Proper Ophthalmic Artery Aneurysms

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Article initiated by:
Agni Kakouri, MD, MBA
All contributors:
Agni Kakouri, MD, MBA
Assigned editor:
Review:
Assigned status Update Pending
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Not to be confused with Ophthalmic Artery Pseudoaneurysm, which addresses false aneurysms from traumatic or iatrogenic arterial wall disruption. For aneurysms arising from the internal carotid artery at or near the ophthalmic artery origin, see ophthalmic-segment (carotid-ophthalmic) aneurysms.

Disease Entity

Proper ophthalmic artery aneurysms (POAAs) arise from the ophthalmic artery trunk or one of its branches after the artery has separated from the internal carotid artery (ICA). The qualifier proper is an anatomic term that distinguishes these lesions from the much more common carotid-ophthalmic or ophthalmic-segment ICA aneurysm.[1][2] POAAs have been reported in the intracranial, intracanalicular, intraorbital, and terminal branch portions of the artery and may be saccular, fusiform, dissecting, traumatic, or flow-related.[1][2][3][4][5][6]

Scope

This article covers saccular, fusiform, and dissecting aneurysms arising from the ophthalmic artery proper, including post-traumatic dissecting lesions. False aneurysms caused by traumatic or iatrogenic arterial wall disruption are addressed in Ophthalmic Artery Pseudoaneurysm.

Disease

POAAs are rare but relevant to ophthalmic practice because they can injure the optic nerve by compression or compromise the central retinal and posterior ciliary circulations by thromboembolism or altered flow. Reported presentations include progressive optic neuropathy, retinal or choroidal ischemia, proptosis, diplopia, painful orbital or orbital apex syndromes, and, less commonly, subarachnoid, intracranial, or intraorbital hemorrhage.[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15]

Definition

A POAA is an aneurysm arising from the ophthalmic artery itself rather than from the adjacent ICA. In contrast, the term “ophthalmic artery aneurysm” is often used in neurosurgical literature for an ICA aneurysm at or near the ophthalmic artery origin.[1][2] Exact localization is therefore essential.

A true aneurysm involves the arterial wall, whereas a pseudoaneurysm follows disruption of the vessel wall with a contained false lumen.[1][16][17] Traumatic and iatrogenic ophthalmic artery lesions are often pseudoaneurysms, although trauma may also produce dissecting or fusiform lesions.[1][2][4][6][16][17][18][19][20][21]

Anatomy

The ophthalmic artery most often arises from the intradural supraclinoid ICA near the anterior clinoid process and courses toward the optic canal. Its relationship to the optic nerve is variable but intimate.[22][23] Anatomical studies show that the artery may enter the optic canal inferomedial or inferolateral to the optic nerve and may have a partially interdural course within the canal.[23][24] The limited space in the optic canal and orbital apex explains why even a small increase in vessel caliber can produce optic nerve compression.[4][9][10]

Classification by ophthalmic artery segment

POAAs may be organized by the segment from which they arise:[1][2][3][4][5][6]

  • Intracranial: after separation of the ophthalmic artery from the ICA and before the optic canal.[1][2]
  • Intracanalicular: within the optic canal.[4][10]
  • Intraorbital: within the orbit after leaving the optic canal.[5][6]
  • Terminal branch: arising from a distal branch of the ophthalmic artery.[1][2]

For a broader review of orbital arterial anatomy, see Vasculature of Orbit.

Epidemiology

There are no reliable incidence or prevalence estimates for POAA.[1][2][6] Qiao et al. identified 35 reported peripheral ophthalmic artery aneurysms across the intracranial, intracanalicular, intraorbital, and terminal branch segments.[1] A 2025 systematic review identified 15 reports classified by the authors as intraorbital aneurysms, although the included anatomy and terminology were heterogeneous.[3] The evidence base remains limited to small case series, case reports, and reviews of those reports.

