Ординатура / Офтальмология / Английские материалы / Handbook of Pediatric Strabismus and Amblyopia_Wright, Spiegel, Thompson_2006
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under bili-lights who were patched bilaterally from several days to 2 weeks showed that they did not have an increased incidence of amblyopia or strabismus. In a separate report by the author,61 a neonate received 17 days of bilateral patching after having 2 weeks of dense vitreous hemorrhage and hyphema. Follow-up at 3 years of age showed visual acuity of 20/30 in each eye and a small accommodative esophoria with good fusion. Bilateral light occlusion remains controversial and, in this author’s opinion, should be used only as a temporary measure in neonates 3 months or younger with ocular opacities such as congenital cataracts. Urgent surgery is still required but, for visually significant cataracts, bilateral occlusion can be used to prevent amblyopia until the retinal image is cleared. The author’s recommendation is to limit bilateral patching to a maximum of 2 weeks.
LEVODOPA/CARBIDOPA IN THE TREATMENT
OF AMBLYOPIA
Levodopa/carbidopa has been traditionally used to treat Parkinson’s disease. Levodopa is a precursor for the catecholamine dopamine, a neurotransmitter/neuromodulator known to influence receptive fields. Levodopa/carbidopa has been studied as an adjunct to patching for the treatment of amblyopia.27,28,29,30 The treatment remains controversial, as the visual acuity improvement has been relatively small, not clearly better than with patching alone, and there are questions regarding long-term stability of vision.
PLEOPTICS
Pleoptics is a method of treating eccentric fixation associated with dense amblyopia. A bright ring of light is flashed around the fovea to temporarily “blind” or saturate the photoreceptors surrounding the fovea, which eliminates vision from the eccentric fixation point and forces fixation to the fovea. Pleoptic treatments are given several times a week to enhance occlusion therapy. Most practitioners have found pleoptics to be no better than standard occlusion therapy.16
ACTIVE STIMULATION
Some investigators have suggested active stimulation of the amblyopic eye as a way to improve vision in the amblyopic eye.
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A high-contrast spinning disc with square-wave grading was one method that has been tried (CAM). The CAM treatment has been found to be no better than standard occlusion therapy.8
PROGNOSIS OF AMBLYOPIA
The prognosis for amblyopia depends upon the age of the patient, severity of amblyopia, and type of amblyopia. The earlier the amblyopia occurs and the longer it remains untreated, the worse the prognosis. In general, bilateral amblyopia responds better than unilateral amblyopia, and myopic anisometropic amblyopia responds better than hypermetropic anisometropic amblyopia. Each case must be evaluated individually as to whether the child is too old to undergo amblyopia therapy. Visual acuity improvement has been documented when children are treated in late childhood after 8 years of age.6,33 This author reported improvement in vision from legally blind to 20/70 and damping of sensory nystagmus in a 14-year-old who underwent late cataract surgery for bilateral congenital cataracts.60 Even adults with dense amblyopia can show visual acuity improvement and prolonged plasticity. Significant visual acuity improvement of the amblyopic eye has been reported in adults who have lost vision in their good eye and relied on the amblyopic eye for their vision.14,45
References
1.Atkinson J. Development of optokinetic nystagmus in the human infant and monkey infant: an analogue to development in kittens. In: Freeman RD (ed) Developmental neurobiology of vision. New York: Plenum Press, 1979.
2.Birch EE, Gwiazda J, Held R. Stereoacuity development of crossed and uncrossed disparities in human infants. Vision Res 1982;22:507.
3.Birch E, Petrig B. FPL and VEP measures of fusion, stereopsis and stereoacuity in normal infants. Vision Res 1996;36(9):1321–1327.
4.Braddick O, et al. Cortical binocularity in infants. Nature (Lond) 1980;288:363–365.
5.Braddick O, Wattam-Bell J. The onset of binocular function in human infants. Hum Neurobiol 1983;2(2):65–69.
6.Brown MH, Edelman PM. Conventional occlusion in the older amblyope. Am Orthopt J 1976;26:54–56.
