Affective dimensions of pain How many and how measured?

Affective dimensions of pain How many and how measured?

Commentary Affective Dimensions of Pain How Many and How Measured? Richard H. Grace/y W ‘bile many authors still refer only to a single dimensio...

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Commentary

Affective

Dimensions

of Pain

How Many and How Measured? Richard H. Grace/y

W

‘bile many authors still refer only to a single dimension of “pain,” the separation of pain experience into sensory-intensity and affective components is well established. In their focus article, Price and Harkins divide the affective component into two parts: primary feelings of immediate unpleasantness and secondary stages, such as despair, that result from intervening thoughts such as concern for the future. This focus on the affective component is needed. Although well established, it is likely that the term “affective” has been a source of confusion. “Affective” has an established psychological-psychiatric usage, such as reference to an affective disorder, or to observable behavior, such as in the phrase, “affect is not appropriate to mood.” The fact that pain affect is commonly described as the “emotional component” reinforces a psychological-psychiatric interpretation of a persistent change in emotional functioning. Thus, there could be three levels of pain affect.

the future (uncertainty, fear, dread). Third, chronic or severe pain can aversely affect psychological health. Terms like the emotional or affective component may refer to changes in mood and personality such as depression, anhedonia, irritability and paranoia.4 Price and Harkins make a strong theoretical argument for both a primary and secondary affective component and buttress their proposal with a body of empirical evidence, much of which has been generated in their laboratory. Their central thesis is supported by the results of both psychophysical and psychological investigations, many of which were not included in this brief article. Indeed, a thorough coverage of the relevant issues would require a book. What follows are a few thoughts stimulated by their article.

THE PRIMARY IMMEDIATE AFFECTIVE COMPONENT: PAIN UNPLEASANTNESS

These various terms can be organized into 3 general types. First are feelings associated with the immediate pain sensation. Psychophysicists have used the term unpleasantness, pain researchers the terms affective, distress, and discomfort, and animal scientists the terms aversive and motivational. Second are feelings associated with human thought, with the way in which pain experiences are cognitively integrated into a patient’s life. These thoughts can be about the past (accumulated effect of chronic suffering), the present (uncertainty), or

Pain hurts; there is no doubt that pain is unpleasant. Pain motivates behaviors of escape and avoidance in all animals, regardless of intelligence. This primary unpleasant quality is very similar to other biological unpleasantries such as hunger or thirst and feelings of overheating or suffocation. These feelings can be extremely powerful, motivating extreme behaviors. The primary unpleasantness of pain is likely to be at least as strong as other feelings that motivate preservation of the organism.

From the Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland. Reprint requests: Richard H. Gracely, PhD, Building 10, Room 1 N103, NIH, Bethesda, MD 20992.

Probably a majority of articles discussing immediate pain unpleasantness refer to “an emotional component.” However, immediate pain unpleasantness is no more an emotion than is hunger or thirst. This

APS Journal

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Pain Unpleasantness Component

Is Not an Emotional

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component feels bad all on its own, it does not need any help from cognitive appraisals. In fact, the term “unpleasantness” was borrowed from psychophysical investigations of the feelings accompanying taste, olfactory, and thermal stimuli.2,6 It was purposefully applied to describe the similar primary component of pain affect. In their model, the primary component is composed of both unpleasantness and (immediate) cognitive appraisals. Their secondary component, associated strongly with chronic pain, is composed of more extensive cognitive appraisals. This classification appears to be based on the difference between acute and chronic pain rather than the distinction between primary pain unpleasantness and secondary cognitively mediated affect. It may be more parsimonious to describe initial and long-term pain as separate constructs, each of which may contain both a primary component of pain unpleasantness, shared by most life forms and independent of cognitions, and a secondary component resulting from cognitive appraisals.

The Magnitude of Pain Unpleasantness Not Emphasized

Is

The tendency to associate the secondary affective component with chronic pain overlooks the contribution of the primary component in protracted pain

THINKING p-0

syndromes. The pain and “state” of backache, headache, and arthritis can certainly engender cognitively mediated feelings. Chronicity can also lead to a high degree of coping as patients become “experts” about their own pain. Although they may experience negative affect related to thoughts about their pain and state, their most significant distress still may be the nagging unpleasantness that will not go away.

