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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.

Objective: To investigate the effect of Wei's triple nine needling therapy on the N2-P2 wave of the flash visual evoked potential (FVEP) in rats of the of the transverse directional pulling model. Methods: Thirty-six Wistar rats were randomly grouped, nine were in normal control group without any treatment, and the remaining 27 were surgically modelled in the right eyes. Eighteen of these rats were randomly divided into a Wei's triple nine needling therapy group and a model group of nine rats each after the TON model was made using the transverse quantitative retraction method. The other 9 rats were sham-operated, and only the optic nerve was exposed without retraction. On the next day of modelling, the Wei's triple nine needling therapy group was treated with Wei's triple nine needling therapy for 20 minutes/1 time/1 day for 14 days. The model group, sham-operated group and normal control group were not intervened. Wei's triple nine acupoints were represented as follows: 1st link: "Jingming" (BL1) and "Chengqi" (ST1); 2nd link: "Sizhukong" (SJ23) penetrating "Taiyang" (EX-HN5); and the third: "Fengchi" (GB 20) and "Taichong" (LV3). The FVEP of each group was observed on 1d, 7d and 14d. The FVEP of each group was observed on 1d, 7d and 14d. Results: Compared with the model group, the N2 wave latency and P2 wave latency were shortened in the Wei's triple nine needling therapy on 1d (P < 0.05, P < 0.01); on 7d, their N2 wave latency was shortened (P < 0.01) and the N2-P2 wave amplitude was increased compared with the model group (P < 0.05); on 14d, their P2 wave latency was shortened (P < 0.05) and the N2-P2 wave amplitude was increased. There was no statistical difference in N2 wave latency, P2 wave latency and N2-P2 wave amplitude in the sham-operated group on 1d, 7d and 14d (P > 0.05). The delayed N2 and P2 wave latencies in the model group did not improve from 1d to 14d (P > 0.05) and the amplitude decreased throughout, showing a significant difference on 14d compared to 1d (P < 0.05). In contrast, the N2 wave latency in Wei's triple nine needling therapy group was not significantly different until 7d to 14d (P < 0.05); its P2 wave latency, although significantly delayed from 1d to 7d (P < 0.05), recovered on 14d and reached a level that was not statistically different from 1d and 7d (P > 0.05). There was also no significant decrease in N2-P2 wave amplitude between 1d and 14d in Wei's triple nine needling therapy group (P > 0.05). Conclusion: In this experiment, the TON rat model was successfully established by the transverse quantitative retraction method, and the treatment of TON rats with Wei's triple nine needling therapy reduced the P2 wave delay of the FVEP electrophysiological signal and increased the N2-P2 amplitude, which had a certain positive effect on the repair of optic nerve injury, probably related to its effect of improving the conduction function of the optic nerve and protecting the retinal ganglion cells that had not been degenerated and necrosed. [ABSTRACT FROM AUTHOR]

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

Retinal ganglion cells (RGCs) are essential to propagate external visual information from the retina to the brain. Death of RGCs is speculated to be closely correlated with blinding retinal diseases, such as glaucoma and traumatic optic neuropathy (TON). Emerging innovative technologies have helped refine and standardize the classification of RGCs; at present, they are classified into more than 40 subpopulations in mammals. These RGC subtypes are identified by a combination of anatomical morphologies, electrophysiological functions, and genetic profiles. Increasing evidence suggests that neurodegenerative diseases do not collectively affect the RGCs. In fact, which RGC subtype exhibits the strongest or weakest susceptibility is hotly debated. Although a consensus has not yet been reached, it is certain that assorted RGCs display differential susceptibility against irreversible degeneration. Interestingly, a single RGC subtype can exhibit various vulnerabilities to optic nerve damage in diverse injury models. Thus, elucidating how susceptible RGC subtypes are to various injuries can protect vulnerable RGCs from damage and improve the possibility of preventing and treating visual impairment caused by neurodegenerative diseases. In this review, we summarize in detail the progress and status quo of research on the type-specific susceptibility of RGCs and point out current limitations and the possible directions for future research in this field. [ABSTRACT FROM AUTHOR]

