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Background: Traumatic optic neuropathy (TON) is a rare complication of facial trauma that results in vision loss. Clinical diagnosis of TON is based on a history of head trauma and an ophthalmic examination; however, the risk factors for TON and the ideal treatment strategy remain undetermined. This study aimed to identify predictive risk factors for TON and evaluate the effectiveness of current treatments with respect to visual outcomes in patients with TON., Methods: This study retrospectively enrolled patients with periorbital facial bone fracture between 2008 and 2019. Initial facial bone computed tomography, ophthalmic exam results, initial Glasgow Coma Scale, and Injury Severity Score were recorded. This study classified patients into 4 intervention groups (i.e., medication, surgery, combination therapy, and observation) to compare the outcome of visual acuity., Results: This study enrolled 1168 patients with facial bone fractures, 93 (7.96%) of whom were diagnosed as having TON. Independent risk factors for TON included optic canal fracture, medial orbital wall fracture, retrobulbar hematoma, and head Abbreviated Injury Scale ≥4. Patients with TON who initially presented with no light perception tended to have poor final visual acuity (VA) outcomes. The results indicated no significant difference in VA improvement among patients receiving observation, megadose corticosteroid therapy, surgical decompression, or combined steroid therapy and decompression., Conclusion: Clinicians can achieve early prediction of TON in patients with an initial unconscious state and the identified risk factors. The results indicated that the conservative observation yielded noninferior VA outcomes in patients with TON compared with those receiving medication or surgical treatment., (Copyright © 2024 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.)

Background: Traumatic optic neuropathy is classically described in up to 8% of patients with traumatic brain injury (TBI), but subclinical or undiagnosed optic nerve damage is much more common. When more sensitive testing is performed, at least half of patients with moderate to severe TBI demonstrate visual field defects or optic atrophy on examination with optical coherence tomography. Acute optic nerve compression and ischaemia in orbital compartment syndrome require urgent surgical and medical intervention to lower the intraocular pressure and diminish the risk of permanent optic nerve dysfunction. Other manifestations of traumatic optic neuropathy have more variable treatments in international practice., Methods: We conducted a systematic review of traumatic optic neuropathy treatments in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement., Results: We included three randomised controlled trials of intravenous methylprednisolone (IVMP), erythropoietin, and levodopa-carbidopa combination, with no evidence of benefit for any treatment. In addition, large studies in TBI have found strong evidence of increased mortality in patients treated with megadose IVMP., Conclusions: There is therefore no evidence of benefit for any medical treatment and strong evidence of harm from IVMP. There is also no evidence of benefit for optic canal decompression for traumatic optic neuropathy. Orbital compartment syndrome is a separate entity that requires both medical and surgical interventions to prevent visual loss., (© 2024. Crown.)

Purpose: To describe a case of a maxillofacial trauma that occurred during a mixed martial arts (MMA) match and to perform a literature review of maxillofacial injuries related to MMA match to determine whether preventive models are applicable., Methods: The authors described a maxillofacial injury with orbital and optic nerve involvement that happened during a professional MMA match. A literature review on maxillofacial trauma in MMA was conducted on Scopus and Pubmed with specific keywords., Results: Open reduction and internal fixation of the maxillofacial complex fractures with right eye optic neuropathy following an MMA match is described. Six articles were selected for the description of trauma in the maxillofacial complex associated with MMA fights., Discussion: Literature has paid little attention to injuries during MMA matches. The most common injury locations that emerged from the literature review were the head, face, and neck. Middle facial third injuries were the most common type. Frequently the injury involved the ophthalmic area., Conclusions: The timing of maxillofacial trauma in MMA is critical. Protective devices should be strongly promoted to prevent catastrophic consequences., Competing Interests: The authors report no conflicts of interest., (Copyright © 2024 by Mutaz B. Habal, MD.)

Introduction: The gold standard treatment for indirect traumatic optic neuropathy (ITON) has not yet been conclusively established, and it is essential to gain an understanding of visual prognosis and to counsel patients regarding the predictive risk factors of poor visual outcomes. Currently, there is limited information regarding ITON in Thai populations; therefore, this study aimed to determine the risk factors of poor visual outcome in patients with this condition., Methods: A retrospective review was conducted of all ITON cases diagnosed at Rajavithi Hospital and Sawanpracharak Hospital between January 2016 and December 2022 in order to determine clinical characteristics and evaluate associated risk factors of poor visual prognosis using binary logistic regression analysis., Results: The mean age of this cohort of 101 patients was 36.17 years, with a male predominance of 73.3 %. Motor vehicle accidents were the most common cause of ITON, with a statistically significant 79.2 % of cases. The patients were categorized into an "improved group" of 29 patients and an "unimproved group" of 72. The unimproved group had a significantly older mean age and poorer initial visual acuity of 20/200 (p-values 0.001 and p < 0.001 respectively). There was no significant difference between Computed Tomography (CT) findings in the two groups. The improved group had significantly better visual acuity (VA) at 1-month and final follow-up visit than the unimproved group (both p < 0.001). Differences between gender, Glasgow coma score, associated underlying diseases, and duration from trauma to intravenous glucocorticoids therapy in the two groups were not statistically significant. Multivariable logistic regression analysis identified patient age of 40 years or more (Odds ratio (OR) 3.447, 95 % CI, 1.085-10.955, p = 0.036) and poor baseline VA (OR 6.628, 95 % Confidence Interval (CI), 2.308-19.036, p < 0.001) as significant risk factors for poor visual outcome in ITON patients., Conclusions: No clear benefit was found of intravenous glucocorticoids in treatment of ITON. Patients aged 40 years or more and/or with poor baseline visual status should be advised that they are at increased risk of poor final visual outcomes., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier Ltd.)

