Evidence Based Physical Therapy for the Pelvic Floor Bridging Science and Clinical Practice

244 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY with a reduced PFM contraction strength and an in- centage in the prospective group who received instruc- creased genital hiatus. Whether reduction of the hiatus tion was not stated, other than that all patients were width in response to PFMT can reduce recurrence of advised to perform PFMT. The authors concluded that POP after surgery has not been shown. Differences as POP recurrence rates were not altered significantly between vaginal, abdominal and laparoscopic surgery, by early return to normal activities, perhaps the risk of and their effect on the PFM are also not known. recurrence might be better reduced through improved instructions on how to do PFMT and how to use PFM EVIDENCE FOR PFMT IN THE PREVENTION contractions before and during increases in abdominal AND TREATMENT OF POP pressure, as well as prophylactic initiatives to protect the pelvic floor. However, due to the limitations in the This section is divided into three parts: design, it cannot be concluded from this study what the role of PFMT in the prevention of recurrence is, nor 1. lifestyle interventions; when is the ideal time or dosage to recommence exer- 2. PFMT in primary and secondary prevention and as cises postoperatively. treatment of POP; Quality of the intervention: 3. PFMT to prevent recurrence after prolapse surgery. dose–response issues Methods As no RCTs have been found based on the outcomes of lifestyle interventions alone on the outcomes of POP, no Computerized searches in PubMed, the Cochrane comment on the quality of the intervention can be made. library, and PEDro were undertaken using the words There is currently no evidence for addressing lifestyle pelvic organ prolapse or genital prolapse in combina- interventions for women with POP, but as recommen- tion with pelvic floor muscle training, pelvic muscle dations on these exist for women with SUI (Wilson et al training, or physical activity. In addition, hand searches 2002), future studies may establish a causal link to POP, from reference lists of general literature on POP were and intervention studies may establish a benefit in conducted. Methodological quality of randomized con- addressing these risk factors in POP. trolled trials (RCTs) was rated with the PEDro scale (Maher et al 2003) The scale is based on the Delphi list, PFMT in primary and secondary prevention and its reliability is supported empirically (Maher et al and as treatment of POP 2003). No studies were found for primary prevention of POP. Lifestyle interventions One uncontrolled study and one RCT were found for treatment of prolapse. In the uncontrolled study, To date, we have been unable to find any RCTs or Mimura et al (2000) followed 32 women with rectocele uncontrolled intervention studies addressing the effect greater than 2 cm below ‘the expected line’ at proctog- of lifestyle interventions in the prevention and treat- raphy. The patients received biofeedback-assisted PFMT ment of POP. Some studies have identified lifestyle risk with a nurse every 2–3 weeks, usually for four to five factors associated with POP, including heavy lifting (Jør- sessions. Twenty-five women met for follow-up assess- gensen et al 1994), constipation and straining at stool ment (drop-out 22%). The results showed that complete (Spence-Jones et al 1994), chronic pulmonary disease resolution of symptoms was achieved in 12%. At (Rinne & Kirkinen 1999) and obesity (Hendrix et al follow-up 14 patients (56%) felt that their constipation 2002). had improved a little and 11 (34%) felt that it had improved a lot. A study by Ottesen et al (2003) considered a mixture of lifestyle interventions and exercise on women who Piya-Anant et al (2003) conducted both a cross- had POP surgery. These authors compared POP recur- sectional study in 682 women and an intervention study rence rates following vaginal surgery in a retrospective of 654 of the same women (mean age 67 years, SD ± 5.6): group of patients (who underwent a ‘normal’ convales- 70% in the cross-sectional study were diagnosed with cence period, median 6 weeks) with a prospective group POP – 30% were classified as severe and 40% as having of patients who were advised to return to normal activi- mild prolapse. The women were randomly allocated to ties much sooner. The 6-month postoperative subjective either an experimental or a control group. Women in the recurrence was 22% in the former group compared to experimental group were taught to contract the PFM 30 17% at 1 year postoperatively in the latter. Only 40% of times after a meal every day. Women not able to contract patients in the retrospective study received instructions in PFMT from a specialized physical therapist. The per-

Pelvic organ prolapse 245 were asked to return to the clinic once a month until they voiding and defecation. Subjects in the treatment group could perform correct contractions. In addition, they received the intervention ‘package’ from a physical ther- were advised to increase their intake of vegetables and apist on three occasions: 2–4 weeks preoperatively, day fruit and to drink at least 2 L of water daily to prevent 2 postoperatively and at 6 weeks postoperatively. A constipation. There were follow-up visits every 6 months blinded investigator measured outcomes at 12 weeks throughout the 2-year intervention period. The results postoperatively. All subjects demonstrated improved showed that the intervention was only effective in the scores postoperatively in the outcomes of urinary leakage group with severe prolapse. The rate of worsening of (paper towel test), urinary symptoms and quality of life POP was significantly greater in the control group than scores (both assessed by King’s Health Questionnaire), the PFMT group: 72.2% versus 27.8%, respectively. Meth- and 48-hour voiding diary. The treatment group demon- odological quality of the study is shown in Table 9.11. strated significantly larger pre- to postoperative differ- The methodological score was 4/10, therefore the results ences than the control group in the urinary symptom should be viewed with some caution. and quality of life scores, and the voiding diary out- comes. Postoperatively, subjects in the treatment group Quality of the intervention: demonstrated an increase in maximum vaginal squeeze dose–response issues pressure compared with subjects in the control group, who showed a decrease in squeeze pressure. The authors The intervention in the Piya-Anant et al (2003) study is recommended preoperative instruction and postopera- not described in detail, but women were taught a correct tive reinforcement by a physical therapist for women contraction of the PFM. However, the method used to undergoing surgery for POPUI. assess correctness of the PFM contraction was not described. Duration and intensity of the contraction Although the surgical population in this study com- were not described and there was neither assessment of prised a mixture of prolapse-only, incontinence-only, adherence to the exercise protocol nor measurement of and combined-POPUI surgery, most subjects in both PFM strength. In addition there was co-intervention groups had prolapse-only surgery, so these results from with change of nutrition and water intake. This may the physical therapy intervention may be generalizable have improved constipation and excessive straining at to a prolapse surgery population. However, no pro- stool in some women. However, no data were presented lapse-specific assessment or outcome measures were on constipation or straining. The evaluation method and reported, therefore the effect of the intervention on the classification categories of POP applied by Piya-Anant presence of any prolapse signs or symptoms postopera- et al (2003) were poorly described and there were no tively is not known. Methodological quality of the study references to studies showing that the evaluation is shown in Table 9.11. The methodological score was systems used had been tested for responsiveness, intra- 6/10, therefore the effectiveness of the treatment can be or inter-test reliability, or validity. accepted with reasonable confidence. Evidence for PFMT to prevent recurrence The second study referred to in the Cochrane review after prolapse surgery is currently investigating the effect of pre- and post- operative physical therapy for women undergoing The Cochrane review investigating conservative man- vaginal POP surgery or hysterectomy (Frawley et al as agement of POP (Hagen et al 2004b) identified two cited in Hagen et al 2004b). This single-blinded RCT will studies in progress that included PFMT following pro- enrol 50 women, randomizing 25 women to receive a lapse surgery. Both of these studies have included life- combination of PFMT and lifestyle modifications. Out- style interventions in addition to PFMT as part of the comes will be assessed at 12 months postoperatively. treatment group protocol. Therefore there are currently The study follow-up period ceased in 2006, and results no completed RCTs that have shown the effect of PFMT of the trial will be available in late 2007. as the sole intervention to prevent POP recurrence postoperatively. Quality of intervention: dose–response issues Jarvis et al (2005) studied the effect of PFMT and The study by Jarvis et al (2005) provided a low but bladder/bowel training on women undergoing surgery pragmatic level of intervention to the treatment group. for POPUI with a RCT of 60 women: 30 women were The frequency of intervention was three visits. The randomized to each of the treatment and control groups. home programme of PFM exercises was stated as ‘indi- The intervention consisted of PFMT, functional bracing vidualized’ with four sets of home exercises per day of PFM before rises in abdominal pressure, bladder/ plus performance of functional bracing at appropriate bowel training and advice to reduce straining during times. No other details of the intensity of exercise or compliance with home training were provided. PFM

246 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Table 9.11 PEDro quality score of RCTs in systematic review E – Eligibility criteria specified 1 – Subjects randomly allocated to groups 2 – Allocation concealed 3 – Groups similar at baseline 4 – Subjects blinded 5 – Therapist administering treatment blinded 6 – Assessors blinded 7 – Measures of key outcomes obtained from over 85% of subjects 8 – Data analysed by intention to treat 9 – Statistical comparison between groups conducted 10 – Point measures and measures of variability provided Study E 1 2 3 4 5 6 7 8 9 10 Total score Piya-Anant et al 2003 + + ? + − − + − − + − 4 Jarvis et al 2005 ++++−−+−? ++ 6 +, criterion is clearly satisfied; −, criterion is not satisfied; ?, not clear if the criterion was satisfied. Total score is determined by counting the number of criteria that are satisfied, except that scale item one ‘eligibility criteria specified’ is not used to generate the total score. Total scores are out of 10. contraction was assessed and trained by continence side-effects, has been shown to be effective in RCTs and physical therapists, so the correctness of the interven- systematic reviews to treat SUI and mixed incontinence tion can be assumed. Assessment of PFM strength was (Hay-Smith et al 2001, Wilson et al 2002), and many recorded via digital palpation and manometry, but no women present with both POP and UI, it is our opinion results for digital palpation were provided. Limited that physical therapists should continue to treat POP results of the manometry scores were provided, which patients with PFMT. Although POP may occur in the restricts interpretation of the clinical significance of the anterior/middle/posterior compartments, the pelvic pre- to post-operative changes in PFM strength. Despite floor should be considered as a single unit in the treat- these limitations, the PFMT intervention resulted in a ment of POP (Thakar & Stanton 2002). As occult SUI positive outcome at 12 weeks postoperatively, which may be a common side-effect of pessary use and surgery represents an encouraging direction for future surgical (Brubaker et al 2002, Clemons et al 2004, Maher et al plus PFMT studies. 2004), PFMT should also be advocated in combination with these other treatments. Until information from Several surveys of rehabilitation guidelines includ- RCTs showing a positive effect of PFMT to prevent ing PFMT for patients undergoing POP or POPUI recurrence of prolapse is available, it is recommended surgery have highlighted the variations in consensus that women undergoing POP surgery receive instruc- among clinicians (Frawley et al 2005, Hibner et al tion from a specialized physical therapist in PFMT to 2004, Ottesen et al 2001). In the absence of evidence to support the prolapse repair and protect against recur- guide these clinical protocols for POP surgery patients, rence or development of de-novo pelvic floor symp- questions remain regarding optimal rehabilitation, toms. There is an urgent need for high-quality RCTs activity restriction, exercise resumption, and PFMT with appropriate training protocols to evaluate the regimens. effect of PFMT to prevent and treat POP. CONCLUSION CLINICAL RECOMMENDATIONS FOR TREATMENT To date there are few published RCTs to support PFMT in the prevention and treatment of POP. However, there • Include questions about POP symptoms in history is a strong rationale that PFMT may be effective both in taking. prevention and treatment. Because PFMT has no known

Pelvic organ prolapse 247 • Assess for POP by use of the POP-Q or simply regis- measures for POP quality of life and symptom dis- ter the prolapse during straining in cm above or tress/bother could include: below the hymen. Record the position used because – the Prolapse Quality of Life (P-QoL) (Digesu et al it may affect reproducibility of the measurement. An upright position may be necessary to reproduce the 2005); extent of the prolapse that bothers the patient (Visco – the Pelvic Floor Distress Inventory (PFDI) (Barber et al 2003). et al 2001); • Explain rationale for PFMT in the prevention and – the Pelvic Floor Impact Questionnaire (PFIQ) treatment of prolapse. (Barber et al 2001); • After thorough instruction of how to perform a – the Urogenital Distress Inventory (Shumaker et al correct PFM contraction, check ability to contract. 1994); • Assess PFM strength and ability to elevate the pelvic – symptoms and bother in POP (Mouritsen & Larsen floor. 2003). • Implement outcome measures to measure effect of intervention for POP symptoms. Suggested outcome • Follow clinical recommendations for PFMT for SUI and lifestyle modifications as may be relevant for each woman. • If no reduction of prolapse severity nor symptom bother after 3 months of supervised training, refer back to the gynaecologist for further management. REFERENCES Balmforth J, Bidmead J, Cardozo L et al 2004 Raising the tone: a prolapse. 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Pelvic pain 249 Pelvic pain INTRODUCTION associated with symptoms suggestive of lower urinary tract, or sexual dysfunction. There is no proven infection Helena Frawley and Dr Wendy Bower or other obvious pathology’ (Fall et al 2004). DEFINITIONS AND CLASSIFICATION OF It has been postulated that pelvic floor pain arises DIFFERENT FORMS from spasm or tension in one or more of the pelvic muscles (levator ani, coccygeus, piriformis), and/or Chronic pelvic pain has been defined as ‘non-malignant referred pain in their attachments to the sacrum, coccyx, pain perceived in structures related to the pelvis of ischial tuberosities or pubic rami (Howard 2000a). either men or women. In the case of documented noci- ceptive pain that becomes chronic, the pain must have Sexual dysfunction and pain are two symptoms of been continuous or recurrent for at least 6 months. If PFM dysfunction (Messelink et al 2005). Pelvic pain of non-acute pain mechanisms are documented, then the PFM origin has been variously labelled as coccygodynia pain may be regarded as chronic irrespective of the time (De Andres & Chaves 2003, Thiele 1937), levator (spasm) period. In all cases, there may be associated negative syndrome (McGivney & Cleveland 1965, Smith 1959), cognitive, behavioral and social consequences’ (Fall tension myalgia of the pelvic floor (Sinaki et al 1977), et al 2004). pelvic floor spasticity (Kuijpers & Bleijenberg 1985) ure- thral/anal sphincter dyssynergia (Whitehead 1996), This definition forms the basis of the classification vaginismus (Masters & Johnson 1970) and shortened system illustrated in Table 9.12. Pelvic pain syndrome pelvic floor (FitzGerald & Kotarinos 2003). has a separate definition, proposed by Abrams et al (2002) and adopted by Fall et al (2004) as ‘the occurrence This chapter considers pelvic pain and/or related of persistent or recurrent episodic pelvic pain associated dysfunction originating (or considered to be originat- with symptoms suggestive of lower urinary tract, sexual, ing) in the PFM (and their bony attachments, fascia and bowel or gynecological dysfunction. There is no proven ligaments), including both deep (levator ani) and super- infection or other obvious pathology’. ficial (perineal muscle) layers. Dysfunction may be primarily from the PFM, occur secondary to visceral Part of the complexity of pelvic pain is that it can be changes (lower urinary tract, reproductive tract or ano- diffuse and felt in more than one area, therefore the rectum), or be referred from other pelvic somatic (cuta- description of pelvic pain should always specify loca- neous and muscular) structures. It is often difficult to tion, duration, identifiable pathology, and other relevant differentially diagnose pain originating from deep pelvic comorbidities (Williams et al 2004). Pelvic pain muscular structures from that emanating from visceral may be reported in the anterior abdominal wall below structures because the symptoms are often similar due the level of the umbilicus, the spine from T10 (ovarian to anatomical proximity and shared innervation, hence and testes nerve supply) or T12 (nerve supply to pelvic pain can be perceived in either location (Perry 2003). musculoskeletal structures) to S5, the perineum, and all of the external and internal tissues within these refer- NEUROANATOMY ence zones. The PFM structures receive somatic innervation from Pelvic pain can be further subclassified into pelvic the pudendal nerve (S2–S4) and sacral nerve roots (S3– pain syndromes of muscular origin, which includes S5) (Barber et al 2002). The pelvic viscera are innervated perineal pain syndrome (Abrams et al 2002, Fall et al by parasympathetic efferent neurons arising from the 2004) and pelvic floor muscle (PFM) pain syndrome, the intermediolateral cell column at spinal levels S2–S4 latter defined as ‘the occurrence of persistent or recur- (Rogers 1998). Pain from viscera is transmitted through rent episodic pelvic floor pain with associated trigger the inferior hypogastric plexus and onwards via either points that is either related to the micturition cycle or the hypogastric, pelvic splanchnic or sacral splanchnic nerves. Nociceptive information may also travel with

Table 9.12 Classification of chronic pelvic pain syndromes. Reprinted from Fall et al 2004, with permission 250 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Chronic Pelvic Urological Painful bladder syndrome Interstitial cystitis pelvic pain pain Urethral pain syndrome (new syndrome Gynaecological Penile pain syndrome (new definition) definition) Prostate pain syndrome (Adapted from NIH) Well-defined Anorectal Scrotal pain syndrome conditions Neurological Testicular pain syndrome (new definition) that produce Muscular Endometriosis-associated pain syndrome Post-vasectomy pain syndrome (new definition) pain, examples Urological (new definition) Epididymal pain syndrome (new definition) include: Gynaecological Vaginal pain syndrome Generalized vulvar pain syndrome (ISSVD 1999) Anorectal Vulvar pain syndrome Neurological Localized vulvar pain Vestibular pain syndrome Other Proctalgia fugax Anorectal pain syndrome (new definition) syndrome (ISSVD (ISSVD 1999) Anism Pudendal pain syndrome (new definition) 1999) Clitoral pain syndrome Perineal pain syndrome Pelvic floor muscle pain syndrome (new definition) (ISSVD 1999) Infective cystitis Infective prostatitis Infective urethritis Infective epididymo-orchitis Endometriosis Proctitis Haemorrhoids Anal fissure Pudendal neuropathy Sacral spinal cord pathology Vascular Cutaneous Psychiatric

Pelvic pain 251 the ovarian vessels or the superior rectal artery. For a reason(s) why pain would be chronically maintained more detailed explanation of the neuroanatomy and in the PFM are not clear. It seems necessary to look neurobiology of the pelvis, see Ch. 4. beyond the PFM in isolation, and consider the inter- relationships with nearby viscera, and the unique and PREVALENCE AND INCIDENCE complex peripheral and central neural control that influ- ences this region, as depicted in Fig. 9.23. The true prevalence and incidence of PFM pain syn- drome alone or coexisting with other chronic pelvic pain Abnormal muscle tone conditions is unknown. Prevalence of chronic pelvic pain of multisystem aetiology (visceral, somatic, pyscho- A physiological and mechanical explanation of muscle neurological) has been estimated at 3.8% of all women tone is presented in Fig. 9.24. Here, muscle tone has two (Howard 2003) or 14.7% of women aged 18–50 years components: the viscoelastic component, which is inde- (Mathias et al 1996). Prevalence estimates of pelvic pain pendent of nervous activity, and the contractile compo- syndromes that overlap with PFM pain syndrome may nent, which is caused by activation of motor units. It is be indicative of PFM pain prevalence. Vaginismus, for possible that abnormalities of both the viscoelastic and example, has been reported to affect up to 21% of women the contractile component may contribute to abnormal- younger than 30 years (Laumann et al 1999). Jamieson ity in PFM tension. Other terms denoting muscle tension & Steege (1996) found higher prevalence figures in their linked to muscle pain, include spasm and cramp. There study of women aged 18–45 years, with 90% reporting is no generally accepted definition of the term ‘spasm’ dysmenorrhea, 46% reporting dyspareunia, 39% report- and no consensus concerning how to differentiate severe ing pelvic pain and 12% reporting irritable bowel muscle contractions from cramps, chronic muscle syndrome. tension, or spasm. AETIOLOGY AND PATHOPHYSIOLOGY Mense et al (2001, p. 111) offer the following defini- tion of muscle spasm: ‘electromyographic (EMG) activ- Acute PFM pain may result from overzealous or unac- ity that is not under voluntary control and is not customed exercise (DeLancey et al 1993), but the dependent on posture. It may or may not be painful’. However if the contraction is painful, it is often called a ‘cramp’. Reissing et al (2004, p. 9) used a working defini- tion of spasm in their study of vaginismus as ‘an invol- Visceral Visceral dysfunction: dysfunction: anorectum bladder Somatic referral: Pelvic pain Sexual dysfunction: – pelvic muscles – dyspareunia – pelvic joints PFM pain Perineal – vaginismus – pelvic soft tissues syndrome pain Gynaecological syndrome disorder Altered tension – deep PFM – superficial PFM Higher centres: – learning – environmental adaption – limbic system Fig. 9.23 Possible factors contributing to pelvic floor muscle pain aetiology.