Relation of Pain Unpleasantness to Pain Intensity: Affective Gain Control Price and Harkins identify several loci likely to be involved in the processing of the affective component and note that it is possible that affective processing could occur both in series and in parallel with sensory-discriminative processing. Figure 1 shows a simplified model that requires a parallel stage of affective processing and does not exclude prior series processing before the affective pathway branches from a common input.5*8 It is useful to think of the affective processor as an amplifier of sensory input with a gain control. Manipulations that increase pain affect, such as anxiety, would do so by increasing the affective gain, resulting in more unpleasantness for a given pain sensation. Manipulations that decrease pain unpleasantness would likewise do so by decreasing the gain. Note that unpleasantness

*

PAIN-UNRELATED SECONDARY AFFECT

*

PAIN-RELATED SECONDARY

AFFECT

bUNPLEASANTNESS -0. AFFECTIVE CONTROL NOCICEPTIVE INPUT -

GAIN

-SENSORY

INTENSlTY

>

Figure 1. The affective pain components. Pain unpleasantness is derived from the output of an affective amplifier (bottom) that receives input from the sensory-discriminative nociceptive system. Pain unpleasantness is related to this input, and thus to sensory intensity, and also related to the gain of the affective amplifier, which is under central control and independent of sensory intensity. Also shown is a secondary affective generator (middle) that receives input from thoughts associated with pain experience. A third affective generator (top) receives input from thoughts unrelated to pain, for example, the knowledge of a life-threatening disease. The affective experience of a patient in pain may be composed of affect from all three sources. Not shown are feedback loops connecting all components to all of the gain controls.

COMMENTARY/Gracely

can also be altered by changing the input signal related to the intensity of the pain sensation. Thus, pain unpleasantness does not originate from an independent parallel affective generator. It is related to both nociceptive input and to a variable affective gain that can be altered independently of sensory input.

SECONDARY, COGNITIVE COMPONENTS The core of cognitive therapy is the concept that emotions and feeling are not evoked by events, but rather by an intervening third variable, the thoughts, interpretations, or “self-talk” about the event. Price and Harkins’ examples of a bee sting (to persons with and without an allergy) or of abdominal pain (with a history of indigestion or a recent diagnosis of cancer) clearly indicate how the feelings associated with similar painful events can result, with the addition of other information, in very different affective responses. The literature on pain cognition contains many more examples and relevant findings. The focus article states that these secondary components can be found only in patients, since laboratory methods cannot duplicate the affective consequences of clinical syndromes. This is only true where ethics and morality prevail; unfortunately the history of man continually provides deplorable examples of secondary affective pain states produced by “laboratory” methods.

Feeling Pain, Feelings About Being in Pain, or Feelings About Being in an Undesirable State Price and Harkins emphasize the difference between pain unpleasantness, the immediate feelings of pain, and the secondary affective component of feeling about being in pain. They recognize that these different components require different measurement techniques and have developed specific scales for each component. It may be important to further distinguish between two types of secondary affective responses (see Fig. 1). The first type would be pain-specific, resulting from direct thoughts about pain, and a future without relief. For example, there are those who may consider themselves especially sensitive to bee stings and anticipate a great deal of pain. The knowledge of abdominal pain and a diagnosis of cancer may result in dread of a future of increasing and unremitting pain. The second type may not be pain-specific, but may originate from general thoughts and feelings about one’s predicament. An allergic recipient of a bee sting and a cancer patient with abdominal pain symptoms may be concerned predominantly with a

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premature end to their lives. Their negative affect may be little related to their pain sensations. Similar affect may be experienced in other life-threatening acute or chronic conditions that are not painful. Unlike either the primary component or the pain-relevant secondary component, this component would not be expected to be related to sensory intensity. The only relevance of these “state” feelings to pain may be via the primary component. Cognitive appraisals, either pain-related or unrelated, may modulate the affective gain of the primary component, resulting in increased pain unpleasantness. Thus, in addition to two types of secondary components, it is also useful to think of two types of affective modulation. First, information or other interventions may directly alter thoughts about experienced pain, resulting in a change in the magnitude of the secondary affective component. Second, cognitive appraisals of either being in pain or of any other undesirable condition may increase the gain of the system mediating primary pain unpleasantness, while other cognitive, pharmacological, etc. interventions may decrease affective gain.

