Ординатура / Офтальмология / Английские материалы / Visual Fields Examination and Interpretation_Walsh_2011
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Smaller-diameter, slower-conducting axons arise throughout the entire retina and terminate in the parvocellular regions of the lateral geniculate nucleus. These are designated as parvocellular (P) cells and are similar to the X-like cells of cats. The parvocellular cells include the midget ganglion cells with small receptive fields that account for central vision acuity and color opponent features. They have low contrast sensitivity.
Optic Nerve Head (2). Lesions of the optic nerve head may involve sufficient numbers of papillomacular axons to cause a central scotoma.
Retrobulbar Optic Nerve (3). Axons arising from the midget ganglion cells of the macula are generally smaller than other axons in the optic nerve. Although they enter on the temporal side of the nerve initially, they mingle with all the bundles from the retinal quadrants within a short distance. The fibers that will cross to the contralateral optic tract are probably segregated a few millimeters prior to the junction of the optic nerve with the optic chiasm. Within the optic chiasm, the macular fibers are generally superior to those from the peripheral retina.
2-3-1-4 Enlarged Physiologic Blind Spot. This pattern of visual field defect results at or in the immediate vicinity of the optic nerve head. It is sometimes designated as a pericecal field defect (Figure 2-11).
Peripapillary Retina (1). Papilledema causes swelling of the optic nerve head axons
(A) in the retina. These axons are not free to expand at the lamina scleralis (B) but
Figure 2-11. Enlarged physiologic blind spot (a pericecal field defect).
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are free to expand at the lamina choroidalis (C) and even more free to expand at the lamina retinalis (D), resulting in displacement of the adjacent retina and choroid. Because the peripapillary receptors are displaced laterally in all directions, this could partially explain the increase in the size of the absolute scotoma that comprises the physiologic blind spot. However, the major cause may be swelling of the axons and intercellular retinal edema (E). This masks some of the light falling on the peripapillary retinal receptors and, in turn, causes a relative scotoma or depression outside the absolute scotoma. Moreover, some of the enlargement of the blind spot is refractive, due to peripapillary hyperopia.8 Increased hyperopic refractive correction usually eliminates or reduces the size of an enlarged blind spot resulting from the optic nerve head swelling of increased intracranial pressure (papilledema). Other peripapillary disorders may cause absolute and relative increases in the size of the physiologic blind spot, but these are not usually as symmetric. Often they result in a pericecal depression or scotoma. Advanced papilledema may be associated with swelling of the outer plexiform layer of the retina (F, Henle’s layer).
The anatomic relationships of the nerve head to the macula are reversed in the visual field, so the nerve head is anatomically superior to the macula on the globe but the blind spot is below the fixation point in the visual field. It is useful to know certain quantitative anatomic relationships of the optic nerve head (Table 2-3), based on the assumption that 1 mm of circumference at the retina corresponds to about 5.0° of visual field.
Optic Nerve (2). Some forms of optic neuropathy, particularly ethanol-induced toxic optic neuropathy, produce centrocecal scotomas.
2-3-1-5 Centrocecal Scotoma or Depression. This phrase describes a visual field abnormality encompassing both the central region of fixation and the physiologic blind spot (Figure 2-12).
Retina (1). The papillomacular bundle can be involved by regional choroidal, outer retinal, and inner retinal layer lesions. Causes can include optic pit with serous retinal detachment, macular degeneration or inflammation, or cilioretinal artery
(1) occlusion. Superior or inferior cilioretinal arteries are present as congenital developmental variations in about 20% of normal eyes. They are retinal branches of the ophthalmic artery via a posterior ciliary artery rather than via a central retinal artery. A cilioretinal artery may be occluded alone, sparing the retinal regions supplied by the central retinal artery, or it may be uninvolved with occlusion of the central retinal artery leaving a small island of vision with good acuity.
