Optic Nerve MRI T2-Hyperintensity: A Nonspecific Marker of Optic Nerve Damage.

BACKGROUND: MRI abnormalities are common in optic neuropathies, especially on dedicated orbital imaging. In acute optic neuritis, optic nerve T2-hyperintensity associated with optic nerve contrast enhancement is the typical imaging finding. In chronic optic neuropathies, optic nerve T2-hyperintensity and atrophy are regularly seen. Isolated optic nerve T2-hyperintensity is often erroneously presumed to reflect optic neuritis, frequently prompting unnecessary investigations and neuro-ophthalmology consultations. Our goal was to determine the significance of optic nerve/chiasm T2-hyperintensity and/or atrophy on MRI. METHODS: Retrospective study of consecutive patients who underwent brain/orbital MRI with/without contrast at our institution between July 1, 2019, and June 6, 2022. Patients with optic nerve/chiasm T2-hyperintensity and/or atrophy were included. Medical records were reviewed to determine the etiology of the T2-hyperintensity and/or atrophy. RESULTS: Four hundred seventy-seven patients (698 eyes) were included [mean age 52 years (SD ±18 years); 57% women]. Of the 364 of 698 eyes with optic nerve/chiasm T2-hyperintensity without atrophy, the causes were compressive (104), inflammatory (103), multifactorial (49), glaucoma (21), normal (19), and other (68); of the 219 of 698 eyes with optic nerve/chiasm T2-hyperintensity and atrophy, the causes were compressive (57), multifactorial (40), inflammatory (38), glaucoma (33), normal (7), and other (44); of the 115 of 698 eyes with optic nerve/chiasm atrophy without T2-hyperintensity, the causes were glaucoma (34), multifactorial (21), inflammatory (13), compressive (11), normal (10), and other (26). Thirty-six eyes with optic nerve/chiasm T2-hyperintensity or atrophy did not have evidence of optic neuropathy or retinopathy on ophthalmologic examination, and 17 eyes had clinical evidence of severe retinopathy without primary optic neuropathy. CONCLUSIONS: Optic nerve T2-hyperintensity or atrophy can be found with any cause of optic neuropathy and with severe chronic retinopathy. These MRI findings should not automatically prompt optic neuritis diagnosis, workup, and treatment, and caution is advised regarding their use in the diagnostic criteria for multiple sclerosis. Cases of incidentally found MRI optic nerve T2-hyperintensity and/or atrophy without a known underlying optic neuropathy or severe retinopathy are rare. Such patients should receive an ophthalmologic examination before further investigations.

Case Report: Indirect Traumatic Optic Neuropathy from Subconcussive Soccer Headers in a 62-year-old Athlete.

SIGNIFICANCE: Traumatic optic neuropathy is an uncommon but devastating cause of vision loss after injury to the head. Soccer players may have a heightened risk because of the game's emphasis on heading the ball, a technique in which a player hits the soccer ball with his/her head. PURPOSE: This article reviews the case of an avid soccer player with traumatic optic neuropathy that occurred after numerous soccer ball headings during a game. This article also (1) provides a summary of the pathophysiology and epidemiology of traumatic optic neuropathy, (2) reviews the current literature on head and eye injuries in soccer, and (3) discusses biomechanical differences in orbital structure throughout aging, which may predispose older patients to traumatic optic neuropathy. CASE REPORT: We present the case of a 62-year-old male patient who reported to the clinic, after repeated subconcussive soccer ball headers the previous day, with symptoms of blurred vision and "seeing stars" in the right eye and a right inferior visual field impairment. Physical examination, subsequent laboratory work, and neurologic consults implicated traumatic optic neuropathy as the primary diagnosis, and halting soccer playing resulted in symptom improvement. CONCLUSIONS: Although not commonly encountered in soccer players, the potential for traumatic optic neuropathy exists. Older athletes may be predisposed because of morphological changes of the orbit. Future direction may look to further investigate hazards promoting traumatic optic neuropathy in older athletes and determine possible protections against injury.

Secondary Degeneration Impairs Myelin Ultrastructural Development in Adulthood following Adolescent Neurotrauma in the Rat Optic Nerve.

