Entheseal pain of levator ani muscle: A novel etiology in chronic pelvic pain and lower urinary tract symptoms—A urodynamic perspective

Abstract

Background:

Although evidence suggests that levator ani muscle (LAM) entheseal pain is a novel etiology of chronic pelvic pain (CPP), its association with lower urinary tract symptoms (LUTS) remains underexplored. This study examined the urodynamic manifestations of LUTS in patients with LAM entheseal pain.

Methods:

In this retrospective cohort, women with chronic pelvic pain (CPP) and LUTS underwent standardized palpation and were divided into three groups: an isolated LAM muscular pain, an isolated LAM entheseal pain, and a combined muscle and entheseal pain group. Between-group differences in symptom prevalence and urodynamic parameters were analyzed.

Results:

A total of 307 female patients were enrolled. Enthesis-related pain groups exhibited significantly higher prevalences of urinary symptoms, including urinary frequency (muscle pain, n = 81 vs entheseal pain, n = 32 vs combined pain, n = 194: 82.7% vs 87.5% vs 85.1%, p = 0.011), residual urinary sensation (46.9% vs 65.6% vs 63.4%, p < 0.001), and painful bladder symptoms (45.7% vs 59.4% vs 61.9%, p < 0.001). Additionally, these groups demonstrated significantly higher rates of pain-related comorbidities, including bearing-down sensation (33.3% vs 37.5% vs 49.0%, p < 0.001), dysmenorrhea (22.2% vs 25.0% vs 35.1%, p < 0.001), irritable bowel syndrome (29.6% vs 32.4% vs 44.3%, p < 0.001), and systemic myofascial pain (28.4% vs 40.6% vs 52.6%, p < 0.001). However, direct comparison between isolated muscular and entheseal pain groups revealed no significant differences in LUTS or pain comorbidities, whereas combined pain group demonstrated the highest symptom prevalence. Notably, no significant intergroup differences were observed in urodynamic parameters.

Conclusion:

LAM entheseal pain represents a distinct, clinically palpable entity in CPP. Its urodynamic similarity to myofascial pain suggests that LUTS reflect a shared final pathway of central sensitization rather than peripheral structural dysfunction. Moreover, its unique association with morning stiffness supports a divergent pathophysiology.

Lay Summary: Entheseal pain refers to pain originating from the compartment to which a muscle is attached. Levator ani muscle entheseal pain is a novel etiology of chronic pelvic pain that may be associated with lower urinary tract symptoms. This study enrolled 307 women with CPP and stratified them into three groups: isolated LAM muscular pain, isolated LAM entheseal pain, and combined muscular and entheseal pain. Participants with enthesis-related pain exhibited significantly higher prevalences of subjective symptoms, including urinary symptoms and pain-related comorbidities. However, no significant differences were observed in any objective urodynamic parameters among the three groups. This dissociation between subjective symptoms and objective findings reflects a shared final pathway of neural remodeling rather than peripheral structural dysfunction as the underlying pathophysiology.

1. INTRODUCTION

Chronic pelvic pain (CPP) is a debilitating condition that affects approximately 24% of women globally, with profound impacts on quality of life.¹ CPP has a multifactorial etiology.^2,3 Pelvic floor myofascial pain (PFMP), characterized by hypertonicity, trigger points, and tenderness of the pelvic floor muscles, accounts for 14% to 22% of CPP cases.^4,5 The levator ani muscle (LAM), a key stabilizer of the pelvic floor, is often implicated in PFMP pathogenesis. Female individuals have a substantially larger LAM compare with male individuals (approximately double the volume).⁶ This structural difference may predispose female individuals to mechanical overload and myofascial dysfunction.

