Search Results (78)

Fatigue and balance disorders are common in people with multiple sclerosis (PwMS), but the neural mechanisms linking them during postural control remain unclear. This cross-sectional study aims to examine associations between fatigue, balance impairment, and task-evoked cortical hemodynamics/connectivity. Sixteen PwMS (relapsing-remitting MS; EDSS < 3.5) and 19 healthy controls (HC) were enrolled. Based on the Modified Fatigue Impact Scale (MFIS), PwMS were classified as fatigued (f_PwMS, MFIS ≥ 38; n = 10) or non-fatigued (nf_PwMS, n = 6). Participants performed five 30 s trials of static stance on foam with eyes closed. fNIRS recorded frontal, temporal, and occipital cortical activity, while stabilometry measured center-of-pressure sway. In PwMS, MFIS showed a trend toward association with sway (r = 0.49; p = 0.06). Sway was higher in f_PwMS than nf_PwMS and HC but not significantly different (ANOVA p = 0.341). Compared with HC, PwMS showed increased bilateral prefrontal and reduced occipital HR. Stratified analyses showed greater HR in f_PwMS versus HC and nf_PwMS in bilateral BA10 and in temporo-parietal regions, with a right-hemisphere predominance. Global coherence did not differ across groups, but exploratory BA10 analysis showed higher prefrontal coherence in f_PwMS than nf_PwMS (p = 0.02). Fatigued PwMS exhibit amplified, right prefrontal and temporo-parietal activation and focal prefrontal hyper-connectivity, consistent with compensatory top–down control to maintain balance. Full article

Background/Objectives: Infective endocarditis (IE) is a life-threatening cardiovascular infection with in-hospital mortality of 15–30% despite modern therapy. Contemporary IE demonstrates non-random valve involvement: aortic and mitral 35–45%, tricuspid 5–10% (30–50% in intravenous drug users [IVDU]), and pulmonary < 1%. These patterns implicate valve-specific anatomy and hemodynamics as central determinants of susceptibility. This narrative review examines the reported distribution of IE across the aortic, mitral, tricuspid and pulmonary valves and summarises the anatomical, haemodynamic, structural, microbial and patient-related factors associated with valve-specific susceptibility. Methods: A structured narrative review of English-language literature was conducted using PubMed/MEDLINE, Embase, Scopus, and Google Scholar (January 1990–March 2026). Search terms included “infective endocarditis,” “valve anatomy,” “hemodynamics,” “bicuspid aortic valve,” “prosthetic valve endocarditis,” and “transcatheter aortic valve replacement (TAVR) endocarditis.” We included anatomical studies, clinical cohorts, surgical series, imaging research, and international guidelines. Evidence was synthesized narratively using Oxford Centre for Evidence-Based Medicine (CEBM) levels. Results: IE susceptibility follows a biologically coherent gradient determined by the interaction between valve anatomy, hemodynamic stress, endothelial injury, and structural substrate. The aortic valve is most vulnerable because of high shear stress, congenital abnormalities such as bicuspid aortic valve, and direct continuity with the cardiac fibrous skeleton, predisposing to peri-annular extension. Mitral valve IE is largely conditional upon pre-existing structural disease, particularly mitral valve prolapse, rheumatic heart disease, and mitral annular calcification, and is characterized by a high risk of systemic embolization. Tricuspid valve IE reflects the interaction between low-pressure hemodynamics and acquired patient-specific modifiers, including intravenous drug use, cardiovascular implantable electronic devices, and congenital heart disease. Pulmonary valve IE remains uncommon because of favorable native hemodynamics but occurs predominantly in repaired congenital heart disease, right ventricular outflow tract reconstruction, and prosthetic pulmonary valves. Across all valve types, multimodality imaging and anatomical assessment consistently influence complication detection, surgical planning, and long-term surveillance. Conclusions: IE involvement is unevenly distributed among the cardiac valves. Aortic and mitral involvement predominate, tricuspid involvement is strongly influenced by injection drug use and intracardiac devices, and pulmonary-valve IE remains rare and is principally associated with congenital abnormalities or prosthetic material. These patterns highlight the possible contributions of haemodynamic stress, pre-existing structural abnormalities, and age-related valvular changes to the greater susceptibility of left-sided valves. Full article

