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Non-Atherosclerotic Fusiform Cerebral Aneurysms

  • J. Max Findlay (a1), Chunhai Hao (a2) and Derek Emery (a3)

Abstract

Background:

Fusiform cerebral aneurysms are dilatations of the entire circumference of a segment of cerebral artery, usually considered due to atherosclerosis in adults. They are relatively thick-walled and elongated, causing neural compression or ischemia when discovered. We have noted a subset of fusiform cerebral aneurysms that vary from this common description.

Patients:

Out of a series of 472 intracranial aneurysms treated over 11 years, 11 patients between the ages 16 and 67 years (mean age 37) were identified who had discrete fusiform aneurysms unassociated with generalized cerebral atherosclerosis, connective tissue disorder or inflammation. Three presented with hemorrhage, six with neural compression by the aneurysm and two were discovered incidentally.

Results:

Nine aneurysms were located in the posterior circulation, the other two in the intracranial carotid artery. Their mean length and width were 16.3 and 11 mm, respectively. Three aneurysms contained thrombus. The eight aneurysms that were exposed surgically were partly or substantially thin-walled with normal appearing parent arteries. Eight were treated with proximal occlusion and three were circumferentially “wrapped”. Parent artery occlusion caused one death and one mild disability and the remaining patients made good recoveries (follow-up 0.5 - 10 years).

Conclusions:

There is a subset of cerebral aneurysms with discrete fusiform morphology, apparently unrelated to cerebral atherosclerosis or systemic connective tissue disease, thin-walled in part or whole, more common in the vertebrobasilar system, and possessing a risk of rupture. Treatments currently available include proximal occlusion or aneurysm “wrapping”, different approaches than neck-clipping or endovascular coiling of side-wall saccular cerebral aneurysms that leave the parent artery intact.

RÉSUMÉ: Introduction:

Les anévrismes cérébraux fusiformes sont des dilatations de toute la circonférence d'un segment d'artère cérébrale, habituellement attribuées à l'athérosclérose chez les adultes, avec une paroi relativement épaisse et allongée, causant des compressions nerveuses ou de l'ischémie lors du diagnostic. Nous avons observé un sous-groupe d'anévrismes cérébraux fusiformes qui diffère de cette description générale.

Patients:

Dans une série de 472 anévrismes intracrâniens traités sur une période de 11 ans, 11 patients entre l'âge de 16 et 67 ans (âge moyen 37 ans) ayant des anévrismes fusiformes discrets non associés à une athérosclérose cérébrale généralisée, à des maladies du tissu conjonctif ou à une maladie inflammatoire, ont été identifiés. Trois patients ont présenté une hémorragie, six une compression neurologique due à l'anévrisme et deux ont été découverts fortuitement.

Résultats:

Neuf anévrismes étaient localisés au niveau de la circulation postérieure, les deux autres dans la carotide intracrânienne. Leur longueur et leur largeur moyennes étaient de 16.3 et 11 mm respectivement. Trois anévrismes contenaient un thrombus. Les huit anévrismes qui ont été explorés chirurgicalement étaient en tout ou en partie des anévrismes à paroi mince et l'artère qui y avait donné naissance était d'apparence normale. Huit ont été traités au moyen d'une occlusion proximale et trois ont été “enveloppés”. L'occlusion de l'artère mère a provoqué un décès et un cas d'invalidité légère; les autres patients ont bien récupéré (suivi de 0.5 à 10 ans).

Conclusions :

Certains anévrismes cérébraux ont une morphologie fusiforme discrète, ne sont apparemment pas en relation avec une athérosclérose cérébrale ou une maladie systémique du tissu conjonctif, ont une paroi mince en tout ou en partie, sont plus fréquents au niveau du système vertébrobasilaire et sont à risque de rupture. Les traitements disponibles présentement sont l'occlusion proximale ou l'enveloppement de l'anévrisme, des approches différentes de la pose d'un clip ou d'une prothèse endovasculaire au niveau des anévrismes cérébraux sacculaires dont l'artère mère est intacte.

