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

We describe the emergency management of a man who experienced acute vision loss diagnosed as direct traumatic optic neuropathy (TON) in his right eye (no light perception) after falling from a height. TON is caused by a high-impact mechanism of injury. Clinical findings include acute vision loss, which is typically immediate, afferent pupillary defect, decreased color vision, and visual field defects. Treatment is controversial because of the lack of strong evidence supporting intervention over observation. In this case report, our treatment strategy comprised immediate hyperbaric oxygen (HBO2) and daily high doses of a steroid. On the second day, minocycline was added to the treatment regimen for its neuroprotective effects. The patient was discharged after receiving six HBO2 treatments and six days of intravenous solumedrol transitioned to oral prednisone. After the third HBO2 treatment, his vision improved to 20/100; after the fourth treatment, it was 20/40 and plateaued. At the time of discharge, it was 20/40. At two-month follow-up, his corrected visual acuity was 20/60+2 in the affected eye. Immediate HBO2 for ischemic and mechanical injury to the optic nerve following trauma is a therapeutic option.

Pathologies of the optic nerve could result as primary insults in the visual tract or as secondary deficits due to inflammation, demyelination, or compressing effects of the surrounding tissue. The extent of damage may vary from mild to severe, differently affecting patient vision, with the most severe forms leading to complete uni- or bilateral visual loss. The aim of researchers and clinicians in the field is to alleviate the symptoms of these, yet uncurable pathologies, taking advantage of known and novel potential therapeutic approaches, alone or in combinations, and applying them in a limited time window after the insult. In this review, we discuss the epidemiological and clinical profile as well as the pathophysiological mechanisms of two main categories of optic nerve pathologies, namely traumatic optic neuropathy and optic neuritis, focusing on the demyelinating form of the latter. Moreover, we report on the main rodent models mimicking these pathologies or some of their clinical aspects. The current treatment options will also be reviewed and novel approaches will be discussed.

Traumatic optic neuropathy (TON) is rare. The heterogeneity of injury patterns and patient condition on presentation makes diagnosis difficult. Fracture patterns associated with TON have never been evaluated. Retrospective review of 42 patients diagnosed with TON at the R. Adams Cowley Shock Trauma Center from May 1998 to August 2010 was performed. Thirty-three patients met criteria for study inclusion of fracture patterns. Additional variables measured included patient demographics and mechanism. Cluster analysis was used to form homogenous groups of patients based on different fracture patterns. Fracture frequency was analyzed by group and study population. Visual depiction of fracture patterns was created for each group. Cluster analysis of fracture patterns yielded five common “groups” or fracture patterns among the study population. Group 1 ( n = 3, 9%) revealed contralateral lateral orbital wall (100%), zygoma (67%), and nasal bone (67%) fractures. Group 2 ( n = 7, 21%) demonstrated fractures of the frontal bone (86%), nasal bones (71%), and ipsilateral orbital roof (57%). Group 3 ( n = 14, 43%) involved fractures of the ipsilateral zygoma (100%), lateral orbital wall (29%), as well as frontal and nasal bones (21% each). Group 4 ( n = 5, 15%) consisted of mid- and upper-face fractures; 100% fractured the ipsilateral orbital floor, medial and lateral walls, maxilla, and zygoma; 80% fractured the orbital roof and bilateral zygoma. Group 5 ( n = 4, 12%) was characterized by fractures of the ipsilateral orbital floor, medial and lateral orbital walls (75% each), and orbital roof (50%). A notably high 15 of 33 patients (45%) sustained penetrating trauma. Our study demonstrates five fracture pattern groups associated with TON. Zygomatic, frontal, nasal, and orbital fractures were the most common. Fractures with a combination of frontal, nasal, and orbital fractures are particularly concerning and warrant close attention to the eye.

