Introduction

A tenet of the psychophysiological approach is that certain disorders affect and are affected by both physiology and emotion, or the mind. Many disorders considered to be strictly physical can be either exacerbated or soothed by cognitive and emotional factors. In these cases, correcting a physical imbalance, such as with medication, is not enough; psychophysiological disorders call for psychophysiological interventions.

It is incomplete to try to alter the physiology without addressing the reason for the condition. Like the acoustic howl when a speaker is moved too close to its microphone, psychophysiological disorders often include a ‘reaction to the reaction’, which in effect traps one in the vicious circle. Thus, anxiety about heartbeat feeds back into the heartbeat, making it faster. Anxiety about breathing further disrupts the breathing. In pelvic pain, anxiety about painful intercourse can alter genital physiology and create the pain that is feared.

In studying the complicated relationship between psychological and physiological factors with regard to chronic pain, researchers have explored certain themes often over the past several decades. Psychological factors, intangible except by their correlates and consequences, may be as objective as blood factors and other physical measures, but they are considered more subjective because of how they must be measured: by self-report, interviews and observation of behaviour, which are all subject to bias. Reliability (consistency of responses over time) and validity of any structured interview or questionnaire can be assessed in the way that blood tests or structural/functional tests can be. For instance, affirmative answers to questions about childhood sexual abuse are far from objective historical data, since they depend first on accurate recall, then willingness to acknowledge and name it as such, and then to acknowledge it in the particular assessment situation. What defines ‘abuse’ differs from person to person; the term is a label for personal experience, and is subject to interpretation.

Psychophysiology in historical perspective

Any study of ‘psychophysiology’, the word itself representing an amalgam of mental and physical, must start with the historical roots of mind–body dualism. Dualism studies the nature of consciousness and its relationship to the physical body, particularly the brain, as the central issue. Dualism argues that the mind is an independently existing substance (physical dualism) or group of independent properties that emerge from (emergent dualism), but cannot be reduced to, the brain. Monism is the position that mind and body are not, by substance, properties, or by development, distinct entities. Reductive physical monism asserts that all mental states and properties will eventually be explained by scientific accounts of physiological processes and states. Most modern philosophers and scientists take a reductive physicalist monism position, asserting that the mind is not separate from the body, and that the physical brain is the fundamental reality. This position has been most influential in the sciences, particularly neurosciences and allied fields such as sociobiology, evolutionary psychology and computer science approaches to artificial intelligence.

Although scientific advances have helped to clarify some mind–body issues, they are far from being resolved. How can the subjective qualities and the essence of a state of consciousness be explained in naturalistic terms? The most recognized modern form of dualism comes from the writings of René Descartes (1641) (see Marenbon 2007), and holds that the mind is a separate mental substance. Descartes clearly identified the mind with consciousness and self-awareness, and distinguished it from the brain, which he identified with intelligence. He was the first to formulate the mind–body problem in the form that it exists today.

Paradoxically, the mind–body issue within the field of psychology became dominated by behaviourism, a form of physical monism, for much of the 20th century. Behaviourism emerged in reaction to the rising popularity of introspection. Introspective reports on one’s own mental life cannot be scrutinized by someone else for accuracy, and cannot form the basis of probabilistic predictions. Behaviourists argued that without the possibility of independent confirmation or generalization, psychological data cannot be scientific. The way out was to eliminate the idea of an internal mental life and focus instead on the objective description of observable behaviour. For the behaviourist, mental events manifest only as objective behaviours or behavioural predispositions, allowing an outside observer to predict and explain behaviour.

This type of behaviourism was ultimately dismissed as mechanistic and counterintuitive, ignoring the richness of internal experience. Cognitive-behavioural psychology arose as a direct reaction to the failure of behaviourism. This new version of behaviourism incorporated thoughts, which often triggered behaviour, and reaffirmed the value of internal experience of consciousness and self. In contrast to pure introspection, however, advances in neurosciences began to define cognitive events as both experiential and neurophysiological phenomena. Considering cognitive events as brain states meant that states of consciousness could be studied both by physical scientific methodology and by subjective, experiential methodology. This included investigation of emotional, cognitive, perceptual and motivational events. The line between physical matter and experiential matter became ever thinner with every scientific advance. The increasing success of biology in explaining mental phenomena led to the gradual acceptance of the fundamental claim that every change in mental state involves a change in brain state.

Psychophysiology studies the interaction of mental faculties with specific anatomical regions of the brain, while evolutionary biology studies the origins and development of the human nervous system. Since the 1980s, sophisticated neuroimaging procedures such as functional MRI have furnished increasing knowledge about the workings of the human brain correlated with mental experience. With the expansion of such technology, it seems inevitable that understanding of mental states will be more and more correlated with observable brain events. In clinical practice, this creates the potential to access and alter states that were not previously available. For example, altering blood flow to rhinencephalic structures (brain state) can alter the perception of pain (state of consciousness). Conversely, creating the expectation of loss of control of a situation (state of consciousness) can lead to synaptic neurochemical changes related to anxiety (brain state).

