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ORIGINAL ARTICLE
Year : 2020  |  Volume : 68  |  Issue : 1  |  Page : 54-60

Endoscopic Endonasal Optic Nerve Decompression with Durotomy: Pis Aller in the Mind of a Blind


1 Department of Neurosurgery, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Neuro-otology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
3 Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
4 Department of Radiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
5 Department of Ophthalmology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication28-Feb-2020

Correspondence Address:
Dr. Arun K Srivastava
Department of Neurosurgery, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.279701

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 » Abstract 


Background: Progressive vision loss is a dismal sequelae of idiopathic intracranial hypertension (IIH) and secondary intracranial hypertension with cerebro-venous sinus thrombosis (CVST). The initial management revolves around weight loss, acetazolamide, steroids, and diuretics. A subset of unfortunate patients, refractory to medical therapy, need surgical intervention in the form of CSF diversion or optic nerve decompression (OND). The ONDd is an emerging alternative with encouraging early results.
Aim: In our study, we share our experience of ONDd by endoscopic endonasal corridor, highlighting the technical nuances of procedure and discuss the indications of the same in the era of advanced technology.
Materials and Methods: A retrospective, noncomparative review of the medical records of all the patients of IIH (ICHD-III criteria) with severe vision loss, refractory to medical treatment, and with established objective evidence of papilledema was done. All the patients were operated in our department by endoscopic endonasal sheath fenestration.
Results: Nine patients (M:F 3:6) underwent endoscopic endonasal optic nerve decompression (2016–2019) approach for medically refractive IIH (n = 6) and CVST (n = 3). The mean age of population was 21.44 ± 5.14 years; 6 patients had improvement in headache and 6 had improvement in visual acuity. The visual acuity deteriorated in two patients (n = 1 IIH and n = 1 CVST with dural AVF). One patient needed postoperative lumbar drain for CSF leak, while none had meningitis.
Conclusion: Endoscopic optic nerve sheath fenestration is minimally invasive and effective alternative with promising outcome in the management of medical refractory IIH or CVST.


Keywords: Cerebro-venous sinus thrombosis, idiopathic intracranial hypertension, optic nerve decompression
Key Messages: Endoscopic endonasal optic nerve decompression with durotomy is a safe and effective procedure for IIH, and should be opted in early in the course of the disease, with an aim to decompress both optic nerves in a single sitting.


How to cite this article:
Srivastava AK, Singh S, Khatri D, Jaiswal AK, Sankar R, Paliwal VK, Neyaz Z, Sharma K, Behari S. Endoscopic Endonasal Optic Nerve Decompression with Durotomy: Pis Aller in the Mind of a Blind. Neurol India 2020;68:54-60

How to cite this URL:
Srivastava AK, Singh S, Khatri D, Jaiswal AK, Sankar R, Paliwal VK, Neyaz Z, Sharma K, Behari S. Endoscopic Endonasal Optic Nerve Decompression with Durotomy: Pis Aller in the Mind of a Blind. Neurol India [serial online] 2020 [cited 2020 Apr 4];68:54-60. Available from: http://www.neurologyindia.com/text.asp?2020/68/1/54/279701




The common clinical presentation of IIH and CVST includes headache, seizures, sixth nerve palsy, and hemiparesis. However, visual deterioration is the most bothersome symptom, both for the treating physician as well as for the patients. CVST and IIH share common pathophysiology and overlapping clinical features in nearly 37%–47% of cases.[1] Nearly one-tenth of IIH patients has radiological evidence of sinus thrombosis.[1],[2] Therefore, visual deterioration is the common thread connecting both the diseases, but the exact incidence or load of symptom is difficult to quote as it has been variably quoted in literature. In the VENOPORT study, visual symptoms were present in 13% of cases, and severe vision loss occurred in only 1.3% of cases.[3] The disease predominantly affects the middle age and thus the socially productive population.[4] The surgical intervention, as a dernier ressort, includes CSF diversion procedures including ventriculo-peritoneal shunt (VPS) or lumbo-peritoneal shunt (LPS) and OND. The surgical results are found better when the pathology is dealt at the local level, i.e., when subarachnoid space around optic nerve is targeted, as compared to targeting intraventricular pressure. The pathophysiological advantage of optic nerve durotomy (ONDd) over bony decompression (OND), in terms of fibroblast proliferation and CSF egress via dural fistula, is a well-established hypothesis. ONSF via medial or lateral orbitotomy or lateral transconjunctival approach is an established procedure. Although the early results were promising, technical difficulty and reported complications (scarring, fibrosis, recti muscle injury, and fat adhesion) made the approach obnoxious among surgeons.[4],[5] With the advent of better optics and endoscopes in armamentarium, the surgery for OND perceives its resurgence. The endoscopic approach has shown great success in traumatic optic neuropathy; however, literature on IIH/CVST is lacking.[6] In our study, we share our experience of endoscopic endonasal ONSF for medically refractive vision loss, in patients of IIH/CVST.


