- •Foreword
- •Preface
- •Contributors
- •Contents
- •1. Epidemiology of Pediatric Strabismus
- •1.1 Introduction
- •1.2 Forms of Pediatric Strabismus
- •1.2.1 Esodeviations
- •1.2.1.1 Congenital Esotropia
- •1.2.1.2 Accommodative Esotropia
- •1.2.1.3 Acquired Nonaccommodative Esotropia
- •1.2.1.4 Abnormal Central Nervous System Esotropia
- •1.2.1.5 Sensory Esotropia
- •1.2.2 Exodeviations
- •1.2.2.1 Intermittent Exotropia
- •1.2.2.2 Congenital Exotropia
- •1.2.2.4 Abnormal Central Nervous System Exotropia
- •1.2.2.5 Sensory Exotropia
- •1.2.3 Hyperdeviations
- •1.3 Strabismus and Associated Conditions
- •1.4.1 Changes in Strabismus Prevalence
- •1.4.2 Changes in Strabismus Surgery Rates
- •1.5 Worldwide Incidence and Prevalence of Childhood Strabismus
- •1.6 Incidence of Adult Strabismus
- •References
- •2.1 Binocular Alignment System
- •2.1.2 Vergence Adaptation
- •2.1.3 Muscle Length Adaptation
- •2.2 Modeling the Binocular Alignment Control System
- •2.2.1 Breakdown of the Binocular Alignment Control System
- •2.2.4 Changes in Basic Muscle Length
- •2.2.6 Evidence Against the “Final Common Pathway”
- •2.3 Changes in Strabismus
- •2.3.1 Diagnostic Occlusion: And the Hazard of Prolonged Occlusion
- •2.3.2.1 Supporting Evidence for Bilateral Feedback Control of Muscle Lengths
- •2.4 Applications of Bilateral Feedback Control to Clinical Practice and to Future Research
- •References
- •3.1 Dissociated Eye Movements
- •3.2 Tonus and its relationship to infantile esotropia
- •3.5 Pathogenetic Role of Dissociated Eye Movements in Infantile Esotropia
- •References
- •4.1 Introduction
- •4.2.1 Binocular Correspondence: Anomalous, Normal, or Both?
- •4.3 MFS with Manifest Strabismus
- •4.3.1 Esotropia is the Most Common Form of MFS
- •4.3.2 Esotropia Allows for Better Binocular Vision
- •4.3.3 Esotropia is the Most Stable Form
- •4.4 Repairing and Producing MFS
- •4.4.1 Animal Models for the Study of MFS
- •References
- •5.1 Esotropia as the Major Type of Developmental Strabismus
- •5.1.2 Early Cerebral Damage as the Major Risk Factor
- •5.1.3 Cytotoxic Insults to Cerebral Fibers
- •5.1.5 Development of Binocular Visuomotor Behavior in Normal Infants
- •5.1.6 Development of Sensorial Fusion and Stereopsis
- •5.1.7 Development of Fusional Vergence and an Innate Convergence Bias
- •5.1.8 Development of Motion Sensitivity and Conjugate Eye Tracking (Pursuit/OKN)
- •5.1.9 Development and Maldevelopment of Cortical Binocular Connections
- •5.1.10 Binocular Connections Join Monocular Compartments Within Area V1 (Striate Cortex)
- •5.1.11 Too Few Cortical Binocular Connections in Strabismic Primate
- •5.1.12 Projections from Striate Cortex (Area V1) to Extrastriate Cortex (Areas MT/MST)
- •5.1.15 Persistent Nasalward Visuomotor Biases in Strabismic Primate
- •5.1.16 Repair of Strabismic Human Infants: The Historical Controversy
- •5.1.18 Timely Restoraion of Correlated Binocular Input: The Key to Repair
