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Giant intracranial aneurysms: morphology and clinical presentation

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Abstract

The purpose of this study was to correlate the morphology of giant intracranial aneurysms (GIA) with their clinical presentation. Eighty patients with GIA, 14 males and 66 females, were studied. Univariate and multivariate analyses were made to test the associations between morphological and clinical features. The main locations of the unruptured GIA included the carotid cavernous segment, and for the ruptured GIA, the most frequent were the carotid supraclinoid and middle cerebral arteries. There was a significant association among communicating arteries (CA) of “bad” quality and presence of thrombus and calcification (TC). The risk of rupture is 8 times higher in patients with CA of “bad” quality and 11 times higher in patients without TC. GIA are more frequent in the cavernous segment. There is a high rupture risk in the middle cerebral artery. CA of “bad” quality are associated with TC. The rupture risk is significantly higher in patients without TC.

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References

  1. Andrews RJ, Spiegel PK (1979) Intracranial aneurysms: age, sex, blood pressure and multiplicity in an unselected series of patients. J Neurosurg 51:27

    Article  PubMed  CAS  Google Scholar 

  2. Barrow DL, Alleyne C (1995) Natural history of giant intracranial aneurysms and indications for intervention. Clin Neurosurg 42:214–244

    PubMed  CAS  Google Scholar 

  3. Barth A, Tribolet N (1994) Growth of small saccular aneurysms to giant aneurysms: presentation of three cases. Surg Neurol 41:277–280

    Article  PubMed  CAS  Google Scholar 

  4. Battaglia R, Pasqualin A, Da Pian R (1988) Italian cooperative study on giant intracranial aneurysms: 1. Study design and clinical data. Acta Neurochir Suppl (Wien) 42:49–52

    Article  CAS  Google Scholar 

  5. Berenstein A, Lasjaunias P, ter Brugge K (2004) Surgical neuroangiography. 2 Clinical and endovascular treatment aspects in adults. Springer, Berlin

    Google Scholar 

  6. Bonilha L, Marques EL, Carelli EF et al (2001) Risk factors and outcome in 100 patients with aneurysmal subarachnoid hemorrhage. Arq Neuropsquiatr 59:676–680

    Article  CAS  Google Scholar 

  7. Cho YD, Park JC, Kwon BJ, Hee Han M (2010) Endovascular treatment of largely thrombosed saccular aneurysms: follow-up results in ten patients. Neuroradiology 52(8):751–758

    Article  PubMed  Google Scholar 

  8. Choi IS, David C (2003) Giant intracranial aneurysms: development, clinical presentation and treatment. Eur J Radiol 36:178–194

    Article  Google Scholar 

  9. Cordeiro JA (1987) Analysis of dependency. Relatório Técnico 48/87. Instituto de Matemática–Unicamp, Campinas

    Google Scholar 

  10. Dashti R, Hernesniemi J, Niemelä M et al (2007) Microneurosurgical management of distal middle cerebral artery aneurysms. Surg Neurol 67:553–563

    Article  PubMed  Google Scholar 

  11. Dimmick SJ, Faulder KC (2009) Normal variants of the cerebral circulation at multidetector CT angiography. RSNA 29:1027–1043

    Google Scholar 

  12. Drake CG (1979) Giant intracranial aneurysms: experience with surgical treatment in 174 patients. Clin Neurosurg 26:12–95

    PubMed  CAS  Google Scholar 

  13. Gonzalez NR, Duckwiler G, Jahan R, Murayama Y, Viñuela F (2006) Challenges in the endovascular treatment of giant intracranial aneurysms. Neurosurgery 59:S113–S124

    Article  PubMed  Google Scholar 

  14. Juvela S, Porras M, Poussa K (2008) Natural history of unruptured intracranial aneurysms: probability of and risk factors for aneurysm rupture. J Neurosurg 108:1052–1060

    Article  PubMed  Google Scholar 

  15. Kato Y, Sano H, Imizu S et al (2003) Surgical strategies for treatment of giant or large intracranial aneurysms: our experience with 139 cases. Minim Invasive Neurosurg 46:339–343

