Chronic pain mechanisms

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3 Chronic pain mechanisms

This chapter looks at some of the definitions and talks about the triggers that may result in chronic pelvic pain (CPP) and some of the predisposition and maintenance factors that may place an individual at risk for developing CPP. Whereas these triggers, predisposing and maintenance factors will have a biological basis, we also have to consider the biological basis of the pain mechanisms, acute and chronic, in their own right.

Defining chronic pelvic pain

Several groups have tried to tackle the issue of defining CPP and discussions are ongoing. The Urogenital Pain Special Interest Group of The International Association for the Study of Pain (IASP) are currently proposing the following:

Chronic Pelvic Pain is chronic/persistent pain perceived * in structures related to the pelvis of either men or women. 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.

^* Perceived indicates that the patient and clinician, to the best of their ability from the history, examination and investigations (where appropriate), have localized the pain as being perceived in the anatomical pelvic area.

They go on to say:

In the case of documented nociceptive pain that becomes chronic/persistent through time, pain must have been continuous or recurrent for at least 6 months. That is it can be cyclical over a six month period, such as the cyclical pain of dysmenorrhoea. Six months is arbitrary; however, six months was chosen because three months was not considered long enough if we include cyclical pain conditions. If non-acute and central sensitization pain mechanisms are well documented, then the pain may be regarded as chronic, irrespective of the time period.

Chronic Pelvic Pain may be subdivided into those conditions with well defined classical pathology (such as infection and cancer) and those where no obvious pathology are found.

For the purpose of this classification the terms Specific Disease Associated Pelvic Pain is proposed for the former and Chronic Pelvic Pain Syndrome is used for the latter.

Chronic Pelvic Pain Syndrome definition

Chronic Pelvic Pain Syndrome (CPPS) is 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.

CPPS is a subdivision of Chronic Pelvic Pain (see above).

The implications of the above for clinical management are huge. Essentially pain perceived to be both chronic and sited within the pelvis is associated with a wide range of causes and associated symptoms that must be investigated and managed in their own right. For this to occur, patients with CPP must have access to the appropriate resources through multispeciality (e.g. urology, urogynaecology, gynaecology, neurology and pain medicine) and multidisciplinary (e.g. medical doctor, nurse, psychology and physiotherapy) teams (Baranowski et al. 2008b) (see Chapter 8.1).

Chronic pelvic pain syndrome: The cause

It is important to realize the difference between trigger, predisposition and maintenance factors and how these may relate to the mechanism for the perceived pain and associated other symptoms.

Over the years there has been a great emphasis on the triggers for the chronic pain and much work has focused on local pathology, such as infection and local irritation with inflammation. This has resulted in a number of inappropriate outcomes (Abrams et al. 2006, Baranowski 2008a):

1. Over-investigation of the end-organ as the source of pain;

2. Inappropriate treatment of the end-organ (e.g. the overuse of antibiotics and even the removal of organs);

3. A spurious classification system that encourages the above.

A small group of patients may be able to identify the exact trigger. However, in many ways triggers are not important, as they are probably numerous, transient and can not be avoided. Ongoing and repeated investigations for the ‘cause’ are associated with a worse prognosis.

Triggers do not result in CPPS in all persons, though the proportion is unknown. It is now accepted that as well as triggers we need to consider predisposing factors and maintenance factors.

Genetics may play a role in predisposing patients to chronic pain, though the exact nature is not fully worked out. Other predisposing factors may include childhood experiences, negative sexual encounters and sexual violence, stress and other social factors, personality traits, as well as physical disability and medical illness. Some of these factors as well as precipitating inappropriate pain responses may also maintain the pain once started.

Maintenance is thus a complex issue. All chronic pain is associated with emotional and behavioural consequences (Sullivan et al. 2006, Nickel et al. 2008). The perceived severity of the pain understandably will be a major decisive factor as to how distressed and disabled the patient is. However, there is a cycle of events, where depression and catastrophizing are poor prognostic factors in their own right and clinical experience suggests that if these issues are not managed no progress in managing the pain will be made. Issues with work, relationships, sex and loss of meaning of life also appear to be as important. All of these factors can produce inappropriate maladaptive coping mechanisms such as inappropriate pain-contingent resting cycling with overactivity and as a result widespread total body pain, increased disability and increased distress.

Chronic pelvic pain syndrome: The mechanisms

There are many texts describing the mechanisms of chronic pain at a cellular level and neurobiological level (Vecchiet et al. 1992, Pezet & McMahon 2006, Nickel et al. 2008). The mechanisms for somatic, visceral and neurological tissue may overlap, but there are some important differences. As well as this science being applied to the patient the biopsychosocial model alluded to above needs to be integrated into the model.

All the structures within the pelvis and some outside of the pelvis (e.g. thoracolumbar junction) may, when stimulated, result in pain perceived in the pelvis. Recurrent activation of the nervous system may be associated with both peripheral and central sensitization.

