Factors predictive of poor visual outcome in indirect traumatic optic neuropathy: A retrospective cohort study.

INTRODUCTION: The gold standard treatment for indirect traumatic optic neuropathy (ITON) has not yet been conclusively established, and it is essential to gain an understanding of visual prognosis and to counsel patients regarding the predictive risk factors of poor visual outcomes. Currently, there is limited information regarding ITON in Thai populations; therefore, this study aimed to determine the risk factors of poor visual outcome in patients with this condition. METHODS: A retrospective review was conducted of all ITON cases diagnosed at Rajavithi Hospital and Sawanpracharak Hospital between January 2016 and December 2022 in order to determine clinical characteristics and evaluate associated risk factors of poor visual prognosis using binary logistic regression analysis. RESULTS: The mean age of this cohort of 101 patients was 36.17 years, with a male predominance of 73.3 %. Motor vehicle accidents were the most common cause of ITON, with a statistically significant 79.2 % of cases. The patients were categorized into an "improved group" of 29 patients and an "unimproved group" of 72. The unimproved group had a significantly older mean age and poorer initial visual acuity of 20/200 (p-values 0.001 and p < 0.001 respectively). There was no significant difference between Computed Tomography (CT) findings in the two groups. The improved group had significantly better visual acuity (VA) at 1-month and final follow-up visit than the unimproved group (both p < 0.001). Differences between gender, Glasgow coma score, associated underlying diseases, and duration from trauma to intravenous glucocorticoids therapy in the two groups were not statistically significant. Multivariable logistic regression analysis identified patient age of 40 years or more (Odds ratio (OR) 3.447, 95 % CI, 1.085-10.955, p = 0.036) and poor baseline VA (OR 6.628, 95 % Confidence Interval (CI), 2.308-19.036, p < 0.001) as significant risk factors for poor visual outcome in ITON patients. CONCLUSIONS: No clear benefit was found of intravenous glucocorticoids in treatment of ITON. Patients aged 40 years or more and/or with poor baseline visual status should be advised that they are at increased risk of poor final visual outcomes.

Optic Nerve Avulsion from Optochiasmal Region Secondary to an Animal Attack: A Case Report.

ABSTRACT: Optic nerve avulsion without bone fracture was observed in four cases in the literature. This case is unique with its cranial effects and complications. A 50-year-old Caucasian female patient attacked by an animal on her left eye was admitted. Traumatic subarachnoid hemorrhage in the suprasellar cistern and epidural hematoma was observed upon brain computed tomography (CT). Enucleation and duraplasty were performed on the patient whose epidural hemorrhage did not increase. Two weeks after being discharged, the patient presented to the emergency room again with numbness on the right side of her face and sensory aphasia. The patient was followed up by medical treatment with left temporoparietal infarction and had completely recovered. Optic nerve avulsion secondary to trauma is a topic that needs to be carefully investigated due to potentially fatal complications. This article was written to share our experience with this rare condition and its case management.

Clinical profile and visual outcome in patients with traumatic optic neuropathy.

Purpose: 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. Methods: 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. Results: 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%). Conclusion: 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 Optic Neuropathy: The Forgotten Concussion.

Cerebral concussions are a well-recognized issue in military and civilian practice. Although most physicians are well versed in recognizing concussion symptoms, many are not as adept at diagnosing and managing comorbid traumatic optic neuropathy (TON). Traumatic optic neuropathy typically follows cerebral concussions but is often not diagnosed as its symptoms are attributed to brain injury or the presence of altered consciousness impedes its recognition. We hereby describe a soldier who sustained a cerebral concussion with an associated unrecognized TON. We review the epidemiology, pathophysiology, diagnosis, and management of TON.

FOCAL RETINAL ISCHEMIA REVEALED BY MULTIMODAL IMAGING AFTER TRAUMATIC PARTIAL OPTIC NERVE AVULSION.