 » Materials and Methods Top


In this retrospective, noncomparative study, a review of the medical records of all the patients of IIH (ICHD-III criteria) with severe vision loss and with established objective evidence of papilledema were included. All these patients were refractory to the medical treatment and operated by endoscopic endonasal ONDd. All the patients included in study were diagnosed as case of medical refractory IIHT/CVST by the senior consultant of Neuro-medicine (VKP) department, in alliance with senior Radiologist (ZN) and Ophthalmologist (KS). The patients of IIH had underwent three trials of lumbar CSF drainage, along with highest dosage (2000 mg/day) of acetazolamide for IIH and oral anticoagulants for CVST, to maintain INR of 2 to 3. Among the patients of CVST, the coagulation parameters were optimized before surgery and LMW heparin was restarted after 6 h of surgery. The visual acuity was tested using Snellen's chart, whereas the visual field assessment was performed using a Humphrey field analyzer using standard 30-2 threshold test. The visual field defects were graded (Wall and George criteria) and scored in a manner that a lower number indicated a better field.[7],[8] The degree of papilledema of each eye was graded using the Frisen's staging scheme (Stage 0 to 5). The ophthalmologic improvement was defined as objective evidence of recovery or the complete resolution of visual deficits [Figure 1]a-f]. Headache improvement was characterized by the patient's subjective self-reporting of their pre and postsurgical symptoms. Postoperative visual assessment was done at 3 months and last available follow-up (range 6–28 months).
Figure 1: Fundus photograph of a patient with IIH showing florid papilloedema in pre operative period in left (a) and right (b) eye which resolved post operatively after bilateral ONDd (c and d). Another photograph of a patient with CVST showing severe papilloedema who showed minimal improvement after surgery (e and f)

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The surgery was done by endoscopic endonasal approach (supplementary video). We used both uni-nostril (n = 2) and bi-nostril (n = 7) corridors. The approach needs additional vigilance during drilling of bone and incising the optic nerve sheath, in a manner that, both the injury to ophthalmic artery and optic nerve axons, is avoided. The anatomical exposure of this medial optic canal wall (bulge in superior-lateral wall of sphenoid) is variable (average 101.3°), so prior CT paranasal sinus is useful, in predicting success of surgery. The presence of Onodi cell is a favorable situation in this regard. As our proximal extent of drilling is zonule of Zinn (ZOZ), optic nerve is still anchored to falciform ligament, and that is our technical limitation.

Once the satisfactory decongestion is achieved, inferior turbinate (IT) is out-fractured, and middle turbinate is medialized. One case had pneumatized middle turbinate (concha-bullosa), so partial turbinectomy was done and MT was removed in flush with ground lamellae [Figure 2]a-f]. Thereafter, lower one-third uncinectomy is done followed by bullectomy. The posterior ethmoidectomy and sphenoidotomy were done. One should be acquainted with important landmarks—lamina paperycea, medial optic nerve bulge, ICA, and optico-carotid recess [Figure 3]a-f]. We used the imaginary line, described by Gogela et al., which represents the point of intersection, where intracanalicular segment passes on to intracranial segment of optic nerve.[9] The ON drilling is done from medial to lateral side, around 180° or more and the sheath was incised with the help of sickle knife from medial to lateral, in a single stroke, on the superior aspect, in order to avoid any inadvertent injury to ophthalmic artery [Figure 4]a-c]. In the bi-nostril approach, posterior septostomy was done to facilitate posterior ethmoidectomy and wide antrostomy for contralateral decompression.
Figure 2: Intraoperative endoscopic photographs showing endoscopic ONDd from the right nostril. The inferior turbinate is out-fractured and mobilized (a) and large middle turbinate is seen head on (due to concae bullosa). Partial middle turbinectomy by vertical lamellotomy is done using sharp knife (b and c). The remaining middle turbinate is medialized and parts of the medial surface of maxillary sinus are seen as uncinate process and bulla ethmoidalis (d). After the lower one-third, incinectomy is done (e), maxillary sinus opening is seen (f), which is further widened in order to avoid postoperative mucocele formation

