Physical Activity as an Intervention for Pain

Based on Gate Control Theory

By Martha E. McDonald

Submitted in partial fulfillment of the requirements for the Doctor of Nursing Science Degree in the School of Nursing Indiana University August, 1987

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. The dissertation entitled, "Physical Activity as an

Intervention for Pain Based on Gate Control Theory" by

Martha E. McDonald is accepted by the faculty of the School

of Nursing, Indiana University, in partial fulfillment of

the requirements for the Doctor of Nursing Science degree.

Dissertation Committee:

Chairperson

Juanita Keck, D.N.S., R.N

Ralph Templeton, Ph.D.

June 25, 1987

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Physical Activity as an Intervention for Pain

Based on Gate Control Theory

Martha E. McDonald, D.N.S. Indiana University, 1987

The purpose of this study was to investigate the

effect of physical activity on pain tolerance and pain

perception. The expectation that physical activity would

reduce the perception of pain was deduced from clinical

observation and propositions of the Gate Control Theory. The

specific proposition tested was that large primary afferent

fiber stimulation would inhibit pain perception. Following

this proposition, stimulation of innocuous fibers by muscle

movement should mediate pain perception. The hypothesis

tested was that there would be no difference in time to

tolerance or descriptors of pain perception among subjects

when they experienced noxious stimulation with no

intervention and when they experienced noxious stimulation

with muscle movement, which stimulated appropriate large

primary afferent fibers.

Subjects were thirty registered nurses and nursing

students. Pain was produced by a pressure finger clip

device. Pain tolerance was measured as the amount of time

from onset of pressure until subjects indicated they could

not tolerate the discomfort any longer. Pain perception was

measured by three scales: (1) the McGill Pain Questionnaire

verbal descriptors, (2) the McGill Pain Questionnaire pain

rating index, and (3) a visual analog scale.

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Cognitive-emotive factors affect pain perception by

altering sensory interpretation and by descending influences

to the spinal cord. Two cognitive-emotive factors that have

been implicated in alterations of pain perception are anxiety

and locus of control. The State-Trait Anxiety Inventory and

Nichols' pain specific locus of control tool were employed to

measure anxiety and locus of control.

The data were analyzed by a 2x2 ANOVA with repeated

measures on the second factor. The null hypothesis was

rejected with all pain measures. When subjects experienced

the intervention they were able to tolerate the pain longer,

selected fewer and less severe pain descriptors, selected

lower pain rating indicators, and indicated less pain on the

visual analog scale than when subjects did not experience the

intervention (control). Anxiety and locus of control

variables were not found to be significant intervening

variables.

The study contributes to theory building by support of

the Gate Control Theory proposition of pain inhibition by

large primary afferent fiber stimulation. The selection of

muscle movement as an effective inhibition technique has been

supported. The study results indicate further investigation

of physical activity as a pain intervention is warranted.

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Approved and accepted by ~€hairperson

of Committee.

Ralph Templeton, Ph.D.

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Acknowledgments

I wish to thank the members of my committee, who became

both mentors and friends; Dr. Carol Deets for her enthusiasm

and encouragement, Dr. Juanita Keck for her gentle, but firm

direction, and Dr. Ralph Templeton, who helped me begin the

long process. I would like to thank the other faculty and

staff of Indiana University for their help, support, and

acceptance.

I would like to thank Dr. Nadine Coudret, University of

Evansville, without whom I would never have attempted

doctoral studies. She instilled faith in my ability to reach

my goals.

I would like to acknowledge the contributions of my

friends at Herrin Hospital, especially Mrs. Shirley Ketter,

Director of Nurses, who provided a flexible environment that

supported my educational pursuits.

My thanks to my fellow doctoral students, companions in

the search for understanding. Their extra efforts to aid my

long distance studies were appreciated. A thank you to my

family members for their help and support. The littlest one

hopes you are all proud.

My special thanks to my good friends Jean and Brandi

Carter who reminded me to stop and smell the roses along the

way.

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. TABLE OF CONTENTS

CHAPTER I - INTRODUCTION...... 1

Purpose...... 3

Theoretical Basis of the Study...... 3

Specificity Theory...... 3

Pattern Theory...... 4

Gate Control Theory...... 5

Hypothesis...... 9

Conceptual Definitions...... 9

Operational Definitions...... 11

Assumptions...... 11

Limitations...... 11

Significance of the Study...... 12

CHAPTER II - REVIEW OF LITERATURE......

Neuroanatomy of Nociception as it Applies

to the Gate Control Theory......

Primary Afferent Fiber Activity...... J ^

Dorsal Horn Cytoarchitecture......

Proposed Physiological Interactions

in the Dorsal Horn...... p-i Rostrad Transmission of Nociceptive Input...... r

Supraspinal Interactions...... 23

Rostral-Caudal Transmission...... 28

Descending Supraspinal Influences...... 28

Pharmacological Considerations...... 30

i

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Inhibition by Muscle Nerve Stimulation...... 35

Previous Applications of the Gate Control Theory...... 36

Historical Background...... 36

Large Primary Afferent Fiber Stimulation...... 37

Previous Applications of Physical Activity

as a Pain Intervention...... ^

Emotional-Cognitive Influences...... ^3

Anxiety...... ^

Locus of Control...... ^

Anxiety and Locus of Control in Interaction...... ^

Summary...... 30

CHAPTER III - METHODOLOGY...... 53

Subjects...... 33

Human Rights, 5lf o, Design...... /lt

Instruments...... ^

Experimental Pain Producing Technique ...... 36

Large Primary Afferent Fiber Stimulus...... 37

Dependent Variables...... 38

Time to Tolerance...... 38

McGill Verbal Descriptors...... 59

McGill Pain Rating Index...... 60

Visual Analog Scale...... 60

Intervening Variables...... 61

Measurement of State Anxiety...... 61

Measurement of Locus of Control...... 62

ii

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Procedures...... 63

Sample Selection...... 63

Data Collection...... 64

Data Analysis...... 66

CHAPTER IV - FINDINGS AND DISCUSSION...... 68

FINDINGS...... 68

Measure of Pain...... 68

Intervening Variables...... 69

Age...... 69

Anxiety...... 69

Locus of Control...... 70

Order of Presentation...... 71

Hypothesis Testing...... 71

Time to Tolerance.. *...... 7^

McGill Verbal Descriptors...... 73

Pain Rating Index...... 73

Visual Analog Scale...... 73

Pearson Correlation of Pain Measures ...... 76

Summary...... -78

DISCUSSION...... 79

Pain Measures...... 79

Intervening Variables...... 81

Summary...... 83

CHAPTER V - SUMMARY, CONCLUSIONS, AND RECOMMENDATIONS...... 84

Summary...... 84

iii

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Conclusions...... 89

Recommendations...... 90

REFERENCES...... 93

APPENDICES...... 113

Appendix A: Participation Announcement...... 113

Appendix B: Consent Form...... 115

Appendix C: Nichols' Locus of Control Tool...... 117

Appendix D: Revised McGill Pain Questionnaire

Pain Rating Index

Visual Analog Scale...... 119

iv

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. LIST OF TABLES

Table 1: Summary of Results for ANOVA with Repeated

Measures on Second Factor for the Pain

Variables...... 7tf

Table 2: Cell Means and Standard Deviations for ANOVAs 75

Table 3: Pearson Correlation for Measures of Pain...... 77

V

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER I

Introduction

The most frequent reason people seek health

professionals' services is for treatment of pain (Kim, 1980)

Over one-third of the U.S. population has acute intermittent

or chronic pain necessitating treatment. Fifty million of

these patients are disabled at some point in their life by

their pain alone. The cost of these disablements is in

excess of 10% of the national budget (Bonica, 1980).

Although great strides have been made in the treatment of

pain, pharmacological and surgical treatments often fail to

satisfactorily relieve pain.

Non-pharmacological interventions have a long history

in nursing. Comfort measures have been utilized throughout

nursing history to substitute for unavailable or to augment

available medications. The role of non-pharmacological

interventions still has much support. The movements toward

more holistic and natural ways of living direct patients to

seek pain relief from sources other than medication. In the

past, non-pharmacological measures have not been utilized if

medication for pain has been ordered, even if the medication

did not give relief or the patient refused the medication

(Graffara, 1981). But the use of medication does not exclud

augmentation by non-pharmacological interventions (Melzack &

Tanzer, 1977). In one study, the Conduct and Utilization of

with permission of the copyright owner. Further reproduction prohibited without permission. 2

Research in Nursing Project (CURN), in the control group

receiving medication only, no one selected ’’marked relief"

the highest category. In the experimental group where

therapeutic communication and comfort measures were utilized,

89% selected "marked relief" (Horseley, Crane, & Reynolds,

1977). Patient Care Standards (Tucker et al., 1984)

contains a range of non-pharmacological nursing

interventions. These begin with a full nursing assessment

and development of a care plan utilizing the patient as an

expert in his own care. Procedures such as positioning,

massage, distraction, imagery, and therapeutic communication

are listed in this and other nursing sources (Abranovich,

1981; Copple,1972; DeCrosta, 1984; Dolon, 1982; Jacob, 1976;

McCaffery, 1979; McCaffery, 1980b; Roy & Tunks, 1980).

Non-pharmacological pain interventions can also serve when

the expected pain is of short duration or of low intensity,

such as needle punctures or catheter insertions. These

interventions may also be utilized during the period of time

from administration to onset of relief from medications for

pain or during lapses in coverage between administrations

(McCaffery, 1980b). Another use is the augmentation of

relief by use of these interventions as well as medication

(Melzack, 1982).

There is a need for theory based research into nursing

interventions for pain. Nurses have been relying on

medication, historical comfort measures, and trial and error

due to the dearth of pain relief research in nursing.

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Studies that add to the knowledge base may provide more

direction to clinical pain management. Of current interest

to nurses is the variety of applications of the Gate Control

Theory (Kim, 1980; Meinhart & McCaffery, 1983).

Purpose

The purpose of this study was to investigate the effect

of physical activity on pain tolerance and perception. The

treatment, physical activity, was deduced from clinical

observations and propositions of the Gate Control Theory

(Melzack & Wall, 1965; Wall, 1978).

Theoretical Basis of the Study

This section includes a discussion of the major theories

of pain perception; specificity, pattern, and The Gate

Control Theory. The rationale for selecting the Gate Control

Theory as the basis for this study is presented.

Specificity Theory. Specificity theory began with

Muller and Volkmann who published descriptions of free nerve

endings and specific transmission to the central nervous

system in 1844 (Nathan, 1976; Procacci, 1980). This theory

proposes that free nerve endings are specific pain receptors

and transmit pain information directly to an area within the

thalamus via A-delta and C fibers and the spinothalamic tract

(Melzack & Wall, 1965; Procacci, 1980). Support for the

specificity theory evolved from the following observations;

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excitation times for pain and touch differ, pain sensation

appears earlier in development than other sensations,

surgical lesions for pain do not necessarily affect touch,

some analgesic drugs affect pain and not other sensations,

dermatomes for pain and other sensations are not identical,

and pressure receptors have been identified that do not

produce pain even when stimulated to maximum levels (Bishop,

1980; Meinhart & McCaffery, 1983; Procacci,1980).

Criticisms of the specificity theory are based on

observations of psychological aspects of pain modulation and

the presentation of neuralgias and causalgias. Beecher

(1946) noted that men wounded in battle often reported little

or no pain from their wounds. Beecher attributed this lack

of sensation to relief of the burden of further fighting.

Pavlov's dogs after repeated painful stimulation associated

with food, no longer responded to the stimulus with

indications of pain (Melzack & Wall, 1965). The

neuropathologies of neuralgias and causalgias refute

specificity theory by demonstrations of pain unrelated to

specific receptors and tract. Specificity theory does not

explain phantom limb pain, causalgias and neuralgias

triggered by gentle touch, unrelated "trigger zones" for

pain, and neuralgic pain lasting long after gentle stimuli

(Melzack & Wall, 1965; Procacci, 1980).

Pattern Theory. In the 1950's Weddell and Sinclair

proposed a new theory of pain transmission, the pattern

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theory. They noted that multiple sensations came from free

nerve endings, and they proposed that spatiotemporal patterns

of transmission from one type of ending signified various

sensations. These patterns of impulses were transmitted to

the thalamus and identified as pain, touch, or other

sensations. (Nathan, 1976; Melzack & Wall, 1965; Meinhart &

McCaffery, 1983, Procacci, 1980).

The pattern theory has been refuted by identification of

various types of receptive units. High threshold

mechanoreceptors, low threshold mechanoreceptors, and

polymodal receptors identified by Perl (1984), and Torbejork

and Hallin (1974) refute the premise of one universal

receptor.

Gate Control Theory. In 1965 Melzack and Wall proposed

the Gate Control Theory of pain. Drawing from previous works

by Barron and Mathews (1938), Melzack and Wall stated a

theory of modulation of sensory transmission within the the

spinal cord. Propositions of this theory are:

1. Injury results in stimulation of small primary

afferent fibers.

2. Transmission of peripheral information is

facilitated or inhibited within the spinal cord

by a gating mechanism.

3. Large fiber input inhibits transmission of

nociception and small fiber input facilitates

tranmission.

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4. Cognitive-emotive processes influence the

modulation within the dorsal horn (Melzack,

1973; Wall, 1978).

Melzack and Wall symbolized this facilitation and

inhibition by describing a gate-like mechanism that opened or

closed to allow transmission of peripheral input (Melzack,

1973; Melzack & Wall, 1965; Wall, 1978). Noxious stimuli

produce stimulation of A-delta (small myelinated) and C

(small unmyelinated) fibers. Innocuous information is

carried by A-B (large myelinated) fibers (Guyton, 1986;

Torebjork, & Hallin, 1973; Wall, 1978).

By the Gate Control Theory, a continuous flow of input

from large and small fibers enters the dorsal horn. The

input is predominantly from small fibers, thus keeping the

gate in a slightly open position (Melzack & Wall, 1965).

This continuous flow was demonstrated by Barron and Mathews

(1938) and Wall (1962). Innocuous stimulation increases

large and small fiber input and a slow increase in

facilitation results. Noxious increases in input result in

large fiber suppression and an acute increase in small fiber

facilitation (Melzack & Wall, 1965; Wall 1978). Stimulation

of large primary afferent fibers will result in inhibition of

transmission to the spinothalamic tract. This inhibition by

large fibers has been demonstrated (Barron & Mathews, 1938;

Iggo, 1980; Kerr, 1976; Wall, 1958).

