UNASSIGNED: Endoscopic transnasal optic canal decompression is widely used in the treatment of traumatic optic neuropathy (TON) following head and craniofacial trauma. Intraoperative hemorrhage is a catastrophic surgical complication during optic canal decompression.
UNASSIGNED: We present two cases of patients with TON who suffered unexpected intra-operative massive bleeding during endoscopic transnasal optic canal decompression. After intraoperative hemostasis was achieved, emergent cerebral angiograms demonstrated the formation of internal carotid pseudoaneurysms, which were immediately embolized with coils combined with or without Onyx with balloon assistance. One of these cases was also complicated by a postoperative cerebrospinal fluid leak, which failed to be treated with lumbar drainage but was successfully repaired with endoscopic transnasal surgery.
UNASSIGNED: The intra-operative rupture of ICA pseudoaneurysm is a rare but catastrophic complication in TON patients. Intraoperative massive bleeding indicates rupture of ICA pseudoaneurysm. Postoperative emergency angiography and endovascular therapy should be arranged to evaluate and repair the cerebral vascular injury. Endoscopic trans-nasal surgery repairing CSF leaks resistant to lumbar drainage could be efficient and safe following pseudoaneurysm embolization.

UNASSIGNED: Traumatic optic neuropathy is known to be a critical condition that can cause blindness; however, the specific mechanism underlying optic nerve injury is unclear. Recent studies have reported that artemisinin, considered vital in malaria treatment, can also be used to treat neurodegenerative diseases; however, its precise role and mechanism of action remain unknown. Therefore, in this study, we aimed to investigate the impact and probable mechanism of action of artemisinin in retinal ganglion cells (RGCs) in a mouse model of traumatic optic neuropathy induced by optic nerve crush (ONC).
UNASSIGNED: ONC was induced in the left eye of mice by short-term clamping of the optic nerve; oral artemisinin was administered daily. The neuroprotective effect of the drug was assessed using Tuj-1 staining in RGCs. In addition, the inflammatory response and the expression levels of phosphorylated tau protein and tau oligomers were observed using RT-qPCR, TUNEL assay, and fluorescence staining to investigate the underlying mechanisms.
UNASSIGNED: Artemisinin increased the survival rate of RGCs 14 days after ONC. Artemisinin significantly reduced the levels of inflammatory factors such as CXCL10, CXCR3, and IL-1β in the retina and decreased the apoptosis of RGCs. Moreover, downregulation of the phosphorylation of tau proteins and the expression of tau oligomers were observed after artemisinin treatment.
UNASSIGNED: Our results suggest that artemisinin can increase the survival rate of RGCs after ONC and reduce their apoptosis. This effect may be achieved by inhibiting the inflammatory response it triggers and downregulating tau protein phosphorylation and tau oligomer expression. These findings suggest the potential application of artemisinin as a therapeutic agent for neuropathy.

UNASSIGNED: Traumatic optic neuropathy (TON) is the optic nerve injury secondary to brain trauma leading to visual impairment and vision loss. Current clinical visual function assessments often fail to detect TON due to slow disease progression and clinically silent lesions resulting in potentially delayed or missed treatment in patients with traumatic brain injury (TBI).
UNASSIGNED: Diffusion basis spectrum imaging (DBSI) is a novel imaging modality that can potentially fill this diagnostic gap. Twenty-two, 16-week-old, male mice were equally divided into a sham or TBI (induced by moderate Closed-Head Impact Model of Engineered Rotational Acceleration device) group. Briefly, mice were anesthetized with isoflurane (5% for 2.5 min followed by 2.5% maintenance during injury induction), had a helmet placed over the head, and were placed in a holder prior to a 2.1-joule impact. Serial visual acuity (VA) assessments, using the Virtual Optometry System, and DBSI scans were performed in both groups of mice. Immunohistochemistry (IHC) and histological analysis of optic nerves was also performed after in vivo MRI.
UNASSIGNED: VA of the TBI mice showed unilateral or bilateral impairment. DBSI of the optic nerves exhibited bilateral involvement. IHC results of the optic nerves revealed axonal loss, myelin injury, axonal injury, and increased cellularity in the optic nerves of the TBI mice. Increased DBSI axon volume, decreased DBSI λ||, and elevated DBSI restricted fraction correlated with decreased SMI-312, decreased SMI-31, and increased DAPI density, respectively, suggesting that DBSI can detect coexisting pathologies in the optic nerves of TBI mice.
UNASSIGNED: DBSI provides an imaging modality capable of detecting subclinical changes of indirect TON in TBI mice.

