Search

AbstractPurposeMethodsResultsConclusionsTo identify risk factors for vision recovery in indirect traumatic optic neuropathy (TON) and to analyze the outcomes associated with surgical treatment for TON.Between 2020 and 2023, a total of 105 patients diagnosed with traumatic optic neuropathy (TON) at Shanghai Ninth People’s Hospital and Shanghai Minhang Hospital were included in a retrospective study. These individuals underwent optic nerve decompression surgery as part of their treatment. To collect comprehensive data, both preoperative and postoperative information was gathered. For analytical purposes, only those patients who had a minimum of one month follow-up post-treatment were considered. The statistical analysis incorporated the use of median values, odds ratios (OR), and 95% confidence intervals (CI) to interpret the data. Any p-values less than 0.05 were deemed to indicate statistical significance, underlining the rigorous criteria set for this study.A total of 105 patients, with a mean age of 31.8 ± 14.9 years, met the inclusion criteria; 89.5% (94) were men, and 10.5% (11) were women. The median time to seek medical attention after injury was 4 days (range: 1 to 15 days). Prognostic factors associated with visual acuity (VA) improvement included a gradual VA loss pattern (OR: 2.22, 95% CI: 0.91–5.67, p = 0.045), while canal fractures (OR: 0.31, 95% CI: 0.095–0.933, p = 0.019) significantly correlated with poor VA outcomes.This study suggested that surgical interventions benefit TON patients with low vision. Gradual VA loss, rather than sudden loss after injury, may be a potential prognostic factor for favorable VA outcomes, while canal fractures, as detected on computed tomography (CT) imaging—especially complex canal fractures, are associated with poor VA outcomes. In the future, more definitive prospective treatment trials are required to identify optimal treatment strategies for TON. [ABSTRACT FROM AUTHOR]

Background: Nonglaucomatous optic neuropathy (NGON) is defined as clinical evidence of optic nerve impairment without glaucomatous field/disc changes. Etiology is diverse and elusive in many patients. Causes of NGON include traumatic, compressive, inflammatory, demyelinating, toxic, nutritional, hereditary, vascular, infiltrative, and idiopathic. NGON disorders can be misdiagnosed as glaucoma and can be preventable or life-threatening. In some, fellow eye involvement is common. This can lead to inadequate management and influence prognosis which can be prevented by multispecialty approach. Physicians and ophthalmologists must be vigilant against threatening NGON forms. It is essential to track burden as most literature focused on particular NGON subtype. AIM: The aim was to study the clinical presentation of NGON in a teaching hospital. Setting and Design: This was a prospective, hospital-based, cross-sectional, observational study. MATERIALS AND METHODS: A total of 86 eyes of 61 NGON patients were studied from January 2021 to June 2022 in a tertiary care hospital. Detailed history and comprehensive ophthalmic examination were performed in ambulatory patients. Nonambulatory patients were examined using torchlight. Ancillary investigations were performed, to confirm the clinical diagnosis wherever applicable. Statistical Analysis: Microsoft Excel was used for statistical analysis. Results: The mean age of study patients was 44.87 ± 16.05 years with a male: female ratio of 2.8:1. Unilateral eye involvement was seen in 36 (59.02%). Best-corrected visual acuity = 3/60–1/60 was noted in 41 (47.67%) patients. Red-green defect and contrast sensitivity were reduced by 59.30% and 66.28%, respectively. Relative afferent pupillary defect (RAPD) was noted in 52.46% of patients with Grade 5 RAPD in 40.63%. The most common visually evoked potential type and visual field defect noted were axonal and central scotoma (n = 31 [36.05%] and n = 26 [30.23%]), respectively. Traumatic optic neuropathy was diagnosed in 15 (24.59%) followed by inflammatory optic neuritis in 11 (18.04%) patients. Conclusion: Diagnosing cause of NGON in clinical practice is challenging, but emerging burden cannot be neglected. Knowledge of various NGON types helps narrow differential diagnoses and execute efficient, targeted workup. Timely recognition alters visual, neurological prognosis and saves the lives of patients sometimes.

Traumatic optic neuropathy (TON) is a rare that causes severe visual impairment usually results from cranial or ocular trauma. TON manifests directly and indirectly, which is more common. The incidence rate ranges from 0.7% to 2.5%. Clinical indicators of TON include the presence of an afferent pupillary defect after trauma, decreased vision acuity and intact ocular structure. Surgical decompression appears to be a feasible option in cases with direct bone compression on the optic nerve or progressive vision impairment in indirect TON. However, the evidence supporting treatment efficacy for improvement in vision is still ambiguous. This review will examine surgical techniques for decompressing the optic canal.

To investigate the effectiveness of optic nerve decompression (OND) in the treatment of severe traumatic optic neuropathy (TON) through pterional and supraorbital approaches, and to identify the prognostic factor for postoperative visual acuity (VA) following OND. Patients with severe TON treated with OND through either pterional or supraorbital approach in our institute from September 2019 to June 2022 were retrospectively reviewed in this study. Demographic information, trauma factors, the interval between trauma and complete blindness, the interval between trauma and surgery, and the associated craniofacial traumas were recorded. Hospitalization days and the postoperative VA of patients in two groups were compared. There were 54 severe TON patients with NLP included in this study; 21 patients underwent OND through the pterional approach, and the other 33 underwent the supraorbital approach. Respectively, in groups of pterional and supraorbital approaches, the average hospitalization days were 9.8 ± 3.2 and 10.7 ± 2.9 days (p = 0.58), the mean durations of follow-up were 18.9 ± 4.3 and 20.8 ± 3.7 months (p = 0.09), and the average circumference of OND were 53.14 ± 15.89 ◦ (range 220 ◦ -278◦) and 181.70 ± 6.56◦ (range 173 ◦ -193◦) (p<0.001). The overall improvement rates of pterional and supraorbital approaches are 57.1% and 45.5% (p = 0.40), respectively. Optic canal fracture (OCF) was revealed to be significantly associated with postoperative VA in the supraorbital approach (Binary: p = 0.014, CI: 1.573–57.087; Ordinal: p = 0.003, CI: 1.517–5.503), but not in the pterional approach. In the group of supraorbital approach, patients with OFC had a higher rate of a better outcome (78.6%) than those without (21.4%). Patients with severe traumatic TON may benefit from OND through either the pterional or supraorbital approach. OCF is a potential prognostic factor for postoperative VA following OND through the supraorbital approach. [ABSTRACT FROM AUTHOR]

