Restorative Neurology and Neuroscience 32 (2014) 655–661 DOI 10.3233/RNN-140395 IOS Press
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Visual improvement and pain resolution in traumatic optic nerve sheath meningocele treated by optic nerve sheath fenestration Chen Huia,b,h,i,1,∗ , Wu Xiaoyunc,1 , Liang Yid,1 , Chen Ningboe,1 , Qiu Xizhonga , Yang Shaoweia , Lin Weia , Zhao Maozhuf , Ma Wubof , Pan Xuefeif , Lai Lic , Tan Haibing , Zeng Daiwenb and Jiang Yongj,∗ a Department
of Ophthalmology, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China b Laboratory Animal Institute, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China c Department of Radiology, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China d Department of Neurology, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China e Emergency Department, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China f Department of Ophthalmology (East Area), Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China g Neurosurgery Department, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China h School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China i School of Materials Science and Engineering, Southwest Jiaotong University, Chengdu, Sichuan, China j Neurosurgery Department, Lu Zhou Medical College, Luzhou, Sichuan, China
Abstract. Purpose: There is no consensus as to the optimum treatment for traumatic optic neuropathy (TON). The decision to intervene medically or surgically, or simply observe was recommended to be on an individual basis. The purpose of this study is to test whether optic nerve sheath fenestration (ONSF) could improve vision in patients with traumatic optic nerve sheath meningocele, although it was reported to be effective in patients with traumatic optic nerve sheath hematoma. Methods: ONSF was performed on two traumatic patients with dilated optic nerve sheath from MRI.
1 Chen Hui, Wu Xiaoyun, Liang Yi and Chen Ningbo contributed
equally to this work. ∗ Corresponding author: Chen Hui, No. 32, 1st ring road, 2nd west section, Chengdu, Sichuan 610072, China. Tel.: +86 028 6708 7565; Fax: +86 028 6708 7557; E-mail: [email protected]; Jiang Yong, Taiping Street 25th, Luzhou, Sichuan 646000, China. Tel.: +86 830 3165 461; Fax: +86 830 2392 753; E-mail: [email protected].
0922-6028/14/$27.50 © 2014 – IOS Press and the authors. All rights reserved
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C. Hui et al. / Visual improvement and pain resolution
Results: Both patients initially suspected as traumatic optic nerve sheath hematoma were diagnosed as traumatic optic nerve sheath meningocele by intraoperative findings of the enlarged optic nerve sheath and clear fluid drained without evidence of blood in the subdural space. Moreover, significant orbit/head pain resolution and visual improvement within a week after ONSF was found. Conclusions: When TON presents with an enlarged optic nerve/sheath on CT or MRI with visual loss, an optic nerve sheath meningocele should be considered with the consideration that ONSF may benefit both visual acuity and post-traumatic pain, if present. Keywords: Traumatic optic neuropathy, optic nerve sheath meningocele, optic nerve sheath fenestration (ONSF), head/orbital pain
1. Introduction Optic nerve injury may result from direct trauma, indirect trauma, or a combination of both. The mechanism of indirect traumatic optic neuropathy (TON) is diverse and complicated. There is no consensus as to the optimum treatment for TON. The largest prospective comparison study of patients of all ages with TON found no difference in outcome among patients treated with surgical optic nerve canal decompression, highdose steroids, or observation (Levin et al., 1999). The decision to intervene medically or surgically, or simply observe has been recommended to be on an individual basis, rather than a simple standard of care (Levin et al., 1994). Optic nerve sheath fenestration (ONSF) was first described by De Wecker in 1872 as an incision in the retrobulbar optic nerve sheath to relieve elevated intracranial pressure (De, 1872). The procedure now is typically performed in instances of papilledema due to idiopathic intracranial hypertension (IIH) with rapid and/or progressive visual loss. ONSF has been anecdotally reported to improve vision in patients with traumatic optic nerve sheath hematoma (Guy et al., 1989; Muthukumar, 1997; Sergott et al., 1990). Herein, we report two cases of traumatic optic nerve sheath meningocele, who were initially suspected to have optic nerve sheath hematomas, and received immediate orbit/head pain resolution with significant visual improvement within a week after ONSF. 2. Methods ONSF was performed using a medial transconjunctival approach under general anesthesia. In detail, a 180◦ peritomy at the nasal limbus is performed with relaxing incisions and dissection down to
bare sclera. The medial rectus muscle is isolated with a muscle hook, and tagged with 6-0 Vicryl suture, then muscle is disinserted. Hemostasis is performed with needle-point cautery. A 5-0 Vicryl suture is passed in a running stitch fashion at the site of the medial rectus disinsertion to be used as a traction suture. The globe is fully and laterally abducted with the traction suture. A careful retraction of the orbital soft tissue is undertaken with a Schepens orbital retractor and cotton-tipped applicators until clear exposure of long posterior ciliary arteries and the optic nerve sheath under the operating microscope. An avascular area of anterior optic nerve sheath was incised using a long 15◦ blade (Sharpoint, the one used for paracentesis in cataract surgery). The incision is made about 4 to 5 mm in length and about 2 mm posterior to the junction of the globe and the nerve. Cerebrospinal fluid is drained on incision of the sheath. The edge of the sheath incision is gently lifted away from optic nerve with a long-handled finetoothed forceps, and a long-handled scissors is used to excise 3 × 5-mm sheath. The traction suture is then removed. The medial rectus muscle is reattached to its insertion point using the 6-0 Vicryl suture. The conjunctiva is then reattached with an 8-0 Vicryl suture. 3. Case reports Case 1: On the 18th of July, 2012, a 48-year-old man suffered a contusion to his left eyeball by a fist. He subsequently suffered left orbital pain and decreased vision. An examination several hours after the injury in a local emergent eye clinic disclosed visual acuity of 0.1 (20/200) on the left and 1.0 (20/20) on the right, left periorbital swelling, with a normal anterior segment and fundus examination. Pupillary reaction was not recorded. He was given oflaxcin eyedrops and observed with no improvement in vision or pain.