We previously identified an underrecognized anatomical feature. We reported that the aponeurosis of the LAM’s iliococcygeus component extends beyond the arcus tendineus levator ani (ATLA), anchoring to the inferior border of the superior pubic ramus.⁶ The site where the iliococcygeus component anchors to the superior pubic ramus qualifies as an enthesis,⁷ and disorders related to this site may contribute to CPP. Although patients with CPP tend to exhibit tenderness at this site, PFMP (particularly with entheseal involvement) is often overlooked in routine evaluations.⁸

Emerging evidence suggests that LAM entheseal pain drives lower urinary tract symptoms (LUTS).^9–11 Nevertheless, this association is poorly addressed in current management paradigms. Women suffering from PFMP may be treated with nonsteroidal anti-inflammatory drugs (NSAIDs). Surprisingly, those who responded well to NSAIDs treatment also reported significant alleviation of their LUTS.¹² Up to 85% of women with CPP exhibit hypertonic pelvic floor dysfunction, such as PFMP and LAM spasms.¹³ Among these women with hypertonic pelvic floor dysfunction, some of them exhibit myofascial urinary frequency syndrome—a phenotype linking LUTS to myofascial dysfunction.⁹ Despite these findings, the urodynamic manifestations of LAM entheseal pain remain unexplored.

This study aimed to bridge the gap between anatomy and clinical practice by investigating the urodynamic profile of LUTS attributable to LAM entheseal pathology.

2. METHODS

2.1. Study design and population

The Joint Institutional Review Board and Ethics Committee of Taipei Medical University Hospital, Taiwan, approved this study (Approval No. N202202006). Data were retrospectively collected from medical records between April 2020 and October 2022. The study protocol adhered to relevant guidelines and regulations.

2.2. Inclusion and exclusion criteria

A total of 307 female patients met the study’s inclusion criteria. Patients were included if they reported experiencing LUTS, including urinary frequency, urgency, incontinence, weak stream, postvoid residual sensation, painful bladder syndrome (PBS), and nocturia. Additionally, patients with LUTS reported varying degrees of CPP localized to the pelvic or lower abdominal area, with some cases classified as PFMP or entheseal pain. All eligible patients underwent a physical examination, including a pelvic examination to identify pain-triggering points in the LAM.

All patients with LUTS were instructed to complete a 3-day urinary diary. This study used these diary entries to identify urinary frequency (>8 voids/day) or nocturia (≥2 voids/night) and determine fluid balance patterns. Data on other symptoms, such as bearing-down sensation, PBS, morning stiffness, and voiding difficulty (eg, weak or interrupted urine stream), were also obtained. These data were identified through physician-patient interactions that had been documented in medical records. Diagnoses of irritable bowel syndrome (IBS), dysmenorrhea, and myofascial pain (MFP) were established on the basis of symptoms, medical history, and physical examination results.

The patients were divided into three groups according to the classifications of CPP: LAM muscular pain group (muscle pain group), which comprised patients who reported tenderness during the palpation of the muscle belly of LAM; LAM entheseal pain group (entheseal pain group), which comprised patients who reported tenderness during the palpation of the inferior border of superior pubic ramus (enthesis of LAM); and combined pain group (muscle plus entheseal pain group), which comprised patients who reported tenderness during the palpation of the muscle belly and the inferior border of superior pubic ramus.

Regardless of the classifications of CPP, the patients were further divided into a nulliparous group (NP group); a spontaneous vaginal birth group (SVB group), which comprised patients who had only ever given birth through spontaneous vaginal delivery; and a cesarean section group (CS group), which comprised patients who had only ever given birth through cesarean section. The nulliparous group comprised gestational-age patients with overactive bladder but without a history of pregnancy beyond 12 weeks of gestation. Patients who had given birth through both spontaneous vaginal delivery and cesarean section.

Patients were excluded if they had a urinary tract infection, pelvic organ prolapse, a pelvic mass or malignancy, active urinary tract stones, intravesical lesions, pelvic inflammation disease or an enlarged uterus (fibroids or adenomyosis). Patients were also excluded if they were on any medications affecting urinary function; if they refused to undergo urodynamic testing; if they had a history of urogenital surgery; or if they had diabetes mellitus, neurogenic lower urinary tract dysfunction, voiding dysfunction, or active interstitial cystitis. Additionally, patients under 20 years of age were excluded.

