TL;DR: This publication deals with automated perimetry and emphasis is on technical aspects of administering the automated test with skill; as well as on interpretation of the result based on an understanding of the text.
Abstract: PART ONE: BASICS 1. Introductory Concepts Anatomy and Function of the Eye Visual Field Correspondence of the Retina and Visual Field Boundaries of the Visual Field 2. Basis of Quantitative Perimetry Visual Characteristics Within the Visual Field Units of Light Intensity Threshold Sensitivity in Terms of Stimulus Intensity Frequency-of-Seeing Curve and Short-Term Fluctuations Long-term Fluctuation Subjective Stimulus Brightness Background Intensity Contrast Sensitivity and Veiling Glare Refractive Error and Retinal Blur Stimulus Size and Spatial Summation Temporal Summation and Stimulus Deviation Learning Effects Fatigue Effects Kinetic and Static Stimuli Chromatic Perimetry Other Types of Perimetry 3. Topographic Classification of Visual Field Defects Anatomical Basis Prechiasmal defects Postchiasmal Defects Stato-kinetic dissociation (Riddoch Phenomenon) 4. Visual Field Loss in Glaucoma Local and diffuse loss Anatomic basis of nerve fiber bundle pattern Hemifield asymmetry and nasal steps Point of Fixation Generalized Depression Summary and Examples PART TWO: OFFICE PERIMETRY 5. Clinical Static Perimetry Basic Goals Mainstream Perimetric Protocols The Original, Classic Central Static Threshold Test New Thresholding Algorithms Determining Test Reliability Current Thresholding Algorithms: Summary Suprathreshold Tests Structuring the Test Conditions 6. The Single Field Printout Basic Identification Reliability Parameters Questions and test time Raw Test Results Total Deviation (From Normal Values For Age) Pattern Deviation (Localized Loss) Global Indices Plain Language Analysis 7. Interpretation of a Single Field Reliability Is The Field Abnormal? How Advanced Is The Disease? Artifacts 8. Selection of Automated Tests Glaucoma Diagnosis in the Office Population Screening for Glaucoma Following the Patient with Glaucoma Neurologic Conditions Retinal Diseases Blepharoptosis Driving Qualification Visual Impairment and Disability Programs That are Obsolete or Rarely Used 9. Follow-Up Examinations Establishing a Baseline Follow-up Visual Field Examinations An Overview Change Analysis Printout Pointwise Changes Interpretation Conclusion 10. Alternate and Supplemental Techniques Amsler Grid Confrontation Techniques PART THREE: TECHNIQUE 11. Administering the Visual Field Test Patient's Perception of the Test Perimetrist's Task Instructing the Patient About the Test Positioning the Patient at the Perimeter Corrective Lenses Monitoring and Modifying the Test After the Test APPENDICES Appendix A - Abbreviations Appendix B - Characteristics and Comparison of the HFA-2 Humphrey Perimeter to the HFA-1 Model Appendix C - Glossary INDEX
TL;DR: Only 4% of eyes with visual loss due to GCA improved, as judged by improvement in both VA and central visual field (by kinetic perimetry and Amsler grid), and the data suggest that there is a better chance of visual improvement with early diagnosis and immediate start of steroid therapy.
Abstract: .
Objectives: (1) To report the incidence and extent of visual improvement achieved by high-dose systemic corticosteroid treatment in eyes with visual loss due to giant-cell arteritis (GCA). (2) To understand the cause of the discrepancies between visual improvement revealed by routine visual acuity (VA) and by the central visual field in kinetic perimetry. (3) To review critically the contradictory literature on the effectiveness of corticosteroid therapy on visual recovery in GCA and to attempt to reconcile differences in the reported results.
Methods: Clinical data were collected systematically on 84 consecutive patients (114 eyes) with visual loss, all of whom had GCA confirmed by temporal artery biopsy and treated by us with high-dose systemic corticosteroid therapy. The patients were treated between 1974 and 1999 and data were compiled retrospectively. All patients underwent a detailed visual and ophthalmic evaluation at the initial visit and at every follow-up. This included visual field testing (with a Goldmann perimeter). All were treated with systemic corticosteroid therapy (intravenous followed by oral in 41 patients and oral only in 43 patients).
Results: Visual loss was due to anterior ischaemic optic neuropathy (91%), central retinal artery occlusion (10.5%), cilioretinal artery occlusion (10%), and/or posterior ischaemic optic neuropathy (4%), either alone or in different combinations. Improvement in both VA (≥ 2 lines) and central visual field was found in only five (4%) eyes of five patients (three treated with intravenous and two with oral steroid therapy). Improvement in VA ≥ 2 lines but not in the central visual field was found in seven eyes (in six patients). Visual improvement was seen in 7% of 41 patients treated initially with intravenous steroids versus 5% (p = 0.672) of 43 patients treated with oral steroids only. Comparison of patients with visual improvement in both VA and fields versus those with no improvement suggested a shorter interval (p = 0.065) between onset of visual loss and start of therapy in the improved patients.
