Author: Rabiller G1,2,3,4, He JW5,6, Nishijima Y7,8,9, Wong A10,11,12, Liu J13,14.
Affiliation: 1Department of Neurological Surgery, University of California at San Francisco and Department of Veterans Affairs Medical Center, 1700 Owens Street, San Francisco, CA 94158, USA. gratianne.rabiller@gmail.com. 2UCSF and SFVAMC, San Francisco, CA 94158, USA. gratianne.rabiller@gmail.com. 3Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, Bordeaux 33000, France. gratianne.rabiller@gmail.com. 4CNRS, Institut des Maladies Neurodégénératives, UMR 5293, Bordeaux 33000, France. gratianne.rabiller@gmail.com. 5Department of Neurological Surgery, University of California at San Francisco and Department of Veterans Affairs Medical Center, 1700 Owens Street, San Francisco, CA 94158, USA. jiwei.he@ucsf.edu. 6UCSF and SFVAMC, San Francisco, CA 94158, USA. jiwei.he@ucsf.edu. 7Department of Neurological Surgery, University of California at San Francisco and Department of Veterans Affairs Medical Center, 1700 Owens Street, San Francisco, CA 94158, USA. nishijima_yasu@yahoo.co.jp. 8UCSF and SFVAMC, San Francisco, CA 94158, USA. nishijima_yasu@yahoo.co.jp. 9Department of Neurosurgery, Tohoku University Graduate School of Medicine 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan. nishijima_yasu@yahoo.co.jp. 10Department of Neurological Surgery, University of California at San Francisco and Department of Veterans Affairs Medical Center, 1700 Owens Street, San Francisco, CA 94158, USA. aaronwong95@gmail.com. 11UCSF and SFVAMC, San Francisco, CA 94158, USA. aaronwong95@gmail.com. 12Rice University, 6100 Main St, Houston, TX 77005, USA. aaronwong95@gmail.com. 13Department of Neurological Surgery, University of California at San Francisco and Department of Veterans Affairs Medical Center, 1700 Owens Street, San Francisco, CA 94158, USA. jialing.liu@ucsf.edu. 14UCSF and SFVAMC, San Francisco, CA 94158, USA. jialing.liu@ucsf.edu.
Conference/Journal: Int J Mol Sci.
Date published: 2015 Oct 26
Other:
Volume ID: 16 , Issue ID: 10 , Pages: 25605-40 , Word Count: 255
Abstract
Brain waves resonate from the generators of electrical current and propagate across brain regions with oscillation frequencies ranging from 0.05 to 500 Hz. The commonly observed oscillatory waves recorded by an electroencephalogram (EEG) in normal adult humans can be grouped into five main categories according to the frequency and amplitude, namely δ (1-4 Hz, 20-200 μV), θ (4-8 Hz, 10 μV), α (8-12 Hz, 20-200 μV), β (12-30 Hz, 5-10 μV), and γ (30-80 Hz, low amplitude). Emerging evidence from experimental and human studies suggests that groups of function and behavior seem to be specifically associated with the presence of each oscillation band, although the complex relationship between oscillation frequency and function, as well as the interaction between brain oscillations, are far from clear. Changes of brain oscillation patterns have long been implicated in the diseases of the central nervous system including ischemic stroke, in which the reduction of cerebral blood flow as well as the progression of tissue damage have direct spatiotemporal effects on the power of several oscillatory bands and their interactions. This review summarizes the current knowledge in behavior and function associated with each brain oscillation, and also in the specific changes in brain electrical activities that correspond to the molecular events and functional alterations observed after experimental and human stroke. We provide the basis of the generations of brain oscillations and potential cellular and molecular mechanisms underlying stroke-induced perturbation. We will also discuss the implications of using brain oscillation patterns as biomarkers for the prediction of stroke outcome and therapeutic efficacy.
KEYWORDS:
CBF; MCAO; action potential; electroencephalography
PMID: 26516838