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RHEUMATOID ARTHRITIS: A PSYCHOLOGICAL INTERVENTION
DISSERTATION
Presented to the Graduate Council of the
North Texas State University in Partial
Fulfillment of the Requirements
For the Degree of
DOCTOR OF PHILOSOPHY
By
Phillip C. McGraw, M. A.
Denton, Texas
May, 1979
McGraw, Phillip C. , Rheumatoid Arthritis: A Psychologi-
cal Intervention. Doctor of Philosophy (Clinical Psychology),
May, 1979, 122 pp., 23 tables, 11 figures, references, 149
titles.
A psychological intervention involving relaxation train-
ing and biofeedback training for the control of peripheral
skin temperature was investigated in this study with 2 7
female rheumatoid arthritics as participants. A two-group
design was used with the only difference being the direction
in which participants were instructed to alter their periph-
eral skin temperature. A temperature increase group was to
use biofeedback to achieve an increase in peripheral skin
temperature, while a temperature decrease group was to
achieve a decrease. Both groups received identical relaxa-
tion training. Based on analysis of the temperature data,
it was concluded that the biofeedback response was not
learned. From electromyographic data, it was concluded that
participants did learn to relax.
The hypothesis that the two treatment components would
have beneficial affects on the physical, functional, and
psychological aspects of rheumatoid arthritis was answered
partially. No differential effects as a function of biofeed-
back training were found as the data for the temperature
increase and temperature decrease groups were statistically
combined in multiple analyses of variance for repeated
measures. Although no differential effects were obtained,
numerous positive changes were found. Correlated with the
relaxation training were decreases in reported subjective
units of discomfort, percentage of time hurting, percentage
of body hurting, and general severity of pain. Improved
sleep patterns were reported as was increased performance of
activities of daily living. Reductions were also found in
psychological tension, and in the amount of time mood was
influenced by the disease. Shifts were not found in imagery,
locus of control, and other psychological dimensions. Con-
stitutional improvements were also absent.
Relaxation training was recommended as an adjunctive
therapy and its implications were discussed. Future research
is suggested.
TABLE OF CONTENTS
Page
LIST OF TABLES iv
LIST OF ILLUSTRATIONS vii
Dissertation
Introduction 1
Clinical Description Stress and Other Diseases Proposed Treatment Components
Biofeedback Verbal Relaxation
Psychological Aspects of Adult Rheumatoid Arthritis
Method 40
Subjects Apparatus
Psychosocial Assessment Tools Physical/Functional Assessment Tools Equipment
Procedure
Results 49
Discussion 83
Appendices 91
References 105
i n
LIST OF TABLES
Table Page
1. The Relationship Between Stress and Rheumatoid Arthritis 7
2. Data on the Efficacy of Verbal Relaxation Training 27
3. Analysis of Variance on Peripheral Skin Temperature for Increase and Decrease Training Groups 50
4. Analysis of Variance for Electromyographic Data Across Blocks 53
5. Analysis of Variance on Pre- and Posttreatment Discomfort Ratings for Increase and Decrease Training Groups Across Blocks 56
6. Analysis of Variance on Reported Percentage of Time Hurting Across Treatment 57
7. Analysis of Variance on Reported Percentage of Body Hurting Across Treatment 59
8. Analysis of Variance on Reported General Severity of Pain • 61
9. Analysis of Variance on Reported Specific Pain Severity 6 3
10. Analysis of Variance of Data from Levinson's Locus of Control Scales 65
11. Analysis of Variance of Data from the Wallston et al. Locus of Control Internal and External Scales 66
12. Analysis of Variance on Image A Data from Raters 1 and 2 68
13. Analysis of Variance on the Reported Number of Hours Slept 69
14. Analysis of Variance on Reported Number of Times Awakened Per Night 71
IV
LIST OF TABLES—Continued
Table P a9 e
15. Analysis of Variance on Reported Changes in Work-Related Activities 73
16. Analysis of Variance on Reported Changes in Leisure-Related Activities 74
17. Analysis of Variance on Reported Changes in Physical Activities 74
18. Analysis of Variance on Measured Changes in Walking Time 75
19. Analysis of Variance on Reported Changes in Functional Performance 77
20. Analysis of Variance on Observed Changes in the Number of Impaired Joints 78
21. Analysis of Variance on Changes in Psycho-logical Configuration as Measured by the Profile of Moods State Test 78
22. Analysis of Variance on Reported Changes in Degree of Disease—Related Mood Affect . . . . 83
v
LIST OF ILLUSTRATIONS
Figure Pa9e
1. Peripheral skin temperature data for combined groups in Sessions 1-4 and 5-9, and plotted separately for Sessions 1-9 52
2. Electromyographic data for combined groups . . . 55
3. Pre- and posttreatment discomfort ratings for combined groups . . . . . . . . . . 58
4. Percentage of time during which disease-related pain is experienced for combined groups 60
5. Percentage of the body experiencing disease-related pain for combined groups . . . . . . . . 62
6. Level of severity of pain generally being experienced across treatment course, rated on a 0-10 scale, for combined groups . . . . . . 64
7. Hours of sleep per night for combined groups . . 70
. 72 8. Number of times awake per night for combined
groups . . .
9. Performance on activities of daily living as measured on the functional evaluation for rheumatoid arthritis for combined groups . . . . 76
10. Level of tension experienced, as measured by the Profile of Moods Scale test, for combined groups 82
11. Percentage of time in which subject's mood was disease-affected for combined groups . . . . 84
vx
RHEUMATOID ARTHRITIS: A PSYCHOLOGICAL INTERVENTION
Recent treatment strategies for many physical disorders
reflect a trend toward an interdisciplinary health care
approach {Williams & Gentry, 1977). It will be suggested
that the treatment of arthritis, particularly rheumatoid
arthritics, should include psychological intervention, A
research review will be presented with special emphasis placed
on the relationship of emotional factors, especially psycho-
logical stress, to the onset and progression of arthritis, as
well as other biological disorders, A treatment strategy for
rheumatoid arthritis will be described in which biofeedback
and verbal relaxation training will be used to reduce the psy-
chological stress and discomfort associated with that disease.
Clinical Description
Arthritis is estimated to be the chief cause of physical
disability in 20-50 million Americans (Pelletier, 19 77; Weiner,
19 77), with approximately a quarter million new cases reported
each year (Pelletier, 1977; Williams, 1974). Due to severe,
chronic pain 17 million arthritics currently are receiving
medical attention. Pelletier (19 77) reports that the economic
impact of arthritis is profound in terms of lost wages and the
expense of chronic medical care. Medical costs directly
attributable to this disease amount to about four billion
dollars per year and are growing rapidly.
Several major types of arthritis may be diagnosed, the
incidence of each varying with factors such as the age and
sex of the afflicted individual. Most arthritics (85%) are
45 years of age or older, and of these 60% have osteoarthri-
tis. Rheumatoid arthritis affects the majority of arthritics
who are 45 years or younger. An estimated five million Amer-
icans fall into this latter diagnostic category, including
approximately 200,000 children and over two million adoles-
cents and young adults (Weiner, 1977). Significantly, rheu-
matoid arthritis afflicts approximately three times more women
than men. Certainly, of all forms of arthritis, rheumatoid
arthritis is the most crippling. It is this subtype of dis-
order which will be the concern in this paper.
Although the term "rheumatoid arthritis" was first used
in the middle of the nineteenth century, a detailed descrip-
tion of the disease has only recently began to emerge. Cur-
rent clinical descriptions of rheumatoid arthritis character-
ize the disease as a generalized systemic illness (Williams,
1974). According to Williams, "multiple extra articular areas
of involvement, the constitutional symptoms, and the interest-
ing generalized prodromata often antedate the illness by years
or months"(p. 31).
Apparently, rheumatoid arthritis begins slowly, usually
in one or two joints at a time. Shoulders, elbows, hips,
wrists, fingers, knees, ankles, and feet are most commonly
involved. Temporomandibular and cricoartenoid joints may
in
uma-
toms
sthe-
ent
ment
not
also be involved and are of some diagnostic significance
that they are rarely affected by diseases other than rhei
toid arthritis. In some patients various prodromal sympl
of fatigue, diffuse muscle stiffness, dysthesias or pare:
sias may occur. A symmetrical pattern of joint involveme
is not unusual, although cases of nonsymmetrical involve]
are also seen. The ultimate severity of the disease can
reliably be predicted by the presence or absence of prodromata
nor by the acuity of onset. As the disease progresses, com-
plaints of joint pain at rest and on moving, swelling of the
involved joints and stiffness after inactivity, and a pro-
nounced limitation of motion are typical. Soft tissue or
periarticular swelling near involved joints is also common.
Muscular atrophy occurs at an alarming rate and subcutaneous
nodules form in approximately one-fifth of all patients. The
severity of the symptoms may fluctuate over time. The most
common complaints of the rheumatoid concern chronic pain, and
the often dramatic reduction of mobility seen in the more
advanced stages.
Underlying this symptomology there is also a predictable
sequence of steps in the progression of the disease at the
physiological level (Williams, 1974). Normally a joint inter-
ior is lined with a synovial membrane which secretes fluid as
a lubricant. Rheumatoid arthritis affects the synovial cells
causing them to multiply at an unnatural rate, thereby creat-
ing swelling. This tissue creeps into the joint, ultimately
4
packing it, destroying the cartilage/ and covering the ends
of the bone until erosion occurs, and the joint is rendered
useless. In the most advanced stages joint deterioration
may cause the formation of scar tissue which in turn produces
a joint that is knobby, deformed, and completely immobilized.
Peripheral manifestations such as vasomotor instability,
exemplified by cold hands or excessive peripheral sweating
are also common.
While this physiological progression is, for the most
part, universally accepted, no single treatment regimen is
so widely endorsed (Williams, 1974). Chemotherapy is the
most typical intervention, but even still there is no gener-
ally accepted pharmaceutical agent. Instead there are cur-
rently five basic medication alternatives for rheumatoid
arthritis (Carpenter & David, 19 76), each using a drug agent
for symptom relief. Aspirin is used most frequently. Dos-
ages are set at a "maintenance" level, i.e., the largest
possible dosage that does not produce counterproductive side
effects. Steroids, gold, penicillamine, and cytotoxins fol-
low as alternative treatment (Johansson & Sullivan, 19 75;
Weiner, 1977). Success rates, in terms of cure or stabiliza-
tion within the five alternatives, vary but are generally
quite low (Williams, 1974).
Alternatives to chemotherapy also are available (Silverman
in Freedman, Kaplan, & Sadock, 1975). A comprehensive inter-
vention often requires a therapy team, which in addition to
a physician, involves a physiotherapist, physical therapist,
occupational therapist, social worker, psychiatric nurse,
and a psychiatrist or psychologist.
The involvement of a psychologist in the treatment pro-
gram may be extremely important since chronic pain and the
loss of mobility may create serious problems of psychological
functioning, including depression, frustration, apathy, and
a helpless outlook (Pelletier, 1977; Weiner, 1977). These
psychological symptoms may act to undermine compliance to the
treatment regimen, blocking any intervention strategy.
Further, psychological distress may antedate or exacerbate
certain diseases, including rheumatoid arthritis (Pelletier,
19 77; Soloman & Moos, 1964; Williams, 19 74; Wolff, 196 8).
Therefore, treatment must involve a process of ever-changing
decisions and goals based on the patient's constantly shift-
ing status of physical and psychosocial functioning (Katy,
Vignos, & Moskowitz, 1968). The psychologist should minimize
maladaptive emotional reactions, and provide an adjunctive
treatment to insure compliance to a medical regime and hope-
fully aid the patient in the management of his or her pain.
