Search Results (514)

Background/Objectives: Implant placement in transnasal and paranasal regions of the severely atrophic maxilla is challenged by complex anatomy and proximity to critical structures, particularly the nasolacrimal duct (NLD). While cortical anchorage is considered important for implant stability, structured methods for evaluating anatomical eligibility and anatomical risk during planning remain limited. This proof-of-concept study aimed to describe a segmentation-assisted workflow for anatomical assessment of potential paranasal implant trajectories. Methods: A single-case proof-of-concept workflow was developed using CBCT imaging and multi-component anatomical bone segmentation (MCABS). Segmented anatomical structures were used to selectively visualize cortical pathways within the anterior maxilla. Implant planning was performed using axial, non-tilted trajectories. Particular attention was directed toward visualization of the spatial relationship between the planned implant pathway and the nasolacrimal duct. Workflow feasibility was further explored through study-model fabrication, guided implant insertion, and axis-based verification. Results: The proposed workflow enabled selective visualization of cortical structures and facilitated identification of anatomically favorable implant trajectories within the paranasal region. The relationship between the planned implant pathway and the nasolacrimal duct could be directly assessed using the segmented anatomical model. Guided insertion in the study model demonstrated concordance between planned and executed implant axes, supporting the technical feasibility of the workflow. Conclusions: Within the limitations of a single-case proof-of-concept study, the proposed segmentation-assisted workflow may contribute to preoperative anatomical assessment of potential paranasal implant trajectories and their relationship to adjacent anatomical structures. The workflow should be regarded as a methodological demonstration rather than a validated clinical protocol. Further anatomical, reproducibility, biomechanical, and clinical studies are required before broader clinical adoption can be considered. Full article

Background: Severe jaw atrophy (Cawood and Howell Class V–VI) often renders conventional endosseous implantation unfeasible due to the lack of medullary bone and vascularization. This study presents a digital workflow for customized subperiosteal implants designed to eliminate bone segmentation errors and ensure optimal passive fit. Methods: Two clinical cases of severe atrophy—a full-arch maxillary rehabilitation and a unilateral partial rehabilitation—were treated using a prosthetic-driven CAD/CAM workflow. Key innovations included densitometric mapping using Hounsfield Units (HU) to identify high-mineralization zones (+1200 to +1800 HU) for strategic screw fixation. Intraoperatively, cobalt–chrome osteoplasty guides and PMMA check-templates were utilized to validate bone segmentation accuracy in vivo and regularize the cortical base. Results: The protocol achieved high precision with a monitored alignment deviation of 0.2 mm. At the 2-year follow-up, clinical and radiographic evaluations (CBCT) confirmed the total absence of gaps at the bone–implant interface. No signs of peri-implantitis, osteolysis, or progressive bone loss were observed, and soft tissues remained stable and healthy. Discussion: Success was driven by the rigorous management of the bone–implant interface and the use of preparatory surgical devices to bridge the gap between digital planning and surgical reality. The mechanical stability achieved through divergent fixation vectors prevented stress shielding by converting shear forces into compression, stimulating basal bone density according to Wolff’s Law. Conclusions: The standardized digital workflow and the use of preparatory surgical devices in this preliminary study showed that complex rehabilitations can be performed with favorable short-term outcomes. While this approach reduces surgical time and biological stress, further prospective studies are required to confirm its clinical predictability and define next-generation subperiosteal implants as a valid alternative for the management of severely atrophic cases. Full article

Background: Action observation (AO) and motor imagery (MI) are widely used cognitive training strategies. Recent evidence suggests that their combination may enhance motor simulation through synergistic neural mechanisms. However, the effects of this approach on complex whole-body movements in elite athletes remain unclear. Methods: Twenty-seven elite ski jumpers performed AO, MI, and concurrent AO + MI tasks, while cortical hemodynamic responses were recorded using functional near-infrared spectroscopy (fNIRS). Channel-level changes in oxygenated hemoglobin (ΔHbO) were analyzed using one-sample and paired-sample t-tests, with false discovery rate (FDR) correction applied for multiple comparisons. Additionally, mixed-design ANOVAs were conducted to examine the potential modulation of athlete level (master-level vs. first-class). Results: Significant activation was observed only in the AO + MIcondition after FDR correction, primarily in channels corresponding to the precentral gyrus, postcentral gyrus, and middle frontal gyrus. No channels in the AO and MI conditions survived FDR correction. Between-condition comparisons revealed significant differences in several channels located in frontoparietal regions, including the inferior parietal lobule, supramarginal gyrus, and middle frontal gyrus, with AO + MIgenerally showing stronger responses. No significant effects related to athlete level were found. Conclusions: These findings indicate that concurrent AO + MI is more effective than AO or MI alone in eliciting cortical activation in elite ski jumpers. This may reflect enhanced engagement of frontoparietal networks involved in action representation and visuomotor integration. These results may be compatible with a neural efficiency interpretation in highly trained athletes, although further studies with behavioral outcomes and broader skill-level comparisons are needed. AO + MI may represent a promising strategy for off-snow cognitive training in high-risk sports. Full article

