- •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
Summary for the Clinician
■Patient with euthyroid GO develop less active/ severe and more asymmetric GO symptoms.
■If present at all GO is mild in childhood and rarely needs treatment.
■Orbital irradiation is possibly contraindicated in patients with diabetic retinopathy and DON occurs more often.
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Index
A
Abducens palsy, 71
Abnormal central nervous system (CNS) esotropia, 2 Abnormal central nervous system (CNS) exotropia, 3 Acquired motor neuropathy, 71–72
Acquired nonaccommodative esotropia, 2 Acquired pulley heterotopy, 63–64 Amblyopia treatment 2009
age e ect, 131 amblyopia management
patch occlusion, 128–129 pharmacological therapy, plano lens, 130
pharmacological treatment, atropine, 129–130 refractive correction, 127–128
Bangerter filters, 132–133 bilateral refractive amblyopia, 131 clinical features, 126
deep unilateral amblyopia, 175–176 diagnosis, 126–127
epidemiology, 125–126 levodopa/carbidopa adjunctive therapy, 133 long-term persistence, 132
maintenance therapy, 131 natural history data, 127 optic neuropathy, 133–134 spectacle correction, 125
Amblyopia, screening
Child Health Promotion Program (CHPP), 96 classification, 95
conventional occlusion, 104 cover-uncover test, 100–101 definition, 95–96 Duane’s/Brown’s syndrome, 97 justification, 98
lay screeners, 102 older children, 104–105
optical penalization, 104 orthoptists, 102 pharmacological occlusion, 104
photorefractive keratectomy (PRK), 105 photoscreening/autorefraction, 101–102 pre-school vision screening, 98–99 quality of life
emotional well-being, 107 impact of treatment, 108 impact on education, 106–107 reading speed and ability, 106 strabismus impact, 107–108
recurrence, 105
refractive adaptation, 103–104 refractive error, 97
sensitivity, 100 stereoacuity test, 101 strabismus, 97
treatment compliance, 105 type of treatment, 103 vision in preschoolers study
(VIP), 100, 101 vision tests, 100
vs. diagnostic test, 97 Anisometropia, 33 Anisometropic amblyopia, 2, 3 Anomalous head posture (AHP)
Anderson–Kesternbaum surgery, 158 binocular visual acuity testing, 161–162 horizontal management, 165–166 idiopathic infantile nystagmus, 158 measurement, 160–161
monocular e ect, 161–162 straightening e ect, head, 162 testing, near vision, 162 vertical management, 166–167
Anomalous retinal correspondence (ARC), 34 Atropine, 129–130
B
Bagolini test, 141 Bangerter foils, 132 Bell’s phenomenon, 88
Bielschowsky head tilt test (BHTT), 181 Bilateral feedback control
applications, 21–22 muscle lengths, 19–21
Bilateral posterior tenectomy, 190 Bilateral refractive amblyopia, 131 Binocular alignment system
control system
A-/V-pattern strabismus, 14 basic muscle length, 15–16 bilateral phenomena, 14–15 breakdown, 14
final common pathway, 17–18 perturbation, 13
sensory torsion, 14
version and vergence stimulation, 16–17 deviation and fixation pattern, 11 long-term maintenance, 11
muscle length adaptation, 12–13
228 Index
vergence adaptation, 12 Binocular vision
angle of strabismus, 140–141 at age six, 140
bilateral recession vs. unilateral recession-resection, 141 Blood–brain barrier, 133
Botulinum toxin A (BTXA), 197, 203, 204 Brown syndrome, 4, 203
Brückner test
amblyopia and amblyogenic disorders, 113–114 corneal light reflex, 114–115
eye movements, alternating illumination, 122 fundus red reflex
ametropia, 116, 118 anisometropia, 118 esotropia, 117–118 foveal dimming, 117 hypermetropia, 118 Mittendorf’s spot, 115
optic coherence tomography, 117 paediatric residents, 119 possibilities and limitations, 120 pupillary constriction, 116
test performance, 119–120 transillumination test, 115 uncorrected ametropia, 118 uni-lateral astigmatismus, 119
uni-lateral spherical ametropia, 118, 119 pupillary light reflex
eccentric vs. central illumination, 121 iris pathology, 120
monocular illumination, 121 possibilities and limitations, 121–122 strabismus diagnostics, 120
test performance, 121
C
Cataract, 2, 3
Child Health Promotion Program (CHPP), 96