Abstract: Optic nerve avulsion without bone fracture was observed in four cases in the literature. This case is unique with its cranial effects and complications. A 50-year-old Caucasian female patient attacked by an animal on her left eye was admitted. Traumatic subarachnoid hemorrhage in the suprasellar cistern and epidural hematoma was observed upon brain computed tomography (CT). Enucleation and duraplasty were performed on the patient whose epidural hemorrhage did not increase. Two weeks after being discharged, the patient presented to the emergency room again with numbness on the right side of her face and sensory aphasia. The patient was followed up by medical treatment with left temporoparietal infarction and had completely recovered. Optic nerve avulsion secondary to trauma is a topic that needs to be carefully investigated due to potentially fatal complications. This article was written to share our experience with this rare condition and its case management., (Copyright © 2023 Copyright: © 2023 Nigerian Journal of Clinical Practice.)

Purpose: To analyze the visual outcome in patients with traumatic optic neuropathy (TON) with respect to different treatment modalities, to study the correlation of initial visual loss with the final visual outcome, and to find out the predictor of final visual outcome in patients with indirect TON., Methods: A retrospective analysis of 36 eyes with TON was done. Data on clinical profile, including demographics, mode of trauma, best corrected visual acuity (BCVA), pupillary reflex examination, and anterior and posterior segment examination, was collected. Presence and location of orbital and cranial fractures were identified from computed tomography scan. Visual outcomes following steroid therapy, optic nerve (ON) decompression, and in untreated patients were analyzed. Pre- and post-treatment BCVA were divided into three groups based on logarithm of the minimum angle of resolution (logMAR) as follows: group A: 3, group B: 2.9-1.3, and group C<1.3. BCVA values at follow-up visits were taken as the primary outcome measure. Association between various risk factors and final visual outcome in patients with indirect TON was also analyzed., Results: Out of 34 patients whose 36 eyes were studied, three (8.8%) patients were females and 31 (91.2%) patients were males. Most common mode of trauma was road traffic accident (RTA; 91.2%), which was followed by fall (8.8%) and assault (2.9%). Pre- and post-treatment BCVA values of 36 eyes were compared, and improvement in BCVA after treatment was found to be statistically significant. Also, 28.6% of patients with presenting BCVA of no light perception showed improvement compared to 94.1% and 100% in groups B and C, respectively. Orbital wall fractures were seen in 80.5% (n = 29) of the patients, with lateral wall fracture being the most common (58.3%) followed by medial wall (33.3%), roof (27.7%), floor (27.7%), and optic strut (5%)., Conclusion: Baseline BCVA had significant association with final vision improvement. Lateral wall fracture was the most common fracture associated with indirect TON. Patients treated with high-dose corticosteroids, irrespective of the time of presentation, had a better visual outcome.

Purpose: This retrospective study aimed to analyze the relationship between the volume of the fractured and the normal orbit in patients with unilateral orbital fractures with and without indirect traumatic optic neuropathy (TON)., Subjects: 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 2 hours of arrival at the emergency room. The subjects were categorized into two groups: unilateral orbital fractures with and without TON., Methods and Measures: 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., Results: The orbital volume of the non-fractured orbit was 27.50  ± 2.26 and 27.48  ±  2.64 cm 3 in the groups with and without TON, respectively. The average volume of the fractured orbit in the TON group was 27.78  ± 2.56 cm 3 , and there 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  ±  3.18 cm 3 , larger than that of the non-fractured orbit (p = 0.016)., Conclusions: 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., (© 2022. The Author(s), under exclusive licence to Springer Nature B.V.)

Cerebral concussions are a well-recognized issue in military and civilian practice. Although most physicians are well versed in recognizing concussion symptoms, many are not as adept at diagnosing and managing comorbid traumatic optic neuropathy (TON). Traumatic optic neuropathy typically follows cerebral concussions but is often not diagnosed as its symptoms are attributed to brain injury or the presence of altered consciousness impedes its recognition. We hereby describe a soldier who sustained a cerebral concussion with an associated unrecognized TON. We review the epidemiology, pathophysiology, diagnosis, and management of TON., (© The Association of Military Surgeons of the United States 2022. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Purpose: Traumatic optic neuropathy can have varying presentations. Blunt focal trauma can lead to optic nerve avulsion with underlying retinal findings. A case of partial optic nerve avulsion after finger poke injury leading to focal retinal ischemia is reported., Methods: Visual acuity, fundus photography with fluorescein angiography, and spectral-domain optical coherence tomography were performed to document the findings in a 16-year-old man who presented after a finger poke injury to the left orbit during a water polo match., Results: On initial presentation, examination revealed decreased visual acuity with a fixed left pupil and afferent pupillary defect by reverse. On slit-lamp examination of the left eye, a hyphema was present. Dilated fundus examination revealed layering vitreous hemorrhage over the posterior pole and an avulsed vitreous base. On follow-up, a gap temporal to the optic nerve head consistent with a partial optic nerve avulsion was noted once the vitreous hemorrhage cleared. Multimodal imaging revealed retinal ischemia temporal to the disc on fluorescein angiography with corresponding changes in the inner retinal layers and retinal nerve fiber layer using spectral-domain optical coherence tomography., Conclusion: Clinicians should have a high suspicion for optic nerve avulsion if a patient presents with new vitreous hemorrhage and afferent pupillary defect after a finger-poke injury. Optic nerve avulsion injury can cause retinal ischemia, likely because of interruption of retinal blood flow as a result of nerve shearing injury. Multimodal imaging can reveal focal retinal injury and aid in proper diagnosis and follow-up.