Unfortunately, psychologists are in no more agreement as to
what to include in their treatment strategy than are their
physician counterparts.
One major problem for both psychologists and physicians
is that criteria used in diagnosing the illness are many and
varied, and often of a dysjunctive nature (Bennett & Burch,
1967; Kellgren, 1968; Ropes, Bennett, Cobb, Jacox, & Jesser,
1958; Weiner, 1977). As a result, research reports are incon-
sistent, as are data obtained from etiology and pathogenesis
investigations. Theories adhering to an epedimiological,
physiological, genetic, or psychological causal basis are
equally frequent, and often contradictory (King, 1955;
Spergel, 1972; Weiner, 1977; Williams, 1968; Wolff, 1968).
Although areas of psychological investigation have varied,
historically the interest in the illness has been of a tradi-
tional nature. Relationships between rheumatoid arthritis
and personality or traits, defense mechanisms and conflicts
are among the most frequently researched areas. Excellent
critical reviews of psychological research methodology in
this area have been offered by King (1955), Moos (1964), and
Scotch and Geiger (1962).
More directly germane to the current paradigm, however,
is the well-documented relationship between psychological
stress and rheumatoid arthritis. Pellitier (19 77) and others
(Cobb, 1959; Cormier & Wittkower, 1957; Crown, Crown, &
Fleming, 1974; Meyerowitz, 1971; Weiner, 1977) report that
the illness may begin, or exacerbations may occur, in associ-
ation with conscious worry, grief, depression, or with expo-
sure to various life events labeled by the patient as
stressful. A review of Table 1 summarizes and leads to the
conclusion that psychological stress may play some role in
initiation or aggravation of symptomology.
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10
The consistent reports of stress as an antedater to
flare-ups of rheumatoid arthritis are rare exceptions to the
usually contradictory evidence reported in the arthritis lit-
erature. Unfortunately, a hypothesis of arthritic pathegene-
sis connecting psychological with physiological functioning
must await elucidation of the exact site at which the process
begins. Clarification of the interaction would also require
discovery of a pathogenetic agent. Currently a variety of
hypotheses exist, all attempting to describe the physiologi-
cal initiating agent. Major hypotheses include infection by
virus (Kilroy, 1970; Phillips & Christian, 1970; Warren,
Marraor, Liebes, & Hollins, 1969) or bacteria (Duthie, Brown,
Knox, & Thompson, 1975; Sharp, 1.971), immunopathology, i.e.,
rheumatoid factors (specifically antibodies directed against
the body's own healthy blood cells)(Kellgren & Ball, 1959;
Lawrence, Valkenburg, Tuxford, & Collard, 1971), and vascular
lesions (Schumacher, 1975).
Without a full understanding of the nature of the inter-
action between the psychological and biological aspects of
rheumatoid arthritis, effective treatment and prevention is
unlikely. However, psychological stress is believed to be an
important piece of the elusive puzzle, and reduction of that
stress a significant treatment adjunct.
Stress and Other Diseases
The relationship of psychological stress to somatic
disease has been recognized for over 2000 years. In the
11
fourth century B.C., Hippocrates prescribed rest and relaxa-
tion for both physiological and psychological complaints
(Silverman, in Freedman et al., 1975). Persian texts written
in the twelth century A.D. have noted the effects of inhib-
ited aggression, grief, sorrow, shock, and general emotional
stress on the course of disease (Shafii, 1973). These early
revelations anticipated development of the more recent study
of "psychosomcitic" (American Psychiatric Association, DSM-II,
1968), and "beihavioral" (Williams & Gentry, 1977) medicine.
In behavioral medicine, the relation of a patient's
attitudes and behavior to the progression of his or her
disease is emphasized. Innovative uses of traditional psy-
chological principles are directed toward the elimination
or reduction of nonproductive emotionality with the belief
that the control of stress will increase the probability of
successful somatic recovery.
It seems logical that stress reduction would be of
benefit to some physiological complaints more than others.
However, predicting the diseases which would be the most
responsive to psychological intervention has been a very
speculative venture (Alexander, 1950; Freedman et al., 1975;
French & Alexander, 1941; Pelletier, 1977; Williams, 1968;
Williams & Gentry, 1977).
Although results are often inconsistent or contradic-
tory, some findings follow an identifiable pattern. Most
notably, there appears to be considerably more evidence that
12
psychological stress may exacerbate a patient's disease
rather than cause or antedate the initial acquisition of that
disease (Weiner, 1977; Wolff, 1968).
Accordingly, Wolff maintains that disease processes
should not be considered to be psychogenic simply because of
a hypothesized origin based on psychological conflict.
Instead the individual's "way of life" may be an exacerbat-
ing factor without specifically being considered causal. He
further hypothesized genetic influences to be of primary
importance, with the individual's attitudes and emotional
life, in part, determining penetrance. However, attempts to
achieve greater specificity by delineating personality pro-
files for each disorder have failed (Williams, 196 8; Wolff,
1968; Spergel, 1972). Of more direct relevance to the cur-
rent project is Spergel's explanation of a patient's response
to his or her disease. He maintains this response is largely
dependent on the premorbid manner in which an individual may
have handled a variety of life problems. Unfortunately,
efforts to differentially predict the onset of, or reaction
to, a specific disease, based on prior behavioral patterns
elicited by stress, have met with little success (Spergel,
1972; Williams, 1968). These failures concern specific pre-
diction, however, and do not obscure the importance of psy-
chological stress to the progression of a disease, whatever
its nature. The following studies will serve to empirically
13
demonstrate the existance of this important, although incom-
pletely understood, relationship.
Holmes and Rahe (1967) constructed a "social readjustment
scale" which could be used to quantify and predict the effects
of psychological stress on disease. An economic and cultural
cross-section of several hundred people were recruited to
assess the stressfulness of 43 common "life events," The
participants assigned each item a stress value based on the
predicted amount of adjustment needed to cope with that event.
These tabulated stress values (labeled as Life Change Units)
ranged from a high of 100 (death of spouse) to a low of 11
(minor violations of the law) , The authors found that an
individual who had accumulated 200 or more life change units
in a single year was later more likely than a similar person
with fewer life changes to succumb to myocardial disorder.
These results were interpreted as clearly supporting the rela-
tionship between psychological stress and onset of disease.
Although the Holmes and Rahe study is correlational, with an
alternate interpretation of the data being that early and
undiagnosed psychiatric or physiological disturbances may
themselves lead to stressful life changes, a caution to ther-
apists is recommended: Treatment programs should be avoided
which might elevate an individual above the 200 unit level.
While the work of Holmes and Rahe began by focusing on
psychological stressors and subsequently monitoring the asso-
ciated incident of disease, others have begun by first looking
14
at a particular disease and then searching retrospectively
for a premorbid personality configuration, or the presence
of certain conflicts which might, consistently antedate that
disease. Treuting (1962) tried to delineate such a profile
for patients with diabetes mellitus. Theorizing that emo-
tional stresses could precipitate the disease, Treuting
hypothesized that diabetes would be disproportionately repre-
sented among highly stressed populations, such as soldiers in
wartime. However, the data did not support this belief
(Hinkle & Wolff, 1952) and Treuting therefore theorized that
perhaps only certain personality types would succumb to dia-
betes mellitus when under stress. Attempts to delineate a
premorbid personality specific to the diabetic, however,
were also unsuccessful (Treuting, 1962).
Although Treuting's data did not verify the hypothesized
relationship between personality type, stress, and the onset
of diabetes mellitus, more positive results have been found
regarding the effect of stress on those already afflicted.
Schless and von Laveren (196 4) confirmed earlier findings by
Rosen and Lidz (1949), that stress can aggravate diabetes,
either through physiological change or by leading the patient
to neglect the proper management of his or her disease.
Hinkle et al. (1952) have demonstrated that a stressful inter-
view designed to threaten the dependency, affectional, and
emotional needs of a diabetic, elevate blood ketosis. A sim-
ilar stress-produced metabolic shoft also is found in nondia-
betics.
15
If such data are accurate, then a treatment strategy
designed to alleviate the stress reaction in favor of a more
homostatic, relaxed state could have a positive effect on
the diabetic's symtomatology. Fowler, Budzynski, and
Vendenbergh (19 76) supported such an observation by using
electromyographic biofeedback relaxation training, and ver-
bal relaxation tapes with a 20-year-old chronic diabetic.
Decreased levels of maintenance medication and fewer episodes
of ketosis resulted. The average dose of insulin needed for
normal functioning was dramatically reduced (approximately
50%) and the patient described herself as decreasing in emo-
tionality and in diabetic fluctuations. Such findings can
be interpreted as suggesting that not only does stress play
an important role in the progression or symptomatology of
diabetes, but also that its impact may be effectively con-
trolled via psychological intervention.
Similar results have been obtained for other endocrine
disorders as well. For example, Koran and Hamburge (in
Freedman et al., 1975) report the presence of high levels of
psychological stress in more than 50% of the patients being
treated for Cushing's syndrome. Mason's (1968a) review of
numerous human and animal studies summarizes reports of con-
sistently high levels of adrenal production of relevant cor-
ticosteroids by organisms exposed to stressful situations
(e.g., novel, unpredictable, or emotionally arousing). Addi-
tionally, psychological stress seems to directly influence
16
certain psychological processes which in turn may exacerbate
the Cushing's syndrome (Gifford & Gunderson, 1970). However,
consistent with research on other diseases is the failure to
delineate a specific personality configuration for sufferers
of Cushing's disease.
Research on the other endocrine disorders shows a simi-
lar pattern. Psychological stress seems to be related to
Addison's disease (Michael & Gibbons, 1963), hypoglycemia
(Marks & Rose, 1965), and amenorrhea (Rakoff, 1968). Yet,
again the relationship of stress to a patient's personality
for these diseases has not been demonstrated reliably.
Although biological predispositioning may be the single
most important factor for expression of coronary or cardio-
vascular disorders (Medalie & Goldbourt, 1976), evidence of
the association of stress and these diseases has been provided
by Szklo, Tonasciand, and Gordis (1976). Specifically,
Bennett, Hoskins, and Hampton (1976) have shown that mental
stress can evoke tachycardia and vasodilatation in the major-
ity of subjects tested.
Stress research, with results similar to those already
reported, has also been conducted with gastrointestinal dis-
orders (Alexander, 1950; Engel, 1975; Weiss, 1972), insomnia
(Dement, 1975) , allergic and skin disorders (Engels &
Wittkower, 1975), asthma (Creer & Renne, in press; Knappe,
1969; Stein & Schiari, 1975), and rheumatoid arthritis
17
(Carpenter & David, 1976? Cobb, 1959; Hartfall, 1955;
Wickramasekera., Truong, Bush, & Orr, 1976).
In summarizing the literature on the relationship of
stress and physiological complaints, three trends emerge.
First, when stress factors antedate or aggravate a disease,
they do not reliably seem to be associated with the assessed
personality of the patient. Second, efforts to demonstrate
that psychological stress can act as a primary precipitant
of a given disease have yielded equivocal results. Third,
psychological stress can have an exacerbating effect on the
majority of the diseases investigated. Although it is tempt-
ing to speculate that these findings could be replicated with
any physiological disorder (Freedman et al., 1975; Spergel,
1972), it is important to note that most of the relevant pub-
lished literature deals only with complaints which can be
categorized as psychosomatic or psychophysiological as a
function of a psychogenic etiology. Perhaps only these types
of illness are prone to exacerbation by psychological stress.
Alexander's (1977) conceptualization of chronic asthma
is in disagreement with such a criticism. Clearly, several
disorders (e.g., peptic ulcers) can be triggered by psycho-
logical stress. However, Alexander claims that research on
asthma, categorized as a psychophysiological disorder (DSM-II,
1968), suggests that psychological factors can influence the
actual biological pathology, i.e., hypersenitive airways.
