- Email: [email protected]
Carotid-Falciform Optic Neuropathy: Microsurgical Treatment
Accepted Manuscript Carotid-falciform optic neuropathy: microsurgical treatment M. Neil Woodall, MD, Cargill H. Alleyne, Jr., MD PII:
S1878-8750(17)30722-2
DOI:
10.1016/j.wneu.2017.05.034
Reference:
WNEU 5728
To appear in:
World Neurosurgery
Received Date: 27 December 2016 Revised Date:
4 May 2017
Accepted Date: 6 May 2017
Please cite this article as: Woodall MN, Alleyne Jr CH, Carotid-falciform optic neuropathy: microsurgical treatment, World Neurosurgery (2017), doi: 10.1016/j.wneu.2017.05.034. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Carotid-falciform optic neuropathy: microsurgical treatment M. Neil Woodall, MD, Cargill H. Alleyne, Jr, MD The Medical College of Georgia at Augusta University, Augusta, Georgia, 30912
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Corresponding author:
SC
M. Neil Woodall, MD [email protected] 1120 15th St. BI-3088 Augusta, GA 30912
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Key Words: Carotid Artery Ectasia; Falciform ligament; Microvascular Decompression; Optic Nerve; Optic Neuropathy
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Abbreviation List: ICA = Internal carotid artery, MVD = Microvascular decompression, ON = Optic nerve
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Abstract Background
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Several recent reports have implicated vascular ectasia and vessel contact with dysfunction of the visual apparatus. A subset of patients with pre-chiasmatic visual deterioration have an ectatic internal carotid artery (ICA) that displaces and flattens the optic nerve (ON) rostrally as the ON exits the skull base. We will offer a proposed pathophysiological mechanism and describe a straightforward surgical technique for dealing with this interesting problem.
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Methods
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Via an ipsilateral pterional craniotomy, the bony roof of the optic canal is removed. The falciform ligament is opened in parallel to the ON. Adhesions between the ICA and ON are then dissected, and a Teflon pledget is placed between the ICA and ON to complete the decompression. Results
Patients both in the literature and in this series experienced an improvement in their vision post-operatively. Conclusion
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We propose that three mechanisms contribute to this carotico-faliciform optic neuropathy: 1) mass effect from ICA ectasia, 2) ON irritation from vessel pulsatility, and 3) indirect compression by the falciform ligament from above. This fascinating disease process can be treated safely using standard microsurgical techniques with excellent outcomes.
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Introduction
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Visual loss due to compression of the optic apparatus by mass lesions such as aneurysms and tumors has been well documented1,2. Cranial neuropathies at other sites have been attributed to either direct compression from neighboring vessels or nerve irritation from vessel pulsitility. Trigeminal neuralgia is the prototypical example, but other examples include hemifacial spasm, hypoglossal neuralgia, and brainstem dysfunction3-6.
SC
Several recent reports have implicated vascular ectasia and vessel contact with dysfunction of the visual apparatus7-11. A subset of patients with pre-chiasmatic visual deterioration have an ectatic internal carotid artery (ICA) that displaces and flattens the optic nerve (ON) rostrally as the ON exits the skull base. This is best appreciated radiographically on coronal MRI images. We present our experience managing three such patients. We will offer a proposed pathophysiological mechanism and describe a straightforward surgical technique for dealing with this interesting problem.
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Methods
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Patients and Indications Three patients presented with progressive pre-chiasmatic visual loss. The first was a 34 year-old male with a monocular hemianopsia affecting the right eye. The second was a 36 year-old female with a monocular inferior temporal quadrantonopsia affecting the right eye. The third was a 69 year-old female with bilateral progressive visual loss worse in the left eye than the right. All patients had MRI evidence of ON flattening/displacement by an ectatic ICA (Figure 1). A multidisciplinary evaluation by neurosurgery, neuro-ophthalmology, and neurology was performed prior to surgical intervention. All three patients were felt to be of an acceptable surgical risk, and common alternative diagnoses that would explain visual loss were ruled out prior to surgical treatment. Research was conducted in accordance with the ethical guidelines put forth by the Medical College of Georgia Institutional Review Board. Due to the number of patients in this case series, the project qualified for an IRB exemption at our institution. Written informed consent for study participation was not required due to the retrospective nature of the study.
