Western Michigan University ScholarWorks at WMU
Master's Theses Graduate College
4-1978
An Investigation of the Role of the Electrodermal Activity in Reduction of Snake Phobia
Mohammad Jaafar Behbehani
Follow this and additional works at: https://scholarworks.wmich.edu/masters_theses
Part of the Psychology Commons
Recommended Citation Behbehani, Mohammad Jaafar, "An Investigation of the Role of the Electrodermal Activity in Reduction of Snake Phobia" (1978). Master's Theses. 2071. https://scholarworks.wmich.edu/masters_theses/2071
This Masters Thesis-Open Access is brought to you for free and open access by the Graduate College at ScholarWorks at WMU. It has been accepted for inclusion in Master's Theses by an authorized administrator of ScholarWorks at WMU. For more information, please contact [email protected]. AN INVESTIGATION OF THE ROLE OF THE ELECTRODERMAL ACTIVITY IN REDUCTION OF SNAKE PHOBIA
By Mohammad Jaafar Behbehani
A Thesis Submitted to the Faculty of the Graduate College in partial fulfillment of the Degree of Master of Arts
Western Michigan University Kalamazoo, Michigan April 1978
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. ACKNOWLEDGEMENT
I wish to thank, in this space, a number of scholars entered
in conducting this research without whose help its fruit-
fullness would not have been fulfilled. I would like to
thank Professor Frederick P. Gault, who has generously
given guidance throughout my education years at Western
Michigan University, and in particular during the con
ducting and writing of this research. I would also like
to offer my appreciation to Professor Malcolm Robertson
and Arthur Snapper for their guidance and constructive
criticism on this project. And, I would like to extend
my thanks to Dr. Robert Freedman, Lafayette Clinic, Detroit,
and Dr. Alan Glaros, Wayne State University, Detroit, who
generously provided the computer facilities at the above
mentioned institutions. This research was in part supported
by a grant from Kuwait University, Kuwait, State of Kuwait,
to which I am indebted.
Mohammad Jaafar Behbehani
ii
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. INFORMATION TO USERS
This material was produced from a microfilm copy of the original document. While the most advanced technological means to photograph and reproduce this document have been used, the quality is heavily dependent upon the quality of the original submitted.
The following explanation of techniques is provided to help you understand markings or patterns which may appear on this reproduction.
1. The sign or "target" for pages apparently lacking from the document photographed is "Missing Page(s)". If it was possible to obtain the missing page(s) or section, they are spliced into the film along with adjacent pages. This may have necessitated cutting thru an image and duplicating adjacent pages to insure you complete continuity.
2. When an image on the film is obliterated with a large round black mark, it is an indication that the photographer suspected that the copy may have moved during exposure and thus cause a blurred image. You will find a good image of the page in the adjacent frame.
3. When a map, drawing or chart, etc., was part of the material being photographed the photographer followed a definite method in "sectioning" the material. It is customary to begin photoing at the upper left hand corner of a large sheet and to continue photoing from left to right in equal sections with a small overlap. If necessary, sectioning is continued again — beginning below the first row and continuing on until complete.
4. The majority of users indicate that the textual content is of greatest value, however, a somewhat higher quality reproduction could be made from "photographs" if essential to the understanding of the dissertation. Silver prints of "photographs" may be ordered at additional charge by writing the Order Department, giving the catalog number, title, author and specific pages you wish reproduced.
5. PLEASE NOTE: Some pages may have indistinct print. Filmed as received.
University Microfiims International 300 North Zeeb Road Ann Arbor, Michigan 48106 USA St. John's Road. Tyler's Green High Wycombe, Bucks. England HP10 8HR
V Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. MASTERS THESIS 13-11,379
BEHBEHANI, Mohammed Jaafar AN INVEST! GATT CN OF THE ROLE OF THE ELECTRQDERMAL ACTIVITY IN REDUCTION OF SNAKE PHOBIA.
Western Michigan University, M.A., 1978 Psychology, experimental
University Microfilms International,Ann Arbor, Michigan 48106
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. TABLE OF CONTENTS
CHAPTER PAGE
AN INVESTIGATION OF THE ROLE OF THE ELECTRODERMAL ACTIVITY IN REDUCTION OF SNAKE PHOBIA...... i
I PROBLEMS AND BACKGROUND 2- 5
II SECTION A. Phobias and Their Nature. . . . 6
Introduction...... 6 - 16
SECTION B. Classification of Phobias . . .17
Introduction...... 17-18
Animal Phobias...... 18-19
III ELECTRODERMAL ACTIVITY AND ITS BASIS. . . .20
Introduction...... 20-32
Pharmacologic Effects ...... 32-33
Current Density and Polarity...... 3^
Anatomical Differences...... 3^-35
Species Differences...... 35-36
EXPERIMENTAL METHODS AND FINDINGS ...... 36
Electrodes and Their Applications . . . -36-37
Size3 Preparation and Location of Site. .37 - 38
Current Strength...... 38-39
PHYSIOLOGICAL BEHAVIOR OF THE SKIN...... 39
Sweat Secretion ...... 39-^0
Epidermal Function...... ^0-41
iii
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER PAGE
Permeability and Water Solutes...... 41-44
The absorption Phenomenon...... 44
Neurophysiological Process and Behavior .44 - 48
IV "REVIEW OF LITERATURE"...... 49
SECTION A. Conditioning of Electrodermal .49
Background and Definition ...... 49-60
SECTION B. EDA as an Indexer of Phobia . .61
Background and Definitions...... 61-68
Electrodermal Activity as an Index of "Phobic" Responding...... 68-72
Imagery versus Direct Experience...... 72 - 93
V HYPOTHESES AND R A T I O N A L ...... 94-96
Hypothesis 1 ...... 96
Hypothesis I I ...... 96
Hypothesis III...... 97
Hypothesis I V ...... 97
Hypothesis V ...... 97
Hypothesis V I ...... 98
Hypothesis VII...... 98
VI METHOD...... 99
Design...... 99 -101
Sub j ects...... 101-103
Aparatus...... 103-106
P r o c e d u r e ...... 106-109
iv
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER PAGE
Experimental Treatment...... 109-110
Phase I (Training)...... 110-113
I n t e r v i e w ...... 114
Phase II (Testing)...... 114-118
Post-Treatment...... 118
VII RESULTS ...... 119
Skin Resistance Response...... 119-147
Tables 1 - 8 ...... 121-129
Tables 25-26 ...... 132-133
Figure 1 ...... 134-135^
Figure 2 ...... 137-138
Figure 3 ...... 139-140
Figure 4 ...... 142-143
Table 2 7 ...... 145
Heart Rate...... 147-172
Table 2 8 ...... 148
Table 2 9 ...... 149
Tables 9-16...... 151-159
Table 3 0 ...... 160
Figures 5-8...... 162-169
Table 3 1 ...... 171
Table 3 2 ...... 172
v
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER PAGE
Respiration Rates ...... 173-198
Tables 17-24 ...... 174-182
Table 3 3 ...... 183
Figure 9 ...... 185-192
Table 3 4 ...... 193
Table 35-37...... 195-197
BAT and Fear Thermometer...... 198-207
Tables 38-41 ...... 199-205
Table 42 ...... 207
VIII DISCUSSION AND CONCLUSIONS...... 208-220
APPENDIX A ...... 221-222
APPENDIX B ...... 223-224
APPENDIX C ...... 225-226
APPENDIX D ...... 227-228
APPENDIX E ...... 229-230
APPENDIX F ...... 231-232
APPENDIX G ...... 233-234
APPENDIX H ...... 235-242
BIBLIOGRAPHY...... 24 3-264
vi
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. AN INVESTIGATION OF THE ROLE OF THE ELECTRODERMAL ACTIVITY IN REDUCTION OF SNAKE PHOBIA
1
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER 1
Introduction
Problem and Background
Since Joseph VJolpe (1958) first described the recip
rocal inhibition principle as a method of training maladap
tive anxiety, its effectiveness has been demonstrated by
many therapists and researchers. Paul (1969 a) reviewed
fifty five different uncontrolled reports, consisting
largely of case histories or single group studies, and
found that definite success of systematic desensitization
therapy was reported in forty-six of fifty-five reports.
In his review of ten poorly controlled experimental studies,
Paul (1969 a) reported that in all ten systematic desensiti
zation was a more effective procedure than no treatment.
Furthermore, when Paul (1969 a) reviewed ten well designed
experimental studies six were poorly controlled, but pro
vided clear evidence to support the effectiveness of systematic
desensitization.
All of these positive studies followed Wolpe's gen
eral outline of systematic desensitization paradigm. How
ever, a close inspection of the procedures reveals wide
variation in actual application of the basic paradigm in
these studies and in even wider general body of the liter
ature on systematic desensitization. For example, training
of the muscle relaxation varied in the muscle groups included,
2
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 3
sequence of muscles, length of training, duration of ten
sion, duration of release, method of executing release and
number of cycles of tension and release. Variation also
existed in the construction of the hierarchy included,
different number of sessions given to this task, different
number of items in the hierarchy, and different types of
hierarchies. Sometimes the standard hierarchies were used.
The desensitization procedure itself varied in length of
time it was administered per session, the number of times
each item was presented, the length of intervals between
scene presentations, the number of items presented each
session, the way in which scenes progressed in a hierarchy,
and the criterion that was used to denote progress. Paul
(1969 h, pp. 151-153) summerized what he saw as the four
major "packages" of approach to these specific parameters,
as applied by four groups of investigators: Wolpe; Lazarus
and Rachman; Lang and Lazovik; and Paul and Shannon. Further
variations in effective application of systematic desensi
tization treatment in groups (Paul 1969 b, p. 131) and via
taped instructions (Donner and Guerney, 1969; Garlington
and Cotier, 1968; Migler and Wolpe, 1967) are well known.
More recent innovations include presentation of only part
of the hierarchy (Clark, 1963; Geer and Katkin, 1966; Suinn,
Edie, and Spineli, 1970), massing of sessions (Ramsay,
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. it
Barends, Breuker, and Kruseman, 1968; Robison and Suinn,
1969; Suinn, 1970; Suinn and Hall, 1970), and disregard
of signalling anxiety (Donner and Guerney, 1969; Suinn,
1970).
Thus, with so many variations in the systematic
desensitization treatment parameters accompanied by the
reported effectiveness of the treatment, the question
which can be proposed is: what components of this treat
ment account for its effectiveness? Lang (1969) thoroughly
reviewed the numerous experimental studies which examined
the separate elements of the desensitization procedure and
which assessed the theoretical explanations underlying
this treatment. He found the research lacking in any defin
itive results regarding the components and the theory of
desensitization. In his conclusion Lang stated that "...
the implication is that fear is a loosely woven fabric of
responses, which many edges where an unraveling process may
be initiated" (p. 190). He suggested "...that both the
organization of the fear responses and the order of their
change is idiosyncratic to the subject and perhaps to the
treatment method employed...", and furthermore, "...the
important therapeutic changes depend on training programs
designed to eliminate specific response components and to
interrupt mutually augmenting feedback between response
systems" (p. 190-191). His implication is that desensiti-
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 5
zation involves a more complex network of variables that
past analysis and theories have emphasized.
Furthermore, Lang (1969) suggested the relevance
of direct instrumental conditioning of automatic nervous
system activity for alleviation of fear responses. In his
review of the presumed mechanisms underlying reciprocal
inhibition, Lang noted that muscle relaxation is supposed
to effect the autonomic outflow. Lang’s notion is that
the role of autonomic activity in regulating and maintain
ing affective responses in other behavioral systems suggests
that it should be dealt with directly, rather that going
through the uncertain medium of muscle relaxation.
Recent research indicates that when appropriate
conditions are present, especially when those which employ
increased sensory feedback, human subjects can learn to
gain direct control of their autonomic activity (Katkin
and Murrya, 1968). This research is directed towards the
point of view of direct autonomic conditioning in investi
gating its role in alleviation of phobic responses.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER 2
Section A. Phobias and Their Nature
Introduction. The word ’fear’ derives its origin from the
Old English ’faer’ for sudden calamity or danger, and was
later used to describe the emotion of uneasiness caused
by the sense of imminent danger (OED). In Middle English
it continued to denote a state of alarm or dread, and does
so still today. Fear is a normal response to active or
imagined portent in higher animals, and comprises an outer
behavioral expression, an inner feeling, and accompanying
physiological changes (Landis, 1964).
Two of the most obvious behavioral effects of fear
present a striking contrast (Miller, 1951)* One Is the
propensity to remain motionless and mute, which in certain
animals reaches Its extreme form of death feigning. The
other is the pattern of startle, withdrawal, running and
vocalization. Both of these incompatible patterns seem to
be stimulated by fear, and behavior may shift rapidly from
one to the other, as when frightened animal first freezes,
then scurries for shelter.
Phobias are a special kind of fear. The term ’phobia’
derived from the Greek word ’phobos’ meaning flight, panic,
fear, terror, and from the diety of the same name who could
6
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 7
provoke panic in one's enemies. The Greeks made ’fear
masks' by depicting likeness of Phobos on weapons such
as shields (Errera, 1962).
Although morbid fears were described by doctors
from Hippocrates onward, its sole medical usage before the
19th century was in Celcus’s term hydrophobia for a prominent
symptom of rabies (Errera, 1962). Only in l801 was 'phobia'
used on its own (OED), and during the next 70 years it
slowly gained acceptance in the same sense as today, that
is, a persistent excessive fear attached to an object or
situation which objectively is not a significant source
of danger.
A phobia can thus be defined as an excessive fear
reaction which is out of proportion to demands of the situa
tion, and is both persistent and unadaptive, and is beyond
voluntary control, leading to avoidance of the feared situa
tion .
This phobic (or fear) reaction can be analyzed into
three components: subjective, autonomic, and motor. The
subjective aspect of phobic (or fear) response is experienced
by the patient as an inner state of alarming feeling of
intense fear, terror, tension or full panic, a great urge
to cry, aggression, irritability, difficulty in breathing,
and a sensation of falling of fainting (Wickert, 19^7).
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 8
The autonomic reaction, which is both an inner state
felt by the patient and outer aspects visible to observers
will include the following physiological changes: pallor,
rapid respiration, pilomotor erection, increased blood flow
through the muscles, pupillary dilation, hypertension,
tachycardia, fluctuations in the skin conductance, failure
of habituation of galvanic skin response, contraction of
bladder and rectum leading to involuntary excretion, dry
ness of the mouth, nausea, muscular tension and/or weak
ness (Marks, 1969). The motor response is usually one of
flight but some patients become inert or "frozen" and feel
too weak to more. Patients who experience these feelings
of muscular weakness seek the support of another person,
or a wall (Rachman, 1968). Biochemical changes also occur
as a result of fear feelings, and these include secretion
of adrenals, non-adrenaline at the peripheral nerve end
ings, and an increase in the plasma free fatty acids (Marks,
1969, pp. 43-44).
Although these different components of fear are
congruent, they are related imperfectly to one another.
Lang (1966) gave a questionnaire to a group of students,
of 20% who reported fear of snakes only 1-2% actually
avoided snakes when tested, and during the avoidance test
subjective reports of fear correlated only .40 (n=23, P^-05)
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 9
with ability to approach the snake. In a study by Agras
(1967) the physiological and behavioral aspects of fear
did not always vary together. In five agora-phobic sub
jects the galvanic skin response only partly reflected
subjects’ ability to enter the phobic situation concerned.
Thus, the subjective, behavioral and physiological ingredients
of fear together form a complex but not necessarily unitary
response.
In general, fear, like other behaviors, develop
through interaction of three kinds of phenomenon: those
which are hereditary, those dependent on maturation, and
those developed through learning from individual and social
experiences. It is perhaps unfashionable to stress the
importance of innate hereditary factors in behavior, but
the evidence regarding their importance is quite conclusive,
especially in lower animals. That is, the more primitive
the species, the more it depends on innate mechanisms of
response.
