Our findings showed a high prevalence of DO (69.68%) and abnormal voiding patterns (65.16%) among NP women with OAB as compared with parous women. Our finding of VD with an abnormal voiding pattern corroborates the findings of Cho et al., who reported that more than half the women in their study presented with OAB symptoms in conjunction with VD, as revealed by UDS8. In addition, Nitti et al. reported the existence of very high overlapping storage (79%) and obstructive symptoms (76%) in 331 non-neurogenic VD women who underwent multichannel video-UDS for non-neurogenic VD17. Our previous study showed that an add-on muscle relaxant (baclofen) to antimuscarinics can improve treatment efficacy among women with OAB who present with abnormal voiding patterns18. These findings imply that voiding dysfunction might be masked by OAB symptoms. The findings also indicate that the co-existence of OAB and VD is an important clinical problem. Our findings imply that an abnormal voiding pattern, which is indicative of voiding dysfunction, might play a role in the etiology of OAB, especially in NP patients as compared with parous women.
A significant relationship was detected between elevated MUCP and the existence of abnormal void patterns, which may provide evidence of a relationship between pelvic floor hypertonicity and VD. MUCP was used to infer the contraction strength of the levator ani muscle because of the increase in MUCP during pelvic floor muscle contraction (Kegel exercise) in UDS examination19. In our study, OAB women with an abnormal voiding pattern presented with significantly higher MUCP compared with those without an abnormal voiding pattern in all groups (Table 4). Thus, women with an abnormal voiding pattern show higher contraction strength of the levator ani muscle or pelvic floor hypertonicity. Our results corroborate those of Zhu et al.4, who found that poor relaxation of the pelvic floor may be involved in the etiology of OAB in NP women. Peng et al. also reported a high prevalence of the co-existence of poor relaxation in pelvic floor muscles and VD20. In addition, abnormal voiding patterns were higher in the NP group (65.16%) than in the CS group (42.11%) and NSD group (38.00%). These findings highlight the importance of the hypertonicity and poor relaxation of the pelvic floor muscles in the etiology of OAB in NP patients.
BOO in women is controversial because of the wide spectrum of symptoms associated with LUTS. Unlike anatomical BOO caused by symptomatic cystocele and uterine prolapse, previous incontinence surgery, or urethral stricture13, functional BOO can occur at different anatomic levels, for example, pelvic floor (dysfunctional voiding) or external urinary sphincter (Fowler’s syndrome), and patients with BOO can present with storage OAB symptoms21. Some studies, such as that by Cho et al., reported that over 90% of women with VD exhibited OAB symptoms associated with obstruction in video-UDS findings8,22,23. Furthermore, Deindl et al. reported that poor relaxation of the levator muscle or urethral sphincter during micturition is a probable cause of functional BOO in women24. Fusco et al. proposed a three-stage model to characterize the changes in hypertrophy, compensation, and decompensation during bladder remodeling induced by BOO11. They showed that increased detrusor contractility during the voiding phase combined with DO during the filling phase characterized the compensation phase of bladder remodeling11. In this study, as shown in Table 3, the relationship between DO and the presence of an abnormal voiding pattern was statistically significant in the NP group (80.56%) compared with the CS (56.25%) and NSD (51.61%) groups. Thus, an abnormal voiding pattern associated with DO may play a role in OAB among NP patients, but not among NSD or CS patients. Functional BOO may be caused by pelvic floor hypertonicity, leading to the compensative phenomenon of DO in NP women.
The feasibility of using MUCP to assess voiding function has not yet been confirmed. High MUCP is detected in in patients with overactive pelvic floor muscles and LUTS. Therefore, MUCP is used as a proxy for assessing the pelvic floor condition25. In our study, MUCP decreased in the order of NP, CS, and NSD, likely indicating the extent of pelvic floor injury caused by pregnancy and birth trauma. Lower MUCP is in concordance with the finding of abnormal voiding patterns. Whether decreasing MUCP could reduce the possibility of abnormal voiding patterns is debatable, and further research is required to clarify the relationship between MUCP and void function.
Uroflowmetry is a potentially useful tool in clinical practice. Pressure flow study (PFS) can be used to differentially diagnose VD as being either due to BOO or detrusor underactivity (DU) based on detrusor pressure measurements9,13. Although PFS can provide more sophisticated measurements, it could induce possible functional urethral obstruction due to the presence of the urethral catheter26. Therefore, VD due to a presumed “obstruction” can be overdiagnosed based solely on PFS13. Because many NP women cannot void with a urethral catheter in place9,13,26, we did not perform PFS in this study. Nonetheless, uroflowmetry, as compared with multi-channel PFS, can be used as a simple, noninvasive, and relatively inexpensive method for assessing VD in patients. Clothier et al. also reported that using noninvasive urodynamics with a staccato-flow pattern could be used to establish a diagnosis of functional obstructed voiding15. Although differentially diagnosing four recognized uroflow patterns (i.e., tower-, staccato-, interrutped-, and pateau-shaped patterns) may be not easy, urofometry is well suited for screening patients, particularly in cases of repeated abnormal flow15,27.
The limitations of our study are as follows. First, because we did not perform PFS on a daily basis, we were unable to obtain detrusor pressure measurements at maximal flow. Second, the effect of age as a confounding factor cannot be excluded as most of the NP patients were relatively young. Excluding the factors of aging and childbirth, our study highlights the relationship between DO and abnormal voiding patterns among NP women with OAB. In conjunction with the correlation between MUCP and abnormal voiding pattern, we concluded that the abnormal voiding pattern due to hypertonicity of pelvic floor muscle is a possible etiology of OAB among NP women. However, further studies with more patients are required to confirm the pathophysiology of OAB in NP patients.
Our data showed a high prevalence of abnormal voiding patterns among NP women with OAB. Based on the significant relationship among high MUCP, DO, and abnormal void patterns, we hypothesized that hypertonicity or poor relaxation of the pelvic muscles in NP women may cause functional BOO, which is related to their OAB.