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operatively, the visual acuity on the left had improved to 0.3 (20/60). The visual acuity continued to improve by the seventh post-operative day to 0.5 (20/40). The patient was examined each day in the following week without continuing visual improvement, and then was discharged. The visual acuity on the left remained 0.5 (20/40) at one year follow-up without orbit/head pain complaint.
Fig. 1. Transverse axial orbital MRI (T2-weighted fat-suppressed sequence) revealing a ballooned left retrobulbar optic nerve sheath (white arrow).
On the 12th of August, 2012, he was referred to an ophthalmologist in another hospital. Examination there showed the same acuity of 0.1 (20/200) on the left and normal anterior segment and fundus, with a left afferent pupillary defect. Intraocular pressure (applanation) was 18 mmHg OD and 16 mmHg OS. Ocular motility was normal without proptosis. A diagnosis of traumatic optic neuropathy with post-traumatic headache was made. He was given prednisone 40 mg per day for one week, then gradually tapered, with no improvement in vision or pain. On the 22nd of August, 2012, he was referred to the ophthalmology department in Sichuan Provincial People’s Hospital (SPPH) for continued decreased vision on the left and severe left-sided headache. Visual acuity and ocular examination was unchanged. A magnetic resonance image (MRI) of the brain and orbits demonstrated the suggestions of a ballooned retrabulbar optic nerve sheath with high signal (Fig. 1). An initial diagnosis of optic nerve sheath hematoma was suspected. On the 28th of August 2012, ONSF was performed on the left under general anesthesia. Under the microscope, the optic nerve sheath was slightly ballooned. A significant amount of clear fluid was noted when the incision was made and a 3 × 5-mm sheath window was excised. Specifically, there was no hematoma or bleeding discovered from the subdural space. Postoperatively, intravenous 10 mg dexamethasone and cefathamidine were given for 5 days. On the first day post-operatively, the patient excitedly reported that the left orbit-front-temporal pain had completely resolved, although the visual acuity on the left remained unchanged. By the fourth day post-
Case 2: On the 9th of January, 2013, a 21-year-old man suffered a contusion to the right face and orbit from a motor vehicle accident with loss of consciousness. One day after injury he was conscious and complained of decreased vision in the right eye. An examination by a local ophthalmologist demonstrated a visual acuity on the right of 0.05 (20/400), a right afferent relative pupillary defect, with a normal anterior segment and fundus examination. He was given prednisone 40 mg per day orally for one week with no improvement of vision, then discontinued. On the 22nd of January, 2013, he was referred to SPPH for further treatment. Examination at that time disclosed a corrected visual acuity of 0.05 (20/400) on the right, and 1.0 (20/20) on the left. The anterior segment and fundus examination were normal bilaterally, with the intraocular pressures (applanation) 16 mmHg OD and 15 mmHg OS. A right afferent relative pupillary defect was present. Ocular motility was full and there was no proptosis. A computed tomography (CT) of the brain and orbit showed a small right frontotemporal epidural hematoma (9.2 mm in thicknesses), multiple fractures of the right lateral and upper orbit walls, and moderate enlargement of both optic nerves (Fig. 2). MRI of orbit suggested an enlarged right optic nerve sheath (Fig. 3). A right optic nerve sheath hematoma was suspected. On the 24th of January 2013, a right ONSF was performed. Under microscope, the optic nerve sheath appeared marked enlarged. A 3 × 5-mm sheath window was excised, and clear fluid was drained without evidence of blood in the subdural space. Postoperatively, intravenous 10 mg dexamethasone and cefathamidine was given for 5 days. On the second day post-operatively, the patient’s vision improved to 0.1 (20/200) OD with resolution of right orbital pressure. The vision gradually improved each day on the right to 0.4 (20/50) until discharge on the seventh post-operative day. The visual acuity on the right maintained at 0.5 (20/40) 8 months postoperatively, without complaints of pain.
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Fig. 2. Axial orbital CT showing multiple fractures in the right lateral and moderate enlargement of bilateral optic nerves (about 6 mm wide).
Fig. 3. Transverse orbital MRI (T2-weighted fat-suppressed sequence) showing an enlarged right retrobulbar optic nerve sheath with a curved borderline (white arrow).
