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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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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

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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

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11.14

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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

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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.

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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.

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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

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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

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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

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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.

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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.

**p < .01.

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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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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