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1. Background
Chronic pelvic pain syndrome (CPPS) is defined as a multifactorial pain disorder that localizes to the anatomic pelvis, anterior abdominal wall at or below the umbilicus, the lumbosacral back or the buttocks. It is of sufficient severity to cause functional disability that may require medical care [1–6]. Structural and functional muscular abnormalities have been suggested as key features of CPPS pathogenesis, specifically hypertonicity of the pelvic floor muscles [7–10], trigger points (TrPs) in the vulvar area [11–13], and shortening of the levator muscles [14]. There are subgroups of CPPS including provoked vestibulodynia (PVD) referred to pain provoked by touch or during vaginal intercourse (dyspareunia) [15, 16] and painful bladder syndrome (PBS) characterized by pelvic pain and urinary storage symptoms (e.g., persistent urge to void, nocturia, and urinary frequency) [17, 18].
CPPS women also characterize by dysfunctional pain system as expressed by hypersensitivity of the peripheral and central pain systems, as well as dysfunctional pain modulation [3, 19–22] as well as psychological distress [23, 24], manifested as high levels of anxiety, pain catastrophizing, depression, and somatization [22, 25–33]. All these factors and the interplay between them may affect the severity of symptoms presented by chronic pain patients such as those with CPPS [34–36].
Hence, the present study is based on the biopsychosocial health model which links between biological, psychological, and social factors in understanding health and disease [37, 38]. From a biological point of view, this model refers to defects in parts and body parts and to functional impairment of body systems. In the psychological dimension, the model relates to the type of personality, attitudes and beliefs, ability to cope, and emotions such as fear, anxiety, depression, anger, and morbid behavior. In the social aspect, it relates to relationships with family members, friends, and work relations, the framework of work, medical advice, support frameworks, emotional and financial compensation, cultural factors, and socioeconomic factors. The perspective of this model serves to explore the complex mechanisms involved in chronic pain disease [39–41].
The dysfunctional pelvic floor muscle, whether originating from the lesioned muscular tissue or secondary to abnormal functioning of the pain system or psychological distress, is the target of physical therapy. This is mainly in the form of myofascial physical therapy (MPT) [42, 43]. MPT involves skillful, hands-on maneuvers directed towards relaxation, elongation, stretching, and massaging of tightened muscles, as well as the relief of myofascial tender points [44, 45]. In addition to these local effects on the pelvic floor, pain attenuation following MPT may be attributed to processes that occur at the systemic pain level, i.e., in the spinal and supraspinal structures. The latter include changes in the activity of the sympathetic nervous system and induction of pain inhibitory effects via supraspinal pathways [46, 47]. We have recently reported that MPT results in attenuation of vulvar pain and pain evoked at trigger points [48]. However, little is currently known on how MPT works and whether reductions in pain and clinical symptoms are associated with improved functioning of the pain system, as well as psychological well-being. The psychological factors, such as somatization, depression, and anxiety, were altered following pain reduction treatments and most often decreased [12, 22, 27, 36]. However, no studies have yet examined the changes of such parameters following MPT in CPPS patients.
The main goal of this prospective longitudinal preliminary study was to shed some light on the biopsychophysiological processes associated with MPT which lead to pelvic pain relief. Our investigational approach included a comprehensive evaluation of both local (morphological parameters of the levator ani pelvic floor muscle) and systemic changes (pain processing and modulation measures, as well as psychological factors) before and after MPT in CPPS patients. An additional goal was to assess the trajectory of the long-term pain relieving effects of MPT.
2. Methods
The data reported in this paper are part of a longitudinal study that examined the prediction and consequences of MPT in CPPS patients [48].
2.1. Study Participants
In this prospective longitudinal study, women diagnosed with CPPS were recruited from the Urogynecology and Pain Clinics at the Rambam Health Care Campus and the Sex Therapy Clinic at the Lis Maternity Hospital. The nontreated by MPT or any other treatment group included age-matched CPPS women (for more detailed information about the study cohort please refer Grinberg et al., 2017) [3]. Inclusion criteria for CPPS were as follows: age >18 years; for painful bladder syndrome (PBS) that is characterized by pelvic pain and urinary storage symptoms: urinary frequency ≥10 times per 24 hours, including one night-time voiding, and complaints of bladder pain ≥3 months [17, 18] for provoked vestibulodynia (PVD); and a distressing genital pain condition provoked by touch and one of the most common causes of pain during intercourse (dyspareunia) in premenopausal women [15, 16]: pain intensity during intercourse ≥4 on a 0–10 numerical pain scale (NPS) during the previous month. Patients were excluded from the study if they had a history of pelvic cancer or radiation therapy; had undergone pelvic or abdominal surgery; suffered from a urinary tract infection within the last month; or had fibromyalgia, irritable bowel syndrome, a neurological disorder, diabetes, or pregnancy. Sociodemographic and medical data including age, marital status, religion, employment status, duration of CPPS symptoms, and pharmacological treatments were recorded.
2.2. Experimental Procedure
The Rambam Medical Center (Haifa, Israel) Review Board, in accordance with the Helsinki Declaration and the IRB of the Haifa University, approved the study. All participants received detailed explanation and provided written informed consent before the start of any testing procedure. All subjects who agreed to participate in the study were instructed to adhere to the study protocol and did not take any medication during treatment. All women were diagnosed by a physician experienced in the field of urogynecology and dyspareunia who performed the clinical evaluation of the pelvic floor and the assessment of vulvar pain (LL and LA). Morphologic assessment of the levator ani was performed by a gynecologist specializing in ultrasonography of the pelvic floor. The psychophysical experimental procedure was conducted during the morning hours by the same investigator (KG) in the Laboratory of Clinical Neurophysiology at the Faculty of Medicine of the Technion (Haifa, Israel).
Women were initially exposed to a training session in order to familiarize them with the psychophysical tests. Thereafter, they completed the sociodemographic and medical history forms and clinical pain and urinary symptoms questionnaires, as well as the psychological questionnaires. They then underwent the psychophysical pain tests. This battery of tests was repeated again on the same women after completion of the 8 weekly session of MPT.
The study’s long-term follow-up was performed after 3 months and again after 9 months (since the end of the treatment). At both time points, patients report their level of pelvic pain intensity using the 0–10 numerical pain scale (NPS) where 0 indicated “no pain” and 10 represented “the worst pain imaginable.” CPPS patients who had enrolled in the first stage of the study but decided not to have MPT served as the nontreated group. They were also asked to similarly report their 0–10 level of pelvic pain intensity at 3 and 9 months following the baseline evaluation session.
2.3. Clinical Evaluation of Symptom Severity
The severity of urgency symptoms among the PBS patients was assessed using the validated Hebrew version of the Urgency, Severity, and Impact life Questionnaire (USIQ) [20]. This questionnaire consists of 13 Likert scale items relating to the intensity of urgency symptoms and the severity of frequency symptoms, as well as the impact of these symptoms on daily life. The α Cronbach of the Hebrew version is 0.85–0.90.
The study’s approach to evaluating the severity of vulvar pain symptoms and evaluation pain evoked at pelvic TrPs has been detailed in an earlier report [49].