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Surgical Technique An ipsilateral pterional craniotomy is performed with the aid of the operating microscope. Subarachnoid dissection is performed to expose the optico-carotid cistern. The dura of the planum sphenoidale is opened in a semi-circular fashion over the optic foramen (Figure 2). This semicircular flap of dura can be reflected posteriorly to protect the intracranial ON during drilling. The bony roof of the optic canal is then removed using a diamond burr to expose the dura of the optic nerve inside the optic canal – frequent breaks during drilling and copious irrigation are critical to avoid thermal injury to the nerve. Next, the falciform ligament is opened with an arachnoid knife or microscissors taking care to cut in parallel to the ON. These maneuvers leave the rostral aspect of the ON free of any potential sources of compression from bone or soft tissue from above (Figure 3). Any adhesions between the ICA and ON are then dissected, and a
ACCEPTED MANUSCRIPT
Teflon pledget is placed between the ICA and ON to complete the decompression. (Video supplement)
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Results Patients 1 and 2 had improvement in subjective vision and visual fields at 4 and 6 month follow up. Patient 3 had improved subjective vision and stable visual fields at 3 months follow up, although her visual fields had been rapidly deteriorating prior to surgery. Representative visual fields pre-operatively and 1 year post-operatively can be seen in Figure 4. There were no complications related to surgical intervention. Discussion
M AN U
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Visual loss due to compression of the optic apparatus by mass lesions such as tumors and aneurysms has been well described in the literature1,2. Vessel pulsatility has been implicated as a causative factor in other cranial neuropathies (trigeminal neuralgia, hemifacial spasm, hypoglossal neuralgia), all of which respond to MVD3,4,6. Oculomotor nerve palsies that occur in the setting of posterior communicating artery aneurysms are thought to be due to both mass effect and pulsatility – this explains why oculomotor nerve palsies can improve following coil embolization, even in the setting of mass effect (although some authors have argued that direct surgical decompression is more efficacious)12-14. Improvement in visual function has also been observed after treatment of a giant ophthalmic aneurysm with flow diversion15. Several authors have recently published cases of ON MVD with good outcomes7-11.
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McClaughlin et al. described a case of a 56 year-old patient with visual loss attributed to compression of the optic chiasm from above by an ectatic anterior cerebral artery. The patient was treated with an MVD with complete resolution of his symptoms. They found four other cases in the literature describing visual loss due to vascular ectasia. They were the first authors to report MVD for this indication7.
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Strom et al. described an important case of a 63 year-old female with a progressive monocular temporal field defect. In this case the ICA was in contact with, but was not displacing or compressing, the ON. The authors performed an MVD with complete resolution of the patient’s symptoms8. Their report supports the notion that vessel pulsatility is involved in this pathophysiological mechanism. The patients in this series differ somewhat from the Strom report in that our patients had rostral displacement and flattening of the ON. The falciform ligament represents a folding-over of dura - as the dura of the planum sphenoidale turns on itself and becomes the dura of the optic foramen. The falciform ligament forms the soft tissue component of the rostral optic canal, and can behave as a knife-like edge in the presence of a mass lesion. Take, for example, this cadaveric specimen seen in Figure 4 that demonstrates an optic nerve that has been nearly transected by the falciform ligament in the presence of mass effect from and underlying ophthalmic segment aneurysm. (Figure 5)
ACCEPTED MANUSCRIPT
RI PT
We suspect that the disease process described in this manuscript results from three pathophysiological factors: 1) direct ON compression from below by a dolicoectatic ICA, 2) ON irritation and dysfunction due to vessel pulsatility, and 3) indirect compression from above by the knife-like edge of the falciform ligament. All three patients in this small case series suffered from visual loss in conjunction with vascular compression of the ipsilateral optic nerve.
M AN U
SC
The proposed surgical technique is designed to address these three proposed pathophysiological mechanisms. The bony optic canal is unroofed and the falciform ligament is opened. This maneuver decompresses the optic foramen, eliminates the edge of the falciform ligament as a possible source of compression, and allows for the nerve to be safely mobilized during the MVD. If the MVD were performed without opening the falciform ligament, it is possible that placement of the Teflon pledget could exacerbate ON compression against the falx in this subset of patients with already flattened and displaced optic nerves. At procedure end, the neurosurgeon can be confident that the affected ON is completely decompressed and protected from the pulsations of the neighboring ICA. Some authors have advocated for the complete removal of the anterior clinoid process during this procedure10,11. For the reasons outlined above, we do not believe that a complete anterior clinoidectomy is necessary to perform this procedure. Drilling of the clinoid can potentially put the clinoidal segment of the ICA at risk and should therefore be avoided unless deemed necessary to achieve adequate exposure.