From Hippocrates to pavlov it has been recognized
that species vary in temperament according to their heredi
tary endowment. Fearfulness is one aspect of temperament,
and therefore, it is reasonable to expect that this trait
depends in part upon genetic makeup. For example, in rats
Broadhurst and Bignami (1965) have described two strains
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 10
of rats bred selectively for slow and for rapid acquisiton
of escape-avoidance conditioned responses in a shuttle-box.
The parents came from two strains of rats preselected for
high and low avoidance. Progressive divergence of the
mean scores for these high and low avoidance strains indicated
a strong genetic control over the development of the con
ditioned avoidance response, especially that to shock.
Autonomic reactivity as measured by emotional elimination
was not important in differentiating the strains, but they
differed in ambulatory activity and in aversion to alcohol
in their drinking water. The selection affected the body
weight.
Another example concerning genetic contribution to
fearfulness is evidence by Murphree and co-workers (Murphree,
et al., 1966; Peters, etal., 1966). These experimenters
succeeded in selectively breeding two separate strains of
dogs, one of which was excessively fearful, the other stable.
They began by two contrasting pair of pointers preselected
by dog breeders, one pair being fearful, the other. By
the F-2 generation excessively fearful behavior was shown
by 90$ of the offspring of the originally timid pair, and
stable behavior was shown by 80 % of the offspring of originally
healthy pair. The differences were best accounted for by
hereditary factors, since the environments were constant
for all dogs. The mode of inheritance was most probably
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 11
polygenetic. Fearful behavior was measured by duration of
immobility after a loud noise, the amount of exploratory
activity in an empty room, several conditioning measures
and standardized field trials with live birds. Repetitive
measures showed that maturation was important, since the
freezing time to noise and active scores became characteris
tic of nervous dogs near the age of 3-^ months, through some
differences between strains were seen earlier.
In higher animals fearfulness becomes more dependent
upon both hereditary and experiences. In humans in particular
it is very difficult to separate the contribution of innate,
maturational and learned elements to the fear, since man
is not a species rich in inborn reactions and evolves more
as a learning machine. By definition, innate elements are
those which appear early in life before there has been
significant experience. Genetical aspects of mental dis
orders have been extensively reviewed by Cowie and Slater
(1959) and Shields and Slater (I960). Though much work has
been carried out on the inheritance of psychotic illness,
the equivalent problem in respect to neuroses has been
relatively neglected. Although genetic aspects of timidity
(fear) in man is not well known, nevertheless, several studies
suggest that hereditary plays as important a role in the
etiology of fear (anxiety) states as it does in the major
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 12
psychosis.
In humans, twin studies are generally regarded as
providing a powerful tool in genetic investigations. If
twin-pairs are examined in respect of a train or illness,
high concordance rates in monozygotic (identical) pairs of
twins with lower concordance rates in the dizygotic (fraternal)
twin-pairs are suggestive of a genetic factor underlying
that train of predisposition of illness. Similarly, for
continuous variables (e.g. height), an estimate can be
made of a genetic influence by comparing the correlations
in the two groups of twin pairs.
In a study by Freedman (1965) the development of
smiling and fear of strangers in a series of twins over
the first year of life was found to be more significant
among monozygotic twins than for dizygotic twins. That is,
greater concordance existed for monozygotic twins than dizy
gotic twins. Shields (1962), in a series of adult twins,
gave a neutoricism questionnaire which included questions
on emotionality, nervousness and shyness. Evidence suggested
a genetic contribution to neuroticism. Neuroticism scores
were closer for monozygotic tv/ins and dizygotic twins.
Furthermore, the discordance between dizygotic twins was
greater than the discordance between monozygotic twins;
the difference between those two groups was much greater
than that between monozygotic twins reared apart and together.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 13
Certainly siblings differ from birth onwards in the inten
sity of their startling and fears, so it is highly likely
that genes affect timidity. But evidence is sparse and
systematic work is needed to delineate the extent of this
influence.
It is much more difficult to separate between the
contributions of maturation and learning to fear in humans.
Although maturation is necessary before learning can begin,
elements due to learning appear mainly as a function of
particular experience. The difficulty in distinguishing
between maturational and learning factors in humans is
compounded by the fact that what appears to be maturation
may in fact be learning, since every species requires
cartain conditions in its environment in order to survive,
and experience of these constant conditions may be the deter
minant of a particular fear rather than maturational changes
within the species itself. And learning may obscure matur
ation in two ways. First, very early experiences of an object
may subsequently inhibit fear to it at the later age when
fear to that object usually appears. Second, at the critical
age at which a response matures very brief experiences can
greatly enhance the maturational response although at an
earlier age such experiences would have had little effect
(Marks, 1969) .
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 14
Therefore, it seems reasonable to assume that learn
ing experiences are best accounted for development of fear
in humans. The phenomena of human phobias in terms of
modern psychological knowledge has been attempted by several
investigators. Of these, the proposal by Wolpe and Rachman
(I960) that phobic disorders can best be regarded as con
ditioned fear (anxiety) reactions seem the most plausible,
since WolpeTs paradigm in cure of phobia, based on this
definition has been most successful. According to Wolpe
(1962), "the distinctive feature of a classical phobia
is the presence of clearly ostensible sources of anxiety
...a behavioristic analysis aims at liquidation of these
sources in every case." According to this view, then,
phobias are anxiety states in which the focus of the anxiety-
producing stimuli is sharpened. Thus, phobic disorders
are regarded as conditioned fear (anxiety) reactions and
are defined as "any neutral stimulus, simple or complex,
that makes an impact on an individual at about the time that
a fear reaction is evoked, acquires the ability to evoke
fear subsequently. If the fear in the original condition
situation was of high intensity, or if the conditioning is
repeated a good many times, the conditioned fear will show
the persistance that is characteristic of neurotic fear;
and there will be generalization of fear reactions to
stimuli resembling the conditioned stimulus” (Wolpe &
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 15
Rachman, 1960).
Therefore, according to the learning theory paradigm,
phobias are acquired by classical conditioning in which the
phobic stimulus (the CS) is paired together with or shortly
before a noxious stimulus (the NCS). Conditioning occurs
through this temporal continguity, and the phobic increases
with the frequency of the pairing, with the strength of the
noxious stimulus and when the pairing occurs in conditions
of confinement or when nothing can be done to stop the
noxious stimulation. Once there is sufficient fear to
cause avoidance of the phobic situation, the phobia is
maintained in part by drive reduction and is hard to extin
guish - this is a form of instructional conditioning (Wolpe,
1958; Eysenck, I960; Marchais and Janson, 1962; Rigal et
al., 1962).
This paradigm regards most, if not all, anxiety
states as complex, multiple phobias, where the stimuli
triggering the anxiety reaction can be identified. In
mono-symptomatic phobias, for example, the triggering stimulus
can be identified in a reasonable manner. The simplier
phobias often begin in a traumatic setting, remain localized
to conditions which surround that setting, and tend to run
a steady course unless they are aggravated by enforced con
tact with the phobic situation, or ameliorated by gradual
retraining. Some varieties of monosymptomatic phobis are
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. animal phobias, height phobia, thunderstorm phobia or
driving phobia after car accidents. In complex phobias,
several types of stimuli are found to elicit the anxiety
reaction. This complexity may arise because the patient
has several interrelated fears. For example, a patient
may complain of several phobias such as claustrophobia,
fear of illness and hospitals, fear of death and its associa
tions, fear of storm, fear of quarrels (Wolpe, 1961). In
treatment of complex phobias the therapist must first
determine the degree of interdependency of these fears, as
best as he can, and then choose the mode of treatment. If
the therapist concludes that the various fears are quite
independent, then his choice of the initial target is merely
a matter of priorities. However, when the phobias appear
to be interdependent, the therapist has to assess the
relative severity of each type of phobia and make a treat
ment program which will integrate the different fear dimen
sion.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 17
Section B. Classification of Phobias
Introduction. Although phobia has been recorded since
Hyppocrates it was not until 1952 that it received a separate
diagnostic label by American Psychiatric Association
(Stengel, 1959)* Sub-division of the phobic disorders
themselves has only just begun. The Camberwell Psychiatric
disorders now lists monosymptomic disorders under separate
heading from other phobias (Wing, 1965).
Pears sufficiently intense to be called phobias
occur only in a small proportion of adults. In a student
population, for example, most subjects might feel mildly
squeamish in presence of non-poisonous snakes, but only
20% reported intense fear, and 1-2% actively avoided a
snake to a degree which might be labeled a phobia (Lang, 1966)-
Marks (1969) divides phobias into two classes.
Class I: phobias of stimuli external to the patient, and
Class II: phobias of stimuli internal to the patient
(pp. 105-106). Class I phobias include agora-phobia, social
phobias, animal phobias, and miscellaneous specific phobias,
e.g., heights, wind darkness, thunderstorms, and so on.
Phobias of stimuli internal to the patient (Class
II) cannot be avoided by the phobics and are divided into
two sub-divisions - illness phobias, such as hypochondria,
and obsessive phobias. Some examples of obsessive phobias
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 18
are fear of contamination by dirt, dust, germs or other
items, a fear of injuring others or oneself.
Animal Phobias
The animal phobias are the most clear cut variety.
They are also the rarest kind seen in hospital practice.
Of all phobias presented at Maudsly Hospital in the decade
1959-1969 only 3 % were animal phobics (Marks, 1969). These
phobias are isolated fears of animals or insects such as
birds (or feathers), cats, dogs, frogs, spiders, moths,
bees and wasps - the commonest of these encounters by psy
chiatrists are of birds and spiders. Specific animal phobias
in adults start generally in childhood even though they may
present themselves for treatment in adult life, run a steady
rather than a fluctuating course, have a different psycho-
physiological correlates and respond quite well to desensiti
zation.
Marks and Gelder (1966) carried out a retrospective
examination of a varieties of phobias presented by 139 un
selected patients. Of the 18 patients who complained of
specific animal phobias, none had acquired abnormal in
adult life even though they only sought treatment in adult
hood. Most of these phobias had started before the age of
five (n=l8, x=4.8, SD=2.8). The age at which the animal
phobics seek treatment is similar to other phobic specific
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 19
patients, which is from 15-40 years of age (x=28.9). How
ever, Marks and Gelder point out that the simple animal
phobias, in addition to having a different age of onset,
are unlike the other phobias in showing a relatively contin
uous course of development and also because they are seldom
associated with other psychiatric disorders. In addition,
Marks and Gelder (1966) note that before puberty animal
phobias are found in both sexes, though by the age of 10-11
they are already much rarer in boys (Rutter, Tizard and
Whitmore, 1968). The few animal phobias which remain after
puberty are usually found in women. These women usually
have a monosympotmatic phobia of single animal species with
little generalization despite persistence of the phobias
over decades. There is no tension or panic in absence of
phobic subject.
Before the psychophysiological features of phobia
is dealt with here, it is necessary to delve into bases
of electrodermal activity so that a clearer understanding
may be obtained in the correlation of the physiological
activity and emotional aspects of fear.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER 3
Electrodermal Activity and Its Bases
Introduction. Skin is one of the seven boundries of the
mammals for their interaction with the external world. The
mouth, lungs, gastro-intestinal tract, eyes, ears and the
nose are the rest of these special structures which function
as boundries. The skin, however, defines the external phy
sical limit of the body, and as such, has a significant
physiological task of keeping bacteria, toxins, and other
undesirable elements out, and keep the body fluid in.
Through its tactile and thermosensitive apparatus it acts
as a primary station for reception of information from
the immediately adjacent outer world. If penetrated by
foreign matter the skin can become "aware" of the location
of penetration and sound appropriate alarm. In response
to signals from higher centers, and sometimes from local
stations it regulates the rate at which the heat generated
within its boundries is lost to outer world. Sometimes it
must expediate this loss by a contribution of its own making,
namely sweat (Edelberg, 1972, p.367)*
The signals which proceed from the control centers
are of electrical nature, as any nerve impulse is, and their
arrival at the skin is heralded by measureable electrical
changes which may be called electrodermal activity. This
20
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 21
electrical activity is, for the most part, an epiphenomenon
of physiological process that ensue. For this reason
Edelberg (1972) suggests this activity be called "neuro-
dermal activity", for it entails the fact that such signals
can be monitored for the activity of the brain.
Galvanic skin response as a response to emotional
stimuli was first discovered by Fere (1838), the French
physiologist. He ascertained that the application of a
small current to the skin, yielded characteristic fluctua
tions in the subject’s resistance to that current. However,
controversy exists among investigators over the nature of
the peripheral process in this response. Sommer (1905)
and Sidis and Nelson (1910) who defended a muscular basis;
McDowall (1933)5 who defended a vascular basis; Veraguth
(1909)5 Darrow (1927) and Jefferess (1928) who argued for
sweat glands; and Richter (1929)5 who supported a combined
sweat gland and ipidermal methanism, have all contributed
to this controversy. The biophysical, physiological and
even the psychological aspects of the "neurodermal" activity
is best understood in the light of the histological organi
zation of the skin, with its four well-defined layers.
The innermost layer, the ’’corneum" or "dermis" is
chiefly composed of connective tissue and also contains
tactile elements, sebaceous glands, hair roots, and bodies
of sweat glands, most of their ducts, and the neural and
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 22
vascular supply, including capillary loops that enter the
little domes or dermal papillae forming roof of this layer.
This stratum, because of its bountiful intercellular spaces
and network of blood vessels, has a high electrical conduc
tivity. Next, the "Malpighian" or "germinating" layer,
directly above corneum, contains its deepest or basal layer
the reproducing cells. The products of cell division meta
morphose as they are displaced toward the surface and are
destined to replace the keratinized cells of the horny layer
or corneum lost through wear and tear. The cells of the
germinating layer are separated by narrow spaces filled
with a fluid in which free diffusion and perhaps circulation
may take place (Nordquist, Olson & Everett, 1966). Cell
membranes usually constitute an effective barrier against
electric current, but it may be surmised that the conductivity
of the layer is enhanced by the presence of this intercel
lular lacework of acqueous channels. Nerve fibers enter
this layer and their concentration varies considerably over
various parts of the body. The cells at the upper level
Malpighian layer contain numerous deeply straining granules,
from which is derived the name of the third or granular
layer.
Above the granular layer lies the "corneum", a com
pact stratum of flattened cell carcasses. In the skin of
the palm and soles, where the corneum is usually thick,
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 23
0.5-1-3 mon (Kuno, 1956), there is a thin glistening layer
the "stratum lucidum", which separates the granular layer
and the corneum, according to Blank and Gould (1959)»
there lies a barrier to the passage of water and solutes.
Two types of sweat glands are found in the dermal
proper. The "eccrine" sweat gland, the type that produces
watery secretions, are found on the palmar and planter sur
faces and over most of the body. This gland is a long tube
with walls consisting of double or triple cell layer. The
deepest two mon of the tube is coiled up to form a compact
body, the sweat gland proper, in which secretion actually
takes place. The remainder is the duct. After a straight
course through the corium and germinating layer, is spirals
through the horny layer and opens to surface as a small
pore. Outside of the epithelial layers of the secretory
region, but not of the duct, are longitudinal smooth muscle
fibers, the myoepithelial cells. Also, surrounding the
secretory portion if a profuse, coiled, nerve supply.
The "aprocrine" glands are the other types of
sweat glands which are located in the axilla, mammary areola,
the labia majora, the mons pubis and circum-anal region.
In these the secretion is formed by pinching off bits of
the protoplasm of the secretory cells. The expulsion of
sweat from apocrine glands is achieved entirely by contrac
tion of the myoepithelial fibers, which are under adrenergic
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 24
control (Hurley & Shelley, 1954).