2.4. Morphologic Assessment of the Levator Ani
The length and width of the levator ani muscle was measured by using a specially designed 3D endovaginal ultrasound (BK Medical Ultrafocus machine (Peabody, MA)), device at a frequency of 4–8 MHz, as depicted in Figure 1. This ultrasound imaging was performed while the women was laying in the dorsal lithotomy position and with the hips flexed and slightly abducted, when a probe is inserted into the vagina. No preparation was required, and the patients were recommended to have a comfortable volume of urine in the bladder. This assessment was performed before and after the MPT by a gynecologist who specializes in ultrasonography evaluation. This test has been extensively described in the article of Rostamina et al. and found to be reliable [49].
[figure omitted; refer to PDF]
2.5. Psychophysical Assessment of Pain
In order to examine the changes in pain sensitivity at the spinal and supraspinal level following MPT, noxious stimuli were delivered to the suprapubis area and forearm, respectively. Notably, no side effect was observed after psychophysical testing. The battery of psychophysical tests (see Grinberg et al., 2017) [3] are as follows:
2.5.1. Mechanical Pain Threshold (MPT)
This was assessed at the referred area (i.e., the suprapubis area) by using von Frey hairs filaments (VFH; Stoeteling Ltd., USA) that evoke pinprick sensation, using the method of levels in an ascending order starting from the lightest VFH force of 3.7 g [50]. The lightest gram weight filament that evoked pain sensation in two out of three trials was considered to be the MPT.
2.5.2. Heat Pain Threshold (HPT)
This was measured via the thermal sensory analyzer (TSA, Medoc, Ramat Yishay, Israel) with a 30 × 30 mm probe, which delivers a contact heat stimulus. Patients received three successive ramps of gradually increasing temperatures delivered to the volar forearm of their dominant hand according to the method of limits [51]. The mean of three successive responses whose variance was less than 0.5°C was calculated as the HPT.
2.5.3. Magnitude Estimation of Painful Mechanical Stimulus
Three stimuli were delivered with a 225 g VFH to the suprapubis area, and women were asked to rate the level of pain intensity on a 0–100 NPS. An average of the three pain ratings was defined as the suprathreshold pain rating.
2.5.4. Magnitude Estimation of Tonic Heat Pain (THP) Stimulation
A thermal stimulus at a temperature perceived to be an intensity of pain rated 50 on a 0–100 NPS (i.e., “pain 50” intensity) was applied to the volar forearm of the dominant hand for one minute. The mean ratings (NPS) of pain at 5, 25, 40, and 55 sec were defined as the suprathreshold pain.
Temporal summation of pain , a sensory phenomenon that represents central sensitization and the functioning of the facilitatory pain pathways:
(a)
Mechanical Temporal Summation (mTS).Two series of 10 repetitive stimuli with a 160 g VFH were applied to the suprapubis with 2-3 sec interstimulus intervals. The differences in 0–100 NPS pain scores between the last and the first stimulus were calculated for each series and averaged across series to calculate the mTS.
(b)
Heat Temporal Summation (hTS). Magnitude was calculated as the difference between the last (at 55 sec) and first 0–100 NPS pain scores (at 5 sec) that were given during the one minute of THP.
2.5.5. The Conditioned Pain Modulation Paradigm (CPM)
This is an advanced psychophysical paradigm to test the efficacy of a dominant supraspinal descending endogenous analgesia mechanism, namely diffuse noxious inhibitory control (DNIC) [51, 52]. This mechanism is based on the “pain inhibits pain” phenomenon, which requires a remote noxious “conditioning stimulus” for pain attenuation of the “test stimulus.” The test stimulus was the 60 sec THP described above. The conditioning stimulus was a 90 sec immersion of the nondominant hand in a hot water bath (46.5°C) (Heto Cooling Bath, Jouan Nordic A/S, Allerod, Denmark). The test stimulus was first given alone, and pain ratings were obtained every 10 sec. After a 10 min break (to allow for nociceptor recovery to resting state), the patients were exposed to the conditioning stimulus for 30 sec after which they immediately rated the pain intensity of the hot water. Then, concomitantly with the conditioning stimulus (hot water bath), the same test stimulus was delivered again and pain ratings of the test stimulus were again recorded every 10 sec. The CPM effect was calculated as the average pain rating for the test stimulus given with the conditioning stimulus minus the average pain rating of the test stimulus given alone. A negative CPM value was considered to indicate effective endogenous pain modulation.
2.6. Psychological Evaluation
Participants completed a battery of psychological questionnaires including (i) the State-Trait Anxiety Inventory [53] using the validated Hebrew version [54]. The first part of the questionnaire assesses the level of state anxiety, and the second part assesses trait anxiety. Each part includes 20 statements that describe the emotional condition (reliability of 0.82–0.91). CPPS patients were asked to rate their feelings about each sentence on a 4 point Likert scale; (ii) the Hebrew version of the Brief Symptom Inventory (BSI) [55], translated by Canetty et al. [56], which assesses the level of somatization symptoms and consists of 13 self-report questions on psychological distress, (reliability of 0.78–0.91); (iii) the Hebrew version of the Pain Catastrophizing Scale (PCS) [57, 58]. This questionnaire includes 13 items representing the three components of pain catastrophizing: rumination, magnification, and helplessness. Items were rated on a Likert scale ranging from 0 (not at all) to 4 (all the time) with a total score range from 0 to 52, (reliability of 0.86); and (iv) the Beck Depression Inventory (BDI), which assesses both the cognitive and affective symptoms of depression [59]. In the BDI, a score of 0–9 is normal, 10–18 means mild depression, scores of 19–26 represent moderate depression, and scores over 26 are considered to indicate severe depression symptoms (reliability of 0.84).
2.7. MPT Intervention
MPT was carried out with the goal to restore pelvic floor muscle length and strength; release TrPs in the muscles and connective tissues of the pelvic floor, pelvic girdle, and abdomen, using pelvic massages (performed by a specialist woman physiotherapist) [60, 61]; and improve blood flow to the pelvic area [62]. Specifically, the MPT intervention included myofascial TrPs release and connective tissue manipulation techniques (manual stretching of the trigger point region and myofascial release). [63]. Furthermore, during treatment, the women also learned control skills and how to self-train their pelvic muscles to contract and relax [64–66]. In this study, the women were scheduled for 8 weekly 1 hour treatments with one specialist pelvic physical therapist. In addition, the patients were asked to perform a minimum of two self exercises at home (every week) in order to maximize the treatment effect and maintained a self diary. The subjective effectiveness of the MPT treatment was examined 3 and 9 months following treatment termination by asking the women to rate their responses on a 0–10 scale where 0 indicated no improvement at all and 10 represented the most effective response. As mentioned previously, the pain intensity was also examined in this period (3 and 9 months following treatment termination) using the 0–10 NPS scale.
