*1.2.2. Non-infectious chronic cystitis — Painful bladder syndrome*

In the elderly, pelvic exercises with biofeedback in the office is more effective than pelvic floor

The first study using rehabilitation assisted with pelvic floor muscles EMG for the treatment of vulvovaginal pain was published in 1995 by Glazer et al. These authors reported a cure rate greater than 50% with an average subjective improvement of 83%. Only changes in the electromyographic signal at rest preceded improvement of pain. These findings confirmed that the efficacy of the treatment depended on muscle stabilization (Glazer, Rodke et al. 1995).

In the following section we shall discuss common conditions, both infectious and non-

Urinary tract infections (UTIs) are the second most common infections in humans (Foxman 2002). A UTI is the presence of microorganisms in the urine (not due to contamination) which can invade the urinary tract or adjacent structures. It is well established the route of infection is ascending in most cases of infections with enteric bacteria which explains why UTIs are more common in females. The development of a UTI is determined by the balance between bacterial virulence, size of the inoculum, local defence mechanisms and anatomical or functional

It is estimated that the prevalence of UTIs in sexually active young women is 0.5-0.7 episodes per year. One fourth of these will recur. Eighteen out 10000 of these women will develop pyelonephritis and 7% will require hospitalization (Andreu, Cacho et al. 2011). This is despite the fact that most young women with UTI have normal urinary tracts (Hooton 2001). The development of infection is determined by the balance between bacterial virulence, size of the inoculum, local defence mechanisms and anatomical or functional alterations of the urinary

Recurrent UTIs are defined as 3 or more culture-documented infections in 1 year or 2 or more in 6 months in women without structural or functional abnormalities. (Grabe, Bjerklund-

Risk factors that predispose to UTIs abnormalities of the urinary tract (such as urinary incontinence or obstruction), sexual behaviour, use of contraceptives, postmenopausal hormonal deficiency, asymptomatic bacteriuria and past urinary tract surgery (Grabe, Bjerklund-Johansen et al. 2011). Risk factors for recurrent UTIs in postmenopausal institution‐ alised women include atrophic vaginitis, incontinence, cystocele and post-voiding residual urine and a history of UTI before menopause (Nicolle 1997). Collagen diseases represent

Systemic diseases, mainly diabetes mellitus and chronic renal failure are also important risk factors (Sharifi, Geckler et al. 1996). Women with diabetes mellitus are prone to UTIs. UTI in both diabetic men and women is more likely to progress to pyelonephritis. Patients with type

**1.2. Chronic inflammatory disorders of the lower urinary tract in females**

exercises alone (Burns, Pranikoff et al. 1990).

290 Electrodiagnosis in New Frontiers of Clinical Research

infectious that can benefit from biofeedback.

alterations of the urinary tract (Andreu, Cacho et al. 2011).

*1.2.1. Recurrent urinary tract infections*

tract.

Johansen et al. 2011).

another extra-urogenital risk factor.

Over the years much of the focus for chronic pelvic pain has been on peripheral-end-organ mechanisms, such as inflammatory or infective conditions (Engeler, Baranowski et al. 2012).

A peripheral stimulus such as infection may initiate the beginning of chronic pelvic pain, and the illness may become self-perpetuating as a result of modulation of the central nervous system, independent of the original cause (Engeler, Baranowski et al. 2012).

Chronic pelvic pain mechanisms may involve on-going acute pain mechanisms, such as those associated with inflammation or infection, which may involve somatic or visceral tissues (Linley, Rose et al.). Nevertheless in most cases, inflammation or infection is not present (van de Merwe, Nordling et al. 2008). However, conditions that produce recurrent trauma, infection or inflammation may result in chronic pelvic pain in a small proportion of cases (van de Merwe, Nordling et al. 2008). Therefore such factors should be ruled out early.

Central sensitisation is responsible for a decrease in threshold and increase in response duration and magnitude of dorsal horn neurons. For instance, with central sensitisation, stimuli that are normally below the threshold may result in a sensation of fullness and a need to void (Nazif, Teichman et al. 2007) and other non-painful stimuli may be interpreted as pain and noxious stimuli may be magnified with an increased perception of pain. Also, somatic tissue hyperaesthesia is associated with recurrent bladder infection.