252 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Muscle tone (general tone) Viscoelastic Contractile (specific tone) activity Elastic Viscoelastic Contracture Electrogenic Electrogenic stiffness stiffness (no EMG spasm contraction activity (normal) (pathologic) Fig. 9.24 Relationship among terms commonly used to characterize muscle tension: tone, stiffness, contracture and spasm (Reprinted from Mense et al 2001, with permission). Abnormal – underactive Normal Abnormal – overactive Fig. 9.25 Terminology used to describe normal and abnormal Decreased resting Normal resting tone Increased resting pelvic floor muscle activity. tone, decreased of PFM tone, increased contractile activity, contractile activity, increased relaxation: Normal contractile decreased relaxation: hypoactive / hypotonic PFM activity of PFM hyperactive / hypertonic / high-tone / shortened PFM Normal relaxation of PFM untary contraction of some or all of the PFM which Pelvic floor muscle pain and overactivity prevents examination’. It has not been clearly established whether pain in the Several terms have been used to denote abnormal PFM causes the overactivity, or whether the overactivity PFM tone or activity linked to PFM pain syndromes. causes the pain. Despite this, several factors have been These appear in Fig. 9.25. This chapter will adopt the postulated to potentiate PFM overactivity and pain, International Continence Society (ICS) recommended including the following: term ‘overactive PFM’ (Messelink et al 2005) to denote a condition where the resting tone of the PFM may be • skeletal muscle overload – repetitive or sustained elevated, the contractile activity (voluntary or involun- (Everaert et al 2001); tary) of the PFM may be increased, or the relaxation control may be reduced. • tethering of fascia overlying skeletal muscle; • trigger points (see below); Not all authors agree with the presumed causal link • local inflammation (Segura et al 1979); between PFM pain and overactivity. Mense et al (2001) • infection (Chung et al 2001); cited clinical and physiological studies indicating that • trauma (Butrick 2000); muscle pain tends to inhibit, not facilitate, voluntary • pelvic surgery (Zermann et al 1998); and reflex contractile activity of the same muscle. These • psychosomatic conditions (Pauls & Berman 2002); authors acknowledge that sufficient spasm can cause • alterations in neural control (Butrick 2003, Perry pain, but something other than the muscle pain is causing the spasm. It could be that the presence of 2003, Zermann et al 1999, 2001a, 2001b): trigger points within a muscle may contribute to the – spinal cord wind-up, hyperalgesia; palpable findings, the pain, and the variable degree of – convergence in the dorsal horn, upregulation, spasm measured in the muscle. central sensitization;

Pelvic pain 253 – dichotomizing neurons; Functional obstruction to complete emptying of the – increase in excitotoxic neurotransmitters; bladder associated with non-relaxation of the PFM – cross-communication between visceral and som- generates increased detrusor pressures (Yeung 2001). Further PFM activity is triggered in an effort to prevent atic structures. additional detrusor pressure rise. Eventually the mictu- rition reflex becomes destabilized during bladder filling, Relationship of PFM pain and myofascial evidenced on urodynamic investigation as an overac- trigger points tive bladder and on a frequency–volume chart as fre- quent low-volume voids. Pelvic floor muscle contraction Several authors have linked PFM pain with myofascial is a common method to inhibit urgency, but in patients pain syndrome (Butrick 2000, Howard 2003). A myofas- with PFM overactivity it is likely that little additional cial pain syndrome is a regional pain syndrome charac- pressure will be generated because the muscle is in its terized by the presence of myofascial trigger points shortened range. Prescription of PFM exercises to in- (Mense et al 2001). The clinical characteristics of trigger crease urethral closure pressure and maximize detrusor points include: inhibition is likely to be inappropriate because it can exacerbate both pain and muscle imbalance. • spot tenderness in a nodule that is part of a palpably tense band of muscle fibres; Patients with PFM overactivity perceive appropriate perineal fullness and fecal urge but have trouble passing • patient recognition of the pain that is evoked by pres- stools. There is delayed initiation of evacuation, pro- sure on the tender spot; longed duration of passage of stool and incomplete emptying of the rectum when compared to control sub- • pain referral in a pattern that is characteristic of that jects (Halligan et al 1995). Smaller more acute straining muscle; angles are seen in symptomatic patients than in normal defecation attempts, a direct consequence of a slowly or • a local twitch response; non-relaxing PFM (Kuijpers & Bleijenberg 1985, Lee • painful limitation of active and passive range of et al 1994). As a consequence defecation may be painful and mechanically difficult, often requiring external motion; assistance (Bleijenberg & Kuijpers 1987). Constipation is • some weakness in that muscle. common in patients with PFM overactivity and can precipitate further anorectal pathology, such as anal The regions of referred pain caused by trigger points fissures and hemorrhoids. Anal manometry indicates in the levator ani and perineal muscles include the essentially normal readings for both resting and squeeze coccyx, anal area, lower part of the sacrum and genital pressure (Halligan et al 1995). However, on straining structures (Travell & Simons 1992). There is no generally there is no obvious perineal descent and marked EMG accepted aetiology for myofascial pain syndrome. It is activity in place of relaxation in puborectalis and the proposed that macrotrauma or microtrauma events may external anal sphincter (Bleijenberg & Kuijpers 1987). disturb the normal or weakened muscle through muscle injury or sustained muscle contraction, leading to trigger Pelvic floor muscle overactivity has been associated points and myofascial pain syndrome. Signs and symp- with vaginal and sexual pain and therefore impaired toms of myofascial pain syndromes resemble other sexual activity or dysfunction. musculoskeletal entities, so differential diagnosis can be difficult. In up to 88% of female patients with pelvic Prevention pain, such trigger points can be identified within the PFM group and also in the abdominal wall and hip No studies addressing the prevention of PFM pain or girdle (FitzGerald & Kotarinos 2003). Despite support in overactivity have been found to date. the literature for the link between PFM pain and trigger points, causation has not been proven. Summary Impact of an overactive PFM on bladder and Pelvic floor muscle pain and/or PFM overactivity are bowel function and sexual activity prevalent and complex conditions that present a chal- lenge to the clinician and the researcher. The exact con- The effect of PFM overactivity on the urinary tract is dition or symptom being addressed should be described dynamic. Symptoms include hesitancy or difficulty ini- precisely, recognizing that overlap with other pelvic tiating a void, slow or intermittent urine flow, pain with pain syndromes commonly occurs. Little is known micturition, significant postvoid residual urine, urgency, regarding the aetiology and pathophysiology of PFM frequency and urethral sphincter hyperalgesia (Meadows 1999, Weiss 2001, Zermann et al 1999). A significant number of patients also have a diagnosis of interstitial cystitis (FitzGerald & Kotarinos 2003).

254 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY pain syndrome. Further studies are required to address Both PFM pain and PFM activity should be specifi- the basic mechanisms of PFM pain and/or overactivity, cally assessed. If no abnormality can be identified in the and to inform effective therapy. PFM that is responsible for the pain, and the symptoms cannot be clinically reproduced, assessment should ASSESSMENT OF PFM PAIN expand to structures that may refer pain to the PFM. AND OVERACTIVITY These include nearby muscles, joints, viscera and the central nervous system. It has been stated that ‘the There are no widely accepted clinical guidelines on the muscle in which the pain and tenderness is located often assessment of pelvic pain syndromes originating spe- serves only as a starting point for finding the source of cifically from the PFM, though several clinical practice the pain’ (Mense et al 2001, p. 84). overviews are available (FitzGerald & Kotarinos 2003, Howard 2000b, 2003, Howard & El-Minawi 2000, Shelly Much information may be gathered by objective et al 2002). There are neither assessment scales nor assessment, but the validity, reliability, responsiveness psychometric outcome measures known to have been and generalizability of this information is limited by a tested specifically for PFM pain/PFM overactivity. lack of normative data especially in subjects with PFM It is desirable that any aspect of PFM dysfunction is pain/overactivity. Despite this, the information that is evaluated using valid, reliable and responsive outcome gathered by careful assessment is of prime clinical use- measures. fulness, and may lead the way to the development of robust assessment tools and normative values of PFM Assessment techniques and outcome measures used activity. Basic PFM observation and objective assess- in studies evaluating pelvic pain (and the effect of inter- ment should be performed as described on pp. 50–55. vention) frequently borrow from other chronic pain fields or continence domains, and adapt these to make In the assessment of a patient with pelvic pain, par- the measures relevant to the presenting symptoms. ticular emphasis is placed on muscle resting tone, con- Commonly used pain scales in PFM assessment include tractile activity, ability to relax, and the presence of pain. the visual analogue scale (Wallerstein 1984) and the Sensitive and careful examination is vital. A suggested McGill Pain Questionnaire (Melzack 1975). A scale pro- process to elicit useful information in the physical posed by Marinoff & Tuner (1991) for dyspareunia com- assessment is as follows. bines both a subjective pain and functional limitation rating, but has not been tested psychometrically. 1. Visually inspect the perineum at rest. The genital hiatus may appear small and the perineal body dis- The subjective history and objective physical assess- placed anteriorly if the PFM are in a shortened ment of PFM pain should be comprehensive and rele- position. vant to the presenting symptoms while keeping in mind the coexistence of possibly one or several other pelvic 2. Observe PFM contraction, relaxation and bearing pain syndromes. A thorough biopsychosocial history down. Movement associated with PFM contraction should be taken. The psychosocial component may may be absent due to an elevated resting level of require multidisciplinary input, especially with respect tone, or display obvious change in recruitment to depression, which is one of several predictors of pain patterning, timing and proprioception. Incomplete, severity in women with chronic pelvic pain and is a abnormal (discordant) or absent relaxation may be significant indicator of response to treatment (Howard observed following attempted contraction, or the 2003). As pain is often the predominant symptom, a woman may need to attempt relaxation several thorough pain history should include the site of pain times before the PFM activity subsides. Bearing confirmed by a pain diagram, the duration of pain, down may be absent or result in an indrawing. Early nature of onset or precipitating event, the pain charac- fatigue may be noted. On attempted location and teristics, and response of pain to activity and associated isolation of a PFM contraction, accessory muscle symptoms (Hopwood 2000). It has been reported that activity is frequently seen in the thigh muscles, hips, pain from a shortened PFM may be perceived as aching buttocks and thorax. It may be helpful to note the or cramping in the coccygeal region or as a heavy feeling presence or absence of PFM indrawing with a voli- in either the vagina or rectum (FitzGerald & Kotarinos tional cough, though this is difficult to measure 2003, Meadows 1999, Shelly et al 2002) and is often objectively. exacerbated after activities that stretch the PFM (Segura et al 1979) and by sitting (Markwell 1998). Some patients 3. Check sensation/neurological integrity: the anal report non-specific tenderness or referred pain in the wink reflex may be absent due to an already con- perineum or labia (Schmidt & Vapnek 1991). tracted PFM. 4. Palpate the external tissues, sites of possible pain referral and the perineum. Palpation of the external

genitalia and perineum is systematic and considers Pelvic pain 255 tissue quality, sensation, temperature and tender- ness. Thickening of subcutaneous connective tissues ° Digital palpation. See Chapter 5, p. 51, with par- around perineal or suprapubic trigger points, or ticular emphasis on the qualitative aspects of their regions of pain referral, may be identified on PFM contractility, symmetry and coordination. palpation as altered tissue bulk, contour, elasticity Per vaginum or per rectum palpation can be and temperature, along with variation in colour used in assessment. (FitzGerald & Kotarinos 2003). Possible referral sites such as the abdomen may become hyperalgesic and ° Surface electromyography (sEMG). From the display trophic changes such as oedema, altered earlier definition of muscle tone, it follows that blood flow, subcutaneous thickening or muscle muscle spasm can be measured by EMG activ- atrophy. A device has been reported that assesses ity, provided other non-contractile sources of sensitivity to light touch in women with urogenital muscle stiffness have been identified. Although pain (Pukall et al 2004) and is reliable in the evalua- some studies have reported good reliability tion of vestibular pain. and predictability of different PFM conditions using sEMG evaluation (Glazer et al 1999), other 5. Palpate the internal vagina/rectum. This examina- studies have found that sEMG is neither diag- tion should always be performed very gently, with nostic of condition nor agrees with palpation a single, well-lubricated digit. There is known to be findings of per vaginum spasm or increased a higher prevalence of previous sexual abuse among PFM tone (Engman et al 2004, Reissing et al patients with functional disorders in comparison to 2004, van der Velde & Everaerd 1999). Surface patients with organic disease (Jacob & DeNardis EMG can also be used per rectum or via elec- 1998), with genitourinary symptoms being one of trodes attached to the perianal skin. the most common somatic complaints (Drossman 1994). Clinicians should be aware of this association ° Manometry. Reports on the use of vaginal when assessing women with pelvic pain. The clini- manometry in the evaluation of PFM pain cian should evaluate: or overactivity are scarce. One study used – Presence of pain. Identify and record site, nature vaginal manometry to screen for PFM ‘hyperto- and whether it is localized or diffuse. The aim is nicity’ (Jarvis et al 2004). These authors defined to reproduce the patient’s pain, at a mild intensity hypertonicity as vaginal resting pressure of only. Severity of pain can be rated on a visual greater than 40 cmH2O. This group of authors analogue scale. A five-point scale has been also reported a case study of a patient reported (Whitmore et al 1998), but there are no with pelvic pain due to painful and overactive reports on the validity of this scale as a scoring PFM, again using vaginal manometry as an system for PFM tenderness, but it has been used assessment tool and an outcome measure in a clinical trial (Oyama et al 2004). (Thomson et al 2005). Anal manometry has – Pelvic floor muscle tone. Mense et al (2001) been used more frequently than vaginal suggest a qualitative definition of muscle tone, manometry, predictably for studies assessing determined by the compliance (compressibility) anal sphincter activity in subjects with pelvic of a muscle. This is assessed by pressing a finger floor dyssynergia (PFD) and anorectal pain into a muscle belly to determine how easily it (levator ani syndrome and proctalgia fugax) indents and how ‘springy’ it is. Stiffness and elas- (Palsson et al 2004). ticity are assessed according to the ease of muscle indentation and return to original shape. This ° Transperineal and transabdominal ultrasound. assessment method has not been tested for valid- No studies have been found that used realtime ity with respect to the PFM. Other scales reported ultrasound as an assessment tool in patients to be relevant to the PFM are yet to undergo valid- with PFM pain or overactivity. ity and/or reliability testing (Devreese et al 2004, Hetrick et al 2003, Lamont 1978, Reissing et al – Spasm. Pelvic floor muscle spasm may be present 2004). during the examination, and may be associated – Muscle contractile activity. Interpretation of mea- with pain. Reissing et al (2004, p. 9) describe surements obtained is limited by lack of norma- spasm occurring during digital palpation as: ‘a tive data, however various tools may contribute prolonged muscle contraction not relieved by information regarding PFM contraction: reassurance’. However this description is not standardized terminology. Spasm may be invoked by vigorous examination; therefore it is para- mount to assess the PFM carefully. Spasm may occur involuntarily or be provoked by a voluntary PFM contraction attempt and therefore override the voluntary attempt.

