Ishii Daisuke, Ishibashi Kiyoshige, Takeda Kotaro, Yuine Hiroshi, Yamamoto Satoshi, Kaku Yuki, Yozu Arito, Kohno Yutaka
Center for Medical Sciences, Ibaraki Prefectural University of Health Sciences, Inashiki-gun, Japan.
Department of Cognitive Behavioral Physiology, Chiba University Graduate School of Medicine, Chiba, Japan.
Front Hum Neurosci. 2021 Nov 1;15:761186. doi: 10.3389/fnhum.2021.761186. eCollection 2021.
Neural plasticity compensates for the loss of motor function after stroke. However, whether neural plasticity occurs in the somatosensory pathways after stroke is unknown. We investigated the left-right somatosensory interaction in two hemorrhagic patients using a paired somatosensory evoked potentials (p-SEPs) recorded at CP3 and CP4, which was defined as an amplitude difference between the SEPs of paired median nerve stimulations to both sides and that of single stimulation to the affected side. Patient 1 (61-year-old, left thalamic hemorrhage) has a moderate motor impairment, severe sensory deficit, and complained of pain in the affected right upper limb. Patient 2 (72-year-old, right thalamic hemorrhage) had slight motor and sensory impairments with no complaints of pain. Single SEPs (s-SEPs) were obtained by stimulation of the right and left median nerves, respectively. For paired stimulations, 1 ms after the first stimulation to the non-affected side, followed by a second stimulation to the affected side. In patient 1, a s-SEP with stimulation to the non-affected side and a p-SEP were observed in CP4. However, a s-SEP was not observed in either hemisphere with stimulation to the affected side. On the other hand, in patient 2, a s-SEP in CP3 with stimulation to the non-affected side and in CP4 with stimulation to the affected side were observed; however, a p-SEP was not observed. In addition, to investigate the mechanism by which ipsilateral median nerve stimulation enhances contralateral p-SEP in patient 1, we compared the SEP averaged over the first 250 epochs with the SEP averaged over the second 250 epochs (total number of epochs recorded: 500). The results showed that in the patient 1, when the bilateral median nerve was stimulated continuously, the habituation did not occur and the response was larger than that of the s-SEP with unilateral median nerve stimulation. In the current case report, the damage to the thalamus may cause neuroplasticity in terms of the left-right interaction (e.g., left and right S1). The somatosensory input from the affected side may interfere with the habituation of the contralateral somatosensory system and conversely increase the response.
神经可塑性可补偿中风后运动功能的丧失。然而，中风后体感通路中是否发生神经可塑性尚不清楚。我们使用在CP3和CP4记录的配对体感诱发电位（p-SEP）研究了两名出血性中风患者的左右体感相互作用，p-SEP被定义为双侧正中神经刺激的SEP与患侧单刺激的SEP之间的幅度差。患者1（61岁，左侧丘脑出血）有中度运动障碍、严重感觉缺陷，并主诉患侧右上肢疼痛。患者2（72岁，右侧丘脑出血）有轻微运动和感觉障碍，无疼痛主诉。分别通过刺激右侧和左侧正中神经获得单SEP（s-SEP）。对于配对刺激，在对非患侧进行首次刺激1毫秒后，接着对患侧进行第二次刺激。在患者1中，在CP4观察到对非患侧刺激的s-SEP和p-SEP。然而，对患侧刺激时，在任一脑半球均未观察到s-SEP。另一方面，在患者2中，观察到对非患侧刺激时CP3的s-SEP和对患侧刺激时CP4的s-SEP；然而，未观察到p-SEP。此外，为了研究患者1中同侧正中神经刺激增强对侧p-SEP的机制，我们将前250个时程平均的SEP与后250个时程平均的SEP进行了比较（记录的时程总数：500）。结果显示，在患者1中，当双侧正中神经持续受到刺激时，习惯化未发生，且反应大于单侧正中神经刺激时的s-SEP。在本病例报告中，丘脑损伤可能在左右相互作用方面（例如，左右S1）引起神经可塑性。来自患侧的体感输入可能干扰对侧体感系统的习惯化，反之增加反应。
