Impaired Visual Function Research Articles

Anterior clinoid process metastasis with sudden loss of vision: role of emergency optic nerve decompression

Abstract Background Anterior clinoid process metastases are rare. We present an unusual case of anterior clinoid process metastasis with sudden deterioration of visual function requiring emergency optic nerve decompression, resulting in visual recovery. Case presentation We report the case of a 41-year-old male patient with a diagnosis of radius leiomyosarcoma, who underwent surgery in 2014, with bone and lung metastases, who had been treated with chemotherapy and appeared to have the disease controlled at his last follow-up. 6 years later, he developed a one month history of progressive unilateral loss of visual acuity and visual field defect (initially quadrantanopia that progressed to nasal hemianopia). Brain imaging showed a contrast-enhancing lesion affecting the left anterior clinoid process with extension to the cavernous sinus and sphenoid sinus, causing compression of the left optic nerve. Although the lesion could have suggested a meningioma given the location, in the context of the patient’s oncological history, the diagnosis of metastasis was considered more likely. The patient was admitted to hospital and, during the hospital stay, developed sudden left retro-orbital pain progressing to left amaurosis over approximately 8 h. Urgent surgery was performed: a pterional craniotomy with partial tumor removal and optic nerve decompression with extradural anterior clinoidectomy. After surgery, the patient had an immediate but partial improvement in visual acuity and in the visual field defect. Conclusions Metastasis to the anterior clinoid process is very uncommon, with only one case previously reported in the literature. In cases of visual impairment, symptoms may deteriorate rapidly to complete loss of vision, so urgent decompressive surgery of the optic nerve may be indicated to recover visual function, although recovery may be partial.

Visual Impairment in Stroke Patients: a Two-Part Review. Part II — Rehabilitation Methods

INTRODUCTION. The search and development of optimal rehabilitation programs for patients who have suffered acute cerebrovascular accident (OMNA) is an urgent problem of modern medicine. The development of scientific and technical capabilities leads to the active introduction of the latest technologies at different stages of medical rehabilitation of cerebral stroke. This article is the second part of a two-part review devoted to the problem of visual impairment in patients with acute cerebrovascular accident, which provides an overview of the methods of rehabilitation of patients in this category. MAIN CONTENT OF THE REWIEW. This overview of rehabilitation methods for patients with impaired visual functions who have undergone OMNA is based on publications in international and domestic databases OpenAlex, Scilit, Lens, PubMed, Cyberleninka and eLibrary available for analysis by 15.08.2024, with a search depth of mainly 15 years. As a result of the search, 66 articles on a given topic were reviewed. In addition, 6 sources dated from an earlier period (1989–2005) were used, as they contain the necessary information within the framework of this review. The rehabilitation methods considered in the review correspond to the accepted basic strategies for restoring impaired visual functions, including those caused by cerebral stroke. Two main strategies include the use of optical devices to adapt to the environment and training of intact structures of the visual analyzer aimed at compensating for lost functions. The third strategy is aimed at increasing the processing of visual information in areas of residual vision. CONCLUSION. The variety of types of visual disorders, the degree of influence on the quality of life of stroke patients, necessitates the search and development of optimal rehabilitation programs. This will significantly expand the choice of recovery options after a cerebral stroke in this category of patients.

Longitudinal assessment of retinal and visual pathway electrophysiology and structure after high altitude exposure.