256 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY – Relaxation of the PFM. PFM relaxation has been ate (Siddall & Cousins 2004). This may incorporate psy- defined as the diminution or termination of PFM chological and/or psychosexual evaluation and should contraction (Messelink et al 2005) and is always be performed by an appropriately skilled person. tested after a contraction. The ICS-proposed quali- tative rating scale has three levels: absent, partial, OUTCOME MEASURES complete. To date this scale has not been tested for validity nor reliability. Another scale for PFM There are no current guidelines for the selection of relaxation is described as 3 for active (good) relax- outcome measures appropriate for the assessment and ation after active contraction, 2 denotes hypertonic treatment of patients with PFM pain or overactivity. muscle with temporary relaxation after elonga- Due to the heterogenous nature of presentations of PFM tion, and 1 indicates a spastic muscle, unable to pain syndromes, outcome measure selection may be relax even after passive elongation (De Ridder et al guided by visceral or somatic perspectives. Hence 1998). This scale has been reported to be reliable in guidelines from the ICS (Lose et al 2001) or chronic (non- a population of patients with multiple sclerosis. It pelvic) pain outcome guidelines may be followed, such is assumed that elongation is achieved by stretch- as the IMMPACT recommendations (Turk et al 2003). ing the PFM, but the technique to perform this The core domains recommended for clinical trials of assessment has not been described. chronic pain treatment efficacy and effectiveness include measurement of pain, physical functioning, emotional If a comprehensive pelvic floor assessment reveals functioning, participant ratings of global improvement, neither PFM overactivity nor elicits reproduction of the symptoms and adverse events, and participant disposi- patient’s symptom(s), further assessment must address tion (Turk et al 2003). structures that have the potential to refer pain to the PFM. A detailed explanation of the mechanisms of how A comprehensive selection of useful outcome pain is referred from other muscles, nearby joints, measures relevant to disease-specific (bladder) and viscera and the central nervous system is beyond the general pain has been published (Hanno et al 2005). scope of this chapter but addressed comprehensively by Other tools exist that include measurements or ques- Mense et al (2001). It is common to find obturator inter- tions on possible PFM-related pain complaints (Litwin nus, psoas, gluteal, abdominal and piriformis muscle et al 1999, Rosen et al 2000, Pukall et al 2004). The clini- abnormality and pain in patients with PFM pain cian and researcher should carefully consider the appro- (Doggweiler-Wiygul & Wiygul 2002, FitzGerald & priateness of the selected outcome measure to the Kotarinos 2003, Hetrick et al 2003, Segura et al 1979, patient or population under review, considering reli- Shelly et al 2002). It is prudent to consider pudendal ability, validity and responsiveness to change of the nerve entrapment in all patients with PFM pain, and to particular tool being used. Outcomes should be selected review pelvic girdle instability in peri- and postnatal that reflect both subjective and objective measures. To women because these problems may present as or con- date, no outcome measures have been specifically tribute to, the presentation of PFM pain. tested for applicability to a PFM pain/overactivity population. The importance of assessing beyond the immediate pelvic floor structures for dysfunction located in other SUMMARY musculoskeletal structures that may impact on the local system has been highlighted (Baker 1993, Brown 2000, Further research is needed to determine the extent to Doggweiler-Wiygul & Wiygul 2002, FitzGerald & Kota- which muscle dysfunction can lead to or exacerbate rinos 2003, Howard 2000a, Prendergast & Weiss 2003, pain, and the extent to which pain and/or guarding Shelly et al 2002, Weiss 2001). Once neurophysiological may lead to muscle dysfunction. Consensus regarding adaptation to the chronic local pain has occurred, the assessment of the dysfunction, whether it is pain alone, sensitized sacral spinal cord is vulnerable to, and influ- overactivity alone, or a combination of both, is urgently enced by other organs and muscles that converge onto required. Reference data of normal PFM activity against the same nerves (somatovisceral convergence) or by which abnormalities in activity may be compared are general factors that increase nerve sensitivity. Dysfunc- lacking. Development and testing of robust assessment tion in other pelvic muscles (abdominal, gluteal, thigh) tools and outcome measures will facilitate well-designed, may therefore perpetuate PFM pain and dysfunction. high-quality intervention studies to measure PFM pain and overactivity. If no somatic or visceral structure can be identified as contributing to the patient’s symptom(s), further assessment of non-organic pelvic pain as the primary disease or pain per se as the primary disease is appropri-

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Pelvic pain 259 Table 9.13 Randomized and controlled trials on treatments for pelvic floor muscle pain and/or pelvic floor muscle overactivity Author Bergeron et al 2001 Design n 3-arm RCT (block randomized): CBT, sEMG BFB, surgery (vestibulectomy) Diagnosis Treatment protocol 87 enrolled, 9 refused allocation group (7 from surgery, 1 from each of CBT and BFB), leaving 78 women Drop-out Adherence Dyspareunia due to VVS Results CBT: 8 × 2 h group sessions over 12 weeks, including education, muscle relaxation, breathing, PFM exercises, vaginal dilators, distraction & imagery, skills training Author Design BFB: 8 × 45 min BFB sessions over 12 weeks, plus 2× day home use of sEMG unit n Diagnosis 13: 3 from surgery group; 10 from BFB group ITT analysis supported general trends of analysis by treatment-received outcomes Treatment protocol Treatment adherence defined as complying with ≥70% of homework sessions: Drop-out CBT: 65%, Adherence BFB: 57% Results Study completers: all groups had significant pain reduction at post-treatment and 6-month follow- up, surgery most significant reduction (surgery: 68.2%; BFB 34.6%; CBT 39.3%) All groups: equally positive and significant improvement in psychological adjustment and sexual function Peters et al 1991 2-arm RCT: laparoscopy + psychological, integrated approach 106 women: 1st arm: n = 49, mean age 35.7 years, duration of pain 3 years; 2nd arm: n = 57, mean age 35.5 years, duration of pain 4 years CPP excluding obvious organic causes Status of PFM pain or tone not detailed for all subjects Positive pain trigger points in 24% of each arm, unclear if abdominal or PFM trigger points 49% of patients in integrated approach received assessment of abdominal and PFM Content of treatment specified as ‘advice’ or ‘treatment’. Some patients received PT + other treatment in integrated approach None specified Not specified Significantly greater reductions in pain (general pain experience, disturbance of daily activities, associated symptoms), p < 0.01, in integrated approach group Not clear what effect of PT treatment alone was BFB, biofeedback; CBT, cognitive behavioural therapy; CPP, chronic pelvic pain; integrated approach, multidisciplinary or multimodal intervention, not always including physiotherapy assessment/treatment; PFM, pelvic floor muscle; sEMG, surface electromyography; VVS, vulvar vestibulitis syndrome. CPP. Physical therapy treatments may add sensory Peters et al (1991) compared two different approaches awareness and change body attitude, movement synergy in women with non-specific CPP of at least 3 months’ and dysfunctional respiration patterns. Cognitive– duration. Randomization was to either laparoscopy behavioural stress management intervention may be (standard procedure) group (n = 49) or to an integrated indicated in a subsample of patients. approach (n = 57), which included physical therapy and

260 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Table 9.14 PEDro quality score of RCT in systematic review E – Eligibility criteria specified 1 – Subjects randomly allocated to groups 2 – Allocation concealed 3 – Groups similar at baseline 4 – Subjects blinded 5 – Therapist administering treatment blinded 6 – Assessors blinded 7 – Measures of key outcomes obtained from over 85% of subjects 8 – Data analysed by intention to treat 9 – Statistical comparison between groups conducted 10 – Point measures and measures of variability provided Study E 1 2 3 4 5 6 7 8 9 10 Total score Bergeron et al 2001 + + + + − − + + + + + 8 Peters et al 1991 ++++−−−++++ 7 +, criterion is clearly satisfied; −, criterion is not satisfied; ?, not clear if the criterion was satisfied. Total score is determined by counting the number of criteria that are satisfied, except that scale item one ‘eligibility criteria specified’ is not used to generate the total score. Total scores are out of 10. dietary, environmental and psychological input: 49% of but it is not known which cognitive–behavioural subjects in the integrated group received unspecified treatment works for which patient (Vlaeyen & physical therapy. Based on outcomes measuring pain, Morley 2005). A theoretical model of cognitive and presence of associated symptoms and functional behavioural pain therapy applicable to patients with limitations, subjects in the integrated therapy approach CPP has been proposed (Reiter 1998) that combines performed better than the laparoscopy group, but a pain control techniques and activities to reduce breakdown of the results from those receiving physical disability and promote wellness (including physical therapy alone was not provided. exercise). LIFESTYLE INTERVENTIONS A randomized study comparing effectiveness of three different treatment regimens (surface electromy- Several published studies have included lifestyle modi- ography [sEMG] biofeedback, group cognitive–behav- fications and/or behavioural interventions, predomi- ioural therapy [GCBT] and surgery) for patients with nantly patient education, stress reduction techniques dyspareunia due to vulvar vestibulitis syndrome (VVS) (improved sleep patterns, breathing relaxation exer- has been reported (Bergeron et al 2001). Kegel exercises, cises), hygiene and dietary factors as part of a multi- education and counselling were included in the GCBT modal intervention for PFM pain/overactivity (Bergeron arm. From the outcomes of this study, all therapies et al 2001, King et al 1991, Peters et al 1991, Weijmar appeared to be effective treatments for patients with Schultz et al 1996). The nature of studies that combine dyspareunia due to VVS, with the surgical group attain- interventions, and the lack of outcomes measuring the ing the greatest improvement in pain reduction. As the effect of each specific lifestyle intervention, precludes GCBT included multiple therapies, the value of any one evaluation of benefit. therapy alone is not clear. In addition, lack of compari- son with a control group limits interpretation of the COGNITIVE BEHAVIOURAL effectiveness of any one of the compared therapies on INTERVENTIONS its own. Cognitive–behavioural treatments are effective in Partially- or non-randomized studies have investi- reducing the suffering of patients with chronic pain, gated the use of cognitive behavioural therapy for PFM pain related to sexual dysfunction (Seo et al 2005, Weijmar Schultz et al 1996). Although positive results were reported for the interventions, application of find- ings is limited due to the study designs.

Pelvic pain 261 EXERCISE have been reported, with varying degrees of method- ological quality (Bergeron et al 2001, FitzGerald & Incorporation of general exercise into a specific PFM Kotarinos 2003, King et al 1991, Oyama et al 2004, Thiele therapeutic approach may be useful because patients 1937, Weiss 2001). Some studies had more than two suffering chronic pain are often deconditioned. Patients arms, and others combined several conservative thera- with pain perceive an equivalent level of exertion at a pies into the treatment arm, rendering it difficult to significantly lower level of performance because of both evaluate the effectiveness of exercise or manual therapy central (cardiorespiratory) and peripheral (strength and directed to the PFM alone. recruitment) factors (Harding et al 1998). Aerobic con- ditioning, strengthening exercises directed to the trunk VOIDING AND DEFECATION TRAINING and limbs, postural correction and emphasis on func- tion rather than impairment may be important in the Women with PFM overactivity are likely to have co- recovery from CPP (Baker 1993, FitzGerald & Kotarinos existing bladder and bowel dysfunction, and therapy 2003, Shelly et al 2002). To date no studies of such treat- should seek to normalize use of both systems. Patients ments specific to PFM pain/overactivity have been are initially instructed in routine hydration to overcome found. voluntary dehydration, create sufficient urine to nor- malize bladder capacity and minimize constipation. Pelvic floor muscle exercises Voiding at regular intervals with a supported posture conducive to PFM relaxation is instituted. Bowel man- As presence of painful PFM spasm and/or overactivity agement may be indicated if stool is passed less than are frequently identified in patients presenting with second-daily or with pain or difficulty, or the patient has CPP, most reported PFM exercise regimens have either poor rectal awareness or fecal soiling. Treatment used a de-training focus (Shelly et al 2002), based on then aims to optimize emptying mechanics of both the the principle that an overactivated muscle should not bladder and bowel. The specific goals are to achieve be further loaded with active exercise until normal, consistent relaxation of the pelvic floor throughout pain-free range and contractile activity have been voiding/defecation, normalize urine flow pattern, ame- restored. Relaxation exercises are often combined with liorate postvoid residual urine and facilitate resolution a cognitive–behavioural approach involving imagery of voiding symptoms and or fecal soiling. Strategies to and de-sensitization. achieve these goals require combination therapy, gener- ally with a sizeable investment of time over a long Methods used to regain normal movement or con- period. No studies have been found that identified tractile activity to the shortened and/or painful PFM voiding or defecation training techniques in isolation include contract/relax, reciprocal inhibition and pro- from other interventions to improve PFM pain or prioceptive neuromuscular facilitation (FitzGerald & overactivity. Kotarinos 2003). The application and evidence of effec- tiveness of these techniques is limited by a lack of ADJUNCTIVE THERAPIES knowledge regarding PFM agonist/antagonist relation- ships, neuromotor control of the PFM and its synergists, Biofeedback modalities and investigation of these interventions in isolation from other techniques. Normal muscle function in Surface electromyography chronic pain conditions may also be restored via gradu- ated loading, with less emphasis on avoidance of pain Surface EMG has been popular in several studies in and more emphasis on restoring normal muscle (con- recent years (Bergeron et al 2001, Glazer 2000, Glazer tractile) activity. Once normalization is restored, PFM et al 1995, McKay et al 2001), particularly in its applica- stabilizing or strengthening exercises facilitate mainte- tion to PFM pain and overactivity impacting on sexual nance of normal function and prevention of recurrence function, but few studies have employed an RCT design, of pain/overactivity. There is currently no evidence to so interpretation of findings is limited. The study by support this assumption in the case of PFM pain. Bergeron et al (2001) adopted randomization to sEMG biofeedback group, but no control group was used. MANUAL THERAPY Post-treatment results showed that subjects receiving the sEMG intervention had improved pain and sexual Several studies investigating a range of manual therapy or exercise interventions for PFM pain/overactivity

262 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY function outcomes compared with pre-treatment levels, Ultrasound imaging but pain reduction percentage was less than that achieved in the surgical and GCBT groups. Transabdominal and transperineal realtime ultrasound are relatively new biofeedback modalities for the PFM. Use of sEMG as a biofeedback treatment for anal The onscreen image of bladder neck (transperineal) or sphincter contractile abnormalities has been reviewed bladder base (transabdominal) resting position and by Bassotti et al (2004). Their recommendations were movement (surrogate markers for PFM activity) dis- limited due to the small number of high-quality trials in plays the elevation and depression components of the the area, and were not differentiated between sEMG PFM to the patient. An overactive PFM may display and other types of biofeedback, but the modality seemed minimal excursion of movement on attempted contrac- promising in the treatment of pelvic floor dyssynergia tion and relaxation and hence may theoretically be (PFD). retrained to relax to a lower resting position following contraction. However, no studies have yet investigated Surface EMG may be a useful modality in the the role of ultrasound as a biofeedback tool in patients treatment of some PFM pain/overactivity disorders with PFM pain or overactivity. because the therapy may assist re-education of the contractile element of muscle tone; however, this Electrical stimulation modality does not address the viscoelastic contribu- tion to muscle tone. Attention to both aspects that Electricity has been a pain treatment modality for many contribute to muscle tone may be required to alleviate centuries. Today, the most common mechanism for the pain/overactivity and provide long-term relief. applying therapeutic electricity is via transcutaneous The sequence of applying the therapies might electrical nerve stimulation (TENS). logically be that muscle extensibility and eradication of trigger points should precede a programme that encour- Transcutaneous electrical (nerve) stimulation ages active muscle contraction and relaxation (Kotari- nos 2003). Generally, muscles that are in a contracted The rationale of the effectiveness of TENS for analgesia state are stretched before active exercise is commenced. is based on the gate control theory of pain modulation. Lack of controlled studies in this area limit the strength The application of TENS has been studied extensively. of recommendation of sEMG as an independent modal- Its use as an analgesic therapy for chronic, non-pelvic ity in the treatment of PFM pain or overactivity pain conditions has been evaluated in a Cochrane review disorders. (Carroll et al 2001). The results of this review were inconclusive because the published trials did not provide Manometry sufficient information on the stimulation parameters that are most likely to provide optimum pain relief Manometry records intravaginal or intra-anal squeeze or long-term effectiveness. The use of TENS for PFM pressure. No studies have been found that used vaginal pain conditions or PFM overactivity has not been manometry as a treatment in patients with PFM pain or investigated. overactivity. Muscle re-education and pain relief The use of anal manometry to treat PFD and anorectal pain has been evaluated in a systematic review Electrogalvanic stimulation (EGS) and electrical muscle by Palsson et al (2004). Only one non-randomized stimulation (ES) induce a sustained contraction, fol- controlled clinical trial (Ger et al 1993), and two lowed by muscle fatigue and eventual release of the uncontrolled trials were found. Using published spasm. guidelines to rate the clinical efficacy of psycho- physiological interventions (La Vaque et al 2002), the Use of EGS applied per rectum for patients with authors of the systematic review (Palsson et al 2004) levator syndrome was first reported in the literature in assigned a level of evidence rating of level 2 (possibly 1982, and several studies appeared in the following efficacious) to the use of pressure biofeedback as a decade (Billingham et al 1987, Ger et al 1993, Hull treatment of anorectal pain. For patients with PFD-type et al 1993, Morris & Newton 1987, Nicosia & Abcarian constipation treated with biofeedback (combined 1985, Oliver et al 1985, Sohn et al 1982). Reported success outcome of sEMG and pressure), the overall average rates ranged from 40 to 90%, but the retrospective nature probability of a successful treatment outcome was of the studies and the lack of both objective measures 62.4%; however, there were insufficient data to warrant such calculation for a treatment outcome for anorectal pain.