Etiology

Traumatic and iatrogenic lesions

Reported contexts include craniofacial trauma, arterial dissection, and iatrogenic injury.[2][6][16][17][18][19][20][21] Post-traumatic dissecting or fusiform lesions arising from the ophthalmic artery proper are included in this article; false aneurysms caused by traumatic or iatrogenic arterial wall disruption are addressed in Ophthalmic Artery Pseudoaneurysm.[16][17][20]

Flow-related and dAVF-associated lesions

Another reported setting is altered hemodynamics from an arteriovenous malformation or dural arteriovenous fistula.[1][2] Kawaguchi et al. documented high-flow, low-resistance ophthalmic artery hemodynamics in two patients with peripheral aneurysms, and Andersson et al. described regression of a flow-related ophthalmic artery aneurysm after treatment of the associated dural arteriovenous shunt.[25][26]

Idiopathic and other associations

Idiopathic or possibly developmental lesions and POAAs associated with multifocal aneurysm disease have also been reported.[1][2][27]

The major POAA reviews used for this article did not identify a confirmed infectious or mycotic aneurysm arising from the ophthalmic artery proper.[1][2][3][5]

Risk Factors

No demographic, inherited, or modifiable risk factor profile has been established specifically for POAA. Conventional intracranial aneurysm risk factors such as hypertension, smoking, family history, older age, and female sex may be relevant background considerations but their association with POAAs has not been validated. Reported associations include blunt or penetrating craniofacial trauma, iatrogenic injury, altered flow from an arteriovenous shunt or vascular malformation, and coexisting intracranial or extracranial aneurysms.[2][3][16][20][25][26][27]

General Pathology and Pathophysiology

The two principal mechanisms of visual injury are mass effect and ischemia. Intracanalicular and orbital-apex lesions can compress the optic nerve in a confined space, causing reduced visual acuity, dyschromatopsia, a relative afferent pupillary defect (rAPD), and visual field loss.[4][9][10][11] More anterior orbital lesions may also affect intraconal structures or cranial nerves III and VI, producing proptosis, ptosis, or diplopia.[9]

Ischemic injury may result from thromboembolism arising within the aneurysm or from reduced flow at or beyond the lesion. Reported ocular ischemic presentations include recurrent retinal artery obstruction, acute central retinal artery occlusion (CRAO), and sequential CRAO with posterior ciliary artery occlusion.[7][8][14][15] In these cases, fundus findings rather than orbital signs may dominate the presentation, and the aneurysm may be discovered only after standard cardiac and carotid workup fails to reveal another embolic source.[14][15]

Reported rupture presentations vary by lesion location.[2][12] Intracranial trunk and anterior ethmoidal branch aneurysms have presented with subarachnoid or intracranial hemorrhage, whereas intraorbital lesions more often produce acute visual loss with intraorbital or periorbital hemorrhage with rupture.[1][2][3][12][13] However, observations are based on few reported cases and should not be treated as a formal risk model.

Primary Prevention

No POAA-specific primary prevention strategy has been established. General intracranial aneurysm risk modification, such as smoking cessation and blood pressure control, may be appropriate as general cerebrovascular care but remains unconfirmed for POAA specifically. Preventive considerations relevant to reported POAA contexts include minimizing orbital or skull-base vascular injury during procedures, prompt evaluation of penetrating orbital trauma, and management of associated high-flow vascular malformations when present.[2][21][25][26]

Diagnosis

POAA is usually diagnosed with vascular imaging after an atypical compressive optic neuropathy, orbital syndrome, or retinal ischemic event.[4][14] Suspicion should rise when the symptoms do not fit common entities such as optic neuritis, ischemic optic neuropathy, thyroid eye disease, or idiopathic orbital inflammation.[4][7][8][9][11][12][14][15]

History

Features in a patient’s history that should raise suspicion for a vascular ophthalmic artery lesion include:

