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

about two thirds of optic radiation lesions, and in less than half of optic tract lesions. However, in this study, only automated and technician Goldmann visual fields were used, again indicating the importance of judging the quality of visual fields with caution.4

Retrochiasmal visual field defects are generally expected to respect the vertical meridian. Occasionally, one encounters a patient whose field is canted several degrees away from the vertical meridian either superiorly or inferiorly. This finding is frequently ignored or explained by a muscle imbalance or a shifting of the patient’s eyes. One observer concluded that the shifting of the vertical hemianopic line was not an artifact but a true finding, that it is unlikely that the developmental process would consistently separate the retina in the same place in everyone, and that some variations of the vertical meridian are likely.5 With automated perimetry, one also finds fields that are shifted slightly into the normal hemifield. This is an artifact of fixation in most cases.

10-3 TEMPORAL LOBE FIELD DEFECTS

The fibers emerging from the ventrolateral portion of the lateral geniculate body form the lower fibers of the optic radiation in the temporal lobe. A lesion in these fibers produces a defect in the upper field. The fibers enter the temporal lobe, turn rostrally, and spread out around the anterior tip of the lateral ventricle, forming Meyer’s loop. This loop of visual fibers varies considerably from person to person. In one relatively recent study, it was determined that there is at least 20 cm from the anterior temporal lobe cortex to the anterior portion of Meyer’s loop.6 In another study, the anterior limit of Meyer’s loop was found to be 24 to 28 mm from the anterior temporal pole and there was involvement of the lower quadrant when resections reached 70 to 79 mm.7 The fibers continue around the lateral aspect of the ventricle and enter the calcarine cortex.

The fibers emerging from the dorsomedial aspect of the lateral geniculate body take a different route in the temporal lobe. They do not spread out but rather travel as a thin bundle medially over the horn of the ventricle and enter the upper portion of the calcarine cortex. These fibers subserve the lower fields and the monocular temporal crescent. They also subserve the central fields and come to lie in the middle third of the radiation. The difference in course, as well as the location of the two groups of fibers, is important in appreciating the characteristic way in which a temporal lobe field defect develops.

The typical field defect caused by a lesion in the temporal lobe is a homonymous, upper altitudinal, incongruous quadrantanopia (see Figure 10-3). This has been called a “pie-in-the-sky” defect. The defect is sector shaped and begins in the upper quadrants. The defect is always densest at the upper vertical meridian.8-10 Because the majority of tumors of the temporal lobe begin in the anterior tip, a patient may have symptoms of temporal lobe disease without interference with the fibers of Meyer’s loop. Repeated experiments measuring visual fields before and after temporal lobectomy have shown that a significant lesion may exist in the anterior tip of the temporal lobe without even the most subtle field defect. When a defect

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does occur, it is densest at the vertical meridian, and the apex of the defect points toward the fixation point (see Figure 10-3).

If the initial test object does not show that the defect reaches the fixation point, smaller or more subtle test objects will enlarge the defect toward fixation. The Chamlin step technique (see Chapter 1) is valuable in situations where the defect is subtle and splits the vertical meridian and, thus, is useful in temporal lobe disease (see Figures 1-19 and 1-20 in Chapter 1). If the Chamlin step is suggestive, but not conclusive, of a defect with small white test objects, the use of red test objects may further enlarge the defect (see Figure 1-21). Because the fibers of Meyer’s loop spread out, the field defect progresses through the upper quadrant of the field in a stepwise fashion.11 The fibers of the lower field, which are in a tight bundle, are affected as a group. The field in the lower quadrant is lost as a unit—a phenomenon that differentiates the defect from one in the upper quadrant, where-the field is lost progressively from the vertical meridian down to the horizontal raphe. The pace of loss of the lower quadrant is different from that of the upper quadrant because of a difference in anatomy, rather than a difference in the growth of the tumor (Figure 10-4).

Most temporal lobe visual field defects are incongruous. The nasal defect tends to be about 15% greater than the temporal defects for all degrees of quadrantanopia.7 One reason for this may be that the fibers leaving the lateral geniculate body rearrange themselves into an incongruous pattern. As the fibers proceed farther into the optic radiation, they rearrange themselves again into a congruous pattern.12 Another possibility is that, when temporal lobe tumors cause incongruous field defects, they do so by pressing medially on the optic tract. Thus, the field defect results more from the tract than from the temporal lobe radiation.

Many field defects in temporal lobe disease have sloping margins, which are indicative of lack of proximity of fibers from corresponding points in the two visual fields in the temporal lobe as opposed to the calcarine cortex, and perhaps also due to the higher incidence of tumors, which cause more diffuse damage than vascular lesions.2,3

Temporal lobe lesions are accompanied by other neurologic deficits. If an infarction of the dominant hemisphere involves the posterior limb of the internal capsule and the temporal isthmus, not only will there be a hemianopia but also agraphia, alexia, hemiplegia, and a supranuclear type of facial weakness. The aphasia may mask some of the other signs, as well as the hemianopia; in that situation, only the threat type of field testing may suggest a defect. If the infarction involves a similar area on the nondominant hemisphere, hemianopia and hemiplegia also occur, as well as anosognosia (the inability to recognize which side of the body is involved).

