Journal articles on the topic 'Consecutive optic atrophy'

<strong>Background:</strong>&nbsp;Optic atrophy is an end stage result of various pathological conditions affecting the visual pathway anywhere from retina to lateral geniculate body. Ophthalmoscopically classified as primary, secondary, consecutive and glaucomatous. It is important to find the underlying etiology and treat at the earliest in order to prevent complete loss of visual function and improve quality of life.&nbsp;<strong>Methodology:</strong>&nbsp;A retrospective observation study included rural population of north Karnataka, who were diagnosed with optic atrophy during the period of 1 year, from July 2023 to June 2024 in Department of Ophthalmology at Gulbarga Institute of Medical Sciences, Kalaburagi.&nbsp;<strong>Results:</strong>&nbsp;A total of 40 patients were diagnosed with optic atrophy. Among them 16 (40%) were females and 24 (60%) were males. 3(7.50%) patients belong to the age group of &lt;20 years, 7 (17.50%) patients to 20-40 years, 14 (35%) patients to 40-60years and 16 (40%) patients to &gt;60years of age groups. Out of 40 optic atrophy cases 3(7.5%) had primary optic atrophy, 7(17.50%) had secondary optic atrophy, 11(27.50%) had consecutive optic atrophy and 19 (47.50%) had glaucomatous optic atrophy.&nbsp;<strong>Conclusion:</strong>&nbsp;Glaucoma followed by retinitis pigmentosa are most common cause of optic atrophy with severe loss of visual function among rural population of north Karnataka. Screening and awareness programme for early diagnosis of glaucoma, genetic counselling for retinitis pigmentosa with improvement in primary health care facility is recommended in order to reduce vision loss due to optic atrophy. &nbsp; &nbsp;

INTRODUCTION: Optic atrophy is usually applied to the condition of the disc following degeneration of the optic nerve. The present study was done to explore the epidemiology and causes of optic atrophy. MATERIAL AND METHODS: A cross-sectional study of 100 cases of optic atrophy patients with convenience sampling was conducted from 1 July 2012 to 23 September 2012. Clinical history was taken including demography. Visual acuity was taken, pupillary reaction tested and posterior segment examined. Optic atrophy was diagnosed by optic disc examination with slit lamp bio-microscopy with aid of 90D lens. Disc pallor with diminution of vision was used as parameter to diagnose optic atrophy. RESULTS: Out of 100 patients, male were 54%. It was bilateral in 26%. The mean age was 53.6 years (+/-18.11 yrs SD). The highest occurrence was seen in 61-70 yrs age range. Glaucoma was the most common cause of optic atrophy involving 58%. Out of 42% non-glaucomatous optic atrophy, 55% manifested primary optic atrophy, 38% secondary optic atrophy and 7% consecutive optic atrophy. The non-glaucomatous causes were trauma, optic neuritis, central retinal vein occlusion, intracranial space occupying lesions, papilloedema and in nine cases cause was unknown. Socially blind patients comprised of 37%. CONCLUSION: Optic atrophy was nearly equal in occurrence in both male and female and common above 4th decade of life. Glaucoma was commonest cause. Non-glaucomatous optic atrophy was also not uncommon and several causal factors should be considered.Journal of Universal College of Medical Sciences (2015) Vol.03 No.02 Issue 10 Page: 26-29

This research was aimed to study the etiology of optic atrophy and comparison of optic disc morphology between compressive and glaucomatous optic atrophy. It included 72 cases of optic atrophy admitted in Maharani Laxmi Bai Medical College, Jhansi between January 2016 to May 2017. Assessment of present complaints, examination of the eyes, visual acuity, refraction, perimetry, Optical Coherence Tomography(OCT) and slit lamp examination was done. The quantitative parameters of Optic Nerve Head (ONH) structure were compared using the Spectralis OCT with an enhanced depth imaging method. Out of 72 cases, 42 were males(58.33%) and 30 were females(41.67%). The disease was bilateral in 55 patients(76.39%). The disease manifested as primary optic atrophy in 36 patients(50%), secondary optic atrophy due to papilloedema in 9 cases(12.5%) and due to papillitis in 9 cases(12.5%). Six cases(8.33.%) had consecutive optic atrophy and 12 cases(16.67%) had glaucomatous optic atrophy. The main causes were meningitis in 12 cases(16.67%), syphilis in 8 cases(11.1%) and intra-cranial space occupying lesions in 6 cases(8.33%). The mean and maximum cup depths of Compressive optic neuropathy(CON) were significantly smaller than those with Glaucomatous optic neuropathy(GON). The distance between Bruch&#39;s membrane opening and anterior surface of the lamina cribrosa (BMO-anterior LC) of CON was also significantly smaller than that of glaucoma. 72 cases of optic atrophy involving 127 eyes have been studied. Measurements of the cup depths and the LC depth showed ability to differentiate between CON with a glaucoma-like disc and glaucoma.

Background: Visual recovery after optic neuritis (ON) used to be defined as good, although patients frequently complain of poor vision. Methods: We carried out a prospective study on 38 consecutive patients with acute ON followed monthly for 6 months and evaluated high- and low-contrast visual acuity (HCVA and LCVA, respectively), quality of vision (National Eye Institute Visual Function Questionnaire-25 (NEI-VFQ-25)), visual fields, and retinal thickness by spectral domain optical coherence tomography (OCT). Results: We found significant impaired LCVA and color vision in ON eyes 6 months after acute ON, which impact on quality of life. LCVA and color vision were correlated with the thicknesses of the ganglion cell and inner plexiform layer (GCIPL; 2.5% LCVA r = 0.65 and p = 0.0001; color vision r = 0.75 and p &lt; 0.0001) and that of the peripapillary retinal nerve fiber layer (pRNFL; LCVA r = 0.43 and p = 0.0098; color vision r = 0.62 and p &lt; 0.0001). Linear regression models that included the change in the GCIPL and pRNFL thicknesses from baseline to month 1 after onset explained 47% of the change in 2.5% LCVA and 67% of the change of color vision acuity. When adjusting for the value of visual acuity at baseline, predictors of the change in vision from baseline to month 6 achieved similar performance for all three types of vision (HCVA, LCVA, and color vision). Conclusion: Monitoring retinal atrophy by OCT within the first month after ON onset allows individuals at a high risk of residual visual impairment to be identified.

ObjectiveTo determine the temporal evolution, morphology, and frequency of macular ganglion cell atrophy in patients with retrochiasmal lesions of the visual pathway.MethodsIn a consecutive retrospective case series, we identified 47 patients with homonymous hemianopia and accessible macular optical coherence tomography scans. We estimated the time of lesion onset and the location of the lesion within the afferent visual pathway. Using semiautomatic layer segmentation, we determined ganglion cell layer thickness in areas projecting to the side of the retrochiasmal lesion and compared it with ganglion cell layer thickness on the healthy side.ResultsWe found that retrochiasmal lesions at any level may be associated with an atrophy of ganglion cells. This atrophy respects the vertical midline through the fovea and thus the anatomic separation of the nasal and temporal visual field. The vertical line separating the affected from the unaffected side has significantly less tilt as compared with the disc–fovea angle. Lesions of the optic tract are associated with earlier macular ganglion cell atrophy than retrogeniculate lesions. Macular ganglion cell atrophy may be present in cases with normal peripapillary nerve fiber layer analysis and vice versa.ConclusionsMacular ganglion cell layer thickness shows a topographic hemiatrophy in retrochiasmal lesions, which manifests earlier for tract lesions than for retrogeniculate lesions. This additional examination of ganglion cell homonymous hemiatrophy has a higher sensitivity in detecting retrograde transsynaptic degeneration than the analysis of the peripapillary nerve fiber layer alone.

AbstractObjective:To investigate differences in orbital involvement in patients with invasive versus non-invasive fungal sinusitis.Method:One hundred consecutive cases of fungal sinusitis were assessed clinically and by computed tomography scan to evaluate orbital involvement.Results:Clinical orbital involvement was more common in invasive (73.5 per cent) than non-invasive (12.1 per cent) fungal sinusitis (p = 0.000). Computed tomography scanning showed similar orbital involvement in both groups, except for erosion of the floor of the orbit, which was more common in patients with invasive fungal sinusitis (p = 0.01). Extra-ocular muscle enlargement (44.4 vs 4 per cent, p = 0.01) and optic atrophy (44.4 vs 0 per cent, p = 0.003) were more common in chronic than acute invasive fungal sinusitis. Four patients (16 per cent) with acute invasive fungal sinusitis had no evidence of orbital involvement on scanning, despite clinical evidence of optic atrophy.Conclusion:Orbital involvement is more common in invasive than non-invasive fungal sinusitis. The difference is more evident clinically than on computed tomography scanning. Patients with acute invasive fungal sinusitis may have limited evidence of orbital involvement on scanning, despite extensive clinical disease.

Introduction: Glaucoma, which is often accompanied by elevated intraocular pressure (IOP), causes progressive optic nerve atrophy and blindness. Among ocular structure parameters abnormalities in central corneal thickness (CCT), cup-to-disc (C/D) ratio, inter-eye C/D ratio asymmetry, optic disc area, and neuro-retinal rim area (N-RRA) appear to be highly correlated with glaucoma. We compare these specific ocular structures in a group of young normal pre-presbyopic patients and in a group of patients being treated for glaucoma.&#x0D; Methods: After written informed consent, 1433 consecutive normal, and 56 consecutive patients being treated for glaucoma were assessed by including age, race, sex, IOP (NCT), C/D ratio, optic disc area, N-RRA (Optos), central center thickness (CCT), and anterior chamber depth.&#x0D; Results: Combinations of findings in CCT, C/D ratio, C/D ratio asymmetry, disc area, and N-RRA (assessed by Z-score) were present in 65.52% of patients being treated for glaucoma and 22.96% of young normal patients. For young normal patients, overall average CCT was 550.37+/-39.47µm. Overall average C/D ratio was 0.39+/-0.11. Inter-eye C/D asymmetry was 0.02+/-0.06. Overall average disc area was 2.46+/-0.49mm2 (7863.54+/1630.42 pixels). Overall average N-RRA was 1.44+/-0.35mm2 (4785.88+/1161.14 pixels). C/D ratio increased modestly with disc area increase, an increase not associated with thinning N-RRA. Thin N-RRA was associated with small optic discs that had large C/D (t=-8.21, p=0.000, DF=93). There was a significant difference between young normal patients and patients being treated for glaucoma in CCT, C/D ratio, C/D ratio asymmetry, disc area, and N-RRA.&#x0D; Conclusion: More than one in five (22.96%) young normal patients has ocular structure findings similar to those found in patients being treated for glaucoma. These results will help refine decisions on which primary eye care patient to screen for glaucoma.