High altitude (HA) exposure induces impairments in visual function. This study was designed to dynamically observe visual function after returning to lowland and elucidate the underlying mechanism by examining the structure and function of retina and visual pathway. Twenty-three subjects were recruited before (Test 1), and one week (Test 2) and three months (Test 3) after their return from HA (4300m) where they resided for 30 days. The clock task was used to assess visual cognition; and pattern-reversal visual evoked potential (p-VEP) and full-field electroretinogram (ff-ERG) were employed to record electrophysiological responses of retinal cells; optical coherence tomography (OCT), color doppler imaging (CDI) and magnetic resonance imaging(MRI) were used to measure structures of retina and visual pathway. In Test 2 vs. Test 1, there was increased reaction time during angle task; the amplitudes of scotopic 3.0cd·s/m2 and scotopic 10.0cd·s/m2 ERG a-wave and scotopic 3.0cd·s/m2 oscillatory potential in the right eye were significantly decreased, all of which were negatively correlated with the increased reaction time during the angle task. In Test 3 vs. Test 1, there were decreased amplitude of scotopic 10.0cd·s/m2 a-wave in the right eye and increased velocity of ophthalmic artery and ocular perfusion pressure in bilateral eyes. The VEP and visual pathway structures remained normal throughout the entire test. HA exposure caused damage to rod and cone responses in both outer and inner retina. After returning to sea level, the damaged visual cell functions gradually recovered over time, coinciding with an increase in the ocular perfusion.

Early diagnosis and prognosis of traumatic optic neuropathy

Traumatic optic neuropathy (TON) caused by blunt eye injuries represents a significant clinical challenge, frequently leading to irreversible vision loss. Early diagnosis and monitoring of retinal and optic nerve changes are crucial for improving patient outcomes. Optical coherence tomography (OCT) offers unparalleled capabilities in detecting and quantitatively assessing such changes. Objective. To evaluate the diagnostic potential of OCT in identifying morphological and functional changes in the retina and optic nerve among patients with TON. Materials and Methods. A total of 40 patients with blunt eye trauma were examined. The diagnostic protocol included OCT, computer perimetry, visual acuity testing, and ophthalmoscopy. Parameters of the RNFL, GCIPL, macula, and optic nerve head were analyzed. Results. Patients with TON demonstrated significant RNFL thickening in the early stages of trauma, optic nerve head swelling, and GCIPL thinning, which correlated with impaired visual function. OCT proved to be highly effective for early diagnosis and monitoring of these changes. Conclusion. OCT is a pivotal tool for assessing retinal and optic nerve damage in TON, enabling improved diagnostics, prognostication, and patient management.

Modeling sacsin depletion in Danio Rerio offers new insight on retinal defects in ARSACS.

Biallelic mutations in the SACS gene, encoding sacsin, cause early-onset autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS), a neurodegenerative disease also characterized by unique and poorly understood retinal abnormalities. While two murine models replicate the phenotypic and neuronal features observed in patients, no retinal phenotype has been described so far. In a zebrafish knock-out strain that faithfully mirrors the main aspects of ARSACS, we observed impaired visual function due to photoreceptor degeneration, likely caused by cell cycle defects in progenitor cells. RNA-seq analysis in embryos revealed dysfunction in proteins related to fat-soluble vitamins (e.g., TTPA, RDH5, VKORC) and suggested a key role of neuroinflammation in driving the retinal defects. Our findings indicate that studying retinal pathology in ARSACS could be crucial for understanding the impact of sacsin depletion and may offer insights into halting disease progression.

Thioredoxin-interacting protein (TXNIP) inhibition promotes retinal ganglion cell survival and facilitates M1-like microglial transformation via the PI3K/Akt pathway in glaucoma

