Papillomacular Bundle Research Articles

Earliest location of glaucomatous retinal nerve fibre layer damage is determined by intact baseline RNFL thickness profile

Background/aimsTo identify whether an intact retinal nerve fibre layer (RNFL) thickness profile could determine the location of the earliest RNFL defect in glaucoma.MethodsRetrospective longitudinal cohort study of patients with initial...

Visual Acuity and Refractive Status in Congenital Macular Coloboma

Purpose We analysed the refractive state and the factors that influence the best-corrected visual acuity (BCVA) in congenital macular coloboma (CMC) to provide new ideas for improving and predicting the vision of patients with CMC. Methods We reported three patients and reviewed 26 cases of CMC reported in the China National Knowledge Infrastructure (CNKI) database. We measured the BCVA, spherical equivalent refraction (SER), the macular coloboma’s diameter and area, and the distance from the macular coloboma’s nasal edge to the optic disc’s temporal edge (DISTANCE). We analyzed the refractive status of CMC and the factors affecting BCVA. Result The three patients with CMC we reported all had myopia. The study also included 26 patients with CMC reported in the CNKI database (9 unilateral, 17 bilateral) and we analyzed the findings of 26 patients with 43 eyes. The mean age at diagnosis was 22.96 ± 2.32 years. All patients underwent a comprehensive eye examination; 39 eyes (91%) had myopia (44% mild myopia; 28% moderate myopia; 28% high myopia); 23 eyes (53%) had a BCVA ≤6/60 and other 20 eyes (47%)>6/60. No correlation was found between SER or BCVA and the macular coloboma’s diameter or area. BCVA correlated positively with DISTANCE (r = 0.603, p < 0.001). No correlation was found between SER and DISTANCE. The study found a significant difference in SER or BCVA between the affected and fellow eyes in patients with unilateral CMC (n = 9, T=-3.259, p = 0.012; Z=-2.521, p = 0.012, respectively). Conclusion CMC seriously affects visual acuity. The refractive state is mostly myopia. We hypothesize that the DISTANCE is related to the integrity of the papillomacular bundle and affects BCVA.

Toxic And Nutritional Optic Neuropathies

Nutritional and toxic optic neuropathies belong to the group of metabolic mitochondrial optic neuropathies together with hereditary optic neuropathies. Nutritional and toxic optic neuropathies are grouped together because they have many common signs and symptoms. Mitochondrial oxidative phosphorylation dysfunction leads to dysfunction of the papillomacular bundle, resulting in optic neuropathy. Common clinical findings include dyschromatopsia, painless bilateral progressive visual loss, central or cecocentral visual field defects, and progressive optic disc pallor. A toxic substance or lacking vitamins and elements critical for mitochondrial function can cause optic neuropathy.

Retinal Nerve Fiber Layer Optical Texture Analysis and 10-2 Visual Field Assessment in Glaucoma

PurposeTo apply retinal nerve fiber layer (RNFL) optical texture analysis (ROTA) to 1) investigate the association between papillomacular and papillofoveal bundle defects with 10-2 visual field (VF) sensitivity abnormalities, and 2) integrate the information from RNFL bundle defect and 24-2 VF central test locations to determine the likelihood of 10-2 VF sensitivity abnormalities. DesignCross-sectional MethodsA total of 841 eyes (144 healthy, 317 glaucoma suspect, and 380 glaucoma) of 442 participants were included. Eyes underwent 24-2, and 10-2 VF testing and OCT for ROTA. The borders of RNFL defects were delineated from ROTA, and the involvement of the arcuate, papillomacular, and papillofoveal bundles was determined for each eye. Multilevel logistic regression analysis was applied to evaluate the structure–function association. ResultsPapillomacular (92.1%) and papillofoveal (37.9%) RNFL bundle defects were prevalent in eyes with glaucoma. A 10-2 VF location that was projected onto a papillomacular or a papillofoveal RNFL bundle defect had a significantly increased likelihood of reduced sensitivity (ORs of 18.61 at PDP < 5%, and 20.17 at TDP < 5%, respectively, P < 0.001 for both). When predicting the likelihood of VF abnormality in a 10-2 test location, noticeably higher odds ratios were observed when overlapping with an RNFL bundle defect, compared to when an abnormal corresponding 24-2 central point was present. ConclusionsPapillomacular and papillofoveal RNFL bundle defects are present in a considerable proportion of eyes with glaucoma. When detected, they significantly increase the likelihood of abnormality in the corresponding central VF test locations assessed by the 10-2 test.

