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Comparison of negative affect, reactivity, and proprioception in chronic low back pain patients and controls

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Title:
Comparison of negative affect, reactivity, and proprioception in chronic low back pain patients and controls
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Gaskin, Melodye Elayne, 1956-
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Language:
English
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vii, 104 leaves : ill. ; 29 cm.

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Anticipation ( jstor )
Anxiety ( jstor )
Chronic pain ( jstor )
Cognitive models ( jstor )
Electromyography ( jstor )
Mental stimulation ( jstor )
Pain ( jstor )
Proprioception ( jstor )
Reactivity ( jstor )
Response bias ( jstor )
Affect ( mesh )
Department of Clinical and Health Psychology thesis Ph.D ( mesh )
Dissertations, Academic -- College of Health Professions -- Department of Clinical and Health Psychology -- UF ( mesh )
Electromyography ( mesh )
Low Back Pain -- physiopathology ( mesh )
Low Back Pain -- psychology ( mesh )
Pain Measurement ( mesh )
Proprioception ( mesh )
Research ( mesh )
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bibliography ( marcgt )
non-fiction ( marcgt )

Notes

Thesis:
Thesis (Ph.D.)--University of Florida, 1998.
Bibliography:
Bibliography: leaves 97-103.
General Note:
Typescript.
General Note:
Vita.
Statement of Responsibility:
by Melodye Elayne Gaskin.

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University of Florida
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Copyright [name of dissertation author]. Permission granted to the University of Florida to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.
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51174907 ( OCLC )

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COMPARISON OF NEGATIVE AFFECT, REACTIVITY, AND PROPRIOCEPTION IN CHRONIC LOW BACK PAIN
PATIENTS AND CONTROLS





















By

MELODYE ELAYNE GASKIN




















A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA 1998













To my mother, Marion Elaine, who gave me life and the treasure of a heritage.



To my grandfather, Charles Henry Robel, who never treated me as

though being a girl should restrict my experience of life.



To my dear friend, Caron, for believing in me and helping me through the tough times.













ACKNOWLEDGMENTS



Electromyographic (ENG) /ergometric lumbar transceiver

(ELT) equipment and software were provided for this study by Physical Health Devices, 417 Corporate Square, 1500 West Cypress Road, Ft. Lauderdale, FL 33309.

Access to subject populations was provided by the

following: Michael Macmillan, MD, Orthopedic Clinic and Pat O'Conner, PT, Department of Physical Therapy at Shands Hospital, University of Florida, Gainesville, FL; Jeff Goode, PT, Sports Medicine Center, Charleston Area Medical Center, General Division, Charleston, WV. Many thanks to these people and their staffs for their support of this project.

Heartfelt thanks are due to the many who have provided support in various ways toward the completion of this project: classmates, friends, family, colleagues, professors, research assistants, my committee. An attempt to name them all would inevitably result in the inadvertent omission of someone.

Much gratitude is due the people who participated in this study, particularly the pain subjects, for sharing of themselves and their experiences. In the end, it is their story.



ift















TABLE OF CONTENTS


pagre
ACKNOWLEDGMENTS................. .. .. ....iii

ABSTRACT ........................ .. .. ...... Vi

CHAPTERS

I INTRODUCTION..........................1

2 CURRENT MODELS OF PAIN.................6

Gate Control Theory of Pain...............7
Information Processing Models of Pain .......8 Sequential Processing Theory...........10
Summary.....................10

3 SENSORY DISCRIMINATION IN PAIN PERCEPTION . 12

Nociception...................12
Sensory-Discrimination Deficits and Pain . . 15 Proprioception and Pain.............23
Sumary.....................27

4 PHYSIOLOGICAL REACTIVITY AND PAIN . . . 28

General Arousal..............................28
EMG Reactivity and Chronic Low Back Pain. o . 30 Summary..........................34

5 COGNITIVE-AFFECTIVE PROCESSES AND PAIN. ......35

Summary.......................39

6 SUMMARY AND HYPOTHESES..............40

7 METHODS.o......................42

Subjects,...................42
Measures.............................43
Procedures.........................47








iv









CHAPTERS

8 RESULTS . . . . . . . . . 51

General Demographic Data . . . . . . 51
Chronic Low Back Pain Subjects . . . . 54 Data Reduction and Analyses . . . . . 57

9 DISCUSSION . . . . . . . . . 74

APPENDIX . . . . . . . . . . . . 83

REFERENCES . . . . . . . . . . . . 97

BIOGRAPHICAL SKETCH . . . . . . . . . 104














Abstract of Dissertation Presented to the Graduate School of
the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Doctor of Philosophy

COMPARISON OF NEGATIVE AFFECT, REACTIVITY, AND PROPRIOCEPTION IN CHRONIC LOW BACK PAIN PATIENTS AND CONTROLS

By

MELODYE ELAYNE GASKIN

May 1998

Chairman: Michael E. Robinson Major Department: Clinical and Health Psychology

Current models of chronic pain view the experience of pain as a complex phenomenon comprised of sensorydiscriminative, cognitive-affective, and physiological components. Several models have proposed that chronic pain involves the dysfunction of a central mechanism that influences as well as is influenced by these components. Previous research has demonstrated higher levels of negative affect (anxiety, anger, and depression) and perceptual deficits in pain patients compared to pain-free controls. A perceptual ability unexamined in the chronic low back pain population is that of trunk proprioception. Studies of physiological reactivity in patients with chronic low back pain (CLBP) have focused on the electromyographic (EMG) activity of the low back with mixed results. The use of stimuli relevant to the patient's clinical pain has been found to influence physiological reactivity.


Vi








This study examined the following variables derived from the components described above: negative affect (anxiety, anger, depression), EMG reactivity of the lumbar paraspinal muscles, trunk proprioception (response accuracy, response bias), and visual analogue scale ratings (VAS) of pain intensity (PIN) and pain unpleasantness (PUN) to an ecologically valid stressor (bending) in 31 CLBP patients and 31 age- and sex-matched pain-free controls. Subjects

were asked to reproduce bending to three angles (-100, 220, 450) over five trials, rating PIN and PUN after each trial. Subjects received no feedback on their performance.

Results of analyses demonstrated that CLBP subjects had higher ratings of negative affect, pain intensity and pain unpleasantness than controls. On measures of proprioception, although there were no differences between groups on response accuracy, there was a difference in the pattern of response bias between groups across angles. Patterns of EMG reactivity also differed by group and angle relative to baseline ENG and were consistent with the biomechanical model of CLBP.

The results of this study provide partial support for the hypotheses generated regarding the components of a proposed dysfunctional central mechanism that mediates the experience of chronic pain.







Vii













CHAPTER 1
INTRODUCTION



Chronic pain is one of the most challenging problems

facing health professionals. Definitions and models of pain have evolved from simplistic sensory stimulus-response explanations to more complex multidimensional ones. The development of theoretical conceptualizations of the psychophysiology of chronic pain have evolved from early research in psychophysiology which relied on generalized activation models, such as those proposed by Duffy (1972) and Selye (1957), to specificity models, such as those proposed by Sternbach and Fahrenberg (Flor & Turk, 1989). In the study of chronic pain, current models must take into account that the experience of pain is a complex phenomenon comprised of sensory-discriminative, cognitive-affective, and physiological components.

In a general theory, Sternbach (1966) proposes that

psychophysiologic disorders such as chronic pain result from the breakdown of homeostatic mechanisms. These mechanisms are unable to keep initial physiological responses and/or rebound to stressful stimuli within normal functioning. This leads to tissue damage and the appearance of symptoms.

For more than 20 years, the gate-control theory of pain has served as a guide to pain research (Price, 1988). It is


I





2


a dynamic model in which the experience of pain is determined by many factors in addition to tissue damage. These factors include personality, culture, and other activities in the nervous system at the time of injury. The gate-control theory proposes that signals from an injury can be radically modified or even blocked at the earliest stages of transmission in the nervous system by a central control mechanism that activates selective cognitive processes involved in evaluating the different aspects of pain (Melzack, 1986; Price, 1988).

In a parallel vein, Chapman (1986) uses an information processing model to provide a way to conceptualize the many facets involved in the experience of pain. In this model, a painful stimulus contains many sources of information so that the barrage of sensory inputs that result are more than simple energy transactions from the pain receptors to the central nervous system. The various classes of information transmitted are filtered and then modulated or inhibited as these inputs are processed through peripheral mechanisms, brainstem, and higher central processing areas (Chapman, 1986). Therefore, the relationship between the intensity of the pain stimulus and the pain reported is subject to individual variation and depends upon the person's perceptual accuracy, previous experience with pain, and attitudes toward pain.

Chapman (1986) also discusses Lundl's cognitiveperceptual model of stimulus equivalence which has





3


implications for chronic pain conditions in which organic findings are absent or inappropriate for the pain reported. In this model, learning processes produce long-term meaning structures relevant to the experience of pain. Through these meaning structures, stimuli that vary considerably in physical properties may take on functional equivalence for the perceiver. Thus, various somatic stimuli could be perceived as equivalent stimuli and, therefore, as painful.

In a discussion of the influence of perceptual

discrimination on pain, Sternbach (1968) described the concept of augmenters and reducers, whereby people display a consistent tendency to over/underestimate magnitude estimations of sensory stimuli. Reducers have been found to tolerate more experimental pain than augmenters (Sternbach, 1968). In a related vein, Barsky and Klerman (1983) suggest that hypochondriacal patients suffer from a perceptual or cognitive abnormality whereby they incorrectly assess and misinterpret the somatic symptoms of emotional arousal and normal bodily function. Barsky and Klerman's concept of hypochondriasis in chronic pain is consistent with Lundl's model of stimulus equivalence in that different somatic sensations may be perceived as equivalent. These conceptualizations as well as that of perceptual augmenters and reducers are consistent with Chapman's information processing model of chronic pain.

Turning from the cognitive-perceptual to the cognitiveaffective dimension of pain, a link between negative affect,





4


such as anger and anxiety, and pain has been emphasized by several writers (Pilowsky, 1986; Merskey, 1986; Gaskin, Greene, Robinson, & Geisser, 1992). Anxiety and anger are associated with the "flight or fight" response which characteristically involves arousal of the autonomic nervous system. Many of these physiological responses are also characteristic of pain. Aides, Cassens, and Stalling (1987) found that normal subjects who scored high on anxiety and were predisposed to attend to somatic symptoms reported more areas of pain and rated these sensations as more noxious. Thus, there is evidence for a link between physiological response, somatic focus, emotional arousal, and pain.

Price (1988) also discusses the role of cognitive

processes in the affective response to pain and proposes a sequential processing theory of pain. This theory proposes that nociceptive input activates arousal, sensorydiscriminative, autonomic, and somatomotor responses in parallel. Emotional responses to pain are then mediated by cognitive-evaluative appraisals of the nociceptive sensations. Thus, the sequential processing theory combines the neurophysiological aspects of the gate-control theory with the cognitive-evaluative components of Chapman's information processing theory. Price (1988) contends that pain affective responses are the end result of several processes, the most salient of which is nociceptive sensation.








The various models of chronic pain described above propose a central process which is responsible for regulating the organism's responses to external and/or internal stimuli. Dysfunction of this process, such as may be the case in chronic pain, could be manifested across several dimensions: 1) the cognitive-affective experience of pain, such as anxiety, anger, and depression; 2) abnormalities in the sensory-discriminative component of pain, such as poor discrimination of somatic stimuli; and 3) altered physiological reactivity due to pain. The current study proposes to explore these dimensions of pain in both chronic pain and pain-free individuals.













CHAPTER 2
CURRENT MODELS OF PAIN



The conceptualization of the experience of pain in a

manner that allows for scientific study has progressed from analyzing pain as a purely sensory phenomenon to viewing it as a multidimensional experience involving cognitiveaffective as well as sensory elements. The currently accepted definition of pain as set forth by the International Association for the Study of Pain is as follows: "pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage, or both (IASP, 1979).11 Chapman (1986) explains that this definition recognizes that the experience of pain is subjective, is more complex than an elementary sensory event, and involves associations between elements of sensory experience and an aversive feeling state as well as the attribution of meaning to the unpleasant sensory events. Therefore, current models must accommodate pain as a complex phenomenon consisting of sensory-discriminative, cognitive-affective, and physiological components.

Current models describe pain as a sensory-perceptual

experience that provides information about both external and internal, or somatic, stimuli. sensory end organs which are


6






7


activated by tissue damage or stress are termed nociceptors. These pain receptors can be either exteroceptors, which provide information about the external environment, or interoceptors, which provide information about body tissues and structures. Chapman (1986) explains that pain is not a simple stimulus energy transduction but appears to be a complex sensory message which results from the information generated in a relatively large interoceptive or exteroceptive receptive field.

Gate-Control Theory of Pain

Meizack's (1986) gate-control theory provides a

neurophysiological perspective of pain that conceptualizes pain as more than just a function of bodily damage. The perception of pain is also influenced by attention, anxiety, suggestion, prior conditioning, and other psychological variables. Melzack (1986) proposes that neural mechanisms in the spinal cord act like a gate to increase or decrease the flow of sensory input to the brain and can be profoundly influenced by descending controls from the brain. Pain occurs when the number of nerve impulses reaching the brain exceeds a critical level.

The gate-control model also contains the concept of a central control mechanism which activates selective cognitive and affective processes (such as memories of prior experiences and response strategies) that then influence, by way of the descending fibers, the modulating properties of the spinal gating mechanism and the experience of pain.





8


Some central processes, such as anxiety, open the gate. The model also proposes that sensory-discriminative processes are influenced by, as well as influence, the central control mechanism which controls the gating mechanism. The central control mechanism is hypothesized to involve higher central nervous system processes, such as those involved in the evaluation of input in terms of past experience.

Despite the initial controversies that the gate-control theory inspired, it has had an important influence on pain research for more than two decades (Price, 1988). Considerable evidence exists to support all but one of the major tenants of the theory (e.g., that ascending rapidly conducting efferents activate cognitive processes that then influence descending efferent pathways), and no one has refuted the basic tenants of the theory. Although Price criticizes the theory for being too general in its explanation of the interactions in the dorsal horn as well as the endogenous pain modulatory systems, he acknowledges that the gate-control theory has heuristic value in understanding pain mechanisms and guiding further research.

Information-Processing Models of Pain

Chapman (1986) discusses the physiological, sensory, and cognitive aspects of pain within an information processing model which parallels the gate-control model. Chapman identifies a central process in the experience of pain which he explains in terms of perceptual organization processes. These processes are influenced by cognitive-





9


affective processes (attention, arousal, emotion), sensory discrimination processes, and perceptions of physical symptoms. He describes the complex sensory modulation of pain as unique to pain since nociceptive signals can be enhanced or diminished at several levels of the neuraxis. This is an important function that apparently serves to protect the information processing centers of the brain from competing nociceptive input during times of danger when complete concentration on the environment is necessary for survival.

Chapman (1986) also describes Lundl's cognitiveperceptual model of stimulus equivalence which provides an explanation for the role of cognitive processes such as memory, beliefs, and expectancy, in the perception of pain. Lundl describes "meaning structures" as the basic determinants of perceptual experience and motor responses. These structures reside in short- or long-term memory and function as predispositions to exercise attentional filtering, vigilance, and readiness for certain types of responses to specific types of stimuli. Certain stimuli may take on functional equivalence for the perceiver in that they elicit identical responses despite notable differences in the stimulus properties. This has implications for somatization disorders as well as chronic pain patients since the patient may misinterpret normal interoceptive stimuli as painful.





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Sequential Processingi Theory

Based upon current knowledge of the neurophysiology and psychology of pain, Price (1988) proposes a sequential processing theory of pain which extends the physiology of the gate-control theory and incorporates the cognitiveaffective components of the information-processing model. In the sequential processing theory, nociceptive input simultaneously activates neural structures involved in arousal, sensory-discriminative, autonomic, and motor responses. Price suggests that the nature and magnitude of the body's responses to nociceptive input undergo cognitiveevaluative appraisal which mediates the affective response to pain. This cognitive appraisal is influenced by attitudes, memories, and the context of the situation in which the pain occurs. In this model, pain affective responses are the end result of nociceptive input.

Summary

In summary, the gate-control theory places emphasis on the neurophysiology of pain, the information-processing model focuses on pain from a cognitive-perceptual perspective, and the sequential processing model incorporates elements of both models with the end result being pain-related affect. All of these models identify a central process which organizes information and modulates the experience of pain through sensory discrimination of nociceptive stimuli, physiological responsivity, and cognitive-affective processes. The following chapters





11


review research which provides evidence in support of these dimensions of pain as well as of a central process as proposed by these models.














CHAPTER 3
SENSORY DISCRIMINATION IN PAIN PERCEPTION



Nociception

Nociceptors are sensory receptors which detect changes in the state of an organism. The most common sensory receptors are the free nerve endings. These afferent nerve endings are distributed throughout almost all parts of the body and are responsible for the sensations of pain, temperature, itch, tickle, movement, and proprioception (Seeley, Stephens, & Tate, 1989). These receptors are activated by three types of stimuli mechanical, thermal, and chemical. Some receptors respond selectively to only one type of stimulus, such as mechanoreceptors in the muscles and joints, whereas others, polymodal receptors, are optimally responsive to all three types of stimuli (Price, 1988).

These receptors can be divided into two functional classes based upon speed of impulse conduction: 1) As afferents which conduct impulses at velocities of between 6 and 30 meters per second over small diameter, myelinated axons, and 2) C afferents which conduct impulses at velocities of between 0.5 and 2 meters per second over large diameter, unmyelinated axons (Guyton, 1991). Price (1988) explains that A nociceptive afferents are relatively 12





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modality specific and often respond optimally to intense mechanical stimuli. They elicit brief latency intense responses critically necessary for rapid withdrawal and escape. These afferents relate to "first pain," which is usually described as sharp or pricking and can be conceptualized as a warning device. C nociceptive afferents tend to be of the polymodal variety and respond to mechanical stimuli (such as muscle stretch and contraction), thermal stimuli, and chemical stimuli, including endproducts of muscle activity such as lactic acid and endogenous chemicals resulting from tissue damage such as bradykinin (Guyton, 1991; Price, 1988). The responses of these afferents are more delayed, and their central actions are prolonged and slowly summate over time. These afferents relate to "second or chronic pain," which is usually described as burning, aching, and chronic and can be conceptualized as a mechanism related to protection and recuperation of injured tissue (Price, 1988).

Nociceptive afferents innervate the skin, muscle

tissue, viscera (such as the heart, lungs, and stomach), and other internal tissues, such as arterial walls and joint surfaces (Guyton, 1991). C polymodal nociceptive afferents make up more than 90% of the unmyelinated cutaneous afferents (Price, 1988). Price (1988) explains that "threshold activation of these afferents may not signal the presence of tissue-threatening stimuli, and there is a distinct possibility that they convey nonnociceptive as well





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as nociceptive information (p. 89)." He concludes that there is evidence that

similar principles of nociceptor functioning extend
across different tissues . that C polymodal
nociceptive afferents similar to those innervating skin
appear to innervate muscle, testes, and perhaps the
lung and cardiovascular system . [and] the latter type of nociceptive afferent [C polymodal] comprises a
large proportion of the nociceptive afferents
innervating different tissues. The physiological
characteristics of polymodal nociceptors are those which may well account for pains that are diffuse,
poorly localized, and poorly discriminated in terms of
modality. (p. 93)

Thus, there is evidence that the physiological

properties of a large number of nociceptors are such that they provide input to the organism that is diffuse and difficult to discriminate, as is frequently the case with chronic pain symptoms. This evidence is consistent with both the hypochondriasis and stimulus-equivalence models of chronic pain.

In a discussion of the results of animal studies

investigating central neurophysiological processing of joint pain in experimentally-induced arthritis, Guilbaud (1991) proposes that changes in the modulary systems may occur in order to allow the central nervous system to locate the source of the pain. Guilbaud proposes that some spinal and/or supraspinal controls might differentially modulate the various peripheral somatic inputs, and she cites several studies which have demonstrated an augmentation in the dorsal horn of both excitatory and inhibitory controls triggered by the inflamed joints.





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Guilbaud's discussion suggests that in an attempt to locate the source of pain, physiological changes may occur in the central nervous system that result in an augmentation of signals from deep somatic receptors and an increase in inhibition of sensory input from peripheral receptors. This is consistent with the gate-control theory of pain, Price's discussion of the diffuse type of input from deep somatic tissues, and studies that have demonstrated poor discriminability of peripheral stimuli in chronic pain subjects. These discriminability studies are discussed in the following section.

Sensory-Discrimination Deficits and Pain

Historically, pain has been evaluated in terms of

threshold (the point at which a person first experiences pain) and tolerance (how much pain the person can endure). The measurement of pain has become more sophisticated, and the application of methods such as signal detection theory (SDT) has allowed researchers to differentiate between discriminability, the ability to distinguish between different levels of stimulation, and response bias, the predisposition to report stimulation as painful.

Lloyd and Appel (1976) have reviewed SDT studies

concerning modification of discriminability and response bias by placebos and suggestion. They report that placebos and suggestion modified response bias (tolerance) but not discriminability. Clark (1974) has also found that suggestion had no effect on subjects' ability to





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discriminate stimuli but did raise their withdrawal criterion (pain tolerance or response bias). Therefore, discriminability has been found to be more closely related to sensory-perceptual processes and does not appear to be subject to the demand characteristics of the situation.

The application of SDT to chronic pain populations has suggested that chronic pain patients are poorer discriminators of experimental stimuli, such as tactual and heat, than controls. Malow, Grimm, and Olson (1980) found that chronic pain patients had lower pain thresholds, were less able to discriminate between varying intensities of pressure stimulation, and had a greater tendency to report pain than controls. Seltzer and Seltzer (1986) also investigated two-point tactual discrimination in chronic pain and pain-free subjects. The results indicated that the chronic pain patients were poorer discriminators of nonpainful, tactual stimuli.

Malow and Olson (1981) looked at changes in pain

threshold, sensitivity, response bias, and discriminability in chronic myofascial pain disorder (MPD) patients before and after conservative treatment with a sedative/hypnotic, muscle relaxant, or placebo; relaxation training; and discussion of the relationship between stress, muscle tension, and pain symptoms. Although there were no differences in the pain measures of subjects prior to treatment, after treatment the improved patients (those without pain symptoms) showed a significant increase in pain





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threshold, sensitivity, and discrimination, and a significant decrease in the tendency to report pain. The authors speculate that these results suggest the involvement of a central mediating process and "that differences in pain responses of MPD patients and normals are not due to permanent psychological or physiological differences, but may be due to the psychophysiologic effects of chronic pain (pp. 70-71)."

Naliboff and colleagues (1981) looked at discrimination and threshold for radiant heat stimuli in chronic low back pain (CLBP) patients, chronic respiratory patients, and nonpatient controls. Their results indicated that the CLBP and respiratory patients had higher pain thresholds, but the CLBP patients demonstrated a discrimination deficit for mildly painful stimuli. Cohen, Naliboff, Schandler, and Heinrich (1983) report that CLBP subjects demonstrated poorer discriminability of radiant heat stimuli but equal discriminability of loud tones compared to age- and sexmatched controls. Lautenbacher, Galfe, Karlbauer, Moltner and Strian (1990) reported reduced somatosensory perception for temperature in chronic back pain (CBP) patients. And although Yang, Richlin, Brand, Wagner, and Clark (1985) found that CLBP patients had a high response bias, the chronic pain group displayed poorer discriminability of experimental heat pain stimuli compared to normals. The authors concluded that these results provided evidence of a perceptual deficit in chronic pain patients.






is

In another study, Flor, Schugens, and Birbaumer (1992) compared the discrimination of muscle tension in patients with CBP and temporomandibular pain and dysfunction (TMPD) with that of age- and sex-matched healthy controls. All subjects were asked to discriminate levels of tension in the masseter and erector spinae muscles. The results demonstrated that chronic pain patients were less able to perceive muscle contraction levels correctly, and they underestimated their actual levels of muscle tension regardless of whether or not the muscle involved in the discrimination task was the site of the chronic pain problem. This deficit in discrimination did not appear to be related to local physiological changes at the site of pain or differences in motivation, attention, or fatigue. The authors concluded that "the present results suggest that the poor discrimination of an internal body process may not merely be the consequence of local changes at the site of pain but might be a more basic deficit (p. 175)."1 Fuller and Robinson (1995) also found that in a relevant but nonpain related modality, CLBP patients underestimated the heaviness of weights lifted with the painful body part, their lower back. Both studies support the notion of a deficit in the processing of nociception at a central level in terms of accurately assessing magnitude.

Gaskin (1991) investigated the relationship of somatic focus, cognitive-affective factors, physiological reactivity, and discrimination of somatic changes to cold





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pressor pain tolerance and threshold as well as to clinical pain in a sample of chronic pain patients. Although no relationship between these components and the experimental pain measures was found, a significant relationship between physiological reactivity and discriminability of reactivity to experimental pain was found suggesting that the subjects with higher levels of reactivity were better discriminators of somatic change. But analysis of the discriminability measure indicated that these chronic pain patients were chance discriminators of somatic changes. The lack of a pain-free control group limits the conclusions which may be drawn from these data, although the results are consistent with other studies that provide evidence of perceptual distortion in chronic pain patients.

Perceptual distortions are also characteristic of

perceptual augmentors and reducers. Along this dimension, people display a consistent tendency to over- or underestimate magnitude estimations of a sensory stimulus after repeated presentations. Augmenters show a tendency to perceive stimulation as greater, whereas reducers tend to perceive stimulation as less. Reducers have been shown to tolerate more radiant heat and electric shock than augmenters (Sternbach, 1968; Weisenberg, 1977).

Further support of the augmentor/reducer perceptual distortion effect in pain perception is suggested by two studies discussed by Schmidt and Arntz (1987) where healthy control subjects were exposed to repeated cold-pressor





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tests. In both studies, two groups emerged: 1) sensitizers, who responded to repeated pain stimulation with decreasing endurance and increasing pain intensity reports, and 2) habituaters, who responded with increasing endurance and decreasing pain intensity reports.

In another study that is also consistent with the

augmentors and reducers model, Peters, Schmidt, and Van den Hout (1989) investigated the responses of CLBP and control subjects to 8 trials of pressure-pain stimulation. They found that the CLBP subjects showed evidence of sensitization to the pain stimuli through decreased pain threshold and tolerance ratings, whereas the controls showed evidence of habituation through increased pain threshold and tolerance ratings. The authors speculated that if CLBP patients have a fundamental inability to habituate to painful experiences, then this could be considered a risk factor for the development of chronic pain. This study does not provide the data to determine if the inability to habituate to pain leads to the development of chronic pain or if chronic pain alters the ability to habituate to painful stimuli.

In a review of clinical and experimental evidence

examining central nervous system (CNS) function in chronic pain patients, Coderre, Katz, Vaccarino, and Melzack (1993) indicate that there is empirical evidence that noxious stimuli or injury can produce alterations in CNS function as well as long-term changes in cellular function. The authors





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concluded that "the effect of these changes includes an expansion of dorsal horn receptive fields and hyperexcitability which, if allowed to persist, would presumably produce prolonged changes in excitability that could be maintained without further noxious peripheral input" (p. 274). Their conclusions support the idea that chronic pain alters the ability to accurately discriminate stimuli.

Also related to the concept of augmentors and reducers, Barsky and Klerman (1983) proposed an information processing model of somatic style which can be conceptualized as perceptual amplification of bodily sensations and their cognitive misinterpretation. In this conceptualization, the perceptual deficit is seen as primary and the hypochondriacal characteristics are the inevitable outcome of these abnormal perceptions. Barsky and Klerman (1983) suggest that attributing an internal perception to a disease is more likely to occur when the person lacks an obvious, immediate and adequate explanation for the symptom. This occurs when the symptom is diffuse, ambiguous, common, and not in a part of the body that is directly observable, as is often the case with chronic pain. These authors discuss a study in which a subgroup of students who scored highest on a hypochondriasis scale were shown to have heightened levels of arousal and heightened perceptual sensitivity to bodily sensations. Other studies have demonstrated that anxiety can cause people to amplify their somatic symptoms and





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experience enhanced sensitivity to pain (Ahles et al., 1987; Malow, West, and Sutker, 1987; Merskey, 1986; Barsky & Klerman, 1983).

Schmidt, Gierlings, and Peters (1989) investigated

interoceptive and operant influences on CLBP behavior. The CLBP patients reported more bodily sensations than controls after treadmill exertion although, objectively the CLBP patients were less fatigued. Under rest conditions, healthy controls reported few bodily sensations, while CLBP patients generally reported as many sensations at rest as after a working-to-tolerance treadmill test. Little direct experimental evidence was found to support the importance of operant factors in the maintenance of poor endurance behavior by CLBP patients on repeated treadmill testing. The authors suggest that these results could be explained by a hypochondriasis theory such as that proposed by Barsky and Klerman (1983) whereby intensified pain perception is part of a general tendency towards augmentation and amplification of normal bodily sensations.

These studies suggest that chronic pain patients may have deficits in discrimination of sensory input. This is consistent with Guilbaud's discussion of the results of animal studies described in the previous section where it was postulated that nociceptive input from deep tissues may be augmented and input from cutaneous afferents may be inhibited in an effort to localize the source of pain, and, in so doing, may actuate a chronic state of pain. This is





23


congruous with the evidence presented in the Coderre et al. (1993) review that pain induces CNS and cellular changes that can maintain pain without additional noxious input.

Proprioception and Pain

Proprioception refers to nociceptive information on

body position provided to the central nervous system through input from muscle, joint, and cutaneous afferents (Grigg, Finerman, & Riley, 1973; Newton, 1982; Proske, Schaible, & Schmidt, 1988; Inglis, Frank, & Inglis, 1991). Revel, Andre-Deshays, and Minguet (1991) investigated the ability to discriminate neck proprioception in 30 patients with cervical pain and in 30 healthy controls. The authors discussed the paradox that although rehabilitation in the field of musculoskeletal diseases aims to improve muscle strength, joint mobility, and "proprioceptive sensibility," proprioceptive ability has not been well documented in healthy subjects and had never been studied in patients with cervical pain. In their study, subjects' ability to relocate the head on the trunk after an active head movement was tested. The results indicated that active head repositioning was significantly less precise in the cervical pain subjects who showed an overshoot in horizontal plane repositioning movements. The authors concluded that patients with neck pain may demonstrate altered proprioceptive sensibility due to "functional alterations of tendinous and muscular proprioceptors related to neck muscle function disturbances (p.291)."






24


In the area of low back pain, many rehabilitation programs include some education and training in body mechanics (Linton & Kamwendo, 1987). Although certain biomechanical positions, such as maintaining forward stooping position, have been found to increase the risk of low back injury (Carlton, 1987; McCauley, 1990), only one study has examined the relationship between injury and proprioception of the lower back (Parkhurst & Burnett, 1994).

Parkhurst and Burnett (1994) tested eighty-eight male, pain-free (no acute pain and not currently under treatment for a back injury) emergency medical service workers for three types of lower back proprioception (passive motion threshold, directional motion perception, and repositioning accuracy) using an apparatus designed by one of the authors. Each type of proprioception was examined in the three primary planes of motion (coronal, sagital, and transverse). Measures of repositioning accuracy did not reach statistical significance in any plane. Age and history of low back injuries within the past 5 years were associated with other proprioceptive deficits. Only 17% (15) of subjects had histories of back pain/injury within the past 5 years and the exclusion criteria screened out chronic pain subjects. Thus, these subjects were essentially pain-free controls, and the lack of deficits in repositioning accuracy would, therefore, be expected in this group. There are no





25


empirical studies evaluating trunk proprioceptive abilities of CLBP patients compared with pain-free controls.

Studies on body mechanics have focused on changes in behavior after instruction. In a review of 16 low back schools, Linton and Kamwendo (1987) concluded that although patients with CLBP demonstrated increased understanding of body mechanics as a result of "back school," there was little indication that this knowledge resulted in behavioral change. In a study of workers without back pain, Carlton (1987) demonstrated that workers who received body mechanics instruction performed better in a laboratory task than those with no training, but there was no difference in the body mechanics between groups (trained and untrained) in the work environment.

Contrary to these findings, a study by McCauley (1990) on the effect of body mechanics instruction on work performance in young workers (without CLBP) demonstrated that the trained workers performed work activities using proper body mechanics significantly better than the untrained workers. Morrison, Chase, Young, and Roberts (1988) investigated the effect of a community hospital outpatient treatment program for CLBP patients and found that observed body mechanics for nine daily living activities had improved dramatically following the program. At a one-year follow-up, gains in observed body mechanics had declined from levels assessed at the end of the program,





26


but were still significantly higher than levels at the beginning of the program.

