Ординатура / Офтальмология / Английские материалы / Visual Fields Examination and Interpretation_Walsh_2011
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Figure 8-2. Prefixed chiasm. The prechiasmal space is 3 mm long, and the chiasm overlies the tuberculum sella. (A) Sagittal section of prefixed chiasm above tuberculum sella. (B) Photograph, top view. (Source: A redrawn by permission from Rhoton AL Jr, Harris FS, Renn WH. Microsurgical anatomy of the sellar region and cavernous sinus. In: Glaser JS, ed. Neuro-Ophthalmology Symposium of University of Miami and Bascom Palmer Eye Institute. St. Louis: CV Mosby; 1977:75-105. B reprinted by permission from Bergland RM, Ray BS, Tornack RM. Anatomical variations in the pituitary gland and adjacent structures in 225 human autopsy cases. J Neurosurg. 1968;28:93-99.)
fibers of the chiasm is compromised by compression as in a pituitary adenoma, resulting in bitemporal hemianopia, which may be reversible if the compression is relieved early enough (Figure 8-4B).9 The proximity of these vessels can also produce other pathologic conditions. Aneurysms of the anterior cerebral and internal carotid arteries can impinge on the optic chiasm, producing visual loss. More uncommonly, the carotid arteries and the anterior cerebral arteries may produce pathologic grooving of the chiasm as they cross above.
8-2-2 Nerve Fiber Anatomy. A large percentage of both crossed and uncrossed chiasmal fibers come from the macular region (Figure 8-5). These fibers are generally
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Figure 8-3. Postfixed chiasm. Prechiasmal space is 12mm long, and tuberculum sella is 6 mm long. Chiasm overlies dorsum sella. (A) Sagittal section of postfixed chiasm above dorsum sellae. (B) Photograph, top view. (Source: A redrawn by permission from Rhoton AL Jr, Harris FS, Renn WH. Microsurgical anatomy of the sellar region and cavernous sinus. In: Glaser JS, ed. Neuro-Ophthalmology Symposium of University of Miami and Bascom Palmer Eye Institute. St. Louis: CV Mosby; 1977:75–105.
B reprinted by permission from Bergland RM, Ray BS, Tornack RM. Anatomical variations in the pituitary gland and adjacent structures in 225 human autopsy cases. J Neurosurg. 1968;28:93–99.)
located in the dorsal and central regions of the chiasm, and lesions affecting the anterior visual pathways can often be detected on automated perimetry, which tests the central 30° of vision.5 The proportion of crossed fibers is greater than that of uncrossed fibers, usually with a ratio of approximately 53 crossed to 47 uncrossed.10 Detailed microscopic anatomy of the fiber paths within the chiasm is based on a limited number of studies, typically with small numbers of specimens. Normal anatomy has been best studied in nonhuman primates and extrapolated to humans, where the conclusions may be fanciful. The crossed and uncrossed fibers separate just as the fibers reach the chiasm. Uncrossed fibers continue laterally
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Figure 8-4. (A) The visual pathways pass through the circle of Willis. ACA = anterior cerebral arteries; PCA = posterior cerebral artery; BA = basilar artery; ICA = internal carotid artery. (B) The visual pathways distorted by pituitary tumor. (Source: Reprinted by permission from Bergland RM, Ray BS. The arterial supply of the human chiasm. J Neurosurg. 1969;31:327-334.)
Figure 8-5. A very substantial portion of the entire chiasm is composed of macular fibers.
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through the chiasm into the ipsilateral optic tract and the lateral geniculate nucleus (LGN). Superior and inferior fibers from the retina and nerve retain their orientation in the chiasm. Crossed fibers from the upper nasal retinal quadrant cross dorsally in the posterior portion of the chiasm; crossed fibers from the lower nasal quadrant tend to cross in the anterior portion of the chiasm (early-crossing fibers). It was previously thought that some of the early-crossing fibers from the inferonasal retina swept into the contralateral optic nerve in a structure known as “Wilbrand’s knee,” although recent experiments suggest that the crossed fibers continue directly into the contralateral optic tract and LGN.11
In 1904 and 1915, Hermann Wilbrand reported his observations, based on two pathologic human specimens after long-standing monocular enucleation, of a bundle of optic nerve fibers arising from the infranasal retina of the good eye, which traveled 1 to 2 mm into the contralateral atrophic optic nerve after entering the optic chiasm to decussate into the contralateral optic tract (Figure 8-6).12 He called these fibers the “knee” of the optic chiasm and theorized that lesions compressing an optic nerve medially, just anterior to the chiasm, would result in a contralateral superior temporal visual field defect due to injury to the “knee fibers” from the contralateral optic nerve. He further theorized that the compression of the ipsilateral nerve would additionally result in an ipsilateral temporal defect or complete blindness. J. Lawton Smith expanded this concept in his popular lectures; he taught that in patients with decreased vision in one eye, the most important part of the workup was to check the other eye’s visual field for an upper temporal defect.”19 This particular combination of visual field loss due to a compression
Figure 8-6. Case E from Wilbrand showing a human chiasm sectioned horizontally after longstanding monocular enucleation of one eye. Nerves are at the bottom, and tracts are on top. The nerve on the right is atrophic following enucleation, showing knee fibers marked K that come from the nerve on the left.
