Psychophysiological Perspective on Chronic Pain

 

By Marek Jantos Ph.D.

Several psychological factors have been identified as strong modulators of pain perception (Keefe et al., 2004). These factors can be divided into two broad categories, those associated with increased pain, psychological distress and physical disability, and those associated with decreased pain, distress and disability:

  • Factors associated with increased pain, psychological distress, and physical disability. These include: pain catastrophizing, pain related anxiety and fear, and helplessness.
    Pain catastrophizing; a tendency to negatively evaluate one’s ability to cope with pain, accounts for 7% to 31% of the variance in pain ratings, and is associated with higher levels of depression, psychological distress, pain-related disability, lower energy levels, and more negative general health status.
    Pain-related anxiety and fear of pain; these patients have a tendency to be anxious about their pain and engage in fear avoidance behaviours. They report high levels of attention to sensations of pain and over-predict the amount of pain they will experience during physical examination. They score higher on self-report measures of disability, depression, pain behaviour and help-seeking, and lower on measures of pain coping.     
    Helplessness; refers to a tendency to view negative outcomes as inevitable, unpredictable and uncontrollable, and is associated with higher levels of pain, depression and disability, and much poorer medical therapy outcomes.

  • Factors associated with decreased pain, psychological distress, and physical disability. These include: self-efficacy, pain coping strategies, readiness to change, and acceptance.
    Self-efficacy; refers to a patient’s confidence in their ability to accomplish desired outcomes, such as control of their pain. It is associated with lower levels of psychological distress and negative medical outcomes. Most importantly, patients who rated their self-efficacy for managing their clinical pain as high, exhibited significantly higher pain thresholds and pain tolerance than patients who rated their self-efficacy for controlling pain as being low. Those scoring high on self-efficacy for clinical pain also rated the laboratory thermal pain stimuli as significantly less unpleasant.
    Pain coping strategies; refers to patient’s ability to utilise a variety of strategies to help them cope with pain. Such pain coping strategies may include pain reduction efforts, relaxation, distraction, redefinition, venting emotions, seeking emotional support, and seeking spiritual comfort. Patients who reported the highest level of coping effort experienced decreasing pain.
    Readiness to change; refers to the patient’s readiness to engage in self-management efforts. Evidence suggests that patients who become actively engaged in self-management efforts are more likely to show improvement in pain management.
    Acceptance; refers to the willingness to engage in meaningful activities in life, regardless of the experience of pain-related sensations. Acceptance refers to a balanced approach of pursuing change if it is likely to assist, and acceptance when change efforts are not likely to succeed. Patients scoring high on acceptance reported significantly lower levels of pain-related anxiety and avoidance, depression, physical and psychosocial disability, and better utilization of time. Acceptance measures were found to explain 24% of variance in measures of adjustment.

It is evident that patient attitudes and beliefs (catastrophizing, passive attitude to treatment), behaviours (active coping strategies, versus high drug intake), emotions (feelings of helplessness, uselessness, anxiety and fear of increased pain) and level of social support (lack of support or over-protectiveness) are all important factors, identified as “yellow flags” in at risk patients (Waddell, 1998).

In examining the role of anxiety and fear in the perception of pain in vestibulodynia patients, cognitive and affective factors were shown to exert a significant influence (Payne et al., 2005). Vestibulodynia patients, when compared with controls, demonstrated hypervigilance in the form of selective attentional bias to pain-relevant stimuli, which in the case of vestibulodynia was coital pain. On self-report measures, patients reported more hypervigilance to pain during sexual intercourse. A further comparison between the patients and the control group showed that the groups differed on measures of hypervigilance, state and trait anxiety, and fear of pain; with anxiety and fear of pain correlating with hypervigilance. However, when controlling for anxiety and fear of pain, the group differences on hypervigilance disappeared. Such selective focus on pain stimuli can lead to an increase in the perceived intensity of pain. In relation to sexual function, the authors suggest that “if attention is preferentially allocated to pain processing during activities such as sexual intercourse, then theoretically, fewer attentional resources will be available for the processing of sexually arousing or pleasurable stimuli”(p 436). This may further exacerbate vulvar pain.

