Coupling between leg muscle activation and EEG during normal walking, intentional stops, and freezing of gait in Parkinson's disease

In this paper, we apply novel techniques for characterizing leg muscle activation patterns via electromyograms (EMGs) and for relating them to changes in electroencephalogram (EEG) activity during gait experiments. Specifically, we investigate changes of leg-muscle EMG amplitudes and EMG frequencies during walking, intentional stops, and unintended freezing-of-gait (FOG) episodes. FOG is a frequent paroxysmal gait disturbance occurring in many patients suffering from Parkinson's disease (PD). We find that EMG amplitudes and frequencies do not change significantly during FOG episodes with respect to walking, while drastic changes occur during intentional stops. Phase synchronization between EMG signals is most pronounced during walking in controls and reduced in PD patients. By analyzing cross-correlations between changes in EMG patterns and brain-wave amplitudes (from EEGs), we find an increase in EEG-EMG coupling at the beginning of stop and FOG episodes. Our results may help to better understand the enigmatic pathophysiology of FOG, to differentiate between FOG events and other gait disturbances, and ultimately to improve diagnostic procedures for patients suffering from PD. Copyright © 2019 Günther, Bartsch, Miron-Shahar, Hassin-Baer, Inzelberg, Kurths, Plotnik and Kantelhardt

Effect of extreme data loss on long-range correlated and anti-correlated signals quantified by detrended fluctuation analysis

We investigate how extreme loss of data affects the scaling behavior of long-range power-law correlated and anti-correlated signals applying the DFA method. We introduce a segmentation approach to generate surrogate signals by randomly removing data segments from stationary signals with different types of correlations. These surrogate signals are characterized by: (i) the DFA scaling exponent $\alpha$ of the original correlated signal, (ii) the percentage $p$ of the data removed, (iii) the average length $\mu$ of the removed (or remaining) data segments, and (iv) the functional form of the distribution of the length of the removed (or remaining) data segments. We find that the {\it global} scaling exponent of positively correlated signals remains practically unchanged even for extreme data loss of up to 90%. In contrast, the global scaling of anti-correlated signals changes to uncorrelated behavior even when a very small fraction of the data is lost. These observations are confirmed on the examples of human gait and commodity price fluctuations. We systematically study the {\it local} scaling behavior of signals with missing data to reveal deviations across scales. We find that for anti-correlated signals even 10% of data loss leads to deviations in the local scaling at large scales from the original anti-correlated towards uncorrelated behavior. In contrast, positively correlated signals show no observable changes in the local scaling for up to 65% of data loss, while for larger percentage, the local scaling shows overestimated regions (with higher local exponent) at small scales, followed by underestimated regions (with lower local exponent) at large scales. Finally, we investigate how the scaling is affected by the statistics of the remaining data segments in comparison to the removed segments

Neuronal noise as an origin of sleep arousals and its role in sudden infant death syndrome

In addition to regular sleep/wake cycles, humans and animals exhibit brief arousals from sleep. Although much is known about consolidated sleep and wakefulness, the mechanism that triggers arousals remains enigmatic. Here, we argue that arousals are caused by the intrinsic neuronal noise of wake-promoting neurons. We propose a model that simulates the superposition of the noise from a group of neurons, and show that, occasionally, the superposed noise exceeds the excitability threshold and provokes an arousal. Because neuronal noise decreases with increasing temperature, our model predicts arousal frequency to decrease as well. To test this prediction, we perform experiments on the sleep/wake behavior of zebrafish larvae and find that increasing water temperatures lead to fewer and shorter arousals, as predicted by our analytic derivations and model simulations. Our findings indicate a previously unrecognized neurophysiological mechanism that links sleep arousals with temperature regulation, and may explain the origin of the clinically observed higher risk for sudden infant death syndrome with increased ambient temperature

Modulations of Heart Rate, ECG, and Cardio-Respiratory Coupling Observed in Polysomnography

