Abstract: Introduction The rising incidence of hepatocellular carcinoma (HCC) in North America mirrors the growing prevalence of metabolic-associated fatty liver disease (MAFLD). Though MAFLD is now a recognized driver of HCC, its precise influence on tumor biology and patient prognosis remains incompletely understood. This study examines whether MAFLD-associated HCC constitutes a distinct clinical phenotype and explores its prognostic and therapeutic implications. Methods We conducted a retrospective cohort study of 154 adult patients who underwent curative-intent hepatic resection for HCC at a leading U.S. university medical center between January 1, 2011, and December 31, 2020, with follow-up through December 31, 2023. Patients were stratified into MAFLD-positive (n=89) and MAFLD-negative (n=67) groups. Demographic, clinical, and oncologic characteristics were compared. Survival outcomes were assessed using Kaplan-Meier estimates, while multivariate Cox regression was employed to adjust for confounding variables and identify independent prognostic factors. Results Compared to their MAFLD-negative counterparts, MAFLD-positive patients were older (mean age 70.1 vs. 67.4 years, p=0.043), more frequently obese (55% vs. 18%, p<0.001), and less likely to have cirrhosis (27% vs. 64%, p<0.001). They also presented with larger tumors (mean diameter 5.6 cm vs. 3.8 cm, p=0.004), although tumor differentiation and T stage were comparable between groups. Progression-free survival (PFS) was longer among MAFLD-positive patients (median 2.80 vs. 1.21 years, p=0.002), with a hazard ratio of 0.64 (95% CI: 0.42–0.96). Median overall survival (OS) was also numerically higher (4.55 vs. 2.54 years), though the difference did not reach statistical significance (p=0.09). After adjustment for confounders, MAFLD was not independently associated with OS or PFS. In contrast, cirrhosis, serum AFP >100 ng/mL, and advanced tumor stage emerged as independent predictors of poorer outcomes. Conclusions Despite prior suggestions of a unique clinical trajectory for MAFLD-associated HCC, our findings suggest that MAFLD status alone does not independently predict survival following curative-intent resection. Once key oncologic factors are accounted for, outcomes appear similar between MAFLD-positive and MAFLD-negative patients. These results underscore the importance of risk stratification based on established prognostic markers rather than liver disease etiology alone.

Abstract: Psychosis constitutes a profound alteration in the individual's relationship with the self and the world, expressed through symptoms signalized by loss of reality testing. Mainstream psychiatric approaches often rely heavily on descriptive psychopathology, which may overlook the multifaceted subjective experiences of affected individuals. This paper outlines an integrative framework to enhance the understanding of psychosis, bringing together phenomenology – the study of structures of consciousness as lived from the first-person perspective - with descriptive psychopathology, which represents the clinical categorization of symptoms. Drawing on phenomenological philosophy, we examine disturbances in the basic structures of selfhood and the perception of the outer world that underpin the observable features of psychotic symptoms along with their clinical course. Through the transdiagnostic description of psychotic features in both primary and secondary psychosis, we aim at bridging the inconsistencies between standartized evaluation and the personal narrative of the individual affected. By focusing on the interplay between symptoms and experiences, we examine the psychopathology of psychosis as a dynamic phenomenon of fundamental disruption in the individual's experiential framework, which is reflected in the clinical manifestations already present from the initial stages of the disorder. The alignment of phenomenological insights with structured clinical observations, enriches the conceptualization and assessment of psychotic phenomena. Moreover, on the basis of an established scientific knowledge regarding recognition and treatment of psychotic disorders, the incorporation of an intersubjective empathic communication in the psychiatric interview further supports a person-centered therapeutic orientation. Integrating phenomenological insights and descriptive psychopathology into assessment and care may advance early intervention, therapeutic alliances and effective treatment strategies in psychosis.

