■就认知障碍而言,磁性癫痫发作疗法(MST)比电惊厥疗法(ECT)更良性。然而,这两种“人工癫痫发作”是否促进中枢运动神经通路和运动皮层效应尚未研究。该研究旨在比较ECT和MST对精神障碍患者运动诱发电位(MEP)的影响。
■49名精神障碍患者(重度抑郁症,双相情感障碍II型,和精神分裂症)在非随机比较临床设计中接受了6次顶点MST治疗,而6次双侧ECT治疗。收集每种治疗的运动性癫痫发作持续时间的数据。在基线和每两次治疗后测量运动诱发电位(MEP)潜伏期和静息运动阈值(rMT)。在组间或组内进行比较。
■与MST组相比,ECT组的癫痫发作持续时间明显更长。与基线(T1)相比,在第四次(T3)和第六次治疗(T4)之后,MST和ECT均显示出在左和右半球的rMT显著降低。然而,在整个治疗期间,组间或组间的MEP潜伏期无显著变化.唯一的区别是,T4后左脑半球的rMT明显低于第二次治疗后(T2)。ECT组和MST组之间的rMT没有差异。
■ECT和MST都有助于中枢运动通路,具有增加运动皮层兴奋性的共同机制。
UNASSIGNED: Magnetic seizure therapy (MST) is more benign than electroconvulsive therapy (ECT) in terms of cognitive impairment. However, whether these two \'artificial seizures\' facilitate the central motor neural pathway and the motor cortical effects have not been investigated. The study aimed to compare the effects of ECT and MST on motor-evoked potential (MEP) in patients with mental disorders.
UNASSIGNED: Forty-nine patients with mental disorders (major depressive disorder, bipolar disorder type II and schizophrenia [SCZ]) received 6 treatment sessions of vertex MST versus 6 bifrontal ECT treatments in a nonrandomized comparative clinical design. Data on the duration of motor seizures were collected for each treatment. MEP latency and the resting motor threshold (rMT) were measured at baseline and after every two treatments. Comparisons were performed between or within the groups.
UNASSIGNED: Seizure durations were significantly longer in the ECT group compared to the MST group across multiple sessions. Both MST and ECT demonstrated a significant reduction in rMT in the left and right hemispheres after the fourth (T3) and sixth treatments (T4) compared to baseline (T1). However, there were no significant changes in MEP latency within or between the groups throughout the treatment sessions. The only difference was that the rMT in the left cerebral hemisphere was significantly lower after T4 than after the second treatment (T2). There was no difference in rMT between the ECT and MST groups.
UNASSIGNED: Both ECT and MST facilitate the central motor pathway, with a shared mechanism of increased motor cortex excitability.