Treatment Of Traumatic Optic Neuropathy Research Articles

Erythropoietin: a novel treatment for traumatic optic neuropathy—a pilot study

To determine the visual outcome and safety of intravenous erythropoietin in patients with indirect traumatic optic neuropathy (TON). In a university-based hospital, from December 2008 to March 2010, seven cases with indirect TON (EPO group) received three intravenous (IV) injections of 10,000 IU of recombinant human erythropoietin in three successive days. They were compared to eight patients with indirect TON who had received no specific treatment from December 2006 to November 2008 (observation group). The primary end point was best-corrected visual acuity (BCVA) in both groups at last follow-up and secondary measure was systemic adverse effects of medication in the EPO group. Mean ages of patients in the observation and EPO groups were 23.3 (SD = 10.8) and 19.7 (SD = 12.1) years, respectively. Mean follow-up in the observation and EPO groups were 5.8 (SD = 3.8) and 7.0 (SD = 5.8) months, respectively. Mean best-corrected visual acuity (BCVA) significantly (p = 0.028) improved from 1.82 logMAR (SD = 1.27) at initial visit to 0.94 logMAR (SD = 0.82) at last follow-up in the EPO group, whereas the observation group showed an insignificant (p = 0.285) improvement from 2.55 log MAR (SD = 0.62) to 2.32 logMAR (SD = 0.83). Mean final BCVA was significantly higher in the EPO group than in the observation group (p = 0.012). Two cases developed mild transient systemic hypotension during EPO injection. Intravenous erythropoietin may be a new effective and safe treatment for patients with indirect TON.

Treatment of traumatic optic neuropathy: our experience of endoscopic optic nerve decompression

Treatment of traumatic optic neuropathy: our experience of endoscopic optic nerve decompression

Assess and analyse on the role of perimetry in diagnosis and prediction of patients with traumatic optic neuropathy

目的 客观评价Octopus 101视野计在外伤性视神经病变诊断和治疗过程中的指导性作用.方法 对86例(86眼)诊断为外伤性视神经病变的临床病例进行Octopus 101视野计检查,分析其图形、MD、EV值,一同时治疗第3d、1周、2周、3周后连续视野检查确定治疗的效果及预后判断.结果 外伤性视神经病变多为单眼受伤,多为单跟视野改变为其特点.其中视野完全缺损20例;视野阈值整体下降15例;局限性视野缺损31例,局限性视野缺损形状不规则,LV值均大于2db;仅存视岛20例.治疗后跟踪MD值下降2db判断为治疗有效.结论 自动电脑视野计对外伤性视神经病变的诊断和疗效、预后判断具有指导作用,具有相对客观性。

Traumatic Optic Neuropathy Therapy: An Update of Clinical and Experimental Studies

Serious injury to the optic nerve, including direct and indirect events, induces significant visual loss and even blindness. For the past decade corticosteroids and/or optic canal decompression surgery have been widely embraced therapeutic paradigms for the treatment of traumatic optic neuropathy. There is little clinical evidence, however, to support the effectiveness of these strategies, raising questions about the efficiency of current therapy for improving visual outcomes. Recently, experimental studies have yielded a wealth of information related to the protection and regeneration of retinal ganglion cells, showing promise for the development of novel and effective treatments for optic nerve injury.

Treatment of traumatic optic neuropathy: our experience of endoscopic optic nerve decompression

Traumatic optic neuropathy can be treated by various methods including steroids and surgical decompression. Endoscopic optic nerve decompression has been suggested to be effective in treating this condition. The aim of this study was to assess the outcome of treating traumatic optic neuropathy with steroids and endoscopic surgical decompression. Two hundred and thirty-seven patients with traumatic optic neuropathy were treated with steroids; 176 also consented to endoscopic optic nerve decompression. The total vision improvement rate was 55 per cent in the 176 patients treated with both steroids and endoscopic optic nerve decompression, compared with 51 per cent in the 61 patients treated with steroids alone; this difference was not statistically significant (p > 0.05). Treatment with steroids plus endoscopic optic nerve decompression resulted in a significantly greater vision improvement in patients with gradual vision loss, compared with those with immediate blindness (68 vs 42 per cent, respectively). Early surgery (within one week) was an important prognostic factor for vision recovery, compared with more delayed surgical treatment (associated vision improvement rates were 60 and 31 per cent, respectively). Endoscopic optic nerve decompression is a minimally invasive, safe and efficient treatment for traumatic optic neuropathy. Used in combination with steroids, it provides effective rescue for some patients suffering visual loss. It should be undertaken as soon as possible.

