Ординатура / Офтальмология / Английские материалы / Handbook of Pediatric Strabismus and Amblyopia_Wright, Spiegel, Thompson_2006
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11.Chrousos GA, O’Neill JF, et al. Accommodative deficiency in healthy young adults. J Pediatr Ophthalmol Strabismus 1988;25: 176–179.
12.Costenbader FD. The physiology and management of divergent strabismus. In: Allen JH (ed) Strabismic ophthalmic symposium, vol I. St. Louis: Mosby, 1950:349.
13.Duane A. Studies in monocular and binocular accommodation with their clinical applications. Am J Ophthalmol 1922;5:865–877.
14.Edelman PM, Murphree AL, Brown MH, Wright KW. Consecutive esodeviation . . . then what? Am Orthopt J 1988;38:111–116.
15.Freeman RS, Isenberg SJ. The use of part-time occlusion for early onset unilateral exotropia. J Pediatr Ophthalmol Strabismus 1989;26: 94.
16.Hardesty H. Management of intermittent exotropia. Binoc Vis Q 1990;5:145.
17.Hardesty HH, Boynton JR, Keenan P. Treatment of intermittent exotropia. Arch Ophthalmol 1978;96:268.
18.Henderson JW, Iacobucci I. Occlusion in the pre-operative treatment of exodeviations. Am Orthopt J 1965;15:42.
19.Hermann JS. Surgical therapy for convergence insufficiency. J Pediatr Ophthalmol Strabismus 1981;18:28.
20.Hiles DA, Davies GT, Costenbader FD. Long-term observations on unoperated intermittent exotropia. Arch Ophthalmol 1968;80: 436.
21.Hunter DG, Ellis FJ. Prevalence of systemic and ocular disease in infantile exotropia: comparison with infantile esotropia. Ophthalmology 1999;106:1951–1959.
22.Kushner BJ. Exotropic deviations: a functional classification and approach to treatment. Am Orthopt J 1988;38:81–93.
23.Mazow ML, Musgrove K, Finkelman S. Acute accommodative and convergence insufficiency. Am Orthopt J 1991;41:102–109.
24.Mazow ML. The convergence insufficiency syndrome. J Pediatr Ophthalmol Strabismus 1971;8:243–244.
25.Moore S. The prognostic value of lateral gaze measurements in intermittent exotropia. Am Orthopt J 1969;19:69.
26.Nawratzi I, Jampolsky A. A regional hemiretinal difference in amblyopia. Am J Ophthalmol 1958;46:339.
27.Parks MM. Comitant exodeviations in children. In: Strabismus symposium, New Orleans Academy of Ophthalmology. St. Louis: Mosby, 1962:45.
28.Parks MM. Cocomitant exodeviations. In: Ocular motility and strabismus. Hagerstown: Harper & Row, 1975:113–122.
29.Pratt-Johnson JA, Barlow JM, Tillson G. Early surgery in intermittent exotropia. Am J Ophthalmol 1977;84:689.
30.Pratt-Johnson J, Wee HS. Suppression associated with exotropia. Can J Ophthalmol 1969;4:136.
31.Raab EL, Parks MM. Recession of the lateral recti: early and late postoperative alignments. Arch Ophthalmol 1969;82:203.
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32.Richard JM, Parks MM. Intermittent exotropia. Surgical results in different age groups. Ophthalmology 1983;90:172.
33.Scott WE, Keech R, Mash J. The postoperative results and stability of exodeviations. Arch Ophthalmol 1981;99:1814.
34.von Noorden GK, Brown DJ, Parks M. Associated convergence and accommodative insufficiency. Doc Ophthalmol 1973;34:393–403.
35.von Noorden GK. Resection of both medial rectus muscles in organic convergence insufficiency. Am J Ophthalmol 1976;81:223.
36.von Noorden GK. Some aspects of exotropia. Presented before meeting of the Wilmer Residents’ Association, Johns Hopkins Hospital, April 26, 1966.
37.von Noorden GK. Divergence excess and simulated divergence excess: diagnosis and surgical management. Ophthalmologica 1969;26:719.
38.von Noorden GK. Binocular vision and ocular motility: theory and management of strabismus. St. Louis: Mosby, 1985.
39.Wiggins RE, von Noorden GK. Monocular eye closure in sunlight. J Pediatr Ophthalmol Strabismus 1990;27:16.
40.Wright KW, De Juan E. Patch test with and without 3.00 near add. Wilmer Eye Institute, Johns Hopkins Hospital, 1981 (unpublished data).