Controversy also exists in interpretation of data
by investigators in terms of the electrical behavior of
the skin. The electrical changes of the skin are probably
the most popular of many measures of autonomic activity
which have attracted the attention of psychologist. One
type of measurements used in determining electrical changes
of the skin is resistance, which is the most widely used
index of level of activation (formerly known as the psycho
galvanic reflex; Veraguth, 1909). By placing two electrodes
on the skin surface and driving a small current through,
the skin will act as a resistor. A voltage develops across
the electrodes and my application of Ohm’s law one can com
pute the apparent resistance. A rapid decrease in the
measured voltage in varying degrees is indicated following
2 sec after a sudden noise, a sharp sniff by the subject,
or a statement made by him. This transient response,
commonly known as the galvanic skin response (GSR), has a
characteristic waveform, taking about 0.5-5 sec to reach
peak, 1-2 sec is typical. Recovery from peak to baseline
is considerably slower and may have a variety of shapes,
from a gently sloping plateau to an expotential - like
descent that is almost as fast as the rising portion. The
time required for the recovery limb to reach its point of
50$ return to baseline varies greatly, from 1-30 sec.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 25
Response latency ranges from 1.2-4 sec, depending on the
temperature (Gildemeister & Ellinghaus, 1923) and site of
the body (Bloch, 1952). A typical latency for palmar
responses at comfortable room temperature Is about 1.8 sec. 2 Apparent resistnace ranges between 10,000 and 500,000 ohms/cm .
There are other types of measurements used in
recording electrodermal activity. Skin conductance is
expressed in terms of reciprocal of resistance. Conductance
measure is favored by many psychophysiologists (see Edelberg,
1967; C. C. Brown, 1967) for the reciprocal transformation
tends to normalize the distribution of resistance changes.
Conductance is expressed in mho (ohm spelled backward).
Since skin conductance varies constantly, the absolute
level at any point in time (baseline conductance) represents
a possible measure of general activation or arousal. It
has not been used as frequently as the transitory increase
in conductance which follows the sudden presentation of
any strong or unusual stimulus. These rapid changes in
skin conductance are superimposed on the baseline and are
generally expressed as a percentage change. Eor the purpose
of such percentage conversions, the baseline measure is
usually taken during a brief period immediately preceding
the presentation of the stimulus.
Other expected values are Skin Conductance Level
(SCL), whose values depend upon the size of electrode used
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 26
and is quoted in micromhos per square centimeter. For p example with 1/cm electrodes and bipolar (two electrodes)
placement, the range of the expected values will be from 2 2 to 100 mho/cm , with most values falling in the range
5-20 mho/cm^ (Ax & Bamford, 1968).
Skin Potential Level (SPL) values will depend upon
concentration of electrolyte used, but with 0.552 KCL values
will range from 10 to -70mV (Ax & Bamford, 1968). Skin
Potential Response (SPR) values range from initial negative
component up to 2 mV to secondary positive component up
to 4 mV.
The above terminology is based on the proposal of
a nomenclature committee of the Society of Psychophysiolo-
gical Research (C. C. Brown, 1967). In these it was sug
gested that SCR, SRR, and SPR should be used to indicate
skin conductance response, skin resistance response, and
skin potential response respectively, while the letters
SC, SR, and SP should indicate levels of activity of the
appropriate variables. Aside from these terms Venables
and Martin (1967) suggest using SRL, SPL, and SCL to
indicate skin resistance level, skin potential level, and
skin conductance level, respectively.
In types of recording electrodermal activities,
use of generic term "exosomatic" for describing those
measurements using an external source (as developed by
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 27
Fere, 1888) and "endosomatie” for describing measurements
with no external current source (as developed by Tarchanoff,
1890) should be followed, appropriately.
These standardizations will, therefore, require the
use of the terms PGR and GSR to be sacrificed for the sake
of unambiquity. However, in this paper the term GSR has
been used at times to represent either electro dermal activity
or SRR (see Method Section).
There exist variables which affect the mechanism
of the skin activity. These peripheral variables include
temperature, humidity, chemical environment, and pharmaco
logic agents. There also exist such variations and anatomical
and species differences.
Temperature and Humidity. Of all the peripheral variables,
temperature has probably contributed more to the variance
of the measure than any other. Resistance increases with
the decrease in temperature by about 3%/°C. Since skin cool
ing of several degrees may accompany vaso-constriction, this
may induce a substantial error into base-level measurements.
The amplitude of the skin resistance response increases by
5%/°0 as the temperature drops, but this effect may be lost
after a few minutes (Maulsby & Edelberg, i960). Lowering
the skin temperature to 20°C for periods of 15 min or more
depresses the resistance response, although this effect is
characterized by great individual differences. The positive
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 28
and negative components of the potential response were
found to behave differently in response to temperature
changes; the positive response was absent from the dorsum
of the hand at 15°C to 20°C, appeared at 30°C, and increased
in amplitude at 40°C. The negative response was most con
spicuous at 20°C (Yokota, Takahash, Kondo, Fujimori, 1959)-
These results were obtained with changes in room temperature.
With changes of skin temperature locally, depression of pos
itive wave at lower temperature was also observed (Fugimori,
1955). Wenger and Collen (1962) reported a positive cor
relation between forearm skin conductance and room temper
ature of .1%, .22, and .12 for three large groups of sub
jects, totalling above 900. Log conductance change showed
a variable relation, and palmer skin conductance a neglig
ible one (pp. 106-112). Venebles (1955) also found an
extremely variable relation between conductance response
and room temperature.
Latency of electrodermal response is markedly in
creased by decreases in skin temperature. Latency can vary
from 1.2 sec at a local temperature of 40°C to 4 sec at
10°C (Gildemeister & Ellinghaus, 1923). There are several
possible implications for the significant portion of the
total delay from stimulus to response due to peripheral
delay. One possibility is due to the time required to
elaborate or express sweat, possibly to the diffusion of
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 29
a chemical menidator, possibly to the spread of an exitation
wave through an epidermal cell layer. Since the skin tem
perature may easily change as a consequence of vaso-con-
struction attending a state of central activation, the
likelihood that latency measurement are spurious seems
high.
Humidity can be expected to exert an effect on skin
conductance; insofar as it influences evaporative water loss,
and consequently, the activity of thermoregulatory system.
One would expect higher humidity to reduce evaporation
and, therefore, to cause a reflex increase in perspiration
to promote heat loss. This would be accompanied by increased
skin conductance. However, the negative correlation report
ed by Venebles (1955) and by Wenger and Cullen (1962),
between palmar skin conductance and relative humidity is
therefore unexpected. It seems to indicate that the palms
are not controlled by thermoregulatory requirements, a
conclusion consistent with the insignificant correlation
reported by these authors between palmar conductance and
room temperature. It may indicate that palmar water output
is in part regulated by the local requirements for main
taining hydration of corneum.
Chemical Environment. The effector organ of the electro
dermal response, whatever it may be, is sensitive to the
composition of the solution at the electrode site and in
this respect manifests the characteristics of a membrane.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 30
Certain slats such as Na^O^, CaCl2, AlCl^ may potentiate
the resistance response significantly, e.g., by 240% in the
case of 1M CaCl2, and 600% for 1M AlCl^. The degree of pot
entiation depends on the polarity of the current at the
experimental site and is greatest when the larger ion of
the electrolyte is tending to move into the skin (Edelberg,
Greiner, & Burch, I960). Thus, in the case of AlCl^s the
increase in response amplitude is twice as great at an
anodal site as at the cathodal one. Conversely, the poten
tiation of response, resistance is decreased by these com
ponents and is only slightly affected by polarity the current
(to a maximum of 15%). Other agents attenuated the response
for example, a cationic detergent miniature, Zephiran
(Winthrop Laboratories), in total concentration of less than
0.005 M, reduced the response amplitude to 45% of control,
and a 1M KC1 solution to 64%.
The specific effects of the various common electro
lytes become weaker with decreasing concentrations of the
order of 0.1M. Acidity of the medium had a pronounced effect,
with the greatest response amplitude occuring at pH7 and
falling off on either side. At pH3 the amplitude was reduced
to 30% of normal at pHll, to 60%.
The effect of electrolyte medium upon the potential
level can be predicted on the basis of the expected behavior
of a surface membrane with a negatively charged, fined struc
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 31
ture. The negative charge is an electrostatic one and is
caused by the ionization of the molecules that form part
of the structure. In case of the skin, the anionic portion
remains fixed, while the cation is free to move. The net
effect for this is a selective permeability of such struc
tures to cation. For the skin the selectivity is evident
but rather imperfect. When a concentrated solution of KC1
is placed on the skin, potassium tends to diffuse through
the membrane, while chloride tends to be excluded, the
result being an increase in external negativity (Rothman,
195^, p. 12). A less concentrated solution produces a lesser
increase. When finger is dipped into 0.1M KC1 and another
into 0.01M KC1, the potential between these sites is of
order of 20mV, as compared a theoretical value of 58mV of
the membranes were perfectly selective (Edelberg, 1963 b).
In addition to the charge the ionic size is also determinant
of the effect. Thus a site exposed to a molar solution of
KC1 is appreciably more negative (by 12 mV) than is one
exposed to a molar solution of AlCl^-
Despite this generally predictable behavior of skin
exposed to such electrolytes, the effect on the trancutaneous
potential is quite unpredictable in the individual case
(Edelberg, 1963 b). For example, the potential level is
sometimes unchanged despite the variation of the external
concentration from 0.005M-0.5M. In other instances the
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 32
surface potential changes but remains highly negatives even
when the external concentration of electrolyte is reduced
to almost zero. These variable results can best be explained
if the site of the potential difference across skin resides
not in a single structure but in two separate structures
having different properties and arranged in parallel. If
one assumes that these are the sweat glands and the epidermis
and, in agreement with Rothman (1954, P-33)j that the sweat
gland membrane is not easily accessible to surface agents,
one can explain such results by allowing for the fact that
the sweat glands may be full or partially empty and may,
therefore, contribute differently to the total surface poten
tial .
Various chemical agents other than inorganic electro
lytes may affect the peripheral apparatus. For example,
ion to phoretically introduce formalin may block sweating
for many days (Kuno, 1956, p. 356). A solution of 5$ acri-
flavin may reduce it to 40% (Edelberg, 1963 b ) .
Pharmacologic Effects. Montagu (1958) devised the reliable
method for local application of cholinergic blocking agents
by ion to phoresis method, which permitted consensual valid
ation of the observation that cholinergic blocking agents
such as atropine (Lader & Montagu, 1963; Wilcott, 1964),
hyoscyamine (Martin & Venables, 1964), and scopolamine
(Edelberg, 1972, p. 376) all effectively block neurodermal
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 33
activity in the human. Reports of the effects of the
catecholamines on sweat secretion are conflicting. Darrow
(1936) has reported a depression of EDA resulting from sys
tematic injection adrenaline. Haimovici’s pharmacological
experiments (1950) on human eccrine glands support the idea
that the normally cholenergic sudomotor fibers manifest
adrenergic activity. He was able to elicit prolonged sweat
ing with the local introduction of adrenaline or non adren
aline and to inhibit spontaneous sweating with dihenamine,
an adrenergic blocking agent. Pilocarpine acts directly
on the end organ and causes profuse, continuing secretion
of sweat and lowering of resistance (Aveling 8c MeDowall, 1925) •
Richter (1927) demonstrated that piolocarpine eliminates
spontaneous responses, but the response to intense startle
stimuli is retained.
Certainly acting agents may produce an indirect
effect on EDA via their action on neurodermal control and
regulatory areas, but a direct effect on the peripheral
apparatus may also be involved, e.g., in case of adrenaline
and mecholy Haimovici, 1950)- In interpreting such effects,
one should consider the possible indirect effect on EDA
resulting from alteration in blood flow, since vasoconstric
tion per se may have a marked effect on the amplitude of
EDA (Edelberg, 1964 a).
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 3^
Current Density and Polarity. The total current applied
to a site is of no significance unless one knows how much
of it passes through each unit area of the skin, i.e., unless
it is expressed in terms of current per unit area (current
density).
The polarity of the current does not have an appreci
able effect on either the base level or the response amplitude
when the electrolyte medium is dilute NaCl on liquid or
paste. With other electrolytes, such as CaC^j AlCl^,
there may be a pronounced polarity effect on response amp
litude, although a minor one on base resistance. With
modern amplifiers employing common-mode rejection, it is
desirable to use a pair of two similar sites, rather than
a large arm reference; this will tend to reduce the polarity
effect.
Anatomical Differences. The palmar and plantar surfaces
are commonly the most active sites in exosomatic as well
as endosomatic responses, although they are not the most
conductive ones on the body. The forehead and scalp are
substantially more so. The rudial affect of the foot over
halusis abductor muscle is highly active. The relative
activity of several other areas can be found in the same
citation (Edelberg, 19675 PP- 14-17). In comparing various
parts of the body, one should bear in mind that the relative
activity changes with the state of activity of individual.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 35
For example, the lateral differences reported by Fisher
(1958) may shift during sleep (Johnson & Luhin, 1966)
or during Hypnosis (Edelberg, 1972, p. 377)• The inactivity
that generally characterizes skin potential and conductance
in such areas as the chest of arm may give to activity under
temperature load or high emotiona stress (Rickies & Day,
1968, Wilcott, 1963) • Neumann (1968) reports interesting
changes in topographical differences in activity during
different seasons. The relation between endosomatic and
exosomatic activity of an area varies considerably; some
areas show little exosomatic response, despite the occurrence
of potential responses of appreciable magnitude the relative
proportion of positive and negative components of the SPR
from different areas also varies considerably (Edelberg,
1965j P- 3^)• It is of interest that the plantar surface
shows very little positive activity; whereas hypothenar and
thenar eminences of the palm show the highest positive activity
of the body, despite the fact that the negative acitvity of
these areas is about equal.
Species Differences. Electrodermal activity has been al
legedly observed in the skin of the frog, toad, and horse,
and from pads and paws of the rabbit, rat, cat, dog, and
monkey (reviewed by Landis & DeWick, 1929). Not all these
exitations are necessarily of genuine responses. For example,
in the study on rabbits, Sidis and Nelson (1910) observed
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 36
that no reflex was produced as long as the legs were held
motionless; they interpreted this as evidence of muscular
basis of the response. Edelberg (1972, p. 378) was unable
to elicit any response from the felt-covered pad of the
rabbit, unless the preperation was such as to permit move
ment artifacts, a likely explanation for the earlier obser
vations. Genuine responses are present in the rat, cat,
and dog (at least in young dogs). The cat, which has been
most studied, resembles man and monkey in its electrodermal
behavior but rarely produces positive SPRs. Wilcott (1965)
observed that the cat behaved differently from these primates
in its response to small currents superimposed on the SPR
(potential "driving").
Experimental Methods and Findings
Electrodes and Their Application. Non-polarizable electrodes
should be used for potential or conductance measurement,
and even for low frequency impedence measurement. The two
most popular types are the zinc/zinc sulphate (Darrow, 1929;
Lacey, Bateman & Van Lehn, 1953; Lykken, 1959; Richter, 1929;
Wenger, Engel, & Clemens, 1957; Wilcott, 1962) and the silver/
silver chloride (A /A Cl) (Edelberg, 1964 b; Johnson & Lubin, s s 1966; Sternback and Tursky, 1965; Venables & Sayer, 1963)*
The zinc sulphate is usually mixed with krobin clay to
provide a non-running electrode paste. The silver/silver
chloride electrode is commonly made by anodizing a silver
electrode in a chloride solution (Geddes, Baker, & Moore,
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 37
1969; Janz & Taniguchi, 1953)-
Since the nature of electrolytes on skin surface
may have a marked effect on base levels and responses ampli
tudes, one does well to use a paste whose electrolyte con
centration resembles that of average sweat, i.e., 0.05M
NaCl.
