Abstract:Objective
To compare bladder sensitivity between pelvic pain and pain-free patients undergoing noninvasive, controlled bladder distension via diuresis. We also sought to measure potential mechanisms underlying bladder sensitivity.
Design
prospective observational study
Setting
community teaching hospital
Population
Reproductive-age women with non-bladder chronic pelvic pain (CPP, n=23), painful bladder syndrome (PBS, n=23) and pelvic pain-free controls (n=42)
Methods
Participants were compared on cysto… Show more
“…3c). Given their reduced bladder volumes 30 , BPS participants reached first urge more rapidly (36 ± 4 min) than dysmenorrheic participants (48 ± 1 min, p = 0.023). The difference in time to reach first urge with dysmenorrhea compared to healthy controls was minimal (55 ± 4 min, p = 0.094).Figure 2The three cohorts have different bladder pain sensitivities during bladder filling.…”
Menstrual pain, also known as dysmenorrhea, is a leading risk factor for bladder pain syndrome (BPS). A better understanding of the mechanisms that predispose dysmenorrheic women to BPS is needed to develop prophylactic strategies. Abnormal autonomic regulation, a key factor implicated in BPS and chronic pain, has not been adequately characterized in women with dysmenorrhea. Thus, we examined heart rate variability (HRV) in healthy (n = 34), dysmenorrheic (n = 103), and BPS participants (n = 23) in their luteal phase across a bladder-filling task. Both dysmenorrheic and BPS participants reported increased bladder pain sensitivity when compared to controls (p’s < 0.001). Similarly, dysmenorrheic and BPS participants had increased heart rate (p’s < 0.01), increased diastolic blood pressure (p’s < 0.01), and reduced HRV (p’s < 0.05) when compared to controls. Dysmenorrheic participants also exhibited little change in heart rate between maximum bladder capacity and after micturition when compared to controls (p = 0.013). Our findings demonstrate menstrual pain’s association with abnormal autonomic activity and bladder sensitivity, even two weeks after menses. Our findings of autonomic dysfunction in both early episodic and chronic visceral pain states points to an urgent need to elucidate the development of such imbalance, perhaps beginning in adolescence.
“…3c). Given their reduced bladder volumes 30 , BPS participants reached first urge more rapidly (36 ± 4 min) than dysmenorrheic participants (48 ± 1 min, p = 0.023). The difference in time to reach first urge with dysmenorrhea compared to healthy controls was minimal (55 ± 4 min, p = 0.094).Figure 2The three cohorts have different bladder pain sensitivities during bladder filling.…”
Menstrual pain, also known as dysmenorrhea, is a leading risk factor for bladder pain syndrome (BPS). A better understanding of the mechanisms that predispose dysmenorrheic women to BPS is needed to develop prophylactic strategies. Abnormal autonomic regulation, a key factor implicated in BPS and chronic pain, has not been adequately characterized in women with dysmenorrhea. Thus, we examined heart rate variability (HRV) in healthy (n = 34), dysmenorrheic (n = 103), and BPS participants (n = 23) in their luteal phase across a bladder-filling task. Both dysmenorrheic and BPS participants reported increased bladder pain sensitivity when compared to controls (p’s < 0.001). Similarly, dysmenorrheic and BPS participants had increased heart rate (p’s < 0.01), increased diastolic blood pressure (p’s < 0.01), and reduced HRV (p’s < 0.05) when compared to controls. Dysmenorrheic participants also exhibited little change in heart rate between maximum bladder capacity and after micturition when compared to controls (p = 0.013). Our findings demonstrate menstrual pain’s association with abnormal autonomic activity and bladder sensitivity, even two weeks after menses. Our findings of autonomic dysfunction in both early episodic and chronic visceral pain states points to an urgent need to elucidate the development of such imbalance, perhaps beginning in adolescence.
“…25 At baseline void and at each of these time points, the bladder volume was quantified with three-dimensional sonographic measurements (GE Voluson 750, Wauwatosa, WI), and participants rated their bladder pain and urgency on a 0–100 VAS on an iPad. 17 The average magnitude of experimental bladder pain was determined by the mean of the pain scores at first sensation, first urge, and maximum capacity.…”
Section: Methodsmentioning
confidence: 99%
“…16 Measures are stable when repeated a month later, closely resembling results in patients with classic BPS. 16,17 One underlying hypothesis for this finding is that repetitive episodes of dysmenorrhea promote cross-organ or central sensitization. This is supported by clinical observations 18 and experimentally in animal models of provoked uterine inflammation.…”
Women experiencing moderate-to-severe dysmenorrhea also harbor a higher pain response to naturally evoked bladder distension. Noninvasive bladder provocation needs to be tested further longitudinally in those with dysmenorrhea to characterize the course of visceral sensitivity and determine if it may help predict individuals at risk for developing subsequent pain in the bladder or elsewhere.
“…[72][73][74] Of note, Hellman and colleagues have recently used noninvasive bladder filling paradigms to identify that many women with heightened dysmenorrhea exhibit silent bladder pain sensitivity; this may be an opportunity to explore for identifying a preclinical phenotype conveying future IC/BPS risk. 75 Central sensitization is increasingly appreciated as a consequence and cause of bladder pain. Sites in the central nervous system, including the rostral ventromedial medulla (RVM), a suspected key regulator of descending sensory inhibition, are inappropriately activated in pathological pain states and facilitate greater transmission of noxious information through spinal cord tracts from persistently inflamed or previously sensitized viscera.…”
Interstitial cystitis/bladder pain syndrome is an uncommon but potentially devastating pelvic pain disorder affecting both women and men. This condition is often confusable and comorbid with other pelvic pain disorders. Although our understanding of the underlying pathophysiology is growing, the exact longitudinal course by which peripheral and central aberrations involving the bladder mucosa, peripheral inflammation, and central dysregulation of bladder sensitivity create painful bladder symptoms remains an area in need of further study. Only a limited number of drugs have been approved for treatment by the Food and Drug Administration, and overall durable efficacy of the many treatments reviewed in recent American Urological Association guidelines remains suboptimal, making awareness, early diagnosis, and use of effective treatments early in the disease course, where neural changes may still be reversible, imperative.
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