Modern psychophysiological research

Much of the current emphasis is on studying either persistent or transient emotional states together with observations of physiological changes: for instance, the effect of experimental stressors on cortisol secretion. Many studies are simply correlational, with no determination of mechanism or direction of causation. In the study of chronic pelvic pain, childhood sexual abuse emerges often as a critical factor, suggesting that having such a history confers a long-term susceptibility to chronic pelvic pain disorders. The thought style of catastrophic thinking is present more often than chance in cases of chronic pain in general. An increased tendency to avoid movement and sexual activity because of fear of pain is another factor contributing to further disability. Chronic depression and anxiety also correlate with chronic pain.

A central question addressed in psychophysiological research is how emotional, behavioural and cognitive characteristics are related to pelvic floor and lower-abdomen susceptibility to pain. Are there observable malfunctions in visceral tonus, in pelvic circulation, or in muscle function and baseline levels? Or do pain thresholds simply fluctuate according to mental and emotional conditions, without objective physiological differences? This simple question has stimulated much investigation.

Psychophysiological research occupies an area on a continuum which can be described with reference to an analogy: hypothetical aliens observing people driving cars but having no knowledge of how such a process could work. From a distance they might – like the Incas first mistaking Spaniards on horseback for Centaur-like beings – perceive the car–driver combination as a single organism. After further observation, one group of aliens might focus on the workings of the automobile, and they would study the steering linkage and the engine’s coupling to the drive train. Another group might study the details of the driver’s arms and hands, and the brain that animated them. Another school of thought might take interest in how the driver decides where to drive, and how fast, and even why. A fourth group might study the ‘behaviour’ of the automobile, how fast, how far, and where it goes, with little concern about how it gets there.

More relevant to clinical concerns, suppose a particular automobile keeps veering out of its lane and hitting the curb. Where should one look for the malfunction? The driver’s intent, the driver’s sensory system, the driver’s muscles and limbs, the steering system, or an uneven road? To the aliens, it might seem that all possibilities should be considered. In this analogy there are several possible levels of analysis, all legitimate, for addressing the fact that people drive cars. Without the existence of both cars and drivers, however, the phenomenon would disappear, so declaring one level of analysis as more objective or closer to the truth seems fanciful.

Psychophysiology’s domain is the entire region between the driver’s mind and the car’s behaviour. An example of a ‘psychophysiological’ disorder in terms of this analogy might be rapid wear of the brake linings, requiring frequent replacement. A mechanic could examine all the component parts for malfunction, but the ultimate reason might be that the driver, fearful of collision, simply rides the brake excessively. Where, in this case, is the fault?

The psychophysiological approach is complex, requires more complete knowledge of a given disorder and organ system, and may not appeal to extremists at either end of the spectrum, but it can provide a comprehensive understanding of any disorder that has both somatic and emotional aspects. This understanding will increase the options for clinical treatment.

The origin and maintenance of medically unexplained chronic pelvic pain appears to be multidetermined and intertwined with psychological factors. Two reviews of the subject reached similar conclusions:

A wide variety of provocative events can lead to localized acute tissue reactions with resulting nociceptive pain. This acute pain most often resolves on resolution of the provocative factors. In the presence of organic and psychological predisposition this pain may become chronic pain with the addition of neuropathic elements to the nociceptive factors. With urogenital pain, psychological, sexual and functional states are adversely affected adding a psychophysiological element to the chronic pain. Figure 4.1 depicts some potential relationships among biological and psychological factors in chronic pelvic pain.

Figure 4.1 • Idiopathic lower urogenital tract disorders model

What follows is a summary of representative research findings in support of the generalizations above, along with some speculations and assumptions guiding both research and treatment.

Prostate and pelvic pain

One recent study (Ullrich et al. 2007) of benign prostate hyperplasia (BPH) implicated the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system reactivity in prostate enlargement. Eighty-three men with BPH underwent an experimental stress task (public speaking, videotaped). The degree of stress was defined physiologically as rises in cortisol and blood pressure. Personal appraisal of the situation was not assessed. Subjects showing stronger stress responses were found to have larger prostate volume and more objective and subjective indications of urinary tract dysfunction. Among the hypotheses for this relationship were decreased apoptosis (slowed prostatic cell death) as a result of chronically greater sympathetic input; increased pelvic floor muscle tension; greater prostate contractility (stimulated by exogenous epinephrine and norepinephrine); and stress-induced hyperinsulinaemia promoting prostate growth. Not all BPH cases involve pain, but when pain is present it can stimulate the sympathetic system, create a feedback loop, and add to the problem.

Anderson et al. (2005, 2008, 2009) compared men with chronic pelvic pain syndrome (CPPS) with asymptomatic controls for evidence of differences in stress levels. Various psychological tests revealed more perceived stress and anxiety in the CPPS patients, plus more somatization, hostility, interpersonal sensitivity and paranoid ideation. Salivary cortisol on awakening was also measured and found to be significantly higher in the pain patients. This rise in cortisol is thought to indicate the hippocampus preparing the HPA axis for anticipated stress. Cortisol has been found to be higher in situations such as waking on the day of a dance competition (Rohleder et al. 2007), in high-school teachers reporting higher job strain (Steptoe et al. 2000), and waking on work days compared with weekends (Schlotz et al. 2004).

Anderson and Wise have advanced an explanation of chronic, otherwise unexplained pelvic pain as frequently stemming from myofascial trigger points (Wise & Anderson 2008) (see Chapter 16). In their view, much long-term pelvic pain develops from the shortening and tensing of pelvic muscles, eventually creating and then aggravating trigger points, and this condition can be treated with manual release techniques. The more complete treatment, however, involves cultivating a skill for dropping into deep relaxation along with changing attention (‘paradoxical relaxation’) in a way that contradicts the usual tensing and bracing against pain. This is achieved (in their programme) by progressively more muscular and emotional self-calming.