Traumatic optic neuropathy (TON) is a rare that causes severe visual impairment usually results from cranial or ocular trauma. TON manifests directly and indirectly, which is more common. The incidence rate ranges from 0.7% to 2.5%. Clinical indicators of TON include the presence of an afferent pupillary defect after trauma, decreased vision acuity and intact ocular structure. Surgical decompression appears to be a feasible option in cases with direct bone compression on the optic nerve or progressive vision impairment in indirect TON. However, the evidence supporting treatment efficacy for improvement in vision is still ambiguous. This review will examine surgical techniques for decompressing the optic canal. [ABSTRACT FROM AUTHOR]

Background: Endoscopic transnasal optic canal decompression is widely used in the treatment of traumatic optic neuropathy (TON) following head and craniofacial trauma. Intraoperative hemorrhage is a catastrophic surgical complication during optic canal decompression. Case description: We present two cases of patients with TON who suffered unexpected intra-operative massive bleeding during endoscopic transnasal optic canal decompression. After intraoperative hemostasis was achieved, emergent cerebral angiograms demonstrated the formation of internal carotid pseudoaneurysms, which were immediately embolized with coils combined with or without Onyx with balloon assistance. One of these cases was also complicated by a postoperative cerebrospinal fluid leak, which failed to be treated with lumbar drainage but was successfully repaired with endoscopic transnasal surgery. Conclusion: The intra-operative rupture of ICA pseudoaneurysm is a rare but catastrophic complication in TON patients. Intraoperative massive bleeding indicates rupture of ICA pseudoaneurysm. Postoperative emergency angiography and endovascular therapy should be arranged to evaluate and repair the cerebral vascular injury. Endoscopic trans-nasal surgery repairing CSF leaks resistant to lumbar drainage could be efficient and safe following pseudoaneurysm embolization. [ABSTRACT FROM AUTHOR]

Introduction: Traumatic optic neuropathy is known to be a critical condition that can cause blindness; however, the specific mechanism underlying optic nerve injury is unclear. Recent studies have reported that artemisinin, considered vital in malaria treatment, can also be used to treat neurodegenerative diseases; however, its precise role and mechanism of action remain unknown. Therefore, in this study, we aimed to investigate the impact and probable mechanism of action of artemisinin in retinal ganglion cells (RGCs) in a mouse model of traumatic optic neuropathy induced by optic nerve crush (ONC). Methods: ONC was induced in the left eye of mice by short-term clamping of the optic nerve; oral artemisinin was administered daily. The neuroprotective effect of the drug was assessed using Tuj-1 staining in RGCs. In addition, the inflammatory response and the expression levels of phosphorylated tau protein and tau oligomers were observed using RT-qPCR, TUNEL assay, and fluorescence staining to investigate the underlying mechanisms. Results: Artemisinin increased the survival rate of RGCs 14 days after ONC. Artemisinin significantly reduced the levels of inflammatory factors such as CXCL10, CXCR3, and IL-1β in the retina and decreased the apoptosis of RGCs. Moreover, downregulation of the phosphorylation of tau proteins and the expression of tau oligomers were observed after artemisinin treatment. Conclusion: Our results suggest that artemisinin can increase the survival rate of RGCs after ONC and reduce their apoptosis. This effect may be achieved by inhibiting the inflammatory response it triggers and downregulating tau protein phosphorylation and tau oligomer expression. These findings suggest the potential application of artemisinin as a therapeutic agent for neuropathy.

Traumatic optic neuropathy (TON) is a condition in which acute injury to the optic nerve from direct or indirect trauma results in vision loss. The most common cause of TON is indirect injury to the optic nerve caused by concussive forces that are transmitted to the optic nerve. TON occurs in up to 5% of closed-head trauma patients and there is currently no known effective treatment. One potential treatment option for TON is ST266, a cell-free biological solution containing the secretome of amnion-derived multipotent progenitor (AMP) cells. We investigated the efficacy of intranasal ST266 in a mouse model of TON induced by blunt head trauma. Injured mice treated with a 10-day regimen of ST266 showed an improvement in spatial memory and learning, a significant preservation of retinal ganglion cells, and a decrease in neuropathological markers in the optic nerve, optic tract, and dorsal lateral geniculate nucleus. ST266 treatment effectively downregulated the NLRP3 inflammasome-mediated neuroinflammation pathway after blunt trauma. Overall, treatment with ST266 was shown to improve functional and pathological outcomes in a mouse model of TON, warranting future exploration of ST266 as a cell-free therapeutic candidate for testing in all optic neuropathies.

IntroductionTraumatic optic neuropathy (TON) is the optic nerve injury secondary to brain trauma leading to visual impairment and vision loss. Current clinical visual function assessments often fail to detect TON due to slow disease progression and clinically silent lesions resulting in potentially delayed or missed treatment in patients with traumatic brain injury (TBI).MethodsDiffusion basis spectrum imaging (DBSI) is a novel imaging modality that can potentially fill this diagnostic gap. Twenty-two, 16-week-old, male mice were equally divided into a sham or TBI (induced by moderate Closed-Head Impact Model of Engineered Rotational Acceleration device) group. Briefly, mice were anesthetized with isoflurane (5% for 2.5 min followed by 2.5% maintenance during injury induction), had a helmet placed over the head, and were placed in a holder prior to a 2.1-joule impact. Serial visual acuity (VA) assessments, using the Virtual Optometry System, and DBSI scans were performed in both groups of mice. Immunohistochemistry (IHC) and histological analysis of optic nerves was also performed after in vivo MRI.ResultsVA of the TBI mice showed unilateral or bilateral impairment. DBSI of the optic nerves exhibited bilateral involvement. IHC results of the optic nerves revealed axonal loss, myelin injury, axonal injury, and increased cellularity in the optic nerves of the TBI mice. Increased DBSI axon volume, decreased DBSI λ||, and elevated DBSI restricted fraction correlated with decreased SMI-312, decreased SMI-31, and increased DAPI density, respectively, suggesting that DBSI can detect coexisting pathologies in the optic nerves of TBI mice.ConclusionDBSI provides an imaging modality capable of detecting subclinical changes of indirect TON in TBI mice.

