1 The University of Auckland, Auckland, New Zealand.
2 Tan Tock Seng Hospital, Novena, Singapore.
Neurorehabil Neural Repair. 2019 Feb;33(2):130-140. doi: 10.1177/1545968319826052.
Stroke is a leading cause of adult disability owing largely to motor impairment and loss of function. After stroke, there may be abnormalities in γ-aminobutyric acid (GABA)-mediated inhibitory function within primary motor cortex (M1), which may have implications for residual motor impairment and the potential for functional improvements at the chronic stage.
To quantify GABA neurotransmission and concentration within ipsilesional and contralesional M1 and determine if they relate to upper limb impairment and function at the chronic stage of stroke.
Twelve chronic stroke patients and 16 age-similar controls were recruited for the study. Upper limb impairment and function were assessed with the Fugl-Meyer Upper Extremity Scale and Action Research Arm Test. Threshold tracking paired-pulse transcranial magnetic stimulation protocols were used to examine short- and long-interval intracortical inhibition and late cortical disinhibition. Magnetic resonance spectroscopy was used to evaluate GABA concentration.
Short-interval intracortical inhibition was similar between patients and controls ( P = .10). Long-interval intracortical inhibition was greater in ipsilesional M1 compared with controls ( P < .001). Patients who did not exhibit late cortical disinhibition in ipsilesional M1 were those with greater upper limb impairment and worse function ( P = .002 and P = .017). GABA concentration was lower within ipsilesional ( P = .009) and contralesional ( P = .021) M1 compared with controls, resulting in an elevated excitation-inhibition ratio for patients.
These findings indicate that ipsilesional and contralesional M1 GABAergic inhibition are altered in this small cohort of chronic stroke patients. Further study is warranted to determine how M1 inhibitory networks might be targeted to improve motor function.
脑卒中是导致成年人残疾的主要原因，主要与运动功能障碍和丧失有关。脑卒中后，初级运动皮层（M1）中的γ-氨基丁酸（GABA）介导的抑制功能可能会出现异常，这可能对残留的运动障碍和慢性期的功能改善有影响。
定量分析同侧和对侧 M1 中的 GABA 神经传递和浓度，并确定其与脑卒中慢性期上肢损伤和功能的关系。
本研究招募了 12 例慢性脑卒中患者和 16 名年龄匹配的对照者。采用 Fugl-Meyer 上肢量表和动作研究上肢测试评估上肢损伤和功能。采用阈值跟踪成对脉冲经颅磁刺激方案检测短程和长程皮质内抑制以及晚期皮质去抑制。磁共振波谱用于评估 GABA 浓度。
患者和对照组之间的短程皮质内抑制相似（P=.10）。同侧 M1 的长程皮质内抑制大于对照组（P<.001）。在同侧 M1 中未出现晚期皮质去抑制的患者，上肢损伤程度更严重，功能更差（P=.002 和 P=.017）。同侧（P=.009）和对侧（P=.021）M1 中的 GABA 浓度低于对照组，导致患者的兴奋-抑制比升高。
这些发现表明，在这一小部分慢性脑卒中患者中，同侧和对侧 M1 的 GABA 能抑制发生了改变。需要进一步研究以确定如何针对 M1 抑制网络来改善运动功能。