In a study which examined both CLBP patients and

control subjects on physical abilities and body mechanics, Naliboff, Cohen, Swanson, Bonebakker, and McArthur (1985) found that controls performed significantly better than the CLBP subjects on endurance walking, the ability to control the low back, and trunk strength and flexibility. Lower extremity strength and flexibility and forward flexion did not differ between the groups. Although the CLBP subjects performed better than controls on the functional test of body mechanics, both groups received less than 25% of the maximum score suggesting that both groups had poor proprioceptive abilities.

In summary, studies on body mechanics show mixed

results in terms of changes in actual behavior in both CLBP patients and control subjects. These studies did not evaluate proprioceptive ability although this could significantly influence the capability to perform proper body mechanics and may account for the mixed outcomes. Although the Naliboff et al. (1985) study indicated that there are differences in physical abilities between CLBP patients and controls, they did not test for differences in proprioceptive abilities. Given that the ability to accurately perceive trunk position would seem to be a prerequisite for successful training in proper body mechanics, and given that Revel et al. (1991) found neck





27


proprioceptive deficits in cervical pain patients as compared to control subjects, the empirical investigation of the ability of CLBP patients and pain-free controls to accurately perceive trunk position seems warranted.

Summary

The studies reviewed in this chapter suggest that

individuals with chronic pain may suffer from a perceptual deficit related to the diffuse nature of input from slow conducting, unmyelinated efferents as well as augmentation of these signals by the central nervous system in an attempt to localize the source of pain. This system, once activated, may also conduct signals that are from non-pain producing stimuli but these stimuli may be interpreted by the central nervous system as painful since they are traveling on the pain-activated system. This is consistent with the theories discussed above and could account for the mixed results in the ability of chronic pain patients to discriminate somatic stimuli due to the nature of the stimuli and whether the stimuli involved the same receptive field as that of the clinical pain. The interpretation of sensory input is a complex process that involves the integration of thoughts, feelings, and memories (including pain-related memories) as well as the arousal level of the person experiencing pain.














CHAPTER 4
PHYSIOLOGICAL REACTIVITY AND PAIN



General Arousal

As discussed in the previous chapter, pain can be

conceptualized as a warning signal and as such is a potent means of producing arousal and widespread cortical activation (Price, 1988). Therefore, physiological responses to pain produce the "flight or fight" reaction that is also characteristic of fear and anger (Sternbach, 1968). This reaction involves arousal of the autonomic nervous system and results in changes across many body systems leading to increases in heart rate, blood pressure, vigilance, and motoric responses enabling the organism to be mobilized in order to escape aversive stimuli.

Sternbach (1966) hypothesized that the development of psychophysiological disorders, such as chronic pain, may be due to frequent and sufficiently intense activation of a body system such that dysregulation of the homeostasis of the affected system occurs and results in the symptoms of the disorder. Flor and Turk (1989) explain that underlying this model, which they referred to as individual response specificity, is the proposition that "psychophysiological disorders develop and are maintained as a consequence of unspecific hyperarousal of the autonomic nervous system.


28





29


Thus, in chronic pain patients, general physiological hyperactivity associated with high levels of sympathetic activation might lead to the development, exacerbation, and maintenance of pain symptoms (p. 216).11

In a study related to this issue, Perry, Heller,

Kamiya, and Levine (1989) compared autonomic functioning in healthy controls to that of patients with arthritis or myofascial pain. The authors also examined differences in autonomic functioning between the two chronic pain groups. Although both pain groups were similar on several parameters, there were differences between these groups. The authors concluded that both pain groups demonstrated similar alterations in autonomic function, although the alterations were not identical, underscoring the importance of investigating different pain syndromes separately. The authors suggest that the changes in autonomic function they observed may have been due "to the presence of pain, to the presence of stress, or to the presence of other psychophysiological concomitants occurring in chronic pain syndromes (p. 82).11 They posit that altered autonomic functioning may contribute to the maintenance of chronic pain syndromes and that further study of this functioning in patients with specific pain syndromes is warranted.

In a review of research on the physiological response patterns of chronic pain patients, Flor and Turk (1989) discuss the theory that aberrant physiological patterns could be an antecedent to chronic pain states, a consequence






30


of chronic pain that maintains the condition, or both. They suggest that regardless of the specific pain condition, chronic pain patients may display nonspecific physiological changes associated with pain, such as increased heart rate, that are indicative of heightened arousal. Peters and Schmidt (1991) found support for this in their study where CLBP subjects reacted to pain stimuli with a greater increase in the number of skin conductance fluctuations, which were also of greater maximal amplitude, than controls. Flor and Turk (1989) also suggest that patients with a particular pain disorder may show specific physiological response patterns, for example, elevated paraspinal electromyographic (EMG) responses in CLBP patients.

EMG Reactivity and Chronic Low Back Pain

A wide range of tasks have been used in studies on the psychophysiology of CLEP, including positioning, movement and lifting tasks, relaxation tasks, mental arithmetic, personally relevant stress, and experimental pain tasks, such as the cold pressor test (Flor & Turk, 1989). In two reviews containing summaries of the results of studies utilizing these various tasks, investigators have found lower EMG levels, no differences in EMG levels, or higher EMG levels in the paraspinal muscles of CLBP patients as compared to healthy controls (Dolce & Raczynski, 1985; Flor & Turk, 1989). These findings have lead some researchers to hypothesize that absolute levels of EMG activity are not as relevant to the development and/or maintenance of back pain





31


as are patterns of EMG activity during dynamic postures (Sherman, 1985; Ahern, Follick, Council, Laser-Wolston, & Litchman, 1988).

In their review, Dolce and Raczynski (1985) provide evidence to support two models of muscular involvement in back pain. One model involves a pain-spasm-pain cycle related to splinting or protective posturing due to physical damage and/or psychological and environmental stress. Splinting or tensing muscles leads to reduced blood flow and results in ischemic pain as well as spasm which can set up a pain-spasm-pain cycle. This pattern predicts higher paraspinal EMG levels in CLBP patients than in healthy controls.

The biomechanical model proposes that muscular

asymmetries and abnormally low levels of paraspinal EMG activity during movement allow the spine to become unstable. This instability results in pain from nerve root, joint, or capsular irritation. This model predicts left-right asymmetries and/or lower EMG levels in CLBP patients as compared to healthy controls. The findings of Ahern et al. (1988) that patients with CLBP demonstrated lower EMG levels during movement than non-patient controls provides support for the biomechanical model.

In a 1985 study, Flor, Turk, and Birbaumer investigated the relationship of paraspinal EMG reactivity to personally relevant and general stress in chronic back pain (CBP) patients, general pain patients, and non-pain medical





32


controls. The results indicated that CBP patients displayed elevations and delayed return to baseline only in their paravertebral musculature and only when discussing a recent personally stressful event or a recent pain episode. Neither of the other groups displayed similar response patterns at the paraspinal EMG site. The authors suggest that the abnormal muscle response of the CBP patients was not part of a general stress reaction, as the other groups indicated comparable levels of arousal in other areas. The results showed that anxiety, pain levels, and EMG elevations were related in the CBP patients, suggesting the involvement of a central process. This study also underscores the importance of using a stimulus that is relevant to the clinical pain of the subjects.

These findings were replicated by Flor, Birbaumer, Schugens, and Lutzenberger (1992) in a study comparing chronic back pain (CBP), temporomandibular pain and dysfunction (TMPD), and controls for symptom-specific psychophysiological responses to personally-relevant stress imagery. The CBP and TMPD patients exhibited elevated EMG activity at the site of pain (erector spinae and m. masseter, respectively).

In a 1989 review, Flor and Turk examined 60 studies which investigated the role of physiological variables in recurrent migraine, tension, and mixed headaches, chronic back pain, and temporomandibular joint (TMJ) disorders. The authors conclude that baseline resting EMG levels do not





33


appear to be a crucial variable in the physiology of pain, but that stress and pain related responses as well as slow return to baseline levels appear to be more relevant. They suggest that slow return to baseline levels is consistent with Sternbach's theory of homeostatic deregulation and warrants further research.

Flor and Turk (1989) further recommend that future research use multiple site, measure, and stressor assessments at several points in time on a well-defined patient sample and that the influence of sensory, cognitive, affective, and behavioral contributions to the pain experience be assessed along with the physiological responses to pain in order to clarify the relationships between these variables. They also encourage the use of potent and ecologically valid stressors.

Sherman (1985) argues for the importance of measuring pain intensity at time of EMG recording. He investigated EMG patterns by recording paraspinal muscle activity of subjects while in motion (bending to approximately 30 degrees and rising) and still (standing upright, sitting supported and unsupported, and prone). He compared these EMG values for subjects with no history of back pain, subjects with past episodes of back pain but no pain during the course of the study, and subjects currently experiencing back pain. He found that the 83 chronic back pain (CBP) patients each produced an unique pattern of muscle activity that was relatively stable over several weekly recording





34


sessions and that pain intensity was positively correlated with ENG levels in the position with the most elevated EMG values as compared to control subjects. He comments that the failure to take pain intensity at time of recording into account may have contributed to the conflicting results of previous EMG studies.

Summary

The research on EMG reactivity in CLBP patients

suggests that there may be several patterns of muscular activity related to back pain. Several researchers suggest that clarification of the role of EMG reactivity in the experience of chronic low back pain requires that future studies investigate patterns of EMG activity from baseline through return to baseline during an ecologically valid stressor. The use of personally relevant stressors or stressors related to patients' clinical pain is critical if the relationship between ENG reactivity and pain is to be understood in a manner which will allow for more efficacious treatment of this disorder. Previous research also indicates the importance of assessing pain intensity, sensory discrimination, and cognitive-affective variables during EMG recording.













CHAPTER 5
COGNITIVE-AFFECTIVE PROCESSES AND PAIN



Regarding the relationship between cognitive-affective processes and pain, evidence is growing to implicate the role of negative affect, especially anxiety, anger, and depression, in the experience of chronic pain (Linton & Gotestam, 1985; Feuerstein, 1986; Wade, Price, Hamer, Schwartz, & Hart, 1990; Jensen, Karoly, & Harris, 1991; Gaskin et al., 1992; Geisser, Gaskin, Robinson, & Greene, 1993). Examining the relationship between anxiety and pain, Sternbach (1968) reports that many studies indicate that persons who are more anxious show greater pain responses. Hall and Stride (1954) found that the appearance of the word "pain" in instructions made anxious subjects report as painful a level of electric shock that they did not regard as painful when the word was absent from the instructions. The authors concluded that the mere anticipation of pain increased anxiety and thereby increased the intensity of perceived pain.

Ables and colleagues (1987) reported that college

students who were attentive to somatic symptoms and scored high on state anxiety reported more areas as painful and rated these sensations as more noxious. Geisser et al. (1993) found that in a mixed group of chronic pain patients,


35






36


attention to somatic symptoms mediated the relationship between depression and the Sensory Pain Rating Index on the McGill Pain Questionnaire (MPQ), whereas depression was directly related to all other subscales of the MPQ. The authors suggest that the "self-report of the sensory experience of pain appears to be related to depression through heightened somatic focus (p.15)." Kremer and Atkinson (1983) describe chronic pain populations as characterized by a high incidence of anxiety and depression and as demonstrating the disruptive effects of affective distress on cognitive tasks.

Empirical studies examining the relationship between anger and pain have been scant until recently. Pilowsky (1986) discussed the results of several clinical case studies and the few controlled studies on pain and anger. He concluded that certain combinations of anger experience and anger inhibition were important elements in the experience of chronic pain for some patients.

A study by Wade et al. (1990) provides additional

support for the role of anger in the experience of pain. Using visual analog scales (VAS), the authors assessed the relationship of depression, anxiety, anger, frustration, and fear to pain-related unpleasantness. Anxiety, anger and frustration were found to predict pain-related unpleasantness. Similarly, Fernandez and Milburn (1994) found that of three weighted sets of emotions, the set comprised of anger, fear, and sadness was the most salient





37


component in ratings of overall pain in a group of 40 chronic pain patients.

In a clinical review, Fernandez and Turk (1995)

concluded that available research indicates that anger is one of the most salient emotional correlates of chronic pain although past research has been focused on depression and anxiety. In addition to discussing cognitive appraisal models of anger in chronic pain patients, the authors suggest that anger in chronic pain patients may be partially explained by a physiological model where anger is an "innate" response triggered via subcortical pathways by aversive stimuli such as pain. A non-cognitive activation of anger in chronic pain patients in response to their pain is a likely concomitant of autonomic arousal to this aversive condition.

Feuerstein (1986) reports that low back pain subjects had greater levels of anger, anxiety, and depression compared to asymptomatic controls. He studied paraspinal skeletal muscle activity (EMG), autonomic nervous system activity (heart rate), gross motor activity, and emotional state in chronic low back pain subjects and asymptomatic age- and sex-matched controls. EMG levels and gross motor activity did not differ between groups, although mood measures indicated greater levels of anxiety, tension, depression, anger, fatigue, confusion, and less vigor in the low back pain subjects. Increased heart rate was modestly correlated with reported pain. Feuerstein concluded that





38


the results question the role of lumbar paraspinal muscle activity in low back pain and suggest the modulating role of autonomic arousal and concomitant mood state in the exacerbation of low back pain. He suggests a model of chronic low back pain consider both cognitive-perceptual processes and autonomic arousal.

Price (1988) discusses the cognitive-evaluative and

affective dimensions of pain and describes emotional states as "complex modes of experience . determined to a large extent by attitudes, images, thoughts, memories, expectations, and desires (p.51).11 Price provides evidence that an emotional state requires some minimal level of physiological arousal and that the specific emotional state that is experienced depends upon the meaning attributed to the situation. Thus, the meaning attributed to somatic sensations, such as pain, determines the type of emotion experienced.

Shacham, Dar, and Cleeland (1984) investigated the

relationship of mood to severity of clinical pain in chronic pain patients. Pain severity was found to be positively correlated to negative mood but was unrelated to positive mood, and negative mood was found to be independent of positive mood. Gaskin et al.(1992) also found that state measures of mood (state anxiety, anger, and depression) were more strongly related to pain ratings in a chronic pain sample than were trait measures. The authors suggest that these findings support the hypothesis that chronic pain





39


adversely affects mood rather than the hypothesis that trait characteristics are a predisposing factor in the development of chronic pain. Both of these studies are consistent with Price's (1988) sequential processing theory that pain results in pain-related affect.

Summary

The literature reviewed indicates that anxiety, anger, and depression as well as increased arousal and somatic focus are associated with the experience of pain. The clarification of the relationship between these factors warrants further study.













CHAPTER 6
SUMMARY AND HYPOTHESES



The previous chapters have provided a review of

research which has investigated the cognitive-affective, sensory-perceptual, and physiological reactivity components of pain. The literature suggests that the experience of pain is modulated via a central process that is influenced by these components. The results of these studies suggest that a dysfunction in this central process may result in the experience of chronic pain as well as increases in negative affect, physiological reactivity, and perceptual deficits. The literature also recommends that physiological reactivity in chronic pain should be assessed in specific pain syndromes, such as CLBP patients, through the use of stressors relevant to patients' clinical pain.

The current study explored group differences between CLBP patients and healthy, pain-free controls on the following aspects of this hypothesized central process:

1) Cognitive-affective processes: Depression, anger and anxiety measured using self-report questionnaires.

2) Subjective experience of pain: Pain intensity and pain related unpleasantness measured using visual Analogue Scales (VAS's).




40





41


3) Sensory-perceptual processes: proprioceptive

discriminability of body position quantified as accuracy of body angle reproduction and response bias, e.g., tendencey to under- or overshoot the target angle..

4) Physiological reactivity: EMG recordings of the lumbar paraspinal muscles during proprioceptive tasks.

Previous research predicts the following group differences:

1) CLBP subjects will exhibit greater levels of negative affect than healthy controls.

2) CLBP subjects will demonstrate higher VAS ratings of pain intensity and unpleasantness than controls.

3) CLBP subjects are expected to be poorer

discriminators of body position, e.g., to be less accurate when reproducing body angle position, and to differ on response bias. Previous research is mixed on the directionality of response bias (overshoot versus undershoot).

4) Although the results of previous research have found that EMG reactivity to some stressors may be the same as that of healthy control subjects, there is evidence that CLBP subjects demonstrate higher EMG reactivity to a stressor relevant to their clinical pain. Therefore, it is predicted that CLBP subjects will demonstrate higher anticipatory and recovery EMG levels than healthy controls.














CHAPTER 7
METHODS



Subjects

Collection Sites

Data was collected from two sites: Gainesville,

Florida and Charleston, West Virginia. Pain subjects were recruited from the outpatients at the orthopedic and Physical Therapy Clinics at Shands Hospital, University of Florida, Gainesville, Florida, and the Sports Medicine Center at Charleston Area Medical Center (CAMC), General Division, Charleston, West Virginia. Control subjects for both sites were recruited from the respective local community.

The University of Florida (UF) sample consisted of 30 subjects: 15 pain-free controls and 15 CLBP subjects with seven females and eight males in each group. The CAMC sample consisted of 32 subjects: 16 pain-free controls and 16 CLBP subjects with five females and eleven males in each group.

Inclusion Criterion

Pain subjects had a CLBP syndrome of at least 6 months' duration and experienced pain on a daily basis. Pain-free controls were free of any pain condition for at least the 42





43


previous 6 months. No subject had any history of psychiatric hospitalization.

Prospective CLBP subjects were initially screened by

consulting with their physician or physical therapist as to their capability to perform the proprioceptive tasks required in this study. Only CLBP subjects who were assessed as capable of performing the proprioceptive tasks were approached for participation in the study.

Measures

Cognitive-Affective Measures

Beck Depression Inventory (BDI). The BDI consists of 21 items that assess the cognitive-affective and neurovegetative signs of depression. The BDI has been standardized on psychiatric and nonpsychiatric populations (Beck, Steer, & Garbin, 1988) with alpha coefficients ranging from .73 to .95. Meta-analyses have reported mean correlations between the BDI and other measures of depression, the Hamilton Psychiatric Rating Scale, the Zung Self-reported Depression Scale, and the Minnesota Multiphasic Personality Inventory Depression Scale, ranging from .60 to .76.

State-Trait Personality Inventory (STPI). The STPI

(Spielberger et al., 1983) consists of six 10-item subscales that assess state and trait anxiety and anger. The state scales measure the intensity of a subject's feelings at the time of administration, e.g., mood. The trait scales assess





44


the frequency with which a subject experiences anxious and angry feelings.

The STPI has been standardized with high school and college students, military recruits, and working adults (Spielberger et al., 1983). Correlations with the parent scales, the State-Trait Anxiety Inventory and the StateTrait Anger Scale, ranged from .93 to .99. Alpha coefficients for each subscale ranged from .76 to .88.

Based upon the results of previous research (Gaskin et al., 1992) indicating the greater impact of state over trait affect measures on pain report, only the state affect subscales were used in this study. Sensory-Perceptual Measure

Body Position Propriocention. Subjects' ability to reproduce 2 body positions during forward flexion and 1 position during backward extension of the trunk was measured using an ergometric lumbar transceiver (ELT) device. The ELT device is a non-invasive, compact, light-weight miniature microcomputer that is worn in a fabric belt which contains EMG sensors. The ELT measures spinal angle from 150 extension (-150) to 1050 forward flexion. Subjects were asked to reproduce forward flexion angles of 220 and 450 and one extension angle of -100.

The ELT device was worn by subjects during the

baseline, guided movement, anticipatory, body position task, and recovery phases of the study and recorded the target






45


angles and the actual performance of subjects as they attempted to reproduce the target angles. The computer monitor was positioned such that subjects could not view it and gain feedback on their performance. Physiologrical Reactivity Measures

ENG reactivity was assessed by measuring muscle

activity of the lumbar paraspinal muscles during the phases of the experiment described above. Sensors for ENG activity were contained in the belt of the ELT device described in the previous section and consisted of 3/4"xl-3/4"1 fabric pads. Integrated EMG data was digitized on-line with equipment and software by Physical Health Devices (Pompano Beach, FL.). This apparatus incorporates proprietary firmware for automated gain adjustment throughout a dynamic range of 7-1,800 uV root mean square (RMS). The bandwidth was 100-540 Hz with a 60 Hz notch filter. Signal processing was as follows: bandpass filtering occurred in front of the RMS conversion, the time constant for the RMS to DC conversion was 40 ins., and the filtered integrated signal was sampled and stored at 128Hz. Average iEMG was computed for each phase of the experimental procedure described below. The computer monitor was positioned such that subjects could not view EMG activity during the experimental procedure.

Pain Measures

McGill Pain Questionnaire (MPO). The MPQ consists of

twenty groups of single word pain descriptors with the words





46


in each group increasing in rank order intensity. The sum of the rank values for each descriptor based on its position in the word set results in a score called the Pain Rating Index (PRI). The MPQ also consists of several subscales: the Sensory PRI, Affective PRI, Evaluative PRI, Miscellaneous PRI, Present Pain Intensity (PPI), and Number of Words Circled. Clinical and experimental data have demonstrated that the MPQ displays acceptable reliability and validity as a method of measuring subjective pain experience (Melzack, 1985; Reading, 1985). Data from this instrument was used to characterize the CLBP sample.

Visual Analogue Scales. Visual analogue scales (VAS's) were used to measure pain intensity and pain-related unpleasantness. Price (1988) stresses the importance of using ratio scales, such as VAS's, in the measurement of pain. Ratio scales are superior to ordinal and interval scales in that ratio scales serve to reflect actual ratios of magnitude. Price (1988) states that VAS's have been shown to demonstrate reliable power functions for ratings of pain intensity and unpleasantness. He concludes from a review of studies comparing the use of different types of VAS;s that "those VAS's that most clearly delineate extremes (i.e., the worst pain, the most intense pain imaginable) and are 10-15 cm in length have been shown to have the greatest sensitivity and are the least vulnerable to distortions or biases in ratings (p. 33)."1





47


The VAS's used in this study consisted of 12.4 cm. lines

whose endpoints were designated as "no sensation" and "the

most intense sensation imaginable" for the pain intensity

(PIN) VAS and "not bad at all" and "the most intense bad

feeling possible for me" for the pain unpleasantness (PUN)

VAS (adapted from Price, Rafii, Watkins, & Buckingham,

1984).

Procedures

After establishing written informed consent in

accordance with Institutional Review Board requirements, all

subjects were administered the BDI and the STPI. The MPQ

was administered to the CLBP patients only. Upon completion

of these questionnaires, subjects were then instructed in

the experimental protocol as follows:



"In a moment I will put a belt around your
waist that measures the muscle activity in your
low back and the angles to which you bend. After
a baseline phase you will be guided through 2
forward bends and 1 backward bend. After you have been guided to a position, you will be asked to do
the bend without guidance, stopping at the same
point to which you were guided. You will repeat
this task without guidance a total of 5 times.
I will give you a 10 second warning ('in 10
seconds I will tell you to bend') before bending,
and I will tell you when to start bending. You
will have 5 seconds to complete the bend. I will
tell you when to return to standing straight.
After each bend, I will show you some scales with
which you will rate your level of pain intensity
and pain unpleasantness at that moment. I will
explain these scales in a moment.
After you have done this bend 5 times without
guidance, you will be guided to another position.
You will be asked to bend to that position 5 times
without guidance, rating your levels of pain intensity and unpleasantness after each bend.





48


After this, you will be guided to one more bend
and will repeat the above procedure."


Then subjects were instructed in the use of the VAS's as

follows:


"There are two aspects of pain which I am
interested in measuring: The intensity, how
strong the pain feels, and the unpleasantness, how unpleasant or disturbing the pain is for you. The
distinction between these two aspects of pain
might be made clearer if you think of listening to
a sound, such as a radio. As the volume of the
sound increases, I can ask you how loud it sounds
or how unpleasant it is to hear it. The intensity
of pain is like loudness; the unpleasantness of
pain depends not only on intensity but also on other factors which may affect you. There are
scales for measuring each of these two aspects of
pain. Although some pain sensations may be
equally intense and unpleasant, I would like you
to judge the two aspects independently." (From
Price et al, 1984; p. 31)
"After each task, I will show you two scales.
The pain intensity scale goes from "no sensation"
to the "most intense sensation imaginable."
Please indicate your judgment by marking the point
on the line which corresponds to your level of
pain intensity at that moment. on the pain
unpleasantness scale, the line goes from "not bad at all" to the "most intense bad feeling possible
for me." Please indicate your judgment by marking
the point on the line which corresponds to your
level of pain-related unpleasantness at that
moment."


The ELT belt was then placed around the subject's waist

with the EMG strips positioned over the subject's lumbar

paraspinal muscles. The ELT was calibrated to zero for each

subject in the standing position after instructing them to

"stand straight." Subjects' understanding of the VAS's and

protocol instructions were verified with several practice

trials during which they were guided to 100 flexion.





49


Subjects were allowed to habituate to the ELT device for a 5 minute baseline phase during which they were instructed to "keep your arms at your sides and remain as still as possible."

Collection of angle and EMG data began during the

baseline phase. Body position angles (-100, 220, 450) and PIN and PUN VAS's were presented in a counterbalanced order to control for possible order effects. After the 5 minute baseline period, subjects were guided to the first target angle and held in place for 5 seconds. They were then instructed to "stand straight." once standing straight, a 10 second recovery period began. After this phase, subjects received the 10 second warning ("in 10 seconds I will tell you to bend"). After this 10 second anticipatory phase, subjects were instructed to "bend." once subjects reached their approximation of the target, they were told to "stand straight." A 10 second recovery phase began at this point during which subjects were presented with the PIN and PUN VAS's and asked to "rate pain intensity and pain unpleasantness" with a pencil on the lines. The VAS's were presented to subjects in such a way as to minimize any gross movement of the arm during this procedure. After the 10 second recovery phase, the next anticipatory phase with a 10 second warning began. The anticipatory, bending, and recovery phases were repeated for a total of 5 trials.

After the last recovery phase for the first target angle, subjects were guided to the next target angle and





50


proceeded through 5 trials as described above. After the last recovery phase for the second target angle, subjects were guided to the third angle and proceeded through 5 trials as above. After the completion of the experiment, the ELT was removed and subjects were fully debriefed. Completion of the questionnaires and body position proprioception task took approximately 45 minutes.













CHAPTER 8
RESULTS



General Demographic Data

Age and Sex

The subjects in this study were age- and sex-matched. Collapsing across sites, there were 31 pain-free control subjects with an average age of 37.6 years (SD=7.9) and 31 CLBP subjects with an average age of 39.6 years (SD=9.8). In each group, there were 12 females and 19 males. Race and Education

All CLEP subjects were Caucasian. There were 29

Caucasians, 1 African-American, and 1 Asian in the control group. All subjects had at least a high school education with a mean of 19 years (SD=2.9) of education for controls and 14.6 years (SD=2.9) for CLBP subjects. Height, Weigrht, and Body-Mass Index

Although there were no differences between groups on height, CLBP subjects and controls differed significantly (t[59]=-2.13, p=0.037) on weight with CLBP subjects weighing 85.2 kilograms (SD=19.2) and controls weighing 75.2 kilograms (SD=17.6) on the average. Since the amount of adipose tissue can effect accuracy of EMG recordings, the body mass index (BMI), a commonly used index of obesity which utilizes weight in relation to height, was calculated 51






52


for all subjects. A t-test of BMI by group indicated a significant difference (p=0.003) in this measure between CLBP subjects (M = 28.3, SD=5.6) and controls (M = 24.4, SD=3.8).

Marital Status

Comparison of groups reveals significant differences in marital status (Fisher's Exact Test, 2-tail, p=0.05) with more control subjects being single and more CLBP subjects being divorced (see Table 8-1).

Table 8-1: Marital Status by Group Marital Status Controls CLBP
Single 11 4
Married 17 21
Divorced 2 6
Widowed 1 0


Employment Status

Comparison of groups reveals significant differences in employment status (Fisher's Exact Test, 2-tail, p=0.00) with more control subjects either employed or students and more CLBP subjects on temporary or permanent disability (see Table 8-2).

Table 8-2: Employment Status by Group
Employment Controls CLBP
Employed 26 12
Unemployed 1 4
Disability 0 5
Retired 0 1
Student 4 1
Temp Disability 0 7






53


Medications

All subjects were asked regarding their medication

usage the day of their participation in the study. None of the control subjects had taken narcotics, analgesics, nonsteroidal anti-inflammatory analgesics (NSAIDs), or muscle relaxers. Ten of the CLBP subjects had taken no medications, while 3 had taken a narcotic, 1 an analgesic/narcotic/sedative drug, 10 had taken NSAIDs, 6 had taken a muscle relaxer, and 7 subjects were on antidepressants.

To determine the impact of medication usage on negative affect and ENG, Cohen's d was calculated for the depression, state anxiety, state anger, and baseline EMG measures comparing pain subjects on medications with those not on medications. The effect sizes and group means indicate that medication usage did not have a dampening affect on any of these measures. The only moderately large effect sizes were for depression (d =0.63) and baseline EMG (d = 0.6). The means for the depression and baseline EMG measures were actually higher for the pain subjects on medications. Present pain and MPQ PPI ratings did not differ between the medication and non-medication groups suggesting that differences in baseline EMG were not related to pain level. Back-Related Surgeries

Only one of the control subjects had undergone a backrelated surgery (laminectomy). Of the CLBP subjects, 24 had no back surgery, 2 had undergone one surgery, 3 had






54


undergone two surgeries, and 2 subjects had undergone 3 or more surgeries. These surgeries consisted of laminectomies, fusions, diskectomy, nerve decompression, and spinal stimulation implant. CLBP subjects with multiple surgeries had undergone more than 1 fusion.

Chronic Low Back Pain Subjects Description of Clinical Pain

Frequency of pain was constant for 26 subjects and intermittent/daily for 5 subjects. Means for ratings of average pain and present pain (on a 0-10 scale where 0=no pain and 10=worst pain imaginable) were 4.9 (SD=1.7) and 4.4 (SD=2.2), respectively. Across sites the average duration of CLBP syndrome was 63.8 months (SD=67.4).

On the McGill Pain Questionnaire (MPQ), CLBP subjects' mean scores (SD) were as follows: Sensory=12.8 (7.1), Affect=l.2 (1.7), Evaluative=l.7 (1.5), Miscellaneous=3.7 (3.0), PRI=I9.5 (10.7), and PPI=2.2 (1.0). Since the MPQ and the negative affect measures were given to pain subjects before beginning the proprioceptive task, it is of interest to examine the correlations between the pain scales and the negative affect measures (see Appendix for the Pearson Correlation Coefficients for these varibles).

The MPQ Sensory scale was significantly correlated with all three negative affect measures, state anxiety (r=0.56, p=0.001), state anger (r=0.46, p=0.011), and BDI (r=0.36, p=0.05). The MPQ Affect scale was significantly correlated only with the BDI (r=0.36, p=0.05). None of the negative





55


affect trio were significantly correlated with the MPQ Evaluative scale, while only state anxiety (r=0.55, p=0.02) was significanly correlated with the MPQ Miscellaneous scale. With the MPQ PRI, correlations with state anxiety (r=0.55, p=0.001) and state anger (r=0.38, p=0.04) were significant while the correlation with the BDI (r=0.38, p=0.056) was marginally significant. The same held true for the correlations with the MPQ PPI: state anxiety (r=0.40, p=0.03) and state anger (r=0.38, p=0.04) were significant while the correlation with the EDI (r=0.34, p=0.06) was marginally significant.

When examined by site (UF versus CAMC), CLBP subjects did not differ on some demographic or medical information such as education, marital status, or medication usage, but these two groups did differ on the following parameters: 1) duration of CLBP syndrome, 2) CLBP diagnosis, 3) presence of additional pain syndrome(s), 4) number of surgeries, 5) employment status.

The average duration of back pain differed

significantly between sites [t(29)=2.45, p=0.02]. The average pain duration for the UF subjects was 92.1 months (SD=73, range 25 to 240 months) whereas the average for the CAMC subjects was 37.3 months (SD=50.6, range 6 to 180 months). Although diagnosis information was missing for 9 of the UF subjects, comparison of the available information showed that 37.5% of the CAI4C sample had the diagnosis of chronic lumbar sprain whereas none of the UF subjects had





56


this diagnosis. The other primary diagnoses in the CAMC sample were bulging disk, herniated disk, spondylolisthesis, degenerative disk disease, and other. In the UF sample, the primary diagnoses were spondylolisthesis, degenerative disk disease, scoliosis, and other. Regarding additional pain syndromes, 10 of the UF subjects (66.7%) reported pain syndromes in addition to CLBP whereas only 5 CAMC subjects (33.3%) had more than one pain syndrome. This is likely related to the difference in duration of pain syndromes between the two groups.

