Tahayori Behdad, Tahayori Bahman, Koceja David
Department of Kinesiology and Program in Neurosciences, Indiana University, Bloomington, Indiana; Department of Physical Therapy, School of Rehabilitation Sciences, Shiraz University of Medical Sciences, Shiraz, Iran; Neurorehabilitation Program, The Crossing Rehabilitation Center, Indiana University Health, La Porte, Indiana;
Neuroengineering Research Laboratory, Department of Electrical and Electronic Engineering, The University of Melbourne, Melbourne, Australia.
J Neurophysiol. 2015 Jun 1;113(10):3751-8. doi: 10.1152/jn.00132.2015. Epub 2015 Apr 22.
Previous activation of the soleus Ia afferents causes a depression in the amplitude of the H-reflex. This mechanism is referred to as postactivation depression (PAD) and is suggested to be presynaptically mediated. With the use of a paired reflex depression paradigm (eliciting two H-reflexes with conditioning-test intervals from 80 ms to 300 ms), PAD was examined in a group of healthy individuals and a group of hemiplegic patients. Healthy individuals showed substantial depression of the test H-reflex at all intervals. Although the patient group showed substantially less depression at all intervals, increasing the interval between the two reflexes sharply reduced the depression. In a separate experiment, we varied the size of the conditioning H-reflex against a constant test H-reflex. In healthy individuals, by increasing the size of the conditioning H-reflex, the amplitude of the test H-reflex exponentially decreased. In the patient group, however, this pattern was dependent on the conditioning-test interval; increasing the size of the conditioning H-reflex caused an exponential decrease in the size of the test reflex at intervals shorter than 150 ms. This pattern was similar to that of healthy individuals. However, conducting the same protocol at a longer interval (300 ms) in these patients resulted in an abnormal pattern (instead of an exponential decrease in the size of the test reflex, exaggerated responses were observed). Fisher discriminant analysis suggested that these two patterns (which differed only in the timing between the two stimuli) were substantially different from each other. Therefore, it is suggested that the abnormal pattern of PAD in hemiplegic stroke patients could be a contributing factor for the pathophysiology of spasticity.
先前对比目鱼肌Ia传入神经的激活会导致H反射幅度降低。这种机制被称为激活后抑制(PAD),并被认为是由突触前介导的。通过使用配对反射抑制范式(以80毫秒至300毫秒的条件-测试间隔诱发两个H反射),对一组健康个体和一组偏瘫患者进行了PAD检测。健康个体在所有间隔下测试H反射均表现出显著抑制。虽然患者组在所有间隔下的抑制程度明显较小,但增加两个反射之间的间隔会大幅降低抑制程度。在另一个实验中,我们在恒定测试H反射的情况下改变条件H反射的大小。在健康个体中,通过增加条件H反射的大小,测试H反射的幅度呈指数下降。然而,在患者组中,这种模式取决于条件-测试间隔;在短于150毫秒的间隔下,增加条件H反射的大小会导致测试反射的大小呈指数下降。这种模式与健康个体相似。然而,在这些患者中以更长的间隔(300毫秒)进行相同的实验方案会导致异常模式(观察到的不是测试反射大小的指数下降,而是夸张的反应)。费舍尔判别分析表明,这两种模式(仅在两个刺激之间的时间上有所不同)彼此有显著差异。因此,有人提出偏瘫中风患者中PAD的异常模式可能是痉挛病理生理学的一个促成因素。