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Figure 3: Intraoperative endoscopic photographs showing steps of endoscopic ONDd. After bulla ethmoidalis is removed, posterior ethmoid cells are cleared, then the ground lamellae is seen (a). Further, the medial corridor is widened and sphenoidectomy is done to coalesce with posterior ethmoid cells (b and c). Lamina papyracea is identified and traced with further identification of medial optico-carotid recess, lateral optico-carotid recess, optic nerve bulge (d and e). The landmark for ZOZ is identified prior to drilling bone over intracanalicular part of optic nerve. Optic canal drilling is done in two parts: initially at the level of zoz and then starting from rest of the optic canal from medial to lateral (f)

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Figure 4: During endoscopic ONDd, once the optic nerve bulge is identified (a), the bone is drilled. Then, sheath is cut from medial to lateral direction, at the superior border, to avoid inadvertent injury to ophthalmic artery. We use sharp endoscopic sickle-shaped knife and cut the sheath in a single stroke from medial to lateral (b) direction. After CSF egress is complete, the oxidized cellulose is kept on the defect for the hemostasis and to facilitate fibroblast growth (c)

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 » Results Top


Seventeen eyes of 9 patients (M:F 3:6), who underwent endoscopic ONDd (2016-2019) for medically refractive IIH (n = 6) and CVST (n = 3), were included. The mean age of population was 21.44 ± 5.14 years; headache was present in six patients and all of them showed improvement in headache and 6 had improvement in visual acuity [Table 1]. Two patients had deterioration in the visual acuity (n = 1 IIH and n = 1 CVST with dural AVF). One patient needed postoperative lumbar drain for CSF leak, while none had meningitis. Among the CVST patients, two were female and one was male. One patient of CVST was on functioning VP shunt, but still presented 3 months after shunt surgery for progressive vision loss. Three patients (4 eyes) had remarkable improvement [n = 2 IIH; n = 1 CVST] from “no perception of light” to “better than 6/60.” In all these patients, bilateral endoscopic ONDd was done. The overall visual field defect score (Wall and George criteria) improved from preoperative median of 3 to postoperative median of 2 (18 eyes). Among the six patients of IIH, mean visual field defect score improved from 2.67 to 1.67. Similarly, the mean papilledema grade improved from 3.22 (median = 3.5) to 2.33 (median = 2.0). Since the sample size of our study is small, statistical significance could not be calculated, but still a trend of improvement was seen [supplementary Figure]. Dural AVF in one patient was coiled by intervention radiologist (ZN) and this patient had the longest postoperative stay (20 days), due to persistent headache and seizure on POD 4. Another patient (CVST) had bleeding from nasal mucosa, as he was on warfarin. The bleeding was managed with nasal packing and INR titration of the drug.
Table 1: Demographic and clinical profile of patients included in our study (n=9)

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 » Discussion Top


IIH is a rare condition, with a prevalence of 0.9/10,000 population [Figure 5]a-d].[10] The usual clinical presentation includes headache, sixth nerve palsy, pulsatile tinnitus, and vision loss. Medical refractory vision loss in IIH or CVST is a dismal situation, with guarded prognosis. The vision loss may be due to hemorrhages, exudates, or subretinal fluid in the macular region, but predominant cause being papilledema. The possible causes of this vision loss revolve around the axoplasmic flow stasis around optic nerve, secondary to raised intracranial pressure.[2],[10] However, there are other causes also like developing venous infarcts in CVST leading to raised ICP, arterial infarcts in territory of occipital lobe, and secondary dural AVF formation. Among these, the patients with axoplasmic flow stasis have been shown to respond to lumbar CSF drainage, lumboperitoneal shunt, thrombolysis and transverse sinus stenting (CVST), and optic nerve sheath fenestration.[11] The idiopathic intracranial hypertension (IH) is termed as secondary IH, once the underlying condition is detected as either CVST or any space occupying lesion.
Figure 5: Magnetic resonance imaging T2 weighted sagittal image left (a) and right (b) eye showing tortuous optic nerve, coronal image (c) of the same patient showing halo sign (increased CSF space around the nerve) marked with black arrow, and coronal computed tomography image (d) of the same patient showing concae bullosa

