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Wiener Klinische Wochenschrift Mar 2022To evaluate potential clinical parameters having an impact on visual outcome after endoscopic optic nerve decompression in acute optic neuropathy patients.
OBJECTIVE
To evaluate potential clinical parameters having an impact on visual outcome after endoscopic optic nerve decompression in acute optic neuropathy patients.
METHODS
A retrospective chart review of patients with acute optic neuropathy, who underwent endoscopic optic nerve decompression between June 2001 and November 2018 at an academic center was performed. Patients were divided into groups according to visual improvement after surgical treatment (yes/no). Following clinical parameters were compared between groups: perioperative steroid use, evidence of optic nerve affection in preoperative neuroimaging, additional optic nerve sheath incision, surgery delay and preoperative C-reactive protein (CRP) levels. Further subgroups analyses were conducted based on etiology (trauma/tumor).
RESULTS
Among 32 included cases, 16 patients (50%) reported visual improvement after endoscopic optic nerve decompression. There was no significant difference in visual improvement between etiology subgroups (trauma: n = 9/20 (45%) vs. tumor: n = 7/12 (58.3%), p = 0.465). Tumor subgroup patients with visual improvement had a significantly higher prevalence of optic nerve affection in preoperative neuroimaging than those without visual improvement (p = 0.018, φ = 0.683). Perioperative steroid administration was negatively associated with visual outcome (p = 0.034, φ = 0.375). Nerve sheath incision, surgery delay and preoperative CRP levels did not have a significant impact on visual outcome (p > 0.05).
CONCLUSION
Radiological findings can help as an indicator for surgical treatment since an affected optic nerve in preoperative neuroimaging resulted in better visual outcome after surgery. The use of steroids should be considered more carefully since it did not show any beneficial effect.
Topics: Decompression, Surgical; Humans; Optic Nerve; Optic Nerve Injuries; Retrospective Studies; Treatment Outcome; Visual Acuity
PubMed: 34342713
DOI: 10.1007/s00508-021-01915-x -
Medical Ultrasonography Jan 2017Our aim was to evaluate the elasticity features of the optic nerve using strain (SE) and shear wave elastography (SWE) in multiple sclerosis (MS) patients in comparison...
AIMS
Our aim was to evaluate the elasticity features of the optic nerve using strain (SE) and shear wave elastography (SWE) in multiple sclerosis (MS) patients in comparison with healthy subjects.
MATERIAL AND METHODS
One hundred and seven optic nerves from 54 MS patients and 118 optic nerves from 59 healthy subjects were examined prospectively by SE and SWE. Optic nerves were divided into three types in accordance to the elasticity designs, as follows: type 1 predominantly blue (hardest tissue); type 2 predominantly blue/green (hard tissue); and type 3 predominantly green (intermediate tissue). Quantitative measurements of optic nerve hardness with SWE were analyzed in kilopascals.
RESULTS
Elastographic images from healthy volunteers showed mostly type 3 optic nerves (61.9%); type 2 was also found (38.1%), but type 1 was not observed. Elastographic examination of MS patients showed mostly type 2 optic nerves (88%), while some type 1 (4.6%) and type 3 optic nerves (6.5%) were rarely observed. There was a statistically significant difference in terms of elasticity patterns between patients and healthy volunteers (p<0.001). Statistically significant differences were observed between patients and healthy volunteers in the analysis of SWE values (10.381±3.48 kPa and 33.87±11.64 p<0.001). The receiver operating characteristic curve analysis was perfect (0.993; 95% confidence interval [CI]=0.971-0.999), and a cut-off value of 18.3 kPa shear had very high sensitivity and specificity for the patient group. No significant differences were observed between patients with and without previous optic neuritis.
CONCLUSION
SE and SWE examination findings concerning the optic nerve in MS patients demonstrated remarkable differences according to the healthy group.
Topics: Adolescent; Adult; Elasticity Imaging Techniques; Female; Humans; Male; Middle Aged; Multiple Sclerosis; Optic Nerve; Sensitivity and Specificity; Young Adult
PubMed: 28180195
DOI: 10.11152/mu-939 -
Investigative Ophthalmology & Visual... Dec 2015Autophagy is a critical process, compromised in neurodegenerative disease, by which terminally differentiated cells like neurons manage cytoskeletal and organelle...
