Ординатура / Офтальмология / Английские материалы / Visual Fields Examination and Interpretation_Walsh_2011
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76 Visual Fields
The fields shown will result if the temporal lobe is amputated more than 4 cm from the tip. The defects are usually congruous and have a sharply defined vertical meridian. The horizontal meridian may be included, with larger lesions yielding a congruous superior quadrantanopia with or without macular sparing. If more than 8 cm of the temporal lobe is amputated, a homonymous hemianopia will result. Tumors usually produce greater incongruity and sloping of isopters than do vascular lesions of the anterior portion of the retrochiasmal visual pathway.
Lingual Gyrus of Occipital Lobe (2). Occipital lesions that produce a pure quadrantanopia do not usually result from pure involvement of the primary visual cortex (area 17), as too long a strip of tissue along the lip of the calcarine cortex would have to be injured. It has recently been demonstrated that the visual association cortex (areas 18 and 19) maps the peripheral visual field along the horizontal meridian in a compact region near the posterior pole of the occipital lobe. Thus, a quadrantanopia can be thought of as resulting from the loss of fibers going to or from the primary visual cortex.
2-4-5-2 Inferior Homonymous, Complete. In this pattern, there is loss of the overlapping inferior right or left visual field of each eye (Figure 2-29).
Parietal Lobe (1). The optic radiation passes posterolaterally from the lateral geniculate body (A) into the parietal lobe. After initial dispersion, the fibers that
Figure 2-29. Complete inferior homonymous quadrantanopia.
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project from the superior retinal quadrants (B) collect into a compact bundle sooner than the temporal lobe fibers serving the inferior retinal quadrants. It is for this reason that complete quadrantic loss occurs more frequently in parietal lobe lesions than in temporal lobe lesions.
Cuneate Gyrus of Occipital Lobe (2). An inferior quadrantanopia of occipital origin involves the visual association area, not just the primary cortex (see earlier section “Lingual Gyrus of Occipital Lobe”).
2-4-6 Bilateral Central Field Defects
2-4-6-1 Scotoma or Depression. The central visual fields of both eyes are abnormal in this pattern of field defect and are usually accompanied by decreased visual acuity (Figure 2-30).
Media Opacities (1). See Section 2-3-1-3.
Macula Denser scotomas occur with lesions that involve the inner retinal layers (2), in contrast to lesser depressions with outer retinal and choroidal disorders in the macular regions. Nutritional and toxic amblyopias may involve ganglion cells originating in the macula.
Figure 2-30. Bilateral central scotomas or depressions.
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Optic Nerve (3). The maculopapillary bundle is in the temporal quadrant of the optic nerve, immediately posterior to the optic nerve head. Axial neuritis results in dense central or centrocecal scotomas.
Optic Nerve, Diffuse (4). After passing 1 cm posterior to the optic nerve head, many of the fibers of the maculopapillary bundle reach the center of the optic nerve while other macular fibers distribute to the peripheral quadrants of the optic nerve.
Calcarine Cortex (5). The macula is represented on the posterior portion of the calcarine sulcus (6) and may extend onto the posterolateral portion of the occipital lobes. This is important in the analysis of trauma to the occipital lobes. Contusion of the superior aspect of both occipital lobes may result in an inferior altitudinal congruous field defect (see Figure 2-27).
2-4-7 Bilateral Peripheral Field Defects
2-4-7-1 Generalized Depression or Peripheral Contraction. In this pattern, the outer isopters of the visual field collapse or contract (Figure 2-31). Because perimetry is a subjective examination, contraction can result from patient or examiner factors. In addition to the lesions noted below, deliberate malingering, too rapid target movement, slow response times, inappropriate contrast of stimulus-target/ background ratio, and an inadequately dilated pupil can all contract the outer isopters.
Figure 2-31. Peripheral contraction.
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Media Opacities (1). Corneal scars, cataracts, Large Vitreous Hemorrhage. Peripheral Retina (2). Quinine, salicylates, thioridazine hydrochloride, and carbon monoxide poisoning are among the causes of contraction of the visual fields. Optic Nerve Head (3). Irregular, progressive constriction may occur. Sector sparing with sector and optic nerve defects may help determine the diagnosis. Glaucoma and optic nerve head swelling may lead to peripheral depressions of the visual fields but usually in combination with other more characteristic field defects.
Optic Nerve (4). Peripheral optic neuritis may occur with tertiary syphilis. When peripheral constriction is combined with central depression, retrobulbar neuritis and optic atrophy from any cause should be considered.
Anterior Calcarine Sulcus (5). To cause a binocular peripheral constriction, paired visual cortical lesions would need to injure the striate cortex or pathways related with the most anterior portions of both calcarine sulci. This portion of the striate cortex serves the visual field of the unpaired temporal crescent visual field of the contralateral eye. Limited extension of the lesion posterior to the junction of the calcarine with parieto-occipital sulcus would involve the nasal field of each ipsilateral eye.
