Background: Stroke burden characterization studies in low‐ and middle‐income countries are scarce. We estimated the burden of stroke and its risk factors in Latin America and the Caribbean (LAC). Methods and Results: We extracted GBD (Global Burden of Disease) study 2019 data on overall stroke and 3 subtypes (ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage) for 20 LAC countries. We estimated absolute and age‐standardized rates of disability‐adjusted life years, years of life lost, years lived with disability, and deaths. The population‐attributable fractions of 17 risk factors were estimated. All analyses were performed at regional and national levels by stroke subtype, sex, and age subgroups. In 2019, the LAC region had the fourth largest stroke burden worldwide (6.8 million disability‐adjusted life years), predominantly attributable to premature deaths (89.5% of disability‐adjusted life years). Intracerebral hemorrhage was the primary cause of the overall stroke burden (42% of disability‐adjusted life years), but ischemic stroke was the leading cause of disability (69% of total years lived with disability). Haiti and Honduras had the highest age‐standardized rates. Older adults and men had the largest burdens, although women had the highest rate of disability. Socioeconomic development level did not influence the burden. The major risk factor clusters were metabolic (high systolic blood pressure [population‐attributable fraction=53%] and high body mass index [population‐attributable fraction=37%]), which were more influential in hemorrhagic events, women, and older adults. Household air pollution was an important risk factor in low‐income countries in LAC. Conclusions: The stroke burden and stroke‐related mortality in LAC are higher than the worldwide averages. However, stroke is a highly preventable disease in this region. Up to 90% of the burden could be reduced by targeting 2 modifiable factors: blood pressure and body mass index. Further research and implementation of primary and secondary prevention interventions are needed, as well as integrated national stroke care programs for acute, subacute, and rehabilitation management in LAC.

Transcutaneous auricular vagus nerve stimulation (taVNS) is a newer delivery system using a non-invasive stimulation device placed at the ear. taVNS research is focused on clinical trials showing potential therapeutic benefits, however the neurophysiological effects of this stimulation on brain activity are still unclear. We propose a systematic review that aims to describe the effects of taVNS on EEG measures and identify taVNS parameters that can potentially lead to consistent EEG-mediated biomarkers for this therapy. A systematic literature review was carried out following the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes (PRISMA) and the Cochrane handbook for systematic reviews. Clinical trials examining EEG parameters were considered, including absolute and relative power, coherence, degree of symmetry, evoked potentials, and peak frequency of all bands. According to our criteria, 18 studies (from 122 articles) were included. Our findings show a general trend towards increased EEG power spectrum activity in lower frequencies, and changes on early components of the ERP related to inhibitory tasks. This review suggests that quantitative electroencephalography can be used to assess the effects of taVNS on brain activity, however more studies are needed to systematically establish the specific effects and metrics that would reflect the non-invasive stimulation through the auricular branch of the vagus nerve.

Background: In this study, we aimed to assess the factors that predict a dysfunctional conditioned pain modulation (CPM) in chronic knee OA. Methods: This is a cross-sectional analysis of patients with chronic knee OA from a prospective cohort study in Brazil (n = 85). We performed linear and logistic multivariate regression models using the purposeful selection approach to test the relationship between the CPM in both knees (average) as a dependent variable and demographics, clinical, and neurophysiological as independent variables. Results: A significant negative association between WOMAC pain scores and CPM (β: −0.13) was found. This association was modified by the subjects’ race, being stronger in the non-white subjects. In our logistic regression models, pain intensity indexed with the WOMAC pain scale remained a significant association with dichotomized CPM. Furthermore, a significant CPM association with balance, indexed with the Berg Balance score, was evidenced (β: 0.04). Neurophysiological variables showed a significant negative relationship with CPM, such as the relative power of delta oscillations in the frontal area (β: −3.11) and central area (β: −3.23). There was no significant relationship between CPM and the following domains: cognitive, emotion, sleep, opioid receptor polymorphisms, and intrinsic variables of OA disease. There was no association of CPM with TMS-indexed inhibitory markers. Conclusions: These results may indicate that less function of the pain descending inhibitory system in patients with OA is correlated with higher activity-related pain (WOMAC), less balance, and cortical plasticity especially with increased low-frequency (delta) brain oscillations. These associations seem modified by race.