Pelvic pain 263 and control groups limits generalizability of the limited evidence reviewed, no recommendations of findings. treatment could be made. A small number of studies have reported the use of Application of heat EGS or ES for anorectal pain, vaginal/sexual PFM pain and levator spasm (Fitzwater et al 2003, Nappi et al Superficial heat may be applied via hot packs (hot water 2003, Park et al 2005, Seo et al 2005). The results are bottle, moist compress), heating pads (electric, chemical encouraging, but the uncontrolled study designs, wide or gel pack), or hydrotherapy. One small controlled range of populations studied and treatment protocols, study considered the effect of immersion in a warm bath and concurrent use of other modalities, limit interpreta- on resting pressures in the anal canal in a group of tions of findings. Further high-quality trials are required patients with anorectal pain (mixed diagnoses) com- to evaluate the benefits of electrical stimulation – both pared to a group of volunteers without pain (Dodi et al analgesic and muscle activation – for PFM pain and 1986). Results were positive for the therapy in the pain overactivity. group, but more rigorously designed studies are required to further test this intervention. Magnetic field therapy Deep heat may be applied via diathermy (shortwave, The use of pulsed electromagnetic fields (PEMF) for microwave) or ultrasound. Ultrasound is the preferred pelvic pain of various origin has been described in a treatment for most painful disorders, especially those small uncontrolled study (Jorgensen et al 1994). Study arising from soft tissues and ligaments because it has design limitations restrict assessment of this therapy for greater penetration and also non-thermal effects, such patients with PFM pain/overactivity. Static magnetic as increasing extensibility of tissues, so is helpful in field therapy for CPP in patients has been investigated treating trigger points. It also has the advantage of in a small double-blind pilot study (Brown et al 2002). being safe around metal and useful over small areas The primary pain site was the abdomen with PFM status (Vasudevan 1997). unknown, so the findings from this study can not be taken to apply to PFM pain/overactivity. The effect of The benefit of therapeutic ultrasound has been evalu- magnetic field therapy on a well-defined PFM pain/ ated with reference to acute perineal pain postpartum. overactivity population has not been investigated. Based on first principles, the application of ultrasound to treat chronic PFM pain or overactivity suggests a Vaginal dilators possible benefit, but studies investigating this aspect are limited. The penetration depth of the ultrasound current Dilators range in size, shape and materials, and gradu- to the target tissue in PFM pain syndromes needs evalu- ate in diameter to allow progressive application through- ation before further intervention studies using this out a course of therapy. The indications for the use of modality are proposed. One retrospective study has vaginal dilators are to stretch or mobilize contracted or investigated the effect of ultrasound on interstitial cys- inflexible soft tissues and to act as a desensitizing tool titis-associated pain (Lilius et al 1973). While favourable to progressively reduce fear and apprehension of the results were reported, application of findings is limited ability of the vaginal tissues to accommodate coital due to the study design. function. There are no published guidelines on the optimal method of application, but clinicians often Application of cold introduce the tool to a patient and encourage continua- tion as part of home therapy. Application of cold is a common and practical treatment for pain, but is used less often in chronic pain conditions Vaginal dilators have been used as part of a multi- than in acute pain conditions. Despite this, it may poten- modal approach directed to PFM pain or overactivity tially be useful due to its analgesic effect, particularly (Bergeron et al 2002, Seo et al 2005) with positive out- when acute-on-chronic flare-ups of pain are experi- comes of combined therapy. A Cochrane review (Denton enced, such as postcoital pain. No studies have been & Maher 2003) evaluated the use of vaginal dilators in found in which cryotherapy has been applied to chronic women following pelvic radiotherapy. They found that PFM pain or overactivity. the use of vaginal dilators to prevent stenosis had level II C evidence. Another Cochrane review (McGuire & PAIN MANAGEMENT Hawton 2003) evaluated interventions for vaginismus, but no studies measuring pain outcomes or PFM con- Perception of visceral (organ) and somatic (muscular) tractile activity were reported. Two trials were reviewed pain may be governed by differing neurological that included systematic desensitization with positive benefit to coital function reported. On the basis of the

264 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY mechanisms. Pelvic pain can receive contributions from SUMMARY both sources. This may explain why some pain manage- ment strategies known to be or not be effective for There is a significant lack of studies addressing the chronic non-pelvic muscular pain syndromes may differ basic elements of PFM therapy for pelvic pain or muscle in their effect on chronic PFM pain syndromes. There is overactivity. In most cases study quality limits insufficient knowledge regarding these issues at confident conclusion about treatment efficacy. There is present. an obvious need for standardized terminology, for studies that consider homogeneous patient groups, No studies were found that specifically addressed single and combination therapies, studies that apply PFM pain in isolation from PFM overactivity. Often no valid and reliable outcome measures, and RCTs to con- organic dysfunction can be identified at which to direct fidently assign evidence to the effectiveness of the local treatment. The clinician must be able to refer the intervention. patient for psychosocial treatment if required. If treat- ment of the pain per se is considered the primary focus, CLINICAL RECOMMENDATIONS TO DATE principles of chronic pain management should be fol- lowed (Siddall & Cousins 2004). The efficacy of the mul- • A comprehensive assessment incorporating a biopsy- tidisciplinary approach to chronic pain treatment has chosocial approach. been reported (Flor et al 1992). • Evaluate the PFM for the presence of overactivity, SUMMARY OF TREATMENT STUDIES trigger points, and reduced elasticity. Aim to repro- duce and quantify the patient’s symptoms. The most promising modalities for treating PFM pain/ overactivity seem to lie in the application of manual • Explain the rationale for proposed treatment moda- therapy techniques for reducing muscle tension, PFM lities. Interventions that may be applied include exercises to reinforce normal muscle contraction and cognitive–behavioural therapy, PFM relaxation and relaxation, the supplementary use of sEMG or mano- re-education exercises, manual therapy, adjunctive metry to achieve this goal, and possibly electrical stimu- therapies and pain management. lation for pain relief and assisted muscle activation and release. Patient advice, education regarding recognition • Direct treatment to the presenting symptoms and of aggravating factors and encouragement to adhere to address objective findings. home programmes of exercise would seem important elements in the success of therapy. Cognitive–behaviour • If there is no response to treatment within a rea- therapy and pain management are likely to be required sonable time frame (allow 3–4 months), refer the to supplement these other methods. patient for either psychosocial evaluation or pain management. REFERENCES Baker P K 1993 Musculoskeletal origins of chronic pelvic pain. Brown C S, Ling F W, Wan J Y et al 2002 Efficacy of static magnetic Diagnosis and treatment. Obstetrics and Gynecology Clinics of field therapy in chronic pelvic pain: a double-blind pilot study. North America 20(4):719–742 American Journal of Obstetrics and Gynecology 187(6):1581–1587 Bassotti G, Chistolini F, Sietchiping-Nzepa F et al 2004 Biofeedback Carroll D, Moore R A, McQuay H J et al 2001 Transcutaneous for pelvic floor dysfunction in constipation. BMJ 328(7436):393– electrical nerve stimulation (TENS) for chronic pain. Cochrane 396 Database of Systematic Reviews 3:CD003222 Bergeron S, Binik Y M, Khalife S et al 2001 A randomized Denton A S, Maher E J 2003 Interventions for the physical comparison of group cognitive–behavioral therapy, surface aspects of sexual dysfunction in women following pelvic electromyographic biofeedback, and vestibulectomy in the radiotherapy. Cochrane Database of Systematic Reviews 1: treatment of dyspareunia resulting from vulvar vestibulitis. Pain CD003750 91(3):297–306 Dodi G, Bogoni F, Infantino A et al 1986 Hot or cold in anal pain? A Bergeron S, Binik Y M, Khalife S 2002 In favor of an integrated study of the changes in internal anal sphincter pressure profiles. pain-relief treatment approach for vulvar vestibulitis syndrome. Diseases of the Colon and Rectum 29(4):248–251 Journal of Psychosomatic Obstetrics and Gynaecology 23(1):5–6 FitzGerald M P, Kotarinos R 2003 Rehabilitation of the short pelvic Billingham R P, Isler J T, Friend W G et al 1987 Treatment of levator floor. II: treatment of the patient with the short pelvic floor. syndrome using high-voltage electrogalvanic stimulation. International Urogynecology Journal and Pelvic Floor Diseases of the Colon and Rectum 30(8):584–587 Dysfunction 14(4):269–275, discussion 275

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266 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Female sexual dysfunction Alessandra Graziottin ASSESSMENT Last, but not least, new insights into the role of the hyperactivity of the pelvic floor in adolescence and, Women’s sexuality has only recently emerged as a possibly, infanthood, as predictors of vulnerability to central concern after years of neglect in the medical further sexual pain disorders (vaginismus and dyspa- world. The current challenge is to blend together the reunia) and to vulvar vestibulitis/vulvodynia open a biological, psychosexual and context-related compo- new preventive window for female sexual dysfunctions nents of women’s sexual response in a comprehensive (FSD) (Chiozza & Graziottin 2004, Graziottin 2005a, and meaningful scenario (Basson et al 2000, 2004). In Harlow et al 2001). Appropriate management of early this perspective, the role of pelvic floor function and hyperactivity of the pelvic floor could hopefully prevent dysfunction is of the highest importance (Alvarez & the urogenital and sexual comorbidities that affect so Rockwell 2002, Bourcier et al 2004, Graziottin 2001a, many young lives. 2005a). In this book, dedicated to physical therapy for the Levator ani’s tone, strength and performance is a pelvic floor, FSD is reviewed paying special attention to major contributor to vaginal receptivity, vaginal respon- the genital components of women’s sexual response in siveness, coital competence and pleasure (for both part- physiological and pathological conditions. However, ners), and for the orgasmic muscular response. Indirectly, the role of the biological and medical factors should pelvic floor disorders (PFD) may impair genital arousal always be considered in the appropriate psychosexual and, through a negative feedback, may affect the poten- and sociocultural context. tial for physical and emotional satisfaction, and for sexual desire and mental arousal, thus potentially affect- THE COMPLEXITY OF ing the whole of a woman’s sexual response, particu- WOMEN’S SEXUALITY larly when coital pain is a disruptive factor (Fig. 9.26) (Graziottin 2000, 2001a, 2004a). Women’s sexuality is multifactorial, rooted in biological, psychosexual and context-related factors (Basson Hyperactivity of the pelvic floor is causally associ- et al 2000, 2004, Binik et al 2002, Dennerstein 2004, ated with sexual pain disorders, namely dyspareunia Dennerstein et al 1999, Levin 2002, Graziottin 2004a, and vaginismus (Abramov et al 1994, Glazer et al 1995, 2004b, Leiblum & Rosen 2000, Klausmann 2002, Plaut et Graziottin et al 2004a, 2005a, Harlow et al 2001; Harlow al 2004, Segraves & Balon 2003), correlated to couple & Stewart 2003, Lamont 1978, McKay et al 2001) and dynamics and family and sociocultural issues. It is mul- overexertion of the pelvic floor muscles (PFM) may lead tisystemic: in men and women, a physiologic response to myalgia and ‘Kegel’ dyspareunia (DeLancey et al requires the integrity of the hormonal, vascular, nervous, 1993). muscular, connective and immune systems; this fact has been too often overlooked in women until recently The pelvic floor is central in understanding how (Bachmann et al 2002, Goldstein & Berman 1998, physiological events such as vaginal deliveries may Graziottin 2000, 2004b, Graziottin & Brotto 2004, Levin modulate levator ani’s sexual competence in a life span 2002, Meston & Frolich 2000, O’Connell et al 1998, 2004, perspective (Baessler & Schuessler 2004, Glazener 1997). Pfaus & Everitt 1995). Pelvic floor disorders are a common denominator in urogenital, proctological and sexual comorbidities Three major dimensions – female sexual identity, (Barlow et al 1997, Cardozo et al 1998, Graziottin sexual function and sexual relationship – interact to give et al 2001a, 2004a, Lauman et al 1999, Weiss 2001, women’s sexual health its full meaning or its problem- Wesselmann et al 1997). Iatrogenic problems, conse- atic profile (Graziottin 2000, 2004a, Graziottin & Basson quent to urogenital surgery, may in parallel affect and 2004). Women’s sexuality is discontinuous throughout impair both a woman’s well-being and sexual response (Graziottin 2001b).

Female sexual dysfunction 267 Dyspareunia Graziottin & Koochaki 2003). Sociocultural factors may vaginismus further modulate the perception, expression and com- plaining modality (i.e. the ‘wording’) of a sexual disor- Resolution/ Libido Arousal/ der. The meaning of sexual intimacy is a strong satisfaction Orgasm receptivity modulator of the sexual response and of the quality of satisfaction a woman experiences besides the simple Fig. 9.26 Circular model of female sexual function and adequacy of the physical response (Basson 2003, Kaplan the interfering role of sexual pain disorders. This model 1979, Klausmann 2002, Levine 2003, Plaut et al 2004). contributes to the understanding of frequent overlapping of The quality of feelings for the partner and the partner’s sexual symptoms reported in clinical practice (comorbidity) health and sexual problems may further contribute to because different dimensions of sexual response are FSD (Dennerstein et al 2003, Dennerstein 2004). Sexual correlated from a pathophysiological point of view. problems reported by women are not discrete and often Potential negative or positive feedback mechanisms operate co-occur, comorbidity being one of the leading charac- in sexual function: dyspareunia and/or vaginismus has a teristics of FSD (Basson et al 2000, 2004). direct inhibiting effect on genital arousal and vaginal receptivity and may have an indirect inhibiting effect on Co-morbidity between FSD and medical conditions orgasm, satisfaction and libido, with close interplay (e.g. urological, gynaecological proctological, metabolic, between biological and psychosexual factors. Pelvic floor cardiovascular and neurological) is increasingly disorders of the hyperactive type causally related to sexual recognized (Graziottin 2000, 2004a, 2004b, 2005b, pain disorders may rapidly affect the sexual response. Wesselmann et al 1997). For example, latent classes Modified from Graziottin 2000, with permission. analysis of sexual dysfunctions by risk factors in women indicate that urinary tract symptoms have a RR = 4.02 the life cycle and is dependent on biological (reproduc- (2.75–5.89) of being associated with arousal disorders tive events) as well as personal, current contextual and and a RR = 7.61 (4.06–14.26) of being associated with relationship variables (Basson et al 2000, 2004). sexual pain disorders according to the epidemiological survey of Laumann et al (1999), credited as being the FSD is age related, progressive and highly prevalent, best survey carried out so far. The attention dedicated affecting up to 20–43% of premenopausal women to pelvic floor related comorbidities – both between FSD (Lauman et al 1999), and 48% of older women who and between FSD and medical conditions – in this paper are still sexually active in the late postmenopause reflects the clinical relevance of this association, espe- (Dennerstein et al 2003, 2007, Graziottin & Koochaki cially in the urogynaecological and proctological 2003). domain. FSD may occur along a continuum from dissatisfac- CLASSIFICATION OF FSD tion (with potential integrity of the physiological response but emotional/affective frustration) to dys- Over the past decades, the classification of FSD has function (with or without pathological modifications), undergone intense scrutiny and revisions that mirrors to severe pathology (Basson et al 2000, 2004). Pelvic floor the new understanding of its complex aetiology. Until a disorders are among the most important and yet decade ago, the classification of FSD, which constitutes neglected medical contributors to FSD (Graziottin 2001a, the frame of reference for an appropriate diagnosis, was 2005a, 2005b). However, sexual dissatisfaction, disinter- focused almost entirely on its psychological and rela- est and even dysfunction may be appropriate for an tional components. Indeed, FSD was included in the ‘antisexual’ context (e.g. a partner affected by male broader manual of ‘psychiatric’ disorders (American sexual disorder or abusive) and they should not be Psychiatric Association 1987, 2000). The first and second labelled per se as ‘diseases’ or dysfunctions requiring consensus conferences on FSD (Basson et al 2000, 2004) medical treatment (Bancroft et al 2003). set out to define FSD with special attention to bringing together the current level of evidence with definitions FSD may occur with or without significant per- to fit women’s wording and experiences. The latest clas- sonal (and interpersonal) distress (Bancroft et al 2003, sification is shown in Box 9.3. CLINICAL HISTORY For a more accurate definition of the sexual symptoms, health care providers should also briefly investigate the

268 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Box 9.3: Classification of female sexual disorders (From Basson et al 2004) WOMEN’S SEXUAL INTEREST/DESIRE DISORDER any type of sexual stimulation as well as complaints of • Absent or diminished feelings of sexual interest or absent or impaired genital sexual arousal (vulvar swelling, lubrication). desire, absent sexual thoughts or fantasies and a lack of responsive desire. Motivations (here defined as PERSISTENT SEXUAL AROUSAL DISORDER reasons/incentives), for attempting to become • Spontaneous, intrusive and unwanted genital arousal sexually aroused are scarce or absent. The lack of interest is considered to be more than that due to a (e.g. tingling, throbbing, pulsating) in the absence of normative lessening with the life cycle and duration sexual interest and desire. Any awareness of subjective of a relationship. arousal is typically but not invariably unpleasant. The arousal is unrelieved by one or more orgasms and the SEXUAL AVERSION DISORDER feelings of arousal persist for hours or days. • Extreme anxiety and/or disgust at the anticipation of/ WOMEN’S ORGASMIC DISORDER or attempt to have any sexual activity • Despite the self-report of high sexual arousal/ SUBJECTIVE SEXUAL AROUSAL DISORDER excitement, there is either lack of orgasm, markedly • Absence of or markedly diminished cognitive sexual diminished intensity of orgasmic sensations or marked delay of orgasm from any kind of stimulation. arousal and sexual pleasure from any type of sexual stimulation. Vaginal lubrication or other signs of DYSPAREUNIA physical response still occur. • Persistent or recurrent pain with attempted or GENITAL SEXUAL AROUSAL DISORDER complete vaginal entry and/or penile vaginal • Complaints of absent or impaired genital sexual intercourse. arousal. Self-report may include minimal vulvar VAGINISMUS swelling or vaginal lubrication from any type of • The persistent or recurrent difficulties of the woman to sexual stimulation and reduced sexual sensations from caressing genitalia. Subjective sexual excitement allow vaginal entry of a penis, a finger, and/or any still occurs from non-genital sexual stimuli. object, despite the woman’s expressed wish to do so. There is often (phobic) avoidance and anticipation/fear/ COMBINED GENITAL AND SUBJECTIVE AROUSAL experience of pain, along with variable involuntary DISORDER pelvic muscle contraction. Structural or other physical • Absence of or markedly diminished subjective sexual abnormalities must be ruled out/ addressed. excitement and awareness of sexual pleasure from so-called ‘descriptors’ of the disorders, as defined by the conditions that may directly or indirectly affect sexual- International Consensus Conferences held in 1998 ity through their multisystemic impact and/or the and 2003 (Basson et al 2000, 2004). They include the consequences of pharmacological, surgical and/or following. radiotherapy treatment should be considered in the dif- ferential diagnosis of potential contributors to the The aetiology of the disorder reported FSD. Loss of sexual hormones, consequent to natural or iatrogenic menopause is a major contributor The aetiology of the disorder is further detailed in pre- to FSD (Dennerstein et al 2003, 2005). It can be addressed disposing, precipitating and maintaining factors (Box with appropriate hormonal replacement therapy 9.4) (Graziottin 2003a, 2003b, Graziottin & Brotto 2004, (Bachmann et al 2002, Graziottin 2000, 2004, Graziottin Graziottin & Leiblum 2005). Each category includes & Basson 2004). Current medication use and substance biological, psychosexual and contextual causes. abuse should be actively investigated (Segraves & Balon 2003). Biological descriptors include hormonal dysfunc- tions, PFDs, cardiovascular problems, neurological con- Psychosexual descriptors refer to emotional/affec- ditions (particularly pain-related) (Binik 2005, Binik et tive/psychic factors such as negative upbringing/ al 2002), metabolic disorders (diabetes mellitus), affec- losses/trauma (physical, sexual, emotional) (Basson tive disorders (depression and anxiety). All the medical 2003, Edwards et al 1997, Rellini & Meston 2004), body

