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Case Report Optic Nerve Vascular Compression in a Patient with a Tuberculum Sellae Meningioma Cezar José Mizrahi, 1 Samuel Moscovici, 1 Shlomo Dotan, 2 and Sergey Spektor 1 1 Department of Neurosurgery, Hadassah-Hebrew University Medical Center, 91120 Jerusalem, Israel 2 Department of Ophtalmology, Hadassah-Hebrew University Medical Center, 91120 Jerusalem, Israel Correspondence should be addressed to Sergey Spektor; [email protected] Received 27 October 2014; Accepted 6 January 2015 Academic Editor: Alexander A. Bialasiewicz Copyright © 2015 Cezar Jos´ e Mizrahi et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Optic nerve vascular compression in patients with suprasellar tumor is a known entity but is rarely described in the literature. Case Description. We present a unique, well-documented case of optic nerve strangulation by the A1 segment of the anterior cerebral artery in a patient with a tuberculum sellae meningioma. e patient presented with pronounced progressive visual deterioration. Following surgery, there was immediate resolution of her visual deficit. Conclusion. Vascular strangulation of the optic nerve should be considered when facing progressive and/or severe visual field deterioration in patients with tumors proximal to the optic apparatus. 1. Introduction It is well known that tuberculum sellae meningiomas cause progressive visual loss by optic nerve compression [15], usually due to mechanical compression by the tumor. We present a rare case, well documented, of severe deterioration in visual function as a result of optic nerve strangulation due to compression of the A1 branch of the anterior cerebral artery against the tumor. 2. Case Presentation 2.1. History and Physical Examination. is 50-year-old woman with no known background disease was referred to our Neurosurgery Department for progressive deterioration of visual function in her leſt eye of 3-4 months duration. Serial visual field examinations with stimulus V showed loss of three quadrants in the leſt eye, with only the superonasal quadrant showing a good degree of preservation (Figure 1). e right visual field was full, suggesting leſt optic neu- ropathy. T1-weighted gadolinium-enhanced MRI revealed a tuberculum sellae meningioma measuring approximately 1.7 cm × 1.9 cm × 1.3 cm (Figure 2). 2.2. Surgical Procedure. e patient underwent a leſt pteri- onal craniotomy. e dura was opened and the Sylvian fissure was split, providing excellent CSF drainage and cerebral relaxation. e leſt frontal lobe was elevated and the tumor came into view. Inspection of the suprasellar region showed total encasement of the leſt optic nerve by the tumor. e tumor was internally decompressed, and the anterior communicating complex was released. Tumor pressing upon the leſt A1 segment of the anterior communicating artery had compressed the leſt optic nerve. When the tumor was removed, the nerve sagged free, exposing a clear impression of the A1 segment (Figure 3). e capsule and the tumor were then removed completely, and the visual apparatus was decompressed. e patient tolerated the procedure well and was discharged 1 week later. 2.3. Followup. A full neuroophthalmologic evaluation per- formed 7 days aſter surgery revealed best-corrected visual acuity of 0.8 in both eyes with no relative afferent papillary defect. Fundal examination in the right eye showed a pink disc of normal appearance, while in the leſt eye there was pallor of the temporal part of the optic disc. e right visual field was normal, while in the leſt visual field there Hindawi Publishing Corporation Case Reports in Ophthalmological Medicine Volume 2015, Article ID 681632, 3 pages http://dx.doi.org/10.1155/2015/681632

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Case ReportOptic Nerve Vascular Compression in a Patient witha Tuberculum Sellae Meningioma

Cezar José Mizrahi,1 Samuel Moscovici,1 Shlomo Dotan,2 and Sergey Spektor1

1Department of Neurosurgery, Hadassah-Hebrew University Medical Center, 91120 Jerusalem, Israel2Department of Ophtalmology, Hadassah-Hebrew University Medical Center, 91120 Jerusalem, Israel

Correspondence should be addressed to Sergey Spektor; [email protected]

Received 27 October 2014; Accepted 6 January 2015

Academic Editor: Alexander A. Bialasiewicz

Copyright © 2015 Cezar Jose Mizrahi et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.

Background. Optic nerve vascular compression in patients with suprasellar tumor is a known entity but is rarely described in theliterature. Case Description. We present a unique, well-documented case of optic nerve strangulation by the A1 segment of theanterior cerebral artery in a patient with a tuberculum sellae meningioma. The patient presented with pronounced progressivevisual deterioration. Following surgery, there was immediate resolution of her visual deficit. Conclusion. Vascular strangulationof the optic nerve should be considered when facing progressive and/or severe visual field deterioration in patients with tumorsproximal to the optic apparatus.

