Treatment Of Traumatic Optic Neuropathy Research Articles

Importance of Preoperative Pupillary Reflex in Traumatic Optic Neuropathy.

Traumatic optic neuropathy (TON) refers to a pathological condition caused by direct or indirect injury to the optic nerves. In the case of patients with traumatic brain injury, adequate vision evaluation is difficult in many cases due to altered mentality. In order to address this problem, we investigated preoperative pupillary light reflex in TON patients as a predictive factor of surgical outcomes after optic nerve decompression. From April 2020 to September 2022, we enrolled patients who were diagnosed with TON and underwent endoscopic optic nerve decompression at our institution. Vision and pupil reflex tests were performed by an ophthalmologist before and after surgery. Seven patients were enrolled. Their ages ranged from 9 to 78 years and all were male. Among the 7 patients, the patient whose pupillary light reflex was 6mm with sluggish and 7mm with fixated pupil before surgery showed no improvement in vision. Patients with some response to direct reflex or contralateral indirect reflex testing preoperative showed vision improvement postoperative. Direct and indirect pupillary reflexes can be important factors determining treatment for TON. In unconscious patients with a fracture involving the optic canal, timely surgical intervention based on pupillary reflex can prevent permanent loss of vision.

Diagnosis and treatment of transnasal endoscopic optic canal decompression for traumatic optic neuropathy.

To investigate the clinical efficacy and prognostic factors of transnasal endoscopic optic decompression in the treatment of traumatic optic neuropathy (TON). A retrospective analysis was performed on 13 TON patients in The Seventh Affiliated Hospital of Sun Yat-sen University and Shenzhen Eye Hospital in Shenzhen City (China) from June 2020 to April 2022. These patients had received transnasal endoscopic optic decompression, and hormonal and neurotrophic drugs were given after surgery. Visual acuity (VA) improvement was used as the criterion to judge clinical efficacy. In a total of 13 patients, 13 injured eyes (12 men and 1 woman; mean age, 28.0 ± 11.8 years) received transnasal endoscopic optic decompression. After surgery, nine patients had improved VA, whereas four patients failed to show any improvement, resulting in a total effective rate of 69.2%. Of the six patients with no light perception preoperatively, three had effective results after the operation, giving an effective rate of 50.0%. Of the seven patients with residual light sensation preoperatively, six had effective results after the operation, giving an effective rate of 85.7%. Of the 10 patients operated on within 7 days after injury, seven had effective results, giving an effective rate of 70%. Of the three patients injured and operated on after 7 days, two had effective results, giving an effective rate of 66.7%. Transnasal endoscopic optic nerve decompression is an effective treatment method for TON. The presence of residual light perception and the timing of surgery within 7 days are crucial to the prognosis.

Green tea extract enhances retinal ganglion cell survival and axonal regeneration in rats with optic nerve injury

Current clinical treatments have not yet effectively cured progressive retinal ganglion cell (RGC) death and axonal degeneration after optic nerve (ON) injury. We previously demonstrated green tea extract (GTE) can reduce RGC death in rats after ischemic injury. Here, we aim to determine the prophylactic and therapeutic effects and mechanisms of GTE on RGC survival and axonal regeneration in rats with ON injury. GTE (275 or 550 mg/kg) was administered intragastrically for 7 d before or 14 d post-ON crush surgery in adult Fischer 344 rats. Rats with pre- or post-operative treatment of 275 mg/kg GTE showed significantly higher numbers of RGCs and regenerated axons post-ON injury with improved pupillary light reflex as compared to saline-treated rats. Akt and Erk p42/44 activation was higher in the retina of rats given 275 mg/kg GTE pre-surgery, whereas Stat3 activation was higher in those with 275 mg/kg GTE post-operation. Less activated microglia were observed in rats with pre-treatment of 275 or 550 mg/kg GTE. RNA sequencing analysis identified the downregulation of inflammation, apoptosis, and microglia activation genes in the retina of rats with pre- or post-treatment with 275 mg/kg GTE as compared to the saline-treated rats. In summary, this study revealed the prophylactic and therapeutic treatment effects of GTE on RGC survival and axonal regeneration in rats with ON injury, indicating a potential alternative treatment for traumatic optic neuropathy.

Oxidative stress in the brain and retina after traumatic injury.

