Acute-Onset Altitudinal Visual Field Defect Caused by Optic Canal Meningioma.
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ABSTRACT:
SUBMITTER: Kim SM
PROVIDER: S-EPMC4596113 | biostudies-literature | 2015 Oct
REPOSITORIES: biostudies-literature
Publications
Acute-Onset Altitudinal Visual Field Defect Caused by Optic Canal Meningioma.
Kim Seung Min SM Lee Jookyung J Joe Soo Geun SG Kim Jong S JS Kwon Sun U SU
Journal of clinical neurology (Seoul, Korea) 20151001 4
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Project description:PurposeTo compare the evolvement of visual field (VF) defect in neuromyelitis optica spectrum disorder-optic neuritis (NMOSD-ON) and idiopathic optic neuritis (IDON).MethodsThis prospective study involved 104 optic neuritis (ON) patients followed up for ≥ 6 months (33 patients with NMOSD-ON and 71 patients with IDON). The pattern and recovery pattern of VF defect, mean defect (MD) and pattern standard deviation (PSD) of VF, as well as BCVA at onset, 1 month (1 m), 3 months (3 m), and ≥ 6 months (6 m) after onset were compared between two groups. Analysis of these indicators in first episode patients was also done.ResultsDiffuse abnormalities and nerve fiber bundle abnormalities were the two most common patterns in both groups. The percentage of neurologic abnormality of VF defect in NMOSD-ON was higher than that of IDON. Compared with the IDON group, the MD and PSD of NMOSD-ON group were significantly worse at each follow-up. While a positive correlation in BCVA was found between 1 m and ≥ 6 m in the NMOSD-ON group only, a positive correlation was found between 1 m and ≥ 6 m in MD and PSD of both groups. A positive correlation was found between 3 m and ≥ 6 m in MD, PSD and BCVA of both groups. The quadrant recovery pattern was the most common pattern in both groups (57.1% in NMOSD-ON and 57.4% in IDON). The analysis of the first episode subgroup further confirmed the observation above.ConclusionsThe NMOSD-ON patients tended to suffer more severe VF damage, VF irregularity and worse prognosis than that of IDON patients. Diffuse abnormalities and nerve fiber bundle abnormalities were the two most common types in both groups, while neurologic abnormality more common in NMOSD-ON and central scotoma more common in IDON. The visual functions of 1 m in NMOSD-ON and 3 m in IDON were related to its prognosis.
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Project description:We investigated optic nerve head factors associated with initial parafoveal scotoma (IPFS) in primary open-angle glaucoma. Eighty (80) patients with an IPFS and 84 patients with an initial nasal step (INS) were compared. Central retinal vascular trunk (CRVT) deviation from the Bruch's membrane opening (BMO) center was measured as a surrogate of lamina cribrosa (LC)/BMO offset, and its obliqueness was defined as the absolute value of angular deviation from the fovea-BMO axis. Proximity of retinal nerve fiber layer defect (RNFLD) was defined as the angular deviation of the inner RNFLD margin from the fovea-BMO axis. Microvasculature dropout (MvD) was defined as a focal sectoral capillary dropout with no visible microvascular network identified in the choroidal layer. Factors associated with IPFS, as compared with INS, were assessed using logistic regression analyses and conditional inference tree analysis. The IPFS group had more oblique CRVT offset (P < 0.001), RNFLD closer to the fovea (P < 0.001), more MvD (P < 0.001), and more LC defects (P < 0.001) compared to the INS group. In logistic regression analyses, obliqueness of CRVT offset (P = 0.002), RNFLD proximity (P < 0.001), and MvD (P = 0.001) were significant factors influencing the presence of IPFS. Conditional inference tree analysis showed that RNFLD closer to the fovea (P < 0.001) in the upper level, more oblique CRVT offset (P = 0.013) and presence of MvD (P = 0.001) in the lower level were associated with the probability of having IPFS. IPFS was associated with closer RNFLD location to the fovea when assessed from the BMO. Oblique LC/BMO offset may not only mask RNFLD proximity to the fovea due to a deviated funduscopic disc appearance, but also potentiate IPFS via focal LC defect and MvD.