He rejects labeling asthma as a psychophysiological disorder.
18
He points out, however, that psychological stress can result
from, and contribute to, the progression of asthma in general
and specifically affectsthe frequency and severity of broncho™
spasms. In concert with other investigators, Alexander views
psychological stress as an exacerbator rather than a precipi-
tor of both somatic as well as psychosomatic diseases.
Apparently the assessment and treatment of subjective
stress is a potentially important component of planned inter-
vention for any physical disorder. For rheumatoid arthritics,
pain is a major source of salient stress with possibly auto-
exacerbating effects. An effective treatment program for
arthritis should therefore minimize subjective distress
whether of an internal (pain) or external origin. Several
possible intervention components will be suggested.
Proposed Treatment Components
An individual's response to' stress is said to be as var-
iable as the situations which produce it (Wolff, 1968),
Regardless of the manner of expression, all stress reactions
are characterized by physiological arousal (Selye, 1950;
Williams & Gentry, 1977; Wolff, 1968)» A detailed descrip-
tion of the autonomic biological mechanisms which underlie
arousal will be omitted in favor of a experientially oriented
description of the phenomenon.
Obviously, short-term physiological arousal would seem
to provide an organism with an adaptive advantage in that
there is a mobilization of biological defenses, such as "fight
3
19
or flight" (Selye, 1950). Increased muscle strength, respir-
ation, heart rate, and vigilance are typically observed in
states of arousal (Coleman, 1968; Williams & Gentry, 19 77;
Wolff, 1968). However, extreme and/or long-term arousal not
only may be nonadaptive, it actually may be counterproductive.
The psychologist's most effective means of combating
inappropriate, maladaptive, physical stress is by training
deep muscle relaxation as a response incompatable to arousal
(Suinn, 1977; Suinn & Richardson, 1971), Although several
indirect approaches, such as jogging, listening to music,
reading, alcohol, etc., yield a degree of relaxation, clini-
cal applications of direct relaxation techniques allow greater
control. These alternatives include physical massage, relax-
ation imagery, meditational instructiont biofeedback, and
verbal relaxation strategies. Of these, biofeedback and
verbal relaxation are the most central to the treatment pro-
grams proposed.
Blofeedback. Several researchers have reported biofeed-
back training to be effective in the control of psychological
stress, Essentially, in biofeedback therapy a preselected
biological response is mechanically or electrically monitored
and transmitted, in amplified form, to the respondent via
visual and/or auditory displays. Using the external feedback
as a guide, the subject tries to alter his or fier physiologi-
cal state in a specified direction (Morris* 1976),
20
Love, Montgomery, and Moeller (19 77) used biofeedback
in an attempt to alleviate the exacerbating influence of
stress on hypertension. It was hypothesized that patients
trained to relax by electromyographic (EMG) feedback subse-
quently would show a reduction in blood pressure. The feed-
back procedure was continued for four weeks, with only one
or two training sessions per week. At the conclusion of
therapy, the subjects who received electromyographic relaxa-
tion training had significantly lower systolic and diastolic
pressures than did a nontreated control group. In a later
paper (Montegomery, Love, & Moeller, 1977), 23 of the origi-
nal subjects were reexamined. Blood pressure readings indi-
cated that earlier progress had been maintained or improved.
Patel (1977) used biofeedback training with three chron-
ically hypertensive subjects and reported results similar to
those found by Love et al. However, Patel suggested that
benefits from relaxation therapy depended on the patient's
daily practicing of the relaxation response for approximately
a year.
Biofeedback also has been applied successfully to Ray-
naud's disease;, using skin temperature as the target response.
Jacobson, Hackett, Surman, and Silverberg (19 73) reported a
case study involving a 31-year-old male with a 3-year history
of Raynaud's. After failing to affect symptomology or periph-
eral skin temperature with three session of hypnosis and
autohypnosis, skin temperature feedback was added to the
21
treatment protocol. The patient was able to elevate skin
temperature up to 4.3°C above a baseline measure, and. color
changes in both hands were observed. When retested 7 months
later, the ability to control skin temperature had been main-
tained.
A 2 8-year-old woman with a chronic case of Raynaud's
disease was successfully treated by Blanchard and Haynes
(19 75). After initial training with skin temperature bio-
feedback, the woman was retested, 2, 4, and 7 months later.
The clinical problem of Raynaud's disease had abated.
Biofeedback also has been used in the specific treatment
of the chronic pain that accompanies a variety of disorders.
Physicians and physical therapists generally accept that mus-
cle tension leads to immobility which then increases the sub-
jective experience of pain (Fowler et al., 1975; Gentry &
Bernal, 1977).. Treatment in these fields often includes mas-
sage, heat, traction, medication, and ultra-sound (Williams &
Gentry, 1977),. Sifnificantly, these techniques do not require
the patient to learn relaxation skills which could be used out-
side of the clinical setting. Compromising generalization
of effect, on the other hand, biofeedback training teaches
the patient a method of breaking the pain-tension^pain cycle.
By providing information about a physiological system that
covaries with tension, such as electrical activity in muscles
or skin temperature, the patient is trained to recognize and
modify deviant states which might exacerbate pain. Relaxation
22
is still the goal, as it is considered incompatible with
physiological tension.
Gentry and Bernal (in Williams & Gentry, 197/) have
reported two case studies which illustrate the use of bio-
feedback-facilitated relaxation as a treatment for chronic
pain. Case One involved a 42-year-old man who complained of
lower back pain. On a scale of 0 (no pain) to 6 (severe pain)
the patient rated himself at an average of 4.82 over a 2—week
pretreatment baseline. After the session of electromyographic
relaxation training, the muscle tension in his subject had
fallen from an average of 7,0 yV to an average of 4.1 yV.
Self ratings of pain fell to an average of 3,62, When reex-
amined 6 weeks after training, the patient's progress had
been maintained.
A 39-year-old woman who complained of neck and shoulder
pain aggravated by phlebitis was involved in the second case.
At the initial treatment session, subjective self ratings of
pain averaged 4.73 on a 7—point scale. Her electromyographic
baseline averaged 10.8 yV. By the end of the first session
the average electromyograph had decreased over 54% when com-
pared to the baseline level. Subjective ratings of pain had
decreased by 31%,
Controlled, experimental evidence showing the efficiency
of biofeedback as a treatment for chronic pain is also avail-
able, Peck and Kraft (19 77) is exemplary. Eighteen patients
with frequent tension headaches, eight with back and shoulder
23
pain, and six with temporomandibular joint pain were treated.
All 32 patients learned to relax via electromyographic bio-
feedback. Pain correspondingly declined significantly in 12
of 18 patients with tension headaches, and one of eight
patients with back pain complaints. Additionally, three head-
ache patients, three back and shoulder pain patients, and two
temporomandibular joint pain patients reported slight relief.
While efficacy varied as a function of the disorder, these
results support electromyographic biofeedback as a viable
treatment for tension-related pain (Hutchings & Reinking,
1976; Reeves, 1976).
Additional support is found in the results of Budzynski,
Stoyva, Adler, and Mullaney (1973). Treating pain from ten-
sion headaches, 18 patients underwent a 2-week baseline
period during which self-report headache evaluations and two
electromyographic baselines were taken daily. Then, patients
were assigned randomly to three groups. Group One received
electromyographic feedback twice a week and was encouraged
to practice the relaxation response at home. Group Two also
was seen twice a week, but received no feedback training and
only was encouraged to relax during the session. Taped audi-
tory feedback generated by the first group's responding was
played, not as sham feedback but with the explanation that
it would help keep out intrusive thoughts. The third group
received no treatment but was required to keep daily headache
data. Data from the 8 weeks of treatment and from a
24
reexamination 3 months later revealed Group One patients
reduced electromyographic base levels below those of controls
and significantly reduced the intensity of reported headaches.
These and othe;r results (Wickramasekera, 1973) seem to justify
the current enthusiasm for biofeedback-facilitated relaxation
as a primary treatment for tension headache.
More debilitating than simple tension headaches, the
migraine headache is another source of severe pain to which
biofeedback therapy has been applied. Reading and Mohr (1976)
trained six patients to voluntarily elevate hand temperature.
It was hypothesized that increased skin temperature would
correlate with muscle relaxation, and lead to a decrease in
severity of the migraines reported by the participants. All
patients learned to raise hand temperature, and data analy-
sis yielded statistically and clinically significant improve-
ment on several indices of migraine activity. Later examina-
tion attested to the stability of these findings. Similar
results are reported by numerous investigators using both
skin temperature and electromyographic level as target phys-
iological responses (Morris, 1976).
Sargent, Watters, and Green (1973) also used temperature
training for treating migraines. Seventy-five patients suf-
fering from migraine pain recorded daily self-rating inven-
tories for one month. Following this, weekly biofeedback
temperature control training sessions were begun. After all
patients could increase hand temperature with feedback, the
25
thermistors were withdrawn and the patients were asked to
practice the response without equipment. Five months after
the beginning of training, 80% of those participants diag-
nosed as true migraine patients reported at least some head-
ache relief.
Although migraine-related pain seems responsive to skin
temperature training techniques, the exact curative elements
of the training are uncertain. Of course, this is crucial in
understanding the disorder and the treatment, but the clini-
cal practitioner must be concerned more with the demonstrated
efficacy of skin temperature biofeedback in reducing the fre-
quency and the pain of severe migraine headaches.
In general, the use of biofeedback in the treatment of
physiological disorders has distinct advantages relative to
the more traditional medical approaches. It may prove to be
a valuable alternative to long-term chemotherapy (with its
attendant counterproductive sides-effects) for disorders such
as Raynaud's disease. The active participation of the patient
in the treatment of his or her illness is probably another
important aspect; patients with a "type A," high—achiever
personalities, or perhaps, with rheumatoid arthritis, possi-
bly experience an exacerbation of symptomotology when rele-
gated to an unaccustomed role of passivity in treatment.
Finally, biofeedback therapy probably elicits from the
patients an increased sense of responsibility and motivation.
Feelings of frustration and helplessness are minimized. For
26
these reasons biofeedback training was included as a major
component of the treatment program proposed for rheumatoid
arthritis.
Verbal relaxation. A treatment strategy often coupled
with biofeedback training is verbally induced relaxation
(Goldfried & Davison, 1976; Rimm & Masters, 1974; Williams
& Gentry, 1977). Broadly conceived, such techniques as
Jacobson's (1948) progressive muscular relaxation, Schutzes
and Luthe's (1969) autogenic training with imagery, and
Benson's (19 75) meditation to elicit the "relaxation response"
are all verbally induced relaxation procedures. It has been
demonstrated repeatedly that voluntary muscular relaxation
markedly reduces subjective stress and anxiety (Bernstein &
Borkovec, 19 73; Goldfried & Trier, 19 74; Jacobson, 1948;
Lang, Melamed, & Hart, 1970; Paul, 1969b). Also of import-
ance, the vocal instructions for relaxation can be tape
recorded and used in clinical training sessions and in home
practice (Achterberg, 1978; Lant et al., 1970). Based on
an impressive pool of positive results and on the simplicity
of the treatment procedure, verbal relaxation (as well as
biofeedback) has been used as least as an adjunctive treat-
ment of numerous physical disorders (Williams & Gentry, 1977).
In Table 2, a brief summary of representative studies demon-
strating the efficacy of verbal relaxation training is pre-
sented. In that the already reviewed literature on biofeed-
back training substantiates the effectiveness of inducing
27
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30
a relaxed state in the treatment of many physical disorders,
and since Table 2 documents that the same state may be induced
with verbal instruction, detailed examples of verbally induced
relaxation as a treatment for physical disease will not be
discussed. However, it should be noted that verbally trained
relaxation is an especially effective intervention strategy
in disorders where immobility or muscular tension are involved.
