4.5 Article

Beta power and movement-related beta modulation as hallmarks of energy for plasticity induction: Implications for Parkinson's disease

期刊

PARKINSONISM & RELATED DISORDERS
卷 88, 期 -, 页码 136-139

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.parkreldis.2021.05.018

关键词

ERD; ERS; Bradykinesia; Learning; Retention

资金

  1. National Institutes of Health [NIH P01 NS083514]
  2. Department of Defense [DOD W81XWH-19-1-0810]

向作者/读者索取更多资源

Research has shown that beta power decreases in sensorimotor areas during movement and transiently increases afterwards, while in neurologically normal subjects, beta power and movement-related modulation increase with practice. Patients with Parkinson's disease do not show such practice-related increases.
Extensive work on movement-related beta oscillations (similar to 13-30 Hz) over the sensorimotor areas in both humans and animals has demonstrated that sensorimotor beta power decreases during movement and transiently increases after movement. This beta power modulation has been interpreted as reflecting interactions between sensory and motor cortical areas with attenuation of sensory afferents during movement and their subsequent reactivation for internal models updating. More recent studies in neurologically normal subjects have demonstrated that this movement-related modulation as well as mean beta power at rest increase with practice and that previous motor learning enhances such increases. Conversely, patients with Parkinson's disease (PD) do not show such practice-related increases. Interestingly, a 2-h inactivity period without sleep can restore beta power values to baseline in normal subjects. Based on these results and on those of biochemical and electrophysiological studies in animals, we expand the current interpretation of beta activity and propose that the practice-related increases of beta power over sensorimotor areas are local indices of energy used for engaging plasticityrelated activity. This paper provides some preliminary evidence in this respect linking findings of biochemical and electrophysiological studies in both humans and animals. This novel interpretation may explain the high level of beta power at rest, the deficient modulation during movement as well as the decreased skill formation in PD as resulting from deficiency in energy consumption, availability and regulation that are altered in this disease.

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