Refining Brainstem-Cortical Connectivity During Natural Bladder Filling in Multiple Sclerosis Patients with Overactive Bladder

Bayer A1, Santoso A2, Lozano V3, High R3, Aazhang B1, Khavari R3

Research Type

Pure and Applied Science / Translational

Abstract Category

Overactive Bladder

Abstract 194
OAB from Laboratory to Clinic
Scientific Podium Short Oral Session 23
Friday 9th October 2026
09:07 - 09:15
Parallel Hall 2
Brightlands Foyer
Capacity: 500
Basic Science Overactive Bladder Multiple Sclerosis Female Imaging
1. Rice University, 2. KU Lueven, 3. Houston Methodist
Presenter
Links

Abstract

Hypothesis / aims of study
Multiple sclerosis (MS) is a common cause of lower urinary tract dysfunction (LUTD), reflecting disruption of neural pathways involved in bladder control. Despite this, brainstem contributions during physiologic bladder filling remain poorly understood. The periaqueductal gray (PAG) and pontine centers are key brainstem hubs that integrate bladder afferent and efferent signaling and coordinate bladder storage and voiding.

We hypothesized that, during the empty bladder state, brainstem-cortical functional connectivity engages supraspinal micturition networks but is obscured by inter-subject variability in bladder physiology. We tested whether incorporating bladder capacity (voided volume + post-void residual, PVR) as a covariate would reveal connectivity not detectable in unadjusted analyses.
Study design, materials and methods
Resting-state functional MRI (rs-fMRI) data were acquired in 14 MS patients (mean age 54 years, range 33-74, OAB-AT ≥ 8) using an oral hydration paradigm. Scans were obtained during full bladder (strong desire to void) and post-micturition (empty bladder). Participants exited the scanner to void, enabling uroflow and PVR measurement prior to the second scan.

Preprocessing included motion correction, denoising, co-registration, and normalization. Five brainstem ROIs (three PAG, two pontine) were defined from prior work [1]. Seed-based functional connectivity (FC) was analyzed using CONN and SPM12. Two models were evaluated during the empty bladder state: (i) unadjusted (FC ~ 1) and (ii) covariate-adjusted (FC ~ 1 + BC). Statistical thresholds were voxel-level p < 0.01 (uncorrected) and cluster-level p < 0.05 (FDR-corrected).
Results
In the unadjusted model, no significant connectivity was observed for any brainstem ROI. After adjusting for bladder capacity (mean 296 mL, range 91–615 mL), significant connectivity emerged: (i) PAG 3 with right middle frontal gyrus (70% overlap) and precentral gyrus (15%), and (ii) Pons 2 with right inferior frontal gyrus (opercular division, 79%). No significant connectivity was observed for PAG 1, PAG 2, or Pons 1 outside seed regions.
Interpretation of results
The absence of findings in the unadjusted model, contrasted with their emergence after covariate inclusion, indicates bladder capacity is a key source of variability that can obscure brainstem–cortical relationships.

Connectivity between PAG and the middle frontal and precentral gyri aligns with established supraspinal pathways linking bladder afferent processing to executive and motor control. The middle frontal gyrus is implicated in higher-order control of continence, while the precentral gyrus contributes to pelvic floor and urethral sphincter regulation.

Pontine connectivity with the inferior frontal region supports involvement of inhibitory control networks. The inferior frontal gyrus, particularly in the right hemisphere, is implicated in motor inhibition and may contribute to the suppression of voiding. Its established structural and functional organization, including interactions with the supplementary motor area and insula, supports integration of inhibitory control and interoceptive processing relevant to bladder function.[2] These findings are also consistent with prior resting-state studies in overactive bladder, demonstrating altered connectivity in frontal and interoceptive networks, supporting a central role for inhibitory control dysfunction.[3]
Concluding message
Brainstem-cortical connectivity in MS is hardly detectable without accounting for bladder physiology, but emerges after adjusting for bladder capacity. These findings highlight the importance of physiologic covariates in neuroimaging of bladder control and suggest that supraspinal networks can be revealed when inter-subject variability is appropriately modeled. Resting-state connectivity may provide a useful framework for identifying neural biomarkers of LUTD in MS.
Figure 1 Schematic of the MRI protocol showing full bladder and post-micturition empty bladder resting-state fMRI acquisitions with intervening voiding and PVR measurement.
Figure 2 Seed-based connectivity of the respective brainstem regions at empty bladder state with bladder capacity covariate. Clusters with connectivity greater than zero are highlighted. The remaining ROIs include PAG 1 (-6,-15,-6), PAG 2 (4, -33, -19) and Pons 1.
References
  1. B. Schott et al., “Is the brainstem activation different between healthy young male and female volunteers at initiation of voiding? A high definition 7-Tesla magnetic resonance imaging study,” International Neurourology Journal, vol. 27, no. 3, p. 174, 2023.
  2. R. Boen, L. Raud, and R. J. Huster, “Inhibitory control and the structural parcelation of the right inferior frontal gyrus,” Frontiers in Human Neuroscience, vol. 16, p. 787079, 2022.
  3. L. Zuo, Y. Zhou, S. Wang, B. Wang, H. Gu, and J. Chen, “Abnormal brain functional connectivity strength in the overactive bladder syndrome: a resting-state fMRI study,” Urology, vol. 131, pp. 64–70, 2019.
Disclosures
Funding Funding is provided by the National Institutes of Health (NIH) grant (1R01DK134340-01). Clinical Trial Yes Registration Number NCT06072703 RCT Yes Subjects Human Ethics Committee This study was approved by the Institutional Review Board of Houston Methodist. Written informed consent was obtained from all participants prior to enrollment. Helsinki Yes Informed Consent Yes AI For simple textual assistance in writing the abstract manuscript
Citation

Continence 19S (2026) 102671
DOI: 10.1016/j.cont.2026.102671

01/11/2026 14:17:30