Size, Preparation, and Location of Site. The size of the
site does not influence potential measurements, but if too
small, its resistance may become appreciable in comparison
with input resistance of the amplifier and attenuation of p the signal results. A site of 1 cm or more is recommended,
unless amplifiers of exceptionally high input impedance are
available. The area is very important in exosomatic meas
ure, since SR and SPR decrease as area increases. SC and
SCR increase with area. To circumscribe a specific area,
one may use either a mask made of plastic, pressure-sensi
tive tape with a cut out, or a cup electrode fastened to
the skin with adhesive or elastic hand (see Day & Lippitt,
1964). If the masking tape method is used, the skin is
cleaned wtih acetone; the mask pressed into place, electrode
paste applied; and a silver/silver chloride electrode some
what larger than the cut out pressed gently over the site
and held in place by pressure sensitive tape with a layer
of 1/4 in sponge rubber between it and the electrode. One
should ensure that the application does not occlude circulation.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 38
For exosomatic measures, a pair of sites on the volar
surfaces of the middle segments of two fingers is a convenient
arrangement. Alternatively, an active area on the foot is
conveniently located just dorsal of the plantar surface,
over the abductor hallucis muscle, midway between point under
the internal malleolus and the first phalange. Two electrodes
may be located 2 cm apart in this region, since it is desir
able when taking exosomatic measures to use similar skin
sites to effect maximal cancellation of endosomatic effects.
The abductor hallucis site is more active than plantar area
and is to be preferred if the subject will be walking at
any time in the course of the experiment (Venables & Christie,
1973).
In endosomatic measures the same sites are recom
mended for the active electrode. There are three preferred
"inactive" areas for reference site: the inner aspect of
ear lobe; over the ulnar bone, one-fifth of the distance
from the elbow to the wrist; and over the tibia bone, one-
fifth the distance from the ankle to the knee (Venables &
Christie, 1973) .
Current Strength. If constant current is used, a current p density of 8 A/cm is recommended. For a pair of sites
the area used in calculation is that of one of the sites.
With constant voltage a source of .75-1.0V across two matched
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 39
sites is recommended. Each of these values is optimum for
general use but will have serious disadvantages under special
conditions (Edelberg, 1967, pp. 22-27).
Physiological Behavior of the Skin
Sweat Secretion. Although sweat glands are found over most
of the body, those on the palmar and plantar surface have
been recognized as responding primarily to emotional or
ideational stimuli, the remainder primarily to thermal stiumli.
The secretion of apocrine glands has been associated with
sexual behavior but appears to respond to a variety of
emotional stimuli (Shelley & Hurley, 1953).
During sweat response, the sweat rises rapidly and
may commonly be seen on the volar surface of the finger,
emerging as a small droplet at the sweat gland pore. Not
all glands are active in any given EDR, nor are all EDRs
necessarily accompanied by any visible sweat. The sweat
glands are applied with sympathetic nervefiliers that are
paradoxically cholingeric. It is commonly believed that
secretion is phasic, occuring at the time of reflex. Kuno
(1956, p. 296), however, argues that secretion is continuous,
the sweat bring stored in the lumen of the gland or duct
until it is forcibly expelled by the contraction of myoepit
helial cells, which are adrenergic. Since atropine blocks
sweating, the production of sweat must be under neural con
trol; but if Kuno is correct, this innervation must act as
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 40
a tonic control that can change its level as the situation
demands. Although apocrine glands appear to require myoepit
helial contraction to force out the contents, it seems pos
sible that secretory pressure in the eccrine gland may be
adequate to force the sweat up the narrow ducts. Although
Edelberg (1972, p. 380) reports evidence of myoepithelial
action in eccrine sweat secretion, and further evidence of
myoepithelial role is provided by Kuno (1956, p. 294) and
Rothman (1954, p. 157) who cite the work of Takahara (1934),
who cannulated single sweat glands on the human plam and
recorded the behavior of the fluid level in capillary tube,
Lobitz and Mason (1943) contend that water absorbtion in
the duct may account for this effect, since solutes in palmar
sweat are found to be more concentrated when secretion is
slow. Contrary to Lobitz and Mason, Robinson and Robinson
(1954) report that solute concentration is increased during
copious sweating. Montagna (1962, pp. 358-359) agrees with
Lobitz and Mason in taking the view that physiological and
histochemical evidence appears to support the occurence of
duct reabsorption.
Epidermal Function. The epidermis function as a barrier
against the movement of water and solutes across the skin,
and in the human represents the area through which most heat
exchange occurs. Kuno (1956), p. 18) estimated that a 9^ - 2 cm area of skin is occupied by sweat gland pores, plus the
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 41
cavity in which they lie. Since the whole body surface is p about 18,000 cm , it can be appreciated that under heavy
heat load the availability of the entire epidermal surface
area for evaporative heat would be highly advantageous,
perhaps imperative. The ease with which the corneum absorbs
sweat secreted at the sweat pores can be readily observed
under low power magnification; it is apparent that the
evaporative surface area may considerably be extended by
this process. According to Kuno (1956, p. 40), except for
the soles and palms, the water loss from the epidermal
layer is far greater than that from sweat gland activity.
This probably can be attributed to loss of water from capil
laries, much like the activity of the capillaries in the
kidneys.
Permeability and Water Solutes. The permeability of the
skin to water is rather low, therefore, maintaining an
effective barrier against the outward movement of the water.
Under average condition of temperature and humidity, the
rate of loss of water to outside is only of the order of
0 5-1 mg/cm^/hr (Kligman, 1964, p. 423)• At this rate it 2 would take 40 days to lose 1 gram of water through 1 cm
of skin. The barrier is not diffuse but seems to be con
centrated in a very thin layer. If one strips off sequen
tial layer of the corneum by applying cellophane tape and
pulling (Szakall, 1958), the water loss rate remains relatively
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 42
constant until about the tenth strip, at which point the
barrier is essentially removed (Blank, 1953)• Buettner
and Odland (1957) regarded this as the level of the stratum
corneum conjunction, in the compact, deepest layer of the
corneum.
As in the case of water, the permeability of the
corneum to electrolytes is relatively high in the most
superficial layers but becomes very low in the layer Just
above the granular layer. Blank and Gould (1959) demonstrated
with skin-stripping technique that this thin super-granular
layer constitutes an effective chemical barrier. The layer
of corneum above this barrier is rather freely permeable
to many solutes. Edelberg (1963 a, pp. 9-17) exposed skin
to silver nitrate for period of 30 min, exposed it to light,
and reduced it with photographic solution. Histological
examination showed the entire corneum to be permeated by
the heavy deposit of reduced silver. The lower boundry of
this dark zone was Just above the granular layer. Rein
(1929) demonstrated that neutral, acidic, or basic dyes per
meated the horny layer freely but came to a sudden halt at
its lower boundry. However, these data appear to contra
dict the recent assertion that the corneum is permeable to
water but not to salts (Rushmer, Buettner, Short, & Odland,
1966).
The question of whether the penetration of the skin
by solutes occur, occurs through epidermis via the corneum
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 43
and the Malpighian layer or via the sweat ducts is another
matter and the subject of controversy. Rothman (1954) argues
on the basis of his studies of percutaneous absorption that
the route of entry on hairy area is primarily through fol
licles and associated sebaceous glands. The epidermal route
per se represents a rather restrictive one. Its permeability
to solutes may, however, be increased by exposure to certain
agents such as dimethyl sulfoxide (Sweeney, Downes, & Matoltsy,
1966) or by increasing the surface alkalinity to pH 10.5
(Blank & Gould), 1959)- Rothman considered the sweat glands
to be an improbable route of entry, a belief consistant with
the poor absorbtive capacity of palmar and plantar skin,
the two areas of the body richest in sweat glands. Although
Kuno (1956, p. 311) defends the role of sweat gland as an
avenue of entry of solutes, but demonstration by Plesch,
Goldstone, and Urbach (1951) pointed to the fact that this
penetration was limited to the upper layers of corneum,even
when strong contophoretic driving was used.
The resolution of this dilemma is of great importance
to the clarification of the electrical properties of the
skin discussed in this chapter. An experiment by Kumo (1956)
strongly suggests that under some conditions the sweat ducts
represents an avenue of entrance to lower levels, even though
perhaps not so far as the secretory portion. By using short
pulses of high intensity current, he was able to drive
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 44
methylene blue down the ducts and out into upper regions
of the corium, as indicated by histological examination.
Suchi (1950) was able to obtain similar results with ferous
sulphate.
The Absorption Phenomenon. The bidirectional nature of
transepidermal movement of water was demonstrated by Buettner
(1959). He placed against the skin, containers that were
partially filled with solutions having a range of vapor pres
sure. By measuring the change in weight he was able to
demonstrate that water diffused from the skin into the
air at relative humidity levels up to 86%. Above this
level water moved into the skin. This simple behavior in
the direction of a concentration gradient did not appear
to be neurally controlled, but a subsequent finding raised
the possibility that the permeability of diffusion barrier
perhaps showed reflex variation.
Neurophysiological Process and Behavior. Both the sympathetic
and parasympathetic division of the autonomic system have
been implicated as mediators of the skin reflex. Now, how
ever, it is generally conceded that the control is, in fact,
sympathetic, but with many parasympathetic characteristic,
especially the involvement of acetylcholine as the mediator
at the neuroeffector junction. The sympathetical nature
of reflex is deduced primarily from anatomical data, namely
that the reflex can be elicited by the stimulation of the
sympathetic trunk, after the sectioning of the rami (Wang
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 45
& Lu, 1930 c), and further that a unilateral sympathetomy
abolishes the reflex in the ipsilateral foot (Schwartz, 1934).
The reflex can be elicited in the spinal animal by tactual
stimulation (Richter, 1930).
Attempts have been made to implicate the parasym
pathetic system, e.g., by stimulation of the dorsal roots,
which have been known to carry fibers of this division
(Hara, 1929). Wang and Lu (1930 b) effectively challenged
these positive results as probably an effect on the blood
vessels, perhaps by the influence of vasomotor changes
on skin temperature and rate of evaporation. As Darrow
(1937 a) pointed out, another reason for suspecting para
sympathetic involvement is seen in the locus of central
sites from which the EDR maybe elicited. The stimulation
of premotor cortex activates not only the EDR but numerous
other autonomic effects, most of which are clearly parasym
pathetic in nature. Moreover, the production of EDA by elec
trical stimulation of the hypothalamus is accomplished not
by stimulating the posterior nuclei known to be associated
with predominent sympathetic effects, but rather the anterior
region (Langworthy & Richter, 1930; Wang & Richter, 1928) .
The stimulation of this area also provokes slowing of the
heart, loss of blood pressure, enhanced gastrointestinal
activity, and other parasympathetic influences. The control
of the sweat activity thus has a paradoxical nature. Possibly
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 46
the reason for this lies in dual function of sweating.
Sweating for thermo-regulatory purposes exerts a cooling
effect that is trophotropic or vegatative in nature, having
a homeostatic function. The posterior regions of hypothalamus
control sympathetic activity, commonly of an emergency nature.
Heat production is simply a by-product of increased metabolism
resulting primarily from intensified tonic activity in skeletal
muscles, the concomitant mobilization of cooling effects
would represent a synergistic activity. If, on the other
hand the heat production is in response to cold stress, the
activation of sudomotor units represent an undesirable antaton-
istic effect.
A second function of sweating is clearly to alter
the physical characteristic of the skin surface (Darrow &
Freeman, 1934). The pliability of the corneum is determined
primarily by the water content of this region, which depends
upon epidermal transpiration or sweat gland activity. Its
importance in fine manipulative and tactile behavior is ap
parent. It is also important in an emergency, when flight,
for example, requires the forceful contact of the extremities
with abrasive objects. At such times it is a distinct advantage
to activate a system for the emergency moisturizing of the
horny layer, at least of the planter and palmar surfaces.
Two somewhat independent systems participate in the
initiation and control of skin reflex. The premotor cortex,
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 47
rea 6 of Brodman, is the best recognized of the cortical
areas capable of eliciting an EDR when stimulated (Schwartz,
1937; Wilcott, 1969)• In addition, there is an area just
posterolateral to the motor area that controls the contra
lateral foot (Langworthy & Richter, 1930), and, of special
significance, another on interior limbic cortex (Isamat,
1961). The limbic area apparently constituted a control
center that is separate from the premotor area. The des
cending pathway from the premotor area courses through the
pyramidal tract, by passing the hypothalamus. Responses
may be elicited by the stimulation of the pyramidal tract
or the cerebral peduncles, and the section of one peduncle
interrupts the responses elicited by the stimulation of
ipsilateral Area 6 (Wall & Davis, 1951). On the other
hand, ablation of the hypothalamus does not prevent the
eliciting of EDRs by the stimulation of Area 6 (Wang & Lu,
1930 a).
The overall control systems of mediating and moderat
ing electrodermal activity have been comprehensively reviewed
by Wang (1957, 1958, 1964) and Bloch (1965)• They involve,
in addition to the premotor corticospiral system and the
limbic hypothalamic system, a control group involving basal
ganglia with a regulatory center in the paldium. Only a
few pathways in those systems have been anatomically identi
fied, namely, those of the facilitatory fibers from lateral
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 48
mesoncephalic reticular formation and from the senorimotor
areas to the spiral sympathetic, neurones, and those of the
inhibitory fibers from the bubar ventrometial formation to
the spinal sympathetics.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Chapter 4
"Review of Literature"
Section A. Conditioning of Electrodermal Activity
Background & Definition. The difference between instru
mental and classical conditioning was first exactly drawn
by Miller and Konorski (1928) and later elaborated by
Schlosberg (1937) and Skinner (1938). This distinction
"rests largely on what is meant by the term reinforcement."
Pavlov refers to reinforcement in terms of presentation
of the unconditioned stimulus (UCS) in close temporal prox
imity following the conditioned stimulus. In classical
conditioning reinforcement is presented "independently
of the subjects behavior." This reinforcement, however,
is neither a reward nor a punishment since in neither case
is its delivery contingent upon the occurence of a response
(reward), the delivery of an aversive stimulus contingent
upon the occurrence of a response (punishment), the delivery
of an appetitive stimulus contingent upon the absence of a
response (omission), the delivery of an aversive stimulus
contingent upon the absence of a response (avoidance), or
the termination of an aversive stimulus contingent upon
the occurrence of a response (escape). The observed effec
tiveness of a response-reinforcement contingency in increasing
49
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 50
or decreasing the tendency to respond determines whether
instrumental reinforcement has, in fact, occured. This
circular definition of reinforcement, commonly referred to
as the empirical law of effect, has the apparent advantage
of avoiding a priori commitment to theoretical conceptions
regarding the reinforcement process. It has the disadvantage
of implying commonality among all forms of instrumental re
inforcement, however.
Instrumental conditioning may involve discrete
trials which are signaled by a regular CS (as in signaled
or "classical" avoidance, excape or straight-alley reward
conditioning), or it may involve no regular signal at all
(as in free operant or unsignaled, Sidman avoidance con
ditioning) . In discriminative operant conditioning, a
continuous signal, referred to as the positive discrimina
tive stimulus (SD ), is present whenever responding is to
be reinforced. Its absence, or the continuous presence of £ the negative discriminative stimulus (S ), identifies a
period of non-reinforcement. Although there is a tendency
for the word "operant" to be used interchangeably with
"instrumental," the latter will be used generically in this
chapter to include all conditioning procedures in which an
explicit response-reinforcement contingency is operative,
while the former will be reserved for those unique instru
mental conditioning procedures which have emerged from the
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 51
work of Skinner (1938) and which normally begin with an
unelicited response.
When Miller and Konorski (1928) first attempted
to identify the differences between classical and instru
mental conditioning (labeled type 1 and type 2 by them),
they proposed that responses mediated by the autonomic
nervous system are modifiable only by classical but not
by instrumental conditioning. Their proposition was based
on the belief that autonomic nervous system responses are
not instrumental in nature. Although expressing some reser
vations based upon the observation that children seem to
learn to cry "real” tears in relation to their consequences,
Skinner (1938) adopted Miller and Konorski's position and
even edited it to the point of questioning whether non-
autonomic behavior can be modified by classical conditioning.
He attempted an exploratory study of instrumental condition
ing of digital vasomotor behavior and reported no evidence
of success. At about the same time Mowrer (1938) found
negative results in an exploratory study of avoidance con
ditioning of the skin resistance response (SRR). In the
content of this meager evidence, the proposition that
autonomic nervous system behavior could not be conditioned
instrumentally was accepted almost universally for more
than 30 years following Miller and Konorski's original
paper, although no systematic empirical evaluation of it
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 52
was undertaken until about 1958.
