Parieto-Occipital Alpha and Low-Beta EEG Power Reflect Sense of Agency

The sense of agency (SoA) is part of psychophysiological modules related to the self. Disturbed SoA is found in several clinical conditions, hence understanding the neural correlates of the SoA is useful for the diagnosis and determining the proper treatment strategies. Although there are several neuroimaging studies on SoA, it is desirable to translate the knowledge to more accessible and inexpensive EEG-based biomarkers for the sake of applicability. However, SoA has not been widely investigated using EEG. To address this issue, we designed an EEG experiment on healthy adults (n = 15) to determine the sensitivity of EEG on the SoA paradigm using hand movement with parametrically delayed visual feedback. We calculated the power spectral density over the traditional EEG frequency bands for ten delay conditions relative to no delay condition. Independent component analysis and equivalent current dipole modeling were applied to address artifact rejection, volume conduction, and source localization to determine the effect of interest. The results revealed that the alpha and low-beta EEG power increased in the parieto-occipital regions in proportion to the reduced SoA reported by the subjects. We conclude that the parieto-occipital alpha and low-beta EEG power reflect the sense of agency.

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Prefrontal Cortex Acetylcholine Release, EEG Slow Waves, and Spindles Are Modulated by M2 Autoreceptors in C57BL/6J Mouse

Journal of Neurophysiology ◽

10.1152/jn.2002.87.6.2817 ◽

2002 ◽

Vol 87 (6) ◽

pp. 2817-2822 ◽

Cited By ~ 27

Author(s):

Christopher L. Douglas ◽

Helen A. Baghdoyan ◽

Ralph Lydic

Keyword(s):

Prefrontal Cortex ◽

Slow Wave ◽

Cortical Activation ◽

Mouse Strains ◽

Potential Contribution ◽

Ach Release ◽

Power Spectral ◽

Eeg Data ◽

Muscarinic Cholinergic ◽

Eeg Power

Recent evidence suggests that muscarinic cholinergic receptors of the M2 subtype serve as autoreceptors modulating acetylcholine (ACh) release in prefrontal cortex. The potential contribution of M2 autoreceptors to excitability control of prefrontal cortex has not been investigated. The present study tested the hypothesis that M2 autoreceptors contribute to activation of the cortical electroencephalogram (EEG) in C57BL/6J (B6) mouse. This hypothesis was evaluated using microdialysis delivery of the muscarinic antagonist AF-DX116 (3 nM) while simultaneously quantifying ACh release in prefrontal cortex, number of 7- to 14-Hz EEG spindles, and EEG power spectral density. Mean ACh release in prefrontal cortex was significantly increased ( P < 0.0002) by AF-DX116. The number of 7- to 14-Hz EEG spindles caused by halothane anesthesia was significantly decreased ( P < 0.0001) by dialysis delivery of AF-DX116 to prefrontal cortex. The cholinergically induced cortical activation was characterized by a significant ( P < 0.05) decrease in slow-wave EEG power. Together, these neurochemical and EEG data support the conclusion that M2 autoreceptor enhancement of ACh release in prefrontal cortex activates EEG in contralateral prefrontal cortex of B6 mouse. EEG slow-wave activity varies across mouse strains, and the results encourage comparative phenotyping of cortical ACh release and EEG in additional mouse models.

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Antithrombotic Treatment After Coronary Intervention: Agreement and Controversy

European Cardiology Review ◽

10.15420/ecr.2019.25.2 ◽

2020 ◽

Vol 15 ◽

Author(s):

Tamara García Camarero ◽

José M de la Torre Hernández

Keyword(s):

Percutaneous Coronary Intervention ◽

Treatment Strategies ◽

Coronary Intervention ◽

New Drugs ◽

Antithrombotic Treatment ◽

The Past ◽

Percutaneous Coronary ◽

The Subject ◽

Clinical Conditions ◽

Combination Regimens

Percutaneous revascularisation has evolved dramatically in the past few decades. The approach to the management of ischaemic heart disease has changed due to the development of new devices and techniques as well as the availability of new drugs and treatment strategies. Its use in combination with antiplatelet therapies has been essential to protect against stent thrombosis. The length of time this combination therapy is used has been modified in recent years and has been the subject of extensive research. The effect of prolonging the time it is taken or shortening it has been evaluated in different clinical conditions. In practice, the decisions regarding antithrombotic therapy after percutaneous coronary intervention are informed by the patient’s profile and the characteristics of the procedures performed. In this article, we review the use of antiplatelet/anticoagulant therapy after percutaneous coronary intervention focusing on trials and guidelines addressing variable durations for combination regimens and the alternatives.

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