2.8. Statistical Analysis
Statistical analyses were performed using SPSS version 23 (SPSS Inc., Chicago, IL). Paired t-tests were used to examine the differences before and after MPT regarding the anatomical muscle changes. MANOVA repeated measure tests were carried out to examine the differences between the experimental pain parameters and the psychological measures following MPT. In addition, a repeated measure ANOVA followed by preplanned contrasts were conducted to examine differences in pelvic pain scores between women with CPPS who received MPT compared with CPPS women who did not receive MPT. To compare difference in the mean difference in the pain score between the before-and-after values between groups who did and did not undergo MPT, ANOVA test was used (for example, pain at 3 and 9 months, with a variable taking into account baseline pain and a variable for the treatment group). Paired t-tests were carried out to examine the differences between the anatomical structure of the levator ani muscle before and after MPT treatment. All statistical tests were corrected for multiple analyses using Bonferroni correction;
3. Results
3.1. Clinical Characteristics of the Patient Population
The sample included 39 CPPS patients (21 with PBS and 18 with PVD) who underwent MPT and 11 nontreated CPPS patients. The mean age of the study group was 37.9 ± 15.4 years (range 22–67 years). The mean disease duration was 5.5 ± 9 years (range 1–30 years). As previously reported, there were no significant differences between PBS and PVD patients neither in their clinical pain ratings and consequent effects on daily functioning nor in their psychophysical and psychological parameters (
3.2. Changes in Outcome Measures following MPT
In line with the reduction in the severity of clinical pain that was recently reported [48], a reduction in USIQ scores was also observed (18.1 ± 4.1 before MPT versus 13.6 ± 3.4 after MPT;
A significant correlation was found between the change in the pain test (CPM test) and the change in the muscle length (r = 0.661,
3.3. Changes in Psychophysical Parameters
MPT significantly impacted the experimental pain parameters as shown from analyzing the changes before and after treatment. Specifically significant reductions in pain sensitivity were observed (F(10, 27) = 5.26,
Table 1
Differences in experimental pain parameters before and after MPT.
Pre-MPT | Post-MPT | Mean difference | F |
|
|
---|---|---|---|---|---|
MPT (gr.) | 5.6 ± 0.5 | 5.7 ± 0.4 | 0.1 | 1.90 | 0.17 |
1st supra-m (NPS) | 29.7 ± 20.5 | 20.7 ± 15.6 | −9.0 | 12.50 | 0.001 |
10th supra-m (NPS) | 41.8 ± 25.5 | 31.3 ± 21.3 | −10.5 | 15.20 | 0.000 |
mTS (NPS) | 10.3 ± 15.2 | 12.2 ± 20.3 | 1.9 | 0.24 | 0.62 |
HPT (°C) | 41.1 ± 2.8 | 41.9 ± 2.7 | 0.8 | 4.81 | 0.035 |
Pain 50 (°C) | 42.7 ± 2.3 | 43.2 ± 2.2 | 0.5 | 10.60 | 0.002 |
Contact THP (NPS) | 46.1 ± 13.3 | 45.6 ± 14.2 | −0.5 | 0.06 | 0.05 |
Immersion THP (NPS) | 67.0 ± 37.9 | 72.8 ± 30.7 | 5.8 | 1.50 | 0.12 |
CPM (NPS) | −0.2 ± 13.9 | 13.8 ± 12.2 | 14 | 34.90 | 0.000 |
Data are shown as mean ± standard deviation. MPT, mechanical pain threshold; 1st supra-m, the mean pain rating of the first mechanical stimuli; 10th supra-m, the mean pain rating of the tenth mechanical stimuli; HPT, heat pain threshold; NPS, 0–100 numerical pain scale; mTS, mechanical temporal summation; hTS, heat temporal summation; Pain 50, the temperature that induces a pain of 50/100 on the NPS; Contact THP, the mean pain rating from the tonic heat stimulus of the thermal sensory probe; Immersion THP, the mean pain rating from the tonic heat stimulus of the hot-water bath; CPM, conditioned pain modulation.
3.4. Changes in Psychological Parameters
MPT significantly improved all pain-related psychological parameters before and after MPT (F(5,32) = 5.72,
Table 2
Differences in psychological factors before and after MPT.
Pre-MPT | Post-MPT | Mean difference | F |
|
|
---|---|---|---|---|---|
Anxiety state | 49.4 ± 7.0 | 46.6 ± 4.9 | −2.8 | 4.42 | 0.043 |
Anxiety trait | 47.7 ± 4.8 | 46.0 ± 5.0 | −1.7 | 4.62 | 0.038 |
PCS | 26.2 ± 13.0 | 21.2 ± 12.2 | −5.0 | 7.32 | 0.001 |
BSI | 13.4 ± 8.7 | 10.1 ± 6.5 | −3.3 | 15.77 | 0.000 |
BDI | 12.0 ± 6.8 | 8.0 ± 6.3 | −4.0 | 17.72 | 0.000 |
Data are shown as mean ± standard deviation. Anxiety state and anxiety trait, from the State-Trait Anxiety Inventory; PCS, pain catastrophizing scale; BSI, brief symptom inventory; BDI, beck depression index.
3.5. Changes in Anatomical Measures
Due to technical problems, data were obtained from only 11 women who were available for the ultrasonographic analysis. An increase in the width of the levator ani (t = 2.28,
Table 3
Anatomical structural differences before and after MPT.
Pre-MPT (N = 11) | Post-MPT (N = 11) | Mean difference | T |
|
|
---|---|---|---|---|---|
Levator ani length (cm) | 5.7 ± 0.7 | 5.2 ± 0.8 | −0.5 | 1.77 | 0.11 |
Levator ani width (cm) | 4.3 ± 0.7 | 4.8 ± 0.9 | 0.5 | 2.28 | 0.04 |
Data are shown as mean ± standard deviation.
3.6. The Long-Term Effects of MPT on Clinical Pain
Repeated measure ANOVA showed significant improvement in self reports of pelvic pain intensity 3 and 9 months following up MPT as compared with baseline pain intensity (F(1, 47) = 7.004,
Table 4
Differences in pain scores (after 3 and 9 months) of women with CPPS who received MPT compared with women with CPPS who did not receive MPT.
CPPS with MPT (N = 39) | CPPS with no MPT (N = 11) | Mean difference | F |
|
|
---|---|---|---|---|---|
NPS at baseline | 7.6 ± 1.4 | 6 ± 1.2 | −1.6 | 3.25 | 0.31 |
NPS at 3 months | 4.4 ± 2.3 | 6.5 ± 1.5 | 2.1 | 2.91 | 0.005 |
NPS at 9 months | 4.1 ± 1.5 | 5.9 ± 1.2 | 1.8 | 3.70 | 0.01 |
Data are shown as mean ± standard deviation. NPS at 3 months, clinical pain ratings after 3 months on a 0–10 numerical pain scale; NPS at 9 months, clinical pain ratings after 9 months on a 0–10 numerical pain scale. There was a significant improvement in clinical pain scores among women receiving MPT compared to women with CPPS who did not undergo any treatment, as assessed at 3 and 9 months.
[figure omitted; refer to PDF]4. Discussion
PVD and PBS represent subgroups of CPPS. They have shared characteristics including muscular abnormalities, a dysfunctional pain system, and psychological distress [3], suggesting a common mechanism-based treatment strategy. Thus, this preliminary study was aimed at investigating how MPT, a pelvic floor-focused treatment, is able to affect biopsychological measures and alleviate symptom severity in women with CPPS from PVD or PBS. The results indicate that MPT has anatomical, neurophysiological, and psychological therapeutic effects alongside long-lasting pelvic pain alleviation. Specifically, MPT works on relieving hypertonicity, reduces the sensitivity to experimental pain, improves the functionality of the endogenous inhibitory system, and decreases psychological distress (i.e., state and trait anxiety levels, pain catastrophizing, somatization, and depressive symptoms). These systemic effects position MPT as a multisystemic therapeutic intervention for patients with CPPS.
Evidence suggests that the MPT approach improves blood flow to the pelvic region and involves the releasing of TrPs [45, 67]. MPT has also been shown to normalize muscle tone, flex the connective and soft tissue around the joints of the pelvic floor, and strengthen the pelvic girdle muscles [45, 68–75]. The fact that women in the current study who were not treated by MPT showed no significant reduction in their clinical pain intensity after 3 and 9 months reinforces the assumption that the short- and long-term effects of MPT cannot be attributed solely to a placebo effect [45, 76]. The combined positive effects on anatomical, neurophysiological, and psychological processes associated with MPT are revealed for the first time in this study.
