Ординатура / Офтальмология / Английские материалы / Handbook of Pediatric Strabismus and Amblyopia_Wright, Spiegel, Thompson_2006
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esotropia and, after 2 years of age, will develop exotropia. This theory has not been borne out, however, as many infants with unilateral visual loss develop exotropia. Surgery for sensory esotropia is a recession of the medial rectus muscle and a resection of the lateral rectus muscle of the blind eye.
References
1.Aiello A, Wright KW, Borchert M. Independence of optokinetic nystagmus asymmetry and binocularity in infantile esotropia. Arch Ophthalmology 1994;112:1580–1583.
2.Archer SM, Sondhi N, Helveston EM. Strabismus in infancy. Ophthalmology 1989;96:133–137.
3.Arthur BW, Smith JT, Scott WE. Long-term stability of alignment in the monofixation syndrome. J Pediatr Ophthalmol Strabismus 1989;26:224–231.
4.Baker JD, Parks MM. Early onset accommodative esotropia. Am J Ophthalmol 1980;90:11.
5.Birch E, Stager D, Wright K, Beck R. The natural history of infantile esotropia during the first six months of life. J AAPOS 1998;2:325– 329.
6.Birch EE, Gwiazda J, Held RR. Stereo acuity development of crossed and uncrossed disparities in human infants. Vision Res 1982;22:507.
7.Birch EE, Petrig BL. FPL and VEP measures of fusion, stereopsis, and stereo acuity. Technical digest series. Noninvasive assessment of the visual system. Washington, DC: Optical Society of America, 1994.
8.Birch EE, Stager DR, Berry P, Everett ME. Prospective assessment of acuity and stereopsis in amblyopic infantile esotropes following early surgery. Investig Ophthalmol Vis Sci 1990;31:758–765.
9.Birch EE, Stager DR, Everett ME. Random dot stereo acuity following surgical correction of infantile esotropia. J Pediatr Ophthalmol Strabismus 1995;32:231–235.
10.Birch EE, Stager DR. Monocular acuity and stereopsis in infantile esotropia. Invest Ophthalmol Vis Sci 1985;26:1624–1630.
11.Birch E, Fawcett S, Stager DR. Why does early surgical alignment improve stereo acuity outcomes in infantile esotropia? J Am Assoc Pediatr Ophthalmol Strabismus 2000;4(1):10–14.
12.Braddick O, et al. Cortical binocularity in infants. Nature (Lond) 1980;288:363–365.
13.Cahill M, Walsh J, McAleer A. Recurrence of cyclic esotropia after surgical correction. J Am Assoc Pediatr Ophthalmol Strabismus 1999;3(6):379–380.
14.Chin NV, Gold AA, Breinin GM. Iris cysts and miotics. Arch Ophthalmol 1964;71:611.
15.Ciancia A. La esotropia en el lactante, diagnostico y tratamiento. Arch Chil Oftalmol 1962;9:117.
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16.Clarke WN, Noel LP. Vanishing infantile esotropia. Can J Ophthalmol 1982;17:100–102.
17.Clarke WN. Current controversies: very early vs. early or late surgery for infantile esotropia. Can J Ophthalmol 1995;30:239–240.
18.Coats DK, Avilla CW, Paysse EA, Sprunger DT, Steinkuller PG, Somaiya M. Early-onset refractive accommodative esotropia. J Am Assoc Pediatr Ophthalmol Strabismus 1998;2(5):275–278.
19.Costenbader FD. Infantile esotropia. Trans Am Ophthalmol Soc 1961;59:397.
20.Crawford ML, Harwerth RS, Smith EL, von Noorden GK. Loss of stereopsis in monkeys following prismatic binocular dissociation during infancy. Behav Brain Res 1996;79(1–2):207–218.
21.Crawford MLJ, von Noorden GK. Optically induced concomitant strabismus in monkeys. Investig Ophthalmol Vis Sci 1980;19:1105.
22.Crawford MLJ, von Noorden GK. The effects of short-term experimental strabismus on the visual system in Macaca mulatta. Investig Ophthalmol Vis Sci 1979;18:496–505.
23.Dell’Osso LF, Ellenberger C Jr, Abel LA, Flynn JT. The nystagmus blockage syndrome. Investig Ophthalmol Vis Sci 1983;24:1580.