Objective: Traumatic optic neuropathy (TON) causes partial or complete blindness because death of irreplaceableretinal ganglion cells (RGCs). Neuroprotective functions of erythropoietin (EPO) in the nervous system have beenconsidered by many studies investigating effectiveness of this cytokine in various retinal disease models. It has beenfound that changes in retinal neurons under conditions of glial cells are effective in vision loss, therefore, the presentstudy hypothesized that EPO neuroprotective effect could be mediated through glial cells in TON model.Materials and Methods: In this experiment study, 72 rats were assessed in the following groups: intact and optic nervecrush which received either the 4000 IU EPO or saline. Visual evoked potential and optomotor response and RGCnumber were assessed and regenerated axons evaluated by anterograde test. Cytokines gene expression changeswere compared by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Density of astrocytes cells,assessed by fluorescence intensity, in addition, possible cytotoxic effect of EPO was measured on mouse astrocyteculture in vitro.Results: In vitro data showed that EPO was not toxic for mouse astrocytes. Intravenous injection of EPO improvedvision, in terms of visual behavioral tests. RGCs protection was more than two times in EPO, compared to the vehiclegroup. More regenerated axons were determined by anterograde tracing in the EPO group compared to the vehicle.Moreover, GFAP immunostaining showed while the intensity of reactive astrocytes was increased in injured retina,systemic EPO decreased it. In the treatment group, expression of GFAP was down-regulated, while CNTF was upregulatedas assessed by qRT-PCR in the 60th day post-crush.Conclusion: Our study showed that systemic administration of EPO can protect degenerating RGCs. Indeed,exogenous EPO exerted neuroprotective and neurotrophic functions by reducing reactive astrocytic gliosis. Therefore,reduction of gliosis by EPO may be considered as therapeutic targets for TON.

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. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) is a major public health concern, particularly in adolescents who have a higher mortality and incidence of visual pathway injury compared to adult patients. Likewise, we have found disparities between adult and adolescent TBI outcomes in rodents. Most interestingly, adolescents suffer a prolonged apneic period immediately post-injury, leading to higher mortality; therefore, we implemented a brief oxygen exposure paradigm to circumvent this increased mortality. Adolescent male mice experienced a closed-head weight-drop TBI and were then exposed to 100% O2 until normal breathing returned or recovered in room air. We followed mice for 7 and 30 days and assessed their optokinetic response; retinal ganglion cell loss; axonal degeneration; glial reactivity; and retinal ER stress protein levels. O2 reduced adolescent mortality by 40%, improved post-injury visual acuity, and reduced axonal degeneration and gliosis in optical projection regions. ER stress protein expression was altered in injured mice, and mice given O2 utilized different ER stress pathways in a time-dependent manner. Finally, O2 exposure may be mediating these ER stress responses through regulation of the redox-sensitive ER folding protein ERO1α, which has been linked to a reduction in the toxic effects of free radicals in other animal models of ER stress. [ABSTRACT FROM AUTHOR]

Background: Traumatic optic neuropathy is one of the major causes for vison loss in patients of head injury. Aim of the study was to determine the surgical outcome of Endoscopic trans-nasal optic nerve decompression performed in patients of Post-Traumatic Optic Neuropathy. Methods: In this retrospective observational study, total 107 patients of Traumatic Optic Neuropathy (TON), treated with corticosteroids and endoscopic trans-nasal optic decompression having no improvement/worsening of vision loss after giving 48 hours of steroid with high dose or had hematoma intra-neurally and in Optic Nerve sheath or those showing bony fragment impinged on Optic Nerve radiologically were included. The pre and postoperative visual acuities (VAs) were noted from the records and the outcome of surgery was determined. Results: Visual improvement was seen in 57.94% patients. 57 out of 79 patients (72.16%), who underwent for surgery TON shown statistically significant improvement (p< 0.001) in vision than those operated after 5 days of injury (17.86%)). 15 out of 19 patients with baseline vision of Finger counting recovered to Visual acuity better than or equal to 6/60. Conclusion: Steroid with Endoscopic Optic Nerve decompression in TON is effective and safe in those with baseline VA of 6/60 or worse if treated as early as possible. [ABSTRACT FROM AUTHOR]

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

Traumatic optic neuropathy is one of the causes of visual loss caused by blunt or penetrating head trauma and is classified as both direct and indirect. Clinical history and examination findings usually allow for the diagnosis of traumatic optic neuropathy. There is still controversy surrounding the management of traumatic optic neuropathy; some physicians advocate observation alone, while others recommend steroid therapy, surgery, or both. In this entry, we tried to highlight traumatic optic neuropathy’s main pathophysiologic mechanisms with the most available updated treatment. Recent research suggests future therapies that may be helpful in traumatic optic neuropathy cases.

AIM: To investigate the effect of different degrees of traction power on the survival rate of retinal ganglion cells(RGCs)and nerve conduction in rats, and to discuss the effect of autophagy level of RGCs on the above parameters.METHODS: A total of 30 healthy male Sprague-Dawley(SD)rats were randomly divided into empty group, sham-operation group, 0.15N, 0.3N and 0.6N group, with 6 rats in each group.Modeling group was performed the transverse quantitative traction to make a rat model of optic nerve injury. In addition, rats in empty group were not operated and rats in sham-operation group only got optic nerve exposed. Flash visual evoked potentials(f-VEP)were performed respectively on 1 and 3d after modeling.The survival of retinal ganglion cells was observed by Brn-3a staining at 3d after modeling, autophagy bodies were observed by transmission electron microscope, and the expression level of LC3B II/I protein was detected by Western blotting.RESULTS: Compared with sham-operation group, the f-VEP P2 peak was significantly delayed and the amplitude reduced at 3d after modeling. In addition, the survival rate of RGCs was decreased, and the expression level of LC3B II/I protein were decreased. Autophagy bodies were observed in the retinal tissue of rats in all groups.CONCLUSION: Optic nerve traction reduced early retinal autophagy level, death of RGCs and corresponding nerve conduction dysfunction in rats,and different traction caused different degrees of injury. In addition,there was a correlation between the autophagy level and the survival of RGCs.