Background/Objectives: Although vascular mechanisms are increasingly implicated in the etiology of sudden sensorineural hearing loss (SSNHL), the inability to directly visualize the labyrinthine artery remains a diagnostic obstacle. Sharing embryological and physiological parallels with the inner ear, the eye represents an accessible surrogate organ capable of reflecting systemic microvascular status. This study aimed to evaluate the diagnostic value of ocular hemodynamic and structural parameters in patients with acute unilateral idiopathic SSNHL. Methods: This prospective, comparative, cross-sectional study enrolled 30 patients with acute unilateral idiopathic SSNHL and 25 age and sex matched healthy controls. Three groups were defined: the affected eye, the contralateral eye, and the control eye. Retrobulbar hemodynamics (PSV, EDV, RI, PI) were assessed by color Doppler imaging; peripapillary choroidal thickness, RNFL, GCC+, and macular thickness by swept-source OCT; and macular microvascular perfusion by OCT angiography. Results: End diastolic velocity in the posterior ciliary arteries was significantly reduced in both patient eye groups relative to controls (p < 0.001), while RI and PI were significantly elevated (p = 0.001 and p = 0.004, respectively). Comparable hemodynamic impairment was observed in the ophthalmic artery. Peripapillary choroidal thickness was bilaterally reduced in the inferior and temporal quadrants in both patient groups (p = 0.003 and p = 0.010). No significant difference was detected between affected and contralateral eyes in any parameter. RNFL, GC+, and macular thickness remained comparable across all groups. Conclusions: The bilateral symmetry of hemodynamic impairment and choroidal thinning suggests that SSNHL arises against a background of systemic microvascular disease. The combined use of OCT and color Doppler ultrasonography holds clinical potential as a non-invasive biomarker panel for defining the vascular phenotype of the condition. Full article

Background: Hemodynamic failure remains a major determinant of mortality in critical illness, yet its detection is often delayed because conventional monitoring relies predominantly on Eulerian measurements that quantify pressure and flow magnitude without resolving the spatial and temporal organization of circulation. Consequently, clinically significant states of dysfunction may persist despite apparently stable hemodynamic indices. The Geometry of Shock is a conceptual and hypothesis-generating multi-scale framework intended to integrate established cardiovascular physiology with emerging computational approaches for the analysis of circulatory dysfunction. Framework: The proposed framework combines Guytonian venous return physiology and cardiopulmonary interactions with Lagrangian flow topology, geometric representations of circulatory equilibrium, topological data analysis, and physics-constrained inverse modeling. Rather than focusing exclusively on static thresholds of pressure and flow, the framework proposes a structural interpretation of circulation centered on the dynamic organization and coherence of blood transport across cardiovascular domains. Within this paradigm, under-recognized hemodynamic phenotypes—including stressed volume failure, oscillatory shock during spontaneous breathing, macro–microcirculatory decoupling, and pulmonary vascular pressure–flow dissociation—may emerge from disrupted coupling between vascular, cardiac, pulmonary, and microcirculatory systems. These states may represent reversible structural transitions in venous return geometry and cardiopulmonary interaction preceding overt circulatory collapse. Conclusions: By reframing shock as a disorder of circulatory structure and coherence rather than solely a deficit in flow, this framework proposes a mechanistic foundation that may support future approaches aimed at earlier recognition of instability, improved physiological characterization of hemodynamic phenotypes, and future development and prospective validation of physiology-informed computational decision-support strategies in critical care. These concepts remain exploratory and hypothesis-generating rather than clinically validated. Full article