Rarely, but often with serious consequences for the patient, the optic nerve is affected during the course of head injuries. Traumatic optic nerve compression is always an emergency situation, which is why time is of the essence for both diagnosis and treatment. Precise knowledge of this accident sequelae but also of the resulting conditions, especially in terms of traumatic optic neuropathy, is indispensable for adequate patient care. The aim of this paper is to provide an overview of this clinical picture, particularly with regard to etiology, diagnosis, and treatment options, and to discuss this in the context of the current literature., (© 2022. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

A 29-year-old man presented with a sudden loss of vision after a closed-globe injury. At presentation, he had no light perception in the right eye and the right pupil was dilated and nonreactive to light. On ophthalmological examination, the area of the optic nerve head was excavated, suggesting optic nerve avulsion. Magnetic resonance imaging scan showed optic nerve avulsion without rupture of the optic nerve sheath. Four months after the injury, the patient's visual acuity remained unchanged. Gliosis developed at the avulsion site. Closed-globe injuries may cause severe posterior injury even if there is no anterior damage in the eye. To prevent unnecessary treatment, trauma patients should be examined carefully appropriate imaging to confirm the diagnosis., Competing Interests: Conflict of Interest: No conflict of interest was declared by the authors., (©Copyright 2022 by Turkish Ophthalmological Association, Turkish Journal of Ophthalmology, published by Galenos Publishing House.)

Clinical Relevance: Traumatic globe luxation is rare vision-threatening event. Besides causing loss of vision in traumatised eye, it may also cause injury to contralateral optic nerve. Any such limitation in a one-eyed patient can make him crippled in his day-to-day activities. Here we hypothesise cause of contralateral field defect in such patients., Background: Traumatic globe luxation is a rare event that leads to profound vision loss due to injury of the ipsilateral optic nerve and rarely a visual field defect in the contralateral eye. Through this communication, we report similar case scenarios and intend to hypothesize the mechanism that results in the occurrence of the contralateral visual field defect., Methods: It is a retrospective, observational study. All cases with traumatic globe luxation were enrolled. Visual field analysis of the contralateral normal eye was main outcome measure., Results: Four patients with traumatic globe luxation and optic nerve injury were studied. There was complete loss of vision in the traumatised eye in all the patients. One patient had complete transection of the optic nerve, whereas in three patients, the course of the optic nerve was intact, on imaging. Three patients had quadrantanopia in the contralateral normal eye for which oral steroids were given. At 1-month follow-up, there was complete recovery of the visual field defect in two patients. We noticed that all the three patients with an intact course of the ipsilateral optic nerve had quadrantanopia in the contralateral normal eye., Conclusion: We hypothesize that in scenarios where globe luxation is associated with incomplete transection or no transection of the optic nerve, a continuous long standing stretch on the optic nerve, transmits the pulling force to the chiasma which might result in a contralateral field defect as compared to those associated with the complete transection of the optic nerve.

Introduction: The aim of the study was to evaluate the associated patterns of orbital wall fractures, diagnostic parameters of Traumatic optic neuropathy and its progress with Mega dose steroid therapy., Materials and Methods: 25 patients with unilateral orbital wall fractures of traumatic aetiology were evaluated with ophthalmologic and radiographic parameters. All patients were prescribed Mega Dose Intravenous steroids irrespective of the timing of presentation. Ophthalmic assessment was repeated for same parameters every alternate day upto 2 weeks., Results: Lateral orbital wall was found to be most commonly involved. Visual acuity, Pupillary Reactivity, Visual Field and Visual Evoked Potential showed statistically significant improvement post steroid therapy in early as well as late presenters., Discussion: Highest incidence of Traumatic optic neuropathy was noted in multiple linear orbital wall fractures with highest incidence with lateral orbital wall involvement. Literature regarding Choice and timing of initiation of steroids based on timing of presentation is inadequate to justify skipping steroids to observe or undertake surgical intervention. In the present study marked improvement was noted post steroid therapy regardless of timing of presentation. The authors conclude that Visual evoked potential should be objectively tested and Mega dose steroid therapy should be initiated for all patients with Traumatic optic neuropathy for maximum benefit to the patient., Competing Interests: Declaration of Competing Interest None., (Copyright © 2021 Elsevier Masson SAS. All rights reserved.)

Background: Head injuries are an important cause of morbidity and mortality in children and young adults. There are multiple sight-threatening complications of head injury, even in closed head injury without visible violation of the globe or orbits. One such entity is traumatic optic neuropathy., Case Report: Herein we describe a case of traumatic optic neuropathy in an otherwise healthy teenage patient who suffered total monocular vision loss after a fall and without any other injuries on examination. Unfortunately, the prognosis for this condition is relatively poor in terms of visual recovery. Though much research has been conducted attempting to treat this condition, to date there have been no studies showing a clear benefit of medical or surgical intervention. Why Should an Emergency Physician Be Aware of This? Although there is no proven treatment for traumatic optic neuropathy, emergency physicians may encounter this in their practice while caring for both pediatric and adult patients presenting with head injury. Having more background knowledge on this condition will enhance emergency physicians' ability to consult with subspecialist providers as well as to educate patients and their families on their condition and prognosis., (Copyright © 2021. Published by Elsevier Inc.)

Background: Traumatic optic neuropathy (TON) is a rare disease but leaves critical sequelae to patient. Purpose of this study is to evaluate the incidence of TON in each orbital wall fracture., Materials and Methods: Retrospective review of 2629 patients with orbital wall fracture was performed in from January 2010 to March 2019, based on diagnostic code, Korean Standard Classification of Diseases, 7th Revision. The orbital wall fractures were divided into 4 subtypes: superior, medial, inferior, and lateral wall. Incidence of TON is analyzed according to subtypes, single and multiple wall fracture., Results: Among 2629 patients with orbital wall fractures, 27 patients were diagnosed with TON with an incidence of 1.02%. In single wall fracture, only lateral wall showed significantly high TON incidence, which only zygomatic fracture was included in single lateral wall fracture. In multiple wall fracture, it was statistically significant in the superior wall., Conclusions: Fracture on lateral and superior orbital wall showed a tendency to increase the incidence of TON. Based on the above results, radiologic evaluation and physical examination is necessary for patient who has lateral and superior orbital wall fracture., Competing Interests: The authors report no conflicts of interest., (Copyright © 2021 by Mutaz B. Habal, MD.)