Tooth-supported fixed partial dentures (FPDs) exhibit complex biomechanical behaviour because occlusal loads are transferred through the periodontal ligament (PDL) and heterogeneous mandibular bone. This pilot study aimed to develop a patient-specific NURBS-based finite element analysis (FEA) workflow for anatomically realistic mandibular reconstruction and to evaluate the biomechanical effect of geometric simplification in tooth-supported FPD simulations. Cone beam computed tomography data from a single subject were segmented and reconstructed into a layered three-dimensional model of the mandible and dentition, including cortical bone, cancellous bone, teeth, and PDL. A high-fidelity reference model (V0) and four simplified variants (V1–V4) were analysed under static 500 N loads applied at 0° and 30°. The reference model yielded a maximum von Mises stress of 507 MPa and a peak displacement of 0.74 mm, with stress concentrations consistently localised at the retainer–pontic connector region. Inclusion of the PDL markedly affected the mechanical response, doubling denture displacement in simplified comparative models. Among the simplified configurations, V4, which preserved cortical morphology and PDL representation while omitting detailed trabecular architecture, showed the closest agreement with the reference model, with mean deviations of 6.1% and 5.8% under the two loading conditions, respectively. These findings suggest that patient-specific NURBS–FEA modelling provides a robust framework for biomechanical assessment of tooth-supported FPDs, while controlled simplification may improve computational efficiency without substantially compromising accuracy under static loading conditions. Full article

Traumatic brain injury (TBI) induces complex molecular and neuroendocrine alterations that extend beyond the site of injury. The hypothalamic–pituitary–adrenal (HPA) axis, a hierarchically organized neuroendocrine system composed of the hypothalamus, pituitary gland, and adrenal glands, plays a central role in coordinating stress and metabolic homeostasis. Despite its critical importance, the temporal transcriptional mechanisms underlying HPA axis dysregulation following TBI remain poorly understood, particularly in relation to coordinated neuronal injury and regeneration processes. This study aimed to investigate the time-dependent transcriptional dynamics of genes associated with neuronal injury and regeneration within the HPA axis following experimental TBI. Moderate-to-severe TBI was induced in Sprague–Dawley rats using a controlled cortical impact (CCI) model. Animals were allocated into sham, acute (24 h), and chronic (30 days) groups. Transcript profiles of 24 HPA axis- and neuroregeneration-related genes were analyzed in hypothalamic, pituitary, and adrenal tissues using quantitative real-time PCR, with normalization to a housekeeping gene and statistical evaluation of differential expression across time points. TBI induced distinct, tissue-specific, and time-dependent transcriptional alterations across the HPA axis. In the acute phase, stress-response genes showed divergent regulation between central and peripheral tissues, whereas the chronic phase was characterized by transcriptional reorganization involving neurotrophic, metabolic, and neuroendocrine pathways. Key regulators such as Hif1a, Rad18, Avp, Gata3, and OxtR exhibited significant and region-specific expression changes. These findings demonstrate that TBI triggers coordinated yet heterogeneous transcriptional responses within the HPA axis, linking central injury to systemic endocrine adaptation. This study provides novel insight into the molecular basis of neuroendocrine dysfunction and recovery after TBI and identifies candidate targets for future therapeutic strategies. Full article