Objective: To investigate the clinical efficacy and prognostic factors of transnasal endoscopic optic decompression in the treatment of traumatic optic neuropathy (TON). Methods: 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. Results: 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%. Conclusion: 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. [ABSTRACT FROM AUTHOR]

Objective: Traumatic optic neuropathy (TON) causes partial or complete blindness because death of irreplaceable retinal ganglion cells (RGCs). Neuroprotective functions of erythropoietin (EPO) in the nervous system have been considered by many studies investigating effectiveness of this cytokine in various retinal disease models. It has been found that changes in retinal neurons under conditions of glial cells are effective in vision loss, therefore, the present study hypothesized that EPO neuroprotective effect could be mediated through glial cells in TON model. Materials and Methods: In this experiment study, 72 rats were assessed in the following groups: intact and optic nerve crush which received either the 4000 IU EPO or saline. Visual evoked potential and optomotor response and RGC number were assessed and regenerated axons evaluated by anterograde test. Cytokines gene expression changes were compared by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Density of astrocytes cells, assessed by fluorescence intensity, in addition, possible cytotoxic effect of EPO was measured on mouse astrocyte culture in vitro. Results: In vitro data showed that EPO was not toxic for mouse astrocytes. Intravenous injection of EPO improved vision, in terms of visual behavioral tests. RGCs protection was more than two times in EPO, compared to the vehicle group. More regenerated axons were determined by anterograde tracing in the EPO group compared to the vehicle. Moreover, GFAP immunostaining showed while the intensity of reactive astrocytes was increased in injured retina, systemic EPO decreased it. In the treatment group, expression of GFAP was down-regulated, while CNTF was upregulated as assessed by qRT-PCR in the 60th day post-crush. Conclusion: Our study showed that systemic administration of EPO can protect degenerating RGCs. Indeed, exogenous EPO exerted neuroprotective and neurotrophic functions by reducing reactive astrocytic gliosis. Therefore, reduction of gliosis by EPO may be considered as therapeutic targets for TON. [ABSTRACT FROM AUTHOR]

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 cm3 in the groups with and without TON, respectively. The average volume of the fractured orbit in the TON group was 27.78 ± 2.56 cm3, 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 cm3, 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. [ABSTRACT FROM AUTHOR]

Definition: Traumatic optic neuropathy is one of the causes of visual loss caused by blunt or penetrating head trauma and is classified as both direct and indirect. Clinical history and examination findings usually allow for the diagnosis of traumatic optic neuropathy. There is still controversy surrounding the management of traumatic optic neuropathy; some physicians advocate observation alone, while others recommend steroid therapy, surgery, or both. In this entry, we tried to highlight traumatic optic neuropathy's main pathophysiologic mechanisms with the most available updated treatment. Recent research suggests future therapies that may be helpful in traumatic optic neuropathy cases. [ABSTRACT FROM AUTHOR]

Background: Since optic neuropathy is the initial manifestation of various systemic disorders, it is essential to do detailed investigations to arrive at the diagnosis. This aids in timely management of underlying systemic disorders and prevents not only the visual disability but also the complications of underlying disease. Many studies focus on individual aetiologies of optic neuropathy, but only few studies provide information about various aetiologies of optic neuropathy. Aim: To determine the clinical profile of patients diagnosed with optic neuropathy and to evaluate the varied aetiologies of optic neuropathies. Methodology: All clinically diagnosed patients of optic neuropathy with defective vision, visual field defect, colour vision defect and abnormal pupillary response attending the neurology and ophthalmology department in Thanjavur Medical College from January 2019 to May 2020 were taken up for the study. Results: Eighty-three patients of clinically diagnosed optic neuropathy, who presented at Thanjavur Medical College, were studied during the period of January 2019–May 2020. The most common aetiology of optic neuropathy was idiopathic optic neuritis followed by ischemic and traumatic optic neuropathy. Conclusion: This study addressed an increase in the incidence of traumatic and ischemic optic neuropathies when compared to other studies. Thus, ischemic and traumatic optic neuropathies need more attention for the future researches.

Purpose: To identify optic nerve (ON) lipid alterations associated with sonication-induced traumatic optic neuropathy (TON). Design: Experimental study. Subjects: A mouse model of indirect TON was generated using sound energy concentrated focally at the entrance of the optic canal using a laboratory sonifier with a microtip probe. Methods: Analyses of datasets generated from high-performance liquid chromatography-electrospray tandem mass spectrometry of ONs dissected from the head of the ON to the optic chiasm at 1 day, 7 days, and 14 days postsonication compared with that in nonsonicated controls. Main Outcome Measures: Lipid abundance alterations in postsonicated ONs were evaluated using 1-way analysis of variance (false discovery rate-adjusted significant P value < 0.01), lipid-related gene sets, biochemical properties, and receiver operating characteristic to identify lipids associated with optic neuropathy. Results: There were 28 lipid species with significantly different abundances across the control and postsonication groups. The 2 most significantly upregulated lipids included a sphingomyelin (SM) species, SM(d40:7), and a hexosylceramide (CerG1) species, CerG1(d18:1/24:2). Hexosylceramide (d18:1/24:2) was noted to have a stepwise increasing trend from day 1 to day 14 after sonication-induced optic neuropathy. Investigation of biophysical properties showed notable enrichment of lipids with high and above-average transition temperatures at day 14 after sonication. Lipid-related gene set analysis revealed enrichment in sphingolipid and glycosphingolipid metabolic processes. The best classifier to differentiate day 14 postsonication from controls, based on area under the receiver operating characteristic curve, was CerG1(d18:1/24:2) (area under the receiver operating characteristic curve: 1). Conclusions: Temporal alterations in sphingolipid metabolism and biochemical properties were observed in the ON of mice after sonication-induced optic neuropathy, with notable elevations in sphingomyelin and hexosylceramide species. Hexosylceramide (d18:1/24:2) may be associated with damage after indirect trauma, indicating that lipid membrane abnormalities may be a mediator of pathology due to trauma.

