Ординатура / Офтальмология / Английские материалы / Visual Fields Examination and Interpretation_Walsh_2011
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36 Visual Fields
1-4-5 Amsler Grid. Although the Amsler grid is sometimes difficult for a patient to learn to use properly, it is particularly useful in subtle foveal problems or in central serous retinopathy.23 I consider using the Amsler grid for a patient who complains of a blur and whose vision is perhaps 20/30. A central scotoma is difficult to demonstrate by the usual field-testing methods. If the patient can learn to fixate steadily on the center of the grid (Figure 1-23), the center lines will appear either distorted or elevated in central serous retinopathy. The image will look as if someone were leaning on the center of a chain-link fence. Two problems the perimetrist may encounter with the test are (1) getting the patient to fixate steadily and to just be aware of the surrounding area rather than looking all around and
(2) instructing the patient as to what he may see without suggesting any defects to him. If both of these problems can be resolved, the Amsler grid is a valuable test device.
1-4-6 Color Testing. The use of color has always been controversial. Even those who subscribe to the use of color do not agree about which technique to use. Some use color as an object of decreased sensitivity, while others use it as color recognition. I prefer to use color recognition. This experience agrees with Kollner’s law even if the law is not perfect. The decreased-sensitivity technique gives varied results even in the same patient from examination to examination. There is even some argument about which color is preferable for detecting central field defects. Red has been the most used and seems the most reliable. If color recognition is the technique, then using the smallest red object defeats the purpose. Certainly, smaller and smaller white test objects can reveal the same scotoma, but the progressive
Figure 1-23. The Amsler grid. This type of field covers about 10° around the fixation point and is used primarily for foveal problems such as central serous retinopathy or subtle changes in macular degeneration.
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decrease in the size of white test objects is governed more by the minimal visual threshold than by any other feature. If rods are affected, blue test objects seem to be more sensitive. If the optic nerve is the location of the defect, then red has traditionally been more sensitive. It is difficult to determine whether this increased sensitivity is due to lower intensity than the same-size white test object or to a different wavelength.
As described previously, color is a useful method for demonstrating a Chamlin step; it is also particularly useful in demonstrating a central scotoma when small white test objects are either inadequate or inconsistent. When it is difficult to establish whether a decrease in acuity is the result of retinal involvement or of optic nerve involvement, colored test plates such as the HRR plates can pinpoint the location. A patient with optic nerve involvement and 20/30 acuity often misses all the HRR plates. Similarly, a patient with retinal disease and an acuity of 20/200 may see almost all the HRR plates. Even if the patient has some degree of color blindness, there will be a significant difference between the two eyes when one has optic nerve involvement. In central scotomas, cones are particularly involved and red test objects are most useful. Because color is the basis of the test, the perimetrist should not use the smallest colored test object in the set because it is too small to see.
One of the more difficult field defects to map is the cecocentral scotoma. Early in the course of the disease, the acuity may still be only moderately depressed. Since a patient with a cecocentral scotoma tends to fixate unsteadily, it is difficult not only to map the defect but also to identify it as a cecocentral rather than a purely central scotoma. The distinction is important because if the examiner can establish it as a cecocentral defect, the etiologic possibilities will be limited. Cecocentral scotomas are usually due to nutritional amblyopia and rarely due to Leber’s optic neuritis or pernicious anemia. Central scotomas have a long list of possible causes.
To overcome the problems of mapping the cecocentral scotoma, the “big pumpkin test,” a method involving a variation on the use of color, has been used at the Yale Medical Center.24 A large piece of orange poster board, about 2 feet square, is placed over the tangent screen so that it covers at least 7° on the nasal side of the fixation point and 20° on the temporal side in order to cover the blind spot (Figure 1-24). The patient is asked to look at a fixation spot and say if any part of the poster board lacks color. Even slight eye movements will generally keep the central and cecocentral areas on the orange board. In essence, the entire central field serves as a colored test object, obviating the need to explore that same area with a colored test object to observe where it is seen and where it is not. To help in this identification, the patient is given a 3-foot dowel rod and is asked to map out the defective area. If he continues to shift fixation, he will be somewhat frustrated in mapping out the scotoma. This, in turn, will encourage the patient to fixate better.