UNASSIGNED: A systematic review and meta-analysis.
UNASSIGNED: Treatment of traumatic optic neuropathy (TON) has been a subject of debate for many decades due to the scarcity of evidence-based treatment protocols. This review compares surgical decompression (SD) and steroid therapy (ST) as treatment approaches in TON patients.
UNASSIGNED: A PRISMA-guided systematic review using PubMed, Embase, Ovid and Scopus databases was performed till the last search date of July 31st 2021. The outcome of interest was an improvement in visual acuity. A meta-analysis of the odds ratio was performed using a random-effect model and sub-group analysis based upon criteria for assessment of improvement in visual acuity.
UNASSIGNED: Sixteen studies (including 1046 patients) were included in the review. The review could identify 590 patients treated with SD and 456 treated with ST. In addition, there was a second cohort of patients presenting with NLP (no light perception). A meta-analysis with a sub-group analysis revealed that there was statistically no significant difference between the two treatment approaches in terms of improvement in VA.
UNASSIGNED: There is no difference in treatment results of SD or ST for TON. Several treatment protocols and different criteria for assessing visual acuity led to difficulty in generating evidence for selecting the correct treatment approach.

UNASSIGNED: The indication for surgical optic canal decompression (OCD) for traumatic optic neuropathy (TON) remains controversial because there is no reliable predictor of a good outcome. We report the case of a blind patient with TON whose remaining visual-evoked potential (VEP) suggested recovery potential of the injured optic nerve after OCD.
UNASSIGNED: A 48-year-old man had fallen from a height of 7 m, striking his head. He immediately complained of right-eye blindness. He had no light perception and the direct light reflex disappeared from the right pupil, although there was no fracture or traumatic lesion on computed tomography and magnetic resonance imaging. Because the amplitude of the VEP with the right eye stimulation remained unchanged, we performed the right OCD. During surgical OCD, the amplitude and latency of VEP began to improve. Finally, the visual field improved in almost all directions, and eyesight improved to 0.2.
UNASSIGNED: The retained VEP activity in TON may suggest the recovery potential of the injured optic nerve, even in cases of blindness. It is possible that VEP is an indicator of aggressive treatment for TON such as OCD.

To analyze the visual outcome in patients with traumatic optic neuropathy (TON) with respect to different treatment modalities, to study the correlation of initial visual loss with the final visual outcome, and to find out the predictor of final visual outcome in patients with indirect TON.
A retrospective analysis of 36 eyes with TON was done. Data on clinical profile, including demographics, mode of trauma, best corrected visual acuity (BCVA), pupillary reflex examination, and anterior and posterior segment examination, was collected. Presence and location of orbital and cranial fractures were identified from computed tomography scan. Visual outcomes following steroid therapy, optic nerve (ON) decompression, and in untreated patients were analyzed. Pre- and post-treatment BCVA were divided into three groups based on logarithm of the minimum angle of resolution (logMAR) as follows: group A: 3, group B: 2.9-1.3, and group C<1.3. BCVA values at follow-up visits were taken as the primary outcome measure. Association between various risk factors and final visual outcome in patients with indirect TON was also analyzed.
Out of 34 patients whose 36 eyes were studied, three (8.8%) patients were females and 31 (91.2%) patients were males. Most common mode of trauma was road traffic accident (RTA; 91.2%), which was followed by fall (8.8%) and assault (2.9%). Pre- and post-treatment BCVA values of 36 eyes were compared, and improvement in BCVA after treatment was found to be statistically significant. Also, 28.6% of patients with presenting BCVA of no light perception showed improvement compared to 94.1% and 100% in groups B and C, respectively. Orbital wall fractures were seen in 80.5% (n = 29) of the patients, with lateral wall fracture being the most common (58.3%) followed by medial wall (33.3%), roof (27.7%), floor (27.7%), and optic strut (5%).
Baseline BCVA had significant association with final vision improvement. Lateral wall fracture was the most common fracture associated with indirect TON. Patients treated with high-dose corticosteroids, irrespective of the time of presentation, had a better visual outcome.

Traumatic brain injury (TBI) is a major public health concern, particularly in adolescents who have a higher mortality and incidence of visual pathway injury compared to adult patients. Likewise, we have found disparities between adult and adolescent TBI outcomes in rodents. Most interestingly, adolescents suffer a prolonged apneic period immediately post-injury, leading to higher mortality; therefore, we implemented a brief oxygen exposure paradigm to circumvent this increased mortality. Adolescent male mice experienced a closed-head weight-drop TBI and were then exposed to 100% O2 until normal breathing returned or recovered in room air. We followed mice for 7 and 30 days and assessed their optokinetic response; retinal ganglion cell loss; axonal degeneration; glial reactivity; and retinal ER stress protein levels. O2 reduced adolescent mortality by 40%, improved post-injury visual acuity, and reduced axonal degeneration and gliosis in optical projection regions. ER stress protein expression was altered in injured mice, and mice given O2 utilized different ER stress pathways in a time-dependent manner. Finally, O2 exposure may be mediating these ER stress responses through regulation of the redox-sensitive ER folding protein ERO1α, which has been linked to a reduction in the toxic effects of free radicals in other animal models of ER stress.

