关键词: amblyopia anisometropia brain function magnetic resonance imaging oculomotor system precortical pathway strabismus structure visual cortex

来  源:   DOI:10.4103/1673-5374.371349   PDF(Pubmed)

Abstract:
Amblyopia is the most common cause of vision loss in children and can persist into adulthood in the absence of effective intervention. Previous clinical and neuroimaging studies have suggested that the neural mechanisms underlying strabismic amblyopia and anisometropic amblyopia may be different. Therefore, we performed a systematic review of magnetic resonance imaging studies investigating brain alterations in patients with these two subtypes of amblyopia; this study is registered with PROSPERO (registration ID: CRD42022349191). We searched three online databases (PubMed, EMBASE, and Web of Science) from inception to April 1, 2022; 39 studies with 633 patients (324 patients with anisometropic amblyopia and 309 patients with strabismic amblyopia) and 580 healthy controls met the inclusion criteria (e.g., case-control designed, peer-reviewed articles) and were included in this review. These studies highlighted that both strabismic amblyopia and anisometropic amblyopia patients showed reduced activation and distorted topological cortical activated maps in the striate and extrastriate cortices during task-based functional magnetic resonance imaging with spatial-frequency stimulus and retinotopic representations, respectively; these may have arisen from abnormal visual experiences. Compensations for amblyopia that are reflected in enhanced spontaneous brain function have been reported in the early visual cortices in the resting state, as well as reduced functional connectivity in the dorsal pathway and structural connections in the ventral pathway in both anisometropic amblyopia and strabismic amblyopia patients. The shared dysfunction of anisometropic amblyopia and strabismic amblyopia patients, relative to controls, is also characterized by reduced spontaneous brain activity in the oculomotor cortex, mainly involving the frontal and parietal eye fields and the cerebellum; this may underlie the neural mechanisms of fixation instability and anomalous saccades in amblyopia. With regards to specific alterations of the two forms of amblyopia, anisometropic amblyopia patients suffer more microstructural impairments in the precortical pathway than strabismic amblyopia patients, as reflected by diffusion tensor imaging, and more significant dysfunction and structural loss in the ventral pathway. Strabismic amblyopia patients experience more attenuation of activation in the extrastriate cortex than in the striate cortex when compared to anisometropic amblyopia patients. Finally, brain structural magnetic resonance imaging alterations tend to be lateralized in the adult anisometropic amblyopia patients, and the patterns of brain alterations are more limited in amblyopic adults than in children. In conclusion, magnetic resonance imaging studies provide important insights into the brain alterations underlying the pathophysiology of amblyopia and demonstrate common and specific alterations in anisometropic amblyopia and strabismic amblyopia patients; these alterations may improve our understanding of the neural mechanisms underlying amblyopia.
摘要:
弱视是儿童视力丧失的最常见原因,在没有有效干预的情况下可以持续到成年期。先前的临床和神经影像学研究表明,斜视性弱视和屈光参差性弱视的神经机制可能不同。因此,我们对这两种弱视亚型患者的脑部改变的磁共振成像研究进行了系统回顾;这项研究在PROSPERO注册(注册ID:CRD42022349191).我们搜索了三个在线数据库(PubMed,EMBASE,和WebofScience)从开始到2022年4月1日;39项研究共633例患者(324例屈光参差性弱视患者和309例斜视性弱视患者)和580例健康对照符合纳入标准(例如,案例控制设计,同行评审的文章),并纳入本综述。这些研究强调,斜视性弱视和屈光参差性弱视患者在基于任务的功能磁共振成像中,在具有空间频率刺激和视网膜异位表现的条纹状和条纹状皮层中,激活和扭曲的拓扑皮层激活图都减少。分别;这些可能是由异常的视觉体验引起的。在静息状态的早期视皮层中,已经报道了对弱视的补偿,这反映在自发脑功能增强中。在屈光参差性弱视和斜视性弱视患者中,背侧通路的功能连接和腹侧通路的结构连接也降低。屈光参差性弱视和斜视性弱视患者的共同功能障碍,相对于控件,其特征还在于动眼神经皮层的自发大脑活动减少,主要涉及额叶和顶叶视野和小脑;这可能是弱视中固定不稳定和异常扫视的神经机制的基础。关于两种形式的弱视的具体改变,屈光参差性弱视患者比斜视性弱视患者在皮质前通路中遭受更多的微结构损伤,如扩散张量成像所反映的,以及腹侧通路中更显著的功能障碍和结构丢失。与屈光参差性弱视患者相比,斜视性弱视患者在纹状体皮质中的激活衰减更大。最后,在成年屈光参差性弱视患者中,脑结构磁共振成像改变倾向于偏侧化,弱视成年人的大脑改变模式比儿童更有限。总之,磁共振成像研究提供了对弱视病理生理学基础的大脑改变的重要见解,并证明了屈光参差性弱视和斜视性弱视患者的常见和特定改变;这些改变可能会提高我们对弱视的神经机制的理解.
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