Describing a "high bladder neck" is common practice, yet it is not a standardized entity, and it lacks an evidence base in diagnostics and therapy. Recent systematic reviews report few trials, yet incision of the bladder neck remains a first-line therapy. The concept insinuates a basis for bladder outlet obstruction, so it is during voiding that such an issue should be assessed. For cystourethroscopy, the urinary tract is in the storage phase. A pressure-flow study in videourodynamics can visualize when the bladder neck is deflected into the proximal prostatic urethra by the force of bladder contraction, but this is rarely undertaken. Standard urodynamics may infer this diagnosis, but only by assuming the cause. Other forms of imaging are being evaluated, though they remain remote from delivering evidence based on therapy outcomes. Proper consensus regarding the "high bladder neck" is needed, primarily for standardization of terminology and agreement on justifiable endoscopic and imaging approaches.

Using multiple statistical methods, this study investigated the core diagnostic information from the four diagnostic methods, the distribution patterns of syndrome elements, and their relationship with laboratory biochemical indicators in diabetic peripheral neuropathy(DPN). The aim is to deepen the understanding of the disease-symptom-syndrome relationship in DPN. A retrospective study was conducted on 1 420 inpatients diagnosed with DPN patients at the Department of Endocrinology, the First Affiliated Hospital of Anhui University of Chinese Medicine, from June 2014 and June 2023. Data mining techniques, including frequency statistics, association rule analysis, factor analysis, cluster analysis, and Bayesian network analysis, were applied to examine general patient information, TCM diagnostic data from the four diagnostic methods, and laboratory biochemical indicators. The core clinical manifestations in DPN patients were dry mouth, limb numbness, blurred vision, fatigue, thirst, and a thready pulse. Association rule analysis indicated Yin deficiency leading to blood stasis is the core pathogenesis. Factor analysis indicated that the disease location primarily involved the spleen, kidney, and liver, while main disease nature elements were Yin deficiency, Qi deficiency, and blood stasis, often complicated by concomitant phlegm turbidity, Yang deficiency, and essence depletion. Cluster analysis identified five syndrome patterns: Yin deficiency with blood stasis syndrome, Qi deficiency with blood stasis syndrome, Yang deficiency with cold aggregation syndrome, phlegm stasis obstructing collateral syndrome, and liver-kidney deficiency syndrome. Among these, Yin deficiency with blood stasis syndrome and Qi deficiency with blood stasis syndrome were the most prevalent. Bayesian network analysis revealed associations between abnormal fasting blood glucose(FBG) and symptoms such as chest tightness, palpitations, dizziness, insomnia, and constipation. Abnormal glycosylated hemoglobin(HbA1c) was associated with frequent urination, polyphagia, polydipsia, thirst and dry mouth. Abnormal total cholesterol(TC) was linked to emaciation, fear of cold and cold limbs, and a weak pulse. Abnormal serum creatinine(SCr) was associated with slow reaction, a wiry pulse, and limb pain. The distribution of TCM syndromes in DPN primarily involves Yin deficiency with blood stasis syndrome and Qi deficiency with blood stasis syndrome. The core pathogenesis is Yin deficiency leading to blood stasis, with the disease location in the spleen, kidney, and liver. The identified associations between FBG, HbA1c, TC, SCr and specific TCM syndromes provide an objective basis for the microscopic syndrome differentiation of DPN and its integrated diagnosis and treatment combining Chinese and western medicine.

Cystitis cystica et glandularis (CCG) is a benign bladder condition driven by chronic mucosal irritation. Although often incidental, extensive disease can cause distal ureteric obstruction and produce radiological and cystoscopic appearances that closely mimic bladder malignancy, creating significant diagnostic and management challenges. We report two men with histologically confirmed CCG whose clinical courses differed markedly. The first presented with bilateral hydronephrosis and bladder distortion, initially suspicious for urothelial carcinoma. Despite repeated resections, stenting and nephrostomy drainage, obstruction persisted and bilateral ureteric reimplantation was ultimately required to preserve renal function. The second presented with recurrent urinary infections and voiding dysfunction refractory to antibiotics. Despite bilateral hydronephrosis, mercaptoacetyltriglycine (MAG3) renography excluded true obstruction. His symptoms reflected a non-prostatic outflow problem, and conservative management was pursued; however, with ongoing symptoms, cystectomy remains under consideration. These cases highlight that clinical outcomes are determined primarily by the level and functional significance of obstruction, rather than histological subtype alone, and that early multidisciplinary assessment and individualised management are key to minimising morbidity.

