Ординатура / Офтальмология / Английские материалы / Visual Fields Examination and Interpretation_Walsh_2011
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contralateral pupil. Because there is equal output from the Edinger-Westfall nucleus, this is unlikely and such pupil size inequality has not been reliably seen in optic tract disease. There is the possibility of pupillary size asymmetry if a lesion affecting an optic tract is large enough to affect the sympathetic fibers in the midbrain or if it were to compress the nearby third cranial nerve.
Optic tract lesions can produce specific ophthalmoscopic findings. Because the tract has fibers from both eyes, any retrograde atrophy will be seen in both optic nerve heads.6 The atrophy, however, will be on the temporal side of the ipsilateral eye and on the nasal side of the contralateral eye—which is usually a striking asymmetric type of atrophy. This type of band atrophy can be seen using red-free light7 during ophthalmoscopy or fundus photography. It is also nicely demonstrated by optical coherence tomography either with retinal nerve fiber analysis or by retinal thickness measurements8 (Figure 9-3).
Other associated findings include pyramidal tract signs, as well as hemianesthesia ipsilateral to the hemianopia. These are similar to findings seen in patients with lateral geniculate body visual field defects (see later).
The most common causes of optic tract lesions are pituitary tumors (Figure 9-2), craniopharyngiomas, and meningiomas of the skull base. Aneurysms of the posterior part of the circle of Willis can compress the optic tract. Occasionally, tumors from the medial portion of the temporal lobe compress the tract. Rarely, optic tract neuritis occurs as a result of demyelinating disease9 (Figure 9-4).
Various infections can affect the optic tract including bacterial and fungal abscesses as well as cytomegalovirus and cryptococci.
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Figure 9-3. (A) Automated visual fields from a 30-year-old nurse who developed memory loss and fatigue showing incongruous left homonymous hemianopia. (B) Optical coherence tomography (OCT) showed a pattern consistent with band optic atrophy. (C) MRI showing a craniopharyngioma causing the findings.
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Figure 9-3. (Continued)
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Figure 9-4. (A) Automated visual fields from a 41-year-old man who noted a left homomymous visual field defect to the left 4 years after having had optic neuritis. (B) Computed tomography scan showing a probable demyelinating lesion involving the right optic tract.
9-2 LATERAL GENICULATE BODY FIELD DEFECTS
As stated previously, the optic tract fibers, which rotate nasally 90° and which represent upper retinal fibers (lower field), make their way to the medial part of the lateral geniculate body. Those from the lower quadrants move to the lateral part of the lateral geniculate body. The macular fibers are wedged in between. Although the lateral geniculate body is rarely the site of an isolated field defect, lateral geniculate anatomy allows for lesions affecting it to result in some very interesting visual field defects.
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Of the six layers of the lateral geniculate body, layers 1, 4, and 6 receive crossed retinal fibers from the contralateral eye, whereas layers 2, 3, and 5 receive uncrossed fibers from the ipsilateral eye. Corresponding retinal areas are vertically represented as well and include all six layers.10,11 This gives a three-dimensional representation of the fields in the lateral geniculate body. Because the layers are not exactly alternating and because a lesion could also affects more bands coming from one eye than the other, visual field defects from partial lesions of the lateral geniculate body are not congruous, and they tend to have a sectoral quality.12-15
When the lateral geniculate body is affected, frequently the damage is partial, with some layers being affected more than others16 because two separate arteries supply it. The anterior and lateral aspects of the nucleus and anterior fibers are supplied by the anterior choroidal artery. Occlusion of that artery produces an upper and a lower sector defect (Figure 9-5).
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Figure 9-5. Occlusion of the anterior choroidal artery produces and loss of the upper and lower quadrants, with sparing of the central part of the visual field and is the same to all test objects in this case. (A) Goldmann representation. (B) Automated representation.
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The remainder of the nucleus, which receives primarily macular input, is supplied by the lateral choroidal artery and occlusion of that artery produces a homonymous horizontal “sectoranopia”14,17-19 (Figure 9-6).
These defects are usually incongruous, but congruous lesions have been found in a few cases.15,17,20,21 Lesions of the optic radiations can mimic a geniculate lesion.18 Involvement of the medial portion of the lateral geniculate body produces a congruous homonymous lower quadrantanopia to the opposite side. Similar involvement of the lateral portion produces a congruous homonymous upper quadrantanopia to the opposite side.19
Involvement of the pyramidal tracts nearby the lateral geniculate body may produce associated contralateral weakness. Concomitant effects on the thalamus may produce a hemianesthesia or, on rare occasions, Déjérine-Roussy syndrome (pain, dysesthesia, paresthesia). In addition to atherosclerotic occlusion, the branches of the posterior cerebral and anterior choroidal arteries can be compressed
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Figure 9-6. Occlusion of the lateral choroidal artery produces loss of the central field up to the fixation point and spares the upper and lower quadrants. (A) Goldmann representation. (B) Automated representation.
