Letters to the Editor / Clinical Neurology and Neurosurgery 131 (2015) 86–91 [16] Flickinger JC, Kondziolka D, Lunsford LD, Kassam A, Phuong LK, Liscak R, et al. Development of a model to predict permanent symptomatic postradiosurgery injury for arteriovenous malformation patients. Arteriovenous Malformation Radiosurgery Study Group. Int J Radiat Oncol Biol Phys 2000;46(5):1143–8. [17] Buell TJ, Ding D, Starke RM, Webster Crowley R, Liu KC. Embolizationinduced angiogenesis in cerebral arteriovenous malformations. J Clin Neurosci 2014;21(11):1866–71. [18] Moftakhar P, Hauptman JS, Malkasian D, Martin NA. Cerebral arteriovenous malformations. Part 1: Cellular and molecular biology. Neurosurg Focus 2009;26(5):E10. [19] Gunel M, Awad IA, Finberg K, Anson JA, Steinberg GK, Batjer HH, et al. A founder mutation as a cause of cerebral cavernous malformation in Hispanic Americans. N Engl J Med 1996;334(15):946–51. [20] Maddaluno L, Rudini N, Cuttano R, Bravi L, Giampietro C, Corada M, et al. EndMT contributes to the onset and progression of cerebral cavernous malformations. Nature 2013;498(7455):492–6. [21] Walker EJ, Su H, Shen F, Choi EJ, Oh SP, Chen G, et al. Arteriovenous malformation in the adult mouse brain resembling the human disease. Ann Neurol 2011;69(6):954–62.

Dale Ding ∗ University of Virginia, Department of Neurosurgery, Charlottesville 22908, USA ∗ Correspondence to: University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, VA 22908, USA. Tel.: +1 434 924 2203; fax: +1 434 982 5753. E-mail address: [email protected]

5 November 2014 Available online 28 January 2015 http://dx.doi.org/10.1016/j.clineuro.2015.01.019

Posterior fossa arteriovenous malformations: Effect of infratentorial location on outcomes after intervention Keywords: Arteriovenous malformations Embolization Intracranial hemorrhages Posterior fossa Stroke

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Table 1 Composition of supplementary AVM grading scale. Factor Patient age Prior AVM hemorrhage AVM nidus morphology

Score in supplementary grading scale 40 years: 3 points Yes: 0 points No: 1 point Compact: 0 points Diffuse: 1 point

Although cerebellar and brainstem AVMs are both located in the posterior fossa, the approaches to their management are notably divergent. Specifically, cerebellar AVMs are surgically favorable lesions, due to the relatively robust neurological tolerance for injury to the cerebellar hemisphere, whereas brainstem AVMs are technically challenging to safely resect and, thus, are generally relegated to treatment with radiosurgery or conservative management [2–11]. The role of embolization is primarily for pre-surgical devascularization or pre-radiosurgical volume reduction. However, its effects on subsequent interventions are incompletely defined [12–18]. Prior studies have shown that the supplementary grading scale (Table 1) may be more accurate than the Spetzler–Martin grading system for predicting the surgical outcomes for cerebellar AVMs [9,19]. The anatomy of the posterior fossa is unique, and thus, AVMs in this region are distinct from those in the supratentorial compartment. Rodriguez-Hernandez et al. found that patients with cerebellar AVMs had significantly worse postoperative outcomes than cerebral AVMs, primarily due to the worse preoperative neurological status of those with cerebellar nidi [9]. In a case–control study of 60 cerebellar AVMs treated with radiosurgery, we found that infratentorial location does not adversely impact radiosurgical outcomes in the same manner as it affects surgical outcomes [20]. Thus, radiosurgery is an effective treatment alternative to resection for cerebellar AVMs, although surgery remains the mainstay of intervention, especially for ruptured nidi.