The brain and the retina share many physiological similarities, which allows the retina to serve as a model of CNS disease and disorder. In instances of trauma, the eye can even indicate damage to the brain via abnormalities observed such as irregularities in pupillary reflexes in suspected traumatic brain injury (TBI) patients. Elevation of reactive oxygen species (ROS) has been observed in neurodegenerative disorders and in both traumatic optic neuropathy (TON) and in TBI. In a healthy system, ROS play a pivotal role in cellular communication, but in neurodegenerative diseases and post-trauma instances, ROS elevation can exacerbate neurodegeneration in both the brain and the retina. Increased ROS can overwhelm the inherent antioxidant systems which are regulated via mitochondrial processes. The overabundance of ROS can lead to protein, DNA, and other forms of cellular damage which ultimately result in apoptosis. Even though elevated ROS have been observed to be a major cause in the neurodegeneration observed after TON and TBI, many antioxidants therapeutic strategies fail. In order to understand why these therapeutic approaches fail further research into the direct injury cascades must be conducted. Additional therapeutic approaches such as therapeutics capable of anti-inflammatory properties and suppression of other neurodegenerative processes may be needed for the treatment of TON, TBI, and neurodegenerative diseases.

Murine adolescent versus adult brain injury outcomes are improved after brief oxygen exposure

<h3>Research Objectives</h3> Traumatic optic neuropathy (TON) is a significant cause of visual impairment after head trauma and has few effective treatment options. In a mouse model of TON we previously noted post-injury apnea led to immediate mortality in adolescents and brief exposure to 100% oxygen reduced the mortality rate. We hypothesized that oxygen exposure may have an effect on the pathophysiology and functional deficits associated with TON and age at injury might modulate these effects. <h3>Design</h3> This was a randomized controlled preclinical intervention study of brief oxygen supplementation after experimental head trauma. Mice were followed for 7 days after injury. <h3>Setting</h3> Preclinical research laboratory. <h3>Participants</h3> Adult (8 week) and adolescent (6 week) male C57BL/6 mice. <h3>Interventions</h3> Brief oxygen exposure consisted of delivery of 100% Oxygen via hood for a total of five minutes immediately after injury; controls received room air and/or anesthesia only. <h3>Main Outcome Measures</h3> Optokinetic Response was assessed over three days. Retinal tissue was analyzed for protein/RNA expression, and serum assayed for cytokine levels. <h3>Results</h3> Although visual impairment after injury was similar between ages, oxygen more reliably improved OKR deficits in adolescents. Oxygen does not prevent retinal cell loss but does reduce pro-apoptotic markers in the retina in both groups. We anticipate a greater increase in injury-associated markers in adolescent mice compared to adults. <h3>Conclusions</h3> Even though pro-apoptotic markers in retinal cells were reduced, visual deficits persisted. Moreover, brief oxygen exposure appeared to be more beneficial for adolescent mice than for adults. Although preliminary, these results may suggest adolescent mice are more amenable to treatment for TON than adults. <h3>Author(s) Disclosures</h3> There are no conflicts to submission from any author.

Comparison of Surgical Decompression and Steroid Therapy for the Management of Traumatic Optic Neuropathy: A Systematic Review and Meta-Analysis.

A systematic review and meta-analysis. Treatment of traumatic optic neuropathy (TON) has been a subject of debate for many decades due to the scarcity of evidence-based treatment protocols. This review compares surgical decompression (SD) and steroid therapy (ST) as treatment approaches in TON patients. A PRISMA-guided systematic review using PubMed, Embase, Ovid and Scopus databases was performed till the last search date of July 31st 2021. The outcome of interest was an improvement in visual acuity. A meta-analysis of the odds ratio was performed using a random-effect model and sub-group analysis based upon criteria for assessment of improvement in visual acuity. Sixteen studies (including 1046 patients) were included in the review. The review could identify 590 patients treated with SD and 456 treated with ST. In addition, there was a second cohort of patients presenting with NLP (no light perception). A meta-analysis with a sub-group analysis revealed that there was statistically no significant difference between the two treatment approaches in terms of improvement in VA. There is no difference in treatment results of SD or ST for TON. Several treatment protocols and different criteria for assessing visual acuity led to difficulty in generating evidence for selecting the correct treatment approach.