7.Carney T. Evidence for an early motion system which integrates information from the two eyes. Vision Res 1997;37(17):2361–2368.
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8.Crandall MA, Gerhard WC, Ellerhorst B. CAM (stripe) therapy for amblyopia, Perspect Ophthalmol 1981;5(1):51–55.
9.Cynader M, Berman N, Hein A. Recovery of function in cat visual cortex following prolonged deprivation. Exp Brain Res 1976:25:139– 156.
10.Cynader M, Mitchell DE. Prolonged sensitivity to monocular deprivation in dark-reared cats. J Neurophysiol 1980;43:1026– 1040.
11.Cynader M. Prolonged sensitivity to monocular deprivation in darkreared cats: effects of age and visual exposure. Dev Brain Res 1983; 8:155–164.
12.Demer JL, von Noorden GK. Optokinetic asymmetry in esotropia. J Pediatr Ophthalmol Strabismus 1988;25:286.
13.Daw N. Critical periods and amblyopia. Arch Ophthalmol 1998; 116(4):502–505.
14.Ellis FD, Schlaegel TF. Unexpected visual recovery: organic amblyopia? Am Orthopt J 1991;31:7.
15.Eustis HS, Chamberlain D. Treatment for amblyopia: results using occlusive contact lens. J Pediatr Ophthalmol Strabismus 1996;33: 319–322.
16.Fletcher MC, Silverman SJ, Boyd J, Callaway M. Biostatistical studies: comparison of the management of amblyopia by conventional patching, intensive hospital pleoptics, and intermittent office pleoptics. Am Orthopt J 1969;19:40.
17.Fox R, Aslin RN, Shea SL, Dumais ST. Stereopsis in human infants. Science 1980;207:323.
18.Garey LJ, De Courten C. Structural development of the lateral geniculate nucleus and visual cortex in monkey and man. Behav Brain Res 1983;10:3–13.
19.Hakim OH, Wright KW. Treatment of anisometropic amblyopia with minimal or no patching. Abstracts Program #2148. ARVO, May/Ft. Lauderdale, FL. 2001.
20.Hendrickson AE, Movshon JA, Eggers HM, Gizzi MS, Boothe RG, Kiorpes L. Effects of early unilateral blur on the macaque’s visual system. II. Anatomical observations. J Neurosci 1987;7:1327– 1339.
21.Horton JC, Hocking DR. Timing of the critical period for plasticity of ocular dominance columns in macaque striate cortex. J Neurosci 1997;17(10):3684–3709.
22.Hoyt CS. The long-term visual effects of short-term binocular occlusion of at-risk neonates. Arch Ophthalmol 1980;98:1970.
23.Hubel KH, Weisel TN. Receptive field, binocular interaction and functional architecture in the cat’s visual cortex. J Physiol 1962;160: 106–154.
24.Ikeda H, Tremain K. Amblyopia and cortical binocularity. Trans Ophthalmol Soc UK 1980;100:452.
25.Keech RV, Kutschke PJ. Upper age limit for the development of amblyopia. J Pediatr Ophthalmol Strabismus 1995;32:89–93.
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26.Leguire LE, Rogers GL, Bremer DL. Visual-evoked response binocular summation in normal and strabismic infants. Investig Ophthalmol Vis Sci 1991;32:126–133.
27.Leguire LE, Rogers GL, Bremer DL, Walson P, HadjiconstantinouNeff M. Levodopa and childhood amblyopia. J Pediatr Ophthalmol Strabismus 1992:29:290–298.
28.Leguire LE, Rogers GL, Bremer DL, Walson P, McGregor ML. Levodopa/carbidopa for childhood amblyopia. Investig Ophthalmol Vis Sci 1993;34:3090–3095.
29.Leguire LE, Rogers GL, Bremer DL, Walson P, McGregor ML. Longitudinal study of levodopa/carbidopa for childhood ambylopia. J Pediatr Ophthalmol Strabismus 1993;30:354–360.