Aphasia is a complex neurological syndrome that includes a multitude of signs and symptoms that describe a patient’s inability to use language (understanding and producing spoken and/or written language) after it has already been acquired, which is caused by cerebral lesions situated in the dominant (left) cerebral hemisphere in right-handed people. Aphasia has a prevalence of 25–30% in acute ischemic stroke (especially in arterial infarcts). In patients who suffered cerebral venous and dural sinuses thrombosis (CVST), aphasia has been noticed in almost 20% of cases, its presence being considered a negative predictive factor. We report the case of a 22-year-old right-handed woman with obesity and active smoking (10 cigarettes/day), undergoing treatment with oral contraceptives who presented to the Emergency Department with an intense headache, resistant to usual analgesic treatment, accompanied by language disorders onset within 24 h. The neurological examination was normal, except for language assessment, which revealed the severe impairment of the repetition domain (she was unable to repeat simple words), and difficulty in naming objects with some hesitations and mild comprehension difficulties (especially in complex orders). She underwent neuroimaging examinations at admission. Native Head Computed Tomography revealed spontaneous hyperdensity (parenchymatous hematoma) in the left temporal lobe. Cranial magnetic resonance imaging (MRI) confirmed venous infarction in the left temporal area and a hypointense signal on MRI T2*SW (susceptibility-weighted) in the region of the left lateral sinus and left jugular vein bulb, which confirmed the thrombosis at this level. Associated cortical vein thrombosis was diagnosed on indirect radiological grounds, since hemorrhagic transformation obscured the direct visualization of the adjacent cortical veins. MR venography was not performed at that time, but instead at the 1-month follow-up, MR venography confirmed the chronic, partial thrombosis of the left lateral sinus and left jugular vein bulb. Laboratory data demonstrated an elevated D-dimer and the presence of homozygosity for MTHFR C677T and PAI-1 4G/4G. Anticoagulation in the form of low-molecular-weight heparin was immediately started, followed by chronic treatment with oral anticoagulant (apixaban) and folic acid. The headaches resolved within three days, and her neurological examination was almost normal: the repetition continued being altered for complex phrases. We did not observe any left lateral sinus thrombosis recurrence, or other extra-cerebral embolic events (deep vein thrombosis or pulmonary embolism) during the follow-up year. The immediate anticoagulation since the admission resulted in a favorable outcome. Taking into consideration our interest in monitoring patients with aphasia secondary to CVST, we also analyzed data from the literature regarding the incidence of conduction aphasia and other aphasic syndromes in this CVST. Due to the limited number of articles identified in the last 21 years (2005–2026) in the literature, we concluded that conduction aphasia is an extremely rare clinical presentation in this kind of pathology and further studies should be conducted in order to identify significant statistical data. Full article

Background: Chronic exposure to addictive substances induces persistent alterations in neural dynamics, reflecting maladaptive brain plasticity. While such changes are well documented using neuroimaging techniques, their electrophysiological signatures—particularly those derived from nonlinear EEG complexity—remain insufficiently explored across diverse substance use profiles. This preliminary study aims to investigate whether nonlinear EEG complexity measures can serve as sensitive biomarkers of maladaptive plasticity in substance use disorder (SUD) across multiple substance categories. Methods: A total of 350 participants were included and categorized into seven groups (n = 50 each): six substance use groups (cannabis, heroin, heroin–cannabis, methamphetamine–cannabis, methamphetamine–heroin, and multi-drug) and one control group without a diagnosis of substance use disorder. Resting state EEG signals were recorded using an eight-channel system. Four nonlinear features, Largest Lyapunov Exponent (LLE), Fractal Dimension (FD), Hurst Exponent (HE), and Kolmogorov Complexity (KC) were extracted. Statistical analysis was performed using two-way ANOVA, and classification was conducted using the K Nearest Neighbour (KNN) algorithm. Results: Significant group differences (p < 0.05) were observed across all nonlinear features. Control participants without a diagnosis of substance use disorder consistently exhibited higher complexity values compared to substance use groups, indicating reduced neural dynamical variability associated with the history of sustained substance uses over multiple years. Region wise analysis revealed that frontal and central cortical areas linked to motor planning and sensorimotor integration were particularly affected. The KNN classifier achieved an accuracy of 98.4%, sensitivity of 100%, and specificity of 96.8%. Conclusions: Nonlinear EEG complexity measures provide a robust electrophysiological marker of substance induced maladaptive brain plasticity. The observed reduction in complexity reflects impaired neural adaptability, particularly within motor control networks. These findings highlight the potential of EEG based complexity metrics for objective assessment, classification, and neurorehabilitation monitoring in substance use disorders. Full article