Optic Nerve (2). Many types of optic nerve lesions including toxic and nutritional amblyopias may produce centrocecal scotomas. The monofixation syndrome results
TABLE 2-3. Quantitative Anatomy of the Optic Nerve Head
Diameter of Optic Nerve Head |
Relation of Nerve Head to Macula |
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Horizontal: 1.1 mm, 5.5° |
Nasal: 3.0 mm, 15.0° |
Vertical: 1.5 mm, 7.5° |
Inferior: 0.3 mm, 1.5° |
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Figure 2-12. Centrocecal scotoma or depression.
in a central scotoma of less than 3° radius in one eye. It can be detected only with binocular perimetry (e.g., red and green targets viewed with a red-filtered right eye and a green-filtered left eye).
2-3-1-6 Equatorial Annular Scotoma or Depression. These visual field defects usually begin as depressions of the field at a 25° to 45° radius from the point of fixation (Figure 2-13).
Preretinal Media (1). An annular, or ring, scotoma can be produced by aphakic spectacle lenses and relieved by removing them. The scotoma is produced by light rays striking the highly convex surface from an oblique direction and their being refracted outside the pupil.
Equatorial Retina (2). The term retinitis pigmentosa describes a heterogeneous group of genetically determined disorders. Although there are notable exceptions (e.g., unilateral pigmentary retinopathy and sector pigmentary retinopathy), the usual pathologic and visual field changes occur in a circular region measuring 25-50° from fixation. The earliest changes of retinitis pigmentosa may be confused with the arcuate and paracentral nerve fiber bundle defects of glaucoma, where the ring scotoma may originate with vertical enlargement and baring of the physiologic blind spot, giving two arcuate scotomas that complete a ring (see Figure 2-9).
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Figure 2-13. Equatorial annular scotoma or depression.
2-3-1-7 Altitudinal Hemianopia. For a discussion of monocular altitudinal hemianopia, see Section 2-4-4-1.
2-3-2 Generalized Defects
2-3-2-1 Generalized Depression or Peripheral Contraction. Generalized depression or peripheral contraction of the visual field results when a focal light stimulus greater than the background light produces less sensory appreciation than normal at any and all locations of the visual field. The depression may be equal in all meridians or may be unequal. An unequal diffuse field abnormality may be the sum of the abnormalities induced by several factors. An extreme example would be a superior altitudinal defect from a ptotic eyelid plus diffuse depression of the media from a cataract plus a central scotoma from a welding burn of the fovea plus a nasal scotoma from glaucoma.
Preretinal Media. The artifact caused by a lens used for central perimetry may often affect the outer points of a central 30° visual field examination and be particularly confusing with programs that merge central and peripheral examinations on a single chart. Body parts such as the nose and upper eyelid frequently cause localized abnormalities. Media opacities include contact lenses, corneal edema, scars, and the astigmatic aspects of keratoconus. Cataracts are the most frequent media opacity and may cause either generalized, localized, or combined depression, contraction,
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or scotomas. Cataracts cause field defects more by scatter and defocusing of the stimulus light with regard to the background light (decreased contrast) than by absorption or backscatter of the stimulus light. Vitreous hemorrhage can also depress the visual field.
Retina. Diffuse disorders of all retinal elements (photoreceptors to ganglion cells) can cause generalized depression of the visual fields. A description of all the disorders that can cause diffuse monocular pathology is beyond the scope of this chapter.
Optic Nerve. Most monocular optic nerve disease is compressive, demyelinating, traumatic, or vascular. A detailed description of these disorders is beyond the scope of this chapter. About half the patients with optic neuritis present with diffuse visual field loss; 20% have altitudinal or other nerve fiber bundle-type defects, while only 8% have central or centrocecal scotomas.
2-4 BINOCULAR FIELD DEFECTS
2-4-1 Homonymous Hemianopias. Any retrochiasmal lesion may present with a congruous homonymous hemianopia. The occipital lobes and the parietal lobes are more frequent than the temporal lobes as the locations of lesions causing the visual field defects.
2-4-1-1 Complete: Macular Splitting. A complete homonymous hemianopia with macular splitting refers to the loss of either the entire right or the entire left visual field of both eyes. The central 5° of the visual field is designated as the macular portion of the visual field. It may be included in the complete hemianopic field defect; thus, the macular region is “split.” Conversely, it may not be included, in which case it is “spared” (Figure 2-14).