Introduction: Ocular and periocular traumatisms may result in loss of vision. Our previous work showed that therapeutic hypothermia prevents retinal damage caused by traumatic neuropathy. We also generated and characterized small molecules that elicit the beneficial effects of hypothermia at normal body temperature. Here we investigate whether one of these mimetic molecules, zr17-2, is able to preserve the function of eyes exposed to trauma. Methods: Intraorbital optic nerve crush (IONC) or sham manipulation was applied to Sprague-Dawley rats. One hour after surgery, 5.0 µl of 330 nmol/L zr17-2 or PBS, as vehicle, were injected in the vitreum of treated animals. Electroretinograms were performed 21 days after surgery and a- and b-wave amplitude, as well as oscillatory potentials (OP), were calculated. Some animals were sacrificed 6 days after surgery for TUNEL analysis. All animal experiments were approved by the local ethics board. Results: Our previous studies showed that zr17-2 does not cross the blood-ocular barrier, thus preventing systemic treatment. Here we show that intravitreal injection of zr17-2 results in a very significant prevention of retinal damage, providing preclinical support for its pharmacological use in ocular conditions. As previously reported, IONC resulted in a drastic reduction in the amplitude of the b-wave (p < 0.0001) and OPs (p < 0.05), a large decrease in the number of RGCs (p < 0.0001), and a large increase in the number of apoptotic cells in the GCL and the INL (p < 0.0001). Interestingly, injection of zr17-2 largely prevented all these parameters, in a very similar pattern to that elicited by therapeutic hypothermia. The small molecule was also able to reduce oxidative stress-induced retinal cell death in vitro. Discussion: In summary, we have shown that intravitreal injection of the hypothermia mimetic, zr17-2, significantly reduces the morphological and electrophysiological consequences of ocular traumatism and may represent a new treatment option for this cause of visual loss. [ABSTRACT FROM AUTHOR]

Erinacine A (EA), a natural neuroprotectant, is isolated from a Chinese herbal medicine, Hericium erinaceus. The aim of this study was to investigate the neuroprotective effects of EA in a rat model of traumatic optic neuropathy. The optic nerves (ONs) of adult male Wistar rats were crushed using a standardized method and divided into three experimental groups: phosphate-buffered saline (PBS control)-treated group, standard EA dose-treated group (2.64 mg/kg in 0.5 mL of PBS), and double EA dose-treated group (5.28 mg/kg in 0.5 mL of PBS). After ON crush, each group was fed orally every day for 14 days before being euthanized. The visual function, retinal ganglion cell (RGC) density, and RGC apoptosis were determined using flash visual-evoked potentials (fVEP) analysis, retrograde Fluoro-Gold labelling, and TdT-dUTP nick end-labelling (TUNEL) assay, respectively. Macrophage infiltration of ON was detected by immunostaining (immunohistochemistry) for ED1. The protein levels of phosphor-receptor-interacting serine/threonine-protein kinase1 (pRIP1), caspase 8 (Cas8), cleaved caspase 3 (cCas3), tumour necrosis factor (TNF)-α, tumour necrosis factor receptor1 (TNFR1), interleukin (IL)-1β, inducible nitric oxide synthase (iNOS), nuclear factor erythroid 2-related factor 2 (Nrf2), haem oxygenase-1 (HO-1), and superoxide dismutase 1 (SOD1) were evaluated by Western blotting. When comparing the standard EA dose-treated group and the double EA dose-treated group with the PBS-treated group, fVEP analysis showed that the amplitudes of P1–N2 in the standard EA dose group and the double EA dose-treated group were 1.8 and 2.4-fold, respectively, higher than that in the PBS-treated group (p < 0.05). The density of RGC in the standard EA dose-treated group and the double EA dose-treated group were 2.3 and 3.7-fold, respectively, higher than that in the PBS-treated group (p < 0.05). The TUNEL assay showed that the standard EA dose-treated group and the double EA dose-treated group had significantly reduced numbers of apoptotic RGC by 10.0 and 15.6-fold, respectively, compared with the PBS-treated group (p < 0.05). The numbers of macrophages on ON were reduced by 1.8 and 2.2-fold in the standard EA dose-treated group and the double EA dose-treated group, respectively (p < 0.01). On the retinal samples, the levels of pRIP, Cas8, cCas3, TNF-α, TNFR1, IL-1β, and iNOS were decreased, whereas those of Nrf2, HO-1, and SOD1 were increased in both EA-treated groups compared to those in the PBS-treated group (p < 0.05). EA treatment has neuroprotective effects on an experimental model of traumatic optic neuropathy by suppressing apoptosis, neuroinflammation, and oxidative stress to protect the RGCs from death as well as preserving the visual function. [ABSTRACT FROM AUTHOR]

Purpose: Our study aims to evaluate the effectiveness of intravenous erythropoietin (EPO) in patients with indirect traumatic optic neuropathy (TON), assess the side effects, and compare the visual function results among three groups of patients who had received different treatment options – EPO, steroids, and observation. Methods: Patients with indirect TON presenting to the neuro-ophthalmology clinic from August 2019 to March 2020, were assigned to three groups, with six patients in each group. In group 1, patients were recruited prospectively and received recombinant human erythropoietin, whereas, in groups 2 and 3, patients were recruited retrospectively and received intravenous methylprednisolone followed by oral steroids and multivitamins, respectively. Groups 1 and 2 included patients presenting within 2 weeks of trauma, whereas group 3 included those presenting beyond that. Best-corrected visual acuity, pupillary reaction, color vision, and visual fields following treatment were measured. Results: Initial visual acuity in the EPO group ranged from 20/80 to no perception of light (No PL). The mean initial BCVA (1.82 logMAR, standard deviation [SD] = 0.847) improved to 1.32, SD = 0.93 logMAR after treatment recorded at the third month (P = 0.0375), with no significant adverse effects. The initial BCVA of group 2 ranged from 20/120 to No PL. The mean initial BCVA (1.95, SD = 0.77 logMAR) improved to 1.45 logMAR, SD = 0.97 after treatment (P = 0.0435) but three patients had side effects of steroids. Initial visual acuity in Group 3 ranged from 20/40 to no PL. The mean initial BCVA (1.09 logMAR, SD = 1.10) worsened to 1.19 logMAR, SD = 1.06 after treatment after treatment (P = 0.0193). The improvement in BCVA when compared between the three groups was not significant. Conclusion: Both erythropoietin and steroids are effective in the management of traumatic optic neuropathy. However, erythropoietin shows lesser or no side effects when compared to steroids. [ABSTRACT FROM AUTHOR]

