Pain is defined as ‘an unpleasant sensory and emotional experience, associated with actual or potential tissue damage, or is described in terms of such damage’ (Merskey & Bogduk 2002) and central neurologic mechanisms will play a major role in the aetiology and pathophysiology of CPP. To emphasize that pathology would not always be found where the pain was perceived and that there would most likely be overlapping mechanisms and symptoms between different CPP conditions, the updated European Association of Urology (EAU) classification of CPP (Fall et al. 2010) reflected a shift from definitions based on assumptions of pathophysiological causes, to one based on recommendations of the International Association for the Study of Pain (IASP) (Merskey & Bogduk 2002) and the International Continence Society (ICS) (Abrams et al. 2003).

Chronic pelvic pain is non-malignant pain perceived in structures related to the pelvis of either men or women. In the case of documented nociceptive pain that becomes chronic, pain must have been continuous or recurrent for at least 6 months. If non-acute and central sensitization pain mechanisms are well documented, then the pain may be regarded as chronic, irrespective of the time period. In all cases, there often are associated negative cognitive, behavioural, sexual and emotional consequences

(Fall et al. 2010)

Chronic pelvic pain is then subdivided into those conditions with well-defined classical pathology, such as infection and cancer, and those where no obvious pathology is found. Chronic pelvic pain syndrome (CPPS) is therefore defined as:

The occurrence of chronic pelvic pain where there is no proven infection or other obvious local pathology that may account for the pain. It is often associated with negative cognitive, behavioural, sexual and emotional consequences as well as with symptoms suggestive of lower urinary tract, sexual, bowel or gynaecological dysfunction.

Therefore in most examples of CPP-related syndromes, and those listed in Box 1.1, marked with an asterisk, it is important to note that they are not the result of infection or pathology, and are characterized by persistent, recurrent or episodic pain (Abrams et al. 2002, Fall et al. 2010).

Box 1.1 Common chronic pelvic pain syndromes

Note: The selection of CPP-associated syndromes on this list does not include acute variants, and the word chronic implies the presence of the symptom for not less than 6 months.

Note: Syndromes marked * have no proven infection or other obvious pathology and are characterized by persistent, recurrent or episodic pain.

• Anorectal pain syndrome: * Persistent or recurrent, episodic rectal pain with associated rectal trigger points/tenderness related to symptoms of bowel dysfunction.

• Bladder pain syndrome: * Suprapubic pain related to bladder filling, accompanied by other symptoms such as increased daytime and night-time frequency, with no proven urinary infection or other obvious pathology. The European Society for the Study of IC/PBS (ESSIC) publication places greater emphasis on the pain being perceived in the bladder (Van de Merwe et al. 2008).

• Clitoral pain syndrome: * Pain localized by point-pressure mapping to the clitoris.

• Endometriosis-associated pain syndrome: Chronic or recurrent pelvic pain where endometriosis is present but does not fully explain all the symptoms (Fall et al. 2010).

• Epididymal pain syndrome: * Persistent or recurrent episodic pain localized to the epididymis on examination. Associated with symptoms suggestive of urinary tract or sexual dysfunction. No proven epididymo-orchitis or other obvious pathology (a more specific definition than scrotal pain syndrome (Fall et al. 2010).

• Interstitial cystitis (IC): Within the EUA guidelines, IC is included within painful bladder pain syndromes. It is frequently diagnosed by exclusion. Positive factors leading to a diagnosis of IC include: bladder pain (suprapubic, pelvic, urethral, vaginal or perineal) on bladder filling, relieved by emptying, and characterized by urgency, and (commonly) the finding of submucosal haemorrhage (glomerulations) on endoscopy. IC is immediately ruled out in the presence of a variety of pathological conditions, including bacterial infection (Hanno et al. 1999, Peeker & Fall 2002).

• Pelvic floor muscle pain: * Persistent or recurrent, episodic, pelvic floor pain with associated trigger points, which is either related to the micturition cycle or associated with symptoms suggestive of urinary tract, bowel or sexual dysfunction.

• Pelvic pain syndrome: Persistent or recurrent episodic pelvic pain associated with symptoms suggesting lower urinary tract, sexual, bowel or gynaecological dysfunction. No proven infection or other obvious pathology (Abrams et al. 2002).

• Penile pain syndrome: * Pain within the penis that is not primarily in the urethra. Absence of proven infection or other obvious pathology (Fall et al. 2010).

• Perineal pain syndrome: * Persistent or recurrent, episodic, perineal pain either related to the micturition cycle or associated with symptoms suggestive of urinary tract or sexual dysfunction.

• Post-vasectomy pain syndrome: Scrotal pain syndrome that follows vasectomy.

• Prostate pain syndrome: Persistent or recurrent episodic prostate pain, associated with symptoms suggestive of urinary tract and/or sexual dysfunction (Fall et al. 2010). This definition is adapted from the National Institutes of Health (NIH) consensus definition and classification of prostatitis (Krieger et al. 1999) and includes conditions described as ‘chronic pelvic pain syndrome’. Using the NIH classification system, prostate pain syndrome may be subdivided into type A (inflammatory) and type B (non-inflammatory).

• Pudendal pain syndrome: A neuropathic-type pain arising in the distribution of the pudendal nerve with symptoms and signs of rectal, urinary tract or sexual dysfunction. (This is not the same as the well-defined pudendal neuralgia.)

• Scrotal pain syndrome: * Persistent or recurrent episodic scrotal pain associated with symptoms suggestive of urinary tract or sexual dysfunction. No proven epididymo-orchitis or other obvious pathology (Abrams et al. 2003). This may be unilateral or bilateral, and is a common complaint in urology clinics.