The increased perception of stimuli in the viscera is known as visceral hyperalgesia, and the underlying mechanisms are thought to be responsible, among, others for bladder pain syndrome and dysmenorrhoea.

Chronic bladder pain may be associated with the presence of Hunner's ulcers and glomeru‐ lation on cystoscopy, whereas other bladder pain conditions may have normal cystoscopic findings. Recent reports about prevalence of bladder pain syndrome show higher figures than earlier ones, ranging from 0.06% to 30% (Parsons and Tatsis 2004).

The conditions associated with the painful bladder include interstitial cystitis, bladder pain syndrome or BPS. The European Urological Association (EUA), the International Society for the study of BPS (ESSIC), the International Association for the Study of Pain (IASP) and several other groups now prefer the term bladder pain syndrome (BPS). Terms that end in "itis" in particular should be avoided unless infection and/or inflammation is proven and considered to be the cause of the pain (Abrams, Baranowski et al. 2006). Chronic pelvic pain may be subdivided into conditions with well-defined classical pathology, such as infection, and those with no obvious pathology.

Methotrexate, Gabapentin, Pregabalin, Suplatast tosilate (IPD-1151T), Quercetin. Antibiotics have a limited role in the treatment of BPS. Cimetidine, prostaglandins, L-Arginine, anticho‐

Biofeedback with Pelvic Floor Electromyography as..

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*Intravesical therapy*: Local anaesthetic (lidocaine), Pentosan polysulphate sodium, intravesical heparin, hyaluronic acid (hyaluronan, chondroitin sulphate, dimethyl sulphoxide (DMSO), bacillus Calmette Guérin (BCG) and vanilloids which disrupt sensory neurons such as

*Interventional management*: Bladder distension with or without electromotive drug adminis‐ tration, transurethral resection (TUR) coagulation and laser, Botulinum toxin A (BTX-A),

*Non-pharmacological*: Behavioural bladder training techniques (Parsons and Koprowski 1991), physiotherapy (Karper 2004), electrical stimulation (de-Oliveira-Bernardes and Bahamondes 2005). Physiotherapy with pelvic floor biofeedback (Borrego-Jiménez, Lorenzo-Gómez et al.

*Surgical:* When all efforts fail to relieve disabling symptoms, surgical removal of the diseased

Urethral pain syndrome is the occurrence of chronic or recurrent episodic pain perceived in the urethra, in the absence of proven infection or other obvious local pathology (Parsons 2011). There pathogenesis of urethral pain syndrome is unknown but it may part of the spectrum of BPS. Some have postulated that neuropathic hypersensitivity can develop following urinary a UTI (Kaur and Arunkalaivanan 2007). The same authors suggested that behavioural therapy including biofeedback and bladder training can be helpful (Kaur and

Pelvic organ prolapse is often an asymptomatic condition, unless it is so marked that it causes

In the past few years, non-absorbable mesh has been used in the pelvic organ prolapse surgery. Although they may have a role in supporting the vagina, they are also associated with several complications including bladder, bowel and vaginal trauma (Niro, Philippe et al. 2010).A subset of these patients may develop chronic pain because mesh insertion causes nerve and

Most patients can be treated by surgical removal of the mesh (Margulies, Lewicky-Gaupp et al. 2008). If appropriate, multidisciplinary pain management strategies can be applied. Another cause of pain is previous surgery for incontinence with transoburator tapes. Chronic perineal pain at 12 months after surgery was reported by 21 trials and metaanalysis of these data showed strong evidence of a higher rate in women undergoing

back strain, vaginal pain and skin excoriation (Roovers, van der Vaart et al. 2004).

Hyperbaric oxygen (HBO), neuromodulation (Engeler, Baranowski et al. 2012).

linergic drugs have also been used (Engeler, Baranowski et al. 2012).

Resiniferatoxin (Engeler, Baranowski et al. 2012).

bladder is the ultimate option (Loch and Stein 2004).