Endoscopically Assisted Transconjunctival Decompression of Traumatic Optic Neuropathy

Traumatic optic neuropathy (TON) is a severe sequel after maxillofacial trauma. Recent clinical experience has suggested that optic canal decompression is beneficial in the treatment of TON. With the advent of endoscopy in orbital reconstruction, we extended this technique to decompress the optical canal and reported its outcome. This technique was applied to 30 patients with TON who did not improve after corticosteroids treatment. The average age of the patients at the time of injury was 26 years. Nine patients presented preoperative vision of light perception (LP) or better and 21 patients had no light perception (NLP). Surgery was performed within 1 week of injury in 10 patients, between 1 and 2 weeks in another 10 patients, and between 2 and 4 weeks in the last 10 patients. Thirteen patients were found to have optic canal fractures during surgery. The average follow-up time was 9.5 months. Vision improved in 12 patients including 6 patients (28.6%) with NLP and in 6 patients (66.7%) with LP or better. The improvement degree of visual acuity was 50% in average. Only patient age reflected differences in improvement of visual acuity when analyzing the effect of optic canal fracture, timing of surgery and initial visual acuity. Two patients experienced postoperative cerebrospinal fluid leakage due to associated skull base fractures. The endoscope-assisted transconjunctival technique successfully decompresses the optic canal and improves visual acuity with minimal morbidity. Younger patients had a significantly better visual outcome.

Treatment of traumatic optic neuropathy with high-dose corticosteroid

Based on the favorable clinical results in acute spinal cord injury, high-dose methylprednisolone at an intravenous loading dose of 30 mg/kg followed by a continuous infusion of 5.4 mg/kg/h for 24 or 48 hours has been adopted for the treatment of acute traumatic optic neuropathy (TON). Although there is anecdotal evidence of the efficacy of high-dose corticosteroid in this condition, there are no prospective, randomized trials to attest to its benefit. On the other hand, the largest retrospective study showed no benefit of high-dose corticosteroid treatment of TON. Moreover, subsequent study of such treatment of acute spinal cord injury has disclosed that the clinical benefit is modest and that treatment is actually harmful if administered more than eight hours after injury. A recently reported placebo-controlled randomized clinical trial of high-dose corticosteroids in head injury was stopped prematurely because of a significantly greater mortality in the corticosteroid-treated patients. Recent experimental studies suggest that methylprednisolone may be harmful to the optic nerve. Considering this clinical and experimental evidence, there is no basis for treating TON with high-dose corticosteroid.

Treatment of Traumatic Optic Neuropathy with High-Dose Corticosteroid

Based on the favorable clinical results in acute spinal cord injury, high-dose methylprednisolone at an intravenous loading dose of 30 mg/kg followed by a continuous infusion of 5.4 mg/kg/h for 24 or 48 hours has been adopted for the treatment of acute traumatic optic neuropathy (TON). Although there is anecdotal evidence of the efficacy of high-dose corticosteroid in this condition, there are no prospective, randomized trials to attest to its benefit. On the other hand, the largest retrospective study showed no benefit of high-dose corticosteroid treatment of TON. Moreover, subsequent study of such treatment of acute spinal cord injury has disclosed that the clinical benefit is modest and that treatment is actually harmful if administered more than eight hours after injury. A recently reported placebo-controlled randomized clinical trial of high-dose corticosteroids in head injury was stopped prematurely because of a significantly greater mortality in the corticosteroid-treated patients. Recent experimental studies suggest that methylprednisolone may be harmful to the optic nerve. Considering this clinical and experimental evidence, there is no basis for treating TON with high-dose corticosteroid.

外傷性視神経症に対する内視鏡下視神経管開放術

We treated 2 patients for traumatic optic neuropathy. Visual acuity remained unchanged following high-dose corticosteroid therapy in both patients. They underwent optic nerve decompression under endoscopic control. One patient with preoperative visual acuity of 0.01 showed an improvement of visual acuity and expansion of visual field. The other was blind preoperatively and did not show any improvement postoperatively. Other authors reported that improvement of vision occurred in approximately half the patients who had no light perception prior to surgery. Therefore, optic nerve decompression can be an option in the treatment of traumatic optic neuropathy, if vision worsens or remains unchanged even after the patient is treated with high-dose corticosteroid therapy.