Trigger points were shown to be exacerbated by stressful emotion (Hubbard & Berkoff 1993, McNulty et al. 1994). EMG was recorded from an upper trapezius trigger point along with a signal from an adjacent area of the muscle without a trigger point. As emotional stress increased, the trigger point EMG increased its voltage even though the rest of the muscle did not. Also, described in Chen et al. (1998) was a demonstration of how electrical activity associated with trigger points in rabbits was abolished by phentolamine, a sympathetic antagonist. This supports the role of the autonomic nervous system in maintaining trigger points, and also is congruent with the cited research on the aggravating effect of negative emotion (anxiety) on trigger points (Simons 2004). Wise and Anderson’s protocol for pelvic pain treatment includes both thorough relaxation training and manual release of trigger points. One is temporarily curative, the other preventive.

Alexithymia and pelvic pain

The word ‘alexithymia’ refers to a relative inability to name feelings, or to verbally elaborate on feeling states. Its Greek roots belie its recent creation, less than 40 years ago, by psychiatrist Peter Sifneos (1973). The phenomenon and the concept existed long before its final naming. Physicians and psychotherapists had noted for many years the tendency of some patients to use very few words to describe their feelings; complex emotional states were reduced to simple terms such as ‘feeling bad’ or ‘upset’ without elaboration. This difficulty with feelings includes reflecting on them, naming them, discussing them and expressing them.

Alexithymia seems to be a trait rather than a state, an enduring and stable aspect of behaviour seen by many as a disability. It is the opposite of the concepts ‘emotional intelligence’ and being ‘psychologically minded’. Alexithymics tend toward concrete thinking and restricted imagination. Knowing when their physical sensations and symptoms are emotionally based (rapid heart beat, changes in face temperature, agitated breathing) is not easy for the alexithymic person.

Researchers have pursued correlations between high scores on alexithymia scales such as the Toronto Alexithymia Scale (Bagby et al. 2006) and other problems such as dissociation, Asperger’s, autism, substance abuse, anorexia nervosa, somatic amplification and somatoform disorders. A functional disconnection between the two cerebral hemispheres or a right hemisphere deficit has been suggested, with incomplete evidence (Tabibnia & Zaidel 2005).

Most research on chronic pain and alexithymia has found a correlation between them. Celikel and Saatcioglu (2006) found that female chronic pain patients scored more than twice as high on alexithymia scales as controls, and there was also a positive correlation between alexithymia scores and duration of pain. Since the study design was not intended to distinguish direction of causation, it is conceivable that prolonged pain damages the right hemisphere, interfering with full experiencing and transfer of emotional material.

Porcelli et al. (1999) found a strong association between alexithymia and functional gastrointestinal disorders (66% had high alexithymia scores, whereas the population average is below 10%), and later (Porcelli et al. 2003) demonstrated that higher alexithymia scores predicted worse treatment outcome. Although anxiety and depression also predicted worse treatment outcome, the alexithymia scores were stable and independent of anxiety and depression, suggesting a unique contribution to failure to improve.

Hosoi et al. (2010) studied 129 patients with chronic pain from muscular dystrophy. Degree of alexithymia was significantly associated with higher pain intensity and more pain interference. Finally, Lumley et al. (1997) compared chronic pain patients to patients seeking treatment for obesity and nicotine dependence, to control for the variable of ‘treatment-seeking’. As predicted, the chronic pain patients scored higher on the alexithymia measures than either of the other groups. They also had higher levels of psychopathology, which can by itself confound and weaken treatment programmes for chronic pain.

There are few theories as to how alexithymia specifically contributes to chronic pelvic pain states; however, the value of patients both naming and differentiating feeling states at the conscious verbal level is emphasized. A person who routinely does this is likely to consider the material objectively, to process, express, and otherwise deal with material that is commonly relegated to the ‘unconscious’ domain. This effective processing of feelings has vast potential influence on automatic (autonomic) functioning by differentiating true physical threat from the much more common triggers for social anxiety or symbolic threats. Local pelvic circulation, adjustments in pelvic floor muscle tension, and changes in breathing are subject to the flux of emotions until they are released from functional service. Strong negative emotions associated with traumatic memories, apprehension, sexual conflict and accidents of elimination can influence the complex structures and functions of the pelvic region.

Processing of emotional experience often involves revisiting traumatic or otherwise disturbing memories, which can be done alone or with the help of a friend, relative or therapist. Psychologist James Pennebaker has led the way in a body of research that repeatedly confirms the value of simply writing about undisclosed experiences and the deep feelings that have been kept private (Berry & Pennebaker 1993; Pennebaker 1997). This process of transforming inchoate memories and feelings into a linear, word-based account of an experience seems to be a key step in ‘adjusting’ to something unpleasant. Part of the value of psychotherapy lies in providing a safe forum for verbalizing one’s feelings about something for the first time, and this activity has therapeutic value regardless of response from another person.