Chronic progressive external ophthalmoplegia (CPEO), 59–60
CNS-associated hypertropia, 4
Complete third nerve palsy hypertropia, 198–199 Congenital cranial dysinnervation disorders (CCDDs), 66
brainstem and cranial nerve development, 77, 78 Brown syndrome
comorbidity, 85 epidemiologic features, 85 incidence and heredity, 86
intra-and postoperative findings, 87 laterality, 85–86
motility findings, 83–85 natural course, 87
neurodevelopmental disorder, 89–90 potential induction, 86–87 radiologic findings, 87
saccadic eye movements, 85 sex distribution, 86
CFEOM, 78–79
congenital fourth nerve palsy, 82
congenital monocular elevation deficiency, 87–89 congenital ptosis, 81
congenital trochlear palsy, 82 Duane retraction syndrome, 79–81 HGPPS, 81
isolated uni-/bilateral facial palsy, 83 vertical retraction syndrome, 88
Congenital esotropia, 2 Congenital exotropia, 3
Congenital fibrosis of the extraocular muscles (CFEOM), 78–79
A-pattern exotropia, 69 motor axonal misrouting, 67 MRI, 67–68
phenotypes, 67 Congenital nystagmus
clinical characteristics, 156–157 compensatory mechanisms
AHP, 160–162
versions and vergence, 160 manifest latent nystagmus (MLN)
clinical characteristics, 157–158 slow phase, 157
periodic alternating nystagmus (PAN), 158–159 sensory deficits
afferent visual defect, 155 causes, 156
horizontal eye movement, 154 idiopathy, 155
phenotypical characteristics, 155 treatment
acupuncture, 164
artificial divergence surgery, 167–168 botulinum toxin-A (Botox), 164 head tilt, 167
horizontal AHP, 165–167 medications, 162–163 prisms, 163
refractive correction, 162 retro-equatorial recession, 168–169
spectacles and contact lenses (CL), 162–163 surgical principles, 164–165
tenotomy procedure, 169 vertical AHP, 166–167
Congenital oculomotor (CN3) palsy, 67 Congenital pulley heterotopy, 62–63 Congenital superior oblique paresis, 20, 21 Congenital trochlear (CN4) palsy, 69 Convergence insu ciency, 3
Cycloplegic drug, 127 Cyclovertical misalignment, 19
D
Diagnostic occlusion, 19 Dissociated eye movements
pathogenetic role, 29 vergence eye movements, 25
dissociated horizontal deviation (DHD), 25–29, 179–180 dissociated torsional deviation (DTD)
inverse and direct head tilt, 181 strabismus, 180
dissociated vertical deviation (DVD) asymmetric vs. symmetric surgeries, 178 bilateral, 175–176
Index 229
hypotropia, nonfixating eye, 178–179 IOOA and V pattern, 176–177 SOOA and A pattern, 177–178 symmetric, 175
Divergence paralysis esotropia, 64–65 Double elevator palsy, 83, 87, 88
Duane’s retraction syndrome (DRS), 69, 79–81 Duane’s syndrome, 19
Dysthyroid optic neuropathy (DON), 214
E
EOM surgery, 216–217 Esotropia (ET)
DHD, 179–180
monofixation syndrome, 35–36 visual cortex mechanisms
binocular input correlation, 50–51 binocular visuomotor behavior
development, 42, 43
cerebral damage risk factors, 41–42 cortical binocular connections, 44–46 cytotoxic insult, cerebral fibers, 42 early-onset (infantile) esotropia, 41 extrastriate cortex, striate cortex, 46 fusional vergence and innate
convergence bias, 44
genetic influence, cerebral connection, 42 high-grade fusion repair, 50
inter-ocular suppression, 46–47
monocular compartments, striate cortex, 44, 46 motion sensitivity and conjugate eye tracking, 44 naso-temporal inequalities, cortical suppression, 47 persistent nasalward visuomotor bias, 47–50 sensorial fusion and stereopsis development, 43 strabismic human infant repair, 50
Essential infantile esotropia. See Congenital esotropia Exotropia (XT)
DHD, 179–180 infantile esotropia
active divergence mechanism, 26
binocular fusion vs. dissociated esotonus, 27, 28 clinical signs, 27
horizontal strabismus, 28
Expected value of perfect information (EVPI), 99 Extraocular muscle (EOM), 196, 197
Eye lid surgery
lower lid lengthening, 218, 219
upper and lower lid blepharoplasty, 218 upper lid lengthening, 217
F
First Purkinje images, 114–115 Fourth nerve palsy hypertropia bilateral involvement, 201
congenital superior oblique palsy, 200 inferior oblique weakening procedure, 203 superior and inferior rectus recession, 209 superior oblique strengthening procedure, 209 superior oblique tendon laxity, 201
