Introduction

This book has a single primary aim – to offer a one-stop source of relevant information for clinicians – specialists, practitioners and therapists – on the subject of non-malignant chronic pelvic pain (CPP), with particular emphasis on current trends in physical medicine approaches to assessment, treatment, management and care.

The purpose of this chapter is to:

Definitions of chronic pelvic pain syndromes

It is suggested that approximately 15–20% of women, aged 18–50 years, have experienced CPP lasting for more than one year (Howard 2000) and a prevalence of 8% CPPS is estimated in the US male population (Anderson 2008). However, overall prevalence rates of CPP are likely to be underdiagnosed, in part due to the lack of agreed-upon definitions and subsequent difficulty in categorizing CPP (Clemens et al. 2005, Fall et al. 2010).

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 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:

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).

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:

Pelvic girdle pain and CPP: To separate or combine?

The American College of Gynecologists (ACOG) has proposed the following definition of CPP (limited to females):

The definitions from ACOG and EUA, include phrases such as ‘structures related to the pelvis’ and ‘involving the pelvis’ which suggests inclusion in such definitions of the structural supporting features of the region – and not only the pelvic organs and soft tissues.

However, many researchers and clinicians make a distinction between pelvic pain and dysfunction that relates to the organs and soft tissues of the region, and those chronic pain problems that involve the structural, osseous and ligamentous structures that frame the pelvis – the pelvic girdle. Pelvic girdle pain (PGP) therefore has its own definition, which specifically excludes gynaecological and/or urological disorders:

A reading of this definition of PGP can be seen to specifically exclude the pelvic organs and soft tissues, while the definition of CPP as provided in Table 1 in Fall et al. (2004, 2010) appears to allow for the consideration of all pelvic structures, including the pelvic framework.

So whilst simultaneously reminding the reader of ‘no brain, no pain’ (Butler & Moseley 2003), one of the aims of this book is to avoid what can be considered to be an artificial separation of the functions and structures of the entire pelvic region.

The urological and gynaecological, as well as the biomechanical (and other), features and functions of the pelvis are therefore considered, throughout this text, as having the potential to mutually influence each other.

Whenever the term chronic pelvic pain (or CPP) is used in this text, unless specifically stated to the contrary, this will refer to pain anywhere in the pelvis, arising from, or being referred to part, or all, of the region that lies inferior to the lumbar spine (although this will be involved at times) and superior to the gluteal folds – whether involving osseous, neurological, ligamentous, or other soft tissues, including the viscera.

Connecting PGP with CPP

O’Sullivan & Beales (2007) suggest that the motor control system can become dysfunctional in a variety of ways, and that such changes may represent a response to a pain disorder (i.e. it may be adaptive), or might promote abnormal tissue strain, and therefore be seen to be ‘mal-adaptive’, or provocative of subsequent pain disorders (see Figure 1.1).

Figure 1.1 • The vicious cycle of pain for centrally mediated pelvic girdle pain.

Adapted from O’Sullivan P, Beales D (2007) Diagnosis and classification of pelvic girdle pain disorders, Part 2: Illustration of the utility of a classification system via case studies. Manual Therapy 12 with permission

Maladaptive changes might in turn lead to reduced force closure (involving a deficit in motor control of, for example, the sacroiliac joint) or excessive force closure (involving increased motor activation) resulting in a mechanism for ongoing peripheral pain sensitization, leading to chronic pain involving the sacroiliac and/or other pelvic structures.

Additionally the pelvic floor itself may be involved in such adaptations – with the possibility of CPP symptoms emerging (O’Sullivan 2005).

Consideration of the biomechanical aspects of CPP and PGP will be found in:

Aetiological features of CPP

Some identifiable aetiological features commonly associated with CPP often involve one or more of the following factors summarized in Box 1.2.