The cardiac component of cardio-respiratory polysomnography is covered by ECG and heart rate recordings. However their evaluation is often underrepresented in summarizing reports. As complements to EEG, EOG, and EMG, these signals provide diagnostic information for autonomic nervous activity during sleep. This review presents major methodological developments in sleep research regarding heart rate, ECG and cardio-respiratory couplings in a chronological (historical) sequence. It presents physiological and pathophysiological insights related to sleep medicine obtained by new technical developments. Recorded nocturnal ECG facilitates conventional heart rate variability analysis, studies of cyclical variations of heart rate, and analysis of ECG waveform. In healthy adults, the autonomous nervous system is regulated in totally different ways during wakefulness, slow-wave sleep, and REM sleep. Analysis of beat-to-beat heart-rate variations with statistical methods enables us to estimate sleep stages based on the differences in autonomic nervous system regulation. Furthermore, up to some degree, it is possible to track transitions from wakefulness to sleep by analysis of heart-rate variations. ECG and heart rate analysis allow assessment of selected sleep disorders as well. Sleep disordered breathing can be detected reliably by studying cyclical variation of heart rate combined with respiration-modulated changes in ECG morphology (amplitude of R wave and T wave)

Asymmetry and basic pathways in sleep-stage transitions

We study dynamical aspects of sleep micro-architecture. We find that sleep dynamics exhibits a high degree of asymmetry, and that the entire class of sleep-stage transition pathways underlying the complexity of sleep dynamics throughout the night can be characterized by two independent asymmetric transition paths. These basic pathways remain stable under sleep disorders, even though the degree of asymmetry is significantly reduced. Our findings demonstrate an intriguing temporal organization in sleep micro-architecture at short time scales that is typical for physical systems exhibiting self-organized criticality (SOC), and indicates nonequilibrium critical dynamics in brain activity during sleep

Network Physiology: How Organ Systems Dynamically Interact

We systematically study how diverse physiologic systems in the human organism dynamically interact and collectively behave to produce distinct physiologic states and functions. This is a fundamental question in the new interdisciplinary field of Network Physiology, and has not been previously explored. Introducing the novel concept of Time Delay Stability (TDS), we develop a computational approach to identify and quantify networks of physiologic interactions from long-term continuous, multi-channel physiological recordings. We also develop a physiologically-motivated visualization framework to map networks of dynamical organ interactions to graphical objects encoded with information about the coupling strength of network links quantified using the TDS measure. Applying a system-wide integrative approach, we identify distinct patterns in the network structure of organ interactions, as well as the frequency bands through which these interactions are mediated. We establish first maps representing physiologic organ network interactions and discover basic rules underlying the complex hierarchical reorganization in physiologic networks with transitions across physiologic states. Our findings demonstrate a direct association between network topology and physiologic function, and provide new insights into understanding how health and distinct physiologic states emerge from networked interactions among nonlinear multi-component complex systems. The presented here investigations are initial steps in building a first atlas of dynamic interactions among organ systems

Random walk model simulates the increased drowsiness of children with obstructive sleep apnea

Obstructive sleep apnea (OSA) is a common sleep disorder, which is particularly harmful to children as it may lead to learning deficits, attention deficit hyperactivity disorder (ADHD) and growth retardation. Furthermore, OSA alters the dynamics of sleep-stage transitions and in particular increases the transition time from being awake to falling asleep (“drowsiness”). In this letter, we show that sleep bout durations during this transient state can be described by an exponential distribution with a longer characteristic time scale for OSA compared to healthy children. This finding can be simulated and better understood by using a random walk model of the integrated neuronal voltage of wake-promoting neurons, and by introducing a new concept of a light sleep threshold parameter L that distinguishes between drowsiness and deeper forms of light sleep. Our analysis also shows that the value of L correlates well with OSA severity. Moreover, we find that after OSA treatment, the parameter L returns to normal values similar to those we detected for healthy children. We anticipate that our methodology can help in better understanding and modeling sleep dynamics, and may improve diagnostics and treatment monitoring of OSA

