Ординатура / Офтальмология / Английские материалы / Visual Fields Examination and Interpretation_Walsh_2011

Abnormalities of the preretinal territory may produce a generalized depression of the visual field, a flattening of the hill of vision, or sometimes a localized depression but rarely a scotoma. Visual field defects relating to a retinal region such as the macula can involve the retinal territory (with a lesion of the outer retinal layers or choroid) or neural territory I (with a lesion of the inner retinal layers). A partialthickness macular hole involving only the internal layers of the retina would be designated as occurring in neural territory I as described by Trobe and Glaser.1 Neural territory I lesions never respect the vertical meridian but reflect the anatomy of the abnormal retinal sensory structures. Lesions of the retinal nerve fiber layer and optic nerve are designated as occurring in neural territory II, perichiasmal lesions as occurring in neural territory III, and retrochiasmal lesions as occurring in neural territory IV.

2-2-1 Occipital Lobe. Occipital lobe lesions may cause visual field defects due to involvement of any or all of these three anatomic sites: the optic radiation, the primary or striate visual cortex, the secondary visual cortex. Studies performed in the 1990s using MR imaging (MRI), functional MRI, and computer graphics have significantly altered our understanding of the retinotopic projection within the visual cortex. These studies have:

1.Demonstrated remarkable variability in the orientation of the calcarine fissure, from almost horizontal to almost vertical in different human brains.

2.Expanded the proportional area of the macular projection so that it takes up almost all but the anterior part of the striate cortex within and adjacent to the calcarine fissure of the occipital lobe2; the striate cortex is designated as VI.

3.Identified the borders of the secondary visual areas, including V2, V3, and others.3,4 The V designations for the visual areas have been carried over from studies in nonhuman primates.

The medial surface of the occipital lobe is bordered anteriorly by the parietooccipital sulcus, which intersects with the anterior portion of the calcarine fissure that divides the occipital lobe into a superior and an inferior portion. The orientation of the calcarine fissure is now routinely observable on the sagittal MRI section. The primary projection of the fovea to the striate cortex is to the most posterior portion of the occipital lobe and usually extends 1 cm onto the lateral convexity of the occipital lobe (Figure 2-4A). The eccentricity of the projection for the fovea can be measured along the calcarine fissure to the junction with the parietooccipital fissure, where the most peripheral visual field is located; this distance is about 80 mm. The linear cortical magnification factor is one way of expressing the weighting given to the retinal projection within the striate cortex. Horton and Hoyt2 have estimated that the linear cortical magnification factor is 9.9 mm/degree at 1° eccentricity, 2.0 mm/degree at 5°, and 1.6 mm/degree at 10°.

A B

Figure 2-4. Representation of the primary visual field on the human striate cortex. Blue, binocular representation; green, monocular representation. (A) The cortical banks surrounding the calcarine fissure have been slightly opened to better expose the borders of this region. The lower vertical visual field meridian is located on or close to the medial cortical surface of the upper bank, while the upper vertical visual field meridian is located on or close to the medial cortical surface of the lower bank. Most of the primary visual cortex is hidden within the fissure. (B) The calcarine fissure has been widely opened so that the horizontal meridian is indicated at the depth of the fissure. The fovea is represented at the most posterior portion of the fissure (the fundus), and the relative location of the physiologic blind spot of the contralateral eye is indicated by the dark ellipse. The most anterior 8-10% of the striate cortex (green area) represents the monocular temporal field of the contralateral eye. The scale bar is calibrated in centimeters. (Source: Redrawn with permission from Horton JC, Hoyt WF. The representation of the visual field in human striate cortex: a revision of the classic Holmes map. Arch Ophthalmol. 1991;109:816–824. Copyright 1991, American Medical Association.)