Pressure waves from explosions or other traumatic events can damage the neurons of the eye and visual centers of the brain, leading to functional loss of vision. There are currently few treatments for such injuries that can be deployed rapidly to mitigate damage. Brain-derived neurotrophic factor (BDNF) and activation of its receptor tropomycin-related kinase B (TrkB) have neuroprotective effects in a number of degeneration models. Small molecule activators of TrkB, such as N-[2-(5-hydroxy-1H-indol-3-yl)ethyl]-2-oxopiperidine-3-carboxamide (HIOC), cross the blood-brain and blood-retina barriers after systemic administration. We characterize the effects of blast-induced ocular trauma on retinal and visual function. We show that systemic administration of HIOC, a potent small molecule activator of the BDNF/TrkB receptor, preserves visual function in mice exposed to ocular blast injury. The HIOC treatment for one week preserves visual function for at least four months. The HIOC treatment effectively protected vision when the initial dose was administered up to 3 h after blast, but not if the initial treatment was delayed for 24 h. We provide evidence that the therapeutic effect of HIOC is mediated by activation of BDNF/TrkB receptors. The results indicate that HIOC may be useful for managing ocular blast injury and other forms of traumatic optic neuropathy.

Purpose: Rapid development in mobile phone technologies increase the average mobile phone usage duration. This increase also triggers exposure to radiofrequency radiation (RF), which is a risk factor for the health. In this study, it was aimed to investigate the effect of mobile phone working with LTE-Advanced Pro (4.5 G) mobile network on the optic nerve, which is responsible for the transmission of visual information., Material and Methods: Thirty-two rats divided into two groups as control (no RF, sham exposure) and experimental (RF exposure using a mobile phone with LTE-Advanced Pro network; 2 hours/day, 6 weeks). The visual evoked potential (VEP) was recorded and determined amplitudes and latencies of VEP waves. Optic nerve malondialdehyde level, catalase and superoxide dismutase activities were determined. Furthermore, ultrastructural and morphometric changes of optic nerve were evaluated., Results: In VEP recordings, the mean VEP amplitudes of experimental group were significantly lower than control group. In ultrastructural evaluation, myelinated nerve fibres and glial cells were observed in normal histologic appearance both in sham and experimental group. However, by performing morphometric analysis, in the experimental group, axonal diameter and myelin thickness were shown to be lower and the G-ratio was higher than in the sham group. In the experimental group, malondialdehyde level was significantly higher and superoxide dismutase and catalase activities were significantly lower than sham group. There was a high correlation between VEP wave amplitudes and oxidative stress markers., Conclusion: Findings obtained in this study support optic nerve damage. These results point out an important risk that may decrease the quality of life.

Purpose: The purpose of this study was to determine the effects of the Sigma-1R (σ-1r) on retinal ganglion cell (RGC) survival following optic nerve crush (ONC) and the signaling mechanism involved in the σ-1r protection., Methods: The overall strategy was to induce injury by ONC and mitigate RGC death by increasing σ-1r expression and/or activate σ-1r activity in σ-1r K/O mice and wild type (WT) mice. AAV2-σ-1r vector was used to increase σ-1r expression and σ-1r agonist used to activate the σ-1r and RGCs were counted. Immunohistochemical and Western blot analysis determined phosphorylated (p)-c-Jun, c-Jun, and Caspase-3. Pattern electroretinography (PERG) determined RGC activity., Results: RGC counts and function were similar in pentazocine-treated WT mice when compared to untreated mice and in WT mice when compared with σ-1r K/O mice. Pentazocine-induced effects and the effects of σ-1r K/O were only observable after ONC. ONC resulted in decreased RGC counts and activity in both WT and σ-1r K/O mice, with σ-1r K/O mice experiencing significant decreases compared with WT mice. The σ-1r transgenic expression resulted in increased RGC counts and activity following ONC. In WT mice, treatment with σ-1r agonist pentazocine resulted in increased RGC counts and increased activity when compared with untreated WT mice. There were time-dependent increases in c-jun, p-c-jun, and caspase-3 expression in ONC mice that were mitigated with pentazocine-treatment., Conclusions: These findings suggest that the apoptotic pathway is involved in RGC losses seen in an ONC model. The σ-1r offers neuroprotection, as activation and/or transgenic expression of σ-1r attenuated the apoptotic pathway and restored RGCs number and function following ONC.

Purpose: To characterize in vivo dendritic changes in retinal ganglion cells (RGCs) after acute (optic nerve transection, ONT) and chronic (experimental glaucoma, EG) optic nerve injury., Methods: ONT and EG (microbead model) were carried out in Thy1-YFP mice in which the entire RGC dendritic arbor was imaged with confocal fluorescence scanning laser ophthalmoscopy over two weeks in the ONT group and over two and six months, respectively, in two (groups 1 and 2) EG groups. Sholl analysis was used to quantify dendritic structure with the parameters: area under the curve (AUC), radius of the dendritic field, peak number of intersections (PI), and distance to the PI (PD)., Results: Dendritic changes were observed after three days post-ONT with significant decreases in all parameters at two weeks. In group 1 EG mice, mean (SD) intraocular pressure (IOP) was 15.2 (1.1) and 9.8 (0.3) mmHg in the EG and untreated contralateral eyes, respectively, with a significant corresponding decrease in AUC, PI, and PD, but not radius. In group 2 mice, the respective IOP was 13.1 (1.0) and 8.8 (0.1) mmHg, peaking at two months before trending towards baseline. Over the first two months, AUC, PI, and PD decreased significantly, with no further subsequent changes. The rates of change of the parameters after ONT was 5 to 10 times faster than in EG., Conclusions: Rapid dendritic changes occurred after ONT, while changes in EG were slower and associated with level of IOP increase. The earliest alterations were loss of inner neurites without change in dendritic field.