It is important to elicit other signs of temporal lobe disease when trying to localize a hemianopic field defect that is not entirely diagnostic on its own. For example, if the lesion is limited to the temporal lobe, the optokinetic nystagmus (OKN) response will be normal.13 Hallucinations are not infrequent in temporal lobe lesions and, theoretically, are usually formed; those occurring in the occipital lobe are unformed, as are those seen in the scintillating scotomas of the migraine syndrome. However, visual hallucinations can be produced in any part of the brain.14,15

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Figure 10-4. (A–C) Progression of visual field defects from right, superior, homonymous, sector loss to (B) right, superior, homonymous quadrantanopia to (C) right, homonymous hemianopia in a patient with a progressively growing temporal lobe tumor.

The significance of color hallucinations versus black-and-white hallucinations is even more of a mystery. There has been one report of a man with a temporal lobe tumor who saw his black-and-white television in color. When the tumor was removed, he saw it in black and white again.2 Other symptoms of temporal lobe lesions are olfactory or gustatory hallucinations (uncinate fits), déjà vu phenomena, and psychomotor seizures.

10-4 PARIETAL LOBE FIELD DEFECTS

Most tumors and vascular lesions are rarely limited to just the parietal lobe. Therefore, “typical” parietal lobe field defects are uncommon. The so-called typical parietal lobe field defect is a homonymous hemianopia, with the densest

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Figure 10-6. This homonymous defect from a parietal lobe lesion appears congruous and denser below. However, in this case, the automated field (B) indicates that it may be more incongruous than depicted by the tangent screen field (A).

no increased intracranial pressure, the lesion is probably located in the parietal lobe, especially the angular gyrus of the dominant hemisphere. If only one or two signs are found, the localization of the lesion is not so specific. When a hemianopia and other signs and symptoms are present, they probably signify more extensive involvement of the cerebral cortex.

Nondominant parietal lobe dysfunction may complicate visual field testing in two ways: motor impersistence and the extinction phenomenon. Motor impersistence limits the patient’s ability to maintain fixation. Therefore, it is important, in patients with suspected parietal lobe disease, to take this into account during the field test and to be careful not to question such patients’ behavior. Also, in any patient who clearly has difficulty with fixation, the possibility that they may have nondominant parietal lobe disease should be raised. Suspicions can be confirmed by asking the patient to close the eyes until told to open them. Within seconds, they will open their eyes, even though they admit to understanding the instruction. The defect of motor impersistence is caused by an inability to perform a willed motor act for any length of time, whether it be closing the eyes or fixating steadily on a target. At that point, the perimetrist should try the confrontation fields outlined in Chapter 1. One can alternately use two hands and project a series of fingers rapidly, first into one field and then into another, before the patient changes his fixation. At this time, a dense homonymous hemianopia may be demonstrated that previously had eluded more sophisticated testing because of the patient’s inability to fixate adequately.

The second sign that affects parietal lobe field testing is the extinction phenomenon.19,20 Patients with this sign may not have a true field defect, but they pay no attention to one half of the field when both sides are simultaneously stimulated.

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They are really ignoring the other half of the body image. This occurs also when the hands or legs are simultaneously stimulated by touch. No matter how careful and exhaustive the testing, the defect will not show up, because only one field is tested at a time with the usual techniques. The extinction phenomenon should be considered when no defect is found by the usual means. When a patient is referred from a nonophthalmologist with the diagnosis of a homonymous hemianopia and, after careful routine testing, no suggestion of a field defect is found, simultaneous testing of tactile sensation can establish the apparent visual field loss as the extinction phenomenon, rather than as a true hemianopia.

The localizing value of OKN responses is somewhat controversial. All agree that OKN abnormalities occur in cerebral hemisphere disease. The traditional view is that abnormal OKN responses occur with targets coming out of the hemianopic field of parietal lobe lesions but not with lesions creating similar field defects from the temporal and occipital lobes.21 On the other hand, others have asserted that the OKN response is only of lateralizing significance to one or the other cerebral hemisphere and not to a single lobe of the brain.22 However, many patients with deep lesions affecting the optic radiations have normal OKN, and a normal OKN response does not rule out the parietal location as much as an abnormal response rules it in.

10-5 OCCIPITAL LOBE FIELD DEFECTS

One cannot always differentiate between lesions of the occipital cortex and lesions of the calcarine cortex. Improved techniques of arteriography, combined with magnetic resonance imaging (MRI), have allowed clinicians to identify small vascular occlusions in these areas, previously only implied, and to map the vascular supply to these areas with more accuracy. The terminal branches of the basilar artery are the posterior cerebral arteries. These, in turn, form the circum-mesencephalic segment as it crosses around the midbrain and the tentorial edge to become the internal occipital branch of the medial aspect of the occipital lobe. The internal occipital branch divides into terminal parieto-occipital and calcarine branches.

