A review of textile-based electrodes developed for electrostimulation

Electrical stimulation can be used for the treatment of various nerve and muscle injuries as well as acute and chronic pain conditions. An electrical pulse is applied to a muscle or nerve to activate excitable tissue using internal or external electrodes with the aim of building muscle strength, artificially creating or supporting limb movement or reducing pain. Textile electrodes offer several advantages over conventionally used disposable surface electrodes: they are flexible and re-usable and they do not require hydrogels, thereby avoiding skin irritation and allergic reactions and enhancing user comfort. This article presents a literature review that assesses the state of research on textile electrode constructions. Based on the review, production approaches and designs are compared, methods for evaluating stimulation discomfort and pain are proposed and issues related to user compliance are discussed. The article concludes with suggestions for future work focused on investigating the impacts of textile-based electrode parameters on comfort, convenience and ease of use.

Suppression of fibrillation consisting of stable rotors by periodic pacing

Recent experimental studies have shown that a sequence of low-energy electrical far-field pulses is able to terminate fibrillation with substantially lower per-pulse energy than a single high-energy electric shock (see S. Luther et al. Nature 475 (7355), 235-239). During this low-energy antifibrillation pacing (LEAP) procedure only tissue near sufficiently large conduction heterogeneities, such as large coronary arteries, is activated. In order to understand the mechanism behind LEAP, We have carried out a statistical study of resetting a medium filled by one or more stable spirals (“rotors”) in a two-dimensional electrophysiological model of cardiac tissue perforated by blood vessels to the resting state (“defibrillation”). We found the highest success probabilities for this defibrillation for underdrive pacing with periods 10 – 20 percent larger than the dominant period of the stable rotors in the unperturbed dynamics. If a sufficiently large number pulses is applied and an optimal pacing period chosen, the energy per pulse required for successful defibrillation is about 75 - 80 percent lower than the energy needed for single-shock defibrillation. Optimal conditions to control and suppress fibrillation based on stable rotors, hence, are similar to the ones in found for the case of an electrophysiological model displaying spatiotemporal chaos (“electrical turbulence”) in an earlier study (see P. Buran et al. Chaos 27, 113110 (2017)). The optimal pacing period is found to increase with increasing strength of the electrical field strength used in the model. The success probability also increases strongly until the fourth or fifth pulse administered, which is strongly correlated to an observed increase of the fraction of re-excitable tissue with each subsequent pulse. Monitoring the fraction of excitable tissue in the model as key quantity of the excitable medium, moreover, enabled us to successfully predict the optimal pacing period for defibrillation.

A Cell-Based Model for Ionic Electrodiffusion in Excitable Tissue

This chapter presents the KNP-EMI model describing ion concentrations and electrodiffusion in excitable tissue. The KNP-EMI model extends on the EMI model by removing the assumption that ion concentrations are constant in time and space, and may as such be more appropriate in connection with modelling e.g. spreading depression, stroke and epilepsy. The KNP-EMI model defines a system of time-dependent, nonlinear, mixed dimensional partial differential equations. We here detail the derivation of the system and present a numerical example illustrating how ion concentrations evolve during neuronal activity.

Variability in electrophysiological properties and conducting obstacles controls re-entry risk in heterogeneous ischaemic tissue

Ischaemia, in which inadequate blood supply compromises and eventually kills regions of cardiac tissue, can cause many types of arrhythmia, some life-threatening. A significant component of this is the effects of the resulting hypoxia, and concomitant hyperklaemia and acidosis, on the electrophysiological properties of myocytes. Clinical and experimental data have also shown that regions of structural heterogeneity (fibrosis, necrosis, fibro-fatty infiltration) can act as triggers for arrhythmias under acute ischaemic conditions. Mechanistic models have successfully captured these effects in silico . However, the relative significance of these separate facets of the condition, and how sensitive arrhythmic risk is to the extents of each, is far less explored. In this work, we use partitioned Gaussian process emulation and new metrics for source-sink mismatch that rely on simulations of bifurcating cardiac fibres to interrogate a model of heterogeneous ischaemic tissue. Re-entries were most sensitive to the level of hypoxia and the fraction of non-excitable tissue. In addition, our results reveal both protective and pro-arrhythmic effects of hyperklaemia, and present the levels of hyperklaemia, hypoxia and percentage of non-excitable tissue that pose the highest arrhythmic risks. This article is part of the theme issue ‘Uncertainty quantification in cardiac and cardiovascular modelling and simulation’.