The anatomical effect of MPT on the width of the levator ani muscle supports the improvements seen in the clinical picture. The levator ani plays a role in supporting the pelvic organs and the functional mechanism of the sphincters. Physical therapy to the pelvic region was focused on imparting patient control of the muscle relaxation and contraction processes, which may contribute to improving muscle relaxation and consequently to changing the muscle width. The literature supports such a causative linkage, as studies have reported a lengthening of the levator ani muscle following MPT in CPPS patients that was correlated with the degree of improvement in clinical pain ratings [45, 77, 78]. The current study did not compare the muscle length and width between women with CPPS and healthy women, which eliminates the possibility to derive any conclusions about a possible anatomical impairment in the muscle prior to the intervention. Yet, it has been suggested that an anatomical defect is one of the mechanisms underlying CPPS that may arise due to stress situations, past events, or perhaps originate from an organic, anatomical, or morphological impairment [4, 32]. An indirect indicator of the anatomical defect might be represented by increased pain ratings in response to contact stimuli at the TrPs, as previously reported in other studies [20, 21], as well as on this cohort [48]. Our findings of reduced pain hypersensitivity following MPT [48], accompanied by the morphological enlargement of the levator ani, may suggest that this anatomical change also contributes to the reduced sensitivity of TrPs.
MPT also affected the systemic pain sensitivity to experimental pain measures. Specifically, we observed an increase in pain thresholds and a decrease in pain ratings in response to noxious stimulation in referred and remote body areas. Two possible central mechanisms may be involved in this treatment-induced plasticity. Firstly we suggest that MPT decreases the level of central sensitization, where sensitization of neurons at the spinal and supraspinal levels contributes to the development and maintenance of referred and remote pain, respectively [79, 80]. It is therefore a fair assumption that in this study, MPT diminished the degree of hypersensitivity at the local level (the pelvic soft tissue), as expressed by a reduction in evoked pain (e.g., TrPs), and thus reduced nociceptive input to the central pain system. The diminished barrage of nociceptive information may have consequently resulted in decreased sensitization at the spinal and supraspinal levels as manifested by the reduced pain sensitivity at referred and remote body areas [20, 81–83].
The second suggested central mechanism is based on the improved endogenous inhibitory capacity following MPT, as demonstrated by an increased CPM response. CPM is the experimental paradigm to test diffuse noxious inhibitory control (DNIC), a descending system that induces top-down modulation on the nociceptive neurons at the spinal level, resulting in a systemic inhibitory effect and pain alleviation. Research has indicated a dysfunctional DNIC system in CPPS [3, 21, 83, 84] and other idiopathic pain conditions [85, 86]. Notably, interventions aimed at pain alleviation (i.e., surgical and pharmacological) have the capability to restore the functioning of the endogenous inhibitory system [85]. For example, Kosek and Ordeberg [87] identified a restoration of the DNIC system in osteoarthritis patients who underwent hip or knee surgery and reported significant pain relief. These results suggest that the dysfunctional pain inhibition is maintained over time by ongoing pain and when the pain is extinguished, and DNIC function may be restored resulting in an attenuation of pain sensitivity. We therefore suggest that following MPT treatment, improved CPM functionality was observed in our patients, probably due to a reduction in the ongoing pain, and such enhanced inhibitory activity contributed to the reduction in the clinical pain.
MPT was also associated with psychological benefits in our patient cohort, as expressed by a reduction in psychological distress and a decrease in the level of state and trait anxiety, as well as decreased ratings of depression, catastrophizing, and somatization after treatment. Previous studies indicate that a reduction in psychological distress can alleviate pain. For example, a decrease in fear, anxiety, and catastrophic thoughts is able to reduce negative feelings and somatic complaints and may affect the response to experimental and clinical pain [36, 58, 88–90]. Furthermore, high levels of catastrophizing have been attributed to clinical pain intensity and experimental pain sensitivity [34, 55, 91, 92]. The literature thus supports the present study’s findings of improved pain-related personality factors in parallel with reduced clinical and experimental pain parameters. Conversely, it is also possible that the chain of events is in the opposite direction and that the reduction in clinical pain improved the psychological distress.
It is important to note an additional perspective to interpreting the observed results of MPT in CPPS patients, namely, the patient-physiotherapist relationship. This may hold therapeutic effects that are above and beyond the direct local influence on the muscular system [45, 69]. Such relationships may involve instilling a sense of control, security, and trust, as well as self-efficacy [93], which are invaluable in improving clinical outcomes of chronic pain disorders. Furthermore, frustration resulting from the failure of previous treatments may have led women to develop negative thoughts in relation to their disease, which also manifested as catastrophic thinking when relating to their pain [94]. An appropriate treatment is therefore likely to reduce such catastrophizing and indeed following MPT, improvements were found in the current study on this psychological factor. Lowered catastrophizing thinking may be also achieved due to the improvement of the patients’ ability to voluntarily contract and relax the pelvic floor muscles and thus control urine functioning. This leads to the adaption of more efficient coping strategies as well as a better sense of control. With regard to the biopsychosocial model, it is therefore likely that MPT also has cognitive-psychological effects that may improve CPPS symptoms beyond its physical influence.
Several limitations that may influence the significance of the findings should be addressed. First, the relatively small sample size limits the generalization of our findings given the variability in psychophysical and pain-related personality measures. The small sample size was due to the restrictive inclusion criteria which reduced the number of CPPS patients that could be enrolled. Second, due to the fact that the 11 women who did not undergo MPT were not randomly selected and that their assignment to this group was based solely on their reports of clinical CPPS symptoms, this nontreated group is not a “true” control group. In order to present an understanding of the mechanistic processes, a real randomized control group should be obtained and tested with both psychophysical and psychological measures. Therefore, the significance of the findings should be carefully interpreted relating to this pilot study. It cannot be ignored that the ability to make decisive conclusions from the findings of this pilot study is limited.
5. Conclusions
This study sheds light on the indirect neurophysiological and psychological effects of MPT that occurred together with pain alleviation and improvement in functioning. The peripherals and systemic effects of MPT position it as a multisystemic therapeutic intervention for patients with CPPS. This suggestion is in line with the notion that CPPS is a multifactorial and complex pain disorder comprised of multiple biopsychosocial components. Therefore, an intervention such as MPT that has multisystemic effects can be recommended as a mechanism-based intervention for CPPS patients. We suggest that future randomized control studies conducted on larger cohorts of patients may allow the reliability of our results to be addressed.
Additional Points
Myofascial manual therapy induces anatomical, neurophysiological, and psychological effects in chronic pelvic pain patients.
Ethical Approval
This study was approved by the Rambam Medical Center Review Board in accordance with the Helsinki Declaration.
Consent
All participants in the study were over 18 years of age and provided written informed consent.
Authors’ Contributions
All authors contributed to the study design. Prof. Lowenstein and Drs. Abramov and Grinberg performed the data collection. Prof. Granot, Dr. Weissman-Fogel, and Dr. Grinberg analyzed the data and wrote the manuscript, and all authors edited it. All authors have read and approved the final manuscript.
Acknowledgments
The authors would like to thank Dr. Ruth Moont for reviewing and editing this manuscript. This study was sponsored by the Chief Scientist Office, Israeli Ministry of Health Grant (300000-7495), and the Israel Pain Association Grant.