Introduction: Ocular injury is the commonest ocular emergency and can vary across geographical and socioeconomic regions. This study was conducted to determine the pattern of ocular injuries presenting to our tertiary care hospital located in Puducherry, Southern India. Methods: A retrospective hospital-based study was performed and analyzed the records of the patients who presented with ocular injuries to the emergency department between January 2016 and December 2017. Data were collected using a structured format and noted the demographic profile and clinical profile of ocular injury. Results: Of the 392 ocular emergencies, 318 (81.1%) were caused by ocular trauma. Mechanical trauma was most common (306; 96.2%). Males were more frequently affected (ratio; 3.7:1). Most cases of trauma belonged to the 21–30 years age group (86, 28.1%) and were caused by road traffic accidents (RTAs) (197; 64.4%). Adnexal injuries were commonest (285; 93.1%). The ocular injury was close globe type in 93 (30.4%) and the open globe in three (1.0%). Serious lid injury was present in 71 cases (23.2%). Serious injuries such as globe rupture and traumatic optic neuropathy were present in three (1.0%) and eleven (3.6%) cases, respectively. Conclusion: Ocular trauma is the most common cause of ocular emergencies and RTA is the commonest cause of ocular trauma. We need to explore strategies to minimize ocular trauma as a priority. [ABSTRACT FROM AUTHOR]

The treatment strategy for traumatic optic neuropathy is mainly high-dose steroid therapy and optic nerve decompression, but no standard treatment has been established. The main symptom of traumatic optic neuropathy is rapid loss of visual acuity, but visual acuity examination can be difficult in cases of impaired consciousness due to head trauma or in children. We report a case of traumatic optic neuropathy with improved visual acuity after transcranial optic nerve decompression. A 14-year-old boy fell into a gutter while jogging and bruised the outer part of his right eyebrows. Immediately after the injury, his right visual acuity was maintained, but the next day, his right visual acuity deteriorated to hand motion. Computed tomography showed a fracture of the lateral wall of the right orbit and of the optic canal. Twenty-seven hours after the injury, a craniotomy was performed to remove a fractured bone fragment. Visual acuity and the visual field improved after the operation. Helpful points for diagnosing traumatic optic neuropathy and transcranial optic nerve decompression surgery are discussed. To make an appropriate diagnosis, it is important to suspect traumatic optic neuropathy if the lateral eyebrows are bruised and to confirm a relative afferent pupillary defect (RAPD) in patients who cannot complain of visual loss. In optic nerve decompression surgery, it is advisable to select the target decompression site based on the fracture and determine the approach route and method according to the surgical experience at each facility. [ABSTRACT FROM AUTHOR]

Background: The indication for surgical optic canal decompression (OCD) for traumatic optic neuropathy (TON) remains controversial because there is no reliable predictor of a good outcome. We report the case of a blind patient with TON whose remaining visual-evoked potential (VEP) suggested recovery potential of the injured optic nerve after OCD. Case Description: A 48-year-old man had fallen from a height of 7 m, striking his head. He immediately complained of right-eye blindness. He had no light perception and the direct light reflex disappeared from the right pupil, although there was no fracture or traumatic lesion on computed tomography and magnetic resonance imaging. Because the amplitude of the VEP with the right eye stimulation remained unchanged, we performed the right OCD. During surgical OCD, the amplitude and latency of VEP began to improve. Finally, the visual field improved in almost all directions, and eyesight improved to 0.2. Conclusion: The retained VEP activity in TON may suggest the recovery potential of the injured optic nerve, even in cases of blindness. It is possible that VEP is an indicator of aggressive treatment for TON such as OCD. [ABSTRACT FROM AUTHOR]

The purpose of this work is to identify mitochondrial optic nerve (ON) lipid alterations associated with sonication-induced traumatic optic neuropathy (TON). Briefly, a mouse model of indirect TON was generated using sound energy concentrated focally at the entrance of the optic canal using a laboratory sonifier (Branson Digital Sonifier 450, Danbury, CT, USA) with a microtip probe. We performed an analysis of a previously generated dataset from high-performance liquid chromatography-electrospray tandem mass spectrometry (LC-MS/MS). We analyzed lipids from isolated mitochondria from the ON at 1 day, 7 days, and 14 days post-sonication compared to non-sonicated controls. Lipid abundance alterations in post-sonicated ON mitochondria were evaluated with 1-way ANOVA (FDR-adjusted significant p-value < 0.01), debiased sparse partial correlation (DSPC) network modeling, and partial least squares-discriminant analysis (PLS-DA). We find temporal alterations in triglyceride metabolism are observed in ON mitochondria of mice following sonication-induced optic neuropathy with notable depletions of TG(18:1/18:2/18:2), TG(18:1/18:1/18:1), and TG(16:0/16:0/18:1). Depletion of mitochondrial triglycerides may mediate ON damage in indirect traumatic optic neuropathy through loss energy substrates for neuronal metabolism. [ABSTRACT FROM AUTHOR]

Although glial scar formation has been extensively studied after optic nerve injury, the existence and characteristics of traumatic optic nerve fibrotic scar formation have not been previously characterized. Recent evidence suggests infiltrating macrophages are involved in pathological processes after optic nerve crush (ONC), but their role in fibrotic scar formation is unknown. Using wild-type and transgenic mouse models with optic nerve crush injury, we show that macrophages infiltrate and associate with fibroblasts in the traumatic optic nerve lesion fibrotic scar. We dissected the role of hematogenous and resident macrophages, labeled with Dil liposomes intravenously administered, and observed that hematogenous macrophages (Dil+ cells) specifically accumulate in the center of traumatic fibrotic scar while Iba-1+ cells reside predominantly at the margins of optic nerve fibrotic scar. Depletion of hematogenous macrophages results in reduced fibroblast density and decreased extracellular matrix deposition within the fibrotic scar area following ONC. However, retinal ganglion cell degeneration and function loss after optic nerve crush remain unaffected after hematogenous macrophage depletion. We present new and previously not characterized evidence that hematogenous macrophages are selectively recruited into the fibrotic core of the optic nerve crush site and critical for this fibrotic scar formation. [ABSTRACT FROM AUTHOR]