Polyetheretherketone (PEEK), a high-performance thermoplastic, is utilized in bone tissue engineering due to its elastic modulus resembling that of human cortical bone. However, toxicological studies on PEEK remain limited. PEEK disrupts bone homeostasis by recruiting macrophages and inducing the aggregation of foreign body multinucleated giant cells, ultimately leading to bone resorption. The lack of effective therapeutic approaches underscores the importance of identifying novel treatments. This study systematically investigated the potential molecular mechanisms underlying PEEK-induced bone resorption using network toxicology, molecular docking techniques, and molecular dynamics simulations. We first conducted a network-based toxicological assessment based on the molecular structure of PEEK. By integrating and screening targets from multiple databases, we identified 139 potential targets associated with PEEK-induced bone resorption and constructed an interaction network diagram of these targets. Gene Ontology (GO)/KEGG enrichment analysis revealed that PEEK may induce bone resorption through pathways such as the PI3K-AKT signaling pathway and TNF signaling pathway. Further analysis using STRING and Cytoscape 3.9.0 software identified 53 core targets, including MAPK3, TNF, IL-6, AKT1, IL-1β, EGFR, and MMP9. We found that enriched highly correlated pathways encompassed core targets, supporting the scientific hypothesis that PEEK induces bone resorption. Furthermore, molecular docking and molecular dynamics simulation results confirmed that PEEK exhibits strong binding affinity with core targets, forming stable complexes. In summary, this study not only reveals the potential biological mechanisms underlying PEEK-induced bone resorption but also provides new evidence for future prevention and treatment of PEEK-induced bone imbalance. Full article

Thyroid hormones (THs) are essential regulators of human brain development, and disrupted TH availability during pregnancy or early life is linked to adverse neurodevelopmental outcomes. Concerns that environmental chemicals interfere with TH signalling have increased the need for human-relevant in vitro systems to identify thyroid hormone system-disrupting chemicals (THSDCs) for risk assessment. Here, we compared two human-induced pluripotent stem cell (hiPSC)-derived brain organoid models for THSDC assessment: (i) human cortical organoids (COs) generated by unguided differentiation, offering higher architectural complexity but lower throughput; and (ii) neural stem cell-derived organoids (NSCOs), designed for scalability with reduced cellular diversity. Both models expressed key TH handling components, including the transporter SLC16A2 (MCT8) and the inactivating enzyme DIO3. Using LC–MS/MS, we show that exogenous T3 is depleted from culture media and metabolized to 3,3′-T2 and 3′-T1 in both models, alongside upregulation of T3-responsive genes (HR, KLF9, DIO3, SEMA3C). Pulse and chronic co-exposures to reference disruptors iopanoic acid (IA, deiodinase inhibitor) and silychristin (SC, MCT8 inhibitor) altered T3 metabolism and modulated T3-responsive transcriptional endpoints. In NSCOs, high-content imaging revealed treatment-associated changes in cell composition, with chronic T3 reducing the SOX2-positive progenitor pool and THSDCs blocking this effect. Together, these findings provide a framework for organoid qualification—linking TH handling, transcriptomic responsiveness, and scalable phenotypic readouts—as a necessary step toward model validation and implementation of brain organoids in THSDC risk assessment pipelines. Full article

Background/Objectives: Mastication is a complex sensorimotor function involving coordination between the brainstem central pattern generator and supraspinal systems, particularly the primary motor cortex (M1). Evidence suggests a link between masticatory activity and corticomotor plasticity, but findings remain fragmented. This scoping review aimed to synthesise the human evidence on the relationships among mastication, tooth loss, dental rehabilitation, ageing, and corticomotor plasticity, with emphasis on M1 mechanisms. Methods: Following PRISMA-ScR guidelines, systematic searches were conducted in MEDLINE/PubMed, Scopus, and Web of Science using terms related to mastication, neuroplasticity, motor cortex, ageing, and rehabilitation. Eligible studies included human experimental, clinical, and observational research employing neuroimaging or neurophysiological methods. Data were extracted and synthesised using a Population–Concept–Context framework across eight conceptual domains. Results: Twenty-two heterogeneous studies (fMRI, TMS, EMG, psychophysical, histological) were included. Mastication consistently activated distributed sensorimotor networks, including M1 and the primary somatosensory cortex (S1). Peripheral sensory input and dental mechanoreception were linked to structural and functional adaptations. Corticomotor excitability was modulated by chewing, oral-motor learning, and rehabilitative interventions. Ageing was associated with altered but preserved cortical responsiveness. Associations between mastication and cognition were reported, though largely cross-sectional. Overall, findings suggested a relationship linking peripheral input, sensorimotor integration, and corticomotor plasticity, but methodological variability limited causal inference. Conclusions: Mastication is linked to modifiable corticomotor activity and supports experience-dependent neuroplasticity. However, the evidence remains largely associative and methodologically heterogeneous. Neural adaptations appear to be preserved with ageing but are influenced by systemic and environmental factors. Longitudinal, multimodal research is needed to clarify the mechanisms, causality, and clinical relevance, particularly in rehabilitation contexts. Full article