2.3. Bimanual examination

According to our previous study, the origin of the LAM (specifically the iliococcygeus component) is a type of aponeurosis that connects with the pubic bone. This aponeurosis involves attachment to the inferior border of the superior ramus of the pubic bone, posterior attachment to the anterior border of the greater sciatic notch, and inferior attachment to the ischial spine and arcus tendinosus fasciae pelvis. In this study, painful sites originating from the enthesis of the LAM were evaluated through digital palpation during regular vaginal examinations. Entheseal pain of the levator ani muscle was defined as tenderness elicited specifically by the digital palpation of the inferior border of the superior pubic ramus, which is the anatomical site where the iliococcygeus aponeurosis anchors. This type of pain was distinguished from generalized myofascial pain, which is characterized by tenderness in the muscle belly of skeletal muscles from any part of the body. Conversely, if the pain was elicited by palpation of the muscle proper of the LAM, it was classified as LAM-related myofascial pain. All pelvic examinations were performed by the same physician, who applied uniform pressure while palpating areas in this newly identified anatomy.

2.4. Urodynamic testing

All patients underwent urodynamic testing. All examinations were performed in the semiseated position by using water media on a urodynamic system (UD-2000; Medical Measurement Systems, Dover, NH). A triple-lumen urethral catheter (8 Fr) was inserted into the urethra and then retracted at 2 mm/s. All examinations were performed by the same physician using the same equipment at the same hospital.

Detrusor overactivity (DO) was defined as a urodynamic observation characterized by involuntary detrusor contractions during the filling phase, which may be spontaneous or be provoked by urinary urgency.¹⁴ Abnormal voiding patterns during uroflowmetry were defined as either an unsmooth curve, the presence of multiple interrupted peaks, or an abnormally low flow rate in the absence of a catheter. Typical uroflowmetry results are those revealing a single smooth curve with a maximum flow rate of >15 mL/s and a voided volume of >200 mL.^14,15 Diagnoses of abnormal voiding patterns were established on the basis of the aforementioned uroflowmetry results regardless of the presence or absence of clinical symptoms. All procedures of urodynamic testing and test result interpretation were performed by one of the study authors (H.Y.C.).

2.5.Statistical analysis

The baseline characteristics were analyzed using the chi-square test for categorical variables, which included age, body mass index (BMI), urinary frequency, urgency, nocturia, urinary incontinence, weak urine stream, residual urine sensation, PBS, bearing-down sensation, dysmenorrhea, IBS, MFP, and morning stiffness. Continuous variables presented as means and SDs and were analyzed using Student’s t test. Data were analyzed in SAS, version 9.4 (SAS Institute, Cary, NC). Significance was indicated by p < 0.05. For the direct comparison between the isolated muscular pain group and the isolated entheseal pain group, the same statistical tests (Chi-square test or Student’s t test) were applied.

3. RESULTS

The patients were divided into a muscle pain group, an entheseal pain group, and a muscle plus entheseal pain group. Although symptom severity was not formally quantified (eg, using a questionnaire), all patients reported that their pain symptoms affected their quality of life. Fig. 1 depicts the flowchart of patient screening and selection process.

Fig. 1.

Flowchart of patient screening and selection.

Table 1 presents the demographic characteristics of the study cohort. No significant intergroup differences were observed in mean age, body height, body weight, or BMI (muscle pain group vs entheseal pain group vs combined pain group: 50.6 ± 15.0 years vs 47.3 ± 12.6 years vs 49.0 ± 14.6 years, p = 0.522; 158.0 ± 6.7 cm vs 160.3 ± 4.5 cm vs 158.6 ± 6.0 cm, p = 0.187; 57.5 ± 10.4 kg vs 56.6 ± 9.0 kg vs 56.5 ± 9.4 kg, p = 0.687; 23.1 ± 4.1 kg/m² vs 22.0 ± 6.1 kg/m² vs 22.5 ± 3.6 kg/m², p = 0.340).

Table 1.