Examining number of surgeries, only 9 of the UF

subjects (60%) had no surgeries compared with 15 (93.8%) of the CAMC subjects. Only one of the CAMC subjects had any back surgery (one laminectomy) whereas 5 of the UF subjects had 2 or more back surgeries.

There were two employment categories on which the CLBP samples differed significantly (Fisher's Exact Test 2-tail, p= 0.00): 9 (64.3%) of the UF subjects were employed compared with 3 (18.8%) of the CAMC subjects and 7 (43.8%) of the CAMC subjects were on temporary disability while none of the UF subjects were.

In summary, these differences between the two CLBP samples reflect the nature of the clinics from which the subjects were solicited. The subjects in the UF sample were mostly patients from an orthopedic surgery clinic whose patients had longer histories of back pain and had received surgical interventions. The CAMC sample consisted of





57


individuals who had been injured relatively recently and were in the early stages of rehabilitation in a physical therapy setting. Despite these differences, there were no significant differences between these samples on measures of proprioception, pain, negative affect, or ENG reactivity.

Data Reduction and Analyses

Zero-order correlations can be seen in the Appendix.

On all measures of negative affect, pain subjects exhibited greater levels than controls, as predicted. Multivariate analysis (MANOVA) of pain subjects' and controls' scores on depression, state anger and state anxiety measures demonstrated that the relationship between the three variables differed by group [F(3,58)=15.11, p=.0001J (see Figure 8-1). See Table 8-3 for means and standard deviations for these measures.

Table 8-3. Means (SD) for Negative Affect Measures
Measures Controls CLBP
Depression (BDI) 3.00 (2.6) 11.13 (6.09)
State Anger (STPI) 10.19 (0.65) 12.68 (5.31)
State Anxiety (STPI) 14.48 (3.05) 18.68 (5.68)

VAS responses, measured in centimeters, were averaged across the 5 trials for each body position. This resulted in an average VAS pain intensity (PIN) and pain unpleasantness (PUN) score for each of the 3 discriminability tasks. Due to the non-normal distribution of the data for the controls subjects for both PIN and PUN responses, nonparametric analyses (Wilcoxon) were performed






58


to compare the groups on these measures. As expected, the pain subjects reported significantly higher levels of pain intensity and pain unpleasantness than controls at all three angles (see Tables 8-4 and 8-5, Figures 8-2 and 8-3).

Table 8-4. Median Ratings in Centimeters (mi max) for PIN
Group *PIN -100 *PIN 220 *PIN 450

Controls 0.8 0.02 0.0
___________ (0,1.7) -(0,0.9) -(0,0.5)
CLBP 5.44.34 4.88
_________ (0.02,11.4) (0.4,12.3) 1(0.9,11.7)
*Wilcoxon 2-sample test, p=0.0001.

Table 8-5. Median Ratings in Centimeters (mm max) for PUN
Group *PU -100 *PU 220 *PU 450

Controls 0.06 0.02 0.02
_______ (0,3.5) (0,1.0) (0,0.8)
CLBP 5.82 4.64 4.30
_____ 1_ (0.1,9.5) (0.2,11.9) 1(0.3,11.8)J
*Wilcoxon 2-sample test, p=0.0001.


Multivariate analyses (MANOVA) of pain intensity and

pain unpleasantness for the CLBP group demonstrated an angle affect for both measures [F(2,29)=4.13, p=0.03; F(2,29)=4.16, p=0.03, respectively]. Univariate analysis of pain subjects' ratings of pain intensity showed that there was no signficant difference in ratings for angles

-100 and 450 (F=0.88, p=0.36) whereas the ratings for angles

-100 and 220 were significantly different (F=7.31, p=0.01) and the difference in ratings for angles 220 and 450 approached significance (F=3.34, p=0.08). Therefore, pain

subjects rated the two angles (-100, 450) most difficult for them to achieve as more painful and the less difficult angle






59


(220) as least painful (see Table 8.6 for means and standard deviations).

Univariate analysis of pain subjects' ratings of pain unpleasantness showed the same pattern (see Table 8.6 for means and standard deviations). There was no significant

difference in ratings for angles -100 and 450 (F=0.91, p=0.35) whereas the ratings for angles -100 and 220 were significantly different (F=6.62, p=0.02) and the difference

in ratings for angles 220 and 450 approached significance (F=3.56, p=0.07). Again, pain subjects rated their pain as more unpleasant at the more difficult angles and least unpleasant at the less difficult angle (see Figure 8-13). These results are consistent with pain subjects' verbal reports (complaints) and/or behavioral difficulties (inability to achieve target angle, increased pain

behaviors) with angles -100 and 450.


Table 8-6. Means (Standard Deviations) for PIN and PUN
-100 220 450
PIN 5.61 (2.7) 4.66 (3.3) 5.24 (3.3)
PUN 5.59 (2.9) 4.58 (3.3) 5.17 (3.5)


Accuracy of subjects' ability to reproduce each body

position was calculated by summing the absolute value of the difference scores from the target angle across the 5 trials for each angle. This yielded a total response accuracy score for each of the 3 body positions with lower scores indicating that a subject's performance was more accurate.






60


On response accuracy, repeated measures ?4ANOVA showed an angle effect [F(2,59)=23.99, p=.0001] but no effect for group or group X angle (see Table 8-7 for means and standard deviations). All subjects were most accurate at angle -100 and least accurate at angle 220 (see Figure 8-4). Collapsing across groups, the difference in response accuracy was statistically significant between angle -100

and both angles 220 and 450 [F(l,60)=38.60, p=0.0001; F(1,60)=20.26, p=0.001] while the difference between angles 220 and 450 was not significant.


Table 8-7. Means (SD) for Response Accuracy
Target Controls CLPBoth Gop
AngleCBPGop
-100 10.90 (6.7) 10l.40 (5.4) 10.70 (6.0) 220 .24.90 (13.5) 23.80 (21.1) 24.40 (17.6) 450 120.10 (16.6) 1 21.10 (15.0) 120.60 (15.7)


Subjects' response bias was calculated by summing the actual value for the angular error from the target angle across the 5 trials. This provided a measure of undershoot or overshoot across the 5 trials for each of the 3 body positions. For example, on a trial with a target angle of 220 flexion where the subject bends to 150 flexion, the amount of undershoot is -70 for that trial. Differences between CLBP subjects and controls on these proprioception measures were assessed by MANOVA.





61


The repeated measures MANOVA for response bias showed no effect for either group or angle but was marginally significant for an angle X group interaction (F(2,59)=2.99, p=.058) (see Table 8-8 for means and standard deviations), while univariate analysis of the interaction of angle X group was significant (p=0.0496). Polynomial contrast demonstrated a subtle but significant difference (p=0.03) in quadratic trends. The curve for the response bias of the pain subjects was an inverted 'IV" with CLBP subjects

overshooting target angle 220 while slightly undershooting target angle -100 and demonstrating almost no response bias at target angle 450. The curve for the controls was almost the inverse with controls slightly overshooting target angle

-100 while demonstrating little response bias at target angle 220 but overshooting target angle 450. (See Figure 8-5). Pain subjects demonstrated the smallest response bias at the two angles which were the most difficult/painful for them.

Table 8-8. Means (SD) for Response Bias
Target Angle Controls CLBP
-100 1.10 (12.8) -1.90 (11.5)
220 0.90 (28.5) 9.60 (30.1)
450 7.8- (24.6) 0.10 (25.8)


Cohen's d was calculated for response accuracy and

response bias (see Table 8-9) to determine effect size. The resulting effect size is so small that it is very likely to






62


be meaningless even with a larger sample with more adequate power.


Table 8-9. Cohen's d
Response Measure Cohen's dAccuracy -100 .08
Accuracy 220 .06
Accuracy 450 .06
Bias -100 .25
Bias 220 .30
Bias 450 .31


Integrated EMG data was averaged across baseline and each phase of the experiment. The mean ENG values for the anticipatory and recovery phases were then averaged across the 5 trials resulting in mean EMG values for these two

phases for each of the 3 body positions (-100, 220, 450). Group differences in anticipatory and recovery mean EMG for the 3 body position tasks were assessed by repeated measures MANCOVA using baseline EMG as the covariate. Results indicated a 3-way interaction between angle, group and the covariate for both anticipatory [F(2,57)=7.58, p=0.001] (Figure 8-6) and recovery [F92,57)=9.02, p=0.0004] ENG (Figure 8-7). As Figures 8-6 and 8-7 illustrate, there is a similarity in pattern of EMG levels by group relative to baseline ENG for angles -100 and 220 but a shift in EMG patterns between groups relative to baseline EMG at angle

450.

For the anticipatory phase at angles -100 and 220, at

higher baseline EMG levels, the CLBP group had higher levels






63


of anticipatory EMG than controls with the more pronounced

differences occurring at angle 220. At angle 450, CLBP subjects had higher anticipatory EMG values than controls at low baseline ENG levels whereas at higher baseline ENG levels, controls had higher anticipatory EMG levels than CLBP subjects. As the means in Table 8-10 demonstrate, the actual differences between groups in anticipatory ENG are very small for a clinical perspective. Table 8-10. Anticipatory EMG Means (SD) Baseline & Trials
Group Baseline -100 220 450

CLBP 6.96 (4.3) 7.64 (5.6) 8.08 (5.9) 7.76 (5.1)

Controls 5.86 (3.6) 5.78 (3.8) 5.81 (3.9) '6.34 (4.9)


For the recovery phase at angle -100, the two

regression lines are almost identical with higher levels of recovery EMG at higher levels of baseline EMG. At angle 220, the two regression lines are parallel with the CLBP group demonstrating higher recovery EMG levels than controls at higher levels of baseline EMG. At angle 450, the pattern demonstrated for anticipatory EMG is repeated: at low baseline EMG levels CLBP subjects had higher recovery EMG levels than controls, but at higher levels of baseline ENG controls had higher recovery EMG levels than CLBP subjects. As with anticipatory ENG, the actual differences between groups in recovery EMG are very small from a clinical perspective (see Table 8-11).





64


Table 8-11. Recovery EMG Means (SD) Baseline & Trials
Group Baseline -100 220 450

CLBP 6.96 (4.3) 8.77 (5.0) 8.97 (5.3) 9.02 (5.1)

Controls 5.86 (3.6) 7.33 (4.3) 6.92 (4.3) 7.37 (5.0)


Since CLBP subjects and controls differed significantly on BMI [t(50.2)=-3.25, p=-0.002; Means: CLBP=28.35 (5.6); controls=24.39 (3.7)], EMG changes from baseline for the anticipatory and recovery phases for the three target angles were examined by repeated measures MANCOVA's using BMI as a covariate to assess the influence of BMI on EMG recordings. Results of these MANCOVA's showed no significant effect on EMG change from baseline for either anticipatory or recovery EMG (Tables 8-12 and 8-13). Only if EMG is collapsed across all three angles does level of BMI marginally affect level of anticipatory (p=0.06) and recovery (p=0.6) EMG change from baseline by group (Figures 8-8 and 8-9). These results suggest the possibility of a slight muting effect on EMG recordings with higher levels of BMI.


Table 8-12. Mean (SD) Anticipatory EMG Change from Baseline
Group -100 220 450
CLBP 0.71 (3.2) 1.14 (2.8) 0.83 (1.6)
Controls -0.08 (1.7) -0.06 (1.3) 0.48 (2.2)


Table 8-13. Mean (SD) Recovery EMG Change from Baseline
Group -100 220 450
CLBP 1.87 (2.1) 2.04 (2.0) 2.11 (1.8)
Controls 1.47 (1.9) 1.06 (1.4) 1.51 (2.0)










U)
C1 -CONTROLS
SCLBP





kn
w
0
(1) o









BDI STATE STATE
ANGER ANXIETY


Figure 8-1. NEGATIVE AFFECT: CLBP vs CONTROLS
(Group Means with Standard Error Bars)









CONTROLS
O -- CLBP






S(0









I I I

10 22 45

ANGLE (degrees)


Figure 8-2. PIN: CLBP vs CONTROLS (Group Medians with Inter-quartile Ranges)











CONTROLS
O CLBP

00


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I I I

10 22 45

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Figure 8-3. PUN: CLBP vs CONTROLS (Group Medians with Inter-quartile Ranges)











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Figure 8-4. RESPONSE ACCURACY: CLBP vs CONTROLS

(Group Means with Standard Error Bars)








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11 CONTROLS CLBP



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Figure8-5. RESPONSE BIAS: CLBP vs CONTROLS
(Group Means with Standard Error Bars)
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ANGLE = 10 DEGREES ANGLE = 22 DEGREES ANGLE = 45 DEGREES

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Figure 8-6. MEAN ANTICIPATORY EMG INTERACTION WITH COVARIATE
0II QIL) X
IL I 0 0
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BASELINE EMVG BASELINE EMVG BASELINE EMG







Figure 8-6. MEAN ANTICIPATORY EMG INTERACTION WITH COVARIATE




















ANGLE = 10 DEGREES ANGLE =22 DEGREES ANGLE =45 DEGREES


-0. ctBw 0 0 00,, 0 .00

0 o
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BASELINE EMVG BASELINE EMVG BASELINE EMG G







Figure 8-7. MEAN RECOVERY EMG INTERACTION WITH COVARIATE









O
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SCLBP
w
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10 22 45

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Figure 8-8. BMI-ADJUSTED CHANGE IN ANTICIPATORY EMG RELATIVE TO BASELINE: CLBP vs CONTROLS (Group Means with Standard Error Bars)









0
cti CONTROLS
CLBP
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10 22 45

ANGLE (degrees) Figure 8-9. BMI-ADJUSTED CHANGE IN RECOVERY EMG RELATIVE TO BASELINE: CLBP vs CONTROLS (Group Means with Standard Error Bars)













Chapter 9
DISCUSSION



The purpose of this study was to explore the hypothesis that the experience of chronic pain is influenced by a dysfunction in a central process that may also result in increases in negative affect, physiological reactivity, and perceptual deficits. Specifically, the current study explored group differences between CLBP patients and healthy, pain-free controls with the following hypotheses: CLBP subjects were expected to exhibit greater levels of

negative affect than controls.

" CLBP subjects were expected to demonstrate higher VAS

ratings of pain intensity and unpleasantness than

controls.

" CLBP subjects were expected to be poorer discriminators

of body position (less accurate) and to differ on

response bias as compared to controls.

" CLBP subjects were expected to demonstrate higher

anticipatory and recovery EMG than controls. Negative Affect

As predicted, negative affect was greater for the CLBP subjects on all three measures as compared to controls. This is consistent with the results of previous studies


74





75


examining depression, anxiety, and anger in chronic pain patients. Also, the relationship between these variables differed by group. Both these findings are consistent with the proposed model of dysfunction of a central process in the experience of chronic pain. Although the statistically significant correlations of the negative affect measures with the MPQ Sensory scale, PPR, and PPI do not allow for discernment of causality and account for only a small amount of the variance in the measures, this data are congruent with the proposed model of a central process dysfunction in chronic pain in that it suggests a relationship between affect and sensory discrimination in pain perception. Pain Ratings

As predicted, CLBP subjects had higher ratings of both pain intensity and pain unpleasantness than controls. CLBP subjects rated the two most difficult angles for them to

achieve, -10' and 450, as being higher on measures of both pain intensity and unpleasantness. Body Position Discrimination

Contrary to what was hypothesized, there were no

differences between CLBP subjects and controls on response accuracy. All subjects were the most accurate at angle

-100, probably due to limited range of motion at this angle. All subjects were the least accurate at angle 220, being on the average, five degrees off target per trial. At angle





76


450, all subjects were, on the average, four degrees off target per trial.

Regarding response bias, the hypothesis was partially supported in that the pattern of response bias across the angles differed between the two groups. CLBP subjects demonstrated the smallest response bias at angles -100 and

450, undershooting -100 but showing almost no response bias at angle 45'. At angle 220, CLBP subjects overshot the target. In contrast, controls showed very little response

bias at angles -100 and 220 but overshot target angle 45*. Undershooting angle -100 by the pain subjects was probably due to limited range of motion and, based upon CLBP subjects' PIN and PUN ratings, increased pain. CLBP subjects' low response bias at angle 450 may be related again to increased pain whereas controls, without pain as a cue, tended to overshoot the target angle. The possibility that this type of discrimination error in pain-free individuals could be related to the acquisition of injuries that result in CLBP requires further investigation.

Several factors could account for the lack of

differences in response accuracy between groups. one source of measurement error is that the ELT belt would shift as some subjects were bending affecting accuracy of readings. Another factor is that for reasons of ecological validity, no standardized bending instructions were given. Thus, some





77

subjects bent from the waist while others bent from their hips. These factors likely contributed to the high amount of variability in both groups on both proprioceptive measures. The use of proprioceptive equipment that is more stable during the bending task as well as standardized control of the bending process through instruction or equipment that stabilizes body position in one plane and controls the range of motion from the lumbar region would help clarify these issues. Another consideration is the use of only one device to measure proprioceptive function in just one plane. As the study by Parkhurst and Burnett (1994) indicates, the measurement of multiple proprioceptive abilities in several planes may better delineate the issue of these abilities in both pain-free controls and CLBP patients. This area warrants further investigation as newer equipment is developed to better assess trunk proprioception. EMG Differences

The hypothesis regarding EMG reactivity was partially supported by the data. Although the differences were, from a clinical perspective, very small, the patterns of EMG are interesting from a theoretical perspective since the results partially support both the pain-spasm-pain model as well as the biomechanical model of muscle activity in chronic pain patients. The higher levels of anticipatory EMG for CLBP subjects at angles -100 and 220 and of recovery EMG for CLBP subjects at angle 220 at higher levels of baseline EMG are





78


consistent with the pain-spasm-pain model. But the lower anticipatory and recovery EMG levels at higher levels of baseline EMG in CLBP subjects at angle 450 is predicted by the biomechanical model.

Peters and Schmidt (1991) discussed several studies

that suggested the generalized participation of uninvolved muscle groups in CLBP patients. The lower levels of recovery EMG (at higher levels of baseline EMG) at 450 in CLBP subjects as compared to controls in this study could be related to the recruitment of what are usually uninvolved muscles during the task for the pain subjects. Although only one EMG site was recorded, the use of multiple EMG site recording or the recording of left and right muscle groups should be used in the future to clarify this issue.

It has been suggested by some authors (Cassisi,

Robinson, O'Conner, MacMillan, 1993; Peters & Schmidt, 1991) that CLBP patients may use their muscles differently than pain-free individuals and that differing patterns of EMG may be more indicative of the biomechanical model. Based upon this reasoning, the pattern of the EMG data of the CLBP subjects relative to the controls in this study is more in line with the biomechanical model of CLBP. Indeed, the data do not demonstrate increased psychophysiological reactivity (as measured by EMG) in the CLBP subjects. This supports the assessment of Flor, Birbaumer, Schugens, and Lutzenberger (1992)that psychophysiological studies of pain should include at least one other psychophysiological





79


measure (besides EMG) in order to assess the generality versus specificity of the observed responses.

From another perspective, one possible reason for the

small group differences in ENG was that the bending task was not adequately arousing for the CLBP subjects. Attaining VAS pain ratings post-baseline in the future could help assess the power of the experimental manipulation. Paradoxically, the verbal warning given at the beginning of the anticipatory phase may have actually reduced the stressfulness of the task, instead of increasing anxiety, due to predictability (Levethal, Brown, Shacham & Engquist, 1979). Arntz, van den H-out, van den Berg, and Meijboom (1991) found that predictability reduced fear and physiological responses. In a more recent study, Crombez, Baeyens, and Eelen (1994) also found that temporal information about impending experimental pain stimuli resulted in lower physiological responsivity to the stimuli. The authors discussed how their findings fit with Seligman's (1968) safety signal hypothesis in that subjects not only could predict when the pain stimulus would occur but also when it would not. Lack of predictability of pain in the everyday life of some patients with chronic pain may contribute to increased levels of physiological reactivity in these patients. This highlights the need for studies using more naturalistic ENG monitoring.

Another possible explanation for the small group

differences in EMG in this study is the suggestion made by





so


several authors (Arena, Sherman, Bruno, & Young, 1989; Flor, Birbaumer et al., 1992; Geisser, Robinson, & Richardson, 1995) that chronic pain patients may be heterogeneous in terms of the development and maintenance of their pain and that different types of CLBP patients may have different patterns of EMG activity in different postures/tasks. Flor, Birbaumer et al. (1992) indicated that there is increasing evidence that the tendency to overrespond in patients' relevant muscles may produce and maintain chronic pain in some patients, whereas in others with low muscle reactivity, the development and maintenance of chronic pain syndromes may be related to factors other than psychophysiological ones, such as operant conditioning. Although the pain subjects from the two sites in this study were different relative to pain diagnoses, they did not differ significantly on EMG reactivity. This suggests the need for more exploration of the factors which may differentiate pain patients on this issue.

Finally, some researchers view surface measurement of EMG as a gross measure of muscle activity (Biedermann cited in Peters & Schmidt, 1991) while others (Wolf, Wolf, & Segal, 1989) caution clinicians against assuming that low levels of integrated surface lumbar EMG recordings provide assurance of lack of activity of deeper muscles. or the relationship between psychophysiological reactivity and muscular pain may be mediated by activity other than ENG.





81


Conclusion

This study provides partial support for the hypotheses generated regarding the components of a proposed central process that mediates the experience of chronic pain as follows: higher levels of negative affect (cognitiveaffective component) and pain ratings in CLBP subjects over controls, differences in patterns of response bias across tasks between groups (sensory-discriminatory component), and different patterns of EMG between groups over the three tasks (physiological reactivity).

Lack of group differences in proprioceptive accuracy could exist because there is no difference between the groups on this measure. If this is the case and taking into account the different patterns of response bias between CLBP subjects and controls, the implications for back injury prevention programs is that proprioceptive awareness may need to be taught in small increments to those without back pain as well as to those who already have back pain. It seems plausible that those with CLBP use pain as one of their cues, whereas those without back pain do not have this cue until they injure themselves due to a tendency to overshoot forward flexion. But, as this is only the second study to examine trunk proprioception, and the development of other trunk proprioception equipment is needed, this issue warrants further exploration before any conclusions can be drawn with certainty.






82


Future studies investigating the cognitive-affective, sensory-discriminatory, and physiological reactivity components of chronic pain could benefit from the following experimental considerations: making use of more stable proprioceptive equipment; assessing multiple proprioceptive measures; use of standardized bending instructions; use of more stressful ecologically valid tasks (considering the issue of lack of predictability of stimulus, e.g., no "safe" zone); assessing both general and specific measures of psychophysiological reactivity; assessment of pain ratings post-baseline; and attending more to diagnostic groups, investigating the EMG patterns of CLBP subgroups as well as patterns of discriminatory function. Also, the use of path analyses (with larger samples) could help delineate the relationship of the hypothesized components of the central process to each other as researchers attempt to unravel the complex and dynamic process that is the experience of pain.















APPENDIX
CORRELATION ANALYSES


Abbreviation Key

ACC10 = Response Accuracy -10* BDI = Beck Depression Inventory
ACC22 = Response Accuracy 220 BMI = Body Mass Index
ACC45 = Response Accuracy 450 BLEMGAV = Average Baseline EMG

DMEMGAI0=Mean EMG Difference from Baseline for Anticipatory Phase -100 DMEMGA22=Mean EMG Difference from Baseline for Anticipatory Phase 220 DMEMGA45=Mean EMG Difference from Baseline for Anticipatory Phase 450

DMEMGRl0=Mean EMG Difference from Baseline for Recovery Phase Angle -100 DMEMGR22=Mean EMG Difference from Baseline for Recovery Phase Angle 220 DMEMGR45=Mean EMG Difference from Baseline for Recovery Phase Angle 450

MEMGA10 = Mean EMG for Anticipatory Phase Angle -100 MEMGA22 = Mean EMG for Anticipatory Phase Angle 220 MEMGA45 = Mean EMG for Anticipatory Phase Angle 450

MEMGR10 = Mean EMG for Recovery Phase Angle -100 MEMGR22 = Mean EMG for Recovery Phase Angle 220 MEMGR45 = Mean EMG for Recovery Phase Angle 450

MPIN10 = Mean Pain Intensity VAS Rating Angle -100 MPIN22 = Mean Pain Intensity VAS Rating Angle 220 MPIN45 = Mean Pain Intensity VAS Rating Angle 450

MPUN10 = Mean Pain Unpleasantness VAS Rating Angle -10 MPUN22 = Mean Pain Unpleasantness VAS Rating Angle 22 MPUN45 = Mean Pain Unpleasantness VAS Rating Angle 450

RB10 = Response Bias Angle -100 STANGER = State Anger
RB22 = Response Bias Angle 220 STANX = State Anxiety
RB45 = Response Bias Angle 450





















83






84


Control Subiects
Correlation Analysis with Demographic Variables Pearson Correlation Coefficients Prob > JR1 under Ho: Rho=0 Number of Observations

AGE
RB45 ACC45 BMI BDI RB22
0.39642 0.32222 -0.20029 0.18986 0.18907
0.0273 0.0771 0.2800 0.3063 0.3084
31 31 31 31 31

HE IGHT
BMI MEMGA45 BLEMGAV REMGR45 MEMGA10
0.38443 0.37354 0.35044 0.34979 0.33487
0.0327 0.0385 0.0533 0.0537 0.0656
31 31 31 31 31

MEMGR22 MEMGA22 MEMGR10
0.33213 0.31593 0.30267
0.0679 0.0834 0.0979
31 31 31

WEIGHT
BMI MEMGA22 MEMGA45 MEMGA10 MEMGR22
0.87074 0.39152 0.38735 0.36295 0.35995
0.0001 0.0294 0.0313 0.0448 0.0467
31 31 31 31 31

BLEMGAV MEMGR45 DMEMGA45
0.33615 0.32085 0.30929
0.0645 0.0784 0.0904
31 31 31

EDUCATION
ACC10 ACC22 RB1O DMEMGR1O
-0.33146 -0.31378 -0.29975 -0.29335
0.0685 0.0856 0.1092 0.1092
31 31 31 31






85


CLBP Sub-jects
Correlation Analysis with Demographic Variables Pearson Correlation Coefficients Prob > JR1 under Ho: Rho=0 Number of Observations

AGE
RB45 BMI MEMGA45 BLEMGAV BDI
-0.54440 0.29755 0.29437 0.28872 -0.28541
0.0015 0.1103 0.1079 0.1152 0.1196
31 30 31 31 31

HEIGHT
MEMGR45 MEMGR22 MEMGR10 BLEMGAV MEMGA45
0.46930 0.44650 0.41286 0.41017 0.40579
0.0089 0.0134 0.0234 0.0244 0.0261
30 30 30 30 30

MEMGA22 DMEMGR45 BDI DMEMGR22
0.39994 0.34412 0.31658 0.30298
0.0285 0.0626 0.0903 0.1036
30 30 30 30

WEIGHT
BMI DMEMGA10 MPIN1O RB10 MPUN10
0.88521 -0.34059 -0.32829 -0.25416 -0.24180
0.0001 0.0655 0.0765 0.1753 0.1980
30 30 30 30 30

YEARS EDUCATION
BDI MEMGA10 BLEMGAV MEMGR10 MEMGA45
-0.33167 0.29801 0.29040 0.28716 0.25712
0.0734 0.1097 0.1195 0.1239 0.1702
30 30 30 30 30

TOTAL SURGERIES
BDI RB45 ACC10 RB10 RB22
0.36018 0.34575 0.26567 -0.23825 0.15538
0.0466 0.0568 0.1486 0.1968 0.4039
31 31 31 31 31

PAIN DIAGNOSES
STANX BDI RB10 ACC22 STANGER
-0.53119 -0.45486 -0.41549 0.33630 -0.30855
0.0110 0.0334 0.0545 0.1259 0.1624
22 22 22 22 22

PAIN DURATION
STANX BDI MEMOAlO STANGER DMEMGA10
-0.44216 -0.32638 0.30623 -0.28686 0.24424
0.0128 0.0731 0.0938 0.1177 0.1855
31 31 31 31 31

PAIN FREQUENCY
MPUN1O MPUN45 MPIN10 MPUN22 MPIN45
-0.48518 -0.46533 -0.46196 -0.40067 -0.37680
0.0057 0.0083 0.0089 0.0255 0.0367
31 31 31 31 31

MPIN22 STANX
-0.35823 -0.30417
0.0478 0.0962
31 31






86


CLBP Subiects
Correlation Analysis with Demographic Variables (Continued) Pearson Correlation coefficients Prob > IR1 under Ho: Rho=0 Number of Observations

AVERAGE PAIN
MPIN45 MPIN10 MPUN10 MPUN45 M4PIN22
0.45589 0.44451 0.40560 0.38952 0.38368
0.0100 0.0122 0.0236 0.0303 0.0331
31 31 31 31 31

MPUN22 BDI DMEMGA10 BMI MEMGA1O
0.35559 0.35284 0.32037 -0.30980 0.27446
0.0496 0.0515 0.0789 0.0957 0.1351
31 31 31 31 31

PRESENT PAIN
MPIN10 MPUN10 MPIN45 DMEMGA10 MPUN45
0.55931 0.50395 0.45883 0.44863 0.44622
0.0011 0.0038 0.0094 0.0114 0.0119
31 31 31 31 31

MPUN22 MPIN22 MEMGA10 RB10 DMEMGR10
0.40279 0.39717 0.34188 0.29131 0.29029
0.0247 0.0269 0.0598 0.1118 0.1132
31 31 31 31 31

ADDITIONAL PAIN
DMEMGA10 RB45 ACC10 DMEMGR10 RB22
0.43254 0.39419 0.38066 0.36714 0.36208
0.0151 0.0282 0.0346 0.0422 0.0453
31 31 31 31 31

ACC22
0. 29931
0.1019
31






87


Control Sublects
Experimental Variables
Pearson Cyrrelation Coefficients/ Prob > RI under Ho: Rho=0/N =31

BDI
BDI DMEMGR10 STANGER DMEMGR45 MPUN22 MPIN10
1.00000 0.31518 0.31264 0.30452 -0.23511 -0.23339
0.0 0.0842 0.0868 0.0958 0.2029 0.2064

STANGER
STANGER ACC22 BDI ACC10 RB22 RB45
1.00000 0.36109 0.31264 -0.22508 0.19973 0.18236
0.0 0.0460 0.0868 0.2235 0.2814 0.3262

STANX
STANX MPIN10 MPIN45 MPUN45 ACC22 M4PUN10
1.00000 -0.35701 -0.33185 -0.31445 -0.28679 -0.26248
0.0 0.0487 0.0682 0.0849 0.1178 0.1537
MP IN 10
MPIN1O MPUN1O MPIN45 MPUN45 MPUN22 MPIN22
1.00000 0.70072 0.65525 0.64237 0.57776 0.56042
0.0 0.0001 0.0001 0.0001 0.0007 0.0010

ACC45 STANX BDI DMEMGA22 DMEMGR22 ACC1O
0.44373 -0.35701 -0.23339 -0.19666 -0.19153 -0.18394
0.0124 0.0487 0.2064 0.2890 0.3020 0.3219

MPIN22
MPIN22 MPUN22 MPUN45 MPIN45 MPUN10 MPIN10
1.00000 0.95920 0.89803 0.85960 0.73625 0.56042
0.0 0.0001 0.0001 0.0001 0.0001 0.0010

DMEMGR22 DMEMGA22 ACC45 DMEMGR10 DMEMGR45 ME14GA22
-0.41601 -0.37594 0.36309 -0.32432 -0.28287 -0.26705
0.0199 0.0371 0.0447 0.0751 0.1231 0.1464

MPIN45
MPIN45 MPUN45 MPIN22 M4PUN22 MPUN1O MPIN10
1.00000 0.94822 0.85960 0.85842 0.73267 0.65525
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

DMEMGR22 DMEMGA22 STANX ACC45 DMEMGR10 DMEMGR45
-0.37403 -0.35342 -0.33185 0.31990 -0.31449 -0.29518
0.0382 0.0511 0.0682 0.0794 0.0849 0.1069

MPUN10
MPUN10 MPUN45 MPUN22 MPIN22 MPIN45 MPIN10
1.00000 0.85314 0.76564 0.73625 0.73267 0.70072
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