Traumatic Optic Neuropathy: Analysis of Demographic and Clinical Parameters Over Three Years in a Tertiary Care Hospital in India.

Background Treatment options for traumatic optic neuropathy (TON) are limited and the role of steroids in the treatment of TON is still controversial. Hence this study was planned to highlight the role of steroids in the treatment of TON. Purpose The study aims to highlight the epidemiological and clinical characteristics, as well as the role of steroids, in TON cases seen during a three-year period at a tertiary care center in India. Methods This was a retrospective study that reviewed records of all cases of TON between January 2018 to January 2020. Results Twenty-three cases of TON were seen representing 1.26% cases of head injuries. The median age was 18 years. One patient (4.34%) had bilateral TON and 18 patients (78.26%) were referred from accident and trauma care. None of the patients presented directly to an ophthalmologist. The most common cause of injury was automobile accident (69.56%). Visual acuity at presentation was 20/80-20/100 in six (26.08%) cases. Fifteen (65.4%) patients had associated closed globe injury. Seven (30.43%) patients had ocular adnexal involvement and 10 (43.47%) patients had orbital fractures. Seventeen (73.91%) received steroid treatment and six of these patients showed visual improvement. Conclusions The study showed that there was no significant association between presenting visual acuity and treatment. The presence of significant ocular injury and orbital injury increased the likelihood of treatment. There was no difference between the treated and untreated groups with respect to final visual acuity.

Affection of Surgical Decompressive Scale of Optic Canal to Traumatic Optic Neuropathy.

Traumatic optic neuropathy (TON) is damage to the optic nerve that is caused by external violence to the optic nerve during cranial and facial trauma. This kind of injury may result in impaired vision, has a high risk of blindness, and significantly impairs the neurological function of the patient. The treatment of TON is controversial, and many different approaches have been suggested. No one is considered best because the traumatic mechanism is not clear. Methods: In this retrospective study, the clinical features of 37 patients diagnosed with TON without light perception who were treated at the Ninth People's Hospital of Shanghai Jiao Tong University School of Medicine were investigated. A comparison was made between the patient's visual results before and after therapy. In addition, using a multifactorial linear regression model, the independent risk variables for the degree of improvement in visual acuity (IDVA) following surgery were determined. Results: After the operation, 17 people's visual acuity (VA) was lightless, 20 people's visual acuity was improved, and 13 people's visual acuity reached the standard of decerebrate. The efficiency of total optic nerve decompression was 54.1%, and the unblinded rate was 35.1%. Multiple linear regression analysis revealed that fractures of the optic canal and orbit were independent predictors of postoperative VA and IDVA. Conclusions: Total optic canal decompression may efficiently and safely enhance the vision of patients who have TON. Patients with TON who do not have fractures of the optic canal and orbit prior to decompression had a more favorable surgical prognosis.

Effect of orbital volume in unilateral orbital fracture on indirect traumatic optic neuropathy.

This retrospective study aimed to analyze the relationship between the volume of the fractured and the normalorbitin patients with unilateral orbital fractures with and without indirect traumatic optic neuropathy (TON). Data of 25 patients with unilateral orbital fractures who underwent computer tomography between January 2016 and December 2020 were investigated. Emergency imaging was performed within 2hours of arrival at the emergency room.The subjects were categorized into two groups: unilateral orbital fractures with and without TON. The assessment of TON was performed during a comprehensive ophthalmologic examination by an ophthalmologist. The stereographic orbit was reconstructed, and the volume was calculated. Other variables examined included age, sex, and cause of orbital trauma.The variables were compared using paired t-tests. Statistical significance was set at p < 0.05. The orbital volume of the non-fractured orbit was27.50 ± 2.26 and 27.48 ± 2.64cm3 in the groups with and without TON, respectively.The average volume of the fractured orbit in the TON group was27.78 ± 2.56cm3, andthere was no significant volumetric difference between the fractured and non-fractured sides in this group. However, the average volume of the fractured orbit without TON was 28.76 ± 3.18cm3, larger than that of the non-fractured orbit (p = 0.016). Non-expansion of the fractured orbit was a risk factor for indirect TON in patients with unilateral orbital fractures. Volumetric analysis from primary imaging would expedite the diagnosis and treatment of TON, resulting in optimal outcomes.

