Eye Movements in Parkinson's Disease and Inherited Parkinsonian Syndromes.
Eye Movements in Parkinson's Disease and Inherited Parkinsonian Syndromes.
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DOI：
10.3389/fneur.2017.00592
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发表时间：
2017
影响因子：
3.4
通讯作者：
Optican LM
中科院分区：
文献类型：
--
作者：
Pretegiani E;Optican LM
尽管有广泛的研究，基底神经节（BG）在运动控制中的功能尚未完全了解。眼球运动，特别是扫视，是BG功能的方便指标。在这里，我们回顾了帕金森病（PD）和遗传性帕金森综合征的主要眼科研究结果。PD是一种进行性神经退行性疾病，由黑质网状部内的多巴胺能细胞损失引起，导致纹状体多巴胺耗竭，随后增加来自内部苍白球和黑质网状部的抑制性BG输出。眼球运动异常是常见的PD：异常是更明显的自愿比反射性扫视在初始阶段，但视觉引导扫视也可能涉及在后期阶段。扫视测量不足（包括异常碎片化的扫视）、准确性降低和潜伏期增加是最突出的缺陷。PD患者也表现出异常频繁和大的方波抽搐和受损的抑制反射性扫视时，自愿镜子扫视是必需的。收敛能力差和改变追求是常见的。遗传性帕金森综合征是一组异质性的罕见综合征，由于基因突变引起的症状类似于PD。研究了某些帕金森病患者的眼动特征。虽然共享一些PD特征，但每种综合征都有独特的特征，这有助于更好地定义帕金森病的临床表型。此外，由于遗传性帕金森病的发病机制和潜在的神经回路故障往往是很好的定义，他们可能提供了一个更好的前景比特发性PD了解BG功能。
Despite extensive research, the functions of the basal ganglia (BG) in movement control have not been fully understood. Eye movements, particularly saccades, are convenient indicators of BG function. Here, we review the main oculomotor findings reported in Parkinson’s disease (PD) and genetic parkinsonian syndromes. PD is a progressive, neurodegenerative disorder caused by dopaminergic cell loss within the substantia nigra pars compacta, resulting in depletion of striatal dopamine and subsequent increased inhibitory BG output from the internal globus pallidus and the substantia nigra pars reticulata. Eye movement abnormalities are common in PD: anomalies are more evident in voluntary than reflexive saccades in the initial stages, but visually guided saccades may also be involved at later stages. Saccadic hypometria (including abnormally fragmented saccades), reduced accuracy, and increased latency are among the most prominent deficits. PD patients show also unusually frequent and large square wave jerks and impaired inhibition of reflexive saccades when voluntary mirror saccades are required. Poor convergence ability and altered pursuit are common. Inherited parkinsonisms are a heterogeneous group of rare syndromes due to gene mutations causing symptoms resembling those of PD. Eye movement characteristics of some parkinsonisms have been studied. While sharing some PD features, each syndrome has a distinctive profile that could contribute to better define the clinical phenotype of parkinsonian disorders. Moreover, because the pathogenesis and the underlying neural circuit failure of inherited parkinsonisms are often well defined, they might offer a better prospect than idiopathic PD to understand the BG function.
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