This article describes the case of a 28-year-old man who suffered an optic nerve evulsion (ONE) after falling from a height of 5 m. On admission visual acuity in the affected left eye was light perception, direct pupillary reaction was unresponsive, and the eye was hypotonic. Because of deep eyelid laceration, hyphemia and severe vitreous hemorrhage a globe rupture was suspected and a surgical exploration with vitrectomy was performed. This resulted in the detection of an ONE. During the following 24 months a painful eyeball due to secondary glaucoma developed and enucleation of the eye became necessary.

Traumatic brain injury (TBI) is frequently described as any head injury ceasing the brain's normal function. Anatomically, developmentally, and physiologically, the eye is deemed as an extension of the brain. Vision in TBI is underrepresented, and the number of active clinical trials in this field are sparse. Frequently, visual problems are overlooked at the time of TBI, often resulting in progressive vision loss, lengthening, and impairing rehabilitation. TBI can be either penetrative or non-penetrative, associated with degeneration of neurons, apoptotic cell death, inflammation, microglial activation, hemorrhage associated with vascular dysfunction; however, precise animal modeling that mimics the extensive visual deficits of TBI pathology remain elusive. Recent works in both the diagnostics and therapeutics fields are starting to make substantial progress in the right direction. Discussion of current advancements in TBI animal models and the recent pathophysiological findings related to the neuro-glia-vascular unit (NVU) will help elucidate novel targets for potential therapeutics lines. Only over the past decade have newer pharmaceutical and stem cell-based treatments begun to come to light. The potency for these new lines of TBI specific curatives will be discussed along with the review of current blast-induced TBI models, providing potential directions for future research.

Considered to be one of the most important non-contagious systemic diseases worldwide, diabetes mellitus is still a topical issue on the health agenda with the problems it causes. Exposure to long-term hyperglycemia causes diabetic complications (diabetic neuropathy, nephropathy and retinopathy). The optic nerve can suffer damage by both diabetic retinopathy and neuropathy during diabetes, both because it is formed by axons of retinal ganglion cells and these axons belong to the central nervous system. The issue of hyperglycemia on the optic nerve have been described as diabetic papillopathy, posterior ischemic optic neuropathy, nonarteritic anterior ischemic optic neuropathy and optic atrophy in clinical studies. Experimental studies indicated axon-myelin degeneration in addition to microvascular and ultrastructural changes caused by the hyperglycemia-induced optic nerve damage. Although there are several proposed biochemical mechanisms to cause these damages, oxidative stress emerges as an important factor among them. Oxidative stress leads to pathological state on the nerve cells by affecting the DNA, protein and lipids at different levels. These are causing deterioration on nerve conduction velocity, myelin sheath and nerve structure, neurotrophic support system, glial cells and nerve function. Curcumin, as an important antioxidant, can be an ideal prophylactic agent to eliminate damages on optic nerve. Curcumin helps to regulate the balance of antioxidant and reactive oxygen species by targeting various molecules (NF-κB, STAT3, MAPK, Mfn2, Nrf2, pro-inflammatory cytokines). In addition, it shows healing or preventive effects on myelin sheath damage via regulating ferritin protein in oligodendrocytes. It is also effective in preventing neurovascular damage., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Ciliary neurotrophic factor (CNTF) is a leading therapeutic candidate for several ocular diseases and induces optic nerve regeneration in animal models. Paradoxically, however, although CNTF gene therapy promotes extensive regeneration, recombinant CNTF (rCNTF) has little effect. Because intraocular viral vectors induce inflammation, and because CNTF is an immune modulator, we investigated whether CNTF gene therapy acts indirectly through other immune mediators. The beneficial effects of CNTF gene therapy remained unchanged after deleting CNTF receptor alpha (CNTFRα) in retinal ganglion cells (RGCs), the projection neurons of the retina, but were diminished by depleting neutrophils or by genetically suppressing monocyte infiltration. CNTF gene therapy increased expression of C-C motif chemokine ligand 5 (CCL5) in immune cells and retinal glia, and recombinant CCL5 induced extensive axon regeneration. Conversely, CRISPR-mediated knockdown of the cognate receptor (CCR5) in RGCs or treating wild-type mice with a CCR5 antagonist repressed the effects of CNTF gene therapy. Thus, CCL5 is a previously unrecognized, potent activator of optic nerve regeneration and mediates many of the effects of CNTF gene therapy., Competing Interests: The authors declare no competing interest.

Purpose: To establish a more sensitive diagnostic tool for traumatic optic neuropathy (TON), we explored the diagnostic efficacy of isolated-check visual evoked potential (ic-VEP) for TON in orbital fracture and compared ic-VEP with pattern-reversal visual evoked potential (P-VEP) testing., Methods: This was a prospective single-center study. A total of 137 eyes from 131 patients diagnosed between December 2016 and October 2019 with orbital fractures were included in the study. Injury history, best-corrected visual acuity (BCVA), visual field, computed tomography (CT), P-VEP, and ic-VEP data were collected. Parameters of ic-VEP (signal-to-noise ratio [SNR]) and P-VEP (peak latency and amplitude of P100) were compared and diagnostic accuracy was analyzed., Results: TON was associated with worse BCVA than non-TON (median 0.52 versus 0.10 logMAR, P < 0.001). SNRs were negatively associated with the P100 peak latency while positively associated with the P100 amplitude. The sensitivity of ic-VEP for TON (79.6%) was higher than that of P-VEP (61.2%, P = 0.049), although this difference was not statistically significant after Bonferroni correction. Using ic-VEP and P-VEP together could increase sensitivity (87.8%). Maximum areas under curve were obtained using the SNR criteria of 1.3, 1.47, and 1.54 at 8%, 16%, and 32% depth of modulation, respectively., Conclusion: ic-VEP was more sensitive than P-VEP in diagnosing TON, and a combination of the two examination tests was recommended. The use of ic-VEP as the new diagnostic standard technique for TON should be considered.