A color defect, or dyschromatopsia, does occur although rarely on a cerebral basis (discussed in Chapter 10).24,25,26 Such a defect requires very careful examination to ascertain that it is not congenital or some expression of aphasia or visual agnosia.
A
B
Figure 1-24. (A) Orange poster board cut out to cover beyond the cecocentral area. The fixation object is large enough to fixate on. It is also displaced away from the center, to leave more room temporally for the cecocentral area. A right eye test circumstance is illustrated here. (B) The patient is pointing at the area on the poster board that is color-desaturated, corresponding to the cecocentral defect.
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REFERENCES
1.Horton J, Hoyt W. The representation of the visual field in human striate cortex. Arch Ophthalmol. 1991;109:816–824.
2.Riddoch G. Dissociation of visual perceptions due to occipital injuries with especial reference to appreciation of movement. Brain. 1917;40:15–29.
3.Chamlin M. Minimal defects in visual field studies. Arch Ophthalmol. 1949;42: 126–139.
4.Chamlin M, Davidoff LM. Choice of test objects in visual field studies. Am J Ophthalmol. 1952;35:381–391.
5.Enoksson P. A study of the visual fields with white and colored objects in cases of pituitary tumors with special reference to early diagnosis. Acta Ophthalmol. 1953;31:505–511.
6.Alexander GL. Diagnostic value of colored fields in neurosurgery. Trans Ophthalmol Soc UK. 1956;76:235–240.
7.Feldman M, Todman L, Bender MB. Flight of color in lesions of the visual system.
J Neurol Neurosurg Psychiatry. 1974;37:1265–1271.
8.Knapp H. The channel by which, in cases of neuroretinitis, the exudation proceeds from the brain into the eye. Trans Am Ophthalmol Soc. 1870;1:118.
9.Wilbrand H, Saenger A, eds. Die pathologie der Netzhaut. In: Neurologie des Augen. Wiesbaden: JF Bergmann; 1909;4(pt 1):568.
10.Paton L, Holmes G. The pathology of papilledema: a histological study of sixty eyes. Brain. 1911;33:389.
11.Stiles WS, Crawford BH. The luminous efficiency of rays entering the eye pupil at different points. Proc R Soc Lond. 1933;12:428.
12.Dailey RA, Mills RP, Stimac GK, et al. The natural history and CT appearance of acquired hyperopia with choroidal folds. Ophthalmology. 1986;93:1336.
13.Corbett JJ, Jacobson DM, Mauer RC, et al. Enlargement of the blind spot caused by papilledema. Am J Ophthalmol. 1988;105:261–265.
14.Reese A. Peripapillary detachment of the retina accompanying papilledema. Trans Am Ophthalmol Assoc. 1930;28:341.
15.Duke-Elder S, Scott GI. Neuro-ophthalmology. In: Duke-Elder S, ed. System of Ophthalmology. St. Louis: CV Mosby; 1971:12:59.
16.Young SE, Walsh FB, Knox DL. The tilted disc syndrome. Am J Ophthalmol. 1976;82:16.
17.Younge BR. Computer-assisted perimetry in visual pathway disease: neuro-ophthalmic applications. Trans Am Ophthalmol Soc. 1984;82:899–942.
18.Welsh RC. Finger counting in the four quadrants as a method of visual field gross screening. Arch Ophthalmol. 1961;66:678–679.
19.Frisén L. A versatile color confrontation test for the central visual field: a comparison with quantitative perimetry. Arch Ophthalmol. 1973;89:3–9.
20.Mindel JS, Safir A, Schare PW. Visual field testing with red targets. Arch Ophthalmol. 1983;101:927–929.
21.Safran BA, Glaser JS. Statokinetic dissociation in lesions of the anterior visual pathways: a reappraisal of the Riddoch phenomenon. Arch Ophthalmol. 1985;98:291–295.