Glossary
Abbreviation
CPPS:Chronic pelvic pain syndrome
MPT:Myofascial physical therapy
TrPs:Trigger points
PVD:Provoked vestibulodynia
PBS:Painful bladder syndrome
NPS:Numerical pain scale
USIQ:Urgency, severity, and impact life questionnaire
MPT:Mechanical pain threshold
VFH:Von Frey hairs
HPT:Heat pain threshold
TSA:Thermal sensory analyzer
THP:Tonic heat pain
mTS:Mechanical temporal summation
hTS:Heat temporal summation
CPM:Conditioned pain modulation paradigm
DNIC:Diffuse noxious inhibitory control
BSI:Brief symptom inventory
PCS:Pain catastrophizing scale
BDI:Beck depression inventory.
[1] A. Ahangari, "Prevalence of chronic pelvic pain among women: an updated review," Pain Physician, vol. 17 no. 2, pp. 41-47, 2014.
[2] D. S. Engeler, A. P. Baranowski, P. Dinis-Oliveira, "The 2013 EAU guidelines on chronic pelvic pain: is management of chronic pelvic pain a habit, a philosophy, or a science? 10 years of development," European Urology, vol. 64 no. 3, pp. 431-439, DOI: 10.1016/j.eururo.2013.04.035, 2013.
[3] K. Grinberg, M. Granot, L. Lowenstein, L. Abramov, I. Weissman-Fogel, "A common pronociceptive pain modulation profile typifying subgroups of chronic pelvic pain syndromes is interrelated with enhanced clinical pain," Pain, vol. 158 no. 6, pp. 1021-1029, DOI: 10.1097/j.pain.0000000000000869, 2017.
[4] J. F. Steege, M. T. Siedhoff, "Chronic pelvic pain," Obstetrics & Gynecology, vol. 124 no. 3, pp. 616-629, DOI: 10.1097/aog.0000000000000417, 2014.
[5] R. W. Stones, Y. C. Cheong, F. M. Howard, S. Singh, "Interventions for treating chronic pelvic pain in women (Review)," Cochrane Database of Systematic Reviews, vol. 11,DOI: 10.1002/14651858.cd000387, 2010.
[6] H. Twiddy, A. Bradshaw, R. Chawla, S. Johnson, N. Lane, "Female chronic pelvic pain: the journey to diagnosis and beyond," Pain Management, vol. 7 no. 3, pp. 155-159, DOI: 10.2217/pmt-2016-0052, 2017.
[7] R. U. Anderson, T. Sawyer, D. Wise, A. Morey, B. H. Nathanson, "Painful myofascial trigger points and pain sites in men with chronic prostatitis/chronic pelvic pain syndrome," Journal of Urology, vol. 182 no. 6, pp. 2753-2758, DOI: 10.1016/j.juro.2009.08.033, 2009.
[8] E. Reissing, C. Brown, M. Lord, Y. Binik, S. Khalifé, "Pelvic floor muscle functioning in women with vulvar vestibulitis syndrome," Journal of Psychosomatic Obstetrics & Gynecology, vol. 26 no. 2, pp. 107-113, DOI: 10.1080/01443610400023106, 2005.
[9] G. White, M. Jantos, H. Glazer, "Establishing the diagnosis of vulvar vestibulitis," Journal of Reproductive Medicine, vol. 42 no. 3, pp. 157-160, 1997.
[10] F. F. Tu, J. Holt, J. Gonzales, C. M. Fitzgerald, "Physical therapy evaluation of patients with chronic pelvic pain: a controlled study," American Journal of Obstetrics and Gynecology, vol. 198 no. 3, pp. 272.e1-277.e7, DOI: 10.1016/j.ajog.2007.09.002, 2008.
[11] R. Bassaly, N. Tidwell, S. Bertolono, L. Hyte, K. Downes, S. Hats, "Myofascial pain and pelvic floor dysfunction in patients with interstitial cystitis," International Urogynecology Journal, vol. 22 no. 4, pp. 413-418, DOI: 10.1007/s00192-010-1301-3, 2011.
[12] L. Lowenstein, K. Kenton, E. R. Mueller, "Patients with painful bladder syndrome have altered response to thermal stimuli and catastrophic reaction to painful experiences," Neurourology and Urodynamics, vol. 28 no. 5, pp. 400-404, DOI: 10.1002/nau.20676, 2009.
[13] A. James, J. Thompson, P. Neumann, K. Briffa, "Change in pain knowledge occurring after a neuroscience education seminar for women with chronic pelvic pain," Australian & New Zealand Continence Journal, vol. 22 no. 4, pp. 90-91, 2016.
[14] K. M. Peters, D. J. Carrico, S. E. Kalinowski, I. A. Ibrahim, A. C. Diokno, "Prevalence of pelvic floor dysfunction in patients with interstitial cystitis," Urology, vol. 70 no. 1, pp. 16-18, DOI: 10.1016/j.urology.2007.02.067, 2007.
[15] L. A. Broto, L. A. Sadownik, S. Thomson, "A comparison of demographic and psychosexual characteristics of women with primary versus secondary provoked vestibulodynia," The Clinical Journal of Pain, vol. 14 no. 30, pp. 428-443, DOI: 10.1097/ajp.0b013e31829ea118, 2014.
[16] B. D. Reed, L. J. Legocki, M. A. Plegue, A. Sen, H. K. Haefner, S. D. Harlow, "Factors associated with vulvodynia incidence," Obstetrics & Gynecology, vol. 123 no. 2, PART 1, pp. 225-231, DOI: 10.1097/aog.0000000000000066, 2014.
[17] C. Cheng, A. Rosamilia, M. Healey, "Diagnosis of interstitial cystitis/bladder pain syndrome in women with chronic pelvic pain: a prospective observational study," International Urogynecology Journal, vol. 23 no. 10, pp. 1361-1366, DOI: 10.1007/s00192-012-1711-5, 2012.
[18] N. F. Davis, C. M. Brady, T. Creagh, "Interstitial cystitis/painful bladder syndrome: epidemiology, pathophysiology and evidence-based treatment options," European Journal of Obstetrics & Gynecology and Reproductive Biology, vol. 175, pp. 30-37, DOI: 10.1016/j.ejogrb.2013.12.041, 2014.
[19] M. Garnot, "Personality traits associated with perception of noxious stimuli in women with vulvar vestibulitis syndrome," The Journal of Pain, vol. 6 no. 3, pp. 168-173, DOI: 10.1016/j.jpain.2004.11.010, 2005.
[20] L. Lowenstein, M. P. Fitzgerald, K. Kenton, "Evaluation of urgency in women, with a validated urgency, severity and impact questionnaire (USIQ)," International Urogynecology Journal, vol. 20 no. 3, pp. 301-307, DOI: 10.1007/s00192-008-0770-0, 2009.
[21] L. Lowenstein, Y. Vardi, M. Deutsch, "Vulvar vestibulitis severity- assessment by sensory and pain testing modalities," Pain, vol. 107 no. 1-2, pp. 47-53, DOI: 10.1016/j.pain.2003.09.012, 2004.
[22] J. J. D. M. Van Lankveld, M. Granot, W. C. M. Weijmar Schultz, "Women’s sexual pain disorders," The Journal of Sexual Medicine, vol. 7 no. 1, pp. 615-631, DOI: 10.1111/j.1743-6109.2009.01631.x, 2010.