| S-EPMC10997601 | biostudies-literature
Project description:Visual field defects interfere with free actions and influence the quality of life of patients with retinitis pigmentosa; the prevalence of this disease is increasing in aging societies. Patients with progressive disease may require visual aids; however, no such devices are currently available. We utilized a retinal projection eyewear system, QD laser eyewear, which includes a projector inside the spectacle frame, to draw the image taken by a connected portable camera with a wide field lens. The images are projected onto the retina using a Maxwellian view optical system, which is not influenced by refractive error or the amount of incident light. Goldmann perimetry and figure recognition tests with the QD laser eyewear showed increased visual field areas and angles, and shortened the time for recognition of the number of figures in a sheet, in a limited visual field model that we developed by using a pin-hole system to simulate the tunnel vision of retinitis pigmentosa in 19 healthy adults. The device supported the quality of vision. Additionally, the visual field defect model used in healthy adults was useful for validating the device in the development stage of the study, to clarify both advantages and future goals for improving the device.
| S-EPMC6353865 | biostudies-literature
Project description:Myopia is significantly growing eye disease which accompanies various ocular pathologies including glaucoma. Understanding visual field (VF) and retinal nerve fiber layer (RNFL) damage observed in myopic eyes is important. Therefore, we evaluated optic disc margin anatomy using spectral-domain (SD) optical coherence tomography (OCT). We enrolled 40 healthy myopic patients and 64 myopic patients with RNFL defects in the superonasal region of the optic disc on red-free photographs and OCT. Optic disc stereophotographs were co-localized to SD-OCT images, and we analyzed the frequency with which the disc margin identified in photographs coincided with Bruch's membrane (BM) opening, BM/border tissue, or border tissue. For each scan, the presence of border tissue overhang beyond the clinical disc margin and the end of Bruch's membrane was identified. Among 64 myopic eyes with RNFL defects, 42 had corresponding inferotemporal VF defects. Border tissue overhang was found from 25 to 60% of myopic eyes with RNFL defect at all clock positions. However, border tissue overhang was found from 86 to 97% at 1, 2, 11 and 12 o'clock position in myopic eyes with VF defects. This was significantly different from myopic healthy eyes. We suggest that the OCT structure at the disc margin might contribute to VF damage in myopic patients.
| S-EPMC6401376 | biostudies-literature
Project description:PURPOSE: Autosomal dominant optic atrophy (ADOA, OMIM 165500), an inherited optic neuropathy that leads to retinal ganglion cell degeneration and reduced visual acuity during the early decades of life, is mainly associated with mutations in the OPA1 gene. Here we report a novel ADOA phenotype associated with a new pathogenic OPA1 gene mutation. METHODS: The patient, a 62-year-old woman, was referred for acute, painless, and severe visual loss in her right eye. Acute visual loss in her left eye occurred a year after initial presentation. MRI confirmed the diagnosis of isolated atrophic bilateral optic neuropathy. We performed DNA sequencing of the entire coding sequence and the exon/intron junctions of the OPA1 gene, and we searched for the mitochondrial DNA mutations responsible for Leber hereditary optic atrophy by sequencing entirely mitochondrial DNA. Mitochondrial respiratory chain complex activity and mitochondrial morphology were investigated in skin fibroblasts from the patient and controls. RESULTS: We identified a novel heterozygous missense mutation (c.2794C>T) in exon 27 of the OPA1 gene, resulting in an amino acid change (p.R932C) in the protein. This mutation, which affects a highly conserved amino acids, has not been previously reported, and was absent in 400 control chromosomes. Mitochondrial DNA sequence analysis did not reveal any mutation associated with Leber hereditary optic neuropathy or any pathogenic mutations. The investigation of skin fibroblasts from the patient revealed a coupling defect of oxidative phosphorylation and a larger proportion of short mitochondria than in controls. CONCLUSIONS: The presence of an OPA1 mutation indicates that this sporadic, late-onset acute case of optic neuropathy is related to ADOA and to a mitochondrial energetic defect. This suggests that the mutational screening of the OPA1 gene would be justified in atypical cases of optic nerve atrophy with no evident cause.