1. Introduction

It is well known that tuberculum sellae meningiomas causeprogressive visual loss by optic nerve compression [1–5],usually due to mechanical compression by the tumor. Wepresent a rare case, well documented, of severe deteriorationin visual function as a result of optic nerve strangulationdue to compression of the A1 branch of the anterior cerebralartery against the tumor.

2. Case Presentation

2.1. History and Physical Examination. This 50-year-oldwoman with no known background disease was referred toour Neurosurgery Department for progressive deteriorationof visual function in her left eye of 3-4 months duration.Serial visual field examinations with stimulus V showed lossof three quadrants in the left eye, with only the superonasalquadrant showing a good degree of preservation (Figure 1).The right visual field was full, suggesting left optic neu-ropathy. T1-weighted gadolinium-enhanced MRI revealeda tuberculum sellae meningioma measuring approximately1.7 cm × 1.9 cm × 1.3 cm (Figure 2).

2.2. Surgical Procedure. The patient underwent a left pteri-onal craniotomy.The dura was opened and the Sylvian fissurewas split, providing excellent CSF drainage and cerebralrelaxation. The left frontal lobe was elevated and the tumorcame into view. Inspection of the suprasellar region showedtotal encasement of the left optic nerve by the tumor.The tumor was internally decompressed, and the anteriorcommunicating complex was released. Tumor pressing uponthe left A1 segment of the anterior communicating arteryhad compressed the left optic nerve. When the tumor wasremoved, the nerve sagged free, exposing a clear impressionof the A1 segment (Figure 3). The capsule and the tumorwere then removed completely, and the visual apparatus wasdecompressed. The patient tolerated the procedure well andwas discharged 1 week later.

2.3. Followup. A full neuroophthalmologic evaluation per-formed 7 days after surgery revealed best-corrected visualacuity of 0.8 in both eyes with no relative afferent papillarydefect. Fundal examination in the right eye showed a pinkdisc of normal appearance, while in the left eye there waspallor of the temporal part of the optic disc. The rightvisual field was normal, while in the left visual field there

Hindawi Publishing CorporationCase Reports in Ophthalmological MedicineVolume 2015, Article ID 681632, 3 pageshttp://dx.doi.org/10.1155/2015/681632

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2 Case Reports in Ophthalmological Medicine

Figure 1: Preoperative left eye visual field. With stimulus V, therewas loss of three quadrants with only the superonasal quadrantshowing a good degree of preservation.

Figure 2: T1-weighted gadolinium-enhancedMRI revealed a tuber-culum sellae meningioma measuring approximately 1.7 cm × 1.9 cm× 1.3 cm.

was a central scotoma and temporal depression (Figure 4).Follow-up visual field examination performed 10 monthsafter surgery showed again a normal right visual field and asolitary paracentral scotoma in the left visual field (Figure 5).There was no evidence of residual tumor on MRI performed6 months after surgery (Figure 6).

3. Discussion

We present a well-documented case of optic nerve stran-gulation by the A1 segment of the anterior cerebral arteryin a patient a with suprasellar tumor. Once the tumor wasdebulked, the optic nerve sagged free presenting a clearimpression of the artery, which had compressed the nervedue to pressure exerted by the meningioma on the anteriorcerebral artery. Preoperative neuroophthalmic examinationrevealed a significant deficit in the left visual function. Therewas dramatic improvement immediately after surgery and

Figure 3: Intraoperative photograph showing a clear impressionof the A1 segment after tumor removal and optic nerve vasculardecompression.

Figure 4: At 1-week postoperative followup, the left eye visualfield examination performedwith normal stimulus revealedmarkedimprovement but residual central scotoma and temporal depression.

near complete resolution in the patient’s visual field at 10-month followup.

Visual loss secondary to the mechanical compressionof the optic nerve by tumors, particularly by tuberculumsellae meningiomas, is well established in the literature [1–5], and it has been reported that vascular elements mayplay a significant role in the mechanism of compression [6–8]. Levatin [7] was a pioneer in 1961 when he describedstrangulation of the optic tract by the anterior cerebral arteryin a patient harboring a suprasellar tumor. In 1989, Steno[8] reported compression of structures in the visual pathwayby arteries of the circle of Willis within suprasellar tumorsin 12 of 34 necropsies of extensive craniopharyngiomas andpituitary adenomas and in three of 109 patients operatedon account of these tumors. In addition, there are severalreports of compression of the optic nerve by an elongatedvascular fusiform enlargement or dolichoectasia [9–12] or anonaneurysmatic idiopathic artery compression [13, 14].

