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Ординатура / Офтальмология / Английские материалы / Essentials in Ophthalmology Pediatric Ophthalmology Neuro-Ophthalmology Genetics_Lorenz, Brodsky_2010.pdf
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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.

References

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2.Gianoukakis AG, Smith TJ (2008) Recent insights into the pathogenesis and management of thyroid-associated ophthalmopathy. Curr Opin Endocrinol Diabetes Obes 15:446–452

3.Feldon SE,Park DJ,O’Loughlin CW,et al (2005) Autologous T-lymphocytes stimulate proliferation of orbital fibroblasts derived from patients with Graves’ ophthalmopathy. Invest Ophthalmol Vis Sci 46:3913–3921

4.Smith TJ (2004) Novel aspects of orbital fibroblast pathology. J Endocrinol Invest 27:246–253

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17.Terwee CB, Prummel MF, Gerding MN, et al (2005) Measuring disease activity to predict therapeutic outcome in Graves’ ophthalmopathy. Clin Endocrinol (Oxf) 62:145–155

18.Mourits MP, Prummel MF, Wiersinga WM, et al (1994) Measuring eye movements in Graves ophthalmopathy. Ophthalmology 101:1341–1346

19.Eckstein AK, Plicht M, Lax H, et al (2006) Thyrotropin receptor autoantibodies are independent risk factors for Graves’ ophthalmopathy and help to predict severity and outcome of the disease. J Clin Endocrinol Metab 91:3464–3470

20.Kahaly GJ (2004) Recent developments in Graves’ ophthalmopathy imaging. J Endocrinol Invest 27:254–258

21.Bartalena L, Baldeschi L, Dickinson A, et al (2008) Consensus statement of the European Group on Graves orbitopathy (EUGOGO) on management of GO. Eur J Endocrinol 158:273–285

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24.Kahaly GJ, Pitz S, Hommel G, et al (2005) Randomized, single blind trial of intravenous versus oral steroid monotherapy in Graves orbitopathy. J Clin Endocrinol Metab 90:5234–5240

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16 27. Bradley EA, Gower EW, Bradley DJ, et al (2008) Orbital radiation for graves ophthalmopathy: a report by the American academy of ophthalmology. Ophthalmology 115:398–409

28.Marcocci C, Bartalena L, Panicucci M, et al (1987) Orbital cobalt irradiation combined with retrobulbar or systemic corticosteroids for Graves’ ophthalmopathy: a comparative study. Clin Endocrinol (Oxf) 27:33–42

29.Marcocci C,Bartalena L,Tanda ML,et al (2001) Comparison of the e ectiveness and tolerability of intravenous or oral glucocorticoids associated with orbital radiotherapy in the management of severe Graves’ ophthalmopathy: results of a prospective, single-blind, randomized study. J Clin Endocrinol Metab 86:3562–3567

30.El Fassi D, Banga JP, Gilbert JA, et al (2009) Treatment of Graves disease with rituximab specifically reduces the production of thyroid stimulating autoantibodies. Clin Immunol 130:252–258

31.Heemstra KA, Toes RE, Sepers J, et al (2008) Rituximab in relapsing Graves disease, a phase II study. Eur J Endocrinol 159:609–615

32.Salvi M, Vannucchi G, Campi I, et al (2007) Treatment of Graves disease and associated ophthalmopathy with the anti-CD20 monoclonal antibody rituximab: an open study. Eur J Endocrinol 156:33–40

33.Paridaens D, van den Bosch WA, van der Loos TL, et al (2005) The e ect of etanercept on Graves’ ophthalmopathy: a pilot study. Eye 19:1286–1289

34.Traisk F, Tallstedt L (2001) Thyroid associated ophthalmopathy: botulinum toxin A in the treatment of upper eyelid retraction–a pilot study. Acta Ophthalmol Scand 79:585–588

35.Baldeschi L (2008) Correction of lid retraction and exophthalmos. Dev Ophthalmol 41:103–126

36.Garrity JA, Bahn RS (2006) Pathogenesis of graves ophthalmopathy: implications for prediction, prevention, and treatment. Am J Ophthalmol 142:147–153

37.Mourits MP, Bijl HM, Baldeschi L, et al (2008) Outcome of orbital decompression for disfiguring proptosis in patients with Graves orbitopathy using various surgical procedures. Br J Ophthalmol

38.Esser J, Eckstein A (1999) Ocular muscle and eyelid surgery in thyroid-associated orbitopathy.Exp Clin Endocrinol Diabetes 107(Suppl 5):S214–S221

39.Eckstein A, Holdt M, Johnson KTM, et al (2008) Tendon elongation: a new surgical technique for large convergent squint after three wall orbital decompression in thyroid associated ophthalmopathy. ESA proceedings

correction of horizontal and vertical squint of value in graves’ ophthalmopathy? Klin Monatsbl Augenheilkd 221:769–775

41.Krzizok T, Efinger K, Kaufmann H (1993) Dosierbarkeit vonAugenmuskeloperationen bei endokriner Orbitopathie. Z prakt Augenheilk 14:273–279

42.Schittkowski M, Fichter N, Gutho R (2004) Strabismus surgery in Graves disease–dose-e ect relationships and functional results. Klin Monatsbl Augenheilkd 221: 941–947