References Dear Editor, I have read, with interest, a recently published article in Clinical Neurology and Neurosurgery by Magro et al. titled ‘Management of ruptured posterior fossa arteriovenous malformations’ [1]. This retrospective cohort study analyzed the outcomes of 34 patients with ruptured posterior fossa arteriovenous malformations (AVM), including those located in the brainstem (21%) or cerebellum (79%). The nidi were managed conservatively (18%), or underwent treatment with single- (35%) or multimodality (32%) therapy. Five patients died (15%), including one from the initial hemorrhage and four from re-hemorrhage. After a mean follow-up period of 31 months, favorable outcome (modified Rankin Scale score of 2 or less) was achieved in 71%. Given that only 10–15% of AVMs are localized to the posterior fossa, the literature pertaining to multimodality treatment outcomes for posterior fossa AVMs is relatively sparse. Thus, the present study improves our understanding of these uncommon lesions by evaluating the long-term functional outcomes for patients with ruptured posterior fossa AVMs, which is the most important impact of this study. In the following discussion, our goals are to (1) analyze the role of multimodality therapy in the modern management of posterior fossa AVMs and (2) determine the effect of infratentorial location on outcomes after intervention for posterior fossa AVMs.

[1] Magro E, Chainey J, Chaalala C, Jehani HA, Fournier JY, Bojanowski MW. Management of ruptured posterior fossa arteriovenous malformations. Clin Neurol Neurosurg 2015;128:78–83. [2] Chen CJ, Chivukula S, Ding D, Starke RM, Lee CC, Yen CP, et al. Seizure outcomes following radiosurgery for cerebral arteriovenous malformations. Neurosurg Focus 2014;37(3):E17. [3] Moosa S, Chen CJ, Ding D, Lee CC, Chivukula S, Starke RM, et al. Volume-staged versus dose-staged radiosurgery outcomes for large intracranial arteriovenous malformations. Neurosurg Focus 2014;37(3):E18. [4] Ding D, Xu Z, Yen CP, Starke RM, Sheehan JP. Radiosurgery for unruptured cerebral arteriovenous malformations in pediatric patients. Acta Neurochir (Wien) 2015;157:281–91. [5] Ding D, Yen C, Starke RM, Xu Z, Sheehan JP. Effect of prior hemorrhage on intracranial arteriovenous malformation radiosurgery outcomes. Cerebrovasc Dis 2014;39(1):53–62. [6] Ding D, Yen CP, Xu Z, Starke RM, Sheehan JP. Radiosurgery for primary motor and sensory cortex arteriovenous malformations: outcomes and the effect of eloquent location. Neurosurgery 2013;73(5):816–24. [7] Starke RM, Yen CP, Ding D, Sheehan JP. A practical grading scale for predicting outcome after radiosurgery for arteriovenous malformations: analysis of 1012 treated patients. J Neurosurg 2013;119(4):981–7. [8] Kelly ME, Guzman R, Sinclair J, Bell-Stephens TE, Bower R, Hamilton S, et al. Multimodality treatment of posterior fossa arteriovenous malformations. J Neurosurg 2008;108(6):1152–61. [9] Rodriguez-Hernandez A, Kim H, Pourmohamad T, Young WL, Lawton MT. Cerebellar arteriovenous malformations: anatomic subtypes, surgical results, and increased predictive accuracy of the supplementary grading system. Neurosurgery 2012;71(6):1111–24. [10] Yen CP, Ding D, Cheng CH, Starke RM, Shaffrey M, Sheehan J. Gamma knife surgery for incidental cerebral arteriovenous malformations. J Neurosurg 2014;121(5):1015–21.