Introduction: Ocular and periocular traumatisms may result in loss of vision. Our previous work showed that therapeutic hypothermia prevents retinal damage caused by traumatic neuropathy. We also generated and characterized small molecules that elicit the beneficial effects of hypothermia at normal body temperature. Here we investigate whether one of these mimetic molecules, zr17-2, is able to preserve the function of eyes exposed to trauma.Methods: Intraorbital optic nerve crush (IONC) or sham manipulation was applied to Sprague-Dawley rats. One hour after surgery, 5.0 µl of 330 nmol/L zr17-2 or PBS, as vehicle, were injected in the vitreum of treated animals. Electroretinograms were performed 21 days after surgery and a- and b-wave amplitude, as well as oscillatory potentials (OP), were calculated. Some animals were sacrificed 6 days after surgery for TUNEL analysis. All animal experiments were approved by the local ethics board.Results: Our previous studies showed that zr17-2 does not cross the blood-ocular barrier, thus preventing systemic treatment. Here we show that intravitreal injection of zr17-2 results in a very significant prevention of retinal damage, providing preclinical support for its pharmacological use in ocular conditions. As previously reported, IONC resulted in a drastic reduction in the amplitude of the b-wave (p < 0.0001) and OPs (p < 0.05), a large decrease in the number of RGCs (p < 0.0001), and a large increase in the number of apoptotic cells in the GCL and the INL (p < 0.0001). Interestingly, injection of zr17-2 largely prevented all these parameters, in a very similar pattern to that elicited by therapeutic hypothermia. The small molecule was also able to reduce oxidative stress-induced retinal cell death in vitro.Discussion: In summary, we have shown that intravitreal injection of the hypothermia mimetic, zr17-2, significantly reduces the morphological and electrophysiological consequences of ocular traumatism and may represent a new treatment option for this cause of visual loss.

Traumatic optic neuropathy (TON) is characterized by impaired visual function due to acute damage to the optic nerve injury related to the trauma. The predictive incidence of TON in children and adolescence is 0.7-2.5% after blunt or penetrating head injuries. Orbital trauma is often accompanied by head injury and is the most common cause of unilateral vision loss. Here, we present a case of 11-year-old child who had the complaint of vision loss in the right eye and developed TON after a motor vehicle accident. The intubated patient was admitted to the pediatric intensive care unit after trauma and was operated due to epidural hemorrhage. Visual loss was detected during follow-up and orbital computed tomography revealed multiple fractures in the orbital walls and magnetic resonance imaging showed effusion of the optic nerve sheath and contrast enhancement of the optic nerve. Clinical and imaging findings suggested TON and as there was no indication for surgery, pulse steroid treatment was given for 5 days. With this treatment, the patient's vision loss and clinical findings improved significantly.In conclusion, TON should be considered in patients with a head injury and post-traumatic vision loss. High-dose steroids should be considered in suitable patients.

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. [ABSTRACT FROM AUTHOR]

Optic neuropathy refers to disease of the optic nerve and can result in loss of visual acuity and/or visual field defects. Combining findings from multiple fMRI modalities can offer valuable information for characterizing and managing optic neuropathies. In this article, we review a subset of resting-state functional magnetic resonance imaging (RS-fMRI) studies of optic neuropathies. We consider glaucoma, acute optic neuritis (ON), discuss traumatic optic neuropathy (TON), and explore consistency between findings from RS and visually driven fMRI studies. Consistent with visually driven studies, glaucoma studies at rest also indicated reduced activation in the visual cortex and dorsal visual stream. RS-fMRI further reported varying levels of functional connectivity in the ventral stream depending on disease severity. ON patients show alterations within the visual cortex in both fMRI techniques. Particularly, higher-than-normal RS activity is observed in the acute phase and decreases as the disease progresses. A similar pattern is observed in the visual cortex of TON-like, open globe injury (OGI), patients. Additionally, visually driven and RS-fMRI studies of ON patients show recovery of brain activity in the visual cortex. RS-fMRI suggests recovery of signals in higher-tier visual areas MT and LOC as well. Finally, RS-fMRI has not yet been applied to TON, although reviewing OGI studies suggests that it is feasible. Future RS-fMRI studies of optic neuropathies could prioritize studying the fine scale RS activity of brain areas that visually driven studies have identified. We suggest that a more systematic longitudinal comparison of optic neuropathies with advanced fMRI would provide improved diagnostic and prognostic information. [ABSTRACT FROM AUTHOR]

Copyright of HNO is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Optic neuropathies are conditions that cause disease to the optic nerve, and can result in loss of visual acuity and/or visual field defects. An improved understanding of how these conditions affect the entire visual system is warranted, to better predict and/or restore the visual loss. In this article, we review visually-driven functional magnetic resonance imaging (fMRI) studies of optic neuropathies, including glaucoma and optic neuritis (ON); we also discuss traumatic optic neuropathy (TON). Optic neuropathy-related vision loss results in fMRI deficit within the visual cortex, and is often strongly correlated with clinical severity measures. Using predominantly flickering checkerboard stimuli, glaucoma studies indicated retinotopic-specific cortical alteration with more prominent deficits in advanced than in early glaucoma. Some glaucoma studies indicate a reorganized visual cortex. ON studies have indicated that the impacted cortical areas are briefly hyperactive. For ON, brain deficits are greater in the acute stages of the disease, followed by (near) normalization of responses of the LGN, visual cortex, and the dorsal visual stream, but not the ventral extrastriate cortex. Visually-driven fMRI is sensitive, at least in ON, in discriminating patients from controls, as well as the affected eye from the fellow eye within patients. The use of a greater variety of stimuli beyond checkerboards (e.g., visual motion and object recognition) in recent ON studies is encouraging, and needs to continue to disentangle the results in terms of change over time. Finally, visually-driven fMRI has not yet been applied in TON, although preliminary efforts suggest it may be feasible. Future fMRI studies of optic neuropathies should consider using more complex visual stimuli, and inter-regional analysis methods including functional connectivity. We suggest that a more systematic longitudinal comparison of optic neuropathies with advanced fMRI would provide improved diagnostic and prognostic information. [ABSTRACT FROM AUTHOR]