Treatment of Traumatic Optic Neuropathy Remains Controversial—Reply

Treatment of Traumatic Optic Neuropathy Remains Controversial—Reply

The treatment of traumatic optic neuropathy: The international optic nerve trauma study

ObjectiveTo compare the visual outcome of traumatic optic neuropathy treated with corticosteroids, treated with optic canal decompression surgery, or observed without treatment. DesignComparative nonrandomized interventional study with concurrent treatment groups. ParticipantsA total of 133 patients with traumatic optic neuropathy (127 unilateral and 6 bilateral) who had an initial visual assessment within 3 days of injury. At least 1 month of follow-up was required for inclusion in the primary analysis. InterventionsOn the basis of treatment received within 7 days of injury, patients with unilateral injuries were categorized as being in one of three treatment groups: untreated (n = 9), corticosteroid (n = 85), or optic canal decompression surgery (n = 33). Main outcome measureVisual acuity. ResultsVisual acuity increased by ≥3 lines in 32% of the surgery group, 57% of the untreated group, and 52% of the steroid group (P = 0.22). The surgery group had more patients whose initial vision was no light perception. After adjustment for the baseline visual acuity, there were no significant differences between any of the treatment groups. There was no indication that the dosage or timing of corticosteroid treatment or the timing of surgery was associated with an increased probability of visual improvement. ConclusionsNo clear benefit was found for either corticosteroid therapy or optic canal decompression surgery. The number of patients studied was sufficient to rule out major effects in the treatment groups, although clinically relevant effects in specific subgroups could have been missed. These results and the existing literature provide sufficient evidence to conclude that neither corticosteroids nor optic canal surgery should be considered the standard of care for patients with traumatic optic neuropathy. It is therefore clinically reasonable to decide to treat or not treat on an individual patient basis.

High-dose steroid therapy of traumatic optic neuropathy may fail to protect the optic nerve permanently

Background: The optimal treatment of traumatic optic neuropathy (TON) is still unresolved due to the poor understanding of the pathology involved and the relatively small number of cases in the published clinical series. It is currently held that the results of conservative treatment with high-dose corticosteroids are similar to those obtained with surgical decompression. Purpose: To assess the late results of conservative treatment for traumatic optic neuropathy. Patients and methods: 15 patients (3 women and 12 men, age 14–64 years) who sustained a direct injury to the optic nerve as a consequence of closed head trauma. All were treated conservatively with high-dose dexamethasone therapy. Ten patients presented for follow-up examination 3–11 years after the injury, on average 5.3±2.4 years (SD). A full ophthalmologic examination and color-coded Doppler (CCD) study of the orbital vessels was performed in all subjects. Results: Full blindness of the affected eye, persisting since the injury, was noted in six patients. Their visual acuity did not improve in spite of vigorous treatment and their eyes remained without sight at the follow-up examination. The finding of an absence of flow in central retinal arteries at follow-up suggests structural damage to the nerve. Moreover, in five of these patients, distinct features of eyeball atrophy had evolved between the time of injury and the follow-up examination. Four patients, who on admission presented only with the ability to perceive light, responded to 2–3 weeks of steroid therapy with improvement of visual acuity to 3/50, 5/50, 5/10, and 5/7. After 4–6 years, however, the visual acuity of all of these patients had deteriorated, resulting in nearly total blindness in one case, light perception in two, and 1/50 in the fourth. Optic nerve atrophy was diagnosed in all of the affected eyes. Conclusion: Conservative treatment of TON, even if giving transient improvement in visual function, may not be reliable in providing permanent relief from the sequelae of traumatic optic neuropathy.

Neuro-ophthalmology of trauma.

This review focuses on neuro-ophthalmic disorders caused by trauma. Most articles discussed were published after 1995. The review is divided into sections according to the anatomical sites that can be affected by trauma and lead to neuro-ophthalmic symptoms. The topics are the oculomotor nerves and the facial nerve, the cavernous sinus, the orbit, the optic nerve, and the brain. Treatment options are discussed, including strabismus surgery, orbital reconstruction, and medical as well as surgical treatment of traumatic optic neuropathy.

Intravenous methylprednisolone in treatment of traumatic optic neuropathy.

Traumatic optic neuropathy is one of true ophthalmic emergencies and there is no proven form of treatment for traumatic optic neuropathy. Here we were presented with 30 cases of sudden visual loss following blunt eye trauma seen in Kaohsiung Medical College Hospital, Taiwan from April 1994 to March 1997. We analyze the treatment style, visual acuity, elapsed time since injury and orbit computed tomography retrospectively. Among them, 21 cases received intravenous methylprednisolone treatment, 2 cases received oral prednisolone, 2 cases underwent optic canal decompression in addition to intravenous methylprednisolone and 5 cases were carefully monitored without any kind of treatment. Thirteen of the 21 cases (62%) in intravenous methylprednisolone group got visual improvement. Patients with initial vision better than light perception benefitted more from treatment than did the patients who with no light perception in medical treatment group (85% VS 20%) (p < 0.05). Thirteen of the 30 cases (53.3%) had orbit fracture and 2 of the 30 cases (6.7%) had a fracture of the optic canal. These two cases also received optic canal decompression surgery in addition to intravenous steroid treatment but the prognosis was poor. In conclusion, intravenous methylprednisolone does offer help in traumatic optic neuropathy. Whether or not initial visual acuity was better than light perception was a key risk factor in the outcome. In this article, we also compare our results with other series in the literature and found that the value of different treatment in traumatic optic neuropathy still needs to be prospectively judged in the future.

