Finally, it is necessary to examine the emotional aspects of pain and to discuss what influence these may have on the assessment and treatment of chronic pain. Pain is a complex physico-emotional experience with its emotional component largely determining how much suffering it causes. It is, therefore, not surprising that in describing pain, no matter whether it is nociceptive, neuropathic or entirely of emotional origin, patients are liable to include not only adjectives like aching, tingling or burning to describe its sensory qualities, but also adjectives like depressing, horrible or excruciating to convey the suffering caused by it.
Melzack & Torgerson (1971), in recognizing that there are three main categories of pain experience – sensory, affective and evaluative – drew up the McGill Pain Questionnaire and this, together with a subsequently introduced shortened version (Melzack 1987) has been shown to be of consider-able value in the assessment of pain. It is, however, because all types of pain experience have an emo-tional component that it must never be assumed that pain is due to some primary psychological disturbance simply because a patient uses a predominance of affective terms to describe it.
Pain may very occasionally be a hallucinatory sensation experienced by schizophrenics. It may also be a manifestation of conversion hysteria or hypochondriasis. It therefore has to be admitted that there is such an entity as psychogenic pain (Feinmann 1990) but there are good grounds for believing that this is relatively rare and that affect-ive disorders such as anxiety or depression are mostly the result of chronic pain rather than the cause of it.
The relationship of emotional factors to chronic pain can be assessed by giving patients with it spe-cially designed standardized questionnaires such as the Minnesota Multiphasic Personality Inventory (MMPI). Sternbach et al (1973) used this inventory
to compare the relative significance of psychologi-cal symptoms occurring in patients with acute (i.e. less than 6 months’ duration) and chronic low-back pain. They found that although those with the shorter history of pain had elevated scores on the scales for depression, anxiety, hysteria and hypochondriasis, the scores were significantly higher in those with chronic pain. The MMPI was also used by Sternbach & Timmermans (1975) in their study of 113 patients with low-back pain of at least 6 months’ duration. An assessment was made before and after either surgery followed by rehabilitation or rehabilitation only. From this assessment it was found that there was a signifi-cant decrease in the hysteria, depression, anxiety and hypochondriasis scales following successful alleviation of the pain.
Observations such as these confirm that chronic pain is usually the cause rather than the result of neurotic symptoms and Melzack & Wall (1988, p. 32) in discussing this conclude:
It is evident from studies such as these that it is unreasonable to ascribe chronic pain to neurotic symptoms. The patients with the thick hospital charts are all too often prey to the physicians’
innuendos that they are neurotic and that their neuroses are the cause of the pain. Whilst psy-chological processes contribute to pain, they are only part of the activity in a complex nervous system. All too often, the diagnosis of neurosis as the cause of pain hides our ignorance of many aspects of pain mechanisms.
The error of failing to recognize pain as being organic in origin and considering it to be entirely psychological most commonly occurs in my experi-ence when myofascial TrP activity causes pain to persist long after all clinical evidence of tissue damage has disappeared (Ch. 7). This error, of course, is particularly likely to be made when the pain has led to the development of appreciable anxiety or depression or both. The reason why this mistake is so frequently made is clearly because of a widespread failure amongst health professionals to search for myofascial TrPs when attempting to find a cause for persistent pain.
It is as a result of this that many injustices are committed concerning the cause of protracted pain in accident compensation cases. Accidents
undoubtedly give rise to much psychological dis-tress (Muse 1985, 1986) but this does not mean that post-accident pain that does not respond readily to some of the more conventional methods of treat-ing organic pain is necessarily psychological in origin and in some way associated with an uncon-scious or even at times a conuncon-scious desire for compensation.
Such an assumption is all too prevalent and in the past has led experienced physicians such as Henry Miller (1961, 1966) to believe that once compensation is awarded, persistent post-accident pain invariably starts to improve. That this is not so has been demonstrated by Mendleson (1982, 1984) who, from a study of accident compensation cases in Australia, concludes that ‘patients are not cured by the verdict’, and that, in general, the pain remains as intense after the financial settlement as before. This is confirmed by Melzack et al (1985) who, in commenting both on Mendelson’s find-ings and their own psychological studies of acci-dent compensation cases, states:
… the phrase ‘compensation neurosis’ is an unwarranted, biased diagnosis. Not only are the disability and pain not cured by the verdict but compensation patients do not exaggerate their pain or show evidence of neurosis or other psy-chopathological symptoms greater than those seen in pain patients without compensation.
From serving on medical appeal tribunals that deal with people seeking compensation for post-accident disablement, it has become evident to me that of those who seek financial assistance because of persistent pain only relatively few are malinger-ers. This observation is in keeping with that of Leavitt & Sweet (1986) in their study of the frequency of malingering amongst patients with low-back pain.
What, however, has become apparent to me is that a disturbingly large number of these claimants are allowed to suffer from the myofascial pain syn-drome for unnecessarily long periods of time sim-ply because the dictum laid down by Livingston as long ago as 1943 is so frequently ignored. He said that in every case of persistent pain following trauma it is essential to search for TrPs. It was because Crue & Pinskey (1984) did not do this that
they failed to find a nociceptive peripheral input in a group of patients with chronic back pain; intro-duced the totally inept diagnostic term ‘chronic intractable benign pain’; and made the unwar-ranted assumption that such pain is a central phenomenon – a polite way of saying ‘it is all in the mind!’ As Rosonoff et al (1989) have now shown, in 96–100% of patients with chronic low-back or neck pain of the type studied by Crue &
Pinskey, the pain emanates from myofascial TrPs.
Finally, it is necessary to reiterate that whilst anxiety is rarely the cause of pain, persistent pain
is commonly associated with the development of anxiety. When this happens, the anxiety causes muscles to be held in a state of tension and with musculoskeletal pain this results in an increase in TrP activity with a consequent exacerbation of the pain (Craig 1989). In all such cases it is not suffi-cient simply to deactivate the TrPs but it is also necessary to reduce the anxiety. My personal pref-erence is to employ hypnotherapy (Orne & Dinges 1989, Hilgard & Hilgard 1994) and to teach the patient how to practise autohypnosis on a regular daily basis.
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