Myelin Oligodendrocyte Glycoprotein Antibody Disease Optic Neuritis: A Structure-Function Paradox?

Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is a demyelinating disorder that most commonly presents with optic neuritis (ON) and affects children more often than adults. We report 8 pediatric patients with MOG-associated ON and characterize focal optical coherence tomography (OCT) abnormalities over time that help distinguish this condition from the trajectories of other demyelinating disorders. These OCT findings are examined in the context of longitudinal visual function testing. This is a retrospective case series of 8 pediatric patients with MOG-associated ON who were referred for neuro-ophthalmic evaluation. Longitudinal data for demographics, clinical history, physical examination, and OCT obtained in the course of clinical evaluations were collected through retrospective medical record review. Patients demonstrated acute peripapillary retinal nerve fiber layer (RNFL) thickening in one or both eyes, consistent with optic disc swelling. This was followed by steady patterns of average RNFL thinning, with 9 of 16 eyes reaching significantly low RNFL thickness using OCT platform reference databases ( P < 0.01), accompanied by paradoxical recovery of high-contrast visual acuity (HCVA) in every patient. There was no correlation between HCVA and any OCT measures, although contrast sensitivity (CS) was associated with global thickness, PMB thickness, and nasal/temporal (N/T) ratio, and color vision was associated with PMB thickness. There was a lower global and papillomacular bundle (PMB) thickness ( P < 0.01) in clinically affected eyes compared with unaffected eyes. There was also a significantly higher N:T ratio in clinically affected eyes compared with unaffected eyes in the acute MOG-ON setting ( P = 0.03), but not in the long-term setting. MOG shows a pattern of prominent retinal atrophy, as demonstrated by global RNFL thinning, with remarkable preservation of HCVA but remaining deficits in CS and color vision. These tests may be better clinical markers of vision changes secondary to MOG-ON. Of the OCT parameters measured, PMB thickness demonstrated the most consistent correlation between structural and functional measures. Thus, it may be a more sensitive marker of clinically significant retinal atrophy in MOG-ON. The N:T ratio in acute clinically affected MOG-ON eyes in our study was higher than the N:T ratio of neuromyelitis optica (NMO)-ON eyes and similar to the N:T ratio in multiple sclerosis (MS)-ON eyes as presented in the prior literature. Therefore, MOG may share a more similar pathophysiology to MS compared with NMO.

Relapsing White Matter Disease and Subclinical Optic Neuropathy: From the National Multiple Sclerosis Society Case Conference Proceedings

A 16-year-old adolescent boy presented with recurrent episodes of weakness and numbness. Brain MRI demonstrated subcortical, juxtacortical, and periventricular white matter T2 hyperintensities with gadolinium enhancement. CSF was positive for oligoclonal bands that were not present in serum. Despite treatment with steroids, IV immunoglobulins, plasmapheresis, and rituximab, he continued to have episodes of weakness and numbness and new areas of T2 hyperintensity on imaging. Neuro-ophthalmologic examination revealed a subclinical optic neuropathy with predominant involvement of the papillomacular bundle. Genetic evaluation and brain biopsy led to an unexpected diagnosis.

Diagnosis of multiple sclerosis using optical coherence tomography supported by explainable artificial intelligence.