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There is differential CSF pressure around the optic nerve and intraventricular region. Progressive visual loss, in the presence of a functioning shunt, has been documented in literature.[11] Nithyanandam et al. showed encouraging results by medial transconjuctival approach.[12] Ever since DeWecker (1872) described optic nerve sheath fenestration, a series of complications has been reported like pupillary atony, transient diplopia, medial rectus muscle injury, traumatic optic nerve neuropathy, and even central retinal artery occlusion.[13] The same principle or pathophysiological advantage can be simulated by minimally invasive endonasal endoscopic approach also. Islands of case reports have shown improvement in headache and visual acuity using the endonasal corridor.[14],[15]

The previous series, abetting transconjunctival optic nerve sheath fenestration, have shown acceptable surgical outcomes.[2],[4],[5],[6],[7] But still, we adopted endoscopic corridor to address optic nerve form medial wall. In our experience, we also observed that endoscopic ONDd has several other advantages like a shorter operative time, bilateral decompression through a single nasal corridor, and assurance of formation larger CSF fistula as compared to fenestrations.

Although the early results of ONDd are promising, a larger data is imperative for recommending the timing of surgery and surgery on both the optic nerve. In our experience, we found a better subjective and objective vision improvement, in all the cases, where early and bilateral ONDd was performed. As of now, two endoscopic approaches exist: optic nerve sheath fenestration and optic nerve decompression. The advantage of dealing local CSF pressure patho-physiologically seems favoring sheath fenestration, because only then, dural fistula formation or fibroblast proliferation may progress; however, clinical outcomes were found similar in both procedures, as these results are from small series. The literature focuses bilateral visual improvement even after single OND/ONSF.[2],[3],[6],[7],[8],[9] In a series of 10 patients, Sencer et al. showed excellent outcomes in both eyes, by unilateral endoscopic decompression.[16] The hypothesis of Sencer and Patrocinio et al. disapproves sheath fenestration, but they could not explain plausible mechanism for improvement in headache and bilateral vision after bony decompression.[16],[17] More than that, Tarrats et al., in their series of endoscopic optic nerve decompression, concluded that the improvement may be a placebo effect.[18] Gupta andGadodia found that pressure in the intracanalicular segment of optic nerve could not decrease by just doing bony decompression, as pressure comes intrinsically from nerve itself and not from any compressive pathology.[19] The optic nerve durotomy (ONDd) has an extra edge over bony decompression (OND), in terms of fibroblast proliferation and CSF egress via dural fistula. We believe that the initial improvement in both eyes was because of CSF egress, while the persistent improvement in the ipsilateral vision is because of fibroblast growth. In background of lacking level-I evidence, we gave benefit of doubt to our rapidly deteriorating patients and did bilateral ONDd. Series showing complications like meningitis or ophthalmic artery injury may be due to technical learning curve, but debate is still a conundrum and prospective randomized study may provide a better answer. Gupta andGadodia also highlighted the fact that open optic nerve fenestration may lead to excessive scarring, fibrosis, and fat adhesion at the surgical site; and possibility of meningitis in endoscopic approach is over-estimated because the fistula gets closed by glial proliferation.[19]

We followed a middle path, which combined the leverage of both ONSF and OND, in terms of bilateral improvement in visual acuity and headache, along with eliminating deficiencies also, in terms of meningitis. The approach being minimally invasive is safe and acceptable, technically easy to adapt, and familiar with most neurosurgeons. The intercanalicular segment of optic nerve is drilled to its maximum safe area, nearly 180° that too from approximately 1 cm anterior to the sphenoid face, upto ZOZ. A Cottle elevator was used to elevate the thin bone of the lamina in a posterior direction. Moreover, the sheath is opened in a single linear fashion along the whole length, using sickle knife. This fulfils the pathophysiological formation of dural fistula with CSF egress and other proponent theories favoring ONSF.