2-4-8 Bilateral Checkerboard Scotomas. This pattern of visual loss consists of two congruous hemianopic scotomas, such as a right superior and left inferior field defect (Figure 2-32).
Figure 2-32. Bilateral checkerboard scotomas.
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Posterior Cerebral Arteries (1). Occlusions of the posterior cerebral arteries may occur simultaneously in severe systemic hypotension or in basilar-vertebral artery disease (“top-of-the-basilar-artery” syndrome); each posterior cerebral artery may be occluded at a different time. Identification of the old or new lesion depends on the history or on other neurologic findings. These are called “checkerboard scotomas” when the hemianopic visual fields are not symmetrically affected.
2-4-9 Bilateral Homonymous Hemianopias. This pattern of field defect consists of complete or incomplete homonymous hemianopias involving both the right and the left visual fields (Figure 2-33).
Posterior Cerebral Arteries (1). The area of damage from occlusion of these arteries is usually more extensive than that described for bilateral checkerboard scotomas.
2-5 JUNCTIONAL FIELD DEFECTS
2-5-1 Complete Monocular Plus Incomplete Contralateral Ocular. This pattern of field loss involves the entire visual field of one eye and a portion (usually superior temporal) of the visual field of the opposite eye (Figure 2-34).
Figure 2-33. Bilateral homonymous hemianopias.
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Figure 2-34. Complete monocular plus an incomplete contralateral ocular (a junctional defect).
Both Eyes or Optic Nerves (1). One reason to perform a complete ocular examination on each patient is to avoid missing a second lesion. However, a complete monocular loss of vision plus an incomplete superior temporal quadrantanopia in the opposite eye with a short vertical meridian passing through fixation is diagnostic of the single lesion described next.
One Optic Nerve at Junction of Optic Chiasm (2). Inferior nasal peripheral fibers from the opposite optic nerve have crossed the optic chiasm and are involved while passing by the junction with the contralateral optic nerve into the contralateral optic tract. (This arrangement was formerly known as the anterior knee of Wilbrand, but it has now been shown that the fibers do not actually enter the contralateral optic nerve.)
2-5-2 Homonymous Hemianopia Plus. This field defect includes a (usually) complete and congruous hemianopia with an additional field defect in one eye (Figure 2-35).
Junction of Optic Tract and Optic Chiasm (1). A complete right homonymous hemianopia of a left postchiasmal lesion may also involve some of the left eye axons that decussate in the optic chiasm. This adds a left eye temporal field defect. The left superior temporal visual field is spared because the inferonasal fibers serving this field decussate anteriorly within the optic chiasm. The fibers from the superior
Figure 2-35. Homonymous hemianopia plus (a junctional scotoma).
Figure 2-36. Bitemporal hemianopia plus (a junctional scotoma).
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nasal retina of the left eye are injured because they decussate posteriorly, giving rise to the left inferior temporal visual field constriction. (Compare this example with Figure 2-34.)
2-5-3 Bitemporal Hemianopia Plus. In this pattern of field defect, there is a nasal field defect in one eye or both eyes in addition to temporal field defects in both eyes (Figure 2-36).
Junction of Optic Chiasm and Optic Nerve (1). A bitemporal hemianopia can still be recognized by the fragment of sharp vertical meridian remaining in the right visual field, but there is also involvement of uncrossed fibers in the optic nerve. This may occur in pituitary tumors if the optic nerves are very long and if the optic chiasm is postfixed with regard to the sella turcica. Sometimes, pituitary tumors progress asymmetrically. Aneurysms of the anterior communicating artery (A) are well situated to produce these fields.
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3
Essentials of Automated Perimetry
GEORGE SHAFRANOV, MD
3-1 INTRODUCTION
Standard automated perimetry is a standard method of measuring peripheral visual function.1 Automated static perimetry gained wide acceptance among clinicians due to the test’s high reproducibility and standardization and ability to store, exchange, and statistically analyze digital data. Advances in the computerized visual field assessment have contributed to our understanding of the role that field of vision plays in clinical evaluation and management of patients. The Humphrey Visual Field Analyzer/HFA II-i is the most commonly used automated perimeter in the United States, and the examples in this chapter have been obtained with this instrument.
3-2 HISTORICAL OVERVIEW
Aubert and Förster2 in the 1860s developed the arc perimeter, which led to the mapping of peripheral neurologic visual field abnormalities and advanced glaucomatous field defects. Analysis of the central visual field was not seen as clinically important by most clinicians until 1889, when Bjerrum2 described a detected arcuate paracentral scotoma. Later, Traquair3 further contributed to kinetic perimetry on the tangent screen. In 1893, Groenouw proposed the term “isopter” for lines with the same sensitivity on a perimetry chart. Rønne further developed kinetic isopter perimetry in 1909 and described the nasal step in glaucoma.
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