- •References
- •6. Neuroanatomical Strabismus
- •6.1 General Etiologies of Strabismus
- •6.2 Extraocular Myopathy
- •6.2.1 Primary EOM Myopathy
- •6.2.2 Immune Myopathy
- •6.2.4 Neoplastic Myositis
- •6.2.5 Traumatic Myopathy
- •6.3 Congenital Pulley Heterotopy
- •6.4 Acquired Pulley Heterotopy
- •6.5 “Divergence Paralysis” Esotropia
- •6.5.1 Vertical Strabismus Due to Sagging Eye Syndrome
- •6.5.2 Postsurgical and Traumatic Pulley Heterotopy
- •6.5.3 Axial High Myopia
- •6.6 Congenital Peripheral Neuropathy: The Congenital Cranial Dysinnervation Disorders (CCDDs)
- •6.6.1 Congenital Oculomotor (CN3) Palsy
- •6.6.3 Congenital Trochlear (CN4) Palsy
- •6.6.4 Duane’s Retraction Syndrome (DRS)
- •6.6.5 Moebius Syndrome
- •6.7 Acquired Motor Neuropathy
- •6.7.1 Oculomotor Palsy
- •6.7.2 Trochlear Palsy
- •6.7.3 Abducens Palsy
- •6.7.4 Inferior Oblique (IO) Palsy
- •6.8 Central Abnormalities of Vergence and Gaze
- •6.8.1 Developmental Esotropia and Exotropia
- •6.8.2 Cerebellar Disease
- •6.8.3 Horizontal Gaze Palsy and Progressive Scoliosis
- •References
- •7.1 Congenital Cranial Dysinnervation Disorders: Facts About Ocular Motility Disorders
- •7.1.1 The Concept of CCDDs: Ocular Motility Disorders as Neurodevelopmental Defects
- •7.1.1.1 Brainstem and Cranial Nerve Development
- •7.1.1.2 Single Disorders Representing CCDDs
- •7.1.1.3 Disorders Understood as CCDDs
- •7.2 Congenital Cranial Dysinnervation Disorders: Perspectives to Understand Ocular Motility Disorders
- •7.2.1.1 Brown Syndrome
- •Motility Findings
- •Saccadic Eye Movements
- •Comorbidity
- •Epidemiologic Features
- •Laterality
- •Sex Distribution
- •Incidence
- •Heredity
- •Potential Induction of the Syndrome
- •Radiologic Findings
- •Natural Course in Brown Syndrome
- •Intra-and Postoperative Findings
- •References
- •8.1 Amblyopia
- •8.2 What Is Screening?
- •8.2.1 Screening for Amblyopia, Strabismus, and/or Refractive Errors
- •8.2.1.1 Screening for Amblyopia
- •8.2.1.2 Screening for Strabismus
- •8.2.1.3 Screening for Refractive Error
- •8.2.1.4 Screening for Other Ocular Conditions
- •8.3 Screening Tests for Amblyopia, Strabismus, and/or Refractive Error
- •8.3.1 Vision Tests
- •8.3.3 Stereoacuity
- •8.3.4 Photoscreening and/or Autorefraction
- •8.3.6 Who Should Administer the Screening Program?
- •8.4 Treatment of Amblyopia
- •8.4.1 Type of Treatment
- •8.4.2 Refractive Adaptation
- •8.4.3 Conventional Occlusion
- •8.4.4 Pharmacological Occlusion
- •8.4.5 Optical Penalization
- •8.4.7 Treatment Compliance
- •8.4.8 Other Treatment Options for Amblyopia
- •8.4.9 Recurrence of Amblyopia Following Therapy
- •8.5 Quality of Life
- •8.5.1 The Impact of Amblyopia Upon HRQoL
- •8.5.3 Reading Speed and Reading Ability in Children with Amblyopia
- •8.5.4 Impact of Amblyopia Upon Education
- •8.5.6 The Impact of Strabismus Upon HRQoL
- •8.5.7 Critique of HRQoL Issues in Amblyopia
- •8.5.8 The Impact of the Condition or the Impact of Treatment?