Adolescence is a critical period of postnatal development characterized by social, emotional, and cognitive changes. These changes are increasingly understood to depend on white matter development. White matter is highly vulnerable to the effects of injury, including secondary degeneration in regions adjacent to the primary injury site which alters the myelin ultrastructure. However, the impact of such alterations on adolescent white matter maturation is yet to be investigated. To address this, female piebald-virol-glaxo rats underwent partial transection of the optic nerve during early adolescence (postnatal day (PND) 56) with tissue collection two weeks (PND 70) or three months later (PND 140). Axons and myelin in the transmission electron micrographs of tissue adjacent to the injury were classified and measured based on the appearance of the myelin laminae. Injury in adolescence impaired the myelin structure in adulthood, resulting in a lower percentage of axons with compact myelin and a higher percentage of axons with severe myelin decompaction. Myelin thickness did not increase as expected into adulthood after injury and the relationship between the axon diameter and myelin thickness in adulthood was altered. Notably, dysmyelination was not observed 2 weeks postinjury. In conclusion, injury in adolescence altered the developmental trajectory, resulting in impaired myelin maturation when assessed at the ultrastructural level in adulthood.

Magnetization transfer saturation reveals subclinical optic nerve injury in pediatric-onset multiple sclerosis.

BACKGROUND: The presence of subclinical optic nerve (ON) injury in youth living with pediatric-onset MS has not been fully elucidated. Magnetization transfer saturation (MTsat) is an advanced magnetic resonance imaging (MRI) parameter sensitive to myelin density and microstructural integrity, which can be applied to the study of the ON. OBJECTIVE: The objective of this study was to investigate the presence of subclinical ON abnormalities in pediatric-onset MS by means of magnetization transfer saturation and evaluate their association with other structural and functional parameters of visual pathway integrity. METHODS: Eleven youth living with pediatric-onset MS (ylPOMS) and no previous history of optic neuritis and 18 controls underwent standardized brain MRI, optical coherence tomography (OCT), Magnetoencephalography (MEG)-Visual Evoked Potentials (VEPs), and visual battery. Data were analyzed with mixed effect models. RESULTS: While ON volume, OCT parameters, occipital MEG-VEPs outcomes, and visual function did not differ significantly between ylPOMS and controls, ylPOMS had lower MTsat in the supratentorial normal appearing white matter (-0.26 nU, p = 0.0023), and in both in the ON (-0.62 nU, p < 0.001) and in the normal appearing white matter of the optic radiation (-0.56 nU, p = 0.00071), with these being positively correlated (+0.57 nU, p = 0.00037). CONCLUSIONS: Subclinical microstructural injury affects the ON of ylPOMS. This may appear as MTsat changes before being detectable by other currently available testing.

Sheath-Preserving Complete Optic Nerve Avulsion Following Closed-Globe Injury: A Case Report.

A 29-year-old man presented with a sudden loss of vision after a closed-globe injury. At presentation, he had no light perception in the right eye and the right pupil was dilated and nonreactive to light. On ophthalmological examination, the area of the optic nerve head was excavated, suggesting optic nerve avulsion. Magnetic resonance imaging scan showed optic nerve avulsion without rupture of the optic nerve sheath. Four months after the injury, the patient's visual acuity remained unchanged. Gliosis developed at the avulsion site. Closed-globe injuries may cause severe posterior injury even if there is no anterior damage in the eye. To prevent unnecessary treatment, trauma patients should be examined carefully appropriate imaging to confirm the diagnosis.

Vision improvement in indirect traumatic optic neuropathy treated by endoscopic transnasal optic canal decompression.

BACKGROUND: Indirect Traumatic optic neuropathy (ITON) is a severe disease characterized by a sudden decline of visual function after craniofacial injury. However, the best treatment for ITON is unknown. Endoscopic transnasal optic canal decompression (ETOCD) has gradually been used for ITON treatment worldwide in recent years. OBJECTIVE: To assess the effect of ETOCD on visual acuity in patients with ITON and identify factors that affect prognosis. METHODS: In this study, clinical characteristics of 44 ITON patients who underwent ETOCD in Qilu Hospital of Shandong University were retrospectively analyzed. Factors affecting prognosis were also evaluated. RESULTS: ETOCD treatment improved the vision of 20 (45.5%) patients with no patient suffering from vision deterioration. The mean value of visual acuity (VA) scores improved from 1.57 to 2.39 (P < 0.001). Patients with residual vision had a better VA improvement percent than those without light perception (66.67% versus 34.48%, χ2 = 4.13, P = 0.042). Although shorter duration before ETOCD was associated with better improvement score in ITON patients (r = -0.30, P = 0.044), optic canal fracture (OCF) and optic nerve sheath incision did not affect the prognosis of these patients. Five ITON patients with cerebrospinal fluid rhinorrhea were treated with free nasal mucosal flap during the surgery, and no other severe surgical complication occurred. CONCLUSIONS: ETOCD can effectively and safely improve the vision of ITON patients, patients with residual vision and those treated earlier may benefit more from this surgery.