Background: Fractures of the orbital roof require high-energy trauma and have been linked to high rates of neurologic and ocular complications. However, there is a paucity of literature exploring the association between injury, management, and visual prognosis., Methods: The authors performed a 3-year retrospective review of orbital roof fracture admissions to a Level I trauma center. Fracture displacement, comminution, and frontobasal type were ascertained from computed tomographic images. Pretreatment characteristics of operative orbital roof fractures were compared to those of nonoperative fractures. Risk factors for ophthalmologic complications were assessed using univariable/multivariable regression analyses., Results: In total, 225 patients fulfilled the inclusion criteria. Fractures were most commonly nondisplaced [n = 118 (52.4 percent)] and/or of type II frontobasal pattern (linear vault involving) [n = 100 (48.5 percent)]. Eight patients underwent open reduction and internal fixation of their orbital roof fractures (14.0 percent of displaced fractures). All repairs took place within 10 days from injury. Traumatic optic neuropathy [n = 19 (12.3 percent)] and retrobulbar hematoma [n = 11 (7.1 percent)] were the most common ophthalmologic complications, and led to long-term visual impairment in 51.6 percent of cases., Conclusions: Most orbital roof fractures can be managed conservatively, with no patients in this cohort incurring long-term fracture-related complications or returning for secondary treatment. Early fracture treatment is safe and may be beneficial in patients with vertical dysmotility, globe malposition, and/or a defect surface area larger than 4 cm2. Ophthalmologic prognosis is generally favorable; however, traumatic optic neuropathy is major cause of worse visual outcome in this population., Clinical Question/level of Evidence: Risk, III., (Copyright © 2020 by the American Society of Plastic Surgeons.)

It is well established that an intravitreal needle poke or injection of buffer is protective to the retina in models of photoreceptor degeneration due to release of endogenous neurotrophic factors. Here we assess the effect of intravitreal injection of buffer in a model of closed globe trauma that causes air-blast induced indirect traumatic optic neuropathy (bITON). We injected animals 1-day after the last bITON or sham procedure and performed assessments 1-month later. Surprisingly, we detected a lower electroretinogram (ERG), greater optic nerve damage, and increased levels of pro-inflammatory cytokines in animals given an intravitreal injection. The effect was sometimes independent of bITON and sometimes exacerbated by the injury. Retina histology appeared normal, however the total number of axons in the optic nerve was lower even in uninjured animals that were injected. The number of degenerative axons was further increased in injured animals that were injected. In contrast, we detected a decrease in the ERG a wave and b wave amplitudes, but no effect on the visual evoked potential. Levels of the pro-inflammatory cytokines, IL-1α and IL-1β were elevated in the mice that received an intravitreal injection. This increase was even greater in animals that also had a bITON. This suggests that intravitreal injections may be injurious to the optic nerve particularly during the acute stage of optic nerve injury. In addition, the data suggests a role for IL-1α and IL-1β in this response., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Traumatic optic neuropathy is sinister sequelae of craniofacial trauma leading to vision loss. The decision between early medical or surgical intervention is usually individualised. Visual evoked potentials may guide the treatment plan. We describe a young male presenting 5 days after a road traffic accident with no perception of light vision in the right eye. He was managed medically with high dose of intravenous steroids. At the 3-month follow-up, he reported a reversal of vision loss with return of visual acuity to 3/60, which improved to 6/36 at 5 months and remained stable at 8 months., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Damage of the optic nerve is the major complication of idiopathic intracranial hypertension. A biomarker indicative for optic nerve damage would help identifying high-risk patients requiring surgical procedures. Here, we studied the potential of cerebrospinal fluid neurofilament to predict idiopathic intracranial hypertension-induced optic nerve damage., Methods: In two centers, serum and cerebrospinal fluid of 61 patients with clinically suspected idiopathic intracranial hypertension were prospectively collected. Neurofilament concentrations were measured and related to ophthalmological assessment., Results: The average cerebrospinal fluid neurofilament concentration in patients with moderate and severe papilledema was increased compared to patients with minor and no papilledema (1755 ± 3507 pg/ml vs. 244 ± 102 pg/ml; p  < 0.001). Cerebrospinal fluid neurofilament concentrations correlated with the maximal lumbar puncture opening pressure (r = 0.67, p  < 0.001). In patients fulfilling the Friedman criteria for idiopathic intracranial hypertension with or without papilledema (n = 35), development of bilateral visual field defects and bilateral atrophy of the optic nerve were associated with increased average age-adjusted cerebrospinal fluid neurofilament concentrations. At last follow-up (n = 30), 8/13 of patients with increased, but only 3/17 with normal, cerebrospinal fluid neurofilament had developed bilateral visual field defects and/or bilateral optic nerve atrophy resulting in a sensitivity of 72.7% and a specificity of 73.7% of cerebrospinal fluid neurofilament to detect permanent optic nerve damage., Conclusions: Cerebrospinal fluid neurofilament is a putative biomarker for optical nerve damage in idiopathic intracranial hypertension.