  • Progressive, fluctuating, transient, or sudden monocular visual loss, including decreased visual acuity
  • Decreased color vision
  • A new visual field complaint or defect
  • Retro-orbital pain or headache
  • New-onset proptosis
  • Pulsatile symptoms
  • Diplopia
  • Ptosis
  • Blunt or penetrating craniofacial trauma, including penetrating orbital injury
  • Prior sinus, orbital, skull-base, or endovascular instrumentation
  • Prominent or delayed epistaxis after trauma or a nearby procedure
  • A known arteriovenous shunt or vascular malformation
  • A previously identified “orbital mass” with vascular imaging features

Symptoms

Compressive lesions typically cause progressive or fluctuating visual loss, dyschromatopsia, or a visual field defect. Diplopia, ptosis, and proptosis suggest orbital apex or intraconal involvement. Ischemic presentations are more often sudden and painless, although pain or headache may accompany aneurysm enlargement, thrombosis, or hemorrhage. RAPD, when present, suggests unilateral optic nerve injury or severe retinal ischemia.

Physical Examination

A complete neuro-ophthalmic and orbital examination is essential. Formal neurologic review should note headache pattern, meningismus, cranial neuropathies, forehead or nasal sensory changes, systemic infectious symptoms if relevant, and signs of trauma. External inspection should look for proptosis, asymmetry, bruit, chemosis, ecchymosis, pulsation, or surgical scars. In ruptured orbital lesions, hemorrhagic swelling may dominate the bedside exam.[12]

Ophthalmic Examination

Baseline testing should include best-corrected visual acuity, pupils, color vision, confrontation visual fields, formal perimetry when feasible, intraocular pressure, ocular motility, and a dilated fundus examination. Eyelid position, exophthalmometry, and external orbital examination are important when proptosis, diplopia, ptosis, or orbital apex involvement is suspected. The optic disc should be assessed for pallor or atrophy, and the retina and choroid should be examined for ischemic change.

Ancillary testing should be selected based on the suspected mechanism. Optical coherence tomography (OCT) of the optic nerve head and macula can document retinal nerve fiber layer (RNFL) and ganglion cell complex/ganglion cell-inner plexiform layer (GCC/GCIPL) thickness, macular structure, inner retinal ischemia, and optic atrophy over time. Fundus photography provides baseline documentation. Fluorescein angiography, indocyanine green angiography, and OCT angiography may help identify retinal or choroidal perfusion defects when ischemia is suspected. Serial perimetry may quantify progression or recovery in compressive optic neuropathy. This approach is based on broader neuro-ophthalmic and retinal ischemia practice instead of dedicated POAA evidence.

Signs

Reported compressive signs include:

  • Reduced visual acuity
  • RAPD
  • Dyschromatopsia
  • Visual field defects
  • Optic disc pallor or atrophy
  • Ophthalmoplegia
  • Ptosis
  • Orbital apex syndrome features[9]

Ischemic signs include:

  • Retinal ischemic whitening
  • Macular cherry-red spot[7][14]
  • Areas of choroidal nonperfusion
  • Arterial attenuation
  • Optic disc pallor

Clinical Diagnosis

The diagnosis is rarely made at the time of examination. The ophthalmologist or neuro-ophthalmologist should recognize a possible vascular compressive or embolic lesion and obtain appropriate imaging. Urgent imaging is warranted for unexplained monocular optic neuropathy with orbital signs, recurrent or sequential retinal arterial occlusion, sudden visual loss after craniofacial trauma, or a suspected orbital mass with flow-related imaging features.

