Center of Functionally Integrative Neuroscience, Aarhus University, Aarhus, Denmark
Radboud University, Donders Institute for Brain, Cognition and Behaviours, Nijmegen, The Netherlands.
J Neurol Neurosurg Psychiatry. 2023 Jun;94(6):448-456. doi: 10.1136/jnnp-2022-329342. Epub 2023 Feb 17.
Parkinson's disease is caused by degeneration of dopaminergic neurons, originating in the and characterised by bradykinesia, rest tremor and rigidity. In addition, visual disorders and retinal abnormalities are often present and can be identified by decreased visual acuity, abnormal spatial contrast sensitivity or even difficulty in complex visual task completion. Because of their early onset in patients with de novo Parkinson's disease, the anatomical retinal changes and electrophysiological modification could be valuable markers even at early stages of the disease. However, due to the concomitant occurrence of normal ageing, the relevance and specificity of these predictive values can be difficult to interpret. This review examines retinal dysfunction arising in Parkinson's disease. We highlight the electrophysiological delays and decreased amplitude in the electroretinography recorded in patients and animal models. We relate this to coexisting anatomical changes such as retinal nerve fibre layer and macular thinning, measured using optical coherence tomography, and show that functional measures are more consistent overall than optical coherence-measured structural changes. We review the underlying chemical changes seen with loss of retinal dopaminergic neurons and the effect of levodopa treatment on the retina in Parkinson's disease. Finally, we consider whether retinal abnormalities in Parkinson's disease could have a role as potential markers of poorer outcomes and help stratify patients at early stages of the disease. We emphasise that retinal measures can be valuable, accessible and cost-effective methods in the early evaluation of Parkinson's disease pathogenesis with potential for patient stratification.
帕金森病是由多巴胺能神经元变性引起的,起源于 ,其特征为运动迟缓、静止性震颤和僵直。此外,常伴有视觉障碍和视网膜异常,可通过视力下降、空间对比敏感度异常甚至复杂视觉任务完成困难来识别。由于新发帕金森病患者的这些视网膜变化很早就出现,因此解剖结构的视网膜变化和电生理改变可能是有价值的标志物,甚至在疾病的早期阶段也是如此。然而,由于正常衰老的同时发生,这些预测值的相关性和特异性可能难以解释。本文综述了帕金森病中出现的视网膜功能障碍。我们强调了在患者和动物模型中记录的视网膜电图中的电生理延迟和振幅降低。我们将其与共有的解剖结构变化相关联,如视网膜神经纤维层和黄斑变薄,这些变化可通过光学相干断层扫描测量,并表明功能测量总体上比光学相干测量的结构变化更一致。我们综述了因视网膜多巴胺能神经元丧失而出现的潜在化学变化,以及左旋多巴治疗对帕金森病中视网膜的影响。最后,我们考虑了帕金森病中的视网膜异常是否可以作为预后较差的潜在标志物,并帮助在疾病早期对患者进行分层。我们强调,视网膜测量可能是一种有价值、可及且具有成本效益的方法,可用于早期评估帕金森病的发病机制,并有可能对患者进行分层。