The aim of this report is to present a patient with traumatic optic nerve sheath hematoma (ONSH), a rare diagnosis with high potential for visual sequelae. This case involves a 41-year-old male who presented promptly following blunt trauma to the right eye and orbit that resulted in acute vision loss. Following computed tomography and ophthalmic examination, a diagnosis of ONSH was made and medical therapy with methylprednisolone was initiated. He reported significant improvements in visual symptoms following intravenous corticosteroid therapy. Although the patient reported significant improvements and had normal Snellen visual acuities in follow-up, he continued to have an inferior visual field defect at 1 week in the affected eye. ONSH causing subsequent localized compression of the optic nerve is a rare mechanism of traumatic optic neuropathy in patients following head trauma. The localized compartment syndrome of the optic nerve and subjective visual symptoms were relieved following corticosteroid therapy with no initial need for surgical decompression. Although central visual acuity returned to baseline, the patient had a persistent visual field defect and relative afferent pupillary defect.

We report a case of an 84-year-old female who presented following a fall from standing height. There was immediate loss of vision in the right eye. On day 3 of admission, the patient described seeing hallucinations in the right eye. She described seeing children playing in the garden while sitting in the hospital bed. She was found to have an indirect traumatic optic neuropathy with an associated Charles Bonnet syndrome. The patient underwent conservative management and on 2 weeks follow-up her right eye vision improved to hand motions. To our knowledge, there is no reported case of this kind in the literature.

AIM: To detect the visual dysfunction, and investigate the changes of Tau and its phosphorylated Ser396/Ser404 forms in retinas and optic nerves in traumatic optic neuropathy(TON)model rats by using FVEP technique.METHODS: Totally 30 SD rats were conducted FVEP electrode implantation. One week later, all rates were implemented TON operation with the optic nerve of left eye crushed and the optic nerve of right eye exposed(sham-operated). FVEP detections were performed respectively in these TON model rats at 1, 3, 7, 14, and 28d post crush, with 5 rats tested at each time point. After FVEP tests were taken, rats were sacrificed and then retinas and optic nerves of left eyes were separated for detecting the expression levels of Tau and pTau-Ser396/404 by Western Blot.RESULTS: Typical FVEP waves were observed in the sham-operated eyes. Compared to the sham group, the N2 waves were significantly delayed and the amplitude of N2-P2 were greatly reduced at each time point in the operation eyes. However, the differences of N2 wave and the amplitude reduction of N2-P2 were not significant at each time point after crush. The contents of total Tau protein in retinas of TON rats sharply decreased at 1d post crush, briefly recovered at 7d post crush, and remained a slightly lower level than normal condition till 28d. The changes of pTau-Ser396/404 were consistent with the changes of total Tau in retains and the Ser396 was the main phosphorylation site. However, the total Tau contents in optic nerves of TON rats increased gradually, and peaked at the 14d post crush and remained till 28d. The changes of pTau-Ser396/404 were similar to the changes of total Tau in optic nerves, which peaked at 7d post crush. However, Ser404 was the main phosphorylation site of Tau in optic nerves.CONCLUSION: The related indexes of N2 and P2 waves in FVEP can be used to detect the visual dysfunction in TON rats. After TON, the content changes of total Tau in retinas and optic nerves were much different while the changes of pTau-Ser396/404 followed the alterations of total Tau in the two locations. However, the main phosphorylation site of Tau was differnet according to the locations.

AIM:To evaluate the clinical efficacy of different interventions of traditional Chinese medicine in the treatment of traumatic optic neuropathy by means of mesh Meta-analysis.METHODS:The Computer searched of Chinese databases(CNKI, VIP, WanFang, SinoMed)and English databases(PubMed, Embase, Cochrane Library). Search time was limited from their inception to March 2020. Randomized controlled clinical trials of traditional Chinese medicine for treatment of traumatic optic neuropathy were subjected to Meta-analysis. Cochrane evaluation tool was used to evaluate the quality of the included studies and Stata 14.2 software was used to conduct network Meta-analysis.RESULTS: Twenty-one RCT studies involving 1 297 patients were included and 7 interventions were involved. Among them, Chinese medicine, Chinese medicine+hormone drugs, acupuncture+Chinese medicine+neurotrophic drugs were better than those with neurotrophic drugs alone. Chinese medicine+hormone drugs, acupuncture+Chinese medicine+neurotrophic drugs, acupuncture+Chinese medicine+hormone drugs were better than that of hormone drugs alone(P