30.Leguire LE, Rogers GL, Bremer DL, Walson P, McGregor ML. Levodopa/carbidopa treatment for the amblyopia in older children. J Pediatr Ophthalmol Strabismus 1995;32:143–151.
31.Lewis TL, Maurer D, Brent HP. Optokinetic nystagmus in normal and visually deprived children: implications for cortical development. Can J Psychol 1989;43:121–140.
32.Naegele JR, Held R. The postnatal development of monocular optokinetic nystagmus in infants. Vision Res 1982;22:341.
33.Oliver M, et al. Compliance and results of treatment for amblyopia in children more than 8 years old. Am J Ophthalmol 1986;102:340– 345.
34.Ottar WL, Scott WE, Holgado SI. Photoscreening for amblyogenic factors. J Pediatr Ophthalmol Strabismus 1995;32:289–295.
35.Parks MM. The monofixational syndrome. Trans Am Ophthalmol Soc 1969;67:609–657.
36.Raab E. Refractive amblyopia. Int Ophthalmol Clin 1971;II:155.
37.Rakic P. Prenatal genesis of connections subserving ocular dominance in rhesus monkey. Nature (Lond) 1976;261:467.
38.Repka MX, Ray JM. The efficacy of optical and pharmacological penalization. Ophthalmology 1993;100:769–775.
39.Sondhi N, Archer SM, Helveston EM. Development of normal ocular alignment. J Pediatr Ophthalmol Strabismus 1988;25:210–211.
40.Timney B, Mitchell DE, Giffin F. The development of vision in cats after extended periods of dark-rearing. Exp Brain Res 1978;31: 547–560.
41.Tychsen L, Lisberger SG. Maldevelopment of visual motion procession in humans who had strabismus with onset in infancy. J Neurosci 1986;6:2495–2508.
42.Tychsen L. Binocular vision. In: Hart WM (ed) Adler’s physiology of the eye: clinical applications, 9th edn. St. Louis: Mosby, 1992:773– 853.
43.Tychsen L, Boothe RG. Latent fixation nystagmus and nasotemporal asymmetries of motion visually evoked potentials in naturally strabismic primate. J Pediatr Ophthalmol Strabismus 1996;33:148–152.
44.van Essen DC, Maunsell JHR. Hierarchical organization and functional streams in the visual cortex. Trends Neurosci 1983:6:370–395.
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45.Vereecken EP, Brabant P. Prognosis for vision in amblyopia after the loss of the good eye. Arch Ophthalmol 1984;102:220.
46.von Noorden GK, Crawford ML. The lateral geniculate nucleus in human strabismic amblyopia. Investig Ophthalmol Vis Sci 1992; 33(9):2729–2732.
47.von Noorden GK, Crawford MLJ, Levacy RA. The lateral geniculate nucleus in human anisometropic amblyopia. Investig Ophthalmol Vis Sci 1983;24:788–790.
48.von Noorden GK, Crawford MLJ. The effects of total unilateral occlusion vs. lid suture on the visual system of infant monkeys. Investig Ophthalmol Vis Sci 1981;21:142–146.
49.von Noorden GK, Crawford MLJ. Form vision deprivation without light deprivation produces the visual deprivation syndrome in Macaca mulatta. Brain Res 1977;129:37–44.
50.von Noorden GK. Amblyopia caused by unilateral atropinization. Ophthalmology 1981;88:131–133.
51.Weakley DR. The association between anisometropia, amblyopia and binocularity in the absence of strabismus. Trans Am Ophthalmol Soc 1999;48:987–1021.
52.Weinacht S, Kind C, Monting JS, Gottlob I. Visual development in preterm and full term infants: a prospective masked study. Investig Ophthalmol Vis Sci 1999;40(2):346–353.
53.Werner DB, Scott WE. Amblyopia case reports: bilateral hypermetropic ametropic amblyopia. J Pediatr Ophthalmol Strabismus 1985; 22:203–205.
54.Westall CA, Woodhouse JM, Brown VA. OKN asymmetries and binocular function in amblyopia. Ophthalmol Physiol Opt 1989;9: 269–276.