Optic Tract (1). Any lesion ascending the visual pathway beyond the first few millimeters of the optic tract may cause a complete homonymous hemianopia. A lesion at the junction with the optic chiasm may cause a junctional scotoma. Optic tract lesions are associated with wedge-shaped retinal axonal degeneration and death of the retinal ganglion cell layer nasal to the fovea of the contralateral eye. Ophthalmoscopy with red-free light reveals homonymous hemiretinal atrophy at the nasal aspect of the contralateral optic nerve head and in a narrow band along the horizontal meridian at the temporal aspect of the nerve head. It should be noted that the nasal aspect of the fovea is represented by fibers in the middle of the papillomacular bundle. The ipsilateral eye will reveal bow-tie atrophy of the superior and inferior arcuate bundles of the retinal nerve fiber layer. The optic tract syndrome consists of a homonymous hemianopia, atrophy of the nasal fibers of the contralateral optic nerve, atrophy of the temporal fibers of the ipsilateral optic nerve, and a contralateral monocular relative afferent pupillary defect. The presumed basis is that about 60% of afferent pupil fibers decussate at the chiasm, giving rise to unequal representation of the two eyes in each optic tract.
Anatomic studies in monkeys have shown that the retinal vertical midline is almost absolute. Above and below the macula, there is only a 1° overlap across the vertically oriented midline strip when the axonally transported tracer horseradish
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Figure 2-14. Complete homonymous hemianopia with macular splitting.
peroxidase is injected into the lateral geniculate body and observed in the retinal ganglion cells. At the macula the overlap widens to 3°. Thus, there is no anatomic basis for macular sparing greater than 3° in patients with a complete retrochiasmal hemianopic lesion. Any macular sparing exceeding this amount must be ascribed to errors in fixation or response. (For further discussion, see Section 2-3-1-3.) There is no evidence of any representation of ipsilateral visual field in the calcarine cortex. Lateral Geniculate Body (2). Both the lateral geniculate body and the optic tract have dual arterial supplies. The lateral and anterior aspect of the lateral geniculate body is supplied by the anterior choroidal artery, a branch of the internal carotid artery (A), while the dorsal and medial aspect is supplied by the lateral choroidal artery (B), a branch of the posterior cerebral artery (C). If both arteries are occluded, a congruous homonymous hemianopia will result.
Optic Peduncle (3). The optic peduncle is the first portion of the optic radiation. It may be considered a part of the internal capsule. It is posterior to the lentiform nucleus (D), the posterior limb of the internal capsule (E, sensory), and the anterior limb (F, motor). Occlusion of the anterior choroidal artery (A) or of the posterior choroidal artery (G) can produce contralateral hemianopia, hemianesthesia, and, sometimes, hemiplegia.
Optic Radiation (4). The optic radiation passes lateral to the inferior horn (H) and the posterior horn (I) of the lateral ventricle. Field defects are often incongruous,
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with anterior lesions becoming more congruous as the fibers in the optic radiation approach the calcarine cortex, except for the portion supplied by the deep optic branch (J) of the middle cerebral artery (K). The optic radiation is supplied by branches of the posterior cerebral artery (C), especially the calcarine branch (L).
Calcarine Cortex (5). Field defects are congruous, except when the lesion involves only the extreme anterior portion of the calcarine cortex (6), where the contralateral temporal crescent is represented. The blood supply to the calcarine cortex is from the posterior cerebral artery (C). Occasionally, the calcarine cortex receives an anastomotic branch (M) from the middle cerebral artery. In many cases, the macular representation on the lateral convexity of the occipital lobe may be supplied by branches of the middle cerebral artery.
2-4-1-2 Incomplete Congruous: Horizontal Sectoranopia. This phrase describes a homonymous, congruous wedge-shaped field defect extending from the point of fixation to the periphery (Figure 2-15).
Lateral Geniculate Body (1). This field defect may result from a vascular lesion (e.g., a lateral choroidal artery infarction) damaging the dorsal portion of the lateral geniculate body that serves the macular function yet causing little damage to the medial portion with the terminations of axons from the inferior retina or to the lateral portion with the terminations of fibers from the superior retina. Frisén9 has presented a case of a congruous homonymous sectoranopia sparing the
Figure 2-15. Horizontal sectoranopia.