Abstract Background Glaucoma is a group of heterogeneous neurodegenerative diseases with abnormal energy metabolism and imbalanced neuroinflammation in the retina. Thioredoxin-interacting protein (TXNIP) is involved in glucose and lipid metabolism, and associated with oxidative stress and inflammation, however, not known whether to be involved in glaucoma neuropathy and its underlying mechanisms. Methods To establish the chronic ocular hypertension (COH) mice model. Western blot, RT-PCR, immunofluorescence and F-VEP were used to detect neuroinflammation level, glial activation and RGCs survival in retina of wild type, TXNIP knockout and MCC950 treatment COH mice. Microglia high-pressure cultured model was constructed. Western blot, RT-PCR and immunofluorescence were used to investigate the proinflammatory cytokines secretion, glucose uptake and phenotype transformation in wild type, TXNIP knockout and overexpressed microglia combined with IL-17A treatment. Finally, we explored the possible underlying mechanisms using relevant pathway inhibitor interventions. Results In this study, for the first time we reported that TXNIP expression was remarkably increased in experimental glaucomatous retina of chronic ocular hypertension (COH) mice, and it was mainly expressed in the ganglion cells layer (GCL). In addition, we found that ablation of TXNIP promoted retinal ganglion cells (RGCs) survival and alleviated visual function impairment in experimental glaucoma. Then, we explored the spatiotemporal consistency between glial activation and retinal inflammation levels in COH mice respectively with TXNIP-deficiency and under treatment of a thermo-containing protein domain 3 (NLRP3) inhibitor MCC950, and the results indicated that TXNIP probably mediated neuroinflammation in glaucomatous retina by activating microglia. Furthermore, upregulation of TXNIP was found in pressure-stimulated microglia, whereas silencing TXNIP facilitated microglial polarization trending towards M1 type and reduced glucose transporter-1 (Glut-1) expression on microglia under high pressure in vitro. Moreover, IL-17A was found to play a role in acting synergistically with TXNIP upon the regulation of microglia polarity transformation. Finally, knockout of TXNIP was revealed to promote PI3K phosphorylation, whereas inhibition of PI3K by LY294002 effectively suppressed Glut-1 expression, glucose uptake, and M1-like transformation tendency in microglia obtained from TXNIP-deficiency mice under high pressure stimulation. Conclusions TXNIP is significantly involved in the inflammation-related neuropathy of experimental glaucoma and probably facilitates M1-like microglial transformation via PI3K/Akt pathway.

Normative prospective data on automatically quantified retinal morphology correlated to retinal function in healthy ageing eyes by two microperimetry devices.

The relationship between retinal morphology, as assessed by optical coherence tomography (OCT), and retinal function in microperimetry (MP) has not been well studied, despite its increasing importance as an essential functional endpoint for clinical trials and emerging therapies in retinal diseases. Normative databases of healthy ageing eyes are largely missing from literature. Healthy subjects above 50 years were examined using two MP devices, MP-3 (NIDEK) and MAIA (iCare). An identical grid, encompassing 45 stimuli was used for retinal sensitivity (RS) assessment. Deep-learning-based algorithms performed automated segmentation of ellipsoid zone (EZ), outer nuclear layer (ONL), ganglion cell layer (GCL) and retinal nerve fibre layer (RNFL) from OCT volumes (Spectralis, Heidelberg). Pointwise co-registration between each MP stimulus and corresponding location on OCT was performed via registration algorithm. Effect of age, eccentricity and layer thickness on RS was assessed by mixed effect models. Three thousand six hundred stimuli from twenty eyes of twenty patients were included. Mean patient age was 68.9 ± 10.9 years. Mean RS for the first exam was 28.65 ± 2.49 dB and 25.5 ± 2.81 dB for MP-3 and MAIA, respectively. Increased EZ thickness, ONL thickness and GCL thickness were significantly correlated with increased RS (all p < 0.001). Univariate models showed lower RS with advanced age and higher eccentricity (both p < 0.05). This work provides reference values for healthy age-related EZ and ONL-thicknesses without impairment of visual function and evidence for RS decrease with eccentricity and increasing age. This information is crucial for interpretation of future clinical trials in disease.

Age-Related Viability of Patients with Ophthalmopathology Depending on Age Dissociation