Background Many authors have reported on therapeutic strategies for traumatic optic neuropathy and their experience with endonasal endoscopic optic nerve decompression for traumatic optic neuropathy. However, to our knowledge, few have described the therapeutic strategies for nontraumatic optic neuropathy and navigation-assisted endoscopic optic nerve decompression as a treatment for nontraumatic, compressive optic neuropathy. The aim of this study was to examine the advantages in treating nontraumatic optic neuropathy with the minimally invasive, image-guided, navigation-assisted, endonasal endoscopic optic nerve decompression. Methods This was a retrospective study of 20 patients (21 eyes) diagnosed with nontraumatic optic neuropathy, undergoing an endonasal endoscopic approach to relieve space-occupying lesions and decompress the optic nerve under image-guided navigation. This article describes our research on the therapeutic strategies for nontraumatic optic neuropathy patients, with special focus on the advantages of navigation-assisted, endonasal, endoscopic optic nerve decompression for the treatment of nontraumatic optic neuropathy. Medical photographs were used to estimate the status of the patients. Results In 18 of the 20 cases, space-occupying lesions were completely resected. In two cases, they were partially resected. All 20 cases (21 eyes) underwent image-guided, navigation-assisted, endonasal endoscopic optic nerve decompression. Visual acuity improved in 20 eyes (95.2%) and remained stable in one eye. There were no intraoperative or postoperative complications. Conclusions Optic nerve decompression is the main treatment strategy for nontraumatic optic neuropathy, to relieve space-occupying lesions and decompress the optic nerve, and to retain and/or improve visual acuity. Image-guided navigation can help doctors pinpoint the optic nerve when facing anatomical deformation caused by a space-occupying lesion. Navigation-assisted, endonasal endoscopic optic nerve decompression is a feasible, safe, practical, and minimally invasive approach.

Purpose. Investigating the efficacy of intravitreal injection of erythropoietin (EPO) in managing indirect traumatic optic neuropathy (ITON) of different durations.Methods. A case series that included two groups of ITON patients: recent ITON group (Results. Significant improvement was found in BCVA, VER amplitude, and latency (P<0.0001, 0.0154, and 0.0291, respectively). Initial values of BCVA, VER amplitude, and latency correlated significantly to the final values. Differences between recent and old trauma groups were insignificant in the three parameters. In patients who received second injection, further clinical but statistically insignificant improvement was noted in BCVA in 60% of patients, VER amplitude in 50% of patients, and in VER latency in 100% of patients. No complications were recorded.Conclusion. Intravitreal injection of EPO may be effective and safe in treatment of recent and old indirect traumatic optic neuropathy.

Ocular trauma can be a common presentation in the emergency department. It is therefore important for a physician to be able to quickly recognize vision-threatening conditions and provide necessary medical management prior to consulting ophthalmology. This article describes the pertinent information that should be gathered during a focused ocular history in a patient with ocular injury, and also provides a systematic approach to evaluating ocular trauma. As an example, a case study of open globe injury is used to illustrate the appropriate pre-ophthalmologic management and common medical errors that must be avoided for a good prognosis. Additional ocular conditions such as traumatic hyphema, traumatic optic neuropathy, traumatic vitreous hemorrhage, orbital compartment syndrome, chemical burns, and eyelid lacerations are also described as differential diagnosis. Ultimately, the aim of this work is to provide medical students with a fundamental understanding in approaching ocular trauma in emergency clinics.

Traumatic optic neuropathy (TON) is an uncommon vision-threatening disorder that can be caused by ocular or head trauma and is categorized into direct and indirect TON. The overall incidence of TON is 0.7–2.5%, and indirect TON has a higher prevalence than direct TON. Detection of an afferent pupillary defect in the presence of an intact globe in a patient with ocular or head trauma with decreased visual acuity strongly suggests TON. However, afferent pupillary defects may be difficult to detect in patients who have received narcotics that cause pupillary constriction and in those with bilateral TON. Mechanical shearing of the optic nerve axons and contusion necrosis due to immediate ischemia from damage to the optic nerve microcirculation and apoptosis of neurons is a probable mechanism. The proper management of TON is controversial. High-dose corticosteroid therapy and decompression of the optic nerve provide no additional benefit over observation alone. Intravenous erythropoietin may be a safe and efficient treatment for patients with TON.