The main consequences of the above science for the clinician are:

1. Lower threshold activation of peripheral nociceptors with increased pain perception;

2. Increased receptive field;

3. Patients become aware of stimuli not normally perceived – hyperaesthesia;

4. Stimuli that are normally not painful become perceived as painful – allodynia;

5. Cross-over hypersensitivity occurs (viscero-visceral hyperalgesia, visceromuscular hyperalgesia);

6. Central-mediated functional abnormalities of the viscera (e.g. abnormal function of the bowel with alternating diarrhoea and constipation);

7. Central-mediated changes in peripheral structure (e.g. Hunner’s ulcers, peripheral oedema and change in vasculature);

8. Neurobiological psychological consequences.

(Vecchiet et al. 1992; Giamberardino 2005; Pezet & McMahon 2006; Baranowski et al. 2008b).

A case history may best illustrate these points:

A patient develops an acute cystitis, infection may never be proven and stress, increased pelvic floor muscle tension is a possible cause for the initial symptoms. Perhaps there is a background of a negative sexual encounter (often there is not) and predisposing genetics, The ongoing pain results in central sensitization involving excitatory amino acid receptors such as N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole epropionic acid (AMPA). The patient feels that their bladder is never empty (aware of stimuli not normally perceived), and holding on to their urine produces pain (stimuli that are normally not painful become perceived as painful). Investigations of the bladder do not reveal infection, but the bladder is inflamed and swollen (central-mediated changes in peripheral structure). The pain appears to spread and the vulvar region becomes very sensitive with evidence of allodynia (increased receptive field). The patient describes erratic bowel habit, this may be due to the treatment; however, irritable-bowel-type symptoms due to central-mediated functional abnormalities of the viscera are also a possibility. The patient develops muscular pain (partly due to visceromuscular hyperalgesia but also due to inappropriate resting and cycles of over- and underactivity). As you might expect, depression, anxiety and anger set in; much of this may be secondary to the low quality of life and the pain but physical neurobiological changes may also be involved.

The initial trigger may involve any structure: somatic (cutaneous/muscular), visceral or neurological. The symptoms may remain well focused in that area, such as in the organ-based pain syndromes (e.g. bladder pain syndrome, vulvar pain syndrome, testicular pain syndrome) or in a specific muscle or local group of muscles. A patient may present at any stage in the above story and with a focus of pain within either a single or multiple system(s)/organ(s). The balance between afferent and efferent (functional) abnormalities is not linear and as a consequence some patients may present with primarily sensory and others with primarily functional phenomena. Patients may present with primarily pain perceived in one area and functional abnormalities in another. As well as these changes occurring or perceived within the pelvis, symptoms may be found elsewhere. For instance, bladder pain syndrome is associated with Sjögren’s and many pelvic pain conditions are associated with endocrine and immune deficiency as well as fibromyalgia and chronic fatigue syndrome (Abrams et al. 2006).

Mechanisms for chronic pelvic pain

Chronic pelvic pain mechanisms may involve:

1. Ongoing acute pain mechanisms (Linley et al. 2010) (such as those associated with inflammation or infection) – which may involve somatic or visceral tissue. This chapter will concentrate primarily on the visceral pain mechanisms;

2. Chronic pain mechanisms, which especially involve the central nervous system (McMahon et al. 1995);

3. Emotional, cognitive, behavioural and sexual responses and mechanisms (Binik & Bergeron 2001, Tripp et al. 2006). These will be covered in Chapter 4.

Table 3.1 illustrates some of the differences between the somatic and visceral pain mechanisms. They underlie some of the mechanisms that may produce the classical features of visceral pain; in particular, the referred pain and the referred hyperalgesias.

Table 3.1 Comparison between visceral and somatic pain

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	Visceral pain	Somatic pain
Effective painful stimuli	Stretching and distension, producing poorly localized pain	Mechanical, thermal, chemical and electrical stimuli, producing well-localized pain
Summation	Widespread stimulation produces a significantly magnified pain	Widespread stimulation produces a modest increase in pain
Autonomic involvement	Autonomic features (e.g. nausea and sweating) frequently present	Autonomic features less frequent
Referred pain	Pain perceived at a site distant to the cause of the pain is common	Pain is well-localized
Referred hyperalgesia	Referred cutaneous and muscle hyperalgesia common, as is involvement of other viscera. This is very important (see below)	Hyperalgesia tends to be localized
Innervation	Low-density, unmyelinated C fibres and thinly myelinated A fibres	Dense innervation with a wide range of nerve fibres
Primary afferent physiology	Intensity coding. As stimulation increases afferent firing increases with an increase in sensation and ultimately pain	Two-fibre coding. Separate fibres for pain and normal sensation
Silent afferents