Rheumatoid arthritis is such a disorder. Thus, in the treat-
ment program proposed, verbally trained relaxation was the
second major component used to manage that disease.
Psychological Aspects of Adult Rheumatoid Arthritis
Before reviewing the arthritis literature, it should be
reemphasized that research conducted on arthritic patients is
fraught with methodological flaws in design and intepretation
(King, 1955; Moos, 1964; Scotch & Geiger, 1962; Weiner, 1977).
These contribute to the inconsistent findings often reported.
Analysis of published results must be attempted cautiously,
with an awareness that in many studies of rheumatoid arthri-
tis scientific rigor was not always maintained.
As described earlier, most psychological investigators
historically have taken a typological or trait-oriented
approach in researching rheumatoid arthritis. Many have
dealt, therefore, with delineating an "arthritic personality"
or at least identifying configurations of traits, demographic
variables, defense mechanisms, or conflicts unique to the
population. The emphasis in this portion of the research has
31
been on identifying high-risk groups and predicting the like-
lihood of rheumatoid arthritis onset. As previously shown m
Table 1, a second large segment of the literature includes
reports on the patient's reaction to certain life events,
including arthritis, as it affects the progression of the
illness.
Among the earliest typological research was that by
Halliday (1941, 1942). Believing he had identified a rheuma-
toid personality, Halliday described a small sample of female
rheumatoids as consistently self-restricted, emotionally calm,
detached, and possessing marked compulsive traits. Also,
according to Halliday, most were independent and self-
sufficient; strict parental discipline was common in child-
hood, and most lived a self-sacrificing, conscientious, quiet
life. The patients reported few intensive friendships, and
often exhibited a domineering personality. Unfortunately,
Halliday*s description of these traits was incomplete and
often vague. Nonetheless Johnson, Shapiro, and Alexander
(1947) reported findings which supported the compulsive
aspect of the proposed configuration. Johnson et al. addi-
tionally identified a proclivity for arthritic patients to
report that they had been vigorous and physically competitive
as children. Supposedly this activity had been an expression
of suppressed rebellious resentment against parental dominance.
Research interest in rheumatoid arthritis accelerated
throughout the 1950s and early 1960s, with each investigator
32
suggesting additional descriptive terms and speculations
about childhood dynamics. For instance, Geist (1966, 1969)
maintained that rheumatoid arthritics repressed hostility
and thus were intrapunitive. These results coincided with
and added to a multitude of earlier studies (Cobb, 1959?
Cormier, 1957; Ludwig, 1954, 1962; Mueller & Lefkowitz, 1956)
characterizing rheumatoids as latently hostile, experiencing
interpersonal difficulties, and as having unemotional mothers
and authoritarian fathers. Eventually, the descriptors became
so numerous that personality measures grew useless as diag-
nostic predictors of arthritis. The utility of these early
reports also is minimized by thei frequent omission of control
procedures by the researchers, and insufficient objectivity
in the definition of crucial terms (Spergel, 19 72).
In the mid 1960s there was a proliferation of more ade-
quately controlled, but still nondefinitive, studies. Several
researchers attempted to delineate an arthritic personality
profile with the relatively objective Minnesota Multiphasic
Personality Inventory (MMPI) replacing the less reliable pro-
jective personality tests (Bourestom & Howard, 1965; Moos &
Soloman, 1964, 1965a, 1965b; Nalven & O'Brien, 1968). Although
many descriptors were again generated, the most consistent
finding was a neurotic pattern characterized by a high degree
of bodily concern, depression, and somatization. However,
these findings were significant only in comparison to a nor-
mal population and were of little use in terms of differential
33
diagnosis when contrasted to patients with other chronic
diseases (Spergel, 19 72). As yet no personality profile
specific to rheumatoid arthritis or any other severe disease
has been found (Weiner, 1977), although there does appear to
be a profile characteristic of individuals suffering from
chronic disease in general. According to reviews by Spergel
(19 72) and Moos and Soloman (196 4) this profile is character-
ized by intrapunitiveness, latent hostility, familial and
interpersonal difficulty, shyness, rigidity, self-conscious-
ness, an inability to express anger, masochism, and a perfec-
tionistic standard of self-evaluation. Emotionally, moderate
depression and a tendency to somatisize are not uncommon.
Personality configurations of rheumatoids (although highly
variable) overlap somewhat with this general chronic disease
profile.
It is evident that attempts to find the arthritic per-
sonality generated much attention to childhood conflicts.
Alexander (1950) and Johnson et al. (1947) hypothesized that
a specific childhood psychological conflict might predispose
an individual to contract rheumatoid arthritis, provided that
the person also possessed a certain (unspecified) physiologi-
cal substrate. Based on clinical findings that were derived
primarily from studies with women, Alexander and his associ-
ates (Alexander, 1950; Alexander, French, & Pallock, 196 8;
Alexander, Stewart, & Duthie, 196 8) currently postulate that
the core conflict in rheumatoid arthritis has its genesis in
34
the restrictive parental attitudes experienced by the patient
in childhood. The child supposedly rebels, but due to an
excessive dependency on the punitive parent (typically the
mother) represses the rebellion for fear of rejection. For
girls, "tomboyish" behavior supposedly provides an outlet
for the repressed emotions of anger and hostility. Later in
life the rebellion is, according to Alexander, transferred to
men and involves rejection of the feminine role in favor of
aggressiveness in sports, work, and environmental control.
Any guilt which may be experienceid is alleviated through
serving others in some way. The disease purportedly has its
onset when the patient can no longer discharge her hostility
by dominating others or relieve her guilt by periodically
serving them.
Although Alexander's data aire used to support his theory,
research by other investigators has been equivocal. For
example, Booth (19 39), Cleveland and Fisher (196), Cobb
(1959), and Meyerowitz, Jacox, and Hess (1968) support the
results showing an active, competitive lifestyle, while Moos
and Soloman (1965a, 1965b) and Rimon (1969) find just the
opposite. Equivocal results not withstanding, the conflict
specificity theory is frequently used to explain the psycho-
genesis of rheumatoid arthritis.
Other investigators adhere to a nonspecific conflict
etiology theory (Blom & Nichols, 1953; Cobb et al., 1965;
Ludwig, 1954; Robinson, 1957; Schochet et al., 1969).
35
Although the advocates of the nonspecific conflict theory
accept hostility, resentment, ovesrcontrol, and inhibited
expression as centrally important, they do not tie these
traits to definite childhood conflicts. This theory is more
easily supported and more difficxilt to empirically refute.
To illustrate, Rimmon (1969) conducted a study with female
rheumatoid patients for whom no explicit environmental or
physiological antecedents of the disease could be found.
These sugjects were significantly more inhibited in their
expression of hostility and aggression than were patients
who had a clear precipitator of arthritis. They were also
less aware of negative emotions. These data support a rela-
tionship between repressed emotionality and the onset of the
disorder in the absence of salient antecedent conditions.
It is not surprising that those interested in identify-
ing the defense mechanisms most common to rheumatoid arthri-
tics consistently find denial and avoidance to be paramount
(Cobb, 1959, 1965; Ludwig, 1954? Schochet et al., 1969).
Reaction formation, isolation, intellectualization and undo-
ing also were common. In related research, Gregg (1939),
King (1955), Nissen and Spencer (1936), Pilkington (1956),
Rothermilch and Phillips (1963), and Trevaham and Tatum
(1954) have reported a lower incidence of psychosis among
rheumatoid arthritics than would be expected in the general
population. Nissen and Spencer (19 36), for instance, did
not find one case of rheumatoid arthritis among 2,200
36
schizophrenic patients, nor did Gregg (19 39) in 3,000 autop
sied psychotics. Since subjects in these and other cited
studies were inpatients, it has been suggested that the pro-
tective atmosphere of the hospital may account for the
absence of the disorder. Such explanations must be considered
speculative due to the lack of carefully controlled research
in this area.
Researchers in an extensive segment of the relevant lit-
erature have dealt with the effect psychological factors may
have on the progress of the established disease, rather than
describing the relationships of the etiology of rheumatoid
arthritis to personality variables. As has already been
demonstrated, considerable data exist which support the con-
clusion that stress, emanating from numerous sources, can
have an exacerbating effect on rheumatoid arthritis, and that
this effect is independent of the specific origin of the
stress. Worry about financial matters, job absentism, anger,
major surgery, divorce, death of a loved one, anxiety about
prognosis or incapacitation, and intense competition have
been shown to be related to a worsened symptom pattern
(Spergel, 1972; Williams, 1968; Wyatt, 1969). A review of
several selected studies should help illustrate this associ-
ation.
Moos and Soloman (1964) examined rheumatoid arthritics
under conditions of intense athletic competition. A rheuma-
toid factor count was determined from blood drawn before and
37
after participation in a highly competitive physical sport.
The subjects who were distressed by the pending competition
had a higher precontest rheumatoid count than those subjects
who displayed little distress, and all participants showed
an increase following their involvement in the very arousing
contest,
Schochet, Lisansky, Schubart, Fiocco, Kurland, and Pope
(1969), in a study of 12 subjects, found a strong relationship
between the occurrence of major life crises (e.g., separation
from a loved person) and the temporary exacerbation of arth-
ritic symptoms. Similarly, Rimon (1969) uncovered an unex-
pected amount of psychological distress in the life-histories
of 100 female patients diagnosed as having rheumatoid arthri-
tis. The families of 25% of the patients had members with
psychiatric disturbances, and 37% of the patients had come
from homes where the parents had separated or divorced.
Marital discord and/or sexual problems in the years immedi-
ately preceding the onset, or serious exacerbation, of the
disorder were reported by 2 3%. Over half (55%) reported
major life conflicts preceding onset and of these, 65%
reported additional exacerbation related to a significant
life crisis. Certainly, it would seem that the frequency
with which stress precedes onset or exacerbation of rheuma-
toid arthritis far exceeds that which would be expected by
chance. Although no unequivocal evidence exists on how this
psychological stress interacts with the physiology of
38
rheumatoid arthritis, it is widely accepted that at least one
mediator is probably increased muscle tension (Alexander,
1950; Barchiton, 1963; Gentry & Bernal, 1977; Weiner, 1977;
Wyatt, 1969) . This seems plausible as it is congruent with
physiological models of the stress reaction (Cannon, 1929,
Selye, 1950), as well as clinical observations that muscular
tension often precedes sudden arthritic outbreaks (Alexander,
1968; Barchiton, 1963; Wyatt, 1969). It is well documented
that muscle tension can be produced by psychological stress
(Barchiton, 1963; Freidman, 1975; Moos & Engle, 1962; Morrison,
Short, Ludwig,, & Schwab, 1974; Rodnan, 1973; Selye, 1950;
Wolff, 196 8). Demonstrations of the translation of stress
into muscle tension have been achieved through the electromy-
ographic monitoring of muscle activity while intermittently
presenting stressful stimuli (Moos & Engel, 1962; Southworth,
1958) . Based on these findings, it may be suggested that
psychological conflicts, such as those espoused by the dynamic
theorists as being central to the onset and/or exacerbation of
illness, are simply nonspecific sources of stress which lead
to muscle tension and a subsequent aggravation of inflammed
joints. A stress-muscle tension-exacerbation cycle seems
plausible. As part of the present study, an attempt was made
to interupt this stress cycle by training patients to respond
to stressful stimuli with a relaxation response rather than
by tension. Unfortunately, too little is known about the
physiological, components responsible for arthritic outbreaks
39
to warrant a high degree of specificity in the design of the
study. Skin temperature biofeedback was used, and since the
curative mechanisms of this technique are uncertain, it would
seem presumptuous to predict that increases in peripheral
skin temperature would be more beneficial than decreases.