Urinary incontinence (UI) is a common and debilitating comorbidity in Alzheimer's disease (AD), yet its underlying pathophysiology remains poorly defined. While UI in dementia has traditionally been attributed to functional impairment, emerging clinical and urodynamic data suggest that neurologic mechanisms may contribute to lower urinary tract dysfunction in this population. Here, we investigated urinary function and neuropathological changes in aged APP/PS1 mice (AD mice), a widely used model of amyloid pathology. Using functional voiding assays, we identified a pattern of urinary dysfunction characterized by increased urinary frequency, small-volume voiding, shortened void duration, and reduced bladder compliance in the absence of bladder outlet obstruction or gross changes in bladder or prostate morphology. These findings are most consistent with a storage-phase abnormality accompanied by impaired voiding coordination rather than classic detrusor overactivity or underactivity. We examined spinal cord and peripheral components involved in bladder innervation and identified amyloid-beta deposition throughout the thoracolumbar and lumbosacral spinal cord, dorsal root ganglia, ventral roots, cauda equina, and associated meningeal structures in AD mice. Importantly, amyloid deposition was accompanied by reduced expression of vesicular acetylcholine transporter and decreased neuronal activation in bladder-innervating pathways, without evidence of increased apoptosis. Taken together, these data demonstrate that AD mice develop a mixed lower urinary tract dysfunction phenotype associated with amyloid-beta deposition and altered neuronal signaling within the spinal cord and peripheral micturition pathways. These findings support a neurogenic contribution to urinary dysfunction in AD and highlight the spinal cord as a novel site of pathology that may influence urinary symptoms in Alzheimer's dementia.

Background: Bladder dysfunction is a complicated condition that substantially impairs quality of life for both men and women. Due to the adverse effects and limited efficacy of current therapies, new strategies must be rapidly developed. Female bladder dysfunction arises from multifaceted etiologies distinct from the predominantly male benign prostatic hyperplasia (BPH) that is the focus of existing drug development. In this study, we investigated the therapeutic potential of Quisqualis indica extract (QIE), a traditional medicinal herb that attenuates BPH-induced lower urinary symptoms (LUTS), to elucidate its underlying mechanisms in a female bladder dysfunction model. Methods and Results: A bladder dysfunction model was established by inducing partial bladder outlet obstruction (pBOO) in female Sprague Dawley rats, followed by the oral administration of QIE for 7 weeks. Voiding pattern analysis and cystometry were conducted to evaluate indicators such as voiding frequency, voiding volume, and intravesical pressure. Histological analysis of excised bladder tissue quantified smooth muscle hypertrophy and collagen deposition. Gene expression profiling of inflammatory cytokines and fibrosis-related markers within the bladder tissue was performed to assess tissue remodeling. Furthermore, pharmacological contraction studies examined the direct effects of QIE on detrusor muscle responsiveness to muscarinic and purinergic agonists. QIE administration significantly improved the elevated voiding pressure and abnormal inter-contraction intervals observed in the pBOO rats, restoring normal voiding patterns. Histological examination revealed a marked decrease in muscle hypertrophy and collagen deposition. Expression levels of pro-inflammatory cytokines (TNFα, IL-1β) and fibrosis-associated genes (TGF-β, α-SMA) were downregulated. Pharmacological contraction assays demonstrated that QIE attenuated the hypercontractile response of bladder smooth muscle to a muscarinic agonist, with concurrent reduced expression of muscarinic receptors (M2, M3) at the mRNA level. Conclusions:QIE ameliorates key aspects of bladder dysfunction, voiding abnormalities, inflammation, fibrosis, and hypercontractility by modulating muscarinic receptor signaling and fibrotic pathways. This study suggests that QIE warrants further investigation as a natural product-based therapeutic candidate for female bladder dysfunction.

Lower urinary tract symptoms (LUTS) and various lower urinary tract dysfunctions (LUTDs) often coexist because their prevalence increases with ageing. In men, benign prostatic obstruction (BPO) is often proposed as a cause of other "secondary" LUTDs. However, causality of BPO in LUTDs, other than voiding LUTS and acute urinary retention, is probably indirect, if present at all. Indirect mechanisms complicate the inference of causality and may reduce the chance of reversibility. BPO is not a unifying explanation for LUTD, but one possible aetiological factor among many age-related, metabolic, neurological, behavioural, and anatomical factors. This mini-review discusses how to evaluate whether associations between BPO and LUTD are causal, reversible, and relevant to treatment decisions. The Bradford Hill viewpoints (strength, consistency, specificity, temporality, biological gradient, plausibility, coherence, experiment, and analogy) remain a useful framework for considering whether observed associations may be causal. However, the potential surgical setting of BPO adds two additional dimensions. First, is BPO needed to maintain the phenotype, such that treating BPO should bring resolution of the secondary problem? Second, if causation appears to apply at a population level, how confidently can that inference be applied to the individual man considering surgery? Association should not be mistaken for causation, causation should not be mistaken for reversibility, and reversibility should not be mistaken for sufficient net benefit for the individual man considering surgery.