Sepsis is a systemic disorder in which infection-induced inflammation progressively disrupts vascular homeostasis and drives organ dysfunction. This review reframes septic pathophysiology as a sequential and self-amplifying process centered on endothelial failure. Early activation of innate immune pathways by pathogen- and damage-associated molecular patterns promotes cytokine release, oxidative stress, and enzymatic degradation of the endothelial glycocalyx. Loss of this protective surface layer exposes endothelial cells to unbuffered inflammatory and mechanical injury, impairing mechanotransduction, increasing leukocyte and platelet adhesion, and destabilizing vascular barrier function. Subsequent disruption of intercellular junctions promotes capillary leakage, tissue edema, and impaired oxygen diffusion, while mitochondrial dysfunction and redox imbalance reduce endothelial repair capacity. In parallel, complement activation, neutrophil extracellular trap formation, platelet–leukocyte interactions, and loss of anticoagulant signaling shift the microvasculature toward a prothrombotic and proinflammatory state. These interconnected mechanisms culminate in microvascular incoherence, characterized by heterogeneous capillary flow, regional hypoxia, impaired oxygen extraction, and progressive organ failure despite apparent restoration of systemic hemodynamics. Within this framework, biomarkers such as syndecan-1, soluble thrombomodulin, angiopoietin-2, von Willebrand factor, and plasminogen activator inhibitor-1 are best interpreted as mechanistic readouts of glycocalyx shedding, endothelial injury, permeability imbalance, and thromboinflammatory activation. Understanding sepsis as an evolving endothelial pathophysiological process provides a coherent framework for integrating inflammation, vascular leakage, hypoxia, coagulation, and organ dysfunction while identifying mechanistic biomarkers that reflect distinct stages of microvascular collapse. Full article

Cardiovascular disease is traditionally interpreted through macrocirculatory parameters such as cardiac output, vascular resistance, and epicardial coronary anatomy. However, clinical outcomes frequently diverge from predictions based solely on these indices, particularly in syndromes such as heart failure with preserved ejection fraction (HFpEF), cardiogenic shock, and sepsis-associated myocardial dysfunction. Increasing evidence suggests that the integrity of the microvascular–immune interface plays a central role in determining tissue perfusion and cardiovascular resilience. This review proposes a staged framework of cardiovascular decompensation centered on progressive failure of this interface. In Stage 1, chronic cardiometabolic and inflammatory stress produces a primed but compensated microvascular state characterized by endothelial activation, glycocalyx vulnerability, pericyte remodeling, platelet sensitization, and reduced lymphatic reserve. Perfusion is preserved at rest, but vasodilatory reserve and microvascular stability are reduced, narrowing the effective perfusion window under physiologic stress. In Stage 2, acute insults such as infection, ischemia, or neurohumoral activation precipitate threshold instability within the microcirculation. Perfusion becomes governed by the arterial pressure–critical closing pressure (Pa − Pcrit) relationship rather than traditional arterial–venous gradients. As this window narrows, segmental capillary derecruitment and heterogeneous flow emerge, producing loss of hemodynamic coherence in which systemic blood pressure and cardiac output may appear preserved despite impaired tissue perfusion. In Stage 3, inflammatory amplification and immunothrombotic processes consolidate microvascular dysfunction. Pericyte contraction, endothelial injury, cytokine escalation, and neutrophil extracellular trap formation promote platelet–fibrin deposition and capillary obstruction, transforming reversible conductance failure into structural microvascular impairment. This framework provides a unifying physiologic lens for diverse cardiovascular syndromes, including Type 2 myocardial infarction, HFpEF decompensation, and cardiogenic shock. It also suggests that therapeutic efficacy may depend less on macrocirculatory normalization alone and more on preserving microvascular integrity before immunothrombotic consolidation occurs. Although this model remains hypothesis-generating, it highlights the microvascular–immune interface as a central determinant of cardiovascular stability and a potential target for future precision hemodynamic and immunomodulatory strategies. Full article