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Given the small patient numbers and lack of collective experience with this poorly understood disease process, firm diagnostic criteria remain unclear. In general, we believe that carotid-falciform optic neuropathy should currently be considered a diagnosis of exclusion: common causes of visual loss must be ruled out prior to the consideration of optic nerve decompression. However, in the absence of an alternative diagnosis, patients with progressive monocular visual loss and displacement and/or flattening of the ipsilateral optic nerve should be considered for microsurgical optic nerve decompression.
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Conclusions A growing body of literature has implicated the ICA in some select cases of monocular visual loss. We propose that three mechanisms contribute to this carotico-faliciform optic neuropathy: 1) mass effect from ICA ectasia, 2) ON irritation from vessel pulsatility, and 3) indirect compression by the falciform ligament from above. This fascinating disease process can be treated safely using standard microsurgical techniques with excellent outcomes. Multidisciplinary pre-operative evaluation is mandatory to ensure proper patient selection. Further study is needed to better define this disease process that is just beginning to be understood.
ACCEPTED MANUSCRIPT
Acknowledgements Special thanks to Colby Polonsky for her illustrations. References Kanagalingam S, Gailloud P, Tamargo RJ, Subramanian PS, Miller NR. Visual Sequelae After Consensus-Based Treatment of Ophthalmic Artery Segment Aneurysms. Journal of Neuro-Ophthalmology. 2012;32(1):27-32. doi:10.1097/WNO.0b013e31823b6c60.
2.
Bor-Shavit E, Hammel N, Nahum Y, Rappaport ZH, Stiebel-Kalish H. Visual disability rates in a ten-year cohort of patients with anterior visual pathway meningiomas. Disability and Rehabilitation. 2014;37(11):958-962. doi:10.3109/09638288.2014.948141.
3.
Jannetta P, Jannetta PJ. Observations on the Etiology of Trigeminal Neuralgia, Hemifacial Spasm, Acoustic Nerve Dysfunction and Glossopharyngeal Neuralgia. Definitive Microsurgical Treatment and Results in 117 Patients. Minim Invasive Neurosurg. 2008;20(05):145-154. doi:10.1055/s-0028-1090369.
4.
Jannetta PJ. Arterial Compression of the Trigeminal Nerve at the Pons in Patients with Trigeminal Neuralgia*. Journal of Neurosurgery. 2007;107(1):216-237. doi:10.3171/JNS-07/07/0216.
5.
Rahimi SY, Shakir AR, Alleyne CH. Brainstem compression by “kissing vertebral arteries.” Neurology. 2008;71(12):954-954. doi:10.1212/01.wnl.0000325997.12607.cd.
6.
Nakahara Y, Kawashima M, Matsushima T, et al. Microvascular Decompression Surgery for Vertebral Artery Compression of the Medulla Oblongata: 3 Cases with Respiratory Failure and/or Dysphagia. World Neurosurgery. 2014;82(34):535.e11-535.e16. doi:10.1016/j.wneu.2014.01.012.
7.
McLaughlin N, Bojanowski MW. Microvascular decompression of the optic chiasm. Journal of Neurosurgery. 2011;114(3):857-860. doi:10.3171/2009.9.JNS081658.
SC
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TE D
EP
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8.
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1.
Strom RG, Fouladvand M, Pramanik BK, Doyle WK, Huang PP. Progressive optic neuropathy caused by contact with the carotid artery: Improvement after microvascular decompression. Clinical Neurology and Neurosurgery. 2012;114(6):812-815. doi:10.1016/j.clineuro.2012.01.001.
9.
Woodall MN, Woodall MN, Alleyne CH, Alleyne CH. Teaching NeuroImages: Microvascular decompression of the optic nerve. Neurology. 2013;81(18):e137e137. doi:10.1212/WNL.0b013e3182a9f40f.
10.
