scholarly journals Chronic Histological Outcomes of Indirect Traumatic Optic Neuropathy in Adolescent Mice: Persistent Degeneration and Temporally Regulated Glial Responses

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3343
Author(s):  
Shelby M. Hetzer ◽  
Emily M. Shalosky ◽  
Jordyn N. Torrens ◽  
Nathan K. Evanson
Keyword(s):  
Optic Nerve ◽  
Optic Neuropathy ◽  
Time Course ◽  
Bimodal Distribution ◽  
Nerve Degeneration ◽  
Traumatic Optic Neuropathy ◽  
Post Injury ◽  
Weight Drop ◽  
Retinal Thinning ◽  
Injury Outcomes

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.

scholarly journals Chronic Histological Outcomes of Indirect Traumatic Optic NEU-Ropathy in Adolescent Mice: Persistent Degeneration and Tem-Porally Regulated Glial Responses

2021 ◽  
Author(s):  
Shelby M. Hetzer ◽  
Emily M. Shalosky ◽  
Jordyn N. Torrens ◽  
Nathan K. Evanson
Keyword(s):  
Optic Nerve ◽  
Time Course ◽  
Bimodal Distribution ◽  
Nerve Degeneration ◽  
Post Injury ◽  
Histological Changes ◽  
Weight Drop ◽  
Retinal Thinning ◽  
Injury Outcomes ◽  
The Brain

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 sus-ceptible 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, as-trogliosis and microglial changes were alleviated between 14-30 DPI in all regions examined, perhaps indicating a potential critical period for intervention/recovery that may determine chronic outcomes.

scholarly journals Exosome-Mediated Delivery of the Neuroprotective Peptide PACAP38 Promotes Retinal Ganglion Cell Survival and Axon Regeneration in Rats With Traumatic Optic Neuropathy

2021 ◽  
Vol 9 ◽  
Author(s):  
Tian Wang ◽  
Yiming Li ◽  
Miao Guo ◽  
Xue Dong ◽  
Mengyu Liao ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Optic Neuropathy ◽  
Axon Regeneration ◽  
Retinal Ganglion ◽  
Traumatic Optic Neuropathy ◽  
Fiber Layer

Traumatic optic neuropathy (TON) refers to optic nerve damage caused by trauma, leading to partial or complete loss of vision. The primary treatment options, such as hormonal therapy and surgery, have limited efficacy. Pituitary adenylate cyclase-activating polypeptide 38 (PACAP38), a functional endogenous neuroprotective peptide, has emerged as a promising therapeutic agent. In this study, we used rat retinal ganglion cell (RGC) exosomes as nanosized vesicles for the delivery of PACAP38 loaded via the exosomal anchor peptide CP05 (EXOPACAP38). EXOPACAP38 showed greater uptake efficiency in vitro and in vivo than PACAP38. The results showed that EXOPACAP38 significantly enhanced the RGC survival rate and retinal nerve fiber layer thickness in a rat TON model. Moreover, EXOPACAP38 significantly promoted axon regeneration and optic nerve function after injury. These findings indicate that EXOPACAP38 can be used as a treatment option and may have therapeutic implications for patients with TON.

Outcomes of Steroid Therapy in Combination with Endoscopic Optic Nerve Decompression Surgery for Direct Traumatic Optic Neuropathy: A Case-Series

2021 ◽  
Vol 104 (7) ◽  
pp. 1166-1171
Keyword(s):  
Visual Acuity ◽  
Optic Nerve ◽  
Optic Neuropathy ◽  
Poor Prognosis ◽  
Combined Treatment ◽  
Treatment Protocol ◽  
Case Series ◽  
Light Perception ◽  
Traumatic Optic Neuropathy ◽  
Nerve Decompression

Background: Direct traumatic optic neuropathy (TON) carries a poor prognosis. However, the outcome of this injury is diverse and is related to time to treatment and treatment protocol. Objective: To evaluate the outcomes of the combined treatment protocol in patients with direct TON. Materials and Methods: The authors retrospectively reviewed the medical records of patients between January 2015 and August 2019. Main outcome was visual acuity (VA) improvement after the treatment. Results: Thirteen patients (15 eyes) were included. The mean age was 38.61 years with a range of 13 to 65 years. Initial VA varied from no light perception (NPL) in seven eyes of six patients, light perception (PL) in one eye, counting fingers in two eyes, 20/200 in three eyes, and 20/60 in two eyes. Average timing to treatment was 2.8 days (range 0 to 7 days). There were no side effects of high-dose corticosteroids treatment in all patients. During a follow-up period of three months, six of 13 patients (46.1%) had VA improvement. Conclusion: Despite poor prognosis of direct TON, the combined treatment protocol provides a favorable successful rate with most patients on having stable vision, and some having visual improvement from reducing intracanalicular pressure of the optic nerve. Keywords: Endoscopic optic nerve decompression; Traumatic optic neuropathy; Visual acuity; Case series

scholarly journals Blunt Facial Trauma Causing Isolated Optic Nerve Hematoma

2013 ◽  
Vol 2013 ◽  
pp. 1-3
Author(s):  
R. Parab ◽  
C. I. Fung ◽  
Gerrit Van Der Merwe
Keyword(s):  
Optic Nerve ◽  
Optic Neuropathy ◽  
Current Literature ◽  
Vision Loss ◽  
Early Recognition ◽  
Facial Trauma ◽  
Traumatic Optic Neuropathy ◽  
Rare Injury

Traumatic optic neuropathy is an uncommon, yet serious, result of facial trauma. The authors present a novel case of a 59-year-old gentleman who presented with an isolated blunt traumatic left optic nerve hematoma causing vision loss. There were no other injuries or fractures to report. This case highlights the importance of early recognition of this rare injury and reviews the current literature and management of traumatic optic neuropathy.

The effect of steroids in combination With optic nerve decompression surgery in traumatic optic neuropathy

2013 ◽  
Vol 123 (5) ◽  
pp. 1082-1086 ◽  
Author(s):  
Thorsten Ropposch ◽  
Bernhard Steger ◽  
Cem Meço ◽  
Martin Emesz ◽  
Herbert Reitsamer ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Optic Neuropathy ◽  
Decompression Surgery ◽  
Traumatic Optic Neuropathy ◽  
Nerve Decompression ◽  
Optic Nerve Decompression ◽  
Nerve Decompression Surgery
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