Background: Hypoplastic left heart syndrome (HLHS) is defined as “a spectrum of congenital cardiovascular malformations with normally aligned great arteries without a common atrioventricular junction, characterized by underdevelopment of the left heart with significant hypoplasia of the left ventricle including atresia, stenosis, or hypoplasia of the aortic or mitral valve, or both valves, and hypoplasia of the ascending aorta and aortic arch”. Without treatment, HLHS is usually lethal in the neonate. Many hypotheses have been advanced to explain the etiology of HLHS; however, no single theory appears to fully explain the phenotypic variability seen in HLHS. Furthermore, many of these theories offer no explanations regarding the precipitating events which lead to the development of HLHS. Objective: This review considers and critically evaluates the strengths and weaknesses of the leading theories proposed to explain the pathogenesis of HLHS—including hemodynamic disturbances, primary myocardial structural defects, valvar malformations, and genetic or epigenetic alterations that may provoke developmental and anatomic abnormalities. After presenting each model, we propose a novel, comprehensive, and data-driven framework which may assist researchers in developing models for the pathogenesis of the various subtypes of HLHS. Methods: Key findings from human fetal imaging, histopathology, genetic studies, and animal models were considered, as well as the hypothetical contribution of each in observed HLHS phenotypes. The rationales for these findings as causal factors initiating individual HLHS patterns, as well as how they might contribute to HLHS in general, were critically analyzed. Results: The flow theory is strongly supported by animal models and in utero interventions that demonstrate the impact of altered hemodynamics on cardiac morphogenesis. However, the flow theory fails to identify initial causes of disturbed flow or related histological features of HLHS like endocardial fibroelastosis. The myocardial and valve-first models suggest an important role in developmental defects, but do not necessarily have a strong experimental basis that provides explanations for how they mediate HLHS. Genetic studies in patients with HLHS have identified several candidate causal mutations. However, such genetic causes of HLHS exhibit incomplete phenotypic penetrance and clinical impact. A multifactorial framework attempts to integrate these diverse mechanisms and may provide the most coherent explanation that can accommodate the heterogeneity and variable presentation of HLHS. Such a framework may identify multiple forces that drive disease but does not provide useful pathways for future research about HLHS. Conclusions: No single hypothesis has fully explained how HLHS is initiated, progresses, and presents with the clinical conditions that are encountered by cardiac surgeons and cardiologists. The most current models suggest that the spectrum of HLHS reflects acomplex interaction between genetic susceptibility, flow-dependent cardiac remodeling, and environmental factors in utero. A multifactorial model integrates these diverse mechanisms and may provide the most coherent explanation for the various phenotypic variations in HLHS. Based on our analysis of the most current data and the strengths and weaknesses of the current theoretical frameworks, we propose a novel research strategy aimed at identifying specific cardiac progenitor cell populations whose dysregulation may represent a unifying explanation for the etiology of the various phenotypes of HLHS. Based on the arguments made throughout this manuscript that evaluate the various genetic, structural, and hemodynamic models of initiation of disease, we believe that the significant phenotypic variability across the spectrum of HLHS (i.e., the different anatomic subtypes for “classic” HLHS) most likely reflects different underlying etiologies and mechanisms. At the very least, it is very likely that the timing of the insult is critical in determining anatomic subtype. Based on the published data and the arguments within this manuscript, it seems naive to think that there is a single unifying mechanism explain all forms of HLHLS. Full article