Imaging

MRI of the brain and orbits with contrast can show a vascular flow void, enhancement, intraluminal thrombus, optic nerve displacement or compression, hemorrhage, or an orbital mass mimic.[4][7][9] CTA and MRA can demonstrate a saccular or fusiform vascular dilation and its continuity with the ophthalmic artery. Chronic intracanalicular lesions may also produce optic canal enlargement or bony remodeling.[4][7][9][10][11]

Catheter angiography with digital subtraction angiography (DSA) remains the most definitive test when noninvasive imaging does not establish the vessel of origin or when intervention is planned. Three-dimensional rotational angiography can clarify that an aneurysm arises from the ophthalmic artery separately from the ICA. Small lesions may be missed on CTA, especially in the presence of artifact or suboptimal spatial resolution.[1][2]

Distinguishing POAA from a carotid-ophthalmic, paraophthalmic, or ophthalmic-segment ICA aneurysm changes treatment planning.[1][2][28] A POAA procedure may require selective ophthalmic artery treatment, preservation of the artery, or, in selected cases, intentional ophthalmic artery occlusion after assessment of collateral ocular perfusion from external carotid branches.[1][6][10] An ICA-based lesion is treated as a paraclinoid ICA aneurysm, with treatment planned to maintain ICA patency while accounting for the ophthalmic artery and adjacent perforators.[28] This distinction is important because it identifies the vessel targeted and the vascular structures that must be preserved.[1][10][28] Therefore, imaging findings should always be interpreted with neurovascular radiology to confirm the vessel of origin and relevant vascular anatomy before intervention.[1][2]

Differential Diagnosis

The differential diagnosis includes:

  • Optic neuritis
  • Nonarteritic or arteritic anterior ischemic optic neuropathy
  • Compressive optic neuropathy from an optic nerve, orbital, or skull-base tumor
  • Orbital apex syndrome from inflammatory, infectious, neoplastic, or vascular causes
  • Cavernous sinus syndrome
  • Carotid-cavernous fistula
  • Orbital varix or orbital venous malformation
  • Cavernous venous malformation
  • Thyroid eye disease
  • Idiopathic orbital inflammatory disease
  • Orbital cellulitis
  • Central retinal artery occlusion
  • Ophthalmic artery occlusion
  • Carotid-ophthalmic, paraophthalmic, or ophthalmic-segment ICA aneurysm
  • Other orbital vascular lesions

Management

General Treatment Principles

Management is individualized because no validated POAA treatment algorithm exists. Important factors include anatomic location, morphology, symptoms, documented growth, rupture, thromboembolic behavior, collateral circulation, visual function, and patient comorbidity.[1][2][3][5][6] A practical team includes cerebrovascular neurosurgery and neurointerventional expertise together with ophthalmology or neuro-ophthalmology. Oculoplastic or orbital surgery may be added when a direct orbital approach is considered.[5][6][9][29]

Observation

Observation may be reasonable for an incidental, asymptomatic, or minimally symptomatic lesion that is stable on imaging, particularly when treatment risk or medical comorbidity is substantial.[1][2][7][29][30] No POAA-specific diameter cutoff has been validated for observation or intervention, and rupture scores developed for common intracranial aneurysms should not be assumed to apply to POAA.[2][3] Documented enlargement, new mass effect, progressive visual loss, embolic events, or hemorrhage should prompt reconsideration of treatment.[1][2][6][29]

Endovascular management

Endovascular approaches reported in the literature include coil embolization, liquid embolization, parent ophthalmic artery occlusion, and internal trapping.[4][6][10][12][19] Treatment planning must balance aneurysm control against retinal and choroidal perfusion. When ophthalmic artery sacrifice is considered, reported approaches include external carotid angiography, assessment of the choroidal blush, and balloon test occlusion to evaluate collateral supply.[4][6][10] Even when collaterals appear adequate, thromboembolic or ischemic visual complications remain possible.[31]

Surgical Management

Published surgical strategies include clipping of intracranial trunk aneurysms, trapping or excision of orbital lesions, and direct orbital or cranio-orbital approaches in selected cases.[5][9][13] In selected compressive lesions, optic canal or orbital decompression may be incorporated into surgery, although visual recovery is variable and the artery may be difficult to preserve because of adherence to the optic nerve.[4][5][9][10]

