Background: Obstructive sleep apnea (OSA) is a common but underrecognized sleep-related breathing disorder characterized by intermittent hypoxemia and autonomic dysfunction. OSA prevalence and clinical relevance in Type 1 Diabetes Mellitus (T1DM), particularly in relation to diabetes-related vascular complications, remain insufficiently explored. Objective: The aim of this study was to evaluate the prevalence of high-risk OSA in adults with T1DM and controls, and to investigate the association between high-risk OSA and microvascular complications among individuals with T1DM. Methods: In this cross-sectional case-control study, 102 adults with T1DM and 126 controls were included. OSA risk was assessed using the modified Berlin Questionnaire (mBQ). Analyses of vascular complications were restricted to participants with T1DM. Multivariable logistic regression models adjusted for age and sex were used to assess associations, with additional adjustments for body mass index, hypertension, current smoking, alcohol use and glycated hemoglobin A1c. Results: High-risk OSA was identified in 18.6% of individuals with T1DM and 11.9% of controls, with no significant difference between groups. Among participants with T1DM, the prevalence of microvascular complications (retinopathy and/or neuropathy) was substantially higher in those with high-risk OSA compared with those at low risk (68.4% vs. 18.07%, p <0.001). In univariate logistic regression analysis, high-risk OSA was significantly associated with microvascular complications (odds ratio [OR] 4.85; 95% confidence interval [CI] 1.65-14.24; p = 0.004). This association remained significant in the fully adjusted model (OR 5.55; 95% CI 1.36-22.65; p = 0.017). Conclusions: High-risk OSA is not more prevalent in adults with T1DM compared with controls; however, among individuals with T1DM, high-risk OSA is strongly and independently associated with microvascular complications. Given the potential contribution of diabetic microvascular and autonomic neuropathy to upper airway dysfunction, the relationship between OSA and vascular complications in T1DM may be bidirectional, warranting further longitudinal investigation.

Impulse sounds such as clinking dishes or slamming objects are often perceived as particularly intense or uncomfortable, yet their perceptual characterization remains insufficiently understood. The present study systematically examined subjective and physiological responses to ecologically valid impulse sounds in young normal-hearing adults. Twenty-seven participants rated nine impulse sounds presented at peak levels between 80 and 120 dB SPL in three acoustic conditions: anechoic, reverberant (room-convolved), and anechoic embedded in the International Speech Test Signal (ISTS) at 65 dB SPL. Loudness and discomfort were assessed using categorical rating scales, and pupil dilation was recorded as an index of autonomic arousal. Both perceptual scales followed Stevens-type growth functions. Loudness increased gradually with level, whereas discomfort showed a delayed onset, but steeper growth once activated. Test-retest reliability was excellent for both scales (ICC ≈0.88). Acoustic condition significantly influenced perception: reverberant stimuli yielded higher perceived intensity and lower 50% thresholds than anechoic presentations for most impulse types, while embedding impulses in speech produced comparatively small effects. Mean pupil dilation increased with presentation level and was significantly associated with both loudness and discomfort ratings. Linear mixed-effects modeling demonstrated that subjective ratings explained pupil dilation more strongly than physical level once both were included in the model. Neither uncomfortable loudness levels nor self-reported sound sensitivity significantly predicted ratings or physiological responses. These findings provide a systematic characterization of impulse sound perception in a normal-hearing population and demonstrate a close correspondence between subjective intensity judgments and autonomic responses under controlled laboratory conditions.

Insufficient or disturbed sleep impairs nocturnal physiological recovery and may negatively affect autonomic nervous system (ANS) regulation. Astronauts are a particularly vulnerable group due to sustained workloads, isolation, and exposure to extreme operational conditions. The present study investigated the interaction between sleep structure and ANS state under different sleep conditions during a prolonged space analogue mission (SAM) conducted as part of the Scientific International Research in a Unique Terrestrial Station (SIRIUS-19) project.

Postural orthostatic tachycardia syndrome (POTS) is characterized by orthostatic tachycardia with associated symptoms including presyncope, fatigue, dizziness, and gastrointestinal complaints, among others. In addition to cardiovascular and neurologic features, autonomic dysfunction may involve other organ systems. We report a rare case of transient evanescent hyperemia occurring during presyncopal episodes in a patient with POTS, highlighting a potentially underrecognized dermatologic sign of autonomic dysfunction. We present a 19-year-old female with known POTS and a complex medical history including pituitary adenoma (prolactinoma), secondary adrenal insufficiency, gastroparesis, severe malnutrition, and pelvic floor dysfunction, who was admitted for recurrent presyncope, syncope, and collapse. Her presentation was multifactorial. Contributing factors included autonomic instability, cabergoline-related effects, and nutritional compromise. During hospitalization, she developed recurrent episodes of transient, sharply demarcated erythematous patches affecting the face, chest, and upper extremities that coincided with presyncope and resolved spontaneously without intervention. Dermatology evaluation supported a diagnosis of evanescent hyperemia in the setting of autonomic dysfunction associated with POTS. Diagnostic workup included serial laboratory testing, electrocardiography, echocardiography, neuroimaging, and multidisciplinary specialty consultations. Transthoracic echocardiography demonstrated a patent foramen ovale with preserved cardiac function, without evidence of structural heart disease contributing to her symptoms. Management required a multidisciplinary approach, including stress-dose intravenous hydrocortisone for adrenal insufficiency, adjustment of cabergoline due to suspected medication-related bradycardia, continuation of fludrocortisone for volume support, and initiation of nasoduodenal tube feeding for nutritional rehabilitation. This case illustrates a transient cutaneous finding temporally associated with presyncope in a patient with POTS and complex comorbidities. Awareness of such skin changes during symptomatic episodes may provide supportive clinical clues to underlying autonomic dysfunction, particularly in diagnostically challenging presentations.