The aim of this study is to describe bilateral optic disc swelling in three consecutive patients with Blau syndrome or cryopyrin-associated periodic syndrome at a single institution. Case 1 was a 30-year-old woman receiving 25 mg etanercept twice weekly who had been diagnosed as early-onset sarcoidosis by biopsy of skin rashes at 5 months old and genetically diagnosed with Blau syndrome with CARD15/NOD2 mutation (N670K) at 13 years old. At 10 years old, she began to have uveitis with optic disc swelling in both eyes, resulting in macular degeneration and optic disc atrophy at 17 years old only when etanercept was introduced. Case 2 was a 21-year-old man receiving adalimumab every 2 weeks who had been diagnosed as early-onset sarcoidosis by biopsy of skin rashes at 1.5 years old and genetically diagnosed as Blau syndrome with CARD15/NOD2 mutation (C495Y) at 5 years old. At 8 years old, around the time of adalimumab introduction, he began to show bilateral optic disc swelling which continued until the age of 16 years when the dose of adalimumab was increased. Case 3 was a 20-year-old woman receiving canakinumab every 8 weeks for systemic symptoms such as fever, headache, vomiting, and abdominal pain and later for sensorineural hearing disturbance on both sides. She had been diagnosed genetically with cryopyrin-associated periodic syndrome with NLRP3 mutation (Y859C) at 7 years old. At 5 years old, she was found to have bilateral optic disc swelling, which continued until the age of 10 years when she began receiving canakinumab (IL-1β inhibitor). Bilateral optic disc swelling might be tentatively designated as a plausible common ocular feature, if it occurred, in autoinflammatory diseases to pay more attention to ophthalmic complications in rare diseases.

Eleven consecutive patients with a first episode of acute optic neuritis were evaluated, using conventional and magnetization transfer (MT) magnetic resonance imaging (MRI), in order to assess the temporal evolution of optic nerve (ON) damage and to investigate the correlation of ON damage with visual outcome and electrophysiological parameters. Patients underwent neuro-ophthalmological, neurological, electrophysiological, and MRI assessments at baseline and after three and 12 months. ON volumes were measured on coronal T1–weighted images using a local thresholding segmentation technique. MT ratio (MTR) from the ON was derived from gradient echo images. No significant volume difference was detected between affected and healthy ON, both at baseline and follow-up. At baseline, mean MTR values were significantly higher in affected ON than in healthy ON (P = 0.001), whereas at months 3 and 12, the mean MTR values were significantly reduced in the affected ON (P = 0.02 and 0.003, respectively). Mean MTR of the affected ON, corrected for healthy ON values, progressively decreased over time (P = 0.04 at month 3 and P = 0.0012 at month 12). On the contrary, MTR values of healthy ON remained stable. No correlations were found between MTR measures and clinical or electrophysiological data. This study shows the presence of subtle pathological changes, possibly due to residual demyelination and subsequent additional demyelination and impaired remyelination, in the ON of patients with a first episode of optic neuritis. In the early phase of optic neuritis, MT MRI is more sensitive than atrophy measurements in detecting disease-related changes. Multiple Sclerosis 2007; 13: 265–268. http://msj.sagepub.com

Objective: To find out the causes of bilateral irreversible blindness in patients of different age groups in District Swabi. Design: It is a prospective observational study of one hundred and eighty nine consecutive blind cases. Place and Duration of Study: The study was conducted from July 2010 to June, 2012 at the Ophthalmology Department of District Headquarter Hospital, Swabi. Subjects and Methods: Informed consent was taken from the patient or guardian of the patient. Patients fulfilling inclusion and exclusion criteria were included in the study. A standard proforma was designed and entries were made regarding present, past and family history, thorough ocular examination of every patient was performed on slit-lamp with relevant biomicroscopic aids and posterior segment examination was conducted with direct as well as indirect ophthalmoscope. Biomicroscopy was performed as and when required. lntraocular pressure using schiotz tonometer, corneal diameters, retinoscopy and ocular mobility were noted and relevant investigations were performed when needed. Children and mentally retarded patients were examined using short general anaesthesia. Results: Of 189 patients 61.4% were males and 38.6% were females. Congenital Causes were present in 49.7% and acquired causes in 50.3%. Diseases accounted for 88.9%, trauma in 10.1% and unknown causes in 1.1% cases. Congenital diseases included congenital glaucoma in 35.1%, retinitis pigmentosa in 29.7% and albinism in 19.1% cases. Acquired diseases included primary glaucoma in 33.8%, diabetic retinopathy 23 %, secondary glaucoma in 17.5% and childhood infection in 10.8% cases. Corneal findings included corneal opacity in 31.2%, corneal edema in 4.8% and absent cornea in 7.4%. Optic nerve findings included optic atrophy in 16.4%, glaucomatous optic atrophy in 16.9%, new vessels in 9.5%. Retina findings included retinal dystrophy in 14.3%, maculopathy in 5.3%, chorioretinopathy in 0.5%, vascular retinopathy and hypopigmentation in 9.5% each respectively. Conclusions: Irreversible blindness is more common in children and young adults and mostly males are affected. Glaucoma is the commonest cause followed by retinitis pigmentosa and albinism in this study.

Background: This study evaluated ocular features and visual outcomes in patients of accidental methanol poisoning at a tertiary centre in Jharkhand, India. Methods: Seven consecutive patients were attended from January 2022 to December 2022 as bedside references in the emergency department of our hospital after accidental ingestion of methanol in the form of adulterated alcoholic beverages. Visual acuity, anterior segment, fundus, and intraocular pressure (IOP) were examined, followed by a magnetic resonance imaging (MRI) of the brain. They were started with intravenous methylprednisolone followed by oral prednisolone. All the patients were followed up for the next three months. Results: The mean age of patients was 36.21±3.3 years (ranging from 29 to 43 years), and all were males. Visual acuity ranged from perception of light to counting fingers at 1 meter. Visual loss was bilateral. The pupillary reaction was sluggish or non-reactive. Fundus pictures ranged from normal to optic disc oedema and tortuous vessels. MRI showed central nervous system involvement in all patients. In follow-up visits, three patients showed normal fundus as in the previous examination, while four patients showed optic atrophy, and none presented with any improvement in visual acuity. Conclusion: It was concluded that methanol causes irreversible visual loss.

Background. Tilted disc syndrome (TDS) is a congenital anomaly characterized by “tilting” of the optic disc tipycally associated with myopic astigmatism, visual field defect, inferior staphyloma, and retinal pigment epithelium atrophy. Associated complications such as macular serous neuroretinal detachment are well described; however, ideal therapy for such complication is unknown.Methods. One interventional case report is hereby described. A patient affected by macular serous neuroretinal detachment-complicated tilted disk syndrome underwent a complete ophthalmic examination. Optical coherence tomography and fluorescein angiography were taken at baseline and at scheduled visits. Two intravitreal treatments of bevacizumab (avastin, 1.25 mg/0.05 mL) were performed at monthly interval.Results. At scheduled visit, one month after the second injection, OCT depicted persistence of neuroretinal detachment. Best-corrected visual acuity remain stable as well as metamorphopsia and functional discomfort.Conclusion. Clinical evidence of this brief interventional case report indicates that one patient affected by recent serous macular detachment-complicated TDS did not benefit from 2 consecutive monthly intravitreal Avastin treatments. Best-corrected visual acuity remained stable over a total observation period of 6 months.

BACKGROUND Relative afferent pupillary defect (RAPD) or Marcus Gunn pupil is a highly sensitive and significant objective clinical finding in eye examination. It can be detected by swinging flashlight test. Its presence indicates unilateral afferent sensory abnormality or an asymmetric bilateral disease. However, it can be determined even in an unconscious patient, requires no complicated gadgets, relies on clinical observation but can be a manifestation of a myriad of disorders affecting the eye or the brain. The goal of our study was to identify the aetiology of relative afferent pupillary defect and ascertain whether the grade of relative afferent pupillary defect correlated with the visual prognosis. METHODS This was a prospective observational hospital-based study. 25 consecutive patients who presented with a clinical diagnosis of relative afferent pupillary defect to the Ophthalmology Department of Kanyakumari Government Medical College in Tamil Nadu from February 2019 to January 2021 were included in the study. The patients were evaluated based on visual acuity, refraction, colour vision, slit lamp, fundus examination, intra ocular pressure (IOP) measurements &amp; fields. Statistical analysis was done by trial version of statistical package for social sciences (SSPS) software. RESULTS Of the 25 cases analysed, 60 % (15) were male, 36 % (9) were females and 4 % (1) children. An analysis of the aetiology revealed that the optic nerve pathology was the predominant aetiology accounting for 60 % (15) of cases, followed by glaucoma 24 % (6) and retinal pathology in 16 % (4). Glaucoma though a bilateral disease has an asymmetrical presentation which led to RAPD. Grade of RAPD correlated well with the visual prognosis. CONCLUSIONS RAPD is a good and valuable clinical tool for any clinician, it is also a useful guide for assessing the management and response to treatment. KEYWORDS Relative Afferent Pupillary Defect, Optic Neuropathy, Retinal Detachment, Glaucomatous Optic Atrophy

Background: Spontaneous vitreous hemorrhage is one of the common causes of ocular emergency. There are very few prospective studies on the clinical profile and surgical outcomes for patients with dense vitreous hemorrhage caused by non-diabetic and non-traumatic till date to our knowledge. Objectives: This study was conducted to better understand the etiologies, clinical profile, surgical outcome, and visual prognosis following pars plana vitrectomy for dense vitreous hemorrhage in adults with non-traumatic and non-diabetic retinopathy. Design: This was a prospective interventional study. Methods: This study was conducted in Mechi Eye Hospital (Birtamod, Nepal) from October 2018 to September 2019. All consecutive cases, 46 eyes of 46 patients, with vitreous hemorrhage that underwent vitrectomy were included in our study. There were 14 (30.4%) female and 32 (69.6%) male patients, and the average age at presentation was 43.74 ± 16.19 (17–84) years. The success rate of surgery in terms of visual outcome was evaluated. Results: The most common cause of vitreous hemorrhage was retinal vasculitis with fibrovascular changes and vascular sheathing 19 (41%). The indication of vitrectomy on patient demand was 20 (43.5%). Success rate of surgery in terms of visual outcome (functional outcome) was defined as final visual acuity of &gt;6/60 which was 86.9%. Conclusion: The most common cause of spontaneous vitreous hemorrhage in our study was retinal vasculitis with fibrovascular changes and vascular sheathing. Vitrectomy has a good surgical outcome for spontaneous vitreous hemorrhage in terms of visual outcome (functional outcome) unless guarded by other factors like chorioretinal atrophy followed by optic atrophy and epiretinal membrane.