- •References
- •9. The Brückner Test Revisited
- •9.1 Amblyopia and Amblyogenic Disorders
- •9.1.1 Early Detection of Amblyopia
- •9.1.2 Brückner’s Original Description
- •9.2.1 Physiology
- •9.2.2 Performance
- •9.2.3 Shortcomings and Pitfalls
- •9.3.1 Physiology
- •9.3.2 Performance
- •9.3.3 Possibilities and Limitations
- •9.4.1 Physiology
- •9.4.2 Performance
- •9.4.3 Possibilities and Limitations
- •9.5 Eye Movements with Alternating Illumination of the Pupils
- •References
- •10. Amblyopia Treatment 2009
- •10.1 Amblyopia Treatment 2009
- •10.1.1 Introduction
- •10.1.2 Epidemiology
- •10.1.3 Clinical Features of Amblyopia
- •10.1.4 Diagnosis of Amblyopia
- •10.1.5 Natural History
- •10.2 Amblyopia Management
- •10.2.1 Refractive Correction
- •10.2.2 Occlusion by Patching
- •10.2.3 Pharmacological Treatment with Atropine
- •10.2.4 Pharmacological Therapy Combined with a Plano Lens
- •10.3 Other Treatment Issues
- •10.3.1 Bilateral Refractive Amblyopia
- •10.3.3 Maintenance Therapy
- •10.4 Other Treatments
- •10.4.1 Filters
- •10.4.2 Levodopa/Carbidopa Adjunctive Therapy
- •10.5 Controversy
- •10.5.1 Optic Neuropathy Rather than Amblyopia
- •References
- •11.1 Introduction
- •11.1.2 Sensory or Motor Etiology
- •11.1.4 History
- •11.1.5 Outcome Parameters
- •11.2 Outcome of Surgery in the ELISSS
- •11.2.1 Reasons for the ELISSS
- •11.2.2 Summarized Methods of the ELISSS
- •11.2.3 Summarized Results of the ELISSS
- •11.2.4 Binocular Vision at Age Six
- •11.2.5 Horizontal Angle of Strabismus at Age Six
- •11.2.6 Alignment is Associated with Binocular Vision
- •11.3 Number of Operations and Spontaneous Reduction into Microstrabismus Without Surgery
- •11.3.1 The Number of Operations Per Child and the Reoperation Rate in the ELISSS
- •11.3.2 Reported Reoperation Rates
- •11.3.3 Test-Retest Reliability Studies
- •11.3.6 Spontaneous Reduction of the Angle
- •11.3.7 Predictors of Spontaneous Reduction into Microstrabismus
- •Appendix
- •References
- •12.1 Overview
- •12.1.2 Manifest Latent Nystagmus (MLN)
- •12.1.2.1 Clinical Characteristics of Manifest Latent Nystagmus (MLN)
- •12.1.3 Congenital Periodic Alternating Nystagmus (PAN)
- •12.1.3.1 Clinical characteristics of congenital periodic alternating nystagmus
- •12.2 Compensatory Mechanisms
- •12.2.1 Dampening by Versions
- •12.2.2 Dampening by Vergence
- •12.2.3 Anomalous Head Posture (AHP)
- •12.2.3.4 Measurement of AHP
- •12.2.3.6 Testing AHP at Near
- •12.3 Treatment
- •12.3.1 Optical Treatment
- •12.3.1.1 Refractive Correction
- •12.3.1.2 Spectacles and Contact Lenses (CL)
- •12.3.1.3 Prisms
- •12.3.1.4 Low Visual Aids
- •12.3.2 Medication
- •12.3.3 Acupuncture
- •12.3.4 Biofeedback
- •12.3.6 Surgical Treatment of Congenital Nystagmus
- •12.3.6.1 Management of Horizontal AHP
- •12.3.6.2 Management of Vertical AHP
- •12.3.6.3 Management of Head Tilt
- •Retro-Equatorial Recession of Horizontal Rectus Muscles
- •The Tenotomy Procedure