With higher levels of anxiety, fear, depression and dysfunction, few models of chronic pain have sought to theoretically conceptualize links between hypervigilance, catastrophizing, fear of activity, avoidance behaviour, disuse, disability and depression (Lame et al., 2005; Boersma & Linton, 2006). Few models have sought to identify the physiological mechanisms that link beliefs, emotions and behaviours to the experience of pain. An extensive discussion of such mechanisms is beyond the scope of this chapter, but a brief discussion will be presented on the mechanisms linking anxiety and depression with pain.

Anxiety can be conceptualized as a sympathetically mediated biological response that prepares the body to threatening situations (Hoehn-Saric & McLeod, 2000). The individual feels tense, experiences increased heart rate, faster but shallower breath, increased skin conductance and increased muscle tension. The expectation that patients who manifest heightened anxiety will also exhibit generalised physiological hyper-arousal at rest has not been confirmed. The majority of individuals show no greater autonomic arousal then normal control subjects, except in relation to stimuli that have been associated with a phobic stimulus (Hoehn-Saric et al., 2000). In relation to a phobic stimulus, anxious subjects were found to be selective in their response and “overreact subjectively and physiologically to stimuli that are anxiety-provoking.” At rest, anxiety levels appear to be associated with a tonic increase in stimulus related physiological arousal, which is also associated with a diminished range of autonomic responsivity, labeled as “diminished physiological flexibility.”

The relationship between anxiety and muscle tension is well documented. Of all the physiological parameters monitored, it is noted that:
“Elevated muscle tension has been the most consistent finding in psychophysiological studies of patients with anxiety disorder. It cannot be attributed to increased restlessness but rather to a tonic increase in tension…It probably represents a peripheral manifestation of central hyperarousal” (Hoehn-Saric et al., 2000, p. 218).

It is further suggested that the anxious patient may be exhibiting increased muscle tension as an expression of hyperalertness but not necessarily generalised autonomic hyperarousal. The authors suggest that strong emotional experiences which initially trigger autonomic responses may be capable of subsequently eliciting similar somatic sensations, even in the absence of physiological triggers. This form of “physiological rigidity”, though not fully understood, may be “a constitutional predisposition, a physiological adaptation to chronic arousal,” or a selective pre-occupation with the patient’s pathophysiological condition. On the other hand, the non-anxious individuals that had lower muscle tension at rest tended to respond to test tasks with “greater increases in muscle activity than the already tense anxiety patients, indicating a task-oriented rather than generalized arousal response.” With elevated anxiety, the subjective perception of bodily states and muscle tension were found not to be congruent with their physical state, with correlations between subjective and physiological measures predictably low. These findings are consistent with the earlier work of Flor and Turk (1989), showing that chronic pain patients show a symptom-specific psychophysiological response and that physiological dis-regulation tends to occur in the affected system.

There are parallels between these findings and the psychophysiological assessments of vulvodynia patients. Increased muscle activity, lower pain thresholds, lower unpleasantness thresholds, significant increases in systolic blood pressure, enhanced perception and increased autonomic reactivity have been documented (Jantos 2008; Granot et al., 2002; Hoehn-Saric et al., 2000).

In the management of vulvodynia the first line of therapy often consists of the use of tricyclics antidepressants, such as imiprimine (Updike & Wisenfeld, 2005). Evidence shows that tricyclic antidepressants result in a decrease in subjective somatic symptoms, while physiological measures such as heart rate, systolic blood pressure and SEMG activity show significant increase (Hoehm-Saric et al., 2000). Patients report varying degrees of benefit from the use of tricyclic antidepressants. The mechanism by which these drugs assist in the management of symptoms remains poorly understood (Updike & Wisenfeld, 2005). Further research needs to examine the benefits of drug therapy as subjective perception of improvement may in fact mask increased autonomic dysregulation and reactivity.

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