P1601N-glycosylation of TREK-1/hK2P2.1 two-pore-domain (K2P) potassium channels

Background and purpose Mechanosensitive hTREK-1 (hK2P2.1) two-pore-domain potassium channels give rise to background currents that control resting membrane potential in excitable tissue. Recently TREK-1 currents have been linked to regulation of cardiac rhythm as well as hypertrophy and fibrosis. Even though pharmacological and biophysical characteristics of hTREK-1 channels have been widely studied, less is known about its posttranslational modifications. This study aims to evaluate whether hTREK-1 channels are N-glycosylated and whether glycosylation may affect channel functionality. Experimental approach Following pharmacological inhibition of N glycosylation, enzymatic digestion or mutagenesis, immunoblots of Xenopus laevis oocytes and HEK-233T cell lysates were used to assess electrophoretic mobility. Two-electrode voltage clamp measurements were employed to study channel function. Key results TREK-1 channels subunits undergo N-glycosylation at asparagine residues 110 and 134. The presence of sugar moieties at these two sites increases channel function. Detection of glycosylation-deficient mutant channels in surface fractions and recordings of macroscopic potassium currents mediated by these subunits demonstrate that non-glycosylated hTREK-1 channels subunits are able to reach the cell surface in general, but seemingly with reduced efficiency. Conclusion and implications hTREK-1 are glycoproteins and N glycosylation at positions 110 and 134 is involved in channel surface trafficking. These findings extend our view on regulation of hTREK-1 currents by posttranslational modifications and provide novel insights into how glycosylation deficiency disorders may promote arrhythmogenesis.

A Measurement Setup and Automated Calculation Method to Determine the Charge Injection Capacity of Implantable Microelectrodes

The design of safe stimulation protocols for functional electrostimulation requires knowledge of the “maximum reversible charge injection capacity” of the implantable microelectrodes. One of the main difficulties encountered in characterizing such microelectrodes is the calculation of the access voltage Va. This paper proposes a method to calculate Va that does not require prior knowledge of the overpotential terms and of the electrolyte (or excitable tissue) resistance, which is an advantage for in vivo electrochemical characterization of microelectrodes. To validate this method, we compare the calculated results with those obtained from conventional methods for characterizing three flexible platinum microelectrodes by cyclic voltammetry and voltage transient measurements. This paper presents the experimental setup, the required instrumentation, and the signal processing.

Investigation of Cortical Signal Propagation and the Resulting Spatiotemporal Patterns in Memristor-Based Neuronal Network

Complexity is the undeniable part of the natural systems providing them with unique and wonderful capabilities. Memristor is known to be a fundamental block to generate complex behaviors. It also is reported to be able to emulate synaptic long-term plasticity as well as short-term plasticity. Synaptic plasticity is one of the important foundations of learning and memory as the high-order functional properties of the brain. In this study, it is shown that memristive neuronal network can represent plasticity phenomena observed in biological cortical synapses. A network of neuronal units as a two-dimensional excitable tissue is designed with 3-neuron Hopfield neuronal model for the local dynamics of each unit. The results show that the lattice supports spatiotemporal pattern formation without supervision. It is found that memristor-type coupling is more noticeable against resistor-type coupling, while determining the excitable tissue switch over different complex behaviors. The stability of the resulting spatiotemporal patterns against noise is studied as well. Finally, the bifurcation analysis is carried out for variation of memristor effect. Our study reveals that the spatiotemporal electrical activity of the tissue concurs with the bifurcation analysis. It is shown that the memristor coupling intensities, by which the system undergoes periodic behavior, prevent the tissue from holding wave propagation. Besides, the chaotic behavior in bifurcation diagram corresponds to turbulent spatiotemporal behavior of the tissue. Moreover, we found that the excitable media are very sensitive to noise impact when the neurons are set close to their bifurcation point, so that the respective spatiotemporal pattern is not stable.