Mai A Mohammed, Ehab Mossallam, Ibrahim Y Allam Ophthalmology Department, Faculty of Medicine, Alexandria University, Alexandria, EgyptCorrespondence: Mai A Mohammed 36 Kamaleldin Salah, Semouha, Alexandria, EgyptTel +201221081590Fax +203 42 444 41Email mai.abdalnabi@yahoo.comPurpose: To assess the value of the flash visual evoked potential (FVEP) in determining final visual prognosis in patients with indirect traumatic optic neuropathy (TON).Subjects and Methods: We included 30 patients diagnosed with indirect TON. Within one week of the onset of the trauma, visual acuity was recorded, pupillary reactions were assessed, FVEP was performed in both eyes. The amplitudes (N1p1 and N2P2) and the latency of P2 for each eye were recorded and amplitude ratio of N2P2 between the affected and normal eye was calculated. In follow-up visits, the cases underwent a complete ophthalmic examination, assessment of visual acuity, pupillary reaction, and FVEP.Results: The study included 22 males (73.3%) and 8 females (26.7%). The right eye was involved in 16 patients (53.3%) and left eye was involved in 14 cases (46.7%). According to the findings of FVEP, there was a direct correlation between final visual acuity and initial amplitude of N1p1 and N2P2 and negative correlation with latency of P2 wave. In 20 patients in whom the N1P1 and N2P2 amplitude was within the normal range and amplitude ratio of N2P2 of normal and fellow eye was at least 0.5 and the P2 implicit time was less than 140 ms, they achieved better visual outcome and visual acuity improved in the affected eye. In other 10 patients in whom the N1P1 and N2P2 amplitude was below normal range and the N2P2 amplitude ratio between the normal and the affected eye was less than 0.5 and the P2 implicit time was more than 140 ms, the visual acuity in the affected eye was less than 0.01 and these patients achieved less or no improvement in their visual function.Conclusion: Cases with TON usually present with severe loss of vision. FVEP is highly predictive of final visual outcome in patients having indirect TON given that the other eye is normal to be used as the patients’ internal control. More studies are needed to confirm these results.Keywords: flash visual evoked potential; FVEP, orbital computed tomography, traumatic optic neuropathy; TON, International Society of Electrophysiology of Vision; ISCEV

Objective Traumatic optic neuropathy (TON) is an important cause of severe vision impairment after sustaining a closed head injury. This study describes the safety and efficacy of combined therapy in the management of TON. Methods A retrospective analysis of 23 consecutive cases of unilateral TON managed with combined therapy (steroid and surgery) were performed. Statistical analysis of patient characteristic, timing of vision loss, radiological and intraoperative findings, and pre- and post-treatment vision were compared to assess the prognostic factors. Results Seventeen patients (85%) had vision improvement with combined therapy. Three patients (15%), who recorded no improvement, initially presented with no perception of light, and loss was sudden and immediate. With steroids, 9 patients improved, all of them presented with perception of light (PL) or better and vision improved to (6/6 in five, 6/9 in one, 6/18 in 3). Eleven patients (6 PL–ve and 5 PL þ ve after failed steroid therapy) underwent endoscopic optic nerve decompression and eight had improvement in vision. The status of vision at presentation was only statically significant prognostic factor (p < 0.02). Others prognostic factors, for example, time of starting treatment, surgery, and presence of fracture in optic canal, were not found statistically significant (p > 0.05). There were no significant intra- and postoperative complications. Conclusion Combined therapy is safe and effective in management of TON. Mild form injury with some preserved vision at presentation respond well to steroids, while endoscopic nerve decompression should be reserved in cases with failed steroid therapy. [ABSTRACT FROM AUTHOR]

