Ординатура / Офтальмология / Английские материалы / Shields Textbook of Glaucoma, 6th edition_Allingham, Damji, Freedman_2010

with superior central nasal step. F: Vertical step (or hemianopic offset).

Figure 5.3 Grayscale of a SITA standard 24-2 achromatic visual field showing superior arcuate defect with corresponding inferior neuro-retinal thinning and retinal nerve fiber layer thinning.

Table 5.1 Differential Diagnosis of Arcuate Scotomas

Chorioretinal lesions

Juxtapapillary choroiditis and retinochoroiditis Myopia with peripapillary atrophy

Retinal pigment epithelium and photoreceptor degeneration Retinal artery occlusions

Optic nerve head lesions

Drusen

Retinal artery plaques

Chronic papilledema

Papillitis

Colobomas (including optic nerve pit)

Anterior optic nerve lesions

Carotid and ophthalmic artery occlusion

Ischemic infarct

Cerebral arteritis

Retrobulbar neuritis

Electric shock

Exophthalmos

Posterior lesions of the visual pathway

Pituitary adenoma

Opticochiasmatic arachnoiditis

Meningiomas of the dorsum sella or optic foramen

Progressive external ophthalmoplegia

Pseudotumor cerebri

Vertical Step

A stepwise defect along the vertical midline, referred to as a vertical step (Fig. 5.2F) or hemianopic offset, is a less common feature of glaucomatous field loss than the nasal step is; it occurs in roughly 20% of cases (27, 28). The mechanism of this field defect is not fully understood, although it may relate

1 - Cellular and Molecular Biology of Aqueous Humor Dynamics Page 167 of 225

to segregation in the optic nerve head of axons from either side of the vertical midline (27). The defect more often appears on the nasal side of the vertical midline (Fig. 5.6). However, healthy eyes have also revealed greater sensitivity temporal to the hemianopic border, and it has been suggested that a small peripheral step at the vertical midline should arouse suspicion of glaucoma only if the defect is located temporally (29). It also has limited diagnostic value because most are associated with other glaucomatous field changes (28), and the main significance of the observation is in distinguishing glaucomatous vertical midline defects from those caused by neurologic lesions.

Generalized and Central Depression of the Visual Field

The increased sensitivity with which newer instruments allow evaluation of vision is changing our understanding of the natural history of progressive visual field loss in glaucoma. Although defects related to loss of retinal nerve fiber bundles are the most familiar visual field changes induced by glaucoma, and central vision is typically one of the last regions to be totally lost, studies have shown mild central and diffuse reduction in the visual field even in the early stages of glaucoma (30, 31, 32, 33, 34 and 35). The mechanism for this is uncertain, although it appears to represent pressure-induced damage with diffuse nerve fiber loss, as evidenced by abnormal light-sense and flicker perimetry, which have been shown to accompany diffuse retinal nerve fiber layer (NFL) loss (33, 34, 36, 37).

Central vision is typically preserved in the early course of glaucoma, but rarely it may be affected by a localized damage involving the fixation point. In these situations, other visual functions, such as visual acuity and color vision, may become abnormal. These central defects should be differentiated from macular disorders.

Although most studies agree that some patients with early glaucoma can have purely diffuse loss in the absence of other causes, other investigators have challenged this concept, suggesting that a generalized depression in glaucoma is rare and that these patients may have other causes for the diffuse loss of perimetric sensitivity, such as media opacity, miosis, or retinal dysfunction (30, 31 and 32, 34, 38, 39, 40, 41 and 42). In any case, the diagnostic value of this finding is currently limited by its nonspecific nature, but it should still be looked for and noted in the course of visual field testing and analysis. Although the measures of generalized reduction in visual function may one day be important in the early detection of glaucoma, they are too inconsistent and nonspecific at present to be of highly significant clinical value. In the future, they may acquire greater diagnostic significance as our knowledge of glaucomatous visual dysfunction expands. The following are some of the perimetric and other measures that can be used to evaluate generalized visual impairment in glaucoma.

Concentric Contraction

Generalized reduction in the visual field may become manifest as a decrease in sensitivity for specific retinal locations or as a concentric constriction of the visual field, both of which precede other detectable glaucomatous field defects in many patients (43, 44). Isopter contraction, as an early field defect of glaucoma, is often more marked in the nasal field, which has been called “crowding of the peripheral nasal isopters” (45).