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of the optic nerve–chiasm junction is often referred to as an “anterior chiasmal syndrome”, and the upper temporal defect in the eye contralateral to the lesion is referred to as a “junctional scotoma.”
Recent work suggests that Wilbrand’s knee is actually an artifact of mononuclear enucleation rather than a structural component of normal chiasmal anatomy. In 1997, Jonathan Horton reported a series of experiments in nonhuman primates and humans in which a radioactive tracer was injected into a single eye of both normal nonhuman primates and those that underwent mononuclear enucleation. No evidence of Wilbrand’s knee appeared in normal subjects; the “knee” could, however, be found to form after long-term mononuclear enucleation (more than 6 months). In his anatomic studies in humans, Horton found that at 6 months after enucleation, crossed fibers from the intact eye were drawn closer to the junction of the atrophic optic nerve and the chiasm. At 27 months post-enucleation, a modest Wilbrand’s knee had formed, and by 28 years after enucleation, a well-developed Wilbrand’s knee of 1 to 2 mm could be seen.11
Horton’s work has since been supported by the notable absence of patients developing a junctional scotoma after surgical resection of the optic nerve at the nerve–chiasm junction.14 One possible explanation for the formation of Wilbrand’s knee is that the optic nerve atrophy following enucleation causes the optic chiasm to shrink, thereby shortening the distance traversed by normal decussating fibers. As a result of their extra slack, the fibers gradually herniate into the contralateral optic nerve. The “anterior chiasmal syndrome,” previously interpreted as compression of the “knee” fibers is now speculated to occur from combined compression of the ipsilateral optic nerve and the body of the chiasm.
8-3 TESTS FOR FIELD DEFECTS
Automated threshold perimetry has become the standard visual field testing technique for diagnosis of chiasmal lesions. It affords several advantages, such as objectivity, reproducibility, and capacity for quantitative analysis. While useful, automated visual fields must be carefully interpreted in the context of the patient, and all test parameters, such as fixation losses and false-positive and false-negative responses, need to be carefully considered. In patients with unreliable results from automated perimetry, confrontation testing, tangent screen, or Goldmann perimetry may be preferable. Testing with multifocal visual evoked potentials may provide an objective measure of visual field function.15
Confrontation techniques remain an essential part of evaluating the patient and can reveal clues that suggest the diagnosis of a chiasmal disorder. Such findings include a patient’s missing temporal letters in each eye, color desaturation of the red Amsler grid in the temporal region, and corrected acuity of less than expected. Subtle central bitemporal hemianopia may be revealed by having the patient compare the relative redness of a red object, such as a red mydriatic bottle cap, across the vertical midline while fixating the examiner’s nose at 1 or more meters. Other findings in the physical examination may suggest bitemporal field defects such as chiasmatic post-fixation blindness or hemifield slide phenomenon.16 Chiasmatic post-fixation
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blindness occurs when the patient with bitemporal hemianopia converges his eyes to look at near. The object of interest is at the convergence of the optic axes of the two eyes, and if the optic axes are projected through the object of interest, they form a triangle beyond fixation; the post-fixational triangle is in the temporal field of each eye. Thus, these patients may experience an area of blindness in the post-fixational triangle. Patients experiencing this may report difficulty with precision tasks such as threading needles, and diminished depth perception, or may report that objects disappear in the area behind fixation. Patients with bitemporal hemianopia may also experience hemifield slide phenomenon, a condition caused by the absence of a physiological linkage between their two nasal half fields. The difficulty in maintaining the two half fields juxtaposed is accentuated in the presence of exophoria, esophoria, or hyperphoria, which can respectively produce the intermittent perception of objects appearing to overlap, separate horizontally, or diverge vertically.
8-4 CHIASMAL VISUAL FIELD DEFECTS
Starting at the anterior junction of the chiasm with the optic nerve and continuing along the chiasm, optic tract, geniculate body, optic radiation, and occipital lobe, the hallmark of visual pathway involvement on the visual field is that the defect respects the vertical midline. This means that the defect is clear on one side and either normal or markedly better on the other side. A vertical step of neurologic origin does not slope across the vertical; that would be a sign of a retinal disorder or a disc anomaly. Vertical defects or steps reflecting chiasmal or further posterior visual pathway involvement typically demonstrate the greatest disparity immediately across the midline. On confrontation, the patient notes a distinct difference in the appearance of the stimulus as it immediately crosses the vertical midline. This is best demonstrated by moving the stimulus from the defective field across the midline to the seeing field. The classic presentation of damage to the optic chiasm is a bitemporal defect, but a variety of visual field defects may suggest chiasmal involvement.