Endoscopic optic nerve decompression for the treatment of traumatic optic neuropathy

Traumatic optic neuropathy complicates approximately 2% of closed head injuries. Although sudden blindness is an infrequent presenting symptom after craniofacial trauma, its consequences are devastating for the patient, thus requiring prompt recognition. Although a uniform approach to the management of traumatic optic neuropathy is not currently available in the literature, the options for therapy consist of observation or a combination of systemic steroids and/or surgical decompression of the optic nerve by intracranial or extracranial approaches. In this article, 12 optic nerve specimens in cadavers were dissected, with anatomic landmarks delineated and measurements taken from the anterior nasal spine. The transnasal approach using endoscopic surgical technique is discussed in this article. Endoscopic optic nerve decompression can be offered as a method of treatment for traumatic optic neuropathy.

Traumatic optic neuropathy. A meta-analysis.

The management of traumatic optic neuropathy remains controversial. Reports of improvement have been published after observation alone, treatment with corticosteroids and surgical decompressions. To systematically review the published literature about traumatic optic neuropathy using a meta-analysis. We performed a retrospective literature review of case series and case reports of traumatic optic neuropathy. They include all English language cases and selected non-English language cases for which patient data were available. The cases were organized into four grades based on visual acuity and the locations and type of fracture. Grade 1 included patients with visual acuity greater than 20/200 in the affected eye and without a posterior orbit fracture; grade 2, patients with visual acuity between 20/200 and light perception; grade 3, patients without light perception or with a nondisplaced posterior orbital fracture and remaining vision; and grade 4, patients with no light perception and a displaced posterior orbital fracture. A meta-analysis was performed, analyzing for each case the recovery of visual acuity for treatment, fracture pattern, and grade. The recovery of vision in treated patients was significantly better than the recovery in patients receiving no treatment. No significant difference in improvement was found among patients treated with corticosteroids alone, with surgical decompression alone, or with corticosteroids and surgical decompression. Recovery was related to the severity of initial injury, as reflected in the grading system. A trend was noted for better improvement of visual acuity in patients without orbital fractures than those with orbital fractures, and also in patients with anterior orbital fractures than in patients with posterior fractures. Treatment with corticosteroids, extracranial decompression, or both, is better than no treatment of traumatic optic neuropathy. Because the data are insufficient to determine whether corticosteroids, surgery, or the use of both treatments is most effective, the findings of the ongoing International Optic Nerve Trauma Study should prove valuable. The standardized grading system we developed is a useful tool for comparing studies and treatment protocols.

Rapid quantification of tissue damage for assessing acute spinal cord injury therapy.

Journal of NeurotraumaVol. 9, No. 2 Rapid Quantification of Tissue Damage for Assessing Acute Spinal Cord Injury TherapyWISE YOUNGWISE YOUNGSearch for more papers by this authorPublished Online:26 Mar 2009https://doi.org/10.1089/neu.1992.9.151AboutSectionsPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail FiguresReferencesRelatedDetailsCited byManagement of Acute Traumatic Spinal Cord Injury: A Review of the Literature13 December 2021 | Frontiers in Surgery, Vol. 8The Efficacy of Progesterone in Treatment of Traumatic Optic Neuropathy (Proton Study)27 June 2017 | Journal of Southeast Asian Medical Research, Vol. 1, No. 1Experimental Models of Partial Lesion of Rat Spinal Cord to Investigate Neurodegeneration, Glial Activation, and Behavior Impairments7 July 2009 | International Journal of Neuroscience, Vol. 111, No. 3-4Traumatismos medulares experimentales: Revisión de la literatura y descripción de un modelo mediante compresión mantenida en la rataNeurocirugía, Vol. 7, No. 3 Volume 9Issue 2Jan 1992 To cite this article:WISE YOUNG.Rapid Quantification of Tissue Damage for Assessing Acute Spinal Cord Injury Therapy.Journal of Neurotrauma.Jan 1992.151-155.http://doi.org/10.1089/neu.1992.9.151Published in Volume: 9 Issue 2: March 26, 2009PDF download

Treatment of Traumatic Optic Neuropathy with Corticosteroids

We treated 21 patients (22 eyes) with traumatic optic neuropathy by using intravenous megadose methylprednisolone (13 patients) or high-dose dexamethasone (eight patients). Of 13 patients treated with megadose methylprednisolone, 12 had improved visual function, as did seven of nine eyes treated with intravenous dexamethasone. This difference was not significant (P = .3). Initial total blindness, mechanism of injury, or time from injury to treatment did not correlate with visual improvement.