This study investigated the cortical activation patterns and functional connectivity underlying human decision-making by comparing two distinct purchasing orientations: other-oriented consumption (OOC) and self-oriented consumption (SOC), using functional near-infrared spectroscopy (fNIRS) as a wearable neuroimaging modality. The results revealed significant temporal concentration differences in $∆\mathrm{H}\mathrm{b}\mathrm{O}$ under the OOC condition in Ch06 ($p$< 0.05). The 15 fNIRS channels were mapped to seven anatomically defined regions of interest ($\mathrm{ROIs}$) to better capture regional activation patterns and functional network properties. While global network metrics showed no significant differences, seed-based connectivity analysis revealed that the OOC condition elicited significantly stronger functional connectivity between the medial prefrontal cortex (${\mathrm{R}\mathrm{O}\mathrm{I}}_4$) and the left lower PFC (${\mathrm{R}\mathrm{O}\mathrm{I}}_6$, $p$ < 0.05, $d$ = 0.45). In summary, while the overall network efficiency remained stable across conditions, our findings highlight a spatially specific enhancement in functional connectivity centered on the PFC, indicating an increased cognitive load from engaging in complex social cognitive processes. These findings advance the understanding of neural correlates underlying human decision-making and demonstrate the utility of wearable monitoring using fNIRS for capturing cognitive state differences in human-centered decision contexts. Full article

Syphilis, caused by the bacterium Treponema pallidum, has a complex evolutionary history, most likely being transferred from the Americas to Europe after the 15th century and subsequently spreading widely through sexual transmission. This work is one of the few studies on the skeletal evidence of probable treponematosis in archaeological populations discovered on the Romanian territory, providing data to better understand the disease history. Pathological lesions identified in three human skeletons of the 15th–19th centuries are described, and a diagnosis of treponematosis is performed. The three analyzed skeletons were discovered during the archaeological excavations in the necropolis of the Roman-Catholic Cathedral in Iasi City (Romania). The investigated skeletons belonged to individuals aged 30–40 years old (two females and one male). Somatoscopic, radiographic, tomographic, and microscopic examinations were used for the differential diagnosis. The results of multiple investigation methods support the diagnosis of probable treponematosis in all three skeletons, showing different stages of caries sicca in skull bones, cortical thickening, and new periosteal bone formation in postcranial bones. Full article

The range of possible inflammatory changes in the oral cavity and in the maxillary and mandibular bones may present with diverse patterns and characteristics in both clinical and radiological evaluation. In most cases, a standard radiological examination, such as dental panoramic radiograph (DPR), has significant limitations in assessing early or complex bone changes associated with chronic bone inflammation. Advanced imaging with multidetector computed tomography or cone-beam computed tomography (MDCT or CBCT) can improve lesion characterization and surgical planning when a detailed evaluation of tooth-bearing structures, tooth apices, cortical plates, and cancellous bone is required. Such imaging allows more detailed assessment of alterations in medullary bone morphology and architecture, as well as identification of possible periosteal reactions adjacent to chronic bone inflammation. Osteomyelitis of the jaws comprises a heterogeneous group of inflammatory bone disorders characterized by variable clinical presentations and a broad spectrum of radiological appearances. Depending on disease chronicity, host factors, and microbial burden, mandibular osteomyelitis may mimic odontogenic tumors, fibro-osseous lesions, or malignant bone pathologies. Quite often, dental treatment affects bone status and condition, leading to unwanted events such as bone inflammation. Imaging plays a central role in diagnosis; however, radiographic findings are often nonspecific, particularly in early or chronic stages. Each case of osteomyelitis underscores the importance of correlating imaging findings with clinical history and highlights the role of repeated imaging in distinguishing inflammatory bone disease from aggressive jaw lesions. This study aims to characterize diverse patterns of chronic mandibular osteomyelitis associated with various prior treatment modalities using CBCT. By presenting a series of illustrative cases from heterogeneous clinical settings, the authors highlight the nonspecific radiographic features and diagnostic challenges inherent in chronic bone inflammation. The focus remains on the interpretation of complex imaging findings rather than a comparative analysis of technical protocols. Full article