24.Dickey CF, Metz HS, Stewart SA. The diagnosis of amblyopia in cross-fixation. J Pediatr Ophthalmol Strabismus 1991;28:171–175.
25.Fawcett S, Leffler J, Birch EE. Factors influencing stereoacuity in accommodative esotropia. J Am Assoc Pediatr Ophthalmol Strabismus 2000;4(1):15–20.
26.Fox R, et al. Stereopsis in human infants. Science 1980;207:323.
27.Friedrich D, de Decker W. Prospective study of the development of strabismus during the first 6 months of life. Orthopt Hor 1987: 21–28.
28.Helveston EM, Ellis FD, Schott J, et al. Surgical treatment of congenital esotropia. Am J Ophthalmol 1983;96:218–228.
29.Helveston EM. Cyclic strabismus. Am Orthopt J 1971;23:4851.
30.Helveston EM, Neely DF, Stidham DB, Wallace DK, Plager DA, Sprunger DT. Results of early alignment of congenital esotropia. Ophthalmology 1999;106:1716–1726.
31.Hiles DA, Watson BA, Biglan AW. Characteristics of infantile esotropia following early bimedial rectus recession. Arch Ophthalmol 1980;98:697–703.
32.Hoyt C, Jastrzebski G, Marg E. Amblyopia and congenital esotropia. Visually-evoked potential measurements. Arch Ophthalmol 1984; 102:58–61.
33.Hubel DH, Wiesel TN. Binocular interaction in striate cortex of kittens reared with artificial squint. J Neurophysiol 1965;28:1041– 1059.
34.Hutcheson KA, Lambert SR. Cyclic esotropia after a traumatic sixth nerve palsy in a child. J Am Assoc Pediatr Ophthalmol Strabismus 1998;2(6):376–377.
35.Ing MR. Early surgical alignment for congenital esotropia. Trans Am Ophthalmol Sci 1981;79:625–663.
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36.Ing M, Costenbader FD, Parks MM. Early surgical treatment for congenital esotropia. Am J Ophthalmol 1966;652:1419–1427.
37.Ing MR. Progressive increase in the angle of deviation in congenital esotropia. Trans Am Ophthalmol Soc 1994;XCII:117–259.
38.Ing MR. Botulinum alignment for congenital esotropia. Ophthalmology 1993;100(3):318–322.
39.Ing MR. Outcome study of surgical alignment before six months of age for congenital esotropia. Ophthalmology 1995;102:2041–2045.
40.Ing MR. Outcome study of stereoacuity in relation to duration of misalignment in congenital esotropia. JAAPOS 2001;Feb.6(1):3–8.
41.Leguire LE, Roger GL, Bremer DL. Visual-evoked response binocular summation in normal and strabismic infants. Investig Ophthalmol Vis Sci 1991;32:126–133.
42.Ludwig IH, Parks MM, Getson PR. Long-term results of bifocal therapy for accommodative esotropia. J Pediatr Ophthalmol Strabismus 1989;26:264–270.
43.Magoon E. Chemodenervation of strabismic children. Ophthalmology 1989;96:931–934.
44.Maumenee IH, Alston A, Mets MB, Flynn JT, Mitchell TN, Beaty TH. Inheritance of congenital esotropia. Trans Am Ophthalmol Soc 1986;84:85–93.
45.Mohoney BG, Erie JC, Hodge DO, Jacobsen SJ. Congenital esotropia in Olmsted County, Minnesota. Ophthalmology 1998;105:846–850.
46.Morris RJ, Scott WE, Dickey CF. Fusion after alignment of longstanding strabismus in adults. Ophthalmology 1993;100:135–138.
47.Mutti DO, Frane SL, Friedman NE, Lin WK, Sholtz RI, Zadnik K. Ocular component changes during emmetropization in infancy (abstract). Investig Ophthalmol Vis Sci 2000;41:S300.
48.Nelson LB, Wagner RS, Simon JW, Harley RD. Congenital esotropia. Surv Ophthalmol 1987;31:363–383.
49.Nixon RB, Helveston EM, Miller K, Archer SM, Ellis FD. Incidence of strabismus in neonates. Am J Ophthalmol 1985;100:798–801.