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References

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1. Boeri, R, Passerini, A. The megadolichobasilar anomaly. J Neurol Sci 1964;1:476484.
2. Sacks, J, Linderberg, R. Dolichoectatic intracranial aneurysms. JohnsHopkins Med J 1969;125:95106.
3. Nishizaki, T, Tamaki, N, Takeda, N, et al. Dolichoectatic basilarartery: a review of 23 cases. Stroke 1986;17:12771281.
4. Echiverri, HC, Rubino, FA, Gupta, SR,Gujrati, M. Fusiform aneurysmof the vertebrobasilar arterial system. Stroke 1989;20:17411747.
5. Pessin, MS, Chimowitz, MI, Levine, SR, et al. Stroke in patients withfusiform vertebrobasilar aneurysms. Neurology 1989;39:1621.
6. Shokunbi, MT, Vinters, HV, Kaufmann, JCE. Fusiform intracranialaneurysms. Surg Neurol 1988;29:263270.
7. Weir, BKA. Special Aneurysms (nonsaccular and saccular). In:Brown, CL, Eckhart, C, eds.Aneurysms Affecting the Nervous System: Williams & Wilkins, 1987:134208.
8. Schievink, WI, Michels, VV, Piepgras, DG. Neurovascularmanifestations of heritable connective tissue disorders. A review. Stroke 1994;25:889903.
9. Stehbens, WE. Etiologyof intracranial berry aneurysms. JNeurosurg 1989;70:823831.
10. Ferguson, GF. Physical factors in the initiation, growth, and ruptureof humanintracranialsaccular aneurysms. J Neurosurg 1972;37:666677.
11. Hayes, W, Bernhardt, H, Young, J. Fusiform arteriosclerotic aneurysmof the basilar artery. Vasc Surg 1967;1:171178.
12. Deeb, Z, Jannetta, P, Rosebaum, A, Kerber, C, Drayer, B. Tortuousvertebrobasilar arteries causing cranial nerve syndromes: screening by computed tomography. J Comp Ass To mog 1979;3:774778.
13. Waga, S, Morikawa, A, Kojima, T. Trigeminal neuralgia: compressionof the trigeminal nerve by an elongated and dilated basilar artery. Surg Neurol 1979;11:1315.
14. Gibson, W, Wallace, D. Basilar artery ectasia. An unusual cause of acerebello-pontine lesion and hemifacial spasm. J Laryng Otol 1975;89:721731.
15. Nakatomi, H, Segawa, H, Kurata, A, et al. Clinicopathological studyof intracranial fusiform and dolichoectatic aneurysms. Stroke 2000;31:896900.
16. Vinters, HV. Pathology of cervical and intracranial atherosclerosisand fibromuscular dysplasia. In: Hunt Batjer, H, ed. CerebrovascularDisease. Philadelphia: Lippincott-Raven, 1997:4151.
17. Vale, F, Hadley, MN. Pathology of intracranial aneurysms andvascular malformations. In:Hunt Batjer, H. ed. Cerebrovascular Disease. Philadelphia: Lippincott-Raven, 1997:65-77.
18. Muhonen, MG, Godersky, JC, VanGilder, JC. Cerebral aneurysmsassociated with neurofibromatosis. Surg Neurol 1991;36:470475.
19. Guha, A, Montanera, W, Hoffman, HJ. Congenital aneurysmaldilatation of the petrous-cavernous carotid artery and vertebral basilar junction in a child. Neurosurgery 1990;26:322327.
20. Sasaki, O, Ogawa, H, Koike, T, Koizumi, T, Tanaka, R. Aclinicopathological study of dissecting aneurysms of the intracranial vertebral artery. J Neurosurg 1991;75:874882.
21. Mizutani, T, Miki, Y, Kojima, H, Suzuki, H. Proposed classification ofnon-atherosclerotic cerebral fusiform and dissecting aneurysms. Neurosurgery 1999;45:253259.
