Anatomic malformation as seen in subclavian steal syndrome leads to an alteration in the body's autonomic regulatory pattern, influencing varying physical manifestations. The autonomic nervous system provides situational regulatory feedback to the body, maintaining the body's desired point of homeostasis. We report the case of a 68-year-old male who initially came in with X-rays indicating retrolisthesis and calcifications in his carotids. A left-sided carotid bruit was also noted, as well as right-sided upper extremity weakness. Continued imaging studies indicated structural changes to his cervical regions and continued calcifications in the remainder of his arterial supply branching off of his carotid arteries. The patient's denial of surgical intervention led to treatments focused on symptomatic control until more conclusive data could be collected and interpreted.

Catatonia is a transdiagnostic syndrome that remains insufficiently recognized despite its clinical impact. Although sleep disturbances are well documented in mood and psychotic disorders, their association with catatonia has only rarely been described. This study aimed to map the available evidence on objective sleep alterations in patients with catatonia, complemented by an illustrative clinical case. A scoping review was conducted in accordance with the PRISMA extension for Scoping Reviews (PRISMA-ScR). Electronic databases were searched in July 2026 for studies reporting objective overnight sleep assessments in patients with catatonia. An illustrative case assessed with polysomnography and psychometric measures was included to contextualize the findings. Six studies met the inclusion criteria, including five case reports describing nine patients and one observational study including three patients with catatonic schizophrenia. Across studies, catatonia was associated with heterogeneous alterations in sleep architecture, while autonomic abnormalities were occasionally reported. In the presented case, polysomnography showed disrupted sleep architecture dominated by N1 and N2 sleep, reduced N3 and REM sleep, and marked sleep fragmentation with frequent micro-arousals. Overall, the available evidence suggests that sleep disturbances may accompany catatonic states. However, the current evidence base remains extremely limited and heterogeneous, precluding any conclusion regarding the specificity of these findings to catatonia or their underlying mechanisms. Further studies using contemporary polysomnographic methods are needed to clarify the clinical and pathophysiological significance of sleep alterations in catatonia.

Thyroid dysfunction (TD) and cardiovascular disease (CVD) commonly coexist in older adults, where age-related vascular, mitochondrial, and autonomic changes heighten sensitivity to even mild hormonal imbalance. Thyroid hormones (THs) regulate cardiac and vascular function through genomic and non-genomic pathways, but aging alters receptor sensitivity, deiodinase (DIO) activity, and epigenetic control, resulting in tissue-specific TH insufficiency despite normal serum levels. Subclinical hypothyroidism (SCH) and low-T3 syndrome are especially prevalent in older adults and are linked to higher risks of heart failure (HF), atherosclerosis, atrial fibrillation, and mortality. Emerging data underscore the role of epigenetic regulators and the gut-thyroid-heart axis in modulating CV responses to TH imbalance. Clinically, routine thyroid function assessment is crucial in CVD, with management tailored to age-related risks. Tissue-selective TH based therapies represent a promising frontier for precision cardioprotection.

Poor sleep quality is closely associated with autonomic dysregulation and increased risks of cardiovascular, metabolic, and mental disorders. Foot reflexology is a widely used complementary therapy; however, its physiological mechanisms and comparative efficacy remain insufficiently explored. This study aimed to compare the effects of manual reflexology treatment (MRT) and foot massage equipment (FEM) on autonomic nervous system function, sleep quality, insomnia severity, and fatigue in adults with poor sleep quality. Using a randomized crossover design, 32 participants with poor sleep quality received MRT and FEM interventions for 6 weeks each (once weekly, 30-40 min/session). Heart rate (HR), blood pressure, and heart rate variability (HRV; time- and frequency-domain indices) were assessed at weeks 1 and 6 before and after each intervention. Subjective outcomes included the Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI), and Fatigue Assessment Scale (FAS). Following MRT, participants demonstrated significantly greater reductions in global PSQI scores and all PSQI components compared with FEM. MRT also resulted in larger improvements in insomnia severity and both mental and physical fatigue. In contrast, FEM primarily improved physical fatigue. Physiologically, MRT induced an immediate decrease in HR and significant increases in HRV time-domain indices (SDNN, RMSSD, pNN50), which were sustained after 6 weeks. Frequency-domain analysis further revealed reduced LF, increased HF, and a lower LF/HF ratio, indicating enhanced parasympathetic activity and cumulative autonomic modulation. In conclusion, programmed manual reflexology, delivered according to the TIDieR framework, is more effective than mechanical foot massage in improving autonomic balance, sleep quality, insomnia severity, and fatigue in individuals with poor sleep quality. These findings support MRT as a feasible and evidence-based non-pharmacological complementary intervention for sleep health promotion. TRIAL REGISTRATION: clinicaltrials.gov; NCT Number: NCT07402460; Registered 3 February 2026.