This self-adjusting activity, however, is precisely what the individuals describable as ‘alexithymic’ are not good at. Their poverty of verbal labels for body sensations related to emotional states is their defining characteristic, and may block necessary processing of experiences in real time. Emotional adjustment and acceptance benefit from review, reflection, hindsight, considering contextual factors, and if possible, ‘normalization’ by an accepting and supportive listener. Pennebaker (2004) has concluded that undisclosed disturbing experiences cause persistent conflict, partly over-suppressing them; the topic stimulates ruminative worry, and this eventually has ill-health effects. Graham et al. (2008) showed that in a large group of chronic pain patients, writing about their anger constructively resulted in better control over both pain and depression, compared with another chronic pain group asked to write about their goals. Junghaenel et al. (2008) also studied the effects of written self-disclosure on chronic pain patients, and found that only those with ‘interpersonally distressed’ characteristics (denoting deficient social support, feeling left alone, etc.) benefited from the expressing of emotional events.

The role of a listener is apparently optional; Pennebaker’s research protocol, extended and repeated by many other researchers over the past 20 years, does not include feedback from another person, but studies only the actual expression, whether through writing, speaking into a tape recorder, or even using sign language or dance. Expression may represent a transfer of affective material from the relatively mute minor (usually right) cerebral hemisphere to the major, speech-dominant hemisphere. The full powers of judgement, rational perspective and philosophical acceptance depend primarily on the major hemisphere, which is dominated by words. So the alexithymic person is at a disadvantage for this process. As a result, strong emotional experiences may remain unprocessed and unexamined. The physiological aspects of this condition may continue to reverberate, causing inappropriate responses to emotion provoking stimuli and situations.

The main thrust of research with alexithymia has been in the areas of somatizing, trying to characterize the ‘psychosomatic’ patient as deficient in this way. One of the largest surveys of this association, studying over 5000 Finnish citizens, found a clear association between somatization and alexithymia (Mattila et al. 2008). Factors such as depression, anxiety and sociodemographic variables were controlled for, and the association remained. The TAS-20 factor scale labeled ‘Difficulty Identifying Feelings’ was the strongest common denominator between alexithymia and somatization.

So an apparent deficit in cognitive processing of emotional material seems firmly associated with somatization in general, and unexplained chronic pain in particular. Why this should be so is a larger research question. Meanwhile, anything that helps lessen the gap for an individual between the non-verbal and verbal domains is likely to help process affects and experiences that otherwise continue to cause bodily distress.

Pain catastrophizing and fear-avoidance

Pain is neither a simple stimulus nor a simple response; it is bound up with expectations, memories, interpretations and emotional associations, and the final experience of pain will be altered by all those factors. For example, changing one’s initial fearful alarm reaction to a new pain by interpreting it differently (‘it’s only a nuisance, but not harmful’) improves the reaction to pain mentally and physically. Consider the shift in mental state when a household smoke alarm goes off. At first the occupants fear a fire and are ‘alarmed’, but if they then discover a malfunction in the alarm system, or perhaps that smoke from cooking has set the alarm off, the distress dissolves into annoyance. Physically the sound is just as loud, but the emotion is completely changed, and most aspects of the physiological response are reversed.

Many instances of chronic pelvic pain have an obscure or unknown aetiology, and are associated with other symptoms such as comorbid psychiatric conditions (anxiety, depression), and a tendency toward emotion-triggered multiple somatic complaints over time (‘somatizing’). Treating such patients as if they have bona fide medical conditions, when such evidence is lacking, is at best incomplete. Such patients may respond to analgesic medications, but they often respond better to a biopsychosocial approach which addresses interpersonal factors, anxiety, apprehension and catastrophic thinking about the meaning of the pain, plus attention to muscle-bracing, movement and breathing patterns, and sensory awareness (Haugstad et al. 2006).

‘Pain catastrophizing’ is a psychological variable easily measured by questionnaires such as the Pain Catastrophizing Scale (PCS) (Sullivan et al. 1995, 2001) or the Pain Anxiety Symptoms Scale (McCracken et al. 1992, Burns et al. 2000). These scales quantify negative expectations about pain and include subfactors such as helplessness, degree of suffering and disability expected, estimated ability to cope with the pain, and feeling overwhelmed.

Sample comments from questions from the PCS include:

The high-catastrophizing pain patient typically feels that the pain justifies their drastic response, and they do not see their reaction as adjustable. Since pain magnitude is entirely subjective and so far not measurable by objective standards, this attitude is hard to dispute. Since there are genetic and other individual differences in pain perception, a one-to-one correspondence between stimulus intensity (degree of damage on X-ray, degree of nerve impingement, etc.) and the subjective response is not likely. Even within the same person, certain factors can augment or diminish pain intensity within seconds. These factors arise from both psychology and physiology.

Pain catastrophizing as a cognitive process may get stronger as pain gets worse, but it also varies independently of pain intensity. For example, in a prospective study, Flink et al. (2009a) studied childbirth and pain. Eighty-eight women were assessed for pain catastrophizing before they gave birth. Those scoring higher in this variable reported subsequent higher pain and poorer physical recovery (measured as activity levels) as compared with those with lower prebirth pain catastrophizing scores. Since this was not an intervention study, it could be argued that the high-scoring women knew that their pain would be worse. But intervention studies which alter pain catastrophizing have been successful in altering various aspects of the reaction to pain (Voerman et al. 2007, van Wilgen et al. 2009).