Female sexual dysfunction 269 Box 9.4: Factors contributing to female sexual dysfunction (modified from Graziottin & Leiblum 2005) PREDISPOSING FACTORS • Postpartum depression • Vulvovaginitis/sexually transmitted diseases Biological • Sexual pain disorders • Endocrine disorders (hypoandrogenism, • Age at menopause hypoestrogenism, hyperprolactinaemia) – premature ovarian failure (POF) – menopause before • Menstrual cycle disorders/premenstrual syndrome age 40 • Recurrent vulvovaginitis and/or cystitis • Pelvic floor disorders: lifelong or acquired – premature menopause – menopause between age • Drug treatments affecting hormones or menstrual 40 and 45 cycle • Biological vs iatrogenic menopause (especially for • Contraceptive methods inappropriate for the woman premature menopause) and couple in that period of life • Iatrogenic menopause • Chronic diseases (diabetes mellitus, cardiovascular, – androgen (besides oestrogen) loss – associated disorder/disease neurological or psychiatric disease etc) • Disorders associated with premature ovarian failure • Extent and severity of menopausal symptoms and impact on well-being (POF): genetic, autoimmune • Benign diseases (e.g. endometriosis) predisposing to • Current disorders • Current pharmacological treatment iatrogenic menopause and dyspareunia • Substance abuse (mainly alcohol and opiates) • Iatrogenic menopause: bilateral oophorectomy, Psychosexual chemotherapy, radiotherapy • Loss of loving feelings toward partner • Persistent residual conditions (e.g. dyspareunia/ • Unpleasant/humiliating sexual encounters or chronic pain associated with endometriosis) experiences • Affective disorders (depression, anxiety) Psychosexual • Relationship of fertility loss to fulfilment of life goals • Inadequate/delayed psychosexual development • Borderline personality traits Contextual • Previous negative sexual experiences: sexual coercion, • Relationship discord • Life-stage stressors (e.g. child’s diseases, divorce, violence, or abuse • Body image issues/concerns separation, partner infidelity) • Affective disorders (dysthymia, depression, anxiety) • Loss or death of close friends or family members • Inadequate coping strategies • Lack of access to medical/psychosocial treatment and • Inadequate sexual education (attitudes towards facilities contraception and sexually transmitted diseases) • Economic difficulties • Dissatisfaction with social/professional role(s) MAINTAINING FACTORS Contextual • Ethnic/religious/cultural messages, expectations, and Biological • Diagnostic omissions: unaddressed predisposing/ constraints regarding sexuality • Social ambivalences towards female sexuality, when precipitating biological aetiologies • Untreated or inadequately treated comorbidities separated from reproduction or marriage • Negative social attitudes towards female – physiatric: pelvic floor disorders – urologic: incontinence, lower urinary tract contraception • Low socioeconomic status/reduced access to medical symptoms (LUTS), urogenital prolapse – proctologic: constipation, rhagades care and facilities – metabolic: diabetes mellitus • Support network – psychiatric: depression, anxiety, phobias • Pharmacological treatments PRECIPITATING FACTORS • Substance abuse • Multisystemic changes associated with chronic disease Biological or secondary to menopause • Negative reproductive events (unwanted pregnancies, abortion, traumatic delivery with damage of the pelvic floor, child’s problems, infertility)

270 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Box 9.4: Factors contributing to female sexual dysfunction—cont’d – hormonal • Diminished affection for or attraction to partner – vascular • Unaddressed affective disorders (depression and/or – muscular – neurological anxiety) – immunological • Negative perception of menopause-associated changes • Contraindications to hormone replacement therapy • Body image concerns and increased body changes (HRT) • Inadequacy of hormone replacement therapy in (wrinkles, body shape/weight, muscle tone) ameliorating menopause-associated biological symptoms Contextual • Omission of menopause and female sexual dysfunction Psychosexual • Low or loss of sexual self-confidence from provider’s diagnostic and therapeutic approach • Performance anxiety • Lack of access to adequate care • Distress (personal, emotional, occupational, sexual) • Partner’s general health or sexual problems or concerns • Ongoing interpersonal conflict (with partner or others) • Environmental constraints (lack of privacy, lack of time) image issues (Graziottin 2006), binge eating disorders Level of distress affecting self-esteem and self-confidence, attachment dynamics (secure, avoidant, anxious) (Clulow 2001) that The level of distress indicates a mild, moderate, or may also modulate the level of trust in the relationship, severe impact of the FSD on personal life (Bancroft et al the intensity of the commitment, and the confidence 2003, Dennerstein et al 2005, Graziottin & Koochaki in loving and attitude towards affective and erotic 2003). Sexual distress should be distinguished from intimacy. non-sexual distress and from depression. The degree of reported distress may have implications for the woman’s Contextual descriptors include past and current sig- motivation for therapy and for prognosis. nificant relationships (Basson 2003, Leiblum & Rosen 2000), cultural/religious restrictions (Basson et al 2000, An interdisciplinary team is the most valuable 2004), current interpersonal difficulties (Klausmann resource for a patient-centred approach, both for diag- 2002, Liu 2003), partner’s general health issues and/or nostic accuracy and tailored treatment. Key professional sexual dysfunctions (Dennerstein et al 1999, 2003, 2004), figures include a medical sexologist, gynaecologist, inadequate stimulation and unsatisfactory sexual and urologist, psychiatrist, endocrinologist, physiatrist, emotional contexts (Levine 2003). anaesthetist, neurologist, proctologist, dermatologist, psychotherapist (individual and couple), and physical Generalized or situational? therapist. Physical therapists are emerging as a key resource in addressing PFDs, which are finally receiving Is the disorder generalized (with every partner and in the attention they deserve as key biological factors in every situation) or situational, specifically precipitated the aetiology of FSD. by partner-related or contextual factors, which should be specified (Basson et al 2000, 2004)? Situational prob- WOMEN’S SEXUAL DESIRE/ lems usually rule out medical factors that tend to affect INTEREST DISORDER the sexual response with a more generalized effect (Graziottin 2004a, 2004b). Hypoactive sexual desire disorder (HSDD) is the sexual dysfunction most frequently reported by women Lifelong or acquired? (Dennerstein et al 2003) The complaint of low desire becomes a sexual disorder when it causes severe per- Has the disorder been lifelong (from the very first sexual sonal distress to the woman. Population data indicate a experience) or is it acquired after months or years of prevalence of low desire in 32% of women between 18 satisfying sexual intercourse? Asking the woman what and 59 years of age (Laumann et al 1999). A recent in her opinion is causing the current FSD may offer European survey of 2467 women, in France, UK, useful insights into the aetiology of the disorder, par- Germany and Italy indicates that the percentage of ticularly when it is acquired (Plaut et al 2004);

Female sexual dysfunction 271 women with low sexual desire is 19% in the age cohort Box 9.5: Sexual history for hypoactive sexual from 20 to 49 years; 32% in the same age cohort in desire disorders and associated sexual women who have experienced surgical menopause; comorbidities. Modified from Graziottin 2004a, 46% in postmenopausal women aged 50 to 70 years with with permission natural menopause; and 48% in the same age cohort, after surgical menopause (Graziottin & Koochaki GENERAL WELL-BEING 2003). • How do you feel (physically and mentally)? • Are you currently sexually active? The percentage of women distressed by their loss of • If not, is that a concern for you? If yes, how’s desire and having a HSDD was 27% in premenopausal women and 28% after surgical menopause, in the age your sex life? cohort 20–49 years, respectively; 11% in women with natural menopause; and 14% in those with surgical SEXUAL FUNCTION menopause aged 50 to 70 years (Graziottin & Koochaki • Have you always suffered from low sexual desire 2003). The likelihood of HSDD increases with age, while the distress associated with the loss of desire is inversely (lifelong) or has it faded recently (acquired)? correlated with age. • Do you suffer from other sexual symptoms? • For example, do you experience vaginal dryness? Surgical menopause secondary to bilateral oophorec- • Do you have difficulty in getting aroused or tomy has a specific damaging effect due to the loss of ovarian oestrogens and androgens. Ovaries contribute lubricated? to more than 50% of total body androgens in the fertile • Do you have difficulty reaching orgasm? age. A European survey on 1356 women indicated that • Do you feel pain during or after intercourse? women with surgical menopause had an odds ratio • Do you suffer from cystitis 24–72 hours after (OR) of 1.4 (CI = 1.1, 1.9; p = 0.02) of having low desire. Surgically menopausal women were more likely to have intercourse and/or other urinary symptoms? HSDD than premenopausal or naturally menopausal • Is there any lifestyle-related factor that may women (OR = 2.1; CI = 1.4, 3.4, p = 0.001). Sexual desire scores and sexual arousal, orgasm and sexual pleasure affect your sexual desire (e.g. body weight, alcohol were highly correlated (p < 0.001). Women with HSDD or drug abuse, little sleep, fatigue, professional were more likely to be dissatisfied with their sex life and distress)? their partner relationship than women with normal • What, in your opinion, is causing or worsening desire (p < 0.001) (Dennerstein et al 2005). your sexual disorder? Is it a psychological problem, a past or current negative event (e.g. The leading biological aetiology of HSDD includes sexual harassment or abuse), something related to not only hormonal factors (low testosterone, low oestro- your physical health or your relationship, or gens, or high prolactin), but also depression and/or something else? comorbidity with major diseases (see Box 9.4). Prema- ture iatrogenic menopause is the most frequent cause of SEXUAL RELATIONSHIP a biologically determined generalized loss of desire; the • Do you have a stable relationship? younger the woman, the higher the distress this loss • How’s your relationship? Are you satisfied with it? causes to her (Dennerstein et al 2005, Graziottin & • How is your partner’s health (general and sexual)? Basson 2004). Key questions to address women’s desire • Do you feel that your current sexual problem is disorders are summarized in Box 9.5. Unaddressed pain associated with sexual pain disorders, and causally more dependent on a physical or couple (loving/ related, among others, to hyperactivity of the pelvic intimacy) problem? floor up to a frank myalgia, is a frequently overlooked • Is your sexual problem present in every context predisposing, precipitating and maintaining factor of and/or with different partners (generalized), or do acquired loss of desire (Graziottin 2000, Graziottin & you complain of it in specific situations or with a Brotto 2004, Graziottin et al, 2001a, 2001b, 2004a). specific partner (situational)? • What made you aware of it and willing to look for What the clinician should look for help (e.g. intolerable personal frustration, fear of losing the partner, partner’s complaints, new hope If a possible biological aetiology is suggested by the for effective treatment, more self-confidence in clinical history, the clinician should assess (Plaut et al reporting)? 2004) the following. • Are you personally interested in improving your sex life?

272 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY • Hormonal profile: acid, with dramatic modification of the vaginal ecosys- – total and free testosterone, dihydroepiandrosterone tem, and an average reduction of vaginal secretions sulfate (DHEAS), prolactin, 17β-estradiol, sex of 50%. hormone binding globulin (SHBG), with a plasma sample on the fifth or sixth day from the beginning Leading biological aetiologies of arousal disorders of the menses in fertile women; include loss of sexual hormones, primarily oestrogen, – follicle stimulating hormone (FSH) and all of the and PFDs. above, in perimenopausal women; – thyroid stimulating hormone (TSH) when indi- • Hyperactivity of the pelvic floor may reduce the vidually indicated. introital opening causing dyspareunia. (Unwanted) pain is indeed the strongest reflex inhibitor of genital • The pelvic floor: in all its components, with an accu- arousal: genital arousal disorders, and the conse- rate gynaecological, sexological and/or physiatric quent vaginal dryness, are often comorbid with examination, particularly when comorbidity with dyspareunia (Graziottin 2001a, 2004a, 2005b). arousal, orgasm and/or sexual pain disorders is Psychosexual and relational factors may also concur reported. in this disorder (Box 9.6); • Psychosexual factors and affective state: depression • A hypoactive or damaged pelvic floor (after trau- first, with referral to a psychiatrist, sex therapist or matic deliveries, with macrosomic children or couples therapist for a comprehensive diagnosis if vacuum extraction) (Baessler & Schuessler 2004) may indicated (Leiblum & Rosen 2000). contribute to genital arousal disorder because it reduces the pleasurable sensations the woman (and AROUSAL DISORDERS partner) feel during intercourse (Graziottin 2004a). Central arousal disorders (‘I do not feel mentally What the clinician should look for excited’) are comorbid with loss of sexual desire and can only be separated from it with difficulty. Genital arousal When a patient complains of an arousal disorder, the disorders with their key subjective symptom, vaginal clinician should check (Plaut et al 2004): dryness, are increasingly reported with age. In epide- miological surveys 19–20% of women complain of • hormonal profile (see above), more so in hypoestro- arousal disorders (Lauman et al 1999). This figure may genic conditions such as longlasting secondary increase to 39–45% in postmenopausal sexually active amenorrhoea, puerperium, menopause (especially patients (Dennerstein et al 2003, 2005). iatrogenic); Mental arousal may be triggered through different • general and pelvic health, focusing on pelvic floor pathways: biologically by androgens and oestrogens, trophism: vaginal, clitoral, vulvar, connective and psychologically by motivational forces such as intimacy muscular (looking for both hypertonic and hypotonic needs, (i.e. the affective needs of love, tenderness, atten- pelvic floor dysfunctions) (Graziottin 2001a, 2004a); tion, bonding and commitment) (Laan & Everaerd 1995). With successful genital arousal, most women produce • vaginal pH with a simple stick because vaginal increased quantities of vaginal transudate. The neu- acidity correlates well with oestrogen tissue levels rotransmitter vasoactive intestinal peptide (VIP) stimu- (Graziottin 2004a); lates this neurogenic transudate production. Oestrogens are believed to be powerful ‘permitting factors’ for VIP • biological factors, such as vulvar vestibulitis or poor (Levin 2002). The neurotransmitter nitric oxide (NO) outcome of perineal/genital surgery causing introital stimulates the neurogenic congestion of the clitoral and and/or pelvic pain (see dyspareunia); vestibular bulb corpora cavernosa. (Levin 2002). Reduc- tion in vaginal lubrication is one of the most common • vascular factors that may impair the genital arousal complaints of postmenopausal women. When the response (smoking, hypercholesterolaemia, athero- plasma oestradiol concentration is below 50 pg/mL (the sclerosis, hypertension, diabetes mellitus) (Goldstein normal range in fertile women being 100–200 pg/mL) & Berman 1998); vaginal dryness is increasingly reported (Sarrel 1998). Physiological studies indicate that after menopause the • relational issues, inhibition and/or erotic illiteracy if vaginal pH increases from 3.5–4.5 to 6.0–7.39 owing to a poor quality of mental arousal, poor or absent fore- decreased glycogen production and metabolism to lactic play are reported; if this is so refer the willing couple to the sexual or couple therapist (Leiblum & Rosen 2000)

Female sexual dysfunction 273 Box 9.6: Aetiology of dyspareunia. Modified ORGASMIC DISORDERS from Graziottin 2004a, with permission Orgasmic disorder has been reported in an average of Many causes may overlap or be associated with 24% of women during their fertile years in the epide- coital pain with complex pathophysiological interplay. miological study of Lauman et al (1999). After the meno- The relative weight of each cause in the individual pause, 39% of women complain of orgasmic difficulties, woman may change with chronicity of pain and with 20% complaining that their clitoris ‘is dead’, accord- progressive involvement of other pelvic organs. ing to Sarrel & Whitehead (1985). BIOLOGICAL Orgasm is a sensorimotor reflex that may be trig- gered by a number of physical and mental stimuli (Mah Superficial/introital and/or mid-vaginal dyspareunia & Binik 2004). • Infectious: vulvitis, vulvar vestibulitis, vaginitis, Genital orgasm requires: cystitis • Inflammatory, with mast cell upregulation • integrity of the pudendal sensory nerve fibres (S2, S3, • Hormonal: vulvovaginal atrophy S4) and corticomedullary fibres; • Anatomical: fibrous hymen, vaginal agenesis • Muscular: primary or secondary hyperactivity of • cavernosal structures that engorged and adequately stimulated convey pleasant sensory stimuli to the levator ani muscle medullary centre and the brain; • Iatrogenic: poor outcome of genital surgery, pelvic • adequate motor response of the PFMs. radiotherapy • Neurological: inclusive of neuropathic pain A short medullary reflex may trigger a muscular • Connective and immunological: Sjögren’s response characterized by involuntary contraction (three to eight times, in single or repetitive sequences) syndrome of the levator ani. The medullary reflex may be eased or • Vascular blocked, respectively, by corticomedullary fibres that convey both excitatory stimuli when central arousal Deep dyspareunia is maximal and inhibitory ones when arousal is poor. • Endometriosis Performance anxiety may activate adrenergic input, • Pelvic inflammatory disease (PID) which disrupts the arousal response. Inhibitory fibres • Pelvic varicocoele are mostly serotonergic: this explains the inhibitory • Chronic pelvic pain and referred pain effects of selective serotonin reuptake inhibitors (SSRIs) • Outcome of pelvic or endovaginal radiotherapy on orgasm in both men and women (Seagraves & • Abdominal nerve entrapment syndrome Balon 2003). Fear of leaking during intercourse may inhibit coital intimacy and/or orgasm (Barlow et al PSYCHOSEXUAL 1997, Cardozo et al 1998): leakage during coital thrust- • Comorbidity with desire and /or arousal disorders, ing is usually associated with stress incontinence, while leakage at orgasm is associated with urge or vaginismus incontinence. • Past sexual harassment and/or abuse • Affective disorders: depression and anxiety Significant age-associated changes in the content of • Catastrophism as leading psychological coping smooth muscle and connective tissue in the clitoral cav- ernosa contributing to age-associated clitoral sexual modality dysfunction causing hypo-anorgasmia, have been dem- onstrated from the first to the sixth decade of life and CONTEXT OR COUPLE RELATED beyond by computer-assisted histomorphometric image • Lack of emotional intimacy analysis (Tarcan et al 1999). • Inadequate foreplay • Conflicts: verbally, physically or sexually abusive What the clinician should look for partner Using the information emerging from the clinical history • Poor anatomical compatibility (penis size and/or as a starting point, the physician should assess: infantile female genitalia) • hormonal balance; • Sexual dissatisfaction and consequent inadequate • signs and symptoms of vulvar dystrophy and, spe- arousal cifically, of clitoral and vaginal involution (Graziottin 2004a);