De Ridder D, Sime MJ, Taylor P, Menovsky T, Vanneste S. Microvascular
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Decompression of the Optic Nerve for Paroxysmal Phosphenes and Visual Field Deficit. World Neurosurgery. 2016;85:367.e5-367.e9. doi:10.1016/j.wneu.2015.09.094. Fargen KM, Blackburn S. Surgical Decompression for Optic Neuropathy From Carotid Artery Ectasia: Case Report with Technical Considerations. World Neurosurgery. 2014;82(1-2):239.e9-239.e12. doi:10.1016/j.wneu.2013.06.023.
12.
Gaberel T, Borha A, di Palma C, Emery E. Clipping Versus Coiling in the Management of Posterior Communicating Artery Aneurysms with Third Nerve Palsy: A Systematic Review and Meta-Analysis. World Neurosurgery. 2016;87(C):498–506.e4. doi:10.1016/j.wneu.2015.09.026.
13.
McCracken DJ, Lovasik BP, McCracken CE, et al. Resolution of Oculomotor Nerve Palsy Secondary to Posterior Communicating Artery Aneurysms. Neurosurgery. 2015;77(6):931-939. doi:10.1227/NEU.0000000000000965.
14.
Chen PR, Amin-Hanjani S, Albuquerque FC, McDougall C, Zabramski JM, Spetzler RF. Outcome of Oculomotor Nerve Palsy from Posterior Communicating Artery Aneurysms: Comparison of Clipping and Coiling. Neurosurgery. 2006;58(6):1040-1046. doi:10.1227/01.NEU.0000215853.95187.5E.
15.
Patel S, Fargen KM, Peters K, Krall P, Samy H, Hoh BL. Return of visual function after bilateral visual loss following flow diversion embolization of a giant ophthalmic aneurysm due to both reduction in mass effect and reduction in aneurysm pulsation. J NeuroIntervent Surg. 2014;7(1):e1-e1. doi:10.1136/neurintsurg-2013-010960.rep.
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Figure 1
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Figure Legends
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Coronal T2-weighted MRI shows flattening and rostral displacement of the optic nerve (arrow). Figure 2
Illustration demonstrating semi-circular incision in the dura of the anterior clinoid and planum. Figure 3 Illustration showing the optic nerve after bony and soft-tissue decompression. Figure 4
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The panel on the left shows pre-operative right eye visual fields in a patient with a partial inferior temporal field defect attributed to carotid-falciform optic neuropathy. The right panel shows visual field measurements taken from the same eye 1-year status post microvascular optic nerve decompression. The physiological punctum caecum (blind spot) is present on both pre-and post-operative visual field measurements.
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Figure 5
Cadaveric specimen demonstrating an ophthalmic segment aneurysm. Note that the ON has been partially transected by the falciform ligament due to aneurysm mass effect. Supplemental content legends
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Video
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Video demonstrating decompression of the optic foramen, opening of the falciform ligament, and placement of Teflon between the ICA and ON.
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Highlights • Vascular compression is the cause for several well described cranial neuropathies • Vascular compression of the optic apparatus can lead to visual loss
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• Nerve dysfunction occurs as a result of compression and vessel pulsatility
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• Release of the falciform ligament and microvascular decompression may alleviate symptoms
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Abbreviation List
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ICA = Internal carotid artery MVD = Microvascular decompression ON = Optic nerve
S1878-8750(17)30722-2
DOI:
10.1016/j.wneu.2017.05.034
Reference:
WNEU 5728
To appear in:
World Neurosurgery
Received Date: 27 December 2016 Revised Date:
4 May 2017
Accepted Date: 6 May 2017
Please cite this article as: Woodall MN, Alleyne Jr CH, Carotid-falciform optic neuropathy: microsurgical treatment, World Neurosurgery (2017), doi: 10.1016/j.wneu.2017.05.034. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Carotid-falciform optic neuropathy: microsurgical treatment M. Neil Woodall, MD, Cargill H. Alleyne, Jr, MD The Medical College of Georgia at Augusta University, Augusta, Georgia, 30912
RI PT
Corresponding author:
SC
M. Neil Woodall, MD [email protected] 1120 15th St. BI-3088 Augusta, GA 30912
M AN U
Key Words: Carotid Artery Ectasia; Falciform ligament; Microvascular Decompression; Optic Nerve; Optic Neuropathy
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Abbreviation List: ICA = Internal carotid artery, MVD = Microvascular decompression, ON = Optic nerve
ACCEPTED MANUSCRIPT
Abstract Background
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Several recent reports have implicated vascular ectasia and vessel contact with dysfunction of the visual apparatus. A subset of patients with pre-chiasmatic visual deterioration have an ectatic internal carotid artery (ICA) that displaces and flattens the optic nerve (ON) rostrally as the ON exits the skull base. We will offer a proposed pathophysiological mechanism and describe a straightforward surgical technique for dealing with this interesting problem.
