Onset Of Visual Field Loss Research Articles

Latanoprostene bunod ophthalmic solution 0.024% for IOP lowering in glaucoma and ocular hypertension

ABSTRACTIntroduction: Intraocular pressure (IOP)-lowering has been demonstrated to slow the progression or onset of visual field loss in open-angle glaucoma (OAG) or ocular hypertension (OHT). Pharmacological lowering of IOP is the most common initial intervention in patients with OAG or OHT, however, many patients will require more than one therapy to achieve target IOP. Latanoprostene bunod is a novel nitric oxide (NO)-donating prostaglandin F2α analog for the reduction of IOP.Areas covered: Current knowledge concerning the mechanism of action of latanoprostene bunod is presented. Additionally, clinical safety and efficacy data from published Phase 1 (KRONUS), Phase 2 (VOYAGER, CONSTELLATION) and Phase 3 (APOLLO, LUNAR, JUPITER) studies are reviewed.Expert opinion: Latanoprostene bunod is a dual mechanism, dual pathway molecule, consisting of latanoprost acid, which is known to enhance uveoscleral (unconventional) outflow by upregulating matrix metalloproteinase expression and remodeling of the ciliary muscle’s extracellular matrix, linked to an NO-donating moiety, which enhances trabecular meshwork/Schlemm’s canal (conventional) outflow by inducing cytoskeletal relaxation via the soluble guanylyl cyclase-cyclic guanosine monophosphate (sGC-cGMP) signaling pathway. Latanoprostene bunod 0.024% solution applied topically once daily appears more effective in reducing IOP in OHT and OAG subjects than either latanoprost or timolol, with a side effect profile similar to that of latanoprost.

Therapeutic targets in glaucoma

AbstractGlaucoma leads to irreversible blindness and is characterized by changes in the optic disc and the visual field. The elevated intraocular pressure is considered the most important factor responsible for the glaucomatous optic neuropathy. There are multiple factors involved in the development of retinal ganglion cell death. The goal of glaucoma treatment is to preserve the visual field of patients and prevent the loss of visual function that is associated with the disease (European Guidelines). We should focus at least on three separate targets of glaucoma treatment (Brubaker RF. Survey of Ophthalmology 2003: Three targets for glaucoma management): Intraocular pressure (IOP), outflow facility, and the retinal ganglion cell (RGC). Elevated IOP is still the primary risk factor for the development and progression of glaucoma, and many studies have shown that IOP reduction can limit the progression of glaucoma and slow the loss of visual function. IOP lowering can be beneficial for normal‐tension as well as high‐tension glaucoma patients, and it may also prevent or delay the onset of visual field loss and optic disk damage in individuals with ocular hypertension. The second target of glaucoma treatment is outflow facility. In a healthy eye, aqueous production (flow) equals aqueous outflow through the trabecular and uveoscleral outflow pathways. Any imbalance between flow and outflow results in a change in IOP, yet even a transient elevation of IOP may cause significant glaucomatous damage. The third target of glaucoma treatment is the RGC itself. RGC death in glaucoma might have many causes, including vascular insufficiency, blockage of axonal transport, diffusion of toxic agents into the nerve cell, or initiation of apoptosis. Treatment that aims to directly protect the RGC from every possible insult might be the ultimate treatment for glaucoma because a strategy of neuroprotection could preserve the visual function of patients regardless of the etiology of their glaucoma.

Predictive Value of Confocal Scanning Laser for the Onset of Visual Field Loss in Glaucoma Suspects

To perform a longitudinal multivariate analysis of the ability of Moorfields Regression Analysis (MRA) to predict the onset of glaucoma in a population of patients with suspected glaucoma due to appearance of the optic nerve head. Prospective longitudinal evaluation of a diagnostic test. Single, randomly selected eye of prospectively recruited patients with suspected glaucoma based on the optic nerve head appearance on stereophotographs and normal baseline visual field results. The MRA was evaluated at baseline (Heidelberg Retina Tomograph; Heidelberg Engineering, Dossenheim, Germany), and visual field tests were repeated every 6 months. A longitudinal multivariate proportional hazard ratio (HR) analysis was performed, and likelihood ratios and positive and negative predictive values were compared. Onset of visual field losses. The study included 230 eyes that were followed up during a mean period of 62±14 months, ranging from 4 to 7 years. The predicted HR (for onset of visual field losses) of the MRA temporal-inferior sector outside normal limits was 3.65 (95% confidence interval [CI], 2.32-5.75; P < 0.0001). An MRA temporal-superior sector outside normal limits had an HR of 3.43 (95% CI, 2.21-5.32; P < 0.0001). The temporal-inferior and temporal-superior positions of the MRA are highly predictive for the onset of visual field loss in glaucoma suspects.