ACC45 DMEMGA22 STANX DMEMGR22 ACC10 EMI
0.69639 -0.26985 -0.26248 -0.20401 -0.17939 0.17303
0.0001 0.1421 0.1537 0.2710 0.3342 0.3519

MPUN22
MPUN22 MPIN22 MPUN45 MPIN45 MPUN10 MPIN10
1.00000 0.95920 0.90994 0.85842 0.76564 0.57776
0.0 0.0001 0.0001 0.0001 0.0001 0.0007

ACC45 DMEMGR22 DMEMGA22 DMEMGR45 DMEMGR1O STANX
0.40699 -0.38117 0.36613 -0.27831 -0.27265 -0.25188
0.0231 0.0344 0.0428 0.1295 0.1378 0.1716







88


Control Subjects
Experimental Variables (Continued) Pearson Cprrelation Coefficients/
Prob > IRI under Ho: Rho=0/N = 31

MPUN45
MPUN45 MPIN45 MPUN22 MPIN22 MPUN10 MPIN10
1.00000 0.94822 0.90994 0.89803 0.85314 0.64237
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

ACC45 DMEMGR22 DMEMGA22 STANX DMEMGR10 DMEMGR45
0.43884 -0.39056 -0.38703 -0.31445 -0.30001 -0.27301
0.0135 0.0298 0.0315 0.0849 0.1011 0.1373

BMI
BMI DMEMGA22 MEMGA22 MEMGR22 MEMGA45 DMZMGR22
1.00000 0.35896 0.32793 0.27058 0.26839 0.26656
0.0 0.0474 0.0717 0.1410 0.1443 0.1472

BLEMGAV
BLEMGAV MEMGR22 MEMGR45 MEMGA22 MEMGA45 MEMGR10
1.00000 0.95264 0.94459 0.93910 0.90688 0.90233
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

MEMGA1O DMEMGR45 DMEMGA45 DMEMGR22 RB1O EMI
0.89876 0.56740 0.38177 0.37703 0.24155 0.22086
0.0001 0.0009 0.0341 0.0365 0.1905 0.2325

MEMGA10
MEMGA1O MEMGA45 MEI4GR1O M4EMGA22 MEMGR22 MEMGR45
1.00000 0.96246 0.94203 0.93768 0.92993 0.92112
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

BLEMGAV D14EMGR45 DMEMGA45 DMEMGR22 DMEMGR10 DMEMGA10 0.89876 0.69098 0.66641 0.56343 0.44454 0.33515
0.0001 0.0001 0.0001 0.0010 0.0122 0.0653

MEMGR10
MEMGR10 MEMGR45 MEMGA10 MEMGR22 MEMGA45 MEMGA22
1.00000 0.94938 0.94203 0.92440 0.92049 0.91087
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

BLEMGAV DMEMGR45 DMEMGR10 DMEMGA45 DMEMGR22 MPIN22
0.90233 0.75543 0.57049 0.56862 0.53757 -0.26545
0.0001 0.0001 0.0008 0.0008 0.0018 0.1489

MEMGA22
MEMGA22 MEMGR22 MEMGR45 MEMGA45 BLEMGAV HEMGA10
1.00000 0.98124 0.95738 0.95712 0.93910 0.93768
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

MEMGR10 DMEMGR45 DMEMGR22 DMEMGA45 DMEMGA22 BMI
0.91087 0.70925 0.61789 0.58986 0.37956 0.32793
0.0001 0.0001 0.0002 0.0005 0.0352 0.0717

MEMGR2 2
MEMGR22 MEMGA22 MEMGR45 MEMGA45 BLEMGAV MEMGA10
1.00000 0.98124 0.98030 0.95814 0.95264 0.92993
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

MEMGR1O DMEMGR45 DMEMGR22 DMEMGA45 DMEMGR10 DMEMGA22 0.92440 0.74234 0.64083 0.57032 0.30151 0.28857
0.0001 0.0001 0.0001 0.0008 0.0993 0.1154







89


Control Sublects
Experimental Variables (Continued) Pearson Cgrrelation Coefficients/
Prob > IRI under Ho: Rho=O/N =31

MEMGA45S
MEMGA45 1MEMGA10 MEMGR45 MEMGR22 MEMGA22 MEMGR10
1.00000 0.96246 0.96170 0.95814 0.95712 0.92049
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

BLEMGAV DMEMGR45 DMEMGA45 DMEMGR22 DMEMGR10 DMEMGA22 0.90688 0.77812 0.73569 0.62883 0.37975 0.34161
0.0001 0.0001 0.0001 0.0002 0.0351 0.0600

MEMGR4 5
MEMGR45 MEMGR22 MEMGA45 MEMGA22 MEMGR10 BLEMGAV
1.00000 0.98030 0.96170 0.95738 0.94938 0.94459
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

MEMGA10 DMEMGR45 DMEMGR22 DMEMGA45 DMEMGR10 ACC10
0.92112 0.80625 0.60117 0.59107 0.37405 -0.24434
0.0001 0.0001 0.0003 0.0005 0.0382 0.1853

DMEMGA1 0
DMEMGA1O DMEMGA45 DMEMGR1O DMEMGA22 DHEMGR22 RB45
1.00000 0.69001 0.66214 0.61290 0.46682 0.42620
0.0 0.0001 0.0001 0.0002 0.0081 0.0168

ACC45 DMEMGR45 MEMGA10 MEMGA45 RB10 MPIN22
0.40605 0.34682 0.33515 0.23261 -0.21990 -0.20113
0.0234 0.0559 0.0653 0.2079 0.2346 0.2779

DMEMGR1 0
DMEMGR1O D1MEMGA10 DMEMGR45 DMEMGA45 MEMGR10 DMEMGR22
1.00000 0.66214 0.64866 0.57458 0.57049 0.51253
0.0 0.0001 0.0001 0.0007 0.0008 0.0032

MEMGA10 DMEMGA22 MEMGA45 MEMGR45 MPIN22 BDI
0.44454 0.42896 0.37975 0.37405 -0.32432 0.31518
0.0122 0.0160 0.0351 0.0382 0.0751 0.0842

DMEMGA2 2
DMEMGA22 DMEMGR22 DMEMGA45 DMEMGA10 DMEMGR45 DMEMGR10
1.00000 0.78166 0.68738 0.61290 0.53480 0.42896
0.0 0.0001 0.0001 0.0002 0.0019 0.0160

MPUN45 MEMGA22 MPIN22 MPUN22 BMI M4PIN45
-0.38703 0.37956 -0.37594 -0.36613 0.35896 -0.35342
0.0315 0.0352 0.0371 0.0428 0.0474 0.0511

DMEMGR2 2
DMEMGR22 DMEMGR45 DMEMGA22 DMEMGA45 MEMGR22 MEMGA45
1.00000 0.82860 0.78166 0.77325 0.64083 0.62883
0.0 0.0001 0.0001 0.0001 0.0001 0.0002

MEMGA22 MEMGR45 MEMGA10 MEMGR10 DMEMGR10 DMEMGA10
0.61789 0.60117 0.56343 0.53757 0.51253 0.46682
0.0002 0.0003 0.0010 0.0018 0.0032 0.0081

MPIN22 MPUN45 MPUN22 BLEMGAV RB45 MPIN45
-0.41601 -0.39056 -0.38117 0.37703 0.37577 -0.37403
0.0199 0.0298 0.0344 0.0365 0.0372 0.0382

ACC10 BMI RB22 MPUN10 MPIN10 RB1O
-0.37299 0.26656 -0.21809 -0.20401 -0.19153 -0.18643
0.0388 0.1472 0.2385 0.2710 0.3020 0.3153






90


Control Subiects
Experimental Variables (Continued) Pearson Cyrrelation Coefficients/ Prob > IRI under Ho: Rho=0/N = 31

DMEMGA4 5
DMEMGA45 DMEMGR45 DMEMGR22 MEMGA45 DMEMGA10 D14EMGA22
1.00000 0.79471 0.77325 0.73569 0.69001 0.68738
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

MEMGA10 MEMGR 45MEMGA 22DMEMGR10 MEMGR22 MEMGR10
0.66641 0.59107 0.58986 0.57458 0.57032 0.56862
0.0001 0.0005 0.0005 0.0007 0.0008 0.0008

RB45 ACC45 BLEMGAV MPIN45 ACCIO MPIN22
0.40703 0.38526 0.38177 -0.26636 -0.25809 -0.24937
0.0231 0.0323 0.0341 0.1475 0.1610 0.1761

DMEMGR45
DMEMGR45 DMEMGR22 MEMGR45 DMEMGA45 MEMGA45 MEMGR1O
1.00000 0.82860 0.80625 0.79471 0.77812 0.75543
0.0 0.0001 0.0001 0.0001 0.0001 0.0001

MEMGR22 MEMGA22M EMGA10 DMEMGR10 BLEMGAV DMEMGA22
0.74234 0.70925 0.69098 0.64866 0.56740 0.53480
0.0001 0.0001 0.0001 0.0001 0.0009 0.0019

ACC10
ACC10 ACC22 DMEMGR22 DMEMGR45 MEMGR22 DMEMGA45
1.00000 0.38130 -0.37299 -0.30580 -0.26372 -0.25809
0.0 0.0343 0.0388 0.0943 0.1517 0.1610

ACC22
ACC22 RB22 ACC10 STANGER RB45 STANX
1.00000 0.47097 0.38130 0.36109 0.30610 -0.28679
0.0 0.0075 0.0343 0.0460 0.0940 0.1178

ACC45
ACC45 MPUN10 RB45 MPIN10 MPUN45 MPUN22
1.00000 0.69639 0.56802 0.44373 0.43884 0.40699
0.0 0.0001 0.0009 0.0124 0.0135 0.0231

DMEMGA10 RB22 DMEMGA45 MPIN22 MPIN45 ACC22
0.40605 0.39601 0.38526 0.36309 0.31990 0.24240
0.0234 0.0274 0.0323 0.0447 0.0794 0.1889

RB1 0
RB10 RB22 BLEMGAV DMEMGA10 REMGR45 MEMGR10
1.00000 0.58717 0.24155 -0.21990 0.21013 0.20555
0.0 0.0005 0.1905 0.2346 0.2566 0.2673

RB2 2
RB22 RB10 RB45 ACC22 ACC45 DMEMGR22
1.00000 0.58717 0.48670 0.47097 0.39601 -0.21809
0.0 0.0005 0.0055 0.0075 0.0274 0.2385

RB4 5
RB45 ACC45 RB22 DMEMGA1O DMEMGA45 DMEMGR22
1.00000 0.56802 0.48670 0.42620 0.40703 0.37577
0.0 0.0009 0.0055 0.0168 0.0231 0.0372

DMEMGA22 ACC22 DMEMGR10 DMEMGR45 MPIN45 MEMGA10
0.31146 0.30610 0.24521 0.22662 -0.20039 0.19898
0.0881 0.0940 0.1837 0.2202 0.2798 0.2832






91


CLBP Sublects
Experimental Variables
Pearson Correlation Coefficients/ Prob > IRI under Ho: Rho=0
/Number of Observations

BDI
BDI STANX STANGER MPUN10 RB45 DMEMGA22
1.00000 0.58953 0.43438 0.28343 0.26941 0.26249
0.0 0.0005 0.0146 0.1223 0.1427 0.1537
31 31 31 31 31 31

STANGER
STANGER STANX BDI BLEMGAV ACC22 MPUN45
1.00000 0.64751 0.43438 -0.26580 -0.26288 0.26145
0.0 0.0001 0.0146 0.1484 0.1531 0.1554
31 31 31 31 31 31

STANX
STANX STANGER BDI ACC22 BLEMGAV HEMGA45
1.00000 0.64751 0.58953 -0.37813 -0.32937 -0.26851
0.0 0.0001 0.0005 0.0360 0.0704 0.1441
31 31 31 31 31 31

MP IN10
MPIN1O MPUN10 MPIN22 MPUN22 MPIN45 MPUN45
1.00000 0.90515 0.80858 0.78983 0.74335 0.71524
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

BMI DMEMGR10 DMEMGA10 MEMGA10 MEMGR10 DMEMGR45
-0.42298 0.37565 0.30765 0.29873 0.29075 0.26695
0.0199 0.0373 0.0923 0.1026 0.1126 0.1466
30 31 31 31 31 31

MPIN2 2
MPIN22 MPUN22 M4PIN45 MPUN45 MPIN10 MPUN10
1.00000 0.95171 0.86049 0.82849 0.80858 0.66687
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

DMEMGR1O REMGR10 MEMGA10 MEMGR45 MEMGR22 MEMGA45
0.36730 0.36138 0.29210 0.27647 0.25845 0.24666
0.0421 0.0458 0.1108 0.1322 0.1604 0.1810
31 31 31 31 31 31
MPIN45
MPIN45 MPUN45 MPIN22 MPUN22 MPIN10 MPUN10
1.00000 0.94281 0.86049 0.84410 0.74335 0.62616
0.0 0.0001 0.0001 0.0001 0.0001 0.0002
31 31 31 31 31 31
DMEMGR10 MEMGR10 M4EMGA10 MEM4GR45 MEMGR22 MEMGA45
0.39448 0.39140 0.36160 0.30013 0.29652 0.28762
0.0281 0.0295 0.0456 0.1009 0.1053 0.1167
31 31 31 31 31 31
MPUN10
MPUN1O MPIN10 MPUN22 MPUN45 MPIN22 MPIN45
1.00000 0.90515 0.75474 0.71202 0.66687 0.62616
0.0 0.0001 0.0001 0.0001 0.0001 0.0002
31 31 31 31 31 31

BMI RB45 DMEMGR10 BDI DMEMGA10 STANGER
-0.36158 0.30397 0.29068 0.28343 0.25583 0.23462
0.0496 0.0964 0.1127 0.1223 0.1648 0.2039
30 31 31 31 31 31







92


CLBP Subjects
Experimental Variables (Continued) Pearson Correlation Coefficients/ Prob > jRI under Ho: Rho=O
/Number of Observations

MPUN22
MPUN22 MPIN22 MPUN45 MPIN45 MPIN10 MPUN10
1.00000 0.95171 0.87378 0.84410 0.78983 0.75474
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

DMEMGR1O MEMGR10 MEMGA10 MEMGR45 BLEMGAV MEMGR22
0.41397 0.39972 0.32868 0.29269 0.26691 0.25362
0.0206 0.0259 0.0710 0.1101 0.1466 0.1686
31 31 31 31 31 31

MPUN45
MPUN45 MPIN45 MPUN22 MPIN22 MPIN10 M4PUN10
1.00000 0.94281 0.87378 0.82849 0.71524 0.71202
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

DMEMGR10 MEMGR10 REMGA10 STANGER BDI MEMGR45
0.35436 0.30873 0.27011 0.26145 0.24455 0.22157
0.0505 0.0910 0.1417 0.1554 0.1849 0.2309
31 31 31 31 31 31

BMI
BMI MPIN10 MPUN10 ACC45 DMEMGA10 DMEMGR10
1.00000 -0.42298 -0.36158 -0.33597 -0.31934 -0.30792
0.0 0.0199 0.0496 0.0695 0.0854 0.0978
30 30 30 30 30 30

BLEMGAV
BLEMGAV M4EMGA45 MEMGR45 MEMGR22 MEMGR10 MEMGA22
1.00000 0.95520 0.94275 0.93696 0.91245 0.90317
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

MEMGA1O DMEMGA22 DMEMGA45 DMEMGR22 STANX MPUN22
0.82175 0.37621 0.33988 0.33229 -0.32937 0.26691
0.0001 0.0370 0.0614 0.0678 0.0704 0.1466
31 31 31 31 31 31

MEMGA10
MEMGA10 MEMGR10 MEMGA45 MEMGR45 MEMGR22 BLEMGAV
1.00000 0.91709 0.83202 0.82832 0.82562 0.82175
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

MEMGA22 DMEMGA1O DMEMGRIO DMEMGA45 DMEMGR22 DMEMGA22
0.77801 0.63320 0.51513 0.42892 0.42334 0.38649
0.0001 0.0001 0.0030 0.0161 0.0176 0.0317
31 31 31 31 31 31

DMEMGR45 MPIN45 MPUN22 ACC45 MPIN10 M4PIN22
0.36890 0.36160 0.32868 0.31056 0.29873 0.29210
0.0411 0.0456 0.0710 0.0891 0.1026 0.1108
31 31 31 31 31 31







93


CLBP Subiects
Experimental Variables (Continued) Pearson Correlation coefficients/
Prob > IRI under Ho: Rho=0
/Number of observations

MEMGR10
MEMGR10 MEMGR45 MEMGR22 MEMGA1O BLEMGAV MEMGA45
1.00000 0.94393 0.92073 0.91709 0.91245 0.91219
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

MEMGA22 DMEMGR10 DMEMGR22 DMEMGR45 DMEMGA45 MPUN22
0.83343 0.52762 0.48080 0.47961 0.43918 0.39972
0.0001 0.0023 0.0062 0.0063 0.0134 0.0259
31 31 31 31 31 31

MPIN45 DMEMGA10 DMEMGA22 MPIN22 MPUN45 MPIN10
0.39140 0.36497 0.36342 0.36138 0.30873 0.29075
0.0295 0.0435 0.0445 0.0458 0.0910 0.1126
31 31 31 31 31 31

MEMGA22
14EMGA22 MEMGA45 MEMGR22 MEMGR45 BLEMGAV MEMGR10
1.00000 0.97649 0.96747 0.94516 0.90317 0.83343
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

MEMGA1O DMEMGA22 DMEMGA45 DMEMGR22 DMEMGR45 ACC45
0.77801 0.73753 0.66855 0.62734 0.50611 0.31563
0.0001 0.0001 0.0001 0.0002 0.0037 0.0837
31 31 31 31 31 31

MEMGR22
MEMGR22 MEMGR45 MEMGA45 MEMGA22 ELEMGAV M4EMGR10
1.00000 0.99003 0.98554 0.96747 0.93696 0.92073
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

MEMGA10 DMEMGR22 DMEMGA22 DMEMGA45 DM4EMGR45 MPIN45
0.82562 0.64092 0.61416 0.60622 0.55257 0.29652
0.0001 0.0001 0.0002 0.0003 0.0013 0.1053
31 31 31 31 31 31

MEMGA4 5
MEMGA45 MEMGR22 MEMGR45 MEMGA22 BLEMGAV MEMGR10
1.00000 0.98554 0.98240 0.97649 0.95520 0.91219
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

MEMGA10 DMEMGA22 DMEMGA45 DMEMGR22 DMEMGR45 MPIN45
0.83202 0.60495 0.60300 0.56183 0.48543 0.28762
0.0001 0.0003 0.0003 0.0010 0.0056 0.1167
31 31 31 31 31 31

MEMGR45
M4EMGR45 MEMGR22 MEMGA45 MEMGA22 MEMGR10 BLEMGAV
1.00000 0.99003 0.98240 0.94516 0.94393 0.94275
0.0 0.0001 0.0001 0.0001 0.0001 0.0001
31 31 31 31 31 31

MEMGA10 DMEMGR22 DMEMGA45 DMEMGR45 DMEMGA22 DMEMGR10
0.82832 0.60129 0.58063 0.56714 0.55691 0.32892
0.0001 0.0003 0.0006 0.0009 0.0011 0.0708
31 31 31 31 31 31




Full Text
63
of anticipatory EMG than controls with the more pronounced
differences occurring at angle 22. At angle 45, CLBP
subjects had higher anticipatory EMG values than controls at
low baseline EMG levels whereas at higher baseline EMG
levels, controls had higher anticipatory EMG levels than
CLBP subjects. As the means in Table 8-10 demonstrate, the
actual differences between groups in anticipatory EMG are
very small for a clinical perspective.
Table 8-10. Anticipatory EMG Means (SD) Baseline & Trials
Group
Baseline
i
i-1
o
o
22
o
IT)
CLBP
6.96 (4.3)
7.64 (5.6)
8.08 (5.9)
7.76 (5.1)
Controls
5.86 (3.6)
5.78 (3.8)
5.81 (3.9)
6.34 (4.9)
For the recovery phase at angle -10, the two
regression lines are almost identical with higher levels of
recovery EMG at higher levels of baseline EMG. At angle
22, the two regression lines are parallel with the CLBP
group demonstrating higher recovery EMG levels than controls
at higher levels of baseline EMG. At angle 45, the pattern
demonstrated for anticipatory EMG is repeated: at low
baseline EMG levels CLBP subjects had higher recovery EMG
levels than controls, but at higher levels of baseline EMG
controls had higher recovery EMG levels than CLBP subjects.
As with anticipatory EMG, the actual differences between
groups in recovery EMG are very small from a clinical
perspective (see Table 8-11).


COMPARISON OF NEGATIVE AFFECT, REACTIVITY,
AND PROPRIOCEPTION IN CHRONIC LOW BACK PAIN
PATIENTS AND CONTROLS
By
MELODYE ELAYNE GASKIN
A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL
OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY
UNIVERSITY OF FLORIDA
1998


79
measure (besides EMG) in order to assess the generality
versus specificity of the observed responses.
From another perspective, one possible reason for the
small group differences in EMG was that the bending task was
not adequately arousing for the CLBP subjects. Attaining
VAS pain ratings post-baseline in the future could help
assess the power of the experimental manipulation.
Paradoxically, the verbal warning given at the beginning of
the anticipatory phase may have actually reduced the
stressfulness of the task, instead of increasing anxiety,
due to predictability (Levethal, Brown, Shacham & Engquist,
1979). Arntz, van den Hout, van den Berg, and Meijboom
(1991) found that predictability reduced fear and
physiological responses. In a more recent study, Crombez,
Baeyens, and Eelen (1994) also found that temporal
information about impending experimental pain stimuli
resulted in lower physiological responsivity to the stimuli.
The authors discussed how their findings fit with Seligman's
(1968) safety signal hypothesis in that subjects not only
could predict when the pain stimulus would occur but also
when it would not. Lack of predictability of pain in the
everyday life of some patients with chronic pain may
contribute to increased levels of physiological reactivity
in these patients. This highlights the need for studies
using more naturalistic EMG monitoring.
Another possible explanation for the small group
differences in EMG in this study is the suggestion made by


19
pressor pain tolerance and threshold as well as to clinical
pain in a sample of chronic pain patients. Although no
relationship between these components and the experimental
pain measures was found, a significant relationship between
physiological reactivity and discriminability of reactivity
to experimental pain was found suggesting that the subjects
with higher levels of reactivity were better discriminators
of somatic change. But analysis of the discriminability
measure indicated that these chronic pain patients were
chance discriminators of somatic changes. The lack of a
pain-free control group limits the conclusions which may be
drawn from these data, although the results are consistent
with other studies that provide evidence of perceptual
distortion in chronic pain patients.
Perceptual distortions are also characteristic of
perceptual augmentors and reducers. Along this dimension,
people display a consistent tendency to over- or
underestimate magnitude estimations of a sensory stimulus
after repeated presentations. Augmenters show a tendency to
perceive stimulation as greater, whereas reducers tend to
perceive stimulation as less. Reducers have been shown to
tolerate more radiant heat and electric shock than
augmenters (Sternbach, 1968; Weisenberg, 1977).
Further support of the augmentor/reducer perceptual
distortion effect in pain perception is suggested by two
studies discussed by Schmidt and Arntz (1987) where healthy
control subjects were exposed to repeated cold-pressor


RESPONSE ACCURACY
ANGLE (degrees)
Figure 8-4. RESPONSE ACCURACY: CLBP vs CONTROLS
(Group Means with Standard Error Bars)
ON
GO


62
be meaningless even with a larger sample with more adequate
power.
Table 8-9. Cohen's d
Response Measure
Cohen's d
Accuracy -10
C0
o

Accuracy 22
.06
Accuracy 45
.06
Bias -10
.25
Bias 22
.30
Bias 45
.31
Integrated EMG data was averaged across baseline and
each phase of the experiment. The mean EMG values for the
anticipatory and recovery phases were then averaged across
the 5 trials resulting in mean EMG values for these two
phases for each of the 3 body positions (-10, 22, 45).
Group differences in anticipatory and recovery mean EMG for
the 3 body position tasks were assessed by repeated measures
MANCOVA using baseline EMG as the covariate. Results
indicated a 3-way interaction between angle, group and the
covariate for both anticipatory [F(2,57)=7.58, p=0.001]
(Figure 8-6) and recovery [F92,57)=9.02, p=0.0004] EMG
(Figure 8-7). As Figures 8-6 and 8-7 illustrate, there is a
similarity in pattern of EMG levels by group relative to
baseline EMG for angles -10 and 22 but a shift in EMG
patterns between groups relative to baseline EMG at angle
45.
For the anticipatory phase at angles -10 and 22, at
higher baseline EMG levels, the CLBP group had higher levels


25
empirical studies evaluating trunk proprioceptive abilities
of CLBP patients compared with pain-free controls.
Studies on body mechanics have focused on changes in
behavior after instruction. In a review of 16 low back
schools, Linton and Kamwendo (1987) concluded that although
patients with CLBP demonstrated increased understanding of
body mechanics as a result of "back school," there was
little indication that this knowledge resulted in behavioral
change. In a study of workers without back pain, Carlton
(1987) demonstrated that workers who received body mechanics
instruction performed better in a laboratory task than those
with no training, but there was no difference in the body
mechanics between groups (trained and untrained) in the work
environment.
Contrary to these findings, a study by McCauley (1990)
on the effect of body mechanics instruction on work
performance in young workers (without CLBP) demonstrated
that the trained workers performed work activities using
proper body mechanics significantly better than the
untrained workers. Morrison, Chase, Young, and Roberts
(1988) investigated the effect of a community hospital
outpatient treatment program for CLBP patients and found
that observed body mechanics for nine daily living
activities had improved dramatically following the program.
At a one-year follow-up, gains in observed body mechanics
had declined from levels assessed at the end of the program,


95
CLBP Sucnects
Experimental Variables (Continued)
Pearson Correlation Coefficients/
Prob > |R| under Hos Rho=0
/Number of Observations
DMEMGR4 5
DMEMGR45
DMEMGR22
DMEMGA45
1.00000
0.92035
0.84175
0.0
0.0001
0.0001
31
31
31
MEMGR22
MEMGA22
MEMGA45
0.55257
0.50611
0.48543
0.0013
0.0037
0.0056
31
31
31
ACC 10
ACC10
MPIN45
DMEMGA10
1.00000
-0.24516
-0.20394
0.0
0.1838
0.2711
31
31
31
ACC22
ACC 2 2
RB22
STANX
1.00000
0.58530
-0.37813
0.0
0.0005
0.0360
31
31
31
ACC 4 5
ACC45
DMEMGA2 2
BMI
1.00000
0.34757
-0.33597
0.0
0.0554
0.0695
31
31
30
RB10
RB10
DMEMGA4 5
DMEMGA22
1.00000
0.32700
0.30877
0.0
0.0726
0.0910
31
31
31
RB22
RB22
ACC22
RB45
1.00000
0.58530
0.53598
0.0
0.0005
0.0019
31
31
31
RB45
RB45
RB22
ACC22
1.00000
0.53598
0.34808
0.0
0.0019
0.0550
31
31
31
DMEMGA22
0.68336
0.0001
31
DMEMGR10
0.62181
0.0002
31
MEMGR45
0.56714
0.0009
31
MEMGR10
0.47961
0.0063
31
MEMGA10
0.36890
0.0411
31
DMEMGA10
0.29219
0.1107
31
MEMGA10
-0.17828
0.3373
31
MPUN45
-0.17754
0.3393
31
RB10
-0.17585
0.3440
31
RB45
0.34808
0.0550
31
STANGER
-0.26288
0.1531
31
MEMGA22
0.23450
0.2042
31
DMEMGA45
0.33344
0.0668
31
MEMGA22
0.31563
0.0837
31
MEMGA10
0.31056
0.0891
31
DMEMGA10
0.30654
0.0935
31
RB22
0.28468
0.1206
31
DMEMGR45
0.25127
0.1727
31
DMEMGA10
0.28542
0.1196
31
RB10
0.28468
0.1206
31
DMEMGA22
0.26825
0.1445
31
MPUN10
0.30397
0.0964
31
BDI
0.26941
0.1427
31
DMEMGA10
0.24795
0.1787
31


26
but were still significantly higher than levels at the
beginning of the program.
In a study which examined both CLBP patients and
control subjects on physical abilities and body mechanics,
Naliboff, Cohen, Swanson, Bonebakker, and McArthur (1985)
found that controls performed significantly better than the
CLBP subjects on endurance walking, the ability to control
the low back, and trunk strength and flexibility. Lower
extremity strength and flexibility and forward flexion did
not differ between the groups. Although the CLBP subjects
performed better than controls on the functional test of
body mechanics, both groups received less than 25% of the
maximum score suggesting that both groups had poor
proprioceptive abilities.
In summary, studies on body mechanics show mixed
results in terms of changes in actual behavior in both CLBP
patients and control subjects. These studies did not
evaluate proprioceptive ability although this could
significantly influence the capability to perform proper
body mechanics and may account for the mixed outcomes.
Although the Naliboff et al. (1985) study indicated that
there are differences in physical abilities between CLBP
patients and controls, they did not test for differences in
proprioceptive abilities. Given that the ability to
accurately perceive trunk position would seem to be a
prerequisite for successful training in proper body
mechanics, and given that Revel et al. (1991) found neck


9
affective processes (attention, arousal, emotion), sensory
discrimination processes, and perceptions of physical
symptoms. He describes the complex sensory modulation of
pain as unique to pain since nociceptive signals can be
enhanced or diminished at several levels of the neuraxis.
This is an important function that apparently serves to
protect the information processing centers of the brain from
competing nociceptive input during times of danger when
complete concentration on the environment is necessary for
survival.
Chapman (1986) also describes Lundl's cognitive-
perceptual model of stimulus equivalence which provides an
explanation for the role of cognitive processes such as
memory, beliefs, and expectancy, in the perception of pain.
Lundl describes "meaning structures" as the basic
determinants of perceptual experience and motor responses.
These structures reside in short- or long-term memory and
function as predispositions to exercise attentional
filtering, vigilance, and readiness for certain types of
responses to specific types of stimuli. Certain stimuli may
take on functional equivalence for the perceiver in that
they elicit identical responses despite notable differences
in the stimulus properties. This has implications for
somatization disorders as well as chronic pain patients
since the patient may misinterpret normal interoceptive
stimuli as painful.


39
adversely affects mood rather than the hypothesis that trait
characteristics are a predisposing factor in the development
of chronic pain. Both of these studies are consistent with
Price's (1988) sequential processing theory that pain
results in pain-related affect.
Summary
The literature reviewed indicates that anxiety, anger,
and depression as well as increased arousal and somatic
focus are associated with the experience of pain. The
clarification of the relationship between these factors
warrants further study.