However, in most cases the aetiology of CPP remains unknown, with no identifiable organic cause (Gomel 2007). Susceptibility to ill-health – in general – and to particular conditions such as those involving CPP, usually has multiple causes, since all manner of features, factors and events can compromise the individual’s ability to self-regulate.

Beyond single causes

A linking of genetic susceptibility with some instances of CPP (discussed further below) suggests an interaction between lifestyle and environmental factors, and the unique genetic make-up of the individual (Dimitrakov & Guthrie 2009).

As to what such environmental factors might be, Tak & Rosmalan (2010) discuss the role of the body’s ‘stress responsive systems’ in what have been termed functional somatic syndromes, for example IBS (Lane et al. 2009), as involving a ‘multifactorial interplay between psychological, biological, and social factors’. They conclude that stress responsive system dysfunction may be involved in the aetiology of such conditions. There is therefore a need to move beyond a search for single causes of most conditions involving CPP, since, like many other complex and difficult-to-treat conditions, CPP commonly has multifactorial aetiological features – possibly interacting with predispositions and altered stress-coping functions.

Beales (2004) has described a scenario that highlights multiple contributory factors to functional somatic syndromes:

Figure 1.2 • Human function curve. Healthy tension is represented by the up slope of the curve, where performance tends to improve in proportion to arousal. In this state of mind and body, activity can be balanced by restoration, and so homeostasis is maintained. On the down slope, effort continues despite fatigue; arousal increases but performance deteriorates, and eventually exhaustion worsens and health breaks down.

Adapted from: Beales (2004) “I’ve got this pain …” Human Givens Journal 11(4):16–18 with permission

Recent research has indicated that there may be a genetic tendency operating in some people with CPP. Dimitrakov & Guthrie (2009) note that:

Interesting as such considerations might be to researchers, a finding of a genetic link to CPP is unlikely to offer solutions to a patient’s current CPP problem. Yet phenotypes result from the expression of an organism’s genes, as well as the influence of environmental factors and the interactions between the two. Understanding the classifications, and possible aetiological features of a particular manifestation of CPP, should help determine a successful therapeutic plan. For example, Baranowski (2009) explains:

Making sense of the multiple clinical features in any individual with CPP and arriving at a therapeutic plan therefore calls for careful evaluation of the evidence. In Chapter 7 the question of the role of clinical reasoning, in the differential diagnosis and management of chronic pelvic pain, is explored in depth. How individuals and organizations set about combining clinical assessment and therapeutic expertise, experience and evidence is clearly of major importance when handling complex problems such as CPP and its multiple associated symptoms.

Treatment aimed at pathology is only part of the answer

There would be little need for this book were current treatment strategies that focus on CPP proving successful. Anderson (2006) notes that traditional medical therapy to treat CPP conditions has failed, ‘whether involving antibiotics, anti-androgens, anti-inflammatories, α-blockers, thermal or surgical therapies, and virtually all phytoceutical approaches’. Shoskes & Katz (2005) concur – demonstrating that a series of monotherapies, used to treat hundreds of men with prostatitis, resulted in only 19% reporting any relief of symptoms. However a randomized clinical trial designed to assess the feasibility of conducting a full-scale trial of physical therapy methods in 48 patients with urological CPPS has shown promise (Fitzgerald et al. 2009). It compared two methods of manual therapy: myofascial physical therapy and global therapeutic massage. The global response rate of 57% in the myofascial physical therapy group was significantly higher than the rate of 21% in the global therapeutic massage treatment group (P = 0.03) suggesting a beneficial effect of myofascial physical therapy.

However, Pontari & Ruggieri (2008) note that the symptoms of CP/CPPS appear to result from interplay between psychological factors and dysfunction in the immune, neurological and endocrine systems. It therefore seems unarguable that therapeutic approaches should adopt strategies that take account of these multiple interacting factors. And this is precisely the approach that this book takes.

