Jaberzadeh Shapour, Sakuma Shigemitsu, Zoghi Maryam, Miles Timothy S, Nordstrom Michael A
Discipline of Physiology, School of Molecular & Biomedical Sciences, The University of Adelaide, Adelaide, SA 5005, Australia; Research Centre for Human Movement Control, The University of Adelaide, Adelaide, SA 5005, Australia.
Department of Fixed Prosthodontics, School of Dentistry Aichi-Gakuin University, Nagoya, Japan.
Clin Neurophysiol. 2008 Mar;119(3):693-703. doi: 10.1016/j.clinph.2007.11.005. Epub 2007 Dec 27.
To determine whether a single hemisphere exerts distinct inhibitory influences over masseter muscles on each side, and to compare features of the masseter cortical silent period (CSP) evoked by transcranial magnetic stimulation (TMS) with previous reports from limb and other cranial muscles.
Focal TMS was applied over the motor cortex jaw area in 14 normal subjects. In one experiment, TMS intensity was constant (1.1 or 1.3x active motor threshold, T) and masseter muscle activation varied from 10% to 100% of maximal. In another experiment, muscle activation was constant (20% maximal) and TMS intensity varied from 0.7 to 1.3T.
In all subjects, TMS evoked a silent period of similar duration in masseter muscles on both sides. Masseter CSP duration increased at higher TMS intensities, but was not affected by muscle activation level or the size of the excitatory response evoked by TMS. Weak TMS produced a bilateral CSP without short-latency excitation. The masseter CSP was short ( approximately 100ms at 1.3T), yet this was not due to maintenance of excitatory drive from the unstimulated hemisphere, as the masseter CSP was not prolonged with dual-hemisphere TMS.
Intracortical inhibitory circuits activated by TMS have a relatively weak effect on corticotrigeminal neurons supplying masseter, and effects are equivalent for corticobulbar efferents directed to contralateral and ipsilateral masseter motoneuron pools.
Trigeminally innervated masseter muscles exhibit weak, bilaterally symmetric inhibition following focal TMS. This method can be used to investigate abnormalities of intracortical inhibition in movement disorders or focal lesions affecting the masticatory muscles in humans.
确定单个半球是否对两侧咬肌施加不同的抑制性影响，并将经颅磁刺激（TMS）诱发的咬肌皮质静息期（CSP）特征与先前关于肢体和其他颅肌的报道进行比较。
对14名正常受试者的运动皮层下颌区域施加局灶性TMS。在一项实验中，TMS强度恒定（1.1或1.3倍主动运动阈值，T），咬肌激活程度从最大激活的10%变化到100%。在另一项实验中，肌肉激活程度恒定（最大激活的20%），TMS强度从0.7T变化到1.3T。
在所有受试者中，TMS在两侧咬肌诱发的静息期持续时间相似。咬肌CSP持续时间在较高TMS强度时增加，但不受肌肉激活水平或TMS诱发的兴奋性反应大小的影响。弱TMS产生双侧CSP且无短潜伏期兴奋。咬肌CSP较短（在1.3T时约为100毫秒），但这并非由于未受刺激半球的兴奋性驱动持续存在，因为双侧半球TMS时咬肌CSP并未延长。
TMS激活的皮质内抑制回路对支配咬肌的皮质三叉神经元的作用相对较弱，且对支配同侧和对侧咬肌运动神经元池的皮质延髓传出纤维的作用相同。
经局灶性TMS后，三叉神经支配的咬肌表现出微弱的双侧对称抑制。该方法可用于研究人类运动障碍或影响咀嚼肌的局灶性病变中皮质内抑制的异常情况。