Diabetic retinopathy and senile cataracts cause not only a significant impairment of visual functions, but also can affect the psychological and emotional status of patients and their age-related viability, which has not been practically studied in patients with the abovementioned ophthalmological diseases.The purpose: to study age–related viability in patients with ophthalmopathology depending on age dissociation. Age viability was studied among 135 patients aged 60–74 years with diabetic retinopathy and cataract with coincidence of calendar and biological age and 142 patients aged 60–74 years with diabetic retinopathy and cataract with accelerated biological age. It was found that diabetic retinopathy and cataract cause a more significant decrease in age viability in patients with an excess of the biological age of the chronological age to 60,1 ± 1,7 points versus 76,4 ± 1,5 points (p &lt; 0,001) in diabetic retinopathy and cataract with the coincidence of biological and calendar age. A similar effect was found for the somatic component of age-related viability, which in patients with diabetic retinopathy and cataract with an excess of the biological age of the chronological value was 4,2 ± 0,5 points relative to 2,2 ± 0,4 points (p &lt; 0,01) in patients with diabetic retinopathy and cataract, who had a coincidence of biological and calendar age. Diabetic retinopathy and cataracts are most affected when the biological age of the calendar value is exceeded among the subdomains of age viability, such as relationship security and positivity of accepted changes, resistance to adverse influences and trust in personal instincts with a significant difference between groups. Diabetic retinopathy and cataracts in patients with exceeding the biological age of the calendar significantly reduce age viability.

Loss of Pigment Epithelium Derived Factor Sensitizes C57BL/6J Mice to Light-Induced Retinal Damage.

Pigment epithelium-derived factor (PEDF) is a neurotrophic glycoprotein secreted by the retinal pigment epithelium (RPE) that supports retinal photoreceptor health. Deficits in PEDF are associated with increased inflammation and retinal degeneration in aging and diabetic retinopathy. We hypothesized that light-induced stress in C57BL/6J mice deficient in PEDF would lead to increased retinal neuronal and RPE defects, impaired expression of neurotrophic factor Insulin-like growth factor 1 (IGF-1), and overactivation of Galectin-3-mediated inflammatory signaling. C57BL/6J mice expressing the RPE65 M450/M450 allele were crossed to PEDF KO/KO and wildtype (PEDF +/+) littermates. Mice were exposed to 50,000 lux light for 5 hours to initiate acute damage. Changes in visual function outcomes were tracked via electroretinogram (ERG), confocal scanning laser ophthalmoscopy(cSLO), and spectral domain optical coherence tomography (SD-OCT) on days 3, 5, and 7 post-light exposure. Gene and protein expression of Galectin-3 were measured by digital drop PCR (ddPCR) and western blot. To further investigate the role of galectin-3 on visual outcomes and PEDF expression after damage, we also used a small-molecule inhibitor to reduce its activity. Following light damage, PEDF KO/KO mice showed more severe retinal thinning, impaired visual function (reduced a-, b-, and c-wave amplitudes), and increased Galectin-3 expressing immune cell infiltration compared to PEDF +/+. PEDF KO/KO mice had suppressed damage-associated increases in IGF-1 expression. Additionally, baseline Galectin-3 mRNA and protein expression were reduced in PEDF KO/KO mice compared to PEDF +/+. However, after light damage, Galectin-3 expression decreases in PEDF +/+ mice but increases in PEDF KO/KO mice without reaching PEDF +/+ levels. Galectin-3 inhibition worsens retinal degeneration, reduces PEDF expression in PEDF +/+ mice, and mimics the effects seen in PEDF knockouts. Loss of PEDF alone does not elicit functional defects in C57BL/6J mice. However, under light stress, PEDF deficiency significantly increases severe retinal degeneration, visual deficits, Galectin-3 expression, and suppression of IGF-1 than PEDF +/+. PEDF deficiency reduced baseline expression of Galectin-3, and pharmacological inhibition of Galectin-3 worsens outcomes and suppresses PEDF expression in PEDF +/+, suggesting a novel co-regulatory relationship between the two proteins in mitigating light-induced retinal damage.

Mettl3-Mediated m6A Modification is Essential for Visual Function and Retinal Photoreceptor Survival.