For example psychological issues are considered in:

As expressed throughout this book, a background of different influences will be found to accompany the evolution of CPP, and its associated symptoms. Identifying the particular influences that have caused, maintained and/or exacerbated a CPP patient’s condition is therefore an appropriate clinical ambition. In the context of this book, a further ambition is the identification of those influences that may be amenable to therapeutic attention involving physical medicine. However, as pain involves many thoughts and emotional contributions, how we treat, talk, listen to and educate our patients about ‘their’ pain requires great skill. Reminiscent of the Indian parable regarding the elephant and a group of six blind men, many clinicians would agree that if there were six therapists examining one chronic pain patient, the most likely outcome would be six different diagnoses and six different treatment approaches. Further resembling the wise man’s explanation, all could be correct but no-one would know the whole truth. The patient may have all the features the therapist individually described, but it would be influenced by the therapist’s perspective and different belief systems. Further complicating matters, any dysfunction observed may not even be relevant to the presenting condition.

So how can the therapist explain CPP to their patient and what makes one patient more susceptible to chronic pain than another? As outlined previously, the aetiology is unclear but it is apparent that multiple factors somehow contribute to the pain experience. With this belief system in mind, a ‘10 points to pain’ model is one concept that a number of patients and clinicians have found useful (Jones 2003) (Figure 1.3). It is an easy way to demonstrate that pain can develop through many different reasons and works on the premise that pain is rarely the result of one single incident, but normally stems from a range of different issues or a whole lifestyle that contribute to the 10 points and painful state.

Figure 1.3 • Accumulate 10 points for pain; some factors that appear to influence the accumulation of a pain experience.

Reproduced, with permission, from Jones (2003)

In this way, the patient and therapist can move away from the solely structural pathological model, to one that considers, for example, the brain in pain, their beliefs about their pain, nutritional issues, in addition to any pathology or motor control issues. For example, there is evidence that understanding pain reduces the threat of it, altering patients’ attitudes and beliefs, increasing pain thresholds and, when combined with physiotherapy, reduces pain and disability (Moseley 2007). It is therefore important to understand what the patient believes the pain means and help explain modern pain biology, thereby reducing the patient’s attitude and beliefs points. For example the patient may have a belief that:

One consequence of these beliefs is that the patient may be afraid to do an activity just in case it hurts or avoid it completely. For example, patients who have been diagnosed with pudendal neuralgia typically are afraid to sit, as they have read that prolonged sitting causes compression to their nerve so if they sit for too long (or at all) they will develop greater compression and more pain. In this way, they avoid sitting at all costs, which can severely affect their work, recreation and quality of life. Similarly sex can be painful, so if the patient equates pain with damage, not only does the patient avoid an activity that can provide great pleasure, cessation of sexual intimacy can produce immense strain on their relationship.

The 10 points for pain is not an exhaustive list, and the patient is encouraged to fill out their own chart, adding in any factor that they believe may contribute to their pain. Furthermore, it is important to emphasize that this is not an absolute scoring system that says that diagnosed pathology is 4 points, having negative beliefs and attitudes is 2 points, having poor motor control is 3 points, being angry or fearful is 2 points. Some patients will accumulate more points in one area than another, or those same factors will have a higher (or lower) weighting in different patients. The task of the therapist and patient is to start piecing the different parts of the puzzle together in order to understand the unique accumulation of factors that tip the patient over the threshold from a pain-free (below 10 points) to a painful (above 10 points) state. Over time the patient then can reduce their points by choosing to change the areas in their life that they believe are contributing to their pain experience and let go of the things that they cannot. The therapist assists by reducing the patient’s accumulated pain points in areas amenable to the therapist’s particular discipline.

It is our hope that some of the ideas contained within this book may be of use in the clinic, either in their current form, or with additional creative input from the reader. However, as stated at the beginning of the chapter, currently most treatment options for CPP are empirical, so there is a great requirement for careful clinical reasoning when approaching the management of a patient with CPP, if indeed we are to do no harm.

The next chapter describes the anatomy of structures that may need to be examined and treated in patients with pelvic pain.