- •References
- •13.1 Dissociated Deviations
- •13.2 Surgical Alternatives to Treat Patients with DVD
- •13.2.1 Symmetric DVD with Good Bilateral Visual Acuity, with No Oblique Muscles Dysfunction
- •13.2.2 Bilateral DVD with Deep Unilateral Amblyopia
- •13.2.3 DVD with Inferior Oblique Overaction (IOOA) and V Pattern
- •13.2.4 DVD with Superior Oblique Overaction (SOOA) and A Pattern
- •13.2.5 Symmetric vs. Asymmetric Surgeries for DVD
- •13.3 Dissociated Horizontal Deviation
- •13.4 Dissociated Torsional Deviation. Head tilts in patients with Dissociated Strabismus
- •13.5 Conclusions
- •References
- •14.1 Introduction
- •14.2 Clinical and Theoretical Investigations
- •References
- •15.1 General Principles of Surgical Treatment in Paralytic Strabismus
- •15.1.1 Aims of Treatment
- •15.1.2 Timing of Surgery
- •15.1.3 Preoperative Assessment
- •15.1.4 Methods of Surgical Treatment
- •15.2 Third Nerve Palsy
- •15.2.1 Complete Third Nerve Palsy
- •15.2.2 Incomplete Third Nerve Palsy
- •15.3 Fourth Nerve Palsy
- •15.4 Sixth Nerve Palsy
- •References
- •16.1 Graves Orbitopathy (GO): Pathogenesis and Clinical Signs
- •16.1.1 Graves Orbitopathy is Part of a Systemic Disease: Graves Disease (GD)
- •16.1.2 Graves Orbitopathy−Clinical Signs
- •16.1.2.1 Clinical Changes Result in Typical Symptoms
- •16.1.3 Clinical Examination of GO
- •16.1.3.1 Signs of Activity
- •16.1.3.2 Assessing Severity of GO
- •16.1.3.3 Imaging
- •16.2 Natural History
- •16.3 Treatment of GO
- •16.3.1.1 Glucocorticoid Treatment
- •16.3.1.2 Orbital Radiotherapy
- •16.3.1.3 Combined Therapy: Glucocorticoids and Orbital Radiotherapy
- •16.3.1.4 Other Immunosuppressive Treatments and New Developments
- •16.3.2 Inactive Disease Stages
- •16.3.2.1 Orbital Decompression
- •16.3.2.2 Extraocular Muscle Surgery
- •16.3.2.3 Lid Surgery
- •16.4 Thyroid Dysfunction and GO
- •16.5.1 Relationship Between Cigarette Smoking and Graves Orbitopathy
- •16.5.2 Genetic Susceptibility
- •16.6 Special Situations
- •16.6.1 Euthyroid GO
- •16.6.2 Childhood GO
- •16.6.3 GO and Diabetes
- •References
41 Epidemiology of Pediatric Strabismus
a
1
b
Fig. 1.3 A child with left fourth nerve palsy showing, (a) right head tilt and (b) left hypertropia with left head tilt
hypertropia include primary inferior oblique overaction, Brown syndrome, and CNS-associated hypertropia [14].
included children with CNS disorders or acquired nonaccommodative esotropia, distinct forms of early-onset esotropia that have been shown to occur more frequently than infantile esotropia. Acquired nonaccommodative esotropia, on the other hand, appears to be relatively prevalent and is a form of esotropia that is much more likely to develop fusion and normal stereopsis with treatment [8]. Intermittent exotropia, the most common form of exodeviation, is more prevalent than any other form of strabismus in Asia and, as a result, may be the most prevalent form of strabismus worldwide.