Although it is believed that the systematic induction of
relaxation will be helpful in controlling arthritis, and
that increases in skin temperature generally coincide with
relaxation, Achterberg (1978b) reports that some patients
may actually experience a decrease in skin temperature when
relaxed. Additionally, although physical therapists tradi-
tionally have endorsed the application of "hot packs to
diseased joints (Jivoff, 19 75-76), many therapists presently
are reporting the application of ice packs (called cryother-
apy) to be successful treatment techniques (Achterberg,
197 8b). It is also possible that skin temperature may
retard the activity of leukocytes in the area of the affected
joint, thus reducing the local inflammation. Therefore,
since it is uncertain whether raising the skin temperature
of arthritic patients would be more beneficial than lowering
it, both techniques were investigated. To better quantify
whether or not muscular relaxation was actually occurring in
either or both treatment groups, electromyographic measures
were taken, in addition to self report. Solely a dependent
variable, no feedback as to changes in muscular activity was
available to patients.
40
Two groups of patients suffering from rheumatoid arthri-
tis were treated. All participants received identical verbal
relaxation training, but one group was taught, via biofeed-
back, to raise peripheral skin temperature, and the other was
taught to lower it. Treatment-related changes in the patients
were measured on physical, functional, and psychological
dimensions. It was hypothesized that the systematic induc-
tion of relaxation and changes in peripheral skin temperature
would influence the symptomology of the subjects. It was
further hypothesized that effects on symptomology would dif-
fer as a function of which biofeedback training was received.
Method
Subjects
A total of 24 female rheumatoid arthritic patients par-
ticipated in this study. The women were recruited from
several sources in Dallas and Wichita Falls, Texas. These
included the arthritic clinic at the Southwestern Medical
School (Parkland), referral by private physicians in Dallas,
and by physician referral and voluntary self-referral in
Wichita Falls. Criteria for inclusion in the sample were:
(a) a medical diagnosis of rheumatoid arthritis, (b) involve-
ment (defined as the clinical observation of inflammation,
pain, and a restricted range of motion for a given joint) in
at least two joints, (c) an ongoing "maintenance" level of
medication, and (d) a minimum of 1-year history of the
disease. Half of the subjects (seven from Wichita Falls,
41
five from Dallas) were randomly assigned to a condition in
which increased peripheral skin temperature training would
be provided. The remaining subjects (eight from Wichita
Falls and four from Dallas) were assigned to a program in
which they would be taught to decrease skin temperature.
When potential participants were initially contacted
they were given a brief letter of explanation about the pro-
posed treatment programs (see Appendix A). Later, the women
were called on the telephone, and those expressing interest
were scheduled for an interview in which a detailed explana-
tion of the experimental program was given. Those who agreed
to participate signed a form on which they certified their
consent (see Appendix B). Following this, the volunteers
were interviewed about themselves, and their medical records,
to determine if the volunteers met the criteria for partici-
pation. For each subject who qualified, the examiner deter-
mined and recorded a subjective evaluation about the severity
of the disease.
Five dollars per visit was paid to some of the more
indigent participants to help defray travel expenses. All
participants remained under the care of their personal physi-
cians throughout the study.
Apparatus
Psychosocial assessment tools. The lifestyle, familial
relationships, modes of emotional expression, and other
aspects of psychosocial development for the patients were
42
explored with a structured social-history interview (see
Appendix C). To assess a patient's tendency to accept or
reject responsibility for life happenings, a scale designed
by Levinson (1973) to measure locus of control was also
administered. The Levinson instrument was chosen because of
demonstrated high reliability and validity. Additionally,
it provides information about the degree to which a respond-
ent is likely to attribute the cause of life happenings to
themselves, to powerful others, or to chance. To facilitate
administration, the scale was retyped so as to provide larger
spaces for marking answers (see Appendix D). A health locus
of control (Wallston, Wallston, Kaplan, & Maides, 1976) was
also administered and is included in Appendix E. The health
locus of control scale consists of 11 items worded either
"internally" or "externally." The scale yields a score indi-
cating a tendency to accept (internal) or assign (external)
responsibility for current health status. The Profile of
Moods State (Educational and Industrial Testing Service) was
additionally given and yields a score on six dimensions of
current mood state and a sample form is included as Appen-
dix F.
Two other diagnostic instruments were used to evaluate
each patient's perceptions about her disease. A questionnaire
labled Image A was patterned after a questionnaire used by
Achterberg and Lawlis (1978) with cancer patients (see
Appendix G). As a second assessment procedure, patients were
43
instructed to draw an image of a healthy and a diseased joint,
as well as their treatment and disease process, as they invi-
sioned them.
Physical/Functional assessment tools. To assess physi-
cal and functional abilities, two protocols for evaluation
were designed. Range-of-motion and strength of affected
joints were considered in accordance with the Physical Ther-
apy Evaluation (see Appendix H). A format was also designed
to measure the performance of daily activities. Ratings of
1 (always can), 2 (sometimes can), or 3 (never can) were
assigned to each of certain tasks in the areas of personal
hygiene, dressing, eating, household chores, locomotion, and
communication. This form was entitled Functional Evaluation
of Rheumatoid Arthritis (see Appendix I),
Equipment. A Biofeedback Technology (BFT), Model 302,
was used to monitor skin temperature and to provide visual
and auditory feedback to patients. Muscle tension was mea-
sured and integrated by a BFT 401, an electromyograph, and
a BFT 215 respectively.
Two standardized cassette tapes were used in the verbal
relaxation portion of the experiment. These tapes were part
of the Perceptual Program in Relaxation and Guided Imagery
(Achterberg, 1978a). One tape (Pre-Biofeedback Relaxation)
was intended for general use with biofeedback patients, and
the other (Arthritis) was designed specifically for arthrit-
ics. The Perceptual Program in Relaxation tape provided
44
instructions on how to achieve the relaxation response. The
emphasis was on reducing tension in major muscle groups.
Relaxing sounds such as an "ocean surf" were included. The
Arthritis tape repeated relaxation instructions and provided
specific information about the arthritic process. Listeners
were given a construct system for conceptualizing their
disease, e.g., white blood corpuscles wrongly attacking
other blood cells and causing inflammation. This tape was
included in order to provide all patients with a minimal
standard explanation of their disease. Copies of both tapes
are available from the author.
The treatment area was a room measuring approximately
2.5 X 3 meters. It contained a standard hospital bed and a
recliner, and a small desk and chair for the therapist.
Procedure
After all subjects had been recruited and assigned to
one of the two experimental conditions, the program began.
It consisted of four phases—pretreatment assessment, treat-
ment, and mid- and posttreatment assessment. In the first
session, each participant met with a trained physical thera-
pist who evaluated her on the severity of her arthritis,
using estimations of range of motion, and strength and number
of effected joints, as guides. The patient also provided
social-history information during rest periods throughout
the examination. Specifically, data were elicited concern-
ing: sleep patterns? work, leisure and physical activity
45
levels; general and specific experiences of pain; mood levels;
percentage of time hurting; and portion of body hurting.
These reports were illicited pre-, mid-, and posttreatment.
Finally, the physical therapist completed the Functional Eval-
uation for Rheumatoid Arthritis form, including a timed 50-
foot walk.
Next, the patient listened to the Arthritis tape after
being told:
Arthritis is a mysterious disease. We do not even
know what causes it. But the real mystery lies in
the different ways it affects each individual. No
one knows better than you how it affects you. First
of all, I am going to ask you to listen to a tape
recording. On the tape will first be some relaxa-
tion instructions. The purpose of the relaxation
is that we have found we can think better about our
bodies when we are relaxed because our minds are
actually more alert to those things. Then, the
tape will give you some information on arthritis
and how it is treated.
Patients then were asked to complete the Image A and to
draw a normal joint, an arthritic joint, a picture of her
disease, and an image of her treatment process. Specifically,
the patient received the following instructions.
Some things are difficult to describe in words, so
I want you to draw for me. It doesn't matter what-
soever how well you draw, but just that you get some
46
ideas on paper. First, draw the worst joint that
has arthritis in it. Do this any way you want—
real or fantasy—as long as it makes sense to you.
Next, show on paper how your disease works inside
your body. Then, draw a picture of a normal joint
as it might look after the treatment had been effec-
tive or you had gotten well for some other reason.
Finally, draw your treatment process as you picture
it in your mind's eye.
At the conclusion of the first session, each participant
was given Levinson's locus of control scale, the mood scale,
and the Wallston et al. health locus of control scale and
asked to complete them at home prior to returning for the
treatment phase.
Patients were then treated individually in 12 30-minute
sessions which occurred over a 4- to 6-week period. With the
exception of the biofeedback manipulation, patients in both
experimental groups received identical instructions and train-
ing.
Immediately upon entering the treatment room, the patient
was asked to rate the severity of her pain on a scale ranging
from 1 (minor, occasional, hardly noticeable pain) to 10
(major, constant, debilitating pain). Upon completion of the
report, the patient was asked to lie down and become comfort-
able. Three surface electromyographic electrodes (two active,
one ground) were placed on the under side of the participant's
47
nondominant arm and connected to the electromyographic ampli-
fier. No attempt was made to position these over specific
muscle groups. A thermistor probe was attached to the tip
of an index finger and the monitoring unit was positioned so
that the patient could view it easily. Since the biofeedback
dial was masked, and the tone generator turned off, informa-
tion about skin temperature was not available to the subject
at this time.
Five minutes elapsed, after which the experimenter
recorded the average integrated muscle tension in microvolts,
and the terminal skin temperature. These scores constituted
a baseline level against which later measurements would be
compared. The peak skin temperature for the baseline period
was also recorded.
Next, the taped prebiofeedback-relaxation instructions
were played for the patient. At the conclusion of the tape,
a second electromyograph and skin temperature measurement was
recorded.
The remainder of the session was devoted to skin temper-
ature training. The mask was removed from the monitor, and
the auditory feedback generator was turned on. The following
instructions were used for both experimental groups with the
words in parenthesis omitted in the group trained to raise
skin temperature or substituted for the immediately preceding
word in the group trying to lower skin temperature.
48
Psychologists have recently learned that patients
can control certain body processes in a way that
may be helpful in overcoming various illnesses.
For example, we believe that skin temperature may
be related to arthritis, and that increasing
(decreasing) it from time to time could lessen
the severity of your symptoms. This machine you
are connected to measures your skin temperature
and the needle and tone will tell you whether it
is staying the same or going up or down. For
instance, if your skin temperature starts to go
up, the tone will go down, and the needle will
move to the right. If your skin temperature
starts going down, the tone will go up and the
needle will move to the left. Just relax and
concentrate on changing the tone and/or the
dial. This will produce the best results. You
are to make the tone and the dial go up (down).
You may listen to the tone and watch the dial or
you may wish to attend to only one or the other.
Please do not pinch the probe on your finger or
press it against your body. Are there any ques-
tion? Okay, let's begin.
At the conclusion of 20 minutes, the therapist recorded
the patient's terminal skin temperature, her most extreme tem-
perature during the training, and her posttreatment muscle
49
tension (averaged over 1 minute). Finally, the patient again
was asked to rate the severity of her pain on the 10-point
scale. After six sessions, the Levinson scale, the health
locus of control scale, and the mood scale were administered.
Upon completion of the last training session, every
patient was reevaluated by both the psychologist and the
physical therapist. This evaluation was identical to the
pretreatment assessment, with the exception that portions of
the social-history interview were omitted.