The article analyzes the surgical treatment of 96 patients who underwent surgery for retinal detachment. The cause of retinal detachment in all cases was an eye contusion. The author analyzed the age, gender, visual acuity before and after surgery, the cause of contusion, the time of onset of retinal detachment, concomitant pathology, type of retinal tear, surgical technique, results of ophthalmological examinations in the pre- and postoperative period, postoperative complications. The factors that affect visual functions in the early and late postoperative period were determined. Visual acuity after surgery depends on the initial visual acuity. Delaying the time of surgery leads to a decrease in visual functions in the postoperative period. Proliferative vitreoretinopathy and traumatic optic neuropathy were the most common complications that led to vision loss 6 months after surgery. Traumatic optic neuropathy is the result of trauma and is not associated with surgery. There are no effective treatments. Proliferative vitreoretinopathy is a complication of surgical treatment of retinal detachment. Repeated surgical treatment does not improve vision. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Traumatic optic neuropathy (TON) is a rare but serious consequence of head injuries. The optimal therapy for TON remains controversial, and standardized recommendations are lacking. The most common therapies used are steroid administration and surgical decompression procedures. The aim of the present study was to compare two common conservative and surgical therapies in a rodent model with a standardized traumatic optic nerve lesion. This study employed 59 male Wistar rats. After exposing the optic nerve, defined trauma was exerted on the optic nerve using a micromanipulator to trigger TON. Rats received either "megadose" methylprednisolone applied perioperatively or decompression via nerve sheath fenestration. The number of neurons was histologically evaluated in retinae explanted as whole mounts. Neuronal size was determined histomorphometrically. Neuronal loss was significantly lower following perioperative "megadose" steroid therapy (p =.017), especially in the central retinal area (p =.025). Compared to the control group without therapy, on average more than 400 neurons/mm2 were saved. In the central retinal area, more than 600 neurons/mm2 were rescued. In contrast, neuronal loss was not significantly affected by surgical decompression; however, this procedure was associated with a reduction in neuron size (p =.003). The present model revealed significant neuroprotective effects following administration of methylprednisolone for TON treatment. Mitigation of neuronal loss may result in functional benefits. Neuroprotective effects were not observed following surgical therapy, suggesting that this approach should be reserved for individual cases such as hematomas in the area of nerve envelopes. [ABSTRACT FROM AUTHOR]

AIM: To evaluate the efficacy and safety of traditional Chinese medicine combined with Western medicine(TCM-WM)in the treatment of traumatic optic neuropathy(TON).METHODS:The computer searched PubMed, EMBASE, Cochrane Library, Chinese Biomedical Literature Database(CBM), Wan-Fang Database, China National Knowledge Infrastructure(CNKI)database and Weipu database. Search time was limited from their inception to May 2020. A comprehensive search strategy was designed to identify all randomized controlled trials(RCTs)comparing TCM-WM therapy versus WM therapy alone. The methodological quality of the included trials was assessed by the quality grade evaluation used in Cochrane handbook. Data extraction and Meta-analysis were performed by RevMan5.3 statistical software.RESULTS: Twelve RCTs were included. The Meta-analysis showed that compared with the WM therapy alone in treating TON, TCM-WM therapy was better in improving the effective rate [RR=1.33, 95% CI(1.23-1.45), P

Objective: To study the spectrum of optic neuropathies in patient’s presenting at AFIO Rawalpindi. Study Design: Descriptive study/retrospective study. Place and Duration of Study: Armed Forces Institute of Ophthalmology, Rawalpindi, from Jan 2017 to Dec 2017. Methodology: Retrospective analysis of hospital record of patients coming to neuro-ophthalmic clinic of Armed Forces Institute of Ophthalmology (AFIO), Rawalpindi, from Jan to Dec 2017 was done. Only patients with clear final diagnosis of neurophthalmic disease were included. Those with vague diagnosis were excluded. Data was entered in SPSS version 22 and grouped into variables before analysis. Chi-square test was used for statistical analysis. The p