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.

Objective: This study aimed to evaluate the outcomes of endoscopic optic nerve decompression (EOND) for adults with traumatic optic neuropathy (TON) and seek factors that might affect surgery outcomes. Methods: From January 2016 to June 2019, 16 adults diagnosed with TON, who underwent endoscopic trans-ethmosphenoid optic canal decompression, were reviewed. All the patients were treated with steroids before the surgery. The main outcome measure was an improvement in visual acuity (VA) after treatment. Results: Eight (50.0%) patients had residual vision before the surgery, while eight (50.0%) had no light perception. After surgical decompression, partial recovery of VA was achieved in three (18.75%) patients who were operated within 10 days and had residual vision before the surgery. However, no improvement in VA was observed for the remaining patients (81.25%) who were operated more than 10 days after injuries. Conclusions: EOND is beneficial for TON not responding to steroid therapy and can prevent permanent disability if earlier intervention is done prior to irreversible damage to the nerve. Endoscopic optic nerve surgery can decompress the traumatic and edematous optic nerve with proper exposure of optic canal and orbital apex without any major complications. The operation timing and residual vision are important factors affecting outcomes.

Study Design: Retrospective chart review of pediatric and globe injuries associated with orbital fractures. Objective: Our study seeks to examine these injuries and their association with orbital fractures at our trauma center to gain a better understanding of how to approach pediatric patients with orbital fractures. Methods: A retrospective review of all facial fractures in pediatric patients at an urban level 1 trauma center was performed for the years 2002 to 2014. Patient demographics were collected, as well as orbital fracture location, mechanism of injury, concomitant injuries, ophthalmologic documentation, imaging, and perioperative records. Results: One hundred sixteen pediatric patients over a 12-year period sustained an orbital fracture. The orbital floor was the most commonly fractured orbital bone in our series (60%). Thirty-four (30%) of the pediatric patients with orbital fractures had documented periorbital and/or globe injuries at the time of presentation. The most common periorbital injury was entrapment related to orbital floor fractures. Significant eyelid lacerations were present in seven patients, with five of these patients had canalicular injuries and two had canthal malposition. Five pediatric patients presented with traumatic optic neuropathy. Two patients had ruptured globes requiring enucleation. Conclusions: Periorbital soft tissue and globe injuries associated with orbital fractures occurs in a substantial number of pediatric patients. There are no guidelines for treatment of these type of injuries in the pediatric population. Further research should be performed to better understand the appropriate management of periorbital injuries in conjunction with surgical management of the orbital fractures.

Traumatic optic neuropathy leads to bidirectional degeneration of retinal ganglion cells and axons and results in optic nerve scaring, which inhibits the regeneration of damaged axons. Compared with its glial counterpart, the fibrotic response causing nerve scar tissue is poorly permissive to axonal regeneration. Using collagen1α1-GFP reporter mice, we characterize the development of fibrotic scar formation following optic nerve crush injury. We observe that perivascular collagen1α1 cells constitute a major cellular component of the fibrotic scar. We demonstrate that extracellular molecules and monocytes are key factors contributing to the pathogenesis of optic nerve fibrotic scar formation, with a previously unrecognized encapsulation of this scar. We also characterize the distribution of collagen1α1 cells in the retina after optic nerve crush injury based on in vivo and whole-mount retinal imaging. Our results identify collagen1α1 cells as a major component of fibrotic scarring following ONC and are a potential molecular target for promoting axonal regeneration after optic nerve injury.