1.4.2Changes in Strabismus Surgery Rates
There have been several reports from the United Kingdom describing a decrease in the incidence of strabismus or strabismus surgery in recent years [21–24]. Explanations for this decline have included the implementation of childhood vision screening programs and the more frequent correction of the full hyperopic refractive error. Contrasting data, however, has come from Louwagie et al.’s population-based cohort study reporting on the incidence of infantile esotropia as well as the incidence of surgery for infantile esotropia in Rochester, Minnesota, US [7]. From 1965 through 1994, there was no significant change in the numbers of children diagnosed with infantile esotropia, and there was no significant change in the number of surgeries performed on these children.
1.3Strabismus and Associated Conditions
A number of studies have demonstrated an association between prenatal and environmental factors and the development of strabismus. Significant independent risk factors for strabismus include: family history, prematurity, low birth weight, low Apgar scores (at 1 and 5min), maternal cigarette smoking, increasing maternal age, retinopathy of prematurity, refractive error, and anisometropia [15–20].
1.4Changing Trends in Strabismus Epidemiology
1.4.1Changes in Strabismus Prevalence
Our understanding of the prevalence of childhood strabismus continues to change. As discussed earlier, congenital esotropia has recently been reported to occur less commonly than once widely believed, comprising only 8.1% of all diagnosed esodeviations [3]. The previously reported higher incidence of infantile esotropia may have
Summary for the Clinician
■Congenital esotropia appears to be less prevalent than previously believed, whereas other forms such as acquired nonaccommodative esotropia are relatively common.
■Intermittent exotropia may be the most prevalent form of strabismus worldwide.
■Therateof pediatricstrabismussurgeryhasrecently been reported to be in decline; however, data from a population-based cohort of children with congenital esotropia in the United States found no change in strabismus incidence or surgical rate over a 30-year period (1965–1994).
1.5Worldwide Incidence and Prevalence of Childhood Strabismus
Recent reports describe the prevalence of pediatric strabismus as ranging from 0.12% in 1.5-year-old Japanese children [25] to 20.1% in a cohort of low birth weight
1.5 Worldwide Incidence and Prevalence of Childhood Strabismus |
5 |
Table 1.1. Pediatric strabismus prevalence rates by regions of the world
|
Reference |
Categorical |
Number |
|
|
descriptions |
of |
|
|
within the |
children |
|
|
study |
examined |
North America |
|
|
|
Canada |
|
|
|
|
[31] |
|
946 |
|
[32] |
|
1,074 |
|
[33] |
|
2,619 |
USA |
[34] |
Caucasian |
306 |
|
|
Hispanic |
548 |
|
[15] |
All races |
39,227 |
|
|
Caucasian |
17,931 |
|
|
African American |
19,619 |
|
[35] |
Caucasian |
119 |
|
|
Asian |
310 |
|
|
Hispanic |
1,781 |
|
|
Black |
9 |
|
[27] |
Hispanic |
3,003 |
|
|
African American |
3,005 |
|
([3]a, [9]a, [14]a) |