| S-EPMC2661005 | biostudies-literature
Project description:PurposeTo investigate the prevalence and risk factors for visual field defect in patients with optic disc drusen (ODD).MethodsWe assessed the visual field status of patients with ODD whose diagnosis were confirmed by spectral-domain optical coherence tomography (SD-OCT). Visual field defects were classified as normal, enlarged blind spot, or other defects. ODD were classified into either type 1 (without hyperreflective border and heterogenic internal reflectance) or type 2 (with hyperreflective border and lower internal reflectance). The prevalence and risk factors for each visual field defect was analyzed using logistic regression analysis and classification and regression tree (CART) modeling.ResultsOf the 40 eyes with ODD, 33 (83%) eyes were categorized as type 1 and 7 (17%) eyes were categorized as type 2 ODD. Regarding the visual field defects, 19 (48%) eyes showed normal visual field, 11 (28%) eyes showed enlarged blind spot, and 9 (24%) eyes showed other defects. The latter was more frequent in type 2 ODD (P = 0.001). Logistic regression analysis revealed that the factor associated with other defects was the thinning of the average retinal nerve fiber layer (RNFL) (per 10 μm decrease, OR = 3.436, P = 0.004), and the factor associated with enlarged blind spot was the height of ODD (per 100 μm increase, OR = 3.956, P = 0.023). CART modeling revealed that the average RNFL thickness lesser than 85.5 μm, and then the ODD height larger than 348 μm were the best split-up factors for predicting the type of visual field defects.ConclusionsIn this study, one-quarter of ODD patients showed abnormal visual field defect other than enlarged blind spot. These other visual field defects appeared to be associated with the axonal loss in the eyes with type 2 ODD.
| S-EPMC5927402 | biostudies-literature
Project description:BackgroundPatients with Leber hereditary optic neuropathy (LHON) have a progressive decrease of their visual acuity which can deteriorate to <0.1. Some patients can have a partial recovery of their vision in one or both eyes. One prognostic factor associated with a recovery of vision is an early-age onset. The purpose of this study was to determine other clinical factors that are predictive of a good visual recovery.MethodsSixty-one Japanese LHON patients, with the 11,778 mutation and a mean age of 23.1 ± 12.1 years at the onset, were studied. All patients were initially examined at an acute stage of LHON and were followed for 3 to 10 years. At 1 year after the onset, the lowest visual acuity was <0.1 in all eyes. We studied the following parameters of patients with/without a final visual acuity of ≥ 0.2: sex; heavy consumption of cigarettes and alcohol; taking idebenone; mean age at onset; mean lowest visual acuity; and distribution of the lowest and the final visual acuity.ResultsFifteen (24.6%) of the 61 patients or 25 (20.5%) of the 122 eyes had a recovery of their visual acuity to ≥ 0.2. The mean age at onset of these 15 patients with visual recovery to ≥ 0.2 was 17.5 ± 7.7 years, and that of the 46 patients without visual recovery to ≥ 0.2 was 25.0 ± 12.8 years (P = 0.02, Mann-Whitney U test). The mean lowest visual acuity of the 25 eyes with visual recovery ≥ 0.2 was 0.04, and that of the 97 eyes without visual recovery to ≥ 0.2 was 0.015 (P < 0.001, Mann-Whitney U test). Fifty percent (15/30) of the eyes whose lowest visual acuity was ≥ 0.04 during 1 year after the onset had a visual recovery to ≥ 0.2, while 11% (10/92) of the eyes whose the lowest visual acuity was ≤ 0.03 had a visual recovery to ≥ 0.2 (P < 0.001, χ 2 test). There were no significant differences in the other clinical factors.ConclusionA final visual acuity of ≥ 0.2 was associated with a less severe reduction of the visual acuity at 1 year after the onset. Our findings can be used to predict the visual prognosis in LHON patients.