Traumatic optic neuropathy (TON) is an important cause of vision loss in the setting of cranial and/or facial trauma. Both direct and indirect variants exist, with the latter being more common. We describe the case of a young male presenting with loss of vision following trauma with an intact globe, an intraorbital foreign body, and Onodi cell hemorrhage. The challenges in diagnoses of type of TON, exact pathology, and management are discussed. We also highlight the role of thin section digital computed tomography imaging which is paramount for timely detection of subtle injuries and their management.

We present our experience following a unique case of coincident intracranial hemorrhage and comminuted fractures of both the squamous temporal bone and zygomaticofrontal orbit. Surgical techniques and outcome for this presentation have yet to be sufficiently described. A 55-year-old male presented following trauma with Glasgow Coma Scale score of 7. Radiographic evaluation revealed comminuted fractures of the squamous temporal bone with extension into the lateral orbit, along with zygomatic process fracture extending 2.5 cm medially into the orbital roof. Zygomaticofrontal orbital roof fragments reached superiorly into the middle cranial fossa and inferiorly into the orbit. Surgical intervention was deemed necessary to address underlying epidural hematoma, subarachnoid hemorrhage, correction of cranial bone defects, and decompression of the optic nerve and other intraorbital nerves. A frontotemporal approach was employed. Repair of temporal and orbital fractures was accomplished using a combination of wire mesh screws and titanium miniplates. Postoperative imaging demonstrated bony approximation and successful evacuation of traumatic hemorrhage. The patient remains functionally and neurologically intact apart from a sluggishly responsive left eye presumed to result from a left optic nerve or ciliary ganglion lesion. Although rapid reconstruction of complex cranial-orbital trauma and hematoma evacuation can permit acceptable gross functional neurological outcome following massive trauma, orbital fracture and subsequent hemorrhagic processes may be the nidus of neurological sequelae in this complex traumatic constellation. Thus, alterations in surgical approach and reconstruction are appropriate in order to maximize neurological function while supporting restoration of cosmetic space.

This study aimed to investigate the clinical outcomes of endoscopic transnasal optic canal decompression (ETOCD) for patients with indirect traumatic optic neuropathy (TON) and identify the relevant prognostic factors.Seventy-two indirect TON patients who underwent ETOCD surgery from August 2017 to May 2019 were analyzed retrospectively. The paired t-test was used to compare the visual acuity (VA) before and after ETOCD, and multiple linear regression analysis was used to distinguish the potential prognostic factors.Among the patients analyzed, postoperative VA (-2.87 ± 0.19) was significantly higher than the preoperative VA (-3.92 ± 0.13) (P 0.05). Multiple linear regression analysis models showed that poor initial VA and longer time to surgery were independent risk factors for VA prognosis (P 0.05), but surgical time alone was significantly associated with the improvement degree of visual acuity (IDVA) (P 0.05). Optic canal fracture, orbital fracture, and hemorrhage within the ethmoid and/or sphenoid sinus were not significantly correlated with IDVA and VA prognosis (P 0.05).ETOCD surgery could salvage VA impairment in patients with indirect TON. A better initial VA indicates better final VA outcomes after surgery. Additionally, shorter time to surgery implies better VA prognosis and higher IDVA.

Traumatic optic neuropathy (TON) is a degenerative process that occurs in a subset of patients following blunt force trauma to the head. This condition is characterized by retinal ganglion cell (RGC) death and axon degeneration within the optic nerve [1]. At the cellular level, mitochondrial changes are associated with many optic neuropathies [2, 3]. Here, we provide a dataset demonstrating changes in the optic nerve mitochondrial lipid profile of a sonication-induced traumatic optic neuropathy (SI-TON) mouse model at 1, 7, and 14 days after injury. 32 C57BL/6J mice were separated into 4 groups (control, 1, 7, and 14 days) of 8, with 4 males and 4 females in each. Mice were exposed to sonication-induced trauma as described previously (by Tao et al) and optic nerves were harvested at 1, 7, or 14 days following injury [4]. Mitochondria were isolated from homogenized optic nerves and lipids were extracted. Extracted mitochondrial lipids were analysed with a Q-Exactive Orbitrap Liquid Chromatography-Mass Spectrometer (LC MS-MS). Further analysis of raw data was conducted with LipidSearch 4.1.3 and Metaboanalyst 4.0. This data is publicly available at the Metabolomics Workbench, http://www.metabolomicsworkbench.org (Project ID: PR000905).