Efficiently suppress of ferroptosis using deferoxamine nanoparticles as a new method for retinal ganglion cell protection after traumatic optic neuropathy.

Traumatic optic neuropathy (TON) is the major contributor to optic nerve damage, where the retinal ganglion cells (RGCs) are substantially lost. However, the underlying pathological mechanisms for these conditions remain largely elusive. Present work conducted a study on TON rat model, where the iron-dependent cyclooxygenase-2 (COX-2) overexpression and lipid peroxidation were observed in RGCs, suggesting ferroptosis, an iron-dependent non-apoptotic cell death, is involved in TON-induced death of RGCs. Hence, the newly formulated hyaluronic acid (HA)-based deferoxamine (DFO) nanoparticles (DFO-NPs) were intravitreally administrated in the rat model. It was hypothesized that the effective delivery of DFO, iron chelator, to the RGCs might rescue RGC ferroptosis from TON-induced injury. Also, since DFO is poor in bioavailability and of very short half-life in vivo, its safe and efficient intravitreal delivery is critical. Therefore, DFO-NPs were prepared by chemical grafting DFO onto HA molecules, and then crosslinking them in microemulsion bubbles for nanoparticles formulation. The nanoparticles were highly accumulated around the ganglionic cells and DFO uptake was increased in RGCs, accompanied by the significantly inhibited the overexpression of COX-2 and inactivation of glutathione peroxidase 4 (GPX4). These results indicate that DFO-NPs acted as an effective ferroptosis inhibitor, for the prevention of TON-induced RGC death. The current study provides new insights into the underlying mechanism of TON-induced RGC death, which may help to explore a novel strategy for the treatment of TON.

Tunable alginate hydrogels as injectable drug delivery vehicles for optic neuropathy.

Many disease pathologies, particularly in the eye, are induced by oxidative stress. In particular, injury to the optic nerve (ON), or optic neuropathy, is one of the most common causes of vision loss. Traumatic optic neuropathy (TON) occurs when the ON is damaged following blunt or penetrating trauma to either the head or eye. Currently, there is no effective treatment for TON, only management options, namely the systematic delivery of corticosteroids and surgical decompression of the optic nerve. Unfortunately, neither option alleviates the generation of reactive oxygen species (ROS) which are responsible for downstream damage to the ON. Additionally, the systemic delivery of corticosteroids can cause fatal off‐target effects in cases with brain involvement. In this study, we developed a tunable injectable hydrogel delivery system for local methylene blue (MB) delivery using an internal method of crosslinking. MB was chosen due to its ROS scavenging ability and neuroprotective properties. Our MB‐loaded polymeric scaffold demonstrated prolonged release of MB as well as in situ gel formation. Additionally, following rheological characterization, these alginate hydrogels demonstrated minimal cytotoxicity to human retinal pigment epithelial cells in vitro and exhibited injection feasibility through small‐gauge needles. Our chosen MB concentrations displayed a high degree of ROS scavenging following release from the alginate hydrogels, suggesting this approach may be successful in reducing ROS levels following ON injury, or could be applied to other ocular injuries.

Traumatic optic neuropathy: a review of current studies.

Traumatic optic neuropathy (TON) is a serious complication of craniofacial trauma that directly or indirectly damages the optic nerve and can cause severe vision loss. The incidence of TON has been gradually increasing in recent years. Research on the protection and regeneration of the optic nerve after the onset of TON is still at the level of laboratory studies and which is insufficient to support clinical treatment of TON. And, due to without clear guidelines, there is much ambiguity regarding its diagnosis and management. Clinical interventions for TON include observation only, treatment with corticosteroids alone, or optic canal (OC) decompression (with or without steroids). There is controversy in clinical practice concerning which treatment is the best. A review of available studies shows that the visual acuity of patients with TON can be significantly improved after OC decompression surgery (especially endoscopic transnasal/transseptal optic canal decompression (ETOCD)) with or without the use of corticosteroids. And new findings of laboratory studies such as mitochondrial therapy, lipid change studies, and other studies in favor of TON therapy have also been identified. In this review, we discuss the evolving perspective of surgical treatment and experimental study.