Study of retinal structure based on optical coherence tomography (OCT) data can facilitate early diagnosis of relapsing-remitting multiple sclerosis (RRMS). Although artificial intelligence can provide highly reliable diagnoses, the results obtained must be explainable. The study included 79 recently diagnosed RRMS patients and 69 age matched healthy control subjects. Thickness (Avg) and inter-eye difference (Diff) features are obtained in 4 retinal layers using the posterior pole protocol. Each layer is divided into six analysis zones. The Support Vector Machine plus Recursive Feature Elimination with Leave-One-Out Cross Validation (SVM-RFE-LOOCV) approach is used to find the subset of features that reduces dimensionality and optimises the performance of the classifier. SVM-RFE-LOOCV was used to identify OCT features with greatest capacity for early diagnosis, determining the area of the papillomacular bundle to be the most influential. A correlation was observed between loss of layer thickness and increase in functional disability. There was also greater functional deterioration in patients with greater asymmetry between left and right eyes. The classifier based on the top-ranked features obtained sensitivity = 0.86 and specificity = 0.90. There was consistency between the features identified as relevant by the SVM-RFE-LOOCV approach and the retinotopic distribution of the retinal nerve fibres and the optic nerve head. This simple method contributes to implementation of an assisted diagnosis system and its accuracy exceeds that achieved with magnetic resonance imaging of the central nervous system, the current gold standard. This paper provides novel insights into RRMS affectation of the neuroretina.

Optic Neuropathy Associated with POLG Mutations: A Case Series and Literature Review.

The clinical characteristics of patients with polymerase gamma (POLG) mutation-associated optic neuropathy remain incompletely characterized. We describe the clinical characteristics of 3 patients with POLG-associated optic neuropathy. We performed a literature review of optic neuropathy cases associated with POLG mutations and compared them with our cohort. Many published cases of POLG-associated optic neuropathy in our literature review lacked details regarding severity of vision loss, visual field defects, and optical coherence tomography analysis. The clinical presentation of POLG mutations remains widely variable in age (from pediatric cases to adults) and associated systemic findings. All patients in our literature review presented with systemic symptoms, most commonly muscle weakness, ptosis, and ophthalmoplegia, whereas many young patients had severe systemic symptoms. In our case series, all 3 cases had isolated optic neuropathy affecting the papillomacular bundle, with signs such as reduced visual acuity and color vision, central visual field defects, temporal retinal nerve fiber layer loss with temporal optic disc pallor, and retinal ganglion cell complex loss. In addition, 2 of the 3 cases had added mitochondrial stressors in addition to the POLG mutation. Clinicians should be aware that POLG mutations can present as isolated optic neuropathy primarily affecting the papillomacular bundle. With mitochondrial failure being the likely underlying pathogenic mechanism in POLG-associated optic neuropathy, helping affected patients eliminate mitochondrial stressors may be important in reducing the risk for progressive vision loss in this otherwise currently untreatable disorder.

Choroid plexus volume as a marker of retinal atrophy in relapsing remitting multiple sclerosis

ObjectiveTo evaluate choroid plexus (CP) volume as a biomarker for predicting clinical disability and retinal layer atrophy in relapsing remitting multiple sclerosis (RRMS). MethodsNinety-five RRMS patients and 26 healthy controls (HCs) underwent 3 T whole brain MRI, expanded disability status scale (EDSS) and optical coherence tomography (OCT). Fully automated intra-retinal segmentation was performed to obtain the volumes of the retinal nerve fiber layer (RNFL), combined ganglion cell layer -inner plexiform layer (GCIPL), inner nuclear layer (INL), outer plexiform layer (OPL), outer nuclear layer (ONL), retinal pigment epithelium (RPE), total macular volume (TMV) and papillomacular bundle (PMB). Automated segmentation of the CP within the lateral ventricles was performed and the choroid plexus volume (CPV) was normalized by total intracranial volume (TIV). Linear regression analysis and generalized estimating equation (GEE) models were applied to evaluate relationships between nCPV and EDSS, T2 lesion volume, disease duration, and retinal layer volumes, followed by Bonferroni correction analysis for multiple comparisons. ResultsRRMS patients had larger tChPV compared to HCs (p < 0.001). After Bonferroni correction, there was a significant positive correlation between tChPV and EDSS (r2 = 0.25, p = 0.0002), disease duration (r2 = 0.30, p = 0.01), and T2 lesion volume (r2 = 0.39, p = 0.0000). A robust negative correlation was found between tChPV and RNFL (p < 0.001), GCIPL (p = 0.003), TMV (p = 0.0185), PMB (p < 0.0001), G (p = 0.04), T(p = 0.0001). ConclusionsOur findings support the association of tChPV with disability and altered retinal integrity in RRMS.