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The clinical implications of this magnified projection of the macula in the primary visual cortex are many. With regard to the selection of the automated visual techniques, this information diminishes the concern that a 24° radius visual field might miss some cortical lesion that could have been detected by a 30° radius examination. Actually, a 30° visual field tests 83% of the cortical area, while a 24° visual field tests 80%. Thus, only 3% of the cortical visual field is lost from the examination by the reduction of the tested area and the test time. Conversely, only the most anterior 10% of the striate cortex is involved in the uniocular temporal crescent, a cortical area equal to that devoted to the central 1° of the visual field. The large proportion of the striate cortex devoted to the macula also explains why the central 8° of stimulation during pattern-shift visually evoked cortical potential testing generates 60% of the voltage of the P100 wave form. The most important implication of this expanded representation of the macula is that there is a large anatomic substrate for the phenomenon of macular sparing. Survival of even a small portion of the striate cortex provides some possibility for retained macular function.

Most of the striate cortex is contained within the superior and inferior banks of the calcarine fissure. The unfolded size of the striate cortex is 40 × 80 mm. The horizontal meridian for V1 is thus buried along the fold line separating the superior and inferior banks, while the lower and upper visual field vertical meridians are represented on the superior and inferior gyri of the calcarine fissure (Figure 2-4B). The horizontal and vertical visual field meridians meet at the posterior pole of the occipital lobe, where the fovea is represented, and again anteriorly at the anterior pole of the calcarine fissure, where the temporal crescent is projected. The reader can conceptualize this representation by imagining the right visual hemifield as an elastic sheet in visual space attached on an opened semicircular fan with a pivot at the fovea (Figure 2-5).

The extrastriate visual cortex is situated above, below, and surrounding the striate cortex on the medial and lateral surfaces of the occipital lobe. This relationship is best seen with computer graphic techniques that unfold, and then cut and flatten the occipital lobe (Figure 2-6).3 These maps can now be made in normal subjects with physiologic, functional MRI and confirm maps made from pathologic cases. While such studies should have many applications with regard to our comprehension of human visual performance, the most immediate application is understanding that an extrastriate lesion that crosses both a horizontal and a vertical meridian of the secondary visual cortex (V2 and/or V3) can cause an inferior homonymous quadrantanopia in the absence of lesions in the parietal lobe or calcarine fissure (Figure 2-7).

2-3 MONOCULAR FIELD DEFECTS

2-3-1 Localized Defects

2-3-1-1 Wedge-Shaped Temporal Field Defect. This pattern of field defect has its apex pointing toward the physiologic blind spot and involves ganglion cell axons from the nasal retina (Figure 2-8).

A B C

Figure 2-5. Topologic representation of the right visual hemifield onto the left visual cortex. (A) The reader can conceptualize by imagining the right hemifield as an elastic sheet in visual space attached on an open semicircular fan with a pivot at the fovea. (B) As the fan collapses around the foveal pivot, the vertical meridians become parallel (and inverted due to the inverted image in the eye) and the elastic sheet collapses along the temporal border. The foveal region is stretched toward the periphery, thus magnifying the proportional area of the representation of the central visual field. (C) The flattened representation of the hemifield in the left visual cortex. The upper and lower vertical meridians are parallel, and the temporal borders collapse at the most anterior part of the calcarine cortex. The green areas correspond to the monocular temporal crescent. HM, horizontal meridian; LTB, lower temporal border; LVM, lower vertical meridian; UTB, upper temporal border; UVM, upper vertical meridian. (Source: Redrawn with permission from Horton JC, Hoyt WF. The representation of the visual field in human striate cortex: a revision of the classic Holmes map. Arch Ophthalmol. 1991;109:816–824. Copyright 1991, American Medical Association.)

Retina (1). In the nasal retina, the ganglion cell layer contains the nuclei of the axons that will travel through the retinal nerve fiber layer to approach the optic nerve head in fan-shaped bundles: the superior (A) and inferior (B) radiating bundles. Any lesion causing complete destruction of a region of the inner retinal layers—retinal nerve fiber, ganglion cell, inner plexiform, or inner nuclear (bipolar cell) layer—is likely to cause a dense field defect.