Melzack and Wall (1965) proposed the site for modulation

to be the substantia gelatinosa of the dorsal horn. The

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interneuron interactions the substantia gelatinosa with

Lamina I, C-fiber afferents, and lamina V dendrites supports

the substantia gelatinosa as a probable site. A-delta

fibers enter the dorsal horn at Lamina I (Basbaura, 1980;

Kumazawa & Perl, 1978; Laraotte, 1979). C— fibers terminate in

the substantia gelatinosa (Basbaum, 1980; Kumazawa & Perl,

1978; Perl, 1984). Large primary afferent fibers terminate

in the substantia gelatinosa (Basbaum, 1980; Bishop, 1980;

Lamotte, 1979). The wide dynamic range neurons of the

nucleus proprius have dendritic terminals in the substantia

gelatinosa (Basbaum, 1980; Kerr, 1976; Szengathai, 1964) and

axons connecting to the spinothalamic tract (Bishop, 1980;

Kerr, 1976). Demonstrations of decreased noxious stimulus

transmission from the dorsal horn to the spinothalamic tract

after large primary afferent fiber stimulation reinforces the

presumption of substantia gelatinosa modulation (Barron &

Mathews, 1938; Iggo, 1980; Kerr, 1976; Melzack & Wall, 1965;

Wall, 1958, 1984).

The proposed transmission sites are the neurons of the

nucleus proprius. Input from the periphery, modulated by the

substantia gelatinosa interneurons, is then be transmitted to

the spinothalamic tract via Lamina V neurons (Melzack, 1973;

Melzack & Wall, 1965; Wall, 1984). Axonal connections of

Lamina V neurons to supraspinal areas have been demonstrated

by Yaksh and Hammond (1981) and Willis (1976).

Melzack and Wall also proposed descending cerebral

modulation, activated by attention, anxiety, awareness, and

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. past experiences. Areas in the cortex, reticular formation,

and limbic system controlling emotional and cognitive

responses could facilitate or inhibit dorsal horn

transmission through neurotransmitter substances(Melzack,

1973; Melzack & Wall, 1965; Wall, 1984). Fiber tracts for

descending transmission from the cortex, reticular formation,

nucleus raphe magnus, and locus coeruleus have been

established by Basbaum and Fields (1982), Fields (1984), and

Zimmerman (1976). Inhibition of noxious responses by

stimulation of the cortex (Coulter, Foreman, Beall, & Willis,

1984; Lineberry & Vierck, 1975; Willis, 1984), reticular

formation (Besson, 1980; Fields, 1984; Willis, 1984), nucleus

raphe magnus (Fields, 1984; Mayer and Liebeskind, 1974;

Willis, 1984), and locus coeruleus (Commissiong, Hellstrom, &

Neff, 1978; Hodge, Apkarian, Stevens, Vogelsang, & Wisnicki,

1981) support the proposal of descending control. Two areas

of emotional and cognitive function that have been

demonstrated to impact pain perception are anxiety (Bronzo &

Powers, 1967; Graffenfried, Afdler, Abt, Neusch, & Spiegel

(1978) and locus of control (Kanfer & Seidner, 1973).

From the propositions of the Gate Control Theory, two

experimental proposals are drawn: 1. That stimulation of

large primary afferent fibers decreases the transmission of

noxious information to supraspinal areas; and 2. that

emotional and cognitive responses modulate dorsal horn

activity through descending controls. This study tested the

first mechanism, large primary afferent fiber inhibition, by

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activation of AB muscle and tendon fibers during noxious

stimulation. The second mechanism of modulation was

considered as an intervening variable. Two

cognitive-emotional factors were measured and evaluated,

anxiety and locus of control.

Hypothesis

If stimulation of large primary afferent fibers by muscle

movement resulted in inhibition of C fiber activity, subjects

utilizing muscle movement during noxious stimulation should

experience increased time to tolerance of the stimulus and

alteration of the perception of the stimulus. The null

hypothesis then is: There will be no difference in time to

tolerance or descriptors of pain perception between a group

experiencing noxious stimulation with no intervention, and a

group experiencing noxious stimulation with muscle movement.

Conceptual Definitions

Pain. Central to this study is the definition of pain.

As with all abstract concepts pain is difficult to define.

It has an individual quality that is learned through

association with noxious stimuli. Although general

categories of stimuli can be proposed that are considered

painful by most people, no one stimulus has the same meaning

for everyone. For the purpose of this study the following

conceptual definition will be considered adequate, but not

perfect. Pain is (1) a personal private sensation of hurt,

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(2) a harmful stimulus which signals current or impending

tissue damage, and (3) a pattern of responses which operate

to protect the organism from harm (Sternbach, 1978).

Nociception is the perception of stimulation of fibers within

the nervous system that produces responses consistent with

pain (Zimmerman,1976). This is generally thought to be

interchangeable with pain.

Anxiety. Anxiety is one of the body’s responses to

stress. It is an emotional response marked by physiological

and psychological symptoms. Anxiety is an unpleasant

emotional state associated with worry,apprehension, and

tension (Kaplan & Saccuzzo, 1982). Spielberger divided

anxiety into two categories, state and trait. State anxiety

is anxiety that varies by situation. Trait anxiety is a

stable personality characteristic (Spielberger and Sarason,

1975).

Locus of control. Rotter postulated a theory of

individual perception of control. Locus of control is the

perception by an individual that change is a consequence of

personal actions, and thereby controllable (internal

control), or that change is not a result of their own

behavior and therefore beyond personal control (external

control) (Rotter, 1982).

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Operational definitions

Pain; unpleasant sensation produced by pressure measured

by time to tolerance in minutes,verbal descriptors of the

McGill tool, and a visual analog scale.

State anxiety; emotional reaction to stress as measured

by the state anxiety tool.

Locus of control: perception of control of situation

during which pain is experienced, as measured by Nichols'

adaptation of Rotter's tool.

Time to tolerance: the interval from beginning of the

stimulus to the point at which the subject requested the

stimulus stop.

Assumptions

There are some basic assumptions necessary to this

experiment. They are that the subjects will honestly report

their perceptions, that the subjects comprehend the language

of the questionnaires, and that other personal factors are

not intervening in the experiment.

Limitations

(1) Due to cognitive influences experimental

pain may differ from pathological pain.

(2) Use of a convenience homogeneous sample limits

generalizability.

(3) The sample may be biased as it precludes

inclusion of subjects who feel they do not wish

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to experience pain.

Significance of the Study

There is a need in nursing for non-pharmacological pain

interventions. The illusion of pain relief from

pharmacological measures fosters the narcotic key reflex

(Pepin & Howe, 1965). In reality pain relief from narcotic

medication is not assured. In cases where narcotics are

indicated, individual responses are often not considered.

Prescribed doses are often ordered by routine, rather than by

the patient's report of relief. The result of this routine

is frequent orders for sub-therapeutic dosages. These doses

may then be reduced by the nursing staff at their discretion,

even when ordered at specific dosages and time intervals.

These phenomena are believed to be the result of the nurses'

fear of patient addiction (Allerton & Exley, 1982; Davis,

1980; DeCrosta, 1984; Eland, 1978; Horsely et al, 1977;

McCaffery & Hart, 1976; Pepin and Howe, 1965). Results of

two studies indicated that 42 of 106 surgical and 27 of 37

medical patients reported minimal pain relief from narcotics

(McCaffery & Hart, 1976). In the Conduct and Utilization of

Research in Nursing Project (CURN) study of 37 medical

patients, in pain and receiving narcotics, 37% continued to

experience severe distress and another 41% continued to

suffer moderate distress (Horsely et al, 1977). In addition,

pharmacological interventions are not without unpleasant side

effects. These effects range from pain at injection sites

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to blood disorders and must be considered as treatment risks.

In the application of most treatment modalities, only

the patient is held accountable for the efficacy of

treatment. No individual professional is responsible for

pain relief. If a treatment is not satisfactory to a

patient, the patient is blamed for the lack of response. The

patient is then considered to be ultra-sensitive to pain or

seeking narcotics for other reasons (Fagerhaugh & Strass,

1980; Meinhart & McCaffery, 1983). Patients should receive

education about the variety of pain measures available to

them as part of the patient education process. The patient

could then be an active participant in the pain relief

program. Selection of pain relief measures from the

orientation of what is effective and acceptable to the

patient would result in greater efficacy of treatment. Fear

of inadequate pain control increases the anxiety level of the

patient and functions as an inhibitory factor in pain

treatment (Fagerhaugh and Strauss, 1980; Isler, 1975;

McCauley & Polomano, 1980).

No interv ention will su cceed for all patients in pain.

A wide range of interacting therapies should be ava ilable for

each pa tient. Non-pharmacol ogical ini:erventions ar e

low-cos t, easi ly instituted, and can 1De controlled by the

patient. If this study is successful, the intervention of

physical activity would have the potential for utilization in

practice settings as a non-nharmacologica lain intervention,

subject to support through replication or similar studies.

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CHAPTER II

Review of Literature

A review was undertaken to identify support for the

application of physical activity as an intervention for pain

based on the Gate Control Theory. Support emanates from

literature regarding neurophysiology of nociception as it

applies to the Gate Control Theory, previous applications of

the gate control theory, and previous applications of

physical activity as an intervention for pain. Of interest

also, are possible interacting variables from

cognitive-emotive influences. The influences of anxiety and

locus of control on the effect of the perception of pain were

reviewed.

The Neuroanatomy of Nociception as it Applies to the Gate

Control Theory.

Neuroanatomical support of the gate control theory can

be divided into nine sections:

1. Primary afferent fiber activity.

2. Dorsal horn cytoarchitecture.

3. Proposed physiological interactions in the dorsal

horn.

4. Rostrad transmission of nociceptive input.

5. Supraspinal interactions.

6 . Rostral-caudal transmission.

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7. Descending supraspinal influences.

8. Pharmacological Considerations.

9. Inhibition by muscle nerve stimulation.

Primary afferent fiber activity. The Gate Control

Theory proposes fiber specific input to the spinal cord.

Primary afferent fiber input includes receptor stimulation by

noxious and innocuous stimuli, and the transmission of

information to the spinal cord.

Nociceptors within the skin and tissue have been shewn

to respond to differing stimuli. Perl (1984, and Torebjork

and Hallin (1974) described neuroreceptors found in human

skin. Low threshold mechanoreceptors are activated by

innocuous, low intensity stimuli (touch). High threshold

mechanoreceptors respond to more intense stimulation with

mechanical displacement (pinch). Other receptors are

activated by chemical, thermal, and mechanical stimuli. The

latter receptors are termed polymodal to describe their range

of function. Wall (1978) agreed that receptors had

specification, but stated high stimulation of any receptor

could result in pain.

Primary af f erent fibers as sociate d with these receptors

are classified by size and myel ination • Myelinated fibers

are classified as Aa (12-20 mic rons), AB (7-14 microns), Ay

(3--8 microns), and A delta (2-5 micron s) C fibers are small

(0.,5-2.0 micro ns) unmy elinated fibers. Speed of transmission

of impulses al ong the fibers is a fact or of size and

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myelination. Larger myelinated fibers transmit impulses

faster than small unmyelinated ones (Collins, Nulsen,

Randt,1960; Guyton, 1986). Low threshold mechanoreceptors

have been shown to be innervated by AB fibers, high threshold

by A delta and polymodal by C fibers (Perl, 1974; Torebjork &

Hallin, 1974; Von Hees & Gybels, 1981). Muscle and tendon

proprioreceptors are innervated by A alpha and A beta fibers

(Guyton, 1986).

Peripheral fibers have been shown to have specific

responses to innocuous and noxious stimuli. Collins et al.,

(1960) stimulated various nerve fibers in human subjects.

Electrical stimulation of AB fibers elicited a touch or

flutter sensation; Ay, a stronger and painful sensation; A

delta, stinging sensation; A delta and C combined,

unbearable pain. Torebjork and Hallin (1973) utilized

preferential blocking to determine responses from human skin

receptors. With noxious stimulation, blocking of C fibers

resulted in weak pain and blocking of A fibers resulted in a

burning sensation.

The Gate Control Theory proposes noxious information is

transmitted via small primary afferent fibers and innocuous

information via large primary afferent fibers. From the

descriptions of sensation produced by specific fibers,

support is shown for transmission of nociception by A delta

and C fibers, and innocuous transmission by larger fibers.

Muscle proprioceptive receptors transmit information to the

dorsal horn by large fibers (Guyton, 1986). Thus, noxious

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mechanical distortion produces small primary afferent fiber

input and muscle movement large fiber input. Impulses from

the peripheral receptors are transmitted along the fibers to

the dorsal horn of the spinal cord via the dorsal root

ganglion.

Dorsal horn cytoarchitecture. The dorsal horn is

divided into layers or laminae by natural divisions of neuron

cytology. Laminae are lateral divisions across the body of

the dorsal horn. The divisions are represented by Roman

numerals from the outermost progressing inward (Bishop, 1980;

Basbaum, 1980; Kerr, 1975. 1976).

Primary afferent fibers from the periphery pass through

dorsal root ganglion and enter the dorsal horn by way of the

tract of Lissauer. Approximately 25% of the fibers in the

tract are primary afferent fibers. The remainder of fibers

in the tract are intrinsic fibers from the dorsal horn.

Afferent fibers branch and enter the dorsal horn at varying

ascending or descending levels. Within the tract, small

fibers align along the lateral border, while large primary

afferent fibers are found in a more medial location (Basbaum,

1980; Kerr, 1976).

The dorsal horn has been divided into sections by the

cytology and appearance of the sections or laminae. The

outermost segment of the dorsal horn has been designated

lamina I or the marginal layer. Primary afferent fibers with

terminals in lamina I are A delta (Basbaum, 1980; Kumazawa

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and Perl, 1978; Lamotte, 1979)

Small primary A delta fibers synapse with interneurons

within lamina I. These interneurons form synapses with the

substantia gelatinosa or rostrad transmission tracts. Gobel

(1978a) described four types of neurons within lamina I, two

types of pyramidal neurons and two types of multipolar

neurons. Gobel did not find dendritic arborizations outside

of lamina I or tract of Lissauer. The dendrites and somas of

these neurons possess multiple terminal boutons with dense

core vesicles (Gobel, 1978a; Kerr, 1976; Szentagathai, 1964).

Kerr (1975,1976) described the penetration of laminae II and

III by dendrites of lamina I neurons, but Gobel described

these fibers as penetrations by stalk cell axons of lamina II

(Gobel, 1978b). Either position describes interconnections

of lamina I and the substantia gelatinosa (Basbaum, 1980),

Axons from lamina I neurons project to the dorsolateral

fasciculus proprius and anterior commissure (Kerr, 1976).

Laminae II and III have been designated the substantia

gelatinosa or translucent layer. Gobel (1978b) described

four types of substantia gelatinosa neurons; stalk, arboreal,

border, and islet cells. Stalk cells with short projecting

branches were found in the outer section of lamina II. There

axons project into lamina I. Islet, arboreal, and border

cells were found to have extensive dendritic arborizations in

laminae II and III. The axons connect mostly with laminae II

and III with some input to lamina I. C fibers enter by the

tract of Lissauer and have terminals in the substantia

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gelatinosa (Basbaum, 1980; Kumazawa & Perl, 1978; Perl,

1984). Large primary afferent fibers course along the

lateral tract of the dorsal horn and re-enter at laminae IV

and V. Their terminals, however, are in the substantia

gelatinosa (Basbaum, 1980; Bishop, 1980; Lamotte, 1979).