It is of more than passing historical interest that
this scientific cul de sac was ever seriously entered,
considering the fact that Bernard (1859) had long before
drawn scientific attention to the significance of the in
ternal environment. When Miller and Konorski (1928) meant
by the phrase "not instrumental in nature" was that auto
nomic responses do not ordinarily have any effect upon
the external environment, except under very unusual cir
cumstances (e.g., when children cry "real" tears and thereby
attain their goals). That these responses may be instru
mental in their influence upon the internal environment
hardly needs to be pointed out.
Beginning in 1958, research on the instrumental
modifiability of autonomically mediated responses was
undertaken by psychologists and physiologists using SRR
and skin potential response (SPR) as well as other autonomic
nervous system responses with human and non-human organisms.
The weight of the experimental findings has resulted in
complete rejection of the earlier erroneous belief that
autonomic responses are not instrumentally conditionable.
Skinner (1938) defined operant behavior as compris
ing those responses whose first occurrence is not preceded
by reliable stimulation. Kimmel and his associates based
several experiments upon this definition in seeking to
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 53
condition unelicited SRR (i.e., operant) by presenting
study Kixnmel 8c Hill C1960) used brief pleasant or un
pleasant odors as potential reinforcers. A series of five
low ampere, low voltage shocks were administered in order
to establish a standard response whose amplitude could be
used for determining when a reinforcable response has
occurred. One-half of the average amplitude of SRRs, which
the shocks elicited, was chosen as the reinforcement criterion
for each subject during conditioning. The effect of shocks
was two-fold: One was to reduce the rate of occurrence of
unelicited SRRs (Kimmel & Hill, 1961), as well as lessening
the frequency with which the reinforcement could be delivered.
The pleasant or unpleasant odors, during 20 minutes of con
ditioning, did not have the effect of influencing the rate
of responding of subjects receiving response-contingent re
inforcement as compared with the controls who received the
same number of pleasant or unpleasant odors per minute, but
at times of nonresponding. At the end of the conditioning
period, an extinction session followed, composed of complete
omission of reinforcement. This resulted in the fact that
contingent-reinforcement subjects increased in response
rate while controls decreased, showing the effect of response-
reinforcement contingency. This effect was true for both
types of odor.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 5h
In an attempt to modify the response-suppressing
effect of the preliminary shocks, in the future rewards
studies of Kimmel and associates, the shock was eliminated.
In addition, a dim white light was used as a reinforcer,
since the use of odor as potential reinforcer required a
2 sec delay and since no apparent difference in effect of
the plesant and unpleasant odors on the conditioning of
SRR was found.
Fowler & Kimmel (1962) presented the dim white light
as reinforcer to subjects in a totally dark room, for which
duration of the white light was explicitly controllable
and its delay reduced to negligible amount. The light
intensity of the reinforcing stimulus was lessened so that
it could only be seen in a dark room. Fowler and Kimmel
(1962) measured the amplitude of unelicited responses for
2 minutes prior to reinforcement presentation and used
one-half of their average amplitude as a reinforcement
criterion. In this study, two response-contingent reinforce
ment groups were used, one receiving the reinforcement for
8 min prior to extinction and the other recieving it for
60 min. In addition, control subjects were matched to
response-contingent Ss in the number of lights received
each minute, which were delivered at times of non-responding.
Both contingent reinforcement groups and both of the control
groups showed a recuction in frequency of response for the
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 55
first 6 minutes of reinforcement. However, response fre
quency began to increase thereafter, particularly notice
able in the 16-min contingent reinforcement group. Both
groups of control continued to decline in responding through
out the reinforcement period. Analysis of the data for the
two 16-min groups indicated that their divergence in the
last several minutes of reinforcement was significant,
as was the difference between the average frequency of
responding during the last 2-min taken separately. In ex
tinction period, the frequency of response was significantly
higher in the contingent groups than in the control groups,
especially following the 16-min of reinforcement. The
response frequency curves of the contingent and control
groups tended to converge during the extinction period,
with the contingent groups showing a reduction in response
frequency and the controls showing an increase.
In both studies, Kimmel and Hill (i960) and Fowler
and Kimmel (1962), a 5-sec period of time-out from reinforce
ment was employed following reinforcement, since the rein
forcing stimulus tends to elicit an SRR. During this time
out period the responses were neither counted nor reinforced,
because they could not be considered unelicited. Kimmel
and Kimmel (1963)a in replication of Fowler and Kimmel
(1962), time-out period was shortened to three seconds
because it was reasoned that the time-out period tends to
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 56
introduce bias against the controls and because it lessens
the number of possible reinforcements. Furthermore, dura
tion of the reinforcing stimulus was reduced from 1 sec. to
.1 sec., and the initial period of non-reinforcement and
the extinction periods were both increased to minutes.
Fowler and Kimmel (1962) had suggested the drop in the
frequency of response during the initial period of reinforce
ment may be dire to the failure to allow the Ss enough time
before conditioning to be acclimated to the experimental
situation. In this study (Kimmel & Kimmel, 1963)s only
one response contingent group was run, itfhich received 20
min of reinforcement and of nonresponse-contingent group
similar to those of the previous studies was included.
The result of the study showed that the difference
in response frequency between the response-contingent groups
and non-response-contingent group was highly significant,
both during acquisition and extinction, and that, the
lengthening of the initial non-reinforcement period had
the desirable effect of eliminating the previously observed
tendency towards an initial decrease in responding. Kimmel
and Kimmel express that because the acquisition response
frequency is expressed relative to average response frequency
of the last 2 min of initial rest period accounts for the
rather high level of responding, since the subjects drop
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 57
to a low level of responding by the last 2 min of the initial
operant period. That the same fact is also true for non
response-contingent group (controls), therefore, does not
reduce the importance of the difference between the two
groups.
The findings of these studies was further confirmed
by Shapiro, Crider and Tursky (1964), who reported the result
of their study using SPR instead of SRR as the reinforced
response, as well as reporting measure of heart rate and
respiration. Shapiro et al (1964) showed that the electro-
dermal changes were independent of skin potential (SP) and
heart rate as well as being unrelated to respiration changes.
The report of heart rate and respiration by Shapiro et al
(1964) was an attempt to deal with the possibility that
observed changes in electrodermal activity resulting from
response-contingent reinforcement might be an artifactual
consequence of operant conditioning of some other response.
Additional importance of the study was the fact that it
showed autonomic responses other than those which are rein
forced are not necessarily also modified by the reinforcement.
Two subsequent studies by Rice (1966) and Van Twyver
and Kimmel (1966) investigated the possibility of reinforce
ment influence on skeletal behavior to then serve as a
mediator of observed changes in autonomic response. Both
studies, using the electromyogram, employed the recording
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 58
of the Ss skeletal response from their arm on the same side
of the body as the hand containing electrodes. Accordingly,
this site was chosen because it is most likely source of
movement - elicited electrodermal changes in the 1 and in
question. In Van Twyver and Kimmel (1966) study, respiration
record were also taken during conditioning session and
both respiration rate and frequency of respiration irreg
ularities were reported. All the SRRs which occurred in
close continguity to EMG responses and respiration ir
regularities were eliminated from consideration. The results
showed that the instrumental conditioning of SRR via reward
training was quite pronounced, even under the highly con
trolled conditions described, and also that no difference
in any of the other measures were found between the two
groups of Ss, nor did any of the other measures change
systemastically during the experimental session.
An important fact to be considered here is that
the delivery of reinforcement at times when Ss were not
making unelicited SRRs (for the control groups) was in
itself an instrumental conditioning procedure. The data
from these cited studies indicate that the nonresponse-con
tingent controls showed a reduction in responding during
conditioning and an increase in responding during extinction.
"The fact that the response rate increases in extinction,
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 59
when the nonresponse-reinforcement contingency is removed,
establishes that the reduction of responding during con
ditioning is not merely attributable to non-associative
decremental process, such as habituation (Kimmel, 1973a pp.
262- 263)."
In the Rice (1966) study, reinforcement was with
held during conditioning unless the SRR occurred in the
absence of an immediately preceeding EMG. The subjects,
in Rice’s study, were divided into two groups based upon
their initial response rates. The high responders showed
instrumental conditioning of SRR, but the low responders
failed to show the conditioning effect.
In a study by Birk, Crider, Shapiro, and Tursky (1966)
bodily movements which could be mediate electrodermal changes
was greatly reduced by use of d-tubocuraine. One subject
(Birk) volunteered to be curarized, although not dramatically
(paralytic) curarized and artifically respirated, for obvious
reasons of safety. Miller (1969) has employed curarization,
on subhumans, sufficient to block the neuromuscular junction
totally and has employed artificial respiration to maintain
the animals during curarization. Nevertheless, the subjects’
skeletal behavior was reduced to minimum, while the subject
could breathe without difficulty (some slight head move
ment, with difficulty, was possible). Instrumental con
ditioning of SDR was found, as in earlier studies without
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 60
curare, and no associated changes in respiration or basal
potential occurred. The majority of published work on
reward of instrumental conditioning (Coffman & Kimmel, 1971;
Crider, Shapiro, & Tursky, 1966; Gavalas, 1967; May & Johnson,
1969; Milstead, 1968; Schwartz & Johnson, 1969s Shapiro &
Crider, 1967)5 a few studies have been reported which do
not fully conform to this pattern. Edelman (1970) found
that only when all Ss responses, including those associated
with EMGs, were reinforced evidence of instrumental condi
tioning was present, but not when responses associated with
EMGs were nonreinforced. Edelman*s subjects reported that
skeletal events were responsible for the reinforcement; a
light which signaled that one cent was earned. However,
an electric shock was used in this study to gain an initial
increase in SP, and there was an observed tendency for
deep breathing following the shock. Two other studies have
been interpreted as negative (Stern, 1967; Stern, Boles,
& Dionis, 1968). Even though the study by Stern et al (1968)
involved findings of differences similar to those found by
others, the results were attributed to cognitive mediation
on the part of the Ss. In the study by Stern (1967)5 the
subjects were aware of reinforcement contingencies, and the
experimenter found no significant differences in support
of an instrumental conditioning.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 61
Section B. EDA as an Indexer of Phobia
Background and Definitions. Jones (1924), who described
elimination of a young boy’s intense fear of small animals
by the procedure of gradually exposing him to a rabbit
while he was eating a favorite food, was first to report
use of systematic desensitization therapy for treatment
of phobias. According to Jones (1924) the reduction of
young boy's fear was caused by the gradual replacement of
fear by the positive responses associated with feeding.
Wolpe (1958) labeled this phenomenon "reciprocal inhibition."
This term was first used by Sherrington (1906) to describe
a much more specific reflex phenomenon. Wolpe has defined
the "reciprocal inhibition" in the following terms: "if
a response inhibitory of anxiety can be made to occur in
the presence of anxiety evoking stimuli, it will weaken
the bond between these stimuli and the anxiety (1964, p. 10)."
Wolpe (I97I3 p. 341) also defined anxiety "as an individual
organisms characteristic constellation of autonomic responses
to noxious stimuli."
In general, Wolpe1s view is that phobic behavior
is manifested by the evocation of anxiety (an autonomic
response), which in turn derives the organism to escape,
or avoid, from the anxiety-eliciting situation, in turn
which escape or avoidance reduces the anxiety. Since Wolpe
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 62
views the anxiety reduction as reinforcing, the escape or
avoidance response, which is continually reinforced, becomes
the overt, observable, characteristic of the phobia. This
view is essentially based on Mowrer’s (19^7) two-factor
theory of avoidance learning.
Solomon and Wynne (195-4) suggest that in order for
fear to extinguish, the organism must remain in contact with
the fear evoking stimulus and not be reinforced, that is,
not experience negative consequences. However, since the
organism's immediate response to the fear-evoking stimulus
is to escape from or otherwise avoid possible negative con
sequences, thereby reducing fear, the fear response never
gets a chance to extinguish. This is the principle of
anxiety conversation, by which the phobic behavior is main
tained over a long period of time. Although the principle
of anxiety conservation has been criticized by Costello
(1970), and the two-factor theory by Herrnstein (1969); it
is evident that many therapists espouse the view of Wolpe
than an enxiety response, a conditioned autonomic response,
remains at the core of phobia behavior and it is the focal
response which must be reciprocally inhibited by desensiti
zation therapy. Aside from Wolpe’s reciprocal inhibition
view, there also have been other explanations offered within
the framework of extinction and habituation, and even in
terms of cognitive change, for the postulated mechanisms
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 63
presumed to underlie the desensitization of acquired fear.
The counter conditioning, or reciprocal inhibition,
notion of systematic desensitization, identified most clearly
by Wolpe (1958), is essentially a restatement of Guthrie’s
(1952) position that responses do not disappear through
the weakening of some associative bond, but are replaced
by new responses. This basically requires the patients to
learn to substitute a response which is incompatible with
fear for the fear response in the presence of fear-eliciting
stimulus. Wolpe’s subject are taught an abbreviated form
of the deep muscle relaxation procedure described by Jacobson
(1938). This relaxation process is presumed not only to
result a state of striate muscular dormancy but an associated
state of reduced autonomic activity, which for Wolpe (1971)
is for the most part synonymous with reduced anxiety. After
learning to relax completely and efficiently, patients are
asked to imagine the phobic object. Initially the therapist
and the patient construct a hierarchy of items relevant to
the phobia, and the patient begins the treatment procedure
by imagining items which are at the lowest hierarchy. Ac
cordingly, the reduced autonomic tonus induced by relaxation
is incompatible with minimal fear which would normally be
elicited by the low hierarchy item, which the patient finds
can imagine without anxiety. Succeedingly the patient
imagines scenes higher on the hierarchy, and gradually all
of his fear is replaced by the induced relaxed state and
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 6H
reduced autonomic tonus. In an ideal situation, there is
adequate or complete transfer of this reciprocal inhibition
from the imagined object to the real object.
The demonstration and relaxation reduces or inhibits
arousal, as reflected in electrodermal activity, and that
this inhibition is maintained in the presence of phobic
stimulus object, supports the extent that the counter-con
ditioning is practicable. Furthermore, if it is to be /
shown that reduced autonomic responsiveness becomes a sub
stitute response for the fear response, one would predict
that for some time after successful desensitization, presen
tation of the phobic object should fail to elicit large or
frequent electrodermal responses (EDRs). Of course, for
the theory counter conditioning theory it is important
that response dimunition with repeated presentation be
unobtainable without paired relaxation, which would other
wise account for an extinction or habituation model.
An extinction explanation of systematic desensitiza
tion is based upon the notion that a conditioned phobic
response will diminish and eventually disappear after re
peated unreinforced presentations of the conditioned stimulus
(phobic subject) which initially elicited it. This model
suggests that relaxation is unnecessary for successful
desensitization and that the important feature of the treat
ment procedure is repeated presentation of the phobic stimulus
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 65
object. In addition, it finds the hierarchy of minimally
threatening to maximally threatening scenes as another
unnecessary element in the extinction process of fear.
The "implosive therapy", asserted by Stampfl and Levis (1967),
employs this view in treatment of the patients. In this
procedure patients are repeatedly exposed to the most
frightening item of the hierarchy without any prior relax
ation training. Clearly, the assumption of implosive therapy
is that the procedure will provide for efficient extinction
of the fear response and the effective generalization from
the treatment environment to real life.
The habituation model, closely follows the extinc
tion view (Lader & Mathews, 1968), except that these investi
gators see the relaxation procedure as a helpful, although
not necessary, supplement to the desensitization process
in that it lowers the patient’s overall arousal level
(Mathews, 1971)• According to Mathews (1971), lowered
arousal level facilitates the habituation process (Katkin
& McCubbin, 1969; Lader, Gelder, & Marks, 1967), and may
facilitate image formation.
Sokolov’s (1963) "neuronal model" has been cited
by the proponents of habituation as the source of their
view. Briefly, Sokolov accords that the repeated presen
tation of a stimulus result in the generation of a "neuronal
model" which matches this stimulus, and the strength of
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 66
that neuronal model determines the extent of the inhibition
of autonomic and skeletal responses to incoming stimuli.