PURPOSE
Autophagy is a critical process, compromised in neurodegenerative disease, by which terminally differentiated cells like neurons manage cytoskeletal and organelle turnover. How autophagy relates to associated neurodegenerative pathologies remain unclear. We examined autophagy in optic neuropathy by investigating cytoskeletal degradation, mitochondria, and autophagic vesicles in the DBA2/J mouse model of glaucoma exhibiting differing levels of axon transport functionality.
METHODS
DBA/2J and DBA/2J(wt-gpnmb) control mice 11 to 14 months of age were injected with cholera toxin-B (CTB) to assay anterograde axonal transport. Axonal mitochondria and autophagic vesicles were analyzed with respect to transport integrity in proximal and distal optic nerve using serial block face scanning electron microscopy (3D EM).
RESULTS
Several indices varied significantly between the DBA/2J and DBA/2J(wt-gpnmb) mice, including mitochondrial volume, average number of autophagic vesicles per axon, and mitochondrial cristae. However, there were no differences in mitochondrial cristae for axons with functional versus dysfunctional CTB transport, suggesting that mitochondrial dysfunction precedes overt transport blockade. Anterograde transport failure was accompanied by a dissociation of the relationship between mitochondrial and axon volumes. Autophagic vesicle profiles were significantly increased in optic nerve with transport deficit, consistent with greater autophagic activity. Mitochondria within autophagosomes, indicative of mitophagy, were observed in both proximal and distal axons.
CONCLUSIONS
Loss of anterograde transport in DBA/2J optic nerve is concomitant with diminished mitochondrial volume, increased cytoskeletal breakdown and autophagic activity, and accumulation of autophagic profiles, including signs of mitophagy, in proximal optic nerve. Axons with transport deficit are metabolically underserved, though not necessarily from mitophagy.
Topics: Animals; Autophagy; Axonal Transport; Axons; Disease Models, Animal; Mice; Mice, Inbred DBA; Microscopy, Electron, Scanning; Optic Nerve; Optic Nerve Diseases
PubMed: 26720474
DOI: 10.1167/iovs.15-17885 -
BMC Ophthalmology Feb 2011The definitive diagnosis of glaucoma is currently based on congruent damage to both optic nerve structure and function. Given widespread quantitative assessment of both...
BACKGROUND
The definitive diagnosis of glaucoma is currently based on congruent damage to both optic nerve structure and function. Given widespread quantitative assessment of both structure (imaging) and function (automated perimetry) in glaucoma, it should be possible to combine these quantitative data to diagnose disease. We have therefore defined and tested a new approach to glaucoma diagnosis by combining imaging and visual field data, using the anatomical organization of retinal ganglion cells.
METHODS
Data from 1499 eyes of glaucoma suspects and 895 eyes with glaucoma were identified at a single glaucoma center. Each underwent Heidelberg Retinal Tomograph (HRT) imaging and standard automated perimetry. A new measure combining these two tests, the structure function index (SFI), was defined in 3 steps: 1) calculate the probability that each visual field point is abnormal, 2) calculate the probability of abnormality for each of the six HRT optic disc sectors, and 3) combine those probabilities with the probability that a field point and disc sector are linked by ganglion cell anatomy. The SFI was compared to the HRT and visual field using receiver operating characteristic (ROC) analysis.
RESULTS
The SFI produced an area under the ROC curve (0.78) that was similar to that for both visual field mean deviation (0.78) and pattern standard deviation (0.80) and larger than that for a normalized measure of HRT rim area (0.66). The cases classified as glaucoma by the various tests were significantly non-overlapping. Based on the distribution of test values in the population with mild disease, the SFI may be better able to stratify this group while still clearly identifying those with severe disease.
CONCLUSIONS
The SFI reflects the traditional clinical diagnosis of glaucoma by combining optic nerve structure and function. In doing so, it identifies a different subset of patients than either visual field testing or optic nerve head imaging alone. Analysis of prospective data will allow us to determine whether the combined index of structure and function can provide an improved standard for glaucoma diagnosis.
Topics: Adult; Aged; Female; Glaucoma; Humans; Male; Middle Aged; Optic Disk; Optic Nerve; ROC Curve; Retinal Ganglion Cells; Tomography; Visual Field Tests
PubMed: 21314957
DOI: 10.1186/1471-2415-11-6 -
Molecular Neurobiology Jun 2020Glaucoma, a multifactorial neurodegenerative disease characterized by progressive loss of retinal ganglion cells and their axons in the optic nerve, is a leading cause...