22.Damgaard-Jensen L. Demonstration of peripheral hemiopic border steps by static perimetry. Acta Ophthalmol. 1977;55:815–819.
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23.Amsler M. Earliest symptoms of diseases of the macula. Br J Ophthalmol. 1953;37: 521–525.
24.Walsh T. Paracentral scotoma testing. Ophthalmic Surg. 1973;4:72–79.
25.Green GJ, Lessell S. Acquired cerebral dyschromatopsia. Arch Ophthalmol. 1977;95:121–128.
26.Zihl J, Van Cramon D. Colour anomia restricted to the left visual hemifield after splenial disconnection. J Neurol Neurosurg Psychiatry. 1980;43:719–724.
2
Anatomic Basis and Differential
Diagnosis of Field Defects
JONATHAN D. WIRTSCHAFTER, MD,
AND THOMAS J. WALSH, MD
2-1 CATEGORIES OF FIELD DEFECTS
The purpose of any medical test is to confirm or rule out a diagnosis based on the clinical facts. In performing perimetry, the printout of the defect is not the end of the test. For even the most experienced reader, the test results at best tell the location of the defect. The next step is to consider the causes of such a defect in that part of the vision system. The experienced perimetrist will look at the results and suggest a differential list of causes. The primary diagnostic list is frequently aided by adding to the perimetry the medical history and other physical signs. The results of both then lead to the next step: ordering tests to confirm the cause of the field defect. It may require the ordering of a magnetic resonance (MR) image, but that may not be the proper test if the original differential diagnosis is faulty. Sedimentation rate and C-reactive protein may be more appropriate tests if the clinical facts suggest cranial arteritis. If carotid disease is suspected, a computed tomography (CT) angiogram may be more appropriate. In the following discussion of these defects, there has been a melding of a discussion explaining anatomically why these defects occur in certain areas.
Because the course and relations of the primary visual sensory pathway have been frequently and well described (including in other chapters of this monograph), this chapter concentrates on the multiple anatomic substrates that may explain each particular pattern of visual field abnormality (Table 2-1).
Visual field abnormalities are represented by three categories: monocular, binocular, and junctional. Monocular field defects include those that can be caused by lesions of one eye or optic nerve. Binocular field defects include those that
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TABLE 2-1. Visual Field Defects
Monocular Field Defects
Localized Defects
Wedge-shaped temporal field defect
Arcuate and paracentral field defects
Central scotoma or depression
Enlarged physiologic blind spot
Centrocecal scotoma or depression
Equatorial annular scotoma or depression
Altitudinal hemianopia
Generalized Defects
Generalized depression or peripheral contraction
Binocular Field Defects
Homonymous Hemianopias
Complete: macular splitting
Incomplete congruous: horizontal sectoranopia
Incomplete congruous: paramidline-sparing vertical hemianopia Incomplete: macular sparing
Incomplete: two scotomas Incomplete incongruous
Incomplete: unilateral sparing of temporal crescent Incomplete: unilateral defect of temporal crescent
Bitemporal Hemianopias
Complete
With central depression, scotomatous
Binasal Field Defects
Complete
Incomplete
Altitudinal Field Defects
Noncongrous and monocular
Congruous
Quadrantanopias
Superior homonymous, incomplete
Inferior homonymous, complete
Bilateral central Field Defects
Scotoma or depression
Bilateral peripheral Field Defects
Generalized depression or peripheral contraction
Bilateral Checkerboard Scotomas
Bilateral Homonymous Hemianopias
Junctional Field Defects
Complete Monocular Plus
Bitemporal Hemianopia plus
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may result from single or multiple lesions at one or more points along the visual pathway. Junctional field defects include three types of visual field defects resulting from a lesion at the junction of the optic nerve and optic chiasm or of the optic tract and optic chiasm.