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

Introduction: Acute injury to the optic nerve resulting in vision loss is known as Traumatic Optic Neuropathy (TON). Optical Coherence Tomography (OCT) documents the progression of damage of axons over time. Aim: To assess visual outcome of patients diagnosed with TON after management with intravenous (IV) steroids and to study Retinal Nerve Fiber Layer (RNFL) using OCT in patients with TON. Materials and Methods: An observational prospective study was conducted in a tertiary care centre, including 29 TON patients. IV steroids, methylprednisolone was administered in indirect TON patients. RNFL was assessed using OCT on the day of discharge. Follow-up for one week and one month after discharge. Paired t-test/Wilcoxon sign rank test was applied to test the mean differences of the study. Results: Patients treated with IV, steroids showed significant improvement over time. Patients with just Perception of Light (PL) or Hand Movements (HM+) did not show much improvement. Another factor for visual recovery was timing of steroid administration. The time limit was within 24 hours after the injury before full-fledged inflammation sets in. RNFL study using OCT showed reductions in circumpapillary RNFL thickness and Retinal Ganglion Cell (RGC) complex began to decrease at two weeks after trauma and plateaued at 20 weeks in all cases. Conclusion: IV steroids can be considered as a treatment of TON rather than wait for spontaneous recovery. But baseline visual acuity played a crucial role in recovery. OCT is a useful follow-up tool to analyse axonal loss. But a standard protocol is still lacking.

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.

Traumatic optic neuropathy (TON) is the affectation of the visual function, secondary to a damage caused by a direct or indirect traumatic mechanism over the optic nerve. It occurs in approximately 0.5 to 5% of closed head injuries, and in 2.5% of patients with maxillofacial trauma and mid-face fractures. The types of TON are direct, anterior indirect, posterior indirect, and chiasmal. This work aims to offer an updating in traumatic optic neuropathy. We made a search in international data bases such as PubMed, ClinicalTrial, Ebsco, Hinari and so on, and found 32 articles which were used in this review article. We used the following keywords: traumatic optic neuropathy, optic nerve, trauma, visual loss, visual disease. 70% of the articles correspond to the last five years. This review was redacted using Microsoft Office Word 2016 in a laptop Asus with Window 10 system. We made a compilation with diverse therapeutic options based principally in axonal regeneration developed by researchers during the last decade. The present review article provides an updating regarding potential strategies for axonal regeneration and optic nerve repair, focusing on the researches of many investigators around the world. Nowadays, therapeutic options have advanced in many fields, but still more researches must be done to find a definitive solution for traumatic optic neuropathy in a near future. Key words: Traumatic optic neuropathy, optic nerve, trauma, visual loss, visual disease.

Key Clinical Message A tumor‐like condition of the optic nerve head of unknown etiology was found in a domestic pig. Clinical and histological manifestations suggest that the unusual tumor‐like condition is probably a variant of proliferative optic neuropathy caused by unknown nonspecific damage (perhaps trauma), which was received earlier.

