Ординатура / Офтальмология / Английские материалы / Field of Vision A Manual and Atlas of Perimetry_Barton, Benatar_2003
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FIELD OF VISION: A MANUAL AND ATLAS OF PERIMETRY / BARTON AND BENATAR |
Fig. 19. Change analysis of same patient as Fig. 18. Box plot (top) shows depression in January 2001, worsening in July 2001, with recovery in August 2001. Short-term fluctuation (SF) increased slightly in July 2001, as expected with any optic neuropathy. Mean deviation (MD) was dramatically worse in July 2001, but pattern deviation (PSD, CPSD) was worse in January 2001, when the defect was confined to a more focal area of the field. In August 2001, with resolution of the second attack, all indices had normalized.
CHAPTER 5 / AUTOMATED PERIMETRY (HUMPHREY FIELD ANALYZER) |
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These change analyses are a convenient way of viewing overall trends, although they do not capture local changes as effectively as the overview; these local effects will be diluted by the normal portions of the field, which ideally should not change. Newer software does try to identify significant regressions for individual points.
REFERENCES
1.Lindenmuth K, Skuta G, Rabbani R, Musch D. Effects of pupillary constriction on automated perimetry in normal eyes. Ophthalmology 1989;96:1298.
2.Bengtsson B, Heijl A, Olsson J. Evaluation of a new threshold visual field strategy, SITA, in normal subjects. Swedish Interactive Thresholding Algorithm. Acta Ophthalmol Scand 1998;76:165–169.
3.Bengtsson B, Heijl A. Evaluation of a new perimetric threshold strategy, SITA, in patients with manifest and suspect glaucoma. Acta Ophthalmol Scand 1998;76:268–272.
4.Schaumberger M, Schäfer B, Lachenmayr B. Glaucomatous visual fields. FASTPAC versus full threshold strategy of the Humphrey visual field analyzer. Invest Ophthalmol Visual Sci 1995;36: 1390–1397.
5.Flanagan J, Wild J, Trope G. Evaluation of FASTPAC, a new strategy for threshold estimation with the Humphrey field analyzer, in a glaucomatous population. Ophthalmology 1993;100:949–954.
6.Bengtsson B, Olsson J, Heijl A, Rootzen H. A new generation of algorithms for computerized threshold perimetry, SITA. Acta Ophthalmol Scand 1997;75:368–375.
7.Bengtsson B, Heijl A. SITA Fast, a new rapid perimetric thres-hold test: description of methods and evaluation in patients with manifest and suspect glaucoma. Acta Ophthalmol Scand 1998;76: 431–437.
8.Wall M, Punke SG, Stickney TL, Brito CF, Withrow KR, Kardon RH. SITA standard in optic neuropathies and hemianopias: a comparison with full threshold testing. Invest Ophthalmol Vis Sci 2001;42:528–537.
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FIELD OF VISION: A MANUAL AND ATLAS OF PERIMETRY / BARTON AND BENATAR |
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INTRODUCTION TO THE ATLAS
Armed with the information from the last two chapters on perimetric technique and interpretation, the reader is presented now with a selection of 120 cases gathered over 12 years. This section is meant not only as a demonstration but also as an exercise, a chance to hone interpretative skills. Each case is presented on two pages.
The first page shows the fields of patient with a brief clinical description. The reader should engage in three tasks. First, they should verbally describe the fields. (How would you communicate the deficit over the phone?) Second, they should estimate the likely location of the lesion. Third, they should consider the clinical history, evolution, and location to arrive at a possible cause of the defect.
The second page, hidden on the reverse side, describes the features of each case, beginning with those three aspects. The fields are discussed in further detail, and relevant points stressed. We also mention what confrontation field testing showed in most cases, so that the reader may obtain a sense of which defects are detectable and which are likely to be missed in the clinic or at the bedside. Photographs, further fields or imaging are provided to illustrate the clinical problem. We also provide a brief discussion about clinical points related to the case. All fields belong to patients with problems. Since we expect that most of the readers of this work are engaged in the clinical care of these patients, we believe that the diagnostic and management issues that arise from these fields should be of interest to the audience.
The first hundred cases are given in anatomic order, beginning with retinal conditions and ending with striate lesions. The last twenty cases are placed in random order within a short “quiz” section. The aim of the quiz is to provide the reader a chance to practice the skills in field analysis and localization that we hope they acquire by reading this book.
GOLDMANN CONVENTIONS:
First, we clarify a few points on our drawing notation with the Goldmann fields. Dots represent points where the patient stated they first saw a moving target. Small ‘x’ marks note where they said they saw a static target. For ease of reading, scotomata are shaded. When there are two shades, the darker, usually inner shade represents a deeper depression of sensitivity than the lighter. In the belief that it is the pattern rather than the actual isopter that is important, we do not label the isopters, except where this may help clarify certain issues. On selected fields there may be dotted lines as well as solid lines. These indicate where an isopter was measured again with the patient using a different lens. The size of that lens in diopters (negative or positive) will be written next to the dashed line.