Follow-up

No standardized POAA-specific follow-up interval has been established. One observed intraorbital aneurysm was followed with neuro-ophthalmic examinations every 3 months and planned angiography at 1 year, while an observed POAA in a modern series underwent DSA at 4, 9, and 21 months.[2][29] Post-treatment imaging in reported cases has ranged from 6 weeks to 6 months, depending on the lesion and procedure.[2][4][6]

Follow-up should be individualized by the treating neurovascular and ophthalmic teams. Each visit should assess visual acuity, pupils, color vision, visual fields, optic disc and retina assessment, and OCT RNFL/GCC when optic neuropathy is present or suspected. Fundus photography and retinal/choroidal perfusion testing are appropriate when ischemia was part of the initial presentation.

Complications

Reported complications include permanent vision loss, optic atrophy, persistent visual field loss, retinal artery occlusion, posterior ciliary ischemia or occlusion, ophthalmic artery occlusion, orbital apex syndrome, ophthalmoplegia, rupture with subarachnoid or orbital hemorrhage, and treatment-related embolic retinal infarction.[3][4][6][7][8][9][11][12][13][14][15][31]

Prognosis

Prognosis is highly heterogeneous and depends on lesion morphology, mechanism, location, and duration of visual symptoms.[1][2][3] Lesions discovered incidentally, without symptoms or before irreversible optic nerve or retinal injury, may do well with observation.[2][29][30] Vision-threatening compressive lesions can improve, but delayed diagnosis can leave patients with permanent atrophy or blindness.[4][6][12][30] Ruptured intracranial and branch lesions add neurologic risk beyond the eye.[12][13]

Relationship to ophthalmic artery pseudoaneurysm

Ophthalmic artery pseudoaneurysm overlaps with this topic because it involves the same artery and can present with similar symptoms.[16][17] It follows arterial wall disruption and is associated with penetrating trauma or iatrogenic injury. However, a pseudoaneurysm is a false aneurysm.[16] For additional information, see Ophthalmic Artery Pseudoaneurysm.