superior rectus contracture, 201 surgical plan, 200
torsional diplopia, 202–203
G
German Institute for Quality and E ciency in Healthcare (IQWIG), 99
Glucocorticoids (GC), 213 Graves orbitopathy
active inflammatory phase combined therapy, 213
dysthyroid optic neuropathy (DON), 214 glucocorticoids (GC), 213 immunosuppressive treatments, 213–214 orbital radiotherapy (OR), 213 sight-threatening corneal breakdown, 214 symptoms, 214–215
childhood, 222 classification, 211–212 clinical assessment
activity signs, 208–209 assess severity, 209–211 orbital imaging, 211
clinical characteristics, 208 diabetes, 222
environmental and genetic influence cigarette smoking, 221 susceptibility genes, 221–222
euthyroid, 222
Graves disease (GD), 207–208 inactive disease stages
extraocular muscle surgery, 216–217 lid surgery, 217–220
orbital decompression, 215–216 management plan, 208, 210 thyroid dysfunction, 220
H
Health-related quality of life (HRQoL), 98, 99, 106–108 Horizontal gaze palsy with progressive scoliosis
(HGPPS), 81 Hypertropia, 3–4, 179
I
Immune myopathy, 60–61
Incomplete third nerve palsy hypertropia, 199 Infantile esotropia (IE)
definition and prevalence, 137 dissociated eye movements
pathogenetic role, 29 vergence eye movements, 25
early vs. late infantile strabismus surgery study (ELISSS)
alignment and fusion, 145 binocular vision, 140
horizontal angle of strabismus, 140–141 methods and results, 139–140 postoperative angle of strabismus, 145 prospective study, 139
random-effects model, 146, 148 reoperation rate, 142–143 spontaneous reduction, 146–148 spontaneous resolution, 146 test-retest reliability, 144–145
esotonus vs. convergence, 28 exotropia
230 Index
active divergence mechanism, 26
binocular fusion vs. dissociated esotonus, 27, 28 clinical signs, 27
horizontal strabismus, 28 outcome parameters, 138–139 pathogenesis, 138 sensory/motor etiology, 137–138 tonus, 25–26
Infantile-onset image decorrelation, 38–39 Inferior oblique (IO) palsy, 71–72
Inferior oblique overaction (IOOA), 4, 176–177 Inflammatory myositis, 61
Intermittent exotropia, 3, 4
L
Levodopa, 133
Logistic regression analysis, 143
Long-term binocular alignment control system, 14
M
Manifest latent nystagmus (MLN) Anderson–Kesternbaum surgery, 158 clinical characteristics, 157–158 idiopathic infantile nystagmus, 158 slow phase, 157
Marcus-Gunn phenomenon, 80–82, 85, 87–89 Marlow occlusion, 19
Meta-regression model, 143 Microstrabismus
number of operations
postoperative angle of strabismus, 145 reoperation rate, 142–143
test-retest reliability, 144–145 random-e ects model, 146, 148 spontaneous reduction, 146–148 spontaneous resolution, 146
Mittendorf’s spot, 115 Möbius syndrome, 83 Moebius syndrome, 70
Monofixation syndrome (MFS) animal models, 37 anisometropia, 33 bi-fixation, 36–37
causes, 33
foveal suppression scotoma elimination, 36 manifest strabismus, 35–36 micro-esotropia
extrastriate cortex, 52–53 neural mechanism, 51 neuroanatomic findings, 52, 53 stereoscopic threshold, 52
subnormal stereopsis and motor fusion, 51 normal and anomalous binocular vision
anomalous retinal correspondence (ARC), 34 binocular correspondence, 34–35 communication, 33
cortical adaptation, 34
ocular dominance column, 33, 34 normal/near-normal fusional vergence, 37 primary MFS, 38–39
Motor skills, 106
Muscle length adaptation, 11–13
N
Neoplastic myositis, 61 Neuroanatomical strabismus
acquired motor neuropathy, 71–72 acquired pulley heterotopy, 63–64 congenital peripheral neuropathy
congenital cranial dysinnervation disorders (CCDDs), 66
congenital fibrosis of the extraocular muscles (CFEOM), 67–69
congenital oculomotor (CN3) palsy, 67 congenital trochlear (CN4) palsy, 69 Duane’s retraction syndrome (DRS), 69 Moebius syndrome, 70
congenital pulley heterotopy, 62–63 divergence paralysis esotropia, 64–65 etiology, 59
extraocular myopathy immune myopathy, 60–61 inflammatory myositis, 61 neoplastic myositis, 61
primary EOM myopathy, 59–60 traumatic myopathy, 61–62
vergence and gaze abnormalities, 72 Normal correspondence (NRC), 34
O
