a posterior cerebral artery (PCA) aneurysm (arrowhead) with an irregular lumen and recanalization . There is a mass effect, seen as displacement of the anterior cerebral artery to the right . d. Early venous phase of the right brachial arteriogram (lateral projection) shows the reformed channel to better advantage(arrows).
strated a reformed channel through the aneurysm; at the time of CT it showed complete thrombosis, and the left posterior cerebral artery was occluded. Two other completely thrombotic aneurysms were confirmed at surgery and postmortem examination, respectively. One case remains unproved. The CT appearance of completely thrombotic aneurysms varied. One (CASE 9) had an isodense center and a slightly hyperdense or calcific peripheral zone with no edema (Fig. 4, a). Following contrast infusion, the scan demonstrated peripheral enhancement of a fibrous wall (Fig. 4, b). A second patient (CASE 1) showed homogeneous contrast enhancement in a surgica11y proved thrombotic aneurysm. There are two possible explanations for this difference: either (a) the section included only the wall of the aneurysm, not the more central isodense thrombus, or (b) revascularization and possibly fibrous
tissue infiltration of the intraluminal thrombus caused the enhancement. Another patient (CASE 19) exhibited prominent calcification of the periphery of the aneurysm but no discernible enhancement. We assume that the calcification was the result of previous bleeding into the highly vascular wall, so that the resultant thrombosis precluded enhancement. Our fourth case (CASE 2) is unproved, but a thrombotic cavernous carotid aneurysm was suspected on the basis of a nonenhanced but slightly hyperdense lesion adjacent to the pituitary fossa, producing focal erosion of the carotid sulcus. The absence of a tumoral blush at angiography and the elevation of the cavernous carotid support this diagnosis. The lack of an enhanced fibrous tissue layer in this patient supports the supposition that arachnoidal irritation is needed for thickening of the connective tissue . The slightly increased density of the lesion on the pre-contrast scan may be the
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e. Selective left vertebral angiogram (frontal projection) obtained at the time of CT(Fig. 3, a and b)reveals occlusion of the left PCA (arrow), aneurysm, and channel. f. The lateralprojection demonstrates a focalthalamic masswith anterior bowing of the left anterior thalamoperforating artery (open arrow)andposterosuperior displacement of both themedial andlateralposterior choroidal arteries (closed arrows). There is no filling of the left PCA, aneurysm, or channel. 5a,b
Fig. 5. a. High-power photomicrograph of the periphery of a giant aneurysm demonstrates a thick layerof granulation tissue with many endothelium-lined vascular channels which do not have the tight junctions of brain vessels. This fibrous layer produces the peripheral enhancement seen in thrombotic aneurysms. (H&E X100) b. High-power photomicrograph of theperiphery of another giant aneurysm shows a thickened layer of fibrous tissue surrounding thelumen (L) and containing many small vessels. The dark purple stain around several small channels represents calcification secondary to microscopic bleeding. result of revascularization or calcification of the intraluminal thrombus or an averaging effect produced by the inclusion of bone within the CT section. Since no discernible enhancement was demonstrated, and since our limited neuropathological study failed to conclusively demonstrate calcification within the intraluminal thrombus, we feel that the latter explanation is more likely. Thus no specific pattern for a completely thrombotic aneurysm was observed in our 4 cases, although a mass with an isodense center with or without peripheral calcification, demonstrating ring enhancement, and lacking edema is highly suspicious. It is very unusual for a primary glioma to have an isodense center within a peripheral zone of enhancement (ring sign) and lack adjacent edema. CT is useful in following up patients who undergo carotid
ligation for a giant aneurysm (Fig. 6). Intraluminal thrombosis is easily assessed by comparing the pre- and postligation scans (Figs. 1 and 6). Since CT is usually performed first in neurological conditions, giant aneurysms are easily detected (12-14). However, they may be mistaken for a neoplasm. When we reviewed our pre-angiographic CT reports, a giant aneurysm was either the prime diagnosis or included in the differential diagnosis in 13 patients, 6 of whom had a clinical history of subarachnoid hemorrhage which may be assumed to influence the diagnosis. In 3 patients, curvilinear peripheral calcification prompted consideration of a giant aneurysm. Of the cases in which a giant aneurysm was not initially suggested, 6 tumors were diagnosed as a meningioma (CASES 4, 10, 14, 15, 17, and 21), one
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Completely thrombotic giant aneurysms lack the central or eccentric zone of hyperdensity and corresponding enhancement. No discernible CT pattern was observed in our small series of patients; however, a mass with an isodense center, with or without peripheral calcification, not surrounded by a zone of edema, and with a ring-shaped zone of enhancement would suggest a completely thrombotic aneurysm . REFERENCES
Fig. 6. Same case as in Fig. 1, a and b, showing the effect of carotid ligation on a nonthrombotic giant aneurysm. a. Pre-contrast scan one week after ligation demonstrates a hyperdense midline area with an adjacent isodense zone representing intraluminal thrombosis (arrow) which was not present on the preoperative study. b. Internal enhancement (i) represents the intraluminal portion of the aneurysm. The isodense region represents partial thrombosis. There is also peripheral enhancement (p) of the fibrous wall.