Identification of the characteristic visual field loss patterns in optic neuropathies

Visual fields support physicians in the diagnosis and progression tracking of optic neuropathies, enabling the visualization of the site of the optic nerve or optic pathways damage. Furthermore, the identification of the underlying patterns of different optic neuropathies can strengthen the diagnosis or help the clinicians for the patient's prognosis. Different abnormalities have been described and associated to neuroophthalmological diseases, such as central and ceco‐central scotomas related to hereditary optic neuropathies as Leber and dominant optic atrophy diseases which are mostly affected in the macular retinal ganglion cells and the papillomacular bundle. Altitudinal defects are usually associated with ischemic optic neuropathies, and in the big field of glaucoma the most commonly abnormalities are the arcuate and the nasal step.Related to this topic, artificial Intelligence is gaining traction, implementing, and testing different approaches to the automatic detection of visual field loss patterns in distinct diseases. For example, application of archetype analysis for the detection of glaucoma progression or for the assessment of efficacy in idiopathic intracranial hypertension treatment trial.

Surgical treatment of small- and medium-sized primary macular holes with preservation of the internal limiting membrane in the papillomacular nerve fiber bundle area

Surgical treatment of small- and medium-sized primary macular holes with preservation of the internal limiting membrane in the papillomacular nerve fiber bundle area

Molecular mechanisms that cause cell death in LHON

Mitochondrial impairments, caused by mtDNA mutations, lead to RGC death and optic atrophy causing blindness in LHON. It was once thought that this was a disease of impaired bioenergetics. More recent thinking, considering the tempo of damage, studies in cybrids and a faithful mouse genetic model of LHON, has led to the realization that the problem is more that of the pathological generation of Reactive Oxygen Species (ROS). For example, synaptosome analysis from the brains of LHON mice show normal levels of ATP, but the blockage of Complex I activity was associated with very high levels of ROS. We hypothesized that the mtDNA mutation, specifically for 3460 in ND1, changed the atomic structures around COQ10 such that ROS were generated. In order to test that hypothesis, we conducted a series of experiments with statistical ensembles, built with Monte Carlo and Boltzmann sampling for simulations in computational chemistry. We began with the single amino acid mutation in ND1 of Complex I that switches hydrophobic alanine to hydrophilic threonine, at the entry of the Coenzyme Q10 binding channel. We explicated the mechanistic consequences of this mutation, using the tools of Molecular Dynamics and Free Energy Perturbation simulations. We showed that the mutant remained capable of binding Coenzyme Q10. Indeed, the mutated channel was even more proficient than the wild type in reducing ubiquinone to ubiquinol due to the closer average proximity of the Coenzyme Q10 headgroup to the chain of iron–sulfur clusters, from which it received electrons via quantum mechanical tunnelling. However, the mutation kinetically hindered the exit of the reduced (ubiquinol) form of Q10 from the ND1 channel, slowing the passage of its headgroup due to unfavourable electrostatics. This effect lead to overproduction of ROS via re‐oxidation of Coenzyme Q10 as electrons were sent back up the Iron–sulfur cluster chain, where the ROS production occurs. Another line of studies has shown that ROS lead to the death of RGCs affecting the smallest axons first. In those areas of the optic nerve in which larger axons are preponderate, the ROS are absorbed by the larger axons and little more happens. However, there is a dearth of large axons inferior temporally where the papillomacular bundle enters the optic nerve. Then, the ROS begins a reiterative and vicious cycle of cell death and the production of more ROS. This explains both the very peculiar spatial and temporal features of the optic neuropathy in LHON.