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 Qiao L, Wang H, Mao L, Chen S, Xie W, Wu Q. Peripheral ophthalmic artery aneurysm. Neurosurg Rev. 2011;34(1):29-38. doi:10.1007/s10143-010-0290-5
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 2.25 2.26 2.27 Hendrix P, Bohan C, Dalal SS, et al. Proper ophthalmic artery aneurysms. Surg Neurol Int. 2023;14:105. doi:10.25259/SNI_1151_2022
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 Al-Shalchy AK, Bani-Saad AA, Badran SA, Bani Saad M, Algabri MH, Ismail M. Intraorbital ophthalmic artery aneurysm: A systematic review. Surg Neurol Int. 2025;16:52. doi:10.25259/SNI_1026_2024
  4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 Choi BK, Lee TH, Choi CH, Lee SW. Fusiform Intracanalicular Ophthalmic Artery Aneurysm; Case Report and Review of Literature. J Korean Neurosurg Soc. 2008;44(1):43. doi:10.3340/jkns.2008.44.1.43
  5. ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 Della Pepa GM, Sabatino G, La Rocca G, et al. Intraorbital and intracanalicular ophthalmic artery aneurysms. Literature review and report of a case. Br J Neurosurg. 2014;28(6):787-790. doi:10.3109/02688697.2014.913776
  6. ↑ 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 6.13 6.14 6.15 Izumihara K, Haruma J, Sugiu K, et al. Endovascular treatment for a symptomatic dissecting ophthalmic artery aneurysm occurring in the orbit: illustrative case. J Neurosurg Case Lessons. 2025;10(13):CASE25483. doi:10.3171/CASE25483
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 Carey AR. Central Retinal Artery Occlusion Due to Intraorbital Ophthalmic Artery Aneurysm. J Neuroophthalmol. 2019;39(1):125-126. doi:10.1097/WNO.0000000000000698
  8. ↑ 8.0 8.1 8.2 8.3 Kumar B, Kanakapura K, Ayachit G, Ayachit A. Sequential central retinal artery and posterior ciliary artery occlusion due to ophthalmic artery aneurysm. BMJ Case Rep. 2024;17(5):e257568. doi:10.1136/bcr-2023-257568
  9. ↑ 9.00 9.01 9.02 9.03 9.04 9.05 9.06 9.07 9.08 9.09 9.10 9.11 Ernemann U, Freudenstein D, Pitz S, Naegele T. Intraorbital aneurysm of the ophthalmic artery: a rare cause of apex orbitae compression syndrome. Graefes Arch Clin Exp Ophthalmol. 2002;240(7):575-577. doi:10.1007/s00417-002-0503-x
  10. ↑ 10.00 10.01 10.02 10.03 10.04 10.05 10.06 10.07 10.08 10.09 Piché SL, Haw CS, Redekop GJ, Heran MKS. Rare Intracanalicular Ophthalmic Aneurysm: Endovascular Treatment and Review of the Literature. Am J Neuroradiol. 2005;26(8):1929-1931.
  11. ↑ 11.0 11.1 11.2 11.3 11.4 Raitta C. Ophthalmic artery aneurysm causing optic atrophy and enlargement of the optic foramen. Br J Ophthalmol. 1968;52(9):707-709. doi:10.1136/bjo.52.9.707
  12. ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 Kirsch M, Henkes H. A Ruptured Intraorbital Ophthalmic Artery Aneurysm, Associated with a Dural Arteriovenous Fistula: Combined Transarterial and Transvenous Endovascular Treatment. Min - Minim Invasive Neurosurg. 2011;54(03):128-131. doi:10.1055/s-0031-1277230
  13. ↑ 13.0 13.1 13.2 13.3 13.4 Yanaka K, Matsumaru Y, Kamezaki T, Nose T. Ruptured Aneurysm of the Ophthalmic Artery Trunk Demonstrated by Three-dimensional Rotational Angiography: Case Report. Neurosurgery. 2002;51(4):1066-1070. doi:10.1097/00006123-200210000-00038
  14. ↑ 14.0 14.1 14.2 14.3 14.4 14.5 14.6 Kim YW, Woo SJ, Ahn J, Park KH, Kwon OK. Ophthalmic Artery Aneurysm: Potential Culprit of Central Retinal Artery Occlusion. Korean J Ophthalmol. 2013;27(6):470-473. doi:10.3341/kjo.2013.27.6.470
  15. ↑ 15.0 15.1 15.2 15.3 15.4 Beiran I, Dori D, Pikkel J, Miller B, Goldsher D. Recurrent retinal artery obstruction as a presenting symptom of ophthalmic artery aneurysm: a case report. Graefes Arch Clin Exp Ophthalmol. 1995;233(7):444-447. doi:10.1007/BF00180950