4. Discussion An optic nerve sheath cyst or meningocele, was first proposed and defined as “dilation of the optic nerve sheath and expansion of the CSF filled space around the optic nerve” by Garrity (Garrity et al., 1990). Similar to an optic nerve hematoma, it presented as an enlarged optic nerve/sheath on CT (Rothfus et al., 1984) and typically as an expanded subarachnoid space around the optic nerve in MRI (Garrity et al., 1990). However, because of the small dimensions of the optic nerve and its subarachnoid space, even high resolution CT and MRI may fail to reveal enlargement of the optic nerve/sheath silhouette (Sergott et al., 1990). In our report, two cases of traumatic optic nerve/sheath enlargement, which were initially mis-diagnosed as
optic nerve sheath hematoma from MRI, but ultimately were suspected as an optic nerve sheath meningocele, received immediate orbit/head pain resolution with significant visual improvement within a week after ONSF. In the past three decades, there have been a total of seven cases of successful treatment of TON with enlarged optic nerve/sheath in imaging through ONSF (Goldenberg-Cohen et al., 2004; Guy et al., 1989; Hupp et al., 1984; Mauriello et al., 1992; Muthukumar, 1997; Sergott et al., 1990). The detailed clinic course, imaging and surgical findings were compared with our two cases in Table 1 (Table 1). Of those seven, three were verified as traumatic optic nerve sheath hematoma by both CT and surgery (Guy et al., 1989; Muthukumar, 1997) or surgery alone (Sergott et al., 1990). One was diagnosed as hematoma through CT presentation without surgical findings (Mauriello et al., 1992) and one was presented with no recording of imaging or surgical findings (Goldenberg-Cohen et al., 2004). The remained two were probable traumatic optic nerve sheath meningoceles (Guy et al., 1989; Hupp et al., 1984). In Hupp’s report, the enlarged optic nerve sheath on CT was verified by the surgical findings of a ballooned optic nerve sheath, with 1.5 ml clear fluid drained by ONSF (Hupp et al., 1984). However as it was associated with progressive venous obstructive retinopathy, the authors were uncertain if the visual loss was from a venous obstructive retinopathy or the meningocele or both (Hupp et al., 1984). It was hard to be completely contributed to the compromise from TON (Guy et al., 1989). Guy also reported two cases of enlarged optic nerve/sheath; one was described as a “cyst” in surgery, but was discussed as a “presumed arachnoid cyst”, with no record of clot evacuated or clear CSF drained in the surgical findings (Guy et al., 1989). In our two cases, the MRI
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Table 1 Comparing reported cases of TON treated by ONSF with our cases Final diagnosis
Time from injury Vision changes to ONSF after trauma
Imaging findings
Surgical findings
Post-operational vision changes
Progressive from “following light” to NLP within 1 day. 6/60 2 days after injury
“A hematoma enlarging ONS” in CT”, no MRI
A small hematoma evacuated
1 D later: CF 1 Y later: 8/30; with optic head atrophy
Enlarged ON in CT 14hs after injury, no MRI
A swollen discolored ONS and a small clot under the ONS.
Progressive from 6/15 to 6/60
Unreported
A subdural hemorrhage and the blood drained
No visual report in the 1st W 3 M later: 6/36 1 Y later: 6/36 6/9, the time to reach 6/9 unreported
CF/1 ft
“ONS hematoma” in CT, no MRI
No blood or fluid drained
20/25; the time to reach 20/25 unreported
unknown
NLP
unreported
unreported
20/200, the time to reach 20/200 unreported
over 3 Ms
Progressive from a large ONS in the 1st CT, A marked ballooned 20/25 to 20/400 further enlargement in ONS, and 1.5 ml clear the 2nd CT; an fluid drained enlarged, fluid-filled ONS 9.3 mm in diameter in the 1st echography, and a further 1.4 mm increase in the 2nd echography Progressive loss enlargement of ONS and A ballooned ONS and the from 20/25 to a orbital floor fracture “cyst” drained (no fluid 20/200 during in CT, no MRI or clot recorded, and the the 1st week term “presumed cyst” was used in discussion) Stable and A ballooned ONSF in Clear fluid drained 0.1(20/200) MRI 2 Ms after trauma
ONS hematoma from Guy’s case 1 (Guy et al., 1989)
1–2 days
ONS hematoma by Muthukumar (Muthukumar, 1997) ONS hematoma by Sergott (Sergott et al., 1990) Imaging diagnosis of ONS hematoma in Mauriello’s 17th case (Mauriello et al., 1992) Unknown by Goldenberg-Cohen (Goldenberg-Cohen et al., 2004) Posttraumatic venous obstructive retinopathy associated with enlarged ONS by Hupp (Hupp et al., 1984)
2 days
3 days
3 to 5 days
A presumed cyst in Guy’s case 2 (Guy et al., 1989)
8 days
Traumatic ONS meningocele (our cases 1)
6W
Traumatic ONS meningocele (our case 2)
2W
Stable and 0.05(20/400)
1 W later: 20/200+ 3 W later: 20/50+ Next 8 Ms follow-up: no change
1 W later: 20/50 1 Y later: 20/25, with optic (head) atrophy
No improvement in the first four days
5 days later: 0.3 (20/60) 7 days later: 0.5 (20/40) 2 weeks later: 0.5 (20/40) 1 year later: 0.5 (20/40) A slightly enlarged ON in A marked ballooned ONS 1 day later:0.1 CT and a ballooned and clear fluid drained (20/200) ONSF in MRI 14 days 3 days later: 0.2 after trauma (20/200) 5 days later: 0.3 (20/60) 7 days later: 0.4 (20/50) 2 weeks later: 0.5 (20/40) 8 Ms later: 0.5 (20/40)
Note: ONS: optic nerve sheath; ONSD: optic nerve sheath fenestration; NLP: no light perception; CF: count fingers; W: week; M: month; Y: year.