PURPOSE: Traumatic optic neuropathy can have varying presentations. Blunt focal trauma can lead to optic nerve avulsion with underlying retinal findings. A case of partial optic nerve avulsion after finger poke injury leading to focal retinal ischemia is reported. METHODS: Visual acuity, fundus photography with fluorescein angiography, and spectral-domain optical coherence tomography were performed to document the findings in a 16-year-old man who presented after a finger poke injury to the left orbit during a water polo match. RESULTS: On initial presentation, examination revealed decreased visual acuity with a fixed left pupil and afferent pupillary defect by reverse. On slit-lamp examination of the left eye, a hyphema was present. Dilated fundus examination revealed layering vitreous hemorrhage over the posterior pole and an avulsed vitreous base. On follow-up, a gap temporal to the optic nerve head consistent with a partial optic nerve avulsion was noted once the vitreous hemorrhage cleared. Multimodal imaging revealed retinal ischemia temporal to the disc on fluorescein angiography with corresponding changes in the inner retinal layers and retinal nerve fiber layer using spectral-domain optical coherence tomography. CONCLUSION: Clinicians should have a high suspicion for optic nerve avulsion if a patient presents with new vitreous hemorrhage and afferent pupillary defect after a finger-poke injury. Optic nerve avulsion injury can cause retinal ischemia, likely because of interruption of retinal blood flow as a result of nerve shearing injury. Multimodal imaging can reveal focal retinal injury and aid in proper diagnosis and follow-up.

Effect of orbital volume in unilateral orbital fracture on indirect traumatic optic neuropathy.

PURPOSE: This retrospective study aimed to analyze the relationship between the volume of the fractured and the normal orbit in patients with unilateral orbital fractures with and without indirect traumatic optic neuropathy (TON). SUBJECTS: Data of 25 patients with unilateral orbital fractures who underwent computer tomography between January 2016 and December 2020 were investigated. Emergency imaging was performed within 2 hours of arrival at the emergency room. The subjects were categorized into two groups: unilateral orbital fractures with and without TON. METHODS AND MEASURES: The assessment of TON was performed during a comprehensive ophthalmologic examination by an ophthalmologist. The stereographic orbit was reconstructed, and the volume was calculated. Other variables examined included age, sex, and cause of orbital trauma. The variables were compared using paired t-tests. Statistical significance was set at p < 0.05. RESULTS: The orbital volume of the non-fractured orbit was 27.50 ± 2.26 and 27.48 ± 2.64 cm3 in the groups with and without TON, respectively. The average volume of the fractured orbit in the TON group was 27.78 ± 2.56 cm3, and there was no significant volumetric difference between the fractured and non-fractured sides in this group. However, the average volume of the fractured orbit without TON was 28.76 ± 3.18 cm3, larger than that of the non-fractured orbit (p = 0.016). CONCLUSIONS: Non-expansion of the fractured orbit was a risk factor for indirect TON in patients with unilateral orbital fractures. Volumetric analysis from primary imaging would expedite the diagnosis and treatment of TON, resulting in optimal outcomes.

[Optic nerve decompression-state of the art]. / Optikusdekompressionen ­ Stand der Technik.

Rarely, but often with serious consequences for the patient, the optic nerve is affected during the course of head injuries. Traumatic optic nerve compression is always an emergency situation, which is why time is of the essence for both diagnosis and treatment. Precise knowledge of this accident sequelae but also of the resulting conditions, especially in terms of traumatic optic neuropathy, is indispensable for adequate patient care. The aim of this paper is to provide an overview of this clinical picture, particularly with regard to etiology, diagnosis, and treatment options, and to discuss this in the context of the current literature.

Sheath-Preserving Complete Optic Nerve Avulsion Following Closed-Globe Injury: A Case Report.

A 29-year-old man presented with a sudden loss of vision after a closed-globe injury. At presentation, he had no light perception in the right eye and the right pupil was dilated and nonreactive to light. On ophthalmological examination, the area of the optic nerve head was excavated, suggesting optic nerve avulsion. Magnetic resonance imaging scan showed optic nerve avulsion without rupture of the optic nerve sheath. Four months after the injury, the patient's visual acuity remained unchanged. Gliosis developed at the avulsion site. Closed-globe injuries may cause severe posterior injury even if there is no anterior damage in the eye. To prevent unnecessary treatment, trauma patients should be examined carefully appropriate imaging to confirm the diagnosis.