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as they pass between the hippocampal gyrus and the base of the lateral geniculate body, and these vessels can be compressed by the firm tentorial edge, either by a tumor displacing the brain or by brain swelling from trauma or hypoxia.
REFERENCES
1.Newman SA, Miller NR: Optic tract syndrome: neuro-ophthalmologic considerations. Arch Ophthalmol. 1983;101:1241–1250.
2.Savino PJ, Paris M, Schatz NJ, et al: Optic tract syndrome: a review of 21 patients. Arch Ophthalmol. 1978;96:656–663.
3.Horton JC, Landau K, Maeder P, Hoyt WF. Magnetic resonance imaging of the human lateral geniculate body. Arch Ophthalmol. 1990;47:1201–1206
4.Wernicke C: Ueber hemiopische Pupillen-reaction. Fortschr Med. 1883;1:49–53.
5.Behr C: Die Untersuchungsmethoden, II: die Lehre von Pupillenbewegungen. In: Graefe A, Saemisehe I, eds: Handbuch der gesamtem Augenheilkunde. Leipzig: Engelmann; 1924:115–117.
6.Hoyt WF, Rios-Montenegro EN, Behrens MM, et al: Homonymous hemioptic hypoplasia: fundoscopic features in standard and red-free illumination in three patients with congenital hemiplegia. Br J Ophthalmol. 1972;56:537–545.
7.Hoyt WF, Schlicke B, Eckelhoff RS: Fundoscopic appearance of a nerve-fibre-bundle defect. Br J Ophthalmol. 1972;56:577–583.
8.Vedel-Jensen N: Optic tract neuritis in multiple sclerosis. Acta Ophthalmol. 1959; 37:537.
9.Moura FC, Medeiros FA, Montiero MLR. Evaluation of macular thickness measurements
for detection of band atropy of the optic nerve using optical coherence tomography. Opthalmology. 2007;114:175–181.
10.Minkowski M: Über den Vertauf die endigung und die zentrale Repräsentation von gekreuzten und ungerkreuzten schnerven Fasern bei einigen Saugertieren und beim Menschen. Schweiz. Arch Psychiatr Nervenkr. 1920;6:201–252; 1921;7:268–303.
11.Mackenzie I, Meighan S, Pollock EN: On the projection of the retinal quadrants on the lateral geniculate bodies and the relationship of the quadrants to the optic radiations.
Trans Ophthalmol Soc UK. 1933;53:142–169.
12.Gunderson CH, Hoyt WF: Geniculate hemianopia: incongruous homonymous field defects in two patients with partial lesions of the lateral geniculate nucleus. J Neurol Neurosurg Psychiatry. 1971;34:1–6.
13.Fite DJ: Temporal lobe epilepsy: association with homonymous hemianopsia. Arch Ophthalmol. 1967;77:71–75.
14.Smith JL, Nashold BS, Kreshoan MJ: Ocular signs after stereotactic lesions in the pallidum and thalamus. Arch Ophthalmol. 1961;65:532–535.
14.Shacklett DE, O’Connor PS, Dorwart RH, et al: Congruous and incongruous sectoral visual field defects with lesions of the lateral geniculate nucleus. Am J Ophthalmol.
1984;98:283–290.
16.Lindenberg R, Walsh FB: Vascular compressions involving intracranial visual pathways.
Trans Am Acad Ophthalmol Otolaryngol. 1964;68:677–694.
17.Frisén L: Quadruple sectoranopia and sectorial optic atrophy: a syndrome of the distal anterior choroidal artery. J Neurol Neurosurg Psychiatry. 1979;42:590–594.
18.Carter JE, O’Connor P, Shacklett D, et al: Lesions of the optic radiations mimicking lateral geniculate nucleus visual field defects. J Neurol Neurosurg Psychiatry. 1985;48:982–988.
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19.Helgason C, Caplan LR, Goodwin J, Hedges TR. Anterior choroidal artery-territory infarction. Arch Neurol. 1986:43:681–686.
20.Frisén L, Holmegaard L, Rosencrantz M: Sectorial optic atrophy and homonymous, horizontal sectoranopia: a lateral choroidal artery syndrome? J Neurol Neurosurg Psychiatry. 1978;41:374–380.
21.Donahue SP, Kardon RH, Thompson HS: Hourglass-shaped visual fields as a sign of bilateral lateral geniculate myelinolysis. Am J Ophthalmol. 1995;119:378–380.
