A neuromorphic model of motor overflow in focal hand dystonia due to correlated sensory input.
A neuromorphic model of motor overflow in focal hand dystonia due to correlated sensory input.
复制标题
由于相关感觉输入而导致局灶性手肌张力障碍的运动溢出的神经形态模型。
DOI：
10.1088/1741-2560/13/5/055001
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Sanger Terence D
中科院分区：
文献类型：
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作者：
Sohn Won J;Niu Chuanxin M;Sanger Terence D
目的肌张力过溢是肌张力障碍的一种常见且令人沮丧的症状，表现为在有意的自主运动中发生的无意识肌肉收缩。尽管人们怀疑运动溢出是由于某些类型的肌张力障碍（如局灶性手肌张力障碍）的皮质紊乱引起的，但仍不清楚是哪种机制引发了运动溢出，更重要的是，是哪种机制使运动溢出持续存在。我们假设，如果不同的运动元素的感觉输入在统计上保持独立，那么它们的运动溢出风险就很低。但是，当有相关的感官输入时，在脉冲时间依赖的可塑性（STDP）下，感官投影之间原有的串扰会增加，最终产生不可逆的电机溢出。我们模拟了一个简化的神经肌肉系统，该系统由两个解剖上不同的指肌组成，由两层具有STDP的尖峰神经元支配。层间的突触连接包括串扰连接。在连续4天的刺激中，输入神经元分别接受独立或相关的感觉驱动。仿真是由我们在以前的工作中创建的神经形态硬件关键启用和加速的。在相关感觉输入的驱动下，串扰突触重量增加，产生明显的运动溢出；串音突触的生长导致感觉表征的扩大，反映了皮层的重组。当输入恢复其原始的不相关统计时，溢出未能消退。对照组未见电机溢出现象。尽管我们的模型是人类感觉运动系统的高度简化和有限的代表，但它使我们能够解释解剖学上不同肌肉的相关感觉输入本身如何足以引起持续和不可逆的运动溢出。需要进一步的研究来确定感觉输入的相关来源。
ObjectiveMotor overflow is a common and frustrating symptom of dystonia, manifested as unintentional muscle contraction that occurs during an intended voluntary movement. Although it is suspected that motor overflow is due to cortical disorganization in some types of dystonia (eg focal hand dystonia), it remains elusive which mechanisms could initiate and, more importantly, perpetuate motor overflow. We hypothesize that distinct motor elements have low risk of motor overflow if their sensory inputs remain statistically independent. But when provided with correlated sensory inputs, pre-existing crosstalk among sensory projections will grow under spike-timing-dependent-plasticity (STDP) and eventually produce irreversible motor overflow.ApproachWe emulated a simplified neuromuscular system comprising two anatomically distinct digital muscles innervated by two layers of spiking neurons with STDP. The synaptic connections between layers included crosstalk connections. The input neurons received either independent or correlated sensory drive during 4 days of continuous excitation. The emulation is critically enabled and accelerated by our neuromorphic hardware created in previous work.Main resultsWhen driven by correlated sensory inputs, the crosstalk synapses gained weight and produced prominent motor overflow; the growth of crosstalk synapses resulted in enlarged sensory representation reflecting cortical reorganization. The overflow failed to recede when the inputs resumed their original uncorrelated statistics. In the control group, no motor overflow was observed.SignificanceAlthough our model is a highly simplified and limited representation of the human sensorimotor system, it allows us to explain how correlated sensory input to anatomically distinct muscles is by itself sufficient to cause persistent and irreversible motor overflow. Further studies are needed to locate the source of correlation in sensory input.