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findings of patulous expansion of CSF-filled space in the retrobulbar optic nerve sheath were consistent with the surgical findings of ballooned optic nerve sheath and the clear, colorless CSF drained. We suggest this may be two cases of post-traumatic optic nerve sheath meningocele. Although spontaneous visual improvement after trauma (Yu-Wai-Man et al., 2007) and the visual improvement from steroids treatment (Spoor et al., 1990) is possible, in our two cases preoperative treatment with steroids and observation for as long as forty days or two weeks respectively did not show visual improvement. It’s of extreme low probability that the visual improvement from pre-operative steroids or spontaneous visual improvement happened to occur just on the post-ONSF weeks. A recent report that optic canal decompression combined with optic sheath incision resulted in a better visual recovery than optic canal decompression alone in TON, especially in subjects without optic canal fracture (Thaker et al., 2009), indicates a potential benefit of ONSF to TON. The clinic course in our two cases suggests that ONSF might have contributed to their marked visual improvement. Actually in our cases after decompression, postoperatively the vision improved mainly in the first week and discontinued two to three weeks later without showing spontaneous improvement in the follow-up period as long as one year or eight months. So, we think that it is the ONSF, not the pre-operative steroids contributes to the patients’ visual improvement. To our knowledge, this was the first report of visual improvement from TON with optic nerve sheath meningoceles through ONSF. The mechanism of ONSF for the treatment of posttraumatic meningocele remains unclear. Jinkins et al. suggested that the obstructed flow of CSF along the optic subarachnoid space plays an important role in various conditions including trauma (Jinkins, 1987). That obstruction might increase the local pressure in the distal optic nerve sheath even with normal intracranial pressure. That has also been suggested in others’ findings (Golnik et al., 1998). Furthermore, Carson (Carson et al., 2010) and Tourtier (Tourtier et al., 2011) suggest that the increase of optic nerve diameter after trauma could be due to raised intracranial pressure. The speculation of direct decompression to the intra-opticnerve-sheath pressure, as well as increased intracranial pressure (ICP) in head trauma (Skoloudik et al., 2011) cannot be excluded. Most importantly, the relief of secondary injury to the optic nerve (Parab et al., 2013)
from recently recognized optic nerve sheath compartment syndrome (Jaggi et al., 2007; Killer et al., 2006), in which the subarachnoid spaces (SAS) of the optic nerve can become separated from other CSF compartments in certain optic nerve disorders, might contribute to the mechanism. Surprisingly, in our two patients the headache and/or orbital pain disappeared post-operatively. Headache and/or retrobulbar pressure or pain as a chief complaint has been described in other non-traumatic meningoceles (Garrity et al., 1990; Golnik et al., 1998). There have been limited reports of resolution of head/orbital pain from ONSD. We believe this is also the first report of headache and/or orbital pressure immediately resolved in a patient with traumatic optic nerve sheath meningocele after ONSF. The mechanism for pain in meningocele and pain relief by ONSF is unclear. Garrity et al. speculated the headache or orbital pain/pressure was most likely produced by the “stretching” or compression to the optic nerve sheath which was innervated by trigeminal nerve (Garrity et al., 1990). We agree with Garrity’s speculation and suggest that the local pressure in meningocele was immediately released by ONSF and the pain was resolved because of relief of stretching or compression to the optic nerve sheath, although it is well-known that ONSF could relieve the headache in idiopathic intracranial hypertension (IIH) with the mechanism thought to be related with the decreased ICP. In summary, we agree with the suggestion by Wojno (Wojno et al., 1986) that ONSF may be of benefit and should be considered when there is no spontaneous improvement of vision or severe headache in traumatic optic neuropathy. Moreover, considering the good results (Guy et al., 1989; Muthukumar, 1997; Sergott et al., 1990) to traumatic optic nerve sheath hematoma by ONSF (reviewed in Table 1), we suggest traumatic optic neuropathy presenting with an enlarged optic nerve or distended retrobulbar optic sheath on neuroimaging, should be treated with ONSF, although optic nerve sheath meningocele should be differentiated from sheath hematoma.
Acknowledgments The present work was jointly funded by the High and New Technology Program in Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital of China (No. 2012-6), National Natural Science
C. Hui et al. / Visual improvement and pain resolution
Foundation of China (81271035/H1205, 81371319), the Program for New Century Excellent Talents in University (NCET-12-1057) and Basic Research Foundation for Public Scientific Research Institutions in Science and Technology Department of Sichuan Province, China. We acknowledge the assistance of Dr. Bradley K. Farris (Dean McGee Eye Institute, USA) for his invaluable surgical introduction.
References Carson, H.J., Lingamfelter, D., & Dudley, M.H. (2010). Optic nerve trauma with unilateral edema as a result of head injury. J Forensic Leg Med, 17(5), 283-284. De, W.L. (1872). On incision of the optic nerve in cases of neuroretinitis. Int Ophthalmol Cong Reps(4), 11-14. Garrity, J.A., Trautmann, J.C., Bartley, G.B., Forbes, G., Bullock, J.D. Jr., & Jones, T.W., et al. (1990). Optic nerve sheath meningoceles. Clinical and radiographic features in 13 cases with a review of the literature. Ophthalmology, 97(11), 15191531. Goldenberg-Cohen, N., Miller, N.R., & Repka, M.X. (2004). Traumatic optic neuropathy in children and adolescents. J AAPOS, 8(1), 20-27. Golnik, K.C., & Kersten, R.C. (1998). Optic nerve head swelling in the Hadju-Cheney syndrome. J Neuroophthalmol, 18(1), 60-65. Guy, J., Sherwood, M., & Day, A.L. (1989). Surgical treatment of progressive visual loss in traumatic optic neuropathy. Report of two cases. J Neurosurg, 70(5), 799-801. Hupp, S.L., Buckley, E.G., Byrne, S.F., Tenzel, R.R., Glaser, J.S., & Schatz, N.S. (1984). Posttraumatic venous obstructive retinopathy associated with enlarged optic nerve sheath. Arch Ophthalmol, 102(2), 254-256. Jaggi, G.P., Mironov, A., Huber, A.R., & Killer, H.E. (2007). Optic nerve compartment syndrome in a patient with optic nerve sheath meningioma. Eur J Ophthalmol, 17(3), 454-458. Jinkins, J.R. (1987). Optic hydrops: isolated nerve sheath dilation demonstrated by CT. AJNR Am J Neuroradiol, 8(5), 867-870. Killer, H.E., Jaggi, G.P., Flammer, J., Miller, N.R., & Huber, A.R. (2006). The optic nerve: a new window into cerebrospinal fluid composition? Brain, 129(Pt 4), 1027-1030.
