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

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Figure 10-9. (A) Automated visual fields showing superior and inferior left paracentral hemianopic scotomas from a 52-year-old woman with a meningioma of the right occipital lobe affecting both upper and lower calcarine areas shown on MRI (B).

Studies using neurosonography and horseradish peroxidase has demonstrated that a 1° strip of cells along the vertical meridian of the dorsal lateral geniculate nuclei represented both ipsilateral and contralateral ganglion cells. In the area of foveal representation, this area increased to 3°. These labeled ganglion cells were found along both the nasal and the temporal rims of the foveola, suggesting bilateral representation.39 Most advocates of the bilateral-representation theory point to surgical cases in which unilateral total occipital lobe removal resulted in a complete homonymous hemianopia with sparing.37-39

Correlation of visual fields and damage to the striate cortex in soldiers with war injuries led to a retinotopic map of the striate cortex that has been the basis of our

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Figure 10-10. (A) Automated visual fields showing superior and inferior mid peripheral scotomas from a 70-year-old woman with probable emboli from recurrent atrial fibrillation to the left superior and left inferior calcarine arteries shown on MRI (B).

thinking since the early 1900s.40,41 The authors of these classic studies assigned 25% of the striate cortex to the central 15° of vision. Early computed tomography studies correlating injury to field loss seem to correlate closely to those figures. However, examination in primates like the macaque monkey suggest that some 15% of central vision is represented by more than 70% of the striate cortex.42 Studies using MRI found a close correlation between the human and the macaque striate cortex.42 These findings compare favorably with estimates that 55% to 60% of striate cortex is devoted to macular vision.43 This has led to the concept of a linear

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Figure 10-11. (A) Automated visual fields showing left inferior midperipheral inferior quadrantic defects from a 43-year-old woman with complicated migraine and infarction of the right anterior occipital region shown on MRI (B).

magnification factor,44 which describes the amount of cortex represented per degree of visual field. This ratio begins at 40:1 and decreases toward the periphery.

Most injuries to the occipital lobe are vascular (see Figures 10-10 through 10-14). The macular vascular supply is primarily conducted by way of the posterior cerebral artery. In about 25% of patients, a supplemental vascular supply is provided by the middle cerebral artery. If the posterior cerebral artery is occluded, the branch from the middle cerebral artery may preserve a part of the macular projection. This is similar in theory to the cilioretinal artery preserving macular vision when the central artery is occluded. As mentioned, the linear magnification factor of the macular projection accounted for the preservation of central vision in only a small area of the striate cortex.

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Figure 10-12. (A) Automated visual fields showing left homonymous hemianopia with macular sparing as seen by preservation of the threshold values to the left of fixation. There is also some preservation of field just to the left of the vertical meridian about 15° above fixation. The patient was able to read without difficulty. The responsible lesion was an infarct seen on MRI (B). The patient noted persistent flashes of light and also saw objects including hands and stools that were not really present.

Conclusive evidence to explain the phenomenon of macular sparing has not yet been put forward. The dense homonymous hemianopia with splitting of fixation is a common form of occipital lobe field defect and usually has a vascular cause. Even if the hemianopia is complete, acuity should remain normal. If acuity is decreased, another cause must be sought. This may represent bilateral, but asymmetric, occipital involvement or disease of the eye itself, such as cataracts or retinal degenerative disease. A bilateral homonymous hemianopia can occur.45,46 When it occurs in the occipital lobes, visual acuity is equal in both eyes. If acuity is not equal, something else is happening, which must be found to explain the discrepancy. In patients who have this sign, the expected site for the lesion is the occipital lobe. A patient with bilateral lesions anywhere else in the radiation would not survive or, at least, would show other defects besides a field defect. As mentioned earlier, one of the causes can be multiple emboli from a mural thrombus of the vertebral basilar system or the heart. Another cause can be sudden and severe anoxia such as might occur with

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Figure 10-13. (A) Automated visual fields showing right superior quadrantanopia with macular sparing, left superior quandrantanopia, left inferior mid peripheral quadrantic loss, and possible peripheral left inferior defects from a 67-year-old woman with bilateral occipital infarcts from an unknown source, presumably cardiac or aortic, shown on MRI (B).

cardiac arrest or drowning. Such patients may have severe loss of visual field and acuity, which may recover some vision after many months.47