A challenge of studying mammalian cardiac embryogenesis is the limited ability to perform experimental manipulations in animal models. The avian embryo is widely accepted as a model for mammalian heart developmental studies. In this study, we establish the methodology and protocols for studying the Japanese quail (Coturnix japonica) heart at embryonic day 10 (HH38) using the FUJIFILM VisualSonics Vevo 3100 ultrasound system equipped with a MX550D small animal cardiology transducer. These protocols were designed to measure right ventricular wall thickness, pulmonary artery diameter, and the outflow velocities of the right ventricular outflow tract (RVOT) and the pulmonary artery (PA), thereby establishing baseline parameters of the normally developing quail morphology. Quail embryos are an ideal model for cardiovascular research due to their short incubation period (16–17 days), experimental accessibility, and strong similarities to mammalian heart development. These developmental similarities include, but are not limited to, looping, chamber septation, and the development of a true four-chamber heart. High-resolution imaging modalities, including ultrasound and optical coherence tomography, enable noninvasive, real-time visualization of cardiac morphology and function throughout development. Echocardiography allows for quantitative and qualitative assessments of myocardial structure and cardiac hemodynamics. The similarity to the mammalian heart, combined with rapid embryogenesis, makes quail embryos a valuable model for investigating congenital heart defects, genetic modifications, and fundamental cardiac developmental processes. In this study, we describe reproducible incubation protocols and baseline echocardiographic parameters used to evaluate morphological and physiological changes in the developing embryonic quail heart on embryonic day 10. Full article

Background/Objectives: Brain death determination in children is clinically challenging. When standard clinical examination cannot be completed or reliably interpreted, ancillary testing is required—yet many established methods depend on infrastructure or patient transport that may not be feasible in critically ill pediatric patients. Orbital ultrasonography is bedside-applicable and non-invasive, but remains poorly characterized in children. Methods: We conducted a single-center retrospective study of 28 pediatric patients evaluated for suspected brain death between January 2021 and February 2025. Patients were classified as brain death-positive [BD(+), n = 20] or brain death-negative [BD(−), n = 8] based on clinical criteria independent of imaging findings. Orbital color Doppler parameters (ophthalmic artery, central retinal artery, posterior ciliary artery) and optic nerve sheath diameter (ONSD) were measured under a standardized protocol by a single experienced operator. Ophthalmic artery resistive index (OA-RI) was defined a priori as the primary outcome; ONSD was the secondary outcome. Group comparisons used the Mann–Whitney U test with Cliff’s delta effect sizes; false discovery rate correction was applied to secondary and exploratory comparisons. ROC analyses were performed to assess discriminative performance. The study was reported in accordance with the STARD 2015 guidelines for diagnostic accuracy research. Results: OA-RI was markedly higher in BD(+) patients (0.84 [IQR 0.80–0.90] vs. 0.65 [0.58–0.69]; p < 0.001; δ = 0.975). ROC analysis yielded an AUC of 0.99 (95% CI: 0.96–1.00); at a cut-off of ≥0.77, sensitivity was 95.0% and specificity 100.0%. ONSD also differed significantly between groups (4.75 [4.15–5.08] mm vs. 3.90 [3.40–4.15] mm; p = 0.012; δ = 0.619; AUC = 0.81, 95% CI: 0.62–1.00; cut-off ≥ 4.2 mm; sensitivity and specificity both 75.0%). Across all three orbital vessels, end-diastolic velocity was consistently reduced and resistive indices elevated in BD(+) patients. Systolic velocities did not differ meaningfully between groups. Cut-off values represent cohort-specific statistical optima and should be interpreted as exploratory. Conclusions: Orbital Doppler ultrasonography demonstrates a coherent high-resistance hemodynamic pattern in pediatric brain death. OA-RI showed strong discriminative performance and may serve as a useful bedside adjunct in selected cases where ancillary testing is indicated. ONSD provides complementary anatomical evidence. These findings are exploratory and require prospective validation in larger, multicenter pediatric cohorts. Full article