Retinal ganglion cells (RGCs) undergo dendritic pruning in a variety of neurodegenerative diseases, including glaucoma and autosomal dominant optic atrophy (ADOA). Axotomising RGCs by severing the optic nerve generates an acute model of RGC dendropathy, which can be utilized to assess the therapeutic potential of treatments for RGC degeneration. Photobiomodulation (PBM) with red light provided neuroprotection to RGCs when administered ex vivo to wild-type retinal explants. In the current study, we used aged (13–15-month-old) wild-type and heterozygous B6;C3-Opa1Q285STOP (Opa1+/−) mice, a model of ADOA exhibiting RGC dendropathy. These mice were pre-treated with 4 J/cm2 of 670 nm light for five consecutive days before the eyes were enucleated and the retinas flat-mounted into explant cultures for 0-, 8- or 16-h ex vivo. RGCs were imaged by confocal microscopy, and their dendritic architecture was quantified by Sholl analysis. In vivo 670 nm light pretreatment inhibited the RGC dendropathy observed in untreated wild-type retinas over 16 h ex vivo and inhibited dendropathy in ON-center RGCs in wild-type but not Opa1+/− retinas. Immunohistochemistry revealed that aged Opa1+/− RGCs exhibited increased nitrosative damage alongside significantly lower activation of NF-κB and upregulation of DJ-1. PBM restored NF-κB activation in Opa1+/− RGCs and enhanced DJ-1 expression in both genotypes, indicating a potential molecular mechanism priming the retina to resist future oxidative insult. These data support the potential of PBM as a treatment for diseases involving RGC degeneration.

Chronic kidney disease (CKD) is a leading public health problem with high morbidity and mortality. However, the therapies remain limited. Traditional Chinese medicine (TCM) has been used for treating kidney disease for thousands of years and is an effective alternative treatment for CKD patients in China and other Asian countries. In the present study, we aimed to investigate the effect and mechanism of Huangqi-Danshen decoction (HDD), a TCM herbal decoction, on treating CKD. CKD rat model was induced by adding 0.75% adenine to the diet for 4 weeks. HDD extract was administrated orally to CKD rats at the dose of 4.7 g/kg/d for consecutive 4 weeks in adenine-induced CKD rats. Kidney function was evaluated by the levels of serum creatinine (Scr) and blood urea nitrogen (BUN). The pathological changes of kidney tissues were observed by periodic acid-Schiff (PAS) and Masson’s trichrome staining. The proteins expression of renal fibrosis and mitochondrial dynamics were determined and quantified by Western blot analysis. CKD rats showed obvious decline in renal function as evidenced by increased levels of Scr and BUN, which were blunted by HDD treatment. HDD could also improve tubular atrophy and interstitial fibrosis of CKD rats. Moreover, HDD downregulated fibronectin, type IV collagen, and α-smooth muscle actin expression in CKD rats. Furthermore, mitochondrial dynamics was disturbed in CKD rats, which manifested as increased mitochondrial fission and decreased mitochondrial fusion. HDD treatment restored mitochondrial dynamics in CKD rats by repressing dynamin-related protein 1 and Mid 49/51 expression, promoting mitofusin 2 expression, and suppressing optic atrophy 1 proteolysis. In conclusion, HDD could significantly retard CKD progression through modulating mitochondrial dynamics.

Background Pathological myopia (PM) is the leading cause for choroidal neovascularization (CNV) in people below 50 years of age, the anti-vascular endothlial growth factor (VEGF) medicine is now available to treat CNV secondary to PM. This study aimed to observe the efficacy of intravitreal ranibizumab for PM associated with subfoveal or juxtafoveal CNV in Chinese patients. Methods Fifty-four eyes of 52 consecutive patients were included, they treated with intravitreal ranibizumab 0.5 mg for PM associated with CNV. The best corrected visual acuity (BCVA) of Snellen chart, letters of ETDRS chart, retinal thickness, leakage of CNV lesion, and complications with surgery were analyzed pre- and post-treatment. Eligibility criteria included diopter ≥-8.0 D or eye axis ≥28 mm with fundus changes of PM (lacquer crack, optic disc atrophy, chorioretinal atrophy, posterior scleral staphyloma); CNV secondary to PM; subfoveal or juxtafoveal CNV. Results For 54 affected eyes of 52 consecutive patients, the average BCVA of Snellen chart and letters of ETDRS chart were 0.29 and 30.4, respectively; fundus fluorescein angiography (FFA)/indocyanine green angiography (ICGA) showed CNV leakage, and average retinal thickness on optical coherence tomography (OCT) was 267.2 μm before treatment. Injections of ranibizumab ranged from 1 to 4 (mean 2.2). Follow-up time varied from 12 to 36 months (mean 31.9 months). At the last visit, the BCVA of Snellen chart was increased by three lines (mean 0.65) (P &lt;0.01); the letters of ETDRS chart were increased to 17.0 letters (mean 47.4, P &lt;0.01); the visual acuity increased more than 15 letters in 30 eyes (55.5%), decreased in 1 eye (1.9%); the retinal thickness on OCT images was decreased by 17.0 μm (mean 250.2 μm) (P=0.082); no active leakage from the CNV lesion occurred in 18 eyes (33.3%), reduced leakage in 30 eyes (55.6%), and no change in 6 eyes (11.1%) as shown by FFA/ICGA. Increased retinoschisis was observed in one eye after the second injection. Conclusions Intravitreal ranibizumab for neovascular PM was well tolerated in Chinese patients, with functional and anatomic improvements in a short-term study, while a long-term study is still needed.

Background: Studies conducted in recent years have reported promising results regarding the treatment of retinoblastoma with the intra-arterial use of melphalan. In the present study, we intended to report the results of intra-arterial chemotherapy with melphalan (IACT) in the treatment of newly diagnosed or relapsed-refractory retinoblastoma patients at the Department of Pediatric Oncology of Hacettepe University, Ankara, Turkey. Materials and Methods: This was a retrospective study of patients with intraocular retinoblastoma who were treated with IACT from December 2011 to May 2014. A total of 56 eyes of 46 consecutive patients (30 males and 16 females) were included in the study. Forty-four eyes received systemic chemotherapy upon diagnosis (systemic chemotherapy group, SCG), and 12 eyes were those of newly diagnosed patients (primary intra-arterial melphalan group, PIAG). The choice of the IACT dose was based on age. Tumor control and globe salvage with IACT were analyzed. Complete blood counts were examined 7 days after the IACT for systemic toxicity. Ocular toxicities such as proptosis, eyelid edema, ocular motility, and retinal and optic atrophy were assessed by an ocular oncologist with regular ophthalmologic examinations. Results: Enucleation was avoided overall in 66% (37/56) of the eyes, including 75% (9/12) in the PIAG and 64% (28/44) in the SCG patients. The 1-year enucleation-free survival rate was 56.7% at a median follow-up time of 11.9 months (range 0.27-27.6). IACT was administered in a total of 124 cycles (ranging from 1 to 7 cycles, mean 2.3). The responses were as follows: regression of the retinal tumor in 27 eyes and improvements in vitreous seeding in 5 of 15 eyes. The further treatment requirements after IACT were as follows: enucleation in 19 eyes (10 with vitreous seeding), radiotherapy in 3 eyes, systemic chemotherapy in 1 eye, and local therapy in 1 eye. No severe systemic side effects occurred. Transient swelling of the eyelids (22 patients), conjunctival chemosis (12 patients), upper eyelid ptosis (5 patients), redness over the frontal area (3 patients), limitation of ocular motility (3 patients) and mild proptosis (1 patient) were detected. Retinal pigment epithelial alterations (30 patients) and optic atrophy (3 patients) were seen in the late follow-up. Conclusions: Globe salvage and avoidance of radiotherapy may be achieved by IACT with limited toxicity. This treatment is efficient, repeatable and safe.

In this study, we investigated medically or surgically actionable genes in inherited eye disease, based on clinical phenotype and genomic data. This retrospective consecutive case series included 149 patients with inherited eye diseases, seen by a single pediatric ophthalmologist, who underwent genetic testing between 1 March 2017 and 28 February 2018. Variants were detected using a target enrichment panel of 429 genes and known deep intronic variants associated with inherited eye disease. Among 149 patients, 38 (25.5%) had a family history, and this cohort includes heterogeneous phenotype including anterior segment dysgenesis, congenital cataract, infantile nystagmus syndrome, optic atrophy, and retinal dystrophy. Overall, 90 patients (60.4%) received a definite molecular diagnosis. Overall, NGS-guided precision care was provided to 8 patients (5.4%). The precision care included cryotherapy to prevent retinal detachment in COL2A1 Stickler syndrome, osteoporosis management in patients with LRP5-associated familial exudative vitreoretinopathy, and avoidance of unnecessary phlebotomy in hyperferritinemia-cataract syndrome. A revision of the initial clinical diagnosis was made in 22 patients (14.8%). Unexpected multi-gene deletions and dual diagnosis were noted in 4 patients (2.7%). We found that precision medical or surgical managements were provided for 8 of 149 patients (5.4%), and multiple locus variants were found in 2.7% of cases. These findings are important because individualized management of inherited eye diseases can be achieved through genetic testing.

