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

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FIGURE 3-16A,B. Prism neutralization. (A) Patient with an esotropia. (B) A prism is introduced to direct the image onto the fovea of the left eye, thus correcting, or neutralizing, the deviation.

deviated right eye is now straight and in alignment with the fixation target. Thus, one can place a prism in front of either eye or even split the prisms between the eyes to neutralize a strabismic deviation.

Prism-Induced Strabismus

A prism placed over one eye in a patient with straight eyes will induce a deviation and produce strabismus. A base-in prism induces esotropia, as the target image is displaced nasal to the fovea (Fig. 3-18). Likewise, a base-up prism induces a hypertropia and a base-out prism induces an exotropia.

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FIGURE 3-17A–C. Neutralization of an esotropia by placing the prism in front of the fixing eye. (A) Esotropia with left eye fixing. (B) Prism is placed base out in front of the fixing eye (left eye), which displaces the image temporally off the fovea. The left eye rotates nasally to refixate to the displaced image. As stated by Hering’s law, both eyes rotate in the direction of the apex of the prism. (C) Patient fixing through the prism, left eye. The left eye has deviated nasally to put the image on the fovea. The right eye has moved temporally and is also in alignment with the fixation target.

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FIGURE 3-18A–C. Prism-induced esotropia. Patient with straight eyes and binocular vision is given an esotropia by placing a base-in prism over one eye. (A) Patient orthotropic with images falling on both foveas. (B) Base-in prism is placed before the left eye causing the image to move nasally off the fovea. Patient is fixing with right eye. (C) Patient now fixates with the left eye, viewing through the base-in prism. Left eye moves temporally to place the image on the fovea and, because of Hering’s law, the right eye moves nasally to displace the right retinal image nasally off the fovea.

Prism-Induced Vergence

Normal adult subjects with binocular fusion will see double when a prism is placed in front of one eye. If the prism is relatively small, the patient’s fusional vergence eye movements will be able to realign the eyes to keep the images appropriately placed on the foveas. The prism will initially invoke diplopia and the patient will realign the eyes within a second or two to replace the diplopia with single binocular vision. A base-out prism evokes fusional convergence, a base-in prism causes fusional divergence, and a base-up or base-down prism will evoke fusional vertical vergence. Figure 3-19 shows the steps of prism-induced convergence. A base-out prism placed over one eye will displace the retinal image off the fovea onto temporal retina, inducing an exotropia (Fig. 3-19A,B). The eye behind the prism moves nasally to refixate to the fovea and the fellow eye moves temporally in a version movement (Hering’s law) (Fig. 3- 19B). Diplopia occurs briefly until fusional convergence is used to realign the eyes so retinal images can fall directly on each fovea (Fig. 3-19C,D). The key aspect of the convergence movement is the nasal fusional movement of the eye without the prism (Fig. 3-19C). Note that, after prism-induced strabismus in a patient with fusion, a compensatory vergence movement will occur in the eye without the prism (Fig. 3-19C). Prism-induced strabismus in a patient without fusion results in a version movement of both eyes without a subsequent vergence movement (see Fig. 3-18C).

Fusional Vergence Amplitudes

Vergence movements compensate for phorias and keep the eyes aligned as targets move in depth throughout space. A patient with an exophoria uses convergence; those with esophorias use divergence, and hypertropias are controlled with vertical vergence. Convergence is by far the strongest of the vergence movements and can be strengthened by eye exercises if convergence is ineffective. Divergence is relatively weak and does not significantly improve with eye exercises. The strength of vergence movements can be measured in prism diopters and is called fusional vergence amplitudes.

Fusional vergence amplitudes are measured by inducing a deviation to stimulate a motor fusion to correct the induced deviation. Induce an exodeviation to test convergence (base-out

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FIGURE 3-19A–B. Four steps of prism convergence. (A) Eyes are well aligned in a patient with good fusional convergence. (B) Exophoria is created by introducing a base-out prism in front of the left eye. Patient initially fixates with the left eye, causing a version movement to the right, thus placing the left fovea on the image.

prism), an esodeviation for divergence (base-in prism), and a hyperdeviation for vertical vergence. Start by inducing a small deviation that can be fused and gradually increase the deviation until vision is blurred (blur point), then increase until fusion breaks (break point). A deviation can be induced by placing prisms (usually in the form of a prism bar) over one eye or by

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FIGURE 3-19C–D. (C) Because of Hering’s law, the right eye also rotates and the image is now off the right fovea. To compensate for this, patient exercises fusional convergence and the right eye rotates nasally to put the image on the fovea; this is a vergence movement in distinction to the version movement seen in (B). (D) Patient is once again fusing, using fusional convergence to maintain eye alignment on the fixation target. Note that the eye behind the prism is deviated nasally. The base-out prism actually induces an exophoria, even though the eye behind the prism is nasally deviated and looks esotropic.