Patient demographic characteristics and clinical symptoms

	Muscle pain n = 81	Entheseal pain n = 32	Muscle plus entheseal pain n = 194	p
Age, y, mean (±SD)	50.6 ± 15.0	47.3 ± 12.6	49.0 ± 14.6	0.522
Height, cm, mean (±SD)	158.0 ± 6.7	160.3 ± 4.5	158.6 ± 6.0	0.187
Weight, kg, mean (±SD)	57.5 ± 10.4	56.6 ± 9.0	56.5 ± 9.4	0.687
Body mass index, mean (±SD)	23.1 ± 4.1	22.0 ± 6.1	22.5 ± 3.6	0.340
Non-nulliparous, %	72.8	65.6	72.7	0.825
Urinary frequency, %	82.7	87.5	85.1	0.011
Urgency, %	49.3	50.0	50.0	0.876
Nocturia, %	55.6	65.6	59.3	0.106
Urinary incontinence, %	55.6	34.4	50.5	0.003
Weak urine stream, %	39.5	37.5	46.9	0.200
Residual urine sensation, %	46.9	65.6	63.4	<0.001
Painful bladder, %	45.7	59.4	61.9	<0.001
Bearing-down sensation, %	33.3	37.5	49.0	<0.001
Dysmenorrhea, %	22.2	25.0	35.1	<0.001
Irritable bowel syndrome, %	29.6	32.38	44.3	<0.001
Myofascial pain from any body part, %	28.4	40.6	52.6	<0.001
Morning stiffness from any body part, %	16.1	25.0	37.1	<0.001

No significant differences were noted between the groups in terms of urinary urgency, nocturia, and weak urine stream (muscle pain group vs entheseal pain group vs muscle plus entheseal pain group: 49.3% vs 50.0% vs 50.0%, p = 0.876; 55.6% vs 65.6% vs 59.3%, p = 0.106; 39.5% vs 37.5% vs 46.9, p = 0.200). Among the LUTS, significant intergroup differences were observed in urinary frequency, urinary incontinence and residual urine sensation (muscle pain group vs entheseal pain group vs combined pain group: 82.7% vs 87.5% vs 85.1%, p = 0.011; 55.6% vs 34.4% vs 50.5%, p = 0.003; 46.9% vs 65.6% vs 63.4%, p < 0.001).

Patients in the enthesis-related pain group exhibited significantly higher prevalence rates of pain-related conditions, including PBS, bearing-down sensation, dysmenorrhea, IBS and general myofascial pain (muscle pain group vs entheseal pain group vs combined pain group: 45.7% vs 59.4% vs 61.9%, p < 0.001; 33.3% vs 37.5% vs 49.0%, p < 0.001; 22.2% vs 25.0% vs 35.1, p < 0.001; 29.6% vs 32.4% vs 44.3%, p < 0.001; 28.4% vs 40.6% vs 52.6%, p < 0.001).

Additionally, comparison among the three groups demonstrated that patients with entheseal involvement (ie, isolated entheseal and combined pain groups) exhibited a stepwise increase in the prevalence of rheumatism-related symptoms, such as morning stiffness, compared with those with isolated muscle pain group (16.1% vs. 25.0% vs. 37.1%, p < 0.001). To determine whether the origin of pain (muscular vs entheseal) independently influences symptom manifestation, a direct comparison of the two isolated pain groups was conducted. As presented in Table 2, this comparison revealed no significant differences in demographic characteristics, LUTS, or pain-related comorbidities, including morning stiffness (p > 0.05).

Table 2.

Patient demographic characteristics and clinical symptoms, exclusively focusing on the comparison between isolated muscle pain and isolated entheseal pain

	Muscle pain n = 81	Entheseal pain n = 32	p
Age, y, mean (±SD)	50.6 ± 15.0	47.3 ± 12.6	0.29
Height, cm, mean (±SD)	158.0 ± 6.7	160.3 ± 4.5	0.06
Weight, kg, mean (±SD)	57.5 ± 10.4	56.6 ± 9.0	0.65
Body mass index, mean (±SD)	23.1 ± 4.1	22.0 ± 6.1	0.24
Non-nulliparous, %	72.8	65.6	0.49
Urinary frequency, %	82.7	87.5	0.78
Urgency, %	49.4	50.0	1.00
Nocturia, %	55.6	65.6	0.50
Urinary incontinence, %	55.6	34.4	0.06
Weak urine stream, %	39.5	37.5	0.85
Residual urine sensation, %	46.9	65.6	0.095
Painful bladder, %	45.7	59.4	0.22
Bearing-down sensation, %	33.3	37.5	0.67
Dysmenorrhea, %	22.2	25.0	0.81
Irritable bowel syndrome, %	29.6	32.4	0.78
Myofascial pain from any body part, %	28.4	40.6	0.26
Morning stiffness from any body part, %	16.0	25.0	0.29