Results
To summarize the effectiveness of the biofeedback train-
ing, an analysis of variance source table for the data from
Sessions 1-4, 5-8, and 9-12 is presented in Table 3. These
data show that while significant skin temperature changes
are found, there are no differential effects relative to the
treatment received. Instead, the differences are basically
in the warming direction regardless of whether the subjects
were in the increase or decrease temperature group during
biofeedback training. One possible exception is seen in the
data obtained from Sessions 9-12. The decrease temperature
group shows an average drop of 3.3 degrees Fahrenheit, which
according to Fisher's T test reaches significance (p < .05).
A review of Figure 1 graphically confirms that the
majority of the change in temperature for both groups took
place between the baseline and postrelaxation measures. It
then appears that the biofeedback training is not a
50
Table 3
Analysis of Variance on Peripheral Skin Temperature for Increase and Decrease Training Groups
Source df MS F
Block 1—Sessions 1-4
Between Subjects 26
Increase vs. Decrease (A) 1 53. 33 < 1
Error B 25 65. 25
Within Subjects 54
Temperature Changes within Blocks (B) 2 56. 66 13.85*'
A X B 2 6. 56 1.59
Error W 25 4. 09
Block 2—Sessions 5-8
Between Subjects 25
Increase vs. Decrease (A) 1 • 09 < 1
Error B 24 53. 17
Within Subjects 52
Temperature Changes within Blocks (B) 2 82. 75 19.85*
A X B 2 10. 88 2.61
Error W 28 4. 17
51
Table 3—Continued
Source df MS F
Block 3—Sessions 9-12
Between Subjects 25
Increase vs. Decrease (A) 1 3.44 < 1
Error B 24 41.20
Within Subjects 52
Temperature Changes within Blocks (B) 2 145.84 24.66**
A X B 2 23.04 3. 89*
Error W 48 5.91
*p < .05.
**p < .01.
significant factor in the control of the peripheral skin tem-
perature.
That all subjects learned the relaxation response, inde-
pendent of the treatment employed, is apparent from the
electromyographic data analysis summarized for Sessions 1-4,
5-8, and 9-12 in Table 4. Figure 2 is a graphic representa-
tion of the linear decline of muscle tension in both groups.
These data, in combination with the skin temperature data,
show that while the relaxation response was learned, and
thus a likely contributor to variance on other dimensions,
52
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53
the biofeedback response was not learned. Further, the learn-
ing of the relaxation response appears to be independent of
the type biofeedback training received.
Table 4
Analysis of Variance for Electromyographic Data Across Blocks
Source df MS F
Block 1—Sessions 1-4
Between Subjects 19
Increase vs. Decrease (B) 1
Error B 18
Within Subjects 40
EMG Changes within Blocks
(A) 2
A X B 2
Error W 36
8.29
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1.56
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< 1
7.21**
2.14
Block 2—Sessions 5-8
Between Subjects 19
Increase vs. Decrease (B) 1
Error B 18
Within Subjects 40
EMG Changes within Blocks (A) 2
9.60
32. 31
11.14
< 1
13.46**
54
Table 4—Continued
Source df MS F
A X B 2 1. 82 2.19
Error W 36 . 83
Block 3—Sessions 9-12
Between Subjects 20
Increase vs. Decrease (B) 1 14.72 < 1
Error B 19 27. 83
Within Subjects 42
EMG Changes within Blocks (A) 2 7.10 8.63*
A X B 2 .49 < 1
Error W 38 .82
*p < .05.
**p < .01.
Table 5 presents the analysis for numerical ratings of
subjective units of discomfort pre- and posttreatment for
increase and decrease groups across blocks. Although the
groups do not differ significantly regarding initial discom-
fort ratings, the combined groups appear to significantly
decline in initial levels across the 12 sessions. Table 5
also shows a similar pattern for posttreatment ratings with
reported discomfort declining across the 12 sessions.
55
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Table 5
Analysis of Variance on Pre- and Posttreatment Discomfort Ratings for Increase and
Decrease Groups Across Blocks
Source df MS F
Pretreatment Discomfort Ratings
Between Subjects 24
Increase vs. Decrease (B) 1 309.19 < 1
Error B 23 659.97
Within Subjects 50
Discomfort Changes within Blocks (A) 2 998.85 14.92**
A X B 2 80.69 1.16
Error W 46 69,24
Posttreatment Discomfort Ratings
Between Subjects 25
Increase vs. Decrease (B) 1 24.10 < 1
Error B 24 430.39
Within Subjects 52
Discomfort Changes within Blocks (A) 2 291.96 6.50**
A X B 2 96.09 2.14
Error W 48 44.90
*p < .05.
**p < .01.
57
Figure 3 graphically represents the linear decline for
pre- and posttreatment discomfort reports. A comparison of
pre- to posttreatment measures reveals that both increase
temperature (t [35] = 8.60, p .01) and decrease tempera-
ture (t [41] = 7.87, p .01) training groups report signif-
icantly less discomfort after treatment than before.
Table 6 presents the analysis of reported percentage of
time during which disease-related pain was experienced and
recorded from all subjects pre-, mid- and posttreatment.
Table 6
Analysis of Variance on Reported Percentage of Time Hurting Across Treatment
Source df MS F
Between Subjects 17
Increase vs. Decrease (B) 1 146.68 < 1
Error B 16 3708.00
Within Subjects 36
Percent Changes for Combined Groups (A) 2 414.02 9.47**
A X B 2 23.57 < 1
Error W 32 43.69
*p < .05.
**p < .01.
58
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59
While there are no differential biofeedback training effects,
there is a general decline in the percentage of time during
which disease-related pain is experienced across sessions
when the two groups are pooled. As shown in Figure 4, the
majority of the improvement occured during the second half
of treatment.
Table 7 presents the analysis of numerical reports of
percentage of the body hurting as a result of rheumatoid
arthritis. Significant differences are indicated both
between and within groups for pre-, mid-, and posttreatment
intervals.
Table 7
Analysis of Variance on Reported Percentage of Body Hurting Across Treatment
Source df MS F
Between Subjects 17
Increase vs. Decrease (B) 1 13632. 66 4.74*
Error (B) 16 2873. 81
Within Subjects 36
Percent Changes for Combined Groups (A) 2 684. 57 7.66**
A X B 2 29. 05 < 1
Error W 32 •
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*p < .05.
**p < .01.
60
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The between-group differences are considered to be of only
minor importance in that significant variance appears to
have been contributed by pretreatment differences between the
groups. Figure 5 represents the decline in the reported per-
centage of body hurting across the treatment sessions.
Table 8 shows pre-, mid-, and posttreatment analysis of
numerical report regarding the general severity of pain exper-
ienced.
Table 8
Analysis of Variance of Reported General Severity of Pain
Source df MS F
Between Subjects 18
Increase vs. Decrease 1 7.79 1. 84
Error B 17 4.22
Within Groups 38
Severity Changes for Combined Group (A) 2 1.75 6.23**
A X B 2 .20 .72
Error W 34 .28
*p < .05.
**p < .01.
Again no significant differences are found between treatment
groups, while a general decline in the average severity of
62
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pain experienced is seen across sessions for the combined
group. Figure 6 is a graphic representation of the pattern.
The data analysis summarizing self-report of specific
(the actual time of the questionning) pain severity yields
no significant results and is presented in Table 9.
Table 9
Analysis of Variance of Reported Specific Pain Severity
Source df MS F
Between Subjects 17
Increase vs. Decrease (B) 1 2386.68 < 1
Error B 16 2907.21
Within Subjects 36
Severity Changes for Combined Groups (A) 2 364.52 2.40
A X B 2 173.40 1.14
Error W 32 151.46
*p < .05.
**p < .01.
Table 10 presents an analysis of the data from the
Levinson locus of control scale. No significant differences
were found.
64
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Table 10
Analysis of Variance of Delta from Levinson's Locus of Control Scales
Source df MS F 1
Internal Scale
Between Subjects 26 1. 12
Increase vs. Decrease (B) 1 245. 00
Error B 25 219. 43
Within Subjects 54
Dimensional Shifts for Combined Groups (A) 2 •
00 WO 92 < 1
A X B 2 36. 92 < 1
Error W 50 93. 60
Powerful Others Scale
Between Subjects 26 < 1
Increase vs. Decrease (B) 1 10. 60
Error B 25 216. 72
Within Subjects 54
Dimensional Shifts for Combined Groups (A) 2 28. 53 < 1
A X B 2 17. 20 < 1
Error W 50 46. 32
66
Table 10—Continued
Source df MS F
Chance Scale
Between Subjects 22
Increase vs. Decrease (B) 1 371.71 2.27
Error B 21 163.58
Within Subjects 46
Dimensional Shifts for Combined Groups (A) 2 24.18 1.16
A X B 2 12.70 < 1
Error W 42 20.76
The analysis of the data from the Walston et al. scale is pre-
sented in Table 11. No significant differences were found.
Table 11
Analysis of Variance of Data from the Walston et al. Locus of Control Internal and External Scales
Source df MS F
Scale I (Internal)
Between Subjects 16
Increase vs. Decrease (B) 1 20.12 < 1
Error B 15 70.92
67
Table 11—Continued
Source df MS F
Within Subjects 34
Dimensional Shifts for Combined Groups (A) 2 10.76 1
A X B 2 18.09 1. 15
Error W 30 15.70
Scale E (External)
Between Subjects 16
Increase vs. Decrease (B) 1 86.65 1. 03
Error B 15 81.45
Within Subjects 34
Dimensional Shifts for Combined Groups (A) 2 30.02 1. 85
A X B 2 25.24 1. 56
Error W 30 16.19
Data regarding measured images of the disease, on both
the Image A questionnaire and on the subjects' drawings, are
equivocal. Two independent raters evaluated each participant
in the study and Section 1 of Table 12 contains a summary of
the analysis of the data derived from Rater 1 which shows no
change. Data generated from a second rater's evaluation are
contained in Section 2 of Table 12 and, while showing no
68
differential effects, a shift in imagery for the combined
groups is evident. Due to the disagreement of the independ-
ent raters, however, the data are considered unreliable.
Table 12
Analysis of Variance on Image A Data from Raters 1 and 2
Rater 1 Rater 2 Source
df MS F df MS
Between Subjects 22 21
Increase vs. Decrease (B) 1 36. 07 <1 1 15. 36 < 1
Error B 21 44. 30 20 46. 56
Within Subjects 23 22
Image Shifts for Combined Groups (A) 1 7. 68 1.21 1 209. 45 15.44*'
A X B 1 • 38 <1 1 2. 27 < 1
Error W 21 6. 35 20 13. 56
*p < .05.
**p < .01.
The six different measures of physical functioning are
noteworthy. Two of the six measures involve sleep patterns,
Table 13 is a summary of the analysis of the data derived
from the subjects' self-reports about the number of hours
spent sleeping each night during pre-, mid-, and posttreat-
ment.
69
Table 13
Analysis of Variance on the Reported Number of Hours Slept
Source df MS F
Between subjects 17
Increase vs. Decrease (B) 1 3.13 < 1
Error B 16 5.40
Within Subjects 36
Shifts in Hours Slept Combined Groups (A)
for 2 1.46 3. 41*
A X B 2 1.68 3.93*
Error W 32 .43
*p < .05.
**p < .01.
As seen in the table, significant differences are shown for
the combined groups and the significant interaction indicates
the patterns are nonparallel. Figure 7 is a graphic repre-
sentation of the reported sleep habits for the two groups
across the 12 treatment sessions, and shows that the increase
temperature group reports a disruption in the number of hours
slept at midtreatment. While the combined groups show a sig-
nificant increase in the number of hours slept each night, no
differential effects are seen.