Implantable patches assembled with mesenchymal stem cells and gelatin/silk fibroin composite microspheres for the treatment of traumatic optic neuropathy

The therapeutic benefits of transplanting mesenchymal stem cells (MSCs) to the injury site of traumatic optic neuropathy (TON) represents a crucial, yet unresolved question, the answer to which may facilitate development of innovative therapies for TON, a frustrating disease with no effective treatment. Herein, we address this issue by showing that MSC transplantation to the injury site is able to promote optic nerve regeneration in terms of retinal ganglion cell survival and axon regeneration using MSC@MS, implantable patches assembled with MSCs and gelatin/silk fibroin composite microspheres, which integrate 3D culture and trypsin-free harvesting, and can increase in vivo retention of transplanted MSCs. In contrast, conventional bolus injection of MSC suspension is not potent enough to produce significant benefits. We also show MSCs in MSC@MS demonstrate superior gene expression profiles over monolayer culture after IGF-1 stimulation. In future study, microspheres in MSC@MS can further be harnessed to deliver therapeutic cargoes that boost the potency of MSCs or treat TON synergistically with MSCs, making MSC@MS a versatile platform to develop tailored MSC-based therapies for TON.

The Retino-Hypothalamic Ultrastructural Changes in Traumatic Optic Neuropathy

Aim: To study the retino-hypothalamic ultrastructural changes in traumatic optic neuropathy’s pathogenesis and treatment. Methods: Four groups of mature rabbits were included in this experiment, 30 in each group, 120 in total. The traumatic crush to the optic nerves was reproduced by surgical clips to 90 mature rabbits. The first group (I) included intact/control animals, the second (II) included animals with traumatic optic neuropathy and two other traumatized groups (III and IV) who were given two different doses of treatment. The animals in group III were given infusions of Methylprednisolone 30mg/kg/day for three days. The group IV animals received infusion of 15mg/kg/ day of Methylprednisolone for 3 days in combination with phosphine electric stimulation (PES), starting from the third until the 13th day of the experiment. The electrical pulse which was used on the affected side of the animal was 800 mА and 300 mА on the opposite side. The morphological analysis of the retina and suprachiasmatic nucleus of the hypothalamus of all the four groups of animals included electron microscopy of the semi-thin and ultrathin sections. This analysis was performed a month following the initial injury while the animals were removed from the experiment. The levels of cortisol and adrenocorticotropic hormone (ACTH) in the blood of all experimental animals was tested up to one month following the injury to the optic nerves. Results: We found that trauma to the orbital part of the optic nerve causes collocative necrosis of ganglion cells and swelling of the nerve fiber layer of the ipsilateral retina. In addition, such traumatic damage causes structural changes in the suprachiasmatic nucleus of the hypothalamus. Combined treatment of methylprednisolone with phosphine electro stimulation in traumatized rabbits reduced the thickness of the retina, reduced the cytokaryometric indices and the regeneration processes of bipolar and ganglion cells of the retina. Histopathologically we found an increased number of neurosecretory granules in the suprachiasmatic nucleus of the hypothalamus. ACTH levels in the blood of the group III rabbits were found to be lower, while the cortisol levels higher, and these hormone levels in the IV group rabbits were quite similar to those of the group which was not treated. Conclusion: The combined treatment of traumatic optic neuropathy in rabbits with phosphine electrostimulation and methylprednisolone can be considered a useful treatment, having a beneficial neuroprotective effect.

The Alteration of M6A-Tagged Transcript Profiles in the Retina of Rats After Traumatic Optic Neuropathy.

Messager RNA (mRNA) can be modified in a variety of ways, among which the modification of N6-methyladenosine (m6A) is one of the most common ones. Recent studies have found that the m6A modification in mRNA could functionally regulate the splicing, localization, translation, and stability of mRNA, which might be closely related to multiple diseases. However, the roles of m6A modification in traumatic optic neuropathy (TON) are unknown. Herein, we detected the expression of m6A-related genes via quantitative real-time PCR (qRT-PCR) and performed methylated RNA immunoprecipitation sequencing (MeRIP-seq) as well as RNA-sequencing to analyze the alteration profiles of m6A modification after TON. The results showed that the expression of m6A-related genes (METTL3, WTAP, FTO, and ALKBH5) were all upregulated after TON. In all, 2,810 m6A peaks were differentially upregulated and 689 m6A peaks were downregulated. In addition, the hypermethylated and hypomethylated profiles of mRNA transcripts were also identified. To sum up, our study revealed the differentially expressed m6A modification in the early stage of TON, which may provide novel insights into the mechanism and treatment of TON.