2-2 OVERVIEW OF THE VISUAL PATHWAY
The layers of the retina are illustrated in Figure 2-1. A general scheme of visual field defects related to the anatomy of the primary visual sensory pathway is depicted in Figure 2-2, and the blood supply of the visual pathway is shown in Figure 2-3. Other relevant anatomic points will be presented with the specific categories of visual field defects.
The visual sensory pathway can be divided into “territories” according to various schemes (Table 2-2). The preretinal territory consists of those anatomic barriers
Figure 2-1. Functional microanatomy of the retina. (A) Cell types: A, amacrine; C, cone; DB, diffuse bipolar; DG, diffuse ganglion; H, horizontal; M, Müller cell; MB, midget bipolar; MG, midget ganglion; R, rod; RB, rod bipolar. (B) Layers and membranes of the retina.
Figure 2-2. Visual field defects related to the anatomy of the visual pathway. The arrow is perpendicular to the horizontal line of the retina throughout the visual pathway. Macular projections are shown as small circles; the monocular temporal crescent field is shown with stipple. Projections from the superior retina (inferior visual field) are shown in red; projections from the inferior retina {superior visual field) are shown in blue. Visual field defects and lesions: (1) Left optic nerve—blind left eye. (2) Vascular lesion of upper aspect of right optic nerve—right inferior altitudinal hemianopia. (3) Left optic nerve involving crossed inferior retinal fibers—junctional scotoma with contralateral superior quadrant field defect. (4) Optic chiasm, crossing fibers—bitemporal hemianopia. (5) Optic chiasm, uncrossed fibers compressed by internal carotid arteries and/or perichiasmal tumor—binasal hemianopia. (6) Optic tract—contralateral relative afferent pupillary defect and contralateral homonymous hemianopia, often incongruous. (7) Lateral geniculate body—contralateral homonymous hemianopia. (8) Optic radiation— contralateral homonymous hemianopia, less congruous anteriorly; optic radiation is external to lateral ventricle. (9) Parietal lobe (and nonstriate occipital visual cortex)— contralateral inferior quadrantanopia. (10) Temporal lobe (and nonstriate occipital visual cortex)—contralateral superior quadrantanopia, often incongruous. (11) Occipital lobe—contralateral homonymous hemianopia. (12) Occipital pole through midportion of calcarine fissure—contralateral hemianopic central scotomas. (13) Anterior portion of calcarine fissure and fibers to it—contralateral hemianopia with macular sparing. (14) Extreme anterior lip of calcarine fissure—contralateral temporal crescent field defect.
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Figure 2-3. Arterial supply of the visual pathway. Left optic nerve and carotid arteries viewed from left; right optic tract, optic radiation, middle and posterior cerebral arteries viewed from their medial surfaces; other cerebral structures removed. Note the dual blood supplies of the optic tract and lateral geniculate body from the anterior choroidal and posterior cerebral artery branches. The temporal isthmus is supplied by the anterior choroidal artery. Inset, Blood supply of the optic nerve head from anastomotic branches of the pial arterioles and posterior ciliary artery branches. The anastomotic vascular circle of Zinn-Haller is thought to be incomplete, explaining the watershed infarctions at the vertical poles of the optic nerve head that are characteristic of anterior ischemic optic neuropathy. Note that the intraneural course of the ophthalmic artery in the optic nerve is longer than that of the central retinal artery.
to the normal focusing of light onto the retina. There are four neural elements in the primary visual sensory pathway. Three are in the retina: the photoreceptor, the bipolar cell, and the retinal ganglion cell (see Figure 2-1). Afferent sensory systems are described as having three orders of neurons excluding the neurosensory transduction cell, which in the retina is the photoreceptor. The first-order neurons are the bipolar cells. The retinal ganglion cells and the axons in the nerve fiber layer of the retina and the optic nerve comprise the second-order neurons. These neurons are also called the anterior visual pathway and include the retinal ganglion cell layer, optic nerves, optic chiasm, and optic tracts. The third-order neurons extend from the lateral geniculate body to the calcarine cortex along the optic radiation. These neurons are often called the posterior visual pathway.