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[11] Starke RM, Sheehan JP, Ding D, Liu KC, Kondziolka D, Crowley RW, et al. Conservative management or intervention for unruptured brain arteriovenous malformations. World Neurosurg 2014;82(5):e668–9. [12] Buell TJ, Ding D, Starke RM, Webster Crowley R, Liu KC. Embolizationinduced angiogenesis in cerebral arteriovenous malformations. J Clin Neurosci 2014;21(11):1866–71. [13] Ding D, Yen CP, Xu Z, Starke RM, Sheehan JP. Radiosurgery for patients with unruptured intracranial arteriovenous malformations. J Neurosurg 2013;118(5):958–66. [14] Ding D, Yen CP, Starke RM, Xu Z, Sheehan JP. Radiosurgery for ruptured intracranial arteriovenous malformations. J Neurosurg 2014;121(2):470–81. [15] Ding D, Yen CP, Starke RM, Xu Z, Sun X, Sheehan JP. Radiosurgery for Spetzler–Martin Grade III arteriovenous malformations. J Neurosurg 2014;120(4):959–69. [16] Ding D, Yen CP, Xu Z, Starke RM, Sheehan JP. Radiosurgery for low-grade intracranial arteriovenous malformations. J Neurosurg 2014;121(2):457–67. [17] Ding D, Yen CP, Starke RM, Xu Z, Sun X, Sheehan JP. Outcomes following singlesession radiosurgery for high-grade intracranial arteriovenous malformations. Br J Neurosurg 2014;28(5):666–74. [18] Mouchtouris N, Jabbour PM, Starke RM, Hasan DM, Zanaty M, Theofanis T, et al. Biology of cerebral arteriovenous malformations with a focus on inflammation. J Cereb Blood Flow Metab 2015;35:167–75. [19] Ding D, Liu KC. Predictive capability of the Spetzler–Martin versus supplementary grading scale for microsurgical outcomes of cerebellar arteriovenous malformations. J Cerebrovasc Endovasc Neurosurg 2013;15(4): 307–10. [20] Ding D, Starke RM, Yen CP, Sheehan JP. Radiosurgery for cerebellar arteriovenous malformations: does infratentorial location affect outcome? World Neurosurg 2014;82(1–2):e209–17.

Dale Ding ∗ University of Virginia, Department of Neurosurgery, Charlottesville, 22908, USA ∗ Correspondence to: University of Virginia, Department of Neurosurgery, P.O. Box 800212, Charlottesville, VA 22908, USA. Tel.: +1 434 924 2203; fax: +1 434 982 5753. E-mail address: [email protected]

gow Outcome Scale at follow-up (P = 0.021) and complications (P = 0.007). Based on these findings, the authors recommend that endovascular therapy is the preferred treatment for non-dorsal paraclinoid aneurysms, whereas microsurgery is the preferred treatment for dorsal paraclinoid aneurysms. The goal of the following discussion is to evaluate the modern management of paraclinoid aneurysms. While the use of flow-diverting stents has become increasingly popular, given their impressive outcomes for large and complex aneurysms of the cavernous and paraclinoid internal carotid artery, they are associated with a unique set of complications, for which the optimal management is ill-defined [2–7]. Nonetheless, many paraclinoid aneurysms which were previously referred for microsurgery due to the failure of conventional endovascular techniques are now being successfully occluded with flow diversion. As the use of clipping for paraclinoid aneurysms progressively wanes, the collective paucity of neurosurgical experience may perpetuate the shift toward endovascular treatment of these lesions. As our understanding of aneurysm biology and treatment outcomes continues to evolve, novel medical therapies or technologies may arise which will reduce the role of microsurgery in the management of paraclinoid aneurysms to the point of extinction [8–14]. Until such time, it remains crucial for vascular neurosurgeons to maintain proficiency in the microsurgical treatment of paraclinoid aneurysms, for which the use of certain maneuvers, such as anterior clinoidectomy and extracranial–intracranial bypass, is becoming increasingly uncommon. However, endovascular training is undoubtedly paramount to the modern development of vascular neurosurgeons, not only to keep abreast of the constantly changing landscape of aneurysm therapy, but also to provide patients with the most prudent management options.

