Traumatic optic neuropathy and second optic nerve injuries

Otolaryngology - Head and Neck Surgery, 1999

The management of traumatic optic neuropathy remains controversial. In this report, we present the results of 45 patients treated with extracranial optic nerve decompression after at least 12 to 24 hours of corticosteroid therapy without improvement. Vision improved in 32 patients after surgery (71%), and the mean percentage of improvement from preoperative visual deficit was 40.7% ± 6.9% (median improvement 41.2%). Worsening of vision occurred in none of the patients as a result of the surgery, and no intraoperative or postoperative complications were encountered. We present a treatment protocol for traumatic optic neuropathy with the use of megadose corticosteroids and optic nerve decompression.

Indian Journal of Neurotrauma, 2021

Objective Traumatic optic neuropathy (TON) is an important cause of severe vision impairment after sustaining a closed head injury. This study describes the safety and efficacy of combined therapy in the management of TON. Methods A retrospective analysis of 23 consecutive cases of unilateral TON managed with combined therapy (steroid and surgery) were performed. Statistical analysis of patient characteristic, timing of vision loss, radiological and intraoperative findings, and pre- and post-treatment vision were compared to assess the prognostic factors. Results Seventeen patients (85%) had vision improvement with combined therapy. Three patients (15%), who recorded no improvement, initially presented with no perception of light, and loss was sudden and immediate. With steroids, 9 patients improved, all of them presented with perception of light (PL) or better and vision improved to (6/6 in five, 6/9 in one, 6/18 in 3). Eleven patients (6 PL–ve and 5 PL + ve after failed steroid th...

British Journal of Ophthalmology, 1992

Twenty three patients with traumatic optic neuropathy were managed by medical and surgical treatment as follows. High dose intravenous steroids were initiated in all patients. If visions did not improve significantly after 24 to 48 hours decompression of an optic nerve sheath haematoma by medial orbitotomy and neurosurgical decompression of the optic canal were considered based on computed tomographic scan findings. Nine of 16 patients who received steroids only showed significant improvement. One of three showed improvement on optic nerve decompression after steroid failure; three or four showed improvement with combined optic nerve sheath decompression by the medial orbitotomy and decompression of the optic canal by frontal craniotomy. A lucid interval of vision after injury and an enlarged optic nerve sheath were associated with an improved prognosis. Five of the 23 patients had a lucid interval and all five had a final improved vision, while only five of 18 patients without a lucid interval improved. Similarly seven of the nine with an enlarged optic nerve sheath showed improvement while only three of 10 patients (three bilateral cases) who presented with no light perception improved with medical and surgical treatment. While a prospective controlled study of the management of traumatic optic neuropathy is necessary this preliminary study suggests that treatment of traumatic optic nerve sheath haematoma by optic nerve sheath decompression should be considered in selected patients.

European Journal of Ophthalmology, 2006

To report the long-term outcome of patients with indirect traumatic optic neuropathy (TON) which showed useful vision for a short period after trauma. METHODS. A cohort of 12 TON patients treated with steroids megadose immediately after trauma was followed every 6 months for an overall period of 5 years. Other than a full neuro-ophthalmologic examination, each visit included quantitative Goldmann perimetry and pattern reversal visual evoked potentials. The results of each examination were compared with the visual function at baseline. The main outcome measures were visual acuity and visual field. Data were analyzed using the Wilcoxon signed-rank test. A p value of less than 0.05 was considered statistically significant. RESULTS. All patients showed a stable visual function 5 years after optic nerve trauma. There was no difference in visual acuity levels (p=0.65) and no visual field surface area between the visit at baseline and the last follow-up. However, a significant improvement in visual field extension (p=0.036) was observed after perimetry evaluation. CONCLUSIONS. This cohort of patients clearly demonstrates that the residual visual function found in the short term after TON is maintained for at least 5 years. These findings add further important clinical information for patients with TON. Furthermore, these data may be helpful to better quantify morbidity related to optic nerve trauma and its permanent sequelae.

Neuro-Ophthalmology, 2014

Traumatic optic neuropathy (TON) refers to an acute injury to the optic nerve secondary to ocular trauma. The study was conducted to evaluate the visual outcome in cases of TON and to study reversal of optic nerve function after emergency ophthalmic intervention. Objectives: To evaluate the visual outcome in cases of TON, study the factors affecting final visual outcome and to evaluate the optic nerve function in cases of TON. Methodology: The present study was a Prospective observational study, 49 patients presented after ocular trauma in the