Population-based |
|
Mexico |
[36] |
|
1,035 |
|
[37] |
|
343 |
Europe |
|
|
|
England |
[38] |
|
4,784 |
|
[39] |
|
6,634 |
|
[40] |
|
7,538 |
Ireland |
[41] |
|
1,582 |
Denmark |
[42] |
|
14,107 |
Sweden |
[43] |
|
6,004 |
|
[44] |
|
1,046 |
|
[45] |
|
3,126 |
|
[46] |
|
143 |
Croatia |
[47] |
All children |
20,045 |
|
|
Term |
17,163 |
|
|
Preterm |
2,882 |
Australia |
|
|
|
|
[20] |
|
1,739 |
|
[48] |
|
2,353 |
Asia |
|
|
|
Malaysia |
[49] |
|
650 |
|
[50] |
Near fixation |
4,634 |
|
|
Distance fixation |
4,634 |
Age of |
Strabismus |
Esotropia |
Exotropia |
Hypertropia |
subjects |
prevalence |
prevalence |
prevalence |
prevalence |
(years) |
(%) |
(%) |
(%) |
(%) |
1.6–11.6 |
4.3 |
|
|
|
<3 |
3.2 |
2.0 |
1.0 |
0.09 |
6 |
4.5 |
2.7 |
1.7 |
0.08 |
6–7 |
1.6 |
|
|
|
6–7 |
0.9 |
|
|
|
0–7 |
4.5 |
3.2 |
1.2 |
|
0–7 |
5.4 |
4.1 |
1.3 |
|
0–7 |
3.6 |
2.3 |
1.3 |
|
8–16 |
3.4 |
|
|
|
8–16 |
2.9 |
|
|
|
8–16 |
1.8 |
|
|
|
8–16 |
1/9 |
|
|
|
0.5–6 |
2.4 |
0.9 |
1.5 |
|
0.5–6 |
2.5 |
1.1 |
1.4 |
|
0–19 |
3.9 |
2.3 |
1.3 |
0.3 |
12–13 |
2.3 |
1.2 |
0.8 |
0.4 |
3–6 |
1.2 |
0.6 |
0.6 |
|
5–6 |
4.4 |
3.6 |
0.8 |
|
2 |
1.5 |
1.1 |
0.4 |
|
7 |
2.3 |
1.7 |
0.5 |
0.1 |
8–9 |
4.0 |
3.4 |
0.6 |
|
0–19 |
4.5 |
3.5 |
0.9 |
0.1 |
0–7 |
3.9 |
3.4 |
0.4 |
0.05 |
12–13 |
2.7 |
1.4 |
0.7 |
0.6 |
≤10 |
2.7b |
1.5 |
0.6 |
|
4–15 |
3.5 |
2.8 |
0.7 |
|
Unspecified |
4.0 |
2.1 |
1.8 |
|
Unspecified |
3.3 |
1.7 |
1.6 |
|
Unspecified |
8.0 |
4.7 |
3.3 |
|
6 |
2.8 |
1.6 |
1.2 |
0 |
12 |
2.7c |
0.9 |
1.1 |
|
8 |
2.2 |
0.2 |
1.8 |
0.2 |
7–15 |
0.7 |
|
0.5 |
|
7–15 |
0.7 |
|
0.6 |
|
(continued)
61 Epidemiology of Pediatric Strabismus
Table 1.1. (continued)
|
|
Reference |
Categorical |
Number |
Age of |
Strabismus |
Esotropia |
Exotropia |
Hypertropia |
|
|
|
descriptions |
of |
subjects |
prevalence |
prevalence |
prevalence |
prevalence |
1 |
|
|
within the |
children |
(years) |
(%) |
(%) |
(%) |
(%) |
|
|
study |
examined |
|
|
|
|
|
|
|
China |
[51] |
Near fixation |
4,364 |
5–15 |
1.9 |
|
1.6 |
|
|
|
|
Distance fixation |
4,364 |
5–15 |
3.0 |
|
2.6 |
|
|
|
[52] |
|
1,084 |
6–14 |
2.5 |
0.4 |
2.1 |
|
|
Japan |
[53] |
Study year 2003 |
86,531 |
6–12 |
1.3d |
0.3 |
0.7 |
|
|
|
[54] |
Study year 2005 |
84,619 |
6–12 |
1.0e |
0.2 |
0.6 |
|
|
|
[25] |
Five consecutive |
33,929 total |
1.5 |
0.01–0.1 |
0–0.03 |
0–0.07 |
|
|
|
|
measurements |
|
|
|
|
|
|
|
|
|
between years |
|
|
|
|
|
|
|
|
|
2000 and 2004 |
|
|
|
|
|
|
|
|
|
Five consecutive |
33,193 total |
3 |
0.2–0.3 |
0.02–0.1 |
0.2–0.3 |
|
|
|
|
measurements |
|
|
|
|
|
|
|
|
|
between years |
|
|
|
|
|
|
|
|
|
2000 and 2004 |
|
|
|
|
|
|
|
Taiwan |
[55] |
|
862 |
6, 8, 11 |
1.6f |
0.5 |
0.9 |
|
|
Thailand |
[56] |
|
3,898 |
1 |
0.6 |
|
|
|
|
India |
[57] |
|
6,447 |
5–15 |
0.5 |
0.3 |
0.2 |
0.02 |
|
|
[58] |
|
10,605 |
≤15 |
0.4 |
|
|
|
|
Nepal |
[59] |
|
1,100 |
5–16 |
1.6 |
0.09 |
1.5 |
|
|
|
[60] |
|
1,816 |
5–16 |
1.3 |
|
|
|
|
Middle East |
|
|
|
|
|
|
|
|
|
Israel |
[61] |
|
38,000 |
1–2.5 |
1.3 |
0.9 |
0.3 |
0.06 |
|
Oman |
[62] |
|
6,292 |
6–7, 11–12 |
0.6 |
0.4 |
0.2 |
|
|
|
[63] |
|
143,112 |
6–7 |
0.5 |
|
|
|
|
Africa |