Abstract: We investigated associations between apolipoprotein E (APOE) alleles and motor mani-festations in Alzheimer’s dementia (AD) capitalizing on NACC data. The baseline evaluations of older adults (≥60years) with a diagnosis of AD were analysed. Those with a concomitant diagnosis Parkinson’s disease or other parkinsonian syndrome, and those treated with anti-parkinsonian agents were excluded. Three APOE groups were formed: APOE2 (APOE2 carriers), APOE3 (APOE3/APOE3) and APOE4 (AP-OE4/APOE4, APOE4/APOE3). UPDRS III was used to assess the presence or absence of motor signs in 9 domains. Adjusted binary logistic models featuring three APOE groups as exposures and motor domains as outcomes were estimated. Of 4979 included individuals, 389 were in the APOE2, 1799 in the APOE3 and 2791 in the APOE4 groups. Compared to the APOE2 group, individuals in the APOE4 group had 36% (18-50%) lower odds of having at least one motor sign; 47% (19-66%) lower odds of rigidity, 44% (23-60%) lower odds of bradykinesia, 44% (22-63%) lower odds of impaired chair rise and 44% (19-64%) lower odds of impaired posture-gait. Exploratory analyses using APOE genotypes suggested dose-response relationships for both APOE2 and APOE4. In conclusion, APOE2 confers a risk towards motor (mainly parkinsonian) signs in AD. APOE4 may have a protective effect.

Abstract: Gastrointestinal dysfunction and microbial dysbiosis are frequently reported in children with autism spectrum disorder (ASD), yet their relationship to systemic metabolic patterns remains incompletely understood. In this study, we assessed urinary levels of four gut-derived uremic toxins—p-cresyl sulfate (PCS), trimethylamine N-oxide (TMAO), indoxyl sulfate (IS), and asymmetric dimethylarginine (ADMA)—in 97 children with ASD and 71 neurotypical controls. Stool consistency was classified using the Bristol Stool Chart (BSC) into hard (BSC 1–2), normal (3–5), and loose (6–7) groups. We introduce two novel composite metrics: The Metabolic Index of Gut Dysfunction (MIGD), defined as (PCS/TMAO × 100 ÷ IS/ADMA), and the Fermentation Skew Index (FSI), defined as PCS/TMAO ÷ IS/ADMA. These indices aim to summarize phenolic and indolic microbial activity in relation to host detoxification status. Results demonstrated median MIGD values of 555.3 in ASD children with hard stools, 404.5 with normal stools, and 109.8 with loose stools. Corresponding FSI values were 5.55, 4.04, and 1.10, respectively. Controls with normal stools showed intermediate values (MIGD 242.5; FSI 2.41). These findings suggest that MIGD and FSI capture distinct gut metabolic phenotypes, with high FSI indicating phenolic-dominant skew and low values suggesting indolic predominance. These indices may support stratification of ASD subtypes and offer non-invasive metabolic biomarkers for microbiota-targeted interventions.

Abstract: Recent data from the CDC indicate that the incidence of Autism Spectrum Disorder (ASD), a neurodevelopmental disorder characterized by deficits in social communication and the presence of restricted interests and repetitive behaviors , has increased to 1 in 31 children. Individuals with ASD have a constellation of neurological, behavioral, sensory, feeding, gastrointestinal, and immunological issues. This manuscript discusses how these can be explained by disruption of the gut-blood and blood-brain barriers due to microbiome dysbiosis which then results in chronic endotoxemia leading to chronic cycle of gut-brain inflammation via mast cell and microglial activation. We present how various environmental, pathogenic and stress factors can disrupt the gut-brain homeostasis to create susceptibility and epigenetic effects contributing to the development of ASD. We also offer a safe, simple, and effective treatment approach to addressing some of the key pathogenetic underpinnings of ASD.

