{"title":"儿童屈光参差:病例系列和回顾","authors":"","doi":"10.31707/vdr2020.6.1.p32","DOIUrl":null,"url":null,"abstract":"Background: The etiology and natural course and history of pediatric anisometropia are incompletely understood. This article reviews the literature regarding pediatric anisometropia with much of the review integrated into a case series. The review and case reports are intended to elevate clinical understanding of pediatric anisometropia including and especially treatment outcomes.\n\nCase Reports: Case one is anisomyopia with amblyopia that resulted in a poor treatment outcome despite outstanding compliance with prescribed spectacles, vision therapy, and occlusion. Case two is anisometropia caused by organic vision loss from optic neuritis early in life. Case three is an infant with hyperopic anisometropia and esotropia. The esotropia did not respond to spectacles and home based vision therapy. Neonatal high bilateral hyperopia that converted to anisometropia because of early onset cosmetically invisible unilateral esotropia is speculated. Case four describes a boy\ndiagnosed with hyperopic anisometropia at age 11 months coincident with a diagnosis\nof pseudoesotropia. His compliance with prescribed spectacles was spotty until age\nthree years. An outstanding visual outcome was achieved by age five years with spectacles only (no occlusion therapy). Case five concerns a boy who acquired hyperopic anisometropia because one eye experienced increasing hyperopia during his toddler years. His response to treatment, spectacles and part time occlusion with home vision therapy, was outstanding. Case six is an infant diagnosed with 2.50 diopters of hyperopic anisometropia at age six months. Monocular home based vison developmental activities, not glasses, were prescribed. Her anisometropia vanished\nthree months later.\n\nConclusions: Pediatric anisometropia presents and responds to treatment in a variety of ways that challenge clinical care. Etiology and age of onset, which usually elude clinicians, can explain this variety. Additional research is required to improve clinical outcomes.","PeriodicalId":91423,"journal":{"name":"Vision development and rehabilitation","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2020-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Pediatric Anisometropia: Case Series and Review\",\"authors\":\"\",\"doi\":\"10.31707/vdr2020.6.1.p32\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Background: The etiology and natural course and history of pediatric anisometropia are incompletely understood. This article reviews the literature regarding pediatric anisometropia with much of the review integrated into a case series. The review and case reports are intended to elevate clinical understanding of pediatric anisometropia including and especially treatment outcomes.\\n\\nCase Reports: Case one is anisomyopia with amblyopia that resulted in a poor treatment outcome despite outstanding compliance with prescribed spectacles, vision therapy, and occlusion. Case two is anisometropia caused by organic vision loss from optic neuritis early in life. Case three is an infant with hyperopic anisometropia and esotropia. The esotropia did not respond to spectacles and home based vision therapy. Neonatal high bilateral hyperopia that converted to anisometropia because of early onset cosmetically invisible unilateral esotropia is speculated. Case four describes a boy\\ndiagnosed with hyperopic anisometropia at age 11 months coincident with a diagnosis\\nof pseudoesotropia. His compliance with prescribed spectacles was spotty until age\\nthree years. An outstanding visual outcome was achieved by age five years with spectacles only (no occlusion therapy). Case five concerns a boy who acquired hyperopic anisometropia because one eye experienced increasing hyperopia during his toddler years. His response to treatment, spectacles and part time occlusion with home vision therapy, was outstanding. Case six is an infant diagnosed with 2.50 diopters of hyperopic anisometropia at age six months. Monocular home based vison developmental activities, not glasses, were prescribed. Her anisometropia vanished\\nthree months later.\\n\\nConclusions: Pediatric anisometropia presents and responds to treatment in a variety of ways that challenge clinical care. Etiology and age of onset, which usually elude clinicians, can explain this variety. Additional research is required to improve clinical outcomes.\",\"PeriodicalId\":91423,\"journal\":{\"name\":\"Vision development and rehabilitation\",\"volume\":\"1 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-03-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Vision development and rehabilitation\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.31707/vdr2020.6.1.p32\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Vision development and rehabilitation","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.31707/vdr2020.6.1.p32","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Background: The etiology and natural course and history of pediatric anisometropia are incompletely understood. This article reviews the literature regarding pediatric anisometropia with much of the review integrated into a case series. The review and case reports are intended to elevate clinical understanding of pediatric anisometropia including and especially treatment outcomes.
Case Reports: Case one is anisomyopia with amblyopia that resulted in a poor treatment outcome despite outstanding compliance with prescribed spectacles, vision therapy, and occlusion. Case two is anisometropia caused by organic vision loss from optic neuritis early in life. Case three is an infant with hyperopic anisometropia and esotropia. The esotropia did not respond to spectacles and home based vision therapy. Neonatal high bilateral hyperopia that converted to anisometropia because of early onset cosmetically invisible unilateral esotropia is speculated. Case four describes a boy
diagnosed with hyperopic anisometropia at age 11 months coincident with a diagnosis
of pseudoesotropia. His compliance with prescribed spectacles was spotty until age
three years. An outstanding visual outcome was achieved by age five years with spectacles only (no occlusion therapy). Case five concerns a boy who acquired hyperopic anisometropia because one eye experienced increasing hyperopia during his toddler years. His response to treatment, spectacles and part time occlusion with home vision therapy, was outstanding. Case six is an infant diagnosed with 2.50 diopters of hyperopic anisometropia at age six months. Monocular home based vison developmental activities, not glasses, were prescribed. Her anisometropia vanished
three months later.
Conclusions: Pediatric anisometropia presents and responds to treatment in a variety of ways that challenge clinical care. Etiology and age of onset, which usually elude clinicians, can explain this variety. Additional research is required to improve clinical outcomes.