    Article  PubMed  CAS  Google Scholar 

  16. Lasjaunias P, Berenstein A, ter Brugge KG (2001) Surgical neuroangiography. 1 Clinical vascular anatomy and variations. Springer, Berlin

    Google Scholar 

  17. Locksley HB (1966) Natural history of subarachnoid hemorrhage, intracranial aneurysms malformations: based on 6368 cases in the cooperative. J Neurosurg 25:219–239

    Article  PubMed  CAS  Google Scholar 

  18. Morley TP, Barr HW (1969) Giant intracranial aneurysms: diagnosis, course, and management. Clin Neurosurg 16:73–94

    PubMed  CAS  Google Scholar 

  19. Nakase H, Shin Y, Kanemoto Y, Ohnishi H, Morimoto T, Sakaki T (2006) Long-term outcome of unruptured giant cerebral aneurysms. Neurol Med Chir 46:379–386

    Article  Google Scholar 

  20. Nixon AM, Gunel M, Sumpio BE (2010) The critical role of hemodynamics in the development of cerebral vascular disease. J Neurosurg 11:1240–1253

    Google Scholar 

  21. Ostergaard JR, Hog E (1985) Incidence of multiple intracranial aneurysms: influence of arterial hypertension and gender. J Neurosurg 63:49

    Article  PubMed  CAS  Google Scholar 

  22. Piepgras DG, Khurana VG, Whisnant JP (1998) Ruptured giant intracranial aneurysms. Part II. A retrospective analysis of timing and outcome of surgical treatment. J Neurosurg 88:430–435

    Article  PubMed  CAS  Google Scholar 

  23. Santos MLT, Demartini Z Jr, Matos LAD, Borges MA, Spotti AR, Tognola WA (2008) Radiculopathy due to iatrogenic fistula between subclavian artery and internal jugular vein. Clin Neurol Neurosurg 110:80–82

    Article  PubMed  Google Scholar 

  24. Santos MLT, Demartini Z Jr, Matos LAD et al (2009) Angioarchitecture and clinical presentation of brain arteriovenous malformations. Arq Neuropsiquiatr 67:316–321

    Article  PubMed  Google Scholar 

  25. Sharma BS, Gupta A, Ahmad FU, Suri A, Mehta VS (2008) Surgical management of giant intracranial aneurysms. Clin Neurol Neurosurg 110:674–681

    Article  PubMed  Google Scholar 

  26. Spotti AR, Lima EG, Santos MLT, Magalhães ACA (2001) Angiografia pela ressonância magnética nos aneurismas intracranianos. Arq Neuropsiquiatr 59:384–389

    Article  PubMed  CAS  Google Scholar 

  27. van Rooij WJ, Sluzewski M (2009) Endovascular treatment of large and giant aneurysms. AJNR 30:12–18

    Article  PubMed  Google Scholar 

  28. Vates GE, Zabramski JM, Spetzler RF, Lawton MT (2004) Intracranial aneurysms. In: Mohr JP, Choi DW, Grotta JC (eds) Stroke: pathophysiology, diagnosis, and management, 4th edn. Churchill Livingstone, Philadelphia, pp 1279–1335

    Google Scholar 

  29. Viñuela F, Fox A, Chang JK, Drake CG, Peerless SJ (1984) Clinico-radiological spectrum of giant supraclinoid internal carotid artery aneurysms: observations in 93 cases. Neuroradiology 26:93–99

    Article  PubMed  Google Scholar 

  30. Wiebers DO, Whisnant JP, Huston J 3rd et al (2003) Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet 362:103–110

    Article  PubMed  Google Scholar 

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Acknowledgments

We would like to thank Prof. José A. Cordeiro, PhD, for statistical assistance and Prof. Renato B. Araujo, PhD, for assistance with data analysis and manuscript preparation.

