Indirect Traumatic Optic Neuropathy Research Articles

Indirect Traumatic Optic Neuropathy with Associated Charles Bonnet Syndrome

Indirect Traumatic Optic Neuropathy with Associated Charles Bonnet Syndrome

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.

Effects of intravitreal injection of siRNA against caspase-2 on retinal and optic nerve degeneration in air blast induced ocular trauma

Ocular repeated air blast injuries occur from low overpressure blast wave exposure, which are often repeated and in quick succession. We have shown that caspase-2 caused the death of retinal ganglion cells (RGC) after blunt ocular trauma. Here, we investigated if caspase-2 also mediates RGC apoptosis in a mouse model of air blast induced indirect traumatic optic neuropathy (b-ITON). C57BL/6 mice were exposed to repeated blasts of overpressure air (3 × 2 × 15 psi) and intravitreal injections of siRNA against caspase-2 (siCASP2) or against a control enhanced green fluorescent protein (siEGFP) at either 5 h after the first 2 × 15 psi (“post-blast”) or 48 h before the first blast exposure (“pre-blast”) and repeated every 7 days. RGC counts were unaffected by the b-ITON or intravitreal injections, despite increased degenerating ON axons, even in siCASP2 “post-blast” injection groups. Degenerating ON axons remained at sham levels after b-ITON and intravitreal siCASP2 “pre-blast” injections, but with less degenerating axons in siCASP2 compared to siEGFP-treated eyes. Intravitreal injections “post-blast” caused greater vitreous inflammation, potentiated by siCASP2, with less in “pre-blast” injected eyes, which was abrogated by siCASP2. We conclude that intravitreal injection timing after ocular trauma induced variable retinal and ON pathology, undermining our candidate neuroprotective therapy, siCASP2.

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

We used optical coherence tomography (OCT) to document the time course of retrograde neuronal degeneration following indirect optic nerve injury. 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 1day and at 1, 2, 3, 4, 6, 8, 12, 24, and 48weeks after trauma. The mean thicknesses of the circumpapillary retinal nerve fiber layer (cpRNFL) and macular retinal ganglion cell-inner plexiform layer (mGCIPL) decreased significantly at 2weeks 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 4weeks and 4 to 6weeks after trauma. The reduction in mGCIPL thickness then slowed, and stabilized at 12weeks after trauma. The proportions of cpRNFL and mGCIPL losses at 2, 4, 6, 8, and 12weeks compared to 24weeks 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. OCT revealed optic atrophy progression 2weeks after trauma, which was most rapid from 2 to 6weeks, 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.

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.

The retinal vasculature pathophysiological changes in vision recovery after treatment for indirect traumatic optic neuropathy patients

PurposeTo evaluate the retinal vasculature pathophysiological changes of indirect traumatic optic neuropathy (ITON) patients after effective surgery.MethodsMonocular ITON patients who underwent endoscopic trans-ethmosphenoid optic canal decompression (ETOCD) or conservative treatments in Zhongshan Ophthalmic Center from January 2017 to June 2020 were recruited. Visual acuity (VA), visual evoked potential (VEP), oxygen saturation of retinal blood vessels (SO2), and optical coherence tomography angiography (OCT-A) were measured. All patients were followed up at least 3 months after treatments.ResultsA total of 95 ITON patients were recruited, including 77 patients who underwent ETOCD and 18 patients who underwent conservative treatments. After treatments, more patients received ETOCD (59/77 = 76.6%) presented with improved VA compared with the patients with conservative treatments (6/18 = 33.3%). Compared with the pre-therapeutic measurements, VEP were significantly improved after surgery in ETOCD-treated patients (P < 0.05). Latent periods of P1 and N2, as well as amplitude of P2 of VEP parameters, showed more sensitive to vision recovery (P < 0.05). Retinal artery SO2 and the differences between arteries and veins were improved in ETOCD-treated patients (P < 0.05). Meanwhile, with OCT-A examination, the retinal thickness and retinal vessel density were notably better in ETOCD-treated patients after surgery than that in patients received conservative treatments (P < 0.05).ConclusionsVision recovery after effective treatment of ITON patients was associated with the increased oxygen saturation of retinal vessels, better availability of oxygen in the retina, greater vessel density, and thicker retinas, which might further underlie the vasculature mechanism of vision recovery in ITON patients.

The Role of the Flash Visual Evoked Potential in Evaluating Visual Function in Patients with Indirect Traumatic Optic Neuropathy.

PurposeTo 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 MethodsWe 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.ResultsThe 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.ConclusionCases 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.

A Systematic Literature Review on Traumatic Optic Neuropathy.

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.

Intravitreal injection worsens outcomes in a mouse model of indirect traumatic optic neuropathy from closed globe injury

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

Interventions for Indirect Traumatic Optic Neuropathy: A Report by the American Academy of Ophthalmology

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 metall 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.