Papillomacular bundle defect (PMBD) in glaucoma patients with high myopia: frequency and risk factors

Little is known about the papillomacular bundle defect (PMBD) in glaucoma. As such, we investigated the frequency of PMBD in glaucoma patients with high myopia, and its risk factors. In this retrospective, cross-sectional study, retinal nerve fiber layer (RNFL) defect was analyzed in 92 glaucomatous eyes with high myopia (axial length of 26.0 mm or more or an average spherical value of − 6.0 diopters or less). After dividing them into two groups with and without PMBD, the clinical characteristics of the groups were compared and analyzed. The mean age of the patients was 52.1 ± 10.5 years, and there were 53 males and 39 females. PMBD were observed in 55 eyes (59.8%). There was no significant intergroup difference in baseline or follow-up intraocular pressure (IOP). Parapapillary atrophy (PPA)-to-disc-area ratio (OR 3.83, CI: 1.58–10.27, p = 0.010), lamina cribrosa defect (LCD; OR 2.92, CI: 1.14–8.13, p = 0.031) and central visual field defect (CVFD; OR 3.56, CI: 1.38–9.58, p = 0.010) were significantly associated with the PMBD..

Choriocapillaris and choroidal thickness in all Leber hereditary optic neuropathy stages using swept source technology.

The role of the choroid in Leber hereditary optic neuropathy (LHON) remains unclear. The literature is scarce, with conflicting results and lacks axial length measurements. Therefore, we aimed to analyse the choriocapillaris (CC) vessel density (VD) and choroidal thickness (ChT) in all stages of LHON using swept source (SS) technology and considering the possible influence of axial length on choroidal parameters. This was a prospective cross-sectional observational study. A total of 119 eyes of 60 patients with molecularly confirmed LHON across all stages and 120 eyes of 60 control participants were included. We obtained the CC VD using optical coherence tomography angiography maps centred on the fovea. ChT was measured from the Bruch's membrane to the choroid-sclera interface in the macular and peripapillary regions. The CC VD was not significantly affected in any sector or average, except for a slight change in the superior region of chronic eyes (52.08 ± 1.62% vs. 53.50 ± 2.29%, p = 0.002). ChT demonstrated a trend towards decreased values in asymptomatic eyes and increased values in the symptomatic stages that failed to reach statistical significance in sectors corresponding to the papillomacular bundle except for the macular nasal inner sector of chronic eyes (281.10 ± 67.12 μm vs. 252.08 ± 70.55 μm, p = 0.045). No significant correlations were observed between visual acuity and CC VD or ChT. The CC VD remained stable across the LHON stages. Choroidal vasculature does not appear to play a role in LHON pathophysiology. Further research is needed on ChT as a potential biomarker of LHON.

Spastic Paraplegia Type 7-Associated Optic Neuropathy: A Case Series.

Hereditary optic neuropathies comprise a group of clinically and genetically heterogeneous disorders. Optic neuropathy has been previously reported in families with spastic paraplegia type 7 (SPG7) gene mutations. However, the typical time course and clinical presentation of SPG7-associated optic neuropathy is poorly understood. We report a series of 5 patients harboring pathogenic SPG7 mutations who originally presented to a neuro-ophthalmology clinic with symptoms of optic neuropathy. Retrospective case series of 5 patients with pathogenic SPG7 mutations and optic atrophy from 3 neuro-ophthalmology clinics. Demographic, clinical, diagnostic, and treatment data were collected and reported by the clinician authors. Five patients ranging in age from 8 to 48 years were evaluated in the neuro-ophthalmology clinic. Although there were variable clinical presentations for each subject, all noted progressive vision loss, typically bilateral, and several also had previous diagnoses of peripheral neuropathy (e.g., Guillain-Barré Syndrome). Patients underwent neuro-ophthalmic examinations and testing with visual fields and optic coherence tomography of the retinal nerve fiber layer. Genetic testing revealed pathogenic variants in the SPG7 gene. Five patients presented to the neuro-ophthalmology clinic with progressive vision loss and were diagnosed with optic atrophy. Although each patient harbored an SPG7 mutation, this cohort was phenotypically and genotypically heterogeneous. Three patients carried the Ala510Val variant. The patients demonstrated varying degrees of visual acuity and visual field loss, although evaluations were completed during different stages of disease progression. Four patients had a previous diagnosis of peripheral neuropathy. This raises the prospect that a single pathogenic variant of SPG7 may be associated with peripheral neuropathy in addition to optic neuropathy. These results support the consideration of SPG7 testing in patients with high suspicion for genetic optic neuropathy, as manifested by symmetric papillomacular bundle damage without clear etiology on initial workup. Applied judiciously, genetic testing, including for SPG7, may help clarify the cause of unexplained progressive optic neuropathies.