Occlusion of one of the nasal branches of the central retinal artery or nasal tributaries of the central retinal vein can cause a wedge-shaped field loss with its apex at the physiologic blind spot. Although the usual pattern of distribution of the branch retinal arteries is quadrantic, it should be noted that the central point of the quadrants is the optic nerve head, not the fovea. When analyzing a visual field defect that involves one or more quadrants of the visual field, one should determine if the quadrants are retinovascular and related to the physiologic blind spot or neurologic and related to the point of fixation. Embolic disease involves the superotemporal branch retinal arterioles more frequently than the nasal branch retinal arteries. The initial finding may consist of a dense scotoma reflecting a complete loss of function of the inner retinal layers, including the nerve fiber layer. Unless recovery occurs within a few days, the field loss may be permanent. The blind spot–based quadrantic field loss may not have its apex extend to the blind spot if the occlusion occurs at a peripheral bifurcation of a retinal arteriole. The inner retinal swelling may first manifest a white appearance (e.g., the cherry-red

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A B

C D

Figure 2-6. Retinotopic projection of human visual areas as derived from functional MRI studies. (A) MRI snowing original cortical surface of right cerebral hemisphere with retinal isoeccentricity indicated by a color code on the cortical surface. Red indicates the fovea, then blue, then green (for the parafovea), then yellow, then brown for the far periphery. (B) The cortical surface is unfolded by computer manipulation, thus expanding the apparent area of the brain. The local areas and local angles are preserved. The sulcal cortex is dark gray and the gyral cortex is light gray. (C) The cortical surface of the occipital lobe is flattened after the occipital lobe has been cut off, and an additional cut (dashed line in B) has been made in the fundus of the calcarine sulcus. (D) The schematic functional representation of the primate (striate, V1) and the secondary visual cortex (extrastriate visual areas, V2, and to some extent V3 are shown as repetitive mirror images surrounding the primary visual cortex). V4 is present only in the lingual gyrus of the inferior occipital lobe and is associated with color recognition. The arrow shows the location of the fovea. VP, ventroposterior area. (Source: Redrawn with permission from Sereno MI, Dale AM, Reppas JB, et al. Borders of multiple visual areas in humans revealed by functional magnetic resonance imaging. Science. 1995;268:889–893.)

spot of the macula that is seen if both the inferior and the superior temporal branch retinal arterioles are occluded). Occlusion of the superior branch retinal arteriole produces an inferior altitudinal field defect. Acute systemic hypotension can have effects similar to those of arterial occlusion.

Thrombosis of the tributary retinal veins usually occurs at and distal to the arteriovenous crossings. Systemic arterial hypotension and ocular hypertension (glaucoma) are predisposing factors. The field defects following venous occlusion are often more peripheral and less dense, giving more hope for late recovery than is

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possible for the field defects of arterial occlusion. Secondary field changes may occur as a result of chronic macular edema or preretinal and vitreous hemorrhages.

Lesions nasal to the optic nerve head will cause wedge-shaped scotomas or peripheral contraction in the field temporal to the blind spot. Lesions of the choroid or outer retinal layers will usually cause less dense defects, because the nerve fibers passing in the overlying nerve fiber layer and some of the input to the bipolar cells in the affected region may be spared. Complete loss of field occurs in regions where retinoschisis has split the retina, thus disconnecting the retinal ganglion cells from the photoreceptors. In contrast, retinal detachments produce milder depressions with less steep margins, at least in their early stages.

Optic Nerve Head (2). The retinal course of the axons is such that the most posterior enter the peripheral portions of the optic nerve head while the most anterior retinal axons enter the central portion. Drusen of the optic nerve head produce local injury to axons at the optic nerve head and may cause progressive (rarely sudden) contraction of the visual field or localized depressions or scotomas. The arterial anatomy of the optic nerve head is invoked to explain various patterns of field loss. The ophthalmic artery is the ultimate source of supply to a continuous capillary bed that extends throughout the optic nerve head. The arterial blood is delivered by three systems:

(1)branches of the short posterior ciliary arteries that enter the medial and lateral peripapillary sclera within 1 mm of the peripheral margin of the optic nerve head,

(2)vessels of the pial plexus and retrobulbar optic nerve, and (3) branches of the central retinal artery. The posterior ciliary artery branches were formerly described as completing the arterial circle of Zinn-Haller, but an anatomically demonstrable arterial circle is generally not complete (see Figure 2-3). The circle of Zinn-Haller may also be supplied by pial arterioles supplying the anterior aspect of the optic nerve. The lack of functional anastomotic continuity is invoked to explain the altitudinal field defects that present in anterior ischemic optic neuropathy. Focal infarctions, usually at the vertical poles of the optic nerve head, may result from infarction in watershed zones between territories served by centripetal optic nerve head branches of the short posterior ciliary arteries (C). The posterior ciliary arteries are generally situated near the horizontal poles of the optic nerve head. They also give rise to centrifugal branches that supply the peripapillary choroid.