Training patients to reduce pain catastrophizing is a standard part of cognitive-behavioural therapy in comprehensive pain management programmes, and the results in many patients are comparable to medication or other medical interventions. Learning to reduce catastrophizing, regardless of the source of the pain, can favourably affect avoidance behaviour, muscle bracing, medication use, general activity and subjective distress.

Smeets et al. (2006) studied chronic low back pain patients going through either physical or cognitive-behavioural treatment, and found that in both intervention groups, pain catastrophizing was a mediating variable for improvement in pain intensity and disability. Thorn et al. (2007) used a RCT design with wait-list control to study the response of chronic headache sufferers to cognitive change techniques, with particular attention to changes in catastrophic thinking. The active treatment group had significant improvements in affect, anxiety and self-efficacy regarding headache management. About half of them also had clinically meaningful reductions in headache indicators that did not occur in the control group.

Tripp et al. (2006) studied certain characteristics in 253 men with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Magnitude of both sensory pain and affective pain could be predicted by degree of what was termed ‘helpless catastrophizing’.

The physiological mediators in pain catastrophizing are largely unknown, but Wolff et al. (2008) showed that the combination of higher paraspinal muscle tension and high catastrophizing predicted high reported pain levels. Muscle tension in this study was not a simple mediating factor, but if resting low back tension was already high, then the co-occurrence of catastrophic thinking amplified the perception of back pain.

Lowering pain intensity is not the only desirable treatment outcome. A study of reducing pain in patients in an emergency deparement (Downey & Zun 2009) instructed patients in slow deep breathing, and in this brief intervention found no significant reduction in pain as estimated by the patients, but there were still significant improvements in rapport with treating physicians, greater willingness to follow the recommendation and numerous statements that the intervention was useful. Another study of back pain patients (Flink 2009b) showed that practising breathing exercises had not so much effect on actual pain levels as it did on less catastrophizing and pain-related distress, along with greater acceptance of the pain condition.

Hypervigilance and fear of movement

One related psychological variable relevant to pain perception is called ‘hypervigilance’. This can be measured in several ways, including magnitude of startle response. The factor of unpredictability, basically an absence of reliable threat cues, seems to amplify vigilance, and the Pain Vigilance and Awareness Questionnaire is designed to measure the vigilance specifically for pain (Roelofs et al. 2003). Hypervigilance was also assessed in a group of 54 young male patients one day before chest-correction surgery (Lautenbacher et al. 2009). Subjective ratings of pain intensity 1 week later were significantly predicted by degree of hypervigilance; the more watchful the patients were, the more pain they reported.

The Tampa Scale of Kinesiophobia (TSK) measures fear of movement instead of fear of pain directly (French et al. 2007). This shows a conditioning effect in which the organism with repeated noxious experiences becomes sensitive to earlier and earlier cues. So if a certain pelvic movement causes pain, the fear of pain will inhibit that movement. Some people generalize from this association more drastically than others: perhaps from only that one particular pelvic movement to all related pelvic movements, or – ‘just to be safe’ – nearly any body movement at all.

Sample items from the TSK scale include:

All these questionnaires seem to tap slightly different aspects of a central quality related to fear and avoidance. As Roelofs et al. put it (2003): ‘With regard to the convergent validity, the Pain Vigilance and Awareness Questionnaire was highly correlated with related constructs such as the Pain Catastrophizing Scale (PCS), Pain Anxiety Symptoms Scale (PASS), and Tampa Scale of Kinesiophobia (TSK)’. What such questionnaires tap is related to anxiety, broadly conceived, and with components of depression such as helplessness and loss of hope. Pain studies may not differentiate subcategories of these broader conditions and so end up blaming anxiety and depression for exacerbating chronic pain.

Avoidance of sexual activity

The correlation between degree of pelvic pain and normal sexual activity is not as great as one might think. Emotional factors that facilitate or inhibit sexual activity are many, and include capacity for sustained intimacy, gender identity, general sense of self-worth, baseline desire, relationship quality and comfort with sex in general. Prolonged avoidance of sex can result from a short-sighted withdrawal from situations associated with pain, past or present. Deconditioning through disuse can occur just as easily in sex organs as in the legs or back muscles. Desrochers et al. (2010) found that baseline fear of pain and catastrophizing were strong predictors of eventual success in a programme targeting provoked vulvodynia, and success included return to normal sexual activity. Desrochers et al. (2009) also presented evidence that psychological variables such as catastrophizing, hypervigilance and fear of pain predicted sexual impairment in women with provoked vestibulodynia. This means that pain magnitude is not linearly correlated with sexual functioning; actual pain is only part of the picture, sometimes overshadowed by cognitive and affective variables. There is a wide range of variability between loss of sexual desire and intensity of sexual pain.

Reissing et al. (2004) investigated the accuracy of the usual criteria for diagnosis of vaginismus, which is usually considered a simple muscle spasm problem. Using the factors of degree of vaginal spasm and pain, women previously diagnosed with vaginismus were not significantly different from women with vulvar vestibulitis syndrome, but they could be differentiated by higher vaginal muscle tone (with lower muscle strength) and more defensive and avoidant distress behaviours. The authors concluded: ‘These data suggest that the spasm-based definition of vaginismus is not adequate as a diagnostic marker for vaginismus. Pain and fear of pain, pelvic floor dysfunction, and behavioral avoidance need to be included in a multidimensional reconceptualization of vaginismus’.