N6-methyladenosine (m6A) modification, one of the most common epigenetic modifications in eukaryotic mRNA, has been shown to play a role in the development and function of the mammalian nervous system by regulating the biological fate of mRNA. METTL3, the catalytically active component of the m6A methyltransferase complex, has been shown to be essential in development of in the retina. However, its role in the mature retina remains elusive. In this study we aim to investigate the in vivo function of Mettl3 in the photoreceptor cells using a conditional knockout allele of Mettl3. Deletion of Mettl3 in rod cells led to progressive retinal degeneration, including progressive retinal thinning, impaired visual function, shortened photoreceptor outer segments (OS), and reduced expression of disk membrane proteins. Similarly, Mettl3 deficiency in cone cells led to the gradual degeneration of cone opsins. Additionally, Mettl3 knockout significantly decreased the expression of the METTL14 subunit and overall m6A methylation levels in the retina. Multi-omics analyses revealed that Mettl3 deletion led to the downregulation of mRNA and protein levels of 10 key target genes in rod cells, ultimately resulting in the progressive death of photoreceptors. Mettl3 controls expression of its target genes by regulating their m6A modification, ultimately leading to rod cell death. These findings highlight critical roles of METTL3 in maintaining retinal photoreceptor function and further elucidate the mechanisms of m6A modification in photoreceptors.

Stirred Not Shaken: A Longitudinal Pilot Study of Head Kinematics and Cognitive Changes in Horseracing

The purpose of this longitudinal pilot study was to add to the body of research relating to head kinematics/vibration in sport and their potential to cause short-term alterations in brain function. In horseracing, due to the horse’s movement, repeated low-level accelerations are transmitted to the jockey’s head. To measure this, professional jockeys (2 male, 2 female) wore an inertial measurement unit (IMU) to record their head kinematics while riding out. In addition, a short battery of tests (Stroop, Trail Making Test B, choice reaction time, manual dexterity, and visual function) was completed immediately before and after riding. Pre- and post-outcome measures from the cognitive test battery were compared using descriptive statistics. The average head kinematics measured across all jockeys and days were at a low level: resultant linear acceleration peak = 5.82 ± 1.08 g, mean = 1.02 ± 0.01 g; resultant rotational velocity peak = 10.37 ± 3.23 rad/s, mean = 0.85 ± 0.15 rad/s; and resultant rotational acceleration peak = 1495 ± 532.75 rad/s2, mean = 86.58 ± 15.54 rad/s2. The duration of an acceleration event was on average 127.04 ± 17.22 ms for linear accelerations and 89.42 ± 19.74 ms for rotational accelerations. This was longer than those noted in many impact and non-impact sports. Jockeys experienced high counts of linear and rotational head accelerations above 3 g and 400 rad/s2, which are considered normal daily living levels (average 300 linear and 445 rotational accelerations per hour of riding). No measurable decline in executive function or dexterity was found after riding; however, a deterioration in visual function (near point convergence and accommodation) was seen. This work lays the foundation for future large-scale research to monitor the head kinematics of riders, measure the effects and understand variables that might influence them.

REMOTE FUNCTIONAL RESULTS PATIENTS WITH MACULAR HOLE AND RHEGMATOGENOUS RETINAL DETACHMENT SURGICAL TREATMENT WITH DIFFERENT VOLUMES OF PRESERVATION OF THE INTERNAL LIMITING MEMBRANE ACCORDING TO MICROPERIMETRY DATA

Rationale: Macular hole is a defect of the retina in the foveolar zone. In combination with rhegmatogenous retinal detachment, this disease can lead to irreversible deterioration of visual functions and requires immediate surgical treatment. One of the trends in modern ophthalmic surgery is to increase the area of preservation of the internal limiting membrane during the macular hole blocking. Despite this, microperimetry data indicate the appearance of microscotomas at the point of peeling initiation and a general decrease in the photosensitivity of the retinal tissue in the membrane removal zone.Objective: to analyze the dynamics of changes in the retinal functional parameters of patients with macular hole and rhegmatogenous retinal detachment according to microperimetry data after surgical treatment in the late postoperative period.Methods: Data from 40 patients (40 eyes) diagnosed with macular hole and rhegmatogenous retinal detachment were prospectively studied. Patients in group 1 (20 patients, 20 eyes) underwent surgical treatment, including three-port 25G vitrectomy, perfluoroorganic compound, vitreous body sanitation at the periphery, and silicone tamponade. Membrane peeling was performed during the second operation to remove silicone. Patients in group 2 underwent vitrectomy, membrane staining under the perfluorine layer, membrane peeling with closure of the macular hole with an inverted flap, vitreous body sanitation during the first intervention. The operation was also completed with silicone tamponade. During the second intervention, silicone oil was removed from the vitreous cavity.Results: When comparing the light sensitivity index of the retinal tissue in the foveolar zone between the groups, a reliable difference in the indices by 1.2 times continued to persist up to one and a half years after the final stage of surgical treatment, there was a predominance of values in patients of the 1st group with a completely preserved membrane (p = 0.043 in comparison with the data of patients of the 2nd group). In three peripheral zones of the macula, during the long-term observation period up to one and a half years after surgery, the indices of patients of the 1st group prevailed by 1.5 times (p = 0.041 in comparison with the data of patients of the 2nd group).Conclusion: based on the analysis of the dynamics of the functional indices of the retina of patients after surgical treatment of macular hole in combination with rhegmatogenous retinal detachment, the refusal to perform membrane peeling on the detached retina during the first stage of surgical intervention allows to avoid aggressive mechanical trauma to the retinal tissue.

