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Body, Mind, and Brain in Pelvic Pain
Carolyn Vandyken and Sandra Hilton
INTRODUCTION
Mind-body connection has been a popular topic over the past decade when looking at persistent pain states in the clinical setting. Despite this shift, the lens used for assessing patients still employs a dominating filter of biomedicalism instead of biopsychosocialism. This chapter will look at historical perspectives, current trends and research to support a significant shift in treatment for persistent pelvic pain towards a biopsychosocial model. Historically, treatment of persistent pelvic pain has been mired in the tissues, and realistically, the tissues should not be ignored. Educating patients about the neurophysiology of pain will allow practitioners to make the shift towards a more comprehensive approach where the biological, psychological and social contributors are all given appropriate consideration. However, we should also exercise caution so that the pendulum does not swing so far in the opposite direction that we only consider the psychosocial characteristics of persistent pain.
BASIC ASPECTS
Mechanisms
Mechanisms underlying persistent pain differ from those underlying acute pain states, and yet from a therapeutic and medical perspective, they are often treated in a similar fashion [21]. In the absence of anatomical causes in persistent pain states, medical subspecialties have historically applied various labels including fibromyalgia, irritable bowel syndrome, interstitial cystitis or somatization [21]. Patients have often been made to feel that their pain is all “in their head” as if they are imagining their symptoms, causing untold despair and frustration. Recent evidence has suggested central pain mechanisms play a considerable role in many patients with persistent pain, even in those that were traditionally thought to have strong peripheral mechanisms, such as rheumatoid arthritis and osteoarthritis [21]. Therefore, the role of central pain mechanisms needs to be considered in all persistent pain states, not as a default diagnostic consideration but as a primary diagnostic indicator in pain that lasts longer than 3–6 months. “The medical profession has unwittingly created a form of mental imprisonment that I call medicalization, when diagnosis and treatment (of pain) causes an increase in pain and suffering” [13].
Definitions
Central Sensitization
As early as 1883, Dr. Sturge envisaged a possible central nervous system “commotion passed up from below” that contributed to the clinical features of ischemic cardiac pain [32]. Indeed, the spinal gate control theory by Melzack and Wall in 1965 highlighted that this sensory relay system could be modulated in the spinal cord by inhibitory controls [15]. Woolf first described central sensitization in the early 1980’s and operationally defined central sensitization 30 years later as an amplification of neural signaling within the CNS that elicits pain hypersensitivity [32]. The structural changes that occur in the nervous system are complex and are the subject of ongoing extensive basic science research. When pain persists, reorganization of the brain may contribute to persistent pain [17]. Central sensitization is a real phenomenon that can contribute to inflammatory, neuropathic and dysfunctional pain disorders. In other words, people experiencing these symptoms are not crazy, and the structural changes that occur in the nervous system in persistent pain are as tangible as the changes that occur in the tissues in acute pain.
DESCRIBING THE SUBJECT
Biopsychosocial Perspective
Thirty years ago, Dr. Waddell introduced the biopsychosocial model of disability for chronic low back pain [31]. Waddell recommended taking a three-pronged approach to the management of chronic low back pain, including the assessment of tissue involvement (biological perspective), illness behavior (psychological perspective) and socio-economic factors (social perspective) as they affect persistent pain. He defined non-organic signs of pain, which have been used extensively in the last thirty years to describe malingers and patients with perceived secondary gain issues. What Waddell put forward as non-organic signs are now recognized as significant factors that suggest central sensitization [25]. Cogwheeling (seen as an absence of smooth movement around a joint) is a classic non-organic sign that presents as a lack of coordination in the sensori-motor cortex, leading to jerky movements within agonist and antagonist muscle groups. Cogwheeling represents an organic change within the central nervous system rather than a poor effort put forth by a patient. Waddell emphasized taking a biopsychosocial approach with patients who demonstrate non-organic signs and symptoms. These patients should be identified as having organic nervous system changes, as defined by central pain mechanisms. Woolf has created a list of syndromes and conditions that have been shown to have a strong basis in central pain mechanisms, and many of those conditions are familiar to the persistent pelvic pain practitioner [32]. These include:
• Fibromyalgia
• Irritable Bowel Syndrome and other functional GI disorders
• Idiopathic Low Back Pain (LBP)
• Primary Dysmenorrhea
• Bladder Pain Syndrome/ Interstitial Cystitis/ Chronic Prostatitis
• Chronic pelvic pain and endometriosis
• Myofascial Pain Syndrome/Regional Soft Tissue Pain Syndrome [21].