[23] N. Adams, L. Field, "Pain management 1: psychological and social aspects of pain," British Journal of Nursing, vol. 10 no. 14, pp. 903-911, DOI: 10.12968/bjon.2001.10.14.5277, 2001.
[24] J. J. Kutch, F. F. Tu, "Altered brain connectivity in dysmenorrhea," Pain, vol. 157 no. 1,DOI: 10.1097/j.pain.0000000000000364, 2016.
[25] R. Basson, "The recurrent pain and sexual sequelae of provoked vestibulodynia: a perpetuating cycle," The Journal of Sexual Medicine, vol. 9 no. 8, pp. 2077-2092, DOI: 10.1111/j.1743-6109.2012.02803.x, 2012.
[26] G. Desrochers, S. Bergeron, T. Landry, M. Jodoin, "Do psychosexual factors play a role in the etiology of provoked vestibulodynia? A critical review," Journal of Sex & Marital Therapy, vol. 34 no. 3, pp. 198-226, DOI: 10.1080/00926230701866083, 2008.
[27] M. Granot, Y. Lavee, "Psychological factors associated with perception of experimental pain in vulvar vestibulitis syndrome," Journal of Sex & Marital Therapy, vol. 31 no. 4, pp. 285-302, DOI: 10.1080/00926230590950208, 2005.
[28] M. Khandker, S. S. Brady, A. F. Vitonis, R. F. MacLehose, E. G. Stewart, B. L. Harlow, "The influence of depression and anxiety on risk of adult onset vulvodynia," Journal of Women’s Health, vol. 20 no. 10, pp. 1445-1451, DOI: 10.1089/jwh.2010.2661, 2011.
[29] J. C. Nickel, D. Shoskes, K. Irvine-Bird, "Clinical phenotyping of women with interstitial cystitis/painful bladder syndrome: a key to classification and potentially improved management," Journal of Urology, vol. 182 no. 1, pp. 155-160, DOI: 10.1016/j.juro.2009.02.122, 2009.
[30] M. M. Kuile, P. T. M. Weijenborg, P. Spinhoven, "Sexual functioning in women with chronic pelvic pain: the role of anxiety and depression," The Journal of Sexual Medicine, vol. 7 no. 5, pp. 1901-1910, DOI: 10.1111/j.1743-6109.2009.01414.x, 2010.
[31] K. A. Payne, Y. M. Binik, C. F. Pukall, L. Thaler, R. Amsel, S. Khalifé, "Effects of sexual arousal on genital and non-genital sensation: a comparison of women with vulvar vestibulitis syndrome and healthy controls," Archives of Sexual Behavior, vol. 36 no. 2, pp. 289-300, DOI: 10.1007/s10508-006-9089-4, 2007.
[32] L. R. Miller- Matero, C. Saulino, S. Clark, M. Bugensk, A. Eshelman, D. Eisenstein, "When treating the pain is not enough: a multidisciplinary approach for chronic pelvic pain," Archives of Women’s Mental Health, vol. 19 no. 2, pp. 349-354, DOI: 10.1007/s00737-015-0537-9, 2015.
[33] A. P. M. S. Romano, R. Gorayeb, S. Romano, "High levels of anxiety and depression have a negative effect on quality of life of women with chronic pelvic pain," International Journal of Clinical Practice, vol. 63 no. 5, pp. 707-711, DOI: 10.1111/j.1742-1241.2009.02034.x, 2009.
[34] T. L. Osborne, M. P. Jensen, D. M. Ehde, M. A. Hanley, G. Kraft, "Psychosocial factors associated with pain intensity, pain-related interference, and psychological functioning in persons with multiple sclerosis and pain," Pain, vol. 127 no. 1, pp. 52-62, DOI: 10.1016/j.pain.2006.07.017, 2007.
[35] M. J. L. Sullivan, B. Thorn, J. A. Haythornthwaite, "Theoretical perspectives on the relation between catastrophizing and pain," The Clinical Journal of Pain, vol. 17 no. 1, pp. 52-64, DOI: 10.1097/00002508-200103000-00008, 2001.
[36] J. Thomtén, A. Karlsson, "Psychological factors in genital pain: the role of fear-avoidance, pain catastrophizing and anxiety sensitivity among women living in Sweden," Scandinavian Journal of Pain, vol. 5 no. 3, pp. 193-199, DOI: 10.1016/j.sjpain.2014.01.003, 2014.
[37] G. E. Engel, "The need for a new medical model," Science, vol. 196 no. 4286, pp. 36-129, DOI: 10.1126/science.847460, 1977.
[38] G. L. Engel, "The biopsychosocial model and the education of health professionals," General Hospital Psychiatry, vol. 1 no. 2, pp. 156-165, DOI: 10.1016/0163-8343(79)90062-8, 1979.
[39] R. Bartz, "The biopsychosocial model. A new approaches to doctor- patients interactions," Journal of Family Practice, vol. 48, pp. 607-610, 1999.
[40] F. Borrel-Carrio, A. L. Suchman, R. M. Epstein, "The biopsychosocial model 25 years later: principles, practice, and scientific inquiry," Annalysis of Family Medicine, vol. 2 no. 6, pp. 576-584, DOI: 10.1370/afm.245, 2004.
[41] R. J. Gatchel, Y. B. Peng, M. L. Peters, P. N. Fuchs, D. C. Turk, "The biopsychosocial approach to chronic pain: scientific advances and future directions," Psychological Bulletin, vol. 133 no. 4, pp. 581-624, DOI: 10.1037/0033-2909.133.4.581, 2007.
[42] L. J. Burrows, A. T. Goldstein, "The treatment of vestibulodynia with topical estradiol and testosterone," Sexual Medicine, vol. 1 no. 1, pp. 30-33, DOI: 10.1002/sm2.4, 2013.
[43] T. Landry, S. Bergeron, M.-J. Dupuis, G. Desrochers, "The treatment of provoked vestibulodynia," The Clinical Journal of Pain, vol. 24 no. 2, pp. 155-171, DOI: 10.1097/ajp.0b013e31815aac4d, 2008.
[44] A. Cox, N. Golda, G. Nadeau, "CUA guideline: diagnosis and treatment of interstitial cystitis/bladder pain syndrome," Canadian Urological Association Journal, vol. 10 no. 5-6, pp. 136-155, DOI: 10.5489/cuaj.3786, 2016.
[45] M. P. FitzGerald, C. K. Payne, E. S. Lukacz, "Randomized multicenter clinical trial of myofascial physical therapy in women with interstitial cystitis/painful bladder syndrome and pelvic floor tenderness," Journal of Urology, vol. 187 no. 6, pp. 2113-2118, DOI: 10.1016/j.juro.2012.01.123, 2012.
[46] G. L. Armstrong, T. G. Vancaillie, "Combined site-specific sacral neuromodulation and pudendal nerve release surgery in a patient with interstitial cystitis and persistent arousal," BMJ Case Reports, vol. 9,DOI: 10.1136/bcr-2015-213513, 2016.
[47] P. Verrills, C. Sinclair, A. Barnard, "A review of spinal cord stimulation systems for chronic pain," Journal of Pain Research, vol. 9, pp. 481-492, DOI: 10.2147/JPR.S108884, 2016.
[48] K. Grinberg, M. Granot, L. Lowenstein, L. Abramov, I. Weissman-Fogel, "Negative illness perceptions are associated with a pro-nociceptive modulation profile and augmented pelvic pain," The Clinical Journal of Pain, vol. 34 no. 12, pp. 1141-1148, DOI: 10.1097/ajp.0000000000000633, 2018.