Atrial fibrillation is the most prevalent type of arrhythmia globally, the incidence of atrial fibrillation continues to rise. Concurrently, as lifestyles modernize, the prevalence of saphenous varicose veins is also increasing significantly. Although both conditions have received considerable clinical attention, previous studies have primarily focused on independent investigations within their respective fields, leaving the potential association between these conditions relatively unexplored. In recent years, retrospective clinical analyses have shown that saphenous varicose veins may constitute a novel risk factor for the onset of atrial fibrillation-a breakthrough discovery that has opened a new dimension of cross-border dialogue in investigating disease mechanisms. Therefore, this study aimed to develop an innovative framework for the pathophysiological association between atrial fibrillation and saphenous varicose veins and to elucidate the associated underlying mechanisms from a multidimensional, evidence-based medical perspective. Available evidence suggests that hemodynamic changes in the lower extremity veins can directly affect right heart preload via central venous pressure transmission, thereby inducing atrial electrophysiological remodeling. Activation of the RAAS (renin-angiotensin-aldosterone system) is involved in venous wall remodeling and in the activation of inflammatory cytokine networks that promote atrial fibrosis. Autonomic dysfunction also exhibits shared pathological features in venous insufficiency and the neural remodeling associated with atrial fibrillation. Moreover, the bidirectional alterations in blood flow shear force may not only accelerate venous valve injury but also trigger abnormal electrical activity in atrial myocytes. The pathophysiological bridging hypothesis proposed in this study not only challenges the traditional single-system research paradigm, but also provides important implications for clinical intervention strategies. Indeed, by integrating a multidisciplinary chain of evidence, this paper systematically demonstrates the potential impact of peripheral venous lesions on cardiac electrophysiological activity, thereby adding a new dimension to screening and identifying a potential therapeutic target for the prevention of atrial fibrillation. These findings both deepen understanding of the nature of the two diseases and lay a theoretical foundation for establishing an integrated cardiovascular-peripheral vascular diagnostic and treatment model.

Background: Bartonella henselae infection has been associated with a broad spectrum of neurological and autonomic manifestations, although its impact on autonomic nervous system function remains insufficiently characterized, and the aim of this study was to evaluate autonomic function in patients with polymorphic symptoms and Bartonella henselae IgM seroreactivity. Methods: In this cross-sectional study, 75 patients were compared with 75 age- and sex-matched healthy controls, and all participants underwent cardiovascular autonomic reflex testing, short-term (5 min) and long-term (24 h) heart rate variability analysis, and 24 h ambulatory blood pressure monitoring, while head-up tilt testing was performed in the Bartonella group. Results: Abnormal autonomic reflex tests were significantly more frequent in the Bartonella IgM-seroreactive group, particularly those reflecting parasympathetic function, while heart rate variability analysis demonstrated reduced high-frequency components and lower long-term variability indices, and head-up tilt testing revealed heterogeneous hemodynamic responses including orthostatic hypotension and pronounced blood pressure variability, with ambulatory monitoring additionally showing higher nighttime blood pressure values and reduced nocturnal dipping. Conclusions: These findings indicate a consistent pattern of autonomic imbalance characterized predominantly by parasympathetic impairment and altered blood pressure regulation in patients with Bartonella henselae IgM seroreactivity, although further studies are required to clarify underlying mechanisms and clinical implications.