Abstract: Respiratory syncytial virus (RSV) remains a leading cause of acute lower respiratory tract infections globally, particularly affecting infants, older adults, and immunocompromised individuals. While recent advances in prophylaxis, such as long-acting monoclonal antibodies and maternal immunization, offer promise for prevention, therapeutic options for active infection remain limited. Severe RSV disease is often driven not solely by viral replication but by dysregulated host immune responses, including excessive cytokine production, T helper type 2 (Th2) and T helper type 17 (Th17) cell polarization, and impaired interferon signaling. RSV has evolved sophisticated immune evasion strategies, such as inhibition of dendritic cell maturation, degradation of signal transducer and activator of transcription 2 (STAT2) via nonstructural proteins 1 and 2 (NS1/NS2), and interference with pattern recognition receptor signaling, particularly Toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors. These mechanisms result in attenuated innate immune responses and defective adaptive immunity, contributing to viral persistence, immunopathology, and recurrent infections. Moreover, age-dependent vulnerabilities, such as immune immaturity in infants and immunosenescence in older adults, exacerbate disease severity. Excessive immune activation leads to bronchiolitis, airway remodeling, and long-term sequelae including wheezing and asthma. Emerging immunomodulatory therapies aim to restore immune balance, targeting cytokines (e.g., interleukin-6 [IL-6], interleukin-1 beta [IL-1β]), the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway, or inflammasome activity. Host-directed therapies and direct-acting antivirals are also under investigation. A better understanding of RSV–host immune interactions is critical for optimizing therapeutic strategies and designing effective vaccines. This review synthesizes current knowledge on RSV immunopathogenesis and highlights immunomodulation as a promising frontier for therapeutic intervention.

Abstract: Even following apparent recovery, musculoskeletal pain and injury patients frequently exhibit persistent muscle weakness (Mw), compromising occupational and athletic performance and increasing risks of ongoing pain, osteoarthritis, and repetitive stress injuries. Current clinical approaches undervalue Mw, inadequately testing for, treating, and explaining the phenomenon. Maladaptive learning (neuroplasticity) is pro-posed as a mechanism for central (pain) sensitization. With separate biomechanical contributions to chronic pain, a "muscle, movement, or motor post-traumatic stress disorder" (mPTSD) Model proposes that persistent Mw also stems from maladaptive neuroplasticity. The model suggests that Mw is induced by predictive processing and/or single-trial, two-stage passive avoidance learning, mechanisms potentially re-lying on cerebellar forward modeling. Affected muscles fail to adapt to incoming force—a binary pathology (present or absent) reflected in similarly binary manual muscle testing (MMT) results, as demonstrated by objective analyses. Preliminary evidence suggests that memory reconsolidation disruption can immediately normalize muscle function by eliminating muscle-pain/trauma associations. Like psychoneuroimmunology, which explores conditioning effects on immune function, this suggests "psychoneurokinesiology": studying conditioning's influence on movement. This neuropsychological reconceptualization may establish a new clinical paradigm for non-specific musculoskeletal disorders while potentially addressing unexplored associations to kinesiophobia and functional weakness.

Abstract: Keywords: Endometriosis-associated infertility; Epigenetics, biomarkers, prevention; Therapeutics.

Abstract: Spine-focused biomedical informatics has emerged as a critical frontier for applying artificial intelligence (AI) to improve diagnosis, prognosis, and intervention in complex musculoskeletal and neurodegenerative conditions. This review synthesizes recent developments in the integration of machine learning (ML), deep learning (DL), and natural language processing (NLP) within spine health ecosystems. We highlight convolutional neural networks for vertebral segmentation and disc classification, radiomic pipelines for quantitative MRI/CT biomarker extraction, and multimodal ML models for outcome prediction across degenerative, neoplastic, and traumatic pathologies. We examine spine-specific clinical decision support systems (CDSSs) that fuse structured EHR data with NLP-parsed reports, wearable biomechanics, and genomic signals to generate real-time, risk-adaptive treatment guidance. Emphasis is placed on explainable AI (XAI) frameworks—e.g., SHAP, LIME, Grad-CAM—that support interpretability and ethical accountability in AI-augmented decision-making. We analyze challenges in generalizability, privacy-preserving federated learning, and regulatory heterogeneity, with attention to evolving U.S. FDA guidance, EU AI Act obligations, and liability frameworks. Integrating epistemic transparency with computational scalability, this review offers a roadmap for translating AI-enhanced spine informatics into safe, equitable, and clinically trustworthy systems—advancing the goals of biomedical informatics by unifying predictive analytics with ethical and patient-centered care.