16
discriminate stimuli but did raise their withdrawal
criterion (pain tolerance or response bias). Therefore,
discriminability has been found to be more closely related
to sensory-perceptual processes and does not appear to be
subject to the demand characteristics of the situation.
The application of SDT to chronic pain populations has
suggested that chronic pain patients are poorer
discriminators of experimental stimuli, such as tactual and
heat, than controls. Malow, Grimm, and Olson (1980) found
that chronic pain patients had lower pain thresholds, were
less able to discriminate between varying intensities of
pressure stimulation, and had a greater tendency to report
pain than controls. Seltzer and Seltzer (1986) also
investigated two-point tactual discrimination in chronic
pain and pain-free subjects. The results indicated that the
chronic pain patients were poorer discriminators of non
painful, tactual stimuli.
Malow and Olson (1981) looked at changes in pain
threshold, sensitivity, response bias, and discriminability
in chronic myofascial pain disorder (MPD) patients before
and after conservative treatment with a sedative/hypnotic,
muscle relaxant, or placebo; relaxation training; and
discussion of the relationship between stress, muscle
tension, and pain symptoms. Although there were no
differences in the pain measures of subjects prior to
treatment, after treatment the improved patients (those
without pain symptoms) showed a significant increase in pain


RECOVERY EMG BASELINE EMG
Figure 8-9. BMI-ADJUSTED CHANGE IN RECOVERY EMG RELATIVE TO BASELINE:
CLBP vs CONTROLS
(Group Means with Standard Error Bars)
LJ


SCORE
m _
CM
CONTROLS
CLBP
BDI STATE STATE
ANGER ANXIETY
Figure 8-1. NEGATIVE AFFECT: CLBP vs CONTROLS
(Group Means with Standard Error Bars)
o\
Ui


88
Control Subjects
Experimental Variables (Continued)
Pearson
Prob > 1
Correlation
r| under Ho:
Coefficients/
Rho=0/N = 31
MPUN45
MPUN45
MPIN45
MPUN22
MPIN22
MPUN10
MPIN10
1.00000
0.94822
0.90994
0.89803
0.85314
0.64237
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
ACC 4 5
DMEMGR22
DMEMGA22
STANX
DMEMGR10
DMEMGR45
0.43884
-0.39056
-0.38703
-0.31445
-0.30001
-0.27301
0.0135
0.0298
0.0315
0.0849
0.1011
0.1373
BMI
BMI
DMEMGA2 2
MEMGA22
MEMGR22
MEMGA45
DMEMGR2 2
1.00000
0.35896
0.32793
0.27058
0.26839
0.26656
0.0
0.0474
0.0717
0.1410
0.1443
0.1472
BLEMGAV
BLEMGAV
MEMGR22
MEMGR45
MEMGA22
MEMGA45
MEMGR10
1.00000
0.95264
0.94459
0.93910
0.90688
0.90233
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
MEMGA10
DMEMGR45
DMEMGA45
DMEMGR22
RB10
BMI
0.89876
0.56740
0.38177
0.37703
0.24155
0.22086
0.0001
0.0009
0.0341
0.0365
0.1905
0.2325
MEMGA10
MEMGA10
MEMGA45
MEMGR10
MEMGA22
MEMGR22
MEMGR45
1.00000
0.96246
0.94203
0.93768
0.92993
0.92112
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
BLEMGAV
DMEMGR45
DMEMGA45
DMEMGR22
DMEMGR10
DMEMGA10
0.89876
0.69098
0.66641
0.56343
0.44454
0.33515
0.0001
0.0001
0.0001
0.0010
0.0122
0.0653
MEMGR10
MEMGR10
MEMGR45
MEMGA10
MEMGR22
MEMGA45
MEMGA22
1.00000
0.94938
0.94203
0.92440
0.92049
0.91087
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
BLEMGAV
DMEMGR45
DMEMGR10
DMEMGA45
DMEMGR22
MPIN22
0.90233
0.75543
0.57049
0.56862
0.53757
-0.26545
0.0001
0.0001
0.0008
0.0008
0.0018
0.1489
MEMGA22
MEMGA22
MEMGR22
MEMGR45
MEMGA45
BLEMGAV
MEMGA10
1.00000
0.98124
0.95738
0.95712
0.93910
0.93768
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
MEMGR10
DMEMGR45
DMEMGR22
DMEMGA45
DMEMGA22
BMI
0.91087
0.70925
0.61789
0.58986
0.37956
0.32793
0.0001
0.0001
0.0002
0.0005
0.0352
0.0717
MEMGR22
MEMGR22
MEMGA22
MEMGR45
MEMGA45
BLEMGAV
MEMGA10
1.00000
0.98124
0.98030
0.95814
0.95264
0.92993
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
MEMGR10
DMEMGR45
DMEMGR22
DMEMGA45
DMEMGR10
DMEMGA2 2
0.92440
0.74234
0.64083
0.57032
0.30151
0.28857
0.0001
0.0001
0.0001
0.0008
0.0993
0.1154


ANTICIPATORY EMG BASELINE EMG
ANGLE (degrees)
Figure 8-8. BMI-ADJUSTED CHANGE IN ANTICIPATORY EMG RELATIVE TO BASELINE:
CLBP vs CONTROLS
(Group Means with Standard Error Bars)
to


CHAPTER 3
SENSORY DISCRIMINATION IN PAIN PERCEPTION
Nociception
Nociceptors are sensory receptors which detect changes
in the state of an organism. The most common sensory
receptors are the free nerve endings. These afferent nerve
endings are distributed throughout almost all parts of the
body and are responsible for the sensations of pain,
temperature, itch, tickle, movement, and proprioception
(Seeley, Stephens, & Tate, 1989). These receptors are
activated by three types of stimuli mechanical, thermal,
and chemical. Some receptors respond selectively to only
one type of stimulus, such as mechanoreceptors in the
muscles and joints, whereas others, polymodal receptors, are
optimally responsive to all three types of stimuli (Price,
1988) .
These receptors can be divided into two functional
classes based upon speed of impulse conduction: 1) As
afferents which conduct impulses at velocities of between 6
and 30 meters per second over small diameter, myelinated
axons, and 2) C afferents which conduct impulses at
velocities of between 0.5 and 2 meters per second over large
diameter, unmyelinated axons (Guyton, 1991). Price (1988)
explains that As nociceptive afferents are relatively
12


91
CLBP Subjects
Experimental Variables
Pearson Correlation Coefficients/
Prob > |R| under Ho: Rho=0
/Number of Observations
BDI
BDI
STANX
STANGER
MPUN10
RB45
DMEMGA22
1.00000
0.58953
0.43438
0.28343
0.26941
0.26249
0.0
0.0005
0.0146
0.1223
0.1427
0.1537
31
31
31
31
31
31
STANGER
STANGER
STANX
BDI
BLEMGAV
ACC22
MPUN45
1.00000
0.64751
0.43438
-0.26580
-0.26288
0.26145
0.0
0.0001
0.0146
0.1484
0.1531
0.1554
31
31
31
31
31
31
STANX
STANX
STANGER
BDI
ACC22
BLEMGAV
MEMGA45
1.00000
0.64751
0.58953
-0.37813
-0.32937
-0.26851
0.0
0.0001
0.0005
0.0360
0.0704
0.1441
31
31
31
31
31
31
MPIN10
MPIN10
MPUN10
MPIN22
MPUN22
MPIN45
MPUN45
1.00000
0.90515
0.80858
0.78983
0.74335
0.71524
0.0
0.0001
0.0001
0.0001
O.OOOl
0.0001
31
31
31
31
31
31
BMI
DMEMGR10
DMEMGA10
MEMGA10
MEMGR10
DMEMGR45
-0.42298
0.37565
0.30765
0.29873
0.29075
0.26695
0.0199
0.0373
0.0923
0.1026
0.1126
0.1466
30
31
31
31
31
31
MPIN22
MPIN22
MPUN22
MPIN45
MPUN45
MPIN10
MPUN10
1.00000
0.95171
0.86049
0.82849
0.80858
0.66687
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
31
31
31
31
31
31
DMEMGR10
MEMGR10
MEMGA10
MEMGR45
MEMGR22
MEMGA45
0.36730
0.36138
0.29210
0.27647
0.25845
0.24666
0.0421
0.0458
0.1108
0.1322
0.1604
0.1810
31
31
31
31
31
31
MPIN45
MPIN45
MPUN45
MPIN22
MPUN22
MPIN10
MPUN10
1.00000
0.94281
0.86049
0.84410
0.74335
0.62616
0.0
0.0001
0.0001
0.0001
0.0001
0.0002
31
31
31
31
31
31
DMEMGR10
MEMGR10
MEMGA10
MEMGR45
MEMGR22
MEMGA45
0.39448
0.39140
0.36160
0.30013
0.29652
0.28762
0.0281
0.0295
0.0456
0.1009
0.1053
0.1167
31
31
31
31
31
31
MPUN10
MPUN10
MPIN10
MPUN22
MPUN45
MPIN22
MPIN45
1.00000
0.90515
0.75474
0.71202
0.66687
0.62616
0.0
0.0001
0.0001
0.0001
0.0001
0.0002
31
31
31
31
31
31
BMI
RB45
DMEMGR10
BDI
DMEMGA10
STANGER
-0.36158
0.30397
0.29068
0.28343
0.25583
0.23462
0.0496
0.0964
0.1127
0.1223
0.1648
0.2039
30
31
31
31
31
31


32
controls. The results indicated that CBP patients displayed
elevations and delayed return to baseline only in their
paravertebral musculature and only when discussing a recent
personally stressful event or a recent pain episode.
Neither of the other groups displayed similar response
patterns at the paraspinal EMG site. The authors suggest
that the abnormal muscle response of the CBP patients was
not part of a general stress reaction, as the other groups
indicated comparable levels of arousal in other areas. The
results showed that anxiety, pain levels, and EMG elevations
were related in the CBP patients, suggesting the involvement
of a central process. This study also underscores the
importance of using a stimulus that is relevant to the
clinical pain of the subjects.
These findings were replicated by Flor, Birbaumer,
Schugens, and Lutzenberger (1992) in a study comparing
chronic back pain (CBP), temporomandibular pain and
dysfunction (TMPD), and controls for symptom-specific
psychophysiological responses to personally-relevant stress
imagery. The CBP and TMPD patients exhibited elevated EMG
activity at the site of pain (erector spinae and m.
masseter, respectively).
In a 1989 review, Flor and Turk examined 60 studies
which investigated the role of physiological variables in
recurrent migraine, tension, and mixed headaches, chronic
back pain, and temporomandibular joint (TMJ) disorders. The
authors conclude that baseline resting EMG levels do not


100
International Association for the Study of Pain
(Subcommittee on Taxonomy). Pain terms: A list with
definitions and notes on usage. Pain 1979; 6,:249-252.
Jensen, M.P., Karoly, P., & Harris, P. (1991). Assessing the
affective component of chronic pain: development of the
pain discomfort scale. Journal of Psychosomatic Research.
35 (2/3), 149-154.
Kremer, E. F. & Atkinson, Jr., J. H. (1983). Pain language
as a measure of affect in chronic pain patients. In R.
Melzack (Ed.), Pain measurement and assessment (pp. 119-
127). New York: Raven Press.
Lautenbacher, S., Galfe, G., Karlbauer, G., Moltner,A. &
Strian, F. (1990). Effects of chronic back pain on the
perception of experimental heat pain. Perceptual and
Motor Skills. 71. 1283-1292.
Leventhal, H., Brown, D., Shacham, & Engquist, G. (1979).
Effects of preparatory information about sensations,
threat of pain, and attention on cold pressor distress.
Journal of Personality and Social Psychology. 37 (5),
688-714.
Linton, S.J. & Gotestam, K.G. (1985). Relations between
pain, anxiety, mood and muscle tension in chronic pain
patients. Psychotherapy and Psvchosomatics. 43. 90-95.
Linton, S.J. & Kamwendo, K. (1987). Low back schools: A
critical review. Physical Therapy. 67 (9), 1375-1383.
Lloyd, M. A. & Appel, J. B. (1976). Signal detection theory
and the psychophysics of pain: An introduction and
review. Psychosomatic Medicine. 38 (2), 79-94.
Malow, R.M., Grimm, L., & Olson, R.E. (1980). Differences in
pain perception between nyofascial pain dysfunction
patients and normal subjects: A signal detection
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Malow, R.M. & Olson, R.E. (1981). Changes in pain perception
after treatment for chronic pain. Pain. 11. 65-72.
Malow, R.M., West, J.A., & Sutker, P.B. (1987). A sensory
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(3), 184-189.
Marschall, P. (1986). Physical complaints, anxiety, and its
body outcomes: A psychophysiological field study. Journal
of Psychopathology and Behavioral Assessment. 9 (4), 353-
367.


8
Some central processes, such as anxiety, open the gate. The
model also proposes that sensory-discriminative processes
are influenced by, as well as influence, the central control
mechanism which controls the gating mechanism. The central
control mechanism is hypothesized to involve higher central
nervous system processes, such as those involved in the
evaluation of input in terms of past experience.
Despite the initial controversies that the gate-control
theory inspired, it has had an important influence on pain
research for more than two decades (Price, 1988).
Considerable evidence exists to support all but one of the
major tenants of the theory (e.g., that ascending rapidly
conducting afferents activate cognitive processes that then
influence descending efferent pathways), and no one has
refuted the basic tenants of the theory. Although Price
criticizes the theory for being too general in its
explanation of the interactions in the dorsal horn as well
as the endogenous pain modulatory systems, he acknowledges
that the gate-control theory has heuristic value in
understanding pain mechanisms and guiding further research.
Information-Processing Models of Pain
Chapman (1986) discusses the physiological, sensory,
and cognitive aspects of pain within an information
processing model which parallels the gate-control model.
Chapman identifies a central process in the experience of
pain which he explains in terms of perceptual organization
processes. These processes are influenced by cognitive-


45
angles and the actual performance of subjects as they
attempted to reproduce the target angles. The computer
monitor was positioned such that subjects could not view it
and gain feedback on their performance.
Physiological Reactivity Measures
EMG reactivity was assessed by measuring muscle
activity of the lumbar paraspinal muscles during the phases
of the experiment described above. Sensors for EMG activity
were contained in the belt of the ELT device described in
the previous section and consisted of 3/4"xl-3/4" fabric
pads. Integrated EMG data was digitized on-line with
equipment and software by Physical Health Devices (Pompano
Beach, FL.). This apparatus incorporates proprietary
firmware for automated gain adjustment throughout a dynamic
range of 7-1,800 uV root mean square (RMS). The bandwidth
was 100-540 Hz with a 60 Hz notch filter. Signal processing
was as follows: bandpass filtering occurred in front of the
RMS conversion, the time constant for the RMS to DC
conversion was 40 ms., and the filtered integrated signal
was sampled and stored at 128Hz. Average iEMG was computed
for each phase of the experimental procedure described
below. The computer monitor was positioned such that
subjects could not view EMG activity during the experimental
procedure.
Pain Measures
McGill Pain Questionnaire (MPO). The MPQ consists of
twenty groups of single word pain descriptors with the words


ACKNOWLEDGMENTS
Electromyographic (EMG)/ergometric lumbar transceiver
(ELT) equipment and software were provided for this study by
Physical Health Devices, 417 Corporate Square, 1500 West
Cypress Road, Ft. Lauderdale, FL 33309.
Access to subject populations was provided by the
following: Michael Macmillan, MD, Orthopedic Clinic and Pat
O'Conner, PT, Department of Physical Therapy at Shands
Hospital, University of Florida, Gainesville, FL; Jeff
Goode, PT, Sports Medicine Center, Charleston Area Medical
Center, General Division, Charleston, WV. Many thanks to
these people and their staffs for their support of this
project.
Heartfelt thanks are due to the many who have provided
support in various ways toward the completion of this
project: classmates, friends, family, colleagues,
professors, research assistants, my committee. An attempt
to name them all would inevitably result in the inadvertent
omission of someone.
Much gratitude is due the people who participated in
this study, particularly the pain subjects, for sharing of
themselves and their experiences. In the end, it is their
story.


34
sessions and that pain intensity was positively correlated
with EMG levels in the position with the most elevated EMG
values as compared to control subjects. He comments that
the failure to take pain intensity at time of recording into
account may have contributed to the conflicting results of
previous EMG studies.
Summary
The research on EMG reactivity in CLBP patients
suggests that there may be several patterns of muscular
activity related to back pain. Several researchers suggest
that clarification of the role of EMG reactivity in the
experience of chronic low back pain requires that future
studies investigate patterns of EMG activity from baseline
through return to baseline during an ecologically valid
stressor. The use of personally relevant stressors or
stressors related to patients' clinical pain is critical if
the relationship between EMG reactivity and pain is to be
understood in a manner which will allow for more efficacious
treatment of this disorder. Previous research also
indicates the importance of assessing pain intensity,
sensory discrimination, and cognitive-affective variables
during EMG recording.


101
McCauley, M. (1990). The effects of body mechanics
instruction on work performance among young workers. The
American Journal of Occupational Therapy. 44 (5), 402-
407.
Melzack, R. (1985). The McGill pain questionnaire. In R.
Melzack (Ed.), Pain measurement and assessment (pp. 41-
47). New York: Raven Press.
Melzack, R. (1986). Neurophysiological foundations of pain.
In R. A. Sternbach (Ed.), The psychology of pain (2nd
ed.), (pp. 1-24). New York: Raven Press.
Merskey, H. (1986). Psychiatry and pain. In R. A. Sternbach
(Ed.), The psychology of pain (2nd ed.), (pp. 97-120).
New York: Raven Press.
Morrison, G.E.C., Chase, W., Young, V., & Roberts, W.L.
(1988). Back pain: treatment and prevention in a
community hospital. Archives of Physical Medicine and
Rehabilitation. 69, 605-609.
Naliboff, B.D., Cohen, M.J., Schandler, S.L., & Heinrich,
R.L. (1981). Signal detection and threshold measures for
chronic back pain patients, chronic illness patients, and
cohort controls to radiant heat stimuli. Journal of
Abnormal Psychology. 90 (3), 271-274.
Naliboff, B.D., Cohen, M.J., Swanson, G.A., Bonebakker,
A.D., & McArthur, D.L. (1985). Comprehensive assessment
of chronic low back pain patients and controls: Physical
abilities, level of activity, psychological adjustment,
and pain perception. Pain. 23., 121-134.
Newton, R.A. (1982). Joint receptor contributions to
reflexive and kinesthetic responses. Physical Therapy. 62
(1), 22-29.
Parkhurst, T.M., & Burnett, C.N. (1994). Injury and
proprioception in the lower back. JOSPT. 19 (5), 282-295.
Pennebaker, J.W. (1982). The psychology of physical symptoms
(Appendix B). New York: Springer-Verlag.
Perry, F., Heller, P.H., Kamiya, J., & Levine, J.D. (1989).
Altered autonomic function in patients with arthritis or
with chronic myofascial pain. Pain. 39. 77-84.
Peters, M.L., & Schmidt, A.J.M. (1991). Psychophysiological
responses to repeated acute pain stimulation in chronic
low back pain patients. Journal of Psychosomatic
Research. 35 (1), 59-74.


the frequency with which a subject experiences anxious and
angry feelings.
44
The STPI has been standardized with high school and
college students, military recruits, and working adults
(Spielberger et al., 1983). Correlations with the parent
scales, the State-Trait Anxiety Inventory and the State-
Trait Anger Scale, ranged from .93 to .99. Alpha
coefficients for each subscale ranged from .76 to .88.
Based upon the results of previous research (Gaskin et
al., 1992) indicating the greater impact of state over trait
affect measures on pain report, only the state affect
subscales were used in this study.
Sensory-Perceptual Measure
Body Position Proprioception. Subjects' ability to
reproduce 2 body positions during forward flexion and 1
position during backward extension of the trunk was measured
using an ergometric lumbar transceiver (ELT) device. The
ELT device is a non-invasive, compact, light-weight
miniature microcomputer that is worn in a fabric belt which
contains EMG sensors. The ELT measures spinal angle from
15 extension (-15) to 105 forward flexion. Subjects were
asked to reproduce forward flexion angles of 22 and 45 and
one extension angle of -10.
The ELT device was worn by subjects during the
baseline, guided movement, anticipatory, body position task,
and recovery phases of the study and recorded the target


52
for all subjects. A t-test of BMI by group indicated a
significant difference (p=0.003) in this measure between
CLBP subjects (M = 28.3, SD=5.6) and controls (M = 24.4,
SD=3.8) .
Marital Status
Comparison of groups reveals significant differences in
marital status (Fisher's Exact Test, 2-tail, p=0.05) with
more control subjects being single and more CLBP subjects
being divorced (see Table 8-1).
Table 8-1: Marital Status by Group
Marital Status
Controls
CLBP
Single
11
4
Married
17
21
Divorced
2
6
Widowed
1
0
Employment Status
Comparison of groups reveals significant differences in
employment status (Fisher's Exact Test, 2-tail, p=0.00) with
more control subjects either employed or students and more
CLBP subjects on temporary or permanent disability (see
Table 8-2).
Table 8-2: Employment Status by Group
Employment
Controls
CLBP
Employed
26
12
Unemployed
1
4
Disability
0
5
Retired
0
1
Student
4
1
Temp Disability
0
7


47
The VAS's used in this study consisted of 12.4 cm lines
whose endpoints were designated as "no sensation" and "the
most intense sensation imaginable" for the pain intensity
(PIN) VAS and "not bad at all" and "the most intense bad
feeling possible for me" for the pain unpleasantness (PUN)
VAS (adapted from Price, Rafii, Watkins, & Buckingham,
1984) .
Procedures
After establishing written informed consent in
accordance with Institutional Review Board requirements, all
subjects were administered the BDI and the STPI. The MPQ
was administered to the CLBP patients only. Upon completion
of these questionnaires, subjects were then instructed in
the experimental protocol as follows:
"In a moment I will put a belt around your
waist that measures the muscle activity in your
low back and the angles to which you bend. After
a baseline phase you will be guided through 2
forward bends and 1 backward bend. After you have
been guided to a position, you will be asked to do
the bend without guidance, stopping at the same
point to which you were guided. You will repeat
this task without guidance a total of 5 times.
I will give you a 10 second warning ("in 10
seconds I will tell you to bend') before bending,
and I will tell you when to start bending. You
will have 5 seconds to complete the bend. I will
tell you when to return to standing straight.
After each bend, I will show you some scales with
which you will rate your level of pain intensity
and pain unpleasantness at that moment. I will
explain these scales in a moment.
After you have done this bend 5 times without
guidance, you will be guided to another position.
You will be asked to bend to that position 5 times
without guidance, rating your levels of pain
intensity and unpleasantness after each bend.


I certify that I have read this study and that in my
opinion it conforms to acceptable standards of scholarly
presentation and is fully adequate, in scope and quality, as
Michael E. Robinson
Associate Professor
Clinical & Health Psychology
I certify that I have read this study and that in my
opinion it conforms to acceptable standards of scholarly
presentation and is fully adequate, in scope and quality, as
a dissertation for the degree of.,Doctor of Philosophy.
Bussell M
Professor
Clinical
. Bauer
& Health Psychology
I certify that I have read this study and that in my
opinion it conforms to acceptable standards of scholarly
presentation and is fully adequate, in scope and quality, as
a dissertation for the degree of Doctor of Philosophy.
Be lar
Professor
Clinical & Health Psychology
I certify that I have read this study and that in my
opinion it conforms to acceptable standards of scholarly
presentation and is fully adequate, in scope and quality, as
a dissertation for the degree of Doctor of Philosophy.
4* I/*-
Michael G. Perri
Professor
Clinical & Health Psychology
I certify that I have read this study and that in my
opinion it conforms to acceptable standards of scholarly
presentation and is fully adequate, in scope and quality,
a dissertation for the degree of Doctor of Philosophy.
law
2
as
Lind R. Shv
Associate Professor
Rehabilitation Counseling


o
CONTROLS
CLBP
10 22 45
ANGLE (degrees)
Figure 8-3. PUN: CLBP vs CONTROLS
(Group Medians with Inter-quartile Ranges)


57
individuals who had been injured relatively recently and
were in the early stages of rehabilitation in a physical
therapy setting. Despite these differences, there were no
significant differences between these samples on measures of
proprioception, pain, negative affect, or EMG reactivity.
Data Reduction and Analyses
Zero-order correlations can be seen in the Appendix.
On all measures of negative affect, pain subjects
exhibited greater levels than controls, as predicted.
Multivariate analysis (MANOVA) of pain subjects' and
controls' scores on depression, state anger and state
anxiety measures demonstrated that the relationship between
the three variables differed by group [F(3,58)=15.11,
p=.0001] (see Figure 8-1). See Table 8-3 for means and
standard deviations for these measures.
Table 8-3. Means (SD) for Negative Affect Measures
Measures
Controls
CLBP
Depression (BDI)
3.00 (2.6)
11.13 (6.09)
State Anger (STPI)
10.19 (0.65)
12.68 (5.31)
State Anxiety (STPI)
14.48 (3.05)
18.68 (5.68)
VAS responses, measured in centimeters, were averaged
across the 5 trials for each body position. This resulted
in an average VAS pain intensity (PIN) and pain
unpleasantness (PUN) score for each of the 3 discrimina-
bility tasks. Due to the non-normal distribution of the
data for the controls subjects for both PIN and PUN
responses, nonparametric analyses (Wilcoxon) were performed


13
modality specific and often respond optimally to intense
mechanical stimuli. They elicit brief latency intense
responses critically necessary for rapid withdrawal and
escape. These afferents relate to "first pain," which is
usually described as sharp or pricking and can be
conceptualized as a warning device. C nociceptive afferents
tend to be of the polymodal variety and respond to
mechanical stimuli (such as muscle stretch and contraction),
thermal stimuli, and chemical stimuli, including end-
products of muscle activity such as lactic acid and
endogenous chemicals resulting from tissue damage such as
bradykinin (Guyton, 1991; Price, 1988). The responses of
these afferents are more delayed, and their central actions
are prolonged and slowly summate over time. These afferents
relate to "second or chronic pain," which is usually
described as burning, aching, and chronic and can be
conceptualized as a mechanism related to protection and
recuperation of injured tissue (Price, 1988).
Nociceptive afferents innervate the skin, muscle
tissue, viscera (such as the heart, lungs, and stomach), and
other internal tissues, such as arterial walls and joint
surfaces (Guyton, 1991). C polymodal nociceptive afferents
make up more than 90% of the unmyelinated cutaneous
afferents (Price, 1988). Price (1988) explains that
"threshold activation of these afferents may not signal the
presence of tissue-threatening stimuli, and there is a
distinct possibility that they convey nonnociceptive as well


36
attention to somatic symptoms mediated the relationship
between depression and the Sensory Pain Rating Index on the
McGill Pain Questionnaire (MPQ), whereas depression was
directly related to all other subscales of the MPQ. The
authors suggest that the "self-report of the sensory
experience of pain appears to be related to depression
through heightened somatic focus (p.15)." Kremer and
Atkinson (1983) describe chronic pain populations as
characterized by a high incidence of anxiety and depression
and as demonstrating the disruptive effects of affective
distress on cognitive tasks.
Empirical studies examining the relationship between
anger and pain have been scant until recently. Pilowsky
(1986) discussed the results of several clinical case
studies and the few controlled studies on pain and anger.
He concluded that certain combinations of anger experience
and anger inhibition were important elements in the
experience of chronic pain for some patients.
A study by Wade et al. (1990) provides additional
support for the role of anger in the experience of pain.
Using visual analog scales (VAS), the authors assessed the
relationship of depression, anxiety, anger, frustration, and
fear to pain-related unpleasantness. Anxiety, anger and
frustration were found to predict pain-related
unpleasantness. Similarly, Fernandez and Milburn (1994)
found that of three weighted sets of emotions, the set
comprised of anger, fear, and sadness was the most salient


87
Control Subiects
Experimental Variables
Pearson Correlation Coefficients/
Prob > IRI under Ho: Rho=0/N = 31
BDI
BDI
DMEMGR10
STANGER
1.00000
0.31518
0.31264
0.0
0.0842
0.0868
STANGER
STANGER
ACC22
BDI
1.00000
0.36109
0.31264
0.0
0.0460
0.0868
STANX
STANX
MPIN10
MPIN45
1.00000
-0.35701
-0.33185
0.0
0.0487
0.0682
MPIN10
MPIN10
MPUN10
MPIN45
1.00000
0.70072
0.65525
0.0
0.0001
0.0001
ACC45
STANX
BDI
0.44373
-0.35701
-0.23339
0.0124
0.0487
0.2064
MPIN22
MPIN22
MPUN22
MPUN45
1.00000
0.95920
0.89803
0.0
0.0001
0.0001
DMEMGR22
DMEMGA2 2
ACC45
-0.41601
-0.37594
0.36309
0.0199
0.0371
0.0447
MPIN45
MPIN45
MPUN45
MPIN22
1.00000
0.94822
0.85960
0.0
0.0001
0.0001
DMEMGR22
DMEMGA22
STANX
-0.37403
-0.35342
-0.33185
0.0382
0.0511
0.0682
MPUN10
MPUN10
MPUN45
MPUN22
1.00000
0.85314
0.76564
0.0
0.0001
0.0001
ACC45
DMEMGA2 2
STANX
0.69639
-0.26985
-0.26248
0.0001
0.1421
0.1537
MPUN22
MPUN22
MPIN22
MPUN45
1.00000
0.95920
0.90994
0.0
0.0001
0.0001
ACC45
DMEMGR22
DMEMGA22
0.40699
-0.38117
0.36613
0.0231
0.0344
0.0428
DMEMGR45
MPUN22
MPIN10
0.30452
-0.23511
-0.23339
0.0958
0.2029
0.2064
ACC 10
-0.22508
0.2235
RB22
0.19973
0.2814
RB45
0.18236
0.3262
MPUN45
-0.31445
0.0849
ACC22
-0.28679
0.1178
MPUN10
-0.26248
0.1537
MPUN45
0.64237
0.0001
MPUN22
0.57776
0.0007
MPIN22
0.56042
0.0010
DMEMGA22
-0.19666
0.2890
DMEMGR22
-0.19153
0.3020
ACC10
-0.18394
0.3219
MPIN45
0.85960
0.0001
MPUN10
0.73625
0.0001
MPIN10
0.56042
0.0010
DMEMGR10
-0.32432
0.0751
DMEMGR45
-0.28287
0.1231
MEMGA22
-0.26705
0.1464
MPUN22
0.85842
0.0001
MPUN10
0.73267
0.0001
MPIN10
0.65525
0.0001
ACC45
0.31990
0.0794
DMEMGR10
-0.31449
0.0849
DMEMGR45
-0.29518
0.1069
MPIN22
0.73625
0.0001
MPIN45
0.73267
0.0001
MPIN10
0.70072
0.0001
DMEMGR22
-0.20401
0.2710
ACC 10
-0.17939
0.3342
BMI
0.17303
0.3519
MPIN45
0.85842
0.0001
MPUN10
0.76564
0.0001
MPIN10
0.57776
0.0007
DMEMGR45
-0.27831
0.1295
DMEMGR10
-0.27265
0.1378
STANX
-0.25188
0.1716


BIOGRAPHICAL SKETCH
Melodye Elayne Gaskin was born on May 28, 1956, in
Omaha, Nebraska. She received a Bachelor of Business
Administration degree from the Stetson University in May,
1978, and entered the University of Florida in August, 1988,
as a graduate student in the Department of Clinical and
Health Psychology. She received the degree of Master of
Science in psychology in December, 1991.
104


Chapter 9
DISCUSSION
The purpose of this study was to explore the hypothesis
that the experience of chronic pain is influenced by a
dysfunction in a central process that may also result in
increases in negative affect, physiological reactivity, and
perceptual deficits. Specifically, the current study
explored group differences between CLBP patients and
healthy, pain-free controls with the following hypotheses:
CLBP subjects were expected to exhibit greater levels of
negative affect than controls.
CLBP subjects were expected to demonstrate higher VAS
ratings of pain intensity and unpleasantness than
controls.
CLBP subjects were expected to be poorer discriminators
of body position (less accurate) and to differ on
response bias as compared to controls.
CLBP subjects were expected to demonstrate higher
anticipatory and recovery EMG than controls.
Negative Affect
As predicted, negative affect was greater for the CLBP
subjects on all three measures as compared to controls.
This is consistent with the results of previous studies
74


APPENDIX
CORRELATION ANALYSES
Abbreviation Key
ACC10 = Response Accuracy -10
ACC22 = Response Accuracy 22
ACC45 = Response Accuracy 45
BDI = Beck Depression Inventory
BMI = Body Mass Index
BLEMGAV = Average Baseline EMG
DMEMGA10=Mean EMG Difference from Baseline for Anticipatory Phase -10
DMEMGA22=Mean EMG Difference from Baseline for Anticipatory Phase 22
DMEMGA45=Mean EMG Difference from Baseline for Anticipatory Phase 45
DMEMGR10=Mean EMG Difference from Baseline for Recovery Phase Angle -10
DMEMGR22=Mean EMG Difference from Baseline for Recovery Phase Angle 22
DMEMGR45=Mean EMG Difference from Baseline for Recovery Phase Angle 45
MEMGA10 = Mean EMG for Anticipatory Phase Angle -10
MEMGA22 = Mean EMG for Anticipatory Phase Angle 22
MEMGA45 = Mean EMG for Anticipatory Phase Angle 45
MEMGR10 = Mean EMG for Recovery Phase Angle -10
MEMGR22 = Mean EMG for Recovery Phase Angle 22
MEMGR45 = Mean EMG for Recovery Phase Angle 45
MPIN10 = Mean Pain Intensity VAS Rating Angle -10
MPIN22 = Mean Pain Intensity VAS Rating Angle 22
MPIN45 = Mean Pain Intensity VAS Rating Angle 45
MPUN10 = Mean Pain Unpleasantness VAS Rating Angle -10
MPUN22 = Mean Pain Unpleasantness VAS Rating Angle 22
MPUN45 = Mean Pain Unpleasantness VAS Rating Angle 45
RB10 = Response Bias Angle -10 STANGER = State Anger
RB22 = Response Bias Angle 22 STANX = State Anxiety
RB45 = Response Bias Angle 45
83


To my mother, Marion Elaine, who gave me life and the treasure
of a heritage.
To my grandfather, Charles Henry Robel, who never treated me as
though being a girl should restrict my experience of life.
To my dear friend, Caron, for believing in me and helping me
through the tough times.