as a pituitary adenoma with suprasellar extension (CASE 7), one as a chordoma (CASE 19), and one as a glioma (CASE 11). A parasellar location, hyperdensity on the pre-contrast scan, calcification, and prominent enhancement all simulate meningioma, especially in patients with thin-walled aneurysms of the cavernous or supraclinoid carotid (CASES 4,7, 10, 14, 17, and 21). However, the lack of edema should rule out meningioma or malignant glioma. SUMMARY AND CONCLUSIONS
CT scanning is highly reliable in the detection of intracranial masses and may suggest a giant aneurysm prior to angiography. Difficulty may arise with thin-walled aneurysms, since the slight hyperdensity of the lesion on the pre-contrast scan and homogeneous enhancement by contrast material may simulate a meningioma. Proximity to the circle of Willis or major intracranial vessels and absence of edema should suggest a thin-walled aneurysm. The CT signs of partially thrombotic aneurysms are highly specific, consisting of (a) a central or eccentric zone of slight hyperdensity, representing the intraluminal component, surrounded by (b) an isodense zone, representing the thrombotic portion, and (c) a peripheral zone of increased density, representing a layer of fibrous tissue ("target" sign). Following contrast infusion, the central and peripheral zones will both be enhanced. The presence of curvilinear wall calcification and the absence of edema support the diagnosis of a partially or completely thrombotic giant aneurysm.
1. Bull J: Massive aneurysms at the base of the brain. Brain 92:535-570, 1969 2. Heiskanen 0 , Nikki P: Large intracranial aneurysms . Acta Neurol Scand 38:195-208, 1962 3. Jefferson G: Compression of the chiasma , optic nerves. and optic tracts by lntracranial aneurysms. Brain 60:444-497, Dec 1937 4. Morley TP, Barr HWK: Giant intracranial aneurysms: diagnosis, course, and management. Clin Neurosurg 16:73-94, 1969 5. Obrador S, Dierssen G, Rodriguez Hernandez J: Giant aneurysm of the posterior cerebral artery . Case report . J Neurosurg 26: 413-416,Apr1967 6. Polis Z, Brzezinski J, Choclak-Gajewicz M: Giant intracranial aneurysm. Case report. J Neurosurg 39:408-411, Sep 1973 7. Rischbieth RHC. Bull JWD: The significance of enlargement of the superior orbital (sphenoidal) fissure. Br J Radiol 31:125-135, Mar 1958 8. Sadik AR, Budzilovich GN, Shulman K: Giant aneurysm of middle cerebral artery : a case report. J Neurosurg 22: 177-181, Feb 1965 9. Sarwar M, Batnitzky S, Schechter MM, et al: Growing intracranial aneurysms. Radiology 120:603-607, Sep 1976 10. White JC, Ballantine HT Jr: Intrasellar aneurysms simulating hypophyseal tumours. J Neurosurg 18:34-50. Jan 1961 11. Sarwar M, Batnitzky S, Schechter MM: Tumorous aneurysms. Neuroradiology 12:79-97, 11 Nov 1976 12. Davis KR, New PFJ, Ojemann RG, et al: Computed tomographic evaluation of hemorrhage secondary to intracranial aneurysms. Am J RoentgenoI127:143-153, Jul1976 13. Pressman BO, Gilbert GE, Davis DO: Computerized transverse tomography of vascular lesions of the brain. Part II: Aneurysms. Am J RoentgenoI124:215-219, Jun 1975 14. Scotti G, Ethier R, Melal)yon D, et al: Computed tomography in the evaluation of intracranial aneurysms and subarachnoid hemorrhage . Radiology 123:85-90, Apr 1977 15. Pool LJ, Potts DG: Aneurysms and Arteriovenous Anomalies of the Brain. Diagnosis and Treatment. New York, Harper & Row, 1965, pp 47-48 16. Cravioto H: Personal communication 17. Bull JWD: Contribution of radiology to the study of intracranial aneurysms . Br Med J 2:1701-1708,29 Dec 1962 18. Schunk H: Spontaneous thrombosis of intracranial aneurysms. Am J RoentgenoI91:1327-1338, Jun 1964 19. Lukin RR, Chambers AA, Mclaurin R, et al: Thrombosed giant middle cerebral aneurysms. Neuroradiology 10:125-129, 19 Dec 1975
Department of Radiology Section of Neuroradiology New York University Medical Center 560 First Ave. New York, N.Y. 10016