41.Wright KW, Min BM, Park C. Comparison of superior oblique tendon expander to superior oblique tenotomy for the management of superior oblique overaction and Brown’s syndrome. J Pediatr Ophthalmol Strabismus 1992;29(2):92–97.
9
Alphabet Patterns and
Oblique Muscle
Dysfunctions
Kenneth W. Wright
In this chapter, A- and V-pattern strabismus and oblique dysfunction are discussed, including management strategies.
Under the category of A- and V-patterns, special subtypes are described. The section on oblique dysfunction includes the following: head tilt test, inferior oblique paresis and inferior oblique overaction, superior oblique paresis and superior oblique overaction, and Brown’s syndrome.
A- AND V-PATTERNS
A significant difference in the horizontal deviation from upgaze to downgaze is described as an A- or V-pattern. An A-pattern is described as more divergence in downgaze versus upgaze of at least 10 prism diopters (PD), whereas a V-pattern is increasing divergence in upgaze versus downgaze by 15 PD or more. A- and V-patterns are often a result of oblique muscle overaction or oblique muscle paresis. Other less common causes include nerve misdirection such as Duane’s syndrome, ectopic muscle course with ectopic muscle pulleys, and a rotated orbit associated with craniofacial abnormalities.5,6,29 Examples of strabismus patterns (1 through 5) follow.
Example 1.
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A-pattern |
V-pattern |
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XT A-pattern |
ET A-pattern |
XT V-pattern |
ET V-pattern |
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Upgaze |
XT 10 |
ET 30 |
XT 30 |
ET 10 |
Primary position |
XT 20 |
ET 20 |
XT 20 |
ET 20 |
Downgaze |
XT 30 |
ET 10 |
XT 10 |
ET 30 |
XT, exotropia; ET, esotropia.
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A- and V-Pattern Subtypes
Look critically at the type of pattern: is it symmetrical or does the change in horizontal deviation occur more in upgaze or downgaze? This is important to know, as the configuration or subtype of the A- or V-pattern can indicate an identifying etiology and can influence the surgical plan. For example, a V-pattern consisting of convergence in downgaze without significant change in horizontal deviation from primary position to upgaze is highly suggestive of a bilateral superior oblique palsy. Listed below are subtypes of A- and V-patterns in which the change in horizontal deviation is asymmetrical.
V-PATTERN SUBTYPES
Y-PATTERN
The Y-pattern is a V-pattern subtype with divergence occurring in upgaze and little change in the horizontal deviation between primary position and downgaze. This pattern is highly suggestive of bilateral inferior oblique overaction, which is often associated with infantile esotropia and may also be seen with intermittent exotropia. Y-pattern can also be seen in patients with Brown’s syndrome, Duane’s syndrome with upshoot, and rarely congenital aberrant innervation of the lateral rectus muscle with the superior rectus nerve (see Example 2).
Example 2.
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ET Y-pattern |
XT Y-pattern |
Upgaze |
ET 10 |
XT 30 |
Primary position |
ET 25 |
XT 15 |
Downgaze |
ET 30 |
XT 10 |
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ARROW PATTERN
Another V-pattern subtype is convergence that largely occurs between primary position and downgaze. This author has termed this pattern “arrow” pattern. The presence of an arrow pattern and extorsion in downgaze is virtually diagnostic for bilateral superior oblique muscle palsy. The lack of abduction and intorsion in downgaze because of weak superior oblique muscles allows unopposed adduction and extorsion by the inferior recti muscles (see Example 3).
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Example 3. |
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ET Arrow Pattern |
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Upgaze |
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Ortho |
Primary Position |
ET 5 |
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Downgaze |
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ET 20 |
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A-PATTERN SUBTYPE
LAMBDA PATTERN
The lambda pattern, an A-pattern subtype, is characterized by a divergence in downgaze without much change in the horizontal deviation from primary position to upgaze. A lambda pattern is most frequently associated with bilateral superior oblique overaction. Overrecessed or slipped inferior rectus muscles will also cause an A-pattern lambda subtype with apparent superior oblique muscle overaction. In contrast, inferior oblique muscle underaction causes an A-pattern with most of the horizontal change as convergence in upgaze (see Example 4).
Example 4.
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XT lambda pattern |
Lambda pattern |
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Upgaze |
XT 15 |
Primary Position |
XT 20 |
Downgaze |
XT 35 |
X-PATTERN
An X-pattern occurs when there is divergence in upgaze and divergence in downgaze, which can occur without a specific cause. Patients with long-standing large-angle exotropia will frequently show an X-pattern, presumably caused by a tight contracted lateral rectus muscle. As the eye adducts against the tight lateral rectus muscle, it acts as a leash and produces lateral forces. If the eye then rotates up or down the tight lateral rectus slips above or below the eye and pulls the eye up and out, or down and out, respectively. This leash effect of the lateral rectus is also seen in Duane’s syndrome, usually type III, with both an upshoot and downshoot present on attempted adduction. Lateral rectus recessions reduce the X-pattern associated with exotropia, and an ipsilateral lateral rectus recession with a Y- split works well to reduce the vertical overshoot and X-pattern associated with Duane’s syndrome type III29 (see Example 5).