Enlargement of the Blind Spot

Enlargement of the blind spot, due to depression of peripapillary retinal sensitivity, is also considered to be an early glaucomatous field change. However, it may be seen with other optic nerve or

P.96

retinal disorders. One example has been called “acu te idiopathic blind spot enlargement” and is relate d to multiple evanescent white-dot syndrome and possibly other retinal diseases (46, 47 and 48). Enlargement of the blind spot can also be produced in healthy persons with threshold targets, so that it is not a pathognomonic sign of glaucoma (49). The relative portion of the blind spot depends on the stimulus value and varies with different testing methods. If the temporal margin of the relative blind spot comes close to the corresponding isopter (in kinetic perimetry), the two boundaries may artifactually become confluent, creating false baring of the blind spot. In addition, because the reduced sensitivity of the peripapillary retina is greater in the upper and lower poles, test objects with small stimulus value may cause vertical elongation of the blind spot, which can break through the isopter, causing true baring

of the blind spot (Fig. 5.7).

Figure 5.4 Grayscale of a SITA standard 24-2 achromatic visual field showing an arcuate defect involving the papillomacular nerve fiber bundle. The corresponding optic nerve with extensive temporal thinning and peripapillary atrophy. HRT-II Moorfields regression analysis calling attention to the temporal rim.

Angioscotomata

Angioscotomata are long, branching scotomas above and below the blind spot, which are presumed to result from shadows created by the large retinal vessels. Retinal vessels may

P.97

P.98

have corresponding representation of angioscotomata in the visual cortex (50). Angioscotomata may

1 - Cellular and Molecular Biology of Aqueous Humor Dynamics Page 169 of 225

represent an early glaucomatous field defect, although it is technically difficult to demonstrate and not highly diagnostic (51, 52, 53 and 54).

Figure 5.5 Grayscale of a SITA standard 24-2 achromatic visual field showing a nasal step. Optic nerve demonstrates significant inferior thinning, which is also called to attention by the HRT-II Moorfields regression analysis.

Figure 5.6 Grayscale of a SITA standard 24-2 achromatic visual field showing a vertical step.

Figure 5.7 False baring (A) and true baring (B) of the blind spot. Temporal Sector Defect

Because the retinal nerve fibers nasal to the optic nerve head converge on the disc by a direct route, a

5.8). This defect usually appears later in the course of glaucomatous field loss (55), but can be the presenting visual field defect. With automated perimetry, glaucomatous defects temporal to the blind spot are not uncommon, but usually add significant information beyond findings of central field testing only in patients with late visual field loss (56).

Advanced Glaucomatous Field Defects

The natural history of progressive glaucomatous field loss involves the eventual development of a complete double arcuate scotoma, which coalesces nasally at the horizontal meridian (57) and may extend to the peripheral limits in all areas except temporally. This results in a central island and a temporal island of vision in advanced glaucoma. With continued damage, these islands of vision progressively diminish in size until the tiny central island is totally extinguished, which may occur abruptly. Glaucoma surgery appears to accelerate the loss of the small central island in some patients, possibly because of the sudden change in intraocular pressure (IOP), although this complication does not occur frequently enough to constitute a contraindication to surgery in these patients (58). The temporal island of vision is more resistant and may persist long after central vision is lost. However, it, too, will eventually be destroyed if the glaucoma is not controlled, leaving the patient with no light perception.

Figure 5.8 Grayscale of a SITA standard 24-2 achromatic visual field showing a temporal wedge defect. Visual Field Changes in Normal-Tension Glaucoma

The nature of visual field defects may be influenced by the IOP, although reports on this are somewhat

1 - Cellular and Molecular Biology of Aqueous Humor Dynamics Page 173 of 225

conflicting. In one study of patients with chronic open-angle glaucoma (COAG) who had early visual field loss, persons with diffuse depression had higher pressures than those with localized defects did (59) (Fig. 5.9). In addition, in some studies patients with COAG whose IOP has never exceeded approximately 21 mm Hg, commonly referred to as normal-tension (or low-tension) glaucoma, had scotomas with steeper slopes, greater depth, and closer proximity to fixation, compared with patients with COAG who had higher IOPs (60, 61). In other studies, however, these two groups did not differ significantly when the same degree of optic nerve damage was present (62, 63). Another study of normal-tension and high-tension glaucoma patients whose automated visual fields were matched to within a 0.3-dB mean deviation (explained later) revealed no significant difference in focal defects in the overall field or superior hemifield, but did show significantly more localized loss in the inferior hemifield among the normal-tension patients, supporting the hypothesis of a vascular mechanism in that group (64).

P.99

Figure 5.9 Grayscale of a SITA standard 24-2 achromatic visual field showing a paracentral defect from a patient with low-tension glaucoma. The optic nerve photograph demonstrates a corresponding notch inferiorly.

One study investigated the effect of trabeculectomy on the rate of visual field progression in patients with normal-tension glaucoma. The authors concluded that surgical lowering of IOP resulted in a decreased rate of visual field loss in the operated eye (65).