Bartonella henselae-Associated Optic Neuropathy Presenting as a Central Scotoma in the Absence of Overt Papillitis - A Multimodal Imaging Study.

To describe the use of multimodal imaging to establish the diagnosis of Bartonella henselae-associated optic neuropathy in a patient who presented with a central scotoma without overt evidence of optic nerve involvement. Case report. Main outcome measures included clinical, optical coherence tomography, and fluorescein angiography findings. A 72-year-old woman presented with a three-day history of central scotoma in the left eye. Her examination was remarkable for faint exudation in the nasal macula of the left eye, but was otherwise normal for her age. Spectral domain optical coherence tomography of the macula revealed mild thickening of the papillomacular bundle with scattered small cystoid spaces and several intraretinal exudates, none of which were visible clinically. Fluorescein angiography revealed localized leakage of the inferotemporal optic disc. When prompted, the patient recalled being scratched multiple times by her two pet kittens. Serial testing showed rising anti-Bartonella henselae (B. henselae) IgG antibody titers to 1:1280, confirming the suspected diagnosis of B. henselae-associated optic neuropathy. and importance: Bartonella-associated optic nerve involvement can occur without overt evidence of optic disc swelling. Multimodal imaging can be used to suggest the diagnosis and support appropriate serologic testing.

Pre-perimetric Optic Neuropathy

We present a case of a 32-year-old male who came with the history of blurring of vision in both eyes. Diagnosed as a glaucoma suspect at another centre, he had a best corrected visual acuity (BCVA) of 20/20 in both eyes and there was no relative afferent pupillary defect (RAPD) in either eye. Intraocular pressure (IOP) was also normal in both eyes. Fundus examination revealed very subtle temporal pallor accompanied by reduced retinal nerve fibre layer (RNFL) striations in the papillomacular bundle (PMB) in both eyes. RNFL optical coherence tomography (OCT) demonstrated thinning of the RNFL in the temporal sector along with thinning of the ganglion cell complex (GCC) on the ganglion cell analysis, whilst his visual fields (24-2) were normal in both eyes. After all necessary laboratory investigations a diagnosis of vitamin B12 and folate deficiency with nutritional optic neuropathy was made and appropriate management was initiated. Hence, diligent clinical evaluation along with a high level of suspicion goes a long way in diagnosing these almost sub clinical cases with pre-perimetric optic neuropathy. Timely diagnosis and appropriate management can help to preserve vision and reverse changes in an otherwise preventable irreversible optic neuropathy.

Predictive potential of optical coherence tomography parameters for the prognosis of decreased visual acuity after trabeculectomy in open-angle glaucoma patients with good vision

BackgroundTrabeculectomy (trab) is the most effective surgical procedure for lowering IOP and preventing glaucoma progression. However, decline in best-corrected visual acuity (BCVA) is one of the most serious postoperative complications of trab. Here, we investigated methods to predict decreased BCVA after trab in glaucoma patients with good preoperative BCVA.MethodsThis study included 35 eyes of 35 open-angle glaucoma (OAG) patients (male / female: 21 / 14, age: 64.0 ± 9.7 years old, preoperative intraocular pressure: 15.9 ± 5.4 mmHg, mean deviation: -18.1 ± 5.6 dB) with preoperative BCVA of 0.7 or better who underwent trab and were observed for more than 12 months. As a preoperative analysis, we measured temporal quadrant circumpapillary retinal nerve fiber layer thickness (cpRNFLT) and ganglion cell complex thickness in a central strip between the disc and fovea (csGCCT), an area that corresponds to the location of the papillomacular bundle (PMB) in swept-source optical coherence tomography (OCT). We defined BCVA decline as a loss of more than 3 lines of BCVA after 12 months. Measurement parameters were compared between the BCVA-decline group and the non-BCVA-decline group.ResultsBCVA decline was detected in 11 cases (31.4%) 12 months after trab. There was a statistically significant difference in axial length (P = 0.049). A single logistic analysis showed that the BCVA-decline group had significantly lower cpRNFLT than the non-BCVA-decline group (27.7 ± 8.0 μm vs. 45.1 ± 5.3 μm, P < 0.001, cut-off value: 33.4 μm), as well as lower csGCCT (72.4 ± 7.7 μm vs. 87.5 ± 5.1 μm, P = 0.002, cut-off value: 82.3 μm). Multivariable logistic analysis showed that the BCVA-decline group had significantly lower temporal quadrant cpRNFLT (P < 0.001) and lower middle csGCCT (P < 0.001) compared to the non-BCVA-decline group.ConclusionsLower temporal quadrant cpRNFLT and middle csGCCT, OCT scan areas that correspond to the location of the PMB, might be biomarkers that predict BCVA decline after trab in OAG patients with good vision.