Glaucoma, a multifactorial neurodegenerative disease characterized by progressive loss of retinal ganglion cells and their axons in the optic nerve, is a leading cause of irreversible vision loss. Intraocular pressure (IOP) is a risk factor for axonal damage, which initially occurs at the optic nerve head (ONH). Complex cellular and molecular mechanisms involved in the pathogenesis of glaucomatous optic neuropathy remain unclear. Here we define early molecular events in the ONH in an inherited large animal glaucoma model in which ONH structure resembles that of humans. Gene expression profiling of ONH tissues from rigorously phenotyped feline subjects with early-stage glaucoma and precisely age-matched controls was performed by RNA-sequencing (RNA-seq) analysis and complementary bioinformatic approaches applied to identify molecular processes and pathways of interest. Immunolabeling supported RNA-seq findings while providing cell-, region-, and disease stage-specific context in the ONH in situ. Transcriptomic evidence for cell proliferation and immune/inflammatory responses is identifiable in early glaucoma, soon after IOP elevation and prior to morphologically detectable axon loss, in this large animal model. In particular, proliferation of microglia and oligodendrocyte precursor cells is a prominent feature of early-stage, but not chronic, glaucoma. ONH microgliosis is a consistent hallmark in both early and chronic stages of glaucoma. Molecular pathways and cell type-specific responses strongly implicate toll-like receptor and NF-κB signaling in early glaucoma pathophysiology. The current study provides critical insights into molecular pathways, highly dependent on cell type and sub-region in the ONH even prior to irreversible axon degeneration in glaucoma.
Topics: Animals; Cats; Cell Proliferation; Disease Models, Animal; Evoked Potentials, Visual; Gene Expression Profiling; Glaucoma; Inflammation; Microglia; Optic Disk; Optic Nerve; Signal Transduction; Transcriptome
PubMed: 32266645
DOI: 10.1007/s12035-020-01910-9 -
The Journal of International Medical... 2008Serious injury to the optic nerve, including direct and indirect events, induces significant visual loss and even blindness. For the past decade corticosteroids and/or... (Review)
Review
Serious injury to the optic nerve, including direct and indirect events, induces significant visual loss and even blindness. For the past decade corticosteroids and/or optic canal decompression surgery have been widely embraced therapeutic paradigms for the treatment of traumatic optic neuropathy. There is little clinical evidence, however, to support the effectiveness of these strategies, raising questions about the efficiency of current therapy for improving visual outcomes. Recently, experimental studies have yielded a wealth of information related to the protection and regeneration of retinal ganglion cells, showing promise for the development of novel and effective treatments for optic nerve injury.
Topics: Animals; Blindness; Clinical Trials as Topic; Crystallins; Decompression, Surgical; Glutamic Acid; Humans; Nerve Growth Factors; Nitric Oxide; Optic Nerve; Optic Nerve Diseases; Optic Nerve Injuries; Retinal Ganglion Cells; Steroids; Tumor Necrosis Factor-alpha
PubMed: 18831880
DOI: 10.1177/147323000803600503 -
Experimental Eye Research Apr 1997Eighteen normal human eye-bank eyes (age: 18-81 years), five fetal eyes (16-24 weeks), 11 primary open-angle glaucoma (POAG) eyes (age: 76-89 years), and two Schnabel's...