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Levin, L.A., Beck, R.W., Joseph, M.P., Seiff, S., & Kraker, R. (1999). The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology, 106(7), 1268-1277. Levin, L.A., Joseph, M.P., Rizzo, J.R., & Lessell, S. (1994). Optic canal decompression in indirect optic nerve trauma. Ophthalmology, 101(3), 566-569. Mauriello, J.A., DeLuca, J., Krieger, A., Schulder, M., & Frohman, L. (1992). Management of traumatic optic neuropathy–a study of 23 patients. Br J Ophthalmol, 76(6), 349-352. Muthukumar, N. (1997). Traumatic haemorrhagic optic neuropathy: case report. Br J Neurosurg, 11(2), 166-167. Parab, R., Fung, C.I., & Van Der Merwe, G. (2013). Blunt facial trauma causing isolated optic nerve hematoma. Case Rep Radiol, 2013, 235209. Rothfus, W.E., Curtin, H.D., Slamovits, T.L., & Kennerdell, J.S. (1984). Optic nerve/sheath enlargement. A differential approach based on high-resolution CT morphology. Radiology, 150(2), 409-415. Sergott, R.C., Savino, P.J., & Bosley, T.M. (1990). Optic nerve sheath decompression: a clinical review and proposed pathophysiologic mechanism. Aust N Z J Ophthalmol, 18(4), 365-373. Skoloudik, D., Herzig, R., Fadrna, T., Bar, M., Hradilek, P., & Roubec, M., et al. (2011). Distal enlargement of the optic nerve sheath in the hyperacute stage of intracerebral haemorrhage. Br J Ophthalmol, 95(2), 217-221. Spoor, T.C., Hartel, W.C., Lensink, D.B., & Wilkinson, M.J. (1990). Treatment of traumatic optic neuropathy with corticosteroids. Am J Ophthalmol, 110(6), 665-669. Thaker, A., Tandon, D.A., & Mahapatra, A.K. (2009). Surgery for optic nerve injury: should nerve sheath incision supplement osseous decompression? Skull Base, 19(4), 263-271. Tourtier, J.P., Lemoullec, D., & Tazarourte, K. (2011). Head injury with unilateral optic nerve enlargement: Could it be caused by increased intracranial pressure? J Forensic Leg Med, 18(1), 44. Wojno, T., Beck, R.W., & Grosserode, R. (1986). Bilateral optic nerve sheath enlargement. Ophthalmic Surg, 17(9), 584-588. Yu-Wai-Man, P., & Griffiths, P.G. (2007). Steroids for traumatic optic neuropathy. Cochrane Database Syst Rev(4), D6032.
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Visual improvement and pain resolution in traumatic optic nerve sheath meningocele treated by optic nerve sheath fenestration Chen Huia,b,h,i,1,∗ , Wu Xiaoyunc,1 , Liang Yid,1 , Chen Ningboe,1 , Qiu Xizhonga , Yang Shaoweia , Lin Weia , Zhao Maozhuf , Ma Wubof , Pan Xuefeif , Lai Lic , Tan Haibing , Zeng Daiwenb and Jiang Yongj,∗ a Department
of Ophthalmology, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China b Laboratory Animal Institute, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China c Department of Radiology, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China d Department of Neurology, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China e Emergency Department, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China f Department of Ophthalmology (East Area), Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China g Neurosurgery Department, Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Chengdu, Sichuan, China h School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China i School of Materials Science and Engineering, Southwest Jiaotong University, Chengdu, Sichuan, China j Neurosurgery Department, Lu Zhou Medical College, Luzhou, Sichuan, China
Abstract. Purpose: There is no consensus as to the optimum treatment for traumatic optic neuropathy (TON). The decision to intervene medically or surgically, or simply observe was recommended to be on an individual basis. The purpose of this study is to test whether optic nerve sheath fenestration (ONSF) could improve vision in patients with traumatic optic nerve sheath meningocele, although it was reported to be effective in patients with traumatic optic nerve sheath hematoma. Methods: ONSF was performed on two traumatic patients with dilated optic nerve sheath from MRI.
1 Chen Hui, Wu Xiaoyun, Liang Yi and Chen Ningbo contributed
equally to this work. ∗ Corresponding author: Chen Hui, No. 32, 1st ring road, 2nd west section, Chengdu, Sichuan 610072, China. Tel.: +86 028 6708 7565; Fax: +86 028 6708 7557; E-mail: [email protected]; Jiang Yong, Taiping Street 25th, Luzhou, Sichuan 646000, China. Tel.: +86 830 3165 461; Fax: +86 830 2392 753; E-mail: [email protected].