Traumatic optic neuropathy management: A survey assessment of current practice patterns

Introduction:The treatment of traumatic optic neuropathy (TON) is highly controversial with a lack of substantiated evidence to support the use of corticosteroids or surgical decompression of the optic nerve. The aim of the study was to determine if there was a general consensus in the management of TON despite controversy in the literature.Methods:An anonymous survey of members of the American Society of Ophthalmic Plastic and Reconstructive Surgery and the North American Neuro-Ophthalmology Society regarding their practice patterns in the management of patients with TON was performed.Results:The majority of 165 respondents indicated that they treated TON with corticosteroids (60%) while a significant minority (23%) performed surgical interventions (P < 0.0001). Subgroup analysis comparing rates of treatment with steroids among oculoplastic surgeons and neuro-ophthalmologists (67% vs. 47%) was not significant (Fisher's Exact test [FET], P =0.11) while results did suggest that a higher proportion of oculoplastic surgeons (33%) than neuro-ophthalmologists (11%) recommended surgical intervention (FET, P =0.004). In cases where visual acuity exhibited a downward trend treatment with steroids was the most commonly employed management. In general, neuro-ophthalmologists trended toward observation over treatment in TON patients with stable visual acuity while oculoplastic surgeons favored treatment with corticosteroids.Conclusions:In spite of the lack of class I evidence supporting intervention of TON, the majority of respondents were inclined to offer corticosteroid treatment to patients whose visual acuity showed progressive decline following injury.

Interventions for Indirect Traumatic Optic Neuropathy: A Report by the American Academy of Ophthalmology

To review the literature on the efficacy and safety of medical and surgical interventions for indirect traumatic optic neuropathy (TON), defined as injury to the nerve that occurs distal to the optic nerve head. A literature search was conducted on October 22, 2019, and updated on April 8, 2020, in the PubMed database for English language original research that assessed the effect of various interventions for indirect TON. One hundred seventy-two articles were identified; 41 met the inclusion criteria outlined for assessment and were selected for full-text review and abstraction. On full-text review, a total of 32 studies metall of the study criteria and were included in the analysis. No study met criteria for level I evidence. Seven studies (1 level II study and 6 level III studies) explored corticosteroid therapy that did not have uniformly better outcomes than observation. Twenty studies (3 level II studies and 17 level III studies) assessed optic canal decompression and the use of corticosteroids. Although visual improvement was noted after decompression, studies that directly compared surgery with medical therapy did not report uniformly improved outcomes after decompression. Four studies (1 level II study and 3 level III studies) evaluated the use of erythropoietin. Although initial studies demonstrated benefit, a direct comparison of its use with observation and corticosteroids failed to confirm the usefulness of this medication. One study (level II) documented visual improvement with levodopa plus carbidopa. Complication rates were variable with all of these interventions. Pharmacologic interventions generally were associated with few complications, whereas optical canal decompression carried risks of serious side effects, including hemorrhages and cerebrospinal fluid leakage. Despite reports of visual improvement with corticosteroids, optic canal decompression, and medical therapy for indirect TON, the weight of published evidence does not demonstrate a consistent benefit for any of these interventions. In summary, no consensus exists from studies published to date on a preferred treatment for TON. Treatment strategies should be customized for each individual patient. More definitive treatment trials will be needed to identify optimal treatment strategies for indirect TON.

Fasudil attenuates glial cell-mediated neuroinflammation via ERK1/2 and AKT signaling pathways after optic nerve crush.