274 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY • traumatic consequences of female genital mutilation From the pathophysiological point of view, vulvar (infibulation); vestibulitis involves the upregulation of: • signs and symptoms of urge, stress or mixed incon- • the immunological system (i.e. of introital mast cells tinence, with either a hypotonic or hypertonic pelvic with hyperproduction of both inflammatory mole- floor (Barlow et al 1997, Cardozo et al 1998); cules and nerve growth factors [NGF]) (Bohm-Starke et al 1999, 2001a, 2001b, Bornstein et al 2002, 2004); • iatrogenic influences when potentially orgasm- inhibiting drugs are prescribed. • the pain system, with proliferation of local pain fibres induced by the NGF (Bornstein et al 2002, 2004, SEXUAL PAIN DISORDERS Westrom & Willen 1998), which may contribute to neuropathic pain (Graziottin & Brotto 2004, Woolf Various degrees of dyspareunia are reported by 15% of 1993); coitally active women, and 22.5–33% of postmenopausal women. Vaginismus occurs in 0.5–1% of premenopausal • hyperactivity of the levator ani, which can be ante- women. However, mild hyperactivity of the pelvic floor, cedent to vulvar vestibulitis (Abramov et al 1994, that could coincide with grade I or II of vaginismus Graziottin 2005a, Graziottin et al 2004a), or second- according to Lamont (1978) may permit intercourse, ary to the introital pain. causing coital pain (Graziottin 2003b, 2005a). In either case, addressing the muscle component is a Vaginal receptiveness is a prerequisite for inter- key part of treatment (Bergeron et al 2001, Glazer et al course, and requires anatomical and functional tissue 1995, McKay et al 2001). Hyperactivity of the pelvic floor integrity, both in resting and aroused states. Normal may be triggered by non-genital, non-sexual causes, such trophism, both mucosal and cutaneous, adequate hor- as urological factors (urge incontinence, when tightening monal impregnation, lack of inflammation, particularly the pelvic floor may be secondary to the aim of reinforc- at the introitus, normal tonicity of the perivaginal ing the ability to control the bladder), or anorectal prob- muscles, vascular, connective and neurological integ- lems (anismus, haemorrhoids, rhagades). Comorbidity rity, and normal immune response are all considered with other sexual dysfunctions – loss of libido, arousal necessary to guarantee vaginal ‘habitability’. Vaginal disorders, orgasmic difficulties, and/or sexual pain- receptiveness may be modulated by psychosexual, related disorders – is frequently reported with persist- mental and interpersonal factors, all of which may result ing/chronic dyspareunia (Graziottin et al 2001b). in poor arousal with vaginal dryness (Plaut et al 2004). What the clinician should look for Fear of penetration, and a general muscular arousal secondary to anxiety may cause a defensive contrac- The diagnostic work-up should focus on: tion of the perivaginal muscles leading to vaginismus (Reissing et al 2003, 2004, van der Velde et al 2001). This • physical examination to define the ‘pain map’ disorder may be the clinical correlate of a primary neu- (Graziottin 2001a, Graziottin & Basson 2004, Graziottin rodystonia of the pelvic floor, as recently proven with et al 2001c), (any site in the vulva, mid-vagina and needle electromyography (Graziottin et al 2004a). It may deep vagina where pain can be elicited) because be so severe as to prevent penetration completely. Vagi- location of the pain and its characteristics are the nismus is the leading cause of unconsummated mar- strongest predictors of type of organicity (Meana et al riages in women. The defensive pelvic floor contraction 1997), and including pelvic floor trophism (vaginal may also be secondary to genital pain of whatever cause pH), muscular tone, strength and performance (Travell & Simons 1983; Wesselmann et al 1997). (Alvarez & Rockwell 2002, Bourcier et al 2004), signs of inflammation (primarily vulvar vestibulitis) Dyspareunia is the common symptom of a variety of (Friedrich 1987, Graziottin & Brotto 2004), poor out- coital pain-causing disorders (see Box 9.6). Vulvar ves- comes of pelvic (Graziottin 2001b) or perineal sur- tibulitis is its leading cause in premenopausal women gery (primarily episiotomy/episiorraphy) (Glazener (Abramov et al 1994, Friedrich 1987, Glazer et al 1995, 1997), associated urogenital and rectal pain syn- Graziottin 2001a, Graziottin & Brotto 2004, Graziottin dromes (Wesselmann et al 1997), myogenic or neuro- et al 2004b). The diagnostic triad is genic pain (Bohm-Starke 2001a, 2001b, Bornstein et al 2002, 2004) and vascular problems (Goldstein & 1. severe pain upon vestibular touch or attempted Berman 1998); vaginal entry; • psychosexual factors, poor arousal and coexisting 2. exquisite tenderness to cotton-swab palpation of the vaginismus (Leiblum 2000, Pukall et al 2005); introital area (mostly at 5 and 7, when looking at the introitus as a clock face); 3. dyspareunia (Friederich 1987).

Female sexual dysfunction 275 • relationship issues (Reissing et al 2003); Box 9.7: Talking with patients about sexual issues. From Plaut et al 2004, with permission • hormonal profile, if clinically indicated, when dyspa- reunia is associated with vaginal dryness. • Ask pointed questions and request clarification that will result in sufficiently specific data about Pain is rarely purely psychogenic, and dyspareunia the patient’s symptoms is no exception. Like all pain syndromes, it usually has one or more biological aetiological factors. Hyperactive • Be sensitive to the optimal time to ask the most PFDs are a constant feature. However, psychosexual emotionally charged questions and relationship factors, generally lifelong or acquired low libido because of the persisting pain, and lifelong • Look for and respond to non-verbal cues that may or acquired arousal disorders due to the inhibitory effect signal discomfort or concern of pain, should be addressed in parallel to provide com- prehensive, integrated and effective treatment. • Be sensitive to the impact of emotionally charged words (e.g. rape, abortion) ETHICAL, LEGAL AND COUNSELLING RELATED CONSIDERATIONS • If you are not sure of the patient’s sexual orientation, use gender-neutral language in The topic of sexuality requires special attention being referring to his or her partner given to confidentiality and informed consent depend- ing on the profession of the clinician and any local laws • Explain and justify your questions and procedures that place limits on confidentiality, such as in the report- • Teach and reassure as you examine ing of sexual abuse. Although the discussion of sexual • Intervene to the extent that you are qualified and matters is often an appropriate part of medical evalua- tion and treatment, it is also important not to sexualize comfortable; refer to qualified medical or mental the clinical setting when it is not necessary. Patients may health specialists as necessary be confused or embarrassed by comments about their attractiveness, disclosure of intimate personal informa- clinical history taking: ‘How’s your sex life’? so offering tion by the clinician, or by sex-related questions that are an opening for current or future disclosure. The wish is neither clinically relevant nor justifiable. The modesty that the new attention to women’s right for a better of the patient should be respected in touching, disrobing sexual life will significantly help increase the physician’s and draping procedures (Plaut et al 2004). Key aspects confidence in asking and listening to complaints of FSD of appropriate counselling attitudes are summarized in and his or her ‘clinical impact factor’ (i.e his or her Box 9.7. ability to appropriately diagnose and effectively treat FSD). CONCLUSION In the tailoring of treatment, the physical therapist To address the complexity of FSD requires a balanced has a crucial role, especially in sexual pain disorders, clinical perspective between biological and psychosex- either lifelong or acquired, and in acquired desire, ual/relational factors. Apart from counselling the FSD arousal or orgasmic disorders secondary to coital pain. complaint in a competent way when the issue is openly The enthusiasm that many physical therapists have raised by the patient, physicians and physical therapists when they can effectively treat or co-treat FSD for which can contribute to improving the quality of (sexual) life a woman has been doctor-shopping for years are mir- of their patients, by routinely asking them during the rored by the woman’s satisfaction in finally feeling lis- tened to, respected in the truth of her coital pain or other sexual complaints, and re-empowered in her body con- fidence, when she is taught how to command and appropriately relax her key muscles for sex and love. REFERENCES American Psychiatric Association 1987 Diagnostic and statistical manual of mental disorders, 3rd edn. American Psychiatric Abramov L, Wolman I, David M P 1994 Vaginismus: An important Association, Washington DC factor in the evaluation and management of vulvar vestibulitis syndrome. Gynecological and Obstetrical Investigations 38:194– American Psychiatric Association 2000 Diagnostic and statistical 197 manual of mental disorders, 4th edn. American Psychiatric Association, Washington DC Alvarez D J, Rockwell P G 2002 Trigger points: diagnosis and management. American Family Physician 65(4):653–660

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In: Weiss J M 2001 Pelvic floor myofascial trigger points: manual Leiblum S R, Rosen R C (eds) Principles and practice of sex therapy for interstitial cystitis and the urgency-frequency therapy, 3rd edn. Guilford, New York, p 181–202 syndrome. Journal of Urology 166:2226–2231 Leiblum S R, Rosen R C (eds) 2000 Principles and practice of sex Wesselmann U, Burnett A L, Heinberg L 1997 The urogenital and therapy, 3rd edn. Guilford, New York rectal pain syndromes. Pain 73(3):269–294 Levin R J 2002 The physiology of sexual arousal in the human Westrom L V, Willen R 1998 Vestibular nerve fiber proliferation female: a recreational and procreational synthesis. Archives of in vulvar vestibulitis syndrome. Obstetrics and Gynecology Sexual Behaviour 31(5):405–411 91:572–576 Levine S B 2003 The nature of sexual desire. Archives of Sexual Woolf C J 1993 The pathophysiology of peripheral neuropathic pain: Behavior 32(3):279–285 abnormal peripheral input and abnormal central processing. Acta Neurochirurgica. Supplementum 58:125–130 Liu C 2003 Does quality of marital sex decline with duration? Archives of Sexual Behavior 32(1):55–60 TREATMENT Mah K, Binik I M 2004 Female orgasm disorders: a clinical Alessandra Graziottin approach. In: Graziottin A (ed) Female sexual dysfunction: a clinical approach. Urodinamica 19(2):99–104. Online. Available: INTRODUCTION http://www.alessandragraziottin.it There is no effective therapy without accurate and McKay E, Kaufman R, Doctor U et al 2001 Treating vulvar comprehensive diagnosis. This is even more true for vestibulitis with electromyographic biofeedback of pelvic female sexual dysfunction (FSD), which usually has a floor musculature. Journal of Reproductive Medicine multifactorial aetiology. Biological, psychosexual and 46:337–342 context-related factors (Basson et al 2000, 2004), further characterized as predisposing, precipitating and main- Meana M, Binik Y M, Khalife S et al 1997 Dyspareunia: sexual taining (Graziottin 2005a, Graziottin & Brotto 2004) may dysfunction or pain syndrome? Journal of Nervous Mental interact to give the FSD that the woman is complaining Diseases 185(9):561–569 about its specific individual characteristics. Meston C M, Frolich P F 2000 The neurobiology of sexual function. Archives of General Psychiatry 57:1012–1030 O’Connell H E, Anderson C R, Plenter R J, Hutson J M 2004 The clitoris: a unified structure. Histology of the clitoral glans, body, crura and bulbs. In: Graziottin A (guest ed.) Female dysfunction: clinical approach. Urodinamica 14:127–132 O’Connell H E, Hutson J M, Anderson C R et al 1998 Anatomical relationship between urethra and clitoris. Journal of Urology 159:1892–1897 Pfaus J G, Everitt B J 1995 The psychopharmacology of sexual behaviour. In: Bloom F E, Kupfer D (eds) Psycho-pharmacology. Raven Press, New York, p 743–758

278 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY The accurate diagnosis of FSD is currently a chal- • accurate examination of the woman, and particularly lenge for researchers and clinicians. The temptation of of the external genitalia, vagina and pelvic floor searching for the aetiology, preliminary to finding the (Graziottin 2004a,b, Graziottin et al 2001a,b,c) – optimal treatment, is usually inappropriate, and con- careful physical examination should be performed tinuously frustrated by the complexity of female because the biological aetiology of FSD is better diag- sexuality. nosed when attention is paid to vulvovaginal tro- phism with pH recording; hypo- or hypertonic pelvic The delay in the medical approach to FSD and the floor conditions, with tender and trigger point evalu- persistent psychological perspective make it difficult to ation; diagnosis of inflammation and infection, with have evidence-based medical treatments of FSD except culture examinations when indicated; and the pain- in the domain of sexual hormones. As a result of diag- map accurate description (Graziottin et al 2001c) nostic delays, inadequacies, and gender biases, no treat- because location of pain and its onset characteristics ment for FSD is currently approved with this specific are the strongest predictors of its biological aetiology indication with the exception of a clitoral device indi- (Meana et al 1997). cated for female arousal disorders (Wilson et al 2001). From the clinical point of view, an integrated diagnostic This is mandatory when genital arousal disorders, and treatment approach is therefore necessary to tailor sexual pain disorders (vaginismus and dyspareunia) treatment according to the individual and couple’s and orgasm disorders are complained of. It may be needs at the best of our current scientific and clinical useful even when sexual desire disorders and/or sub- knowledge (Basson et al 2000, 2004, Graziottin 2001a, jective sexual arousal disorders (‘I do not feel mentally 2004a, 2004b, Plaut et al 2004). excited’) are the leading complaints to diagnose biologi- cally rooted comorbidities with other FSD. Comorbidity The available evidence for treatment of FSD will be should be accurately recorded with attention to which reviewed. Special focus will be given to the role of the sexual disorder came first. On the positive side, the physical therapist in addressing the muscle and pelvic cascade of positive feedback when a treatment is effec- floor-related contributors to FSD. tive may cause a significant improvement in all domains of sexual response as several studies have proven DIAGNOSTIC KEY POINTS (Alexander et al 2004, Graziottin & Basson 2004, Laan et al 2001, Shifren et al 2000, Simunic et al 2003). Key points in the FSD diagnosis, preliminary to a well tailored treatment, should be: In stable couples, current feelings for the partner (i.e. quality of the relationship, and the quality of the part- • accurate listening to the complaint’s wording, to ner’s sexuality [inclusive of general and sexual health]) verbal and non-verbal messages, with: should be investigated as well (Dennerstein et al 1999, – definition of the nature of the disorders; 2003, 2007, Klausmann 2002). – is it lifelong or acquired? – is it generalized or situational? The woman’s general health should be examined, – is it organic, psychogenic, contextual or, as in most with special focus on conditions that may directly or cases, mixed? with definition of key predisposing, indirectly impair the woman’s mental and/or genital precipitating and maintaining factors; response (Basson et al 2000, 2004, Graziottin 2000, 2003a, – how severe is the distress it causes? 2004a,b). – are there sexual and/or medical (e.g. urogenital, proctological) associated comorbidity – comorbidi- PRINCIPLES OF FSD THERAPY ties may be other types of FSD, but also other medical conditions, such as urological, gynaeco- A growing body of evidence implicates hormonal factors logical, proctological, metabolic, cardiovascular in the genesis of FSD (Alexander et al 2004, Graziottin and neurological diseases – for example, urinary & Basson 2004, Laan et al 2001, Sarrel 1998, Shifren et al tract symptoms have a relative risk (RR) of: 2000, Simunic et al 2003,). Indeed, during a woman’s ° 4.02 (2.75–5.89) of being associated with arousal entire reproductive life span, sex hormones exert both disorders organizational and activational effects on sexual behav- ° 7.61 (4.06–14.26) of being associated with sexual iour. The action of hormones is mediated by non- pain disorders (Laumann et al 1999) genomic and genomic pathways. Current evidence – partner’s related issues; indicates that there is a specific place in the treatment – the personal motivation the woman has (or does of FSD for pharmacological hormones, for the most part not have) to treatment of FSD, which includes the in postmenopausal women (Alexander et al 2004, meaning of the symptom for the woman;

Female sexual dysfunction 279 Graziottin & Basson 2004, Laan et al 2001, Sarrel 1998, at or below the lowest quartile of the normal range for Shifren et al 2000, Simunic et al 2003). Sexual hormones women in their reproductive years also suggest a diag- may be delivered by various routes: oral, transdermal, nosis of androgen insufficiency syndrome. A recent, nasal, vaginal, through subcutaneous implants or intra- systematic review of all available data from randomized uterine devices. The most important difference between and placebo-controlled trials of treatment for FSD in the oral route and those that bypass the first hepatic pass postmenopausal women concluded that use of many is that the oral treatment induces an increase of sex frequently used treatments is not supported by ade- hormone-binding globulin (SHBG) by as much as quate evidence (Madelska & Cummings 2003). In their 133%, thus significantly reducing free testosterone review of randomized, controlled trials involving the (Vehkavaara et al 2000). Levels of SHBG seem to be use of T in oestrogen-replete women, Alexander et al unaffected by hormones delivered via transdermal, (2004) found general support for the positive effect of T nasal, and vaginal routes. on different dimensions of women’s sexuality. One limit of this analysis is that some of the reviewed studies Depending on the aetiological diagnosis of the involved supraphysiological doses. In a study by Shifren leading disorder, the therapy should consider one or et al (2000), the total T was raised above the normal more of the following leading options. range, but the free and bioavailable T remained within the normal range. Sherwin (2002) and more recently Libido disorder Alexander et al (2004) in their reviews of randomized, controlled trials, found that adding androgens to the Libido and subjective sexual arousal disorder (‘I do not standard oestrogen replacement had added sexual feel mentally excited’), often diagnosed in comorbidity, benefit in different domains, sexual desire first. either lifelong or, more frequently, acquired, may benefit from the following. Ostrogens and progestogens In naturally postmeno- Medical treatment pausal women, progesterone or progestogens protect the endometrium. The positive effect of oestrogens on Hormones the well-being and sexuality of postmenopausal women Androgen The major androgens in women include may be variably modulated according to the type of progestogens added in the hormonal replacement testosterone (T) and dihydrotestosterone (DHT), therapy (Graziottin & Leiblum 2005). Progesterone, the dehydroepiandrosterone sulphate (DHEA-S), dehydro- physiological hormone, may have a mildly inhibiting epiandrosterone (DHEA), and androstenedione (A) effect on sexual desire. Progestogens, synthetic mole- (Bachmann et al 2002). T is the most potent androgen. cules with progestinic action, have a wide spectrum of Plasma T levels range from 0.2 to 0.7 ng/mL (0.6– actions from strongly antiandrogenic to neutral to 2.5 nmol/L), with significant fluctuations related to the androgenic, according to: phase of the menstrual cycle. T is converted to DHT, but can also be aromatized to estradiol (E2) in target tissues; • their structure (whether they are derived from 17- DHT is the principal ligand to androgen receptors in OH-progesterone, 19-nortestosterone or 17-alpha- women as well. Androgens peak in the early 20s, then spironolactone) and their consequent varying pattern decline steadily (Burger et al 2000). of interaction with different hormonal receptors (Graziottin & Leiblum 2005, Schindler 1999, Stanczyk T in premenopausal women: evidence concerning 2002) – progestogens may interact with progestinic, the role of hormones, particularly T, in premenopausal oestrogenic, androgenic, glucocorticoid, and miner- women is limited. Very few studies have been done in alcorticoid receptors, so the consequent metabolic premenopausal subjects. Goldstat et al (2003) focused and sexual profile differs; their controlled study on a small group of premeno- pausal women; subjects with lifelong hypoactive sexual • their variable binding affinity to SHBG, which modu- desire disorder with T levels in the lower one-third or lates the quantity of free T available for its biological less of the normal range may significantly benefit from action; T cream when compared to placebo. • the variable inhibition of the type 2,5-alpha- T in postmenopausal women: menopause can be reductase, which activates T into DHT. natural or iatrogenic. Iatrogenic menopause may result from surgery, chemotherapy, or radiation therapy. The To assimilate progestogens in a unique category most common surgical cause of menopause is bilateral focusing on a generalized ‘class effect’ is wrong and oophorectomy, which leads to a sudden 50% fall in cir- may lead to inappropriate conclusions (Graziottin & culating T levels (Bachmann et al 2002). Plasma T values