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

Therapeutic hypothermia (TH) is potentially an important therapy for central nervous system (CNS) trauma. However, its clinical application remains controversial, hampered by two major factors: (1) Many of the CNS injury sites, such as the optic nerve (ON), are deeply buried, preventing access for local TH. The alternative is to apply TH systemically, which significantly limits the applicable temperature range. (2) Even with possible access for ‘local refrigeration’, cold-induced cellular damage offsets the benefit of TH. Here we present a clinically translatable model of traumatic optic neuropathy (TON) by applying clinical trans-nasal endoscopic surgery to goats and non-human primates. This model faithfully recapitulates clinical features of TON such as the injury site (pre-chiasmatic ON), the spatiotemporal pattern of neural degeneration, and the accessibility of local treatments with large operating space. We also developed a computer program to simplify the endoscopic procedure and expand this model to other large animal species. Moreover, applying a cold-protective treatment, inspired by our previous hibernation research, enables us to deliver deep hypothermia (4 °C) locally to mitigate inflammation and metabolic stress (indicated by the transcriptomic changes after injury) without cold-induced cellular damage, and confers prominent neuroprotection both structurally and functionally. Intriguingly, neither treatment alone was effective, demonstrating that in situ deep hypothermia combined with cold protection constitutes a breakthrough for TH as a therapy for TON and other CNS traumas.

Objective: We used optical coherence tomography (OCT) to document the time course of retrograde neuronal degeneration following indirect optic nerve injury. Methods: We retrospectively studied patients diagnosed with unilateral indirect traumatic optic neuropathy (TON). Patients with total or near-total optic atrophy were included. All patients underwent complete ophthalmological examinations, including OCT imaging, within 1 day and at 1, 2, 3, 4, 6, 8, 12, 24, and 48 weeks after trauma. Results: The mean thicknesses of the circumpapillary retinal nerve fiber layer (cpRNFL) and macular retinal ganglion cell-inner plexiform layer (mGCIPL) decreased significantly at 2 weeks after trauma (p = 0.027 and p = 0.043). Changes in mGCIPL thickness preceded changes in cpRNFL thickness. The rates of reduction in mGCIPL and cpRNFL thicknesses were greatest between 2 to 4 weeks and 4 to 6 weeks after trauma. The reduction in mGCIPL thickness then slowed, and stabilized at 12 weeks after trauma. The proportions of cpRNFL and mGCIPL losses at 2, 4, 6, 8, and 12 weeks compared to 24 weeks were 17.1, 33.7, 59.8, 77.9, and 87.9% and 30.0, 73.3, 76.1, 88.3, and 97.9%, respectively. Conclusions: OCT revealed optic atrophy progression 2 weeks after trauma, which was most rapid from 2 to 6 weeks, and then gradually stabilized. Loss of retinal ganglion cell bodies and dendrites seemed to precede the axonal degeneration. Observations of morphological changes in retinal layers using OCT in TON patients improve our understanding of retrograde neuronal degeneration of the central nervous system. [ABSTRACT FROM AUTHOR]

Introduction: To compare the optic nerve head (ONH) structure and microvasculature in patients with optic atrophy due to non-arteritic anterior ischemic optic neuropathy (NAION), compressive optic neuropathy (CON), methanol-induced optic neuropathy (MION), and traumatic optic neuropathy (TON) using optical coherence tomography angiography. Methods: In this comparative, cross-sectional study, 32 eyes with NAION, 18 eyes with CON, 32 eyes with MION, 23 eyes with TON, and 55 normal eyes were enrolled. Radial peripapillary capillary (RPC) vessel density, peripapillary retinal nerve fiber layer (RNFL) thickness, disc area, cup volume, and cup/disc area ratio were obtained using the RTVue XR Avanti system (Optovue Inc., Fremont, CA, USA). Results: RPC vessel density and peripapillary RNFL thickness in all patients were significantly lower than normal subjects. A positive correlation was found between the RPC vessel density and peripapillary RNFL thickness in normal subjects and all study groups. The positive correlation between the inside and outside disc RPC vessel density was only found in the NAION (r = 0.36, P =.042) and MION (r = 0.42, P =.018) groups. No significant difference was found among the groups in terms of peripapillary and inside disc vascular densities (all P >.05). Disc area and cup volume in patients with MION was larger than the values in patients with NAION (P =.018) and TON (P =.044) and normal subjects (P =.015). The discriminating features among the study groups were the larger cup volume and cup/disc area ratio in patients with MION, and lower RNFL thickness in patients with TON. Conclusions: There was a positive correlation between the RNFL thickness and peripapillary RPC vessel density regardless of the cause of optic disc pallor. Structural evaluation of the ONH seems to be a better way to differentiate the cause of optic nerve head atrophy than the microangiographic changes. [ABSTRACT FROM AUTHOR]