55.Westall CA, Eizenman M, Kraft SP, Panton CM, Chatterjee S. Cortical binocularity and monocular optokinetic asymmetry in early onset esotropia. Investig Ophthalmol Vis Sci 1998;39(8):1352– 1360.
56.Wiesel TN, Hubel DH. Single-cell responses in striate cortex of kittens deprived of vision in one eye. J Neurophysiol 1963;26:1003– 1017.
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58.Wright KW, Fox BES, Erikson KJ. PVEP evidence of true suppression in adult onset strabismus. J Pediatric Ophthalmol Strabismus 1990; 27:196–201.
59.Wright KW, Guyton DL. A test for predicting the effectiveness of penalization on amblyopia. In: Henkind P (ed) Acta: XXIV international congress of ophthalmology. Philadelphia: Lippincott, 1983: 896–901.
60.Wright KW, Christensen LE, Noguchi BA. Results of late surgery for presumed congenital cataracts. Am J Ophthalmol 1992;114(4):409– 415.
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61.Wright KW, Wehrle MJ, Urrea PT. Bilateral total occlusion during the critical period of visual development. Letter to the editor. Arch Ophthalmol 1987;105:321.
62.Wright KW, et al. Reliability of fixation preference testing in diagnosing amblyopia. Arch Ophthalmol 1986;104:549–553.
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64.Zipf RF. Binocular fixation pattern. Arch Ophthalmol 1976;94:401– 405.
5
The Ocular Motor
Examination
Kenneth W. Wright
EVALUATION OF THE STRABISMIC PATIENT
The goals of the strabismus examination are to (1) diagnose amblyopia; (2) establish a strabismus diagnosis (e.g., pseudoesotropia, congenital esotropia, cranial nerve palsy, or restrictive strabismus); (3) assess the binocular status (e.g., bifoveal fusion, monofixation–peripheral fusion, anomalous retinal correspondence, no fusion–large suppression, diplopia, and fusion potential); and (4) measure and characterize the deviation. A well-focused, goal-oriented evaluation helps prevent a laborious exhaustive examination that results in patient fatigue, examiner fatigue, and the collection of spurious data. Even after a full evaluation, a patient’s strabismus may not clearly fall into a specific category, and the diagnosis may be nebulous. In these cases, the patient can still be appropriately managed if evaluated for amblyopia, sensory status, size of the deviation, and the possibility of an underlying neurological problem or systemic disease. As in all aspects of medicine, the combination of detailed history and careful physical examination provides the foundation for making the correct diagnosis and taking the appropriate action.
HISTORY
The character and onset of the strabismus provides information about binocular fusion potential. The earlier the onset and longer the duration of the strabismus, the worse the prognosis for binocular vision. Older children with congenital strabismus
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who have never experienced fusion have a poor fusion prognosis, whereas an acquired strabismus of a few months duration usually indicates the patient has developed at least some binocular vision and has the potential to recover binocular fusion. A history of compensatory head posturing speaks for binocular fusion, as does a history of an intermittent strabismus. In the real world of clinical practice, however, these general rules do not hold 100% of the time as some patients will obtain binocular fusion after late surgery for a presumed congenital strabismus. The history of an acquired strabismus is important because it may indicate a neurological or systemic disease, especially when the strabismus is incomitant and associated with limited ductions. An unexplained acquired incomitant strabismus requires neurological evaluation. Examining baby photographs, the family album, or a patient’s driver’s license under magnification can facilitate documenting the onset and type of strabismus. Additionally, patients should be questioned about the presence of diplopia, as diplopia usually indicates acquired strabismus with onset usually after 4 to 6 years of age.
History regarding birth weight, complications of birth, the health of the child, and developmental milestones are also an integral part of a complete evaluation. Finally, the family history is very important. Although the exact hereditary pattern of strabismus is unclear, most types of strabismus are familial.