IntroductionGlaucoma is one of the most common causes of blindness and affects more than 70 million people worldwide. The disease is characterised by the loss of retinal ganglion cells associated with a progressive optic neuropathy, resulting in an impairment of visual functions, for example, visual field loss. Nowadays, the only modifiable risk factor is the increase in intraocular pressure, and its treatment is to lower this pressure by medication, laser treatment or surgery to avoid disease progression. New methods for preventing and reversing vision loss are thus urgently needed. Several small and two multicentre studies have presented evidence that repetitive transorbital alternating current stimulation (rtACS) can lead to long-lasting visual field improvement. This could open a new and inexpensive therapeutic option for optic atrophy. However, the level of evidence for this method is still fairly rather poor, and further trials are needed. Therefore, this clinical trial aims to prove the effectiveness of rtACS compared with sham stimulation in patients with primary open-angle glaucoma (POAG).Methods and analysisVIRON (Vision Restoration in Optic Neuropathy) is a national, multicentre, prospective, randomised, placebo-controlled, double-blind trial with three arms. The primary objective is to assess the effectiveness of rtACS in patients with POAG compared with sham stimulation. The primary outcome is the change in mean defect (MD) in the visual field immediately after 10 sessions of rtACS (days 9, 16 and 23) compared with the values of initial perimetry (days −21 to –14 and 0) after applying electrical stimulation with a classical montage, compared with sham and electrical stimulation using individualised montage. Secondary outcome measures comprise a long-term effect with changes in MD at 24 weeks after stimulation, and data from the National Eye Institute Visual Function-25 and quality of life (Short Form 36) questionnaires. The target population are patients with glaucomatous optic atrophy and significant glaucomatous visual field defects (MD of 5–22 dB) due to POAG.After randomisation, patients received either classical rtACS (group 1), individual rtACS (group 2) or sham stimulation (group 3) in daily 25 min stimulation sessions in two series of five consecutive days separated by a weekend interval. In group 1, active stimulation will be via the routinely applied montage using two electrodes affixed on the right and left side of the head, next to the eyes, with straightforward fixation. In group 2, the current flow will be individually modelled (MRI-based) to target areas of partial visual field defects by optimising electrode positions in conjunction with an optimised visual fixation direction. Group 3 with sham stimulation will serve as control.The calculated sample size required to achieve a statistical power of 80% for a relevant effect size and allow for dropouts was 300 (100 per group). The trial has already begun with the first patient in July 2023. The planned recruitment period is 24 months with an estimated end of the study in November 2025 (last patient out). An adjusted extension of the study period is planned.Ethics and disseminationVIRON was approved by the Central Ethics Committee of the University Medical Center Göttingen (19 October 2022) and those of the individual participating centres (Bonn: 446/23-EP, Hamburg: 2023-200889-BO-bet, Cologne: 23-1487 and Mainz: 2023-17399-§23b). The study protocol complies with the Declaration of Helsinki, the national medicine device regulation (MDR) laws and the international standards of good clinical practice (GCP).The study protocol (V.5, 24 November 2023) was designed following the Standard Protocol Items: Recommendations for Interventional Trials guidelines and is registered onhttps://drks.de/search/de/trial/DRKS00029129.As study initiatior the University Medical Center Göttingen (UMG) is responsible for data ownership and data management of the VIRON study. The study data will be published within 6 months of the study being completed. After the publication of the primary results, all data are anonymised and published in an open-access journal to ensure access to the data for third parties.Trial registration numberhttps://drks.de/search/de/trial/DRKS00029129.

Abstract Background Idiopathic intracranial hypertension (IIH) is a disorder of unknown origin, characterized by features of raised intracranial pressure (ICP). Existing literature is inconclusive about the role of transcranial Doppler (TCD) in the management of IIH. Objective To study the TCD changes in IIH patients, pre- and post-cerebrospinal fluid (CSF) drainage. Materials and Methods This was a prospective study, conducted between July 2017 and December 2019, in a tertiary care referral center in South India. Sixteen consecutive patients, suspected to have IIH, underwent magnetic resonance imaging ofthe brain, a baseline TCD, and lumbar puncture with CSF drainage and pressure monitoring. Post-CSF drainage, TCD was repeated and mean flow velocities, peak systolic velocities, end-diastolic velocities, and pulsatility index (PI), in the middle cerebral artery (MCA), vertebral artery, and basilar artery (BA) were noted. Thirteen patients had elevated CSF pressure, and fulfilled the diagnostic criteria for IIH. These patients were included in the final analysis and pre- and post-CSF drainage TCD blood flow velocities and PI were compared. Results The mean age of study participants was 29.92 ± 6.92 years. There was a significant reduction in the cerebral flow velocities in bilateral MCA, after CSF drainage and normalization of ICP. Flow velocities in posterior circulation and PI in MCA, PCA, and BA showed an insignificant reduction. Two patients, who did not show any reduction in flow velocities after CSF drainage, developed optic atrophy on follow-up. Conclusion TCD-derived systolic blood flow velocities can be used in the management and follow-up of patients with IIH.

Abstract OBJECTIVE Recent reports have shown promising short- to medium-term results in patients with refractory idiopathic intracranial hypertension (IIH) treated using the stereotactic ventriculoperitoneal shunting (SVPS) technique. However, the long-term clinical efficacy of this technique remains questionable. This report provides the long-term results of SVPS in treating refractory IIH patients. METHODS We reviewed the medical charts of nine consecutive patients (mean age, 26.4 yr; range, 4–63 yr) treated using either a frame-based or frameless SVPS technique for IIH. RESULTS The mean postoperative follow-up period was 44.3 months (range, 6–110 mo). Before shunting procedures were performed, each patient presented with intractable headache, and five patients (55.6%) had mild to moderate visual deficits. The last follow-up assessment showed that after shunting was performed, eight patients (89%) were headache-free. Only one patient had recurrent headache; however, this patient's pain was much less frequent and severe than before the shunting procedure was completed and was concomitant with recent weight increase. Visual deficits were resolved in three patients and remained stable in two who already had optic nerve atrophy before shunting was completed. Twelve SVPS procedures were performed on our patients. Nine shunt revisions were needed in six patients because of infection (n = 5, including two revisions in one patient), valve dysfunction (n = 2), distal obstruction (n = 1), and ventricular catheter malpositioning (n = 1). No patient had proximal catheter obstruction. CONCLUSION Given the favorable long-term outcome of the SVPS technique for refractory IIH, we are encouraged to apply this procedure on our patients. More invasive approaches should be reserved for patients who have SVPS failure.

Background: Anecdotally, Ghanaians with brain tumours present late with visual impairment. Contributory factors are unclear.Purpose: To determine the degree of visual impairment in Ghanaians with brain tumours, factors affecting this and their prognostic significance.Methods: A prospective study of 70 consecutive patients newly diagnosed with brain tumours seen from November 2010 to July 2013, at Korle-Bu Teaching Hospital(KBTH), Accra, Ghana. Patients had clinical diagnosis of brain tumour with confirmation by Computerized tomography(CT) or Magnetic Resonance Imaging(MRI).Outcome measures: presenting visual acuity, prepresentation symptom interval (PPSI), tumour size and location at presentation.Results: Data on 70 patients was analyzed. Ages ranged from 8 days to 70 years, mean(SD) 41.8±1.8. Fortyseven (67.1%) were females. Histology was confirmed in 22(75.9%) of 29 who had surgery, comprising: pituitary adenoma, 17(77.3%) meningioma, 2(9.1%)craniopharyngioma, 2(9.1%) and combined pituitary adenoma and meningioma,1(4.5%). Common presenting symptoms were blurred vision, 65(92.9%), headache, 51(72.9%) and ocular pain, 22(31.4%). Common signs were impaired colour vision in 97(79.5%) of 122 eyes and optic atrophy in 49(35%) of 140 eyes. Fourteen (20%) patients were visually impaired and 18(25.7%) blind. Visual impairment20(14.3%) and blindness, 61(43.6%) were present in 140 eyes. Pre-presentation symptom interval(PPSI) was longer in the blind than the visually impaired. However, no significant association was found between PPSI and visual impairment or blindness (p=0.660). Noassociation was found between diagnosis and visual status at presentation (p=0.629)Conclusions: Early detection of brain tumours to avoid blindness and visual impairment is needed in this population since majority (57.9%) of eyes were blind or visually impaired at presentation.

Abstract Background: Vitreous hemorrhage is one of the most common ocular emergencies encountered in the eye care setup. Presenting features may vary from decreased visual acuity to floaters. We present a case series of a profile of pars plana vitrectomy patients and their surgical outcome in a tertiary care setup. Objectives: This study is designed to better analysis of etiologies, clinical presentation, and outcome measurements following pars plana vitrectomy for various causes. Design: It is a single-centric interventional study. Materials and Methods: The study was conducted at a tertiary care setup in the Hooghly district of West Bengal for 1 year (from December 2021 to November 2022). In all consecutive cases, 30 eyes of 30 patients underwent pars plana vitrectomy in our study. Detailed history and examination were done in all patients with routine blood and serological testing. Details of all patients with pre- and postoperative data were collected and analyzed with SPSS for quantitative evaluation. Results: Most patients were male in the age group of 40–60 years; the total number of females was 8. The median age of presentation was 49.5 ± 6.2 years in males and 41.2 ± 3.2 years in females. Surgical outcomes were evaluated in each patient. Twenty-eight patients responded with a single-step procedure, two patients required second-step surgery. The most common cause of surgical intervention was advanced diabetic eye disease in our study (43.33%) followed by hypertensive retinopathy (20%). Functional visual outcome was taken in this study as visual acuity of &gt;6/60, achieved in 76.6% of patients. Conclusion: Most of the patients had good surgical outcomes unless had preoperative additional risk factors such as extensive proliferation, optic atrophy, secondary glaucoma, and long-standing cases where functional outcome did not correlate with anatomical outcome.

ABSTRACT Background: Tuberculosis is an important cause of morbidity and mortality in children, especially in endemic countries. The diagnosis of tuberculosis in these patients is challenging due to various reasons. The outcome of treatment in these patients is also varied. Aims and Objectives: Our study aims to determine the various types of presentations of tuberculosis; describe the clinical, radiological and microbiological characteristics and also study the outcome of treatment in patients ≤ 18 years of age. Materials and Methods: It was a prospective study. We included all newly diagnosed consecutive cases of pulmonary or extra pulmonary TB in patients (up to 18 years of age). After a detailed history and complete physical examination, AFB smear and CBNAAT of samples and radiology were performed. Follow-up of all cases was done at the end of intensive phase (IP) and at the end of treatment or at any time as needed. All statistical analyses were performed using SPSS version 19.0. Results: A total of 105 cases were included in our study. Most cases belonged to the age group of 7–14 yrs. Pulmonary tuberculosis (PTB) was diagnosed in 37 cases (35.2%), followed by TB lymphadenitis (31.4%). Microbiological confirmation could be obtained only in 53 cases (50.47%). Joint pain and a derangement in liver function test were the most common adverse effects (4 cases) and 1 case developed optic atrophy. Conclusion: A combination of history, signs and symptoms, and radiology may help reach a diagnosis in children. The risk of serious adverse events in children associated with the use of the recommended treatment regimens is also very low. Children and their family members should be educated about TB and the importance of completing treatment.