Therapeutic Strategies for Retinal Artery Occlusion-A Literature Review.

Retinal artery occlusion (RAO) is an emergency condition causing acute retinal ischemia and is considered an equivalent of ischemic stroke. The occurrence of an episode of RAO is associated with significant impairment of visual functions and correlates with an increased risk of future vascular events. Although RAO requires immediate diagnosis and treatment, there are currently no clear guidelines specifying optimal management. This review discusses current and future therapeutic strategies following an episode of RAO, including secondary prevention.

SURGICAL TREATMENT OF CYSTIC FILTRATION BLEBS AFTER SINUSTRABECULECTOMY: CASES FROM PRACTICE

The article presents two similar clinical cases. Patients with complaints of bulbar conjunctiva neoplasm, which grew on the cornea, caused a pronounced feeling of discomfort and partially impaired visual functions, turned to the department of surgical treatment of glaucoma of the MNTC “Eye Microsurgery”. It should be noted that previously these patients underwent a sinustrabeculectomy at their place of residence in order to reduce intraocular pressure. After examination and additional instrumental research methods, the presence of a cystic filtration bleb was diagnosed and the area of anti-glaucoma surgery was revised with individual characteristics in each case. As a result of the treatment, a positive effect was achieved. At a repeat visit a month after surgery, patients did not complain, intraocular pressure was compensated, and there were no relapses.

A preliminary exploration of quantitative models for evaluating binocular visual perception impairments among patients diagnosed with stroke.

The objective of this study is to formulate and implement graded biological models pertaining to binocular visual perception function with the use of computer algorithms. We aim to quantitatively assess the location, severity, and degree of impairment in binocular visual perception among patients who have suffered stroke, thereby providing valuable insights into the repercussions of cerebral tissue damage on the visual system. To overcome the shortcomings of previous instruments used to assess binocular function in terms of stereoscopic effects and the challenges posed by physiological and psychological interference during examinations, this study optimized its approach by integrating polarized stereovision technology with computer graphic modeling techniques. This study employed computer models to assess binocular visual perception function in stroke patients. Computer models refer to psychophysical testing methods used to measure binocular visual perception function, including various assessment tasks such as recognizing inverted letters and assessing stereopsis during high-speed movements. The cross-into-circle test was used as a means to quantify perceptual eye position. Subsequently, the collected data was analyzed to assess the magnitude of impairment in binocular visual perception. The results of the study revealed a spectrum of binocular visual perception impairment among patients diagnosed with stroke, demonstrating discernible variations in the recognition of inverted letters and stereopsis across different movement speeds. Importantly, perceptual eye position measurements offered valuable insights into ocular misalignment. The computational models effectively quantified both the spatial distribution and severity of these identified impairments. Damage to brain tissue resulting from a stroke can give rise to notable impairments in binocular visual perception function. Graded biological models, formulated through computer algorithms, provide a systematic framework for the comprehensive evaluation and quantification of these impairments. The comprehension of the nature and extent of visual impairments observed in patients with stroke establishes a basis for the development of personalized visual perception learning methodologies. Based on such tailored approaches, we aim to facilitate the recovery of impaired visual function, thereby contributing to the broader objective of neural system rehabilitation.

