Measurement of human organ volumes has been extensively applied in clinical functional assessment. Muscle volume has been a crucial function assessment indicator of the muscles. To determine the relationship between psoas muscle volume and acute osteoporosis or low bone mass compression fractures in postmenopausal women, Huang et al. have retrospectively analyzed the spinal MRI images and dual-energy X-ray absorptiometry data from postmenopausal women. Their results have uncovered that acute compression fractures are positively correlated with the muscle volume/fat volume ratio and that postmenopausal women with underlying osteoporosis/low bone mass are susceptible to compression fractures due to the small volume of paraspinal muscles. Also, lumbar muscle volume is regarded as the main quantitative and qualitative indicator of its function [5].

Using MRI, de Figueiredo Melke et al. have segmented and reconstructed the total head, upper head, and lower head images of the LPM, and performed 3D quantitative measurement of its volume and insertion patterns, which has shown different volumes of the LPM in the closed and open-mouth positions. Gender may affect muscle volume, especially the upper head, the insertion type of which also affect muscle volume [6]. Jeppe Hvedstrup et al. have measured the volume of the rectus capitis posterior minor muscle through the MRI images of patients with migraine and have revealed no correlations of its volume with migraine, frequency of headache or migraine, and age or BMI, suggesting no pathological structural changes in migraine patients [11].

Therefore, muscle volume is closely linked to its function and disease state, which contributes to accurate diagnosis of diseases, functional assessment, and treatment efficacy evaluation. Through the cutoff value based on the ROC curve, we can diagnose the OAB through directly calculating volume and thickness based on 3D MRI, which is an easy way to diagnose the OAB. In some extent, we may find the OAB through thickness and volume measurement which is higher than the cutoff value of bladder detrusor, and through thickness and volume measurement which is lower than the cutoff value of main part of urethra sphincter.

OAB has been previously reported to cause UUI, which is closely relevant to the dysregulated central nervous system. Functional MRI (fMRI) analyses of OAB by Yuko M. Komesu et al. have unraveled the relevance of urinary urgency in OAB patients to limbic cortex (LC) activation, which is likely to be aberrant processing of sensory input in the brain region linked to emotional responses to uncomfortableness [12]. Thus, urinary urgency in OAB is linked to the abnormality in the central nervous system. Matthias Walter et al. observed supraspinal activity responding to bladder distention and cold stimuli, providing a better understanding of the neuropathophysiology of OAB in females. They found impairment in sensory processing and regulation in the OAB patients, which is potentially attributed to insufficient motor activity in the fundamental sensory processing areas, such as the brain insula. Conversely, the cerebellum exhibits considerably enhanced activation of cortical regions, which may support the pelvic floor muscle motor activity to curb urinary incontinence (UI) [13]. However, whether OAB is primarily attributed to abnormal regulation of the central nervous system or impaired anatomical components of urination and UC remains unclear.

Our preliminary study and Christian Wallner's study have shown that the bladder detrusor is a key urination anatomical component and that the LAM and USC such as the main part of urethral sphincter, the compressor urethral, and the urethrovaginal sphincter are important UC anatomical components. Based on the previous anatomical research results, this study additionally unraveled the increased volume of urination anatomical component detrusor in the OAB patients versus the healthy volunteers. This is attributable to long-term muscle tension or contraction of the bladder and its hypercontraction, leading to significantly thickened bladder detrusor and increased volume. The increase of the muscle is more likely to induce a long-term continuous urge to urinate, resulting in UI.

However, the general topology and volume of the LAM showed no noteworthy difference between the OAB patients and the volunteers. Also, no obvious structural damage and changes of the LAM were found in OAB patients, accompanied by no LAM atrophy and volume reduction. From the perspectives of the anterior, middle, and posterior pelvic widths of the LAM hiatus, the hiatus of anterior pelvis was generally wide while the middle and posterior pelvises were almost unaffected, indicating a certain morphological change of the anterior pelvic part of the LAM. Due to long-term UI, the anterior pelvic part of the LAM is loose, but it is far from functional disorders of the pelvic floor such as POP. The LAM is significantly damaged in the patients with long-term prolapse, characterized by relatively large structural damage, and obvious compensatory hypertrophy of the LAM, significantly increased volume, and obvious widen LAM hiatus. MRI study of DeLancey et al. have illustrated that vaginal delivery may cause LAM damage [14], whereas, their research is only limited to the two-dimensional MRI images but lacks either 3D localization or 3D quantification. DeLancey et al. have shown noticeable LAM injury, a significant increase in width of the LAM hiatus, and notably weakened muscle strength in the POP patients as compared to conventional normal volunteers by MRI [15]. DeLancey et al. have measured the volume of the puborectalis muscle in healthy volunteers and POP patients using MRI and 3D reconstruction techniques, demonstrating no notable difference between groups and no puborectalis muscle defect. As illustrated in their article, although there is little difference in the puborectalis muscle between the two groups, the proportion of thickened puborectalis in the POP patients was much higher than in the volunteers. Birth trauma is an important cause of LAM damage, a crucial inducer of POP [14, 16].

We also found weakened main part of urethral sphincter and the compressor urethral in the USC of OAB patients than healthy volunteers except that it is difficult to identify and segment the urethrovaginal sphincter in MRI images [1, 2]. The volume and thickness were markedly smaller in OAB patients than in healthy volunteers, which led to weakened continence muscles and easy leakage of urine, causing or aggravating UUI. Our findings are in agreement with the results of Wu et al. and Wallner et al. [1, 2]. Therefore, the volume of the USC can serve as a quantitative parameter for female UC. Additionally, the results of this study also validated prominently lower pelvic floor muscle strength of OAB patients than the normal values.

MRI measurement by Cevdet Adıgüzel et al. has elucidated no significant difference regarding the thicknesses of the left and right uterosacral ligament (USL) between the OAB patients and the control group, indicative of no relation between the condition of OAB and the USL [17]. Therefore, the occurrence and symptoms of OAB are mainly related to the female urination and continence muscles, instead of the uterine ligaments.

These results offered the first quantitative evidence for pelvic floor imaging studies. Our data of Spearman correlation analysis further unveiled that OAB was strongly linked to age, BMI, pregnancies, and vaginal deliveries, rather than abortions. The incidence of OAB increases with the age, which correlates with the decline of estrogen and autonomic disorders [18]. More pregnancies correlate with a longer cumulative time of compression over the pelvic floor, which is easier to cause disorders in the autonomic nervous system and resultant urodynamic disorders, increased frequency of urination, as well as tore and damaged pelvic floor muscles and widened LAM hiatus, resulting in a risk of the organs prolapse. Besides, the LAM hiatus is easily damaged following vaginal delivery, which will widen the LAM hiatus and lead to the LAM fiber destruction, ultimately contributing to UI. Also, obese patients with higher BMI are at a higher risk of OAB, and more severe symptoms are related to high incidence of POP. As the bladder is compressed by the larger body weight, the prolapse and UI may be aggravated. Obesity (BMI greater than 30 kg m2) and overweight (BMI greater than 25–30 kg m2) are associated with increased prevalence of pelvic floor disorders including UI and OAB. OAB can be triggered by several obesity-related disorders, such as mechanical compression over the bladder caused by weight gain, type 2 diabetes, or metabolic syndrome, the latter two of which elicit an underlying metabolic defect during the occurrence of OAB [2, 19]. Moreover, excessive fat in obese patients will destroy the dense junctions between the pelvic floor muscles and alter the dense connective tissues with tight junctions into fat with loose junctions, resulting in pelvic floor relaxation and UI [20].