Objectives: Traumatic optic neuropathy (TON), a relatively rare condition, can cause visual functional impairment and permanent functional damage. Surgeons should be familiar with its diagnostic criteria and treatment to effectively manage cases of facial trauma with TON. We investigated the feasibility of navigation-assisted endoscopic trans-nasal optic nerve decompression (ETOND) to treat TON in maxillofacial trauma patients. Patients and., Methods: We retrospectively analyzed data from the clinical investigation of four consecutive patients, two males and two females with an average age of 75 years, with midfacial fractures and TON between April 2021 and September 2023. All patients had swelling and subcutaneous periorbital hemorrhage accompanied by optic nerve canal and zygomaticomaxillary complex fractures on the affected side. Three patients had lacerations on the lateral eyebrow or upper eyelid. All patients were evaluated by an ophthalmologist for visual impairment; two patients could see hand motion at a 30 cm distance, one patient could perceive light, and one did not have any loss of visual acuity. Among the four patients, three had visual impairment immediately after the injury, and one showed delayed impairment., Results: The patients were treated with navigation-assisted ETOND conducted by an endoscopic rhinologist. Three of the ETONDs were performed along with open reduction and internal fixation (ORIF); the other ETOND was delayed. Orbital reconstruction was performed in three patients. Steroid therapy was administered to two patients, one pre-operatively and one post-operatively. The two patients with pre-operative vision loss showed improved visual acuity post-operatively, and the two patients with no pre-operative visual impairment had no vision loss associated with ORIF for their midfacial fractures. No patient had post-operative complications., Conclusion: Navigation-assisted ETOND can be performed easily by endoscopic rhinologists; and prompt examination, diagnosis, and treatment are important in patients with facial trauma and TON.

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.)

Traumatic optic neuropathy (TON) is a common cause of irreversible blindness following head injury. TON is characterized by axon damage in the optic nerve followed by retinal ganglion cell death in the days and weeks following injury. At present, no therapeutic or surgical approach has been found to offer any benefit beyond observation alone. This is due in part to the lack of translational animal models suitable for understanding mechanisms and evaluating candidate treatments. In this study, we developed a rat model of TON in which the eye is rapidly rotated, inflicting mechanical stress on the optic nerve and leading to significant visual deficits. These functional deficits were thoroughly characterized up to one week after injury using electrophysiology and immunohistochemistry. The photopic negative response (PhNR) of the light adapted full field electroretinogram (LA ffERG) was significantly altered following injury. This correlated with increased biomarkers of retinal stress, axon disruption, and ganglion cell death. Together, this evidence suggests the utility of our model for mimicking clinically relevant TON and that the PhNR may be an early diagnostic for TON. We also found indirect evidence that ketamine, which was used for anesthesia, may ameliorate TON. Future studies will utilize this animal model for evaluation of candidate treatments., Competing Interests: Author(s’) Disclosure Statements: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Optic neuropathy refers to disease of the optic nerve and can result in loss of visual acuity and/or visual field defects. Combining findings from multiple fMRI modalities can offer valuable information for characterizing and managing optic neuropathies. In this article, we review a subset of resting-state functional magnetic resonance imaging (RS-fMRI) studies of optic neuropathies. We consider glaucoma, acute optic neuritis (ON), discuss traumatic optic neuropathy (TON), and explore consistency between findings from RS and visually driven fMRI studies. Consistent with visually driven studies, glaucoma studies at rest also indicated reduced activation in the visual cortex and dorsal visual stream. RS-fMRI further reported varying levels of functional connectivity in the ventral stream depending on disease severity. ON patients show alterations within the visual cortex in both fMRI techniques. Particularly, higher-than-normal RS activity is observed in the acute phase and decreases as the disease progresses. A similar pattern is observed in the visual cortex of TON-like, open globe injury (OGI), patients. Additionally, visually driven and RS-fMRI studies of ON patients show recovery of brain activity in the visual cortex. RS-fMRI suggests recovery of signals in higher-tier visual areas MT and LOC as well. Finally, RS-fMRI has not yet been applied to TON, although reviewing OGI studies suggests that it is feasible. Future RS-fMRI studies of optic neuropathies could prioritize studying the fine scale RS activity of brain areas that visually driven studies have identified. We suggest that a more systematic longitudinal comparison of optic neuropathies with advanced fMRI would provide improved diagnostic and prognostic information.

Optic neuropathies are conditions that cause disease to the optic nerve, and can result in loss of visual acuity and/or visual field defects. An improved understanding of how these conditions affect the entire visual system is warranted, to better predict and/or restore the visual loss. In this article, we review visually-driven functional magnetic resonance imaging (fMRI) studies of optic neuropathies, including glaucoma and optic neuritis (ON); we also discuss traumatic optic neuropathy (TON). Optic neuropathy-related vision loss results in fMRI deficit within the visual cortex, and is often strongly correlated with clinical severity measures. Using predominantly flickering checkerboard stimuli, glaucoma studies indicated retinotopic-specific cortical alteration with more prominent deficits in advanced than in early glaucoma. Some glaucoma studies indicate a reorganized visual cortex. ON studies have indicated that the impacted cortical areas are briefly hyperactive. For ON, brain deficits are greater in the acute stages of the disease, followed by (near) normalization of responses of the LGN, visual cortex, and the dorsal visual stream, but not the ventral extrastriate cortex. Visually-driven fMRI is sensitive, at least in ON, in discriminating patients from controls, as well as the affected eye from the fellow eye within patients. The use of a greater variety of stimuli beyond checkerboards (e.g., visual motion and object recognition) in recent ON studies is encouraging, and needs to continue to disentangle the results in terms of change over time. Finally, visually-driven fMRI has not yet been applied in TON, although preliminary efforts suggest it may be feasible. Future fMRI studies of optic neuropathies should consider using more complex visual stimuli, and inter-regional analysis methods including functional connectivity. We suggest that a more systematic longitudinal comparison of optic neuropathies with advanced fMRI would provide improved diagnostic and prognostic information.