22. Mizutani, T, Kojima, H. Clinicopathological features of non-atherosclerotic cerebral arterial trunk aneurysms. Neuropathology 2000;20:9197.
23. Haddad, FS, Haddad, GF, Taha, J. Traumatic intracranial aneurysmscausedby missiles:their presentation and management. Neurosurgery 1991;28:107.
24. Murata, J, Sawamura, Y, Takahashi, A, Abe, H, Saitoh, H. Intracerebralhemorrhage caused by a neoplastic aneurysm from small-cell lung carcinoma: case report. Neurosurgery 1993;1:124126.
25. Furuya, K, Sasaki, T, Yoshimoto, Y, Kirinio, T. Histologically verifiedcerebral aneurysm formation secondary to embolism from cardiac myxoma. J Neurosurg 1995;83:170173.
26. Hashimoto, N, Handa, H, Taki, W. Ruptured cerebral aneurysms inpatients with systemic lupus erythematosus. Surg Neurol 1986;26:512516.
27. Sasaki, T, Morimoto, T, Utsumi, S. Cerebral transmural angiitis andruptured cerebral aneurysms in patients with systemic lupus erythematosus. Neurochir 1990;33:132135.
28. Venger, BH, Aldama, AE. Mycotic vasculitis with repeatedintracranial aneurysmal hemorrhage. J Neurosurg 1988;69:775779.
29. Brust, JCM, Dickinson, PCT, Hughes, JEO, Holtzman, RNN. Thediagnosis and treatment of cerebral mycotic aneurysms. AnnNeurol 1990;27:238246.
30. Kurino, M, Kuratsu, J, Yamaguchi, T, Ushio, Y. Mycotic aneurysmaccompanied by aspergillotic granuloma: a case report. SurgNeurol 1994;42:160164.
31. Barami, K, Ko, K. Ruptured mycotic aneurysm presenting as anintraparenchymal hemorrhage and nonadjacent acute subdural hematoma: case report and review of the literature. Surg Neurol 1994;41:290293.
32. Scodary, DJ, Tew, JM Jr, Thomas, GM, Tomsick, TH, Liwnicz, BH. Radiation-induced cerebral aneurysms. Acta Neurochir 1990;102:141144.
33. Drake, CG, Peerless, SJ. Giant fusiform intracranial aneurysms:review of 120 patients treated surgically from 1965 to 1992. J Neurosurg 1997;87:141162.
34. Kumabe, T, Kaneko, U, Ishibashi, T, Kaneko, K, Uchigasaki, S. Twocases of giant serpentine aneurysm. Neurosurgery 1990;26:10271033.
35. Isla, A, Alvarez, F, Roda, JM, et al Serpentine aneurysm: regrowthafter a superficial temporal artery-middle cerebral artery bypass and internal carotid artery ligation. Neurosurgery 1994;34:10721074.
36. Horowitz, MB, Yonas, H, Jungreis, C, Hung, TK. Management of agiant middle cerebral artery fusiform serpentine aneurysm with distal clip application and retrograde thrombosis: case report and review of the literature. Surg Neurol 1994;41:221225.
37. Bederson, JB, Zabramski, JM, Spetzler, RF. Treatment of fusiformintracranial aneurysms by circumferential wrapping with clip reinforcement. Technical note. J Neurosurg 1992;77:478480.
38. Anson, JA, Lawton, MT, Spetzler, RF. Characteristics and surgicaltreatment of dolichoectatic and fusiform aneurysms. J Neurosurg 1996;84:185193.
39. Jennett, B, Bond, M. Assessment of outcome after severe braindamage. A practical scale. Lancet 1975;1:480484.

Non-Atherosclerotic Fusiform Cerebral Aneurysms

  • J. Max Findlay (a1), Chunhai Hao (a2) and Derek Emery (a3)

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