Corticosteroids and glaucoma: How do treatments trigger ocular nerve damage? - A systematic literature review

Corticosteroids are steroid hormone derivatives produced by the adrenal glands. Corticosteroids in the health sector have been widely utilized as anti-inflammatory agents because of their strong and rapid effects. This study aimed to identify the impact of long-term corticosteroid use on eye damage. This study uses a systematic literature review, which is guided by the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) to the article screening process. The data of this study, in the form of demographic variables, route of administration, steroid type, comorbidities, and patient risk factors, were descriptively analyzed. As a result, 15 of the 22 articles were selected for analysis. Chronic corticosteroid administration may precipitate optic neuropathy, manifesting as glaucoma, which is characterized by progressive structural degeneration of retinal ganglion cells (RGCs) and concomitant visual function deterioration. The locus of primary pathological insult in glaucomatous conditions is the optic nerve head, specifically at the optic disc. This anatomical site is notable for the abrupt 90-degree angular deviation of RGC axons as they transition from the retinal nerve fiber layer to their trajectory within the optic nerve proper. The use of corticosteroids can damage ocular nerve tissue through an increase in intraocular pressure (IOP) beyond 21 mmHg. This increase in IOP is due to changes in the microstructure of the trabeculum webbing, resulting in increased obstruction to the outflow of aqueous humor.

Demyelination and neurodegeneration early in experimental autoimmune encephalomyelitis contribute to functional deficits in the anterior visual pathway

Impaired visual function is a prevalent feature of optic neuritis (ON) in multiple sclerosis (MS). Abnormal visual evoked potential (VEP) findings of increased latencies, reduced amplitudes and abnormal waveforms as well as decreased retinal nerve fiber layer (RNFL) assessed by optical coherence tomography (OCT) are hallmarks of ON-induced visual dysfunction. Here we utilized the experimental autoimmune encephalomyelitis (EAE) mouse model of MS to investigate the functional and pathological progression during early (before any clinical symptoms), peak (initial maximal clinical symptoms), and late (chronic disease for > 3 weeks) disease stages. Demyelination and initial stages of axon damage were observed in early EAE. Significant demyelination, inflammation, increased axon damage and impaired P1/N2 amplitudes and latencies by VEP were seen in middle and late EAE groups. A decrease in RNFL thickness by OCT was observed only during late EAE. NanoString analysis of optic nerves from late EAE indicated elevated inflammation-related genes, reduced myelin-related genes, and changes in axon degeneration-related genes. Early inflammatory demyelination and functional deficits of the visual pathway, if untreated, may lead to severe irrecoverable axon damage in EAE. These studies potentially help explain the progression of visual dysfunction during MS.

Transcriptional responses in a mouse model of silicone wire embolization induced acute retinal artery ischemia and reperfusion.

Acute retinal ischemia and ischemia-reperfusion injury are the primary causes of retinal neural cell death and vision loss in retinal artery occlusion (RAO). The absence of an accurate mouse model for simulating the retinal ischemic process has hindered progress in developing neuroprotective agents for RAO. We developed a unilateral pterygopalatine ophthalmic artery occlusion (UPOAO) mouse model using silicone wire embolization combined with carotid artery ligation. The survival of retinal ganglion cells and visual function were evaluated to determine the duration of ischemia. Immunofluorescence staining, optical coherence tomography, and haematoxylin and eosin staining were utilized to assess changes in major neural cell classes and retinal structure degeneration at two reperfusion durations. Transcriptomics was employed to investigate alterations in the pathological process of UPOAO following ischemia and reperfusion, highlighting transcriptomic differences between UPOAO and other retinal ischemia-reperfusion models. The UPOAO model successfully replicated the acute interruption of retinal blood supply observed in RAO. 60 min of Ischemia led to significant loss of major retinal neural cells and visual function impairment. Notable thinning of the inner retinal layer, especially the ganglion cell layer, was evident post-UPOAO. Temporal transcriptome analysis revealed various pathophysiological processes related to immune cell migration, oxidative stress, and immune inflammation during the non-reperfusion and reperfusion periods. A pronounced increase in microglia within the retina and peripheral leukocytes accessing the retina was observed during reperfusion periods. Comparison of differentially expressed genes (DEGs) between the UPOAO and high intraocular pressure models revealed specific enrichments in lipid and steroid metabolism-related genes in the UPOAO model. The UPOAO model emerges as a novel tool for screening pathogenic genes and promoting further therapeutic research in RAO.