70
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A second sleep-related measure involves the subjects'
self-reports of the number of times they awoke during a typi-
cal night. Table 14 is a summary of the analysis of the
data.
Table 14
Analysis of Variance on Reported Number of Times Awakened Per Night
Source df MS F
Between Subjects 18
Increase vs. Decrease (B) 1 23. 88 1.69
Error B 17 14.13
Within Subjects 38
Times Awake for Combined Group (A) 2 2.73 3.43*
A X B 2 .06 < 1
Error W 34 .79
*p < .05.
A significant change for the combined groups is shown in
Figure 8. Again, while there is a positive and significant
change for the combined group, no differential effects are
seen.
A third measure involves the subjects' self-reported
level of participation in work-related activities. Table 15
72
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is a summary of the analysis of these data. No significant
changes across treatment sessions are in evidence.
Table 15
Analysis of Variance on Reported Changes in Work-Related Activities
Source df MS F
Between Subjects 18
Increase vs. Decrease (B) 1 .55 < 1
Error B 17 3.43
Within Subjects 38
Changes for Combined Groups (A) 2 .22 1.45
A X B 2 .15 < 1
Error W 34 .15
*p < .05.
**p < .01.
Table 16 presents the analysis for numerically rated
changes in subjects' reported participation in leisure-
related activities. No significant changes occurred on this
dimension throughout the course of treatment.
74
Table 16
Analysis of Variance on Reported Changes in Leisure-Related Activities
Source df MS F
Between Subjects 18
Increase vs. Decrease (B) 1 8.27 3.42
Error B 17 2.42
Within Subjects 38
Changes for Combined Groups (A) 2 .23 < 1
A X B 2 .02 < 1
Error W 34 .24
Table 17 presents the analysis for numerically rated
changes in physical activities. No significant changes are
evident.
Table 17
Analysis of Variance on Reported Changes in Physical Activities
Source df MS F
Between Subjects 17
Increase vs. Decrease (B) 1 27.63 < 1
Error B 16 1101.16
Within Subjects 36
Changes for Combined Groups (A) 2 17.13 < 1
A X B 2 19.90 < 1
Error W 5 3 74. 77
75
Table 18 is an analysis of times required to walk a dis-
tance of 50 feet. No significant differences are apparent
within or between groups.
Table 18
Analysis of Variance on Measured Changes in Walking Time
Source df MS F
Between Subjects 22
Increase vs. Decrease (B) 1 10.13 < 1
Error B 21 20.75
Within Subjects 2 3
Changes for Combined Groups (A) 1 9.02 1.67
A X B 1 1.71 < 1
Error W 21 5.41
*p < .05.
**p < .01.
Table 19 presents the analysis for numerical ratings of
functional performance pre-, and posttreatment. While no
differences between groups are evident, there is a signifi-
cant change in functional performance across the duration of
treatment when the two groups are pooled. Figure 9 shows the
positive direction of change, i.e., functional performance
improved from pretreatment to posttreatment.
76
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Table 19
Analysis of Variance on Reported Changes in Functional Performance
Source df MS
Between Subjects 21
Increase vs. Decrease (B) 1 26. 27 1. 37
Error B 20 19. 12
Within Subjects 22
Changes for Combined Groups (A) 1 17. 82 9. 29**
A X B 1 • 82 < 1
Error W 20 1. 92
*p < .05.
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Table 20 presents the analysis of the number of diseased
joints recorded pre- and posttreatment. No significant
changes are evident.
A second and broader-based physical therapist's assess-
ment of each patient, pre- and posttreatment, indicates an
absence of discernable improvement. A t test for differences
between groups yields nonsignificant results (t [22] = 1.4).
78
Table 20
Analysis of Variance on Observed Changes in the Number of Impaired Joints
Source df MS F
Between Subjects 2 3
Increase vs. Decrease (B) 1 1416.36 3.12
Error B 22 453.43
Within Subjects 24
Changes for Combined Groups (A) 1 21.04 3.11
A X B 1 .04 < 1
Error W 22 6.75
Table 21 summarizes the data analysis generated from the
subjects' responding to the Profile of Moods State test admin-
istered pre-, mid-, and posttreatment. Of the six dimensions
assessed, significant changes are seen only in the area of
subjective tension.
Table 21
Analysis of Variance on Changes in Psychological Configuration as Measured by the Profile of Moods State Test
Source df MS F
Tension
Table 21—Continued
79
Source df MS F
Between Subjects 2 3
Increase vs. Decrease (B) 1 70. 17 1. 13
Error B 22 62. 30
Within Subjects 48
Changes for Combined Groups (A) 2 32. 07 6. 43**
A X B 2 57. 89 1. 16
Error W 44 49. 81
Depression
Between Subjects 2 3
Increase vs. Decrease (B) 1 20. 64 < 1
Error B 22 71. 26
Within Subjects 4 8
Changes for Combined Groups (A) 2 32. 90 < 1
A X B 2 117. 15 2. 54
Error W 44 46. 06
Anxiety
Between Subjects 23
Increase vs. Decrease (B) 1 69. 35 < 1
Error B 22 95. 86
Table 21—Continued
80
Source df MS F
Within Subjects 48
Changes for Combined Groups (A) 2 224. 45 3. 05
A X B 2 117. 95 1. 60
Error W 44 73, 54
Vitality
Between Subjects 23
Increase vs. Decrease (B) 1 231. 54 1. 12
Error B 22 205. 95
Within Subjects 48
Changes for Combined Groups (A) 2 1. 61 < 1
A X B 2 102. 39 1. 32
Error W 44 77. 40
Fatigue
Between Subjects 23
Increase vs. Decrease (B) 1 58. 33 < 1
Error B 22 204. 01
Within Subjects 48
Changes for Combined Groups (A) 2 239. 47 2. 33
81
Table 21—Continued
Source df MS F
A X B 2 223.80 2.17
Error W 44 102.86
C Scale
Between Subjects 23
Increase vs. Decrease (B) 1 1.26 < 1
Error B 22 58.43
Within Subjects 48
Changes for Combined Groups (A) 2 68.06 1.96
A X B 2 41. 78 1.21
Error W 44 34.64
*p < .05.
**p < .01.
Figure 10 graphically illustrates this linear decline for the
combined groups.
A second psychological measure involves the subjects'
self-reports of the percentage of time during which they feel
their mood is affected by their disease. Table 22 is a sum-
mary of the analysis of these data. A significant decline
in the affected-mood time is seen for the combined groups.
82
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83
Table 22
Analysis of Variance on Reported Changes in Degree of Disease-Related Mood Affect
Source df MS F
Between Subjects 17
Increase vs. Decrease (B) 1 2660.02 < 1
Error B 16 3025.71
Within Subjects 36
Changes for Combined Groups (A) 2 501.41 3.78*
A X B 2 5. 85 < 1
Error W 32 132.59
*p < .05.
**p < .01.
Figure 11 is a graphic illustration of the pattern. The
majority of the improvement appears to be between mid- and
posttreatment measures.
Discussion
The results of this research are interpreted as par-
tially answering the question of whether relaxation training
and biofeedback training of peripheral skin temperature can
positively influence the functional, physical, and psycholog-
ical aspects of rheumatoid arthritis. Contrary to the belief
that both the relaxation and skin temperature control response
would be learned and yield positive effects, only the
84
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85
relaxation response appears to be correlated with improvement
of the disease on certain of the considered dimensions.
Although statistically significant changes in skin
temperature are shown for both the increase and decrease
temperature groups, the changes are generally in the warmer
direction. Further, the majority of the change is associated
with relaxation training, and only statistically nonsignifi-
cant changes are recorded subsequent to the addition of the
biofeedback training. A suggestive trend is seen in the per-
formance of the decrease group in the last four training ses-
sions. The data for the period shows that rheumatoids may,
in fact, be able to consciously lower peripheral skin temper-
ature. Electromyographic data for the same period are inter-
preted as confirming that these subjects were concomitantly
relaxed, relative to baseline levels, and were in fact able
to further decrease muscular tension during the biofeedback
training. Admittedly, the performance of 12 subjects across
only four sessions is scant evidence, and the overall data
do support the general notion that an increase in peripheral
skin temperature typically occurs in a relaxed state. However,
from examining the data, it appears possible that with the
application of biofeedback training this peripheral skin
temperature pattern might be reversed for the rheumatoid pop-
ulation. The occurrence of this pattern is apparently neither
widespread nor dramatic enough to differentiate the two
treatment groups, as there are no reliable between-group
86
differences. Whether such a reversal would be desirable has
yet to be answered.
The learning of the relaxation response is confirmed by-
examining the electromyographic data collected at baseline
and subsequent to relaxation and biofeedback training. The
issue of whether the relaxation methodology is efficacious
is clear from the differences between baseline and post-
training relaxation measures.
The impact of the unsuccessful biofeedback training is
apparent since the biofeedback training is the only factor
differentiating the two treatment groups. With this factor
being essentially removed, between-group differences would
not be expected and, in fact, are not substantiated.
Although there are no differential shifts on measures
of discomfort and incapacitation, positive changes do occur
generally, and are encouraging. Apparently muscular relaxa-
tion is the only active treatment component and its applica-
tion may well have positive implications regarding the way
in which a rheumatoid experiences her disease. Reportedly,
the subjective level of pain, percentage of time spent hurt-
ing, and percentage of the body hurting all indicate reduc-
tion within and/or across treatment session with some relief
being perceived by the subjects. This relief is noteworthy
because of the consistent achievement without medication.
The absence of shifts, differential or otherwise, on
the two locus of control measures is believed to be partially
87
related to the subjects1 failure to learn the biofeedback
response. It is possible that some subjects may have per
ceived themselves as failing, a perception which may well
have undermined any increasing sense of mastery or internal
locus of control- It should also be noted that many of the
subjects had suffered for years and had been exposed to num-
erous treatments and "cures," so were consequently not easily
swayed in their perceptions or expectations. Some success
experienced in the relaxation training segment possibly
averted complete frustration or perceived helplessness, per-
haps offsetting any tendencies to move in the external
direction.
The failure to determine any reliable changes in disease-
related imagery is believed to be due to a lack of sophisti-
cation for both the subject and the experimenter. A review
of the Image A protocols and the patients1 drawings reveals a
rather impoverished ideational system specific to the disease.
Concomitantly, it is believed that the evaluation mechanisms
lacked in the control and specificity necessary for quantita-
tive analysis. Perhaps patient education would be helpful,
with an aim toward achieving a level of understanding con-
cerning both disease and treatmemt.
Of the six measures employed as physical criteria behav-
ior, four are measures of active, and two are indices of more
passive endeavors. Positive results are confined to the pas-
sive measures, with improvement seen in the increased number
88
of hours slept and decrease in the number of times a subject
awoke during the night. It appears that although some
changes in the life patterns occur, the subjects either are
not motivated to initiate more actively oriented changes or
they do not perceive themselves as improved enough to support
the endeavor. It is speculated that the subjects are not
motivated to attempt new patterns because increased activity
levels have historically antedated exacerbations of pain and
discomfort. Based on such history, this restraint may be
well advised.
The subjects' tendency to initiate new physical, work,
or leisure-related activities may be lacking, but they report
improved performance regarding day-to-day tasks on the func-
tional evaluation for rheumatoid arthritis. It should be
noted that the data patterns for pain and discomfort are
continually in the positive direction showing that increases
in activity do not necessarily lead to exacerbations. Many
of these tasks, however, are quite simple and the improvement
might be a function of the reductions in muscular tension
leading to greater flexibility of the joints. This flexibil-
ity would allow better performance without necessarily requir-
ing greater muscular output.