The Collaborative Normal-Tension Glaucoma Study investigators also concluded that IOP reduction decreases glaucoma progression in normal-tension glaucoma (66).

Visual Field Changes with Acute Pressure Elevation

The preceding discussions have dealt with field changes that are associated primarily with chronic forms of glaucoma. When the IOP elevation is sudden and marked, as in acute angle-closure glaucoma, various associated field changes have been reported, including general depression, early loss of central vision, arcuate scotomas, and enlargement of the blind spot (67). After the acute attack is brought under control, the fields return to normal in some patients, but other patients may have reduced color vision, generalized decreased sensitivity, or constriction of isopters, especially superiorly (68).

When the IOP is artificially elevated, by compression of the globe or administration of topical steroids, typical glaucomatous field defects or constriction of central isopters occur in some eyes (69, 70, 71, 72, 73, 74 and 75). The changes are reversible when the IOP returns to normal and are dependent on the

1 - Cellular and Molecular Biology of Aqueous Humor Dynamics Page 174 of 225

ocular perfusion pressure (73, 74, 76). This response to artificial pressure elevation is said to occur more commonly in patients with glaucoma (69, 70, 76)—esp ecially normal-tension glaucoma (67)— although one study found no difference between patients with and without glaucoma (71).

Correlation between Optic Nerve Head and Visual Field Defects

In most patients with glaucoma, clinically recognizable disc changes precede detectable field loss, and the presence or absence of glaucomatous field defects can usually, but not always, be predicted from the appearance of the optic nerve head (77, 78, 79, 80, 81 and 82). Quigley and coworkers (83, 84) attempted to correlate axon loss in the optic nerve head with visual field defects. Although limited by small sample size, their work suggested that not only does nerve fiber loss occur before reproducible field defects in some patients with elevated IOP, but the extent of axonal loss may be much greater than the corresponding visual field change. With standard perimetric techniques, 25% to 35% of the retinal ganglion cells may be lost in an eye with a normal field by the time reproducible early field defects are found (85), and 10% or fewer axons may remain by the stage of severe field loss (83). When correlating retinal ganglion cell atrophy with automated perimetry in patients with glaucoma, a 20% loss of cells, especially large ganglion cells in the central 30 degrees of the retina, correlated with a 5-dB sensitivity loss (discussed later), whereas a 40% loss corresponded with a 10-dB decrease, and some ganglion cells remained in areas with 0-dB sensitivity (84).

The nature of optic nerve head cupping can also be used to predict the type (in addition to the presence) of field loss. Extensive or focal absence of neural rim tissue, especially at the inferior or superior poles, is the most reliable indicator of visual field disturbance and is usually associated with a field defect in the corresponding arcuate area (79, 86, 87, 88 and 89). In some eyes, field loss may occur before the pallor reaches the disc margin (86), and unusual cases have been reported with field damage despite round, symmetric cups (79). Quantitative measures of the retinal NFL also correlate with the visual field loss in patients with glaucoma (90).

The ability to predict impending glaucomatous visual field loss by the appearance of the optic nerve head is less accurate than correlating disc damage with established field loss. No single parameter or combination of parameters in glaucomatous optic atrophy is totally satisfactory for this purpose. The parameters that correlate best with visual field loss are magnification-corrected measurements of neuroretinal rim area and defects in the retinal NFL (91, 92, 93, 94, 95, 96, 97, 98 and 99). Diffuse structural changes in the optic nerve head or retinal NFL are more often associated with diffuse depression of visual function, whereas localized changes correlate more with localized visual field changes (98). In some cases, the early field loss associated with retinal NFL defects can be detected with automatic perimetry when it has been missed with manual perimetry (100, 101).

P.100

The correlation between optic nerve head and visual field defects in glaucoma is close enough to prompt a search for other underlying disease processes, such as neurologic disorders, if a correlation is not found. Nevertheless, the absence of a perfect correlation indicates that both disc and field examinations are essential in managing the glaucoma patient (102). In general, optic nerve head and retinal NFL changes have their greatest value in the early stages of glaucoma, whereas progressive visual field loss becomes the more useful guide to therapy in advanced cases (77, 103).

BASIC PRINCIPLES OF VISUAL FIELD TESTING Stimuli

The typical stimuli used in clinical perimetry are spots of light of various predefined combinations of diameter and intensity projected on the background. The visibility of the stimulus also depends on how far the eye is positioned from the screen and the brightness of the background. The other factors affecting perception of the stimulus include the length of time the stimulus is presented, the color of the stimulus and the background, whether kinetic or static techniques are used, and the condition of the eye and the patient.

The absolute light intensity is measured in units of luminance, called apostilbs, but the measured light sensitivity is expressed in logarithmic units referred to as decibels (dB), which provides a more linear