JNK/c-Jun-driven NLRP3 inflammasome activation in microglia contributed to retinal ganglion cells degeneration induced by indirect traumatic optic neuropathy

BackgroundIndirect traumatic optic neuropathy (ITON) is a major cause of permanent loss of vision after blunt head trauma. Neuroinflammation plays a crucial role in neurodegenerative diseases. The present study concentrated on JNK/c-Jun-driven NLRP3 inflammasome activation in microglia during the degeneration of retinal ganglion cells (RGCs) in ITON. MethodsAn impact acceleration (IA) model was employed to induce ITON, which could produce significant neurodegeneration in the visual system. Pharmacological approaches were employed to disrupt JNK and to explore whether JNK and the microglial response contribute to RGC death and axonal degeneration. ResultsOur results indicated that the ITON model induced significant RGC death and axonal degeneration and activated JNK/c-Jun signaling, which could further induce the microglial response and NLRP3 inflammasome activation. Moreover, JNK disruption is sufficient to suppress NLRP3 inflammasome activation in microglia and to prevent RGC death and axonal degeneration. ConclusionsITON could promote JNK/c-Jun signaling, which further activates the NLRP3 inflammasome in microglia and contributes to the degeneration of axons and death of RGCs. JNK inhibition is able to suppress the inflammatory reaction and improve RGC survival. Although further work is needed to determine whether pharmacological inhibition of the NLRP3 inflammasome can prevent ITON, our findings indicated that such intervention could be promising for translational work.

Treatment of Optic Canal Decompression Combined with Umbilical Cord Mesenchymal Stem (Stromal) Cells for Indirect Traumatic Optic Neuropathy: A Phase 1 Clinical Trial

Purpose: This study was aimed to investigate the safety and feasibility of umbilical cord-derived mesenchymal stem cell (MSC) transplantation in patients with traumatic optic neuropathy (TON). Methods: This is a single-center, prospective, open-labeled phase 1 study that enrolled 20 patients with TON. Patients consecutively underwent either optic canal decompression combined with MSC local implantation treatment (group 1) or only optic canal decompression (group 2). Patients were evaluated on the first day, seventh day, first month, third month, and sixth month postoperatively. Adverse events, such as fever, urticarial lesions, nasal infection, and death, were recorded at each visit. The primary outcome was changes in best-corrected visual acuity. The secondary outcomes were changes in color vision, relative afferent pupillary defect, and flash visual evoked potential. Results: All 20 patients completed the 6-month follow-up. None of them had any systemic or ocular complications. The change in best-corrected visual acuity at follow-up was not significantly different between group 1 and group 2 (p > 0.05); however, group 1 showed better visual outcome than group 2. Both groups showed significant improvements in vision compared with the baseline (p < 0.05); however, there were no statistically significant differences between the groups (p > 0.05). In addition, no adverse events related to local transplantation were observed in the patients. Conclusions: A single, local MSC transplantation in the optic nerve is safe for patients with TON.

Microsphere antioxidant and sustained erythropoietin-R76E release functions cooperate to reduce traumatic optic neuropathy

Wild-type erythropoietin (EPO) is promising for neuroprotection, but its therapeutic use is limited because it causes a systemic rise in hematocrit. We have developed an EPO-R76E derivative that maintains neuroprotective function without effects on hematocrit, but this protein has a short half-life in vivo. Here, we compare the efficacy and carrier-induced inflammatory response of two polymeric microparticle (MP) EPO-R76E sustained release formulations based on conventional hydrolytically degradable poly(lactic-co-glycolic acid) (PLGA) and reactive oxygen species (ROS)-degradable poly(propylene sulfide) (PPS). Both MP types effectively loaded EPO-R76E and achieved sustained release, providing detectable levels of EPO-R76E at the injection site in the eye in vivo for at least 28 days. Testing in an in vitro oxidative stress assay and a mouse model of blast-induced indirect traumatic optic neuropathy (bITON) showed that PPS and PLGA MP-mediated delivery of EPO-R76E provided therapeutic protection. While unloaded PLGA MPs inherently increase levels of pro-inflammatory cytokines in the bITON model, drug-free PPS MPs have innate antioxidant properties that provide therapeutic benefit both in vitro and in vivo. Both PLGA and PPS MPs enabled sustained release of EPO-R76E, providing therapeutic benefits including reduction in inflammation and axon degeneration, and preservation of visual function as measured by electroretinogram. The PPS-based MP platform is especially promising for further development, as the delivery system provides inherent antioxidant benefits that can be harnessed to work in complement with EPO-R76E or other drugs for neuroprotection in the setting of traumatic eye injury.

Traumatic Brain Injury: a Case Report and Its Contribution to Understanding the Underlying Mechanisms - Alpha-Emitting Nanoparticulates Proven as Key

This case report on a mild traumatic brain injury (self-diagnosis of the author on his own brain) leads to alpha-emitting nanoparticulates whose major contribution to TBI is confirmed by the extremely strong occurrence of TBIs in war veterans (with wideranging administrative data available to confirm the extremely strong typicality of the case). This allows a better and clearer understanding of the secondary injury events following TBI such as blood-brain barrier damage, mitochondria dysfunction and massive neuron death, of the various neurodegenerative disorders usually diagnosed following TBI such as chronic traumatic encephalopathy, chronic traumatic brain inflammation and indirect traumatic optic neuropathy, and of the risks of ischemic stroke following TBI.