[49] G. Rostaminia, J. Manonai, E. Leclaire, "Interrater reliability of assessing levator ani deficiency with 360° 3D endovaginal ultrasound," International Urogynecology Journal, vol. 25 no. 6, pp. 761-766, DOI: 10.1007/s00192-013-2286-5, 2014.
[50] D. Yarnitsky, "Quantitative sensory testing," Muscle & Nerve, vol. 20 no. 2, pp. 198-204, DOI: 10.1002/(sici)1097-4598(199702)20:2<198::aid-mus10>3.3.co;2-4, 1997.
[51] D. Le Bars, A. H. Dickenson, J.-M. Besson, "Diffuse noxious inhibitory controls (DNIC). I. Effects on dorsal horn convergent neurones in the rat," Pain, vol. 6 no. 3, pp. 283-304, DOI: 10.1016/0304-3959(79)90049-6, 1979.
[52] D. Yarnitsky, L. Arendt-Nielsen, D. Bouhassira, "Recommendations on terminology and practice of psychophysical DNIC testing," European Journal of Pain, vol. 14 no. 4,DOI: 10.1016/j.ejpain.2010.02.004, 2010.
[53] C. D. Speilberger, R. L. Gorsuch, R. Luchene, The State- Trait Anxiety Inventory, 1969.
[54] Y. Teichman, F. Malineck, Manual for the Hebrew State- Trait Anxiety Inventory: Tel Aviv, 1978.
[55] R. R. Edwards, C. M. Campbell, R. B. Fillingim, "Catastrophizing and experimental pain sensitivity: only in vivo reports of catastrophic cognitions correlate with pain responses," The Journal of Pain, vol. 6 no. 5, pp. 338-339, DOI: 10.1016/j.jpain.2005.02.013, 2005.
[56] L. Canetty, A. Y. Shalev, K. Caplan De-Nour, "Israeli adolescent’s norms of the Brief Symptom Inventory," Israel Journal of Psychiatry and Related Sciences, vol. 31 no. 1, pp. 13-18, 1994.
[57] M. J. L. Sullivan, S. R. Bishop, J. Pivik, "The pain catastrophizing scale: development and validation," Psychological Assessment, vol. 7 no. 4, pp. 524-532, DOI: 10.1037/1040-3590.7.4.524, 1995.
[58] M. Granot, S. G. Ferber, "The roles of pain catastrophizing and anxiety in the prediction of postoperative pain intensity," The Clinical Journal of Pain, vol. 21 no. 5, pp. 439-445, DOI: 10.1097/01.ajp.0000135236.12705.2d, 2005.
[59] A. T. Beck, R. W. Beck, "Screening depressed patients in family practice: a rapid technique," Postgraduate Medicine, vol. 52 no. 2, pp. 81-85, DOI: 10.1080/00325481.1972.11713319, 1972.
[60] I. M. Chiu, C. A. Von Hehb, C. J. Woolf, "Neurogenic inflammation- the peripheral nervous system’s role in host defense and immunopathology," Natural Neuroscience, vol. 15 no. 8, pp. 1063-1067, 2013.
[61] K. M. Peters, D. J. Carrico, I. A. Ibrahim, A. C. Diokno, "Characterization of a clinical cohort of 87 women with interstitial cystitis/painful bladder syndrome," Urology, vol. 71 no. 4, pp. 634-640, DOI: 10.1016/j.urology.2007.11.013, 2008.
[62] S. Heymen, W. Maixner, W. E. Whitehead, R. R. Klatzkin, B. Mechlin, K. C. Light, "Central processing of noxious somatic stimuli in patients with irritable bowel syndrome compared with healthy controls," The Clinical Journal of Pain, vol. 26 no. 2, pp. 104-109, DOI: 10.1097/ajp.0b013e3181bff800, 2010.
[63] J. Q. Clemens, S. O. Brown, E. A. Calhoun, "Mental health diagnoses in patients with interstitial cystitis/painful bladder syndrome and chronic prostatitis/chronic pelvic pain syndrome: a case/control study," Journal of Urology, vol. 180 no. 4, pp. 1378-1382, DOI: 10.1016/j.juro.2008.06.032, 2008.
[64] T. Graven-Nielsen, T. Wodehouse, R. M. Langford, L. Arendt-Nielsen, B. L. Kidd, "Normalization of widespread hyperesthesia and facilitated spatial summation of deep-tissue pain in knee osteoarthritis patients after knee replacement," Arthritis & Rheumatism, vol. 64 no. 9, pp. 2907-2916, DOI: 10.1002/art.34466, 2012.
[65] M. Jantos, "Underdtanding chronic pelvic pain," Pelviperineol, vol. 26, pp. 66-69, 2007.
[66] C. F. Pukall, Y. M. Binik, S. Khalife, R. Amsel, F. V. Abbott, "Vestibular tactile and pain thresholds in women with vulvar vestibulitis syndrome," Pain, vol. 96 no. 1-2, pp. 163-175, DOI: 10.1016/s0304-3959(01)00442-0, 2002.
[67] R. K. Kotarinos, "Myofascial pelvic pain: rationale and treatment," Current Bladder Dysfunction Reports, vol. 10 no. 1, pp. 87-94, DOI: 10.1007/s11884-014-0287-y, 2015.
[68] M. H. Bardley, A. Rawlins, C. A. Brinker, "Physical therapy treatment of pelvic pain," Physical Medicine and Rehabilitation Clinics of North America, vol. 28 no. 3, pp. 589-601, DOI: 10.1016/j.pmr.2017.03.009, 2017.
[69] S. Bergeron, Y. M. Binik, S. Khalifé, "A randomized comparison of group cognitive-behavioral therapy, surface electromyographic biofeedback, and vestibulectomy in the treatment of dyspareunia resulting from vulvar vestibulitis," Pain, vol. 91 no. 3, pp. 297-306, DOI: 10.1016/s0304-3959(00)00449-8, 2001.
[70] G. Chiarioni, A. Nardo, I. Vantini, A. Romito, W. E. Whitehead, "Biofeedback is superior to electrogalvanic stimulation and massage for treatment of levator ani syndrome," Gastroenterology, vol. 138 no. 4, pp. 1321-1329, DOI: 10.1053/j.gastro.2009.12.040, 2010.
[71] N. Cozean, J. Cozean, The Interstitial Cystitis Solution, 2016.
[72] M. P. FitzGerald, R. U. Anderson, J. Potts, "Randomized multicenter feasibility trial of myofascial physical therapy for the treatment of urological chronic pelvic pain syndromes," Journal of Urology, vol. 182 no. 2, pp. 570-580, DOI: 10.1016/j.juro.2009.04.022, 2009.
[73] S. Loving, T. Thomsen, P. Jaszczak, J. Nordling, "Pelvic floor muscle dysfunctions are prevalent in female chronic pelvic pain: a cross-sectional population-based study," European Journal of Pain, vol. 18 no. 9, pp. 1259-1270, DOI: 10.1002/j.1532-2149.2014.485.x, 2014.
[74] I. A. Oyama, A. Rejba, J. C. Lukban, "Modified Thiele massage as therapeutic intervention for female patients with interstitial cystitis and high-tone pelvic floor dysfunction," Urology, vol. 64 no. 5, pp. 862-865, DOI: 10.1016/j.urology.2004.06.065, 2004.