1.At the anterior angle of the chiasm, small lesions nasal to an optic nerve at the junction of the nerve and chiasm may produce an ipsilateral monocular temporal scotoma respecting the vertical midline. Harry Moss Traquair, who called it a “junctional scotoma,” first identified this monocular temporal scotoma with careful tangent screen testing.17 It is now referred to as the “junctional scotoma of Traquair” (Figure 8-7).5 Traquair, who practiced prior to the availability of computed tomography, referred to these defects in 1927, saying, “I have termed this type ‘junction’ scotoma on account of the probable situation of the lesion at the junction of nerve and the chiasm.” He accounted for these lesions, theorizing that “[i]f on careful analysis hemianopic features are found, indicating that either the crossed or uncrossed macular fibers are purely or mainly affected, it may be inferred that the lesion is situated at a point where these fasciculi are anatomically separated… .”
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Figure 8-7. (A) Traquair’s illustration of a series of tangent screen visual fields from a patient with a resolving junctional scotoma. (B) Tangent screen visual field demonstrating monocular central temporal defect in the left eye ipsilateral to a pituitary adenoma compressing the junction of left optic nerve and chiasm (junctional scotoma of Traquair). The right eye is normal. (C) Coronal MRI scan demonstrating the pituitary adenoma compressing the junction of the left optic nerve and chiasm causing the visual defect from B.
2.The other junctional scotoma syndrome is an upper temporal visual field defect contralateral to a cecocentral scotoma or large central scotoma incorporating the blind spot or other optic nerve type defect. Prior to Horton’s work on Wilbrand’s knee, the upper temporal defect (scotoma) was attributed to injury to knee fibers that were originating from the contralateral optic nerve. Since Horton, we believe the body of the chiasm and the optic nerve ipsilateral to
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the central defect are compressed. Whatever the anatomical point, one of the most important practical concepts in visual field testing as emphasized by J. Lawton Smith is that in a patient with decreased vision in one eye, extra care should be taken to look for an upper temporal defect in the contralateral eye as this would localize the lesion to the anterior chiasmal region. (See Figure 8-10 for left eye demonstrating a junctional scotoma.)
3.Lesions affecting the body of the chiasm often produce bitemporal hemianopia that may be peripheral, central, or a combination of both with or without splitting of the macula (Figures 8-8 and 8-9). Visual acuity may or may not be affected.5
4.Lesions at the posterior angle of the chiasm typically produce bitemporal hemianopic scotomas. Lesions here may also involve the optic tracts and result in homonymous hemianopia.5,18
5.At the lateral aspect of the chiasm, compression from internal carotid artery aneurysms or other lesions can produce a distinctive pair of field defects.
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Figure 8-8. (A) Humphrey 24-2 visual field OS from patient with a craniopharyngioma compressing the body of the chiasm from below showing marked temporal defect which is densest below with intact foveal sensation. (B) Humphrey 24-2 OD from same patient as in A.
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Figure 8-8 (Continued).
Figure 8-9. Coronal T2-weighted MRI image of patient from Figure 8-8 demonstrating craniopharyngioma distorting the chiasm roughly in the midline.
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The eye ipsilateral to the lateral chiasmal compression has an upper and lower nasal defect and an inferior temporal defect, but the upper temporal field is relatively spared because the fibers from the ipsilateral inferior nasal retina have crossed early or anteriorly in the chiasm and have avoided the compression. The early-crossing fibers from the contralateral eye have crossed already and are exposed to the compression (Figure 8-10).19
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Figure 8-10. (A) Humphrey 24-2 visual field from the left eye of a patient with right lateral chiasmal compression from a meningioma demonstrating subtle upper temporal defect from compression of the early crossing fibers, originating in the left inferior nasal retina, as they cross in the anterior chiasmal region. (B) Humphrey 24-2 visual field from right eye of patient in A. This field demonstrates an upper and lower nasal defect from compression of uncrossed fibers originating in the right temporal retina passing through the chiasm laterally. It also demonstrates relative sparing of the upper temporal quadrant caused by sparing of the fibers from the inferior nasal retinal that have crossed to the left anteriorly at the optic nerve junction and chiasm. (C) Axial T1-weighted MRI with contrast; bold arrow points to enhancing meningioma lateral to chiasm indicated by thin arrow.