{"title":"Neural Plasticity in Amblyopia","authors":"B. Thompson","doi":"10.1093/acrefore/9780190236557.013.702","DOIUrl":null,"url":null,"abstract":"Early in life, the brain has a substantial capacity for change, often referred to as neuroplasticity. Disrupted visual input to the brain during an early “critical” or “sensitive period” of heightened neuroplasticity induces structural and functional changes within neural systems and causes amblyopia, a sensory disorder associated with abnormal development of the brain areas involved in perception. Amblyopia impairs a broad range of visual, multisensory, and motor functions, and recovery from amblyopia requires a substantial change in visual information processing within the brain. Therefore, not only is amblyopia caused by an interaction between visual experience and heightened neuroplasticity, recovery from amblyopia also requires significant neuroplastic change within the brain. A number of evidence-based treatments are available for young children with amblyopia whose brains are still rapidly developing and have a correspondingly high level of neuroplasticity. However, adults with amblyopia are often left untreated because of the idea that the adult brain no longer has sufficient neuroplasticity to relearn how to process visual information. In the early 21st century, it became clear that this idea was not correct. A number of interventions that can enhance neuroplasticity in the mature visual cortex have been identified using animal models of amblyopia and are now being translated into human studies. Other promising techniques for enhancing visual cortex neuroplasticity have emerged from studies of adult humans with amblyopia. Examples of interventions that may improve vision in adult amblyopia include refractive correction, patching of the amblyopic eye (reverse patching), monocular and binocular perceptual learning, noninvasive brain stimulation, systemic drugs, and exercise. The next important stage of research within this field will be to conduct fully controlled randomized clinical trials to assess which, if any, of these interventions can be translated into a mainstream treatment for amblyopia in adulthood.","PeriodicalId":339030,"journal":{"name":"Oxford Research Encyclopedia of Psychology","volume":"5 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2021-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oxford Research Encyclopedia of Psychology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/acrefore/9780190236557.013.702","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
Abstract
Early in life, the brain has a substantial capacity for change, often referred to as neuroplasticity. Disrupted visual input to the brain during an early “critical” or “sensitive period” of heightened neuroplasticity induces structural and functional changes within neural systems and causes amblyopia, a sensory disorder associated with abnormal development of the brain areas involved in perception. Amblyopia impairs a broad range of visual, multisensory, and motor functions, and recovery from amblyopia requires a substantial change in visual information processing within the brain. Therefore, not only is amblyopia caused by an interaction between visual experience and heightened neuroplasticity, recovery from amblyopia also requires significant neuroplastic change within the brain. A number of evidence-based treatments are available for young children with amblyopia whose brains are still rapidly developing and have a correspondingly high level of neuroplasticity. However, adults with amblyopia are often left untreated because of the idea that the adult brain no longer has sufficient neuroplasticity to relearn how to process visual information. In the early 21st century, it became clear that this idea was not correct. A number of interventions that can enhance neuroplasticity in the mature visual cortex have been identified using animal models of amblyopia and are now being translated into human studies. Other promising techniques for enhancing visual cortex neuroplasticity have emerged from studies of adult humans with amblyopia. Examples of interventions that may improve vision in adult amblyopia include refractive correction, patching of the amblyopic eye (reverse patching), monocular and binocular perceptual learning, noninvasive brain stimulation, systemic drugs, and exercise. The next important stage of research within this field will be to conduct fully controlled randomized clinical trials to assess which, if any, of these interventions can be translated into a mainstream treatment for amblyopia in adulthood.