Biomedical versus Biopsychosocial Perspective
A biopscychosocial approach is not neurocentric, focusing only on the brain and central processing. Peripheral pathology certainly needs to be considered, and a careful assessment of the balance of peripheral and central drivers should be completed for the person experiencing persistent pelvic pain. It is reasonable to assume that central pain mechanisms play a part in persistent pelvic pain, just as they do in all pain, even though we do not have the growing body of evidence underpinning other complex pain states such as Complex Regional Pain Syndrome (CRPS).
It can be challenging to change paradigms. We have identified 3 likely barriers to adopting a biopshycosocial approach to persistent pelvic pain.
First, the diagnostic terminology for persistent pelvic pain remains biomedical. Diagnostic labels include such conditions as levator ani syndrome, piriformis syndrome, coccydynia, vaginismus, vulvodynia, vestibulodynia and pudendal neuralgia. The labelled anatomical parts in these diagnoses encourage the clinician to consider the anatomical tissues as the main driver of the pain state. It may be sensible to follow the lead of other complex pain syndromes, such as Complex Regional Pain Syndrome, which was renamed from Reflex Sympathetic Dystrophy, in recognition that this syndrome is more complex and not limited to the autonomic nervous system. This re-labeling approach is beginning to occur in persistent pelvic pain as evidenced by renaming Interstitial Cystitis to Bladder Pain Syndrome (BPS). Phenotyping is the next logical step in this identification process, which would then help to direct appropriate treatment within the syndrome. This phenotypic approach is currently being studied in BPS [27]. Perhaps a change from the biomedical labels of pelvic pain as described previously to Chronic Pelvic Pain Syndrome would emphasize the need to approach this complex population from a biopsychosocial framework. Within Chronic Pelvic Pain Syndrome, it would then be prudent to determine if the predominant expression of the pain presentation is urological, gynaecological, gastrointestinal, sexual, or orthopaedic in order to direct treatment efforts and team member involvement.
Second, educational and training programs are biomedical. Domenech compared biomedical training versus biopsychosocial training of second-year physiotherapy (PT) students in the treatment of chronic LBP and how it drove their beliefs and clinical reasoning [2]. When trained in the commonly held biomedical approach, PT student interactions with chronic LBP patients were more limiting with regards to fear avoidance beliefs and had weaker return to work recommendations than those trained in a biopsychosocial approach [2]. Dr. Goldstein reports that gynaecologists are not taught a biopsychosocial perspective either in their residency programs [6]. He reports that in his training, he had one hour of education in a 20,000-hour residency on the nature of pelvic pain. It should also be noted that many patients hold very strong biomedical beliefs even before their visit to a physiotherapist or physician. Research has shown treatment expectancy and credibility to be of significant prognostic value to rehabilitation outcomes in patients with chronic low back pain [26]. The clinicians’ beliefs and attitudes account for the communication between the clinician and patient, including patient education, which in turn modulates treatment expectancy and credibility. The patient’s expectancy and beliefs of treatment credibility can be positively influenced by the clinician, but focusing on the biomedical model will result in inadequate illness perceptions in patients, which in turn leads to more negative initial response to treatment [29].
Third, randomized clinical trials (RCT) published in persistent pelvic pain are biomedical. Clinical RCT’s are not common in pelvic pain. However, Fitzgerald published a RCT looking at tissue-based treatment for urological pain including connective tissue massage, internal trigger point massage and external trigger point massage vs. generalized whole body massage [3