Laminae IV, V, and VI, or nucleus proprius, contain

large neurons and numerous myelinated fibers. Dendrites from

the neurons extend into the substantia gelatinosa. These

neurons are described as wide dynamic range neurons due to

their response to a large variety of stimuli. Projection

axons connect the nucleus proprius to the spinothalamic tract

and dorsolateral fasiculus proprius (Bishop, 1980; Kerr,

1976). Within the substantia geilatinosa, the interneuron

dendritic endings of stalk cells are arranged in lobules with

interspaced dendrites from nucleus proprius neurons

(Basbaum,1980; Kerr, 1979; Szengathai, 1964).

Proposed physiological interactions in the dorsal horn.

The Gate Control Theory proposes a modulating mechanism

within the substantia gelatinosa of the spinal cord. Input

from the peripheral fibers is integrated and modulated before

transmission to supraspinal areas. Integration and

modulation is dependent upon the ability of neurons within

substantia gelatinosa to affect transmission. The substantia

gelatinosa neurons synapse with the T (transmission) cells of

the nucleus proprius to transmit to supraspinal areas.

A delta fibers from the tract of Lissauer enter the

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dorsal horn and transmit information to the marginal neurons.

C fibers transmit to the neurons of the substantia gelatinosa

(Basbaum, 1980; Kumazawa et al, 1978). Stalk cells within

the substantia gelatinosa act as excitatory interneurons that

receive information from other neurons in laminae II and III

and relay to laminae I and V. Islet, arboreal, and border

cells are inhibitory interneurons upon laminae I and V

dendrites. Laminae I and V then transmit impulses to the

spinothalamic tract (Gobel, 1978b; Kerr, 1976).

Large primary afferent fibers that carry innocuous

information have terminals in the substantia gelatinosa which

activate dendrites of neurons of the nucleus proprius which

transmit the information to the ascending spinothalamic tract

(Bishop, 1980; Kerr, 1975, 1976). Inhibition of dorsal horn

cells by stimulation of large primary afferent fibers has

been noted (Kerr, 1976, Iggo,1980; Wall, 1984). Morris

(1987) demonstrated inhibition of laminae V-VII nociceptive

neurons by stimulation of muscle nerve fibers.

The complexity and structural connections indicate that

rather than a simple relay system, the dorsal horn performs

integrative and modulating functions in nociception. Small

primary afferent fibers transmit information to marginal and

substantia gelatinosa neurons (Wall, 1984). Large primary

afferent fibers relay innocuous information to the

spinothalamic tract. These large fibers also activate the

substantia gelatinosa neurons that are believed to inhibit

discharge from lamina V neurons (Kerr, 1976). Both pre and

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post synaptic influences may work to inhibit transmission of

impulses(Melzack, 1973; Wall, 1984).

The substantia gelatinosa is considered to be the

modulating area of the Gate Control Theory. The location and

interactions of interneurons of the substantia gelatinosa

with lamina I and nucleus proprius neurons support

designation of the substantia gelatinosa as the modulation

site. The nucleus proprius projection cells act as T

(transmission) cells for relay to supraspinal areas (Melzack,

1973).

Rostrad Transmission of Nociceptive Input. Responses to

pain, other than simple withdrawal reflexes, depend upon

transmission to supraspinal sites for interpretation and

response formation. Three major pathways serve to transmit

nociceptive information to higher brain centers; the

spinothalamic, spinoreticular, and spinomesencephalic.

The spinothalamic tract can be subdivided into the

lateral and ventral tracts. The ventral spinothalamic tract

originates from cells in laminae I, IV, V, VI, and VII. This

tract ascends to the mesencephalon and thalamus. The tract

has not been clearly defined, but is believed to carry

information of nonspecific nociceptive type (Bishop, 1980;

Kerr, 1975; Kerr, 1976; Willis, 1976).

The lateral spinothalamic tract is believed to be the

major tract for relay of information. Spinothalamic neurons

in the dorsal horn are found in laminae I, IV, V, and VII.

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Four types of spinothalamic neurons have been identified:

those in laminae IV and V neurons that respond to innocuous

tactile stimuli, laminae IV and V that respond to

proprioception, lamina V wide dynamic range neurons, and

lamina I neurons that respond to high intensity noxious

stimuli (Yaksh & Hammond, 1982; Willis, 1976). The majority

of fibers of the lateral spinothalamic tract traverse to the

thalamus. Studies of degeneration of fibers in animals have

established synaptic connections in the

ventroposteriorlateral nucleus, medial division of the

posterior group, nucleus centralis lateralis, and nucleus

submedius. The tract also possesses synaptic connections

with the nucleus cuniformis, periaquaductal grey, and

reticular system (Angerbauer & Dostrovsky, 1984; Kerr, 1979;

Ralston, 1984; Willis, 1976).

The spinoreticular tract fibers originate in laminae V

through VIII. The fibers course in the ventrolateral

funiculus both ipsalaterally and contralaterally with the

majority being ipsalateral (Fields & Anderson, 1976; Yaksh &

Hammond, 1982). The fibers terminate in the reticular

formation in the areas of n. reticularis

paragigantocellularis, n. reticularis pontis caudalis, n.

subcerulus, n. raphe magnus, and n. pallidus (Gallager &

Perl,1978; Yaksh & Hammond, 1982). Neurons of the

spinoreticular tract are of the wide dynamic range type and

respond to innocuous stimuli, but increase their response

frequency with noxious stimuli (Yaksh & Hammond, 1982).

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The spinomesencephalic tract fibers also originate from

neurons in laminae V through VIII as do the spinoreticular

fibers (Yaksh & Hammond, 1982; Yezierski & Schwartz, 1984).

The tract also progresses ipsalaterally and contralaterally.

Degeneration studies have established connections in the

reticular formation, n. cuneiformis, inferior and superior

colliculi, periaquaductal grey, and mesencephalon (Yaksh &

Hammond, 1982).

These fibers connect lamina I and nucleus proprius

neurons to supraspinal areas. Rostrad transmission from the

spinal cord is demonstrated by these tracts to sites within

the thalamus, reticular formation, nucleus raphe magnus, and

periaquaductal grey.

Supraspinal interactions. According to the Gate Control

Theory supraspinal areas interpret and formulate responses to

nociceptive input from the spinal cord. Various sites within

the brain receive nociceptive input frcra the spinal tracts.

These are the reticular formation, thalamus, limbic system,

and cortex. These areas have many interacting channels and

are believed to perform integrative, assessment, and

modulating functions.

The reticular formation begins at the superior spinal

cord and extends rostrad through the medulla, pons,

mesencephalon, and thalamus. This formation fulfills

excitatory, equilibrium, and nociceptive functions (Bishop,

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1980; Guyton, 1986; Noback & Demarest, 1975). As previously

described, the reticular formation receives input from the

spinoreticular tract primarily and receives connecting tracts

from the spinothalamic and spinomesencephalic tracts.

Both wide dynamic range neurons and nociceptive specific

neurons have been found in the reticular formation

(Casey,1980; Yaksh & Hammond, 1982; Zimmerman, 1976).

Nishikawa & Yokota (1985) identified wide dynamic range

neurons and subnucleus reticularis ventralis neurons in the

bulbar lateral reticular formation of cats. The subnucleus

reticularis ventralis neurons were response specific to

noxious stimuli. The nucleus gigantocellularis has been

identified by some authors as the primary site within the

reticular formation for nociceptive activity and learned

aversive behavior (Casey, 1980; Gallager & Pert, 1978;

Nishikawa et al., 1985; Yaksh & Hammond, 1982). Stimulation

of the reticular formation results in increased activity

within the thalamus, indicating neural pathways connecting

these structures (Bowsher, 1974, 1976; Yaksh & Hammond,

1982). The locus coeruleus, a central nucleus, has ascending

projections to the hypothalmus, thalamus, and global cortex

(Jones & Yang, 1985; Noback & Demarest, 1975). This area

contains catecholamine bodies that serve as relay neurons

from the globis pallidus to the thalamus and cortex (Noback &

Demarest, 1975).

The thalamus lies at the superior pole of the reticular

activating system and at the base of the cortex. It serves

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many integrative functions for somatic input to the cortex

and associated areas (Guyton, 1986). Three areas within the

thalamus have been indicated in nociceptive functions;

posterior, ventrobasal, and intralaminar (Bowsher, 1974,

1976; Casey, Keene, & Morrow, 1974; Yaksh & Hammond, 1982;

Zimmerman, 1976). The thalamus receives input from the

ventral spinothalamic and reticular formation (Bishop, 1980;

Casey, 1973; Guyton, 1986; Pay & Barasi, 1982; Peschanski &

Besson, 1984; Yaksh & Hammond, 1982). Nuclei in these areas

respond to a wide range of noxious and innocuous stimuli.

Lesions within these areas relieve the affective dimension of

pain , but preserve somatosensory discrimination (Bishop,

1980; Casey,1973; Casey, et al., 1974; Guyton,1986; Yaksh &

Hammond, 1981;).

The posterior nuclear complex is the main terminus for

the spinothalamic tract (Bowsher, 1974, 1976; Curry, 1972;

Ralston, 1984; Yaksh & Hammond, 1982; Zimmerman, 1976).

Sixty percent of the neurons in the posterior complex respond

to noxious stimuli (Yaksh & Hammond, 1982; Zimmerman, 1976).

Nishikawa, Koyama, & Yokota (1984) found trigeminal

nociceptive neurons projected to the posterior group. The

posterior complex has been shown by stimulation and

regeneration studies to have projections to the somatosensory

II area of the cortex (Bowsher, 1974; Curry, 1972; Burton &

Jones, 1968; Ralston, 1984; Yaksh & Hammond, 1982).

Connections to the somatosensory II area suggest

somatoesthetic functions for the posterior complex.

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The ventrobasal complex also receives input from the

spinothalamic tract (Bishop, 1980; Casey, 1973; Guyton, 1986;

Kerr, 1975; Ralston, 1984; Willis, 1976). Ventrobasal

neurons have been shown to respond to noxious thermal and

mechanical stimuli (Yaksh & Hammond, 1982; Zimmerman, 1976).

Ventrobasal neurons also project to the somatosensory II

area. The major function of the ventrobasal area is believed

to be leminscal (Bowsher, 1974; Yaksh & Hammond, 1982;

Zimmerman, 1976).

Intralaminar neurons receive input from the reticular

formation and the spinothalamic tract. The majority of

neurons respond to noxious stimuli and perform an integrative

function between the reticular formation and thalamus

(Bowsher, 1984; Ralston, 1984; Yaksh & Hammond, 1982;

Zimmerman, 1981).

The limbic system consists of the hypothalamus, and

associated areas of the subcortex, including the amygdala.

It controls the subconscious balancing of vegetative

functions, sleep cycles, and emotional behavior responses.

The limbic system is concerned with the affective sensations

associated with nociception. The limbic area also serves as

a connection between the thalamus and cortex. Studies of

reward and punishment have led to the establishment of pain,

punishment, and negative reactions in the limbic area

(Guyton, 1986; Noback & Demarest, 1975). The limbic system

is thought to contribute memory and learned behavior to the

thalamic and cortical interpretation of pain (Casey, 1973;

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Guyton, 1986).

The cerebral cortex serves as the ultimate integrative

and interpretive center of sensory input. It also organizes

the chemical and motor responses of the organism to sensory

input (Guyton, 1986; Noback & Demarest, 1975). Nociceptive

input to the cortex is primarily thought to be through

thalamic-somatosensory connections (Casey,1973; Zimmerman,

1976). The somatosensory cortex lies in the postcentral

gyrus. The somatosensory area can be divided into anterior

and posterior sections or somatosensory I and II. The

anterior portion receives input from the ventrobasal thalamic

nuclei. This area receives innocuous tactile and

proprioceptive information (Guyton, 1986; Yaksh & Hammond,

1982). Input to somatosensory I is from low threshold

mechanoreceptors. Small numbers (2%) of nociceptive neurons

have been observed in this area and it will respond to

nociceptive stimulation (Guyton, 1986; Zimmerman, 1976).

Somatosensory II is located posterior and basally to

somatosensory I. It lies at the base of the postcentral

gyrus (Guyton, 1986). Somatosensory II receives input from

the posterior and ventrobasal thalamic areas. The responsive

properties of neurons in this group are similar to the

posterior thalamus. They respond to noxious stimuli from

wide receptive fields (Curry,1972; Yaksh & Hammond, 1981;

Zimmerman, 1976). Several studies of noxious electrical

stimulation produced responses in somatosensory II neurons

(Guyton, 1986; Vyklicky & Keller, 1974; Zimmerman, 1976).

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Thus, pain fibers travel to the reticular formation,

thalamus, and cerebral cortex. Integration of nociceptive

information is possible by connecting tracts to these areas.

Cerebral influences on pain perception, interpretation, and

responses are possible through this system.

Rostral-caudal transmission. The rostral-caudal

transmission of nociceptive information and

facilitation-inhibition follows similar pathways as the

ascending system. Some accessory pathways augment

communication. Pathways from the cortex to the reticular

activating system and limbic sites have been demonstrated

(Basbaum, Clayton, & Fields, 1978, Fields, 1984). Generally

the progression is from cortex to thalamus, through the

reticular formation or on separate thalamic-spinal tracts to

the funicular tracts and returning to the spinal column as

part of the tracts that carry ascending fibers (Basbaum &

Fields, 1982; Fields, 1984; Zimmerman, 1976).

Descending supraspinal influences. The Gate Control

Theory incorporates a central intensity monitor that

modulates nociceptive perception by feedback to the dorsal

horn (Melzack, 1973; v,\ll, 1978). Facilitation or inhibition

of nociceptive transmission can occur at multiple supraspinal

sites. This section will review studies of facilitation and

inhibition of nociception by stimulation of various central

sites. Facilitory and inhibitory responses from stimulation

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of the nucleus raphe raagnus and reticular formation, locus

coeruleus, periaquaductal grey, and sensory cortex are

discussed.

Stimulation of raphe nuclei neurons in the reticular

formation has been demonstrated to result in preferential

inhibition of nociceptive spinothalamic tract neurons

(Fields, 1984; Mayer & Liebeskind, 1974; Willis, 1984).

Inhibition of Laminae I and V nociceptive neurons has been

shown (Anderson, Basbaum & Fields, 1977; Basbaum, 1978;

Fields, Basbaum, Clanton, & Anderson, 1977). Excitation of

dorsal horn neurons by electrical stimulation of the nucleus

raphe was shown by Basbaum et al. (1978). Other areas in the

reticular formation have been shown to produce excitation in

the dorsal horn that resulted in aversive behavior in animal

studies (Basbaum, et al, 1978; Casey, 1973; Willis, 1984).