Performance-based approach for movement artifact removal from electroencephalographic data recorded during locomotion

<div><p>The appreciation for the need to record electroencephalographic (EEG) signals from humans while walking has been steadily growing in recent years, particularly in relation to understanding gait disturbances. Movement artefacts (MA) in EEG signals originate from mechanical forces applied to the scalp electrodes, inducing small electrode movements relative to the scalp which, in turn, cause the recorded voltage to change irrespectively of cortical activity. These mechanical forces, and thus MA, may have various sources (e.g., ground reaction forces, head movements, etc.) that are inherent to daily activities, notably walking. In this paper we introduce a systematic, integrated methodology for removing MA from EEG signals recorded during treadmill (TM) and over-ground (OG) walking, as well as quantify the prevalence of MA in different locomotion settings. In our experiments, participants performed walking trials at various speeds both OG and on a TM while wearing a 32-channel EEG cap and a 3-axis accelerometer, placed on the forehead. Data preprocessing included separating the EEG signals into statistically independent additive components using independent component analysis (ICA). We observed an increase in electro-physiological signals (e.g., neck EMG activations for stabilizing the head during heel-strikes) as the walking speed increased. These artefact independent-components (ICs), while not originating from electrode movement, still exhibit a similar spectral pattern to the MA ICs–a peak at the stepping frequency. MA was identified and quantified in each component using a novel method that utilizes the participant’s stepping frequency, derived from a forehead-mounted accelerometer. We then benchmarked the EEG data by applying newly established metrics to quantify the success of our method in cleaning the data. The results indicate that our approach can be successfully applied to EEG data recorded during TM and OG walking, and is offered as a unified methodology for MA removal from EEG collected during gait trials.</p></div

Plasticity of brain wave network interactions and evolution across physiologic states

Neural plasticity transcends a range of spatio-temporal scales and serves as the basis of various brain activities and physiologic functions. At the microscopic level, it enables the emergence of brain waves with complex temporal dynamics. At the macroscopic level, presence and dominance of specific brain waves is associated with important brain functions. The role of neural plasticity at different levels in generating distinct brain rhythms and how brain rhythms communicate with each other across brain areas to generate physiologic states and functions remains not understood. Here we perform an empirical exploration of neural plasticity at the level of brain wave network interactions representing dynamical communications within and between different brain areas in the frequency domain. We introduce the concept of time delay stability (TDS) to quantify coordinated bursts in the activity of brain waves, and we employ a system-wide Network Physiology integrative approach to probe the network of coordinated brain wave activations and its evolution across physiologic states. We find an association between network structure and physiologic states. We uncover a hierarchical reorganization in the brain wave networks in response to changes in physiologic state, indicating new aspects of neural plasticity at the integrated level. Globally, we find that the entire brain network undergoes a pronounced transition from low connectivity in Deep Sleep and REM to high connectivity in Light Sleep and Wake. In contrast, we find that locally, different brain areas exhibit different network dynamics of brain wave interactions to achieve differentiation in function during different sleep stages. Moreover, our analyses indicate that plasticity also emerges in frequency-specific networks, which represent interactions across brain locations mediated through a specific frequency band. Comparing frequency-specific networks within the same physiologic state we find very different degree of network connectivity and link strength, while at the same time each frequency-specific network is characterized by a different signature pattern of sleep-stage stratification, reflecting a remarkable flexibility in response to change in physiologic state. These new aspects of neural plasticity demonstrate that in addition to dominant brain waves, the network of brain wave interactions is a previously unrecognized hallmark of physiologic state and function

Decaying harmonics at 0.5 multiples of the stepping frequency.

<p>Frequency spectrum of an exemplary AMICA component, decomposed from a 1.6 m/s TM trial. Each spectral peak’s frequency and amplitude are depicted in the data-tips. The stepping frequency, as derived from the accelerometer, is shown as a red dashed line.</p