CHAPTER 6
SUMMARY AND HYPOTHESES
The previous chapters have provided a review of
research which has investigated the cognitive-affective,
sensory-perceptual, and physiological reactivity components
of pain. The literature suggests that the experience of
pain is modulated via a central process that is influenced
by these components. The results of these studies suggest
that a dysfunction in this central process may result in the
experience of chronic pain as well as increases in negative
affect, physiological reactivity, and perceptual deficits.
The literature also recommends that physiological reactivity
in chronic pain should be assessed in specific pain
syndromes, such as CLBP patients, through the use of
stressors relevant to patients' clinical pain.
The current study explored group differences between
CLBP patients and healthy, pain-free controls on the
following aspects of this hypothesized central process:
1) Cognitive-affective processes: Depression, anger
and anxiety measured using self-report questionnaires.
2) Subjective experience of pain: Pain intensity and
pain related unpleasantness measured using Visual Analogue
Scales (VAS's).
40


RESPONSE BIAS
ANGLE (degrees)
Figure 8-5. RESPONSE BIAS: CLBP vs CONTROLS
(Group Means with Standard Error Bars)
ON


102
Peters, M.L., Schmidt, A.J.M., & Van den Hout, M.A. (1989).
Chronic low back pain and the reaction to repeated acute
pain stimulation. Pain. 39. 69-76.
Pilowsky, I. (1986). Psychodynamic aspects of the pain
experience. In R.A. Sternbach (Ed.), The psychology of
pain (2nd ed.), (pp. 189-190). New York: Raven Press.
Portenoy, R.K. (1989). Mechanisms of clinical pain:
Observations and speculations. Neurologic Clinics. 7(2),
205-230.
Price, D.D. (1988). Psychological and neural mechanisms of
pain New York: Raven Press.
Price, D.D., Rafii, A., Watkins, L.R., & Buckingham, B.
(1984). A psychophysical analysis of acupuncture
analgesia. Pain. 19 (1). 27-42.
Proske, U., Schaible, H.-G., Schmidt, R.F. (1988). Joint
receptors and kinaesthesia. Experimental Brain Research.
72, 219-224.
Reading, A.E. (1985). The McGill pain questionnaire: An
appraisal. In R. Melzack (Ed.), Pain measurement and
assessment (pp. 55-61). New York: Raven Press.
Revel, M., Andre-Deshays, C., & Minguet, M. (1991).
Cervicocephalic kinesthetic sensibility in patients with
cervical pain. Archives of Physical Medicine and
Rehabilitation. 72, 288-291.
Schmidt, A.J.M. & Arntz, A. (1987). Psychological research
and chronic low back pain: A stand-still or breakthrough?
Social Science and Medicine. 25 (10), 1095-1104.
Schmidt, A.J.M., Gierlings, R.E.H., & Peters, M.L. (1989).
Environmental and interoceptive influences on chronic low
back pain behavior. Pain. 38 (2),137-143.
Seeley, R.R., Stephens, T.D., & Tate, P. (1989). Anatomy and
physiology (pp. 389, 431). St. Louis: Mosby College
Publishing.
Seligman, M.E.P. (1968). Chronic fear produced by
unpredictable shock. Journal of Comparative Physiology
and Psychology. 66. 402-411.
Seltzer, S.F. & Seltzer, J.L. (1986). Tactual sensitivity of
chronic pain patients to non-painful stimuli. Pain. 27,
291-295.
Seyle, H. (1957). The stress of life. New York: McGraw-Hill.


21
concluded that "the effect of these changes includes an
expansion of dorsal horn receptive fields and
hyperexcitability which, if allowed to persist, would
presumably produce prolonged changes in excitability that
could be maintained without further noxious peripheral
input" (p. 274). Their conclusions support the idea that
chronic pain alters the ability to accurately discriminate
stimuli.
Also related to the concept of augmentors and reducers,
Barsky and Klerman (1983) proposed an information processing
model of somatic style which can be conceptualized as
perceptual amplification of bodily sensations and their
cognitive misinterpretation. In this conceptualization, the
perceptual deficit is seen as primary and the
hypochondriacal characteristics are the inevitable outcome
of these abnormal perceptions. Barsky and Klerman (1983)
suggest that attributing an internal perception to a disease
is more likely to occur when the person lacks an obvious,
immediate and adequate explanation for the symptom. This
occurs when the symptom is diffuse, ambiguous, common, and
not in a part of the body that is directly observable, as is
often the case with chronic pain. These authors discuss a
study in which a subgroup of students who scored highest on
a hypochondriasis scale were shown to have heightened levels
of arousal and heightened perceptual sensitivity to bodily
sensations. Other studies have demonstrated that anxiety
can cause people to amplify their somatic symptoms and


TABLE OF CONTENTS
page
ACKNOWLEDGMENTS iii
ABSTRACT vi
CHAPTERS
1 INTRODUCTION 1
2 CURRENT MODELS OF PAIN 6
Gate Control Theory of Pain 7
Information Processing Models of Pain 8
Sequential Processing Theory 10
Summary 10
3 SENSORY DISCRIMINATION IN PAIN PERCEPTION ... 12
Nociception 12
Sensory-Discrimination Deficits and Pain. ... 15
Proprioception and Pain 23
Summary 27
4 PHYSIOLOGICAL REACTIVITY AND PAIN 28
General Arousal 28
EMG Reactivity and Chronic Low Back Pain. ... 30
Summary 34
5 COGNITIVE-AFFECTIVE PROCESSES AND PAIN 35
Summary 39
6 SUMMARY AND HYPOTHESES 40
7 METHODS 42
Subjects 42
Measures 43
Procedures 47
IV


93
CLBP Subjects
Experimental Variables (Continued)
Pearson Correlation Coefficients/
Prob > |R| under Ho: Rho=0
/Number of Observations
MEMGR10
MEMGR10
MEMGR45
MEMGR22
MEMGA10
BLEMGAV
MEMGA45
1.00000
0.94393
0.92073
0.91709
0.91245
0.91219
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
31
31
31
31
31
31
MEMGA22
DMEMGR10
DMEMGR22
DMEMGR45
DMEMGA45
MPUN22
0.83343
0.52762
0.48080
0.47961
0.43918
0.39972
0.0001
0.0023
0.0062
0.0063
0.0134
0.0259
31
31
31
31
31
31
MPIN45
DMEMGA10
DMEMGA2 2
MPIN22
MPUN45
MPIN10
0.39140
0.36497
0.36342
0.36138
0.30873
0.29075
0.0295
0.0435
0.0445
0.0458
0.0910
0.1126
31
31
31
31
31
31
MEMGA22
MEMGA22
MEMGA45
MEMGR22
MEMGR45
BLEMGAV
MEMGR10
1.00000
0.97649
0.96747
0.94516
0.90317
0.83343
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
31
31
31
31
31
31
MEMGA10
DMEMGA2 2
DMEMGA45
DMEMGR22
DMEMGR45
ACC45
0.77801
0.73753
0.66855
0.62734
0.50611
0.31563
0.0001
0.0001
0.0001
0.0002
0.0037
0.0837
31
31
31
31
31
31
MEMGR22
MEMGR22
MEMGR45
MEMGA45
MEMGA22
BLEMGAV
MEMGR10
1.00000
0.99003
0.98554
0.96747
0.93696
0.92073
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
31
31
31
31
31
31
MEMGA10
DMEMGR22
DMEMGA22
DMEMGA45
DMEMGR45
MPIN45
0.82562
0.64092
0.61416
0.60622
0.55257
0.29652
0.0001
0.0001
0.0002
0.0003
0.0013
0.1053
31
31
31
31
31
31
MEMGA45
MEMGA45
MEMGR22
MEMGR45
MEMGA22
BLEMGAV
MEMGR10
1.00000
0.98554
0.98240
0.97649
0.95520
0.91219
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
31
31
31
31
31
31
MEMGA10
DMEMGA22
DMEMGA45
DMEMGR22
DMEMGR45
MPIN45
0.83202
0.60495
0.60300
0.56183
0.48543
0.28762
0.0001
0.0003
0.0003
0.0010
0.0056
0.1167
31
31
31
31
31
31
MEMGR45
MEMGR45
MEMGR22
MEMGA45
MEMGA22
MEMGR10
BLEMGAV
1.00000
0.99003
0.98240
0.94516
0.94393
0.94275
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
31
31
31
31
31
31
MEMGA10
DMEMGR22
DMEMGA45
DMEMGR45
DMEMGA22
DMEMGR10
0.82832
0.60129
0.58063
0.56714
0.55691
0.32892
0.0001
0.0003
0.0006
0.0009
0.0011
0.0708
31
31
31
31
31
31


56
this diagnosis. The other primary diagnoses in the CAMC
sample were bulging disk, herniated disk, spondylolisthesis,
degenerative disk disease, and other. In the UF sample, the
primary diagnoses were spondylolisthesis, degenerative disk
disease, scoliosis, and other. Regarding additional pain
syndromes, 10 of the UF subjects (66.7%) reported pain
syndromes in addition to CLBP whereas only 5 CAMC subjects
(33.3%) had more than one pain syndrome. This is likely
related to the difference in duration of pain syndromes
between the two groups.
Examining number of surgeries, only 9 of the UF
subjects (60%) had no surgeries compared with 15 (93.8%) of
the CAMC subjects. Only one of the CAMC subjects had any
back surgery (one laminectomy) whereas 5 of the UF subjects
had 2 or more back surgeries.
There were two employment categories on which the CLBP
samples differed significantly (Fisher's Exact Test 2-tail,
p= 0.00): 9 (64.3%) of the UF subjects were employed
compared with 3 (18.8%) of the CAMC subjects and 7 (43.8%)
of the CAMC subjects were on temporary disability while none
of the UF subjects were.
In summary, these differences between the two CLBP
samples reflect the nature of the clinics from which the
subjects were solicited. The subjects in the UF sample were
mostly patients from an orthopedic surgery clinic whose
patients had longer histories of back pain and had received
surgical interventions. The CAMC sample consisted of


7
activated by tissue damage or stress are termed nociceptors.
These pain receptors can be either exteroceptors, which
provide information about the external environment, or
interoceptors, which provide information about body tissues
and structures. Chapman (1986) explains that pain is not a
simple stimulus energy transduction but appears to be a
complex sensory message which results from the information
generated in a relatively large interoceptive or
exteroceptive receptive field.
Gate-Control Theory of Pain
Melzack's (1986) gate-control theory provides a
neurophysiological perspective of pain that conceptualizes
pain as more than just a function of bodily damage. The
perception of pain is also influenced by attention, anxiety,
suggestion, prior conditioning, and other psychological
variables. Melzack (1986) proposes that neural mechanisms
in the spinal cord act like a gate to increase or decrease
the flow of sensory input to the brain and can be
profoundly influenced by descending controls from the brain.
Pain occurs when the number of nerve impulses reaching the
brain exceeds a critical level.
The gate-control model also contains the concept of a
central control mechanism which activates selective
cognitive and affective processes (such as memories of prior
experiences and response strategies) that then influence, by
way of the descending fibers, the modulating properties of
the spinal gating mechanism and the experience of pain.


CHAPTERS
8 RESULTS 51
General Demographic Data 51
Chronic Low Back Pain Subjects 54
Data Reduction and Analyses 57
9 DISCUSSION 74
APPENDIX 83
REFERENCES 97
BIOGRAPHICAL SKETCH 104
v


98
Coderre, T.J., Katz,J., Vaccarino, A.L. & Melzack, R.
(1993). Contribution of central neuroplasticity to
pathological pain: review of clinical and experimental
evidence. Pain, 52, 259-285.
Cohen, J. (1977). Statistical power analysis for the
behavioral sciences. Orlando, Florida: Academic Press,
Inc.
Cohen, M.J., Naliboff, B.D., Schandler, S.L., & Heinrich,
R.L. (1983). Signal detection and threshold measures to
loud tones and radiant heat in chronic low back pain
patients and cohort controls. Pain. 16, 245-252.
Crombez, G., Baeyens, F., & Eelen, P. (1994). Sensory and
temporal information about impending pain: the influence
of predictability on pain. Behavior Research and Therapy.
32 (6), 611-622.
Dolce, J.J. & Raczynski, J.M. (1985). Neuromuscular activity
and electromyography in painful backs: Psychological and
biomechanical models in assessment and treatment.
Psychological Bulletin. 97 (3), 502-520.
Duffy, E. (1972). Activation. In N.S. Greenfield & R.A.
Sternbach (Eds.), Handbook of psychophysiology (pp. 577-
622). New York: Holt, Rinehart & Winston.
Fernandez, E. & Milburn, T.W. (1994). Sensory and affective
predictors of overall pain and emotions associated with
affective pain. Clinical Journal of Pain. 10. 3-9.
Fernandez, E. & Turk, D.C. (1995). The scope and
significance of anger in the experience of chronic pain.
Pain. 61, 165-175.
Feuerstein, M. (1986). Ambulatory monitoring of paraspinal
skeletal muscle, autonomic and mood-pain interaction in
chronic low back pain. Paper presented at the 7th Annual
Meeting of the Society of Behavioral Medicine, San
Francisco, CA.
Flor, H., Birbaumer, N., Schugens, M.M., & Lutzenberger, W.
(1992). Symptom-specific psychophysiological responses
in chronic pain patients. Psychophysiology. 29 (4), 452-
460.
Flor, H., Schugens, M.M., & Birbaumer, N. (1992).
Discrimination of muscle tension in chronic pain patients
and healthy controls. Biofeedback and Self-Regulation. 17
(3), 165-177.


3
implications for chronic pain conditions in which organic
findings are absent or inappropriate for the pain reported.
In this model, learning processes produce long-term meaning
structures relevant to the experience of pain. Through
these meaning structures, stimuli that vary considerably in
physical properties may take on functional equivalence for
the perceiver. Thus, various somatic stimuli could be
perceived as equivalent stimuli and, therefore, as painful.
In a discussion of the influence of perceptual
discrimination on pain, Sternbach (1968) described the
concept of augmenters and reducers, whereby people display a
consistent tendency to over/underestimate magnitude
estimations of sensory stimuli. Reducers have been found to
tolerate more experimental pain than augmenters (Sternbach,
1968). In a related vein, Barsky and Klerman (1983) suggest
that hypochondriacal patients suffer from a perceptual or
cognitive abnormality whereby they incorrectly assess and
misinterpret the somatic symptoms of emotional arousal and
normal bodily function. Barsky and Klerman's concept of
hypochondriasis in chronic pain is consistent with Lundl's
model of stimulus equivalence in that different somatic
sensations may be perceived as equivalent. These
conceptualizations as well as that of perceptual augmenters
and reducers are consistent with Chapman's information
processing model of chronic pain.
Turning from the cognitive-perceptual to the cognitive-
affective dimension of pain, a link between negative affect,


23
congruous with the evidence presented in the Coderre et al.
(1993) review that pain induces CNS and cellular changes
that can maintain pain without additional noxious input.
Proprioception and Pain
Proprioception refers to nociceptive information on
body position provided to the central nervous system through
input from muscle, joint, and cutaneous afferents (Grigg,
Finerman, & Riley, 1973; Newton, 1982; Proske, Schaible, &
Schmidt, 1988; Inglis, Frank, & Inglis, 1991). Revel,
Andre-Deshays, and Minguet (1991) investigated the ability
to discriminate neck proprioception in 30 patients with
cervical pain and in 30 healthy controls. The authors
discussed the paradox that although rehabilitation in the
field of musculoskeletal diseases aims to improve muscle
strength, joint mobility, and "proprioceptive sensibility,"
proprioceptive ability has not been well documented in
healthy subjects and had never been studied in patients with
cervical pain. In their study, subjects' ability to
relocate the head on the trunk after an active head movement
was tested. The results indicated that active head
repositioning was significantly less precise in the cervical
pain subjects who showed an overshoot in horizontal plane
repositioning movements. The authors concluded that
patients with neck pain may demonstrate altered
proprioceptive sensibility due to "functional alterations of
tendinous and muscular proprioceptors related to neck muscle
function disturbances (p.291)."


54
undergone two surgeries, and 2 subjects had undergone 3 or
more surgeries. These surgeries consisted of laminectomies,
fusions, diskectomy, nerve decompression, and spinal
stimulation implant. CLBP subjects with multiple surgeries
had undergone more than 1 fusion.
Chronic Low Back Pain Subjects
Description of Clinical Pain
Frequency of pain was constant for 26 subjects and
intermittent/daily for 5 subjects. Means for ratings of
average pain and present pain (on a 0-10 scale where 0=no
pain and 10=worst pain imaginable) were 4.9 (SD=1.7) and 4.4
(SD=2.2), respectively. Across sites the average duration
of CLBP syndrome was 63.8 months (SD=67.4).
On the McGill Pain Questionnaire (MPQ), CLBP subjects'
mean scores (SD) were as follows: Sensory=12.8 (7.1),
Affect=1.2 (1.7), Evaluative=l.7 (1.5), Miscellaneous=3.7
(3.0), PRI=19.5 (10.7), and PPI=2.2 (1.0). Since the MPQ
and the negative affect measures were given to pain subjects
before beginning the proprioceptive task, it is of interest
to examine the correlations between the pain scales and the
negative affect measures (see Appendix for the Pearson
Correlation Coefficients for these varibles).
The MPQ Sensory scale was significantly correlated with
all three negative affect measures, state anxiety (r=0.56,
p=0.001), state anger (r=0.46, p=0.011), and BDI (r=0.36,
p=0.05). The MPQ Affect scale was significantly correlated
only with the BDI (r=0.36, p=0.05). None of the negative


15
Guilbaud's discussion suggests that in an attempt to
locate the source of pain, physiological changes may occur
in the central nervous system that result in an augmentation
of signals from deep somatic receptors and an increase in
inhibition of sensory input from peripheral receptors. This
is consistent with the gate-control theory of pain, Price's
discussion of the diffuse type of input from deep somatic
tissues, and studies that have demonstrated poor
discriminability of peripheral stimuli in chronic pain
subjects. These discriminability studies are discussed in
the following section.
Sensory-Discrimination Deficits and Pain
Historically, pain has been evaluated in terms of
threshold (the point at which a person first experiences
pain) and tolerance (how much pain the person can endure).
The measurement of pain has become more sophisticated, and
the application of methods such as signal detection theory
(SDT) has allowed researchers to differentiate between
discriminability, the ability to distinguish between
different levels of stimulation, and response bias, the
predisposition to report stimulation as painful.
Lloyd and Appel (1976) have reviewed SDT studies
concerning modification of discriminability and response
bias by placebos and suggestion. They report that placebos
and suggestion modified response bias (tolerance) but not
discriminability. Clark (1974) has also found that
suggestion had no effect on subjects' ability to


50
proceeded through 5 trials as described above. After the
last recovery phase for the second target angle, subjects
were guided to the third angle and proceeded through 5
trials as above. After the completion of the experiment,
the ELT was removed and subjects were fully debriefed.
Completion of the questionnaires and body position
proprioception task took approximately 45 minutes.


as nociceptive information (p. 89)." He concludes that
there is evidence that
14
similar principles of nociceptor functioning extend
across different tissues .... that C polymodal
nociceptive afferents similar to those innervating skin
appear to innervate muscle, testes, and perhaps the
lung and cardiovascular system . [and] the latter
type of nociceptive afferent [C polymodal] comprises a
large proportion of the nociceptive afferents
innervating different tissues. The physiological
characteristics of polymodal nociceptors are those
which may well account for pains that are diffuse,
poorly localized, and poorly discriminated in terms of
modality, (p. 93)
Thus, there is evidence that the physiological
properties of a large number of nociceptors are such that
they provide input to the organism that is diffuse and
difficult to discriminate, as is freguently the case with
chronic pain symptoms. This evidence is consistent with
both the hypochondriasis and stimulus-equivalence models of
chronic pain.
In a discussion of the results of animal studies
investigating central neurophysiological processing of joint
pain in experimentally-induced arthritis, Guilbaud (1991)
proposes that changes in the modulary systems may occur in
order to allow the central nervous system to locate the
source of the pain. Guilbaud proposes that some spinal
and/or supraspinal controls might differentially modulate
the various peripheral somatic inputs, and she cites several
studies which have demonstrated an augmentation in the
dorsal horn of both excitatory and inhibitory controls
triggered by the inflamed joints.


99
Flor, H. & Turk, D.C. (1989). Psychophysiology of chronic
pain: Do chronic pain patients exhibit symptom-specific
psychophysiological responses? Psychological Bulletin.
105 (2), 215-259.
Flor, H., Turk, D.C., & Birbaumer, N. (1985). Assessment of
stress-related psychophysiological reactions in chronic
back pain patients. Journal of Consulting and Clinical
Psychology. 53 (3), 354-364.
Fuller, A. & Robinson, M.E. (1995). Perceptual differences
between patients with chronic low back pain and healthy
volunteers using magnitude matching and clinically
relevant stimuli. Behavior Therapy. 26. 241-253.
Gaskin, M.E. Chronic pain: Evidence of a central processing
mechanism? Unpublished master's thesis, University of
Florida, Gainesville, FL, 1991.
Gaskin, M.E., Greene, A.F., Robinson, M.E.,& Geisser, M.E.
(1992). Negative affect and the experience of chronic
pain. Journal of Psychosomatic Research. 36. 707-713.
Geisser, M.E., Gaskin, M.E., Robinson, M.E., & Greene, A.F.
(1993) The relationship of depression and somatic focus
to experimental and clinical pain in chronic pain
patients. Psychology and Health. 8 (6), 405-415.
Geisser, M.E., Robinson, M.E. & Richardson, C. (1995). A
time series analysis of the relationship between
ambulatory EMG, pain, and stress in chronic low back
pain. Biofeedback and Self-Regulation. 20 (4), 339-355.
Grigg, P., Finerman, G.A., Riley, L.H. (1973). Joint-
position sense after total hip replacement. Journal of
Bone and Joint Surgery. 55-A (5), 1016-1025.
Guilbaud, G. (1991). Central neurophysiological processing
of joint pain on the basis of studies performed in normal
animals and in models of experimental arthritis. Canadian
Journal of Physiological Pharmacology. 69. 637-646.
Guyton, A.C. (1991). Textbook of medical physiology (8th
ed.), (pp. 478-531). Philadelphia: W.B. Saunders.
Hall, K. R. L. & Stride, E. (1954). The varying response to
pain in psychiatric disorders: a study in abnormal
psychology. British Journal of Medical Psychology. 27,
48-60.
Inglis, J.T., Frank, J.S., Inglis, B. (1991). The effect of
muscle vibration on human position sense during movements
controlled by lengthening muscle contraction.
Experimental Brain Research. 84. 631-634.


84
Control Subjects
Correlation Analysis with Demographic Variables
Pearson Correlation Coefficients /
Prob > |R| under Ho: Rho=0 /
Number of Observations
AGE
RB45
0.39642
0.0273
31
ACC45
0.32222
0.0771
31
BMI
-0.20029
0.2800
31
BDI
0.18986
0.3063
31
RB22
0.18907
0.3084
31
HEIGHT
BMI
0.38443
0.0327
31
MEMGA45
0.37354
0.0385
31
BLEMGAV
0.35044
0.0533
31
MEMGR45
0.34979
0.0537
31
MEMGA10
0.33487
0.0656
31
MEMGR22
0.33213
0.0679
31
MEMGA22
0.31593
0.0834
31
MEMGR10
0.30267
0.0979
31
WEIGHT
BMI
0.87074
0.0001
31
MEMGA22
0.39152
0.0294
31
MEMGA45
0.38735
0.0313
31
MEMGA10
0.36295
0.0448
31
MEMGR22
0.35995
0.0467
31
BLEMGAV
0.33615
0.0645
31
MEMGR45
0.32085
0.0784
31
DMEMGA45
0.30929
0.0904
31
EDUCATION
ACC10
-0.33146
0.0685
31
ACC22
-0.31378
0.0856
31
RB10
-0.29975
0.1092
31
DMEMGR10
-0.29335
0.1092
31



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81,9(56,7< 2) )/25,'$


30
of chronic pain that maintains the condition, or both. They
suggest that regardless of the specific pain condition,
chronic pain patients may display nonspecific physiological
changes associated with pain, such as increased heart rate,
that are indicative of heightened arousal. Peters and
Schmidt (1991) found support for this in their study where
CLBP subjects reacted to pain stimuli with a greater
increase in the number of skin conductance fluctuations,
which were also of greater maximal amplitude, than controls.
Flor and Turk (1989) also suggest that patients with a
particular pain disorder may show specific physiological
response patterns, for example, elevated paraspinal
electromyographic (EMG) responses in CLBP patients.
EMG Reactivity and Chronic Low Back Pain
A wide range of tasks have been used in studies on the
psychophysiology of CLBP, including positioning, movement
and lifting tasks, relaxation tasks, mental arithmetic,
personally relevant stress, and experimental pain tasks,
such as the cold pressor test (Flor & Turk, 1989). In two
reviews containing summaries of the results of studies
utilizing these various tasks, investigators have found
lower EMG levels, no differences in EMG levels, or higher
EMG levels in the paraspinal muscles of CLBP patients as
compared to healthy controls (Dolce & Raczynski, 1985; Flor
& Turk, 1989). These findings have lead some researchers to
hypothesize that absolute levels of EMG activity are not as
relevant to the development and/or maintenance of back pain


2
a dynamic model in which the experience of pain is
determined by many factors in addition to tissue damage.
These factors include personality, culture, and other
activities in the nervous system at the time of injury. The
gate-control theory proposes that signals from an injury can
be radically modified or even blocked at the earliest stages
of transmission in the nervous system by a central control
mechanism that activates selective cognitive processes
involved in evaluating the different aspects of pain
(Melzack, 1986; Price, 1988).
In a parallel vein, Chapman (1986) uses an information
processing model to provide a way to conceptualize the many
facets involved in the experience of pain. In this model, a
painful stimulus contains many sources of information so
that the barrage of sensory inputs that result are more than
simple energy transductions from the pain receptors to the
central nervous system. The various classes of information
transmitted are filtered and then modulated or inhibited as
these inputs are processed through peripheral mechanisms,
brainstem, and higher central processing areas (Chapman,
1986). Therefore, the relationship between the intensity of
the pain stimulus and the pain reported is subject to
individual variation and depends upon the person's
perceptual accuracy, previous experience with pain, and
attitudes toward pain.
Chapman (1986) also discusses Lundl's cognitive-
perceptual model of stimulus equivalence which has


96
CLBP Subjects
Negative Affect Variables and
McGill Pain Questionaire (MPQ) Scales
Pearson Correlation Coefficients /
Prob > |R| under Ho: Rho=0 / N = 31
MPQ
SENSORY SCALE
STANX
STANGER
BDI
0.56338
0.44738
0.35452
0.0010
0.0116
0.0504
MPQ
AFFECTIVE SCALE
BDI
STANGER
STANX
0.35569
0.29077
0.28577
0.0496
0.1125
0.1191
MPQ
EVALUATIVE SCALE
BDI
STANX
STANGER
0.11655
0.08196
0.02953
0.5324
0.6611
0.8747
MPQ
MISCELLANEOUS SCALE
STANX
BDI
STANGER
0.43308
0.14630
0.11195
0.0149
0.4323
0.5488
MPQ
PRI (PAIN RATING
INDEX)
STANX
STANGER
BDI
0.55063
0.37615
0.34694
0.0013
0.0370
0.0559
MPQ
PPI (PRESENT PAIN
INDEX)
STANX
STANGER
BDI
0.39533
0.37952
0.34007
0.0277
0.0352
0.0612


This study examined the following variables derived
from the components described above: negative affect
(anxiety, anger, depression), EMG reactivity of the lumbar
paraspinal muscles, trunk proprioception (response accuracy,
response bias), and visual analogue scale ratings (VAS) of
pain intensity (PIN) and pain unpleasantness (PUN) to an
ecologically valid stressor (bending) in 31 CLBP patients
and 31 age- and sex-matched pain-free controls. Subjects
were asked to reproduce bending to three angles (-10, 22,
45) over five trials, rating PIN and PUN after each trial.
Subjects received no feedback on their performance.
Results of analyses demonstrated that CLBP subjects had
higher ratings of negative affect, pain intensity and pain
unpleasantness than controls. On measures of proprio
ception, although there were no differences between groups
on response accuracy, there was a difference in the pattern
of response bias between groups across angles. Patterns of
EMG reactivity also differed by group and angle relative to
baseline EMG and were consistent with the biomechanical
model of CLBP.
The results of this study provide partial support for
the hypotheses generated regarding the components of a
proposed dysfunctional central mechanism that mediates the
experience of chronic pain.
vii


CHAPTER 5
COGNITIVE-AFFECTIVE PROCESSES AND PAIN
Regarding the relationship between cognitive-affective
processes and pain, evidence is growing to implicate the
role of negative affect, especially anxiety, anger, and
depression, in the experience of chronic pain (Linton &
Gotestam, 1985; Feuerstein, 1986; Wade, Price, Hamer,
Schwartz, & Hart, 1990; Jensen, Karoly, & Harris, 1991;
Gaskin et al., 1992; Geisser, Gaskin, Robinson, & Greene,
1993). Examining the relationship between anxiety and pain,
Sternbach (1968) reports that many studies indicate that
persons who are more anxious show greater pain responses.
Hall and Stride (1954) found that the appearance of the word
"pain" in instructions made anxious subjects report as
painful a level of electric shock that they did not regard
as painful when the word was absent from the instructions.
The authors concluded that the mere anticipation of pain
increased anxiety and thereby increased the intensity of
perceived pain.
Ahles and colleagues (1987) reported that college
students who were attentive to somatic symptoms and scored
high on state anxiety reported more areas as painful and
rated these sensations as more noxious. Geisser et al.
(1993) found that in a mixed group of chronic pain patients,
35


85
CLBP Subjects
Correlation Analysis with Demographic Variables
Pearson Correlation Coefficients /
Prob > |R| under Ho: Rho=0 /
Number of Observations
AGE
RB45
-0.54440
0.0015
31
BMI
0.29755
0.1103
30
MEMGA45
0.29437
0.1079
31
BLEMGAV
0.28872
0.1152
31
BDI
-0.28541
0.1196
31
HEIGHT
MEMGR45
0.46930
0.0089
30
MEMGR22
0.44650
0.0134
30
MEMGR10
0.41286
0.0234
30
BLEMGAV
0.41017
0.0244
30
MEMGA45
0.40579
0.0261
30
MEMGA22
0.39994
0.0285
30
DMEMGR45
0.34412
0.0626
30
BDI
0.31658
0.0903
30
DMEMGR22
0.30298
0.1036
30
WEIGHT
BMI
0.88521
0.0001
30
DMEMGA10
-0.34059
0.0655
30
MPIN10
-0.32829
0.0765
30
RB10
-0.25416
0.1753
30
MPUN10
-0.24180
0.1980
30
YEARS EDUCATION
BDI
-0.33167
0.0734
30
MEMGA10
0.29801
0.1097
30
BLEMGAV
0.29040
0.1195
30
MEMGR10
0.28716
0.1239
30
MEMGA45
0.25712
0.1702
30
TOTAL SURGERIES
BDI
0.36018
0.0466
31
RB45
0.34575
0.0568
31
ACC 10
0.26567
0.1486
31
RB10
-0.23825
0.1968
31
RB22
0.15538
0.4039
31
PAIN DIAGNOSES
STANX
-0.53119
0.0110
22
BDI
-0.45486
0.0334
22
RB10
-0.41549
0.0545
22
ACC22
0.33630
0.1259
22
STANGER
-0.30855
0.1624
22
PAIN DURATION
STANX
-0.44216
0.0128
31
BDI
-0.32638
0.0731
31
MEMGA10
0.30623
0.0938
31
STANGER
-0.28686
0.1177
31
DMEMGA10
0.24424
0.1855
31
PAIN FREQUENCY
MPUN10
-0.48518
0.0057
31
MPUN45
-0.46533
0.0083
31
MPIN10
-0.46196
0.0089
31
MPUN22
-0.40067
0.0255
31
MPIN45
-0.37680
0.0367
31
MPIN22
-0.35823
0.0478
31
STANX
-0.30417
0.0962
31