Spinal Cord Injury (SCI) causes persistent autonomic dysregulation, which is not merely a clinical epiphenomenon, but a mechanistic condition shaping the neurochemical, neurovascular, and immuno-endocrine milieu in which plasticity unfolds. Yet, the modulatory role of the Autonomic Nervous System (ANS) in post-injury circuit reorganization remains insufficiently integrated in rehabilitation paradigms. This narrative review synthesizes emerging evidence (2020-2025) describing how sympatho-vagal dynamics constrain or enable adaptive plasticity following SCI, and surveys therapeutic strategies that intentionally leverage autonomic modulation to amplify recovery. Mechanistically, autonomic tone influences neuronal excitability, perfusion, neurotrophin signaling (notably Brain-Derived Neurotrophic Factor (BDNF)/Tropomyosin receptor kinase B (TrkB)), and microglia-dependent inflammatory states. Recurrent sympathetic surges during Autonomic Dysreflexia (AD) bias networks toward maladaptive phenotypes, whereas enhanced vagal flexibility promotes neurotrophin availability, homeostatic excitability, and synaptic strengthening. Interventions including Vagus Nerve Stimulation (VNS), paired with task-specific training, respiratory-based protocols, Heart Rate Variability (HRV) biofeedback, and individualized aerobic exercise demonstrate promising autonomic and functional effects. Altogether, these observations support the view that autonomic modulation is a mechanistic boundary condition for post-injury plasticity, rather than a secondary consequence of SCI. Future work requires rigorously powered, multimodal trials integrating autonomic biomarkers-especially HRV-with neurophysiological endpoints to refine dose-specific protocols and accelerate translation into precision-based rehabilitation.

Women are disproportionately affected by disorders of gut-brain interaction (DGBI), including esophageal, gastroduodenal, bowel, and anorectal conditions, and frequently experience overlapping pain syndromes. This review synthesizes clinical and preclinical evidence on sex- and gender-related differences in DGBI, highlighting alterations in central pain processing, autonomic regulation, stress, microbiota composition, epithelial permeability, motility, genetic and epigenetic factors, and immune responses that may underlie observed disparities. Emerging data indicate that gonadal hormones, interacting with environmental stressors across the lifespan, modulate symptom severity and disease course. Social determinants of health, inadequate patient-provider communication, and disorder-associated stigma further exacerbate inequities in diagnosis and care. Research remains limited by lack of standardized definitions of sex and gender, under-representation of men and gender minorities, and insufficient consideration of hormonal changes and exogenous hormone exposure. Addressing these gaps is essential to advance our understanding of DGBI and guide gender-informed diagnostic and therapeutic strategies for DGBI management.

Background: Chronic low-grade inflammation plays a central role in the pathogenesis of type 2 diabetes (T2DM) and its complications. Neopterin, a marker of macrophage activation and Th1-mediated immune response, has been associated with cardiovascular disease and metabolic disorders. However, its relationship with diabetic autonomic neuropathy remains insufficiently investigated. Methods: We conducted a cross-sectional study including 129 participants (93 with T2DM and 36 with obesity without carbohydrate disturbances). Clinical, anthropometric, and biochemical assessments were performed. Cardiovascular autonomic neuropathy was evaluated using Ewing cardiovascular reflex tests and sudomotor dysfunction scoring. Neopterin concentrations were measured in serum. Correlation, ROC, and logistic regression analyses were performed. Results: Neopterin levels were not significantly different between T2DM and obesity groups. No differences were observed in patients with versus without peripheral neuropathy, nephropathy, or retinopathy. However, neopterin levels were significantly higher in individuals with cardiovascular autonomic neuropathy (p = 0.013). Neopterin correlated with cardiovascular autonomic neuropathy score, sudomotor dysfunction, fasting glucose, fasting insulin, and HOMA-IR. It showed a moderate negative monotonic correlation with eGFR (Spearman's rho = -0.41, p< 0.001). In multivariable logistic regression adjusted for age, HbA1c, BMI, eGFR, and diabetes duration, each 1-SD increase in neopterin was associated with 2.67-fold higher odds of cardiovascular autonomic neuropathy (95% CI 1.21-5.89; p = 0.015). Conclusions: Circulating neopterin is independently associated with cardiovascular autonomic neuropathy in T2DM but not with classical microvascular complications. These findings suggest a potential role of immune-mediated mechanisms in the pathogenesis of diabetic cardiovascular autonomic neuropathy.