It is relevant that sexual desire and arousal are autonomically regulated functions which are physiologically and psychologically mutually exclusive. Acute fear can cause extreme pelvic floor muscle relaxation and urinary and bowel incontinence because bodily resources are redirected to ‘fight or flight’ mechanisms, and away from regulation of elimination and reproductive organs. Therefore the psychological factors, including conditioned avoidance and biased expectations of discomfort, are integral to female pelvic pain problems. They should be addressed along with strictly physiological factors, which even if normalized do not automatically heal problems in the psychological realm which impair natural sexual function.

For instance, a large study in China surveyed 291 men with chronic prostatitis and pelvic pain for degree of anxiety and depression as they underwent a 6-week treatment programme. Other factors expected to affect treatment outcome were also assessed: age, a prostatitis symptom index, and leukocyte count. None of these were predictive of treatment success, but the psychological variables of anxiety and depression were. The authors concluded: ‘Such psychological obstacles as anxiety and depression play an important role in the pathogenesis, development and prognosis of CP/CPPS’. The psychophysiological link in this case is unknown, but may involve chronic restriction of pelvic or prostate circulation (Li et al. 2008).

Finally, the variable of self-efficacy has been found to be correlated with both chronic pain and alexithymia. Physical self-efficacy – meaning roughly self-confidence in one’s physical capacity – is modifiable to a degree, with favourable health consequences. A study by Pecukonis (2009) found two initial differences between a sample of patients with chronic intractable back pain and a matched control group. The pain group was significantly higher in alexithymia and lower in physical self-efficacy (self-estimate of strength, endurance and ability to perform physically). Foster et al. (2010) found that ‘pain self-efficacy’ was a strong predictor of recovery from chronic pain, independently of depression, pain catastrophizing and fear of movement. Having a self-concept that includes resilience and capacity to recover is important for participating fully in treatment programmes for any kind of chronic pain.

This quality was pinpointed also in Albert Bandura’s 1987 study teaching subjects to withstand experimental pain, using cognitive techniques to boost self-efficacy. The study design included the opioid-blocking chemical naloxone to control for the effects of opiate pain medication administered at certain points. The outcome supported the value of cognitive training to boost pain control. In the author’s words: ‘…subjects who expressed efficacious judgments regarding their ability to manage pain experienced as much relief from their symptoms as subjects receiving opioid analgesics or placebo’ (Bandura et al. 1987).

Experimentally induced pain differs from natural chronic pain in that it is usually introduced into a non-compromised nervous system. Research subjects can be screened out if they have a chronic pain condition. As pain persists over time, phenomena such as central and peripheral sensitization, kindling, windup and allodynia typically develop, amplifying and complicating the pain sensations. All this constitutes malfunction of the pain-detection system.

The advantage of an experimental pain stimulus is that its intensity and location can be adjusted in order to measure pain thresholds, usually via a thermal stimulus or by intramuscular hypertonic saline infusions. In one such study (Chalaye et al. 2009) pain intensity diminished, as measured by subject ratings (subjective thresholds), in response to slow deep breathing at a rate of six per minute. Another result in that study was the increase in heart rate variability, which correlates with increased vagal tone and general lowering of arousal.

In the varied populations targeted above (headache, back pain and childbirth) there was clear evidence of a specific cognitive variable affecting both pain intensity and degree of disability. In most cognitive-behavioural interventions for any kind of pain, catastrophic thinking and its variants are not addressed in isolation, but as part of an array of techniques including relaxation, re-appraisal, controlled breathing, acceptance, cognitive reframing, distraction and general education about mind–body influences in chronic pain. Much of the important pain-related psychophysiological research has been done on chronic back pain, but patients with pelvic pain are probably not substantially different to the other patient populations discussed; they have the same brain and nervous system, and are presumably subject to the same emotional stresses and imbalances. So until more pelvis-specific research is done, it is reasonable to tentatively generalize the conclusions and treatment methods to patients with pelvic pain.

Identifying these psychological factors in chronic pain patients does not imply the presence of mental illness or require psychotherapy. It simply acknowledges the role of emotions in the pain-modulating system. In the absence of an organized, multidisciplinary treatment team, the essential facts may be conveyed one-on-one, along with suggestions for changing the emotional factors. Such an intervention is far better than none, and can bring about lasting improvements in chronic pain – improvements which medication alone may never achieve. For example, it may be helpful for the patient with CPP to consider the following principles of chronic pain treatment programmes:

Defensiveness, emotional denial and repression

This group of inter-related psychological variables refers to how individuals manage negative emotions, whether personally related (shame, guilt, blame), by denying faults and stress, or by denying negative feelings such as anger and hostility. Burns (2000a) thoroughly reviewed the concept of emotional repression in relation to chronic pain, updating it from its roots in psychoanalysis, and incorporated modern research to make it relevant to current understandings of chronic pain. The conceptual gap between such subjective variables as blocking or denying negative feelings and experiencing somatic pain has been narrowed by psychophysiological research. The evidence supports such a connection in cases where denial of negative feelings coincides with high physiological and/or behavioural reactivity to stress. This mismatch apparently gives rise to conflict, with physiological effects, and correlates with increased pain and poor response to multidisciplinary pain management programmes (Burns 2000b).