64
Table 8-11. Recovery EMG Means (SD) Baseline & Trials
Group
Baseline
i
H
O
o
22
45
CLBP
6.96 (4.3)
8.77 (5.0)
8.97 (5.3)
9.02 (5.1)
Controls
5.86 (3.6)
7.33 (4.3)
6.92 (4.3)
7.37 (5.0)
Since CLBP subjects and controls differed significantly
on BMI [t(50.2)=-3.25, p=-0.002; Means: CLBP=28.35 (5.6);
controls=24.39 (3.7)], EMG changes from baseline for the
anticipatory and recovery phases for the three target angles
were examined by repeated measures MANCOVA's using BMI as a
covariate to assess the influence of BMI on EMG recordings.
Results of these MANCOVA's showed no significant effect on
EMG change from baseline for either anticipatory or recovery
EMG (Tables 8-12 and 8-13). Only if EMG is collapsed across
all three angles does level of BMI marginally affect level
of anticipatory (p=0.06) and recovery (p=0.6) EMG change
from baseline by group (Figures 8-8 and 8-9). These results
suggest the possibility of a slight muting effect on EMG
recordings with higher levels of BMI.
Table 8-12. Mean (SD) Anticii
oatory EMG Change from Baseline
Group
-10
22
45
CLBP
0.71 (3.2)
1.14 (2.8)
0.83 (1.6)
Controls
-0.08 (1.7)
-0.06 (1.3)
0.48 (2.2)
Table 8-13. Mean (SD) Recovery EMG Change from Baseline
Group
M
O
o
22
45
CLBP
1.87 (2.1)
2.04 (2.0)
2.11 (1.8)
Controls
1.47 (1.9)
1.06 (1.4)
1.51 (2.0)


61
The repeated measures MANOVA for response bias showed
no effect for either group or angle but was marginally
significant for an angle X group interaction [F(2,59)=2.99,
p=.058] (see Table 8-8 for means and standard deviations),
while univariate analysis of the interaction of angle X
group was significant (p=0.0496). Polynomial contrast
demonstrated a subtle but significant difference (p=0.03) in
quadratic trends. The curve for the response bias of the
pain subjects was an inverted "V" with CLBP subjects
overshooting target angle 22 while slightly undershooting
target angle -10 and demonstrating almost no response bias
at target angle 45. The curve for the controls was almost
the inverse with controls slightly overshooting target angle
-10 while demonstrating little response bias at target
angle 22 but overshooting target angle 45. (See Figure
8-5). Pain subjects demonstrated the smallest response bias
at the two angles which were the most difficult/painful for
them.
Table 8-8. Means (SD) for Response Bias
Target Angle
Controls
CLBP
i
M
O
o
1.1 (12.8)
-1.9 (11.5)
o
CS]
CN
0.9 (28.5)
9.6 (30.1)
45
7.8 (24.6)
0.1 (25.8)
Cohen's d was calculated for response accuracy and
response bias (see Table 8-9) to determine effect size. The
resulting effect size is so small that it is very likely to


103
Shacham, S., Dar, R., & Cleeland, C.S. (1984). The
relationship of mood state to the severity of clinical
pain. Pain. 18 187-197.
Sherman, R.A. (1985). Relationships between strength of low
back muscle contraction and reported intensity of chronic
low back pain. American Journal of Physical Medicine. 64
(4), 190-200.
Spielberger, C.D. (1988). State-Trait Anger Expression
Inventory professional manual. Psychological Assessment
Resources, Inc.: Odessa.
Spielberger, C.D., Jacobs, G., Crane, R. Russell, S.,
Westberry, L., Barker, L., Johnson, E., Knight, J.,
Marks, E. (1983) Preliminary manual for the State-Trait
Personality Inventory (STPI). unpublished manuscript.
Sternbach, R. A. (1966). Principles of psychophysiology. New
York: Academic Press.
Sternbach, R. A. (1968). Pain: A psychological analysis.
(pp. 1-24). New York: Academic Press.
Wade, J.B., Price, D.D., Hamer, R.M., Schwartz, S.M., &
Hart, R.P. (1990). An emotional component analysis of
chronic pain. Pain. 40. 303-310.
Weisenberg, M. (1977). Pain and pain control. Psychological
Bulletin. 84 (5), 1008-1044.
Williams, R.B., Jr., Kuhn, C.M., Melosh, W., White, A.D., &
Schanberg, S.M. (1982). Type A behavior and elevated
physiological and neuroendocrine responses to cognitive
tasks. Science. 218 (29), 483-485.
Wolf, S.L., Wolf, L.B., & Segal, R. L. (1989). The
relationship of extraneous movements to lumbar paraspinal
muscle activity: implications for EMG biofeedback
training applications to low back pain patients.
Biofeedback and Self-Regulation. 14 (1), 63-74.
Yang, J.C., Richlin, D., Brand, L., Wagner, J., & Clark,
W.C. (1985). Thermal sensory decision theory indices and
pain threshold in chronic pain patients and healthy
volunteers. Psychosomatic Medicine. 47 (5), 461-468.


CHAPTER 7
METHODS
Subjects
Collection Sites
Data was collected from two sites: Gainesville,
Florida and Charleston, West Virginia. Pain subjects were
recruited from the outpatients at the Orthopedic and
Physical Therapy Clinics at Shands Hospital, University of
Florida, Gainesville, Florida, and the Sports Medicine
Center at Charleston Area Medical Center (CAMC), General
Division, Charleston, West Virginia. Control subjects for
both sites were recruited from the respective local
community.
The University of Florida (UF) sample consisted of 30
subjects: 15 pain-free controls and 15 CLBP subjects with
seven females and eight males in each group. The CAMC
sample consisted of 32 subjects: 16 pain-free controls and
16 CLBP subjects with five females and eleven males in each
group.
Inclusion Criterion
Pain subjects had a CLBP syndrome of at least 6 months'
duration and experienced pain on a daily basis. Pain-free
controls were free of any pain condition for at least the
42


5
The various models of chronic pain described above
propose a central process which is responsible for
regulating the organism's responses to external and/or
internal stimuli. Dysfunction of this process, such as may
be the case in chronic pain, could be manifested across
several dimensions: 1) the cognitive-affective experience of
pain, such as anxiety, anger, and depression; 2)
abnormalities in the sensory-discriminative component of
pain, such as poor discrimination of somatic stimuli; and 3)
altered physiological reactivity due to pain. The current
study proposes to explore these dimensions of pain in both
chronic pain and pain-free individuals.


46
in each group increasing in rank order intensity. The sum
of the rank values for each descriptor based on its position
in the word set results in a score called the Pain Rating
Index (PRI). The MPQ also consists of several subscales:
the Sensory PRI, Affective PRI, Evaluative PRI,
Miscellaneous PRI, Present Pain Intensity (PPI), and Number
of Words Circled. Clinical and experimental data have
demonstrated that the MPQ displays acceptable reliability
and validity as a method of measuring subjective pain
experience (Melzack, 1985; Reading, 1985). Data from this
instrument was used to characterize the CLBP sample.
Visual Analogue Scales. Visual analogue scales (VAS's)
were used to measure pain intensity and pain-related
unpleasantness. Price (1988) stresses the importance of
using ratio scales, such as VAS's, in the measurement of
pain. Ratio scales are superior to ordinal and interval
scales in that ratio scales serve to reflect actual ratios
of magnitude. Price (1988) states that VAS's have been
shown to demonstrate reliable power functions for ratings of
pain intensity and unpleasantness. He concludes from a
review of studies comparing the use of different types of
VAS;s that "those VAS's that most clearly delineate extremes
(i.e., the worst pain, the most intense pain imaginable) and
are 10-15 cm in length have been shown to have the greatest
sensitivity and are the least vulnerable to distortions or
biases in ratings (p. 33)."


59
(22) as least painful (see Table 8.6 for means and standard
deviations).
Univariate analysis of pain subjects' ratings of pain
unpleasantness showed the same pattern (see Table 8.6 for
means and standard deviations). There was no signficant
difference in ratings for angles -10 and 45 (F=0.91,
p=0.35) whereas the ratings for angles -10 and 22 were
significantly different (F=6.62, p=0.02) and the difference
in ratings for angles 22 and 45 approached significance
(F=3.56, p=0.07). Again, pain subjects rated their pain as
more unpleasant at the more difficult angles and least
unpleasant at the less difficult angle (see Figure 8-13).
These results are consistent with pain subjects' verbal
reports (complaints) and/or behavioral difficulties
(inability to achieve target angle, increased pain
behaviors) with angles -10 and 45.
Table 8-6. Means (Standard Deviations) for PIN and PUN
O
O
rH
1
22
o
in
PIN
5.61 (2.7)
4.66 (3.3)
5.24 (3.3)
PUN
5.59 (2.9)
4.58 (3.3)
5.17 (3.5)
Accuracy of subjects' ability to reproduce each body
position was calculated by summing the absolute value of the
difference scores from the target angle across the 5 trials
for each angle. This yielded a total response accuracy
score for each of the 3 body positions with lower scores
indicating that a subject's performance was more accurate.


49
Subjects were allowed to habituate to the ELT device for a 5
minute baseline phase during which they were instructed to
"keep your arms at your sides and remain as still as
possible."
Collection of angle and EMG data began during the
baseline phase. Body position angles (-10, 22, 45) and
PIN and PUN VAS's were presented in a counterbalanced order
to control for possible order effects. After the 5 minute
baseline period, subjects were guided to the first target
angle and held in place for 5 seconds. They were then
instructed to "stand straight." Once standing straight, a
10 second recovery period began. After this phase, subjects
received the 10 second warning ("in 10 seconds I will tell
you to bend"). After this 10 second anticipatory phase,
subjects were instructed to "bend." Once subjects reached
their approximation of the target, they were told to "stand
straight." A 10 second recovery phase began at this point
during which subjects were presented with the PIN and PUN
VAS's and asked to "rate pain intensity and pain
unpleasantness" with a pencil on the lines. The VAS's were
presented to subjects in such a way as to minimize any gross
movement of the arm during this procedure. After the 10
second recovery phase, the next anticipatory phase with a 10
second warning began. The anticipatory, bending, and
recovery phases were repeated for a total of 5 trials.
After the last recovery phase for the first target
angle, subjects were guided to the next target angle and


29
Thus, in chronic pain patients, general physiological
hyperactivity associated with high levels of sympathetic
activation might lead to the development, exacerbation, and
maintenance of pain symptoms (p. 216)."
In a study related to this issue, Perry, Heller,
Kamiya, and Levine (1989) compared autonomic functioning in
healthy controls to that of patients with arthritis or
myofascial pain. The authors also examined differences in
autonomic functioning between the two chronic pain groups.
Although both pain groups were similar on several
parameters, there were differences between these groups.
The authors concluded that both pain groups demonstrated
similar alterations in autonomic function, although the
alterations were not identical, underscoring the importance
of investigating different pain syndromes separately. The
authors suggest that the changes in autonomic function they
observed may have been due "to the presence of pain, to the
presence of stress, or to the presence of other
psychophysiological concomitants occurring in chronic pain
syndromes (p. 82)." They posit that altered autonomic
functioning may contribute to the maintenance of chronic
pain syndromes and that further study of this functioning in
patients with specific pain syndromes is warranted.
In a review of research on the physiological response
patterns of chronic pain patients, Flor and Turk (1989)
discuss the theory that aberrant physiological patterns
could be an antecedent to chronic pain states, a consequence


37
component in ratings of overall pain in a group of 40
chronic pain patients.
In a clinical review, Fernandez and Turk (1995)
concluded that available research indicates that anger is
one of the most salient emotional correlates of chronic pain
although past research has been focused on depression and
anxiety. In addition to discussing cognitive appraisal
models of anger in chronic pain patients, the authors
suggest that anger in chronic pain patients may be partially
explained by a physiological model where anger is an
"innate" response triggered via subcortical pathways by
aversive stimuli such as pain. A non-cognitive activation
of anger in chronic pain patients in response to their pain
is a likely concomitant of autonomic arousal to this
aversive condition.
Feuerstein (1986) reports that low back pain subjects
had greater levels of anger, anxiety, and depression
compared to asymptomatic controls. He studied paraspinal
skeletal muscle activity (EMG), autonomic nervous system
activity (heart rate), gross motor activity, and emotional
state in chronic low back pain subjects and asymptomatic
age- and sex-matched controls. EMG levels and gross motor
activity did not differ between groups, although mood
measures indicated greater levels of anxiety, tension,
depression, anger, fatigue, confusion, and less vigor in the
low back pain subjects. Increased heart rate was modestly
correlated with reported pain. Feuerstein concluded that


60
On response accuracy, repeated measures MANOVA showed
an angle effect [F(2,59)=23.99, p=.0001] but no effect for
group or group X angle (see Table 8-7 for means and standard
deviations). All subjects were most accurate at angle -10
and least accurate at angle 22 (see Figure 8-4).
Collapsing across groups, the difference in response
accuracy was statistically significant between angle -10
and both angles 22 and 45 [F(1,60)=38.60, p=0.0001;
F(l,60)=20.26, p=0.001] while the difference between angles
22 and 45 was not significant.
Table 8-7.
Means (SD)
for Response Accuracy
Target
Anqle
Controls
CLBP
Both
Groups
-10
10.9 (6.7)
10.4 (5.4)
10.7
(6.0)
22
24.9 (13.5)
23.8 (21.1)
24.4
(17.6)
o
in
20.1 (16.6)
21.1 (15.0)
20.6
(15.7)
Subjects' response bias was calculated by summing the
actual value for the angular error from the target angle
across the 5 trials. This provided a measure of undershoot
or overshoot across the 5 trials for each of the 3 body
positions. For example, on a trial with a target angle of
22 flexion where the subject bends to 15 flexion, the
amount of undershoot is -7 for that trial. Differences
between CLBP subjects and controls on these proprioception
measures were assessed by MANOVA.


ANTICIPATORY EMG
ANGLE = 10 DEGREES ANGLE = 22 DEGREES ANGLE = 45 DEGREES
Figure 8-6. MEAN ANTICIPATORY EMG INTERACTION WITH COVARIATE
^4
O
kJI 1Z3 AQUlVai^Ullv


10
Sequential Processing Theory
Based upon current knowledge of the neurophysiology and
psychology of pain, Price (1988) proposes a sequential
processing theory of pain which extends the physiology of
the gate-control theory and incorporates the cognitive-
affective components of the information-processing model.
In the sequential processing theory, nociceptive input
simultaneously activates neural structures involved in
arousal, sensory-discriminative, autonomic, and motor
responses. Price suggests that the nature and magnitude of
the body's responses to nociceptive input undergo cognitive-
evaluative appraisal which mediates the affective response
to pain. This cognitive appraisal is influenced by
attitudes, memories, and the context of the situation in
which the pain occurs. In this model, pain affective
responses are the end result of nociceptive input.
Summary
In summary, the gate-control theory places emphasis on
the neurophysiology of pain, the information-processing
model focuses on pain from a cognitive-perceptual
perspective, and the sequential processing model
incorporates elements of both models with the end result
being pain-related affect. All of these models identify a
central process which organizes information and modulates
the experience of pain through sensory discrimination of
nociceptive stimuli, physiological responsivity, and
cognitive-affective processes. The following chapters


90
Control Subnects
Experimental Variables (Continued)
Pearson Correlation Coefficients/
Prob > IR1 under Ho: Rho=0/N = 31
DMEMGA45
DMEMGA45
1.00000
0.0
DMEMGR45
0.79471
0.0001
DMEMGR22
0.77325
0.0001
MEMGA10
0.66641
0.0001
MEMGR
0.59107
0.0005
45MEMGA
0.58986
0.0005
RB45
0.40703
0.0231
ACC45
0.38526
0.0323
BLEMGAV
0.38177
0.0341
DMEMGR45
DMEMGR4 5
1.00000
0.0
DMEMGR22
0.82860
0.0001
MEMGR45
0.80625
0.0001
MEMGR22
0.74234
0.0001
MEMGA22M
0.70925
0.0001
EMGA10
0.69098
0.0001
ACC 10
ACC10
1.00000
0.0
ACC22
0.38130
0.0343
DMEMGR22
-0.37299
0.0388
ACC22
ACC22
1.00000
0.0
RB22
0,47097
0.0075
ACC10
0.38130
0.0343
ACC45
ACC45
1.00000
0.0
MPUN10
0.69639
0.0001
RB45
0.56802
0.0009
DMEMGA10
0.40605
0.0234
RB22
0.39601
0.0274
DMEMGA45
0.38526
0.0323
RB10
RB10
1.00000
0.0
RB22
0.58717
0.0005
BLEMGAV
0.24155
0.1905
RB22
RB22
1.00000
0.0
RB10
0.58717
0.0005
RB45
0.48670
0.0055
RB45
RB45
1.00000
0.0
ACC45
0.56802
0.0009
RB22
0.48670
0.0055
DMEMGA2 2
0.31146
0.0881
ACC22
0.30610
0.0940
DMEMGR10
0.24521
0.1837
MEMGA45
DMEMGA10
DMEMGA2 2
0.73569
0.69001
0.68738
0.0001
0.0001
0.0001
22DMEMGR10
MEMGR22
MEMGR10
0.57458
0.57032
0.56862
0.0007
0.0008
0.0008
MPIN45
ACC10
MPIN22
-0.26636
-0.25809
-0.24937
0.1475
0.1610
0.1761
DMEMGA45
MEMGA45
MEMGR10
0.79471
0.77812
0.75543
0.0001
0.0001
0.0001
DMEMGR10
BLEMGAV
DMEMGA2 2
0.64866
0.56740
0.53480
0.0001
0.0009
0.0019
DMEMGR45
MEMGR22
DMEMGA45
-0.30580
-0.26372
-0.25809
0.0943
0.1517
0.1610
STANGER
0.36109
0.0460
RB45
0.30610
0.0940
STANX
-0.28679
0.1178
MPIN10
0.44373
0.0124
MPUN45
0.43884
0.0135
MPUN22
0.40699
0.0231
MPIN22
0.36309
0.0447
MPIN45
0.31990
0.0794
ACC22
0.24240
0.1889
DMEMGA10
-0.21990
0.2346
MEMGR45
0.21013
0.2566
MEMGR10
0.20555
0.2673
ACC22
0.47097
0.0075
ACC45
0.39601
0.0274
DMEMGR22
-0.21809
0.2385
DMEMGA10
0.42620
0.0168
DMEMGA45
0.40703
0.0231
DMEMGR22
0.37577
0.0372
DMEMGR45
0.22662
0.2202
MPIN45
-0.20039
0.2798
MEMGA10
0.19898
0.2832


75
examining depression, anxiety, and anger in chronic pain
patients. Also, the relationship between these variables
differed by group. Both these findings are consistent with
the proposed model of dysfunction of a central process in
the experience of chronic pain. Although the statistically
significant correlations of the negative affect measures
with the MPQ Sensory scale, PPR, and PPI do not allow for
discernment of causality and account for only a small amount
of the variance in the measures, this data are congruent
with the proposed model of a central process dysfunction in
chronic pain in that it suggests a relationship between
affect and sensory discrimination in pain perception.
Pain Ratings
As predicted, CLBP subjects had higher ratings of both
pain intensity and pain unpleasantness than controls. CLBP
subjects rated the two most difficult angles for them to
achieve, -10 and 45, as being higher on measures of both
pain intensity and unpleasantness.
Body Position Discrimination
Contrary to what was hypothesized, there were no
differences between CLBP subjects and controls on response
accuracy. All subjects were the most accurate at angle
-10, probably due to limited range of motion at this angle.
All subjects were the least accurate at angle 22, being on
the average, five degrees off target per trial. At angle


82
Future studies investigating the cognitive-affective,
sensory-discriminatory, and physiological reactivity
components of chronic pain could benefit from the following
experimental considerations: making use of more stable
proprioceptive equipment; assessing multiple proprioceptive
measures; use of standardized bending instructions; use of
more stressful ecologically valid tasks (considering the
issue of lack of predictability of stimulus, e.g., no "safe"
zone); assessing both general and specific measures of
psychophysiological reactivity; assessment of pain ratings
post-baseline; and attending more to diagnostic groups,
investigating the EMG patterns of CLBP subgroups as well as
patterns of discriminatory function. Also, the use of path
analyses (with larger samples) could help delineate the
relationship of the hypothesized components of the central
process to each other as researchers attempt to unravel the
complex and dynamic process that is the experience of pain.


41
3) Sensory-perceptual processes: proprioceptive
discriminability of body position quantified as accuracy of
body angle reproduction and response bias, e.g., tendencey
to under- or overshoot the target angle..
4) Physiological reactivity: EMG recordings of the
lumbar paraspinal muscles during proprioceptive tasks.
Previous research predicts the following group
differences:
1) CLBP subjects will exhibit greater levels of
negative affect than healthy controls.
2) CLBP subjects will demonstrate higher VAS ratings of
pain intensity and unpleasantness than controls.
3) CLBP subjects are expected to be poorer
discriminators of body position, e.g., to be less accurate
when reproducing body angle position, and to differ on
response bias. Previous research is mixed on the
directionality of response bias (overshoot versus
undershoot).
4) Although the results of previous research have found
that EMG reactivity to some stressors may be the same as
that of healthy control subjects, there is evidence that
CLBP subjects demonstrate higher EMG reactivity to a
stressor relevant to their clinical pain. Therefore, it is
predicted that CLBP subjects will demonstrate higher
anticipatory and recovery EMG levels than healthy controls.


UNIVERSITY OF FLORIDA


22
experience enhanced sensitivity to pain (Ahles et al., 1987;
Malow, West, and Sutker, 1987; Merskey, 1986; Barsky &
Klerman, 1983).
Schmidt, Gierlings, and Peters (1989) investigated
interoceptive and operant influences on CLBP behavior. The
CLBP patients reported more bodily sensations than controls
after treadmill exertion although, objectively the CLBP
patients were less fatigued. Under rest conditions, healthy
controls reported few bodily sensations, while CLBP patients
generally reported as many sensations at rest as after a
working-to-tolerance treadmill test. Little direct
experimental evidence was found to support the importance of
operant factors in the maintenance of poor endurance
behavior by CLBP patients on repeated treadmill testing.
The authors suggest that these results could be explained by
a hypochondriasis theory such as that proposed by Barsky and
Klerman (1983) whereby intensified pain perception is part
of a general tendency towards augmentation and amplification
of normal bodily sensations.
These studies suggest that chronic pain patients may
have deficits in discrimination of sensory input. This is
consistent with Guilbaud's discussion of the results of
animal studies described in the previous section where it
was postulated that nociceptive input from deep tissues may
be augmented and input from cutaneous afferents may be
inhibited in an effort to localize the source of pain, and,
in so doing, may actuate a chronic state of pain. This is


58
to compare the groups on these measures. As expected, the
pain subjects reported significantly higher levels of pain
intensity and pain unpleasantness than controls at all three
angles (see Tables 8-4 and 8-5, Figures 8-2 and 8-3).
Table 8-4. Median Ratings in Centimeters (min, max) for PIN
Group
*PIN -10
*PIN 22
*PIN 45
Controls
0.8
(0,1.7)
0.02
(0,0.9)
0.0
(0,0.5)
CLBP
5.94
(0.02,11.4)
4.34
(0.4,12.3)
4.88
(0.9,11.7)
Wilcoxon 2-sample test, p=0.0001.
Table 8-5. Median Ratings in Centimeters (min, max) for PUN
Group
*PUN -10
*PUN 22
*PUN 45
Controls
0.06
(0,3.5)
0.02
(0,1.0)
0.02
(0,0.8)
CLBP
5.82
(0.1,9.5)
4.64
(0.2,11.9)
4.30
(0.3,11.8)
*Wilcoxon 2-sample test, p=0.0001.
Multivariate analyses (MANOVA) of pain intensity and
pain unpleasantness for the CLBP group demonstrated an angle
affect for both measures [F(2,29)=4.13, p=0.03;
F(2,29)=4.16, p=0.03, respectively]. Univariate analysis of
pain subjects' ratings of pain intensity showed that there
was no signficant difference in ratings for angles
-10 and 45 (F=0.88, p=0.36) whereas the ratings for angles
-10 and 22 were significantly different (F=7.31, p=0.01)
and the difference in ratings for angles 22 and 45
approached significance (F=3.34, p=0.08). Therefore, pain
subjects rated the two angles (-10, 45) most difficult for
them to achieve as more painful and the less difficult angle


Abstract of Dissertation Presented to the Graduate School of
the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Doctor of Philosophy
COMPARISON OF NEGATIVE AFFECT, REACTIVITY,
AND PROPRIOCEPTION IN CHRONIC LOW BACK PAIN
PATIENTS AND CONTROLS
By
MELODYE ELAYNE GASKIN
May 1998
Chairman: Michael E. Robinson
Major Department: Clinical and Health Psychology
Current models of chronic pain view the experience of
pain as a complex phenomenon comprised of sensory-
discriminative, cognitive-affective, and physiological
components. Several models have proposed that chronic pain
involves the dysfunction of a central mechanism that
influences as well as is influenced by these components.
Previous research has demonstrated higher levels of negative
affect (anxiety, anger, and depression) and perceptual
deficits in pain patients compared to pain-free controls. A
perceptual ability unexamined in the chronic low back pain
population is that of trunk proprioception. Studies of
physiological reactivity in patients with chronic low back
pain (CLBP) have focused on the electromyographic (EMG)
activity of the low back with mixed results. The use of
stimuli relevant to the patient's clinical pain has been
found to influence physiological reactivity.
VI


4
such as anger and anxiety, and pain has been emphasized by
several writers (Pilowsky, 1986; Merskey, 1986; Gaskin,
Greene, Robinson, & Geisser, 1992). Anxiety and anger are
associated with the "flight or fight" response which
characteristically involves arousal of the autonomic nervous
system. Many of these physiological responses are also
characteristic of pain. Ahles, Cassens, and Stalling (1987)
found that normal subjects who scored high on anxiety and
were predisposed to attend to somatic symptoms reported more
areas of pain and rated these sensations as more noxious.
Thus, there is evidence for a link between physiological
response, somatic focus, emotional arousal, and pain.
Price (1988) also discusses the role of cognitive
processes in the affective response to pain and proposes a
sequential processing theory of pain. This theory proposes
that nociceptive input activates arousal, sensory-
discriminative, autonomic, and somatomotor responses in
parallel. Emotional responses to pain are then mediated by
cognitive-evaluative appraisals of the nociceptive
sensations. Thus, the sequential processing theory combines
the neurophysiological aspects of the gate-control theory
with the cognitive-evaluative components of Chapman's
information processing theory. Price (1988) contends that
pain affective responses are the end result of several
processes, the most salient of which is nociceptive
sensation.


76
45, all subjects were, on the average, four degrees off
target per trial.
Regarding response bias, the hypothesis was partially
supported in that the pattern of response bias across the
angles differed between the two groups. CLBP subjects
demonstrated the smallest response bias at angles -10 and
45, undershooting -10 but showing almost no response bias
at angle 45. At angle 22, CLBP subjects overshot the
target. In contrast, controls showed very little response
bias at angles -10 and 22 but overshot target angle 45.
Undershooting angle -10 by the pain subjects was probably
due to limited range of motion and, based upon CLBP
subjects' PIN and PUN ratings, increased pain. CLBP
subjects' low response bias at angle 45 may be related
again to increased pain whereas controls, without pain as a
cue, tended to overshoot the target angle. The possibility
that this type of discrimination error in pain-free
individuals could be related to the acquisition of injuries
that result in CLBP requires further investigation.
Several factors could account for the lack of
differences in response accuracy between groups. One source
of measurement error is that the ELT belt would shift as
some subjects were bending affecting accuracy of readings.
Another factor is that for reasons of ecological validity,
no standardized bending instructions were given. Thus, some


27
proprioceptive deficits in cervical pain patients as
compared to control subjects, the empirical investigation of
the ability of CLBP patients and pain-free controls to
accurately perceive trunk position seems warranted.
Summary
The studies reviewed in this chapter suggest that
individuals with chronic pain may suffer from a perceptual
deficit related to the diffuse nature of input from slow
conducting, unmyelinated afferents as well as augmentation
of these signals by the central nervous system in an attempt
to localize the source of pain. This system, once
activated, may also conduct signals that are from non-pain
producing stimuli but these stimuli may be interpreted by
the central nervous system as painful since they are
traveling on the pain-activated system. This is consistent
with the theories discussed above and could account for the
mixed results in the ability of chronic pain patients to
discriminate somatic stimuli due to the nature of the
stimuli and whether the stimuli involved the same receptive
field as that of the clinical pain. The interpretation of
sensory input is a complex process that involves the
integration of thoughts, feelings, and memories (including
pain-related memories) as well as the arousal level of the
person experiencing pain.


31
as are patterns of EMG activity during dynamic postures
(Sherman, 1985; Ahern, Follick, Council, Laser-Wolston, &
Litchman, 1988).
In their review, Dolce and Raczynski (1985) provide
evidence to support two models of muscular involvement in
back pain. One model involves a pain-spasm-pain cycle
related to splinting or protective posturing due to physical
damage and/or psychological and environmental stress.
Splinting or tensing muscles leads to reduced blood flow and
results in ischemic pain as well as spasm which can set up a
pain-spasm-pain cycle. This pattern predicts higher
paraspinal EMG levels in CLBP patients than in healthy
controls.
The biomechanical model proposes that muscular
asymmetries and abnormally low levels of paraspinal EMG
activity during movement allow the spine to become unstable.
This instability results in pain from nerve root, joint, or
capsular irritation. This model predicts left-right
asymmetries and/or lower EMG levels in CLBP patients as
compared to healthy controls. The findings of Ahern et al.
(1988) that patients with CLBP demonstrated lower EMG levels
during movement than non-patient controls provides support
for the biomechanical model.
In a 1985 study, Flor, Turk, and Birbaumer investigated
the relationship of paraspinal EMG reactivity to personally
relevant and general stress in chronic back pain (CBP)
patients, general pain patients, and non-pain medical


38
the results question the role of lumbar paraspinal muscle
activity in low back pain and suggest the modulating role of
autonomic arousal and concomitant mood state in the
exacerbation of low back pain. He suggests a model of
chronic low back pain consider both cognitive-perceptual
processes and autonomic arousal.
Price (1988) discusses the cognitive-evaluative and
affective dimensions of pain and describes emotional states
as "complex modes of experience . determined to a large
extent by attitudes, images, thoughts, memories,
expectations, and desires (p.51)." Price provides evidence
that an emotional state requires some minimal level of
physiological arousal and that the specific emotional state
that is experienced depends upon the meaning attributed to
the situation. Thus, the meaning attributed to somatic
sensations, such as pain, determines the type of emotion
experienced.
Shacham, Dar, and Cleeland (1984) investigated the
relationship of mood to severity of clinical pain in chronic
pain patients. Pain severity was found to be positively
correlated to negative mood but was unrelated to positive
mood, and negative mood was found to be independent of
positive mood. Gaskin et al.(1992) also found that state
measures of mood (state anxiety, anger, and depression) were
more strongly related to pain ratings in a chronic pain
sample than were trait measures. The authors suggest that
these findings support the hypothesis that chronic pain


CHAPTER 8
RESULTS
General Demographic Data
Age and Sex
The subjects in this study were age- and sex-matched.
Collapsing across sites, there were 31 pain-free control
subjects with an average age of 37.6 years (SD=7.9) and 31
CLBP subjects with an average age of 39.6 years (SD=9.8).
In each group, there were 12 females and 19 males.
Race and Education
All CLBP subjects were Caucasian. There were 29
Caucasians, 1 African-American, and 1 Asian in the control
group. All subjects had at least a high school education
with a mean of 19 years (SD=2.9) of education for controls
and 14.6 years (SD=2.9) for CLBP subjects.
Height, Weight, and Body Mass Index
Although there were no differences between groups on
height, CLBP subjects and controls differed significantly
(t[59]=-2.13, p=0.037) on weight with CLBP subjects weighing
85.2 kilograms (SD=19.2) and controls weighing 75.2
kilograms (SD=17.6) on the average. Since the amount of
adipose tissue can effect accuracy of EMG recordings, the
body mass index (BMI), a commonly used index of obesity
which utilizes weight in relation to height, was calculated
51


RECOVERY EMG
ANGLE = 45 DEGREES
ANGLE = 10 DEGREES
ANGLE = 22 DEGREES
BASELINE EMG
Figure 8-7. MEAN RECOVERY EMG INTERACTION WITH COVARIATE
-4
RECOVERY EMG


33
appear to be a crucial variable in the physiology of pain,
but that stress and pain related responses as well as slow
return to baseline levels appear to be more relevant. They
suggest that slow return to baseline levels is consistent
with Sternbach's theory of homeostatic dysregulation and
warrants further research.
Flor and Turk (1989) further recommend that future
research use multiple site, measure, and stressor
assessments at several points in time on a well-defined
patient sample and that the influence of sensory, cognitive,
affective, and behavioral contributions to the pain
experience be assessed along with the physiological
responses to pain in order to clarify the relationships
between these variables. They also encourage the use of
potent and ecologically valid stressors.
Sherman (1985) argues for the importance of measuring
pain intensity at time of EMG recording. He investigated
EMG patterns by recording paraspinal muscle activity of
subjects while in motion (bending to approximately 30
degrees and rising) and still (standing upright, sitting
supported and unsupported, and prone). He compared these
EMG values for subjects with no history of back pain,
subjects with past episodes of back pain but no pain during
the course of the study, and subjects currently experiencing
back pain. He found that the 83 chronic back pain (CBP)
patients each produced an unique pattern of muscle activity
that was relatively stable over several weekly recording


48
After this, you will be guided to one more bend
and will repeat the above procedure."
Then subjects were instructed in the use of the VAS's as
follows:
"There are two aspects of pain which I am
interested in measuring: The intensity, how
strong the pain feels, and the unpleasantness, how
unpleasant or disturbing the pain is for you. The
distinction between these two aspects of pain
might be made clearer if you think of listening to
a sound, such as a radio. As the volume of the
sound increases, I can ask you how loud it sounds
or how unpleasant it is to hear it. The intensity
of pain is like loudness; the unpleasantness of
pain depends not only on intensity but also on
other factors which may affect you. There are
scales for measuring each of these two aspects of
pain. Although some pain sensations may be
equally intense and unpleasant, I would like you
to judge the two aspects independently." (From
Price et al, 1984; p. 31)
"After each task, I will show you two scales.
The pain intensity scale goes from "no sensation"
to the "most intense sensation imaginable."
Please indicate your judgment by marking the point
on the line which corresponds to your level of
pain intensity at that moment. On the pain
unpleasantness scale, the line goes from "not bad
at all" to the "most intense bad feeling possible
for me." Please indicate your judgment by marking
the point on the line which corresponds to your
level of pain-related unpleasantness at that
moment."
The ELT belt was then placed around the subject's waist
with the EMG strips positioned over the subject's lumbar
paraspinal muscles. The ELT was calibrated to zero for each
subject in the standing position after instructing them to
"stand straight." Subjects' understanding of the VAS's and
protocol instructions were verified with several practice
trials during which they were guided to 10 flexion.


