Ординатура / Офтальмология / Английские материалы / Handbook of Pediatric Strabismus and Amblyopia_Wright, Spiegel, Thompson_2006

compare agonist and antagonist muscle strength, as well as comparing the muscle strength of fellow eyes, to assess muscle function.

Cycloplegic Refraction

Cycloplegic refraction should be performed on every new strabismus patient. The standard regimen is 1 drop of cyclopentolate 1% and neosynephrine 2.5% in each eye, times two, 5 min apart; then, perform the refraction 30 min after the last drop. In patients with dark eyes, the drops should be repeated three times. Patients with blue eyes, or patients with pigment dilution syndrome such as ocular albinism, should receive one set of drops. Remember that mydriasis does not mean cycloplegia. The mydriatic effect comes on sooner and lasts longer than the cycloplegic effect. If the patient shows varying refractive error during retinoscopy, then it is likely that the patient has only partial cycloplegia and requires more drops. In cases of heavily pigmented eyes or in patients with variable refractions, it may be advisable to have the patient return for a 1% atropine refraction. In these patients, atropine should be given to both eyes twice a day for 3 days before the refraction. (See Chapter 3 for details on cycloplegic agents.)

Fundus Examination (Objective Torsion)

See Chapter 3 and Figure 3-14 for details on fundus examination.

References

1.Bahill AT, Brockenbrough A, Troost BT. Variability and development of normative data base for saccadic eye movements. Investig Ophthalmol Vis Sci 1981;21:116–125.

2.Biedner et al. Stereopsis testing: at the beginning or the end of orthoptic examination. Binoc Vis Q 1992;7:37–39.

3.De Respinis PA, Naidu E, Brodie SE. Calibration of Hirschberg test photographs under clinical conditions. Ophthalmology 1989;96: 944–949.

4.Guyton DL. Exaggerated traction test for the oblique muscles. Ophthalmology 1981;88:1035.

5.Mitchell PR, Wheeler MB, Parks MM. Kestenbaum surgical procedure of torticollis secondary to congenital nystagmus. J Pediatr Ophthalmol Strabismus 1987;24:87–92.

6.Paliaga GP. Linear strabismometric methods. Binoc Vis 1992;7:134– 154.

7.Ruttum MS, Shimshak KJ, Chesner M. Photographic measurement of the angle of strabismus. In: Campos EC (ed) Strabismus and ocular motility disorders. Basingstoke: Macmillan, 1990:155–160.

in younger children with acquired strabismus, but it is usually transient and lasts only 2 to 4 weeks before the diplopia is cortically suppressed. The patient with diplopia will fixate on an object with one fovea, and see a diplopic image of that object that comes from the perifoveal retina of the deviated eye (Figs. 6-1, 6-2). The fovea of the deviated eye is suppressed to avoid simultaneously seeing two different objects, one from each fovea (see below: Confusion). Thus, the patient with one eye fixing on

Perception

FIGURE 6-1. Esotropia with uncrossed diplopia. The image of the skier falls on the fovea of the left eye and on the nasal retina of the deviated right eye. A red filter over the right eye causes the diplopic image from the right eye to be red. Note at the bottom of the figure: the patient perceives the red image from the right eye to be located to the right of the clear image, resulting in uncrossed diplopia.

Patient's

FIGURE 6-2. Exotropia with image falling on the fovea of the left eye and on temporal retina of the right eye, causing crossed diplopia. A red filter over the deviated right eye causes the diplopic image from the right eye to be red. Note at the bottom of the figure: the patient perceives the red image from the right eye to be located to the left of the clear image, resulting in crossed diplopia.

a painting and the deviated eye pointed to a lamp will see two paintings, not a painting superimposed on a lamp. The image from the fixing eye will be in clear focus located directly in front of the patient, while the diplopic image from the deviated eye will appear blurred and off center because it comes from the peripheral retina.

FIGURE 6-3. Patient with a left hypertropia. A red filter over the deviated left eye causes the diplopic image from the left eye to be red. The X projects to the fovea of the fixing right eye and to the superior retina of the deviated left eye. Because the superior retina views the inferior visual field, the red diplopic image in the left eye is seen below the clear image from the right eye.

Esotropia causes the image to fall on the nasal retina of the esotropic eye, which projects temporally and causes uncrossed diplopia because diplopic image is on the same side as the deviated eye (see Fig. 6-1). Exotropia causes the image to fall temporal to the fovea of the exotropic eye, which projects to the nasal field, producing crossed diplopia (see Fig. 6-2). We can remember the s in esotropia means same side diplopia (uncrossed), and the x in exotropia means a cross for crossed diplopia. In cases of vertical strabismus, the hypertropic eye perceives the object as being below the image from the fixing eye (Fig. 6-3).

Aniseikonia is a difference in image size between eyes and is a cause of diplopia. Aniseikonia is usually caused by anisometropia and is treated with spectacles. An acquired retinal image size disparity up to 7% is usually tolerated, but aniseikonia over 10% may result in diplopia.

