traumatic optic neuropathy
Recently Published Documents


TOTAL DOCUMENTS

374
(FIVE YEARS 103)

H-INDEX

30
(FIVE YEARS 3)

Author(s):  
Bin Chen ◽  
Hengsen Zhang ◽  
Qing Zhai ◽  
Huaipeng Li ◽  
Chunxia Wang ◽  
...  

Author(s):  
Bincy Joseph ◽  
Sapna S. Nambiar ◽  
K. Ramachandran ◽  
Suma Radhakrishnan

<p><strong>Background: </strong>Traumatic optic neuropathy (TON) a vision threatening disorder requires early diagnosis and prompt treatment. High dose steroid injections, optic nerve decompression or combined therapy are the available current treatment options. This study aims to determine the visual outcome with transnasal endoscopic optic nerve decompression in patients with TON having no improvement in vision despite high dose steroids.</p><p><strong>Methods:</strong> A prospective study was conducted at the department of ENT, government medical college Kozhikode; on patients who presented with loss of vision following history of trauma. All patients suspected of compressive optic neuropathy received injection methyl prednisolone (30 mg/kg/day) with assessment of vision and HRCT scan. Patients with deterioration or no improvement in vision despite high steroid therapy were taken up for trans-nasal endoscopic optic nerve decompression.</p><p><strong>Results:</strong> In our study 19 patients with TON underwent trans-nasal endoscopic optic nerve decompression. 11(57.9%) patients had improvement of vision, 7 (36.8%) patients had no improvement of vision and 1 (5.3%) patient had worsening of vision. The visual improvement was seen in 8 (80%) patients when treatment was initiated within 7 days and in only 3(33.3%) patients when treatment was initiated after 7 days. The visual acuity at presentation and time interval between trauma and intervention are factors that determine better visual outcomes.</p><p><strong>Conclusions:</strong> The decreased visual acuity in TON requires prompt treatment. High dose steroid must be started at once when it is suspected or diagnosed. The timely surgical intervention with trans-nasal endoscopic optic nerve decompression is a relatively safe and effective technique enabling better visual prognosis.</p>


Author(s):  
Sudesh Kumar ◽  
Amit Joshi ◽  
Rajeev Tuli ◽  
Narvir Chauhan

Abstract 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 therapy) underwent endoscopic optic nerve decompression and eight had improvement in vision. The status of vision at presentation was only statically significant prognostic factor (p < 0.02). Others prognostic factors, for example, time of starting treatment, surgery, and presence of fracture in optic canal, were not found statistically significant (p > 0.05). There were no significant intra- and postoperative complications. Conclusion Combined therapy is safe and effective in management of TON. Mild form injury with some preserved vision at presentation respond well to steroids, while endoscopic nerve decompression should be reserved in cases with failed steroid therapy.


Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1934
Author(s):  
Chin-Te Huang ◽  
Yao-Tseng Wen ◽  
Tushar Dnyaneshwar Desai ◽  
Rong-Kung Tsai

Traumatic optic neuropathy (TON) may cause severe visual loss following direct or indirect head trauma which may result in optic nerve injuries and therefore contribute to the subsequent loss of retinal ganglion cells by inflammatory mediators and reactive oxygen species (ROS). Granulocyte colony-stimulating factor (G-CSF) provides the anti-inflammatory and anti-oxidative actions but has a short half-life and also induces leukocytosis upon typical systemic administration. The purpose of the present study was to investigate the relationship between the anti-oxidative response and neuroprotective effects of long-acting pegylated human G-CSF (PEG-G-CSF) in a rat model of optic nerve crush (ONC). Adult male Wistar rats (150–180 g) were chosen to have a sham operation in one eye and have ONC in the other. PEG-G-CSF or phosphate-buffered saline (PBS control) was immediately administered after ONC by intravitreal injection (IVI). We found the IVI of PEG-G-CSF does not induce systemic leukocytosis, but increases survival of RGCs and preserves the visual function after ONC. TUNEL assays showed fewer apoptotic cells in the retina in the PEG-G-CSF-treated eyes. The number of sorely ED1-positive cells was attenuated at the lesion site in the PEG-G-CSF-treated eyes. Immunoblotting showed up-regulation of p-Akt1, Nrf2, Sirt3, and HO-1 in the ON of the PEG-G-CSF-treated eyes. Our results demonstrated that one IVI of long-acting PEG-G-CSF is neuroprotective in the rONC. PEG-G-CSF activates the p-Akt1/Nrf2/Sirt3 and the p-Akt1/Nrf2/HO-1 axes to provide the antioxidative action and further attenuated RGC apoptosis and neuroinflammation. This provides crucial preclinical information for the development of alternative therapy with IVI of PEG-G-CSF in TON.


Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3343
Author(s):  
Shelby M. Hetzer ◽  
Emily M. Shalosky ◽  
Jordyn N. Torrens ◽  
Nathan K. Evanson

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.


2021 ◽  
Author(s):  
Yikui Zhang ◽  
Mengyun Li ◽  
Bo Yu ◽  
Shengjian Lu ◽  
Lujie Zhang ◽  
...  

Therapeutic hypothermia (TH) is potentially an important therapy for central nervous system (CNS) trauma. However, its clinical application remains controversial, hampered by two major factors: 1) Many of the CNS injury sites, such as the optic nerve (ON), are deeply buried, preventing access for local TH. The alternative is to apply TH systemically, which significantly limits the applicable temperature range. 2) Even with possible access for "local refrigeration", cold-induced cellular damage offsets the benefit of TH. Here we present a clinically translatable model of traumatic optic neuropathy (TON) by applying clinical trans-nasal endoscopic surgery to goats and non-human primates. This model faithfully recapitulates clinical features of TON such as the injury site (pre-chiasmatic ON), the spatiotemporal pattern of neural degeneration, and the accessibility of local treatments with large operating space. We also developed a computer program to simplify the endoscopic procedure and expand this model to other large animal species. Moreover, applying a cold-protective treatment, inspired by our previous hibernation research, enables us to deliver deep hypothermia (4°C) locally to mitigate inflammation and metabolic stress (indicated by the transcriptomic changes after injury) without cold-induced cellular damage, and confers prominent neuroprotection both structurally and functionally. Intriguingly, neither treatment alone was effective, demonstrating that in situ deep hypothermia combined with hibernation-mimicking cold protection constitutes a breakthrough for TH as a therapy for TON and other CNS traumas.


Sign in / Sign up

Export Citation Format

Share Document