55
affect trio were significantly correlated with the MPQ
Evaluative scale, while only state anxiety (r=0.55, p=0.02)
was significanly correlated with the MPQ Miscellaneous
scale. With the MPQ PRI, correlations with state anxiety
(r=0.55, p=0.001) and state anger (r=0.38, p=0.04) were
significant while the correlation with the BDI (r=0.38,
p=0.056) was marginally significant. The same held true for
the correlations with the MPQ PPI: state anxiety (r=0.40,
p=0.03) and state anger (r=0.38, p=0.04) were significant
while the correlation with the BDI (r=0.34, p=0.06) was
marginally significant.
When examined by site (UF versus CAMC), CLBP subjects
did not differ on some demographic or medical information
such as education, marital status, or medication usage, but
these two groups did differ on the following parameters:
1) duration of CLBP syndrome, 2) CLBP diagnosis, 3) presence
of additional pain syndrome(s), 4) number of surgeries,
5) employment status.
The average duration of back pain differed
significantly between sites [t(29)=2.45, p=0.02]. The
average pain duration for the UF subjects was 92.1 months
(SD=73, range 25 to 240 months) whereas the average for the
CAMC subjects was 37.3 months (SD=50.6, range 6 to 180
months). Although diagnosis information was missing for 9
of the UF subjects, comparison of the available information
showed that 37.5% of the CAMC sample had the diagnosis of
chronic lumbar sprain whereas none of the UF subjects had


77
subjects bent from the waist while others bent from their
hips. These factors likely contributed to the high amount of
variability in both groups on both proprioceptive measures.
The use of proprioceptive equipment that is more stable
during the bending task as well as standardized control of
the bending process through instruction or equipment that
stabilizes body position in one plane and controls the range
of motion from the lumbar region would help clarify these
issues. Another consideration is the use of only one device
to measure proprioceptive function in just one plane. As
the study by Parkhurst and Burnett (1994) indicates, the
measurement of multiple proprioceptive abilities in several
planes may better delineate the issue of these abilities in
both pain-free controls and CLBP patients. This area
warrants further investigation as newer equipment is
developed to better assess trunk proprioception.
EMG Differences
The hypothesis regarding EMG reactivity was partially
supported by the data. Although the differences were, from
a clinical perspective, very small, the patterns of EMG are
interesting from a theoretical perspective since the results
partially support both the pain-spasm-pain model as well as
the biomechanical model of muscle activity in chronic pain
patients. The higher levels of anticipatory EMG for CLBP
subjects at angles -10 and 22 and of recovery EMG for CLBP
subjects at angle 22 at higher levels of baseline EMG are


CHAPTER 1
INTRODUCTION
Chronic pain is one of the most challenging problems
facing health professionals. Definitions and models of pain
have evolved from simplistic sensory stimulus-response
explanations to more complex multidimensional ones. The
development of theoretical conceptualizations of the
psychophysiology of chronic pain have evolved from early
research in psychophysiology which relied on generalized
activation models, such as those proposed by Duffy (1972)
and Selye (1957), to specificity models, such as those
proposed by Sternbach and Fahrenberg (Flor & Turk, 1989).
In the study of chronic pain, current models must take into
account that the experience of pain is a complex phenomenon
comprised of sensory-discriminative, cognitive-affective,
and physiological components.
In a general theory, Sternbach (1966) proposes that
psychophysiologic disorders such as chronic pain result from
the breakdown of homeostatic mechanisms. These mechanisms
are unable to keep initial physiological responses and/or
rebound to stressful stimuli within normal functioning.
This leads to tissue damage and the appearance of symptoms.
For more than 20 years, the gate-control theory of pain
has served as a guide to pain research (Price, 1988). It is
1


20
tests. In both studies, two groups emerged: 1)
sensitizers, who responded to repeated pain stimulation with
decreasing endurance and increasing pain intensity reports,
and 2) habituaters, who responded with increasing endurance
and decreasing pain intensity reports.
In another study that is also consistent with the
augmentors and reducers model, Peters, Schmidt, and Van den
Hout (1989) investigated the responses of CLBP and control
subjects to 8 trials of pressure-pain stimulation. They
found that the CLBP subjects showed evidence of
sensitization to the pain stimuli through decreased pain
threshold and tolerance ratings, whereas the controls showed
evidence of habituation through increased pain threshold and
tolerance ratings. The authors speculated that if CLBP
patients have a fundamental inability to habituate to
painful experiences, then this could be considered a risk
factor for the development of chronic pain. This study does
not provide the data to determine if the inability to
habituate to pain leads to the development of chronic pain
or if chronic pain alters the ability to habituate to
painful stimuli.
In a review of clinical and experimental evidence
examining central nervous system (CNS) function in chronic
pain patients, Coderre, Katz, Vaccarino, and Melzack (1993)
indicate that there is empirical evidence that noxious
stimuli or injury can produce alterations in CNS function as
well as long-term changes in cellular function. The authors


92
CLBP Subjects
Experimental Variables (Continued)
Pearson Correlation Coefficients/
Prob > |R| under Ho: Rho=0
/Number of Observations
MPUN22
MPUN22
MPIN22
MPUN45
MPIN45
MPIN10
MPUN10
1.00000
0.95171
0.87378
0.84410
0.78983
0.75474
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
31
31
31
31
31
31
DMEMGR10
MEMGR10
MEMGA10
MEMGR45
BLEMGAV
MEMGR22
0.41397
0.39972
0.32868
0.29269
0.26691
0.25362
0.0206
0.0259
0.0710
0.1101
0.1466
0.1686
31
31
31
31
31
31
MPUN45
MPUN45
MPIN45
MPUN22
MPIN22
MPIN10
MPUN10
1.00000
0.94281
0.87378
0.82849
0.71524
0.71202
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
31
31
31
31
31
31
DMEMGR10
MEMGR10
MEMGA10
STANGER
BDI
MEMGR45
0.35436
0.30873
0.27011
0.26145
0.24455
0.22157
0.0505
0.0910
0.1417
0.1554
0.1849
0.2309
31
31
31
31
31
31
BMI
BMI
MPIN10
MPUN10
ACC45
DMEMGA10
DMEMGR10
1.00000
-0.42298
-0.36158
-0.33597
-0.31934
-0.30792
0.0
0.0199
0.0496
0.0695
0.0854
0.0978
30
30
30
30
30
30
BI.EMGAV
BLEMGAV
MEMGA45
MEMGR45
MEMGR22
MEMGR10
MEMGA22
1.00000
0.95520
0.94275
0.93696
0.91245
0.90317
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
31
31
31
31
31
31
MEMGA10
DMEMGA22
DMEMGA45
DMEMGR22
STANX
MPUN22
0.82175
0.37621
0.33988
0.33229
-0.32937
0.26691
0.0001
0.0370
0.0614
0.0678
0.0704
0.1466
31
31
31
31
31
31
MEMGA10
MEMGA10
MEMGR10
MEMGA45
MEMGR45
MEMGR22
BLEMGAV
1.00000
0.91709
0.83202
0.82832
0.82562
0.82175
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
31
31
31
31
31
31
MEMGA22
DMEMGA10
DMEMGR10
DMEMGA45
DMEMGR22
DMEMGA22
0.77801
0.63320
0.51513
0.42892
0.42334
0.38649
0.0001
0.0001
0.0030
0.0161
0.0176
0.0317
31
31
31
31
31
31
DMEMGR45
MPIN45
MPUN22
ACC45
MPIN10
MPIN22
0.36890
0.36160
0.32868
0.31056
0.29873
0.29210
0.0411
0.0456
0.0710
0.0891
0.1026
0.1108
31
31
31
31
31
31


18
In another study, Flor, Schugens, and Birbaumer (1992)
compared the discrimination of muscle tension in patients
with CBP and temporomandibular pain and dysfunction (TMPD)
with that of age- and sex-matched healthy controls. All
subjects were asked to discriminate levels of tension in the
masseter and erector spinae muscles. The results
demonstrated that chronic pain patients were less able to
perceive muscle contraction levels correctly, and they
underestimated their actual levels of muscle tension
regardless of whether or not the muscle involved in the
discrimination task was the site of the chronic pain
problem. This deficit in discrimination did not appear to
be related to local physiological changes at the site of
pain or differences in motivation, attention, or fatigue.
The authors concluded that "the present results suggest that
the poor discrimination of an internal body process may not
merely be the consequence of local changes at the site of
pain but might be a more basic deficit (p. 175)." Fuller
and Robinson (1995) also found that in a relevant but non
pain related modality, CLBP patients underestimated the
heaviness of weights lifted with the painful body part,
their lower back. Both studies support the notion of a
deficit in the processing of nociception at a central level
in terms of accurately assessing magnitude.
Gaskin (1991) investigated the relationship of somatic
focus, cognitive-affective factors, physiological
reactivity, and discrimination of somatic changes to cold


REFERENCES
Ahern, D.K., Follick, M.J., Council, J.R., Laser-Wolston,
N., & Litchman, H. (1988). Comparison of lumbar
paravertebral EMG patterns in chronic low back pain
patients and non-patient controls. Pain. 34. 153-160.
Ahles, T.A., Cassens, H.L., & Stalling, R.B. (1987). Private
body consciousness, anxiety and the perception of pain.
Journal of Behavioral Therapy and Experimental
Psychiatry. 18 (3), 215-222.
Arena, J.G., Sherman, R.A., Bruno, G.M. & Young, T.R.
(1989). Electromyographic recordings of 5 types of low
back pain subjects and non-pain controls in different
postitions. Pain. 37. 57-65.
Arntz, A., van den Hout, M., van den Berg, G., Meijboom, A.
(1991). The effects of incorrect pain expectations on
acquired fear and pain responses. Behavior Research and
Therapy. 29 (6), 547-560.
Barsky, A.J. & Klerman, G.L. (1983). Overview:
Hypochondriasis, bodily complaints, and somatic styles.
The American Journal of Psychiatry. 140 (3), 273-283.
Beck, A.T., Steer, R.A., & Garbin, M.G. (1988). Psychometric
properties of the Beck Depression Inventory: Twenty-five
years of evaluation. Clinical Psychology Review. 8, 77-
100.
Carlton, R.S. (1987). The effects of body mechanics
instruction on work performance. The American Journal of
Occupational Therapy. 47 (1), 16-20.
Cassisi, J.E., Robinson, M.E., O'Conner, P., & MacMillan, M.
(1993). Trunk strength and lumbar paraspinal muscle
activity during isometric exercise in chronic low-back
pain patients and controls. Spine. 18 (2), 245-251.
Chapman, C. R. (1986). Pain, perception, and illusion. In R.
A. Sternbach (Ed.), The psychology of pain (2nd ed.),
(pp. 153-179). New York: Raven Press.
Clark, W. C. (1974). Pain sensitivity and the report of
pain. Anesthesiology. 40 (3), 272-287.
97


94
CLBP Subjects
Experimental Variables (Continued)
Pearson Correlation Coefficients/
Prob > |R| under Ho: Rho=0
/Number of Observations
DMEMGA10
DMEMGA10
DMEMGR10
MEMGA10
MEMGR10
BMI
MPIN10
1.00000
0.71936
0.63320
0.36497
-0.31934
0.30765
0.0
0.0001
0.0001
0.0435
0.0854
0.0923
31
31
31
31
30
31
RB10
DMEMGR45
DMEMGR22
DMEMGA45
RB22
MPIN45
0.30654
0.29219
0.28923
0.28869
0.28542
0.27046
0.0935
0.1107
0.1145
0.1152
0.1196
0.1411
31
31
31
31
31
31
DMEMGR10
DMEMGR10
DMEMGA10
DMEMGR45
MEMGR10
MEMGA10
DMEMGR22
1.00000
0.71936
0.62181
0.52762
0.51513
0.47461
0.0
0.0001
0.0002
0.0023
0.0030
0.0070
31
31
31
31
31
31
MPUN22
MPIN45
MPIN10
MPIN22
DMEMGA45
MPUN45
0.41397
0.39448
0.37565
0.36730
0.35805
0.35436
0.0206
0.0281
0.0373
0.0421
0.0480
0.0505
31
31
31
31
31
31
DMEMGA22
DMEMGA2 2
DMEMGA45
DMEMGR22
MEMGA22
DMEMGR45
MEMGR22
1.00000
0.90826
0.83128
0.73753
0.68336
0.61416
0.0
0.0001
0.0001
0.0001
0.0001
0.0002
31
31
31
31
31
31
MEMGA45
MEMGR45
MEMGA10
BLEMGAV
MEMGR10
ACC45
0.60495
0.55691
0.38649
0.37621
0.36342
0.34757
0.0003
0.0011
0.0317
0.0370
0.0445
0.0554
31
31
31
31
31
31
DMEMGR22
DMEMGR22
DMEMGR45
DMEMGA45
DMEMGA22
MEMGR22
MEMGA22
1.00000
0.92035
0.88965
0.83128
0.64092
0.62734
0.0
0.0001
0.0001
0.0001
0.0001
0.0002
31
31
31
31
31
31
MEMGR45
MEMGA45
MEMGR10
DMEMGR10
MEMGA10
BLEMGAV
0.60129
0.56183
0.48080
0.47461
0.42334
0.33229
0.0003
0.0010
0.0062
0.0070
0.0176
0.0678
31
31
31
31
31
31
DMEMGA45
DMEMGA4 5
DMEMGA2 2
DMEMGR22
DMEMGR45
MEMGA22
MEMGR22
1.00000
0.90826
0.88965
0.84175
0.66855
0.60622
0.0
0.0001
0.0001
0.0001
0.0001
0.0003
31
31
31
31
31
31
MEMGA45
MEMGR45
MEMGR10
MEMGA10
DMEMGR10
BLEMGAV
0.60300
0.58063
0.43918
0.42892
0.35805
0.33988
0.0003
0.0006
0.0134
0.0161
0.0480
0.0614
31
31
31
31
31
31


24
In the area of low back pain, many rehabilitation
programs include some education and training in body
mechanics (Linton & Kamwendo, 1987). Although certain
biomechanical positions, such as maintaining forward
stooping position, have been found to increase the risk of
low back injury (Carlton, 1987; McCauley, 1990), only one
study has examined the relationship between injury and
proprioception of the lower back (Parkhurst & Burnett,
1994) .
Parkhurst and Burnett (1994) tested eighty-eight male,
pain-free (no acute pain and not currently under treatment
for a back injury) emergency medical service workers for
three types of lower back proprioception (passive motion
threshold, directional motion perception, and repositioning
accuracy) using an apparatus designed by one of the authors.
Each type of proprioception was examined in the three
primary planes of motion (coronal, sagital, and transverse).
Measures of repositioning accuracy did not reach statistical
significance in any plane. Age and history of low back
injuries within the past 5 years were associated with other
proprioceptive deficits. Only 17% (15) of subjects had
histories of back pain/injury within the past 5 years and
the exclusion criteria screened out chronic pain subjects.
Thus, these subjects were essentially pain-free controls,
and the lack of deficits in repositioning accuracy would,
therefore, be expected in this group. There are no


This dissertation was submitted to the Graduate Faculty
of the College of Health Professions and to the Graduate
School and was accepted as partial fulfillment of the
requirements for the degree jgf^-Doctfir of Philosophy.
May 1998
Dean, College of Health
Professions
Dean, Graduate School


o
CONTROLS
CLBP
00 -
C\J -
O -
I 1 1
10 22 45
ANGLE (degrees)
Figure 8-2. PIN: CLBP vs CONTROLS
(Group Medians with Inter-quartile Ranges)


81
Conclusion
This study provides partial support for the hypotheses
generated regarding the components of a proposed central
process that mediates the experience of chronic pain as
follows: higher levels of negative affect (cognitive-
affective component) and pain ratings in CLBP subjects over
controls, differences in patterns of response bias across
tasks between groups (sensory-discriminatory component), and
different patterns of EMG between groups over the three
tasks (physiological reactivity).
Lack of group differences in proprioceptive accuracy
could exist because there is no difference between the
groups on this measure. If this is the case and taking into
account the different patterns of response bias between CLBP
subjects and controls, the implications for back injury
prevention programs is that proprioceptive awareness may
need to be taught in small increments to those without back
pain as well as to those who already have back pain. It
seems plausible that those with CLBP use pain as one of
their cues, whereas those without back pain do not have this
cue until they injure themselves due to a tendency to
overshoot forward flexion. But, as this is only the second
study to examine trunk proprioception, and the development
of other trunk proprioception equipment is needed, this
issue warrants further exploration before any conclusions
can be drawn with certainty.


89
Control Subjects
Experimental Variables (Continued)
Pearson Correlation Coefficients/
Prob >
1RI under Ho:
Rho=0/N =
31
MEMGA45
MEMGA45
MEMGA10
MEMGR45
MEMGR22
MEMGA22
MEMGR10
1.00000
0.96246
0.96170
0.95814
0.95712
0.92049
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
BLEMGAV
DMEMGR45
DMEMGA45
DMEMGR22
DMEMGR10
DMEMGA22
0.90688
0.77812
0.73569
0.62883
0.37975
0.34161
0.0001
0.0001
0.0001
0.0002
0.0351
0.0600
MEMGR45
MEMGR45
MEMGR22
MEMGA45
MEMGA22
MEMGR10
BLEMGAV
1.00000
0.98030
0.96170
0.95738
0.94938
0.94459
0.0
0.0001
0.0001
0.0001
0.0001
0.0001
MEMGA10
DMEMGR45
DMEMGR22
DMEMGA45
DMEMGR10
ACC 10
0.92112
0.80625
0.60117
0.59107
0.37405
-0.24434
0.0001
0.0001
0.0003
0.0005
0.0382
0.1853
DMEMGA10
DMEMGA10
DMEMGA45
DMEMGR10
DMEMGA22
DMEMGR22
RB45
1.00000
0.69001
0.66214
0.61290
0.46682
0.42620
0.0
0.0001
0.0001
0.0002
0.0081
0.0168
ACC45
DMEMGR45
MEMGA10
MEMGA45
RB10
MPIN22
0.40605
0.34682
0.33515
0.23261
-0.21990
-0.20113
0.0234
0.0559
0.0653
0.2079
0.2346
0.2779
DMEMGR10
DMEMGR10
DMEMGA10
DMEMGR4 5
DMEMGA45
MEMGR10
DMEMGR22
1.00000
0.66214
0.64866
0.57458
0.57049
0.51253
0.0
0.0001
0.0001
0.0007
0.0008
0.0032
MEMGA10
DMEMGA22
MEMGA45
MEMGR45
MPIN22
BDI
0.44454
0.42896
0.37975
0.37405
-0.32432
0.31518
0.0122
0.0160
0.0351
0.0382
0.0751
0.0842
DMEMGA22
DMEMGA2 2
DMEMGR2 2
DMEMGA45
DMEMGA10
DMEMGR45
DMEMGR10
1.00000
0.78166
0.68738
0.61290
0.53480
0.42896
0.0
0.0001
0.0001
0.0002
0.0019
0.0160
MPUN45
MEMGA22
MPIN22
MPUN22
BMI
MPIN45
-0.38703
0.37956
-0.37594
-0.36613
0.35896
-0.35342
0.0315
0.0352
0.0371
0.0428
0.0474
0.0511
DMEMGR22
DMEMGR22
DMEMGR45
DMEMGA22
DMEMGA45
MEMGR22
MEMGA45
1.00000
0.82860
0.78166
0.77325
0.64083
0.62883
0.0
0.0001
0.0001
0.0001
0.0001
0.0002
MEMGA22
MEMGR45
MEMGA10
MEMGR10
DMEMGR10
DMEMGA10
0.61789
0.60117
0.56343
0.53757
0.51253
0.46682
0.0002
0.0003
0.0010
0.0018
0.0032
0.0081
MPIN22
MPUN45
MPUN22
BLEMGAV
RB45
MPIN45
-0.41601
-0.39056
-0.38117
0.37703
0.37577
-0.37403
0.0199
0.0298
0.0344
0.0365
0.0372
0.0382
ACC 10
BMI
RB22
MPUN10
MPIN10
RB10
-0.37299
0.26656
-0.21809
-0.20401
-0.19153
-0.18643
0.0388
0.1472
0.2385
0.2710
0.3020
0.3153


CHAPTER 2
CURRENT MODELS OF PAIN
The conceptualization of the experience of pain in a
manner that allows for scientific study has progressed from
analyzing pain as a purely sensory phenomenon to viewing it
as a multidimensional experience involving cognitive-
affective as well as sensory elements. The currently
accepted definition of pain as set forth by the
International Association for the Study of Pain is as
follows: "pain is an unpleasant sensory and emotional
experience associated with actual or potential tissue
damage, or described in terms of such damage, or both (IASP,
1979)." Chapman (1986) explains that this definition
recognizes that the experience of pain is subjective, is
more complex than an elementary sensory event, and involves
associations between elements of sensory experience and an
aversive feeling state as well as the attribution of meaning
to the unpleasant sensory events. Therefore, current models
must accommodate pain as a complex phenomenon consisting of
sensory-discriminative, cognitive-affective, and
physiological components.
Current models describe pain as a sensory-perceptual
experience that provides information about both external and
internal, or somatic, stimuli. Sensory end organs which are
6


78
consistent with the pain-spasm-pain model. But the lower
anticipatory and recovery EMG levels at higher levels of
baseline EMG in CLBP subjects at angle 45 is predicted by
the biomechanical model.
Peters and Schmidt (1991) discussed several studies
that suggested the generalized participation of uninvolved
muscle groups in CLBP patients. The lower levels of
recovery EMG (at higher levels of baseline EMG) at 45 in
CLBP subjects as compared to controls in this study could be
related to the recruitment of what are usually uninvolved
muscles during the task for the pain subjects. Although
only one EMG site was recorded, the use of multiple EMG site
recording or the recording of left and right muscle groups
should be used in the future to clarify this issue.
It has been suggested by some authors (Cassisi,
Robinson, O'Conner, MacMillan, 1993; Peters & Schmidt, 1991)
that CLBP patients may use their muscles differently than
pain-free individuals and that differing patterns of EMG may
be more indicative of the biomechanical model. Based upon
this reasoning, the pattern of the EMG data of the CLBP
subjects relative to the controls in this study is more in
line with the biomechanical model of CLBP. Indeed, the data
do not demonstrate increased psychophysiological reactivity
(as measured by EMG) in the CLBP subjects. This supports
the assessment of Flor, Birbaumer, Schugens, and
Lutzenberger (1992)that psychophysiological studies of pain
should include at least one other psychophysiological


CHAPTER 4
PHYSIOLOGICAL REACTIVITY AND PAIN
General Arousal
As discussed in the previous chapter, pain can be
conceptualized as a warning signal and as such is a potent
means of producing arousal and widespread cortical
activation (Price, 1988). Therefore, physiological
responses to pain produce the "flight or fight" reaction
that is also characteristic of fear and anger (Sternbach,
1968). This reaction involves arousal of the autonomic
nervous system and results in changes across many body
systems leading to increases in heart rate, blood pressure,
vigilance, and motoric responses enabling the organism to be
mobilized in order to escape aversive stimuli.
Sternbach (1966) hypothesized that the development of
psychophysiological disorders, such as chronic pain, may be
due to frequent and sufficiently intense activation of a
body system such that dysregulation of the homeostasis of
the affected system occurs and results in the symptoms of
the disorder. Flor and Turk (1989) explain that underlying
this model, which they referred to as individual response
specificity, is the proposition that "psychophysiological
disorders develop and are maintained as a consequence of
unspecific hyperarousal of the autonomic nervous system.
28


86
CLBP Subjects
Correlation Analysis with Demographic Variables (Continued)
Pearson Correlation Coefficients /
Prob > |R| under Ho: Rho=0 /
Number of Observations
AVERAGE PAIN
MPIN45
MPIN10
MPUN10
MPUN45
MPIN22
0.45589
0.44451
0.40560
0.38952
0.38368
0.0100
0.0122
0.0236
0.0303
0.0331
31
31
31
31
31
MPUN22
BDI
DMEMGA10
BMI
MEMGA10
0.35559
0.35284
0.32037
-0.30980
0.27446
0.0496
0.0515
0.0789
0.0957
0.1351
31
31
31
31
31
PRESENT PAIN
MPIN10
MPUN10
MPIN45
DMEMGA10
MPUN45
0.55931
0.50395
0.45883
0.44863
0.44622
0.0011
0.0038
0.0094
0.0114
0.0119
31
31
31
31
31
MPUN22
MPIN22
MEMGA10
RB10
DMEMGR10
0.40279
0.39717
0.34188
0.29131
0.29029
0.0247
0.0269
0.0598
0.1118
0.1132
31
31
31
31
31
ADDITIONAL PAIN
DMEMGA10
RB45
ACC 10
DMEMGR10
RB22
0.43254
0.39419
0.38066
0.36714
0.36208
0.0151
0.0282
0.0346
0.0422
0.0453
31
31
31
31
31
ACC22
0.29931
0.1019
31


53
Medications
All subjects were asked regarding their medication
usage the day of their participation in the study. None of
the control subjects had taken narcotics, analgesics,
nonsteroidal anti-inflammatory analgesics (NSAIDs), or
muscle relaxers. Ten of the CLBP subjects had taken no
medications, while 3 had taken a narcotic, 1 an
analgesic/narcotic/sedative drug, 10 had taken NSAIDs, 6 had
taken a muscle relaxer, and 7 subjects were on
antidepressants.
To determine the impact of medication usage on negative
affect and EMG, Cohen's d was calculated for the depression,
state anxiety, state anger, and baseline EMG measures
comparing pain subjects on medications with those not on
medications. The effect sizes and group means indicate that
medication usage did not have a dampening affect on any of
these measures. The only moderately large effect sizes were
for depression (d = 0.63) and baseline EMG (d = 0.6). The
means for the depression and baseline EMG measures were
actually higher for the pain subjects on medications.
Present pain and MPQ PPI ratings did not differ between the
medication and non-medication groups suggesting that
differences in baseline EMG were not related to pain level.
Back-Related Surgeries
Only one of the control subjects had undergone a back-
related surgery (laminectomy). Of the CLBP subjects, 24 had
no back surgery, 2 had undergone one surgery, 3 had


17
threshold, sensitivity, and discrimination, and a
significant decrease in the tendency to report pain. The
authors speculate that these results suggest the involvement
of a central mediating process and "that differences in pain
responses of MPD patients and normals are not due to
permanent psychological or physiological differences, but
may be due to the psychophysiologic effects of chronic pain
(pp. 70-71)."
Naliboff and colleagues (1981) looked at discrimination
and threshold for radiant heat stimuli in chronic low back
pain (CLBP) patients, chronic respiratory patients, and non
patient controls. Their results indicated that the CLBP and
respiratory patients had higher pain thresholds, but the
CLBP patients demonstrated a discrimination deficit for
mildly painful stimuli. Cohen, Naliboff, Schandler, and
Heinrich (1983) report that CLBP subjects demonstrated
poorer discriminability of radiant heat stimuli but equal
discriminability of loud tones compared to age- and sex-
matched controls. Lautenbacher, Galfe, Karlbauer, Moltner
and Strian (1990) reported reduced somatosensory perception
for temperature in chronic back pain (CBP) patients. And
although Yang, Richlin, Brand, Wagner, and Clark (1985)
found that CLBP patients had a high response bias, the
chronic pain group displayed poorer discriminability of
experimental heat pain stimuli compared to normals. The
authors concluded that these results provided evidence of a
perceptual deficit in chronic pain patients.


80
several authors (Arena, Sherman, Bruno, & Young, 1989; Flor,
Birbaumer et al., 1992; Geisser, Robinson, & Richardson,
1995) that chronic pain patients may be heterogeneous in
terms of the development and maintenance of their pain and
that different types of CLBP patients may have different
patterns of EMG activity in different postures/tasks. Flor,
Birbaumer et al. (1992) indicated that there is increasing
evidence that the tendency to overrespond in patients'
relevant muscles may produce and maintain chronic pain in
some patients, whereas in others with low muscle reactivity,
the development and maintenance of chronic pain syndromes
may be related to factors other than psychophysiological
ones, such as operant conditioning. Although the pain
subjects from the two sites in this study were different
relative to pain diagnoses, they did not differ
significantly on EMG reactivity. This suggests the need for
more exploration of the factors which may differentiate pain
patients on this issue.
Finally, some researchers view surface measurement of
EMG as a gross measure of muscle activity (Biedermann cited
in Peters & Schmidt, 1991) while others (Wolf, Wolf, &
Segal, 1989) caution clinicians against assuming that low
levels of integrated surface lumbar EMG recordings provide
assurance of lack of activity of deeper muscles. Or the
relationship between psychophysiological reactivity and
muscular pain may be mediated by activity other than EMG.


11
review research which provides evidence in support of these
dimensions of pain as well as of a central process as
proposed by these models.


43
previous 6 months. No subject had any history of
psychiatric hospitalization.
Prospective CLBP subjects were initially screened by
consulting with their physician or physical therapist as to
their capability to perform the proprioceptive tasks
required in this study. Only CLBP subjects who were
assessed as capable of performing the proprioceptive tasks
were approached for participation in the study.
Measures
Cognitive-Affective Measures
Beck Depression Inventory (BDI). The BDI consists of
21 items that assess the cognitive-affective and
neurovegetative signs of depression. The BDI has been
standardized on psychiatric and nonpsychiatric populations
(Beck, Steer, & Garbin, 1988) with alpha coefficients
ranging from .73 to .95. Meta-analyses have reported mean
correlations between the BDI and other measures of
depression, the Hamilton Psychiatric Rating Scale, the Zung
Self-reported Depression Scale, and the Minnesota
Multiphasic Personality Inventory Depression Scale, ranging
from .60 to .76.
State-Trait Personality Inventory STPI). The STPI
(Spielberger et al., 1983) consists of six 10-item subscales
that assess state and trait anxiety and anger. The state
scales measure the intensity of a subject's feelings at the
time of administration, e.g., mood. The trait scales assess