Heat exposure is an increasingly important climate-related determinant of mental health, yet the biological mechanisms linking heat to psychiatric outcomes remain insufficiently integrated. This narrative review synthesizes evidence from climate medicine, thermoregulation, neuroscience, psychoneuroimmunology, sleep research, psychopharmacology, epidemiology, and psychiatry to examine how acute and chronic heat exposure may influence mental health. Heat acts as a multi-system biological stressor by challenging thermoregulation, increasing autonomic and cardiovascular strain, disrupting hydration, impairing sleep and circadian rhythms, activating stress-response systems, and contributing to neuroinflammation, oxidative stress, mitochondrial dysfunction, blood-brain barrier disruption, and neurotransmitter alterations. These pathways may interact with psychotropic medication exposure and impaired behavioral thermoregulation, particularly among people with severe mental illness, older adults, individuals receiving lithium, people with cognitive impairment, substance use disorders, outdoor workers, and those living in poorly cooled environments. Heat-related psychiatric vulnerability is therefore transdiagnostic but heterogeneous, with relevance to distress, depression, anxiety, mood instability, psychosis, substance-related crises, cognitive dysfunction, delirium, and suicide-related outcomes. The review also distinguishes pathways supported by stronger human evidence from mechanisms supported mainly by experimental, preclinical, severe-spectrum, or indirect evidence. It proposes an integrative biological model and an evidence-informed translational agenda focused on exposure assessment, biomarkers, sleep and circadian monitoring, medication safety, risk prediction, physiological adaptation, heat-mitigation strategies, heat-health action plans, and implementation-oriented evaluation.

Cardiac neuromodulation includes various methods, such as vagus nerve stimulation, baroreflex activation therapy, renal denervation, and stellate ganglion intervention, and targets the autonomic imbalance contributing to the pathophysiology of many cardiovascular diseases. Despite promising mechanistic evidence, several landmark trials, including INOVATE-HF, NECTAR-HF, and SYMPLICITY HTN-3, did not meet their primary clinical outcomes, with substantial numbers of non-responders observed across therapies. Variation in patient response is attributed to several unresolved issues, including insufficient stimulation dosing, off-target or non-selective fiber activation, and differences in autonomic phenotypes between patients. Both problems highlight the need for individualized approaches to patient selection, therapy delivery, and monitoring. Artificial intelligence (AI) offers tools to address these problems. In this narrative review, we describe seven families of AI techniques relevant to cardiac neuromodulation: supervised machine learning, deep learning, representation learning, reinforcement learning, multimodal fusion, digital twins with physics-informed AI, and explainable AI with federated learning. For each family, we summarize how the method works, the cardiac neuromodulation problem it addresses, and the available evidence in the field of cardiac electrophysiology. We then map these techniques to the three core problems of patient selection, real-time stimulation control, and longitudinal response monitoring. The strongest evidence to date supports representation learning for VNS responder identification, reinforcement learning for closed-loop VNS control, and digital twins for in silico testing of stimulation protocols. The opportunity for the field is to translate these methods, most of which were developed in adjacent fields, into prospective cardiac neuromodulation trials.

Diabetes mellitus is increasingly recognized as a systemic disorder associated with a broad spectrum of neurological complications, including diabetic peripheral neuropathy, autonomic neuropathy, cerebrovascular disease, cognitive impairment, and neurodegenerative disorders. Because neurological injury may develop before the onset of overt clinical manifestations, the identification of reliable biomarkers for early risk assessment remains an important challenge in diabetes care. This narrative review summarizes current evidence regarding molecular biomarkers implicated in diabetes-related neurological complications. A literature search was conducted using major biomedical databases, with emphasis on human studies, systematic reviews, prospective cohorts, and clinically relevant translational research. Biomarker categories reviewed include inflammatory mediators, oxidative stress markers, advanced glycation end-products, neuronal injury proteins, metabolomic signatures, circulating microRNAs, extracellular vesicles, and multi-omics approaches. Current evidence suggests that several biomarkers are associated with neurological injury and adverse neurological outcomes in patients with diabetes. However, the strength of evidence varies substantially across biomarker classes. While some biomarkers demonstrate biological plausibility and consistent associations with disease burden, most remain at an exploratory stage and lack sufficient prospective validation for routine clinical implementation. Major barriers include study heterogeneity, assay variability, limited reproducibility, uncertainty regarding incremental predictive value, and insufficient evaluation in diabetes-specific populations. Future research should focus on rigorous validation of candidate biomarkers, standardization of analytical methods, and assessment of their added value beyond established clinical risk factors. The integration of molecular biomarkers with clinical variables, neuroimaging findings, and advanced analytical approaches may contribute to future risk stratification strategies; however, substantial validation is required before clinical implementation can be considered.

Heart rate recovery (HRR) and oxygen uptake (VO₂) recovery provide complementary information regarding autonomic and metabolic recovery following exercise; however, their integrated assessment remains insufficiently explored in patients with coronary artery disease (CAD).