Background/Objectives: Systematically elucidating the neural mechanisms of bowel and bladder control is crucial for developing closed-loop brain-computer interface (BCI) neurorehabilitation for patients with spinal cord injury (SCI). This study aims to characterize the spatiotemporal Electroencephalography (EEG) dynamics and compensatory cortical reorganization underlying continence motor intentions across healthy aging and SCI cohorts. Methods: 32-channel EEG signals were collected from healthy young adults, healthy older adults, and SCI patients during motor attempt paradigms of suppressed urination and defecation (SUD) and active urination and defecation (UD). Data were analyzed utilizing event-related spectral perturbation (ERSP) and phase-locking value (PLV) functional connectivity across alpha (8-13 Hz), beta1 (13-20 Hz), and beta2 (20-30 Hz) bands. Results: All cohorts exhibited generally consistent broadband event-related desynchronization (ERD) in the sensorimotor cortex (SMC) during visceral motor attempt. Conversely, the frontal cortex (FC) demonstrated marked frequency-band differentiation. During the SUD task, healthy older adults showed significantly greater SMC beta2 ERD than young adults, whereas SCI patients showed a similar but non-significant trend. Frontal beta2 findings were preliminary and should be interpreted with caution due to potential residual artifacts. Network analysis revealed that physiological aging and SCI are associated with large-scale topological reconfigurations, prominently featuring enhanced long-range frontal functional connectivity to compensate for sensory or peripheral deficits. Conclusions: High-level cortical intentions for continence are preserved after SCI, with frontal high-frequency activity possibly reflecting a compensatory process for sensorimotor disruption. These findings substantiate that visceral intentions exhibit discernible characteristics at the cortical level, establishing a spatiotemporal framework for targeted pelvic nerve modulation via brain-machine interfaces.

Background: Kidney transplant recipients are particularly vulnerable to severe infections because of chronic immunosuppression, impaired wound healing, repeated healthcare exposure, and the potential nephrotoxicity of antimicrobial therapy. We report a complex case of multidrug-resistant (MDR) sepsis in a kidney transplant recipient with two concomitant potential infectious sources: an infected sacral pressure ulcer and recurrent urinary tract infection. Case Presentation: A 31-year-old kidney transplant recipient developed traumatic paraplegia following a road traffic accident. Prolonged immobilization was complicated by a progressive sacral pressure ulcer and recurrent urinary tract infections in the setting of neurogenic bladder dysfunction. During hospitalization, wound and urinary cultures identified MDR Gram-negative organisms, including Klebsiella pneumoniae, Acinetobacter baumannii, and Proteus mirabilis. Blood cultures obtained during systemic deterioration were positive for K. pneumoniae. Diagnostic Assessment and Therapeutic Intervention: Severe systemic infection developed with hemodynamic deterioration and markedly elevated inflammatory biomarkers. Because both the urinary tract and infected sacral wound represented plausible infectious reservoirs, the primary source of bacteremia could not be established unequivocally. Management required extensive surgical debridement, negative pressure wound therapy with instillation, culture-directed antimicrobial therapy, and close monitoring of renal allograft function. Gentamicin was used as a culture-directed therapeutic option in the setting of limited antimicrobial alternatives and impaired renal function. Conclusions: This case illustrates the diagnostic and therapeutic complexity of severe MDR infection in kidney transplant recipients when multiple potential infectious sources coexist. Successful management required early source control, microbiological assessment, individualized antimicrobial selection, and multidisciplinary monitoring aimed at controlling infection while preserving renal allograft function.

BACKGROUND Xanthogranulomatous pyelonephritis (XGP) is a rare chronic inflammatory renal infection associated with urinary obstruction, recurrent infections, and progressive renal parenchymal destruction. Bilateral involvement is exceedingly uncommon and associated with substantial morbidity and mortality, particularly in patients with neurogenic bladder and impaired longitudinal urologic follow-up. CASE REPORT A 30-year-old man with spina bifida complicated by neurogenic bladder requiring intermittent catheterization presented with respiratory distress, profound anemia, and progressive functional decline. Imaging demonstrated severe bilateral hydronephrosis, diffuse renal parenchymal destruction and calcifications, and right-sided staghorn calculi, consistent with advanced bilateral XGP. The patient rapidly developed septic shock and acute-on-chronic hypercapnic respiratory failure requiring mechanical ventilation and vasopressor support. Percutaneous nephrostomy drainage yielded purulent material, and cultures grew Morganella morganii, Candida parapsilosis, and Candida tropicalis. His hospital course was complicated by dialysis-dependent renal failure, recurrent respiratory failure, and prolonged ventilatory dependence. Definitive surgical intervention was considered but deferred because of severe anatomical deformities, clinical instability, and prohibitive operative risk. After prolonged hospitalization, he was discharged to a long-term acute care facility but later died from complications related to tracheostomy. CONCLUSIONS This case illustrates the severe clinical consequences of advanced bilateral XGP in a high-risk patient with neurogenic bladder. The coexistence of recurrent infection, urinary obstruction, and disrupted longitudinal follow-up is consistent with recognized risk factors for upper urinary tract deterioration, although their individual contribution to this patient's disease progression cannot be established. The case underscores the management challenges that arise when bilateral renal destruction and systemic instability limit definitive source-control options.

Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic inflammatory disorder characterized by urothelial barrier disruption, neurogenic inflammation, and persistent pelvic pain. However, the upstream molecular mechanisms linking epithelial dysfunction with inflammatory and vascular alterations remain incompletely understood. In this study, we investigated the involvement of STING-associated signaling in experimental cystitis and evaluated the therapeutic potential of the anti-inflammatory marine-derived briareane diterpenoid excavatolide B (EXCB) and its derivative EXCB79 in a cyclophosphamide (CYP)-induced rat model. CYP-induced cystitis was accompanied by increased immunoreactivity of STING together with elevated TBK1 and NF-κB immunostaining, urothelial barrier disruption, CD11b[+] myeloid cell infiltration, increased expression of the inflammatory mediators COX-2 and IL-1β, angiogenesis-associated changes, and enhanced pelvic hypersensitivity. At the concentrations selected for subsequent analyses, EXCB (20 µg/mL) and EXCB79 (5 µg/mL) attenuated pelvic hypersensitivity and were associated with reduced bladder inflammation and partial preservation of epithelial barrier integrity. Double immunofluorescence analysis demonstrated altered spatial associations between STING and CD11b, CD31, VEGF, ZO-1, E-cadherin, and vimentin following CYP administration. Pharmacological modulation of STING-associated signaling was accompanied by reduced immunoreactivity of STING-associated markers together with attenuation of inflammatory, vascular, and epithelial barrier-related alterations, including reduced VEGF immunoreactivity. Collectively, these findings support an association between STING-associated signaling and inflammatory, vascular, and epithelial alterations in experimental cystitis and suggest that pharmacological modulation of this pathway may represent a potential therapeutic strategy for bladder inflammation and pain-related symptoms.

An ileal conduit represents a surgical method of urinary diversion where the ureters are anastomosed to an isolated segment of the distal ileum, which is subsequently exteriorized as a stoma. Stones in ileal conduits are a recognized late complication of urinary diversion, arising from mucus production, urease-producing infection, and impaired drainage due to uretero-ileal stenosis. We report a 30-year-old male with Down syndrome, neurogenic bladder, and chronic kidney disease who presented with bilateral staghorn calculi, stent encrustation, and a conduit calculus following prolonged loss to follow-up. He was managed with a staged, multimodal endoscopic approach combining percutaneous and transconduit techniques, achieving complete stone clearance with significant improvement in renal function. Such cases are technically challenging and require individualized management strategies, underscoring the importance of regular surveillance and early recognition of complications to prevent silent disease progression.

Stress urinary incontinence (SUI), defined as involuntary leakage with effort, exertion, sneezing, or coughing, remains a significant cause of morbidity. While well characterized in the general population, SUI in the setting of neurogenic lower urinary tract dysfunction (NLUTD) poses unique diagnostic and management challenges. This review outlines sex-specific epidemiology, diagnostic strategies, and evolving management approaches for SUI in NLUTD, emphasizing individualized and mechanism-based care.

The coexistence of diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS), known as mixed hyperglycemic crisis, is a rare but potentially fatal metabolic emergency in pediatrics, and is frequently underrecognized because it is misclassified as isolated DKA. It carries a higher risk of complications than either entity alone, particularly in patients with complex comorbidities. We describe the case of a 16-year-old female with myelomeningocele, neurogenic bladder, obesity, and insulin resistance, who had self-discontinued treatment with metformin, atorvastatin, and allopurinol one year prior and presented with sudden neurological deterioration. Initial workup revealed extreme hyperglycemia (1,777 mg/dL), severe hyperosmolarity (431 mOsm/kg), decompensated metabolic acidosis (pH 7.13), and positive urine ketones (+++), consistent with a mixed DKA-HHS presentation. She subsequently developed septic shock of urinary origin, acute kidney injury, and acute pancreatitis (lipase 3,911 U/L). Despite intensive management guided by International Society for Pediatric and Adolescent Diabetes-ISPAD recommendations, she progressed to refractory shock and multiorgan failure, dying within 48 hours of admission. To the best of our knowledge, this represents one of the most extreme metabolic derangements reported in pediatric mixed hyperglycemic crisis. The convergence of extreme hyperosmolarity, concurrent sepsis, and structural comorbidities created a lethal risk phenotype in which sepsis, rather than the degree of metabolic derangement alone, appeared to determine the fatal outcome. Early recognition and an individualized therapeutic approach are essential to improve outcomes in vulnerable pediatric patients.

PurposeSpina bifida (SB) is the most common neural tube defect, often accompanied by neurogenic bladder and bowel dysfunction, hydrocephalus, and orthopedic sequelae. As life expectancy increases for individuals with SB, understanding disparities in healthcare utilization becomes crucial. This study examined colorectal cancer (CRC) screening colonoscopy utilization rates among adults living with SB.MethodUsing the California Health Care Access and Information database (2005-2017), a matched control group was established to compare colonoscopy utilization. Multivariable logistic regression analysis was performed to identify predictors of screening colonoscopy utilization.ResultsAmong individuals aged ≥50 years, 9.5% of those living with SB underwent screening colonoscopy compared to 13.0% of matched controls. After adjustment, SB was independently associated with lower odds of screening colonoscopy (OR 0.84, 95% CI 0.76-0.93).ConclusionFindings underscore the need for targeted interventions to improve CRC screening accessibility for this vulnerable population. Addressing structural barriers and enhancing patient-centered approaches may improve preventative care delivery and long-term health outcomes in individuals with SB.