280 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Leiblum 2005). The progestogen with the most favour- or secondary to sexual pain disorders such as dysp- able effect on sexual function in hormonal replacement areunia associated with vulvar vestibulitis (Graziottin et therapy is norethisterone, with a positive impact on al 2001b), in which defensive contraction of levator ani desire, arousal, orgasm, and satisfaction in natural post- is common (Bergeron et al 2001, Glazer et al 1995, menopausal women with an intact uterus. Controlled Graziottin et al 2004b, McKay et al 2001). head-to-head studies are necessary to evaluate the cor- relation between the pharmacological profile and the Antalgic treatment When loss of desire is acquired clinical effect. and secondary to persistent chronic coital pain, antalgic Tibolone Tibolone is a 19-nortestosterone derivate treatment aimed at reducing or eliminating pain (espe- cially if neuropathic) is preliminary to effective normal- with mild oestrogenic, progestinic and androgenic ization of sexual desire (Vincenti & Graziottin 2004). activity. It lowers SHBG, thus increasing free E2, T, and DHEA-S levels. It is not available in the USA, but is Psychosexual treatment widely used in Europe. In randomized studies compar- ing it with placebo, tibolone (2.5 mg/day) alleviated Individual psychosexual or behavioural vaginal dryness and dyspareunia, increasing libido, therapy Individual psychosexual or behavioural arousal, and sexual satisfaction in postmenopausal women with natural or surgical menopause (Laan et al therapy is the approach of choice if the FSD aetiology 2001, Madelska & Cummings 2002). includes sexual inhibitions, poor erotic skills, poor body image, low self-confidence or previous abuse (Leiblum DHEA-S Studies conducted in elderly women have & Rosen 2000, Rellini & Meston 2004). shown a positive effect of DHEA-S on mental well-being Couple therapy Couple therapy is used when sym- and on motivational aspects of sexuality with a mild relief of climacteric symptoms (Labrie et al 2001, Stomati biotic dynamics with poor differentiation according to et al 2000). Schnarch (2000) or conflicts and/or destructive dynam- ics are reported. Hypoprolactinaemic drugs Prolactin is the most Referral powerful inhibiting hormone when sexual desire is con- sidered, with increasing inhibiting effect with increas- The multisystemic and multifactorial aetiology of FSD ing plasma levels. Hypoprolactinaemic drugs are useful requires a professional multidisciplinary team. Appro- to improve sexual desire when the prolactin level is priate referral is a key part of successful treatment (Box supraphysiological. 9.8) (Plaut et al 2004). For example, referral of the partner to the uroandrologist should be recommended when Antidepressants Affective disorders, namely depres- male disorders (premature ejaculation, erectile deficit, libido disorders) emerge as critical co-factors in the aeti- sion and anxiety, when associated with sexual desire ology of FSD (i.e. if the partner appears to be the disorders should be addressed with a mixed approach, ‘symptom inducer’ and the woman is the ‘symptom both pharmacological and psychodynamic (Alexander carrier’ [Kaplan 1979, Plaut et al 2004]). & Kotz 2004). Among antidepressants, bupropion seems to have the most positive effect on sexual desire (Clayton Acquired libido disorder should be treated on the et al 2004, Seagraves & Balon 2003). Comorbidity basis of the leading aetiological factor, especially if it is between low testosterone and depression should be comorbid with other lifelong or acquired FSD, such as considered and appropriately treated. pain disorder, arousal disorder or orgasm disorder (Graziottin et al 2001b), or biological factors such as iat- Pelvic floor rehabilitation A few physicians and rogenic menopause (Graziottin & Basson 2004). medical sexologists recommend careful physical exami- Arousal disorders nation of the woman complaining of low desire on the wrong assumption that the disorder is either ‘all psy- Subjective sexual arousal disorders, either lifelong or chogenic and/or couple dependent’ or at best ‘hormone- acquired, usually in comorbidity with sexual desire dis- dependent’. Low desire can result from negative orders, should be treated as mentioned above. Post- feedback from disappointing arousal, coital pain, coital menopausal mixed genital and subjective arousal anorgasmia, dissatisfaction (see Fig. 9.26, p. 267). Indeed, disorders may benefit from systemic hormonal replace- low desire may be concomitant to sexual aversion dis- ment therapy, especially androgens (see above) orders associated with vaginismus (with a variable (Alexander et al 2004, Traish et al 2002). hyperactivity of the pelvic floor) (Graziottin et al 2004a)

Female sexual dysfunction 281 Box 9.8: Referral resources. Modified from 140 mL to 180 mL (p < 0.048); and bladder volume at Plaut et al 2004, with permission strong urgency increases from 130 mL to 170 mL (p < 0.045). The comorbidity between urogenital and • Medical sexologist or gynaecologist trained in sexual symptoms in postmenopausal women may sexual medicine: FSD requires appropriate medical therefore be effectively addressed with a topical vaginal diagnosis and treatment treatment that is easy to use and safe both for the endo- metrium and the breast. • Urologist or andrologist: when the partner has erectile or ejaculatory dysfunction that requires Topical testosterone Testosterone propionate medical intervention powder 1% or 2% in vaseline jelly applied in minimal • Family physician trained in sexual medicine: for daily quantity to the clitoris and the vulvar region sexual dysfunctions in either partner may improve genital arousal in the external genitalia (Notelovitz 2002). Controlled studies, however, are • Oncologist: when hormonal treatment is lacking. considered for patients who have had cancer Vasoactive drugs Evidence on the effectiveness of • Psychiatrist: when depression and anxiety are associated with FSD vasoactive drugs (sildenafil, vardenafil, tadalafil) in addressing genital arousal disorders in women is nega- • Sex therapist: to carry out the psychosexual tive or at best controversial, with one exception (Berman therapy et al 2003). The frequent comorbidity with desire disorders, the frequent couple issues, the difficulty in • Couple therapist: when relationship issues are a diagnosing a ‘pure’ genital arousal disorder and the lack primary contributor to the sexual dysfunction of a personal motivation for a pharmacological treat- ment of genital arousal disorder may explain the sub- • Individual psychotherapist: when personal stantial lack of efficacy in comparison to men’s genital psychodynamic issues are inhibiting sexual arousal disorders (i.e. erectile deficit of vascular function aetiology). • Physical therapist: when hyper- or hypotonicity of Clitoral vacuum device Clitoral vacuum device is pelvic floor is contributory the only FDA-approved treatment for genital arousal Isolated acquired genital arousal disorders may ben- disorders with a vascular and/or neurogenic aetiology efit from the following. (Wilson et al 2001). It may be useful in women treated for invasive carcinoma of the cervix who have under- Medical treatment gone surgery and pelvic radiotherapy. Topical oestrogens A number of studies suggest that Pelvic floor rehabilitation Genital arousal disorders topical vaginal oestrogens may significantly reduce may be secondary to coital pain: unwanted pain is the vaginal dryness, increase genital arousal, and reduce strongest reflex inhibitor of vaginal congestion and dyspareunia (Dessole et al 2004, Rioux et al 2000, lubrication. Diagnosing and treating the muscular com- Simunic et al 2003). A multicentre, double-blind, ran- ponent of coital pain (both in vaginismus and dyspareu- domized, placebo-controlled study (n = 1612 postmeno- nia) is a key part of the medical treatment (Bergeron et al pausal women with urogenital and sexual complaints) 2001, Glazer et al 1995, Graziottin 2004d, McKay indicates that 25 μg of estradiol applied vaginally twice et al 2001) and is preliminary to resuming a normal a week for a year may significantly improve six vaginal vasocongestive response (Graziottin & Brotto 2004). symptoms and signs: vaginal dryness (p < 0.0001), itching/burning (p < 0.0001), recurrent vaginitis Psychosexual treatment (p < 0.0001), petechiae (p < 0.0002), dyspareunia (p < 0.0001), and vaginal atrophy (p < 0.0001), and five Indications for psychosexual treatment of subjective bladder symptoms and signs: dysuria (p < 0.003), fre- sexual arousal disorders overlap with those for desire quency/nocturia (p < 0.001), urinary tract infection disorders. Co-treatment may therefore effectively (p < 0.034), urinary incontinence, urge mostly (p < 0.002), address comorbidity. However, treatment of the poten- and urinary atrophy (p < 0.001) (Simunic et al 2003). tial parallel biological aetiology of the genital arousal Furthermore, cystometry performed at baseline and disorder is mandatory if cure for the reported FSD is to after 12 months indicates that the maximal cystometric be achieved (Plaut et al 2004). Couple psychotherapy capacity increases from 200 mL to 290 mL (p < 0.023); should be proposed when relational dynamics are con- the bladder volume at first urgency increases from

282 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY tributing to maintenance of the sexual problem (Clulow benefit from a behavioural educational treatment, 2001, Leiblum & Rosen 2000). encouraging self-knowledge and eroticism with the experience of higher arousal sensations, use of vibrators Orgasm disorders or of a clitoral device up to orgasm (Meston et al 2004). More often, however, the orgasmic disorder is associ- Orgasm disorders have a prevalent psychogenic aetiol- ated with poor arousal with or without performance ogy in young women (Mah & Binik 2004). Biological anxiety. These conditions should therefore be treated factors – age, menopause-related loss of sexual hor- together (Leiblum & Rosen 2000). mones, pelvic floor disorders, iatrogenic issues (such as antidepressant serotoninergic drugs inhibiting orgasm), Couple therapy Lifelong orgasm difficulties may and comorbidities (mainly with stress and urge inconti- nence) – become increasingly important with increasing need a couple therapy when sexual inhibitions, poor age (Graziottin 2004a). According to the aetiologic diag- erotic skills and/or low self-confidence are shared by nosis, the main therapeutic options include the the couple (Meston et al 2004). following. Appropriate behavioural and pharmacological treat- Medical treatment ment of premature ejaculation should be proposed to the partner when it causes inadequate coital stimulation Systemic and/or topical hormonal replacement and increasing erotic dissatisfaction in the female therapy Systemic and/or topical hormonal replace- partner. ment therapy is discussed above. Testosterone has a If all of the sexual response is impaired, with signifi- special role in the treatment of orgasmic disorders asso- cant comorbidity with desire and arousal disorders, ciated with loss of sexual hormones, especially after accurate treatment of predisposing, precipitating and bilateral oophorectomy (Alexander et al 2004, Sherwin maintenance factors, biological, psychosexual and/or 2002, Shifren et al 2000). It behaves as ‘initiator’ in the contextual, should be proposed (Plaut et al 2004). brain and as ‘modulator’ in the cavernosal bodies, where it works as ‘permitting factor’ for nitric oxide Sexual pain disorders (NO), in women as well as in men (Graziottin 2004d). Dyspareunia and vaginismus because of coital pain Change of pharmacological treatment inhibiting directly inhibit genital arousal and vaginal receptivity. orgasm (e.g.antidepressants such as selective serotonin Indirectly, they may affect orgasm potential, the physi- reuptake inhibitor [SSRI] or tricyclics) should be consid- cal and emotional satisfaction, causing loss of desire up ered when feasible from the medical point of view if to avoidance of sexual intimacy. Dyspareunia may have orgasm inhibition is reported as a side-effect. Bupropion many biological aetiologies: the leading cause of coital seems to be a better choice (Clayton et al 2004, Segraves pain in premenopausal women is vulvar vestibulitis, & Balon 2003). whereas postmenopausally it is vaginal dryness. Pelvic floor rehabilitation Pelvic floor rehabilitation Dyspareunia may benefit from the following (Box 9.9). is of the highest importance for hypotonic conditions of the pelvic floor, as pioneered by Kegel (1952), after Medical treatment delivery (Baessler & Schuessler 2004, Glazener 1997); even more so when incontinence is a strong inhibiting Multimodal therapy Vulvar vestibulitis should be orgasmic factor. Fear of leaking during thrusting in stress incontinence and at orgasm in urge incontinence treated with a combined treatment aimed at reducing: is an often under-reported and yet powerful disruptor of orgasm potential. Orgasm inhibition may also be sec- • upregulation of mast cells, both by reducing the ondary to coital pain (Graziottin et al 2001b). Again, agonist stimuli (such as candida infections, micro- accurate diagnosis of comorbidity and appropriate co- abrasions of the introital mucosa because of inter- treatment with relaxation of the pelvic floor in this latter course with a dry vagina and/or a contracted pelvic case is key. floor, chemicals, allergens etc) that cause degranula- tion leading to chronic tissue inflammation, and/or Psychosexual treatment with antagonist modulation of its hyper-reactivity, with amitriptyline or aliamides gel (Graziottin & Individual psychosexual or behavioural Brotto 2004, Graziottin et al 2004b); therapy Lifelong ‘isolated’ orgasmic disorders may • upregulation of the pain system secondary to prolif- eration of introital pain fibres (Bohm-Starke et al 1999, 2001a,b, Bornstein et al 2002, 2004) induced by nerve

Female sexual dysfunction 283 Box 9.9: Treatment of the medical causes of dyspareunia INFLAMMATORY AETIOLOGY (UPREGULATION OF NEUROLOGICAL AETIOLOGY (UPREGULATION OF THE MAST CELLS) PAIN SYSTEM) Pharmacological modulation of mast cell Systemic analgesia hyper-reactivity • Amitriptyline • Antidepressants: amitriptyline • Gabapentin • Aliamides topical gel • Pregabalin Reduction of agonist factors causing mast cell Local analgesia hyper-reactivity • Electroanalgesia • Recurrent candida or Gardnerella vaginitis • Ganglion impar block • Microabrasions of the introital mucosa Surgical therapy – from intercourse with a dry vagina • Vestibulectomy – from inappropriate lifestyles • Allergens/chemical irritants HORMONAL AETIOLOGY • Physical agents • Neurogenic stimuli Hormonal therapy • Local: MUSCULAR AETIOLOGY (UPREGULATION OF THE MUSCULAR SYSTEM) – vaginal oestrogens • Self-massage and levator ani stretching – testosterone for the vulva • Physical therapy of the levator ani • Systemic: • Electromyographic biofeed-back – hormonal replacement therapies • Type A botulinum toxin *Aliamides is a class of endogenous molecules with an anti-inflammatory activity. The most important is the palmitoiletanolamide, belonging to the class of fatty acid amides, chemically known as N-(2-idrossietil)- esadecanamide. They work through the down-regulation of the hyperactive mast cells. In Italy they are available in the form of vaginal gel and now of pills. They constitute an innovative approach to the vaginal and bladder chronic inflammation, secondary to mast cells’ upregulation. growth factor produced by the upregulated mast massage, pelvic floor stretching and physical therapy cells, and the lowered central pain threshold (Pukall may also reduce the muscular component of coital et al 2006) – a thorough understanding of the patho- pain (Graziottin 2004a, Graziottin & Brotto 2004), but physiology of pain in its nociceptive and neuropathic high-quality randomized controlled trials are needed component, is mandatory – antalgic treatment should to determine the true effect of such interventions; for be prescribed: locally, with electroanalgesia (Nappi et hyperactivity of the pelvic floor, treatment with type al 2003) or, in severe cases, with the ganglion impar A botulinum toxin has been proposed (Bertolasi 2004, block; systemically with tricyclic antidepressant or personal communication) – individually tailored gabapentin in the most severe cases (Graziottin & combinations of this approach are useful for treating Brotto 2004, Vincenti & Graziottin 2004). introital dyspareunia with different aetiologies from vulvar vestibulitis. • upregulation of the muscular response, with hyper- actvity of the pelvic floor (Graziottin et al 2004a), Deep dyspareunia, secondary to endometriosis, which may precede vulvar vestibulitis when the pre- pelvic inflammatory disease (PID), chronic pelvic pain disposing factor is vaginismus (Abramov et al 1994, and other less frequent aetiologies requires specialistic Graziottin et al 2001b) or be acquired in response to treatment that goes beyond the scope of this chapter. genital pain (Graziottin et al 2004a,b) – in controlled studies, electromyographic feedback (Bergeron et al Topical hormones Vaginal oestrogen treatment is 2001, Glazer et al 1995, McKay et al 2001) has proven to significantly reduce pain of vulvar vestibulitis; self mandatory when vaginal dryness is causing postmeno- pausal dyspareunia, either spontaneous or iatrogenic