Retinal ganglion cell (RGC) axons converge at the optic nerve head to convey visual information from the retina to the brain. Pathologies such as glaucoma, trauma, and ischemic optic neuropathies injure RGC axons, disrupt transmission of visual stimuli, and cause vision loss. Animal models simulating RGC axon injury include optic nerve crush and transection paradigms. Each of these models has inherent advantages and disadvantages. An optic nerve crush is generally less severe than a transection and can be used to assay axon regeneration across the lesion site. However, differences in crush force and duration can affect tissue responses, resulting in variable reproducibility and lesion completeness. With optic nerve transection, there is a severe and reproducible injury that completely lesions all axons. However, transecting the optic nerve dramatically alters the blood brain barrier by violating the optic nerve sheath, exposing the optic nerve to the peripheral environment. Moreover, regeneration beyond a transection site cannot be assessed without reapposing the cut nerve ends. Furthermore, distinct degenerative changes and cellular pathways are activated by either a crush or transection injury. The method described here incorporates the advantages of both optic nerve crush and transection models while mitigating the disadvantages. Hydrostatic pressure delivered into the optic nerve by microinjection completely transects the optic nerve while maintaining the integrity of the optic nerve sheath. The transected optic nerve ends are reapposed to allow for axon regeneration assays. A potential limitation of this method is the inability to visualize the complete transection, a potential source of variability. However, visual confirmation that the visible portion of the optic nerve has been transected is indicative of a complete optic nerve transection with 90-95% success. This method could be applied to assess axon regeneration promoting strategies in a transection model or investigate interventions that target the axonal compartments.

Competing Interests: Competing interests: None declared.

Traumatic operative injury of the optic nerve in an endoscopic sinus surgery may cause immediate or delayed blindness. It should be cautioned when operating in a sphenoethmoidal cell, or known as Onodi cell, with contact or bulge of the optic canal. It remains unclear how frequent progression to visual loss occurs and how long it progresses to visual loss because of a diseased sphenoethmoidal cell. Research to discuss these questions is expected to help decision making to treat diseased sphenoethmoidal cells. From July 2001 to June 2017, 216 patients received conservative endoscopic sinus surgery without opening a diseased sphenoethmoidal cell. We used their computed tomography images of paranasal sinuses to identify diseased sphenoethmoidal cells that could be associated with progression to visual loss. Among the 216 patients, 52.3% had at least one sphenoethmoidal cell, and 14.8% developed at least one diseased sphenoethmoidal cell. One patient developed acute visual loss 4412 days after the first computed tomography. Our results show that over half of the patients have a sphenoethmoidal cell but suggest a rare incidence of a diseased sphenoethmoidal cell progressing to visual loss during the follow-up period., Competing Interests: All authors declare no conflict of interest., (Copyright © 2020 Ethan I. Huang et al.)

Traumatic optic neuropathy (TON) is commonly associated with head trauma, and thus is a known comorbidity of traumatic brain injury (TBI). TON has not received much attention in basic research despite being associated with permanent vision loss, color blindness, and loss of visual fields. This mini-review discusses the importance of studying TON in the context of TBI and mechanisms that may be involved in the ongoing optic nerve degeneration of TON. We focus particularly on endoplasmic reticulum (ER) and redox stress processes because of the overlapping presence of these degenerative mechanisms in both TBI and various retinopathies, even though these stress pathways have not yet been used to explain retinal degeneration in a model of TON. We propose that future research is needed to uncover whether ER and redox stress function independently or whether one precedes the other. This understanding is necessary in order to understand the time frames of potential treatment and the prognosis of ongoing secondary effects of TBI including optic nerve injury., (© 2019 Wiley Periodicals, Inc.)

Background: Traumatic optic neuropathy (TON) is a rare cause of severe permanent visual impairment after injury. Traumatic optic neuropathy may occur due to sharp trauma (direct injury) that damages the optic nerve directly or due to damage from the transmitted forces after a concussive blow to the head or orbit (indirect injury). The management of indirect TON remains controversial. Either surgical decompression or mega dose corticosteroid is used for managing indirect TON. However, no consensus exists regarding the definitive treatment., Materials and Methods: We designed a randomized controlled trial study to investigate this issue. Only patients with indirect TON and normal vision before the injury were enrolled. The patients' data were recorded, and fine cut facial computed tomography scan was performed to exclude those with retrobulbar hematoma. All the study subjects were randomly allocated to either the mega dose steroid (30 mg/kg stat and 15 mg/kg every 6 hours for 3 days) group or the surgical decompression group. The patients were followed up at 1 week, 1 month, 3 months, 6 months, and 9 months. During each follow-up, the Snellen visual acuity (VA), visual field, color change, fundus findings, and intraocular pressure were evaluated. These data were compared and analyzed using the Mann-Whitney U test and odds ratio. The short form questionnaire was used to analyze the lift quality difference between the two groups., Results: Thirty patients were enrolled, 12 in the surgical group and 18 in the steroid treatment group. There were no significant differences in the improvement rate, improvement degree, and life quality between the groups. However, the odds ratios are 5, 10, 2.5, and nonavailable in the cutoff points of no light perception (NLP), light perception (LP), hand movement, and counting finger in surgery group. In steroid group, they are 1, 1, 1, 1.83 in each cutoff points. Patients with better VA than NLP had better life quality than those with NLP VA (P = 0.005). Other cutoff point groups had no significant difference., Conclusions: Patients with worse initial VA (eg, NLP and LP) had a higher chance of benefiting from surgical treatment and experiencing improvements in the life quality.

Glaucoma is a multifactorial blinding disease with a major inflammatory component ultimately leading to apoptotic retinal ganglion cell (RGC) death. Pharmacological treatments lowering intraocular pressure can help slow or prevent vision loss although the damage caused by glaucoma cannot be reversed. Recently, nutritional approaches have been evaluated for their efficacy in preventing degenerative events in the retina although mechanisms underlying their effectiveness remain to be elucidated. Here, we evaluated the efficacy of a diet supplement consisting of forskolin, homotaurine, spearmint extract, and vitamins of the B group in counteracting retinal dysfunction in a mouse model of optic nerve crush (ONC) used as an in vivo model of glaucoma. After demonstrating that ONC did not affect retinal vasculature by fluorescein angiography, we determined the effect of the diet supplement on the photopic negative response (PhNR) whose amplitude is strictly related to RGC integrity and is therefore drastically reduced in concomitance with RGC death. We found that the diet supplementation prevents the reduction of PhNR amplitude ( p < 0.001) and concomitantly counteracts RGC death, as in supplemented mice, RGC number assessed immunohistochemically is significantly higher than that in non-supplemented animals ( p < 0.01). Major determinants of the protective efficacy of the compound are due to a reduction of ONC-associated cytokine secretion leading to decreased levels of apoptotic markers that in supplemented mice are significantly lower than in non-supplemented animals ( p < 0.001), ultimately causing RGC survival and ameliorated visual dysfunction. Overall, our data suggest that the above association of compounds plays a neuroprotective role in this mouse model of glaucoma thus offering a new perspective in inflammation-associated neurodegenerative diseases of the inner retina.

