Evaluation of the neuroprotective effects of methylprednisolone and surgical decompression in a rodent model of traumatic optic neuropathy

Author(s):  
Philippe Korn ◽  
Nils-Claudius Gellrich ◽  
Simon Spalthoff ◽  
Philipp Jehn ◽  
Ulf T. Eysel ◽  
...  
2007 ◽  
Vol 84 (2) ◽  
pp. 293-301 ◽  
Author(s):  
Nataliya O. Danylkova ◽  
Sandra R. Alcala ◽  
Howard D. Pomeranz ◽  
Linda K. McLoon

Author(s):  
Rafael Martinez-Perez ◽  
Thiago Albonette-Felicio ◽  
Douglas A. Hardesty ◽  
Ricardo L. Carrau ◽  
Daniel M. Prevedello

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Zuohuizi Yi ◽  
Liao Chen ◽  
Xiaoling Wang ◽  
Changzheng Chen ◽  
Yiqiao Xing

Purpose. We sought to explore the effects of intravitreal injection of the Rho-kinase inhibitor Y-27632 in a rodent model of nonarteritic anterior ischemic optic neuropathy (rAION). Methods. The rAION model was established by using laser-induced photoactivation of intravenously administered Rose Bengal in rats. The rats received intravitreal injections of Y-27632 or PBS 1, 3, and 6 days after rAION induction. Optical coherence tomography (OCT) was performed at 2 days and 4 weeks after induction. Visual evoked potential (VEP) was used to evaluate the visual function at 4 weeks. Brn3a immunofluorescence staining of surviving RGCs and apoptosis assays of RGCs were performed at 4 weeks. Results. Optic nerve head (ONH) width was significantly reduced in the Y-27632 group compared with that in the PBS group at 2 days after induction (p<0.05). At 4 weeks, the P1 amplitude of flash-VEP (FVEP) in the Y-27632 group was significantly higher than that of the PBS group (p<0.05). The RGC densities in the central and midperipheral retinas in the Y-27632 group were significantly higher than those in the PBS group (p<0.05). Furthermore, there was a significant decrease in apoptotic RGCs in the Y-27632 group than in the PBS group (p<0.05). Conclusions. Intravitreal injection of Y-27632 had neuroprotective effects on ONH edema, RGC survival, and visual function preservation in rAION.


2008 ◽  
Vol 122 (12) ◽  
pp. 1325-1329 ◽  
Author(s):  
H Li ◽  
B Zhou ◽  
J Shi ◽  
L Cheng ◽  
W Wen ◽  
...  

AbstractObjective: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.Methods:Two hundred and thirty-seven patients with traumatic optic neuropathy were treated with steroids; 176 also consented to endoscopic optic nerve decompression.Results: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).Conclusions: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.


2020 ◽  
Vol 84 ◽  
pp. S80-S83
Author(s):  
Hsin-Hung Chen ◽  
Min-Chao Lee ◽  
Chia-Hsuan Tsai ◽  
Chun-Hao Pan ◽  
Yu-Te Lin ◽  
...  

2002 ◽  
Vol 80 (3) ◽  
pp. 287-293 ◽  
Author(s):  
Thomas-Michael Wohlrab ◽  
Stefan Maas ◽  
J.P. De Carpentier

2019 ◽  
pp. 709-712
Author(s):  
Janet L. Alexander ◽  
◽  
Matthew D. Shulman ◽  
Kinjal N. Sethuraman ◽  
◽  
...  

We describe the emergency management of a man who experienced acute vision loss diagnosed as direct traumatic optic neuropathy (TON) in his right eye (no light perception) after falling from a height. TON is caused by a high-impact mechanism of injury. Clinical findings include acute vision loss, which is typically immediate, afferent pupillary defect, decreased color vision, and visual field defects. Treatment is controversial because of the lack of strong evidence supporting intervention over observation. In this case report, our treatment strategy comprised immediate hyperbaric oxygen (HBO2) and daily high doses of a steroid. On the second day, minocycline was added to the treatment regimen for its neuroprotective effects. The patient was discharged after receiving six HBO2 treatments and six days of intravenous solumedrol transitioned to oral prednisone. After the third HBO2 treatment, his vision improved to 20/100; after the fourth treatment, it was 20/40 and plateaued. At the time of discharge, it was 20/40. At two-month follow-up, his corrected visual acuity was 20/60+2 in the affected eye. Immediate HBO2 for ischemic and mechanical injury to the optic nerve following trauma is a therapeutic option.


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.


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