Traumatic optic neuropathy (TON) is a condition in which acute injury to the optic nerve from direct or indirect trauma results in vision loss. The most common cause of TON is indirect injury to the optic nerve caused by concussive forces that are transmitted to the optic nerve. TON occurs in up to 5% of closed-head trauma patients and there is currently no known effective treatment. One potential treatment option for TON is ST266, a cell-free biological solution containing the secretome of amnion-derived multipotent progenitor (AMP) cells. We investigated the efficacy of intranasal ST266 in a mouse model of TON induced by blunt head trauma. Injured mice treated with a 10-day regimen of ST266 showed an improvement in spatial memory and learning, a significant preservation of retinal ganglion cells, and a decrease in neuropathological markers in the optic nerve, optic tract, and dorsal lateral geniculate nucleus. ST266 treatment effectively downregulated the NLRP3 inflammasome-mediated neuroinflammation pathway after blunt trauma. Overall, treatment with ST266 was shown to improve functional and pathological outcomes in a mouse model of TON, warranting future exploration of ST266 as a cell-free therapeutic candidate for testing in all optic neuropathies.

OBJECTIVE: Traumatic optic neuropathy (TON) causes partial or complete blindness because death of irreplaceable retinal ganglion cells (RGCs). Neuroprotective functions of erythropoietin (EPO) in the nervous system have been considered by many studies investigating effectiveness of this cytokine in various retinal disease models. It has been found that changes in retinal neurons under conditions of glial cells are effective in vision loss, therefore, the present study hypothesized that EPO neuroprotective effect could be mediated through glial cells in TON model.
METHODS: In this experiment study, 72 rats were assessed in the following groups: intact and optic nerve crush which received either the 4000 IU EPO or saline. Visual evoked potential and optomotor response and RGC number were assessed and regenerated axons evaluated by anterograde test. Cytokines gene expression changes were compared by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Density of astrocytes cells, assessed by fluorescence intensity, in addition, possible cytotoxic effect of EPO was measured on mouse astrocyte culture in vitro.
RESULTS: in vitro data showed that EPO was not toxic for mouse astrocytes. Intravenous injection of EPO improved vision, in terms of visual behavioral tests. RGCs protection was more than two times in EPO, compared to the vehicle group. More regenerated axons were determined by anterograde tracing in the EPO group compared to the vehicle. Moreover, GFAP immunostaining showed while the intensity of reactive astrocytes was increased in injured retina, systemic EPO decreased it. In the treatment group, expression of GFAP was down-regulated, while CNTF was upregulated as assessed by qRT-PCR in the 60th day post-crush.
CONCLUSIONS: Our study showed that systemic administration of EPO can protect degenerating RGCs. Indeed, exogenous EPO exerted neuroprotective and neurotrophic functions by reducing reactive astrocytic gliosis. Therefore, reduction of gliosis by EPO may be considered as therapeutic targets for TON.

UNASSIGNED: To investigate the clinical efficacy and prognostic factors of transnasal endoscopic optic decompression in the treatment of traumatic optic neuropathy (TON).
UNASSIGNED: A retrospective analysis was performed on 13 TON patients in The Seventh Affiliated Hospital of Sun Yat-sen University and Shenzhen Eye Hospital in Shenzhen City (China) from June 2020 to April 2022. These patients had received transnasal endoscopic optic decompression, and hormonal and neurotrophic drugs were given after surgery. Visual acuity (VA) improvement was used as the criterion to judge clinical efficacy.
UNASSIGNED: In a total of 13 patients, 13 injured eyes (12 men and 1 woman; mean age, 28.0 ± 11.8 years) received transnasal endoscopic optic decompression. After surgery, nine patients had improved VA, whereas four patients failed to show any improvement, resulting in a total effective rate of 69.2%. Of the six patients with no light perception preoperatively, three had effective results after the operation, giving an effective rate of 50.0%. Of the seven patients with residual light sensation preoperatively, six had effective results after the operation, giving an effective rate of 85.7%. Of the 10 patients operated on within 7 days after injury, seven had effective results, giving an effective rate of 70%. Of the three patients injured and operated on after 7 days, two had effective results, giving an effective rate of 66.7%.
UNASSIGNED: Transnasal endoscopic optic nerve decompression is an effective treatment method for TON. The presence of residual light perception and the timing of surgery within 7 days are crucial to the prognosis.