Traumatic Brain Injury-Related Optic Nerve Damage.

Vision disorders are associated with traumatic brain injury (TBI) in 20%-40% of clinical cases and involve a diverse set of potential symptoms that can present acutely or chronically. Due to its structure and position, the optic nerve is vulnerable to multiple forms of primary injury, which can result in traumatic optic neuropathy (TON). Multiple studies have shown that the optic tract may also be injured during TBI, though data regarding the temporospatial resolution of injury to the optic nerve are sparse. We evaluated the time course of optic nerve injury and visual impairments in our closed head impact acceleration mouse model of mild TBI (mTBI) designed to mimic repetitive injuries experienced in the context of sport. Our results show that inflammation and gliosis occur acutely in response to injury. Additionally, indications of optic nerve degeneration and functional loss of vision beginning at 1-month postinjury, and retinal ganglion cell loss at 7 months, revealed that the degeneration is continuous and permanent. Together, this study demonstrated that the optic nerve is vulnerable to damage during mTBI, which can cause TON and vision loss. These findings will be important for clinicians to consider to determine whether optic nerve is injured in the TBI patients with vision problems.

Progression of optic atrophy in traumatic optic neuropathy: retrograde neuronal degeneration in humans.

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.

Contralateral field defect in traumatic globe luxation with optic nerve injury.

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

Optic nerve injury in preoperative imaging is associated with visual improvement outcome in endoscopic optic nerve decompression.

OBJECTIVE: To evaluate potential clinical parameters having an impact on visual outcome after endoscopic optic nerve decompression in acute optic neuropathy patients. METHODS: A retrospective chart review of patients with acute optic neuropathy, who underwent endoscopic optic nerve decompression between June 2001 and November 2018 at an academic center was performed. Patients were divided into groups according to visual improvement after surgical treatment (yes/no). Following clinical parameters were compared between groups: perioperative steroid use, evidence of optic nerve affection in preoperative neuroimaging, additional optic nerve sheath incision, surgery delay and preoperative C-reactive protein (CRP) levels. Further subgroups analyses were conducted based on etiology (trauma/tumor). RESULTS: Among 32 included cases, 16 patients (50%) reported visual improvement after endoscopic optic nerve decompression. There was no significant difference in visual improvement between etiology subgroups (trauma: n = 9/20 (45%) vs. tumor: n = 7/12 (58.3%), p = 0.465). Tumor subgroup patients with visual improvement had a significantly higher prevalence of optic nerve affection in preoperative neuroimaging than those without visual improvement (p = 0.018, φ = 0.683). Perioperative steroid administration was negatively associated with visual outcome (p = 0.034, φ = 0.375). Nerve sheath incision, surgery delay and preoperative CRP levels did not have a significant impact on visual outcome (p > 0.05). CONCLUSION: Radiological findings can help as an indicator for surgical treatment since an affected optic nerve in preoperative neuroimaging resulted in better visual outcome after surgery. The use of steroids should be considered more carefully since it did not show any beneficial effect.

Chronic Histological Outcomes of Indirect Traumatic Optic Neuropathy in Adolescent Mice: Persistent Degeneration and Temporally Regulated Glial Responses.

Injury to the optic nerve, termed, traumatic optic neuropathy (TON) is a known comorbidity of traumatic brain injury (TBI) and is now known to cause chronic and progressive retinal thinning up to 35 years after injury. Although animal models of TBI have described the presence of optic nerve degeneration and research exploring acute mechanisms is underway, few studies in humans or animals have examined chronic TON pathophysiology outside the retina. We used a closed-head weight-drop model of TBI/TON in 6-week-old male C57BL/6 mice. Mice were euthanized 7-, 14-, 30-, 90-, and 150-days post-injury (DPI) to assess histological changes in the visual system of the brain spanning a total of 12 regions. We show chronic elevation of FluoroJade-C, indicative of neurodegeneration, throughout the time course. Intriguingly, FJ-C staining revealed a bimodal distribution of mice indicating the possibility of subpopulations that may be more or less susceptible to injury outcomes. Additionally, we show that microglia and astrocytes react to optic nerve damage in both temporally and regionally different ways. Despite these differences, astrogliosis and microglial changes were alleviated between 14-30 DPI in all regions examined, perhaps indicating a potentially critical period for intervention/recovery that may determine chronic outcomes.