Conclusions: In our study, only 4% of eyes with visual loss due to GCA improved, as judged by improvement in both VA and central visual field (by kinetic perimetry and Amsler grid). The data also suggest that there is a better (p = 0.065) chance of visual improvement with early diagnosis and immediate start of steroid therapy. Improvement in VA without associated improvement in the central visual field or Amsler grid may simply represent a learned ability to fixate eccentrically with more effective use of remaining vision: this factor could help explain a number of reported cases in the literature of improved VA after steroid treatment for GCA. To prevent further visual loss in either eye and for management of systemic manifestations of GCA, all patients must be treated on a long-term basis with adequate amounts of systemic corticosteroids.
TL;DR: Amsler grid reports have poor validity and cannot be accurately interpreted for use in the clinical diagnosis of retinal defects.
Abstract: • Objective. —To compare the reports of scotomas and metamorphopsia in standard and threshold Amsler grid testing with the location and extent of scotomas in the macular region as determined by standard and threshold fundus perimetry. Design. —Fundus perimetry determined the existence, size, and retinal location of macular scotomas. Amsler grid testing was performed with the scanning laser ophthalmoscope and the TA-300 system (Stereo Optical, Chicago, III). All testing was done at both standard and threshold light conditions. Patients. —Fifty-five patients with vision loss in the macular region and 10 normally sighted subjects. Results. —Nearly half of the standard and threshold scotomas were not detected by Amsler grid testing. For scotomas of 6° or less in diameter, 77% of standard and 87% of threshold scotomas were not detected by Amsler grid testing. Of the eyes with central scotomas involving the fovea, 66% used an eccentric preferred retinal locus for fixating the center of the grid. Finally, more than half of the distortion reported in Amsler grids was at the retinal area that corresponded to the scotoma area, not a nonscotoma retinal area. Conclusion. —Amsler grid reports have poor validity and cannot be accurately interpreted for use in the clinical diagnosis of retinal defects.
TL;DR: Late-onset Stargardt's disease STGD1 is at the mild end of the spectrum of retinal dystrophies caused by ABCA4 mutations, and the VA is frequently preserved in late-ONSet STGD 1 patients owing to foveal sparing.
TL;DR: A new method of performing scanning laser ophthalmoscope perimetry that compensates for eye movements so that the correct retinal location is tested even if fixation changes, which allows for accurate and repeatable measures of retinal sensitivity in specific locations.
Abstract: Visual field measurement provides important information regarding the diagnosis, progression, and management of many ocular diseases. Most notably, visual fields are extremely important in glaucoma to diagnose and evaluate the progression of disease, in neuroophthalmologic disorders to aid in the determination of the site of involvement in the eye, optic nerve, or brain, and in some retinal diseases, such as retinitis pigmentosa, to assess the extent of involvement and visual disability. These evaluations are well served by our current methods of visual field determination, herein referred to as conventional visual field testing, which include Goldmann kinetic perimetry, Humphrey static perimetry, and similar techniques.
However, conventional visual field determination is inadequate for the accurate evaluation of macular disorders or any retinal disorder in which foveal vision is compromised and the patient may have unstable fixation or extrafoveal fixation. Accuracy of the conventional visual field relies on the assumption that fixation is foveal and stable. If fixation is not foveal, the conventional visual field will still be mapped as though fixation is at the center (0°) of the field, so that all points tested will be shifted relative to their true retinal location. (A perimeter that uses the blind spot to test fixation may register fixation losses, but it is unable to correct for these.) If central fixation is unstable and there is significant eye movement during testing, scotoma size will be incorrect. Often, eccentric fixation and unstable fixation coexist, and there is a combination of these errors in scotoma location and size. In addition, there is often perceptual “filling in” of the area of the scotoma so that even the Amsler grid, used as a screening test for changes in central vision, may not detect the presence of a scotoma.1,2 Pericentral fixation lines to facilitate a patient’s centering on the fovea often still result in eccentric fixation. 3,4
Fundus perimeters are devices that provide for visualization of the fundus and the precise location of the stimulus on it. One can then see the exact test site on the retina and can correlate visual field defects to their true retinal positions.5 Several fundus perimeters have been designed and used in the past 30 years.6–14 The scanning laser ophthalmoscope (SLO) is the most recent and well-known fundus perimeter. It has allowed us to gain new information regarding the nature of visual loss in various macular diseases, including age-related macular degeneration and macular holes.1,6,7,15–25 However, because of difficulties in dealing with the additional data provided by SLO testing, methods of performing fundus perimetry have not used and have even ignored the advantage of viewing the fundus during testing. These difficulties include how to evaluate data correctly when the stimulus does not fall on the desired retinal location because of eye movement, how to ensure that the desired retinal areas are tested, and how to summarize the data. An additional problem is how to test for scotomas that might not correspond to observable lesions rather than simply testing over or at borders of retinal lesions. A number of investigators have shown that in diabetes26–28 and other macular diseases,29 scotomas may be present that do not correspond to observed retinal lesions; this is undoubtedly true in other retinal diseases, and these areas would be missed by testing only over observed retinal lesions. Finally, there must be a reliable method to test over the same retinal points when testing is repeated, even if fixation has shifted, to assess change over time.