Transorbital and intra-sphenoidal traumas are relatively uncommon, can be challenging to manage, and are associated with a high risk of complications and potentially fatal outcome. Transorbital and intra-sphenoidal trauma pose a medical challenge due to close relationship to delicate and critical anatomical structures, such as the globe, optic nerve, the ophthalmic internal carotid arteries, and central nervous system. Rapid admission to a level 1 trauma center with a high surgical expertise level is essential to ensure the best possible treatment and outcome. We present a case of a 75-year-old man who had a severe orbital trauma, where a wooden foreign object penetrated the orbit into the sphenoid sinus without penetrating its posterior wall. This case is important because of the rare trauma presentation with a wooden foreign object, which can easily be missed on computed tomography. The case also illustrates the importance of close collaboration between ophthalmologists and rhinologists when challenged with severe orbital sphenoid sinus trauma.

Aims: The aim of this study was to analyze the clinical profile, visual outcome, factors predicting the visual outcome, and response to systemic methylprednisolone as per the Optic Neuritis Treatment Trial (ONTT) protocol in patients with traumatic optic neuropathy (TON). Study Design: This was a prospective observational study. Subjects and Methods: All cases who had decreased visual acuity (VA) following impact head/orbital injury were evaluated with detailed history, and ophthalmic evaluation was done. Those who were diagnosed to have indirect TON were treated with intravenous methylprednisolone 500 mg twice daily for 3 days, followed by oral prednisolone 1 mg/kg for 11 days. Visual outcome was assessed at 1 week, 1 month, 3 months, and 6 months. The results were statistically analyzed. Results: 34.65% had severe loss of vision (

The vision loss in the Traumatic Optic Neuropathy is the impact of deformational forces. This occurs due to direct or indirect injuries during trauma to skull. The use of high dose corticosteroids is the primary line of treatment in such injuries still remains a matter of debate. Traumatic Optic Neuropathy is yet an unexplored topic of study in Ayurveda. The Traumatic Optic Neuropathy can be correlated with Abhighatajanya Vataprakopaj Drishtinash. The treatment principles of Vataprakopaj Vyadhi are Snehan (massage), Swedan (sudation), Basti (enema) and Nasya (oleation through nasal route). A 50 year old male patient came to outpatient department suffered from motorcycle accident and had a forehead trauma followed by loss of vision in both eyes after 5 days and diagnosed as Traumatic Optic Neuropathy. An electrophysiological assessment showed absence of waveform in Visual Evoked Potential (VEP). According to Ayurveda patient was diagnosed primarily as Abhighatajanya Vataprakopaj Drishtinash and started to follow the protocol of Vataprakopaj Vyadhi. Patient received Ayurvedic formulations in morning, after meal and at night for 12 months and a course of Yapan Basti (medicated decoction enema) followed by Netratarpan (eye satiation), Nasya and Abhyanga (body and foot massage). Patient showed an improvement in the visual quality from no perception of light to perception of light and rays in right eye in 9 month. Patient had improvement in P100 latencies of right eye in VEP report and subjective improvement in quality of vision to perceive the images and objects. Application of Ayurvedic principles and Panchakarma therapy resulted in improvement of the case. An early management of Traumatic Optic Neuropathy with Ayurvedic treatment can have a significant impact on the clinical/visual outcome in terms of recovery in damaged optic nerve fibers.

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.

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

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.

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., Competing Interests: 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., (Copyright © 2024 Yu, Qi, Wang, Yang, Liu, Chen, Xu, Li, Chen, Dai and Gu.)

Traumatic brain injury (TBI) causes structural and functional damage to the central nervous system including the visual pathway. Defects in the afferent visual pathways affect visual function and in severe cases cause complete visual loss. Visual dysfunction is detectable by structural and functional ophthalmic examinations that are routine in the eye clinic, including examination of the pupillary light reflex and optical coherence tomography (OCT). Assessment of pupillary light reflex is a non-invasive assessment combining afferent and efferent visual function. While a assessment using a flashlight is relatively insensitive, automated pupillometry has 95% specificity and 78.1% sensitivity in detecting TBI-related visual and cerebral dysfunction with an area under the curve of 0.69–0.78. OCT may also serve as a noninvasive biomarker of TBI severity, demonstrating changes in the retinal ganglion cell layer and nerve fiber layer throughout the range of TBI severity even in the absence of visual symptoms. This review discusses the impact of TBI on visual structure and function. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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.