Inhibition of dorsal horn neurons by reticular stimulation

has also been demonstrated (Anderson et al, 1977; Basbaum et

al, 1978; Fields, 1984; Liebeskind, Mayer, & Akil, 1974;

Mayer & Liebeskind, 1974). The locus coeruleus projects to

the substantia gelatinosa (Commissiong et al., 1978; Hodge et

al., 1981) cerebellum, hypothalamus, and cortex (Commissiong

et al; 1978). Stimulation of the locus coeruleus led to

inhibition of neurons in laminae IV, V, and VI (Commissiong

et al., 1978; Hodge et al., 1981).

Stimulation of periaquaductal grey has been shown to

result in inhibition of dorsal horn nociceptive neurons and

analgesia to peripheral pain stimuli (Fields, 1984;

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Liebeskind et al, 1973; Mayer & Liebeskind, 1974; Willis,

1984; Zimmerman, 1976). Richardson (1982) and Liebeskind et

al. (1973) reported relief of pain mediated by noxious

mechanical stimuli by periventricular grey stimulation.

Stimulation of the somatosensory cortex has been

demonstrated to produce both excitatory and inhibitory

affects on dorsal horn nociceptive neurons (Curry, 1972;

Fields et al, 1977; Lineberry & Vierck, 1975; Liebeskind et

al., 1974; Mayer & Liebeskind, 1974; Willis, 1984).

Modulation of dorsal horn neurons by the cortex is described

as a function of connections in the pyramidal tracts (Willis,

1984; Zimmerman, 1976). Oliveras, Besson, Guilbaud, and

Liebeskind (1974) described inhibition in lamina IV and V

neurons specific to noxious stimuli after electrical cortical

stimulation.

Support has been shown for supraspinal excitatory and

inhibitory influences on dorsal horn pain transmission.

Cognitive-emotive factors have ability to enhance or reduce

transmission of peripheral noxious stimulation to supraspinal

areas and thus, affect the perception of pain. Two

cognitive-emotive factors that have the potential of

descending influence through supraspinal modulation are

anxiety and locus of control. These factors were chosen as

primary influences on pain perception, and as such were

included as intervening variables within this study.

Pharmacological considerations. The Gate Control Theory

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is based upon interactions that occur in the dorsal horn and

at supraspinal levels. These interactions require

neurotransmitters to facilitate or modulate neuron responses.

To be considered for inclusion as a neurotransmitter, any

substance must be (a) identified as present at the site, and

(b) identified as a stimulant or inhibitor of neuronal

function at the site. Five neurotransmitters and

neurohormones are discussed in this section; substance P,

enkephalin, endorphins, serotonin, and norepinephrine.

Substance P is the primary candidate for the excitatory

neurotransmitter for small primary afferent fibers.

Substance P is an undecapeptide found in the cell bodies of

primary afferent fibers. Substance P has been found in

quantity in 15-20% of the dorsal root ganglion cell bodies of

fibers that terminate in laminae I, II, III, and V; areas of

nociceptive terminations (Dodd, Jahr, & Jessell, 1984; Salt,

Morris, & Hill, 1983; Yaksh, 1979). Substance P was found in

the vesicles of axons within the spinal cord (Basbaum, 1980;

Yaksh & Hammond, 1982). Substance P is released following

nociceptive stimulation of small primary afferent fibers

(Basbaum, 1980; Dodd et al., 1984; Kurashi, Hirota, Sata et

al., 1985; Yaksh, Jessell, Gamse, Mudge & Leeman, 1980), but

innocuous stimulation did not result in a release of

substance P (Kurashi, Hirota, Sata et al., 1985). Following

injection of capsacin, an extreme irritant, substance P

levels were depleted in the dorsal horn, indicating release

of sustance P with noxious stimulation (Yaksh & Hammond,

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1982). Injections of substance P have been shown to have a

depolarizing effect on dorsal horn nociceptive interneurons

(Dodd et al., 1984; Yaksh and Hammond, 1982).

Substance P is found in small primary afferent fibers,

released by noxious stimulation, and results in excitation of

dorsal horn nociceptive neurons. The preceding factors

indicate substance P is the primary excitatory

neurotransmitter of small afferent fibers.

The Gate Control Theory proposition of inhibition from

large primary afferent fibers presupposes an inhibitory

neurotransmitter exists to inhibit substance P excitation of

nociceptive neurons. Enkephalin, an opoid peptide, is the

candidate for consideration as the small afferent fiber

inhibitor. Enkephalin has been demonstrated as present in

stalk and islet cell interneurons of the substantia

gelatinosa; and Laminae I and V spinothalamic tract neurons

(Basbaum, 1980; Dubner et al., 1984; Fredrikson, & Geary,

1982; Miller, 1981). Opoid receptors have been identified in

Laminae I, II, and III (Duggan, 1884; Pert, Kuhm, & Snyder,

1975; Yaksh & Hammond, 1982).

A delta and C fiber stimulation was depressed by

injections of morphine, an opoid compound (Cavillo, Henry &

Neuman, 1974; LeBars, Guilbaud, Jurna & Besson, 1976).

Substance P release was suppressed by injection of morphine

(Yaksh, 1978, 1979; Yaksh et al., 1980). Noxiously

stimulated neurons in Laminae I and V were suppressed by

iontophoretic administration of enkephalins, but innocuous

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transmission was not affected (Kitohata, Kosaka, Taub,

Bonikos & Hoffert, 1974; Yaksh et al, 1980). Administration

of enkephalin near cell bodies of rat dorsal horn neurons

delayed responses to noxious heat stimulation, depressed

excitation of the cells, and depressed wide dynamic range

neuron response in the nucleus proprious (Duggan, 1984).

The effects of enkephalin were reversed by naloxone injection

(Dubner, Cavillo, Henry, & Neuman, 1984; Duggan, 1984; LeBars

et al., 1976; Yaksh & Hammond, 1982).

Enkephalin is found in the dorsal horn, depresses

substance P release, and reverses nociceptive responses.

Therefore, enkephalin is considered the neuro inhibitor of

small primary afferent fiber activity.

Supraspinal influences on nociception transmission are

modulated by three neurochemical substances; endorphins,

serotonin, and norepinephrine. Stimulation of the

periaquaductal-periventricular grey (PAG/PVG) areas of the

brain results in naloxone reversible analgesia (Hosobuchi,

Rossier, Bloom & Guilleraan, 1979). The PAG/PVG areas have no

direct spinal cord projections, suggesting supraspinal areas

of action (Gebhardt, 1982). Supraspinal action is supported

by studies of lesion or naloxone blockage in the nucleus

raphe raagnus. The analgesia produced by morphine was negated

by nucleus raphe magnus blockage (Gebhardt, 1982; Oliveras,

Hosobuchi, Redjemi, Guilbaud & Besson, 1977; Proudfit &

Anderson, 1975).

Stimulation of the PAG/PVG resulted in release of B

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. endorphin, an opoid compound (Fredrickson et al, 1982).

Endorphin stores have been found in the pituitary and

hypothalamus (Fields, 1984; Gebhardt, 1982). Pert, Kuhar,

and Snyder (1975) located endorphin receptor sites in the

nucleus caudatus putamen, locus coeruleus, and amygdala, as

well as several other limbic sites. Morphine injections to

the PAG/PVG resulted in decreased laminae V-VII response to

noxious stimulation, but not to innocuous stimuli (Calvillo

et al., 1974; Kitahata et al., 1974; LeBars et al., 1976).

Serotonin is released with stimulation of the nucleus

raphe magnus. Stimulation of the nucleus raphe magnus

produces inhibition of marginal and stalked cells in laminae

I and II of the dorsal horn (Belcher, Ryall & Schaffner,1978;

Dubner et al.,1984). Stimulation of the nucleus raphe magnus

produces release of serotonin in substantia gelatinosa area

of the dorsal horn and decreased response to noxious stimuli

(Rivot et al., 1984). Iontophoretic administration of

serotonin in the dorsal horn inhibits neurons excited by

noxious stimuli (Dubner et al., 1984).

Norepinephrine is released with stimulation of the locus

coeruleus (Koda, Schulman & Bloom, 1978). Norepinephrine has

been found to inhibit the release of substance P in dorsal

horn neurons excited by noxious stimuli (Engberg & Ryall,

1966; Headley, Duggan & Griersmith, 1978; Jones & Olpe, 1986;

Kurashi, Hirota, Hino et al., 1984; Pang & Vasko, 1986).

Iontophoretic administraion of norepinephrine decreased

dorsal horn neuron response to noxious stimulation (Akil &

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Liebeskind, 1975; Kurashi, Hirota, Hino, 1984). Dorsal horn

inhibition was not found to be naloxone reversible, and

therefore, not a product of opiate transmission to the locus

coeruleus (Headley et al., 1978; Jones & Olpe, 1986; Reddy &

Yaksh, 1980; Pang & Vasko, 1986).

Inhibition by muscle stimulation. The review of

literature has shown support for large primary afferent

inhibition of pain transmission. Stimulation of

proprioreceptors in muscles and tendons is transmitted to the

spinal cord via large primary afferent fibers (Guyton, 1986).

These large primary afferent fibers transmit innocuous

information to the dorsal horn. The fibers enter by way of

the nucleus proprius, but have terminals in the substantia

gelatinosa (Basbaum, 1980; Bishop, 1980; LaMotte, 1979). In

the substantia gelatinosa interneuron dendritic endings from

substantia gelatinosa neurons are interspaced with dendrites

from the nucleus proprius (Basbaum, 1980; Kerr, 1979;

Szengathtai, 1964).

Inhibition of transmission of noxious stimulation in the

dorsal horn by large primary afferent stimulation has been

shown (Kerr, 1976; Iggo, 1980; Wall, 1984). Morris (1987)

demonstrated inhibition of nucleus proprius nociceptor

transmission by muscle nerve stimulation. These studies

provide neurophysiological support for pain inhibition by

muscle movement.

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Previous Applications of the Gate Control Theory.

Historical background. From ancient times, scientists

have attempted to treat pain by methods that utilized

innocuous stimulation of nerves to interfere with pain

responses. The use of peripheral stimulation for analgesia

began in classical Greece. The Greeks found that use of

electrical stimulation through application of live torpedo

fish to an affected area produced numbness and subsequent

relief of pain. Other fish similarly used by ancients were

eels and electric catfish (Kane & Taub, 1975). Development

of the Leyden jar to produce and store electricity allowed

Galvani in the 1790's to extend his studies of the torpedo

fish and experiment with nerve and muscle conduction of

electricity in frogs. His works complemented Franklin's and

led to development of the two electrode metal stimulator.

Galvani noted that current traveled faster along nerve fibers

and the contraction produced was greatest when the spinal

cord was stimulated (Galvani, 1791/1953).

Electrical stimulation for analgesia gained popularity

in the late 1800's with the development of small generators

for use in dentistry. Althaus in 1858 in England was the

first to intentionally utilize electricity for transcutaneous

stimulation of peripheral nerves. He promoted the use of

electroanalgesia for pathological conditions, for example,

neuritis. Several surgeons in the late 1800's utilized

electroanalgesia for various procedures. Guenot in 1953

reported a post inhibitory effect to noxious stimuli after

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use of electroanalgesia (Kane & Taub, 1975). In oriental

cultures, acupuncture with or without electrical stimulation

had been developed (Kane & Taub, 1975; Melzack, 1973).

Large primary afferent fiber stimulation. In early

observations by Barron and Mathews, (1938), oscillograph

recordings were made of dorsal column discharges in cats and

frogs. An intermittent pattern of discharges was noted.

Then several stimuli were introduced to examine the effect of

these stimuli on the discharge rate. An animal with good

muscle tone experienced more intervals of interruption of

discharge patterns while anesthetized animals produced an

almost continuous discharge pattern. Mechanical stimulation

of the contralateral leg produced a complete block of

discharges for the duration of the stimulus. Toe flexion

also blocked the discharge. Barron and Mathews concluded

that a block in dorsal column transmission could be produced

by peripheral stimulation, Wall (1958) studied the effects

of stimulation of proprioceptive and skin nerve fibers on

dorsal and ventral roots and dorsal horn cells in cats.

Transcutaneous electrical nerve stimulation (TENS) was

developed in the 1970's from these early experiments with

electrical stimulation. TENS is based on the Gate Control

Theory (Lampe, 1979; Wall, 1978). Electrodes are placed

along nerve tracts from pain sites and low level electrical

current is supplied. Although TENS is believed to function

through stimulation of large primary afferent fibers,

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specific mechanisms of action have not been shown (Lampe,

1979; Wolf, 1979; Wall, 1978).

Wall and Sweet (1967) investigated a study of electrical

stimulation of large primary afferent fibers to inhibit pain

perception. Eight subjects with chronic cutaneous pain

received electrical stimulation by needle electrodes placed

at the pain site or near nerve tracts proximal to the pain

site. Low level electrical stimulation was employed as large

primary afferent fibers have the lowest electrical threshold

for stimulation. Square form stimulation at 100 Hz for 0.1

msec, was used. All subjects reported relief during

stimulation, but the relief experienced post stimulation fell

into two categories. One group of four subjects experienced

relief for more than 30 minutes after two minutes of

stimulation. The second group reported pain relief for less

than two minutes after the stimulation. Wall and Sweet felt

short term relief was experienced by subjects with intact

peripheral axons that transmitted continuing intense stimuli

from peripheral pathology. Worthy of note is that two

subjects reported relief lasting several months.

Melzack (1975b) studied pain relief by somatic

stimulation in 53 patients with chronic nerve or muscle pain.

Electrical stimulation of peripheral nerves was carried out

with a 60 Hz sine wave stimulator with a 35V current. The

McGill Pain Questionnaire was utilized to measure pain

perception. Stimulators were placed on trigger points, nerve

tracts, or acupuncture points. The stimulators were adjusted

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to a level immediately preceding painful stimulation.

Placebo effects were tested by counterfeit stimulation in

seven subjects. After stimulation, the McGill Pain

Questionnaaire was repeated. Pain relief was also evaluated

by a generalized estimate of pain relief; 67-100% was

excellent, 34-66% was good, and < 33% was unsatisfactory.

The conclusions of the study were that stimulation was

effective for pain from peripheral nerve injury, low back

pain, phantom-limb, and shoulder - arm pain. Relief

produced was immediate and often long lasting. Placebo

effect was not supported. Melzack, Jeans, Stratford, and

Monks (1980) compared transcutaneous electrical stimulation

to ice massage with 44 men and women with chronic back pain.

Subjects were given two treatments with each. The McGill

Pain Questionnaire was administered after each treatment.

Comparisons of mean and range scores from each group yielded

similar results, both groups reported significant relief.

Ice was felt to be a cheaper and easier stimulant for self

care.