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horizontal sector. Computed tomography (CT) scanning demonstrated changes in the lateral geniculate body that followed ligation of the distal portion of the anterior choroidal artery. Incongruity with lesions of the lateral geniculate body is rare and, if present, may result from simultaneous involvement of the optic tract. Wedge-shaped defects that do not fully extend from fixation to the periphery have been reported with occipital infarction (2).
2-4-1-3 Incomplete Congruous: Paramidline-Sparing Vertical Hemianopia. This phrase describes an incomplete congruous hemianopia in which the paramidline portion of the visual field is spared. The spared portion is bordered by a vertical line tangent to a horizontal radius (Figure 2-16).
Posterior and Middle Cerebral Arteries. After recovery from coronary artery bypass surgery, cardiac arrest, or similar hypoxic events, dysfunction may be present in the watershed zones (1) at the borders of perfusion of the middle (A) and posterior
(B) cerebral arteries. Thus, occlusion can give rise to a field defect stretching from the top to the bottom of the visual field about 5-10° from the vertical midline and may coincide with the lateral border of cortical area 17. Prenatal and infantile hypoxia in these regions may lead to a dense incomplete hemianopic field defect associated with a porencephalic cyst (2). The injured fibers of the optic radiation are the most medial fibers, especially those at its upper and lower margins, while the more lateral and intermediate regions of the optic radiation are spared.
Figure 2-16. Paramidline-sparing vertical hemianopia.
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Figure 2-17. Homonymous hemianopia with macular sparing.
2-4-1-4 Incomplete: Macular Sparing. If a congruous homonymous hemianopia is complete except for the central radius of less than approximately 5°, it is said to have sparing of the macular representation of the visual field (Figure 2-17).
Immediately Postchiasmal Optic Tract (1). Lesions such as craniopharyngiomas may cause a homonymous hemianopia with macular sparing, a rare form of congruous field defect. When it occurs, the region of sparing is likely to be less than 2°; perhaps only a few macular fibers remain.
Calcarine Cortex (2). The more anterior the lesion of the calcarine cortex, the more the central field is spared. Lesions with macular sparing are usually the result of calcarine artery occlusion or tumors. The anastomotic branch of the middle cerebral artery (A) may supply the posterior lateral portion of the calcarine cortex.
2-4-1-5 Incomplete: Two Scotomas. These field defects result from two separate lesions in one retrochiasmal visual pathway (Figure 2-18).
Postchiasmal Visual Pathway (1). While any location may be involved, the most typical location would be due to occlusions of two branches of one posterior cerebral artery or to occlusion of the ipsilateral posterior and middle cerebral arteries. One or both of the hemianopic homonymous scotomas may involve or spare the macula, as illustrated.
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Figure 2-18. Two ipsilateral homonymous hemianopic scotomas.
2-4-1-6 Incomplete Incongruous. Incongruity results when the retrochiasmal fibers of the projection of one eye are differentially positioned or injured than the fibers of the opposite eye (Figure 2-19).
Anterior Optic Tract (1). Extreme incongruity, especially near the vertical meridian, is usually related to the difference in the projections of fibers from the two eyes in the anterior portion of the optic tracts. The lesions are usually caused by tumors of adjacent structures. The field defects may have steeply sloping isopter borders as well as incongruity.
Optic Radiation (2). After the fibers of the optic radiation leave the lateral geniculate body through the optic peduncle of the internal capsule (A), they enter the external sagittal striatum to form the midportion of the optic radiation, which lies in the temporal and temporoparietal lobes (B). Incongruous defects may occur in the temporal lobe, because fibers serving homologous points in the visual fields of the two eyes are not adjacent. The blood supply to the temporal lobe comes mostly from branches of the middle cerebral artery.
The fibers of the optic radiation become more compact and the arrangement more homologous as the fibers pass into the posterior portion of the optic radiation in the parietal and parieto-occipital lobes (C). Incongruity and sloping margins are less frequent here. Field defects may result from tumors or middle cerebral artery disease. Because the more medial aspects of the parietal lobe are supplied