The urodynamic testing results for each group are presented in Table 3. No significant differences were observed between the groups in cystometric parameters, including first sensation of bladder filling volume, normal desire-to-void volume, maximum cystometry capacity, and detrusor overactivity (muscle pain group vs entheseal pain group vs combined pain group: 142.1 ± 65.2 mL vs 142.2 ± 61.8 mL vs 130.4 ± 65.1 mL, p = 0.314; 213.3 ± 83.9 mL vs 213.8 ± 89.9 mL vs 195.7 ± 78.4 mL, p = 0.184; 362.1 ± 114.4 mL vs 368.7 ± 121.5 mL vs 338.1 ± 108.0 mL, p = 0.140; 58.0% vs 43.8% vs 45.4%, p = 0.232). Additionally, no significant differences were observed between the groups in uroflowmetry parameters, including peak flow and mean flow (muscle pain group vs entheseal pain group vs combined pain group: 21.8 ± 29.8 mL/sec vs 19.8 ± 7.5 mL/sec vs 18.6 ± 8.4 mL/sec, p = 0.348; 9.1 ± 4.4 mL/sec vs 10.7 ± 5.1 mL/sec vs 9.5 ± 5.3 mL/sec, p = 0.344). However, a significant intergroup difference was observed in abnormal voiding patterns (muscle pain group vs entheseal pain group vs combined pain group: 63.0% vs 50.0% vs 62.9%, p = 0.033). No significant differences were observed between the groups in urethral pressure profile, including maximum urethral closure pressure (MUCP) and functional length (muscle pain group vs entheseal pain group vs combined pain group: 80.6 ± 34.0 cmH₂O vs 81.8 ± 32.6 cmH₂O vs 80.1 ± 31.4 cmH₂O, p = 0.963; 2.3 ± 0.6 cm vs 2.3 ± 0.5 cm vs 2.3 ± 0.9 cm, p = 0.949). In summary, no significant intergroup differences were observed in the majority of urodynamic parameters (p > 0.05), regardless of whether pain originated from muscular or entheseal sources.

Table 3.

Urodynamic parameters in patients with myofascial pain, entheseal pain, or combined pain of muscle proper and enthesis of levator ani muscle

	Muscle pain n = 81	Entheseal pain n = 32	Muscle plus enthesesal pain n = 194	p a
Peak flow, mL/s, mean (±SD)	21.8 ± 29.8	19.8 ± 7.5	18.6 ± 8.4	0.348
Mean flow, ml/s, mean (±SD)	9.1 ± 4.4	10.7 ± 5.1	9.5 ± 5.3	0.344
MUCP, cmH2O, mean (±SD)	80.6 ± 34.0	81.8 ± 32.6	80.1 ± 31.4	0.963
FL, cm, mean (±SD)	2.3 ± 0.6	2.3 ± 0.5	2.3 ± 0.9	0.949
FS, mL, mean (±SD)	142.1 ± 65.2	142.2 ± 61.8	130.4 ± 65.1	0.314
ND, mL, mean (±SD)	213.3 ± 83.9	213.8 ± 89.9	195.7 ± 78.4	0.184
MCC, mL, mean (±SD)	362.1 ± 114.4	368.7 ± 121.5	338.1 ± 108.0	0.140
DO, %	58.0	43.8	45.4	0.232
Abnormal voiding patterns, %	63.0	50.0	62.9	0.033

DO = detrusor overactivity; FL = functional urethral length; FS = first sensation of bladder filling; MCC = maximum cystometric capacity; MUCP = maximum urethral closure pressure; ND = normal desire to void.

^aMean (±SD): ANOVA; n(%): χ² test.

Birth delivery mode has been noted to potentially influence urodynamic outcomes. Therefore, we conducted subgroup analyses stratified by parity status and birth delivery mode (Table 4). We accounted for parity status by stratifying patients into nulliparous and parous groups. Parity status subgroups did not significantly differ in MUCP (muscle pain group vs entheseal pain group vs combined pain group: 92.3 ± 36.3 cmH₂O vs 88.9 ± 32.3 cmH₂O vs 95.6 ± 28.1 cmH₂O, p = 0.778 among nulliparous patients; 76.2 ± 32.4 cmH₂O vs 78.0 ± 32.8 cmH₂O vs 74.3 ± 30.7 cmH₂O, p = 0.839 among parous patients).