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Example 5. |
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XT X-Pattern |
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Upgaze |
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XT40 |
Primary position |
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XT30 |
Downgaze |
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XT40 |
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Treatment of A- and V-Patterns
A- and V-patterns with minimal or no oblique overaction can be managed by offsetting, or transposing, the horizontal rectus muscles superiorly or inferiorly. Transpose the medial recti insertions toward the apex of the pattern (up for an A-pattern and down for a V-pattern) and the lateral recti insertions to the wide part of the pattern (down for an A-pattern and up for a V- pattern) (Fig. 9-1). An A-pattern exotropia, for example, can be treated by recessing both lateral rectus muscles and transposing them inferiorly (Fig. 9-2). Vertical transposition of horizontal muscles in the treatment of A- or V-patterns changes vector forces and muscle tension as the eyes rotate up and down. For example, when the medial recti are infraplaced for a V-pattern, they gain increased function as the eyes rotate up, thus collapsing the V-pattern. Conversely, when the eyes rotate down, the infraplaced medial rectus muscles slacken, resulting in divergence of the apex of the V-pattern. One-half-tendon-width
FIGURE 9-1. Direction to transpose the rectus muscles to correct for A- and V-patterns. Left diagram: transposition for a V-pattern, with the lateral rectus muscles moved up and medial rectus muscles moved down. Right diagram: transposition for an A-pattern, with the medial rectus muscles moved up and the lateral rectus muscles moved down. The medial rectus is moved toward the apex of the A or V and the lateral rectus is moved away from the apex of the A or V. This transposition holds true whether the muscles are recessed or resected.
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FIGURE 9-2. Drawing of a one-half-tendon-width inferior transposition of the lateral rectus muscle with recession for an A-pattern associated with an intermittent exotropia. A Insertion to limbus distance. B Recession measured from the insertion.
(5 mm) of vertical displacement results in approximately 15 PD of pattern correction. A full-tendon-width vertical displacement results in approximately 25 PD of correction and is reserved for extremely large A- or V-patterns. Vertical transposition of a horizontal rectus muscle by one full-tendon-width reduces the vector forces at the horizontal plane and, in this author’s opinion, often results in unpredictable horizontal alignment. For example, a full-tendon-width infra-placement of the lateral rectus muscles for an A-pattern would predispose to an overcorrection (esotropia) in primary position. This author rarely performs a horizontal rectus muscle transposition more than one-half tendon-width (5 mm) except in cases of a large A- or V- pattern associated with craniofacial disorders or absent muscles. Monocular supraplacement of one rectus muscle and infraplacement of the partner antagonist muscle can be used to correct an A- or V-pattern in a patient with amblyopia to avoid surgery on the only good eye. Monocular A- or V-pattern horizontal muscle offsets can cause significant torsional changes and should be done only on amblyopic eyes in patients with poor binocular fusion to avoid inducing torsional diplopia. Thus, monocular horizontal offsets can be used to correct torsional diplopia.
In cases with significant inferior or superior oblique overaction and an A- or V-pattern, the appropriate oblique muscles should be weakened rather than performing a horizontal rectus muscle transposition. An exception exists for patients with
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superior oblique overaction and binocular fusion. These patients are at risk for developing cyclovertical diplopia after superior oblique tenotomy.23 Patients with binocular fusion and mild superior oblique overaction are best treated with transposition of the horizontal recti rather than a superior oblique tenotomy. Another surgical option for the fusing patient is a controlled tendon elongation procedure, such as the Wright superior oblique tendon expander or a split-tendon elongation. For large A- and V-patterns ( 25 PD) with 3 or more oblique overaction, consider combining oblique weakening with a half-tendon- width horizontal rectus muscle transposition.