Differential Retinal Protein Expression in Primary and Secondary Retinal Ganglion Cell Degeneration Identified by Integrated SWATH and Target-Based Proteomics.

To investigate the retinal proteins associated with primary and secondary retinal ganglion cell (RGC) degeneration and explore their molecular pathways, SWATH label-free and target-based mass spectrometry was employed to identify the proteomes in various retinal locations in response to localized optic nerve injury. Unilateral partial optic nerve transection (pONT) was performed on adult Wistar rats and their retinas were harvested 2 weeks later. To confirm the separation of primary and secondary RGC degeneration, immunohistochemistry of RNA binding protein with multiple splicing (RBPMS) and glial fibrillary acidic protein (GFAP) was performed on retinal whole-mounts. Retinal proteomes in the temporal and nasal quadrants were evaluated with high resolution hybrid quadrupole time-of-flight mass spectrometry (QTOF-MS), and SWATH-based acquisition, and their expression was compared to the corresponding retinal quadrant in contralateral control eyes and further validated by multiple reaction monitoring mass spectrometry (MRM-MS). A total of 3641 proteins (FDR < 1%) were identified using QTOF-MS. The raw data are available via ProteomeXchange with the identifier PXD026783. Bioinformatics data analysis showed that there were 37 upregulated and 25 downregulated proteins in the temporal quadrant, whereas 20 and five proteins were upregulated and downregulated, respectively, in the nasal quadrant, respectively (n = 4, p < 0.05; fold change ≥ 1.4-fold or ≤0.7). Six proteins were regulated in both the temporal and the nasal quadrants, including CLU, GFAP, GNG5, IRF2BPL, L1CAM, and CPLX1. Linear regression analysis indicated a strong association between the data obtained by means of SWATH-MS and MRM-MS (temporal, R2 = 0.97; nasal, R2 = 0.96). Gene ontology analysis revealed statistically significant changes in the biological processes and cellular components of primary RGC degeneration. The majority of the significant changes in structural, signaling, and cell death proteins were associated with the loss of RGCs in the area of primary RGC degeneration. The combined use of SWATH-MS and MRM-MS methods detects and quantifies regional changes of retinal protein expressions after localized injury. Future investigation with this integrated approach will significantly increase the understanding of diverse processes of progressive RGC degeneration from a proteomic prospective.

Nursing Research of Optic Canal Decompression Operation under Nasal Endoscopic Medical Treatment Based on Intelligent Internet of Things for Traumatic Vision Disorders.

Traumatic vision is an important factor that causes people to have a vision. In our country, the vast majority of vision is caused by trauma. To understand the role of optic nerve decompression in the treatment of traumatic visual disturbances based on the pathological states of traumatic visual disturbances and intelligent Internet of tumors medical nasal endoscopy optic nerve decompression. This article collects relevant information by investigating patients, investigating relevant literature, interviewing professionals, etc., constructing a case template and using a comprehensive quantitative and qualitative analysis method to create a damage assessment matrix. The results of the study found that most traumatic vision disorders occur in the young and middle-aged stage, which is more than three times that of other age groups. The permanent blindness rate of patients reaches 8%, which is extremely harmful. Optic canal decompression surgery can play a great role in the treatment of patients. It can greatly reduce the patient's neurological damage. The effect is about 30% higher than that of general treatment methods, and it can also play a certain role in the prognosis of rehabilitation. It can effectively prevent related postoperative complications. This shows that optic canal decompression in the treatment of traumatic vision disorders should attract people's attention and increase research and development efforts and promotion efforts so that optic canal decompression can be used in the diagnosis and treatment of patients with traumatic vision disorders based on smart Internet of things China can play a greater role.

Traumatic Optic Neuropathy Is Associated with Visual Impairment, Neurodegeneration, and Endoplasmic Reticulum Stress in Adolescent Mice.

