Sacral Neuromodulation Improves Abnormal Prefrontal Brain Activity in Patients with Overactive Bladder: A Possible Central Mechanism. Issue 6 (24th June 2022)

• Record Type: Journal Article
• Authors: Pang, Dongqing; Liao, Limin; Chen, Guoqing; Wang, Yiming
• Is Part Of: Journal of urology. Volume 207:Issue 6(2022)
• Page Start: 1256
• Page End: 1267
• Publication Date: 2022-06-24
• Subjects: spectroscopy, near-infrared -- brain mapping -- urination -- urodynamics; Genitourinary organs -- Periodicals; Urology -- Periodicals; Urology -- Periodicals; Urologie -- Périodiques; Urologie; 616.6
• DOI: 10.1097/JU.0000000000002445
• Languages: English
• ISSNs: 0022-5347

Abstract

Abstract : Purpose: We explored the central pathogenesis of overactive bladder (OAB) and the central mechanism of action of sacral neuromodulation (SNM). Materials and Methods: We prospectively enrolled patients with OAB who chose SNM and healthy controls (HCs). At baseline, all subjects completed a 72-hour voiding diary, OAB symptom score and prefrontal cortex functional near-infrared spectroscopy scan synchronous urodynamic monitoring. All OAB patients were tested after implantation of the SNM electrode, and both success and failure groups were reevaluated. NIRS_KIT software was used to analyze prefrontal activity (p <0.05 and corrected by false discovery rate). SPSS® 22.0 was used to analyze clinical parameters, and p <0.05 was considered statistically significant. Results: A total of 16 HC and 20 OAB patients were enrolled. SNM treatment was successful in 18 OAB patients and failed in 2. The parameters of the voiding diary, OAB symptom score and urodynamic monitoring of OAB group were significantly improved after SNM treatment in success group, not in the failure group. Compared with HCs, Brodmann's area 9 (left dorsolateral prefrontal cortex [DLPFC]) was significantly deactivated in the preoperative OAB success group and significantly activated after SNM treatment. Before surgery, compared with the success group, the failure group showed significantly deactivated Brodmann's area 9 (left DLPFC). Conclusions: Our study provides novel neuroimaging evidence for the possible central pathogenesis of OAB (ie abnormal deactivation of the left DLPFC) and the possible central mechanism of action of SNM (ie restore activation of the left DLPFC).