50.Parks MM. Congenital esotropia with a bi-fixation result: report of a case. Doc Ophthalmol 1984;58:109–114.
51.Pediatric Eye Disease Investigator Group. The clinical spectrum of early-onset esotropia. Experience of the Congenital Esotropia Observational Study. Am J Ophthalmol 2002;133:102–108.
52.Pediatric Eye Disease Investigator Group. Spontaneous resolution of early-onset esotropia: experience of the Congenital Esotropia Observational Study. Am J Ophthalmol 2002;133:109–118.
53.Petrig B, Juless B, Kropff W, Baumgartner G, Anliker M. Development of stereopsis and cortical binocularity in human infants: electrophysiological evidence. Science 1981;213:1402–1405.
54.Pillai P, Dhand UK. Cyclic esotropia with central nervous system disease: report of two cases. J Pediatr Ophthalmol Strabismus 1987;24(5):237–241.
55.Podgor MJ, Remaley NA, Chew E. Associations between siblings for esotropia and exotropia. Arch Ophthamol 1996;114:739–744.
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56.Pollard ZF. Accommodative esotropia during the first year of life. Arch Ophthalmol 1976;94:1912.
57.Prieto-Diaz J. Large bilateral medial rectus recession in early esotropia with bilateral limitation of abduction. J Pediatr Ophthalmol Strabismus 1980;17:101–105.
58.Prism Adaptation Research Group. Efficacy of prism adaptation in the surgical management of acquired esotropia. Arch Ophthalmol 1990;108:1248–1256.
59.Robb RM, Rodier DW. The variable clinical characteristics and course of early infantile esotropia. J Pediatr Ophthalmol Strabismus 1987;24:276–281.
60.Scott WE. Temporary surgical overcorrection of infantile esotropia. Transactions of the New Orleans Academy of Ophthalmology. New York: Raven Press, 1986.
61.Shauly Y, Prager TC, Mazow ML. Clinical characteristics and longterm postoperative results of infantile esotropia. Am J Ophthalmol 1994;117:183–189.
62.Shirabe H, Mori Y, Dogru M, Yamamoto M. Early surgery for infantile esotropia. Br J Ophthalmol 2000;84:536–538.
63.Smith JT, Scott WE. Long-term stability of alignment in the monofixation syndrome. J Pediatr Ophthalmol Strabismus 1989;Sep.–Oct. 26(5):224–231.
64.Sondhi N, Archer S, Helveston EM. Development of normal ocular alignment. J Pediatr Ophthalmol Strabismus 1988;25:210.
65.Tychsen L, Lisberger SG. Maldevelopment of visual motion processing in humans who had strabismus with onset in infancy. J Neuroci 1986;6:2495–2508.
66.von Noorden GK. The nystagmus compensation (blockage syndrome). Am J Ophthalmol 1976;82:283.
67.von Noorden GK, Munoz M, Wong SY. Compensatory mechanisms in congenital nystagmus. Am J Ophthalmol 1987;104:387–397.
68.Wilson ME, Parks MM. Primary inferior oblique overaction in congenital esotropia, accommodative esotropia, and intermittent exotropia. Ophthalmology 1989;96:950–955.
69.Wright KW. Clinical optokinetic nystagmus asymmetry in treated esotropes. J Pediatr Ophthalmol Strabismus 1996;33(3):153–155.
70.Wright KW, Bruce-Lyle L. Augmented surgery for esotropia associated with high hypermetropia. J Pediatr Ophthalmol Strabismus 1993;30:167–170.
71.Wright KW, Edelman PM, McVey JH, Terry AP, Lin M. High-grade stereoacuity after early surgery for congenital esotropia. Arch Ophthalmol 1994;112:913–919.
72.Wright KW, Edelman PM, Walonker F, Yiu S. Reliability of fixation preference testing in diagnosing amblyopia. Arch Ophthalmol 1986; 104:549.
73.Zubcov AA, Reinecke RD, Gottlob I, Manley DR, Calhoun JH. Treatment of manifest latent nystagmus. Am J Ophthalmol 1990;110:160– 167.