According to Sokolov, repeated presentations of any stimulus
should ultimately result in diminished response to it.
Mathew (1971) holds the view that the value of relaxation
in systematic desensitization facilitates habituation and
that reciprocal inhibition is fiction.
The habituation model is usually applied to uncon
ditional stimuli, and not to conditional stimuli, which
possess signal value for the organism. Thus, the ultimate
appropriateness of the habituation model may be questioned
for most of the phobic stimulus subjects employed in desen
sitization therapy, on the grounds that they are most
usually construed to be conditioned stimuli. Systematic
desensitization, after all, attempts to eliminate acquired
fears, not innate ones.
Page (1955) has provided evidence from the animal
laboratory that the extinction of underlying fear responses
may not be closely related to the extinction of overt
avoidance behavior as is predicted from two-factor theory
(Mowrer, 19^7). In other words, while support for the
extinction view could be drawn from demonstration, that
the repeated presentation of a phobic object results in
the dimunition of autonomic responding without use of relax
ation, the extinction of avoidance behavior may not
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 67
necessarily be evidence for corollary extinction of the
fear component of phobic behavior.
Page (1955) trained rats to go from one side of a
box to another in order to avoid shock. After this training,
half of the rats were given normal extinction and half were
restrained in the starting box for 15 sec during the first
five extinction trials. The results showed the restraint
facilitated extinction; the restrained group showed extinc
tion after 8 trials and unrestrained group after 30 trials.
Later, page trained both groups plus an additional group
which had never been trained to avoid to run back to the
starting box to obtain food. Average latencies for the
first five training trials indicated for the new group a
latency of 25 sec, the group that had extinguished in 30
trial showed a latency of 60 sec, and the restrained group
which had showed the most rapid extinction showed a latency
of 125 sec. The starting box, distinctly, still posessed
cues which interfered with new learning even though avoid
ance of the box had been extinguished. Also, the group
which had it extinction facilitated by restraint (an analog
of therapeutic intervention) showed the most interference
with new learning. Thus, extinction procedure, while effec
tive with respect to the avoidance response, actually increased
the apparent fear level of the animals. It is evident from
demonstrating such as Page’s procedure the theoretical
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 68
importance of assessing autonomic as well as behavioral com
ponents of the desensitization process in human subjects
because it is otherwise unclear whether therapy is changing
only motor behavior or both the motor behavior and the fear
presumed to underlie it.
Finally, a number of theorists have postulated that
the observed improvement following systematic desensitization
may be explained as a function of a change in the patient's
expectancy about the phobic object and/or a cognitive re
appraisal of his own ability to cope with the obj'ect.
Efran and Marcia (1972) suggested that instructional set
manipulation was effective as an analog of desensitization
therapy in alleviating spider phobias (Efran & Marcia, 1967;
Marcia, Rubin, Efran, 1969). A related idea, derived from
Lazarus’ theoretical view (1966); has been proposed con
cerning the importance of cognitive coping processes in the
modulation of fear responses (Folkins, Lawson, Opton, and
Lazarus, 1968).
In order to determine the relationship of electro-
dermal activity as an index of therapeutic effectiveness
one needs to investigate the empirical findings which have
compared the electrodermal activity of phobic and non-phobic
subj'ects to noxious stimuli.
Electrodermal Activity as an Index of "Phobic” Responding.
As Lang (1969) has pointed out, defining anxiety solely
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 69
in terms of one of its attributes is a dangerous oversimpli
fication of a complex construct. Nevertheless, Wolpe’s
emphasis on the organism’s characteristic pattern of autonomic
responses to noxious stimulation and his adherence to a
two-factor interpretation of phobic avoidance behavior has
led behavior therapists to place special emphasis on the
autonomic components of fear. Given that this position
is tenable, there has been a sufficient accumulation of
evidence that show electrodermal responsiveness is a valid
index of a subject’s autonomic response to a noxious stimulus.
Geer (1966) has demonstrated that spider phobic
subjects emitted greater skin conductance responses (SCRs)
to pictures of spiders than they did to pictures of snakes,
which he assumed to be generally negative stimuli unrelated
to the spider phobia. Geer’s spider phobics also gave
greater SCRs to the pictures of spiders than did a matched
group of subjects who reported being unafraid of spiders.
Thus, Geer (1966) demonstrated that the SCR reflected the
distress elicited by the pictorial representation of a
noxious object.
Wilson (1967) reported essentially the same findings
with a sample of ten spider phobics and ten subjects who
reported no fear of spiders. A set of tachistoscopically
presented slides of spiders and neutral landscapes was
presented to these 20 subjects, and their skin resistence
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 70
responses (SRRs) were monitored. Wilson found that the
ratio between SRR to the spider slides and SRR to the
landscape slides yielded a perfect discrimination between
the groups.
In discussing the findings of his study, Geer (1966)
suggested that it was not possible to conclude that the
SCRs reflected fear per se, as they might also have reflected
orienting responses to the noxious pictures. In his recent
review of psychological approaches to desensitization.
Mathews (1971) also has raised questions with respect to
both Geer’s (1966) and Wilson’s (1967) data, suggesting
that some concurrent measurement of a subject’s experiential
state would be necessary to determine whether the EDR reflected
fear or attention. This question has concerned psychophy
siologists for some time, and there has been a great deal
of discussion on question of whether EDA reflects attention,
arrousal, or emotion (Duffy, 1962; Flanagan, 1967; Malmo,
1959)- It is not clear that this quesiton is pertinent to
the current issue, for it is not obvious that one can dis
tinguish between the attentional component and the fearful
component of a phobic response to a phobic object. Certainly
it seems reasonable that a phobic person will attend to
the object of his fear, and that increased attention is in
fact an essential component of the entire phobic response.
In that case it seems reasonable that the findings of Geer
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 71
(1966) and Wilson C1967) reflect some autonomic component
of differential "fearfulness" on the part of their subjects.
It must be noted at this point that both Geer (1966)
and Wilson (1967) observed differential EDRs to the phobic
and non-phobic objects only during early presentations of
the stimuli. Both investigators reported relatively rapid
habituation of the EDRs after a few presentations. This
is of a potentially great importance, for it is just such
a diminution in response strength which might be interpreted
as evidence of therapeutic success. Of course, there is
a distinct difference between the procedure followed by
Geer (1966) and by Wilson (1967) and the procedure employed
in systematic desensitization therapy. In systematic desen
sitization therapy, as usually employed, the patient is not
presented with pictures of the phobic object or even with
the actual phobic objects; rather, in the therapeutic situa
tion the patient is asked to imagine the phobic object in
a variety of different configurations. The research cited
above indicates that pictorial representations of phobic
objects elicit differentially large EDRs from phobic and
non-phobic subjects. Other recent research (Barlow, Agras,
Leitenberg & Wincze, 1970; Barlow, Leitenberg, Agras &
Wincze, 1969) indicates that the presentation of actual
phobic stimulus objects also elicit differential EDRs from
phobic and non-phobic subjects. Yet, it remains of con
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 72
siderable importance for Wolpe’s theory of systematic
desensitization to demonstrate that imagined stimulus objects
can also elicit EDRs of differential magnitude from phobic
and non-phobic subjects.
According to Wolpe, "there is almost invariably a
one-to-one relationship between what the patient can imagine
without anxiety and what he can experience in reality with
out anxiety" (1963a P- 1063). In systematic desensitization
therapy, visualization of the phobic object is assumed to
produce autonomic reactions similar to those produced by
direct contact with the phobic object, but differing in
intensity. Several investigators have tested the assumption
that imagining fearful scenes produces physiological arousal,
although the experiments have not always been directly re
lated to desensitization therapy.
Imagery versus Direct Experience. Barber and Hahn (1964)
studied comparative physiological effect of real and imagined
pain in 48 female subjects randomly assigned to one of four
conditions. During the first 20 minutes of the experiment,
subjects were asked to sit quietly ("waking" condition),
while subjects in a fourth condition were given a "hypnotic
induction" procedure for 15 min, followed by a 5-min "test
suggestion" period to assess the "hypnotic" state. During
a cold pressor test (water at 2°C applied to the left hand
for 1 min) following the 20-min period, all subjects showed
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 73
decreased skin resistance level (SRL); there were no signi
ficant differences between the groups in either physiological
or subjective responses to the painful stimulus.
Following this, subjects in the "hypnotic" condition
and in one of the "waking" groups were told that they would
be exposed to an innocuous stimulus (immersing hand in tepid
water) but instructed to imagine that they were once again
experiencing the painful stimulus. Subjects in a second
"waking" condition were administered the cold pressor test
again, without specific instructions to imagine the painful
stimulus, and subjects in the third "waking" condition
received the innocuous stimulus, also without instructions
to imagine. Tonic levels of SR were recorded for 1-min
period preceding the test. Mean SRL scores obtained during
the base-line and test periods indicated no significant
differences between the four groups; however, there was a
tendency for both groups instructed to imagine pain to show
decreases in SRL similar to the group actually experiencing
the painful stimulus. Thus, these data suggested that
instructions to imagine a painful stimulus elicited physio
logical arousal in the same manner as direct experience.
Further evidence for this notion was reported by
Craig (1968), who studied physiological arousal to direct
aversive stimulation (a cold pressor test), a vicarious
stress experience (viewing a confederate undergoing cold
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 74
pressor test), and an imagined stress experience (immersing
a hand in cold water, with instructions to imagine that the
water was "cold as ice" and "very painful"). Craig’s (1968)
results indicated that direct aversive stimulation did not
result in significantly different skin conductance levels
(SCL) than did the imagined stress experience.
Another aspect of systematic desensitization, that
of hierarchy and its relation to EDR has also been investi
gated. Lang, Melamed, and Hart (1970), investigated the
notion that the subjective steps of an anxiety hierarchy
are related to physiological responsivity. Their first
experimental group consisted of 5 male and 5 female sub
jects afraid of spiders. During the first two experimental
sessions a tentative anxiety hierarchy was constructed for
each subject; during the third session each subject was
trained in visualization with neutral scenes, and in the
fourth session each subject was presented randomly with a
series of five fearful scenes chosen from his anxiety hier
archy, alternating with four neutral scenes. After the
presentation of each item, subjects were asked to rate both
the vividness of their imagery and their experienced anxiety
on a scale from 0 to 4. Throughout the fourth session
physiological recordings were made. The results revealed
an overall association between SCR magnitude and hierarchy
position although a significant linear trend was revealed
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 75
only for the spider phobic group.
Similarly, Van Egeren, Feather, and Hein (1971)s
in a study of 30 male subjects with public speaking phobias
demonstrated both increases in SCL from a prestimulus period
to the imagining of threatening scenes and a direct relation
ship between the position of an item in the anxiety hier
archy and a number of magnitude of SCRs to the visualization
of that item.
Grossberg and Wilson (1968) investigated the effects
upon autonomic activity of imagining both neutral and fear
ful stimuli, which were selected individually for each
subject on the basis of responses to Wolpe and Lang’s (19 64)
Fear Survey Schedule (FSS). A group of control subjects
was also selected who showed no unusual attitude toward
either the items that were neutral or fearful for the
experimental subjects. "For example, if the experimental
subject was disturbed by injections but neutral toward
high places, she would be matched with a control subject
who had indicated no disturbance for injection or high
places" (Grossberg 8c Wilson, 1968, p. 126).
Base-line physiological levels were recorded for
all subjects during a 10-min adaptation period, after which
the experimenter read a fearful or a neutral scene and then
instructed the subjects to imagine it vividly. The reading
and instructions were repeated eight times, once each for
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 76
four neutral and four fearful scenes. Mean SCLs obtained
during the reading were compared with adaptation period SCLs
and expressed as ratio of amount of change. Fearful scenes
produced significantly greater increases in mean SCL than
neutral scenes during imagination, whereas no significant
differences were found between fearful and neutral scenes
during the reading interval. These results support Wolpe’s
assumption that the imagination of a fearful stimulus is
sufficient to elicit physiological arousal. Further find
ings of Grossberg and Wilson, however, raise important ques
tions concerning the necessity of the relaxation component
in systematic desensitization. They report that in their
finding "...successive reading trials produced significantly
decreasing amounts of arousal for the...SC measures, and
this effect was also evident for SC during successive Imagin
ing trials. The number of...SC increases over trials...
showed a similar decline. This adaptation or extinction
effect occurred without deliberate relaxation training,
and raises the question of the role of relaxation training
in Wolpe’s desensitization procedure" (Grossberg & Wilson,
1968, p. 131).
The data reviewed so far indicated that the imagina
tion of a phobic stimulus object does, in fact, tend to elicit
the autonomic response which Wolpe has called anxiety.
Thus, one necessary precondition for the effective utiliza-
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 77
tion of systematic desensitization seems to be met - the
anxiety response can be elicited in the absence of actual
stimulus. Yet, Grossberg and Wilson’s conclusion coupled
with the findings of Geer (1966) and Wilson (1967) indicate
that the "anxiety response" seems to diminish after repeated
exposures of the phobic object, even when the other elements
of desensitization procedure are absent. These findings
are inconsistent with Wolpe's theory about mechanism of
desensitization therapy and lend credence to the extension
notion, insofar as they suggest that response dimunation
can be obtained without associated relation.
The role of progressive relation in desensitization
process has been investigated in terms of physiological
effects of brief relaxation training. These investigators
have reported contradictory findings. Although Jacobson
(1938) has shown that prolonged training in muscular relax
ation produces a general reduction in autonomic arousal,
it is essential for the counter conditioning position that
brief training in muscular relaxation also can be shown
to result in reduced autonomic tonus.
Grossbert (1965 ) compared a number of physiological
measures, including SRLs of 30 male subjects assigned to
one of three groups: a group trained in relaxation by
recorded instructions, a group that listened to relaxing
music, and a self-relaxation control group that received
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 78
no specific instructions in relaxation. Grossberg (1965)
found no significant differences between groups in either
SRL and or other measure of autonomic activity; indicating
that the relaxation technique possesses no particular
advantage in effecting autonomic change. Similar results
have been reported by Barber and Hahn (1963), who reported
no particular advantage of hypnotically suggested relaxa
tion as compared with instructions to just sit quietly,
and by Lehrer (1970) who also found that brief relaxation
training was apparently no more effective than normal rest
ing for reducing autonomic activity.
Paul (1969) compared physiological effects of brief
relaxation training, hypnotically suggested relaxation, and
a self-relaxation control procedure for 60 female subjects.
Following specific instructions for each condition, subjects
were asked to sit quietly, for a 10-min adaptation period,
the last minute of which served as a basal period. All
subjects were instructed to practice their respective tech
niques for about 15 min, twice a day, for the week separating
the first and second sessions, at which time they were told
briefly that the procedure would be similar to that of the
first session. Paul's result for SCL were entirely consistent
with those of Barber and Hahn (1963), Grossberg (1965), and
Lehrer (1970); no differences between groups were obtained.
Paul's (1969) results for the heart rate, muscle tension,
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 79
and respiration showed significant effects in favor of
relaxation training, and inconsistent with his SCL results.
Paul and Trimble (1970) ran 30 additional subjects
after the completion of Paul (1969) study, using prerecorded
instructions, instead of a live experimenter, in order to
assess the effect of the experimenter's presence on the
efficiency of the instructions. In general they found that
recorded instructions were not as effective as live instruc
tions in reducing physiological arousal. Paul and Trimble's
(1970) findings added nothing new to the observation that
there were no differences in SC between the brief relaxation,
hypnotically suggested relaxation, and self-induced relaxation
procedures.