|
|
|
|
|
|
|
|
|
Cameroon |
[64] |
|
11,230 |
≤26 |
1.2 |
0.5 |
0.8 |
|
|
Nigeria |
[65] |
|
1,144 |
4–24 |
0.3 |
|
|
|
|
Ghana |
[66] |
|
957 |
6–22 |
0.2 |
|
|
|
|
Tanzania |
[67] |
|
1,386 |
7–19 |
0.5 |
|
|
|
|
Madagascar |
[68] |
|
1,081 |
8–14 |
0.7 |
0.5 |
0.3 |
|
aStudy of incidence rather than prevalence
bStrabismus prevalence includes 19 cases of microtropia cStrabismus prevalence includes 16 cases of microtropia
dStrabismus prevalence includes 245 cases of “unknown” and 20 cases of “other” types of strabismus eStrabismus prevalence includes 110 cases of “unknown” and 23 cases of “other” types of strabismus fStrabismus prevalence includes two cases of “other” strabismus
English children [26]. Prevalence studies, reporting on the number of people with a specific disease at a prescribed point in time, are found most commonly in the pediatric strabismus literature. However, this type of study may only capture a snapshot of childhood ocular deviations. Incidence reports, on the other hand, by including the number of new cases diagnosed during a
specific period of time, may survey any number of characteristics and their changes over time.
Table 1.1 includes recent strabismus prevalence and incidence data organized by regions of the world. One overarching trend is that strabismus prevalence rates differ based on racial and ethnic background. Esodeviations are found with a relatively higher prevalence among
Caucasian populations, while exodeviations are more commonly reported among Asian and African children. As shown, North American, European, and Australian data contrast with epidemiologic information gathered from multiple studies in Asia and Africa. This trend is additionally evident among non-Caucasians in the US. In the Multi-Ethnic Pediatric Eye Disease Study group’s work describing strabismus prevalence among Hispanic and African-American children, for instance, exotropia was diagnosed more commonly than esotropia [27]. The basis of this di erence may be in part linked with popula- tion-based di erences in refractive error. Esotropia is commonly associated with hyperopia, whereas exotropia is more often diagnosed in children with myopia [28].
Summary for the Clinician
■The prevalence of strabismus subtypes varies based on racial and ethnic background; Asians are primarily diagnosed with exotropia whereas Europeans, Australians, and Americans are predominantly diagnosed with esotropia.
1.6Incidence of Adult Strabismus
Although there is substantially less epidemiological information regarding adult strabismus, its prevalence has been reported as approximately 4% in the United States [29]. In a study of strabismus patients over 60 years of age, 29% developed their ocular deviation in childhood [30]. Beauchamp and colleagues similarly found that a minority, or 38%, of strabismus patients between 17 and 92 years of age developed their deviation before visual maturation [29]. Common causes of adult strabismus in descending order include neuroparalytic, restrictive, and sensory factors [30].
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