Some patients, even in our series, did not improve after CSF diversion, highlighting the fact that there is a difference in CSF pressure, at peri-optic region and intraventricular region. Killer et al. did a dynamic CSF CT-cisternography sequences and found that patients of IIH had remarkable pressure differences at both sites.[14] Therefore, this pathology should be better dealt at intracanalicular level, rather than intraventricular level. With increase in intracranial pressure, there is preponderant increase in subarachnoid space of optic nerve, leading to unfolding of optic nerve sheath and swelling of optic nerve axons.

We observed several interesting facts in our experience that our average age of patients was nearly a decade younger than what it is reported in literature. Second, none of them has shown any improvement in the vision following multiple therapeutic lumbar drains but showed improvement in headache. Third, there was hardly any symmetricity in the visual loss, indirectly hypothesizing some local pathophysiology in or around optic nerve. Finally, few patients showed remarkable improvement, better than reported in literature, highlighting the need of bilateral decompression, but a larger sample size is needed for any justifiable recommendation.

Possible pathophysiology of papilledema in IIH/CVST

There are three acceptable pathophysiologies leading to papilledema and all of them consider the distal optic nerve as the most important pathological target getting involved.[14],[15] The first mechanism refers the increased and fluctuating pressure in the distal optic nerve sheath as a cause. Second refers the persistent elevation of the central retinal venous pressure and the third refers the impaired perfusion of the nerve fibers traversing the lamina cribrosa. Papilledema is, therefore, possible only if the subarachnoid space surrounding the optic nerve is patent. The transmitted CSF pressure to the optic nerve is lowered either by creating a fistula or fenestration which divert the CSF and thus preventing it from damaging the distal ON. The mechanism by which, this may occur is either via formation of a permanent CSF fistula or by the obliteration of the subarachnoid space through fibroblast proliferation. To understand this, we have noticed that all of our patients complained of minor CSF leak or PND till postoperative day 2-3, but later the problem resolved spontaneously. In five patients where CT brain was advised to see the ventricular system, we did CT-cisternography also, and to our surprise we have found that none of these patients had obvious leaking CSF fistula. Therefore, we believe that the final common pathway of healing of these fistulas is fibroblast formation and sealing the medial ONS, thus alleviating the pressure from the distal ON. The direct CSF fistula and CSF egress was useful in the early postoperative period and it lasts till the fibroblast sealing is formed. Late failure of the procedure could be because of failure of proper fistula formation due to faulty surgical technique or later on improper fibroblast growth.[20],[21]

Limitations of study

Our study has a small sample size, but the rarity of disease precludes a large size surgical data. With only nine patients, our series is largest of its kind. Selection and referral bias may be an additional limitation, but we just wanted to highlight feasibility and credibility of the procedure, not exactly comparing it with any established standard procedure. The approach is cost-effective with unsubstantial learning curve.


 » Conclusion Top


The endoscopic endonasal ONDd is a safe and effective procedure to address the rapid visual deterioration in cases of medical refractory IIHT/CVST. The bilateral decompression gave us better results. We believe that it is the local pathophysiology in and around the optic nerve which is responsible for the vision loss, and hypothesize that the CSF egress is an initial mechanism, which was further followed and supplemented by fibroblast formation at fistula site, leading to alleviation of CSF pressure from distal ON as factors in improving the vision in these cases.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Satti SR, Leishangthem L, Chaudry MI. Meta-analysis of CSF diversion procedures and dural venous sinus stenting in the setting of medically refractory idiopathic intracranial hypertension. AJNR Am J Neuroradiol 2015;36:1899-904.  Back to cited text no. 1
    
2.
Scherman DB, Dmytriw AA, Nguyen GT, Nguyen NT, Tchantchaleishvili N, Maingard J, et al. Shunting, optic nerve sheath fenestration and dural venous stenting for medically refractory idiopathic intracranial hypertension: Systematic review and meta-analysis. Ann Eye Sci 2018;3:26.  Back to cited text no. 2
    
3.
Ferro JM, Lopes MG, Rosas MJ, Ferro MA, Fontes J. Cerebral Venous Thrombosis Portugese Collaborative Study Group. Long-term prognosis of cerebral vein and dural sinus thrombosis. Results of the VENOPORT study. Cerebrovasc Dis 2002;13:272-8.  Back to cited text no. 3
    
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Fonseca PL, Rigamonti D, Miller NR, Subramanian PS. Visual outcomes of surgical intervention for pseudotumour cerebri: Optic nerve sheath fenestration versus cerebrospinal fluid diversion. Br J Ophthalmol 2014;98:1360-3.  Back to cited text no. 4
    