2009 Jan).

*1.2.2.1. Urethral pain syndrome*

Arunkalaivanan 2007).

*1.2.2.2. Other causes of chronic pelvic pain*

muscle irritation (Daniels, Gray et al. 2009).

BPS is the occurrence of persistent or recurrent pain perceived in the urinary bladder region, accompanied by at least one other symptom, such as pain worsening with bladder filling and day-time and/or night-time urinary frequency. There is no proven infection or other obvious local pathology. BPS is believed to represent a heterogeneous spectrum of disorders. There may be specific types of inflammation as a feature in subsets of patients (Engeler, Baranowski et al. 2012).

Pelvic floor muscle pain syndrome is the occurrence of persistent or recurrent episodic pelvic floor pain. It is often associated with symptoms suggestive of lower urinary tract dysfunction (Engeler, Baranowski et al. 2012).

BPS should be diagnosed on the basis of pain, pressure or discomfort associated with the urinary bladder, accompanied by at least one other symptom, such as daytime and/or nighttime increased urinary frequency, the exclusion of confounding diseases as the cause of symptoms, and if indicated, cystoscopy with hydrodistension and biopsy (van de Merwe, Nordling et al. 2008). Hunner's lesion and inflammation is referred to as BPS type 3. Current thought implicates an initial unidentified insult to the bladder, triggering inflammatory, endocrine and neural phenomena (Warren, Wesselmann et al.).

No infection aetiology has been implicated since BPS patients and controls have equal UTI frequency (Nickel, Shoskes et al. ; Warren, Brown et al. 2008). Of interest however is the fact that UTI and urgency are significantly more frequent during childhood and adolescence in patients who later develop BPS in adulthood (Peters, Killinger et al. 2009).

Cystoscopic and biopsy findings in both ulcer and non-ulcer BPS are consistent with defects in the urothelial glycosaminoglycan (GAG) layer. Urinary uronate, and sulphated GAG levels are increased in patients with severe BPS (Lokeshwar, Selzer et al. 2005).

The physiopathologic relationship between interstitial cystitis and rheumatic, autoim‐ mune, and chronic inflammatory diseases has been investigated. (Lorenzo Gomez and Gomez Castro 2004).

Biological markers have been explored as an attractive idea to support or, even better, to confirm the clinical diagnosis and prognosis (Lokeshwar, Selzer et al. 2005).

The therapeutic modalities currently available for BPS include the following:

*Medical management:* Analgesics, corticosteroids, anti-allergic medications, Amitriptyline, Pentosan polysulphate sodium.Immunosuppressants such as Azathioprine, Cyclosporin A, Methotrexate, Gabapentin, Pregabalin, Suplatast tosilate (IPD-1151T), Quercetin. Antibiotics have a limited role in the treatment of BPS. Cimetidine, prostaglandins, L-Arginine, anticho‐ linergic drugs have also been used (Engeler, Baranowski et al. 2012).

*Intravesical therapy*: Local anaesthetic (lidocaine), Pentosan polysulphate sodium, intravesical heparin, hyaluronic acid (hyaluronan, chondroitin sulphate, dimethyl sulphoxide (DMSO), bacillus Calmette Guérin (BCG) and vanilloids which disrupt sensory neurons such as Resiniferatoxin (Engeler, Baranowski et al. 2012).

*Interventional management*: Bladder distension with or without electromotive drug adminis‐ tration, transurethral resection (TUR) coagulation and laser, Botulinum toxin A (BTX-A), Hyperbaric oxygen (HBO), neuromodulation (Engeler, Baranowski et al. 2012).

*Non-pharmacological*: Behavioural bladder training techniques (Parsons and Koprowski 1991), physiotherapy (Karper 2004), electrical stimulation (de-Oliveira-Bernardes and Bahamondes 2005). Physiotherapy with pelvic floor biofeedback (Borrego-Jiménez, Lorenzo-Gómez et al. 2009 Jan).

*Surgical:* When all efforts fail to relieve disabling symptoms, surgical removal of the diseased bladder is the ultimate option (Loch and Stein 2004).