Total Isolated Monocular Vision Loss in a Patient Who Suffered Closed Head Injury.

BACKGROUND: Head injuries are an important cause of morbidity and mortality in children and young adults. There are multiple sight-threatening complications of head injury, even in closed head injury without visible violation of the globe or orbits. One such entity is traumatic optic neuropathy. CASE REPORT: Herein we describe a case of traumatic optic neuropathy in an otherwise healthy teenage patient who suffered total monocular vision loss after a fall and without any other injuries on examination. Unfortunately, the prognosis for this condition is relatively poor in terms of visual recovery. Though much research has been conducted attempting to treat this condition, to date there have been no studies showing a clear benefit of medical or surgical intervention. Why Should an Emergency Physician Be Aware of This? Although there is no proven treatment for traumatic optic neuropathy, emergency physicians may encounter this in their practice while caring for both pediatric and adult patients presenting with head injury. Having more background knowledge on this condition will enhance emergency physicians' ability to consult with subspecialist providers as well as to educate patients and their families on their condition and prognosis.

Traumatic optic neuropathy in orbital wall fractures- diagnostic parameters and treatment outcomes: A prospective observational study.

INTRODUCTION: The aim of the study was to evaluate the associated patterns of orbital wall fractures, diagnostic parameters of Traumatic optic neuropathy and its progress with Mega dose steroid therapy. MATERIALS AND METHODS: 25 patients with unilateral orbital wall fractures of traumatic aetiology were evaluated with ophthalmologic and radiographic parameters. All patients were prescribed Mega Dose Intravenous steroids irrespective of the timing of presentation. Ophthalmic assessment was repeated for same parameters every alternate day upto 2 weeks. RESULTS: Lateral orbital wall was found to be most commonly involved. Visual acuity, Pupillary Reactivity, Visual Field and Visual Evoked Potential showed statistically significant improvement post steroid therapy in early as well as late presenters. DISCUSSION: Highest incidence of Traumatic optic neuropathy was noted in multiple linear orbital wall fractures with highest incidence with lateral orbital wall involvement. Literature regarding Choice and timing of initiation of steroids based on timing of presentation is inadequate to justify skipping steroids to observe or undertake surgical intervention. In the present study marked improvement was noted post steroid therapy regardless of timing of presentation. The authors conclude that Visual evoked potential should be objectively tested and Mega dose steroid therapy should be initiated for all patients with Traumatic optic neuropathy for maximum benefit to the patient.

Contralateral field defect in traumatic globe luxation with optic nerve injury.

CLINICAL RELEVANCE: Traumatic globe luxation is rare vision-threatening event. Besides causing loss of vision in traumatised eye, it may also cause injury to contralateral optic nerve. Any such limitation in a one-eyed patient can make him crippled in his day-to-day activities. Here we hypothesise cause of contralateral field defect in such patients. BACKGROUND: Traumatic globe luxation is a rare event that leads to profound vision loss due to injury of the ipsilateral optic nerve and rarely a visual field defect in the contralateral eye. Through this communication, we report similar case scenarios and intend to hypothesize the mechanism that results in the occurrence of the contralateral visual field defect. METHODS: It is a retrospective, observational study. All cases with traumatic globe luxation were enrolled. Visual field analysis of the contralateral normal eye was main outcome measure. RESULTS: Four patients with traumatic globe luxation and optic nerve injury were studied. There was complete loss of vision in the traumatised eye in all the patients. One patient had complete transection of the optic nerve, whereas in three patients, the course of the optic nerve was intact, on imaging. Three patients had quadrantanopia in the contralateral normal eye for which oral steroids were given. At 1-month follow-up, there was complete recovery of the visual field defect in two patients. We noticed that all the three patients with an intact course of the ipsilateral optic nerve had quadrantanopia in the contralateral normal eye. CONCLUSION: We hypothesize that in scenarios where globe luxation is associated with incomplete transection or no transection of the optic nerve, a continuous long standing stretch on the optic nerve, transmits the pulling force to the chiasma which might result in a contralateral field defect as compared to those associated with the complete transection of the optic nerve.