Glaucoma is a chronic neurodegenerative disease of the optic nerve and a leading cause of irreversible blindness, worldwide. While the experimental research using animal models provides growing information about cellular and molecular processes, parallel analysis of the clinical presentation of glaucoma accelerates the translational progress towards improved understanding, treatment, and clinical testing of glaucoma. Optic nerve axon injury triggers early alterations of retinal ganglion cell (RGC) synapses with function deficits prior to manifest RGC loss in animal models of glaucoma. For testing the clinical relevance of experimental observations, this study analyzed the functional correlation of localized alterations in the inner plexiform layer (IPL), where RGCs establish synaptic connections with retinal bipolar and amacrine cells. Participants of the study included a retrospective cohort of 36 eyes with glaucoma and a control group of 18 non-glaucomatous subjects followed for two-years. The IPL was analyzed on consecutively collected macular SD-OCT scans, and functional correlations with corresponding 10–2 visual field scores were tested using generalized estimating equations (GEE) models. The GEE-estimated rate of decrease in IPL thickness (R = 0.36, P&lt;0.001) and IPL density (R = 0.36, P&lt;0.001), as opposed to unchanged or increased IPL thickness or density, was significantly associated with visual field worsening at corresponding analysis locations. Based on multivariate logistic regression analysis, this association was independent from the patients’ age, the baseline visual field scores, or the baseline thickness or alterations of retinal nerve fiber or RGC layers (P&gt;0.05). These findings support early localized IPL alterations in correlation with progressing visual field defects in glaucomatous eyes. Considering the experimental data, glaucoma-related increase in IPL thickness/density might reflect dendritic remodeling, mitochondrial redistribution, and glial responses for synapse maintenance, but decreased IPL thickness/density might correspond to dendrite atrophy. The bridging of experimental data with clinical findings encourages further research along the translational path.

Objective: To assess the relationship between Helicobacter pylori (Hp) infection and primary open-angle glaucoma (POAG); and meantime, to explore the possible mechanism of POAG induced by Hp. Methods: 30 consecutive POAG patients, 30 primary angle-closure glaucoma (PACG) and cataract patients were recruited and divided into three groups according to different diseases. The sera and aqueous humor samples were collected and used to detect Hp-specific IgG antibody (Hp-Ab) with dot immunogold filtration assay (DIGFA). 14C-urea breath test (14C-UBT) was carried out to detect Hp infection of all participants. Results: The Hp-Ab positive rate respectively was 76.7% (23/30) and 66.7% in sera samples and aqueous humor samples for POAG group, which was significantly higher than the corresponding data of the other two groups (all P&lt;0.05). In 14C-UBT, the Hp-Ab positive rate was 63.3% in POAG group and it was close to that of serological result detected by DIGFA (P&gt;0.05). There were little numbers of positive ANA and ENA in the three groups and no meaning to make statistically analysis. Conclusions: There is positive association between Hp infection and POAG, and the autoimmune is suggested as one of the key mechanisms in our opinions.&#x0D; Introduction&#x0D; Glaucoma is one of the commonest causes for blindness in the world. Generally, glaucoma is divided into primary open-angle glaucoma (POAG) and primary angle-closure glaucoma (PACG).1 As a leading causes for blindness, the study of POAG causes more and more attention.2,3To our understand, POAG is a chronic optic neuropathy characterized by atrophy and increased cupping of optic disk. To date, many aspects of its pathogenesis remain unknown but some significant risk factors are advanced age, African origin, familial history of glaucoma and elevated intraocular pressure.4,5&#x0D; Helicobacter pylori (Hp) is a Gram-negative and microaerophilic bacterium which plays an important role in the development of various upper gastrointestinal diseases. With the development of studies, some researchers reported that Hp was also associated with some extragastric diseases, such as ischemic heart disease,6 iron-deficient anemia,7 diabetes mellitus,8 and so on. In 2001, Kountouras et al9 established a higher prevalence of Hp infection in the sera of patients with POAG in a Greek population, and suggested a possible causal link between Hp and glaucoma. Subsequently, this finding was evidenced by some scholars in their own studies.10 But the significance of such an association remains uncertain because of the conflicting findings reported by various studies.11-13 Aiming to such a discrepancy, further studies are necessary.14&#x0D; In this study, we just do detect Hp-specific IgG antibodies (Hp-Ab) in the sera and aqueous humor of patients with different ocular diseases, including POAG, PACG and cataract, and attempt to further determine the relationship between Hp infection and POAG and to analyze the possible mechanism of POAG induced by Hp.&#x0D; Abbreviations&#x0D; ANA, antinuclear antibody; ENA, Extractable nuclear antigen; DIGFA, dot immunogold filtration assay; Hp, Helicobacter pylori; Hp-Ab, Hp-specific IgG antibodies; PACG, primary angle-closure glaucoma; POAG, primary open-angle glaucoma; 14C-UBT: 14C-urea breath test.&#x0D; &#x0D; Subjectsand methods&#x0D; Subjects&#x0D; 30 consecutive POAG patients were enrolled with the average age of 68±7.3 y (ranged from 47 to 78 y). The ratio of the male and the female was 11: 19. Meantime, 30 PACG patients and 30 cataract patients were also recruited, and who were matched by age and sex with the POAG patients. According to different diseases, the participants were divided into POAG, PACG and cataract groups, respectively. All of them were excluded from tumor, immunodeficiency, autoimmune and infectious diseases in clinic, and also had no antibiotics and other medicines related to immunopotentiator or immunosuppressive agents in the six months before the experiment. Written informed consents were obtained from all the participants. The study was approved by the local ethics committee.&#x0D; Hp-Ab detection of sera samples&#x0D; 2 ml venous blood was collected from each of the participants. The serum was obtained after centrifugation and used to detect Hp-Ab with dot immunogold filtration assay (DIGFA) according to the manufacturer’s instruction of the reagent kit (MP Biomedicals Asia-Pacific Pte. Ltd., Singapore).&#x0D; Hp-Ab detection of aqueous humor samples&#x0D; About 50 μl aqueous humor sample was aspirated at the beginning of glaucoma surgery from the each of the patients in the three groups, respectively. Hp-Ab was assayed with DIGFA as same as the detection process of venous blood samples.&#x0D; Detection of Hp infection with 14C-urea breath test&#x0D; Referring to Tang’s report,1514C-urea breath test (14C-UBT) was carried out in POAG group with Hp detection instrument-YH04 (Yanghe Medical Equipment Co. Ltd., China).&#x0D; Sera auto-antibodies detection&#x0D; Serum antinuclear antibody (ANA) was detected with the indirect immunofluorescence assay by a commercialized ANA kit. Extractable nuclear antigen (ENA) was assayed with line immunoassay. All reagents were bought from Jiangsu HOB Biotech Group, China.&#x0D; Statistic analysis&#x0D; Using T-test and Chi-square test, all analyses were performed with SPSS 13.0 software. P value less than 0.05 were considered significant.&#x0D; Results&#x0D; 3.1 Hp infection detection in sera and aqueous humor &#x0D; Of the sera samples, there were 23 cases exhibited Hp-Ab-positive in POAG group, and the positive rate was 76.7% which was significantly higher than those of PACG and cataract group (43.3% and 36.6% respectively). In the aqueous humor samples, there were 18 patients with positive Hp-Ab in POAG group, and the positive rate was 66.7%. Compared to each data of the other two groups, the difference was statistically significant (Table 1). In POAG group, the mean positive rate of sera samples was similar to that of aqueous humor and no difference existed between them (P = 0.287).&#x0D; Table 1. The serum and aqueous humor qualitative test results of the patients with glaucoma&#x0D; Hp infection detection with 14C-UBTAH: aqueous humor; a: POAG group vs cataract group; b: POAG group vs PACG group; c: PACG group vs cataract group.&#x0D; In 14C-UBT, there were 19 patients with Hp-Ab-positive, and the positive rate was 63.3%. Compared to the data detected with DIGFA, the difference was not significant (Table 2).&#x0D; Table 2. Comparison of DIGFA and 14C-UBT for diagnosis of Hp infection in POAG group&#x0D; ANA and ENA detection* represents comparison of the positive rate detected with the two methods.&#x0D; There were 4, 2 and 1 patients with ANA-positive in POAG, PACG and cataract group, respectively. The positive ENA in POAG group were SSA, SSB and Ro-52, and the corresponding numbers were 2, 2 and 1. Only Ro-52 showedpositive in PACG group while there was no positive ENA in cataract group (Table 3).&#x0D; Table 3. The results for sera ANA, ENA of the patients of each group&#x0D; Discussion&#x0D; In Greece, a very active research group led by J. Kountouras published several original contributions as well as the reviews concerning the connection between Hp infection and POAG.14,16 In other counties, there were also several papers containing the similar arguments issued, such as India,17 Turkey,18 Korea19 and so on. In China, Hong et al20 detected Hp infection and POAG through 13C-UBT, and also found the positive correlation between them. Since then, there was no relative article issued by Chinese could be found in PubMed and other well-known scientific database. In this study, referring to other researchers’ reports, we designed and carried out the experiments. In the results, we found that the positive rate of sera Hp-Ab was high to 76.7% in POAG patients, which was significantly higher than those of the other two groups. This finding was close to the data of the previous reports2,21 and further verified that there was a positive relation between Hp infection and POAG.&#x0D; In the present study, we also assayed Hp infection with 14C-UBT. Encouragingly, the positive rate of Hp infection was 63.3%, which was very close to 76.7% detected with DIGFA. This result further indicated the existence of the relation between Hp infection and POAG. However, Bagnis et al22 thought that the studies based on Hp serological assessment might be misleading, since serum antibodies were not the sensitive markers of active Hp infection; while 13C-UBT could clarify the actual prevalence of POAG among patients infected by Hp. In fact, there were still deficiencies for 13C- or 14C -UBT, because it was more suitable for the detection of gastrointestinal Hp infection, and to an extent, there were false-negatives in the test.23 This probably was the just reason for what the positive rate in DIGFA was little higher than that in 14C-UBT in this study. As to the cresyl fast violet staining on the histology preparations of tissue samples of trabeculum and iris introduced by Zavos et al,24 although it could provide the direct and strong evidence for Hp infection in the pathophysiology of POAG, the difficult harvest of the sample limited its application. Therefore, in our opinions, the serological assay is suitable to detect Hp infectionand used to assess the relationship between Hp prevalence and POAG.&#x0D; Except for detecting sera Hp-Ab, we also detected Hp-Ab in the aqueous humor collected from the majority of participants. As the results shown, the positive rate of the POAG group was statistically higher than each of the other groups, respectively. This result was consistent with that of the serological assessment and again showed the positive relation between Hp infection and POAG. However, in another similar study, Deshpande et al17 also found a statistically significant difference between the POAG patients and the controls in the concentration of serum Hp-Ab, but they did not find any significant correlations between the Hp concentrations of the aqueous humor of the different patient groups. This disagreement probably associated with the damage degree of blood-brain barrier (BBB), because the sera Hp-Ab could reach the trabeculum and iris under the condition of the BBB disruption.25 According to the results of the present study, we supported the hypothesis related to POAG onset that Hp-Ab in circulation might get through the blood-aqueous humor barrier, further condensed in aqueous humor and finally induced or aggravated glaucomatous damage.2&#x0D; As to the occurrence of POAG, we thought another autoimmune mechanism was most probable and should not be ignored: Hp infection initiated autoimmune response because of the common genetic components shared in Hp and human nerve tissue; and then, cell destruction which mediated by apoptosis direct caused glaucoma.26 Just based on the theory, we designed and detected sera ANA and ENA of the POAG patients and the control participants, and hoped to find any evidences related to autoimmune. As a result, we found that the positive rate of every group was rather low and there was no difference between them. However, this seronegative result can’t deny the hypothesis of autoimmune mechanism in POAG; and the auto-antibodies specific to eyes, such as trabeculum and iris, were suggested to be detected in future study in our opinions.&#x0D; Conclusion&#x0D; The positive association between Hp infection and POAG not only using serum sample but also aqueous humor sample is found in this study. And further, through the experimental data, it is suggested that the autoimmune induced by Hp infection probably is the key mechanism for POAG onset, and Hp detection should be taken as a routinized index applied to the prevention and therapy of POAG in clinic. However, we can not sufficiently investigate the possible mechanism of POAG relates to Hp infection. Is it true that Hp infection only relative to POAG but not a causative factor for POAG?18 What are the initial mechanisms of Hp in POAG if the pathogen takes part in the onset of the disease? Such questions will be the study topics to the medical researchers worldwide in future.&#x0D; Funding&#x0D; This work is supported by the Research Fund for Lin He’s Academician Workstation of New Medicine and Clinical Translation in Jining Medical University(JYHL2018FMS08), and the Project of scientific research support fund for teachers of Jining Medical University (JYFC2018FKJ023).&#x0D; Conflicts of interest&#x0D; There is no any conflict of interest between all of the authors.&#x0D; References:&#x0D; &#x0D; Chan H. H.; Ng Y.F.; Chu P. H. Clin Exp Optom. 2011, 94, 247.&#x0D; Kountouras J.; Mylopoulos N.; Konstas A. G.; Zavos C.; Chatzopoulos D.; Boukla A. Graefe’s Arch Clin Exp Ophthalmo. 2003, l241, 884.&#x0D; Kim E. C.; Park S. H.; Kim M. S. A. J. Pharmacol. Ther. 2010, 26, 563.&#x0D; Cantor L.; Fechtner R. D.; Michael A. J. San Francisco: Foundation of American Academy of Ophthalmology. 2005, 8.&#x0D; Bron A.; Chaine G.; Villain M.; Colin J.; Nordmann J. P.; Renard, J.P.; et al. Fr. Ophtalmol. 2008, 31, 435.&#x0D; Suzuki H.; Franceschi F.; Nishizawa T.; Gasbarini A. Helicobacter. 2011, 16, 65.&#x0D; Xia W.; Zhang X.; Wang J.; Sun C.; Wu L. Br. J. Nutr. 2011, 18, 1.&#x0D; Schimke K.; Chubb S. A.; Davis W. A.; Davis T. M. Atherosclerosis. 2010, 212, 321.&#x0D; Kountouras J.; Mylopoulos N.; Boura P.; Bessas C.; Chatzopoulos D.; Venizelos J.; et al. Opthalmology. 2001, 108, 599.&#x0D; Zaidi M.; Jilani A.; Gupta Y.; Umair S.; Gupta M. Nep. J. Oph. 2009, 1, 129.&#x0D; Galloway P. H.; Warner S. J.; Morshed M. G.; Mikelberg F. S. Ophthalmology. 2003, 110, 922.&#x0D; Abdollahi A.; Zarei R.; Zare M.; Kazemi A.Iran J. Opththalmol. 2005, 18, 15.&#x0D; Kurtz S.; Regenbogen M.; Goldiner I.; Horowitz N.; Moshkowitz M. Glaucoma. 2008, 17, 223.&#x0D; Tsolakin F.; Gogaki E.; Sakkias F.; Skatharoudi C.; Lopatatzidi C.; Tsoulopoulos V.; et al. Ophthalmol. 2012, 6, 45.&#x0D; Tang H. R.; Fan Y. J.; Liu S. Sichuan Da Xue Xue Bao Yi Xue Bao. 2014, 45, 823.&#x0D; Zavous, C.; Kountouras, J. Ophthalmol. 2012, 6, 243.&#x0D; Deshpande N.; Lalitha P.; Krishna das S. R.; Jethani J.; Pillai R. M.; Robin A.; et al. Glaucoma. 2008, 17, 605.&#x0D; Öztürk F.; Kurt E.; Inan U. U.; Erm S. S.; Çetinkaya Z.; Altýndi M. African J. Res. 2009, 3, 560.&#x0D; Kim J. M.; Kim S. H.; Park K. H.; Han S. Y.; Shim H. S. Invest Ophthalmol. Vis. Sci. 2011, 52, 665.&#x0D; Hong Y.; Zhang C. H.; Duan L.; Wang E. Asian J. Ophthalmol. 2007, 9, 205.&#x0D; Samarai V.; Shrif N.; Nateghi S. Glob. J. Health Sci. 2014, 6, 13.&#x0D; Bagnis A.; Izzotti A.; Saccàn S. C. Diagestive and Liver Disease. 2012, 44, 962.&#x0D; Gao F.; Li W. X. Chin. J. 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Background: MRI abnormalities are common in optic neuropathies, especially on dedicated orbital imaging. In acute optic neuritis, optic nerve T2-hyperintensity associated with optic nerve contrast enhancement is the typical imaging finding. In chronic optic neuropathies, optic nerve T2-hyperintensity and atrophy are regularly seen. Isolated optic nerve T2-hyperintensity is often erroneously presumed to reflect optic neuritis, frequently prompting unnecessary investigations and neuro-ophthalmology consultations. Our goal was to determine the significance of optic nerve/chiasm T2-hyperintensity and/or atrophy on MRI. Methods: Retrospective study of consecutive patients who underwent brain/orbital MRI with/without contrast at our institution between July 1, 2019, and June 6, 2022. Patients with optic nerve/chiasm T2-hyperintensity and/or atrophy were included. Medical records were reviewed to determine the etiology of the T2-hyperintensity and/or atrophy. Results: Four hundred seventy-seven patients (698 eyes) were included [mean age 52 years (SD ±18 years); 57% women]. Of the 364 of 698 eyes with optic nerve/chiasm T2-hyperintensity without atrophy, the causes were compressive (104), inflammatory (103), multifactorial (49), glaucoma (21), normal (19), and other (68); of the 219 of 698 eyes with optic nerve/chiasm T2-hyperintensity and atrophy, the causes were compressive (57), multifactorial (40), inflammatory (38), glaucoma (33), normal (7), and other (44); of the 115 of 698 eyes with optic nerve/chiasm atrophy without T2-hyperintensity, the causes were glaucoma (34), multifactorial (21), inflammatory (13), compressive (11), normal (10), and other (26). Thirty-six eyes with optic nerve/chiasm T2-hyperintensity or atrophy did not have evidence of optic neuropathy or retinopathy on ophthalmologic examination, and 17 eyes had clinical evidence of severe retinopathy without primary optic neuropathy. Conclusions: Optic nerve T2-hyperintensity or atrophy can be found with any cause of optic neuropathy and with severe chronic retinopathy. These MRI findings should not automatically prompt optic neuritis diagnosis, workup, and treatment, and caution is advised regarding their use in the diagnostic criteria for multiple sclerosis. Cases of incidentally found MRI optic nerve T2-hyperintensity and/or atrophy without a known underlying optic neuropathy or severe retinopathy are rare. Such patients should receive an ophthalmologic examination before further investigations.

