3 Chronic pain mechanisms
Chronic pelvic pain syndrome: The cause
Chronic pelvic pain syndrome: The mechanisms
Mechanisms for chronic pelvic pain
Ongoing peripheral visceral pain mechanisms as a cause of chronic pelvic pain
Spinal mechanisms of visceral pain and sensitization: Central sensitization
Supraspinal modulation of pain perception
Higher-centre modulation of spinal nociceptive pathways
Neuromodulation and psychology
Defining chronic pelvic pain
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.
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
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.
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.
The main consequences of the above science for the clinician are:
1. Lower threshold activation of peripheral nociceptors with increased pain perception;
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);
(Vecchiet et al. 1992; Giamberardino 2005; Pezet & McMahon 2006; Baranowski et al. 2008b).
A case history may best illustrate these points:
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
| 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 |
