Reflex

Transcutaneous auricular vagus nerve stimulation (taVNS) has recently emerged as a focal noninvasive neuromodulatory approach in anti-inflammatory therapeutics. The vagus nerve functions as a critical neuroimmune interface, tonically suppressing proinflammatory cytokine release via the cholinergic anti-inflammatory pathway (CAP). This mechanism provides substantial therapeutic potential across a spectrum of inflammatory disorders, including postoperative systemic inflammation. Clinical trials have demonstrated the anti-inflammatory efficacy of taVNS, supporting its expanded use in rheumatoid arthritis, systemic lupus erythematosus, gout, inflammatory bowel disease (IBD), and other immune-mediated disorders. Investigations into postoperative inflammation and metabolic syndrome are now emerging. In this review, we synthesize the anatomical substrate, mechanistic framework, and disease-specific applications of taVNS, with a particular emphasis on how stimulation parameters influence therapeutic outcomes. Finally, we outline current challenges and propose future directions to advance research and clinical translation.

Electrodermal activity (EDA) and heart rate variability (HRV) offer opportunities to grasp critical manifestations of the nervous autonomic system using low-intrusive sensing tools. A key question relies on the capacity to adequately process EDA and HRV signals to extract cognitive load markers, a multifaceted construct with intricate neural networks functioning, where emotions interfere with cognition. Here, 34 participants (20 males, 19.2 ± 1.3 years) were exposed to two-back mental tasking and watching emotionally charged images while recording EDA and HRV. HRV signals were processed using variable frequency complex demodulation (VFCDM) and wavelet packet transform (WPT) to provide high- and low-frequency (HF and LF) markers. Three methods were used to extract EDA indices: VFCDM (EDATVSYMP), WPT (EDAWPT), and convex-optimization (EDACVX). Cognitive load and emotion epochs were distinguished by significant differences in NASA-TLX scores, mental fatigue, and stress, on the one hand; and by EDACVX and, remarkably, EDATVSYMP and HF-HRVVFCDM on the other hand. A linear mixed-effects model and stepwise backward selection procedure showed that these two markers were main predictors of the NASA-TLX score (cognitive load). The individual perception of cognitive load was finally discriminated by k-means clustering, showing three profiles of autonomic responses relying, respectively, on EDATVSYMP, HF-HRVVFCDM, or a mix of these two markers. The existence of EDA-, HRV-, and EDA/HRV-derived profiles might explain why previous attempts that have predominantly employed a single biosignal often remained unconclusive in evaluating the perceived cognitive load, thereby demonstrating the added value of the present approach to monitor mental-related workload in human operators.

The chemoreflex is a vital protective reflex that is crucial in restoring normal blood gas and pH levels. The carotid bodies are peripheral chemoreceptors activated by hypoxia (primarily), hypercapnia, acidaemia, temperature, lactate and potassium fluctuations. They are crucial for maintaining physiological conditions based on underlying causes and blood gas abnormalities. Central chemoreceptors in the brain stem are responsive to hypercapnia and contribute to blood gas regulation. Chemoreceptors regained attention during the SARS-CoV-2 (COVID-19) pandemic, potentially contributing to disease severity. In conditions like chronic intermittent hypoxia, chemoreflex sensitization may lead to respiratory disorders, impacting quality of life. There has been substantial research/evidence linking chemoreflex dysfunction to cardiovascular illnesses such as heart failure and hypertension. However, little emphasis has been placed on the role of the chemoreflex in mediating cardiopulmonary dysfunction during and after pulmonary disorders such as acute lung injury. The current review summarizes recent advances in the study of chemoreflex malfunction and the underlying mechanisms in acute and chronic lung diseases such as COVID-19 infection, chronic obstructive pulmonary disease, asthma, obstructive sleep apnoea and acute lung injury.

Sensory conflicts are widely recognized as the primary drivers of motion sickness (MS), though the underlying integrative processes remain poorly understood. This study investigated sensory reweighting following exposure to two different sensory conflict paradigms. Visual and vestibular reflexes were assessed before and after sensory conflict. In the first paradigm, participants were exposed to a visuo-vestibular conflict using visually induced illusory motion (vection) in two environments in immersive virtual reality. In the second paradigm, vestibular conflict was induced by gravitational changes in parabolic flight. Semi-circular canal integration was measured via the vestibulo-ocular reflex (VOR) suppression task, while visual weight was assessed through optokinetic nystagmus (OKN). Our findings revealed that, following virtual reality exposure, VOR response decreased by 12%, indicating a reduced reliance on vestibular inputs. Conversely, after parabolic flight, OKN performance was diminished by 13%, indicating a diminished weight of visual inputs. These findings suggest that the sensory modality failing to detect the motion was considered less reliable and therefore assigned a reduced contribution during the integration process, regardless of its actual accuracy. Additionally, visual sensitivity was associated with increased susceptibility to cybersickness, whereas vestibular sensitivity seemed to correlate MS severity in parabolic flight. Altogether, our data suggest that the sensitivity of the most stimulated sensory modality during a sensory conflict may predict an individual's susceptibility to MS.