Background: Monitoring patients with idiopathic intracranial hypertension (IIH) and optic atrophy may be difficult as papilledema may not be appreciable on ophthalmoscopy. This retrospective chart review evaluated whether papilledema recurrence can be detected in this population using optical coherence tomography (OCT). Methods: Serial clinical assessments, ophthalmoscopy, and peripapillary OCT were reviewed in a cohort of patients with IIH and optic atrophy. Atrophy was defined as moderate if average peripapillary retinal nerve fiber layer (pRNFL) thickness was ≤80 μm and severe if average pRNFL thickness was ≤60 μm on at least 2 consecutive high-quality OCT scans. Based on the upper tolerance limit of test–retest variability, mean pRNFL elevation of ≥6 μm with subsequent decrease to baseline thickness was considered papilledema. Results: In a cohort of 165 patients with IIH, 32 eyes of 20 patients and 22 eyes of 12 patients demonstrated moderate and severe optic atrophy, respectively. Over a median follow-up of 198.5 weeks (range, 14.0–428.9), 63.3% (19 of 30) of patients had at least 1 episode of relapse, and 50.0% (15 of 30) had at least 1 episode of papilledema. There was a total of 36 relapse episodes, of which 7 occurred in patients with clinical signs and symptoms but no OCT evidence of relapse, 12 occurred in patients with OCT changes but no clinical signs and symptoms of relapse, and 17 occurred in patients with both clinical and OCT evidence to support relapse. The median percent pRNFL increase in the latter 2 groups was 13.7% (range, 7.5–111.8), and 7 eyes (13.0%) of 5 patients (16.7%) showed thickening greater than 20.0% from baseline. The rate, magnitude, and concordance of pRNFL swelling were similar between moderately vs severely atrophic eyes. Conclusions: Papilledema recurrence can be detected in atrophic optic discs using OCT. All patients with atrophic IIH should be longitudinally monitored with pRNFL measurement. Concurrence of other relapse-suggestive features should prompt further evaluation.

Abstract Purpose The aim of this study was to find out whether the vascular architecture of untreated macular neovascularisations (MNV) in neovascular age-related macular degeneration (nAMD) as visualised with optic coherence tomography angiography (OCTA) is associated with functional and known morphological alterations of the retina in optic coherence tomography (SD-OCT). Methods The study design was retrospective with consecutive patient inclusion. In 107 patients with newly diagnosed nAMD, MNV were detected by means of OCTA and automated quantitative vascular analysis was performed. The MNV characteristics measured were area, flow density, total vascular length (sumL), density of vascular nodes (numN), fractal dimension (FD) and average vascular width (avgW). These parameters were assessed for associations with vision (BCVA), central retinal thickness (CRT), fluid distribution, the elevation of any pigment epithelial detachment (PED), the occurrence of subretinal haemorrhage and atrophy. Results BCVA was significantly worse with greater MNV area and sumL. Fluid distribution differed significantly in relation to area (p &lt; 0.005), sumL (p &lt; 0.005) and FD (p = 0.001). Greater PED height was significantly associated with higher numN (p &lt; 0.05) and lower avgW (p &lt; 0.05). Atrophy was present significantly more often in MNV with larger area (p &lt; 0.05), higher sumL (p &lt; 0.05) and higher flow density (p = 0.002). None of the MNV parameters had a significant association with CRT or the occurrence of haemorrhage. Conclusion OCTA is not restricted to evaluation of secondary changes but offers the opportunity to analyse the vascular structure of MNV in detail. Differences in vascular morphology are associated with certain secondary changes in retinal morphology. There are thus grounds for optimism that further research may identify and classify OCTA-based markers to permit more individualised treatment of nAMD.