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Authors and Affiliations

  1. Department of Neurological Sciences, Medical School of São José do Rio Preto, São José do Rio Preto, SP, Brazil

    Marcio L. Tostes dos Santos, Antonio Ronaldo Spotti, Moacir Alves Borges & Waldir Antônio Tognola

  2. Neuropsychology Diagnostic and Treatment Center, São José do Rio Preto, SP, Brazil

    Rosangela M. Tostes dos Santos

  3. Department of Neurosurgery, Medical School of Presidente Prudente, Presidente Prudente, SP, Brazil

    Antonio Fernandes Ferrari

  4. Division of Neurosurgery, Department of Surgery, Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil

    Benedicto Oscar Colli

  5. Unit of Vascular and Endovascular Neurosurgery, Service of Neurosurgery, Hospital de Base of São José do Rio Preto, Avenida Brig. Faria Lima 5544, São José do Rio Preto, SP, Brazil, 15090-000

    Marcio L. Tostes dos Santos

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  1. Marcio L. Tostes dos Santos
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  2. Antonio Ronaldo Spotti
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Correspondence to Marcio L. Tostes dos Santos.

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Comments

Yavor Enchev, Varna, Bulgaria

Santos et al. analyzed the correlation between the morphology of GIA with their clinical presentation in a series of 80 patients. They applied univariate and multivariate statistical tests. Expectedly, most frequently, the unruptured GIA were located at the carotid cavernous segment and the ruptured GIA at the carotid supraclinoid and middle cerebral arteries. 
The authors found out that the risk of rupture is 8 times higher in patients with CA of the so-called “bad” quality and 11 times higher in patients without TC. At this point, by my opinion, there exists a very interesting discrepancy between both facts: first, that the risk of rupture is eight times higher in patients with CA of the so-called “bad” quality and, second, the statement that “there was a significant association, suggesting that deficiency patterns of communicating arteries are related to the formation of thrombus and calcification, possibly related to unidirectional flow patterns [11, 20],” page number 7 in the manuscript. So, the so-called “bad” quality of CA is beneficial for the TC formation, which is protective, but at the same time, it is associated with several times higher risk for rupture. The analysis of this fact, unfortunately not obtainable in the paper, probably will be an object of future studies. Why in some patients the CA of the so-called “bad” quality caused GIA rupture and in other patients are related with TC formation seems to be an intriguing unanswered question. 
Other important authors' conclusions were that GIA are more frequent in the cavernous segment and that there is a high rupture risk in the middle cerebral artery.

Divaldo Camara Junior, Recife, Brazil

The authors presented an excellent paper with valuable information regarding giant intracranial aneurysms. It can be inferred from the data presented that the risk of rupture is higher in bad-quality communicating arteries. The latter were also significantly associated with presence of thrombus and calcification. On the other hand, the risk of rupture of GIA is 11 times higher in patients without thrombus and calcification. Therefore, other studies are necessary to precisely evaluate the risk of rupture and understand the role of the aforementioned three parameters (quality, thrombus/calcification, status of rupture) as well as other morphological features of GIA. Whether the term “good- and bad-quality arteries” will be of practical use is a matter for the future.

Kazuhiro Hongo, Matsumoto, Japan

This is a paper on the relation of the morphology and clinical presentation of the giant intracranial aneurysms. They concluded that giant intracranial aneurysm in the region of the middle cerebral artery showed high risk of rupture and that with regard to vascular pattern of communicating arteries, these arteries are associated with presence of thrombus and calcification. Also, they mentioned that the rupture risk is significantly higher in patients without thrombus and calcification in relation to those with thrombus and calcification.

They conducted meticulous analyses using univariate and multivariate statistical tests. The results seem quite reasonable. To select an appropriate treatment option in each patient with a giant intracranial aneurysm, a detailed neuroimaging study should be examined; however, the information the authors demonstrated must be useful to know the behavior of the giant aneurysm in general.

NSR-09-11-0180.R1

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dos Santos, M.L.T., Spotti, A.R., dos Santos, R.M.T. et al. Giant intracranial aneurysms: morphology and clinical presentation. Neurosurg Rev 36, 117–122 (2013). https://doi.org/10.1007/s10143-012-0407-0

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  • DOI: https://doi.org/10.1007/s10143-012-0407-0

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