0922-6028/14/$27.50 © 2014 – IOS Press and the authors. All rights reserved
656
C. Hui et al. / Visual improvement and pain resolution
Results: Both patients initially suspected as traumatic optic nerve sheath hematoma were diagnosed as traumatic optic nerve sheath meningocele by intraoperative findings of the enlarged optic nerve sheath and clear fluid drained without evidence of blood in the subdural space. Moreover, significant orbit/head pain resolution and visual improvement within a week after ONSF was found. Conclusions: When TON presents with an enlarged optic nerve/sheath on CT or MRI with visual loss, an optic nerve sheath meningocele should be considered with the consideration that ONSF may benefit both visual acuity and post-traumatic pain, if present. Keywords: Traumatic optic neuropathy, optic nerve sheath meningocele, optic nerve sheath fenestration (ONSF), head/orbital pain
1. Introduction Optic nerve injury may result from direct trauma, indirect trauma, or a combination of both. The mechanism of indirect traumatic optic neuropathy (TON) is diverse and complicated. There is no consensus as to the optimum treatment for TON. The largest prospective comparison study of patients of all ages with TON found no difference in outcome among patients treated with surgical optic nerve canal decompression, highdose steroids, or observation (Levin et al., 1999). The decision to intervene medically or surgically, or simply observe has been recommended to be on an individual basis, rather than a simple standard of care (Levin et al., 1994). Optic nerve sheath fenestration (ONSF) was first described by De Wecker in 1872 as an incision in the retrobulbar optic nerve sheath to relieve elevated intracranial pressure (De, 1872). The procedure now is typically performed in instances of papilledema due to idiopathic intracranial hypertension (IIH) with rapid and/or progressive visual loss. ONSF has been anecdotally reported to improve vision in patients with traumatic optic nerve sheath hematoma (Guy et al., 1989; Muthukumar, 1997; Sergott et al., 1990). Herein, we report two cases of traumatic optic nerve sheath meningocele, who were initially suspected to have optic nerve sheath hematomas, and received immediate orbit/head pain resolution with significant visual improvement within a week after ONSF. 2. Methods ONSF was performed using a medial transconjunctival approach under general anesthesia. In detail, a 180◦ peritomy at the nasal limbus is performed with relaxing incisions and dissection down to
bare sclera. The medial rectus muscle is isolated with a muscle hook, and tagged with 6-0 Vicryl suture, then muscle is disinserted. Hemostasis is performed with needle-point cautery. A 5-0 Vicryl suture is passed in a running stitch fashion at the site of the medial rectus disinsertion to be used as a traction suture. The globe is fully and laterally abducted with the traction suture. A careful retraction of the orbital soft tissue is undertaken with a Schepens orbital retractor and cotton-tipped applicators until clear exposure of long posterior ciliary arteries and the optic nerve sheath under the operating microscope. An avascular area of anterior optic nerve sheath was incised using a long 15◦ blade (Sharpoint, the one used for paracentesis in cataract surgery). The incision is made about 4 to 5 mm in length and about 2 mm posterior to the junction of the globe and the nerve. Cerebrospinal fluid is drained on incision of the sheath. The edge of the sheath incision is gently lifted away from optic nerve with a long-handled finetoothed forceps, and a long-handled scissors is used to excise 3 × 5-mm sheath. The traction suture is then removed. The medial rectus muscle is reattached to its insertion point using the 6-0 Vicryl suture. The conjunctiva is then reattached with an 8-0 Vicryl suture. 3. Case reports Case 1: On the 18th of July, 2012, a 48-year-old man suffered a contusion to his left eyeball by a fist. He subsequently suffered left orbital pain and decreased vision. An examination several hours after the injury in a local emergent eye clinic disclosed visual acuity of 0.1 (20/200) on the left and 1.0 (20/20) on the right, left periorbital swelling, with a normal anterior segment and fundus examination. Pupillary reaction was not recorded. He was given oflaxcin eyedrops and observed with no improvement in vision or pain.
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operatively, the visual acuity on the left had improved to 0.3 (20/60). The visual acuity continued to improve by the seventh post-operative day to 0.5 (20/40). The patient was examined each day in the following week without continuing visual improvement, and then was discharged. The visual acuity on the left remained 0.5 (20/40) at one year follow-up without orbit/head pain complaint.
Fig. 1. Transverse axial orbital MRI (T2-weighted fat-suppressed sequence) revealing a ballooned left retrobulbar optic nerve sheath (white arrow).
On the 12th of August, 2012, he was referred to an ophthalmologist in another hospital. Examination there showed the same acuity of 0.1 (20/200) on the left and normal anterior segment and fundus, with a left afferent pupillary defect. Intraocular pressure (applanation) was 18 mmHg OD and 16 mmHg OS. Ocular motility was normal without proptosis. A diagnosis of traumatic optic neuropathy with post-traumatic headache was made. He was given prednisone 40 mg per day for one week, then gradually tapered, with no improvement in vision or pain. On the 22nd of August, 2012, he was referred to the ophthalmology department in Sichuan Provincial People’s Hospital (SPPH) for continued decreased vision on the left and severe left-sided headache. Visual acuity and ocular examination was unchanged. A magnetic resonance image (MRI) of the brain and orbits demonstrated the suggestions of a ballooned retrabulbar optic nerve sheath with high signal (Fig. 1). An initial diagnosis of optic nerve sheath hematoma was suspected. On the 28th of August 2012, ONSF was performed on the left under general anesthesia. Under the microscope, the optic nerve sheath was slightly ballooned. A significant amount of clear fluid was noted when the incision was made and a 3 × 5-mm sheath window was excised. Specifically, there was no hematoma or bleeding discovered from the subdural space. Postoperatively, intravenous 10 mg dexamethasone and cefathamidine were given for 5 days. On the first day post-operatively, the patient excitedly reported that the left orbit-front-temporal pain had completely resolved, although the visual acuity on the left remained unchanged. By the fourth day post-
Case 2: On the 9th of January, 2013, a 21-year-old man suffered a contusion to the right face and orbit from a motor vehicle accident with loss of consciousness. One day after injury he was conscious and complained of decreased vision in the right eye. An examination by a local ophthalmologist demonstrated a visual acuity on the right of 0.05 (20/400), a right afferent relative pupillary defect, with a normal anterior segment and fundus examination. He was given prednisone 40 mg per day orally for one week with no improvement of vision, then discontinued. On the 22nd of January, 2013, he was referred to SPPH for further treatment. Examination at that time disclosed a corrected visual acuity of 0.05 (20/400) on the right, and 1.0 (20/20) on the left. The anterior segment and fundus examination were normal bilaterally, with the intraocular pressures (applanation) 16 mmHg OD and 15 mmHg OS. A right afferent relative pupillary defect was present. Ocular motility was full and there was no proptosis. A computed tomography (CT) of the brain and orbit showed a small right frontotemporal epidural hematoma (9.2 mm in thicknesses), multiple fractures of the right lateral and upper orbit walls, and moderate enlargement of both optic nerves (Fig. 2). MRI of orbit suggested an enlarged right optic nerve sheath (Fig. 3). A right optic nerve sheath hematoma was suspected. On the 24th of January 2013, a right ONSF was performed. Under microscope, the optic nerve sheath appeared marked enlarged. A 3 × 5-mm sheath window was excised, and clear fluid was drained without evidence of blood in the subdural space. Postoperatively, intravenous 10 mg dexamethasone and cefathamidine was given for 5 days. On the second day post-operatively, the patient’s vision improved to 0.1 (20/200) OD with resolution of right orbital pressure. The vision gradually improved each day on the right to 0.4 (20/50) until discharge on the seventh post-operative day. The visual acuity on the right maintained at 0.5 (20/40) 8 months postoperatively, without complaints of pain.