Abstract: Prostate-specific antigen (PSA) has been the main biomarker used for the detection and monitoring of prostate cancer for decades. However, its limited specificity and prognostic accuracy have prompted the development of novel molecular and imaging biomarkers to improve the clinical characterization of localized disease. This review critically examines recent advances in urinary biomarkers (e.g., PCA3, SelectMDx), tissue-based genomic assays (Oncotype DX Prostate, Prolaris, Decipher), and imaging techniques such as multiparametric magnetic resonance imaging (mpMRI) and prostate-specific membrane antigen positron emission tomography (PET-PSMA). We evaluate their diagnostic performance, prognostic relevance, and clinical utility in risk stratification and individualized treatment decision-making. Methodological and clinical barriers to their routine implementation are also discussed. Current evidence supports a multidisciplinary integration of these biomarkers to address the limitations of PSA, improve biopsy decision-making, better distinguish indolent from aggressive tumors, and optimize therapeutic strategies. Finally, future research directions aimed at validating and incorporating emerging biomarkers into clinical practice are outlined, with the goal of improving outcomes in patients with localized prostate cancer.

Abstract: Background: Left ventricular (LV) summit is important origin for ventricular arrhythmias (VAs). However, the complex electroanatomic structure of LV summit and the surrounding anatomic sites, makes ablation of this arrythmia challenging. Aim: In this paper, we review the main strategies to mapping and ablation of LV summit VAs and summarize our experience in this challenging ablation. Methods: to summarize our experience, we included All consecutive patients with outflow VAs referred to ablation in our institute between 2019 and 2024 who eventually diagnosed to have LV summit origin based on electroanatomical mapping and ablation result using stepwise and sequential ablation approach Results: A total of 38 patients were found to have VAs from LV summit origin. Overall 5 patients had history of at least 1 failed ablation. V1 transition was seen in 15 patients, V2 transition in 12 patients, V3 transition in 11 patients. Four patients had R wave pattern break in lead V2. Ablation was performed from the earliest activation and or from one of the adjacent sites using stepwise and sequential approach. Acute suppression of VAs occurred in 35 patients without complications except one case of pseudoaneurysm of femoral artery. Conclusion: stepwise and sequential ablation approach can suppress VAs originated from LV summit in most of patients.

Abstract: Background/Objectives: In recent years, research has highlighted the heterogeneity of corticotroph pituitary neuroendocrine tumors (CPitNETs), which are linked to Cushing’s disease. Purpose of the study is to determine stable postgenomic markers depending on maximum diameter on MRI (without visualization of the pituitary tumor on MRI/less than 6 mm (group 1a) and with visualization on MRI/more than 6 mm (group 1b). Methods: Immunohistochemically determined granulation pattern (group 2a densely granulated, 2b Crooke cell tumor) and proliferation levels based on Ki-67 with a threshold of 3% (group 3a high proliferation, 3b low proliferation), and biological behavior (group 4a indolent, 4b aggressive). Our study analyzed fresh tissue samples of CPitNETs from 34 patients with Cushing’s disease. Total RNA was extracted and sequenced using Cap Analysis Gene Expression (CAGE) on the Illumina HiSeq2500 platform, followed by bioinformatics analysis. Results: Differentially expressed genes were identified in group 1a tumors (EN1, EFS,) versus group1b (LCN1, BMP3). An inverse relationship was found between tumor volume and the expression of the RBM24 and ADGRD2 genes. A direct relationship was found between tumor volume and the expression of the PFN2 and CNTNAP5 genes. Identical gene signatures were found both in densely granulated and Crooke cell variants. Samples from group 3a, 4b and with bigger volume presented upregulated CT45A3, CT45A, CT45A1 genes. Samples from group 3b were enriched with PI3K/Akt pathway. Samples from group 4a showed expression of FXYD3, FGFR3 and FZD9 genes. Conclusions: Identified postgenomic markers in the studied subgroups of CPitNETs can potentially become biomarkers and allow to predict big volume and type of biological behavior at the early stages of diagnosis and treatment of patients with Cushing's disease.