Retrobulbar Optic Nerve (3). Monocular wedge-shaped nerve fiber bundle defects can occur with infarction, inflammation, tumors, or trauma anywhere between the optic nerve head and the optic chiasm. However, the likelihood of involving only the nasal fibers decreases at 1 cm behind the globe as fibers from the papillomacular bundle disperse throughout the optic nerve.

2-3-1-2 Arcuate and Paracentral Field Defects. Pericentral (within 5° of the fovea) or paracentral (within 20° of the fovea) scotomas or depressions in the Bjerrum region result from injury to retinal ganglion cell arcuate axons arising from the temporal retina (Figure 2-9). These arcuate nasal defects are often referred to as “nerve fiber bundle defects,” although they are just one particular pattern of nerve fiber bundle defect. Injury to either the superior or the inferior nerve fiber bundle will produce an arcuate scotoma terminating at the horizontal meridian. If the superior and inferior fibers are injured asymmetrically, a nasal step field defect will result.

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Figure 2-9. Arcuate and paracentral field defects.

Retina (1A and 1B). During the embryogenesis of the eye, the fovea develops at the temporal periphery. At that time, all the nerve fibers have a fan-shaped radiation from the optic nerve head. Later in development, the fovea migrates toward the optic nerve head. As a result, the temporal nerve fiber layer arches around the fovea, causing the nerve fiber layer to assume an arcuate shape—the superior (1A) and inferior (1B) arcuate bundles. Peripheral axons in the arcuate bundles originate in ganglion cells on either side of the horizontal retinal raphe. The initial course of these axons is parallel to the horizontal raphe (C) where the axons are in the superior or inferior temporal retinal raphe. The arcuate portion of the retinal nerve fiber layer also contains the blood vessels coursing around the macular region. The arcuate portion of the retinal nerve fiber layer is the thickest (0.5 mm), and its bundles reflect bright white striations especially when viewed with red-free (green-filtered) light. The thickness of the nerve fiber layer decreases 1 or 2 disc diameters from the optic disc margin. Loss of the retinal nerve fiber layer may occur in various patterns ranging from diffuse atrophy to highly localized atrophic wedge defects. The minimum ophthalmoscopically detectable wedge defect is the loss of a 50-μ thickness of nerve fibers adjacent to 50 μ of intact nerve fibers. This would represent a loss of 15,000, or about 1% of retinal axons.5

Optic Nerve Head (2). The retinal ganglion cell axons pass as nerve fiber bundles through the pores of the collagenous scleral lamina within the scleral canal.

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Figure 2-10. Central scotoma or depression field defect.

photocoagulation is likely to cause a field defect. The papillomacular bundle contains more than half the optic nerve axons.

Significant depressions of visual acuity, central visual fields, spatial contrast sensitivity, and color perception may follow lesions in the macular region. The differential diagnosis of anatomic lesions in the macular region is beyond the scope of this chapter.

The projection of human retinal ganglion cell axons of various sizes and physiologic characteristics must be deduced from studies in monkeys and cats, and these studies have not given wholly consistent results. It is generally agreed that the largest, fastest-conducting axons, including 25% of the axons originating in the parafoveal region, terminate in the magnocellular layers of the lateral geniculate nucleus. These are designated as magnocellular (M) cells and in many respects are similar to the Y cells of cats. The larger-diameter axons are thought to be important in such functions as achromatic vision, blue-yellow vision, and high temporal frequency vision (loss of the larger-diameter axons results in lowering of the critical flicker fusion frequency). Glaucoma seems to be a disorder whose initial effects are on the more peripheral M (Y-like) cells. Contrast-sensitivity testing seems to be particularly sensitive to M-cell dysfunction because M cells have large receptive fields, high contrast sensitivity, and a broad band of spectral response.