Trans-synaptic degeneration in the optic pathway: Exploring the role of lateral geniculate nucleus in early stages of relapsing-remitting multiple sclerosis.

Optic pathway is considered an ideal model to study the interaction between inflammation and neurodegeneration in multiple sclerosis (MS). Optical Coherence Tomography (OCT) and 3.0 T magnetic resonance imaging (MRI) were acquired in 92 relapsing remitting (RR) MS at clinical onset. Peripapillary RNFL (pRNFL) and macular layers were measured. White matter (WM) and gray matter (GM) lesion volumes (LV), lateral geniculate nucleus (LGN) volume, optic radiations (OR) WM LV, thickness of pericalcarine cortex were evaluated. OCT and MRI control groups (healthy controls [HC]-OCT and HC-MRI) were included. A significant thinning of temporal pRNFL and papillo-macular bundle (PMB) was observed (p<0.001) in 16 (17%) patients presented with monocular optic neuritis (MSON+), compared to 76 MSON- and 30 HC (-15μm). In MSON-, PMB was reduced (-3μm) compared to HC OCT (p<0.05). INL total volume was increased both in MSON+ (p<0.001) and MSON- (p=0.033). Inner retinal layers volumes (macular RNFL, GCL and IPL) were significantly decreased in MSON+ compared to HC (p<0.001) and MSON- (p<0.001). Reduced GCL volume in the parafoveal ring was observed in MSON- compared to HCOCT (p < 0.05). LGN volume was significantly reduced only in MSON+ patients compared to HC-MRI (p<0.001) and MSON- (p<0.007). GCL, IPL and GCIP volumes associated with ipsilateral LGN volume in MSON+ and MSON-. Finally, LGN volume associated with visual cortex thickness with no significant difference between MSON+ and MSON-. Anterograde trans-synaptic degeneration is early detectable in RRMS presenting with optic neuritis but does not involve LGN.

Changes in Thresholds of Electrically Evoked Phosphene and Electrical Lability of the Optic Nerve in the Ground Station Crew in the International Experiment SIRIUS 20/21

In the ground sealed station crew, during the 8 months international experiment SIRIUS 20/21 simulating an interplanetary flight, electrically induced phosphene (EIP) thresholds, which reflected the electrical sensitivity (ES) of the retina, and the optic nerve. ES&amp;L was assessed using the “ESOM” device (“Neuron”, Ufa, Russia) once a month, twice a day (morning/evening), under mesopic conditions. An increase in ES and other patterns of changes in ES&amp;L parameters during period of isolation were established, reflecting the adaptation of the crew to the conditions of the experiment and the reaction of the visual system to physical and psycho-emotional stress. Further study of the thresholds of the EIP and L of the optic nerve in experiments of increasing duration will make it possible to determine the biomarkers that differentiate the individual adaptive reaction of astronauts from dysfunction of the retina and optic nerve under real space flight conditions. The L of the optic nerve showed greater resistance to experimental conditions than the ES of the retina. The results suggest that the determination of the L in the ES&amp;L test can become an express test on board the ISS to assess the functional state of the papillomacular bundle of optic nerve fibers, the risk of developing or diagnosing SANS (flight-associated neuro-ocular syndrome) in long-term space missions.