The International Continence Society (ICS) defines overactive bladder (OAB) as a “symptom-based syndrome suggestive of lower urinary tract dysfunction,” characterised by “urgency, with or without urgency incontinence, usually combined with frequency and nocturia”. Despite these symptoms, a substantial proportion of patients do not demonstrate clear detrusor overactivity (DO) during urodynamics [1]. Current diagnostic assessment relies primarily on intravesical pressure measurements, which detect global increases in detrusor pressure. However, spatially confined bladder wall contractions (or micro-contractions) may not generate sufficient global pressure change to exceed standard detection thresholds yet may still contribute to urgency sensations [1,2].
We hypothesised that bladder overactivity may originate from ‘epicenters’ of the bladder wall, and that spatially resolved intravesical volume measurements could help detect and localise these micro-contractions. Identification of a dominant/triggering contracting region could improve DO diagnosis and support the development of more targeted therapeutic strategies.

Viable ex-vivo porcine bladders were harvested immediately following euthanasia and maintained in oxygenated Krebs solution. Ethical approval was not required as the specimens were sourced postmortem from other approved research projects. Removal of central neural inhibition resulted in spontaneous, localised micro-contractions resembling those described in OAB pathophysiology [3]. A multielectrode pressure-volume (PV) catheter (Ventri-Cath 512, Millar, Texas, US), originally designed for cardiac applications,  was adapted for intravesical application. In addition to pressure, this catheter measures segmental impedance to derive spatially resolved volume changes along the bladder axis. (Figure 1A). This enables the detection of regional volume redistribution during spontaneous bladder contractions. Bladder motion was also recorded using a camera and optical tracking of fiducial markers placed on the bladder surface. This provided independent validation of regional wall displacement and allowed identification of the epicenter of the bladder contraction. The maximum displacement vector of each marker was used to identify the epicenter of the bladder contraction (Figure 1B).

The ex-vivo bladders showed consistent spontaneous micro-contractions, which generated intravesical pressure levels below 1 cmH2O (Figure 2A). This generated intravesical pressure level would be indistinguishable from baseline noise, where amplitudes of up to 5 cmH2O are considered normal. In contrast, PV segmental volume measurements (Figure 2B) clearly demonstrated localised volume redistribution during these events and identified the upper bladder segment as exhibiting the greatest relative volume change, as confirmed from the reference optical tracking (Figure 1B).

These findings suggest that the bladder can have dominant contraction regions without detectable intravesical pressure changes, due to volume redistributions within the bladder. Introducing PV catheters into clinical practice may therefore help improve diagnosis in patients with OAB symptoms who do not show DO on conventional urodynamics. Current therapies, including intra-detrusor botulinum toxin injections, reduce global detrusor contractility. While effective for urgency symptoms, such treatments impair voiding efficiency and lead to urinary retention or the need for intermittent catheterisation. The identification of the epicenter of the bladder contraction raises the possibility that OAB, at least in some patients, may be driven by local pathophysiology rather than diffuse detrusor dysfunction. If similar regional patterns are confirmed in in-vivo animal models and in patients, this could also enable spatially targeted treatment approaches, potentially reducing total toxin dose while preserving global bladder contractility.

We have demonstrated that spatially resolved intravesical volume measurement can detect and localise low-amplitude bladder micro-contractions that are invisible to pressure-based urodynamic assessment. In this study on an ex-vivo bladder, a reproducible dominant contraction region was identified in the upper bladder segment. These findings support the concept that bladder overactivity may originate from epicenters and suggest that localisation of contractile activity could provide a foundation for more precise, bladder-preserving therapeutic strategies in OAB.

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