Acupuncture is thought to be another method of

stimulating afferent fibers. Of 309 acupuncture points

evaluated in a study in Shanghai in 1975, all are either at

or near nerve tracts (Chan, 1984). Acupuncture is thought to

operate by stimulation of muscle nerve fibers (Langyan, &

Shaoying, 1985; Mannheimer,1878)

Lundeberg (1983, 1984) conducted a series of experiments

to compare vibratory stimulation to electrical or cold

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thermal stimulation for pain relief. In the first study

(1983) 731 patients, 135 with acute pain and 596 with chronic

pain, all with a history of previous unsuccessful treatment

were evaluated. Pain was measured by the McGill Pain

Questionnaire, a seven interval graded scale, and a visual

analog scale. The subjects were also asked to rate the pain

by moving a lever attached to an ink writer during the

experiment. Vibratory stimulation of peripheral nerves was

provided by a covered probe applied to the skin with

sufficient pressure to contact underlying bony prominences,

using 100 Hz vibrations. Electrical stimulation was produced

by a high frequency - low interval square wave unit at 0.2

msec and 100Hz. Cold stimulation was produced with a gauze

covered ice cube. Pharmacological comparisons of pain relief

were made with 1 Gm. dose of ASA. Various sites of

stimulation were compared for effectiveness. Lundeberg found

that the site of pain was the most effective simulation

point, with durations of vibratory stimulation of 30 to 45

minutes giving the most relief. In comparison ratings of

pain relief; 31 of 51 subjects experienced relief of 70% or

greater with vibratory stimulation, 28 with long electrical

stimulation, and 23 with short electrical stimulation.

Thirty-five percent experienced some relief with placebo

compared with 62% with vibratory treatment. Lundeberg was

unable to determine if the effect of vibratory stimulation

was due to diffuse noxious stimulation, large primary

afferent fiber stimulation, or autonomic effects of increased

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circulation to the area.

Lundeberg (1984) investigated the long-term effects of

vibratory stimulation. Lundeberg compared vibratory and

electrical stimulation pain relief in 267 chronic pain

patients. Sixty-eight percent of the subjects reported

short-term relief, 30% relief after 3 months, 9% after 18

months, and in 14% pain had never returned. The results were

the same for electrical stimulation.

Lundeberg, Nordeman, and Ottoson (1984) studied 366

acute and chronic pain patients. Sixty-nine percent of these

patients reported long term relief with vibratory

stimulation. Lundeberg felt that vibratory stimulation was

more economical, easier, and more natural than electrical

stimulation. He concluded that the results were due to large

primary afferent stimulation in keeping with the Gate Control

Theory.

Keck (1983) investigated the effect on pain perception

of large primary afferent stimulation by light touch. With a

convenience sample of 32 subjects, pain was produced by the

submaximal effort tourniquet technique. Innocuous

stimulation was employed using a towel with light strokes

over the forearm. Time to tolerance and description of

experience were analyzed. No significant difference was

found in the time to tolerance of the total sample, but order

of presentation was found to be a confounding variable. Two

sub-groups were identified, a group for whom the intervention

was successful and a group for whom it was not. These groups

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differed in the number of cognitive strategies utilized. The

successful group utilized fewer cognitive strategies than the

unsuccessful group. Keck concluded that large primary-

afferent stimulation by touch was effective for approximately

50% of the population sampled, a similar finding as the

effectiveness of TENS.

Previous Applications of Physical Activity as a Pain

Intervention.

The use of muscle movement to stimulate large primary

afferent fibers was suggested by clinical observations of

pain relief by ambulation in women with labor pain. Read,

Miller, and Paul (1981) investigated the relative effects of

oxytocin and ambulation on labor patients. Pain responses

were measured by verbal reports. This study found all

oxytocin patients reported increased pain, four of the

ambulation patients reported less pain, three ambulation

patients reported the same level of pain, and one patient

had increased pain. The subjects all had progression of

labor which is reported to increase pain.

Langyan and Shaoying (1985) investigated the effect of

arm movement on pain thresholds in humans. In acupuncture

techniques of limb movements and stretching to enhance

relief, muscle electrical activity is believed to provide

the relief obtained. Langyan and Shaoying noted traditional

Chinese medicine acupoints are located between muscles and

sinews. Subjects were 50 volunteers in good health, 28 males

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and 22 females, with ages ranging from 20 to 57. Pain was

induced to the hand with a spring painmeter with applied

needle pressure of 60 to 600 Gins. The pressure was increased

every 2 seconds by 100 Gms. Theshold of pain was measured at

the Hegu point between the first and second metacarpals.

Subjects were then asked to wave the wrist two to four times

per second for about ten seconds. Pain threshold was again

measured after stopping. Threshold was measured every minute

for five minutes after the intervention testing to measure

post movement inhibition. Measurements of pain thresholds

indicated significantly higher pain thresholds for the

exercise intervals (p <0.01). One minute after the exercise

ended, values were comparable to those before exercise.

Langyan and Shaoying concluded that arm movement increased

the threshold of pain.

Clinical experience has shown that muscle movement is

effective as a pain relief measure in primary dysmenorrhea

and in patients with joint replacement surgeries, but no

research was found in the review. Further investigation of

muscle movement as a pain relief measure is warranted.

Emotional-Cognitive Influences

The focus on emotional-cognitive influences to pain

perception was inaugurated by Beecher's (1946) classic study

of men injured at Anzio in World War II. Wounded men often

failed to notice their injuries until a lull in the fighting.

The men injured in war required less analgesia than similarly

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. injured civilians. Beecher proposed that the overwhelming

input of battle blocked perception of pain. When injuries

were perceived, the significance to a soldier was a trip home

and an end to fighting. The influences of decreased

attention to pain and positive benefit decreased pain

perception. Melzack and Casey (1968) proposed that

activation of limbic, reticular, and cortical areas assigns

motivational-discriminative qualities to the pain experience.

The reticular formation determines the alertness of the

person to input signals, the limbic area discrimination, and

the cortex assesses the input in relation to other

non-noxious stimuli and memory comparisons. Two areas of

emotional-cognitive influence on pain indicated by the

literature review are anxiety and locus of control. These

are intertwining variables with separate contributions and a

combined effect.

Anxiety. Anxiety is an emotional state marked by worry,

apprehension, and tension (Kaplan, et al., 1982). Increased

anxiety leads to a hypersympathetic state in which the

organism is unable to function well due to a barrage of

stimuli. The organism initially marshals forces to ’’fight"

or "flight" from noxious stimuli, but soon exhausts

physiological and psychological resources (Guyton, 1986;

Weisenberg, 1984). Evaluation of the anxiety component in

pain perception is indicated as one mechanism of supraspinal

influence.

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Bronzo and Powers (1967) studied a single subject in a

pilot test of pain threshold and anxiety. They tested a 20

year old female student using a heat stimulus. The subject

was tested under control, non-anxious, and anxious

situations. Non-anxiety situations (control) were tested by

telling the student she was doing well. In anxiety

situations, the student would be told that the machine was

broken, but the test would continue. Tolerance for heat was

measured by highest degree tolerated. During the low anxiety

procedure she was able to tolerate higher heat settings than

in the control test. In the high anxiety procedure the

subject experienced tolerance at settings lower than the

control test. The conclusion was that increased anxiety

decreased pain tolerance.

Graffenfried, Adler, Abt, Nuesch, and Spiegel (1978)

studied the relationship of anxiety and pain using 32 males

with ischemic pain. The submaximal effort tourniquet

technique was utilized to produce pain. Pain intensity was

measured by a visual analog scale and aspirin pain relief

dosages. Anxiety was measured by questionnaires and verbal

report. Findings were that the greater the increase in

anxiety levels, the shorter the interval before pain

tolerance.

Martinez-Urrutia examined the effect of anxiety on pain

perception pre and post surgery. Subjects were 59 male

surgical patients. The State Trait Anxiety Scale (STAI) and

Fear of Surgery Scale (FSS) were administered pre and post

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surgery. Pain was measured by the McGill Pain 1 uestionaire.

Anxiety was found to have a significant positive correlation

with pain intensity in the post surgical patients.

Spielberger (Spielberger & Sarason, 1975; Spielberger,

Gorsch, & Luchene, 1970) developed a theory of a two

dimensional aspect to anxiety, state and trait. Starting

with Freud's objective vs. neurotic anxiety, or fear of an

object versus free floating fears, Spielberger began to study

situational anxiety in the form of test anxiety. Spielberger

found that increased anxiety increased performance of

complicated tasks, but interfered with completion of

complicated tasks. Extreme levels of anxiety blocked

cognitive processes. Two types of anxiety, state and trait,

were indicated by Cattell & Scherer (1958). Spielberger

characterized state (A-state) as a subjective feeling of

apprehension associated with autonomic nervous system

activation. This type varies with each situation and the

meaning of the interaction to the individual. Trait anxiety

(A-trait) refers to the general disposition toward anxiety

inherent in the individual. This leads to the reaction of

high trait anxiety scorers to be more anxious in situations

of threats to their ego. Trait anxiety did not appear to

affect reactions to physical danger. Spielberger then

developed the State-Trait Anxiety Inventory to measure

relative levels of anxiety in various situations (Spielberger

& Sarason, 1975; Spielberger, et al., 1970). Supraspinal

influence on pain perception by anxiety would appear to be

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centered in state anxiety levels that fluctuate with

situational changes. Stimulation by increased anxiety would

provide feedback to spinal cord transmission neurons and

increase pain perception.

Locus of control. Rotter defined locus of control as

how individuals perceive events in their lives as being the

results of their own actions, and thereby controllable

(internal control), or as the results of external forces and

therefore beyond personal control (external control) (Rotter,

1982). In studying psychological factors influencing pain

perception, Kanfer and Goldfoot (1966) tested 60 students

with ice water as a noxious stimulus. Subjects were divided

into groups and each group received one of following

instructions: (a) the stimulus would be uncomfortable, but

they could end it at will; (b) the stimulus would be very

painful, but could be ended at will; (c) the stimulus would

be uncomfortable and they were to verbally describe the

experience; (d) the stimulus would be uncomfortable, but

there was a clock for distraction; (e) the stimulus was

uncomfortable, but there were slides to view as a distractor

and they controlled the rate of slide changes. In the

findings, the distractors controlled by the subject (c,e)

provided the greatest aid in tolerating noxious stimuli. The

researchers did remark that subjects reported utilizing

self-help distractors that they had previously learned to

cope with stress. The indications were that perceived

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control of a painful situation increased pain tolerance.

Rotter, Seeman, and Liverant (Rotter, 1982) developed a

scale for measuring locus of control traits as a range of

internal-external tendencies. Lefcourt (1966) examined

studies of applications of locus of control and determined

that high external scores were correlated with less

responsible members of society (mentally ill, children,

criminals). Internal controlled persons were more active in

controlling their own lives and seeking to change.

Reliability and validity of the concepts of locus of control

have been tested in a variety of settings. Hersch and

Sciebe (1967) and Williams and Warchal (1981) validated the

social adjustment found by Lefcourt. Phares, Rithchie, and

Davis (1968) tested a reaction to threat by negative feedback

after a test and noted the focus on negative factors by high

external scorers. Remedial actions were more likely to be

undertaken by internal controlled subjects.

Craig and Best (1977) investigated the relationship of

locus of control and modeling on pain tolerance. Subjects

were 50 female volunteer students. Pain was induced by

electrical shocks to the forearm. The Rotter I-E Scale and

Subjective Stress Scale were administered and then pain was

induced with an inactive model present. Subjects were then

instructed in internal or external control terms as to the

subject's control over the pain. Another set of shocks were

then delivered. Internal control subjects tolerated more

shocks than external control subjects in both settings.

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Nichols (1983) developed a pain-specific locus of

control tool. This study was undertaken to validate a

situation specific and general conceptions of locus of

control. The 24 item tool was derived from Rotter's

modified tools. Pain was produced by the submaximal

tourniquet technique. Sixty-three nurses and students

experienced the pain producing procedure and then completed

the tool measuring situation and general expectancy locus of

control. Nichols concluded that general expectancy scores

were not altered by pain experiences, the situation specific

scores were altered by the pain experience, and no

correlations between reported level of pain and general or

specific score were noted.

Anxiety and Locus of Control in Interaction. As

previously stated, anxiety and locus of control are not only

of significance as separate influences, but they also

interact. Researchers have investigated this relationship

with subjects in various settings. Watson (1967) sampled 648

subjects with Rotter's I-E, the Manifest Anxiety Scale, and

the Alber-Haber Achievement Anxiety Test. Watson found a

relationship of the more external the subject the more likely

to report high anxiety scores. Lowery, Jacobsen, and Keane

(1975) tested 91 pre-surgical patients with Rotter' I-E and

Zuckerman's Multiple Affect Adjective Checklist. All

subjects scored high on anxiety levels, as would be

expected. A slight increase in anxiety levels was found in

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external controlled subjects, but it was not significant.

Bowers (1968) hypothesized that lack of control over a

stressor was an antecedant to anxiety. Thirty-two subjects

received electrical shocks and were told either that they

could avoid shocks by certain learned responses or that the

shocks were unavoidable. Students then completed pain

rating, anxiety and locus of control forms. Partial support

for the hypothesis was found in that subjects without control

reported pain at lower shock levels than those with control

and higher anxiety scores.

From these studies it can be concluded that of the

psychological factors influencing pain perception, two of

note are anxiety and locus of control. These interacting

factors are of concern when determining variables that could

influence pain perception through the feedback of cognitive-

lective information to the gate control areas.

Summary,.

The results of this review of literature support an

investigation of physical activity as a pain intervention.

Neurophysical support provides transmission of pain stimuli

to the dorsal horn by small primary afferent fibers.

Innocuous stimuli activate large primary afferent fibers.

Muscle and tendon nerves are large primary afferent fibers.

Large and small primary afferent fibers have terminations in

the substantia gelatinosa of the dorsal horn. Axo-dendritic

connections from the substantia gelatinosa interneurons to

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the transmission neurons of the nucleus proprius affect

transmission to supraspinal areas. Although interactions in

the dorsal horn have not been fully explicated, stimulation

of large primary afferent fibers has been shown to inhibit

transmission of from nociceptive lamina V neurons. Substance

P release is associated with nociceptive stimuli. Large

fiber stimulation activates enkephalin release. Enkephalin

has been shown to inhibit nociceptive responses.

Support for large fiber stimulation as a mechanism of

pain inhibition was shown by studies of electrical,

vibratory, touch, and acupuncture stimulation. Although

direct inhibition of lamina V neurons was demonstrated in

only one study, all of these mechanisms activate large

primary afferent fibers and each mechanism has been shown to

be effective as a nociceptive inhibitor.

Despite clinical observation of pain inhibition by

physical activity, few studies support muscle movement as an

intervention. There are frequent clinical reports of pain

inhibition by ambulation with labor and primary dysmenorrhea

patients. The Read et al. (1981) study supported the

ambulation of labor patients, not only for labor progression,

but to reduce pain. The study by Langyan and Shaoying (1985)

utilized muscle movement as a pain inhibitor. The need for

further exploration of physical activity is indicated by the

active utilization of the technique in clinical activities

without empirical testing.