Background/Objectives: This study aimed to evaluate macular choroidal blood flow dynamics and structural alterations in children with hyperopic anisometropic amblyopia and compare these findings with those of the fellow eyes. Methods: This retrospective observational study included 36 eyes from 18 children (mean age: 4.9 years) with unilateral hyperopic anisometropic amblyopia. Central choroidal thickness (CCT) was measured using enhanced depth imaging optical coherence tomography. Macular choroidal hemodynamics were assessed using laser speckle flowgraphy. Mean blur rate (MBR) was used as an index of blood flow, whereas beat strength (BS) was used as a measure of pulsatility. Ocular perfusion pressure (OPP) was also calculated. All parameters were compared between amblyopic and fellow eyes. Results: Amblyopic eyes demonstrated significantly greater CCT compared with fellow eyes (407.6 ± 84.9 µm vs. 326.4 ± 79.1 µm). Conversely, macular MBR was significantly lower in amblyopic eyes (9.28 ± 3.60 AU vs. 10.94 ± 4.68 AU), as was BS (5.73 ± 3.07 AU vs. 7.28 ± 3.59 AU). No significant differences were observed in central retinal thickness or OPP between amblyopic and fellow eyes. In amblyopic eyes, CCT was not significantly correlated with macular MBR or BS. Conclusions: Amblyopic eyes exhibited significant central choroidal thickening accompanied by reduced macular blood flow and pulsatility. These findings suggest that localized macular hemodynamic dysregulation may contribute to the pathophysiology of hyperopic anisometropic amblyopia. Full article

Background and Objectives: Septic shock is marked by profound circulatory and cellular dysfunction, with mortality rates of 25–40% despite guideline-based resuscitation. Normalization of macrohemodynamic variables often fails to restore tissue perfusion, a concept known as hemodynamic incoherence. Persistent microcirculatory dysfunction is associated with organ failure and poor outcomes, underscoring the limitations of systemic monitoring alone. This focused narrative review synthesizes current evidence on microcirculatory monitoring in septic shock, with emphasis on bedside and emerging optical technologies, and evaluates their role as adjuncts to traditional hemodynamic assessment for perfusion-targeted resuscitation. Materials and Methods: A concept-driven search of PubMed/MEDLINE (January 2015 to January 2026) was performed, incorporating MeSH and free-text terms for septic shock, microcirculation, hemodynamic coherence, and monitoring modalities. Foundational pre-2015 studies were included for context. Articles were screened using predefined inclusion/exclusion criteria to minimize bias, with thematic qualitative synthesis. A PRISMA-inspired flow diagram was used to summarize the study selection process. Results: Microcirculatory alterations in septic shock include reduced functional capillary density, perfusion heterogeneity, and impaired oxygen extraction, persisting despite macrohemodynamic correction. Bedside markers, such as capillary refill time (CRT) and mottling, track microvascular recovery more closely than lactate. When used to guide resuscitation, CRT-based strategies show a non-significant mortality trend in randomized evaluation, with later studies reporting benefit in composite clinical outcomes. Optical technologies offer non-invasive insights: photoplethysmography (PPG) and perfusion index (PI) show prognostic value and early detection of incoherence; automated CRT (aCRT) enhances reproducibility; advanced modalities, such as laser speckle contrast imaging (LSCI), near-infrared spectroscopy (NIRS), and sublingual videomicroscopy, provide detailed physiological data but face standardization challenges. Recent interventional evidence, including peripheral perfusion-targeted RCTs, supports improved outcomes, though large-scale trials remain limited. Conclusions: Microcirculatory monitoring provides complementary, physiologically relevant information to macrohemodynamic assessment in septic shock. Emerging bedside tools, such as PI and aCRT, are poised for routine use, while multimodal integration may enable personalized management. Future research should prioritize standardization, AI-driven analysis, and randomized trials to confirm outcome benefits. Full article