Abstract: Background/Objectives: Endometrial cancer (EC) is the most common gynecological tumor in developed countries and presents a wide variety of histological and molecular characteristics that make its treatment increasingly complex. In recent years, advances in molecular imaging, particularly with [¹⁸F]FDG-PET/CT and PET/MRI, have changed clinicians management of diagnosis, treatment planning, and prognosis of EC. Methods: In this narrative review, a search was conducted for current evidence on the role of [¹⁸F]FDG-PET/CT and PET/MRI throughout the treatment of EC, focusing on their diagnostic performance, clinical relevance, and prognostic implications. Their use in areas such as initial staging, treatment monitoring, recurrence detection, and individualized risk assessment was also discussed. Results: [¹⁸F]FDG-PET/CT is effective in detecting lymph node and distant metastases, while [¹⁸F]FDG-PET/MRI offers greater accuracy for T and N staging. In addition, [¹⁸F]FDG-PET/CT provides early metabolic indicators of therapeutic response and facilitates differentiation between viable tumors and post-treatment changes. Radiomics-derived parameters have shown promising associations with tumor aggressiveness, lymphovascular invasion and survival, supporting their role as prognostic imaging biomarkers. In addition, the use of non-FDG radiotracers, as well as predictive models based on machine learning, can further refine preoperative stratification and treatment planning in certain subtypes of EC. Conclusions: Molecular imaging enhances the accuracy of TNM staging in EC. The incorporation of molecular imaging biomarkers into daily clinical practice could significantly improve personalized decision-making in EC. However, large prospective studies are needed to confirm their efficacy.

Abstract: Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently emerged as the predominant aetiology of chronic liver disease worldwide. This condition can progress to hepatocellular carcinoma (HCC) through various pathogenetic mechanisms. Briefly, metabolic dysfunction, which may occur in genetically susceptible individuals, disrupts lipid metabolism homeostasis. This imbalance leads to increased oxidative stress and DNA damage. Concurrently, chronic inflammation intensifies, impairing immune surveillance and facilitating HCC progression. Recent research has shed light on the significant role of Protease-activated receptor 2 (PAR2) in metabolic regulation. PAR2 is not only pivotal in inflammatory and fibrotic process but has also been identified as a key metabolic regulator. Given its multifaceted functions, PAR2 has become a focal point in studies exploring obesity, MASLD progression and HCC development. This review aims to synthesize the major findings from this growing field of research, offering insights into the intricate relationship between PAR2, metabolic dysfunction, and liver disease progression.

Abstract: Background Breast cancer is the most common malignancy among women and more female patients fall within genetic testing guidelines indications. Therefore, a larger number of patients will be identified as BRCA mutation carriers. Conflicting results have been published previously regarding the feasibility and safety of conception after breast cancer treatment, and analyses are scarce regarding the BRCA positive population. The present study aims to asses the impact of BRCA status on reproductive and disease-specific outcomes of breast cancer patients. Methods This was a single-center retrospective cohort. Eligible patients were women aged 40 and below, diagnosed with stage I-III invasive breast cancer between 1995 and 2017, and who were tested for BRCA mutations. For all eligible patients, data on breast cancer history, treatment, type of BRCA mutation, reproductive outcomes, recurrence, survival status and the achievement of pregnancy after breast cancer were collected and statistical analyses were performed accordingly. Results One hundred eighteen young patients diagnosed with breast cancer were eligible to be included in the current analysis, of whom 15 had at least one pregnancy after breast cancer. Although groups were quite homogenous, statistically significant differences were observed between BRCAmut and wildtype subgroups regarding the tumor grade, hormone receptor status, HER2 receptor status and types of treatment. BRCA status did not seem to have a statistically significant effect on the reproductive outcomes or disease-specific outcomes such as overall survival, or disease free survival. Conclusion The present analysis, although limited by the bias of selection and small number of patients, did not associate BRCA mutation with a worse prognosis in the setting of pregnancy, nor did pregnancy outcomes seemed to be affected by the BRCA status. Larger, prospective, multicentric studies are needed in order to confirm the safety of pregnancy in BRCA mutated breast cancer patients.