The Incidence of Traumatic Optic Neuropathy Associated With Subtypes of Orbital Wall Fracture.

BACKGROUND: Traumatic optic neuropathy (TON) is a rare disease but leaves critical sequelae to patient. Purpose of this study is to evaluate the incidence of TON in each orbital wall fracture. MATERIALS AND METHODS: Retrospective review of 2629 patients with orbital wall fracture was performed in from January 2010 to March 2019, based on diagnostic code, Korean Standard Classification of Diseases, 7th Revision. The orbital wall fractures were divided into 4 subtypes: superior, medial, inferior, and lateral wall. Incidence of TON is analyzed according to subtypes, single and multiple wall fracture. RESULTS: Among 2629 patients with orbital wall fractures, 27 patients were diagnosed with TON with an incidence of 1.02%. In single wall fracture, only lateral wall showed significantly high TON incidence, which only zygomatic fracture was included in single lateral wall fracture. In multiple wall fracture, it was statistically significant in the superior wall. CONCLUSIONS: Fracture on lateral and superior orbital wall showed a tendency to increase the incidence of TON. Based on the above results, radiologic evaluation and physical examination is necessary for patient who has lateral and superior orbital wall fracture.

A Tropomycin-Related Kinase B Receptor Activator for the Management of Ocular Blast-Induced Vision Loss.

Pressure waves from explosions or other traumatic events can damage the neurons of the eye and visual centers of the brain, leading to functional loss of vision. There are currently few treatments for such injuries that can be deployed rapidly to mitigate damage. Brain-derived neurotrophic factor (BDNF) and activation of its receptor tropomycin-related kinase B (TrkB) have neuroprotective effects in a number of degeneration models. Small molecule activators of TrkB, such as N-[2-(5-hydroxy-1H-indol-3-yl)ethyl]-2-oxopiperidine-3-carboxamide (HIOC), cross the blood-brain and blood-retina barriers after systemic administration. We characterize the effects of blast-induced ocular trauma on retinal and visual function. We show that systemic administration of HIOC, a potent small molecule activator of the BDNF/TrkB receptor, preserves visual function in mice exposed to ocular blast injury. The HIOC treatment for one week preserves visual function for at least four months. The HIOC treatment effectively protected vision when the initial dose was administered up to 3 h after blast, but not if the initial treatment was delayed for 24 h. We provide evidence that the therapeutic effect of HIOC is mediated by activation of BDNF/TrkB receptors. The results indicate that HIOC may be useful for managing ocular blast injury and other forms of traumatic optic neuropathy.

Sigma-1R Protects Retinal Ganglion Cells in Optic Nerve Crush Model for Glaucoma.

Purpose: The purpose of this study was to determine the effects of the Sigma-1R (σ-1r) on retinal ganglion cell (RGC) survival following optic nerve crush (ONC) and the signaling mechanism involved in the σ-1r protection. Methods: The overall strategy was to induce injury by ONC and mitigate RGC death by increasing σ-1r expression and/or activate σ-1r activity in σ-1r K/O mice and wild type (WT) mice. AAV2-σ-1r vector was used to increase σ-1r expression and σ-1r agonist used to activate the σ-1r and RGCs were counted. Immunohistochemical and Western blot analysis determined phosphorylated (p)-c-Jun, c-Jun, and Caspase-3. Pattern electroretinography (PERG) determined RGC activity. Results: RGC counts and function were similar in pentazocine-treated WT mice when compared to untreated mice and in WT mice when compared with σ-1r K/O mice. Pentazocine-induced effects and the effects of σ-1r K/O were only observable after ONC. ONC resulted in decreased RGC counts and activity in both WT and σ-1r K/O mice, with σ-1r K/O mice experiencing significant decreases compared with WT mice. The σ-1r transgenic expression resulted in increased RGC counts and activity following ONC. In WT mice, treatment with σ-1r agonist pentazocine resulted in increased RGC counts and increased activity when compared with untreated WT mice. There were time-dependent increases in c-jun, p-c-jun, and caspase-3 expression in ONC mice that were mitigated with pentazocine-treatment. Conclusions: These findings suggest that the apoptotic pathway is involved in RGC losses seen in an ONC model. The σ-1r offers neuroprotection, as activation and/or transgenic expression of σ-1r attenuated the apoptotic pathway and restored RGCs number and function following ONC.