Table 4.

Maximum urethral closure pressure in patients with levator ani muscle-related pain, stratified by parity status

Nulliparous, n = 86
	Muscle pain n = 22	Entheseal pain n = 11	Muscle plus entheseal pain n = 53	p
MUCP, cmH2O	92.3 ± 36.3	88.9 ± 32.3	95.6 ± 28.1	0.778

Parous, n = 221
	Muscle pain n = 59	Entheseal pain n = 21	Muscle plus entheseal pain n = 141	p
MUCP, cmH2O	76.2 ± 32.4	78.0 ± 32.8	74.3 ± 30.7	0.839

MUCP = maximum urethral closure pressure, expressed as mean ± SD. Reference ranges from prior studies: nulliparous women (90-100 cmH₂O), cesarean delivery (80-90 cmH₂O), and vaginal delivery (70–80 cmH₂O).¹⁶

We next examined whether an association existed between MUCP and abnormal voiding patterns (Table 5). No significant correlation between MUCP and abnormal voiding patterns was observed between the three groups (NP group, p = 0.180; vaginal delivery group, p = 0.069; cesarean group: p = 0.230).

Table 5.

Association between maximum urethral closure pressure and abnormal voiding patterns, stratified by delivery mode

Delivery variable	Abnormal voiding patterns	No abnormal voiding patterns	p
Nulliparous no.	61	25
MUCP, cmH2O	96.80 ± 29.94	86.72 ± 31.61	0.180
Vaginal delivery no.	103	78
MUCP, cmH2O	77.67 ± 27.99	69.01 ± 29.94	0.069
Cesarean delivery no.	29	16
MUCP, cmH2O	81.79 ± 27.99	72.69 ± 21.47	0.230

MUCP = maximum urethral closure pressure, expressed as mean ± SD.

We also analyzed the correlation between abnormal voiding patterns and DO as shown in Table 6. No significant correlation was observed between the three pain groups, regardless of their parity status (NP group vs parous group: p = 0.460 vs p = 0.626). These findings suggest that abnormal voiding patterns are not associated with the presence of DO in patients with LAM-related pain.

Table 6.

Association between detrusor overactivity and abnormal voiding patterns in patients with levator ani muscle-related pain, stratified by parity status

	Voiding pattern in urodynamic testing			p
Nulliparous, n = 86
	Abnormal voiding patterns		No abnormal voiding patterns	p
DO (no.)	29		9	0.460
Without DO (no.)	32		16

Parous, n = 221
	Abnormal voiding patterns	No abnormal voiding patterns		p
DO (no.)	62		49	0.626
Without DO (no.)	66		44

DO = detrusor overactivity.

4. DISCUSSION

Patients who reported pain originating from the enthesis of the LAM had a significantly higher prevalence of LUTS than patients who reported pain originating from the muscle proper of the LAM. Nevertheless, no significant differences were observed in any urodynamic parameters, including cystometric and uroflowmetric parameters and urethral pressure measurements (all p > 0.05). These findings indicate that LAM-related pain does not alter the urinary tract structure or fundamental micturition physiology. Instead, the abnormalities observed in voiding perception may originate from central sensitization mechanisms.^17,18

Notably, direct comparison of patients with isolated muscle pain and those with isolated entheseal pain revealed no significant differences in the prevalence of LUTS or systemic pain-related comorbidities. This finding suggests that when pain is present in isolation, its anatomical origin (muscle belly vs enthesis) does not lead to distinct symptomatic phenotypes in this population. In the present study, patients with both muscle and entheseal pain consistently had the highest prevalence of subjective symptoms, such as postvoid residual sensation, PBS, systemic myofascial pain, and morning stiffness, which confirms the presence of an additive or potentially synergistic effect when multiple sources of pain coexist.^19,20 Despite this increased subjective symptom burden, no significant differences were observed in any objective urodynamic parameters between the three groups, which underscores a marked dissociation between patient-reported symptoms and objective measures of lower urinary tract function.