Traumatic brain injury (TBI) results in a number of impairments, often including visual symptoms. In some cases, visual impairments after head trauma are mediated by traumatic injury to the optic nerve, termed traumatic optic neuropathy (TON), which has few effective options for treatment. Using a murine closed-head weight-drop model of head trauma, we previously reported in adult mice that there is relatively selective injury to the optic tract and thalamic/brainstem projections of the visual system. In the current study, we performed blunt head trauma on adolescent C57BL/6 mice and investigated visual impairment in the primary visual system, now including the retina and using behavioral and histologic methods at new time points. After injury, mice displayed evidence of decreased optomotor responses illustrated by decreased optokinetic nystagmus. There did not appear to be a significant change in circadian locomotor behavior patterns, although there was an overall decrease in locomotor behavior in mice with head injury. There was evidence of axonal degeneration of optic nerve fibers with associated retinal ganglion cell death. There was also evidence of astrogliosis and microgliosis in major central targets of optic nerve projections. Further, there was elevated expression of endoplasmic reticulum (ER) stress markers in retinas of injured mice. Visual impairment, histologic markers of gliosis and neurodegeneration, and elevated ER stress marker expression persisted for at least 30 days after injury. The current results extend our previous findings in adult mice into adolescent mice, provide direct evidence of retinal ganglion cell injury after head trauma and suggest that axonal degeneration is associated with elevated ER stress in this model of TON.

Outcome of the surgical decompression for traumatic optic neuropathy: a systematic review and meta-analysis.

There exists a persisting controversy regarding the indications for optic nerve surgical decompression (ONSD) in traumatic optic neuropathy (TON). A meta-analysis is warranted to help guiding therapeutic decisions and address gaps in knowledge. The authors conducted a search of PubMed and MEDLINE electronic databases. Primary endpoint was the improvement in the visual function with ONSD in comparison with the conservative management. Secondary endpoint was visual function improvement when surgery was performed within the first 7 days. A random effects model meta-analysis was conducted. Data from each study were used to generate log odds ratio and 95% confidence intervals, to compare post-operative visual improvement. Nine studies met the inclusion criteria for analysis, comprising 766 patients. Visual improvement occurred in 55% (198/360) of patients treated with ONSD, and in 40% (164/406) of those who underwent conservative treatment. Forest plot revealed significant differences in the visual function improvement among these two groups, although further analysis revealed the studies were heterogeneous (log OR, 0.81; CI, 0.07-1.55; I2, 62.8% p = 0.015). Overall, patients who underwent early surgery had better visual outcomes (log OR, 0.94; CI, 0.29-1.60; I2, 0% p = 0.9). ONSD is an effective technique to improve the outcome in the visual function in patients with TON. A lack of randomized controlled trial-and inherent surgical selection and publication bias-limits direct comparison between surgical decompression and conservative management. Suitably designed prospective cohort studies may be useful in identifying patients more likely to receive benefit from ONSD.

CT Features of Posttraumatic Vision Loss.

Clinical evaluation of patients with trauma is challenging, especially in the presence of neurologic injuries. Vision loss after trauma is a harmful and usually overlooked consequence that may be avoided with a prompt and accurate intervention. Head CT is commonly performed in patients with trauma. However, radiologists may be unfamiliar with the CT findings associated with injuries that may affect eyesight. Understanding the visual pathway anatomy and its critical landmarks is paramount for recognizing these findings. This article describes the use of head CT to evaluate the visual pathway to help avoid vision loss in patients with trauma. Injuries are presented in terms of those affecting the globe (rupture, hemorrhage, and lens trauma), optic nerve (direct and indirect traumatic optic neuropathy), orbit (orbital compression syndrome), and vasculature (traumatic carotid-cavernous sinus fistula and posterior cerebral artery injury or ischemia). Techniques for measuring the globe on CT to assess for injury are illustrated. Indications for screening CTA of the head and neck in patients with suspicion for blunt traumatic vascular injury are summarized. Emphasis is placed on the CT findings that warrant an emergency intervention to prevent traumatic visual impairment.

Combination analysis on the impact of the initial vision and surgical time for the prognosis of indirect traumatic optic neuropathy after endoscopic transnasal optic canal decompression.