There are three varieties of bilateral homonymous hemianopia that can occur. The first type is represented by the patient who says he is blind or so severely impaired visually that he is functionally blind. The patient says that he is blind and acts as if he is blind. The pupils are essentially normal and so is the fundus

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Figure 10-14. (A) Automated visual fields showing primarily right superior quadrantic loss as well as left superior quadrantic loss from a 78-year-old man with bilateral strokes involving both occipital regions shown on MRI (B).

examination, as would be expected. The only objective evidence of the severe visual loss is the loss of the blink reflex to the threat type of field testing. The second type is that found in a patient who has an identical type of field defect but does not admit to having blindness. If the deficit is demonstrated to them, they create an excuse for their lack of visual function—there may be a certain Korsakoff-like quality to their personality. This denial of blindness, referred to as Anton syndrome, probably represents involvement not only of the visual cortex of

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area 17 of Brodmann but also of the association areas. The last variety of bilateral homonymous hemianopia is the most misunderstood. Patients with this type say, and act as if, they are functionally blind. They admit to seeing light. They cannot see the largest letters on the chart. The examiner then logically goes to countingfingers and finally to hand-motion tests for visual acuity. At times, however, the patient appears to identify small test objects correctly, which is inconsistent with his inability to see large test objects or to count fingers. The diagnosis of hysteria or of malingering is often considered at this point. The real answer may be that the tip of the visual cortex has been spared from infarction, leaving a field remnant of only 3° to 5°. A residual field may be too small for the patient to see the entire 20/400 letter “E,” for instance, but he may see a smaller letter if he can find it. In situations where this type of defect is suspected, it may be easier to have the patient hold a card. The proprioceptive effect of holding the card will allow the patient to direct his residual field to the correct place in space, namely, the handheld card. Using his finger as a proprioceptive guide, the patient should move his gaze down the card until his residual field can encompass the appropriate-size letter. This will distinguish the patient with hysteria from the patient with a residual 3° to 5° central field.

10-5-2 Field Defects Unique to the Occipital Cortex. The temporal crescent syndrome is a very rare form of occipital lobe defect.48-50 In each radiation there is an unpaired group of fibers. When these are interrupted, they cause only a monocular defect— probably the only true monocular visual defect behind the chiasm. The fibers of the temporal crescent are not isolated sufficiently as a unit until they reach the anterior visual cortex, so they are not affected individually as a unit anterior to that location. The monocular temporal crescent extends from about 60° out to the peripheral field. This is the part of the field that does not overlap with the other eye. It may either be preserved in the face of an otherwise complete homonymous hemianopia51 (see Figure 10-18) or be lost when the rest of the field is preserved52 (see Figure 10-19). The most anterior portion of the calcarine cortex is where information from the temporal crescent is initially processed. This phenomenon demonstrates the value of obtaining peripheral as well as central fields. If only central fields were obtained, the defect would be missed, and if only peripheral fields were done, the impression would be one of a monocular field defect, and investigation of the cause would be directed erroneously to the particular eye or optic nerve.

The Riddoch phenomenon is a visual field sign that has been ascribed to occipital visual field defects.53 Riddoch believed that patients with severe field loss from occipital lobe involvement perceive form and movement separately. He postulated that perception of movement recovers before perception of form and that this phenomenon was of some prognostic value for recovery of field. The phenomenon is illustrated in the patient with an extensive, dense homonymous hemianopia as a result of an occipital lobe lesion: Such a patient cannot see a large stationary object in the blind field but can see a much smaller object if it is moving. The Riddoch phenomenon was originally described as a sign of a recovering occipital lobe field defect. The patient would perceive movement before light in their peripheral field. This can be best demonstrated with the projection type of perimeter. The patient

perceives the movement of the test light but does not see that same object when projected into that same field without movement. However, others have found that the Riddoch phenomenon is not anatomically specific and can be demonstrated in most field defects using kinetic red stimuli.54,55

Postictal hemianopia is rare, whereas postictal (Todd’s) paralysis is not. When postictal visual loss does occur, the duration varies and may be related to cerebral tumor.56 If the occipital seizures are frequent, affected patients can lose vision or visual field for periods of days.

Transient cerebral blindness after seemingly minor head trauma occurs more frequently in children than in adults.57 It lasts from several minutes to several hours, depending on the degree of trauma, and the patient may have other neurologic deficits. This condition also occurs when there is a history of migraine or epilepsy.58 The latter diagnoses should be kept in mind when there is only minimal trauma.

