神经可塑性补偿中风后运动功能的丧失。然而,卒中后的体感通路中是否存在神经可塑性尚不清楚.我们使用在CP3和CP4记录的成对体感诱发电位(p-SEP)研究了两名出血性患者的左右体感相互作用,这被定义为成对的正中神经刺激对两侧的SEP与对患侧的单次刺激之间的幅度差异。患者1(61岁,左丘脑出血)有中度运动障碍,严重的感觉缺陷,并抱怨受影响的右上肢疼痛。患者2(72岁,右丘脑出血)有轻微的运动和感觉障碍,没有疼痛的抱怨。通过刺激左右正中神经获得单个SEP(s-SEP),分别。对于配对刺激,第一次刺激后1ms到非患侧,然后对患侧进行第二次刺激。在患者1中,在CP4中观察到具有对非患侧的刺激的s-SEP和p-SEP。然而,在任一半球均未观察到s-SEP,并刺激患侧.另一方面,在患者2中,观察到CP3中刺激未患侧和CP4中刺激患侧的s-SEP;然而,未观察到p-SEP。此外,为了研究患者1的同侧正中神经刺激增强对侧p-SEP的机制,我们比较了前250个时期的平均SEP和后250个时期的平均SEP(记录的时期总数:500).结果显示,在患者1中,当连续刺激双侧正中神经时,没有发生习惯性现象,且反应大于s-SEP伴单侧正中神经刺激的反应.在目前的病例报告中,丘脑的损伤可能会在左右相互作用方面引起神经可塑性(例如,左和右S1)。来自患侧的体感输入可能会干扰对侧体感系统的习惯化,并反过来增加反应。
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.