43.Neoh C, Eckstein A (2007) Eyelid surgery. In: Wiersinga WM, Kahaly GJ (eds) Graves orbitopathy: a multidiscplinary approach. Karger, Basel, pp 188–198

44.Tallstedt L, Lundell G, Torring O, et al (1992) Occurrence of ophthalmopathy after treatment for Graves’ hyperthyroidism. The thyroid study group. N Engl J Med 326: 1733–1738

45.Marcocci C, Bruno-Bossio G, Manetti L, et al (1999) The course of Graves’ ophthalmopathy is not influenced by near total thyroidectomy: a case-control study. Clin Endocrinol (Oxf) 51:503–508

46.Dralle H, Sekulla C (2004) Morbidity after subtotal and total thyroidectomy in patients with Graves disease: the basis for decision-making regarding surgical indication and extent of resection. Z Arztl Fortbild Qualitatssich 98(Suppl 5):45–53

47.Bartalena L, Marcocci C, Bogazzi F, et al (1998) Relation between therapy for hyperthyroidism and the course of Graves’ ophthalmopathy. N Engl J Med 338:73–78

48.Perros P, Kendall-Taylor P, Neoh C, et al (2005) A prospective study of the effects of radioiodine therapy for hyperthyroidism in patients with minimally active graves’ ophthalmopathy. J Clin Endocrinol Metab 90: 5321–5323

49.Carella C, Mazziotti G, Sorvillo F, et al (2006) Serum thyrotropin receptor antibodies concentrations in patients with Graves disease before, at the end of methimazole treatment, and after drug withdrawal: evidence that the activity of thyrotropin receptor antibody and/or thyroid response modify during the observation period. Thyroid 16:295–302

50.Schott M, Morgenthaler NG, Fritzen R, et al (2004) Levels of autoantibodies against human TSH receptor predict relapse of hyperthyroidism in Graves disease. Horm Metab Res 36:92–96

51.Orgiazzi J, Madec AM (2002) Reduction of the risk of relapse after withdrawal of medical therapy for Graves disease. Thyroid 12:849–853

52.Khoo DH, Ho SC, Seah LL, et al (1999) The combination of absent thyroid peroxidase antibodies and high thyroidstimulating immunoglobulin levels in Graves disease iden-

tifies a group at markedly increased risk of ophthalmopathy. Thyroid 9:1175–1180

53.Gerding MN, van der Meer JW, Broenink M, et al (2000) Association of thyrotrophin receptor antibodies with the clinical features of Graves’ ophthalmopathy. Clin Endocrinol (Oxf) 52:267–271

54.Noh JY, Hamada N, Inoue Y, et al (2000) Thyroidstimulating antibody is related to Graves’ ophthalmopathy, but thyrotropin-binding inhibitor immunoglobulin is related to hyperthyroidism in patients with Graves disease. Thyroid 10:809–813

55.Eckstein AK, Plicht M, Lax H, et al (2004) Clinical results of anti-inflammatory therapy in Graves’ ophthalmopathy and association with thyroidal autoantibodies. Clin Endocrinol (Oxf) 61:612–618

56.Eckstein AK, Plicht M, Lax H, et al (2006) TSH-receptor autoantibodies are independent risk factors for Graves’ ophthalmopathy and help to predict severity and outcome of the disease. J Clin Endocrinol Metab 91(9):3464–3470

57.Pfeilschifter J, Ziegler R (1996) Smoking and endocrine ophthalmopathy: impact of smoking severity and current vs lifetime cigarette consumption. Clin Endocrinol (Oxf) 45:477–481

58.Eckstein A, Quadbeck B, Mueller G, et al (2003) Impact of smoking on the response to treatment of thyroid associated ophthalmopathy. Br J Ophthalmol 87:773–776

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59.Cawood TJ, Moriarty P, O’Farrelly C, et al (2007) Smoking and thyroid-associated ophthalmopathy: a novel explanation of the biological link. J Clin Endocrinol Metab 92:59–64

60.Brix TH, Kyvik KO, Christensen K, et al (2001) Evidence for a major role of heredity in Graves disease: a populationbased study of two Danish twin cohorts. J Clin Endocrinol Metab 86:930–934

61.Manji N, Carr-Smith JD, Boelaert K, et al (2006) Influences of age, gender, smoking, and family history on autoimmune thyroid disease phenotype. J Clin Endocrinol Metab 91:4873–4880

62.Ban Y, Tomer Y (2005) Genetic susceptibility in thyroid autoimmunity. Pediatr Endocrinol Rev 3:20–32

63.Aust G, Krohn K, Morgenthaler NG, et al (2006) Graves disease and Hashimoto’s thyroiditis in monozygotic twins: case study as well as transcriptomic and immunohistological analysis of thyroid tissues. Eur J Endocrinol 154:13–20

64.Eckstein A, Loesch C, Glowacka D, et al (2009) Euthyroid and primarily hypothyroid patients develop milder and significantly more asymmetric Graves ophthalmopathy. Br J Ophthalmol 93:1052–1056

65.Krassas GE, Gogakos A (2006) Thyroid-associated ophthalmopathy in juvenile Graves disease–clinical, endocrine and therapeutic aspects. J Pediatr Endocrinol Metab 19:1193–1206

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