Support was shown for supraspinal influences on pain

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transmission. Dorsal horn activity is transmitted via nerve

tracts to the thalamus, reticular formation, limbic areas,

and cortex. Interpretation of the stimulus is affected by

responses in the supraspinal structure from attention,

memory, personality, and physical health. Supraspinal areas

influence pain transmission from the dorsal horn.

Stimulation of the cortex, reticular formation, limbic

system, and periaquaductal-periventricular gray areas

activates facilitory and inhibitory pain transmission to the

dorsal horn. Inhibition of dorsal horn activity was shown by

an opoid and non-opoid system.

The effects of two cognitive-emotive factors were

supported by the literature; anxiety and locus of control.

Anxiety was shown to increase the perceived severity of pain

and decrease tolerance of pain. The individual locus of

control, or perception of personal control, affects pain

perception. Internal orientation is associated with higher

pain tolerance.

In conclusion, the studies reviewed support an

investigation of pain inhibition by muscle movement. Anxiety

and locus of control are indicated as possible intervening

variables in pain perception. A test of one proposition of

the Gate Control Theory will increase the knowledge base of

pain perception and intervention.

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CHAPTER III

Methodology

The methodology utilized in the study is described.

Information is explicated concerning the subjects,

instruments, procedures, data collection, and data analysis

methods.

Sub jects

A convenience sample of 30 subjects was sought from two

groups: registered nurses from a community hospital, and

registered nurses and students in their last six months of

training from a university nursing school. Prior study

samples were from graduate nursing students, subjects were

sought from a community hospital, thus broadening the scope

of the study. Exclusion criteria included poor general

health, peripheral neuropathy, peripheral vascular disease,

diabetes, arthritis, recent injury to the non-dominant arm or

hand, coagulapathies, current psychiatric treatment, and any

use of medications that would effect blood coagulation or

pain sensitivity.

A total of 32 subjects was obtained. Data from two

subjects were not usable. One experienced difficulty with

the language of the tools and one experienced muscle spasms

not related to the stimulus or intervention.

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Human Rights

The study was reviewed by the Indiana University School

of Nursing Committee for the Protection of Human Rights.

Informed consent was obtained from each subject (see Appendix

B). Complete anonymity and confidentiality were assured for

all participants.

Design

The effect of physical activity on pain perception was

tested utilizing a split-plot factorial design (Kirk, 1982)

in which subjects were randomly assigned to the intervention

procedure, with one group experiencing the intervention

procedure first and one the control procedure first. Each

subject served as her own control, reducing the effect of

subject heterogeneity.

Chapman et al. (1985) and Keck (1983) found that the

order of presentation affected the pain perception

measurement. Chapman et al. (1985) also found familiarity

with the procedure to be a confounding variable. Randomly

assigning subjects to begin with either the intervention or

control should offset order of presentation as a confounding

variable. One group experienced the pain producing procedure

first without the intervention and the other group

experienced the procedure with the intervention first. To

control for subject familiarity, the procedure was explained

to each subject and the pain producing instrument

demonstrated to each subject at the beginning of the

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procedure.

Extremes of age, sex, and testing with dominant or

non-dominant hand have been found to effect pain thresholds

(Weisenberg, 1977). Because of these previous findings, all

subjects were female, between the ages of 18 and 60, and the

non-dominant hand exclusively was utilized for testing.

Diurinal variations in pain perception were found by

Rogers and Vilkin (1978). Student subjects had significantly

higher pain tolerance in the evening hours. For the current

study, subjects included nurses from all three shifts.

Although testing took place at various times during the day,

each subject’s testing was completed within a two hour

period. This precaution should have eliminated the effect of

diurinal variations.

Due to factors such as the meaning of the experience,

anxiety levels, and other health factors, experimental pain

differs from clinical pain (Beecher, 1956). In order to

accurately measure the influence of the intervention while

limiting extraneous variables, experimental pain was utilized

for this study.

Instruments

The mechanical device used to produce experimental pain,

the technique of physical activity to stimulate the LPAs, and

the instruments to measure anxiety and locus of control are

described in this section. The dependent variable

instruments are also presented.

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Experimental pain producing technique. Pressure

devices were first used in Victorian times as a pain

producing technique for experimentation. Air pressure

devices, screws, and graters were some methods of pressure

production. The pressure algometer was developed to produce

a measurable amount of pressure. Generally this device

consists of a plunger attached to a spring device that is

applied to the bony surfaces of the body. This device

produces pain by activation of small primary afferents by

noxious pressure (Merskey & Spear, 1964). Wolfe (1984)

tested the pressure algometer finding varying degrees of

response at various bony surfaces. The difficulties

experienced with the pressure algometer have been the

awkwardness of the device and uneven increments of pressure.

The standard pressure algometer would have been too heavy to

allow for the arm movement necessary for large primary

afferent stimulation in this experiment. Therefore, a

clip-on pressure device was developed. Several types of

clips were tested on volunteers. The final choice was a

modification of a large barrel-type paper holder. It was

reduced in size to a weight of one ounce and a surface of 1.5

inches. In pilot testing, all subjects reported pressure

developing into pain within a five minute interval. The pain

was reportedly progressive with some subjects unable to

withstand more than two minutes of the pressure. The clip

was tested before and after the study by use of a pressure

balloon and manometer. The surface pressure produced was

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123mmHG or 2psi at the beginning and 118mmHg at the end of

the study. Flucuations did occur at varying widths of the

balloon indicating a variance of pressure with finger size,

but it did not vary more than lOmmHg. Utilizing subjects as

their own control offset this problem, as the pressure would

be the same for the same finger size.

Each subject was tested twice, once with the

intervention and once without. To prevent carryover of pain

or pain produced neuromodulators, a resting period was

inserted between the two testing times. Mediating

neuromodulators may be neurotransmitters or neurohormones.

Neurotransmitters are degradated in within a short time.

Neurohormones are degraded to near normal levels within a 30

minute time frame (Fredrickson & Geary, 1982). For the

purposes of this study a 20 minute resting period between

testing times was used.

Large primary afferent fiber stimulus. According to

the Gate Control Theory the stimulation of large primary

afferent fibers modulates pain perception. The method

employed in that stimulation is detailed.

Large primary afferent fibers, Alpha a and alpha B, are

found in muscle sheaths and tendons (Guyton, 1986).

Stimulation of these fibers can be accomplished by movement

of the muscle group. The bicep muscle was selected due to

location in the same dermatome as the intervention. Subjects

were asked to flex the bicep of the non-dominant arm during

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the intervention testing. The arm was rested on a soft

surface at mid-chest height during the control testing

period.

To prevent stimulation of noxious muscle receptors the

intervention was self-paced by the subject. However, all

subjects maintained a near one per second movement rate

naturally. The testing arm was rested on a soft towel during

the procedure to prevent stimulation of noxious receptors

from the hard surface of the table.

Dependent Variables; Time to Tolerance. McGill Verbal

Descriptors, McGill Pain Rating Index, and Visual Analog

Scale

To measure the influence of LPA stimulation on pain

perception the time to tolerance was measured. As additional

indicators, the McGill Pain Questionnaire with a Visual

Analog Scale were also used.

Time to tolerance. Time to tolerance was measured as

the time, in minutes, from initiation of the pressure

stimulus to the time the subjects report they no longer can

endure the pain. Procedures altering the pain perception

are expected to alter the time the subject tolerates the pain

(Chapman et al, 1985). For the purposes of this study,

subjects were instructed to stop the procedure when they felt

they no longer wished to continue. The maximum time allowed

for the pain producing procedure was 20 minutes for each

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testing time. Twenty minutes would not result in tissue

damage from pressure, but would allow for development of pain

(Guyton, 1981).

McGill verbal descriptors. The Gate Control Theory has

indicated a change in the perception of pain at higher

brain centers. In order to measure the affective componet of

pain, the McGill Pain Questionnaire was selected. This tool

was developed by Melzack and Torgerson in 1971 (Melzack,

1975a) to specify the qualities of pain perception. One

hundred and two words were classified into 3 major classes

and 16 subclasses. The classes contained sensory, affective,

or evaluative words (see Appendix D for pain tool). Words

within the subclasses are ordered by intensity. The first

page of the questionnaire has questions of demographic

information and history of pain.

This tool has been widely used to measure and describe

experimental and clinical pain (Melzack, 1975a; Reading,

1984; Turk, Rudy, & Salovey, 1985). Reliability of the tool

was established by multiple utilizations over time (Melzack,

1975a; Reading, 1984). Turk, et al . (1985) reported a .84

internal reliability for the tool. Words selected by

subjects reflected the general selection and subgroups of the

McGill Questionnaire. The validity of the scale has been

confirmed both for subgroup distinction and correlations with

other measuraments of pain perception (Melzack, 1975;

Reading, 1984; Turk et al, 1985). The pain tool including

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verbal descriptors, pain rating index, and visual analog

scale was administered immediately after the control and

intervention pain stimulus testings. For the purposes of

this study, the verbal pain desciptors and pain rating index

were used. The words in each subclass were numbered with one

indicating the least severe word. The verbal subclasses were

then summed for a total score.

McGill pain rating index. The McGill tool includes a

five word summary scale. Each word is scored one to five,

with five indicating intense pain. The reliablities for this

scale were tested with the total McGill and a sum reliability

of .84 was reported (Melzack, 1975a; Turk et al., 1985).

Visual analog scale. An additional pain level indicator

was sought to add a visual dimension to the measurement of

the pain produced. Time to tolerance may not reflect the

perceived intensity of the pain. A Visual Analog Scale (VAS)

has been used both alone and with other measures to indicate

the level of pain perceived. The VAS consists of a line

with end point identifications of maximum and minimum points.

The subject is asked to indicate a point along that line that

relates to the intensity of the pain. It has been suggested

that linear scales with no artificial divisions are

preferable to sectionally divided scales (Scott & Hutchinson,

1976). Woodforde and Merskey (1972) and Reading (1984)

found correlations of .60 between visual analog and verbal

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report measures of pain. Scott and Hutchinson (1976) found

the VAS eight times as sensitive to changes in pain

perception as verbal scales. Kremer, Atkinson, and Ignelzi

(1981) demonstrated the VAS scores were reliable over time,

sensitive to pain change, and did not force certain choices

as verbal scales did. Criticisms of visual analog scales

have centered on their inability to reflect the sensory

component of pain (Chapman et al, 1985; Reading, 1984)(see

Appendix D). The scale was divided into thirty increments

for analysis.

Intervening Variables

Measurement of state anxiety. Pain has been described

as an affective feeling as well as sensory experience. One

of the emotions that has had a demonstrable effect on pain

perception is anxiety. Bronzo and Powers (1967), and Bowers

(1968) demonstrated that anxiety lowered the pain threshold

to electrically stimulated pain. Graffenfried et al, (1978)

reported a similar increase in pain sensitivity to ischemic

pain with increased anxiety.

Anxiety was measured by the A-State Anxiety Scale of the

State-Trait Anxiety Inventory (STAI). State anxiety

fluctuates in response to situational stressors (Spielberger

et al, 1970). The STAI was administered to each subject

prior to pain stimulus procedures. Subjects were instructed

to fill out the questionnaire in response to how they felt at

the time. The STAI was utilized to measure the influence of

anxiety on time to tolerance and verbal report scores. The

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The A-State Anxiety Scale is a self-report, 20 item, Likert

type scale. The scores on the items were summated for each

subject for an anxiety index score. Low scores reflected low

state anxiety.

Spielberger measured state and trait anxiety as separate

dimensions, although reactions to stress measured by state

were affected by the subjects trait levels (Spielberger et

al., 1970). Allen and Potkay (1981) discussed the

interaction of state-trait influences. They felt that state

and trait were not only dependent on the perception of the

situation by the investigator, but that the two concepts were

so interwoven as to be inseparable. Zuckerman in 1983

reputed that argument citing several of his own studies to

support a separate state-trait measurement.

Spielberger et al. (1970) validated the tool by testing

in several stress situations. Results of these tests allowed

distincions of differing anxiety levels with associated

stress situations. Spielberger reported reliablility

coefficients of .93 with both working and college women 19 to

39, .94 for working women 39 to 49, and .90 for working women

50 to 69 with the A-State tool. Test-retest reliabilities

were .27 to .31 reflecting the changing nature of state

anxiety.

Measurement of locus of control. Rotter (1982) proposed

that people develop expectancies of whether positive outcomes

are based on internal or external forces. Rotter developed a

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scale to measure individual expectancy of personal control.

Hersch and Scheibe (1967) tested the Rotter I-E tool. They

found test re-test reliabilities of .72, comparable to those

of Rotter (1966). Correlation scores for the I-E with other

measures were significant.

Kanfer and Seidner (1971) reported higher noxious

stimuli tolerance in subjects who had perceived control over

the experiment. Craig and Best (1977) validated the

relationship of locus of control and pain by an experiment

with electrical shock and measurements of Rotter I-E scores.

Significant differences were found with internal high scorers

tolerating more noxious stimuli.

Rotter's original tool was modified by Nichols in 1983

to measure perception of internal and external control of

pain. The tool is a 25 item Likert type scale with 5 choices

from strongly agree to strongly disagree. Nichols reported a

reliability of .81 and .85 for this tool. Items were scaled

1 to 5 for analysis (see Appendix C).

Procedures

Sample selection. Subjects were obtained in a variety

of ways. First, faculty in the school of nursing were

approached for permission to address their classes. If

permission was granted the students were the read Student

Form (see Appendix A). Those students consenting to

participate were asked to contact the school of nursing or

leave information on the form for follow-up. All Student

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Forms were collected after read. Faculty at the university

were approached individually as potential subjects. Finally,

registered nurses in a community hospital were approached

(see Appendix A) by form letter. Those consenting to part

lpate were asked to contact the investigator through a form

letter for an appointment.

Data collection. Testing sites were small rooms at

Indiana University and the community hospital. Plain drapes

covered the windows. The investigator was seated to the side

of the subject and did not move or distract the subject

during testing.

Data collection procedure was as follows:

1. Subjects were seated in a comfortable chair

with a chest high table in front of them.

2. Subjects were asked to draw a number from a

container to be assigned to group 1 or 2.

Control and intervention session

presentations were reversed with group 2.

3. Subjects were given a booklet containing the

instructions for that group.

4. Subjects were instructed to inform the

investigator if any of the following items

pertained to them: diabetes,arthritis,

peripheral vascular disease, peripheral

neuropathy, medications for pain,

medications that effect coagulapathy,

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treatment for psychiatric disorder,

or poor general health.

5. Subjects were instructed to read and sign the

consent form in front of them. Any

questions about the form would be answered.