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Corbett JJ, Nerad JA, Tse DT, Anderson RL. Results of optic nerve sheath fenestration for pseudotumor cerebri: The lateral orbitotomy approach. Arch Ophthalmol 1988;106:1391-7.  Back to cited text no. 5
    
6.
He ZH, Lan ZB, Xiong A, Hou GK, Pan YW, Li Q, et al. Endoscopic decompression of the optic canal for traumatic optic neuropathy. Chin J Traumatol 2016;19:330-2.  Back to cited text no. 6
    
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Wall M, George D. Idiopathic intracranial hypertension. A prospective study of 50 patients. Brain 1991;114:155-80.  Back to cited text no. 7
    
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Keltner JL, Johnson CA, Cello KE, Wall M; NORDIC Idiopathic Intracranial Hypertension Study Group. Baseline visual field findings in the Idiopathic Intracranial Hypertension Treatment Trial (IIHTT). Invest Ophthalmol Vis Sci 2014;55:3200-7.  Back to cited text no. 8
    
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Gogela SL, Zimmer LA, Keller JT, Andaluz N. Refining operative strategies for optic nerve decompression: A morphometric analysis of transcranial and endoscopic endonasal techniques using clinical parameters. Oper Neurosurg (Hagerstown) 2018;14:295-302.  Back to cited text no. 9
    
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Jensen RH, Radojicic A, Yri H. The diagnosis and management of idiopathic intracranial hypertension and the associated headache. Ther Adv Neurol Disord 2016;9:317-26.  Back to cited text no. 10
    
11.
Kelman SE, Sergott RC, Cioffi GA, Savino PJ, Bosley TM, Elman MJ. Modified optic nerve decompression in patients with functioning lumboperitoneal shunts and progressive visual loss. Ophthalmology 1991;98:1449-53.  Back to cited text no. 11
    
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Nithyanandam S, Manayath GJ, Battu RR. Optic nerve sheath decompression for visual loss in intracranial hypertension: Report from a tertiary care center in South India. Indian J Ophthalmol 2008;56:115-20.  Back to cited text no. 12
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13.
Spitze A, Lam P, Al-Zubidi N, Yalamanchili S, Lee AG. Controversies: Optic nerve sheath fenestration versus shunt placement for the treatment of idiopathic intracranial hypertension. Indian J Ophthalmol 2014;62:1015-21  Back to cited text no. 13
    
14.
Killer HE, Jaggi GP, Miller NR, Huber AR, Landolt H, Mironov A, et al. Cerebrospinal fluid dynamics between the basal cisterns and the subarachnoid space of the optic nerve in patients with papilloedema. Br J Ophthalmol 2011;95:822-7.  Back to cited text no. 14
    
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Pircher A, Montali M, Pircher J, Berberat J, Remonda L, Killer HE. Perioptic cerebrospinal fluid dynamics in idiopathic intracranial hypertension. Front Neurol 2018;9:506.  Back to cited text no. 15
    
16.
Sencer A, Akcakaya MO, Basaran B, Yorukoglu AG, Aydoseli A, Aras Y, et al. Unilateral endoscopic optic nerve decompression for idiopathic intracranial hypertension: A series of 10 patients. World Neurosurg 2014;82:745-50.  Back to cited text no. 16
    
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Patrocínio JA, Patrocínio LG, Júnior FB, da Cunha AR. Endoscopic decompression of the optic nerve in pseudotumor cerebri. Auris Nasus Larynx 2005;32:199-203.  Back to cited text no. 17
    
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Tarrats L, Hernández G, Busquets JM, Portela JC, Serrano LA, González-Sepúlveda L, et al. Outcomes of endoscopic optic nerve decompression in patients with idiopathic intracranial hypertension. Int Forum Allergy Rhinol 2017;7:615-23.  Back to cited text no. 18
    
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Gupta D, Gadodia M. Transnasal endoscopic optic nerve decompression in post traumatic optic neuropathy. Indian J Otolaryngol Head Neck Surg 2018;70:49-52.  Back to cited text no. 19
    
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Kilpatrick CJ, Kaufman DV, Galbraith JE, King JO. Optic nerve decompression in benign intracranial hypertension. Clin Exp Neurol 1981;18:161-8.  Back to cited text no. 20
    
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