Abstract: Lung transplantation remains the standard of care for end-stage lung disease, yet a persistent gap exists between donor lung availability and growing clinical demand. Expanding the donor pool and optimising donor lung management are therefore critical priorities. However, no universally accepted management protocols are currently in place. This narrative review examines evidence-based strategies to improve lung utilisation across three donor categories: donors after brain death (DBD), controlled donors after circulatory death (cDCD), and uncontrolled donors after circulatory death (uDCD). A systematic literature search was conducted to identify interventions targeting lung preservation and function, including protective ventilation, recruitment manoeuvres, fluid and hormonal management, and ex vivo lung perfusion (EVLP). Distinct pathophysiological mechanisms—sympathetic storm and systemic inflammation in DBD, ischaemia-reperfusion injury in cDCD, and prolonged warm ischaemia in uDCD—necessitate tailored approaches to lung preservation. In DBD donors, early application of protective ventilation, bronchoscopy, and infection surveillance is essential. cDCD donors benefit from optimised pre- and post-withdrawal management to mitigate lung injury. uDCD donor lungs, uniquely vulnerable to ischaemia, require meticulous post-mortem evaluation and preservation using EVLP. Implementing structured, evidence-based lung management strategies can significantly enhance donor lung utilisation and expand the transplantable organ pool. Integration of such practices into clinical protocols is vital to addressing the global shortage of suitable lungs for transplantation.

Abstract: Background/Objectives: Patients with adrenal insufficiency (AI) are at an increased risk of adverse events (AEs) during cardiovascular hospitalization. However, the association between AI and takotsubo cardiomyopathy (TCM) remains unclear. This study investigated the association between AI and cardiovascular outcomes in patients with TCM. Methods: We analyzed data on patients with TCM included in the 2016–2020 Nationwide Readmissions Database to compare in-hospital outcomes between patients with and without AI. The primary outcome measure was inpatient mortality. Secondary outcomes included the odds of all-cause 90-day readmission, acute kidney injury (AKI), mechanical ventilation use, vasopressor use, cardiogenic shock, length of stay (LOS), and total hospitalization charges (THC). Multivariate regression models were used to adjust for confounding variables. Results: Among 30,987 cases, 0.59% (n=183) had concomitant AI. AI was associated with higher odds of in-hospital mortality (adjusted odds ratio [aOR] 3.32, 95% confidence interval [CI] 1.43–7.74, p=0.005), cardiogenic shock (aOR 5.28, 95% CI 3.16–8.82, p&lt;0.001), mechanical ventilation use (aOR 3.20, 95% CI 1.78–5.74, p&lt;0.001), AKI (aOR 1.96, 95% CI 1.11–3.48, p=0.021), vasopressor use (aOR 4.59, 95% CI 1.56–13.47, p=0.006), longer LOS (6.84 vs. 3.67 days, p&lt;0.001) and higher THC ($97,419 vs. $54,574, p&lt;0.001). Additionally, AI was associated with lower odds of all-cause 90-day readmissions (aOR 0.44, 95% CI 0.25–0.79, p=0.006). Conclusions: Among patients with TCM, AI was associated with higher odds of fatal and non-fatal adverse events. Further studies are required to confirm these findings and better understand how to improve outcomes in this high-risk population.

Abstract: Stunting is a chronic growth disorder that not only affects height but may also impair craniofacial development. Facial proportions, especially in the vertical dimension, may provide additional anthropometric insight into growth status among children. Objectives: To assess and compare the vertical and horizontal facial proportions of stunted and non-stunted children, and to explore the potential of facial dimensions as supportive indicators for early stunting detection in community-based settings. Methods: This cross-sectional analytical study involved 266 children aged 7–72 months from several community health centers in Bandung, Indonesia. Children were categorized as stunted or non-stunted based on WHO height-for-age Z-scores. Facial dimensions were measured directly by calibrated pediatric dentistry residents using manual instruments. The vertical dimensions included Nasion–Subnasale (N–SN) and Subnasale–Menton (SN–M), while horizontal dimensions included zygomatic width and intergonion width. Data were analyzed using the Mann–Whitney U test and Spearman correlation. Results: Significant differences were found in vertical facial dimensions between stunted and non-stunted children: median N–SN (32.4 mm vs. 33.6 mm; p = 0.003) and SN–M (42.5 mm vs. 45.1 mm; p &lt; 0.001). No significant differences were observed in horizontal dimensions. All facial parameters showed a positive correlation with age (p &lt; 0.001). No significant differences were found based on sex. Conclusions: Stunted children exhibited shorter vertical facial dimensions compared to their non-stunted peers, while horizontal dimensions remained stable across groups. Vertical facial proportions may serve as supportive indicators in the screening and monitoring of childhood stunting. This method has potential for integration into community-based growth monitoring using simple or digital anthropometric tools.

