The clinical syndromes of Progressive Supranuclear Palsy (PSP) may be mediated by abnormal temporal dynamics of brain networks, due to the impact of atrophy, synapse loss and neurotransmitter deficits. We tested the hypothesis that alterations in signal complexity in neural networks influence short-latency state transitions. Ninety-four participants with PSP and 64 healthy controls were recruited from two independent cohorts. All participants underwent clinical and neuropsychological testing and resting-state functional MRI. Network dynamics were assessed using hidden Markov models and neural signal complexity measured in terms of multiscale entropy. In both cohorts, PSP increased the proportion of time in networks associated with higher cognitive functions. This effect correlated with clinical severity as measured by the PSP-rating-scale, and with reduced neural signal complexity. Regional atrophy influenced abnormal brain-state occupancy, but abnormal network topology and dynamics were not restricted to areas of atrophy. Our findings show that the pathology of PSP causes clinically relevant changes in neural temporal dynamics, leading to a greater proportion of time in inefficient brain-states.

由于萎缩、突触丧失和神经递质缺乏的影响，进行性核上性麻痹 (PSP) 的临床综合征可能由脑网络的异常时间动态介导。我们测试了神经网络中信号复杂性的变化会影响短延迟状态转换的假设。从两个独立的队列中招募了 94 名 PSP 参与者和 64 名健康对照者。所有参与者都接受了临床和神经心理学测试以及静息状态功能磁共振成像。使用隐马尔可夫模型和根据多尺度熵测量的神经信号复杂性来评估网络动态。在这两个队列中，PSP 均增加与高级认知功能相关的网络中的时间比例。这种影响与通过 PSP 评分量表测量的临床严重程度相关，并且与神经信号复杂性降低有关。区域性萎缩影响了异常的脑状态占用，但异常的网络拓扑和动态并不局限于萎缩区域。我们的研究结果表明，PSP 的病理学会导致神经时间动力学的临床相关变化，从而导致更大比例的时间处于低效的大脑状态。