Anger suppression was found to increase pain sensitivity in normal subjects without chronic pain. Subjects were asked to perform an arithmetic task and suppress both their experience and expression of anger during an experimentally manipulated ‘harassment’ condition. Compared to subjects not given such instructions, the anger-suppressors reported higher pain levels in response to the cold pressor (ice water) test. Whether this would also apply to chronic pelvic pain is unknown, but the manipulation may be generalizable to naturally occurring situations involving the need to conceal anger and frustration.

Placebo-nocebo chemistry as psychophysiology

The information presented so far about psychological influences on pain may seem to be floating in conceptual space, lacking a link to physiology. But in the case of pain, much is known about the interaction between mind and body, and relaxation, broadly defined, is at the centre of the pain mechanisms. Relaxation seems effective for reducing and coping with pain of any sort. This includes not only releasing muscles, but also creating greater peace of mind: lower anxiety, less stress, and less apprehension about the pain getting worse. Although multidisciplinary pain programmes routinely teach cognitive change techniques and various kinds of relaxation, they usually operate empirically without too much concern about how the techniques work physiologically.

The relaxation effect acts like a mental lever, affecting the entire pain modulation system. Pain intensity can be adjusted not only with opiates, but also by altering the naturally occurring endogenous opiates (endorphins) and their receptors (Hoffman et al. 2005). Emotional changes accompanying relaxation also affect the proportions of other pain-related biochemicals, such as GABA, cholecystokinin (CCK), dopamine and adrenaline (epinephrine).

Work with mu-opioid receptors has revealed that endorphins serve a more complex role than simply muffling pain. Endorphins also affect motivation and behaviour: low endorphin levels stimulate more alertness and vigilance, preparation for defence, sharper memory, faster reflexes for actions such as limb withdrawal, and a general increase in qualities favouring survival and mobilization of energy. High endorphin levels, in contrast, are associated with somnolence, reduced vigilance, and a sense of well-being. Memory and alertness are reduced, as well as pain sensitivity (Fields 2004).

Endorphins and other pain-related chemicals can be manipulated by triggering expectations in experimental subjects, both humans and animals. Conditioned placebos of any sort will diminish pain (for instance, a cue that has been associated with a pain-relieving injection). Using a ‘nocebo’ (an inert substance or stimulus that creates the expectation of worse pain) will make pain worse (Benedetti 2006, Benedetti et al. 2005, 2007). Even words of warning before an injection – ‘This might hurt a little’ – will increase pain perception more than will reassurance or distraction. These rapid adjustments to pain intensity are created by alterations in mu-opioid receptor sensitivity as well as changes in endorphin release. There are also changes in the anterior cingulate cortex, periaqueductal grey, and other brain sites known to be involved in pain modulation. Finally, administering morphine also turns off certain pain-gating cells in the rostral ventromedial nucleus and facilitates descending inhibitory circuits which inhibit dorsal horn neurons (Wager 2007). fMRI and PET scans of opioid receptor sites have confirmed the actions of pain-gating neurons (Scott et al. 2007).

Other chemicals involved in pain-modulation include adrenaline (epinephrine), which also stimulates alertness and lowers sensory thresholds, and CCK, which blocks morphine and stimulates not only pain but bodily changes collectively termed ‘fight or flight’. CCK is actually used in research to stimulate panic attacks. Dopamine raises the expectation of pleasure or relief, and helps to enhance placebo effect.

Table 4.1 shows the relevant chemistry and interactions.

Expecting relief, some version of ‘help is on the way!’ reduces the sense of danger and emergency, and tips the balance of pain-related chemicals away from pain and suffering, toward pain suppression. One notable exception is fear-induced analgesia, which occurs when stress is intense and current rather than anticipatory. Sustaining an injury, for example, brings temporary numbness, and presumably allows the animal to cope with the situation without distraction from pain. But anxiety and apprehension will do the opposite: increase pain along with all the other survival-related changes.

So relaxation, distraction, meditation and cognitive change are all to a degree pain-reducers, while apprehension, bracing, worrying, etc. agitate the organism. This agitation prompts stronger pain as a part of a general boosting of the behavioural and psychological changes to maximize survival. The psychological variables previously discussed – pain catastrophizing, pain vigilance, low self-efficacy, and kinesiophobia – all have similar effects on the pain modulation system: they stimulate the survival system at the expense of rest and recovery. This is the modern psychophysiology of pain, far beyond tight muscles and fast breathing. So teaching chronic pain patients to create positive expectations, confidence and relaxation modifies the pain-alarm system, ultimately calming the biochemistry and brain activity that supports continued pain.

Effects of physical and sexual abuse

Researchers examining this variable sometimes distinguish early from later (adult) physical abuse and sexual abuse, although they can overlap. Lampe et al. (2003) concluded that ‘Childhood physical abuse, stressful life events, and depression had a significant impact on the occurrence of chronic pain in general, whereas childhood sexual abuse was correlated with CPP only’.

Vulvodynia may be a distinctly different disorder than CPP. Reed et al. (2000), generalizing from a small sample, described evidence that vulvodynia patients were not significantly different from control subjects in most psychological or historical variables. Those with chronic pelvic pain, however, were more likely to report a history of sexual or physical abuse, depression and more somatic complaints. Bodden-Heidrich et al. (1999) supported this distinction between the two diagnoses, finding in a comparison of vulvodynia with CPP patients that the latter as a group showed more history of sexual abuse and ‘severe psychological problems’.