Cortical blindness has also been reported with ventriculography or with ventricular decompression.59 The exact cause is unknown and, fortunately, the condition is rare. One theory holds that there is a shift of the brain when the cerebrospinal fluid is exchanged for air, causing herniation and compression of the blood supply to the occipital cortex.60,61 More commonly seen now is reversible leukomalacia from various drugs and with severe elevations in blood pressure, especially with eclampsia.62

In multiple sclerosis, a homonymous hemianopia is much rarer than optic neuritis. This is not to say that the retrochiasmal pathway is not frequently involved in this disease—an observation made in 1890 by Uhthoff. However, as mentioned previously, small lesions of the radiation and of the striate cortex may not produce any demonstrable field defect.

A bilateral homonymous hemianopia must be even rarer in multiple sclerosis. In one study of 300 patients, only 4 had a homonymous field defect and only 1 had a bilateral homonymous field defect.63 The incidence of a homonymous field defect in this series was 1.3%. The patients all had multiple sclerosis, diagnosed by other criteria. The site of the lesions causing homonomous hemiaopia in multiple sclerosis may occur anywhere from the optic tracts to the occipital regions.64

Headache can occur in patients with occipital vascular lesions as well as tumors. In one report, the authors commented that headaches occurred more often with a hemianopia in the occipital lobe than in other parts of the radiation. They believed that the headache was caused by irritation of dural branches of the first division of the trigeminal nerve.65

The occipital lobe can be affected by more remote lesions. Frontal tumors can displace the brain posteriorly, compressing the blood supply to the visual cortex as the vessel posterior cerebral arteries cross the tentorial edge. The frontal lobe tumor may have been inconspicuous up to that point, but when an infarction of one of the occipital lobes caused a sudden hemianopia, it became symptomatic. There may be confusion when a brain scan shows two widely separated lesions. These may incorrectly be interpreted as metastatic lesions, and tumor resection will not be indicated. In reality, there is only one tumor in the frontal lobe, and it may be accessible surgically. MRI or CT usually shows the different densities of the lesions and indicates whether they have the same cause. A similar mechanism

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of tentorial herniation with compression of the posterior cerebral arteies can occur from epidural hematoma after trauma.66

A false localizing hemianopia in the chiasmal area may also occur when, distant from the chiasm, obstruction of the aqueduct of Sylvius causes enlargement of the third ventricle. This will, in turn, cause compression of the chiasm and the bitemporal type of defect typical of chiasmal lesions.

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Figure 10-15. (A) Automated visual fields from a 75-year-old woman who noted visual loss after resection of an atrial myxoma, showing apparent superior nasal paracentral loss in the right visual field and apparent inferior temporal paracentral loss on the left. However, tangent screen fields (B) show that there really is a congruous, left inferior homonymous paracentral scotoma. This was due to a right posterior occipital infarct associated with other infarcts on the opposite side seen on MRI (C).

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Figure 10-15. (Continued)

Visual hallucinations, as mentioned previously, can originate in any part of the visual system. They are not necessarily confined to the temporal and occipital lobe areas.14 The explanation accepted generally is that formed and organized hallucinations are attributed to a temporal lobe location, whereas unformed hallucinations originate in the occipital lobe. A classic example of an unformed hallucination of the occipital lobe is the scintillating fortification scotoma in migraine.66

The optokinetic nystagmus response is generally considered to be normal in temporal and occipital lobe lesions associated with a homonymous hemianopia. However, the OKN response can be abnormal in known occipital lobe lesions. However, this more often occurs with a mass lesion, perhaps because tumors are rarely confined to such a small area without involving the parietal lobe (the distance covered by the occipital lobe is only 50 mm).13

Conjugate-gaze deviations in occipital lobe lesions are rarely seen. When they are, they are small and the deviation is toward the side of the lesion or away from the hemianopia. Another explanation for this mild gaze paresis is reticence to look into the hemianopic field defect.

10-5-3 Color Field Defects in the Occipital Lobe. Color used as a reduced stimulus for measuring subtle field defects is well known. However, lack of appreciation of a colored stimulus can take several other forms. It may also be due to a greater effect of the disease on fibers sensitive to color such as is seen in early stages of optic nerve disease. Another form of color defect is the congenital variety, which is seen to varying degrees in about 6% of the male population. This type of color defect persists throughout the entire visual field and should not cause a localized field defect. These defects in color testing are commonly known to any perimetrist. A more rarely encountered form is a color loss secondary to a lesion of the central