8
Exotropia
Kenneth W. Wright
Exodeviations are quite common, and they are not necessarily pathological. A small intermittent exotropia is normal in most newborns, as 70% of normal newborns have a transient
exodeviation that resolves by 2 to 4 months of age.1 Another type of exodeviation that is considered normal is a small exophoria, usually less than 10 prism diopters (PD). Most normal adults have a small exophoria when fully dissociated. Exodeviations are controlled with our innate strong fusional convergence, typically measuring 30 PD or more. The most common form of divergent strabismus is intermittent exotropia, which probably accounts for more than 90% of all exodeviations. Table 8-1 lists the different categories of pathological exodeviations, with the one most frequently occurring listed first.
INTERMITTENT EXOTROPIA
Intermittent exotropia is a large phoria that is intermittently controlled by fusional convergence. Unlike a phoria, intermittent exotropia spontaneously breaks down into a manifest exotropia (Fig. 8-1).
Clinical Features
Intermittent exotropia is usually first observed by the parents in early childhood or late infancy as an infrequent drifting or squinting of one eye. 12 Patients with intermittent exotropia tend to manifest their deviation when they are tired, have a cold or the flu, or when they are daydreaming. Adult patients will often become exotropic after imbibing alcoholic beverages or taking sedatives.
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TABLE 14.1. Classifications of Exodeviations.
Intermittent exotropia (common)
Convergence insufficiency (common)
Sensory exotropia (common)
Congenital exotropia (rare)
Signs of intermittent exotropia include blurred vision, asthenopia, visual fatigue, and, rarely, diplopia in older children and adults. Many patients with intermittent exotropia have photophobia (squinting to bright light). Photophobia was originally thought to be a way for eliminating diplopia or confusion, but Wiggins and von Noorden have shown that the photophobia may not be related to diplopia avoidance.39
As a rule, during the phoric phase of intermittent exotropia, the eyes are perfectly aligned and the patient has bifoveal fusion with excellent stereoacuity ranging between 40 and 50 s arc. This excellent bifoveal fusion develops because the eyes are well aligned in early infancy when the critical binocular cortical connections are being established. A minority of patients with intermittent exotropia are primary monofixators and do not develop normal bifoveal fusion with good stereopsis. Rarely a patient will even have significant amblyopia. The poor fusion in these cases is associated with a predominance of the tropia phase. During the tropia phase of intermittent exotropia, patients will show large hemiretinal or regional suppression of the temporal retina.26,30 Anomalous retinal correspondence in the tropia phase and normal retinal correspondence in the phoria phase have been demonstrated in some patients with intermittent exotropia.4,38
Natural History
The natural history of intermittent exotropia remains obscure, as there are no longitudinal prospective studies and only a few retrospective studies of untreated intermittent exotropia. Von Noorden found that 75% of 51 untreated patients showed progression over an average follow-up period of 3.5 years, whereas 9% worsened and 16% improved.36,38 Hiles et al.,20 in their study of 48 patients, found no significant change in the deviation after an average of 11 years follow-up, and 2 patients progressed to a constant tropia. The most we can say about the natural history is that, in the majority of cases, intermittent exotropia does not get better; it either stays the same or progresses. If the tropic phase increases, patients may develop dense suppression and,
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A
B
FIGURE 8-1A–B. (A) Patient with intermittent exotropia and straight eyes in the phoric phase. Patient has 40 s arc stereoacuity. (B) Occlusion of the right eye disrupts fusion and manifests the exotropia. Under the occluder, the right eye is deviated temporally.
over time, may progress to a constant exotropia with loss of fusional potential.
Classifications
Intermittent exotropia has been classically categorized into three subtypes based on the difference between the distance
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C
FIGURE 8-1C. (C) Occluder is removed and the right eye is deviated temporally, showing the exotropia. Patient is in the tropic phase and suppresses right eye.
deviation and the near deviation. These three “older” classic categories are (1) basic, (2) pseudodivergence excess, and (3) true divergence excess. It is important to note that the older terminology uses the term divergence excess, and pseudodivergence excess is only descriptive as to the difference of the deviation distance versus near; it is not meant to imply a mechanism for the distance–near disparities. The mechanism for the dis- tance–near disparities seen in patients with intermittent exotropia is most likely caused by superimposed overconvergence on the basic exodeviation. These convergence mechanisms include tonic fusional convergence (tenacious proximal fusion),22 accommodative convergence (AC/A ratio), and proximal convergence (instrument convergence).