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Fig. 2. Axial orbital CT showing multiple fractures in the right lateral and moderate enlargement of bilateral optic nerves (about 6 mm wide).
Fig. 3. Transverse orbital MRI (T2-weighted fat-suppressed sequence) showing an enlarged right retrobulbar optic nerve sheath with a curved borderline (white arrow).
4. Discussion An optic nerve sheath cyst or meningocele, was first proposed and defined as “dilation of the optic nerve sheath and expansion of the CSF filled space around the optic nerve” by Garrity (Garrity et al., 1990). Similar to an optic nerve hematoma, it presented as an enlarged optic nerve/sheath on CT (Rothfus et al., 1984) and typically as an expanded subarachnoid space around the optic nerve in MRI (Garrity et al., 1990). However, because of the small dimensions of the optic nerve and its subarachnoid space, even high resolution CT and MRI may fail to reveal enlargement of the optic nerve/sheath silhouette (Sergott et al., 1990). In our report, two cases of traumatic optic nerve/sheath enlargement, which were initially mis-diagnosed as
optic nerve sheath hematoma from MRI, but ultimately were suspected as an optic nerve sheath meningocele, received immediate orbit/head pain resolution with significant visual improvement within a week after ONSF. In the past three decades, there have been a total of seven cases of successful treatment of TON with enlarged optic nerve/sheath in imaging through ONSF (Goldenberg-Cohen et al., 2004; Guy et al., 1989; Hupp et al., 1984; Mauriello et al., 1992; Muthukumar, 1997; Sergott et al., 1990). The detailed clinic course, imaging and surgical findings were compared with our two cases in Table 1 (Table 1). Of those seven, three were verified as traumatic optic nerve sheath hematoma by both CT and surgery (Guy et al., 1989; Muthukumar, 1997) or surgery alone (Sergott et al., 1990). One was diagnosed as hematoma through CT presentation without surgical findings (Mauriello et al., 1992) and one was presented with no recording of imaging or surgical findings (Goldenberg-Cohen et al., 2004). The remained two were probable traumatic optic nerve sheath meningoceles (Guy et al., 1989; Hupp et al., 1984). In Hupp’s report, the enlarged optic nerve sheath on CT was verified by the surgical findings of a ballooned optic nerve sheath, with 1.5 ml clear fluid drained by ONSF (Hupp et al., 1984). However as it was associated with progressive venous obstructive retinopathy, the authors were uncertain if the visual loss was from a venous obstructive retinopathy or the meningocele or both (Hupp et al., 1984). It was hard to be completely contributed to the compromise from TON (Guy et al., 1989). Guy also reported two cases of enlarged optic nerve/sheath; one was described as a “cyst” in surgery, but was discussed as a “presumed arachnoid cyst”, with no record of clot evacuated or clear CSF drained in the surgical findings (Guy et al., 1989). In our two cases, the MRI
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Table 1 Comparing reported cases of TON treated by ONSF with our cases Final diagnosis
Time from injury Vision changes to ONSF after trauma
Imaging findings
Surgical findings
Post-operational vision changes
Progressive from “following light” to NLP within 1 day. 6/60 2 days after injury
“A hematoma enlarging ONS” in CT”, no MRI
A small hematoma evacuated
1 D later: CF 1 Y later: 8/30; with optic head atrophy
Enlarged ON in CT 14hs after injury, no MRI
A swollen discolored ONS and a small clot under the ONS.
Progressive from 6/15 to 6/60
Unreported
A subdural hemorrhage and the blood drained
No visual report in the 1st W 3 M later: 6/36 1 Y later: 6/36 6/9, the time to reach 6/9 unreported
CF/1 ft
“ONS hematoma” in CT, no MRI
No blood or fluid drained
20/25; the time to reach 20/25 unreported
unknown
NLP
unreported
unreported
20/200, the time to reach 20/200 unreported
over 3 Ms
Progressive from a large ONS in the 1st CT, A marked ballooned 20/25 to 20/400 further enlargement in ONS, and 1.5 ml clear the 2nd CT; an fluid drained enlarged, fluid-filled ONS 9.3 mm in diameter in the 1st echography, and a further 1.4 mm increase in the 2nd echography Progressive loss enlargement of ONS and A ballooned ONS and the from 20/25 to a orbital floor fracture “cyst” drained (no fluid 20/200 during in CT, no MRI or clot recorded, and the the 1st week term “presumed cyst” was used in discussion) Stable and A ballooned ONSF in Clear fluid drained 0.1(20/200) MRI 2 Ms after trauma
ONS hematoma from Guy’s case 1 (Guy et al., 1989)
1–2 days
ONS hematoma by Muthukumar (Muthukumar, 1997) ONS hematoma by Sergott (Sergott et al., 1990) Imaging diagnosis of ONS hematoma in Mauriello’s 17th case (Mauriello et al., 1992) Unknown by Goldenberg-Cohen (Goldenberg-Cohen et al., 2004) Posttraumatic venous obstructive retinopathy associated with enlarged ONS by Hupp (Hupp et al., 1984)
2 days
3 days
3 to 5 days
A presumed cyst in Guy’s case 2 (Guy et al., 1989)
8 days
Traumatic ONS meningocele (our cases 1)
6W
Traumatic ONS meningocele (our case 2)
2W
Stable and 0.05(20/400)
1 W later: 20/200+ 3 W later: 20/50+ Next 8 Ms follow-up: no change
1 W later: 20/50 1 Y later: 20/25, with optic (head) atrophy
No improvement in the first four days
5 days later: 0.3 (20/60) 7 days later: 0.5 (20/40) 2 weeks later: 0.5 (20/40) 1 year later: 0.5 (20/40) A slightly enlarged ON in A marked ballooned ONS 1 day later:0.1 CT and a ballooned and clear fluid drained (20/200) ONSF in MRI 14 days 3 days later: 0.2 after trauma (20/200) 5 days later: 0.3 (20/60) 7 days later: 0.4 (20/50) 2 weeks later: 0.5 (20/40) 8 Ms later: 0.5 (20/40)
Note: ONS: optic nerve sheath; ONSD: optic nerve sheath fenestration; NLP: no light perception; CF: count fingers; W: week; M: month; Y: year.