Introduction: Massage therapy delivers structured mechanosensory input that can influence brain function, yet the central mechanisms and potential for neuroplastic change have not been synthesized across neuroimaging modalities. This mechanistic review integrates evidence from electroencephalography (EEG), functional MRI (fMRI), and functional near-infrared spectroscopy (fNIRS) to map how massage alters human brain activity acutely and over time and to identify signals of longitudinal adaptation. Materials and Methods: We conducted a scoping, mechanistic review informed by PRISMA/PRISMA-ScR principles. PubMed/MEDLINE, Cochrane Library, Google Scholar, and ResearchGate were queried for English-language human trials (January 1990–July 2025) that (1) delivered a practitioner-applied manual massage (e.g., Swedish, Thai, shiatsu, tuina, reflexology, myofascial techniques) and (2) measured brain activity with EEG, fMRI, or fNIRS pre/post or between groups. Non-manual stimulation, structural-only imaging, protocols, and non-English reports were excluded. Two reviewers independently screened and extracted study, intervention, and neuroimaging details; heterogeneity precluded meta-analysis, so results were narratively synthesized by modality and linked to putative mechanisms and longitudinal effects. Results: Forty-seven studies met the criteria: 30 EEG, 12 fMRI, and 5 fNIRS. Results: Regarding EEG, massage commonly increased alpha across single sessions with reductions in beta/gamma, alongside pressure-dependent autonomic shifts; moderate pressure favored a parasympathetic/relaxation profile. Connectivity effects were state- and modality-specific (e.g., reduced inter-occipital alpha coherence after facial massage, preserved or reorganized coupling with hands-on vs. mechanical delivery). Frontal alpha asymmetry frequently shifted leftward (approach/positive affect). Pain cohorts showed decreased cortical entropy and a shift toward slower rhythms, which tracked analgesia. Somatotopy emerged during unilateral treatments (contralateral central beta suppression). Adjuncts (e.g., binaural beats) enhanced anti-fatigue indices. Longitudinally, repeated programs showed attenuation of acute EEG/cortisol responses yet improvements in stress and performance; in one program, BDNF increased across weeks. In preterm infants, twice-daily massage accelerated EEG maturation (higher alpha/beta, lower delta) in a dose-responsive fashion; the EEG background was more continuous. In fMRI studies, in-scanner touch and reflexology engaged the insula, anterior cingulate, striatum, and periaqueductal gray; somatotopic specificity was observed for mapped foot areas. Resting-state studies in chronic pain reported normalization of regional homogeneity and/or connectivity within default-mode and salience/interoceptive networks after multi-session tuina or osteopathic interventions, paralleling symptom improvement; some task-based effects persisted at delayed follow-up. fNIRS studies generally showed increased prefrontal oxygenation during/after massage; in motor-impaired cohorts, acupressure/massage enhanced lateralized sensorimotor activation, consistent with use-dependent plasticity. Some reports paired hemodynamic changes with oxytocin and autonomic markers. Conclusions: Across modalities, massage reliably modulates central activity acutely and shows convergent signals of neuroplastic adaptation with repeated dosing and in developmental windows. Evidence supports (i) rapid induction of relaxed/analgesic states (alpha increases, network rebalancing) and (ii) longer-horizon changes—network normalization in chronic pain, EEG maturation in preterm infants, and neurotrophic up-shifts—consistent with trait-level recalibration of stress, interoception, and pain circuits. These findings justify integrating massage into rehabilitation, pain management, mental health, and neonatal care and motivate larger, standardized, multimodal longitudinal trials to define dose–response relationships, durability, and mechanistic mediators (e.g., connectivity targets, neuropeptides). Full article