FACTORS AFFECTING VISUAL OUTCOME IN INDIRECT TRAUMATIC OPTIC NEUROPATHY – A RETROSPECTIVE NON-RANDOMIZED STUDY

Purpose To study the demographic profile and factors associated with visual outcome in patients with indirect traumatic optic neuropathy. Methods A retrospective study of patients admitted with indirect traumatic optic neuropathy, in a tertiary care centre in South India, from February 2016 to February 2018 was conducted. Patients with bony impingement on the optic nerve were treated with endoscopic surgical decompression and the rest were treated with low dose steroids. Visual acuity was assessed at presentation, 2 weeks and 3 months. Results The mean age of the patients was 31.6 years (13-75 years). 19(90.4%) patients were male and road traffic accident (95.23%) was the most common cause of injury. Mean time of presentation was 3.6 hours ( 1-7 hours) Vision at presentation was perception of light and above in 8(3.1%) and no perception of Light in 13(61.9%) patients. Visual improvement was seen in 4 out of 18 patients (22.2%) in the steroid group and 1 out of 3 patients (33.3%) in the surgery group. Visual acuity at presentation was significantly associated with final visual outcome (P=0.047). Conclusion Our study demonstrated that visual acuity at presentation was the only factor associated with final vision, irrespective of associated injuries and treatment modalities.

The Biomechanics of Indirect Traumatic Optic Neuropathy Using a Computational Head Model With a Biofidelic Orbit.

Indirect traumatic optic neuropathy (ITON) is an injury to the optic nerve due to head trauma and usually results in partial or complete loss of vision. In order to advance a mechanistic understanding of the injury to the optic nerve, we developed a head model with a biofidelic orbit. Head impacts were simulated under controlled conditions of impactor velocity. The locations of impact were varied to include frontal, lateral, and posterior parts of the head. Impact studies were conducted using two types of impactors that differed in their rigidity relative to the skull. The simulated results from both the impactors suggest that forehead impacts are those to which the optic nerve is most vulnerable. The mode and location of optic nerve injury is significantly different between the impacting conditions. Simulated results using a relatively rigid impactor (metal cylinder) suggest optic nerve injury initiates at the location of the intracranial end of the optic canal and spreads to the regions of the optic nerve in the vicinity of the optic canal. In this case, the deformation of the skull at the optic canal, resulting in deformation of the optic nerve, was the primary mode of injury. On the other hand, simulated results using a relatively compliant impactor (soccer ball) suggest that primary mode of injury comes from the brain tugging upon the optic nerve (from where it is affixed to the intracranial end of the optic canal) during coup countercoup motion of the brain. This study represents the first published effort to employ a biofidelic simulation of the full length of the optic nerve in which the orbit is integrated within the whole head.

Analysis of Prognostic Factors for the Indirect Traumatic Optic Neuropathy Underwent Endoscopic Transnasal Optic Canal Decompression.

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.

Visual Outcome In Patients of Indirect Traumatic Optic Neuropathy Treated with Steroids

Visual Outcome In Patients of Indirect Traumatic Optic Neuropathy Treated with Steroids

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 ofpatients with residual vision and blindness, respectively. VA was improved in 60.9% of patients treated within 3days, 61.5% treated within 7days, and 35.0% treated later than 7days. Of the blindness patients, 50.0%, 37.5%, and 0.0% were treated within 3days, 3-7days, and later than 7days, respectively. Of patients with residual vision, 85.7%, 92.3%, and 70.0% were treated within 3days, 3-7days, and later than 7days, 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 7days and those who received ETOCD later than 7days (P = 0.043). The improvement rate of blindness patients managed within 3days (P = 0.008) and 3-7days (P = 0.035) was significantly higher than that for patients managed beyond 7days. 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 7days. For blindness patients, it is necessary to carry out the surgery within 7days with increased benefit seen before 3days.

Newly onset indirect traumatic optic neuropathy-surgical treatment first versus steroid treatment first.

To investigate the efficacy and safety of the treatment of endoscopic trans-ethmosphenoid optic canal decompression (ETOCD) with combination of steroid in patients with newly onset indirect traumatic optic neuropathy (ITON) and compare the outcome between immediate ETOCD treatment and ETOCD with preoperative steroid treatment. Patients presented as newly onset ITON (suffered trauma within 3d) at a tertiary medical center between Mar 1st, 2016 and Mar 1st, 2018 were enrolled in this study. All patients were equally and randomly divided into 2 groups. Cases in group A were performed ETOCD immediately after admition while cases in group B were prescribed by methylprednisolone (20 mg/kg · d) for 3d before ETOCD. Methylprednisolone (20 mg/kg · d) was used after surgery for 6d in group A and 3d in group B. Follow-up was up to 3mo in all cases. Visual acuity (VA) before and after treatment between the two groups were taken into comparison. Complete postoperative data were acquired from 34 patients in group A and from 32 patients in group B. Group A had significantly higher effective rate in VA than group B (χ 2=4.905, P=0.027). For patients with newly onset ITON, combination treatment of ETOCD with high-dose steroid is an effective and safe way. Immediate surgery will lead to better prognosis for these cases.