SC
Methods
M AN U
Via an ipsilateral pterional craniotomy, the bony roof of the optic canal is removed. The falciform ligament is opened in parallel to the ON. Adhesions between the ICA and ON are then dissected, and a Teflon pledget is placed between the ICA and ON to complete the decompression. Results
Patients both in the literature and in this series experienced an improvement in their vision post-operatively. Conclusion
AC C
EP
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We propose that three mechanisms contribute to this carotico-faliciform optic neuropathy: 1) mass effect from ICA ectasia, 2) ON irritation from vessel pulsatility, and 3) indirect compression by the falciform ligament from above. This fascinating disease process can be treated safely using standard microsurgical techniques with excellent outcomes.
ACCEPTED MANUSCRIPT
Introduction
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Visual loss due to compression of the optic apparatus by mass lesions such as aneurysms and tumors has been well documented1,2. Cranial neuropathies at other sites have been attributed to either direct compression from neighboring vessels or nerve irritation from vessel pulsitility. Trigeminal neuralgia is the prototypical example, but other examples include hemifacial spasm, hypoglossal neuralgia, and brainstem dysfunction3-6.
SC
Several recent reports have implicated vascular ectasia and vessel contact with dysfunction of the visual apparatus7-11. A subset of patients with pre-chiasmatic visual deterioration have an ectatic internal carotid artery (ICA) that displaces and flattens the optic nerve (ON) rostrally as the ON exits the skull base. This is best appreciated radiographically on coronal MRI images. We present our experience managing three such patients. We will offer a proposed pathophysiological mechanism and describe a straightforward surgical technique for dealing with this interesting problem.
M AN U
Methods
EP
TE D
Patients and Indications Three patients presented with progressive pre-chiasmatic visual loss. The first was a 34 year-old male with a monocular hemianopsia affecting the right eye. The second was a 36 year-old female with a monocular inferior temporal quadrantonopsia affecting the right eye. The third was a 69 year-old female with bilateral progressive visual loss worse in the left eye than the right. All patients had MRI evidence of ON flattening/displacement by an ectatic ICA (Figure 1). A multidisciplinary evaluation by neurosurgery, neuro-ophthalmology, and neurology was performed prior to surgical intervention. All three patients were felt to be of an acceptable surgical risk, and common alternative diagnoses that would explain visual loss were ruled out prior to surgical treatment. Research was conducted in accordance with the ethical guidelines put forth by the Medical College of Georgia Institutional Review Board. Due to the number of patients in this case series, the project qualified for an IRB exemption at our institution. Written informed consent for study participation was not required due to the retrospective nature of the study.
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Surgical Technique An ipsilateral pterional craniotomy is performed with the aid of the operating microscope. Subarachnoid dissection is performed to expose the optico-carotid cistern. The dura of the planum sphenoidale is opened in a semi-circular fashion over the optic foramen (Figure 2). This semicircular flap of dura can be reflected posteriorly to protect the intracranial ON during drilling. The bony roof of the optic canal is then removed using a diamond burr to expose the dura of the optic nerve inside the optic canal – frequent breaks during drilling and copious irrigation are critical to avoid thermal injury to the nerve. Next, the falciform ligament is opened with an arachnoid knife or microscissors taking care to cut in parallel to the ON. These maneuvers leave the rostral aspect of the ON free of any potential sources of compression from bone or soft tissue from above (Figure 3). Any adhesions between the ICA and ON are then dissected, and a
ACCEPTED MANUSCRIPT
Teflon pledget is placed between the ICA and ON to complete the decompression. (Video supplement)
RI PT
Results Patients 1 and 2 had improvement in subjective vision and visual fields at 4 and 6 month follow up. Patient 3 had improved subjective vision and stable visual fields at 3 months follow up, although her visual fields had been rapidly deteriorating prior to surgery. Representative visual fields pre-operatively and 1 year post-operatively can be seen in Figure 4. There were no complications related to surgical intervention. Discussion
M AN U
SC
Visual loss due to compression of the optic apparatus by mass lesions such as tumors and aneurysms has been well described in the literature1,2. Vessel pulsatility has been implicated as a causative factor in other cranial neuropathies (trigeminal neuralgia, hemifacial spasm, hypoglossal neuralgia), all of which respond to MVD3,4,6. Oculomotor nerve palsies that occur in the setting of posterior communicating artery aneurysms are thought to be due to both mass effect and pulsatility – this explains why oculomotor nerve palsies can improve following coil embolization, even in the setting of mass effect (although some authors have argued that direct surgical decompression is more efficacious)12-14. Improvement in visual function has also been observed after treatment of a giant ophthalmic aneurysm with flow diversion15. Several authors have recently published cases of ON MVD with good outcomes7-11.