The physical therapists' general conclusion (that the
subjects did not significantly differ as a function of treat-
ment received) is considered valid. Such a finding does not,
however, undermine the general conclusion that the rheumatoids
89
felt better. Results indicate that while joint parameters
are unchanged, the experience of pain in those joints is,
and functional performance did improve. This finding leads
to the suggestion that relaxation therapy be considered as
an adjunct to medical or physical treatment, and not neces-
sarily be employed singularly.
Consistent with all other data, no differential shifts
emerge among psychological measures. Concomitant with decre-
ments in muscular tension, however, is the general decline in
psychological tension measured on the mood scale. This,
coupled with the decrease in time in which the subjects'
mood are disease-affected, adds to the list of indices sup-
porting the conclusion that gains are evident regarding the
patients' personal experience with rheumatoid arthritis.
While it may be that the progress reflected in the
reported data is associated with relaxation training, it is
possible that other factors contribute to the variance. It
is possible that expectancy sets or the demand characteris-
tics of the situation are causitive. Future research should
consider the inclusion of control and/or attention/control
groups.
Further consideration of biofeedback training is encour-
aged, as previous researchers have demonstrated that skin
temperature control (at least in the warming direction) is a
learnable response (Blanchard & Haynes, 19 75; Jacobson et al.,
1973). Further experimentation with the rheumatoid population
90
is necessary to determine if the manipulation, in fact, is
helpful. Biofeedback training of the electromyographic con-
trol response should also be considered as a possible facil-
itation to learning the relaxation response.
In conclusion, it seems that relaxation training should
be given serious consideration as an adjunct to other modes
of treatment for the rheumatoid arthritic. It should also
be noted that the relaxation training in the present study
is basically automated; the training could be negotiated
easily by technicians or other support personnel, or adapted
to and implemented in the patient's home.
91
Appendix A
Letter of Explanation
Title of Study: A Comparison of the Psychological Effects
of Two Adjunctive Treatments for the Rheu-
matoid Arthritic
Investigator's Name: Phillip C. McGraw, M. A.
Lay Statement of Insure Informed Consent:
You have been diagnosed as having Rheumatoid Arthritis.
Very often patients with this diagnosis have problems in
adjusting to the disease, the pain and stiffness, and the
medication. This can interfere with your outlook on life.
Sometimes, however, patients are able to live quite well with
their disability. Regardless of how arthritis has affected
you, we would like to ask your help in investigating these
emotional aspects and xn studying the effect of physical
therapy on adjusting the problem arthritics may encounter.
Physical therapy has been used for a long time with
arthritic patients, and includes such things as exercises,
heat or cold packs, paraffin baths, and instruction as to
improving your activities of daily living. There are no
obvious risks to your health, and many patients find it
helps them move and feel better.
You will be asked to participate in the study twice a
week for 45 minutes each time, for about six weeks. Your
progress will be checked by extensive testing by the physical
Appendix A—Continued 9 2
the psychologist and the physician and your records will be
kept confidential. You will be asked to come in for follow-
up examinations three, six, and nine months after your treat-
ment.
93
Appendix B
Consent Form
Your participation in this study will help us better
understand the emotional difficulties of having rheumatoid
arthritis and how it can change your life, as well as to
learn techniques which are most effective in dealing with
these problems. With this information we can then provide
more comprehensive treatment for other patients.
You are under no responsibility to continue in the treat-
ment study should you wish to withdraw your consent, nor
would failure to sign the consent form influence the care
you will receive in this hospital.
Any questions you have will be fully answered.
Consent;
Having read the information statement and had the oppor-
tunity to ask questions, I hereby willingly consent to be
tested.
Date Signed (Patient - if 18 or older)
Time Witness
94
Appendix C
Social History Interview Questionnaire
I.
II.
Name
Date of First Symptoms
Sudden Onset
Insidious Onset
Comments (ask patient details)
Age Date
Education
Religion
Occupation
III. Birth Order 1. first born 2. second born ~3. third born "4. fourth born
5. other middle siblings
6. last born (of how many )
IV. What makes you angry?
V. What do you do when you get angry (you may answer never, sometimes, always)?
Pre Now 25
1. withdraw, pout, get quiet
2. yell or curse
3. fight
4. throw things
5. work very hard at something to help get
over it
6. punish yourself, dislike yourself
7. cry
VI. Physical activities when young
Appendix C—Continued 95
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CD -p 0 0 -P CD -p rH rH •H £ w rH i—1 a 0 0 0 H 00 PM p-l
I. How many hours a day do you experi-ence pain?
1. I do not have pain
2. 1-8 hours per day
3. 9-16 hours per day
4. 17-2 3 hours per day
5. Constantly
II. How many hours sleep do you get each night?
III. How many times do you wake up?
IV. Check changes in work (including housework) activities since diagno-sis .
1. do more
2. no change
3. considerable change
4. drastic change, I cannot do what I did before
V. Changes in leisure activities
1. Some activities I engaged in more (Specify)
2. No change. I participate in the same activities as before.
3. Some activities (but not all) I engage in less frequently.
4. I have had to curtail or decrease all leisure activities
VI. Pain/discomfort scales (0-100)
1. pain severity
2. physical activity
3. percent of time pain felt
Appendix C—Continued 96
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4. effect on mood
5. percent of body hurting
97
Appendix D
Levinson Locus of Control Scale*
1. Whether or not I get to be a leader depends mostly on my ability.
Strongly disagree Disagree somewhat Slightly disagree Slightly agree Agree somewhat Strongly agree
To a great extent, my life is controlled by accidental happenings.
Strongly disagree Disagree somewhat Slightly disagree Slightly agree Agree somewhat Strongly agree
I feel like what happens in may life is mostly determined by powerful people.
Strongly disagree Disagree somewhat Slightly disagree Slightly agree Agree somewhat
~~~~ Strongly agree
4. Whether or not I get into a car accident depends mostly on how good a driver I am.
Strongly disagree Disagree somewhat Slightly disagree Slightly agree Agree somewhat
~~~~ Strongly agree
5. When I make plans, I am almost certain to make them work.
Strongly disagree Disagree somewhat Slightly disagree
*Revis ion of form used here to show sample of items and responses.
Appendix D--Continued
Slightly agree Agree somewhat Strongly agree
98
6. Often there is no chance of protecting my personal inter-est from bad luck happenings.
Strongly disagree Disagree somewhat Slightly disagree Slightly agree Agree somewhat Strongly agree
7. When I get what I want, it's usually because I'm lucky,
Strongly disagree Disagree somewhat Slightly disagree Slightly agree Agree somewhat Strongly agree
8. Although I might have good ability, I will not be given leadership responsibility without appealing to those in positions of power.
Strongly disagree Disagree somewhat Slightly disagree Slightly agree Agree somewhat Strongly agree
9. How many friends I have depends on how nice a person I
Strongly disagree Disagree somewhat Slightly disagree Slightly agree Agree somewhat Strongly agree
am.
10. My life is chiefly controlled by powerful others
Strongly disagree Disagree somewhat Slightly disagree Slightly agree Agree somewhat Strongly agree
99
Appendix E
cl Health Locus of Control
1. If I take care of myself, I can avoid illness.
2. Whenever I get sick it is because of something I've done
or not done.
3. Good health is largely a matter of good fortune.
4. No matter what I do, if I am going to get sick, I will
get sick.
5. Most people do not realize the extent to which their
illnesses are controlled by accidental happenings.
6. I can only do what my doctor tells me to do.
7. There are so many strange diseases around that you can
never know how or when you might pick one up.
8. When I feel ill, I know it is because I have not been
getting the proper exercise or eating right.
9. People who never get sick are just plain lucky.
10. People's ill health results from their own carelessness.
11. I am directly responsible for my health.
^Wallston, Wallston, Kaplan, & Maides, 1976
100
Appendix F
Profile of Moods State*
Name Date
Below is a list of words that describe feelings people have. Please read each one carefully. Then fill in one space under the answer to the right which best describes how you have been feeling during the past week including today.
1. Friendly
2. Tense
3. Angry
4. Worn out
5. Unhappy
6. Clear-headed
7. Lively
8. Confused
9. Sorry for things done
10. Shaky
11. Listless
12. Peeved
13. Considerate
14. Sad
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*Revision of form used here to show sample of items.
101
Appendix G
Image A Questions
1. If you had x-ray vision and could see your most diseased joint; what would it look like? (Elicit as complete a description as possible).
2. How strong is that joint? (How many lbs. can it lift, etc.).
3. What would the joint feel like if you could touch it? (hard, soft, rough, porous, smooth, etc.) (let patient supply several adjectives)
4. Describe what your white blood cells around your damaged joint look like.
5. Describe the movement of your white blood cells. How fast, etc.
6. Describe the fluid around your abnormal joints. What consistency? What does it do?
7. How do healthy vs. unhealthy joints look different? Act different? Feel different?
8. Describe your treatment? What does it do?
9. Do you think it works to cure arthritis? (How?)
10. Do you think it relieves pain? How?
11. Do you think it reduces swelling? How?
12. Describe any healing you think is taking place.
13. What do you think your chances (percentage) are of returning to health? (Ask patient to be extremely honest about this)
14. (Score on symbolism)
15. (Score on overall strength/weakness of ability to do image task)
16. (Score on clinical impression of disease process)
102
Appendix H
Physical Therapy Evaluation (Sample Items)
Name
Age
Date
Sex Occupation
Diagnosis
Any Pain
How Long
Is is Constant
When is it Worse
Rate Pain on a Scale of 1 to 10
1 = minor, offasional, hardly noticeable pain 10 = major, constant, debilitating pain
501 walking time
SHOULDER Flexion (160) L RC )M R L STRE INGTH
K, Extension (40) Abduction (160) Abduction Internal rotation (90) External rotation (90)
ELBOW Flexion (140) Extension
FOREARM Pronation (90) Supination (90)
WRIST Flexion (60) Extension (65) Ulnar deviation (45) Radial deviation (25)
ANKLES Dorsiflexion Plantarflexion Inversion Eversion
103
Appendix I
Functional Evaluation for Rheumatoid Arthritis (Sample Items)
Name Date
Dominant Hand
Score Activities on Scale of 1 to 3
1 = Always can 2 = Sometimes can 3 = Never can
ACTIVITIES SCORE: COMMENTS
PERSONAL HYGIENE 1. Wash hands, face 2. Brush teeth 3. Shave or make up DRESSING 1. Take clothes from closet 2. Put on, remove button blouse
socks or hose slacks or shorts
3. Wind watch EATING 1. Pass food at table 2. Use salt shaker 3. Cut with knife HOUSEHOLD 1. Pick up object from table 2. Wash, dry dishes (heavy pans) 3. Empty trash 4. Dust, wax furniture 5. Hang up wash 6. Carry grocery bag LOCOMOTION 1. Ambulate unassisted 2. Ambulate with crutches, cane 3. Propell wheelchair COMMUNICATION 1. Write name 2. Use eraser 3. Dial phone APPARATUS 1. Put on, remove adaptive apparatus
Appendix I—Continued 104
Limits Activity
Concomitant Diseases: None Some Greatly
1)
2 )
3)
Onset of disease Duration of disease_
Patient's subjective assessment of disease:
crippled somewhat disabled
almost crippled few problems
disabled no problems
Nonsteroidal antiinflammatory
agents
Gold
Penicillamine
Steroids
Cytoxan/Immuran
Other - Past Psychoactive Drugs: Ever 3 Mo. Present
Benzodiazepams
Tricyclic antidepressants
Barbiturates
Phenothiazines
Steroids
Other -
Patient's present meds.:
1)
2)
3 )
4 )
5)
105
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