BASIC INTERMITTENT EXOTROPIA
With this type of exotropia, there is no significant distance–near disparity, and the distance deviation is within 10 PD of the near deviation. Patients with a basic deviation have normal convergence, so their deviation is essentially the same for distance and near.
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PSEUDODIVERGENCE EXCESS
This is an exodeviation that is measured larger for distance fixation than near fixation by brief alternate cover testing (distance 10 PD greater than near); however, with prolonged monocular occlusion (patch test for 30–60 min), the near deviation increases and becomes similar to the distance deviation (within 10 PD). For example, an exodeviation measures 30 PD in the distance and 10 PD at near to alternate cover testing. One eye is patched for 30 min, and now the patient measures 30 PD in the distance and 25 PD at near. This change occurs because patients with pseudodivergence excess have increased tonic near fusional convergence that dissipates slowly after monocular occlusion. Prolonged monocular occlusion of 30 to 60 min is required in these patients to dissipate tonic near fusional convergence and disclose the full latent deviation (see Patch Test, below). The relatively brief period of monocular occlusion that occurs with alternate cover testing is not enough to break up the tonic near fusional convergence and disclose the full deviation at near. Surgery is performed for the full distance deviation.
Pseudodivergence excess is quite common. More than 80% of patients with an apparent divergence excess actually have pseudodivergence excess, as the near deviation will increase to within 10 PD of the distance deviation after the patch test.5,22,37
PATCH TEST (OCCLUSION TEST)
The patch test consists of placing an occlusive patch over one eye for at least 30 to 60 min, then measuring the deviation without letting the patient restore binocular fusion. The idea is to totally suspend all tonic fusional convergence by occluding one eye, forcing the full latent deviation to become manifest. When performing the patch test, be sure the patient does not peek around the patch and regain fusion before the deviation is measured. To measure the deviation, first cover the unpatched eye with a paddle occluder, then remove the patch and measure the deviation with alternate cover testing. This method ensures the patient will not sneak a peek with both eyes and reestablish fusion before the deviation is measured.
TRUE DIVERGENCE EXCESS
In these cases, the distance deviation is greater than the near deviation by more than 10 PD, even after performing the patch
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test. For example, the distance deviation would measure 30 PD, near deviation 10 PD and, after a 30-min patch test, the distance deviation would be 30 PD and the near deviation 15 PD. This author and Eugene De Juan (Los Angeles, CA) studied the cause of true divergence excess at the Wilmer Clinic at Johns Hopkins Hospital in Baltimore in 1981. They found that most of the patients with true divergence excess had a high AC/A (accommodative convergence/accommodation) ratio as determined by a 3.00 add after a 60-min patch test. The patch test relaxes tonic fusional convergence, and the 3.00 add relaxes accommodation. The high AC/A ratio patients do not show an increase in the near exotropia to the patch test, but the near deviation increases dramatically with a 3.00 near add.40 In a similar study, Kushner22 found approximately 60% of patients with a true divergence excess had a high AC/A ratio and 40% had a normal AC/A ratio. The group with a high AC/A ratio was prone to postoperative overcorrection (75% overcorrection) at near if the distance measurement is used as the surgical target angle. The 40% of true divergence excess patients with a normal AC/A ratio had relatively good results using the distance measurement. Patients with true divergence excess are a difficult group to surgically correct as they are prone to having a consecutive esotropia at near, and some will require bifocals or additional surgery. Following is a summary of the causes of overconvergence that produce true divergence excess.
CAUSES OF TRUE DIVERGENCE EXCESS
HIGH AC/A RATIO
This condition occurs when the distance deviation is larger than the near deviation even after the patch test, but the near deviation increases close to the distance deviation with a 3.00 add. High AC/A ratio intermittent exotropia has normal tonic fusional convergence but has a high AC/A ratio that causes the distance–near disparity. Surgery is usually performed for a deviation somewhere between the distance and near deviation measured without near add. Some of these patients require bifocals after surgery if there is an esotropia at near.
INCREASED PROXIMAL CONVERGENCE
This situation arises when the distance deviation is larger than the near deviation after the patch test and a 3.00 add OU. These patients have a normal tonic fusional convergence and a