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findings of patulous expansion of CSF-filled space in the retrobulbar optic nerve sheath were consistent with the surgical findings of ballooned optic nerve sheath and the clear, colorless CSF drained. We suggest this may be two cases of post-traumatic optic nerve sheath meningocele. Although spontaneous visual improvement after trauma (Yu-Wai-Man et al., 2007) and the visual improvement from steroids treatment (Spoor et al., 1990) is possible, in our two cases preoperative treatment with steroids and observation for as long as forty days or two weeks respectively did not show visual improvement. It’s of extreme low probability that the visual improvement from pre-operative steroids or spontaneous visual improvement happened to occur just on the post-ONSF weeks. A recent report that optic canal decompression combined with optic sheath incision resulted in a better visual recovery than optic canal decompression alone in TON, especially in subjects without optic canal fracture (Thaker et al., 2009), indicates a potential benefit of ONSF to TON. The clinic course in our two cases suggests that ONSF might have contributed to their marked visual improvement. Actually in our cases after decompression, postoperatively the vision improved mainly in the first week and discontinued two to three weeks later without showing spontaneous improvement in the follow-up period as long as one year or eight months. So, we think that it is the ONSF, not the pre-operative steroids contributes to the patients’ visual improvement. To our knowledge, this was the first report of visual improvement from TON with optic nerve sheath meningoceles through ONSF. The mechanism of ONSF for the treatment of posttraumatic meningocele remains unclear. Jinkins et al. suggested that the obstructed flow of CSF along the optic subarachnoid space plays an important role in various conditions including trauma (Jinkins, 1987). That obstruction might increase the local pressure in the distal optic nerve sheath even with normal intracranial pressure. That has also been suggested in others’ findings (Golnik et al., 1998). Furthermore, Carson (Carson et al., 2010) and Tourtier (Tourtier et al., 2011) suggest that the increase of optic nerve diameter after trauma could be due to raised intracranial pressure. The speculation of direct decompression to the intra-opticnerve-sheath pressure, as well as increased intracranial pressure (ICP) in head trauma (Skoloudik et al., 2011) cannot be excluded. Most importantly, the relief of secondary injury to the optic nerve (Parab et al., 2013)
from recently recognized optic nerve sheath compartment syndrome (Jaggi et al., 2007; Killer et al., 2006), in which the subarachnoid spaces (SAS) of the optic nerve can become separated from other CSF compartments in certain optic nerve disorders, might contribute to the mechanism. Surprisingly, in our two patients the headache and/or orbital pain disappeared post-operatively. Headache and/or retrobulbar pressure or pain as a chief complaint has been described in other non-traumatic meningoceles (Garrity et al., 1990; Golnik et al., 1998). There have been limited reports of resolution of head/orbital pain from ONSD. We believe this is also the first report of headache and/or orbital pressure immediately resolved in a patient with traumatic optic nerve sheath meningocele after ONSF. The mechanism for pain in meningocele and pain relief by ONSF is unclear. Garrity et al. speculated the headache or orbital pain/pressure was most likely produced by the “stretching” or compression to the optic nerve sheath which was innervated by trigeminal nerve (Garrity et al., 1990). We agree with Garrity’s speculation and suggest that the local pressure in meningocele was immediately released by ONSF and the pain was resolved because of relief of stretching or compression to the optic nerve sheath, although it is well-known that ONSF could relieve the headache in idiopathic intracranial hypertension (IIH) with the mechanism thought to be related with the decreased ICP. In summary, we agree with the suggestion by Wojno (Wojno et al., 1986) that ONSF may be of benefit and should be considered when there is no spontaneous improvement of vision or severe headache in traumatic optic neuropathy. Moreover, considering the good results (Guy et al., 1989; Muthukumar, 1997; Sergott et al., 1990) to traumatic optic nerve sheath hematoma by ONSF (reviewed in Table 1), we suggest traumatic optic neuropathy presenting with an enlarged optic nerve or distended retrobulbar optic sheath on neuroimaging, should be treated with ONSF, although optic nerve sheath meningocele should be differentiated from sheath hematoma.
Acknowledgments The present work was jointly funded by the High and New Technology Program in Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital of China (No. 2012-6), National Natural Science
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Foundation of China (81271035/H1205, 81371319), the Program for New Century Excellent Talents in University (NCET-12-1057) and Basic Research Foundation for Public Scientific Research Institutions in Science and Technology Department of Sichuan Province, China. We acknowledge the assistance of Dr. Bradley K. Farris (Dean McGee Eye Institute, USA) for his invaluable surgical introduction.
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