This persistent dissociation, characterized by pronounced symptoms in the absence of corresponding urodynamic abnormalities, strongly suggests that LUTS in this context are not primarily mediated by structural or functional changes in the bladder or urethra. Instead, our findings point toward central nervous system mechanisms, including nociceptive sensitization and altered sensory processing, as key contributors. Although entheseal involvement was associated with a higher prevalence of urinary frequency in the initial three-group comparison, this association was not corroborated by objective indices such as bladder sensation volumes. This discrepancy further supports the notion that subjective urinary frequency may reflect chronic pain states, heightened central arousal, or concomitant psychological factors, rather than diminished bladder capacity or increased peripheral sensory sensitivity.^17,18

Among all the patients in the present study, those with both muscle and entheseal pain exhibited the greatest symptom burden. This finding is clinically significant and suggests that the coexistence of muscular and entheseal pain may reflect a more severe or complex phenotype of chronic pelvic floor disorder, which potentially involves broader neuroinflammatory pathways or a higher degree of central sensitization. Overall, these results underscore the clinical importance of comprehensive palpation-based examinations to identify all potential sources of pain, which may collectively serve as a marker of increased symptom burden.

Patients with isolated entheseal pain had a lower prevalence of urinary incontinence compared with those with isolated muscle pain, despite having higher rates of other LUTS and systemic comorbidities. This may reflect a pain-induced guarding mechanism, wherein entheseal discomfort leads to compensatory pelvic floor contraction during stress to stabilize the area,^21,22 which in turn reduces leakage. Alternatively, entheseal pain pathology may selectively sensitize bladder afferents,²³ which in turn may precipitate urinary frequency and urgency without impairing urethral closure, in contrast to muscular pain, which may more directly affect sphincteric function. Further research with larger sample sizes and detailed incontinence subtyping is warranted to clarify this paradoxical finding.

Our analysis revealed no significant differences between the three pain groups in MUCP (p = 0.963). This lack of significance remained even after we adjusted for obstetric history variables (Table 4). These findings are consistent with those of another study,¹⁶ which reported that MUCP typically ranges from 90 to 100 cmH₂O in nulliparous women and from 70 to 80 cmH₂O in parous women after vaginal or cesarean delivery. Notably, none of the participants of the present study exhibited pelvic floor hypertonicity or impaired muscle relaxation secondary to LAM-related pain, regardless of whether the origin of their pain was muscular or entheseal. These findings further support that LAM-related pain does not result in measurable alterations in urethral sphincter function or pelvic floor contractility that can be detected through conventional urodynamic testing.

Patients with abnormal voiding patterns did not exhibit higher-than-normal MUCP values (Table 5), an observation that held even after we accounted for parity status and birth delivery mode. This result is consistent with our previous findings,^16,24 suggesting that the abnormal voiding patterns that we observed are unlikely to result from poor urethral relaxation or pelvic floor hypertonicity. In other words, LAM-related pain appears to primarily affect neurological sensation rather than muscle function. Moreover, no significant association was discovered between abnormal voiding patterns and DO, regardless of parity status (Table 6). This further supports the notion that LAM-related voiding dysfunction and DO may not be mechanistically linked to pelvic floor hypertonicity. Further research is required to more comprehensively examine the underlying pathophysiology.

Although the sensation of residual urine was more frequently reported in the overall enthesis-related pain cohort, this difference may be primarily driven by the high prevalence in the combined pain group. Nevertheless, the lack of corresponding urodynamic abnormalities supports the concept of cross-sensitization between entheseal pain and bladdery sensory nerves. Yoshikawa et al²⁵ described a similar pathological mechanism, arguing that enthesopathy may alter urination perception through distinct neuromuscular mechanisms. Additionally, Aredo et al²⁶ demonstrated that certain pelvic tendon entheses are richly innervated with substance P-positive nerve fibers, whose inflammatory mediators can directly activate bladder afferent nerves. Taken together, these findings suggest that urinary symptoms are more accurate than urodynamic parameters in reflecting the mechanisms underlying neuropathological pain in patients with LAM-related pain. Specifically, chronic pelvic floor pain appears to influence lower urinary tract function primarily through sensory nerve remodeling rather than through structural alterations.²⁷ This finding may explain the dissociation that we observed, wherein pain subtypes did not significantly affect objective urodynamic measures yet contributed to distinct subjective symptom profiles.