OBLIQUE DYSFUNCTION
Clinical Evaluation of Oblique Dysfunction
When an oblique muscle overacts or underacts, all three functions of the muscle are involved: torsional, vertical, and horizontal. Clinical quantification of oblique dysfunction, however, is primarily based on the vertical hyperor hypofunction seen on version testing. To assess oblique function, move the eye under examination into adduction and make an observation. Then move the eye into the field of action of the muscle: adduction and elevation for the inferior oblique muscle, and adduction and depression for the superior oblique muscle. The amount of overaction or underaction can be graded on a scale of 1 to4 for overaction and 1 to 4 for underaction. A measurement of 1 overaction is recorded if there is no hypertropia with horizontal versions, but there is slight overaction when the eye is moved into the field of action of the oblique muscle vertically. With 2 overaction, there is a slight hypertropia in horizontal gaze, and with 3 overaction, there is obvious hypertropia on direct horizontal gaze. In 4 overaction, there is a large hypertropia in horizontal gaze with an abduction movement as the eye moves vertically into its field of action. Figure 5-3 in Chapter 5 shows degrees of inferior oblique overaction on version testing. The amount of A- or V-pattern and amount of fundus torsion are additional parameters to help quantitate the amount of oblique dysfunction.
When evaluating oblique dysfunction, the abducting eye should be fixing so the adducting eye is free to manifest oblique dysfunction. For example, when the right inferior oblique is
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being evaluated, a version movement to the left is directed, the right eye is partially covered, and the right eye is observed behind the cover for an upshoot (see Chapter 5, Fig. 5-4). Discussion of the characteristics of individual oblique muscle dysfunctions follows.
Primary Oblique Overaction Versus Paresis
Overaction of an oblique muscle can be primary (i.e., unknown etiology) or can be secondary to a muscle paresis. Primary oblique muscle overaction is commonly found in association with A- and V-pattern horizontal strabismus. One possible etiology for what appears to be primary oblique muscle overaction is ectopic location of rectus muscles and their pulleys.5,6 A transient congenital oblique muscle paresis could also cause secondary overaction of its antagonist muscle. A congenital superior oblique paresis, for example, produces ipsilateral inferior oblique overaction. Oblique overaction can also be caused by paresis of its yoke vertical rectus muscle of the contralateral eye (Hering’s law of yoke muscles). For example, a left inferior rectus paresis causes apparent overaction of the right superior oblique muscle and is best observed when the patient fixes with the paretic left eye, down and in abduction.
In general, acquired oblique muscle paresis is associated with underaction of the agonist and with relatively mild overaction of the antagonist oblique muscle. Congenital and longstanding oblique muscle paresis are usually associated with minimal superior oblique underaction and significant overaction of the antagonist oblique muscle. The head tilt test, described below, is used to distinguish primary oblique dysfunction from oblique dysfunction secondary to a vertical or oblique muscle paresis. A positive head tilt test is a strong indication that there is a vertical rectus or oblique muscle paresis whereas a negative head tilt usually indicates a primary oblique overaction. If the vertical deviation changes by more than 5 PD on right tilt versus left tilt, then the head tilt test is said to be positive. If there is no significant difference in the deviation (5 PD or less) from right tilt to left tilt, then the head tilt test is said to be negative.
BIELSCHOWSKY HEAD TILT TEST
Tilting the head stimulates the utricular reflex and invokes torsional eye movements to correct and maintain the appropriate
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retinal orientation. A tilt right, for example, invokes intorsion of the right eye and extorsion of the left eye. The intortors are the superior oblique and the superior rectus muscles, and the extortors are the inferior oblique and the inferior rectus muscles. This arrangement keeps vertical forces balanced during the head tilt. If one of the torsional muscles is paretic, then there will be an imbalance of vertical forces and a vertical deviation will occur on head tilt testing. Figure 9-3 demonstrates this concept for a right superior oblique paresis. As the head tilts to the right, the right superior oblique and right superior rectus contract to intort the right eye. Because the superior oblique is paretic, the superior rectus has unopposed vertical force and elevates the eye, creating an increasing right hyperdeviation on head tilt to the right.
The head tilt test is used in patients with a vertical deviation to determine if either a vertical rectus or oblique muscle is paretic. When a patient presents with a vertical deviation, first perform the head tilt test to see if a paretic muscle is present. If the head tilt test is positive ( 5 PD difference in right tilt vs. left tilt), then it is likely there is a vertical rectus or oblique muscle paresis. To determine which muscle is paretic, measure the deviation in sidegaze and use the three-step test as described next.
FIGURE 9-3. Diagram of a right superior oblique paresis with a positive head tilt in tilt right. As the head tilts to the right, the left eye extorts and the right eye intorts. The extorters of the left eye are the inferior rectus and the inferior oblique. Their vertical functions cancel each other, so there is no vertical overshoot. The intortors of the right eye are the superior rectus (SR) and superior oblique (SO) muscles. Because the right superior oblique is paretic, the elevation effect of the superior rectus is unopposed, and a right hypertropia occurs on tilt to the right.