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

PURPOSE: The aim of the study was to assess the efficacy of virtual planning and surgical guide jig to improve surgical outcomes of open reduction and internal fixation with restoration and correction of orbital volume (OV) in unilateral orbital wall fractures. METHODS: Fifteen patients with unilateral orbital fractures were assessed with ophthalmologic and radiographic parameters. The orbit was divided into three zones on computed tomography to localize defects. Fractures were coded into Fx Mx Rx Lx (F = Orbital Floor, M = Medial Wall, L = Lateral wall, R = Orbital Roof) based on pattern and specific wall involved. 1-mm sections were used to make stereolithographic models, design the custom fabricated surgical jig for intraoperative use as a guide. RESULTS: Pre- and postoperative ophthalmological parameters, OV, were compared with the contralateral normal orbit serving as the reference. Postoperative ophthalmological parameters showed significant improvement in terms of visual acuity, enophthalmos, dystopia, and traumatic optic neuropathy. OV changes were concentrated in Zones 2 and 3. OV showed adequate restoration postoperatively. CONCLUSION: The surgical jig served as an efficient guide to improve surgical outcomes of open reduction internal fixation. Preplanned intraoperative positioning helped achieve adequate anatomical reduction and fixation with an adequate reconstruction of OV aiding the effective transfer of virtual surgical plan on the table with improved surgical outcomes in clinical performance and functional restitution. Clinical trial registration: The Clinical Trials Registry of India (CTRI) Registration No.: CTRI/2019/11/021929. [ABSTRACT FROM AUTHOR]

Background: Direct traumatic optic neuropathy (TON) carries a poor prognosis. However, the outcome of this injury is diverse and is related to time to treatment and treatment protocol. Objective: To evaluate the outcomes of the combined treatment protocol in patients with direct TON. Materials and Methods: The authors retrospectively reviewed the medical records of patients between January 2015 and August 2019. Main outcome was visual acuity (VA) improvement after the treatment. Results: Thirteen patients (15 eyes) were included. The mean age was 38.61 years with a range of 13 to 65 years. Initial VA varied from no light perception (NPL) in seven eyes of six patients, light perception (PL) in one eye, counting fingers in two eyes, 20/200 in three eyes, and 20/60 in two eyes. Average timing to treatment was 2.8 days (range 0 to 7 days). There were no side effects of high-dose corticosteroids treatment in all patients. During a follow-up period of three months, six of 13 patients (46.1%) had VA improvement. Conclusion: Despite poor prognosis of direct TON, the combined treatment protocol provides a favorable successful rate with most patients on having stable vision, and some having visual improvement from reducing intracanalicular pressure of the optic nerve. [ABSTRACT FROM AUTHOR]

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

We report a case of intraconal grease gun injury along with traumatic optic neuropathy in a 20-year-old male. He presented with dimness of vision and proptosis of the left eye (LE) following an accidental injury at work place. The computer tomography of orbit revealed hypodense grease orbit. Cream colored grease was continually exuding from the conjunctival wound. Patient improved rapidly after the surgical removal of the grease by anterior orbitotomy. Grease gun injuries to the orbit have rarely been reported. The present case is the eighth report throughout the world, and the first in India as per our knowledge.

Abstract Background Traumatic optic neuropathy (TON) is a form of optic nerve injury that occurs secondary to trauma and is etiologically associated with acute axonal loss with severe vision loss. Here, we reported longitudinal changes in the peripapillary retinal nerve fiber layer (RNFL) and macular ganglion cell complex (GCC) using wide-field swept source optical coherence tomography (SS-OCT) in two cases of TON and identified the source of the damage. Case presentation (Case 1) A 65-year-old man was admitted to the hospital due to an injury in the right eye (OD) and was subsequently diagnosed with indirect TON. He was then treated with high-doses of intravenous steroids. Wide-field SS-OCT was performed at the baseline and after 1 day, 2 days, 1 week, 1 month, and 4 months. The wide-field deviation map detected thinning earlier in the macular GCC than in the peripapillary RNFL. (Case 2) A 63-year-old man was admitted to the hospital with a fractured left maxilla-zygomatic complex attributed to blunt-force trauma to the head and loss of vision in his left eye (OS). He was diagnosed with indirect TON and treated with high-doses of intravenous steroids. Wide-field SS-OCT was performed at the baseline and after 1 week, 2 weeks, 2 months 5 months, and 7 months. The wide-field deviation map detected thinning earlier in the peripapillary RNFL than in the macular GCC. Conclusions Wide-field SS-OCT facilitated the identification of various sequential progression patterns in patients with TON. Furthermore, the area in which the structural damage was first detected was seen differently in the peripapillary and macular deviation maps for each case. Thus, wide-field imaging, which includes the macular and peripapillary areas, are useful in monitoring TON.

