背景:帕金森病(PD)是一种常见的神经退行性疾病。经颅磁声刺激(TMAS)是一种新疗法,将经颅聚焦声压场与磁场相结合,以激发或抑制目标区域的神经元。抑制PD状态下异常升高的β带振幅,具有高空间分辨率和非侵入性。
目的:研究TMAS单核和多核刺激治疗β带能量降低的PD的有效刺激参数,改进了异常同步,没有热损伤。
方法:TMAS模型是基于志愿者的计算机断层扫描构建的,128阵列的相位控制传感器,和永久磁铁。在Izhikevich模型和声学模型的基础上,构建了PD状态的基底神经节-丘脑(BG-Th)神经网络模型。基于Hodgkin-Huxley模型构建超声刺激神经元模型。经颅聚焦声压场的数值模拟,使用STN的位置进行了单目标和双目标的温度场和感应电场,GPi,和GPe在人脑中作为主要的刺激目标区域。并提取焦点处的声电参数以激发BG-Th神经网络中的单核和多核。
结果:当忽略超声的刺激作用时,TMAS-STN同时抑制GPi核的β带振幅,而TMAS-GPi不能同时对STN有抑制作用。TMAS-STN&GPi可以降低β波段振幅。TMAS-STN&GPi&GPe在更大程度上抑制了每个核的PD病理β带振幅。当考虑超声波的刺激效应时,较低的超声声压不影响神经元放电状态,但是较高的声压可能会促进或抑制感应电流的刺激作用。
结论:在9T静磁场下,0.5-1.5MPa和1.5-2.0MPa超声对单个STN和GPi神经元具有协同作用。具有适当超声强度的TMAS多核刺激在抑制PD中病理性β振荡的幅度方面最有效,并且可能在临床上有用。
BACKGROUND: Parkinson\'s disease (PD) is a common neurodegenerative disease. Transcranial magnetoacoustic stimulation (TMAS) is a new therapy that combines a transcranial focused acoustic pressure field with a magnetic field to excite or inhibit neurons in targeted area, which suppresses the abnormally elevated beta band amplitude in PD states, with high spatial resolution and non-invasively.
OBJECTIVE: To study the effective stimulation parameters of TMAS mononuclear and multinuclear stimulation for the treatment of PD with reduced beta band energy, improved abnormal synchronization, and no thermal damage.
METHODS: The TMAS model is constructed based on the volunteer\'s computed tomography, 128 arrays of phase-controlled transducers, and permanent magnets. A basal ganglia-thalamic (BG-Th) neural network model of the PD state was constructed on the basis of the Izhikevich model and the acoustic model. An ultrasound stimulation neuron model is constructed based on the Hodgkin-Huxley model. Numerical simulations of transcranial focused acoustic pressure field, temperature field and induced electric field at single and dual targets were performed using the locations of STN, GPi, and GPe in the human brain as the main stimulation target areas. And the acoustic and electric parameters at the focus were extracted to stimulate mononuclear and multinuclear in the BG-Th neural network.
RESULTS: When the stimulating effect of ultrasound is ignored, TMAS-STN simultaneously inhibits the beta-band amplitude of the GPi nucleus, whereas TMAS-GPi fails to simultaneously have an inhibitory effect on the STN. TMAS-STN&GPi can reduce the beta band amplitude. TMAS-STN&GPi&GPe suppressed the PD pathologic beta band amplitude of each nucleus to a greater extent. When considering the stimulatory effect of ultrasound, lower sound pressures of ultrasound do not affect the neuronal firing state, but higher sound pressures may promote or inhibit the stimulatory effect of induced currents.
CONCLUSIONS: At 9 T static magnetic field, 0.5-1.5 MPa and 1.5-2.0 MPa ultrasound had synergistic effects on individual STN and GPi neurons. TMAS multinuclear stimulation with appropriate ultrasound intensity was the most effective in suppressing the amplitude of pathological beta oscillations in PD and may be clinically useful.