Background: Optic nerve injuries occur in the setting of head injury which is often a consequence of road traffic accidents or falls. Traumatic optic neuropathy (TON) is a potentially blinding complication of head and orbital trauma. Different treatment approaches like different dosages of steroids, surgical decompression and observation alone have been suggested but there is no standardized protocol till date. Object: To study the clinical profile, risk factors, visual outcome in a series of forty five patients of Traumatic Optic Neuropathy (TON) after medical management at our tertiary centre. Methods: Forty five patients reported to outpatient department from January 2018 to June 2019 who have a history of trauma were studied prospectively. After relevant and detailed ocular examination, Intravenous methyl prednisolone 1 gram for 5days and thenoral prednisolone 1 mg/kg in tapering doses for two weeks was administered in all patients irrespective of duration of presentation to the hospital after trauma. Results: The age group involved was predominantly 16 to 45years (80%) with a mean age of 35.31 years. Range of follow up was seen from 5days to 5 months. Males (91%) were outnumbered. Road traffic accidents (73.33%) were found to be the most common cause for TON in our series. Of 45, 10 patients were lost to follow up, rest 35 patients who have been followed steroid regime, 18 (51.43%) showed visual improvement (12 patients had >/=2 line improvement, rest 06 patient had one line improvement). 17(48.57%) patients did not show any improvement. 08 patients were same (no perception of light) till the final follow up. Conclusion: IV methyl prednisolone along with oral steroids as proposed by ONTT has been found effective in our case series of TON even in patients who have very low initial visualacuity and who presented late even after 24 hours of injury till the irreversible damage to optic nerve.No major side effects have been encountered with this steroid regimen. High dose steroid has proven its role in traumatic optic neuropathy.

Acta Clinica Croatica

Traumatic optic neuropathy (TON) is a serious vision threatening condition that can be caused by ocular or head trauma. Indirect damage to the optic nerve is the most common form of TON occurring in 0.5% to 5% of all closed head trauma cases. Although the degree of visual loss after indirect TON may vary, approximately 50% of all patients are left with 'light perception' or 'no light perception' vision, making TON a signifi cant cause of permanent vision loss. We present a 47-year-old male patient with a history of right eye keratoconus following a motorcycle crash. Visual acuity was of 'counting fi ngers at 2 meters' on the right eye due to keratoconus and 'counting fi ngers at 1 meter' on the left eye as a consequence of trauma. Th e Octopus visual fi eld showed diff use reduction in retinal sensitivity and the Ishihara color test indicated dysfunction of color perception on the left eye. Relative aff erent pupillary defect was also present. Computed tomography revealed multifragmentary fracture of the frontal sinus and the roof of the left orbit without bone displacement. Based on the fi ndings, conservative corticosteroid therapy without surgery was conducted. Th e patient responded well to treatment with complete ophthalmologic recovery.

IOSR Journals , 2019

BACKGROUD: Traumatic optic neuropathy (TON) refers to an acute injury of the optic nerve secondary to trauma. The optic nerve axons may be damaged either directly or indirectly and the visual loss may be partial or complete. Optic nerve decompression with steroids or surgical interventions or both has therefore been advocated as a means of improving visual prognosis in TON.OBJECTIVES:The aim of the study is to retrospectively analyse the most common cause ,age group ,gender,fracturerate,presenting visual acuity and postmedicaltreatment visual acuity.METHODS: Inclusion criteria:isolated traumatic optic neuropathy with atleast one follow up visit.A retrospective study of 50 patients with isolated traumatic optic neuropathy with atleast one followup was done.They were given iv methylprednisolone,iv steroids and oral steroids and tab.methycobalamine based on severity at the time of presentation.RESULTS:Most common gender affected were males(98%) than females.Most common age group was 33yrs(range 4yrs to 66yrs) and cause was roadtraffic accident around 81.6%,fracture rate about 53%.Left eye was most commonly affeceted (around 60.4%).22% presented with vision with No PL,24% from PL+ to ( ½)/60,20% with vision 1/60 to 5/60,27% presented with vision ranging 6/60 to 6/9,6% with 6/6.Post treatment vision ranged:10%-NO PL,24%-PL+ to (½)/60,24%-1/60 to5/60,18%-6/60 to 6/9,22%-6/6

Objective: To investigate a possible correlation between final visual acuity and the presence at baseline of various systemic and local (orbital/ocular) signs in patients affected by indirect traumatic optic neuropathy. Methods: 35 cases of traumatic optic neuropathy were examined retrospectively and 13 variables were tested. Univariate analysis with " no recovery of visual acuity " as the primary outcome was performed. Relative risk (RR) and 95% confidence intervals (CI) were calculated. Fisher's exact test was used for two variables to test differences between proportions. Results: Four variables showed a significantly increased risk for no recovery of visual acuity: presence of blood within the posterior ethmoidal cells (RR = 2.25, 95% CI 1.25 to 4.04); age over 40 years (RR = 1.79, 1.07 to 2.99); loss of consciousness associated with traumatic optic neuropathy (RR = 2.21, 1.17 to 4.16); and absence of recovery after 48 hours of steroid treatment (p < 0.01, Fisher's exact test). Recovery documented at the first follow up visit after treatment was significantly associated with recovery at the last follow up visit (p < 0.01, Fisher's exact test). Conclusions: These four negative prognostic signs in patients affected by traumatic optic neuropathy may be useful in predicting the visual outcome in patients developing visual loss after head trauma and in deciding on the need for surgical treatment.