PHYSICAL EXAMINATION
Try to obtain as much information as possible by inspection without touching the child. Use toys to play with the child to observe eye alignment and eye movements. Save the more intrusive parts of the examination for last. The steps for the strabismic examination are listed in order in Table 5-1. Traditionally, binocular sensory testing is performed before tests that require occluding one eye, such as visual acuity testing and the cover/ uncover tests. Covering one eye dissociates the eyes and may disrupt fusion in a patient with latent strabismus (large phoria or intermittent tropia). This may be more of a theoretical consideration, as Biedner et al.2 found no significant difference in stereopsis tested at the beginning versus at the end of the exam. This author prefers testing vision early, before sensory testing, as knowledge of the visual acuity sets the tone for the rest of the examination.
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TABLE 5-1. Order of Examination.
1.Inspection: Evaluation and measurement of face turns
2.Amblyopia assessment/visual acuity
3.Sensory tests (see Chapter 6)
4.Ductions and versions
5.Measurement of deviation
6.Special tests for identifying restriction and paresis
7.Cycloplegic refraction
8.Fundus examination (objective torsion)
ORDER OF EXAMINATION
Inspection
The physical examination actually starts as the patient enters the room. While taking the history, it is important to observe the patient’s visual behavior, eye alignment, eye movements, fixation, and head posturing. By the time the history is recorded, a good observer will often have established a preliminary differential diagnosis. An initial differential diagnosis helps guide the direction of the physical examination and minimize extraneous test. However, be careful not to overanticipate: keep an open mind.
Much can be learned about the patient’s sensory status from simple inspection. Do the eyes appear straight? Is there a face turn or head posturing? The presence of straight eyes with a face turn in a patient with strabismus can indicate the presence of binocular fusion even if this cannot be demonstrated by sensory testing. Often, patients with weak fusion will break down to a tropia after even a brief cover test or during sensory tests. Therefore, it is important to observe the patient’s alignment and face posturing before formal testing.
Amblyopia Assessment/Visual Acuity
Techniques for diagnosing amblyopia are covered in Chapter 4. Always try to document visual function even in neonates or developmentally delayed children who are unable to cooperate with standard testing. Preverbal children can be tested for amblyopia by examining the quality of monocular fixation or binocular fixation preference. When evaluating amblyopia in older cooperative children, use linear acuity because single opto-
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type presentation lacks crowding and slightly underestimates the degree of amblyopia. In young preliterate children, however, single optotype testing is quicker, easier, and probably more accurate than linear optotypes. Crowding bars around an optotype or using the Wright figures have inherent crowding and may be useful for diagnosing amblyopia with single optotypes. There are many ways to test visual acuity in preschool children including Wright figures, Allen picture cards, HOTV, and the illiterate E game.
Sensory Tests
A description of sensory tests is provided in Chapter 6. Evaluation of the sensory status should be part of every strabismus examination and usually includes a haploscopic fusion/suppression test (e.g., Worth 4-dot test) and a test for stereoacuity (e.g., Titmus).
Ductions and Versions
Ductions test monocular movements and are examined with one eye occluded, forcing fixation to the eye being examined. Ductions evaluate the ability for the eye to move into extreme fields of gaze. Figure 5-1 shows both normal and limited abduction; this is a scale of 0 to 4, with 1 limitation meaning slight limitation and 4 indicating severe limitation with inability of the eye to move past midline. This scale can be used to measure horizontal and vertical ductions.
Versions test binocular eye movements and show how well the eyes move together in synchrony. Versions will detect subtle imbalance of eye movements and oblique muscle dysfunction missed on ductions. Evaluation of versions should include eye movements through the nine cardinal positions of gaze: from primary position to straight right, straight left, straight up, straight down, up to the right, up to the left, down to the right, and down to the left (Fig. 5-2). Abnormal versions can be noted on a scale of 4 to 4 with 0 indicating normal and 4 indicating maximum overaction (Fig. 5-3A), whereas 4 indicates severe underaction (Fig. 5-3B). It is important to remember, when observing for oblique dysfunction, to make sure the abducting eye is fixing so the adducting eye is free to manifest the oblique dysfunction; this can be accomplished by partially occluding the adducting eye (with your thumb or occluder) and