To analyze the impact of the initial vision and surgical time for endoscopic transnasal/transethmosphenoid optic canal decompression (ETOCD) in the treatment of indirect traumatic optic neuropathy (TON). This retrospective case series analysis included 72 patients with indirect TON who underwent ETOCD from August 2017 to May 2019. Visual acuity (VA) was compared before and after surgery to estimate the improvement rate. The overall VA improvement rate of ETOCD was 54.2%. There were 83.3% and 33.3% improvement rate of patients with residual vision and blindness, respectively. VA was improved in 60.9% of patients treated within 3 days, 61.5% treated within 7 days, and 35.0% treated later than 7 days. Of the blindness patients, 50.0%, 37.5%, and 0.0% were treated within 3 days, 3-7 days, and later than 7 days, respectively. Of patients with residual vision, 85.7%, 92.3%, and 70.0% were treated within 3 days, 3-7 days, and later than 7 days, respectively. A statistically significant difference was found between patients with residual vision and those with blindness (P < 0.01), as well as between patients who received ETOCD within 7 days and those who received ETOCD later than 7 days (P = 0.043). The improvement rate of blindness patients managed within 3 days (P = 0.008) and 3-7 days (P = 0.035) was significantly higher than that for patients managed beyond 7 days. Indirect TON patients can directly benefit from ETOCD, and patients with residual vision have better improvement rates. ETOCD should be performed as soon as possible to salvage the patient's VA, especially within the first 7 days. For blindness patients, it is necessary to carry out the surgery within 7 days with increased benefit seen before 3 days.

Traumatic Globe Subluxation Accompanied by Traumatic Optic Neuropathy.

A 52-year-old, alcohol-intoxicated woman suffered periorbital trauma to the left eye and presented to the emergency department with proptosis and complaints of decreased vision in the left eye. Physical examination revealed loss of light perception (LP), relative afferent pupillary defect (RAPD), pupil dilatation, and corneal epithelial defect of the left eye. In addition, the fundus of the left eye was not easily visible due to severe corneal abrasion and edema, but there was no retinal detachment or vitreous hemorrhage on B-scan ultrasonography. Hertel exophthalmometric values differed by 7 mm between the eyes and measured 13 mm in the right eye and 20 mm in the left eye. In addition, she had severely limited left eye movement in all directions. Computerized tomography (CT) imaging of the orbit showed that the left optic nerve extended 15 mm further than the optic nerve of the right eye and retrobulbar hemorrhage of the left eye. The patient underwent emergency lateral canthotomy, cantholysis, and conjunctival incision to release the optic nerve extension and reduce the eyeball subluxation of the left eye. An intraoperative examination demonstrated that all extraocular muscles of the left eye were intact. The left eyeball returned to its normal position after surgery. Two days after surgery, proptosis of the left eye improved significantly, and there was no difference in Hertel exophthalmometric values between the eyes, both eyes measured 13 mm. However, the patient continued to suffer LP, RAPD, and pupil dilatation of the left eye.

Acute monocular nasal hemianopia following a mild traumatic brain injury: A case report.

INTRODUCTION: Monocular hemianopia is a visual field defect with an uncommon pattern. The etiology of monocular temporal hemianopia has been well-evaluated and has been suggested to result from an optic nerve or chiasmal lesion. However, the etiology of monocular nasal hemianopia remains unclear. PATIENT CONCERNS: Here, we present the case of a 41-year-old male who was punched on the head with fists during a fight and then suffered from painless blurred vision in the left eye after mild traumatic brain injury. An ophthalmic examination revealed a conjunctival chemosis, periorbital hematoma, and a relative afferent pupillary defect in the left eye. Automated perimetry indicated there was a left side nasal hemianopia along the vertical meridian. DIAGNOSIS: Examination of the fundus showed there was a normal appearing retina and disc bilaterally. Fluorescein angiography revealed no delayed filling of the vessels. Computed tomography and magnetic resonance imaging showed unremarkable findings of the visual pathways, orbit, and brain. A diagnosis of left traumatic optic neuropathy was made. INTERVENTIONS: Systemic steroid pulse therapy (1 gram of intravenous methylprednisolone per day) was given to the patient for 3 days. OUTCOMES: An ophthalmologic examination after treatment indicated there was no obvious improvement in the relative afferent pupillary defect, best corrected visual acuity, and color sense. A second set of automated perimetry results showedno changes after 3 months. CONCLUSION: Monocular nasal hemianopia caused by traumatic optic neuropathy is uncommon. In this case, monocular nasal hemianopia was likely due to ischemic changes from impairment of the prechiasmal arterial anastomotic network or indirect injury to the lateral prechiasmal nerve fiber.