A study (Heim et al. 1998) of CPP using neuroendocrine assessment of HPA axis activity implicated blunted cortisol response. Compared with normals, a large proportion of CPP subjects reported physical and/or sexual abuse history, and post-traumatic stress disorder-like symptoms were commonly reported. There were similarities to other long-term disorders such as fibromyalgia, rheumatoid arthritis and chronic fatigue syndrome. Reduced cortisol response to stressful conditions impairs energy availability, promotes pain and inflammation by allowing prostaglandins to rise, and permits more of the damaging effects of the stress response, including autoimmunity and susceptibility to chronic pain. The authors concluded that abuse history seems to promote, in many cases, a long-term maladjustment in endocrine aspects of the stress response system, making chronic pain disorders, including CPP, more likely.

Collett et al. (1998) found that the lifetime incidence of sexual abuse was significantly higher in women with CPP, but physical abuse history was comparable in CPP patients and women with non-pelvic chronic pain complaints. Walker et al. (1992) studied psychological characteristics of women with CPP and noted a higher likelihood of dissociation as a coping mechanism, compared with a control group. Women with CPP had more evidence of current psychological distress, somatization, lower vocational and social functioning, and amplification of physical symptoms. In this study also, they were significantly more likely to have experienced severe childhood sexual abuse.

Somatization

Two articles from Austria recommended routine evaluation for psychological aspects of CPP. Maier et al. (1999) summarized experience with 220 women with CPP who were examined in collaboration between the Department of Obstetrics & Gynaecology and the Psychosomatic Department in the St. Johann’s Hospital of Salzburg. The patients received both laparoscopic examination and psychological evaluation; the researchers found that somatization was a frequent explanation for the symptoms. Standard somatic medicine, according to the authors, could not explain the discrepancies between the intensity of reported pain and the pathophysiology. They recommended continued engagement of the patients in order to facilitate psychotherapy or consideration of psychological input to the problem. The alternative outcome, ignoring psychological features, carries the risk of ‘chronification of CPP in patients approached only in somatic terms’.

Greimel & Thiel (1999), at the University Hospital in Graz, Austria, put forth a similar view: that emphasizing medical approaches to CPP increases the patient’s belief that medical (pharmaceutical, surgical) remedies will give them relief. In their view, the majority of CPP patients have evidence of somatoform disorder, which calls for psychological interventions rather than medical.

In making decisions about CPP treatment, psychosocial factors could be considered from the beginning, but more usually the medical approach is started first, to ‘rule out’ physical aetiology before psychological and behavioural intervention is even considered. This issue was addressed by one study by Peters et al. (1991) which compared the outcomes of these two approaches. One group of CPP patients began with laparoscopic examination to look for somatic problems before doing anything else. The second group was examined for many factors simultaneously: psychological, physiotherapeutic, dietary, environmental and somatic. At one-year follow-up, those receiving the second (‘integrated’) approach had done significantly better with pain management, and laparoscopic assessment seemed to add little to the results. This conclusion may indicate the advantage of not biasing patients toward a medical solution; otherwise, if no clear-cut medical disorder is found, the patients must re-orient to considering psychological, behavioural and experiential history factors. They can easily feel prematurely cast out and stereotyped.

Carrico et al. (2008) approached interstitial cystitis as amenable to guided imagery, and mounted a study in which guided imagery specific to interstitial cystitis (IC) was developed, recorded and given to IC patients. The recordings contained imagery and suggestions for healing the bladder, relaxing pelvic floor muscles and quieting the nerves supplying the pelvic area. Recordings were to be listened to twice a day for 25 minutes, while the control group simply relaxed for the same amount of time. Results clearly favoured the imagery group, who had significantly more reduced pain, urinary urgency and other symptoms of IC compared with the control group. This approach is remarkably simple and inexpensive, yet brought respectable results to many of the participants.

In the above summaries, researchers nearly always make a dichotomous distinction between ‘medical’ and ‘psychological’, or ‘somatic’ and ‘psychogenic’. This distinction perpetuates the notion that a given disorder has its source in either one or the other domain. Yet most of these studies at least speculate about a biological mechanism responsible for the clinical improvements, and also acknowledge the physiological ramifications of trauma, anxiety, depression, etc.

An improvement on the ‘somatic/psychogenic’ dichotomy might be to estimate the relative contributions of somatic and emotional factors. Given that the HPA axis responds to cognitive changes such as expecting danger or anticipating pain, it could be the primary mind-to-body transduction system. Cognitions can trigger a rapid switch to sympathetic dominance, withdraw vagal tone, initiate appropriate emotions and prepare the body for a physical challenge. Muscle bracing, altered breathing and circulation patterns, endocrine changes, and aggravation of trigger points are all biological responses to psychological shifts. Trying to suppress these factors pharmaceutically may be insufficient to affect the more central source of the problem.

Acknowledgement

We acknowledge with gratitude the help from Dr. Hallie Robbins DO, in the initial conceptualization and organization of this chapter.

This chapter has described how CPP is affected by both physiology and emotion, and suggested that cognitive and emotional factors can both exacerbate or sooth nociception. It appears that biological, socio-cultural and psychosocial aspects determine an individual’s response to a variety of potential pain triggers. The next chapter describes the relationship between gender and pain, including the role of sex hormones in CPP, and questions whether women are in general more susceptible than men to experience CPP.