Longitudinal In Vivo Changes in Retinal Ganglion Cell Dendritic Morphology After Acute and Chronic Optic Nerve Injury.

Purpose: To characterize in vivo dendritic changes in retinal ganglion cells (RGCs) after acute (optic nerve transection, ONT) and chronic (experimental glaucoma, EG) optic nerve injury. Methods: ONT and EG (microbead model) were carried out in Thy1-YFP mice in which the entire RGC dendritic arbor was imaged with confocal fluorescence scanning laser ophthalmoscopy over two weeks in the ONT group and over two and six months, respectively, in two (groups 1 and 2) EG groups. Sholl analysis was used to quantify dendritic structure with the parameters: area under the curve (AUC), radius of the dendritic field, peak number of intersections (PI), and distance to the PI (PD). Results: Dendritic changes were observed after three days post-ONT with significant decreases in all parameters at two weeks. In group 1 EG mice, mean (SD) intraocular pressure (IOP) was 15.2 (1.1) and 9.8 (0.3) mmHg in the EG and untreated contralateral eyes, respectively, with a significant corresponding decrease in AUC, PI, and PD, but not radius. In group 2 mice, the respective IOP was 13.1 (1.0) and 8.8 (0.1) mmHg, peaking at two months before trending towards baseline. Over the first two months, AUC, PI, and PD decreased significantly, with no further subsequent changes. The rates of change of the parameters after ONT was 5 to 10 times faster than in EG. Conclusions: Rapid dendritic changes occurred after ONT, while changes in EG were slower and associated with level of IOP increase. The earliest alterations were loss of inner neurites without change in dendritic field.

The effect of 4.5 G (LTE Advanced-Pro network) mobile phone radiation on the optic nerve.

PURPOSE: Rapid development in mobile phone technologies increase the average mobile phone usage duration. This increase also triggers exposure to radiofrequency radiation (RF), which is a risk factor for the health. In this study, it was aimed to investigate the effect of mobile phone working with LTE-Advanced Pro (4.5 G) mobile network on the optic nerve, which is responsible for the transmission of visual information. MATERIAL AND METHODS: Thirty-two rats divided into two groups as control (no RF, sham exposure) and experimental (RF exposure using a mobile phone with LTE-Advanced Pro network; 2 hours/day, 6 weeks). The visual evoked potential (VEP) was recorded and determined amplitudes and latencies of VEP waves. Optic nerve malondialdehyde level, catalase and superoxide dismutase activities were determined. Furthermore, ultrastructural and morphometric changes of optic nerve were evaluated. RESULTS: In VEP recordings, the mean VEP amplitudes of experimental group were significantly lower than control group. In ultrastructural evaluation, myelinated nerve fibres and glial cells were observed in normal histologic appearance both in sham and experimental group. However, by performing morphometric analysis, in the experimental group, axonal diameter and myelin thickness were shown to be lower and the G-ratio was higher than in the sham group. In the experimental group, malondialdehyde level was significantly higher and superoxide dismutase and catalase activities were significantly lower than sham group. There was a high correlation between VEP wave amplitudes and oxidative stress markers. CONCLUSION: Findings obtained in this study support optic nerve damage. These results point out an important risk that may decrease the quality of life.

Chemokine CCL5 promotes robust optic nerve regeneration and mediates many of the effects of CNTF gene therapy.