284 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY (Graziottin 2001a,b, 2004a, Simunic et al 2003). Vulvar • levator ani tender and/or trigger points with referred treatment with testosterone may be considered when pain (Alvarez & Rockwell 2002, Travell & Simons vulvar dystrophy and/or lichen sclerosus contribute to 1983); introital dyspareunia. • levator ani hyperactivity associated with recurrent Psychosexual treatment cystitis, urge incontinence and dyspareunia (Graziottin 2004a); Psychosexual and/or behavioural therapy Psycho- • systemic postural problems in chronic pelvic pain, sexual and/or behavioural therapy is the leading treat- dyspareunia and vaginismus; ment of lifelong vaginismus (Leiblum 2000). It should be offered in parallel with progressive rehabilitation of • chronic pelvic pain and chronic coital pain-associated the pelvic floor and pharmacological treatment to mod- myalgias and pertinent antalgic treatment (Bourcier ulate the intense systemic arousal in the subset of et al 2004). intensely phobic patients (Plaut et al 2004). In this latter group, comorbidity with sexual aversion disorder Hypoactivity/hypotonus of the pelvic floor should be investigated and treated first. The physical therapist should diagnose and address: Psychosexual and/or behavioural therapy contrib- utes to the multimodal treatment of lifelong dyspareu- • pelvic floor damage after delivery; nia, which is reported in one-third of our patients • hypotonicity worsening after the menopause; (Graziottin et al 2001b). Anxiety, fear of pain and sexual • pelvic floor hypotonus in comorbidity with urogeni- avoidant behaviours should be addressed as well. The shift from pain to pleasure is key from the sexual point tal and/or proctological disorders (Bourcier et al of view. Sensitive and committed psychosexual support 2004, Wesselmann et al 1997); to the woman and the couple is mandatory. The physical therapist may also help the patient to WHEN THE PHYSICAL THERAPIST COUNTS increase awareness of the levator ani role in sexual receptivity and vaginal sensitivity to increase the Pelvic floor muscles are critically involved in the woman’s and her partner’s coital pleasure. physiology and pathophysiology of women’s sexual response. The physical therapist should be part of the CONCLUSIONS multidisciplinary team involved in the centre of sexual medicine. He or she should diagnose and address the The complexity of FSD requires a dedicated diagnostic following. and therapeutic team, sharing a common pathophysio- logical and psychodynamic cultural scenario with the Hyperactivity/hypertonus aim of offering the most integrated understanding of of the pelvic floor the meaning of the symptoms and the most effective comprehensive treatment. The physical therapist should diagnose and address: Pelvic floor muscles are critically involved in the • primary pelvic floor hyperactivity in children and physiology and pathophysiology of a women’s sexual adolescents, thus preventing one of the most response. Physical therapists may therefore greatly con- neglected predisposing factors to dyspareunia and tribute to improving women’s sexual health. They vulvar vestibulitis (Chiozza & Graziottin 2004, deserve appreciation and an increasing role in the mul- Graziottin 2005a, Harlow et al 2001); timodal treatment of FSD. There is, however, an urgent need for high-quality randomized controlled trials to • acquired hyperactivity with levator ani myalgia by evaluate the effect of different physical therapy inter- overexertion (i.e. ‘Kegel dyspareunia’; DeLancey ventions for FSD. A collaboration between physical et al 1993); therapists and sexologists/gynaecologists in future research projects in this important field is highly • lifelong hyperactivity of the pelvic floor in vaginis- recommended. mus and lifelong or acquired hyperactivity in dyspa- reunia of any aetiology (Graziottin 2003a);

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288 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Classification of different forms men and significantly greater numbers of men with existing comorbidities such as hypertension (15%), dia- Men can be classified as having low or absent libido. betes mellitus (28%) and heart disease (39%) (Feldman et al 1994, Wagner et al 1996). The number of men with Prevalence erectile dysfunction is predicted to rise with increased life expectancy and with a growing population of elderly The exact prevalence of men who have low libido people. remains unknown. It is estimated that at 40 years of age, there will be a 10% decline of total testosterone every Aetiology decade, though the mechanisms are not fully under- stood (1st Latin American Erectile Dysfunction Consen- The causes of erectile dyfunction are listed in Table sus Meeting 2003a). 9.15. Aetiology Anatomy of the penis The cause of diminished libido is a result of ageing and The internal structure of the penis consists of three cylin- a gradual decline in androgen production. The testis drical bodies: dorsally, the two corpora cavernosa com- produces 95–98% of androgen with the adrenal glands municate with each other for three-quarters of their producing the remaining 2–5% (1st Latin American length and ventrally the corpus spongiosum surrounds Erectile Dysfunction Consensus Meeting 2003a). the penile portion of the urethra (Fig. 9.27). The proxi- mal end of the corpus spongiosum forms a bulb attached ERECTILE DYSFUNCTION to the urogenital diaphragm and at the distal end expands to form the glans penis (Kirby et al 1999). The Erectile dysfunction is a common condition linked to tunica albuginea, which is composed of two layers of increasing age and age-related diseases. Men with elastic and collagen fibres, surrounds the erectile erectile dysfunction suffer from depression and low bodies. self-esteem and experience difficulties establishing and maintaining relationships. The erectile tissue in the corpora cavernosa and the corpus spongiosum is comprised of vascular lacunar Definition spaces, which are surrounded by smooth muscle (Fig. 9.28). The lacunar spaces derive blood from the helicine Erectile dysfunction is defined as ‘the inability to achieve arteries, which open directly into these sinusoids. Sub- or maintain an erection sufficient for satisfactory sexual tunical veins between the inner and outer tunica albu- performance (for both partners)’ (National Institutes of ginea form a network, which drains blood from the Health (NIH) Consensus Development Conference in erectile tissue. 1993). Neurophysiology of penile erection Classification of different forms From a neurophysiological aspect, erection can be clas- The severity of erectile dysfunction has been classified sified into three types (Brock & Lue 1993). as mild, moderate or severe. Men who achieve satisfac- tory sexual performance 7–8 attempts out of 10 are clas- Corpus Glans sified as having mild erectile dysfunction, those who cavernosum penis achieve 4–6 out of 10 are classified moderate, and those who achieve 0–3 out of 10 are classified severe (Albaugh Urethral Corpus & Lewis 1999). bulb spongiosum Prevalence Fig. 9.27 Anatomy of the penis. Pelvic floor muscles The exact prevalence of erectile dysfunction is unknown. It is common and strongly age-related (Feldman et al 1994) affecting more than 20% of men under 40 years of age, more than 50% of men over 40 years of age, and more than 66% of men over 70 years of age (Feldman et al 1994, Heruti et al 2004). It may affect 10% of healthy

Table 9.15 Risk factors for erectile dysfunction Male sexual dysfunction 289 Risk factor Possible components Reference Psychological Feldman et al (1994) Marital conflict Vascular Depression Feldman et al (1994) Neurological Poor body image Feldman et al (1994) Performance related Endocrinological Bereavement Feldman et al (1994) Diabetic Benet & Melman (1995) Drug-related Arterial Surgical trauma Venous Benet & Melman (1995) Lower urinary tract symptoms (LUTS) Prostatic Spinal cord trauma Lewis & Mills (1999) Lifestyle related Multiple sclerosis Spinal tumour Frankel et al (1998) Weak pelvic floor musculature Parkinson’s disease Baniel et al (2000) Bortolotti et al (1997) Hormonal deficiency Andersen & Bovim (1997) Rosen et al (1991) Peripheral neuropathy Lewis & Mills (1999) Hypertension Fabra & Porst (1999) Renal failure Dorey et al (2004) Colpi et al (1999) Some antihypertensives Some psychotropics Hormonal agents Transurethral and radical prostatectomy Pelvic surgery Radiotherapy Severity of LUTS, particularly incontinence Benign prostatic hyperplasia Trauma to the perineum Bicycling Nicotine abuse Drug abuse Alcohol abuse Weak pelvic floor muscles Ageing Reflexogenic erection Reflexogenic erection origi- Nocturnal erection Nocturnal erection occurs nates from tactile stimulation to the genitalia. Impulses mostly during the rapid eye movement stage of sleep. reach the spinal erection centre via sacral sensory nerves Most men experience three to five erections lasting up (S2–S4) and thoracic nerves (T10–L2) and some follow to 30 minutes in a normal night’s sleep (Fisher et al the ascending tract culminating in sensory perception, 1965). Central impulses descend the spinal cord (through whereas others activate the autonomic nuclei of the an unknown mechanism) to activate the erection efferent nerves that induce the erection process. process. Psychogenic erection Psychogenic erection origi- Pathophysiology of penile erection nates from audiovisual stimuli or fantasy. Signals Penile erection occurs following a series of integrated descend to the spinal erection centre to activate the erec- vascular processes culminating in the accumulation of tion process.

290 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Dorsal vein Corpora cavernosa (A) Flaccid state Trabecular Outflow smooth muscle Helicine artery Subtunical space Inflow through cavernosal Corpus spongiosum Outflow artery surrounding urethra Lacunar Fig. 9.28 Cross-section of the penis. space blood under pressure and end-organ rigidity (Moncada (B) Erect state Iribarren & Sáenz de Tejada 1999). This vascular process can be divided into six phases: No outflow • Flaccidity: A state of low flow of blood and low pres- Tunica Dilated helicine sure exists in the penis in the flaccid state (Fig. 9.29a). albuginea artery The ischiocavernosus and bulbocavernosus muscles are relaxed. Inflow through dilated • Filling phase: when the erection mechanism is initi- cavernosal ated, the parasympathetic nervous system provides artery excitatory input to the penis from efferent segments S2–S4 of the sacral spinal cord; the penile smooth No outflow Lacunar arterial muscle relaxes and the cavernosal and heli- space cine arteries dilate enabling blood to flow into the lacunar spaces. Compressed subtunical • Tumescence: the venous outflow is reduced by com- pression of the subtunical venules against the tunica venule albuginea (corporal veno-occlusive mechanism) causing the penis to expand and elongate but with a Fig. 9.29 Veno-occlusive mechanism of penile erection. scant increase in intracavernous pressure. lacunar spaces and contraction of the smooth trabec- • Full erection: the intracavernous pressure rapidly ular muscle leads to a collapse of the lacunar spaces increases to produce full penile erection. and detumescence. • Rigidity: the intracavernous pressure rises above Pathophysiology of erectile dysfunction diastolic pressure and blood inflow occurs with the systolic phase of the pulse enabling complete rigidity Three types of erectile dysfunction are acknowledged: to occur. Contraction or reflex contraction of the psychogenic, organic and mixed. They may be primary ischiocavernosus and bulbocavernosus muscles or secondary after a period of normal erectile function produce changes in the intracavernous pressure. (1st Latin American Erectile Dysfunction Consensus When full rigidity is achieved, no further arterial Meeting 2003b). In organic erectile dysfunction, the flow occurs (Fig. 9.29B). events leading to full erection do not happen due to insufficient blood reaching the penis or blood escaping • Detumescence: the sympathetic nervous system is from the penis. responsible for detumescence via thoracolumbar seg- ments (T10–T12, L1–L2) in the spinal cord. Contraction Role of the pelvic floor muscles of the smooth muscle of the penis and contraction of the penile arteries lead to a decrease of blood in the The ischiocavernosus and bulbocavernosus muscles are active during penile erection (Fig. 9.30). Contractions of the ischiocavernosus muscles increase intracavernous pressure and influence penile rigidity. The area of the corpora cavernosum compressed by the ischiocavernosus muscle ranges from 35.6 to 55.9% (Claes et al 1996). The middle fibres of the bulbocaver-

Male sexual dysfunction 291 Ischiocavernosus Bulbocavernosus Prevalence The prevalence of anejaculation is muscle muscle unknown. Transverse Levator perineal muscle ani Aetiology Ejaculatory dysfunction can be due to con- Gluteus genital abnormalities, surgical trauma, genital infection, maximus muscle stones in the ejaculatory duct, paraplegia, dilatation of the seminal vesicles, or functional (Hendry et al 2000). Fig. 9.30 Anal Functional ejaculatory dysfunction includes congenital sphincter anorgasmia, where an excessively strict upbringing may produce an inability to achieve orgasm, premature ejac- Superficial pelvic floor muscles. ulation and the side-effects of some antihypertensive and psychotropic drugs. nosus muscle assist in erection of the corpus spongio- sum penis by compressing the erectile tissue of the bulb Anorgasmia of the penis. The anterior fibres spread out over the side of the corpus cavernosum and are attached to the fascia Definition Anorgasmia is defined as ‘the inability to covering the dorsal vessels of the penis and contribute to erection by compressing the deep dorsal vein of the achieve orgasm during conscious sexual activity, penis, thus preventing the outflow of blood from the although nocturnal emission may occur’ (Hendry et al penis. 2000). Weak pelvic floor muscles compromise penile erec- Classification of different forms Anorgasmia may tion (Colpi et al 1999, Dorey et al 2004). be congenital, acquired and/or psychological (Hendry ORGASMIC AND EJACULATORY 1999). DISORDERS Prevalence The exact prevalence of anorgasmia is The final phase of sexual response in men culminates in orgasm and ejaculation. Although erection and ejacula- unknown. However, 37% of men reported anorgasmia tion are coordinated, they are produced by different after radical prostatectomy, and a further 37% reported mechanisms. a decreased intensity of orgasm (Barnas et al 2004). Classification of different forms Aetiology There are a number of causes of anorgas- Orgasmic and ejaculatory disorders may be classified as mia. These range from congenital abnormalities, surgi- anejaculation, anorgasmia, premature ejaculation, retro- cal trauma following imperforate anus, para-aortic grade ejaculation and delayed ejaculation (Hendry et al lymphadenectomy or prostate surgery, genital infec- 2000). Ejaculatory disorders such as anejaculation, tions such as gonorrhoea or non-specific urethritis, delayed ejaculation and premature ejaculation may lead spinal cord injury, antidepressants, antipsychotics and to complete or partial loss of the ejaculate needed for polycystic kidney associated with dilatation of the impregnation of the female partner. seminal vesicles (Hendry 1999). Anejaculation Retrograde ejaculation Definition Anejaculation is defined as ‘the absence of Definition Retrograde ejaculation is defined as ‘back- ejaculation during orgasm’ (Hendry et al 2000). ward passage of semen into the bladder after emission usually due to failure of closure of the bladder neck Classification of different forms Anejaculation mechanism, demonstrated by presence of spermatozoa in the urine after orgasm’ (Hendry et al 2000). may be congential or acquired and/or psychological (1st Latin American Erectile Dysfunction Consensus Classification of different forms Retrograde ejacu- Meeting 2003c). lation can be congential or acquired and/or psychologi- cal (1st Latin American Erectile Dysfunction Consensus Meeting 2003c). Prevalence The prevalence of retrograde ejaculation is unknown.

292 PELVIC FLOOR DYSFUNCTION AND EVIDENCE-BASED PHYSICAL THERAPY Aetiology Retrograde ejaculation can be due to Premature ejaculation is typically defined by three char- acteristics: short latency to ejaculation, lack of self- damage of the bladder neck during prostate surgery, efficacy regarding the rapid ejaculation, and distress or bladder neck disorder from alpha-adrenergic, neurolep- dissatisfaction with the condition (Rowland 2003). In tic or antidepressant blocking agents, diabetes mellitus, some men ejaculation occurs before or within 1 minute and some neuropathies (1st Latin American Erectile of the beginning of intercourse (Waldinger et al 1998). Dysfunction Consensus Meeting 2003c). Rowland et al (2001) believed that the latency for men with premature ejaculation varied from 1 to 5 minutes. Retarded ejaculation However, a study investigating the ejaculatory time of ‘normal’ men in different countries showed that the Retarded ejaculation is defined as ‘undue delay in reach- average time to ejaculation varies between 7 and 14 ing a climax during sexual activity’ (Hendry et al minutes (Montorsi 2005). Therefore, the definition of 2000). premature ejaculation should not be counted in minutes but acknowledge three core components: short ejacula- Prevalence The prevalence of retarded ejaculation is tory time, lack of control over ejaculation and lack of sexual satisfaction (Montorsi 2005). It may occur in the unknown. absence of sufficient erection and the problem is not the result of prolonged abstinence from sexual activity. Classification of different forms Retarded ejacula- Classification of different forms There are several tion can be drug related or psychological (Hendry et al 2000). different subtypes of biogenic and psychogenic prema- ture ejaculation according to aetiological features (Metz Aetiology Retarded ejaculation can be due to emo- & Pryor 2000). Physiological types of premature ejacula- tion are due to neurological constitution, acute physical tional suppression, an inability to relax, relationship dif- illness, physical injury, and pharmacological side-effects. ficulties, medications, societal and religious attitudes, Psychological types are due to psychological constitu- and the use of alcohol and recreational drugs (1st Latin tion, acute psychological distress, relationship distress, American Erectile Dysfunction Consensus Meeting and deficient psychosexual skills. Premature ejaculation 2003c). may be labelled psychogenic when the physical cause is unknown. Role of the pelvic floor muscles During sexual Prevalence The prevalence of premature ejaculation activity, rhythmic contractions of the bulbocavernosus muscle along with the other pelvic floor muscles result is 16.3 to 32.5% (Rowland et al 2004). There is no evi- in ejaculation (Gerstenberg et al 1990). The external ure- dence that ejaculation latency increases with age. In a thral sphincter and deep pelvic floor muscles relax stopwatch study of 110 men aged 18 to 65 years, 76% rhythmically to allow the ejaculate to pass through the reported their ejaculation to be as rapid at their first urethra. An ability to relax may compromise this sexual contacts with 23% reporting increasing rapidity process. and only 1% reporting a delay (Waldinger et al 1998). Premature ejaculation Aetiology The aetiology of premature ejaculation is Premature ejaculation is one of the commonest forms of unknown, but psychological, behavioural and biogenic sexual dysfunction (Rosen 2000). It is characterized by components are likely (Montague et al 2004). There may a lack of ejaculatory control and is associated with sig- be an organic basis for some forms. The causes can be nificant effects on sexual functioning and satisfaction congenital or acquired and/or psychological (1st Latin (Rowland et al 2004). American Erectile Dysfunction Consensus Meeting 2003). Definition Premature ejaculation has been defined as Pathophysiology Data suggest that men with prema- ‘recurrent ejaculation that occurs with minimal stimula- tion and earlier than desired, before or soon after pene- ture ejaculation have hypersensitivity and hyperexcit- tration, which causes bother or distress, and upon which ability of the glans penis and the dorsal nerve (Xin et al the sufferer has little or no control’ (World Health Orga- 1996, 1997). nization 1992). It is also defined as ‘the inability to delay ejaculation sufficiently to enjoy lovemaking. Persistent Role of pelvic floor muscles During sexual activity, or recurrent occurrence of ejaculation with minimal sexual stimulation before, on, or shortly after penetra- rhythmic contractions of the bulbocavernosus muscle tion and before the person wishes it’ (Hendry et al 2000).

Male sexual dysfunction 293 along with the other pelvic floor muscles result in ejacu- voluntary use of the pelvic floor muscles could delay lation (Gerstenberg et al 1990). Contraction of the pelvic ejaculation. floor muscles combined with intermittent relaxation of the external urinary sphincter and urogenital diaphragm SEXUAL PAIN allows ejaculation (Krane et al 1989). The bladder neck sphincter under involuntary control remains closed. Sexual pain is any pain that affects the ability to gain and maintain an erection and achieve orgasm and It is hypothesized that weak pelvic floor musculature ejaculation. affords little control to delay ejaculation and that the REFERENCES 1st Latin American Erectile Dysfunction Consensus Meeting 2003a Gerstenberg T C, Levin R J, Wagner G 1990 Erection and ejaculation Androgen deficiency in the aging male. International Journal of in man. 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