  16. ↑ 16.0 16.1 16.2 16.3 16.4 16.5 16.6 Czyz CN, Piehota PG, Strand AT, Stein M. Post-traumatic ophthalmic artery pseudoaneurysm from orbital projectile. Can J Ophthalmol. 2017;52(4):e130-e132. doi:10.1016/j.jcjo.2016.12.007
  17. ↑ 17.0 17.1 17.2 17.3 17.4 Kelly ME, Fiorella D. Traumatic Ophthalmic Artery Pseudoaneurysm Coiled with a Steerable Microcatheter. Can J Neurol Sci J Can Sci Neurol. 2009;36(4):496-499. doi:10.1017/S0317167100007861
  18. ↑ 18.0 18.1 Matsunaga K, Tanaka Y, Kato D, Hashimoto T, Kohno M. Clinical features and management of traumatic ophthalmic artery aneurysm: a case report and literature review. Br J Neurosurg. 2023;37(4):709-713. doi:10.1080/02688697.2019.1587382
  19. ↑ 19.0 19.1 19.2 Shim YS. Coil Embolization of Traumatic Ophthalmic Artery Aneurysm: Case Report. Korean J Neurotrauma. 2022;18(1):98. doi:10.13004/kjnt.2022.18.e2
  20. ↑ 20.0 20.1 20.2 20.3 Selcuk H, Soylu N, Albayram S, et al. Endovascular Treatment of Persistent Epistaxis due to Pseudoaneurysm Formation of the Ophthalmic Artery Secondary to Nasogastric Tube. Cardiovasc Intervent Radiol. 2005;28(2):242-245. doi:10.1007/s00270-004-0206-2
  21. ↑ 21.0 21.1 21.2 Li Y, Song W xian, Zhang T ming, Fu J di, Sun S, Zhao J zong. Intraorbital traumatic ophthalmic artery aneurysm: Case report. Neurol India. 2012;60(6):657. doi:10.4103/0028-3886.105213
  22. ↑ Govsa F, Erturk M, Kayalioglu G, Pinar Y, Ozer MA, Ozgur T. Neuro-arterial relations in the region of the optic canal. Surg Radiol Anat. 1999;21(5):329-335. doi:10.1007/BF01631334
  23. ↑ 23.0 23.1 Zoli M, Manzoli L, Bonfatti R, et al. Endoscopic endonasal anatomy of the ophthalmic artery in the optic canal. Acta Neurochir (Wien). 2016;158(7):1343-1350. doi:10.1007/s00701-016-2797-1
  24. ↑ Tayebi Meybodi A, Borba Moreira L, Lawton MT, et al. Interdural course of the ophthalmic artery in the optic canal. J Neurosurg. 2020;132(1):277-283. doi:10.3171/2018.6.JNS18856
  25. ↑ 25.0 25.1 25.2 Kawaguchi S, Sakaki T, Okuno S, Uchiyama Y, Nishioka T. Peripheral ophthalmic artery aneurysm: Report of two cases. J Neurosurg. 2001;94(5):822-825. doi:10.3171/jns.2001.94.5.0822
  26. ↑ 26.0 26.1 26.2 Andersson T, Kihlström L, Söderman M. Regression of a Flow-Related Ophthalmic Artery Aneurysm after Treatment of a Frontal DAVS: A Case Report. Interv Neuroradiol. 2004;10(3):265-268. doi:10.1177/159101990401000310
  27. ↑ 27.0 27.1 Hong Z, Noonan JE, Mitchell PJ, Hardy TG. Peripheral Ophthalmic Artery Aneurysm Associated with Multifocal Intracranial and Extracranial Aneurysms: Case Report and Literature Review. Case Rep Ophthalmol. Published online June 22, 2023:257-266. doi:10.1159/000530475
  28. ↑ 28.0 28.1 28.2 Day AL. Aneurysms of the ophthalmic segment: A clinical and anatomical analysis. J Neurosurg. 1990;72(5):677-691. doi:10.3171/jns.1990.72.5.0677
  29. ↑ 29.0 29.1 29.2 29.3 29.4 Dehdashti A, Safran A, Martin J, Rüfenacht D, De Tribolet N. Intraorbital ophthalmic artery aneurysm associated with basilar tip saccular aneurysm. Neuroradiology. 2002;44(7):600-603. doi:10.1007/s00234-002-0786-y
  30. ↑ 30.0 30.1 30.2 Garala P, Virdee J, Qureshi M, Gillow T. Intraorbital aneurysm of the ophthalmic artery. BMJ Case Rep. 2019;12(4):e227044. doi:10.1136/bcr-2018-227044
  31. ↑ 31.0 31.1 Park H, Nakagawa I, Yokoyama S, et al. Central Retinal Artery Thromboembolism without Ophthalmic Artery Occlusion During Stent-Assisted Coil Embolization of Ophthalmic Artery Aneurysm. World Neurosurg. 2019;121:77-82. doi:10.1016/j.wneu.2018.09.184
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