The significantly higher prevalence of morning stiffness in groups with entheseal involvement (ie, patients with either isolated entheseal pain or combined muscular and entheseal pain) warrants attention. Morning stiffness is a well-recognized marker of rheumatologic diseases,²⁸ and this finding in the current study may reflect the presence of localized inflammatory responses or systemic immune activation,²⁸ which underscores the importance of clinical screening for potential comorbid autoimmune diseases.²⁹ Notably, 30% to 50% of patients with CPP have undiagnosed rheumatologic disorders,^30,31 highlighting the clinical value of rheumatologic referral before the initiation of invasive pelvic treatment.³¹ Similarly, the higher prevalence of general MFP in patients with entheseal involvement may indicate overlapping pain mechanisms, such as central sensitization, fibromyalgia, or potential comorbid autoimmune diseases.²⁹ Despite having distinct underlying pathological mechanisms, enthesopathy and MFP may coexist and interact, which may in turn influence clinical presentations.¹⁹ MFP syndrome is typically localized to specific muscles,³² whereas enthesopathy is typically associated with widespread systemic MFP.^33,34 Increased awareness of these overlapping mechanisms is essential for comprehensive assessment and appropriate multidisciplinary management.

Although this study observed no significant differences between the groups in cystometric parameters (first sensation of bladder filling, normal desire to void, and maximum cystometric capacity), all measured values were lower than standard guideline averages.^35,36 This finding suggest that CPP, regardless of its anatomical origin, may be associated with a tendency toward reduced functional bladder capacity, potentially mediated by chronic afferent signaling or behavioral adaptation. Notably, this association appears to be independent of whether the pain arises from muscular or entheseal sources.

This study has several limitations. First, we did not quantitatively examine correlations between pain intensity and urodynamic parameters. This lack of quantitative symptom assessment (eg, through validated pain or LUTS scales) constrains the correlation between symptom intensity and urodynamic parameters or pain subtypes. Future studies incorporating validated instruments such as the Visual Analogue Scale (VAS) for pain or the Pelvic Pain and Urgency/Frequency (PUF) questionnaire would help elucidate whether symptom severity aligns with nociceptive sensitization patterns. Such data would strengthen the hypothesis that entheseal pain drives symptom perception through afferent sensitization, independent of detectable urodynamic changes. Second, our study cohort did not include a healthy control group. Although our cohort’s cystometric parameter values are lower than established guideline averages, the absence of a healthy, age-matched control group precludes definitive conclusions regarding whether LAM-related pain, regardless of it’s subtype, shifts urodynamic parameters away from a normative baseline. To address this limitation, future studies should include asymptomatic controls to establish reference ranges and better distinguish between pain-related changes and normal physiological variations. Third, we did not assess differences in treatment response.³⁷

In conclusion, this study demonstrates that entheseal pain of the LAM represents a distinct and clinically identifiable pain source in women with CPP. Although the LUTS associated with LAM entheseal pain are clinically comparable to those observed in LAM myofascial pain, the inability of urodynamic assessment methods to reliably differentiate between these entities indicates that these symptoms are unlikely to arise from peripheral structural or functional abnormalities of the lower urinary tract. Instead, the uniform dissociation observed between symptom severity and normal urodynamic findings across all pain subtypes supports the presence of a shared downstream mechanism, most probably central sensitization. Additionally, the specific association between entheseal pain and morning stiffness implies a divergent, potentially inflammatory, pathophysiological component. Accordingly, the diagnosis of LAM-related pain should primarily rely on targeted physical examination rather than on urodynamic testing. Moreover, future therapeutic strategies should incorporate approaches addressing this central neuropathic dimension, particularly in patients with combined pain phenotypes, who exhibit the greatest symptom burden.

ACKNOWLEDGMENTS

We would like to thank Ms. Yu-Chuan Tsai for her contribution to urodynamic examinations at Taipei Country Hospital. We would also like to thank Wallace Academic Editing for editing and proofreading this manuscript.