Transcriptional responses in a mouse model of silicone wire embolization induced acute retinal artery ischemia and reperfusion

Acute retinal ischemia and ischemia-reperfusion injury are the primary causes of retinal neural cell death and vision loss in retinal artery occlusion (RAO). The absence of an accurate mouse model for simulating the retinal ischemic process has hindered progress in developing neuroprotective agents for RAO. We developed a unilateral pterygopalatine ophthalmic artery occlusion (UPOAO) mouse model using silicone wire embolization combined with carotid artery ligation. The survival of retinal ganglion cells and visual function were evaluated to determine the duration of ischemia. Immunofluorescence staining, optical coherence tomography, and haematoxylin and eosin staining were utilized to assess changes in major neural cell classes and retinal structure degeneration at two reperfusion durations. Transcriptomics was employed to investigate alterations in the pathological process of UPOAO following ischemia and reperfusion, highlighting transcriptomic differences between UPOAO and other retinal ischemia-reperfusion models. The UPOAO model successfully replicated the acute interruption of retinal blood supply observed in RAO. 60 min of Ischemia led to significant loss of major retinal neural cells and visual function impairment. Notable thinning of the inner retinal layer, especially the ganglion cell layer, was evident post-UPOAO. Temporal transcriptome analysis revealed various pathophysiological processes related to immune cell migration, oxidative stress, and immune inflammation during the non-reperfusion and reperfusion periods. A pronounced increase in microglia within the retina and peripheral leukocytes accessing the retina was observed during reperfusion periods. Comparison of differentially expressed genes (DEGs) between the UPOAO and high intraocular pressure models revealed specific enrichments in lipid and steroid metabolism-related genes in the UPOAO model. The UPOAO model emerges as a novel tool for screening pathogenic genes and promoting further therapeutic research in RAO.

Relationship between Age-Related Hearing Loss and Age-Related Macular Degeneration

Background: With the aging of the population, the deterioration of visual and auditory functions amongst the elderly has attracted much attention. Age-related hearing loss (ARHL) and age-related macular degeneration (AMD) are common eye and ear diseases that seriously affect the quality of life of elderly population. Methods: This study utilised a whole cohort sampling method, with a total of 713 participants aged 50 years and older in the community from June 2022 to October 2023, resulting in the inclusion of 620 participants. Demographic information was collected from these participants, and eye and hearing examinations were conducted at Ningde Municipal Hospital affiliated of Fujian Medical University. Spearman’s correlation analysis was utilised to investigate the association between ARHL and AMD in patients. Multivariate logistic regression analysis was employed to identify the factors influencing ARHL to provide insights for preventing and treating ARHL and AMD in older individuals. Results: Correlation analysis indicated a significantly positive relationship between ARHL and AMD (P &lt; 0.001). The results showed that age, medical history, AMD and chronic noise exposure were risk factors for ARHL. Conclusions: There were 196 cases of AMD in ARHL patients (82.35%). Spearman’s correlation analysis revealed that ARHL was associated with AMD; logistic regression analysis revealed that age, medical history, macular degeneration and history of prolonged noise exposure were risk factors for ARHL. Among them, age, medical history (hypertension, hyperlipidaemia and diabetes mellitus), noise and AMD influence the development of ARHL in the elderly population. Therefore, attention should be paid to controlling risk factors in this population to prevent or reduce the development of ARHL.