To investigate the functional role of fasudil in optic nerve crush (ONC), and further explore its possible molecular mechanism. After ONC injury, the rats were injected intraperitoneally either with fasudil or normal saline once a day until euthanized. RGCs survival was assessed by retrograde labeling with FluoroGold. Retinal glial cells activation and population changes (GFAP, iba-1) were measured by immunofluorescence. The expressions of cleaved caspase 3 and 9, p-ERK1/2 and p-AKT were detected by western blot. The levels of the pro-inflammatory cytokines were determined using real-time polymerase chain reaction. Fasudil treatment inhibited RGCs apoptosis and reduced RGCs loss demonstrated by the decreased apoptosis-associated proteins expression and the increased fluorogold labeling of RGCs after ONC, respectively. In addition, the ONC + fasudil group compared had a significantly lower expression of GFAP and iba1 compared with the ONC group. The levels of pro-inflammatory cytokines were significantly reduced in the ONC + fasudil group than in the ONC group. Furthermore, the phosphorylation levels of ERK1/2 and AKT (p-ERK1/2 and p-AKT) were obviously elevated by the fasudil treatment. Our study demonstrated that fasudil attenuated glial cell-mediated neuroinflammation by up-regulating the ERK1/2 and AKT signaling pathways in rats ONC models. We conclude that fasudil may be a novel treatment for traumatic optic neuropathy.

Diagnosis and management of three optic neuropathies: a national survey.

We aimed to evaluate the current practice patterns of neuro-ophthalmologists in diagnosis and management of three optic neuropathies using a national survey in South Korea and to further compare the practices of neuro-ophthalmologists divided into junior and senior groups based on their clinical practice experience. An anonymous, 15-question survey on the diagnosis and treatment of traumatic optic neuropathy (TON), nonarteritic anterior ischemic optic neuropathy (NAION), and Leber's hereditary optic neuropathy (LHON) was sent to all neuro-ophthalmologists registered with the Korean Neuro-ophthalmology Society. The questions addressed physician's practice duration as neuro-ophthalmologist, choices of MRI scans and laboratory tests for the diagnosis in suspected optic neuropathy, clinical experiences with steroids (e.g., side effects), and choices of treatment modalities and reason in in each optic neuropathy. All participants were classified into senior (≥ 10years) and junior (< 10years) groups. A total of 63 responders (response rate 78.8%) answered the questionnaire. All responders performed the basic blood tests and brain imaging for evaluating optic neuropathy. Observation was the most preferred option for TON (47.6%) and NAION (63.5%). Steroid use was the second most preferred, and the most selected indication of steroid was "when the patient wants" (58.7%) for TON and "severe visual loss or last eye" (66%) for NAION. The most preferred treatment for LHON was "prescribing idebenone" (69.7%) with a dose of 900mg/day (63.8%). Forty-nine respondents (77.8%) experienced side effects of steroids. There was no significant difference between the senior and junior groups in all questionnaire answers (all p > 0.05). Optic neuropathies are being managed similarly by the two groups in South Korea, and many of them still use steroids. We provided reliable reasons for our results compared with other countries.

Outcome of optic nerve decompression through neuroendoscopic transethmoidal-sphenoidal approach in the treatment of traumatic optic neuropathy

Objective To investigate the outcome of optic nerve decompression through neuro-endoscopic transethmoidal-sphenoidal approach in the treatment of traumatic optic neuropathy (TON). Methods The consecutive clinical data of 29 patients (32 sides) with TON who were treated at Department of Neurosurgery, Shanghai General Hospital, Shanghai Jiao Tong University from December 2013 to February 2018 were retrospectively analyzed. Preoperative visual acuity results were as follows: no light perception (NLP) in 15 sides, light perception in 14 sides, and hand moving in 3 sides. All patients underwent optic nerve decompression through neuroendoscopic transethmoidal-sphenoidal approach assisted with intraoperative neuronavigation. High-resolution skull CT scan was performed before the operation. These aspects were documented including the anatomic landmark observed during operation, visual changes of the patients and operative complications. Results The follow-up periods were 5.2±1.1 months (range: 3 to 6 months). Postoperative visual acuity results were as follows: NLP in 10 sides, light perception in 4 sides, hand moving in 4 sides, counting finger in 5 sides, and logMAR≥0.02 in 9 sides. The effective rate of operation was 59.4% (19/32). No surgical complications such as internal carotid artery injury, cerebrospinal fluid rhinorrhea or anosmia occurred. Conclusion Optic nerve decompression through transethmoidal-sphenoidal approach seems to be an effective method for the treatment of TON. The anatomic landmarks of the surgical approach are clearly defined, and intraoperative neuronavigation contributes to the safety of operation and reduces the occurrence of complications. Key words: Optic nerve injuries; Natural orifice endoscopic surgery; Treatment outcome; Optic nerve decompression; Transethmoidal-sphenoidal approach