6. Subjects were instructed to fill out the

Self-evaluation questionnaire. They were

to think about how they felt about

experiencing pain as they filled out the form.

7. Subjects were instructed to fill out the

Nichol's locus of control questionnaire.

8. (A towel was placed under the subject's

non-dominant arm.) Subjects were instructed

to indicate when they were ready to proceed

with the experimental testing. A finger clip

was placed on the index finger of the

subject's non-dominant hand. During control

sessions subjects were instructed to leave

the arm resting on the table in a relaxed manner

and not to rest the finger clip on the table.

During intervention sessions they were instructed

to move the arm by flexing at the elbow, bringing

the hand up towards the face. They were to

continue flexing until they reached their

tolerance point for the pain.

9. Subjects were asked to say ,,stopl,when they

felt they had reached their tolerance point

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for the pain, and the investigator would

remove the clip. Subjects were told not to

remove the clip themselves. Subjects were

asked to concentrate on the sensations

produced by the pressure.

10. Subjects were instructed to complete the

Revised McGill Pain Questionnaire, describing

the sensations they felt during testing.

A list of definitions was available on the

table for reference, if needed.

11. There was a 20 minute break. During this

break subjects could not leave the room,

smoke, or eat. Water was available.

12. After testing subjects were asked if they

had used any cognitive method to control

the pain.

13. Subjects were thanked for their

participation at the end of testing.

Data analysis. Data were analyzed by use of SPSSX and

BMDP statistical software. Descriptive statistics were

obtained. Reliabilities were measured for the A-state

anxiety tool, Nichols' locus of control tool, and the McGill

verbal descriptor tool. A correlation matrix for all

measures was obtained. Age scores were divided at 33% and

67% for grouping as low, medium, and high . State anxiety

scores were divided at 33% and 67% population scores for

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grouping as low, medium, and moderately high scores. Locus

of control scores were divided at 33% and 67% of the

population for grouping as internal, central, and external.

Age, anxiety and locus of control variables were analyzed by

ANOVA with the dependent variables. The hypothesis was

tested utilizing ANOVA with repeated measures with control

for order of presentation.

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CHAPTER IV

Findings and Discussion

The findings of the study are presented and discussed in

this chapter. Included in this section are analysis of pain,

age, anxiety, locus of control, and hypothesis testing. The

findings are presented first, followed by a discussion of the

findings.

Findings

Findings will be presented in the following order: (1)

measure of pain, (2)intervening variables, (3) hypothesis

testing, and (4) summary of findings.

Measure of Pain.

This study examined the effect of an intervention on the

subject's perception of pain. It was therefore necessary to

establish that the pain producing procedure was painful to

the subjects. As the pain producing instrument had not been

previously tested, acknowledgements of pain sensation were

established within the study. No subject denied pain.

Reports varied from "irritating" to "unbearable". No

subjects indicated a "0" score on the visual analog scale, a

rating of "no pain". Of the verbal descriptors of the McGill

Pain Questionnaire, the most frequently chosen items were

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throbbing, pinching, aching, annoying, and squeezing. These

terms describe the aching pain associated with C-fiber

activation (Collins, et. al., 1960; Torebjork, & Hallin,

1973).

Intervening Variables.

Age. Due to the wide age range of the subjects, 21 to

52, M = 37.16, modes = 34 and 43, analysis of pain by age was

performed. An analysis of variance was performed. Age was

divided at one-third and two-thirds percentage levels.

Categories were created with young (21-32), mid-range (33-45)

and middle age (46-60). The analysis revealed no

significant differences in time to tolerance, McGill Pain

verbal descriptors, pain rating index, or visual analog

scale scores for the control or intervention procedures.

Anxiety. Anxiety has been implicated as an influence on

the perception of pain and was, therefore, considered as a

possible intervening variable in the study. Anxiety was

measured using the A-State Anxiety tool of the STAI. The

tool was administered after descriptive information was

obtained and before the locus of control tool. Internal

consistency reliability of the instrument was examined

utilizing the Cronbach Alpha. The alpha was .93. This was

the same as the alpha reported by Spielberger, et al. (1970)

for working women 19-38.

Scores from the A-State tool ranged from 21 to 77

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(possible range 20-80), a mean of 40.5, and a S.D. of 11.7.

There was a single score of 77, with the next lowest score

58. Low scores indicated low anxiety. The effect of anxiety

was tested utilizing a one-way analysis of variance.

Anxiety was divided into one-third percentage levels for

analysis. Categories of low (21-33), medium (35-42), and

high (42-77) were created. No significant difference was

found for time to tolerance, McGill verbal descriptors,

McGill pain rating index, or visual analog scale in the

control or intervention groups. Scattergram analyses were

performed to examine the relationships. The scattergram

revealed a non-linear relationship between anxiety and the

pain measures. Small sample size may have altered the

significance of the relationship.

Locus of control. The review of the literature revealed

perception of control as an influence on pain perception.

Locus of control was; therefore, considered as a possible

intervening variable in the study. Locus of control was

measured by the Nichols' specific expectancy tool for pain

(Nichols, 1983). The tool was administered after the A-State

tool and prior to pain testing. The reliability of the tool

was assessed by use of the Cronbach Alpha. The initial alpha

was .76. Items were then deleted that had a reported

corrected item-total correlation of <.20, resulting in an

alpha of .84. This was consistent with Nichols’ alphas of

.81 and .85. Scores for the locus of control tool had a

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range of 47-84 (possible of 24-120), M = 64.0, and a S.D. =

8.36. High scores were indicative of an externally oriented

locus of control. The effect of the locus of control

variable was tested by an analysis of variance. No

significant difference was found for time to tolerance,

McGill verbal pain descriptors, McGill pain rating index, or

visual analog scale in the control or intervention groups.

Scattergrams were performed to analyze the relationships.

Scattergram analyses revealed a non-linear relationship

between locus of control and the pain measures. Small sample

size may have altered the significance of the relationship.

Locus of control and anxiety were found to have a r(29) =

-.49, p = <.05.

Order of presentation. The pain stimulus was

introduced twice during the testing with a 20 minute interval

between tests. It is possible that a carry-over effect of

pain sensation or modulation could effect the second testing.

Order of presentation effect was counteracted by randomly

deciding whether the intervention was offered during the

first or last time pain was presented (30 subjects in each

group). This variable was also controlled for in the

statistical analysis used for hypothesis testing.

Hypothesis Testing.

The null hypothesis tested was that there would be no

sigificant difference in time to tolerance or pain perception

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. between the control and intervention groups. Separate

ANOVA's were completed to test pain perception as measured by

the four indicators of pain; the McGill pain questionnaire

verbal descriptors, McGill pain questionnaire pain rating

index, the visual analog scale, and time to tolerance

variable. The hypothesis was tested by two-way analysis of

variance with repeated measures for all four pain perception

measures. The analysis considered order of presentation as a

possible intervening variable and found no significant

influence by presentation order with the dependent variables.

As indicated in the methods section, four pain measures were

implemented to study the range of sensory and affective

perception.

Time to tolerance. Time to tolerance scores for the

control group had a M = 14. 4 minutes with a S. D. = 6. 80 and

a— -ranc----o p of 2 to 20 , whi ch was sig nif icantly different from

the int ervention group M = 16 .1 minutes with S. D. = 5 .76 and

range of 3 to 20. The resu It s of time to tolerance te stin 8

allowed for the re j e c t ion of the null hypothesis; subj ects in

the intervention group were able to tolerate the stimu lus

longer than those in th e co nt rol gro up (see Tables 1,2 ).

A ceiling eff ect was created by 16 of the control (N=30)

and 17 of the inte rvent ion (N=30) 8roups completing the 20

minute interval. There is no way to estimate how long the

subject s who compl eted the 20 minute interval could ha ve

continu ed.

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McGill Verbal Descriptors. The McGill scores were

assessed for reliability by Cronbach Alpha. The control and

intervention data were analyzed separately and both had

alphas of .89. The McGill verbal descriptor scores had a M =

21.4, SD = 12.24,and range of 3 to 54 for the control group,

which was signifcantly different from intervention group M =

17.8, SD = 11.60,and range of 2 to 46. Scores were obtained

by numbering the rank of a word within the group and adding

the totals for words selected. If no word was selected

within a group, a 0 was indicated. The results of this test

were significant and thus, permitted rejection of the null

hypothesis. Subjects in the intervention group selected

fewer and less severe descriptors than the subjects in the

control group (see Tables 1,2).

Pain rating index. The McGill pain rating index

produced a M = 2.23, SD = .679, and range of 1 to 4 for the

control group, which was significantly different from the

intervention group M = 1.90, SD = .662, and range of 1 to 3.

The five words were numbered 1 to 5 in increasing intensity.

The analysis permitted the rejection of the null hypothesis.

Subjects in the intervention group selected words indicating

less pain than the subjects in the control group (see Tables

1,2).

Visual Analog Scale. Visual analog scores reported a M

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= 12.2, SD = 7.07, and range of 1 to 28 for the control

group, which was significantly different from the

intervention group M = 9.8, SD = 6.13, and range of 1 to 23.

The scale was divided into 30 increments in increasing pain

intensity (0 = no pain, 30 = unbearable pain). The analysis

permitted rejection of the null hypothesis. The intervention

group indicated less severe pain than the control group (see

Tables 1-2).

Table 1 Summary of Results for ANOVA with Repeated Measures on Second Factor for the Pain Variables

Variable Source df MS F Prob

Tolerance Order 1 38.40 0.53 .47 Intervention 1 38.40 4.66 .04 Error (within) 28 72.40 Error (subjects) 28 8.23

Verbal Order 1 365.07 1.46 .24 Intervention 1 194.40 7.91 .009 Error (within) 28 249.75 Error (subjects) 28 24.57

Rating Order 1 1.67 2.45 .13 Intervention 1 1.67 10.94 .003 Error (within) 28 .68 Error (subjects) 28 .15

Visual Order 1 260.42 3.78 .06 Intervention 1 88.82 10.30 .003 Error (within) 28 68.82 Error (subjects) 28 8.62

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Table 2 Cell Means and Standard Deviations for ANOVA 's

Variable Group M-S.D. Control Intervention

Tolerance 1 M 15.80 16.33 SD 6.06 5.27 2 M 13.13 15.80 SD 7.44 6.43

Verbal 1 M 17.1 17.20 SD 9.46 12.58 2 M 25.73 18.47 SD 13.47 10.93

Rating 1 M 1.93 1.87 SD .59 .74 2 M 2.53 1.93 SD .64 .59

Visual 1 M 8.80 9.07 SD 6.18 5.97 2 M 15.67 10.53 SD 6.32 6.41

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Pearson Correlation of Pain Measures

As indicated in the methods section four pain measures

were implemented to study the range of sensory and affective

perception. A Pearson correlation analysis was performed to

examine the relationships between the pain measures. The

pain measures did correlate in the direction anticipated,

with low tolerance correlated to high pain perception scores.

The pain rating index did not correlate with the time to

tolerance (r=-,10 to -.24), but did with the VAS (r=.48 to

.76). Only the visual analog scale significantly correlated

with time to tolerance. Moderately high correlations (.59

to .80) were found between control and intervention groups in

each pain measure (see Table 3).

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Table 3

Pearson Correlation for Measures of Pain

Variable Time Verbal Rating Visual

Control - Intervention

CI CI CC

Time-C

Time-I .80* i o • Verbal-C -.07 vO

Verbal-I -.00 -.19 .79*

Rating-C -.17 -.10 .50* .31*

Rating-I -.10 -.24 .13 .40* .59*

Visual-C -.19 -.32* .54* .40* .76* .60*

Visual-I -.15* -.37* .31* .56* .48* .73*

* p<.05

Note: Time = Time to Tolerance

Verbal = McGill Verbal Descriptors

Rating = McGill Pain Ratin Index

Visual = Visual Analog Scale

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Summary

The study attempted to measure pain perception. Pain

measurement tools indicated all subjects perceived the

stimulus as painful. The selection of descriptors indicated

C-fiber activation, the type of pain targeted for modulation

by the Gate Control Theory.

Age, anxiety, locus of control, and order of

presentation have been indicated as intervening variables in

pain perception. Age, anxiety levels, and locus of control

orientation were measured prior to stimulus testing. The

variables did not produce significant differences in any of

the measures.

The null hypothesis that there would be no significant

difference between the control and intervention groups in

time to tolerance was rejected. All measures of pain

perception reported significant differences between the

control and intervention groups. The intervention group was

able to tolerate the pain stimulus longer and selected less

severe pain indicators than the control group on all

measures,

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Discussion

This discussion relates findings to the use of physical

activity as a means of large primary afferent fiber

activation in accordance with the Gate Control Theory of

Pain. All measures of pain tolerance and perception

produced indications of reduced pain with muscle movement.

Physical activity by moving muscle groups activates large

primary afferent fibers. Based on the Gate Control Theory of

Pain, large primary afferent fiber activation should inhibit

the rostrad transmission of pain impulses from the spinal

cord dorsal horn. This study tested a proposition of the

Gate Control Theory, pain perception inhibition by large

primary afferent fiber stimulation.

Pain measurement is limited to the perception of the

individual. There is no method of objectively analyzing

pain, except by report or behaviors of the subjects.

Analysis of these results depends upon the report of the pain

perceived by the individuals in the study. Naivete to the

anticipated result of the study by subjects was assumed. The

method of pain stimulation was a simple pressure device.

Although the device produced pain in all subjects and

appeared to produce the same pressure in all subjects,

variations in subject finger size may have affected results.

Pain Measures.

Four pain measures were obtained to reflect differing

aspects of pain perception. The time to tolerance measure

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would reflect a gross indicator of the degree of

unpleasantness of the experience. The pain rating index is a

similar tool. The McGill verbal descriptors were included to

measure the change in character of the sensation. Although

time to tolerance may be the same, the affective-cognitive

sensation may change. The Visual Analog Scale (VAS) was

included to add a visual conceptual 17tion to the pain

experience.

All four measures of pain allowed for rejection of the

null hypothesis. THe subjects in the intervention procedure

tolerated the pain longer, selected less severe pain verbal

indicators, choose lower pain rating indicators, and

indicated less severe pain on the visual analog scale than

subjects during the control procedure. A ceiling effect was

found with the time to tolerance measure in both control and

intervention procedures. This not only did not permit a full

exploration and measurement of tolerance, but precluded

measurement of full perception on the other tools. No

estimate of the perception that would have been encountered

with full tolerance was permitted.

A Pearson correlation was obtained to evaluate the

similarities of measurement from the scales. In the

correlation analysis, less pain perception correlated

negatively with lower tolerance times. Control and

intervention groups correlated at moderately high levels to

indicate similar measurement, but a difference obtained from

the intervention. The pain rating index did not correlate

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. well with any other measure or between its two groups (r=

.59). Only the VAS was significantly correlated with time to

tolerance. The finding indicates that the sensory sensation

is separate from the affective-cognitive perception. The

highest correlations were the VAS and pain rating index (.48

and .76), indicating similar measurement of gross sensation.

