Computational models to delineate 3D gaze-shift strategies in Parkinson's disease.
Computational models to delineate 3D gaze-shift strategies in Parkinson's disease.
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DOI：
10.1088/1741-2552/ac123e
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发表时间：
2021-07-19
影响因子：
4
通讯作者：
Shaikh AG
中科院分区：
文献类型：
--
作者：
Gupta P;Beylergil S;Murray J;Kilbane C;Ghasia FF;Shaikh AG
帕金森病(PD)经常影响眼球的会聚运动，干扰对减轻跌倒至关重要的深度和维度的感知。我们研究了补偿异常收敛的神经策略及其在帕金森病中的机制基础。先验假设是，通过结合快速眼动(扫视)来实现不同深度的凝视转移，受损的聚光率得到补偿。我们的实验通过模拟帕金森病患者眼跳-眼动相互作用的生物学上可信的计算模型并验证实际患者数据中的预测来检验这一假设。我们发现了四种完成3D凝视转移的策略：纯眼球运动、纯眼球跳动、先眼球后眼跳和先眼跳后眼球跳动的组合。帕金森病患者双眼的注视转移策略不一致。眼跳潜伏期延长，且当眼跳先于眼跳或眼跳仅使3D视线移动时，这种延长更为明显。计算模型预测，至少有两种可能的机制会触发眼跳和眼球收敛。一种是基于当收敛增益不是最优时中心凹精确度的缺乏。第二种机制反映了门控机制中的噪声，即全食道神经元，用于发散和眼跳。这两个模型的预测都没有完全得到患者数据的支持。然而，一个包含异常会聚速度增加和门控受损的组合模型准确地模拟了PD患者的结果。这一组合策略在生物学上是可行的，原因有两个：1)在帕金森病中显著受影响的基底节通过小脑投射到中脑的收敛速度神经元。投影直接影响收敛速度增益。2)基底节通过上丘影响更年期神经元的活动模式。异常的基底节活动可能会在更年期神经元中引入噪声。
Parkinson's disease (PD) frequently affects vergence eye movements interfering with the perception of depth and dimensionality critical for mitigating falls. We examined neural strategies that compensate for abnormal vergence and their mechanistic underpinning in PD. The a priori hypothesis was that impaired vergence is compensated by incorporating rapid eye movements (saccades) to accomplish gaze shifts at different depths. Our experiments examined the hypothesis by simulating biologically plausible computational models of saccade-vergence interactions in PD and validating predictions in the actual patient data. We found four strategies to accomplish 3D gaze shift; pure vergence eye movements, pure saccadic eye movements, combinations of vergence followed by a saccade, and combination of saccade followed by vergence. The gaze shifting strategy of the two eyes was incongruent in PD. The latency of vergence was prolonged, and it was more so when the saccades preceded the vergence or when the saccades only made 3D gaze shift. Computational models predicted at least two possible mechanisms triggering saccades along with vergence. One is based on the lack of foveal accuracy when the vergence gain is suboptimal. The second mechanism reflects the noise in the gating mechanism, the omnipause neurons, for vergence and saccades. None of the two model predictions alone were completely supported by the patient data. However, a combined model incorporating both abnormal vergence velocity gain and impaired gating accurately simulated the results from PD patients. The combined strategy is biologically plausible for two reasons: 1) The basal ganglia that is prominently affected in PD projects to the vergence velocity neurons in the midbrain via the cerebellum. The projection directly affects the vergence velocity gain. 2) The basal ganglia, via superior colliculus, influences the pattern of omnipause neuronal activity. Abnormal basal ganglia activity may introduce noise in the omnipause neurons.
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影响因子：
4.1
作者：
Hanuska, Jaromir;Bonnet, Cecilia;Ruzicka, Evzen
通讯作者：
Ruzicka, Evzen
影响因子：
0.8
作者：
Lepore, FE
通讯作者：
Lepore, FE
影响因子：
4.1
作者：
Ghasia, Fatema F.;Otero-Millan, Jorge;Shaikh, Aasef G.
通讯作者：
Shaikh, Aasef G.
影响因子：
2.9
作者：
HENN, V;COHEN, B
通讯作者：
COHEN, B
影响因子：
2.5
作者：
MAYS, LE
通讯作者：
MAYS, LE