Resting-state functional connectivity (rsFC) provides insight into the intrinsic organization of brain networks and is increasingly recognized as a sensitive marker of age-related neural changes. Functional near-infrared spectroscopy (fNIRS) offers a portable and cost-effective approach to measuring rsFC, including in naturalistic settings. However, its sensitivity to age-related alterations in network topology remains poorly characterized. Here, we applied graph-based analysis to resting-state fNIRS data from 57 healthy participants, including 26 young adults (YA, 18–30 years) and 31 older adults (OA, 50–77 years). We observed that older adults exhibited a marked attenuation of low-frequency oscillation (LFO) power across all hemoglobin contrasts, corresponding to a 5–6-fold reduction in spectral power. In addition, network analysis revealed altered topological organization under matched sparsity conditions, characterized by reduced degree heterogeneity and increased segregation in older adults, with the strongest differences observed in the default mode (DMN), auditory, and frontoparietal control (FPC) networks. Network visualizations further indicated a shift toward more right-lateralized and posterior hub organization in older adults. Together, the coexistence of reduced oscillatory power and increased connectivity suggests that fNIRS-derived rsFC reflects combined neural and non-neural hemodynamic influences, including increased coherence arising from age-related vascular and systemic physiological processes. Overall, our findings demonstrate that fNIRS is sensitive to age-related changes in large-scale hemodynamic network organization. At the same time, sensitivity to non-neural hemodynamics highlights the need for cautious interpretation, but it may provide complementary, clinically relevant signatures of aging-related changes. Full article

Background/Purpose: Four patients independently reported episodes of seeing a dimly flickering overlay on an otherwise intact part of their binocular visual field. The aim of the study was to describe the clinical characteristics of this episodic phenomenon, which we call dim flicker. Methods: Retrospective chart review and patient evaluation of an animated reference simulation. Results: The patients described repeated episodes of a seeing a patch of rhythmically oscillating dim flicker overlaid on a circumscribed patch of their otherwise normal binocular visual field. The flicker was typically seen at low ambient light levels and disappeared in bright light or when one or both eyes were covered. Episodes lasted seconds to minutes. Some flicker patches crossed the vertical midline. The flicker was subjectively experienced as coming from one specific eye. Compared to a 7 Hz flicker simulation, patients reported differences in location, prominence, and frequency, with the latter ranging from 3 to 10 Hz. In three patients, the flicker was sometimes experienced during aerobic exercise and in two patients sometimes when they rose at night in the dark. In one patient, the flicker corresponded to an area of ischemic macular edema secondary to central retinal vein occlusion. There was no headache during or after the flicker. Associated maladies included retinal venous congestion, central serous chorioretinopathy, arterial hypertension, atrial fibrillation, and migraine with visual aura distinctly different from the dim flicker. Conclusions: Episodes of seeing an endogenous, rhythmically oscillating transparent overlay within a confined, non-expanding part of an otherwise intact binocular visual field appears to be a distinct nosological entity that can be associated with ocular and systemic vascular disease. Full article

Background: Coronary artery aneurysm and ectasia (CAAE) represent uncommon forms of coronary artery disease characterized by abnormal arterial dilatation and complex remodeling. The mechanisms underlying their development remain poorly defined. Optical coherence tomography (OCT) provides high-resolution evaluation of plaque morphology and vessel wall structure, offering insights into the pathophysiology of CAAE. Methods: We analyzed 21 patients with angiographically confirmed CAAE who underwent intracoronary OCT. Dilated segments were compared with adjacent non-dilated reference segments. Quantitative measurements included the maximal dilated segment’s diameter, reference diameter, and intima–media thickness. Qualitative assessment focused on plaque composition, calcification, neovascularization, fibrous cap characteristics, and thrombus. Results: Aneurysmal segments displayed larger lumen dimensions but no proportional increase in plaque burden, consistent with exaggerated positive remodeling. Compared with non-aneurysmal regions, CAAE segments exhibited significantly smaller calcification arcs and a lower prevalence of lipid plaques and neovascularization, suggesting a heterogeneous and potentially more fibrotic remodeling pattern. Classical features of plaque vulnerability were not consistently present in dilated segments, suggesting that hemodynamic factors, such as disturbed flow and stenosis, may contribute substantially to the thrombotic risk. Conclusions: OCT reveals distinct structural and compositional characteristics in CAAE, supporting the concept of maladaptive remodeling rather than uniformly unstable plaque. High-resolution intracoronary imaging enhances understanding of CAAE pathophysiology and may facilitate individualized clinical assessment and management. Full article