Ciliary neurotrophic factor (CNTF) is a leading therapeutic candidate for several ocular diseases and induces optic nerve regeneration in animal models. Paradoxically, however, although CNTF gene therapy promotes extensive regeneration, recombinant CNTF (rCNTF) has little effect. Because intraocular viral vectors induce inflammation, and because CNTF is an immune modulator, we investigated whether CNTF gene therapy acts indirectly through other immune mediators. The beneficial effects of CNTF gene therapy remained unchanged after deleting CNTF receptor alpha (CNTFRα) in retinal ganglion cells (RGCs), the projection neurons of the retina, but were diminished by depleting neutrophils or by genetically suppressing monocyte infiltration. CNTF gene therapy increased expression of C-C motif chemokine ligand 5 (CCL5) in immune cells and retinal glia, and recombinant CCL5 induced extensive axon regeneration. Conversely, CRISPR-mediated knockdown of the cognate receptor (CCR5) in RGCs or treating wild-type mice with a CCR5 antagonist repressed the effects of CNTF gene therapy. Thus, CCL5 is a previously unrecognized, potent activator of optic nerve regeneration and mediates many of the effects of CNTF gene therapy.

Visual deficits after traumatic brain injury.

Traumatic brain injury (TBI) is frequently described as any head injury ceasing the brain's normal function. Anatomically, developmentally, and physiologically, the eye is deemed as an extension of the brain. Vision in TBI is underrepresented, and the number of active clinical trials in this field are sparse. Frequently, visual problems are overlooked at the time of TBI, often resulting in progressive vision loss, lengthening, and impairing rehabilitation. TBI can be either penetrative or non-penetrative, associated with degeneration of neurons, apoptotic cell death, inflammation, microglial activation, hemorrhage associated with vascular dysfunction; however, precise animal modeling that mimics the extensive visual deficits of TBI pathology remain elusive. Recent works in both the diagnostics and therapeutics fields are starting to make substantial progress in the right direction. Discussion of current advancements in TBI animal models and the recent pathophysiological findings related to the neuro-glia-vascular unit (NVU) will help elucidate novel targets for potential therapeutics lines. Only over the past decade have newer pharmaceutical and stem cell-based treatments begun to come to light. The potency for these new lines of TBI specific curatives will be discussed along with the review of current blast-induced TBI models, providing potential directions for future research.

How curcumin affects hyperglycemia-induced optic nerve damage: A short review.

Considered to be one of the most important non-contagious systemic diseases worldwide, diabetes mellitus is still a topical issue on the health agenda with the problems it causes. Exposure to long-term hyperglycemia causes diabetic complications (diabetic neuropathy, nephropathy and retinopathy). The optic nerve can suffer damage by both diabetic retinopathy and neuropathy during diabetes, both because it is formed by axons of retinal ganglion cells and these axons belong to the central nervous system. The issue of hyperglycemia on the optic nerve have been described as diabetic papillopathy, posterior ischemic optic neuropathy, nonarteritic anterior ischemic optic neuropathy and optic atrophy in clinical studies. Experimental studies indicated axon-myelin degeneration in addition to microvascular and ultrastructural changes caused by the hyperglycemia-induced optic nerve damage. Although there are several proposed biochemical mechanisms to cause these damages, oxidative stress emerges as an important factor among them. Oxidative stress leads to pathological state on the nerve cells by affecting the DNA, protein and lipids at different levels. These are causing deterioration on nerve conduction velocity, myelin sheath and nerve structure, neurotrophic support system, glial cells and nerve function. Curcumin, as an important antioxidant, can be an ideal prophylactic agent to eliminate damages on optic nerve. Curcumin helps to regulate the balance of antioxidant and reactive oxygen species by targeting various molecules (NF-κB, STAT3, MAPK, Mfn2, Nrf2, pro-inflammatory cytokines). In addition, it shows healing or preventive effects on myelin sheath damage via regulating ferritin protein in oligodendrocytes. It is also effective in preventing neurovascular damage.