[75] J. M. Weiss, "Pelvic floor myofascial trigger points: manual therapy for interstitial cystitis and the urgency-frequency syndrome," The Journal of Urology, vol. 166 no. 6, pp. 2226-2231, DOI: 10.1016/s0022-5347(05)65539-5, 2001.
[76] T. Y. Rosenbaum, A. Owens, "Continuing medical education: the role of pelvic floor physical therapy in the treatment of pelvic and genital pain-related sexual dysfunction (CME)," The Journal of Sexual Medicine, vol. 5 no. 3, pp. 513-523, DOI: 10.1111/j.1743-6109.2007.00761.x, 2008.
[77] S. G. R. Klotz, M. Schön, G. Ketels, B. Löwe, C. A. Brünahl, "Physiotherapy management of patients with chronic pelvic pain (CPP): a systematic review," Physiotherapy Theory and Practice, vol. 35 no. 6, pp. 516-532, DOI: 10.1080/09593985.2018.1455251, 2019.
[78] S. A. Prendergast, "Pelvic floor physical therapy for vulvodynia," Obstetrics and Gynecology Clinics of North America, vol. 44 no. 3, pp. 509-522, DOI: 10.1016/j.ogc.2017.05.006, 2017.
[79] L. Arendt-Nielsen, D. Yarnitsky, "Experimental and clinical applications of quantitative sensory testing applied to skin, muscles and viscera," The Journal of Pain, vol. 10 no. 6, pp. 556-572, DOI: 10.1016/j.jpain.2009.02.002, 2009.
[80] R. H. LaMotte, C. N. Shain, D. A. Simone, E. F. Tsai, "Neurogenic hyperalgesia: psychophysical studies of underlying mechanisms," Journal of Neurophysiology, vol. 66 no. 1, pp. 190-211, DOI: 10.1152/jn.1991.66.1.190, 1991.
[81] M. A. Giamberardino, C. Tana, R. Costantini, "Pain thresholds in women with chronic pelvic pain," Current Opinion in Obstetrics and Gynecology, vol. 26 no. 4, pp. 253-259, DOI: 10.1097/gco.0000000000000083, 2014.
[82] S. Kaya, L. Hemans, T. Willems, "Central sensitization in urogynecological chronic pelvic pain: a systematic literature review," Pain Physician, vol. 16 no. 4, pp. 291-308, 2013.
[83] C. F. Pukall, M. Meana, K. S. Sutton, "Psych evalu & measur dyspareunia," Female Sexual Pain Disorders: Evaluation and Measurement, pp. 21-26, 2009.
[84] C. F. Pukall, Y. M. Binik, S. Khalifé, "A new instrument for pain assessment in vulvar vestibulitis syndrome," Journal of Sex & Marital Therapy, vol. 30 no. 2, pp. 69-78, DOI: 10.1080/00926230490275065, 2004.
[85] A. Gerhardt, W. Eich, R.-D. Treede, J. Tesarz, "Conditioned pain modulation in patients with nonspecific chronic back pain with chronic local pain, chronic widespread pain, and fibromyalgia," Pain, vol. 158 no. 3, pp. 430-439, DOI: 10.1097/j.pain.0000000000000777, 2017.
[86] D. Yarnitsky, M. Granot, Y. Granovsky, "Pain modulation profile and pain therapy: between pro- and antinociception," Pain, vol. 155 no. 4, pp. 663-665, DOI: 10.1016/j.pain.2013.11.005, 2014.
[87] E. Kosek, G. Ordeberg, "Lack of pressure pain modulation by heterotopic noxious conditioning stimulation in patients with painful osteoarthritis before, but not following, surgical pain relief," Pain, vol. 88 no. 1, pp. 69-78, DOI: 10.1016/s0304-3959(00)00310-9, 2000.
[88] B. R. Goodin, L. McGuire, M. Allshouse, "Associations between catastrophizing and endogenous pain-inhibitory processes: sex differences," The Journal of Pain, vol. 10 no. 2, pp. 180-190, DOI: 10.1016/j.jpain.2008.08.012, 2009.
[89] L. Katz, D. A. Tripp, J. C. Nickel, R. Mayer, M. Reimann, A. van Ophoven, "Disability in women suffering from interstitial cystitis/bladder pain syndrome," BJU International, vol. 111 no. 1, pp. 114-121, DOI: 10.1111/j.1464-410x.2012.11238.x, 2012.
[90] K. Whitmore, J. F. Siegel, S. Kellogg-Spadt, "Original research-sexual pain disorders: interstitial cystitis/painful bladder syndrome as a cause of sexual pain in women: a diagnosis to consider," The Journal of Sexual Medicine, vol. 4 no. 3, pp. 720-727, DOI: 10.1111/j.1743-6109.2007.00497.x, 2007.
[91] M. Hubstcher, N. Moloney, T. Rebbeck, A. Traeger, K. Refshauge, "Contributions of mood, pain catastrophizing, and cold hyperalgesia in acute and chronic low back pain: a comparison with pain-free controls," The Clinical Journal of Pain, vol. 30 no. 10, pp. 886-993, DOI: 10.1097/ajp.0000000000000045, 2014.
[92] J. L. Rhudy, A. E. Williams, K. M. McCabe, J. L. Russell, L. J. Maynard, "Emotional control of nociceptive reactions (ECON): do affective valence and arousal play a role?," Pain, vol. 136 no. 3, pp. 250-261, DOI: 10.1016/j.pain.2007.06.031, 2008.
[93] S. E. George, S. C. Clinton, D. F. Borello-France, "Physical therapy management of female chronic pelvic pain: anatomic considerations," Clinical Anatomy, vol. 26 no. 1, pp. 77-88, DOI: 10.1002/ca.22187, 2013.
[94] C. P. Van Wilgen, M. W. Van Ittersum, A. A. Kaptein, M. Van Wijhe, "Illness perceptions in patients with fibromyalgia and their relationship to quality of life and catastrophizing," Arthritis & Rheumatism, vol. 58 no. 11, pp. 3618-3626, DOI: 10.1002/art.23959, 2008.
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Abstract
Background. Chronic pelvic pain syndrome (CPPS) is a multifactorial disorder comprising structural and functional muscular abnormalities, a dysfunctional pain system, and psychological distress. Myofascial physical Therapy (MPT) that is targeted at improving pelvic muscle functioning is considered a first line nonpharmacological treatment for CPPS, although the precise mechanisms that lead to symptoms alleviation have not yet been elucidated. Purpose. This longitudinal study aimed to examine the local and systemic effects of MPT intervention, including biopsychophysiological processes, among CPPS patients. Methods. The study included 50 CPPS women. Morphologic assessment of the levator ani and quantitative sensory testing of the pain system were applied alongside with evaluation of pain-related psychological factors using designated questionnaires. All measures were evaluated both before and after MPT in 39 patients. The long-term effects of MPT were evaluated by clinical pain reports obtained at 3 and 9 months following MPT that were compared with a nontreated group of 11 untreated CPPS women. Results. Along with an improvement in the clinical pain intensity (
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Details

1 Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel; The Department of Nursing, Ruppin Academic Center, Emek Hefer, Israel
2 Department of Physical Therapy, Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel
3 The Department of Obstetrics and Gynecology, Rambam Medical Center and Faculty of Medicine, Technion, Haifa, Israel
4 Lis Maternity Hospital, Tel Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, The Sex Therapy Clinic, Tel Aviv, Israel
5 Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel; The Laboratory of Clinical Neurophysiology, Faculty of Medicine, Technion, Haifa, Israel