• Testicular pain syndrome: * Persistent or recurrent episodic pain localized to the testis on examination, which is associated with symptoms suggestive of urinary tract or sexual dysfunction. No proven epididymo-orchitis or other obvious pathology. This is a more specific definition than scrotal pain syndrome (Abrams et al. 2002).

• Urethral pain syndrome: * Recurrent episodic urethral pain, usually on voiding, with daytime frequency and nocturia (Abrams et al. 2003).

• Vaginal pain syndrome: * Persistent or recurrent episodic vaginal pain associated with symptoms suggestive of urinary tract or sexual dysfunction.

• Vestibular pain syndrome (formerly vulval vestibulitis): Refers to pain that can be localized by point-pressure mapping to one or more portions of the vulval vestibule.

• Vulvar pain syndrome: Subdivided into generalized and localized syndromes:

• Generalized (formerly dysaesthetic vulvodynia): Refers to vulval burning or pain that cannot be consistently and tightly localized by point-pressure ‘mapping’ by probing with a cotton-tipped applicator or similar instrument. The vulval vestibule may be involved but the discomfort is not limited to the vestibule. Clinically, the pain may occur with or without provocation (touch, pressure or friction) (Abrams et al. 2002).

• Localized: Refers to pain that can be consistently and tightly localized by point-pressure mapping to one or more portions of the vulva. Clinically, the pain usually occurs as a result of provocation (touch, pressure or friction) (Abrams et al. 2002).

(Fall et al. 2010, Abrams et al. 2003)

This shift in definition is important to avoid incorrect diagnostic terms and descriptors as erroneous diagnostic terms are frequently associated with inappropriate investigations, treatments, patient expectations and potentially a worse prognostic outlook (Fall et al. 2010).

Terms that imply infection or inflammation should be avoided unless these are known to exist. For example, treatment choices for chronic prostate pain are often based on anecdotal evidence, with most patients requiring multimodal treatment aimed at their symptoms and comorbidities. Only between 5% and 7% of all chronic prostatitis complaints yield evidence of bacterial involvement (Anderson 2008), and the concept of chronic pain deriving from inflammatory conditions of the prostate is questionable (Nickel et al. 2003). Similarly, a diagnosis of interstitial cystitis (IC) suggests that the bladder interstitium is inflamed, despite evidence to the contrary in most cases.

Additional confusion results from the presence of lesions necessary for diagnosis of type 1 IC in healthy women following bladder distension (Waxman et al. 1998). It appears that urologic chronic pelvic pain syndromes (UCPPS) frequently evolve in otherwise healthy men and women, with no obvious pathogenic aetiological evidence, or objective biological markers of disease (Anderson 2008). EAU guidelines have therefore moved away from using ‘prostatitis’ and ‘interstitial cystitis’ in the absence of proven inflammation or infection.

Baranowski (2009) suggests that where pain is a major feature of a condition it is appropriate to name the region/area/organ where the individual perceives the pain – for example painful bladder syndrome. Such a label does not imply any mechanism, merely a location, while inclusion of the word syndrome takes account of any ‘emotional, cognitive, behavioural and sexual [associations or] consequences of the chronic pain’. The mechanisms involved may be associated with local, peripheral or central neural behaviour, and may involve psychological and/or functional influences, reaction and effects. None of these aspects are however implied by the name ‘bladder pain syndrome’, although all are subsumed into its potential aetiology and presentation.

In general management of CPP Fall et al. (2010) suggest a sequence in which initial consideration is given to the organ system in which the symptoms appear to be primarily perceived. Where a recognized pathological process exists (infection, neuropathy, inflammation, etc.), this should be diagnosed and treated according to national or international guidelines. However, when such treatment is ineffectual in relation to the pain, additional tests, such as cystoscopy or ultrasound, should be performed. If such tests reveal pathology this should be treated appropriately; however, if such treatment has no effect, or no pathology is found by additional tests, investigation via a multidisciplinary approach is called for (see Chapters 6, 7 and 8).

Chronic pain

As practitioners working with people in chronic pain, we therefore need to remind ourselves that the structural–pathology model for explaining chronic pain is outdated, particularly as the relationship between pain and the state of the tissues becomes weaker as pain persists (Moseley 2007). A summary of the sensitization processes involved in CPP (Fall et al. 2010) suggests that persistent pain is associated with changes in the central nervous system (CNS) that may maintain the perception of pain in the absence of acute injury. The CNS changes may also magnify non-painful stimuli that are subsequently perceived as painful (allodynia), with painful stimuli being perceived as more painful than expected (hyperalgesia). For example, pelvic floor muscles may become hyperalgesic, and may contain multiple trigger points. This process may lead to organs becoming sensitive, for example the uterus with dyspareunia and dysmenorrhoea, or the bowel with irritable bowel syndrome (IBS). Berger et al. (2007) have indicated that men with chronic prostatitis have more generalized pain sensitivity, and current thinking suggests that if there has been an inciting event, such as infection or trauma, it results in neurogenic inflammation in peripheral tissues and the CNS (Pontari & Ruggieri 2008). Later chapters – particularly Chapter 3 – will consider both the local and the general influences on, as well as the nature of, pain, occurring in pelvic structures.

The following chapters include pain-oriented discussion:

• Chapter 3: Chronic pain mechanisms;

• Chapter 8: Multispeciality and multidisciplinary practice; Chronic pelvic pain and nutrition;

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