TE D
McClaughlin et al. described a case of a 56 year-old patient with visual loss attributed to compression of the optic chiasm from above by an ectatic anterior cerebral artery. The patient was treated with an MVD with complete resolution of his symptoms. They found four other cases in the literature describing visual loss due to vascular ectasia. They were the first authors to report MVD for this indication7.
AC C
EP
Strom et al. described an important case of a 63 year-old female with a progressive monocular temporal field defect. In this case the ICA was in contact with, but was not displacing or compressing, the ON. The authors performed an MVD with complete resolution of the patient’s symptoms8. Their report supports the notion that vessel pulsatility is involved in this pathophysiological mechanism. The patients in this series differ somewhat from the Strom report in that our patients had rostral displacement and flattening of the ON. The falciform ligament represents a folding-over of dura - as the dura of the planum sphenoidale turns on itself and becomes the dura of the optic foramen. The falciform ligament forms the soft tissue component of the rostral optic canal, and can behave as a knife-like edge in the presence of a mass lesion. Take, for example, this cadaveric specimen seen in Figure 4 that demonstrates an optic nerve that has been nearly transected by the falciform ligament in the presence of mass effect from and underlying ophthalmic segment aneurysm. (Figure 5)
ACCEPTED MANUSCRIPT
RI PT
We suspect that the disease process described in this manuscript results from three pathophysiological factors: 1) direct ON compression from below by a dolicoectatic ICA, 2) ON irritation and dysfunction due to vessel pulsatility, and 3) indirect compression from above by the knife-like edge of the falciform ligament. All three patients in this small case series suffered from visual loss in conjunction with vascular compression of the ipsilateral optic nerve.
M AN U
SC
The proposed surgical technique is designed to address these three proposed pathophysiological mechanisms. The bony optic canal is unroofed and the falciform ligament is opened. This maneuver decompresses the optic foramen, eliminates the edge of the falciform ligament as a possible source of compression, and allows for the nerve to be safely mobilized during the MVD. If the MVD were performed without opening the falciform ligament, it is possible that placement of the Teflon pledget could exacerbate ON compression against the falx in this subset of patients with already flattened and displaced optic nerves. At procedure end, the neurosurgeon can be confident that the affected ON is completely decompressed and protected from the pulsations of the neighboring ICA. Some authors have advocated for the complete removal of the anterior clinoid process during this procedure10,11. For the reasons outlined above, we do not believe that a complete anterior clinoidectomy is necessary to perform this procedure. Drilling of the clinoid can potentially put the clinoidal segment of the ICA at risk and should therefore be avoided unless deemed necessary to achieve adequate exposure.
EP
TE D
Given the small patient numbers and lack of collective experience with this poorly understood disease process, firm diagnostic criteria remain unclear. In general, we believe that carotid-falciform optic neuropathy should currently be considered a diagnosis of exclusion: common causes of visual loss must be ruled out prior to the consideration of optic nerve decompression. However, in the absence of an alternative diagnosis, patients with progressive monocular visual loss and displacement and/or flattening of the ipsilateral optic nerve should be considered for microsurgical optic nerve decompression.
AC C
Conclusions A growing body of literature has implicated the ICA in some select cases of monocular visual loss. We propose that three mechanisms contribute to this carotico-faliciform optic neuropathy: 1) mass effect from ICA ectasia, 2) ON irritation from vessel pulsatility, and 3) indirect compression by the falciform ligament from above. This fascinating disease process can be treated safely using standard microsurgical techniques with excellent outcomes. Multidisciplinary pre-operative evaluation is mandatory to ensure proper patient selection. Further study is needed to better define this disease process that is just beginning to be understood.