PD, prism diopter.

moving the amblyoscope arms off parallel. Measure nearconvergence amplitudes by placing a base-out prism bar over one eye, starting with 4 PD, having the patient fixate on an accommodative target at a distance of 33 cm. Then, move the bar up slowly to increase the base-out prism. The eye behind the prism bar will progressively turn in to converge as the prism is increased. The greatest prism that the patient can fuse is the fusional vergence amplitude. Prisms larger than this will break fusion and one eye will turn out, usually causing diplopia. Have the patient note when the fixation target blurs (i.e., blur point), and when it becomes double (i.e., break point). Table 3-2 shows normal fusion vergence amplitudes based on the break point.

The maximum base-out prism that can be fused is around 30 PD (convergence), the maximum base-in prism that can be fused is 6 to 10 PD (divergence), and the maximal vertical prism that can be fused is usually 2 to 3 PD (vertical vergence). In certain conditions, divergence and vertical vergence fusional amplitudes can be quite large. Patients with congenital superior oblique palsy, for example, can have vertical fusion vergence amplitudes up to 25 to 30 PD.

Types of Convergence

There are various mechanisms of convergence; these include fusional convergence, accommodative convergence, tonic convergence, voluntary convergence, and proximal or instrument convergence.

FUSIONAL CONVERGENCE

Fusional convergence is based on binocular vision. Occluding, or severely blurring the image of one eye, will disrupt fusional convergence; however, convergence mechanisms still function when binocular vision is suspended.

PROXIMAL OR INSTRUMENT CONVERGENCE

This type of convergence is induced by a psychological awareness of an object at near, or when one views an object through an instrument such as a microscope.

Comitant Versus Incomitant Strabismus

Strabismus can be classified into two broad categories: comitant and incomitant. Comitant strabismus is when the deviation measures the same in all fields of gaze. Most types of congenital and childhood strabismus are comitant. With comitant strabismus, both eyes move together equally well and there is no significant restriction or paresis. Comitant strabismus is usually a “good” sign and indicates that the strabismus is not secondary to a neurological problem. Occasionally, however, acquired neurological disease processes, such as early-onset myasthenia gravis, chronic progressive external ophthalmoplegia (CPEO), or even a mild bilateral sixth nerve palsy, can initially present as a clinically comitant strabismus.

Incomitant strabismus means the deviation is different in different fields of gaze. In the vast majority of cases, incomitance is caused by a limitation of ocular rotations secondary to ocular restriction or extraocular muscle paresis. Causes of ocular restriction include a tight or stiff muscle and periocular adhesions to the eye. Muscle paresis can be caused by a lack of innervation (i.e., third, sixth, or fourth nerve paresis), traumatic muscle damage, an overrecessed or lost muscle, or neuromuscular junction disease such as myasthenia gravis.

Figure 3-20 shows an example of an incomitant esotropia secondary to limited abduction of the left eye. When the patient in Figure 3-20 looks to the left, the left eye cannot fully abduct; thus, the right eye overshoots and creates an esotropia (ET) that increases in leftgaze (Hering’s law of yoke muscles). In this example, the limited abduction could be due to either restriction (e.g., a tight left medial rectus muscle or a nasal fat adherence scar to the globe) or paresis (e.g., left sixth nerve palsy or left slipped lateral rectus muscle). Methods for diagnosing restriction and paresis are presented in Chapter 5.

CHAPTER 3: BINOCULAR VISION AND INTRODUCTION TO STRABISMUS 101

FIGURE 3-20. Left lateral rectus paresis. In primary position, there is a moderate esotropia. In right gaze, the esotropia (ET ) diminishes, and in left gaze the esotropia increases. A tight left medial rectus muscle would give the same pattern of incomitance.

Primary Versus Secondary Deviation

Patients with incomitant strabismus secondary to ocular restriction or muscle paresis will show a larger deviation when the eye with limited ductions is fixing (secondary deviation) than when the eye with full ductions fixates (primary deviation); this is in accord with Hering’s law. As shown in Figure 3-21, the primary deviation is small because relatively little innervation ( 1) is needed to keep the eye in primary position when the nonparetic

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FIGURE 3-21A,B. Left sixth nerve palsy. (A) Normal right eye fixating with little effort. Only 1 innervation is needed to put the eye on target; there is a small esotropia of 25 PD. (B) Change of fixation to the left eye. Because the left lateral rectus muscle is weak, it requires 4 innervation to bring the left eye to primary position to view the target. The right medial rectus muscle is the yoke muscle to the weak left lateral rectus muscle, so the right medial rectus muscle also gets 4 innervation. The4 innervation of the normal right medial rectus results in a large esotropia of 50 PD.