A TERTIARY PSYCHOLOGICALPSYCHIATRIC AFFECTIVE COMPONENT? The term “affective” connotes a change in personality and mood. It is well documented that chronic pain is associated with a number of measurable changes, such as increased somatization, hostility, irritability, and depression. Price and Harkins include these affective changes in an overall secondary factor. Although there is considerable overlap, there is likely to be a sufficient reason to label these changes as an additional subset of secondary pain affect, or as a separate tertiary factor. For example, following a procedure that essentially cures a chronic pain problem, the primary and secondary affect associated with the pain sensation should disappear along with the pain sensation. The psychological changes acquired during the period with chronic pain, however, will likely persist for some time. The pain is gone but the patient’s affective state lingers on.

MEASUREMENT OF PAIN UNPLEASANTNESS The measurement of immediate unpleasantness, and also pleasantness, is well established in psychophysical evaluations of the sensory intensity and subjective feelings produced by thermal, taste, and olfactory stimuli during various internal states. My own early studies used these methods as a starting point for the development and validation of separate scales

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of intensity and unpleasantness. Verbal descriptor scales were chosen for several reasons, including an assumption, supported by some empirical evidence ls3 that they might facilitate the discrimination of these two pain dimensions.6,7 Price and colleagues have used visual analog scales and careful instructions to separately rate these dimensions. Both methods satisfy the criterion of similar structure for the sensory and unpleasantness scales.’ With parallel scales, differences can be attributed to the dimension, and not to a method variance associated with a confound between dimensions and a different type of scale.’ Regardless of scale type, the validity of differential scales must be firmly established. Only then can one be confident that similar effects measured by sensory and affective scales indicate a lack of a differential effect and not a lack of a differential scale.

Validity: Different Functions Price and Harkins cite the two lines of evidence proposed by Gracely et al.‘to support the validity of separate scales of the intensity and unpleasantness of pain sensations. The first uses different psychophysical functions as evidence for the validity of the sensory intensity and unpleasantness. While such differences are suggestive, it should be noted that this line of evidence does not stand alone. For example, the use of different labels for two visual analog scales of sensory intensity also could result in different functions. Different descriptor scales of sensory intensity could also show different functions, although methods exist for quantifying the descriptors on the same common scale.6s13 Thus, difference in psychophysical functions may indicate the assessment of different dimensions, but it can also indicate distortions of the same dimension. Conversely, it is also possible that valid scales of sensory intensity and unpleasantness could produce similar psychophysical functions. This caveat also applies to the identification of neurons involved in affective processing. In addition, the variance and nonlinear characteristics of neuronal responses would probably prevent any meaningful differential correlations with sensory or affective responses. As Price and Harkins note, stronger support is provided by the second, empirical, line of evidence.

pain affect. Selective affective responses were demonstrated in the early psychophysical studies of the thermal and chemical senses; hunger or satiety altered ratings of the unpleasantness or pleasantness of taste or olfactory stimuli without changing intensity ratings.’ Likewise, raising or lowering body temperature altered unpleasantness-pleasantness ratings of thermal stimuli without altering intensity ratings.’ As the focus article notes, this validation method has been applied to both verbal descriptor and visual analog scales. It provides a validation gold standard both for new subjective scales and for investigations of the neural basis of pain affect.