Confusion

Under rare circumstances, instead of diplopia, patients with acquired strabismus see two different images superimposed on each other, one image from each fovea. If the right eye is looking at a painting and the left eye is pointed at a lamp, the patient with confusion will see the lamp superimposed on the painting. This simultaneous perception from the fixing fovea and the devi-

ated fovea is termed confusion. Most patients with acquired strabismus do not experience confusion because they suppress the foveal area of the deviated eye and see the diplopic image from the peripheral retina. Confusion is exceedingly rare; however, this author has reported a patient with tunnel vision secondary to glaucoma and acquired strabismus who had confusion rather than diplopia.10 The peripheral visual field loss associated with the glaucoma probably forced foveal fixation of the deviated eye. It is likely that suppression of the fovea of the deviated eye is dependent on peripheral retinal stimulation by the diplopic image and, therefore, foveal suppression is not possible when the peripheral field is eliminated.

IMMATURE VISUAL SYSTEM

Sensory adaptations occur when the binocularity is disrupted by strabismus or a blurred retinal image during the first few years of life, usually before 6 years of age. The specific type of sensory adaptation depends on many factors, including the size of the strabismus, whether it is intermittent or constant, the age of onset of the strabismus, and the age when the strabismus is corrected. Once childhood sensory adaptations are acquired, they are usually present throughout the patient’s life. Cortical suppression is a basic mechanism present in virtually all sensory adaptations to strabismus and a unilateral blurred retinal image. Cortical suppression and amblyopia are discussed in Chapter 4. Herein is a discussion of specific patterns of suppression and abnormal binocular vision.

The following discussion of sensory abnormalities presumes that strabismus is the primary event and that the brain develops sensory adaptations in response to the abnormal visual stimulation. In this author’s view, this is probably true for the majority of strabismus cases; however, strabismus can also occur as a secondary consequence of poor binocular fusion. Examples of a primary fusion deficit and secondary strabismus include sensory strabismus (i.e., unilateral congenital cataract) and central fusion loss associated with closed head trauma. It should be pointed out that some would argue that most types of childhood strabismus are a consequence of congenitally abnormal fusion centers within the brain, not motor misalignment degrading binocular fusion. The answer to this controversy— which came first, the strabismus or the sensory fusion abnor-

mality?—remains unanswered. The fact that one can recover excellent binocular fusion and stereoscopic vision with early and aggressive treatment suggests that, at least in some cases, the sensory abnormality is secondary to the strabismus.

Monofixation Syndrome (Peripheral Fusion)

Small-angle strabismus ( 10 prism diopters, PD) or mild to moderate unilateral retinal image blur in young children and infants causes a suppression of the central visual field of the deviated or blurred eye. The small suppression scotoma allows for peripheral fusion (Fig. 6-4). This sensory adaptation, first described by Marshall Parks, is termed the “monofixation syndrome.”3 Suppression is localized to within the central 4° to 5° because the central retina has small receptive fields and high spatial resolution potential; therefore, relatively small differences in image clarity or retinal image position are recognized. In the peripheral fields, however, slight interocular image differences are not detected, as the peripheral retina has large receptive fields and relatively low spatial resolution. Thus, small retinal image discrepancies between the eyes are not disruptive in the peripheral fields, and peripheral fusion occurs. The size of the suppression scotoma is directly proportional to the amount of image blur and size of the strabismus. If the interocular image disparity is too great, even peripheral fusion will be disrupted. Thus, strabismus greater than 10 PD or severe unilateral image blur (e.g., unilateral dense cataract) will disrupt even peripheral fusion. These patients will lack binocular fusion and will not have the monofixation syndrome.

Because patients with the monofixation syndrome have motor fusion, they often have a relatively large underlying phoria in addition to a small tropia, giving rise to the term phoria-tropia syndrome. Patients with monofixation syndrome usually have stereoacuity in the range of 3000 to 70 s arc, and the central suppression scotoma measures between 2° and 5°. The Bagolini striated lens test is a sensory test that presents a linear streak of light to each eye oriented 90° apart and centered on the fixation light (Fig. 6-5). Patients with normal binocular vision describe a cross through the center of a fixation light (Fig. 6-5A). In contrast, patients with the monofixation syndrome will describe a cross with a gap in the center of the line presented to the deviated eye (Fig. 6-5B). The gap represents a central suppression scotoma of the nonfixing eye. It is impor-

FIGURE 6-4A,B. (A) Diagram of monofixation syndrome secondary to a small-angle esotropia. (B) Hypermetropic anisometropia with amblyopia. In both cases, patient perceives a clear single image, as the suppression scotoma eliminates the discrepancy from the esotropia and blurred image, respectively. Because of the suppression scotoma, the patient sees one clear image.

tant to note that as soon as the dominant fixing eye is occluded, the suppression scotoma vanishes and the patient fixes with the fovea (Fig. 6-5C). The suppression scotoma is often referred to as a facultative scotoma, because its presence is dependent upon fixation with the dominant eye. Worth 4-dot testing is another good method to document the monofixation syndrome. Patients with the monofixation syndrome will fuse the near Worth 4-dot

A

B

C

FIGURE 6-5A–C. Monofixation with microtropia and visual perception with Bagolini lenses. (A) Bagolini lenses over right small-angle esotropia and suppression scotoma, right eye. (B) Retinal images from (A). Note the patient’s perception is one continuous line LE, and one line with an interruption in the center RE. (C) Covering the fixing eye (LE) eliminates the suppression scotoma, and the patient sees a single, continuous line from RE.