The calcarine artery, which is the main blood supply to the calcarine cortex, arises on the lateral aspect of the parieto-occipital branch as one of two trunks. The striate area is frequently supplied with additional blood from the posterior temporal and parieto-occipital branches. It is difficult to predict the size of the field defect resulting from an injury of the visual cortex, regardless of its cause. Postmortem23 and refined arteriography24 studies demonstrated collateral circulation to this area, indicating that visual field defects from posterior cerebral artery occlusions are much smaller than one might expect.

The areas usually spared in posterior cerebral artery occlusion are the macular projection and the far periphery. The former receives additional blood from the posterior temporal and angular branches of the middle cerebral artery from the carotid system in over 50% of cases. The peripheral strip is preserved by its proximity to adjacent pial blood supply. The area most consistently lost through posterior cerebral artery occlusion is the paracentral field, which is supplied preponderantly,

if not exclusively, by the posterior cerebral artery and is in the central part of the calcarine cortex. Angiography has demonstrated that the vascular bed of the occipital cortex is perfused not only by the vertebral basilar system but also by the posterior temporal branch of the middle cerebral artery, accounting for a smaller field defect than expected.25-28

There are many causes of the vascular occlusion of one posterior cerebral artery, which, in turn, causes a homonymous hemianopia. The development of a bilateral hemianopia, presumably from bilateral posterior cerebral artery occlusion, is less common but does occur from multiple emboli from a cardiac, vertebral, or basilar arterial source.24 Similar field defects can occur during open-heart surgery, particularly if there is any complication such as hypotension or cardiac arrest, no matter how brief.

Refined angiographic techniques showing the capillary details shed light on why the macular projection in the striate area is preserved in some of these cases. In cases involving avascularity of the anterior striate cortex, as well as of the posterior occipital pole, the central macular projection is involved. If, in another instance, the same avascular anterior striate area had late capillary filling of the occipital pole, there is less involvement of the macular area. Late filling represents collateral filling from the parieto-occipital and posterior temporal branches of the posterior cerebral artery and through posterior temporal and angular branches of the middle cerebral artery.

The anatomy of the visual cortex studied in detail on postmortem specimens has shown variations in the amount of both total visual cortex and exposed visual cortex not buried in the calcarine fissure. An average of 67% of the visual cortex appears to be buried in the calcarine fissure. The deeper areas of the fissure are considered to represent the visual field along the horizontal axis.29

Evaluation of visual fields of patients who had penetrating bullet wounds of the radiation and the visual cortex indicated that the central vision is located in the most posterior tip of the visual striate area and is large in area, covering not only a posterior area but also a posteromedial area. Within the calcarine fissure is the horizontal meridian field, which also is located above and below the fissure. The peripheral field is located anteriorly in the striate cortex. 24,25,30,31

10-5-1 Types of Occipital Cortex Field Defects. The types of field defects seen in the occipital radiation or the striate cortex vary from very small congruous scotomas32 to congruous quadrantanopia and homonymous hemianopia from unilateral occipital lesions (Figures 10-7 through 10-12) and apparent altitudinal hemianopia, severe visual field constriction, and even checkerboard quadrantanopia when there are bilateral lesions33 (Figures 10-13 through 10-19).

Regardless of the type of visual field defect, most lesions are associated with macular sparing from 2° to 10° around the fixation point (see Figures 10-7 and 10-12). Most hemianopic field defects that occur from lesions in the optic tract and optic radiations cut directly through fixation and split the macula and only occasionally spare part of fixation. The method of testing for macular splitting is explained in Chapter 1. False sparing of the macula occurs when fixation is poor or shifts a few degrees. This type of sparing is spurious, because it occurs all along

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Figure 10-7. (A) Automated visual fields showing congruous left inferior quadrantanopia with macular sparing from a 60-year-old man with metastatic carcinoma of the lung to the right occipital lobe shown on MRI (B).

the vertical meridian, not just around fixation. Automated perimetry, especially programs that test the central 30° or 24° of the visual field, frequently give the impression of macular splitting, and careful evaluation of the threshold values may be needed to identify macular sparing (see Figure 10-12).

One explanation for the phenomenon of macular sparing in occipital lesions is bilateral representation of the macula in the cortex. Proponents of unilateral representation point to failure to produce bilateral geniculate degenerative changes after unilateral removal of the cerebral cortex.34 This evidence seems to indicate that there are no crossing fibers. Also, sectioning the corpus callosum causes no

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Figure 10-8. (A) Automated visual field showing congruous right inferior quadrantic scotoma from a 55-year-old man with a meningioma of the right superior occipital lobe shown on MRI (B).

ocular defect,35 indicating that there are no crossing fibers from one geniculate body to the other through the corpus callosum. On the other hand, one patient has been described who had unilateral occipital lobe destruction, producing a complete homonymous hemianopia with macular sparing. After subsequent surgical resection went as far forward as the splenium of the corpus callosum, the defect changed from one of macular sparing to one of macular splitting.36 Another theory of a chessboard type of foveal innervation with ganglion cells projecting to both ipsilateral and contralateral dorsal lateral geniculate bodies from each side of the fovea has been postulated but not substantiated.36