The endoscopic transethmoidal approach is favored for the lack of external scars, a wide field of view, and rapid recovery time. But the effect of iatrogenic trauma should not be ignored due to the removal of the uncinate process and anterior and posterior ethmoidal sinus. Anatomically, the optic nerve is close to the sphenoid sinus and Onodi cell. In order to preserve the uncinate process and ethmoidal sinus, we perform endoscopic transsphenoidal optic canal decompression (ETOCD), which is less invasive. However, the anatomy of sphenoid sinus is quite variable, and the anatomical landmarks are rare. Therefore, identifying the position of optic canal is particularly important during surgery. To solve this, we use a postprocessing technique to identify the position of the optic nerve and internal carotid artery on the sphenoid sinus wall. Our results find that VA in 13 patients improved, with a total improve rate of 59.1%. No serious complications were found. We also found that the length of optic canal is different and the medial wall of the optic canal was the longest (p<0.05). The middle section of the optic canal is the narrowest, which was significantly different from cranial mouth and orbital mouth (p<0.05). We assumed that decompression may not require removal of all medial wall. If we remove the length of the shortest wall on the medial wall of the optic canal, the compression may be relieved. Thus, ETOCD was a feasible, safe, effective, and less-invasive approach for patients with TON. The CT postprocessing imaging facilitated recognition of the optic canal during surgery. The decompression length of the medial wall may not need to be completely removed, especially near the cranial mouth.

Traumatic visual pathway injuries are often associated with severe head trauma and can have profound deleterious effects in developing children and their rehabilitation. We sought to elucidate the epidemiology of pediatric visual pathway injuries in the United States.This study is a retrospective evaluation of pediatric patients (less than 21 years of age) with visual pathway injuries that were submitted to the National Trauma Data Bank between 2008 to 2014. Patients were identified using the International Classification of Diseases, Ninth Revision Clinical Modification codes. Statistical analysis was performed with SPSS software. Variables were correlated using Student t test, chi-squared test, and logistic regression analyses.Of the 58,765 pediatric patients (1.7%) who were admitted with ocular injuries, 970 had visual pathway injuries. The majority of these patients were male (69.2%), and the mean age was 11.6 years (±7.2). Traumatic optic neuropathy was the most common (86.1%) visual pathway injury. It had the greatest odds of occurring with oculomotor nerve injury (odds ratio = 3.84; P 0.001). Associated ocular injuries were open adnexal wounds (87.4%) and orbital fractures (23%). Common mechanisms were motor vehicle occupant (21.5%) and firearms (15.6%). Motor vehicle occupants were most likely white and firearms injury, black. In the zero to three years age group, most injuries were due to falls; injuries in the 19 to 21 years age group had the greatest association with firearms. Overall mortality was 17.6%.Visual pathway injuries may have devastatating sequelae and should be considered in pediatric ocular injuries. The clear majority were traumatic optic neuropathies. The common mechanisms, motor vehicle occupant and firearms, revealed age and race disparities.

Background The optimal management of indirect traumatic optic neuropathy (TON) is controversial. We aimed to compare the differences in visual improvement by treatment option in patients presenting with TON and no light perception (NLP). We also wanted to identify any patient-related factors that might favor the use of steroid pulse therapy or optic nerve decompression (OND). Methods We retrospectively identified 46 consecutive patients with indirect TON treated at Chang Gung Memorial Hospital between 2007 and 2015. The outcome was the improvement in visual acuity by improvement rate and degree of improvement. Results Females had a better improvement rate than did males. Compared with delayed treatment, patients receiving steroid pulse therapy within 14 hours or receiving OND within 26 hours had a better improvement rate/degree. In patients with an initial intraocular pressure (IOP) of 17–23 mm Hg, the improvement rate/degree was significantly better than for patients with an IOP outside this range. For patients treated by OND, an initially normal IOP (11–21 mm Hg) suggested a significantly better prognosis in the improvement rate/degree. Conclusions For patients with indirect TON, initial NLP implies a poor prognosis, but steroid pulse therapy or OND are both feasible treatment options. These results emphasize the importance of timely treatment for patients with indirect TON and NLP. Females and patients with an initial IOP of 17–23 mm Hg were more likely to recover. The results of our study indicate that normal initial IOP (11–21 mm Hg) is good prognostic factor for patients with indirect TON treated with OND.