Introduction: One of the primary motivations for studying the human brain is to comprehend how external sensory input is processed and ultimately perceived by the brain. A good understanding of these processes can promote the identification of biomarkers for the diagnosis of various neurological disorders; it can also provide ways of evaluating therapeutic techniques. In this work, we seek the minimal requirements for identifying key stages of activity in the brain elicited by median nerve stimulation.
Methods: We have used a priori knowledge and applied a simple, linear, spatial filter on the electroencephalography and magnetoencephalography signals to identify the early responses in the thalamus and cortex evoked by short electrical stimulation of the median nerve at the wrist. The spatial filter is defined first from the average EEG and MEG signals and then refined using consistency selection rules across ST. The refined spatial filter is then applied to extract the timecourses of each ST in each targeted generator. These ST timecourses are studied through clustering to quantify the ST variability. The nature of ST connectivity between thalamic and cortical generators is then studied within each identified cluster using linear and non-linear algorithms with time delays to extract linked and directional activities. A novel combination of linear and non-linear methods provides in addition discrimination of influences as excitatory or inhibitory.
Results: Our method identifies two key aspects of the evoked response. Firstly, the early onset of activity in the thalamus and the somatosensory cortex, known as the P14 and P20 in EEG and the second M20 for MEG. Secondly, good estimates are obtained for the early timecourse of activity from these two areas. The results confirm the existence of variability in ST brain activations and reveal distinct and novel patterns of connectivity in different clusters.
Discussion: It has been demonstrated that we can extract new insights into stimulus processing without the use of computationally costly source reconstruction techniques which require assumptions and detailed modeling of the brain. Our methodology, thanks to its simplicity and minimal computational requirements, has the potential for real-time applications such as in neurofeedback systems and brain-computer interfaces.
Introduction: Parkinson’s disease (PD) is a neurodegenerative disorder affecting the whole brain, leading to several motor and non-motor symptoms. In the past, it has been shown that PD alters resting state networks (RSN) in the brain. These networks are usually derived from fMRI BOLD signals. This study investigated RSN changes in PD patients based on maximum phase-amplitude coupling (PAC) throughout the cortex. We also tested the hypothesis that levodopa medication shifts network activity back toward a healthy state.
Methods: We recorded 23 PD patients and 24 healthy age-matched participants for 30 min at rest with magnetoencephalography (MEG). PD patients were measured once in the dopaminergic medication ON and once in the medication OFF state. A T1-MRI brain scan was acquired from each participant for source reconstruction. After correcting the data for artifacts and performing source reconstruction using a linearly constrained minimum variance beamformer, we extracted visual, sensorimotor (SMN), and frontal RSNs based on PAC.
Results: We found significant changes in all networks between healthy participants and PD patients in the medication OFF state. Levodopa had a significant effect on the SMN but not on the other networks. There was no significant change in the optimal PAC coupling frequencies between healthy participants and PD patients.
Discussion: Our results suggest that RSNs, based on PAC in different parts of the cortex, are altered in PD patients. Furthermore, levodopa significantly affects the SMN, reflecting the clinical alleviation of motor symptoms and leading to a network normalization compared to healthy controls.
Burst suppression is a brain state consisting of high-amplitude electrical activity alternating with periods of quieter suppression that can be brought about by disease or by certain anesthetics. Although burst suppression has been studied for decades, few studies have investigated the diverse manifestations of this state within and between human subjects. As part of a clinical trial examining the antidepressant effects of propofol, we gathered burst suppression electroencephalographic (EEG) data from 114 propofol infusions across 21 human subjects with treatment-resistant depression. This data was examined with the objective of describing and quantifying electrical signal diversity. We observed three types of EEG burst activity: canonical broadband bursts (as frequently described in the literature), spindles (narrow-band oscillations reminiscent of sleep spindles), and a new feature that we call low-frequency bursts (LFBs), which are brief deflections of mainly sub-3-Hz power. These three features were distinct in both the time and frequency domains and their occurrence differed significantly across subjects, with some subjects showing many LFBs or spindles and others showing very few. Spectral-power makeup of each feature was also significantly different across subjects. In a subset of nine participants with high-density EEG recordings, we noted that each feature had a unique spatial pattern of amplitude and polarity when measured across the scalp. Finally, we observed that the Bispectral Index Monitor, a commonly used clinical EEG monitor, does not account for the diversity of EEG features when processing the burst suppression state. Overall, this study describes and quantifies variation in the burst suppression EEG state across subjects and repeated infusions of propofol. These findings have implications for the understanding of brain activity under anesthesia and for individualized dosing of anesthetic drugs.