Anterior Ischemic Optic Neuropathy After Strabismus Surgery

We report a case of nonarteritic anterior ischemic optic neuropathy (NAION) in a healthy young woman after strabismus surgery. A 26-year-old woman with no medical history underwent uneventful left medial rectus recession and lateral rectus resection for a long-standing esotropia under general anesthesia. Preoperatively, visual acuity had been 20/20 in the right eye and 20/200 in the left eye (amblyopia). Thirteen days postoperatively, she noticed loss of vision superiorly in the left eye on awakening without any other symptoms. On our examination the next day, visual acuity was 20/20 in the right eye and 20/400 in the left eye. She had a superior nerve fiber bundle (altitudinal) visual field defect on confrontation, a left relative afferent pupillary defect, and mild left optic disc swelling, mainly inferiorly (Fig. 1). The right optic disc had a normal appearance. Both discs had a cup-to-disc ratio of 0.1. All other aspects of the ophthalmic examination were normal.FIG. 1: Fundus photography performed 1 day after onset of visual field loss shows left optic disc swelling.Results of standard laboratory tests, including a full blood cell count, serum electrolytes, erythrocyte sedimentation rate, C-reactive protein, thyroid function, blood glucose, and anti-nuclear, anti-mitochondrial, anti-smooth muscle, and anti-parietal cell antibodies, were normal. MRI of the brain and orbits was unremarkable. Four weeks later, visual acuity in the left eye had returned to its baseline level of 20/200, but the altitudinal field defect persisted (Fig. 2). A diagnosis of left NAION was made. Six months later, field testing showed a persistent defect with some improvement (Fig. 3).FIG. 2: Late-phase fluorescein angiography demonstrates areas of pinpoint hyperfluorescence without marked optic disc hyperfluorescence.FIG. 3: Visual field examination performed 7 months after the onset of field loss shows minimal improvement.NAION has been reported after anterior segment (mainly cataract) surgery (1), vitrectomy (2), scleral buckling surgery (3), and post-LASIK (4). We have found no reports of NAION occurring either immediately or after an interval following strabismus surgery, although a case of posterior ischemic optic neuropathy has been reported (5). Our patient had no risk factors for NAION apart from a low cup-to-disc ratio, and her youth makes her an unlikely candidate for spontaneous NAION. The ages of patients reported with NAION occurring at an interval after ocular surgery range from 48 to 94 (2,4). A case has been reported after intraocular lens implantation in a 33-year-old woman, but this occurred immediately after surgery rather than after an interval (6). The delayed onset of symptoms in our young patient raises the possibility of an inflammatory etiology. However, the lack of pain and normal MRI scan suggest that optic neuritis was unlikely. Given our patient's left amblyopia, we cannot exclude preexisting structural anomalies that might have increased her susceptibility to NAION. Also, from one case, we cannot conclude that the optic neuropathy and strabismus surgery were necessarily related. O. A. R. Mahroo, MB, BChir, PhD C. J. Hammond, MB, BChir, MD, FRCOphth West Kent Eye Centre Princess Royal University Hospital Farnborough Common Orpington, UK [email protected]

Drusenpapille

Optic disc drusen (ODD) are an initially symptom-free, usually bilateral, progressive type of optic neuropathy with genetic disposition. We observed visual field loss (VFL) in 64% (49 of 77) of our patients. Vascular complications such as AION are common. Initially, papilledema is often diagnosed and the diagnosis of ODD is confirmed by means of ultrasound examination. We found an average time interval of 7 years between groups of patients with preperimetric stage and onset of VFL. We also observed more advanced stages of VFL, faster progression of visual field loss and greater visibility of ODD with increasing age. VFL frequently results in loss of driving ability according to driving permission regulations. The aim of our therapy concept is to reduce intraocular pressure (IOP). In a pilot study we found that patients who underwent IOP-lowering therapy showed significantly less progression of VFL than patients who did not undergo this therapy. The present article summarizes current knowledge on epidemiology, pathogenesis, clinical presentation, diagnostics and therapy of optic disc drusen.