Background: The features of the application of neuroprotective therapy for traumatic optic neuropathy (TON) in the clinical setting are not known. Methods: Forty-nine TON patients (49 eyes) with MRI evidence of no compressive optic nerve injury were divided into group A (25 patients) and group B (24 patients) and underwent treatment. Patients of group A were treated with 1000 mg of pre-intravenous methylprednisolone daily for 3 days with subsequent gradual tapering of the dose. Patients of group B were treated with a 1000-mg methylprednisolone infusion daily for 3 days and bilateral electric phosphene stimulation (EPS) for 10 days. Results: We demonstrated in the clinical setting that, compared to steroid-only treatment, steroids plus EPS treatment for TON is characterized by greater improvements in (a) visual acuity, (b) selectivity of action depending on the ophthalmoscopic form of TON, and (c) atrophic processes in the axial bundle of the optic nerve. After combination treatment for TON, visual acuity improved by 0.6 to 0.8, and critical frequency of phosphene disappearance (CFPD) improved by 35 to 45 Hz. Compared with combined or inverse form of TON, ischemic form of TON is seen in the earlier period after the traumatic event. Steroids plus EPS treatment effect was greater in the last form than in the two former forms. Conclusion: Our steroids plus EPS treatment may be an alternative to conventional treatment (megadose steroid-only therapy) for TON in the clinical setting.

Traumatic optic neuropathy (TON) refers to optic nerve damage caused by trauma, leading to partial or complete loss of vision. The primary treatment options, such as hormonal therapy and surgery, have limited efficacy. Pituitary adenylate cyclase-activating polypeptide 38 (PACAP38), a functional endogenous neuroprotective peptide, has emerged as a promising therapeutic agent. In this study, we used rat retinal ganglion cell (RGC) exosomes as nanosized vesicles for the delivery of PACAP38 loaded via the exosomal anchor peptide CP05 (EXOPACAP38). EXOPACAP38 showed greater uptake efficiency in vitro and in vivo than PACAP38. The results showed that EXOPACAP38 significantly enhanced the RGC survival rate and retinal nerve fiber layer thickness in a rat TON model. Moreover, EXOPACAP38 significantly promoted axon regeneration and optic nerve function after injury. These findings indicate that EXOPACAP38 can be used as a treatment option and may have therapeutic implications for patients with TON.

Purpose: Traumatic injury to the optic chiasm is rare and most frequently caused by high-velocity head trauma. It classically results in bitemporal hemianopsia and often presents in conjunction with multiple other traumatic injuries, such as skull fractures and cerebrospinal fluid leaks. We present the case of a 40-year-old woman with pre-existing thyroid orbitopathy who struck her forehead after a fall from standing height. Observations: This patient suffered immediate profound unilateral vision loss from traumatic optic neuropathy and possible optic nerve avulsion. The fellow eye manifested a temporal hemianopsia with delayed retinal nerve fiber layer and nasal hemimacular ganglion cell layer thinning on optical coherence tomography, consistent with chiasmal pathology. Magnetic resonance imaging showed no definitive lesions at the optic chiasm or more posteriorly along the afferent visual pathway. Conclusions and importance: This patient's severe vision loss suggests that proptosis from thyroid orbitopathy can sensitize the anterior visual pathway to trauma. In this case, we propose that the lack of laxity in the intra-orbital optic nerves allowed transmission of stretching forces to the optic chiasm in the setting of low-velocity blunt trauma.