Background: Chronic pain is highly burdening and multifactorial in etiology. The endogenous-pain-healing system restores body tissue to a non-painful state after an injury leading to pain, and its disruption could represent a relevant mechanism, especially for nursing interventions. Aim: To review the literature and summarize the results that support this hypothesis. Methods: We hypothesized that the mechanism behind this system mainly depends on the endogenous pain modulatory system (EPMS), which is responsible for inhibiting pain after tissue healing is complete and facilitating it when tissue damage is still present. Different biomarkers can quantify EPMS functioning. We reviewed the literature and included relevant information regarding this hypothesis. Results: First, conditioned pain modulation (CPM) measures pain inhibition and is a possible predictor for pain chronification. Second, motor cortex excitability measures the cortical control of the EPMS, which can be assessed through transcranial magnetic stimulation (using intracortical inhibition) or electroencephalography. Modifiable factors disrupt its functioning, such as sleep deprivation, medication overuse, and mental health status, but could be protective, such as exercise, certain medications, mind–body techniques, and non-invasive neuromodulation therapies. The acquisition of neurophysiological knowledge of how the chronicity of pain occurs and the EPMS involvement in this process may allow for better management of these patients. Conclusions: We raised the hypothesis that the impairment of the EPMS (altered cortical excitability and descendent pain modulation pathways) seems to be related to the disruption of the pain healing process and its chronicity. Further longitudinal studies evaluating the relationship between these biomarkers and chronic pain development are necessary.

Background/Objectives: Knee osteoarthritis (KOA) is one of the most common causes of chronic pain and disability in older adults. Its mechanisms are both peripheral and central, causing discordance between pain intensity and disease severity. To provide better, mechanism-driven treatments for KOA, it is important to understand the emotional, physical, and neurophysiological factors that influence pain intensity. Thus, we proposed a multivariate model investigation of the multimodal predictors of pain intensity in patients with chronic KOA pain. Methods: We conducted an extensive assessment of 105 KOA patients. We used two different types of outcomes: (i) activity-related (Western Ontario and McMaster Universities Osteoarthritis [WOMAC] pain scale), and (ii) non-specific (visual analog scale [VAS]) pain assessments. Results: We found the following. (1) A higher WOMAC pain score was predicted by sensory–motor markers (lower intracortical inhibition [p = 0.021] and higher beta-band oscillations [p = 0.027]) and central sensitization (dysfunctional CPM response [p < 0.001]), in addition to the psychological and peripheral sensitization factors (adjusted R² = 52%, F (5, 99) = 22.81, p < 0.0001). (2) Conversely, higher VAS pain intensity was only predicted by psychological factors (higher depression [p = 0.021] and pain catastrophizing [p = 0.003]), peripheral sensitization (lower pain thresholds), and worse motor function (balance test) (adjusted R² = 36%, F (5, 99) = 12.57, p < 0.0001). Interestingly, no TMS or EEG markers were associated with VAS pain. Conclusions: Our study supports the notion that pain during physical activity is associated with a neural signature that demonstrates a lack of compensatory mechanisms for pain (decreased cortical inhibition, higher beta-band oscillations, and defective CPM), and it is different from the pain at rest, measured by the VAS, which is related mostly to emotional circuit dysregulation. These findings are important for developing better-targeted neural therapies given the contribution of different neural mechanisms to OA pain.

Neuromyelitis optica spectrum disorder (NMOSD) is a severe central nervous system (CNS) inflammatory disease. New immunobiological therapies have emerged a