10
Retrogeniculate Visual
Field Defects
THOMAS R. HEDGES III, MD
10-1 TESTING FOR RETICULOGENICULATE VISUAL FIELD DEFECTS
Automated perimetry has changed visual field testing considerably in recent years. What was considered an art has become an exercise in interpreting a set of data points obtained mechanically. Automated perimetry saves ophthalmologists time, which ideally should allow for more visual fields to be obtained on patients with unexplained vision loss. However, one must still keep in mind that automated perimetry still depends on the subjective responses from the patient. More important, automated perimetry has made interpretation of visual field defects, especially those due to occipital lesions, more difficult.1 For example, macular sparing may not be reflected, especially with programs limited to the central 24° or 30°. A 10° field may be required to show macular sparing. Also, sparing or involvement of the temporal crescent will not be shown with 24° or 30° visual fields. The limitation of most programs may lead to the appearance of incongruity when in fact the field is indeed congruous. Sometimes, a small homonymous hemianopic scotoma will be detected when one eye is tested but will be completely missed when the other eye is tested, giving the false impression that the visual loss is monocular. This is especially problematic if the patient also falsely interprets his or her homonymous loss of vision as monocular. Such individuals may complain of loss of vision in one eye when in fact it is one half of their visual field that is defective. The strategy of automated testing on either side the vertical and horizontal meridians may lead to the false impression that field defects respect the vertical or horizontal meridian when they do not.
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Automated perimetry should make it possible to test more patients with unexplained vision loss, but all automated visual fields must be interpreted with caution and, when necessary, substantiated with some other method, such as the tangent screen, which remains the most powerful method of detecting the size, shape, and density of visual field defects. Because most ophthalmologists no longer use tangent screen testing, at least an Amlser grid should be used to qualify the nature of a paracentral visual field defect.
10-2 LOCALIZATION AND CONGRUITY OF OPTIC RADIATION AND CALCARINE CORTEX VISUAL FIELD DEFECTS
Localizing the site as well as cause of a lesion in the optic radiations and occipital lobe depends on certain characteristics of the visual field as well as associated neurological signs and symptoms. In one series of 100 consecutive cases of homonymous hemianopia, 24% were due to lesions in the temporal lobe, 33% were due to lesions in the parietal lobe, 39% were due to lesions in the occipital lobe, and the remaining 4% were due to lesions in the optic tract and the lateral geniculate body.2 In a later series of 104 cases, occipital lobe cases accounted for 62%.3 Tumors occurred in 18% of the occipital lobe cases,3 as opposed to only 3% in a previous series.2 There were also differences in the incidence of congruity and in sparing versus splitting. The fact that the investigators used different patient selection techniques may have caused differences in the results. One can conclude that the exact cause and anatomic location may not always be ascertained merely by conducting the field, finding a homonymous hemianopia, and depending on statistical guidelines. In each of the three lobes through which the visual fibers pass, there are not only specific characteristics of the hemianopia but other neurologic signs that may help in localizing the responsible lesion.
A complete homonymous hemianopia has only lateralizing value. Loss of the left half of the field of each eye signifies loss of function of the right half of the visual pathway somewhere behind the chiasm but gives no more information than that. Figure 10-1 shows the perimetric fields of a patient who had a vascular infarction of the left occipital lobe. All this chart discloses, however, is that the right half of the visual pathway is completely interrupted by the lesion. It gives no information as to whether the difficulty lies in the tract, the radiation, or the occipital lobe. Some of the characteristics of hemianopias that have localizing value include congruity and the presence or absence of macular sparing. It should be noted that, with the almost constant use of automated perimetry in current use, many of the subtleties of classic perimetry, either Goldmann or tangent screen, are not usually seen, or they are less apparent.
When judging whether a field defect is congruous or incongruous, the defect must be incomplete. If it is complete, any test object, large or small, will show the same complete, homonymous hemianopic field defect as demonstrated in Figure 10-1. Looking at the peripheral field in Figure 10-2, one’s initial impression might be of “incongruity,” because one half-field is about two times the size of the defect in the other eye. To determine of there is congruity, the field defect must spare some
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Figure 10-1. A right homonymous hemianopia is the same to all test objects; it is absolute. It can be seen in complete lesions of the optic tract, lateral geniculate body, optic radiation, or visual cortex. Under these conditions and with splitting of the macula, there are no distinguishing features to localize the field defect to any one of these anatomical locations. (A) Tangent screen representation. (B) Computerized representation.
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Figure 10-2. Peripheral fields from both eyes were performed with a 1-mm white test object. The homonymous field in the right eye is larger than the field from the left eye and appears to be incongruous. However, this is only apparent; the temporal visual field of the right eye is normally larger than the right nasal visual field. (A) Tangent screen representation. (B) Computerized representation.
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