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Case Reports in Ophthalmological Medicine 3

Figure 5: At 10-month postoperative followup, the left eye visualfield showed a solitary paracentral scotoma.

Figure 6: T1-weighted gadolinium-enhanced MRI performed 6months after surgery showed no evidence of residual tumor.

We found only one paper by Bejjani et al. [6] describingvascular compression of the optic nerve due to pressureexerted by a tuberculum sellae meningioma, with intraoper-ative illustration of the mechanism of ON strangulation.

Our illustration provides further documentation that thismechanism of strangulation exists and may play role in thepathogenesis of visual loss in patients with infrachiasmatictumors.

In summary, optic nerve vascular strangulation shouldbe considered when facing progressive and/or severe visualfield deterioration patients with tumors proximal to the opticapparatus.

Conflict of Interests

The authors have no conflict of interests to declare.

References

[1] O. Al-Mefty, A. Holoubi, A. Rifai, and J. L. Fox, “Microsurgicalremoval of suprasellar meningiomas,”Neurosurgery, vol. 16, no.3, pp. 364–372, 1985.

[2] B. T. Andrews and C. B. Wilson, “Supresellar meningiomas:the effect of tumor location on postoperative visual outcome,”Journal of Neurosurgery, vol. 69, no. 4, pp. 523–528, 1988.

[3] R. Fahlbusch and W. Schoot, “Pterional surgery of menin-giomas of the tuberculum sellae and planum sphenoidale:surgical results with special consideration of ophthalmologicaland endocrinological outcomes,” Journal of Neurosurgery, vol.96, no. 2, pp. 235–243, 2002.

[4] N. Margalit, A. Kesler, H. Ezer, S. Freedman, and Z. Ram,“Tuberculum and diaphragma sella meningioma—surgicaltechnique and visual outcome in a series of 20 cases operatedover a 2.5-year period,” Acta Neurochirurgica, vol. 149, no. 12,pp. 1199–1204, 2007.

[5] N. S. Margalit, J. B. Lesser, J. Moche et al., “Meningiomasinvolving the optic nerve: technical aspects and outcomes fora series of 50 patients,”Neurosurgery, vol. 53, no. 3, pp. 523–533,2003.

[6] G. K. Bejjani, K. P. Cockerham, J. S. Kennerdell et al., “Visualfield deficit caused by vascular compression from a suprasellarmeningioma: case report,”Neurosurgery, vol. 50, no. 5, pp. 1129–1132, 2002.

[7] P. Levatin, “Eye findings in strangulation of the optic nerve,”American Journal of Ophthalmology, vol. 51, no. 6, pp. 1308–1312,1961.

[8] J. Steno, “Compression of structures in the visual pathwayby arteries of the circle of Willis in suprasellar tumors,”Ceskoslovenska Neurologie a Neurochirurgie, vol. 52, no. 2, pp.143–147, 1989.

[9] E. V. Colapinto, M. A. Cabeen, and L. N. Johnson, “Optic nervecompression by a dolichoectatic internal carotid artery: casereport,” Neurosurgery, vol. 39, no. 3, pp. 604–606, 1996.

[10] K.Matsuo, S. Kobayashi, and K. Sugita, “Bitemporal hemianop-sia associated with sclerosis of the intracranial carotid arteries.Case report,” Journal of Neurosurgery, vol. 53, no. 4, pp. 566–569,1980.

[11] N. McLaughlin and M.W. Bojanowski, “Microvascular decom-pression of the optic chiasm: case report,” Journal of Neuro-surgery, vol. 114, no. 3, pp. 857–860, 2011.

[12] M. G. Mitts and J. D. McQueen, “Visual loss associated withfusiform enlargement of the intracranial portion of the internalcarotid artery,” Journal of Neurosurgery, vol. 23, no. 1, pp. 33–37,1965.

[13] D. M. Jacobson, “Symptomatic compression of the optic nerveby the carotid artery: clinical profile of 18 patients with 24affected eyes identified by magnetic resonance imaging,” Oph-thalmology, vol. 106, no. 10, pp. 1994–2004, 1999.

[14] D. M. Jacobson, J. J. Warner, and S. K. Broste, “Optic nervecontact and compression by the carotid artery in asymptomaticpatients,”American Journal of Ophthalmology, vol. 123, no. 5, pp.677–683, 1997.

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