11 January 2015 Available online 2 February 2015 http://dx.doi.org/10.1016/j.clineuro.2015.01.024

Modern management of paraclinoid aneurysms: Rise of flow diversion and fall of microsurgery Keywords: Endovascular procedures Intracranial aneurysms Flow diversion Microsurgery Stents

Dear Editor, I have read, with interest, a recently published article in Clinical Neurology and Neurosurgery by Oh et al. titled ‘Management strategy of surgical and endovascular treatment of unruptured paraclinoid aneurysms based on the location of aneurysms’ [1]. This retrospective cohort study of 176 patients with 185 unruptured paraclinoid aneurysms analyzed the treatment outcomes after microsurgical clipping (17%) or endovascular therapy (83%). The paraclinoid aneurysms were classified, based on anatomic location, into dorsal (27%) and non-dorsal (73%) cohorts. After a mean follow-up of 27 months, the complete occlusion rate was significantly higher in aneurysms treated with microsurgery (97% vs. 60%, P < 0.001). The clinical outcomes were similar between dorsal aneurysms treated with either approach. However, the clinical outcomes for non-dorsal aneurysms were significantly better for endovascular therapy, with respect to Glas-

References [1] Oh SY, Lee KS, Kim BS, Shin YS. Management strategy of surgical and endovascular treatment of unruptured paraclinoid aneurysms based on the location of aneurysms. Clin Neurol Neurosurg 2015;128:72–7. [2] Ding D, Liu KC. Microsurgical extraction of a malfunctioned pipeline embolization device following complete deployment. J Cerebrovasc Endovasc Neurosurg 2013;15(3):241–5. [3] Ding D, Starke RM, Liu KC. Microsurgical strategies following failed endovascular treatment with the pipeline embolization device: case of a giant posterior cerebral artery aneurysm. J Cerebrovasc Endovasc Neurosurg 2014;16(1):26–31. [4] Hu YC, Deshmukh VR, Albuquerque FC, Fiorella D, Nixon RR, Heck DV, et al. Histopathological assessment of fatal ipsilateral intraparenchymal hemorrhages after the treatment of supraclinoid aneurysms with the Pipeline Embolization Device. J Neurosurg 2014;120(2):365–74. [5] Liu KC, Ding D, Starke RM, Geraghty SR, Jensen ME. Intraprocedural retrieval of migrated coils during endovascular aneurysm treatment with the Trevo Stentriever device. J Clin Neurosci 2014;21(3):503–6. [6] Ding D, Liu KC. Management strategies for intraprocedural coil migration during endovascular treatment of intracranial aneurysms. J Neurointerv Surg 2014;6(6):428–31. [7] Fargen KM, Velat GJ, Lawson MF, Mocco J, Hoh BL. Review of reported complications associated with the Pipeline Embolization Device. World Neurosurg 2012;77(3–4):403–4. [8] Ding D, Liu KC. Applications of stenting for intracranial atherosclerosis. Neurosurg Focus 2011;30(6):E15. [9] Ding D, Starke RM, Dumont AS, Owens GK, Hasan DM, Chalouhi N, et al. Therapeutic implications of estrogen for cerebral vasospasm and delayed cerebral ischemia induced by aneurysmal subarachnoid hemorrhage. Biomed Res Int 2014;2014:727428. [10] Ding D, Starke RM, Crowley RW, Liu KC. Role of stenting for intracranial atherosclerosis in the post-SAMMPRIS era. Biomed Res Int 2013;2013:304320. [11] Starke RM, Chalouhi N, Ding D, Raper DM, McKisic MS, Owens GK, et al. Vascular smooth muscle cells in cerebral aneurysm pathogenesis. Transl Stroke Res 2014;5(3):338–46. [12] Starke RM, Raper DM, Ding D, Chalouhi N, Owens GK, Hasan DM, et al. Tumor necrosis factor-alpha modulates cerebral aneurysm formation and rupture. Transl Stroke Res 2014;5(2):269–77. [13] Starke RM, Turk A, Ding D, Crowley RW, Liu KC, Chalouhi N, et al. Technology developments in endovascular treatment of intracranial aneurysms.

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Posterior fossa arteriovenous malformations: effect of infratentorial location on outcomes after intervention.

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