To examine the difference between primary and secondary retinal ganglion cell (RGC) degeneration, the protein expression at four regions of retina including superior, temporal, inferior and nasal quadrant in a rat model of partial optic nerve transection (pONT) using 2‑D Fluorescence Difference Gel Electrophoresis (DIGE) were investigated. Unilateral pONT was performed on the temporal side of optic nerves of adult Wistar rats to separate primary and secondary RGC loss. Topographical quantification of RGCs labeled by Rbpms antibody and analysis of axonal injury by grading of optic nerve damage at 1 week (n=8) and 8 weeks (n=15) after pONT demonstrated early RGC loss at temporal region, which is considered as primary RGC degeneration and progressing RGC loss at nasal region, which is considered as secondary RGC degeneration. Early protein expression in each retinal quadrant (n=4) at 2 weeks after pONT was compared with the corresponding quadrant in the contralateral control eye by DIGE. For all comparisons, 24 differentially expressed proteins (>1.2‑fold; P<0.05; ≥3 non‑duplicated peptide matches) were identified by mass spectrometry (MS). Interestingly, in the nasal retina, serum albumin and members of crystallin family, including αA, αB, βA2, βA3, βB2 and gamma S indicating stress response were upregulated. By contrast, only αB and βA2 crystallin proteins were altered in temporal quadrant. In the superior and inferior quadrants, βB2 crystallin, keratin type I, S‑arrestin and lamin‑B1 were upregulated, while heat shock cognate 71 kDa protein and heterogeneous nuclear ribonucleoproteins A2/B1 were downregulated. In summary, the use of DIGE followed by MS is useful to detect early regional protein regulation in the retina after localized optic nerve injury.

Background: An orbitocranial injury with a penetrating Intraorbital Foreign Body (IOFB) is listed as a rare cause of penetrating trauma. Since this type of trauma is considered a surgical emergency, taking a thorough history along with careful examination to find out the mechanism and cause of the trauma is crucial towards correct diagnosis and management of the disease., Case Presentation: A 35-year-old male patient was presented to the ER with an occupational craniofacial injury because of an IOFB. The patient underwent an extra-dural orbitocranial craniotomy procedure to remove the foreign body. Interestingly, a plastic foreign body (a piece of a plastic pipe) was removed from the orbital cavity, which was suspected to be a fractured orbital bone, at first place., Conclusion: In this study, we demonstrated that plastics could mimic bone structure in a Computerized Tomography (CT) scan leading to possible initial misdiagnosis. Hence high clinical suspicion is necessary for the correct diagnosis of such cases. However, despite the prompt intervention, our patient ended up with permanent vision loss in his injured eye.

We examined the effect of repeat exposure to a non-damaging insult on central nervous system axons using the optic projection as a model. The optic projection is attractive because its axons are spatially separated from the cell bodies, it is easily accessible, it is composed of long axons, and its function can be measured. We performed closed-system ocular neurotrauma in C57Bl/6 mice using bursts of 15 or 26-psi (pounds per square inch) overpressure air that caused no gross damage. We quantified the visual evoked potential (VEP) and total and degenerative axons in the optic nerve. Repeat exposure to a 15-psi air blast caused more axon damage and vision loss than a single exposure to a 26-psi air blast. However, an increased VEP latency was detected in both groups. Exposure to three 15-psi air blasts separated by 0.5 sec caused 15% axon degeneration at 2 weeks. In contrast, no axon degeneration above sham levels was detected when the interinjury interval was increased to 10 min. Exposure to 15-psi air blasts once a day for 6 consecutive days caused 3% axon degeneration. Therefore, repeat mild trauma within an interinjury interval of 1 min or less causes synergistic axon damage, whereas mild trauma repeated at a longer interinjury interval causes additive, cumulative damage. The synergistic damage may underlie the high incidence of traumatic brain injury and traumatic optic neuropathy in blast-injured service members given that explosive blasts are multiple injury events that occur in a very short time span. This study also supports the use of the VEP as a biomarker for traumatic optic neuropathy.

Purpose: To analyze the clinical presentation and optical coherence tomography (OCT) findings in indirect traumatic optic neuropathy (ITON) in veterans with chronic mild traumatic brain injury (mTBI)., Methods: This retrospective study is the first to describe the OCT pattern of subclinical to mild ITON in veterans with chronic mTBI. The thicknesses of the macular ganglion cell layer (mGCL), peripapillary retinal nerve fiber layer (pRNFL), and subfoveal choroidal layer were analyzed in young veterans who had mTBI of >6 months' duration and either blunt head injury or improvised explosive device (IED) concussions., Results: Three major OCT findings were demonstrated: (1) temporal pRNFL thinning was associated with subclinical TON in the eyes of chronic mTBI patients compared with controls; within mTBI subjects, nasal mGCL thinning at the 3-mm modified Early Treatment Diabetic Retinopathy Study circle diameter distance from the fovea correlated with the corresponding temporal retinal nerve fiber layer thinning; (2) inner (1 mm) superior thinning was greater than that of the temporal mGCL in blunt head injury and could potentially distinguish it from IED concussive head trauma; and (3) subfoveal choroidal thinning was significantly worse in eyes of mTBI patients compared with those of controls., Conclusions: These OCT findings may contribute to the understanding of the spectrum of visual injuries resulting from head trauma.