ACCEPTED MANUSCRIPT
Acknowledgements Special thanks to Colby Polonsky for her illustrations. References Kanagalingam S, Gailloud P, Tamargo RJ, Subramanian PS, Miller NR. Visual Sequelae After Consensus-Based Treatment of Ophthalmic Artery Segment Aneurysms. Journal of Neuro-Ophthalmology. 2012;32(1):27-32. doi:10.1097/WNO.0b013e31823b6c60.
2.
Bor-Shavit E, Hammel N, Nahum Y, Rappaport ZH, Stiebel-Kalish H. Visual disability rates in a ten-year cohort of patients with anterior visual pathway meningiomas. Disability and Rehabilitation. 2014;37(11):958-962. doi:10.3109/09638288.2014.948141.
3.
Jannetta P, Jannetta PJ. Observations on the Etiology of Trigeminal Neuralgia, Hemifacial Spasm, Acoustic Nerve Dysfunction and Glossopharyngeal Neuralgia. Definitive Microsurgical Treatment and Results in 117 Patients. Minim Invasive Neurosurg. 2008;20(05):145-154. doi:10.1055/s-0028-1090369.
4.
Jannetta PJ. Arterial Compression of the Trigeminal Nerve at the Pons in Patients with Trigeminal Neuralgia*. Journal of Neurosurgery. 2007;107(1):216-237. doi:10.3171/JNS-07/07/0216.
5.
Rahimi SY, Shakir AR, Alleyne CH. Brainstem compression by “kissing vertebral arteries.” Neurology. 2008;71(12):954-954. doi:10.1212/01.wnl.0000325997.12607.cd.
6.
Nakahara Y, Kawashima M, Matsushima T, et al. Microvascular Decompression Surgery for Vertebral Artery Compression of the Medulla Oblongata: 3 Cases with Respiratory Failure and/or Dysphagia. World Neurosurgery. 2014;82(34):535.e11-535.e16. doi:10.1016/j.wneu.2014.01.012.
7.
McLaughlin N, Bojanowski MW. Microvascular decompression of the optic chiasm. Journal of Neurosurgery. 2011;114(3):857-860. doi:10.3171/2009.9.JNS081658.
SC
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8.
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1.
Strom RG, Fouladvand M, Pramanik BK, Doyle WK, Huang PP. Progressive optic neuropathy caused by contact with the carotid artery: Improvement after microvascular decompression. Clinical Neurology and Neurosurgery. 2012;114(6):812-815. doi:10.1016/j.clineuro.2012.01.001.
9.
Woodall MN, Woodall MN, Alleyne CH, Alleyne CH. Teaching NeuroImages: Microvascular decompression of the optic nerve. Neurology. 2013;81(18):e137e137. doi:10.1212/WNL.0b013e3182a9f40f.
10.
De Ridder D, Sime MJ, Taylor P, Menovsky T, Vanneste S. Microvascular
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Coronal T2-weighted MRI shows flattening and rostral displacement of the optic nerve (arrow). Figure 2
Illustration demonstrating semi-circular incision in the dura of the anterior clinoid and planum. Figure 3 Illustration showing the optic nerve after bony and soft-tissue decompression. Figure 4
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The panel on the left shows pre-operative right eye visual fields in a patient with a partial inferior temporal field defect attributed to carotid-falciform optic neuropathy. The right panel shows visual field measurements taken from the same eye 1-year status post microvascular optic nerve decompression. The physiological punctum caecum (blind spot) is present on both pre-and post-operative visual field measurements.
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Figure 5
Cadaveric specimen demonstrating an ophthalmic segment aneurysm. Note that the ON has been partially transected by the falciform ligament due to aneurysm mass effect. Supplemental content legends
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Video demonstrating decompression of the optic foramen, opening of the falciform ligament, and placement of Teflon between the ICA and ON.
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Highlights • Vascular compression is the cause for several well described cranial neuropathies • Vascular compression of the optic apparatus can lead to visual loss
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• Nerve dysfunction occurs as a result of compression and vessel pulsatility
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• Release of the falciform ligament and microvascular decompression may alleviate symptoms
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Abbreviation List
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ICA = Internal carotid artery MVD = Microvascular decompression ON = Optic nerve