Eighteen normal human eye-bank eyes (age: 18-81 years), five fetal eyes (16-24 weeks), 11 primary open-angle glaucoma (POAG) eyes (age: 76-89 years), and two Schnabel's cavernous optic atrophy eyes were examined using a biotinylated-hyaluronan binding protein to study the changes in the distribution of hyaluronic acid (HA) in the fetal, adult and glaucomatous optic nerve head. The vitreous body served as a positive control. Sections treated with Streptomyces hyaluronidase were used to confirm specificity. Monoclonal antibodies to myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP) were used as additional controls. In fetal optic nerve, HA was localized in blood vessels, peripapillary sclera and the pial septae in the retrolaminar nerve. No staining was associated with axons. Staining for MBP was negative. In adults, HA was found surrounding the myelin sheaths in the retrolaminar nerve; staining decreased with age. In contrast, HA staining in myelinated peripheral nerves (e.g. ciliaries) remained unchanged with age. HA also was localized to the adventitia of arteries and veins throughout the posterior segment. Compared to age-matched normal eyes, HA staining was virtually absent around myelin sheaths of the retrolaminar nerve in POAG eyes. Similar changes were not found in other HA positive structures. In Schnabel's cavernous optic atrophy. HA was present in increased amount in the atrophic area, but virtually absent in the remaining retrolaminar nerve. HA staining was invariably positive in vitreous, and Streptomyces hyaluronidase treated sections were negative. In adults, staining of MBP was associated with the myelin sheath in the retrolaminar nerve. In contrast to HA, staining of MBP was unchanged with age and in POAG. In Schnabel's atrophy, MBP staining disappeared only in the atrophic area. HA in the retrolaminar optic nerve appears to be associate with the space-filling matrix between myelin sheaths. HA is not present in the axon bundles prior to myelination of the optic nerve. HA in the retrolaminar optic nerve appears to decrease with age and is further reduced in POAG; however, corresponding changes are not found in MBP or in peripheral nerves. Perhaps, decreased amounts of HA is related to a higher susceptibility to elevated intraocular pressure or to optic nerve atrophy. In Schnabel's cavernous optic atrophy, HA is present in increased amount only in the atrophic area while MBP is markedly decreased, suggesting in situ production of HA in areas of optic nerve atrophy.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Aging; Fetus; Glaucoma, Open-Angle; Glial Fibrillary Acidic Protein; Histocytochemistry; Humans; Hyaluronic Acid; Middle Aged; Myelin Basic Protein; Myelin Sheath; Optic Nerve; Optic Nerve Diseases; Vitreous Body
PubMed: 9227277
DOI: 10.1006/exer.1996.0245 -
Asian Journal of Surgery Feb 2024
Topics: Humans; Optic Chiasm; Optic Nerve; Foot; Lower Extremity
PubMed: 37945403
DOI: 10.1016/j.asjsur.2023.10.090 -
JAMA Network Open Jun 2020
Topics: Diagnosis, Differential; Humans; Optic Nerve; Papilledema
PubMed: 32484550
DOI: 10.1001/jamanetworkopen.2020.7159 -
Arquivos Brasileiros de Oftalmologia 2019To test the hypothesis that Chagas disease predisposes to optic nerve and retinal nerve fiber layer alterations.
PURPOSE
To test the hypothesis that Chagas disease predisposes to optic nerve and retinal nerve fiber layer alterations.
METHODS
We conducted a cross-sectional study including 41 patients diagnosed with Chagas disease and 41 controls, paired by sex and age. The patients underwent ophthalmologic examinations, including intraocular pressure measurements, optic nerve and retinal nerve fiber layer screening with retinography, optical coherence tomography, and standard automated perimetry.
RESULTS
All of the patients with Chagas disease had a recent cardiologic study; 15 (36.6%) had heart failure, 14 (34.1%) had cardiac form without left ventricular dysfunction, and 12 (29.3%) had indeterminate form. Optic nerve/retinal nerve fiber layer alterations were observed in 24 patients (58.5%) in the Chagas disease group and 7 controls (17.1%) (p£0.01). Among these, optic nerve pallor, optic nerve alterations suggestive of glaucoma, notch, peripapillary hemorrhage, and localized retinal nerve fiber layer defect were detected. Alterations were more prominent in patients with Chagas disease and heart failure (11 patients), although they also occurred in those with Chagas disease without left ventricular dysfunction (7 patients) and those with indeterminate form (6 patients). Optical coherence tomography showed that themean of the average retinal nerve fiber layer thickness measured 89 ± 9.7 mm, and the mean of retinal nerve fiber layer superior and inferior thickness measured 109 ± 17.5 and 113 ± 16.8 mm, respectively were lower in patients with Chagas disease. In controls, these values were 94 ± 10.6 (p=0.02); 117 ± 18.1 (p=0.04), and 122 ± 18.4 mm (p=0.03).
CONCLUSION
Changes in optic nerve/ retinal nerve fiber layer were more prevalent in patients with Chagas disease.
Topics: Aged; Analysis of Variance; Case-Control Studies; Chagas Disease; Cross-Sectional Studies; Female; Humans; Intraocular Pressure; Male; Middle Aged; Nerve Fibers; Optic Nerve; Optic Nerve Diseases; Reference Values; Retina; Retinal Diseases; Tomography, Optical Coherence; Visual Field Tests
PubMed: 31116301
DOI: 10.5935/0004-2749.20190036