Mathews and Gelder (1969) evaluated the effects of
relaxation training on a sample of 14 clinically defined
phobic patients, rather than on a sample of fearful under
graduates. In addition, Mathews and Gelder (1969) employed
a relaxation procedure more consistent with that used in
actual therapeutic situations than did most other Investi
gators. All patients initially were trained in relaxation
for a period of 1 hour, with instructions to practice the
relaxation technique during the following week. A second
session consisted of 30 min of practice in passive concen
tration on muscle groups, including instructions and sug
gestions from the therapist, followed by 30 min of similar
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 80
tape-recorded standardized instructions. In a third session,
patients were exposed to: (1) the same relaxation recording
followed by a control recording in which the patients were
asked to rest, but were not told to relax in the formal
manner in which they had been trained; or (2) the control
recording followed by relaxation recording. Results of
this experiment indicated a significantly faster rate of
SCL adaptation during relaxation periods, when compared
with control periods, but no main effect of treatments on
overall SCL. Additionally, Mathews and Gelder (1969) found
a significant main effect of treatment on the rate of spon
taneous SC fluctuations, indicating that the number of such
fluctuations was generally lower during the relaxation period.
Furthermore, this experiment yielded a significant product -
moment correlation between number of SC fluctuations and
subjective report of "anxiety tension" and "relaxation".
These findings on SC fluctuations are consistent with the
experimental findings of Katkin (1965, 1966) and Rappaport
and Katkin (1972) which showed a relationship between experi
mental induction of stress and number of spontaneous SR
fluctuations.
Mathews and Gelder’s (1969) positive findings are
somewhat inconsistent with the other findings on relaxation,
although it must be remembered that they, too, were unable
to demonstrate a clear main effect of relaxation on SCL.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 81
The positive results which they obtained may be explained
in part by the more intensive relaxation training they
employed (Mathews, 1971)5 or by the fact that a genuinely
phobic population may respond differently to relaxation
instructions than a population of fearful undergraduates.
Finally, the results of Mathews and Gelder were most clear
for spontaneous fluctuation rate, an index not used by
other investigators. Recent evidence on the utility of
this measure as an index of arousal (Burch & Greiner, I960;
Katkin, 19655 1966; Katkin & McCubbin, 1969; Silverman,
Cohen & Shmavonian, 1959) suggests that it might be a sub
stantial importance in evaluating the therapeutic effects
of relaxation training as well as other aspects of the
desensitization procedure.
Grings and Uno (1968) have conducted a detailed and
critical evaluation of the counter conditioning Hypothesis,
in an experiment that was theoretically precise, but did
not address itself directly to the problems of clinically
phobic behavior. Grings and Uno (1968) performed an analog
experiment in which they essentially induced a phobic
response in the laboratory and then studied the effect of
reciprocally inhibiting it. In short, what Grings and Uno
did was to train 12 volunteer subjects in muscle relaxation.
After all subjects had learned to relax completely, they
were instructed to initiate relaxation when they saw the
word NOW projected on a screen. On the following day,
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 82
subjects were presented with a pure color flashed on the
screen, followed by a painful electric shock. Thus, the
color became a conditional stimulus for the elicitation of
EDR.
After both training in relaxation and conditioning
of the EDR to color was completed, test trials were intro
duced in which subjects were exposed to the fear cue alone,
and to the fear cue with the verbal cue for relaxation super
imposed on it. "The magnitude of response to the compound
composed of the ’fear’ cue and the ’relaxation’ cue, was
consistently less than the response to the ’fear’ cue alone"
(C-rings & Uno, 1968, p. M83)-
These results, while impressive, do not necessarily
suggest that progressive relaxation will function in the
same way for phobic subjects in the course of desensitization
therapy, nor even that relaxation will have similar inhibit
ing effects on autonomic response to threatening stimuli
of more personal significance or more complex origin.
Davidson and Hiebert (1971) studied the effects of
relaxation on the inhibition of autonomic responses to a
stressful film. Using a noxious film which depict a care
less shopworker being mutillated by a circular saw, Davidson
and Hiebert set out to evaluate the effects on SC responses
of differentially specific instructions to relax. One-third
of their subjects receive specific instructions in abbreviated
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 83
progressive relaxation; a second group of their subjects
received instructions to relax without any specific training;
and a third group of subjects, the control group, received
no instructions to relax. All subjects were then shown a
.92 - sec segment of the distressing film ten times in
succession with approximately 2 min between showings. Sub
jects in the two relaxation groups were requested to main
tain as much relation as possible throughout the showings.
Skin conductance levels were recorded every 2 sec, yielding
46 scores per showing. Davidson and Hiebert (1971) found
that on the first showing of the film there was no difference
in SC response among subjects in the three groups. However,
after the fifth showing of the film, a clear pattern emerged
in which SCLs for subjects in the two relaxation groups began
to decrease, ultimately reaching their prefilm level, while
SCL for subjects in the control group did not decrease.
Thus, these data indicated that relaxation instructions,
whether specifically describing progressive relaxation or
simply being casual instructions to relax, have an inhibitory
effect upon overall SCL in the presence of a noxious stimulus.
No significant difference was found between the two relaxa
tion groups. These findings are similar in quality to those
of Grings and Uno (1968) and support the notion that relaxa
tion inhibits autonomic response to noxious stimulation.
Yet Davidson and Hiebert’s (1971) study is also somewhat
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 84
different in content from the situation usually found in
desensitization therapy.
A study which more closely approximated the actual
desensitization procedure, although it uses actual instead
of imaginary stimuli, has been reported by Barlow et al
(1969). Barlow et al (1969) investigated what they have
termed the "transfer gap" in systematic desensitization,
i.e., the observation that progress in the imagination of
successive steps on a phobic hierarchy does not necessarily
reflect progress in the real-life situation. Twenty female
subjects, who indicated that they would feel "definitely
tense" in the presence of a harmless snake at a distance
of 2 ft, were assigned to either a standard desensitization
procedure involving relaxation while a live caged snake was
moving progressively closer to the subject. Tonic SCL was
obtained for all subjects under two conditions: (1) while
imagining five scenes from a hierarchy, and (2) in the
presence of the snake at distance of 10, 5* and 2 ft.
A comparison of pretreatment and post-treatment
mean SC scores revealed that subjects in the systematic
desensitization group showed reduced SCRs to imagined scenes,
but no change in SCR to the real snake. In contrast, the
analog group exhibited significantly reduced SCRs to both
and imagined situation. Behavioral approach measures in
dicated additional support for the superiority of the group
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 85
that experienced contact with the real phobic stimulus,
The results of this study suggest that standard
desensitization procedure, employing imagined rather than
real objects, may not be the most efficient techniques for
the reduction of autonomic components of the phobic response.
Several studies have evaluated the role of relaxation in
standard desensitization paradigms.
Wolpe and Flood (1970) compared changes in SR for
five subjects administered a standardized desensitization
technique with relaxation training (RT group) and five
subjects receiving desensitization with no training in relax
ation nor instructions to relax at any time during the pro
cedure (NR group). After an initial interview, during which
anxiety hierarchies were constructed, five evenly separated
items from each subject's hierarchy were chosen. During
the next four sessions, subjects were presented with the
five stimulus items in ascending order, while physiological
recordings were made. Skin resistance levels during the
stimulus periods were compared with baseline SRLs obtained
1 sec prior to the reading of a stimulus item, and the SRR
was expressed as a percentage change score.
Although Wolpe and Flood (1970) provided no statis
tical analysis of their data, the curves which they presented
suggest that subjects in the RT group showed a systematic
decrease in SRR magnitude over four desensitization sessions
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 86
while subjects in the NR groups showed no change in SRR to
five items selected from their hierarchies. While these
data seem to indicate the general effectiveness of relaxation
in desensitization procedures* they also raise some questions.
First of all* Wolpe and Flood reported that by chance the
five subjects assigned to the RT group showed larger initial
SRRs to the imagined stimuli than did the five subjects
assigned to the NR group. In fact* the smaller SRR ever
obtained from subjects in the RT group after treatment
never was as small as the initial pretreatment response
elicited from the NR group. Consequently, the results may
be nothing more than an artifact of had sampling and a floor
effect for subjects in the NR group. Second of all, Wolpe
and Flood (1970) were surprised themselves to discover that
subjects in their RT group showed SRR decrements as rapidly
to high hierarchy items as they did to lower hierarchy items
and were moved to comment, "the question must be faced
whether the standard technique of desensitization is neces
sarily the best" (1970, p. 200).
Hyman and Gale (1973) studied electrodermal, sub
jective, and behavioral responses of 24 female snake phobics,
divided into three groups: systematic desensitization with
relaxation (D), systematic desensitization without relaxation
(Ext), and relaxation with the visualization of neutral
scenes (R). The electrodermal measure consisted of the
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 87
visualization compared with tonic SRL just prior to each
visualization. Significant negative linear trends were
found for all groups; however, the rate of habituation of
the EDR to repeated presentations of the phobic stimulus
appeared to be greater for the D group than for the other
groups. In addition, self-report and behavioral outcome
measures (fear survey schedule, fear thermometer scores,
and a runway task) indicated a superiority for the D group
over the Ext group, with the R group falling between the
two. Thus, Hyman and Gale (1973) reported limited support
for the counter-conditioning explanation of systematic de
sensitization, as did Van Egeren et al (1971)-
In contrast to these findings, Waters, McDonald
and Koresco (1972), utilizing an analog desensitization
procedure, compared SRRs, and SRLs for 40 female rat phobics.
One group of subjects (SD group) received training in relaxa
tion, to be paired with instructions to imagine themselves
in the phobic situation while viewing five slides of a girl
progressively approaching the rat in a cage; the second
group (NRC) received a procedure identical to that of the
SD group except they received no training in progressive
relaxation. Both the SD and NRC groups exhibited decreased
arousal to phobic stimulus across trials and significant
changes in avoidance behavior from pretest to post test.
No difference between the groups were reported for either
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 88
physiological or behavioral measures; however, subjects in
the SD group reported significantly lower subjective fear
during the procedure (fewer signals of anxiety) and thus
required significantly few trials to obtain a criterion
level of reduced fear than did the nonrelaxation controls
(NRC). Waters, et al. (1972 concluded that while relaxa
tion tends to accelerate the process of systematic desensi
tization, it is not a necessary component of the procedure,
a view which is similar to that put forth by Mathews (1971).
In another analog study, Polkins et al. (1968) com
pared SC measures of 51 female and 58 male subjects during
exposure to a stressful film depicting an industrial accident.
Prior to viewing the film, subjects were randomly divided
into four groups: an analog of systematic desensitization,
relaxation along, cognitive rehearsal (visualization of
stressful scenes), or a no-training control group. Both
the analog desensitization and cognitive rehearsal groups
received training in imagining scenes from stressful film
prior to viewing the film; however, in place of relaxation
training, the cognitive rehearsal group listened to a tape
concerning study habits. On both SCL and self-report
measures during the accident scene, the no-treatment control
group exhibited the greatest amount of "anxiety," followed
by the desensitization group, and relaxation group. Arousal
(i.e., SCL) was lowest for the cognitive rehearsal group.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 89
Thus, Folkins et al. (1968) concluded that the separate com
ponents of systematic desensitization, i.e., relaxation
and cognitive rehearsal alone, were more effective in
reducing physiological stress reactions to the accident
film than they were when combined as they are in reducing
physiological stress reactions to the accident film than
they were when combined as they are in systematic desensiti
zation, further supporting the notion that the relaxation
component, while useful, may not be essential for autonomic
change.
Lomont and Edwards (1967), in an attempt to evaluate
the reciprocal inhibition and extinction hypothesis of
systematic desensitization, compared five measures of snake
fear change including SRL in 22 female snake phobics. Half
of their subjects were assigned to a treatment condition
which received systematic desensitization, including standard
relaxation, and half were assigned to a group which received
systematic desensitization without any relaxation. The
latter group was defined as an extinction treatment. In
order to guarantee that subjects in extinction condition
would not independently practice muscle relaxation, they
were instructed after each stimulus visualization to tense
their muscle. All subjects were presented with a live
snake at a distance of 6 feet before treatment began and
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 90
after having received ten sessions. During the pretreat
ment and post-treatment snake presentations, SRLs were
obtained.
Lomont and Edwards (1967) found no significant dif
ferences between the two groups in SRL, although measure
of subjective responses to snake fear items (including rat
ings on a 10-point "fear thermometer") yielded results favor
ing the desensitization group. However, Lomont and Edwards
(1967) found marked decreases in SRL across trials for both
the desensitization and extinction groups, results similar
to those of Grossberg and Wilson (1968) and Gale, Hyman,
and Ayer (1970). All three of these studies found habitua
tion of the EDR across trials, irrespective of relacation.
It must be noted, however, that Lomont and Edwards’ (1967)
technique was unique in that pre and post therapy SRLs were
obtained during presentation of the real phobic object,
although the treatment procedure employed imagined phobic
objects as desensitization stimuli. In that sense, Lomont
and Edwards (1967) have most closely approximated the con
ditions that constituted the critical test of clinical
effectiveness in a real-life therapy situation.
Edelman (1971) also conducted a study on the effec
tiveness of progressive relaxation, comparing the standard
progressive relaxation technique with an instructional set
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 91
designed to elicit relaxation, but not involving the standard
ized relaxation procedure utilized the desensitization therapy.
Edelman*s subject were not selected on the basis of any
specific phobia, but were rather selected on the basis of
general anxiety level as measured by Taylor Manifest Anxiety
Scale (Taylor, 1953)- Half the subjects were then placed
in a group which was asked to visualize a scene very high
in an individually generated fear hierarchy and half the
subjects were placed in a group which was asked to visualize
a scene very low in their hierarchy. In addition, half of
each of these groups was trained in progressive relaxation,
while another half was exposed to the nonstructured instruc
tions to relax. The training or relaxation instructional
sessions were spaced at 1-week intervals, and each subject
was given two sessions. Subsequent to relaxation, all sub
jects xtfere asked to visualize the selected scene from their
fear hierarchy (e.g., the high fear or the low fear scene)
five successive times. The procedure followed was similar
to that of Grossberg and Wilson (1968) in that an interval
of 30 sec was allotted for the experimenter to read the
scene to the subject and then 30 sec more for the subject
to visualize it.
Edelman*s basic findings were that SC habituated
as a function of successive presentations of the visual
ized scenes irrespective of the relaxation technique
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 92
employed. Thus Edelman’s findings are consistent with
earlier findings which indicate that the diminution in
autonomic responding found with repeated presentations of
fear-eliciting stimuli do not necessarily result from the
use of progressive relaxation. Edelman interpreted his
findings as a support for a central rather than peripheral
theory of reciprocal inhibition, based upon his belief
that his casual relaxation procedure did not focus upon
specific control of the skeletal masculature and there
fore must have been mediated by more central processes.
It is not altogether clear that Edelman’s conclusion is
justified for a variety of reasons, not the least of which
is that he had no means of assessing the manner in which
subjects acted upon his casual relaxation instructions.
Nevertheless, Edelman’s data, when taken together with
the findings Grossberg and Wilson (1968), Davidson and
Hiebert (1971), Waters et al. (1972), and Gale et al. (1970)
indicated that even if relaxation facilitates habituation
of autonomic responses to phobic objects, or even if it is
a necessary component in counterconditioning, there is
little reason to think that the standardized ritual associated
with the progressive relaxation technique is necessary.
These above mentioned studies show that there seems
to be good reason to believe that minimal generalize
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 93
instructions to relax have as much effect upon the habitu
ation of electrodermal components of the response to the
phobic object as more precise training in progressive
relaxation does.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER 5
HYPOTHESES AND RATIONAL
The preceeding review of literature has noted the
emphasis that many investigators have placed on instrumental
conditioning of the electrodermal activity. Similarly,
several researchers investigating the psychophysiology of
fear have suggested the possibility of the electrodermal
activity as an autonomic reaction index in the presence
of phobic stimuli. As has been reviewed, investigators
have shown that electrodermal activity can be used as an
index of phobic responding, in wit, phobic stimuli —
whether in reality or imagination — tend to elicit the
autonomic responding to that which Wolpe has called anxiety.
