脑电图
磁刺激
静息状态功能磁共振成像
听力学
痴呆
心理学
神经科学
医学
内科学
心脏病学
刺激
疾病
作者
Hiba Alhabbal,Gifty Asare,Renee P Lawson,Hamed Azami,Reza Zomorrodi,Robert Chen,Daniel M. Blumberger,Benoit H. Mulsant,Bruce G. Pollock,Tarek K. Rajji,Sanjeev Kumar
摘要
Abstract Background Previous literature has identified slowing of resting state electroencephalography (EEG) rhythm and abnormal cortical excitation in Alzheimer’s Dementia (AD). However, the relationship between these two divergent functional abnormalities and cognitive symptoms of AD are not well understood. Method Resting state EEG signal was recorded in participants with AD and HCs for 5 minutes with eyes closed. Relative resting state EEG power was measured for the five frequency bands. Participants underwent a single pulse transcranial magnetic stimulation (TMS) combined with EEG. Cortical evoked activity (CEA) was assessed using TMS‐evoked potential (TEP) rectified area under the curve (AUC) from 25 to 80 ms post‐TMS stimulus, and the TEPs peak amplitudes were calculated by taking the maximal peak in the following time windows: 25 – 35 ms (P30), 40 – 50 ms (N45), and 55 – 65 ms (P60). Result Compared to 32 HC (18 females; mean ± SD age: 69.3 ± 7.9 years), 52 participants with AD (32 females; 74.2 ± 8.5 years) had higher relative theta power than HCs (t(66.6) = 5.34, p<0.001). AD participants also had a significantly lower alpha power (t(76) = ‐3.03, p=0.003) and beta power (t(76) = ‐2.51, p=0.014) than HCs. Controlling for sex, age and years of education, AD participants showed a positive association between theta power and CEA (r partial =0.573, p=0.008); and an inverse association between alpha power and CEA (r partial =‐0.471, p=0.036). Theta power in AD participants showed a positive association with P60 (r partial =‐0.637, p=0.003) and an inverse association with N45 (r partial =‐0.512, p=0.025), while alpha power was inversely associated with P60 (r partial =‐0.531, p=0.016). Conclusion This study showed a positive association between resting state EEG slowing and increased cortical excitability in AD, indicating a possible shared mechanistic pathway between these abnormalities.
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