Abstract Background Immunologic and inflammatory adverse effects following vaccination against COVID-19 are being reported. While some reactions may develop denovo others concern its immunogenic effect in patients with pre-existing inflammatory conditions. Methods Retrospective consecutive patients diagnosed with ocular inflammatory manifestations within 8 weeks of receiving COVID-19 vaccination who presented to a tertiary eye care centre in South India. Results Ninety-eight eyes of 67 patients presenting with ocular inflammatory manifestations within 8 weeks following COVID-19 vaccination were studied. The mean age was 43 years (+/- 14.82; range 19–80 years). The most common presentations were anterior uveitis (n = 31, 31.7%), followed by panuveitis (n = 24, 24.5%). The mean time to onset of symptoms was 25 days (+/- 15.48; range 2–55 days) following a dose of vaccine. Among all patients, 39 (58.2%) had a previous history of ocular inflammation. Mean presenting visual acuity was 0.4 (0-4) logMAR units and mean final visual acuity was 0.2 (0-4) logMAR units. The causes for reduced vision included of cystoid macular edema (n=2, 2%), chorioretinal atrophy (n=2.2%), optic atrophy (n=1.1%), retinal vascular occlusion (n=1.1%) and acute retinal necrosis (n=1.1%). Conclusion Infective and immunogenic adverse events should be watched out for after COVID-19 vaccination. It is difficult to establish causality for such manifestations, nevertheless, most of them were mild and had good final visual outcomes.

AbstractThe study aimed to evaluate the ocular motility and visual and optic disc abnormalities in children diagnosed with periventricular leukomalacia (PVL). A retrospective analysis was performed on 51 consecutive children who had ophthalmic symptoms and were diagnosed with PVL by using magnetic resonance imaging. The patients were assessed for visual function, strabismus, cycloplegic refraction, fundus examination, and if appropriate, spectral-domain optical coherence tomography and visual field testing were applied. The primary outcome measures were the prevalence and visual and ocular motility dysfunctions. Mean age was 5.72 ± 2.6 years (range = 1–12), median birth weight was 2,740 g (range = 1,240–3,460), and median gestational age was 34 weeks (range = 28–38). In total, 21 patients (39.6%) had neurological deficit, 11 (21.5%) had intellectual disability, and 19 (37.2%) had no neurological symptom. In the spherical equivalent refractive error and cylinder power analysis, 10 patients had ≥3.0 D myopia, 15 had ≥3.0 D hyperopia, and eight had ≥2.50 D astigmatism. Thirteen (25.4%) children had a best-corrected visual acuity between 20/40 and 20/20 for Snellen card, while 9 (17.6%) had strabismic amblyopia and 6 (11.7%) had anisometropic amblyopia. Manifest strabismus was present in 35 patients (68.6%); of whom 12 had esotropia (23.5%), 16 had exotropia (31.3%) and 6 had vertical deviation (11.7%). Manifest or latent nystagmus was detected in 14 patients (27.4%). In 28 patients (54.9%), there was optic nerve abnormality. Two patients had hypoplastic disc, 14 had optic disc pallor, 7 had large cupping, and 5 had total optic atrophy. Six subjects underwent reliable visual field (VF) examinations, and all six had abnormal VFs, with inferior fields being most affected. Ocular motility disorders, optic nerve abnormalities, VF defects, and low visual acuity are common findings in this cohort of PVL patients and maybe the only presenting signs of the disease. The recognition of the visual disabilities and implementation of early rehabilitation may have a significant benefit in these children.

Abstract Purpose To examine the ophthalmic data from a large database of people attending a general medical survey institute, and to investigate ophthalmic findings of the eye and its adnexa, including differences in age and sex. Methods Retrospective analysis including medical data of all consecutive individuals whose ophthalmic data and the prevalences of ocular pathologies were extracted from a very large database of subjects examined at a single general medical survey institute. Results Data were derived from 184,589 visits of 3676 patients (mean age 52 years, 68% males). The prevalence of the following eye pathologies were extracted. Eyelids: blepharitis (n = 4885, 13.3%), dermatochalasis (n = 4666, 12.7%), ptosis (n = 677, 1.8%), ectropion (n = 73, 0.2%), and xanthelasma (n = 160, 0.4%). Anterior segment: pinguecula (n = 3368, 9.2%), pterygium (n = 852, 2.3%), and cataract or pseudophakia (n = 9381, 27.1%). Cataract type (percentage of all phakic patients): nuclear sclerosis (n = 8908, 24.2%), posterior subcapsular (n = 846, 2.3%), and capsular anterior (n = 781, 2.1%). Pseudophakia was recorded for 697 patients (4.6%), and posterior subcapsular opacification for 229 (0.6%) patients. Optic nerve head (ONH): peripapillary atrophy (n = 4947, 13.5%), tilted disc (n = 3344, 9.1%), temporal slope (n = 410, 1.1%), ONH notch (n = 61, 0.2%), myelinated nerve fiber layer (n = 94, 0.3%), ONH drusen (n = 37, 0.1%), optic pit (n = 3, 0.0%), and ON coloboma (n = 4, 0.0%). Most pathologies were more common in males except for ONH, and most pathologies demonstrated a higher prevalence with increasing age. Conclusions Normal ophthalmic data and the prevalences of ocular pathologies were extracted from a very large database of subjects seen at a single medical survey institute.

Abstract Introduction Trigeminal schwannoma surgery has shown a remarkable improvement in functional recovery and tumor resection. In the era of radiosurgery, these outcomes need to be characterized for tumors which are outside the realm of being treated with radiosurgery. We present a series of trigeminal schwannomas larger than 3 cm, surgical approaches used, and outcomes with an emphasis on functional recovery in a high-volume center with radiosurgery facilities. Method All consecutive cases of trigeminal schwannoma from January 2012 to May 2021 which were more than 3 cm in size and underwent microsurgery were included in this series. The surgical approach, neurological outcomes, and extent of resection were defined objectively with pre/postoperative magnetic resonance imaging. Results A total of 83 such cases (&gt;3 cm) were found, with cranial nerve symptoms (5th most common) being the commonest. Twenty three percent cases had blindness due to secondary optic atrophy and eighteen percent had long tract motor symptoms signifying the tumor burden in our series. Radiological gross total excision was achieved in 75.9% cases. Conclusions Large-volume schwannomas present with cranial nerve involvement and may need extensive skull base approaches. Functional outcomes need to be prioritized and can be achieved albeit with lesser gross resection rates. Hearing and facial preservation in addition to relief of trigeminal symptoms should be the goal of resection with minimal additional morbidity.

Abstract Background Lumbar puncture (LP) is a common and relatively safe neurological procedure. It can be complicated by post-dural puncture headache (PDPH) after both diagnostic and therapeutic procedures. The aim of this study is to identify the incidence, risk factors and clinical characterization of PDPH in the inpatient setting of the main tertiary neurology hospital in Kuwait. Methods We conducted a prospective observational cohort study that included patients who were admitted to neurology department at Ibn Sina hospital, Kuwait, from January 1, 2019 to December 31, 2020, on whom, LP was performed for diagnostic and/or therapeutic reasons. Multivariate logistic regression analysis was performed to evaluate the association between PDPH and different clinical parameters. Results A total of 285 patients were included; 225 females (78.9%), mean age of 32.9 ± 11.7 years. PDPH was reported by 84 patients (29.5%), with mean headache onset of 1.7 ± 0.8 days, and mean duration of 2.4 ± 2.1 days. The commonest headache type was dull aching in 49 patients (58.3%). Headache severity was mild to moderate in 64 patients (76.2%), with mean NRS of 4.1 ± 0.9. Most PDPH (99.3%) resolved with conservative medical management, with only 2 patients (0.7%) requiring epidural blood patch. In multivariate logistic regression model, there was a statistically significant correlation between development of PDPH and young age (p = 0.001), female gender (p = 0 .001), low BMI (p &lt; 0 .001), pre-LP headache (p = 0.001), history of previous PDPH (p = 0.001), and number of LP attempts (p &lt; 0.001). PDPH was statistically significantly higher in patients with optic neuritis (p = 0.009), and cerebral venous thrombosis (p = 0.007), and lower in patients with peripheral neuropathy (p = 0.011) and spinal muscular atrophy (p = 0.042). Conclusions Findings from clinical practice in the main tertiary neurology hospital in Kuwait were in line with literature findings. Younger age, female gender, lower BMI, pre-procedural headache, previous history of PDPH, and number of LP attempts were found to be independent risk factors for developing PDPH. To our knowledge, this study represents the first comprehensive description of PDPH in a population from the Arabian Gulf Region.

AbstractKIF1A‐related disorders (KRDs) encompass recessive and dominant variants with wide clinical variability. Recent genetic investigations have expanded the clinical phenotypes of heterozygous KIF1A variants. However, there have been a few long‐term observational studies of patients with heterozygous KIF1A variants. A retrospective chart review of consecutive patients diagnosed with spastic paraplegia at Miyagi Children's Hospital from 2016 to 2020 identified six patients with heterozygous KIF1A variants. To understand the long‐term changes in clinical symptoms, we examined these patients in terms of their characteristics, clinical symptoms, results of electrophysiological and neuroimaging studies, and genetic testing. The median follow‐up period was 30 years (4–44 years). This long‐term observational study showed that early developmental delay and equinus gait, or unsteady gait, are the first signs of disease onset, appearing with the commencement of independent walking. In addition, later age‐related progression was observed in spastic paraplegia, and the appearance of axonal neuropathy and reduced visual acuity were characteristic features of the late disease phenotype. Brain imaging showed age‐related progression of cerebellar atrophy and the appearance of hyperintensity of optic radiation on T2WI and FLAIR imaging. Long‐term follow‐up revealed a pattern of steady progression and a variety of clinical symptoms, including spastic paraplegia, peripheral neuropathy, reduced visual acuity, and some degree of cerebellar ataxia. Clinical variability between patients was observed to some extent, and therefore, further studies are required to determine the phenotype–genotype correlation.