The Pearson correlation analysis would have also been

affected by the ceiling effect on time to tolerance. The

correlations might have been altered by changes in perception

with increased tolerance.

Indications are that no reasonable limit will allow for

a full range of time to tolerance. If an increased pain

stimulus is utlilized, subjects in the low tolerance range

will not have measureable times. Indications are that the

McGill verbal descriptors and visual analog scale would be

the most accurate measures of pain and would allow for

sensory and affective componets to be measured.

Intervening Variables.

Extraneous variables were identified as age, anxiety,

locus of control, and order of presentation. None of these

variables was found to influence pain perception. The age

range should not present a physiological effect, but could

have cognitive-emotive significance as an indicator of pain

experience. The selection of a homogenous sample in a low

anxiety laboratory situation could have led to the lack of

significance of anxiety. The subjects were informed of their

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ability to stop the experiment at any time and the pain

experience had no secondary meaning; permanent damage, loss

of income, or monetary loss. The anxiety score mean was

well within the low anxiety range (<50), although one subject

did report a very high score (77). Locus of control scores

were slightly internal, as might be expected in a sample of

working women and college students. There was a significant

correlation between anxiety and locus of control (r= -.49).

Further studies in clinical pain may reveal a relationship

between anxiety and locus of control. The reliabilities of

the A-State Anxiety tool of the STAI and Nichols' Specific

Expectancy tool for locus of control were supported by the

highly acceptable Cronbach alphas reported. This supports

the utilization of these tools in further studies. Order of

presentation 40s controlled for in the study design and

analysis.

The non-linearity of the relationship of anxiety and

locus of control with the pain factors warrants further

investigation. Anxiety has been shovrn to be non-linear with

pain, but not locus of control. Muscle movement may impact

the perception of control in interaction with increasing

pain.

It is possible that other variables contributed to the

pain perception experience. Influences of distraction,

cognitive control, or perception of the study could have

influenced the results. A wider search for intervening

variables may reveal other modifying influences.

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Summary. The study supported further investigation of

physical activity as an intervention for pain. Large primary

afferent fiber for alteration of pain transmission as a

proposition of the Gate Control Theory was supported. Of the

pain measures utilized, the verbal descriptors and visual

analog scale proved most effective. The ability to tolerate

the pain stimulus for the maximum time interfered with full

tolerance investigation.

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CHAPTER V

Summary, Conclusions, and Recommendations

Summary.

The purpose of this study was to investigate the effect

of physical activity on p.\in tolerance and pain perception.

The application of physical activity as a pain intervention

was suggested by clinical observation and propositions of

the Gate Control Theory. The propositions of the Gate

Control Theory have stated:

1. Injury results in stimulation of small primary

afferent fibers.

2. Transmission of peripheral information is

facilitated or inhibited within the spinal

cord by a gating mechanism.

3. Large fiber input inhibits transmission of

nociception and small fiber input facilitates

transmission.

4. Cognitive-emotive processes influence the

modulation within the dorsal horn.

From these propositions two experimental proposals were

drawn:

1. That stimulation of large primary afferent

fibers will decrease the transmission of

noxious stimuli to supraspinal areas.

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2. That emotional and cognitive responses

modulate dorsal horn activity through

descending influences.

From clinical reports, physical activity was indicated

as a pain relief measure. Support for the intervention came

from the propositions of the Gate Control Theory. The review

of literature supported an investigation of this intervention

from neurophysiological review, previous applications of the

Gate Control Theory, and previous applications of physical

activity as a pain intervention.

Neurophysiological support for the Gate Control Theory

propositions is indicated by:

1. Pain stimuli activate small primary afferent

fibers.

2. Muscle and tendon movements activate large

primary fibers.

3. Large and small fibers terminate in the

substantia gelatinosa of the dorsal horn.

4. Stimulation of large primary afferent fibers

was shown to inhibit transmission from

nociceptive neurons in the spinal cord.

5. Muscle movement was shown to release

enkephalin, an inhibitor of substance P,

a neurotransitter in the dorsal horn.

Previous applications of large fiber stimulation were

electrical stimulation, including TENS, vibratory

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stimulation, touch, and acupuncture. Although there is some

disagreement on the mechanism of inhibition, these mechanisms

are assumed to be based on the Gate Control Theory. Each of

the mechanisms have been reported to be effective as a pain

inhibitor.

Physical activity as a pain intervention has not been

widely tested. Only two studies were found relating to the

implementation of muscle stimulation. Read et al. (1981)

focused on pain as a secondary factor to labor progression in

a comparison of ambulation and oxytocin. All patients in the

ambulatory group reported less pain, despite progression of

labor. Langyan and Shaoying (1985) investigated muscle

movement as an intervention to augment acupuncture

treatments. Pain was induced in the hand. The intervention

group moved the wrist and the control group held the hand

still. Significant reduction of pain was noted. Further

analysis of physical activity as a pain intervention is

indicated by these studies.

The second proposal drawn from the Gate Control Theory

indicates supraspinal influences on pain perception.

Supraspinal descending influences were indicated by:

1. Establishment of tracts transmitting

nociceptive information to the reticular

formation, thalamus, and cortex.

2. Demonstration of facilitation and inhibition

of transmission from dorsal horn nociceptive

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neurons following supraspinal stimulation.

3. Demonstration of inhibitory properties of

opoids,serotonin, and norepinephrine on

pain perception.

4. Proposed interactions of the cortex, PAG/PVG,

nucleus raphe magnus and locus coeruleus

in descending inhibtory pathways.

Two cognitive-emotive supraspinal influences indicated

in the review of literature were anxiety and locus of

control. Anxiety has been shown to decrease pain tolerance.

Internal locus of control has been associated with higher

pain tolerance.

The influence of physical activity as a pain

intervention was tested by use of a pressure device. The

device was placed on the index finger of the non-dominant arm

of each subject. Time to tolerance was measured. The

subjects then filled out the McGill Verbal Descriptor

Questionnaire, McGill Pain Rating Scale, and a visual analog

scale. The subjects were then tested again for time to

tolerance and filled out the questionnaires. During the

control testing they were requested to rest their arm on the

table and during the intervention testing they flexed the

elbow.

The review of literature indicated two possible

supraspinal influences on pain perception, anxiety and locus

of control. These influences were considered as possible

intervening variables in the study. Anxiety was measured by

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the use of the STAI A-State Anxiety Tool. Locus of control

was measured by Nichols' specific expectancy tool for pain.

Previous studies had indicated order of presentation as

an intervening variable in pain perception. Subjects were

randomly assigned to one of two groups with alternate

sequencing of control and intervention testing.

The experience under consideration was pain perception.

The stimulus was validated as painful by analysis of the pain

ratings and verbal descriptors selected by the subjects of

the study. The subjects indicated the type of pain

identified with C-fiber activation.

Anxiety as an intervening variable was evaluated by

statistical analysis. The subjects indicated a low level of

anxiety and no significant difference in pain tolerance or

perception was found due to anxiety levels. The non-linear

relationship between anxiety and the pain measures is an area

for future exploration with a larger sample.

Locus of control as an intervening variable was

evaluated by statistical analysis. The subjects indicated a

slightly internal locus of control orientation. No

significant difference was found in pain perception or

tolerance due to locus of control levels. The non-linear

relationship between locus of control and the pain measures

is an area for further investigation with a larger sample.

The correlation between anxiety and locus control should be

analyzed further.

Order of presentation was considered as an intervening

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variable. Statistical analyses of the scores for time to

tolerance and pain perception were structured to analyze the

influence of order of presentation. No significant

difference was found due to order.

The null hypothesis was tested by an analysis of

variance with repeated measures design. The hypothesis was

rejected by all four measures of pain perception: Time to

tolerance was significantly longer for the intervention

group, the intervention group selected fewer and less intense

word descriptors from the McGill verbal descriptors, the

intervention group had significantly lower scores on the

McGill pain rating index, and the intervention group

indicated significantly lower scores on the visual analog

scale.

Conclusions

The results of this study have supported the Gate

Control Theory proposition of pain inhibition by large

primary afferent fiber stimulation. The Gate Control Theory

has been supported through numerous studies. This study adds

to that knowledge by exploration of a another pain

intervention based on the theory. The use of physical

activity has been supported as a effective method of LPA

stimulation. LPA stimulation has been explored in the past

through the use of massage, TENS, vibratory stimulation,

touch, and acupuncture. Further investigation of physical

activity as a method of LPA stimulation is supported.

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The study results support further investigation of

physical activity as a pain intervention and the addition of

physical activity to the repertoire of nursing interventions

for pain. Support for this conclusion is derived from the

knowledge that; (1) physical activity is a natural human

operation that requires no extra equipment or personnel, (2)

the intervention is within the realm of nursing activity and

requires no specialized training, (3) the client can be

taught home interventions specific to their situations, and

(4) the intervention can be used in conjunction with

pharmacological and other modalities of pain treatment.

Recommendations

Based on the findings of this study the following

investigations are recommended:

1. This was the only study found to directly test physical

activity as a pain intervention. Therefore, replications

with different samples are indicated.

2. The pressure device utilized in this study was a simple

instrument which did not control pressure on an individual

basis. Replication of the study with a more sophisticated

pressure algometer is indicated.

3. One of the supraspinal influences that may alter pain

perception is distraction (Barber & Cooper, 1972). The

movement of the arm during testing may serve as a distracting

influence. Studies utilising a distractor in the control

group should be initiated.

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4. Studies have indicated possible contralateral inhibitory

influences of LPA stimulation. Based on the success of this

study, studies utilizing contralateral movement are

indicated.

5. No effort was made to determine the optimum rate of

movement to produce inhibition. Studies should be conducted

which identify the relationship between rate of movement and

pain inhibition.

6. This study did not address the phenomena of pain

inhibition following termination of intervention. There is a

need to investigate the length of inhibition produced by

various intervals of movement.

7. Although no difference was found in pain perception due

to anxiety levels in this study, this may be reflective of

the sample selection and testing situation. Studies with a

mechanism for introduction of anxiety to the testing are

indicated.

8. Locus of control was indicated as a possible intervening

variable. No alteration in pain perception from the

influence of locus of control was indicated in this study.

This may reflect the sample selection and subject control in

the study methodology. The need for studies utilizing the

introduction of various control levels is indicated.

9. This study collected data in a laboratory setting with

artificially induced pain. There are clinical settings, such

as labor and delivery, in which patients with pain experience

muscle movement. Studies of these natural clinical settings

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are indicated.

10. A multivariate analysis 18the pain measures and

intervening variables is recommended, because the four

indicators apparently measure slightly different aspects of

the pain sensation.

Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 9 3

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state scales is not arbitrary: comment on Allen and Potkay's "On the arbitrary distinction between state and traits". Journal of Personality and Social Psychology, 44(5), 1083-1086.

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Paricipation Announcement

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Participation Announcement: My name is Martha McDonald. I am a graduate student in the doctoral program of the Indiana University School of Nursing. I am conducting a study to investigate an intervention which may be effective for the care of persons with acute pain. Your taking part in this study would allow me to test the usefulness of the intervention in a controlled laboratory situation. If the intervention is successful, it can then be tested with patients with acute clinical pain. If you agree to take part in the study, you will be asked to experience an experimental pain producing procedure which is expected to cause discomfort in your hand. A pressure transducer finger clip will be attached to the index finger of your non-dominant hand. The discomfort should increase over time. You will be free to end the procedure at any time you feel you have reached your tolerance point for the procedure, regardless of the amount of discomfort you are feeling. The intervention for this study consists of flexing your bicep muscle. During the session the clip will be placed on your finger and left until you request its removal or twenty minutes have elapsed. After a 20 minute rest the clip will again be placed on your finger. One time you will experience the intervention and one time you will not. The experiment will last approximately one hour. Each testing will last for twenty minutes if you do not feel the need to have the clip removed before then. You will be asked to complete two short questionnaires before the testing and one questionnaire after each testing. Other than the discomfort you will feel, there are no risks involved with the experimental procedure. The finger clip will not cause damage in a twenty minute time period. Blood flow should not be hampered by the clip. The discomfort should be relieved as soon as the clip is removed. I am not interested in how much discomfort you can take. You are free to stop the procedure at any time. I will remain with you during the testing times and will answer any questions you have at any time during the procedure. All result of the study will remain confidential. Your name will not be used at any time. Instead you will be assigned an identification number which will be used to identify all information resulting from your participation. I will be testing on Monday, Tuesday, Friday, Saturday, and Sunday during June and July. Please contact me at work or home for an appointment.

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Appendix B

Consent Form

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Consent Form Procedure explanation: Thank you for agreeing to participate in this study to investigate the effectiveness of a possible nursing intervention for people with acute pain. The experiment will take place in two parts which are exactly alike except that during one I will ask you to move your arm. Both times you will experience a procedure which is expected to produce discomfort in your non-dominant hand. The intervention consists of stimulation of the receptors of your arm by muscle movement. You will provide the stimulus by flexing your arm at the elbow to move the bicep muscle. It is important that the two testing times be as alike as possible except for the intervention. Therefore, you will lay your arm across the table during the time with no intervention. You will be asked not to move your arm during this testing time. Each session will last for no longer than twenty minutes, with a twenty minute rest period between times. You are free to end the procedure at any time before the end of the twenty minute testinf period, whenever you feel your tolerance for the procedure has been reached or for any other reason. You can get up an walk around the room between testing times, but I would like for you not to rub your finger or leave the room. Magazines are available to help you pass the time. Please refrain from eating or drinking anything but water between the testing times. Before you begin the experimental procedure, you will be asked to complete two short questionnaires about how you feel prior to the experiment. During the experimental procedure, you will be asked to sit comfortably at a table with yur non-dominant hand resting on the table top. I will place a small pressure clip on your index finger. You will be told if you are to leave your arm on the table or begin flexing your arm at the elbow with the upper arm resting on the table. Please do not move your fingers or hand during either test. You will be asked to pay attention to the sensations in your finger while the test lasts. Most people will begin to feel discomfort as soon as the clip is placed on their finger. The amount of discomfort usually increases over time. The clip will remain on until you tell me you want to have it removed or twenty minutes has elapsed. After each testing time you will be asked to fill out a questionnaire describing the sensations felt. Remember, you may end the procedure at any time you feel you have reached your tolerance or for any other reason. All information about you will be strictly confidential. Only I will know what occurred during the procedure.

"I have read the above and understand my role and rights in this study. I am willing to participate by experiencing the pain producing procedure and completing the questionnai T~es

Witness Investigator

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Nichols Locus of Control Tool

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Appendix C p. 113______

Appendix D p. 120

University M icrofilm s International 300 N. ZEEB RD.. ANN ARBOR. Ml 48106 (313) 761-4700

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Appendix D

Revised McGill Pain Questionnaire

Pain Rating Index

Visual Analog Scale

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