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ATLAS / CASE #1 |
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HISTORY AND EXAM
This 80-yr-old man complained of a hazy line located just left of center in the vision of the left eye, gradually increasing in width over the last 10 years. The haze did not distort vision and he could read through it. Earlier medical history was significant for coronary artery disease, peripheral vascular disease, and hypertension. There was no history
of smoking. Visual acuity was 20/20 OD and 20/30 OS, not improving with pinhole. Ishihara color plates were 12/14 OD and 1/14 OS. There was no relative afferent pupillary defect (RAPD).
ATLAS / CASE #1 |
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DISCUSSION
Field description: Incongruous relative central scotomata OU. Localization: Bilateral macula.
Pathology: Age-related macular degeneration, late atrophic form.
Confrontation testing was normal OU, but tangent screen perimetry showed small areas of haze centrally OU.
The patient has central defects OU, larger OS, where the defect extends to the blind spot. Bilateral central defects can occur at any level of the visual system. The incongruity and lack of a step at the vertical meridian are against bilateral occipital lesions. Instead, bilateral optic neuropathy (see Case 38) or bilateral maculopathy are most likely. Fundoscopy showed macular pigmentary changes, making the diagnosis of age-related macular degeneration.
Age-related macular degeneration causes progressive loss of acuity, central holes in vision, and metamorphopsia, or distorted vision, caused by fluid and scarring in the retina
(1). This latter complaint is best shown on Amsler grid. These central defects impair the fine spatial resolution needed for tasks such as reading, face recognition, and driving, although patients can walk without help because of their good peripheral vision. Macular changes are subtle in the early stage, consisting mainly of drusen and mild pigmentary changes. The late stage is associated with visual loss and has two forms (2). In “dry” macular degeneration, there is atrophy of the photoreceptors, retinal pigment epithelium, and choriocapillaris, in a patchy “geographic” arrangement, as here. Acuity tends to be about 20/40 or better. In “wet” macular degeneration, there is serous or hemorrhagic detachment of the retinal pigment epithelium with choroidal neovascularization, leakage, and scarring, with more severe loss of acuity, sometimes abrupt. Smoking and a diet low in antioxidant vitamins and zinc are identified risk factors that can be modified. Progression is usually slow. There is no known treatment, but laser photocoagulation and photodynamic therapy are being evaluated (2).
See Color Plate after page 180
ATLAS / CASE #2 |
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HISTORY AND EXAM
This 39-yr-old man noted slowly progressive patchy holes in his vision for 4 years in both eyes. These interfered with his reading and seemed better in dim light. There was no family history of neurologic disease. Visual acuity was 20/20 OU and color vision was impaired at 1/14 OD and 3/14 OS. There was no RAPD. Maculopathy was suspected
although the retina appeared normal, even on fluorescein angiography. He did not return for follow-up until 4 years later, when his acuity had declined to 20/200 OU. Neurologic examination was otherwise normal.
ATLAS / CASE #2 |
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DISCUSSION
Field description: Incongruous central scotomata OU, worse OS.
Localization: Bilateral macula.
Pathology: Cone dystrophy.
Amsler grid showed incongruous perifoveal scotomata in both eyes (see below).
The patient’s initial small central defects were measured with a 10-2 program. These are quite different in the two eyes and progressed slowly over the next 2 years, mainly OD, (see follow-up field), with pigmentary darkening of the maculae. The slow progression, small initial scotomata, and markedly impaired color vision suggested a maculopathy. He was referred for electroretinography. The main features of electroretinography are an a wave, a negative potential originating in photoreceptors, and a subsequent b wave, a positive potential generated by potassium currents in the Müller cells, a glial cell in the outer retina. Dysfunction of the photoreceptors reduces the amplitude of both a and b waves because photoreceptor transmission creates the potassium currents in the Müller cells. Rod and cone function is assessed separately by varying the stimulus parameters. The electroretinogram recorded under bright (photopic) conditions reflects mainly cone function, whereas that in dark (scotopic) conditions is generated primarily by rods. In this patient, electroretinography showed reduced a- and b-wave amplitudes under photopic conditions, suggesting a cone dystrophy.
Cone and cone-rod dystrophies are degenerative conditions often beginning in childhood or young adulthood. Cones are most heavily concentrated in the fovea, and central scotomata with reduced acuity and impaired color vision are the hallmarks of cone dystrophy. The retina may appear normal initially. Cone-rod dystrophies, or pigmentary retinopathies, are of neurologic interest because of their association with conditions such as Kearns-Sayre syndrome, Bassen Kornzweig syndrome, and Refsum disease (3). They should not be confused with retinitis pigmentosa (see Case 12).
ATLAS / CASE #3 |
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HISTORY AND EXAM
This 47-yr-old man had central dimming of vision OD 7 years earlier, resolving over a few months. Since then he has had four recurrences, the most pronounced episode 2 years earlier, which lasted 5 months. In between episodes he notes micropsia, in that when he looks at people’s heads with his right eye only they are quite a bit smaller than either
their bodies or their heads viewed with his other eye. For 8 months he was also aware of small holes in his vision just nasal and temporal to fixation. These were stable. Visual acuity was 20/20 OU but the photostress test was prolonged OD, being more than 2 min compared with 60 s OS. There was no RAPD.