Objectives:NLRP3-associated autoinflammatory disease (NLRP3-AID) and Behçet's syndrome (BS) both belong to autoinflammatory diseases and rarely co-occur. Here we reported a Chinese pedigree of NLRP3-AID presented with BS.Methods: We recorded a Chinese pedigree of NLRP3-AID presented with BS. Whole-exome sequencing was performed to find the hereditary susceptibility gene, and Sanger sequencing was performed on a consecutive cohort of 30 BS patients. We also reviewed the English literature on vasculitis associated with NLRP3-AID.Results: The proband was a 45-year-old Chinese Han woman. She and her 12-year-old daughter presented with recurrent fevers, cold-induced urticaria, oral, and genital ulcers, conjunctivitis, uveitis, optic atrophy, erythema nodosum, headache, and hearing loss. They were initially suspected of having BS, and both responded poorly to corticosteroids and immunosuppressants, while anti-TNF therapy was moderately effective. Pedigree analysis revealed another four relatives with similar symptoms, and a heterozygous NLRP3 gene mutation c.1316C&amp;gt;T, p.Ala439Val was identified by whole-exome sequencing and Sanger sequencing. However, we did not discover NLRP3 gene mutation by Sanger sequencing in a confirmative cohort of 30 BS cases. A few case reports of vasculitis coexisting with NLRP3-AID, including a case of glomerulonephritis, and five cases of retinal vasculitis, were summarized through literature review.Conclusions: Our study is the first report of NLRP3-AID associated with BS. The coexistence of NLRP3-AID and BS reveals the extensive heterogeneity of the pathogenesis of systemic autoinflammatory diseases and calls for specific therapeutics.

Abstract Background Exposure to particulate matter (PM) with an aerodynamic diameter less than 2.5 μm (PM2.5) is a risk factor for developing pulmonary diseases and the worsening of ongoing disease. Mitochondrial fission and fusion are essential processes underlying mitochondrial homeostasis in health and disease. We examined the role of mitochondrial fission and fusion in PM2.5-induced alveolar epithelial cell damage and lung injury. Key genes in these processes include dystrophin-related protein 1 (DRP1) and optic atrophy 1 (OPA1) respectively. Methods Alveolar epithelial (A549) cells were treated with PM2.5 (32 µg/ml) in the presence and absence of Mdivi-1 (10µM, a DRP1 inhibitor) or BGP-15 (10µM, an OPA1 activator). Results were validated using DRP1-knockdown (KD) and OPA1-overexpression (OE). Mice were injected intraperitoneally with Mdivi-1 (20 mg/kg), BGP-15 (20 mg/kg) or distilled water (control) one hour before intranasal instillation of PM2.5 (7.8 mg/kg) or distilled water for two consecutive days. Results PM2.5 exposure of A549 cells caused oxidative stress, enhanced inflammation, necroptosis, mitophagy and mitochondrial dysfunction indicated by abnormal mitochondrial morphology, decreased mitochondrial membrane potential (ΔΨm), reduced mitochondrial respiration and disrupted mitochondrial fission and fusion. Regulating mitochondrial fission and fusion pharmacologically using Mdivi-1 and BGP-15 and genetically using DRP1-KD and OPA1-OE prevented PM2.5-induced celluar damage in A549 cells. Mdivi-1 and BGP-15 attenuated PM2.5-induced acute lung injury in mice. Conclusion Increased mitochondrial fission and decreased mitochondrial fusion may underlie PM2.5-induced alveolar epithelial cell damage in vitro and lung injury in vivo.

Abstract Rationale Alteration of the NAD+ metabolic pathway is proposed to be implicated in lipopolysaccharide (LPS)-induced neurotoxicity and mitochondrial dysfunction in neurodegenerative diseases. Apigenin, a naturally-occurring flavonoid, has been reported to maintain NAD+ levels and to preserve various metabolic functions. Objectives This study aimed to explore the effect of apigenin on mitochondrial SIRT3 activity as a mediator through which it could modulate mitochondrial quality control and to protect against intracerebrovascular ICV/LPS-induced neurotoxicity. Methods Mice received apigenin (40 mg/kg; p.o) for 7 consecutive days. One hour after the last dose, LPS (12 µg/kg, icv) was administered. Results Apigenin robustly guarded against neuronal degenerative changes and maintained a normal count of intact neurons in mice hippocampi. Consequently, it inhibited the deleterious effect of LPS on cognitive functions. Apigenin was effective in preserving the NAD+/NADH ratio to boost mitochondrial sirtuin-3 (SIRT3), activity, and ATP production. It conserved normal mitochondrial features via induction of the master regulator of mitochondrial biogenesis, peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α), along with mitochondrial transcription factor A (TFAM) and the fusion proteins, mitofusin 2 (MFN2), and optic atrophy-1 (OPA1). Furthermore, it increased phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and parkin expression as well as the microtubule-associated protein 1 light chain 3 II/I ratio (LC3II/I) to induce degradation of unhealthy mitochondria via mitophagy. Conclusions These observations reveal the marked neuroprotective potential of apigenin against LPS-induced neurotoxicity through inhibition of NAD+ depletion and activation of SIRT3 to maintain adequate mitochondrial homeostasis and function. Graphical abstract

Background: Ocular trauma and its complications are a significant contributor to global visual impairment and often present as an ophthalmic emergency in medical care facilities. Timely intervention is crucial for final visual outcome. Aims and Objectives: This study aimed to identify the factors that are correlated with the final visual outcome in cases of traumatic hyphema in a closed globe injury (CGI). Materials and Methods: A single-centric, prospective, interventional study was conducted in a tertiary care hospital. Fifty-three consecutive patients were enrolled in the study over a period of 1 year 5 months who presented with traumatic hyphema due to blunt trauma. Patients with a head injury, any blood dyscrasia, on blood thinners, associated with eye injury other than traumatic and unwilling patients were excluded from the study. Data analysis was done using statistical package for the social sciences software. Results: There was male preponderance. Majority of the study population were in the second decade. Best-corrected visual acuity (BCVA) was affected more among those who had hyphema of Grade-II or higher (P = 0.017). BCVA on presentation, posterior segment injury (P = 0.001) was found to be major determinant. Conclusion: We conclude traumatic cataract, corneal blood staining, secondary hemorrhage, time interval between the injury and presentation, BCVA at presentation, posterior segment injuries such as retinal detachment, berlin’s edema, optic atrophy, glaucoma are the major factors that determine the visual outcome. A handful of studies are available in literature regarding the visual outcome in patients with hyphema in CGI due to blunt trauma, but no such study is available from this part of the country.

BackgroundOcular ischemic syndrome (OIS), attributable to chronic hypoperfusion caused by marked carotid stenosis, is one of the important factors that cause ocular neurodegenerative diseases such as optic atrophy. The current study aimed to detect blood flow perfusion in a visual pathway by arterial spin labeling (ASL) and magnetic resonance imaging (MRI) for the differential diagnosis of OIS.MethodsThis diagnostic, cross-sectional study at a single institution was performed to detect blood flow perfusion in a visual pathway based on 3D pseudocontinuous ASL (3D-pCASL) using 3.0T MRI. A total of 91 participants (91 eyes) consisting of 30 eyes with OIS and 61 eyes with noncarotid artery stenosis-related retinal vascular diseases (39 eyes with diabetic retinopathy and 22 eyes with high myopic retinopathy) were consecutively included. Blood flow perfusion values in visual pathways derived from regions of interest in ASL images, including the retinal-choroidal complex, the intraorbital segments of the optic nerve, the tractus optics, and the visual center, were obtained and compared with arm-retinal circulation time and retinal circulation time derived from fundus fluorescein angiography (FFA). Receiver operating characteristic (ROC) curve analyses and the intraclass correlation coefficient (ICC) were performed to evaluate the accuracy and consistency.ResultsPatients with OIS had the lowest blood flow perfusion values in the visual pathway (all p &amp;lt; 0.05). The relative intraorbital segments of optic nerve blood flow values at post-labeling delays (PLDs) of 1.5 s (area under the curve, AUC = 0.832) and the relative retinal–choroidal complex blood flow values at PLDs of 2.5 s (AUC = 0.805) were effective for the differential diagnosis of OIS. The ICC of the blood flow values derived from the retinal–choroidal complex and the intraorbital segments of the optic nerve between the two observers showed satisfactory concordance (all ICC &amp;gt; 0.932, p &amp;lt; 0.001). The adverse reaction rates of ASL and FFA were 2.20 and 3.30%, respectively.Conclusion3D-pCASL showed that the participants with OIS had lower blood flow perfusion values in the visual pathway, which presented satisfactory accuracy, reproducibility, and safety. It is a noninvasive and comprehensive differential diagnostic tool to assess blood flow perfusion in a visual pathway for the differential diagnosis of OIS.

ObjectiveIdiopathic intracranial hypertension (IIH) is a neurometabolic disease with an increasing incidence. The pathophysiology is unknown, but improvement of diagnosis and management requires discovery of novel biomarkers. Our objective was to identify such candidate biomarkers in IIH, and secondarily, test for associations between identified metabolites and disease severity.MethodsThis is a prospective case–control study with collection of cerebrospinal fluid (CSF), serum, and clinical data from new‐onset, treatment‐naïve patients with IIH (n = 60). Patients were included consecutively from 2 tertiary headache centers in Denmark, and age, sex, and body mass index (BMI) ‐matched healthy controls (n = 35) were recruited. Clinical data were retrieved at ocular remission (n = 55). Samples were analyzed using non‐targeted mass spectrometry.ResultsSerum sphingosine 1‐phosphate (S1P), adenosine, and glutamate were 0.46‐fold (q &lt; 0.0001), 0.25‐fold (q = 0.0048), and 0.44‐fold (q &lt; 0.0001) lower, respectively, in IIH. CSF stearoyl‐lysophosphatidylcholine (LysoPC‐18) and 2‐palmitoyl‐lysophosphatidylcholine (LysoPC‐16) were 0.42 (q = 0.0025) and 0.37 (q &lt; 0.001) ‐fold lower. LysoPC‐18 was higher in patients with moderate–severe versus mild papilledema (p = 0.022). LysoPC‐18 correlated positively with retinal nerve fiber layer thickness (p = 0.0012, r = 0.42) and inversely with mean deviation on automated perimetry (p = 0.01, r = −0.35). Higher baseline serum S1P (p = 0.018) and lower CSF LysoPC‐16 (p = 0.003) were associated with optic nerve atrophy at ocular remission. Pathway analysis suggests dysregulated lipid metabolism and redox disturbances in new‐onset IIH.InterpretationWe identify perturbed metabolism in new‐onset IIH. S1P and LysoPC‐16 demonstrate potential prognostic value due to association with subsequent optic nerve atrophy. This association between specific, differential metabolites and outcome provides substantial evidence for novel biomarkers of clinical significance that should be the focus of further targeted studies. ANN NEUROL 2024