Affective Ratios In affective ratio models, both the primary and secondary affective components can be compared to sensory intensity. It is useful to quantify an “affective ratio” defined as the amount of unpleasantness or secondary affect associated with a specific magnitude of pain sensation. This model was first developed with verbal descriptor scale responses of painful electrical stimuli’ and the ratio using verbal descriptor responses varied over experimental electrical tooth pulp stimulation (0.15) clinical stimulation of exposed dentin with cold spray (0.72) and chronic myofascial pain (0.82).l” The absolute value of these ratios can vary with the type of scale; the important relation is the relative ratio between conditions obtained with a consistent scaling method. The affective ratio, describing the affective gain (both primary and secondary), is an extremely useful concept that can be used to quantify an important dimension of pain, or the characteristics of a patient or a treatment. Its use also clarifies the relationship between sensory-discriminative and affective components. For example, the importance of the distinction between sensory intensity and unpleasantness has been challenged because of a high correlation between these dimensions.“*12 This high correlation reflects the sensory input into the “affective amplifier.” Flgure 1 shows that the true affective variable is the affective gain, not the output of the affective system. This gain is measured by the affective ratio and should be relatively independent (and thus uncorrelated) with sensory intensity.5v8

Validity: Empirical Test

MEASUREMENT OF OTHER AFFECTIVE COMPONENTS

Price and Harkins describe in detail the most important evidence for validity of affective scales: the selective response to manipulations assumed to alter

Price, Harkins, and colleagues have made a compelling theoretical case for secondary components, and they have derived and used scales to measure them.

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They found an association between secondary components and variables such as neuroticism and depression that is not shared by either the sensory dimensions or the primary unpleasantness component. They have, in addition, described a strategy for further identification of both of these psychological constructs and the underlying neural structures involved in affective responses. Their preliminary results are very promising. However, the surface has just been scratched. For example, what is the role of clinical scales such as the McGill Pain Questionnaire in the evaluation of secondary affective attributes? What is the relation of their secondary components to the affective and evaluative components of this instrument? How do visual analog scales compare to more complex measures of pain cognition? What do psychometric validation studies indicate about visual analog scales of secondary pain affect? For example, a pain-independent secondary component such as fear of death may be related to psychological variables directly without an intermediary conduit of pain sensation. Price and Harkins should be lauded for asking the right questions. They must be good ones because they lead to many more.

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Fessard D (eds): Advances in pain research and therapy. Vol. 3. Raven Press, New York, 1979 Gracely RH: Theoretical and practical issues in pain assessment in central pain syndromes. pp. 85-101. In Casey KL (ed): Pain and central nervous system disease. Raven Press, New York, 1991 Gracely RH: Evaluation of multidimensional pain scales. Pain 48:297-300, 1992 Gracely RH, McGrath PA, Dubner R: Ratio scales of sensory and affective verbal pain descriptors. Pain 5: 5-18,1978 Gracely RH, McGrath PA, Dubner R: Validity and sensitivity of ratio scales of sensory and affective verbal pain descriptors. Pain 5:9-29, 1978 Gracely RH, Smith WB: Psychological modification of cranial nociception. In Schmidt RF, Olesen J (eds): Proceedings of the International Symposium on the Pathophysiological Mechanisms of Migraine, (in press) Gracely RH, Taylor F, Schilling RM, Wolskee PJ: The effect of a simulated analgesic on verbal descriptor and category responses to thermal pain. Pain Suppl2: 173, 1984 Heft MW, SharavY, Gracely RH: Assessment of chronic pain using verbal descriptor scaling procedures. J Dent Res 58 (Special issue A):216, 1979 Holroyd KA, Holm JE, Keefe FJ et al: A multi-center evaluation of the McGill Pain Questionnaire: results from more than 1700 chronic pain patients. Pain 48: 301-312, 1992 Turk DC, Rudy TE, Salovey P: The McGill Pain Questionnaire reconsidered: confirming the factor structure and examining appropriate uses. Pain 21: 385-397, 1985 Tursky B: The development of a pain perception profile: a psychological approach. pp. 171-l 94. In Weisenberg M, Tursky B (eds): Pain: new perspectives in therapy and research. Plenum Press, New York, 1976