Objectives: Autism spectrum disorder (ASD) is increasingly conceptualized as a neurodevelopmental condition with prenatal origins. Advances in fetal magnetic resonance imaging (MRI), including high-resolution structural imaging and resting-state functional connectivity analysis, now enable in vivo characterization of the developing human brain before birth. This review examines whether fetal MRI biomarkers are associated with later ASD diagnosis or autistic traits. Methods: We conducted a PRISMA-informed narrative review of human studies identified through MEDLINE, EMBASE, SCOPUS, and Web of Science. Eligible studies included original human investigations using fetal MRI to assess brain structure and/or function, with postnatal ASD diagnosis or standardized autistic-trait outcomes. Results: Eight eligible studies provide converging evidence that neurodevelopmental divergence associated with ASD may be detectable in utero. Structural analyses consistently report prenatal volumetric alterations, particularly enlargement of the insular cortex between the second and third trimesters. Additional findings of regional overgrowth and hemispheric asymmetries suggest distributed deviations in cortical maturation. Functional fetal MRI studies further demonstrate atypical large-scale network organization prior to birth. Altered connectivity within cingulate, prefrontal, temporal, and cerebellar circuits has been prospectively associated with later autistic traits, indicating that network-level integration may diverge before behavioral symptoms emerge. Evidence from high-risk conditions, including isolated ventriculomegaly and tuberous sclerosis complex, reinforces the association between prenatal structural abnormalities and increased ASD risk. Conclusions: Current evidence suggests that structural and functional brain alterations identifiable by fetal MRI may precede the clinical manifestation of ASD. These findings support a model of ASD as a condition potentially rooted in prenatal neurodevelopmental divergence. However, larger, standardized, multicenter studies are required before fetal MRI biomarkers can be translated into predictive or clinical applications. Full article

Background: Migraine is a complex neurovascular disorder with a substantial genetic component, yet many contributing loci remain poorly characterised. Methods: This study investigated the association between 21 biologically prioritised single nucleotide variants (SNVs) and migraine susceptibility in a case-control cohort of 548 individuals of European ancestry, of whom 304 (164 cases, 140 controls) remained after quality control and principal component analysis (PCA). Genotyping was performed using a targeted Sequenom MassARRAY platform, and substantial missingness (mean 30.3% per SNV) was addressed using multiple imputation by chained equations (MICE). Association testing was conducted using three complementary logistic regression frameworks: unadjusted single-variant analysis, covariate-adjusted marginal models, and a multivariable joint model incorporating all SNVs with L2 regularisation. Results: Across analyses, two variants in ASTN2 (rs1052053 and rs6478241) showed the most robust associations with migraine, surviving Bonferroni correction in the joint model (p = 0.001 and p = 0.002, respectively) and false discovery rate (FDR) correction in marginal models (q = 0.003 for both). A third variant, rs7304841 (12p12), demonstrated a risk-increasing effect that reached FDR significance in marginal analysis (q = 0.035) and remained nominally significant in the joint model. In contrast, rs62624978 in CTC1 showed a strong signal in unadjusted analysis (OR = 0.217, p = 0.0014) and remained nominally significant after adjustment (p = 0.011), although it did not survive multiple-testing correction in imputed models. The joint model demonstrated good discriminatory performance (AUC = 0.822), though this is not intended as a predictive tool. Biologically, implicated loci suggest contributions from both neuronal circuit organisation (ASTN2) and telomere and vascular maintenance pathways (CTC1), supporting a broader neurovascular model of migraine susceptibility. Conclusions: These findings are consistent with shared genetic architecture between migraine and microvascular dysfunction, potentially involving endothelial integrity, neurovascular coupling, and cortical excitability mechanisms. Full article