Abstract: Introduction Nervus hypoglossus stimulation implants are a well-known second-line option for the treatment of obstructive sleep apnea (OSA). Similar to other implants, postoperative radiological positional evaluation serves as a quality control measure for the surgical procedure and as a reference point for future adjustments. Furthermore, the impact of artifacts on the visual assessment of the adjacent structures might be of clinical importance. This study aimed to evaluate postoperative positional implant control and CT-generated artifacts of a bilateral hypoglossal nerve stimulation device. Material and methods We retrospectively evaluated postoperative radiological imaging of 9 patients on the first day after implantation of a bilateral nervus hypoglossus stimulation device. A variety of radiological imaging procedures were utilized: 8 CT scans (in sagittal and axial planes) and 9 X-ray examinations were conducted. Eight patients (89%) received postoperative X-ray and CT scans, and one patient (11%) received postoperative X-ray control only. Radiological imaging was analysed regarding the position of the implant, anatomy, and artifacts. The age range of patients varied from 59 to 87 years (mean, 68.9 years; SD, 8.6 years). Preoperative Apnoe-Hypopnoea Index (AHI) varied from 16.5 to 64 (mean 40.1) and Body Mass Index (BMI) ranged from 25 to 34 kg/m2 (mean 29.2 kg/m2). Results Evaluation of X-ray images did not reveal artifacts that affected the diagnostic accuracy of postoperative position control. In contrast, CT images showed artifacts in the coronal, sagittal, and axial planes, making radiological assessment more difficult. We observed a high variation of device position without any effect on functionality. Paddle asymmetry was found in 78% of cases (7 out of 9). Conclusion Postoperative radiologic monitoring after implantation of a bilateral hypoglossal nerve stimulator is recommended. A high variation of device position could be found. The variability in implant position observed in our study group does not affect the implant's functionality. CT artifacts need to be considered.

Abstract: Background: This study aimed to assess the cranial morphometric features of patients with idiopathic syringomyelia by conducting comparative analyses with individuals diagnosed with Chiari Type I, Chiari Type I accompanied by syringomyelia, and healthy controls, in order to elucidate the potential structural contributors to the pathogenesis of idiopathic syringomyelia. Methods: In this retrospective and comparative study, a total of 172 patients diagnosed with Chiari Type I and/or syringomyelia between 2016 and 2024, along with 156 radiologically normal individuals, were included. Participants were categorized into four groups: healthy controls, Chiari Type I, Chiari Type I with syringomyelia, and idiopathic syringomyelia (defined as syringomyelia without an identifiable cause). Midline sagittal T1-weighted MR images were used to obtain quantitative measurements of the posterior fossa, cerebellum, intracranial area, and foramen magnum. All measurements were stratified and statistically analyzed by sex. Results: In cases with idiopathic syringomyelia, both the posterior fossa area and the cerebellum/posterior fossa ratio differed significantly from those of healthy controls. In male patients, the foramen magnum diameter was significantly larger in the Chiari + syringomyelia group compared to the idiopathic group. A significant correlation was found between the degree of tonsillar descent and selected morphometric parameters in female subjects, whereas no such correlation was observed in males. Both Chiari groups exhibited significantly smaller posterior fossa dimensions compared to the healthy and idiopathic groups, indicating greater neural crowding. Additionally, a paradoxical decrease in syringomyelia incidence was observed with increasing tonsillar descent in Chiari Type I cases. Conclusions: Anatomical variations such as a reduced posterior fossa area or altered foramen magnum diameter may contribute to the pathogenesis of idiopathic syringomyelia. Cranial morphometric analysis appears to offer diagnostic value in these cases. Further prospective, multicenter studies incorporating advanced neuroimaging modalities, particularly those assessing cerebrospinal fluid dynamics, are warranted to better understand the mechanisms underlying syringomyelia of unknown etiology.