Ocular albinism (OA), 155 Ocular motility disorders, CCDD
brainstem and cranial nerve development, 77, 78 Brown syndrome
comorbidity, 85 epidemiologic features, 85 incidence and heredity, 86
intra-and postoperative findings, 87 laterality, 85–86
motility findings, 83–85 natural course, 87
neurodevelopmental disorder, 89–90 potential induction, 86–87 radiologic findings, 87
saccadic eye movements, 85 sex distribution, 86
CFEOM, 78–79
congenital fourth nerve palsy, 82
congenital monocular elevation deficiency, 87–89 congenital ptosis, 81
congenital trochlear palsy, 82 Duane retraction syndrome, 79–81 HGPPS, 81
isolated uni-/bilateral facial palsy, 83 vertical retraction syndrome, 88
Ocular motor control system, 18 Oculocutaneous albinism (OCA), 155 Oculomotor palsy, 71
Optic neuropathy, 133–134
Optical coherence tomography (OCT), 155, 156 Orbital radiotherapy (OR), 213
P
Paralytic strabismus
complete third nerve palsy, 198–199
Index 231
fourth nerve palsy hypertropia bilateral involvement, 201
congenital superior oblique palsy, 200 inferior oblique weakening procedure, 203 superior and inferior rectus recession, 209 superior oblique strengthening procedure, 209 superior oblique tendon laxity, 201
superior rectus contracture, 201 surgical plan, 200
torsional diplopia, 202–203 incomplete third nerve palsy, 199 principles
preoperative assessment, 196–197 surgery timing, 195–196
surgical treatment, 197–198 sixth nerve palsy hypertropia
lateral and medial rectus resection, 204 medial rectus weakening, sound eye, 204–205
Pediatric strabismus adult strabismus, 7
associated conditions, 4 esodeviation, 1–2 exodeviation, 3 hyperdeviation, 3–4 surgery rates, 4
worldwide incidence and prevalence, 4–7 Periodic alternating nystagmus (PAN), 158–159 Pharmacological occlusion, 104 Photorefractive keratectomy (PRK), 105
Plano lens, 130 Posner’s maneuver, 174
Posterior partial tenectomy, 190
Primary extraocular muscle (EOM) myopathy, 59–60 Primary oblique muscle overaction, 14
Prism adaptation, 12
Q
Quality adjusted life years (QALY), 99
R
Reversed fixation test (RFT), 179
S
Sensory esotropia, 2, 3 Sensory exotropia, 3
Sixth nerve palsy hypertropia
lateral and medial rectus resection, 204 medial rectus weakening, sound eye, 204–205
Stereoacuity skills, 106
Superior oblique overaction (SOOA), 176–177 Superior oblique (SO) surgery
clinical investigation
6–0 Polyglactin 910 sutures, 186 asymmetric effects, 189 enucleation, 186
Jampolsky’s recommendations, 187
measurement technique, 188
superior rectus muscle recession effects, 186–188 suspension technique, 188–189
tendon incarceration syndrome, 185 frenulum, 185
theoretical e ect anterior–posterior axis, 189 posterior tenectomy, 190 SO anatomy, 190, 191
SO tendon, 189, 192 threefold function, 189
two-dimensional trigonometry, 192
T
Thyroid-stimulating hormone receptor (TSHR), 208 Traumatic myopathy, 61–62
Trochlear palsy, 71
TSHR antibodies (TRAb), 208 Two-dimensional trigonometry, 192
U
Unilateral strabismus changes cyclovertical deviation, 20, 21 head-tilt changes, 21
ipsilateral medial and contralateral rectus muscle, 19 torsional position, 20
vertical recordings, 21
V
Vergence adaptation, 11, 12 Vertical retraction syndrome, 88 Visual cortex mechanisms esotropia
binocular input correlation, 50–51
binocular visuomotor behavior development, 42, 43 cerebral damage risk factors, 41–42
cortical binocular connections, 44–46 cytotoxic insult, cerebral fibers, 42 early-onset (infantile) esotropia, 41 extrastriate cortex, striate cortex, 46
fusional vergence and innate convergence bias, 44 genetic influence, cerebral connection, 42 high-grade fusion repair, 50
inter-ocular suppression, 46–47
monocular compartments, striate cortex, 44, 46 motion sensitivity and conjugate eye tracking, 44 naso-temporal inequalities, cortical suppression, 47 persistent nasalward visuomotor bias, 47–50 sensorial fusion and stereopsis development, 43 strabismic human infant repair, 50
micro-esotropia extrastriate cortex, 52–53 neural mechanism, 51
neuroanatomic findings, 52, 53 stereoscopic threshold, 52
subnormal stereopsis and motor fusion, 51