Background: COVID-19 has been associated with persistent impairments in autonomic modulation of heart rate variability (HRV). However, whether disease severity during the acute phase influences the magnitude of these impairments remains insufficiently explored. In turn, aerobic physical training (APT) has been proposed as a countermeasure to autonomic dysfunction of HRV in different conditions, although its effects in individuals with COVID-19 are not yet well established. To address these gaps, this study investigated the consequences of COVID-19 on autonomic modulation of HRV according to disease severity and evaluated the effects of APT on this parameter. Methods: One hundred and sixteen individuals (58 men and 58 women) aged between 30 and 55 years were included, allocated into three groups according to the severity of the disease in the acute phase: Mild group (n = 38, mean age: 48 ± 7 years); Moderate group (n = 52, mean age: 43 ± 5 years); and Severe group (n = 26, mean age: 45 ± 6 years). All groups had anthropometric and hemodynamic parameters evaluated before and after the 16-week APT period, as well as parameters of autonomic modulation of HRV analyzed using linear (time and frequency domain) and non-linear (symbolic analysis) methods obtained from R-R interval (RRi) recordings in the supine position for 30 min. Results: Initially, all groups presented similar anthropometric and hemodynamic values. In contrast, the Moderate and Severe groups presented lower values for standard deviation of normal RRi (SDNN; Moderate: 38 ± 14 ms; Severe: 33 ± 12 ms vs. Mild: 55 ± 28 ms; p < 0.001), root mean square difference between adjacent normal RRi (RMSSD; Moderate: 28 ± 13 ms; Severe: 22 ± 7 ms vs. Mild: 47 ± 38 ms; p < 0.001), total variance (Moderate: 203 ± 127 ms2; Severe: 303 ± 157 ms2 vs. Mild: 526 ± 347 ms2; p < 0.001), and high-frequency (HF) oscillations in absolute units (Moderate: 259 ± 270 ms2; Severe: 153 ± 74 ms2 vs. Mild: 438 ± 421 ms2; p < 0.001), both compared to the Mild group. In turn, the Severe group, when compared to the other groups, also presented lower HF oscillations (Severe: 29 ± 12 nu vs. Mild: 44 ± 17 nu and Moderate: 42 ± 17 nu; p < 0.001) and higher low-frequency (LF) oscillations (Severe: 71 ± 12 nu vs. Mild: 60 ± 17 nu and Moderate: 58 ± 17 nu; p < 0.001), but in normalized units. After the 16-week APT, all groups showed increases in HF oscillations (Mild: -206 ms2 and -19.12 nu; Moderate: -236 ms2 and -26.7 nu; Severe: -211 ms2 and -31.0 nu; p < 0.001) and reductions in LF oscillations (Mild: 198 ms2 and 19.01 nu; Moderate: 98 ms2 and 26.7 nu; Severe: 218 ms2 and 31.1 nu; p < 0.001), both in absolute and normalized units. In this case, there were no further differences in LF and HF oscillations between the groups. Conclusions: Individuals who had COVID-19 and developed moderate to severe cases showed greater impairments in the autonomic modulation of HRV, characterized by increased sympathetic autonomic modulation and reduced vagal modulation. In turn, APT as a countermeasure appears to increase vagal autonomic modulation and reduce sympathetic autonomic modulation of HRV, regardless of the previous severity of COVID-19.

Diabetic peripheral neuropathy (DPN) is one of the most common and disabling complications of diabetes mellitus (DM), affecting up to 50% of patients during the course of their disease. The condition manifests predominantly as a distal symmetric polyneuropathy, with early involvement of small fibers and progressive sensory loss. Epidemiological data show high prevalence not only in type 1 and type 2 diabetes but also in prediabetic populations, highlighting the need for early detection. The pathophysiology of DPN is complex, involving metabolic dysregulation, oxidative stress, vascular insufficiency, inflammation, and mitochondrial dysfunction. Diagnostic tools range from clinical examination and nerve conduction studies (NCS) to magnetic resonance imaging. Recent advances in plasma and neuroimaging biomarkers offer promising avenues for earlier and more accurate diagnosis. Management focuses on strict glycemic control, risk factor modification, symptomatic treatment of neuropathic pain, and lifestyle interventions. Despite ongoing research, no curative therapy currently exists, underscoring the urgent need for disease-modifying strategies. A multidisciplinary, patient-centered approach is essential to mitigate complications and improve quality of life. This review provides a comprehensive overview of DPN, covering its epidemiology, pathogenesis, diagnostic approaches, emerging biomarkers, and current management strategies. Future research should emphasize biomarker validation, longitudinal monitoring, and personalized therapeutic interventions.