Baseline visual field characteristics in the ocular hypertension treatment study

PurposeThe Ocular Hypertension Treatment Study (OHTS) seeks to evaluate the safety and efficacy of topical ocular hypotensive medication in preventing or delaying the onset of visual field loss and/or optic nerve damage in ocular hypertensive subjects at risk for developing primary open-angle glaucoma. This study evaluates the baseline visual field test characteristics (visual field status, reliability properties, etc.) of patients who underwent eligibility visual field testing for entry to the OHTS. DesignCross-sectional study of baseline data as part of a longitudinal randomized clinical trial. ParticipantsTwo thousand eight hundred nineteen ocular hypertensive individuals, aged 40 to 80 (mean age, 55). MethodsSubjects underwent at least two Humphrey Field Analyzer Program 30-2 Full Threshold visual field examinations in both eyes for study eligibility. A third examination was performed if a prior test was abnormal, questionable, or unreliable. For final eligibility, two sets of visual field examinations had to meet OHTS criteria for reliability and had to be classified as “normal.” All OHTS visual field tests of potential subjects were submitted for eligibility assessment to the OHTS Visual Field Reading Center. Main Outcome MeasuresThe percentage of visual fields that were normal and reliable according to OHTS criteria. ResultsOf the subset of 2304 subjects who completed the eligibility assessments, 1828 (79%) were OHTS-eligible based on visual field test requirements. A third eligibility test was required for 11% of all eyes because of unreliable, questionable, or abnormal test results. With the 33% fixation loss cutoff in the OHTS, 97% of all eligibility visual field examinations were reliable and 3% were unreliable. The most frequent cause (69.5%) of unreliability was excessive fixation losses. ConclusionsPermitting one repeat test after an abnormal or unreliable test allowed an extra 560 patients to be “eligible” for the study based on visual field tests. A clinical screening review of otherwise normal and reliable tests was not restrictive. The adoption of a 33% fixation loss cutoff significantly reduced the number of required retests and prevented study rejection of 89 patients.

Acute annular outer retinopathy: report of four cases

PURPOSE: To describe the clinical findings and course in four patients with acute annular outer retinopathy. METHODS: Four patients were evaluated during the course of acute annular outer retinopathy, and the historical and clinical findings were retrospectively collected. RESULTS: Four healthy patients developed the acute onset of visual field loss associated with a localized, white annular outer retinopathy. All patients were caucasian; two were women, aged 29 and 32 years, and two were men, aged 71 and 79 years. The mean follow-up was 3.9 years (range, 1 to 6 years). On presentation, four eyes had an irregular, incomplete, peripapillary, annular band of gray-white, deep retinal opacification with visual acuities that varied from 20/25 without foveal involvement to counting fingers with foveal involvement. Laboratory serologies were unremarkable. Two patients did not receive any treatment, and two received varying courses of oral corticosteroids with subjective improvement. Of the four eyes, two eyes developed ophthalmoscopic sequelae, one eye did not, and one had evidence of retinal pigment epithelial damage and narrowing of the retinal vessels on presentation. CONCLUSIONS: These four cases of acute annular outer retinopathy expand our knowledge of this disorder. Acute annular outer retinopathy may be a distinct entity or it may represent a variant of acute zonal occult outer retinopathy. As more cases are recognized, the characteristic features of the disease spectrum, the etiology, and treatment options may be better elucidated.

A third locus (GLC1D) for adult-onset primary open-angle glaucoma maps to the 8q23 region

Purpose: Two genes for adult-onset primary open-angle glaucoma have been mapped to chromosomes 2cen-q13 and 3q21-q24. We studied a family with adult-onset primary open-angle glaucoma in which the disease did not map to these two chromosomal regions. Methods: We ascertained a four-generation family with adult-onset primary open-angle glaucoma in which the disease status of individuals was objectively assigned using defined criteria. Complete ophthalmologic examinations, visual field testing, optic nerve head photographs, and venous blood samples were obtained. Family members were genotyped using polymerase chain reaction amplification of microsatellite polymorphic markers. Linkage analysis was performed and lod scores were calculated. Haplotype transmission data were analyzed. Results: A total of 20 subjects in three successive generations agreed to participate in the study. This included samples from eight affected subjects, one glaucoma suspect, one normal individual, and two spouses in generations II and III, and an additional eight individuals in generation IV. The phenotype in this family appears to be variable, with onset of visual field loss in middle age, followed by modest elevation of intraocular pressure and progression of the disease in older individuals. Linkage was established with a group of DNA markers located in the 8q23 region. A lod score value of 3.61 was obtained using marker D8S1471. Three other markers from the same region gave lod score values of over 3.0. Haplotype transmission data identified two recombination events that placed the gene in a 6.3-cM region flanked by D8S1830 and D8S592. The disease-bearing haplotype was inherited by eight affected subjects and three glaucoma suspects. Conclusion: We present evidence for a third adult-onset primary open-angle glaucoma locus (GLC1D) on chromosome 8q23. The genetic heterogeneity of adult-onset glaucoma is evident from the multiplicity of chromosomal loci associated with this disease.

Closed-angle glaucoma: diagnosis and management.

Open-angle glaucoma Is not a benign disease; untreated, it can lead to total blindness. If intraocular tension is controlled early, before onset of visual field loss or optic nerve degeneration, the prognosis is good.

Open-angle glaucoma: diagnosis and management.

Open-angle glaucoma is not a benign disease; untreated, it can lead to total blindness. If intraocular tension is controlled early, before onset of visual field loss or optic nerve degeneration, the prognosis is good.