| S-EPMC5648487 | biostudies-literature
Project description:PurposeVision loss in glaucoma is not only associated with elevated intraocular pressure and neurodegeneration, but vascular dysregulation (VD) is a major factor. To optimize therapy, an improved understanding of concepts of predictive, preventive, and personalized medicine (3PM) is needed which is based on a more detailed understanding of VD pathology. Specifically, to learn if the root cause of glaucomatous vision loss is of neuronal (degeneration) or vascular origin, we now studied neurovascular coupling (NVC) and vessel morphology and their relationship to vision loss in glaucoma.MethodsIn patients with primary open angle glaucoma (POAG) (n = 30) and healthy controls (n = 22), NVC was studied using dynamic vessel analyzer to quantify retinal vessel diameter before, during, and after flicker light stimulation to evaluate the dilation response following neuronal activation. Vessel features and dilation were then related to branch level and visual field impairment.ResultsRetinal arterial and venous vessels had significantly smaller diameters in patients with POAG in comparison to controls. However, both arterial and venous dilation reached normal values during neuronal activation despite their smaller diameters. This was largely independent of visual field depth and varied among patients.ConclusionsBecause dilation/constriction is normal, VD in POAG can be explained by chronic vasoconstriction which limits energy supply to retinal (and brain) neurons with subsequent hypo-metabolism ("silent" neurons) or neuronal cell death. We propose that the root cause of POAG is primarily of vascular and not neuronal origin. This understanding can help to better personalize POAG therapy of not only targeting eye pressure but also vasoconstriction to prevent low vision, slowing its progression and supporting recovery and restoration.Trial registrationClinicalTrials.gov, # NCT04037384 on July 3, 2019.
| S-EPMC9971397 | biostudies-literature
Project description:BackgroundHemianopia is a complete or partial blindness in the visual fields of both eyes, commonly caused by cerebral infarction. It has been hypothesized that systematic audio-visual (AV) stimulation of the blind hemifield can improve accuracy and search times, probably due to the stimulation of bimodal representations in the superior colliculus (SC), an important multisensory structure involved in both the initiation and execution of saccades.MethodsA narrative synthesis of the findings is presented to highlight how AV rehabilitation impacts on patients with hemianopia including visual oculomotor function, functional ability in activities of daily living, hemianopic dyslexia, visual scanning and searching tasks, maintaining of functional ability post training and the effect on brain multisensory integration by using neuroimaging.ResultsSixteen studies were included (fourteen articles (188 participants) and two literature reviews). Results were grouped into AV training of hemianopia in adults and in children and then further grouped according to the AV task type: tasks measuring the training effects by comparing visual stimulation training to audio-visual training, localization abilities in homonymous hemianopia (HH) and AV integration in patients with HH.ConclusionSystematic AV training may improve the processing of visual information by recruiting subcortical pathways, and because most of the patients with visual cortex damage have an intact SC, it might be useful to use the bimodal AV training to activate retinotectal functions. Nevertheless, the underlying mechanisms supporting the reported positive effects are not currently understood. Systematic functional and/or structural imaging studies may help in understanding the underlying mechanism and inform the design of optimal training paradigms.
| S-EPMC8918177 | biostudies-literature
Project description:AIMS/PURPOSE: To determine and correlate the long-term changes in retinal nerve fibre layer (RNFL) thickness, optic nerve head (ONH) morphology, and visual fields after a single episode of acute primary angle closure (APAC). METHODS: This was a cross-sectional comparative study of patients at National University Hospital (Singapore) from 2000 to 2006 after an episode of unilateral APAC. The peripapillary and macular RNFL were measured using Stratus optical coherence tomography (OCT) and ONH configuration was assessed using Heidelberg Retina Tomography (HRT)-III. Humphrey perimetry was also performed, and the presence of disc pallor was noted. APAC eyes were compared with fellow eyes as matched controls. RESULTS: Twenty-five patients were assessed at a median of 33 months (range, 11-85 months) after APAC. OCT showed that there was a reduction in the peripapillary and outer macular RNFL thickness in APAC eyes compared with controls. Humphrey perimetry revealed significantly reduced mean deviation (P=0.006) and increased pattern standard deviation (P=0.045) in APAC eyes compared with controls. HRT-III showed no difference in mean rim area, rim volume, or cup-disc ratio between APAC eyes and controls. Disc pallor was present in nine APAC eyes (36%) but was absent in fellow eyes (P=0.002), and was associated with peripapillary RNFL thinning, visual field loss, and an increased interval between the onset of symptoms and normalization of intraocular pressure (P=0.023). CONCLUSION: APAC results in peripapillary and outer macular RNFL loss, visual field defects, and optic disc pallor, even in cases in which the ONH configuration remains unchanged.
| S-EPMC3171266 | biostudies-other