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Traumatic brain injury (TBI) can induce a coma and directly affect the pathways that help control lower urinary tract (LUT) function. This paper reviews the clinical and urodynamic data from the literature on LUT function after TBI in the acute, rehabilitation and chronic phases. The number of papers available on LUT function after TBI is very limited, but the studies have been well conducted, and the sample size is acceptable. The interpretation of reported data is complex due to heterogeneity in the items studied and the level of detail. During the early phase, indwelling catheters are needed for critical care, but spontaneous voiding is possible in most patients as soon as the catheter can be removed. The ability to void is primarily independent of the Glasgow Coma Scale value. During rehabilitation, spontaneous voiding is observed in the majority, but re-learning of voluntary control may be needed. In the follow-up, complete recovery of continence and voiding is possible, but overactive bladder and other LUT symptoms (LUTS) have been described. The data show that afferent and sensory functions related to the LUT remain active in many TBI patients, making long-term use of indwelling catheters unnecessary. There are no studies that follow the evolution in the same patient over a long period. Urodynamic studies show that LUT function varies after TBI and that variables such as age, previous dysuria, diabetes and local anatomic pathologies can also influence the outcome. Personalized management after an evaluation is therefore needed in TBI patients.

The pelvic floor biomechanics and sphincter functioning are essential for understanding pelvic floor dysfunction and the pathophysiology of the pelvic organs. The pelvic floor consists of muscles, fascial connections and ligaments. The Integral Theory Paradigm (ITP) explains the musculoskeletal entity of the sphincter mechanism and the pathophysiology of pelvic organ function. The ITP explains the pelvic floor function determined by 3 directional muscle forces: forward, backwards and downward-acting muscle vector forces that form an anterior and posterior resultant. The resultant equilibrium is essential for urinary continence, voiding and defecation. Loose ligaments disturb the equilibrium of the pelvic floor's muscular function with consequences for the organ function's continence, evacuation, and sensory perception. [ABSTRACT FROM AUTHOR]

Objectives: Several central nervous system (CNS) centers affect muscle groups of the lower urinary tract (LUT) and anorectal tract (ART) via autonomic and somatic pathways, working in different modes (storage or expulsion). Hence spinal cord dysfunction can affect the LUT and ART by several possible mechanisms. Methods: This review reports the discussions of a workshop at the 2023 meeting of the International Consultation on Incontinence Research Society, which reviewed uncertainties and research priorities of spinal dysfunction. Results: Discussion focussed on the levator ani nerve, mechanisms underpinning sensory function and sensation, functional imaging, dyssynergia, and experimental models. The following key research questions were identified. (1) Clinically, how can we evaluate the levator ani muscle to support assessment and identify prognosis for effective treatment selection? (2) How can we reliably measure levator ani tone? (3) How can we evaluate sensory information and sensation for the LUT and the ART? (4) What is the role of functional CNS imaging in development of scientific insights and clinical evaluation? (5) What is the relationship of detrusor sphincter dyssynergia to renal failure? Conclusions: Spinal cord dysfunction can fundamentally disrupt LUT and ART function, with considerable clinical impact. The evaluation needs to reflect the full scope of potential problems, and new clinical and diagnostic approaches are needed, for prognosis and treatment. The preclinical science evaluating spinal cord function in both LUT and ART storage and elimination remains a major priority, even though it is a challenging experimental context. Without this underpinning evidence, development of new clinical evidence may be held back. [ABSTRACT FROM AUTHOR]

To critically analyse the relationship of bladder pain syndrome (BPS/IC), as defined, to the posterior fornix syndrome, "PFS" predictably co-occurring bladder urgency, frequency, nocturia, chronic pelvic pain, emptying symptoms/retention, caused by uterosacral ligament (USL) laxity and cured by USL repair. The starting and end points of this paper are the questions, "Are there arguments that BPS/IC can, in some cases, be linked to PFS?" And if so, "To what extent?" We used the criteria required by Ueda for proper diagnosis: "understanding symptoms, detecting abnormal findings and verifying them as a cause of the symptoms." Literature, diagnostic and surgical, indicate that chronic pelvic pain "of unknown origin" can be caused by unsupported visceral pelvic plexuses because of weak USLs; these cause fire of afferent impulses, which the brain mistakenly interprets as coming from the end-organ itself (i.e., genitourinary pain, lower urinary tract symptoms). The same lax USLs can also weaken the pelvic muscles which contract to stretch the vagina to support the urothelial stretch receptors from below: these may prematurely fire off afferent impulses to activate micturition at lower bladder volumes, interpreted as urgency. A speculum placed in the vagina can relieve pain and urgency by mechanically supporting the vaginal wall and USLs, thus predicting an eventual cure by USL repair. There is need to evaluate what percentage of women with known BPS/IC also pass the criteria for PFS. Identifying a significant percentage of BPS/IC women with the causative relation between PFS pathogenesis and BPS/ IC may open a new way of diagnosing and treating BPS/IC in some women. [ABSTRACT FROM AUTHOR]