Wolpe’s theory of acquisition of fear, as an anxiety response,
and his method of counterconditioning has been criticized
by different investigators, most notably by Lang (1969)9
who implied that desensitization involves a more complex
network of variables than past analyses and theory of
emphasized. Lang (1969) has discussed the relevance of
direct instrumental conditioning of autonomic nervous system
activity of the alleviation of fear responses. In reviewing
the presumed mechanisms underlying reciprocal inhibition,
Lang noted that muscle relaxation is supposed to affect the
autonomic outflow. He continued to suggest that the "role
94
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 95
of autonomic activity in modulating and maintaining emotional
responses in other behavioral systems suggest that it should
be dealt with directly, rather than going through the un
certain medium of muscle relaxation..." (Lang 1969, p.l83)-
Recent research has indicated that under appropriate condi
tions, especially those which utilized augmented sensory
feedback, human subjects can learn to gain direct control
over their autonomic responses (Katkin and Murray, 1968).
As Lang has noted, not only does the instrumental control
of autonomic responses provide an interesting potential
technique for direct alteration of autonomic response to
a phobic stimulus, it also provides a potentially important
theoretical tool. For if subjects who are taught to vol
untarily reduce autonomic nervous system responses to stress
ful stimuli also show reduced verbal and behavioral evidence
of fear response in the presence of those stimuli, it would
provide for the reciprocal inhibition notion of therapeutic
effect.
It would appear that the next step would be a dir
ect experimental investigation of the above theory. Instru
mental conditioning of electrodermal activity will be used
as a criteria to investigate the relationship between EDR
as an autonomic response, and reduce fear in the presence
of phobic stimulus as a notion for therapeutic effectiveness.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 96
The primary aim of this study is not to offer for
consideration a new mode of therapy, but to investigate
the role of conditioned autonomic activity in reciprocal
inhibition theory. It should be noted that the working
conceptual model presented in this section is admittedly
fragile, based for the most part on tenuous inference, and
quite lacking in specific details. For example, no pre
diction can be made regarding the relative importance of
EDR conditioning in inhibition of fear and, therefore,
what importance should be attached to this activity in
relationship to various aspects of phobic behavior. Yet
in the absence of previous research on this topic the fol
lowing hypotheses will be tested.
Hypothesis I
Instrumental conditioning of electrodermal activity
in either increase or decrease direction is possible, under
the current procedure, despite the previous studies' dis
similarities with this procedure.
Hypothesis II
Phobic groups will demonstrate statistically the
same conditioning ability as the nonphobic, for either
directions.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 97
Hypothesis III
There will be a statistical demonstration of signi
ficant difference between the phobic group in the increase
direction and the phobic group in the decrease direction of
the rate of conditioned electrodermal responding. Also,
there will be a significant difference between nonphobics
in the increase direction and nonphobics in the decrease
direction of electrodermal responding.
Hypothesis IV
The increase groups will respond more frequently
during the training periods than during the rest periods.
The decrease groups will respond less frequently during
the training periods than the rest periods.
Hypothesis V
There will be significant difference between testing
and rest periods within all groups. The increase groups
will have a higher responding rate of electrodermal activity,
and conversly, the decrease group will have a lower rate
of electrodermal responding during testing than during
rest periods.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 98
Hypothesis VI
There will be a statistically significant difference
in the rate of electrodermal responding between the increase
groups and the decrease groups during testing periods.
Hypothesis VII
The phobic increase group will respond with the
same absolute difference as the nonphobic increase group
in electrodermal activity. Similarly, the phobic decrease
group will respond with the same absolute difference as
the nonphobic decrease group in electrodermal activity.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER 6
Method
Design. The basic experimental design was a 2x2 factorial
analysis of variance with repeated measure on one factor
(time), for the two treatment phases of the experiment,
with two subjects assigned at random to each cell, with
the restriction that the male/female ratio be equal between
cells. Subjects were divided into four groups, or Phobic-
Increase Group (PI), nonphboic Increase group (NPI), phobic
decrease group (PD), and a nonphobic decrease group (NPD).
Subjects were selected according to their responses on the
criterion based on the pre-treatment session, and the fear
survey schedule BAT and MMPI. The independent variables
were the contingency of reinforcement, duration of the
reinforcement period. A reinforcement light was presented
contingent upon a subject emitting a GSR of 500 ohms or more
in the group-designated-direction. A non-contingent light
indicated rest periods.
The experiment was conducted in the following man
ner: (a) Pretreatment assessment, (b) Phase I, (c) Phase
II, and (d) Post-treatment assessment.
Pre-treatment session consisted of conducting a
Behavioral Avoidance Test (BAT), to determine the level of
subject’s approach to the phobic stimulus (Appendix A).
99
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 100
The experimental treatment consisted of two sequen
tial phases; Training (Phase I), and Testing (Phase II).
The first phase was conducted in six consecutive 40 -
minute sessions. Each session was conducted with a 10-min
baseline, and three Training-Rest (T-R) periods of 10-min
each. During each training period (T) of 5-min interval
all the GSRs which met the criterion were reinforced by a
green light for a duration of .1-sec. The training period
(T) was followed by a 5-min rest period during which subjects
were to simply relax. This combination of Training-Rest
periods were conducted for a total of three consecutive times
within each session (Appendix C).
Phase II, consisted of three consecutive sessions.
The sessions were conducted in the same exact manner as
the sessions in Phase I, except that (a) the 5-min period
previously designated for GSR training (T) was now designated
for presenting the phobic stimulus (snake) and (b) Reinforce
ment, i.e., green light, was not presented during these
periods. The sequence and number of Phobic-Rest (P-R)
periods were the same as T-R periods for each session in
Phase I. The difference between sessions in Phase II was
the distance of the phobic stimulus to the subject, which
changed closer by an increment of 3-ft. each day, i.e.,
8-ft., 5-ft., 2-ft., (Appendix D).
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 101
Post-treatment session consisted of a Behavioral
Avoidance Test (BAT), to test the effect of the Treatment
on the subject, and a comprehensive questionnaire about
the experiment (Appendix H).
Sub.jects. All subjects were comprised of Caucasian adults,
male and female, university student volunteers. They were
apparently healthy, and on normal mixed diets. They vol
unteered to participate in a bio-feedback study, which
required the subjects not to be under medication. The
original pool of volunteers (N=60) were given the Minnesota
Multiphasic Personality Inventory, Fear Survey Schedule,
and the Autonomic Perception Inventory (Appendix E).
Selection criterion of the phobic subjects for the
experiment included a subject’s fear rating of 4 (much)
or 5 (very much) on the snake item of the Fear Survey
Schedule. Seven subjects responded in this direction on
the test and were given the Behavioral Avoidance Test (BAT).
One subject completed the test and therefore, was dismissed
from the experiment, of the two other subjects after taking
the test, one refused to participate in the experiment, and
the other was dismissed because of several high scores
(greater than 70) on the scale. Thus, the total number of
the phobic subjects was N 4, two males, and two females.
The mean age of the group was 22.5 (s.d.=l.l).
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 102
The selection criteria of non-phobic subjects for
the experiment included a subject’s fear rating of 1 (none-
at-all) on the Fear Survey Schedule, the successful comple
tion of BAT (holding the snake against one’s chest for the
period of 10-sec). They were randomly drawn, with the res
triction of only two males and two females for the non-phobic
group, from the original pool of "none-at-all" subjects.
The mean age of this experiment, and at the end of the study,
were rewarded the amount of $25-00 for their participation
in the experiment.
The purpose of the study was explained to the sub
jects separately for each of two treatment phases in the
experiment. Phase I was explained as a biofeedback procedure
to train subject in the control of their GSR.
Before the start of Phase II, explanation was given
as to a test to measure their ability to control the other
learned GSR in presence of an emotion eliciting stimulus.
The reason for separate explanation was to minimize hypnotic
suggestibility and alteration of motivation.
Subjects were assigned randomly to four groups
subjected to the homogeneity of male/female ratio per cell.
Therefore, two subjects were in phobic-increase group (PI),
two in phobic-decrease group (PD), two subjects assigned
to nonphobic increase group (NPI) and two were assigned to
nonphobic decrease group (NPD).
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 103
Each subject signed a consent form, for participating
in the experiment, immediately prior to the pre-treatment
session.
Apparatus. The experiment was conducted in an electrically-
shielded room designed for psychophysiological research.
The room was thermostatically maintained at ambient tem
perature of 22.64°C (s.d.=.65°C) at which value palmar
thermoregulatory activity could be presumed absent and
vasomotor regulation operant (Brengelman 8c Brown, 1966).
The average relative humidity was 70.33 (s.d.-5-03)- A
two-way intercom system facilitated any necessary communi
cation between subject and experimenter, as well as per
mitting partial monitoring of subject’s gross movement,
and unusual breathing (e.g., sneezing, and sighing). A
cushioned chair was provided for the subjects so that they
could comfortably situate themselves and rest their arms
on the padded arms of the chair. Conditions were of optimal
comfort and minimal random stimulation, lighting was absent,
and the air conditioning unit provided a convenient masking
hume.
Two lights, which were mounted 20 cm apart and
approximately 290 cm from the subjects at eye level served
as reinforcement (contingent light), the rest feedback
(non-contingent light). The contingent reinforcement light 2 was a 25 w green light of 210 cd/f at source. A 25 w
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. lob
2 blue light of 180 ce/f at source served as a non-contingent
light. The contingent-reinforcement stimulus (green light)
was presented for .1-sec time-interval, by means of an
electronic remote-control switch operated by experimenter
immediately after the criterion voltage change. The non
contingent stimulus (blue light) was operated by a separate
remote-control switch for 1-sec tlme-interval. The switches
also automatically operated the ink-writing time-marker pen
of the polygraph, thus, recording the occurrence of the
reinforcing stimulus and non-contingent stimulus for their
duration of time-interval.
All physiological data were recorded on a six channel
Grass model 7 Polygraph located in an instrumentation room
adjacent to the subject room.
Skin resistance response (SRR) were recorded through
a direct coupled DC pre-amplifier (Grass type Model 7 PI)3
having an input time of 1.5 megohms of 50 microamperes.
Hence, skin resistance in ohms was recorded directly. Bi
polar palm-to-palm recordings were obtained with the use
of zinc disc-type electrodes placed in lucite cups of 21
mm inside diameter, filled with saline (.05M NaCl) zinc-
sulfate electrode paste. Prior to attaching the electrodes
to the active sweating area on the thenar eminence, both
palms were cleansed with distilled water. The electrodes
were then covered with small gauzes saturated with saline
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 105
(.05M NaCl) and were attached and held in position by elastic
hands. A response was defined as a change of 500 ohms or
greater in designated direction.
Respiration rate (RR) and amplitude were measured
through a direct coupled Grass Model 7 PI preamplifier
having an input of 1.5 megohms at PGR position via a Fen-
wal Electronics thermistor with a resistance of 50,000
to 150,000 ohms at 25°C. The thermistor was secured under
the right nostril of the subject by a head set.
The raw heart rat (HR) was recorded by means of a
Grass Model 7 P5 preamplifier, having an input time con
stant of .45 sec. Two Grass silver electrodes were attached
to dorsal side of both wrists by Grass electrode paste,
for biopolar recording.
Forearm muscle tension (superficial finger flexor
group) was recorded through a Grass Model 7P5 preamplifier,
having an input time constant of .1 sec. Grass electrodes
were attached to the dorsal part of each forearm about two
thirds of the distance from the wrist to the elbow. The
location of the electrode varied slightly for different
subjects, and was determined by having each subject move
his fingers up and down rapidly. The electrodes were attached
directly over the point of maximum muscle response.
Occipital activity was recorded monopolary through
a Grass type Model 7 P5 preamplifier, having an input time
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 106
constant of .1 sec. One electrode was attached to location
Oz (Jasper, 1958) with the reference electrode attached to
the right earlobe. A ground electrode was attached to the
inner lobe left ear of subject.
All the electrode sites, with the exception of the
GSR electrode sites, were cleansed with alcohol before
electrode placement. In addition, except for the GSR and
respiration sensors, all other sensors were attached to
an electrode plug-board located directly behind the subject
and attached to the ploygraph in the instrumentation room.
Appendix C- shows the general setting of the preampliers,
amplifiers, for all the sensors. The polygraph was calibrated
immediately before and after each experimental session.
Procedure. Treatment phases extended over nine consecutive
days. Pre and post assessment sessions were conducted
7-10 days before and after the experimental treatment ses
sions. Two subjects (24, & 58) were not tested continuously
because of illness. The interruption for subject 24 occurred
between sessions 3 and 4 of Phase I, for two days. One
day interruption occurred for subject 58 between session
4 and 5.
Pre-treatment assessment was conducted approximately
7-10 days before the experimental treatment. Subject was
asked to approach as closely as he could a live Florida
King Snake (Lampropeltis getulus floridana), described to
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 107
subject as harmless and thin, measuring approximately
177-8 cm in length and securely enclosed in a glass cage.
The glass cage was a 26.7 (w) x 39-5 (1) x 27-45 (h) cm
acquarium covered by wire grating, which could be entirely
removed from the cage. A room was divided in two by a
floor-to-ceiling partition. In one side, the caged snake
was situated at the end of a runway marked off the floor
with strips of white tape of 5 (w) x 45 (1) cm. The length
of the runway was approximately 390 cm marked off at 30 cm
increments. All the strips were clearly marked with 5 cm
size numbers, from 1 to 13- The subject's score was deter
mined by proximity to the snake, on a scale of 22, ranging
from complete refusal to enter the laboratory to picking
up the snake barehanded and placing it against his chest
for a 10-sec interval.
A phobic subject qualified for the experiment by
failing to reach Point 17 which consisted of reaching into
the cage barehanded. A non-phobic subject qualified for
the experiment by completing Point 22, which consisted of
picking up the snake barehanded and placing it against
his chest for duration of 10 sec. In addition, the latency
of the subject's approach in the test was recorded by the
experimenter using a stop watch.
Upon arrival at the laboratory subjects were given
the following verbal instructions:
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 108
"In the next room a completely harmless snake is situated at the end of a runway, securely enclosed in a glass cage. The purpose of this session is simply to find out how afraid of a snake you are. To do this, we simply ask you to enter the next room and stand in front of the runway and follow the steps on the instruction sheet as far as you can see. You may terminate the test at any time you feel like you should. Please make sure you follow the steps according to the instruction sheet. Any questions?"
An instruction sheet was provided to the subject
which included all the points to be followed during the
test. Subject was requested to score himself on those
points which he successfully completed, after the session
was concluded (Appendix A ) .
After answering only those questions regarding the
instruction sheet, the experimenter entered the room and
situated himself so that he could notice all the subject’s
movements. In order to insure some conformity of the activity,
the snake was poked just before the assessment to provide
some movement during the test. The experimenter also scored
the scale of subject’s approach and in addition, the latency
of subject’s approach in the test was determined by a timer.
After the subject had finished the test, they were asked
to leave the room, score themselves on the BAT scale. The
subject was given a Fear Thermometer scale. Fear Thermometer
is a 10-point scale on which subject judged his decree of
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 109
fear during the test, from a low of "not scared at all" to
a high of "very much scared" (Appendix F ) . The subject
was then thanked for his participation in the session, and
asked not to discuss the session to anyone. Those phobic
subjects who were selected were then scheduled for the next
two phases of the experiment.
Experimental Treatment. During these two phases, the record
ing of the physiological variables was the same for all
sessions and all subjects. Subjects were tested for nine
consecutive days, except for al interruption of two days
between sessions 3 and 4, and interruption of one day bet
ween sessions 4 and 5, for subject 24 and 58, respectively.
Subjects were instructed that before each recording
session to spend at least 30 minutes within the University
in a moderate temperature abstaining from arousing activity
and from food, drink, and empty bladder. The experimenter
also inquired a record of their activity within the past
twenty four hours that each recording session was conducted
(Appendix G).
When subject arrived at the laboratory, he was
seated in a cushioned chair, located in an air conditioned,
sound attentuated, electrically shielded room. The experi
menter explained the procedure as follows:
"In this experiment, I will be recording some physiological measures, which include your galvanic skin
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 110
response (sweating), heart rate, respiration, electroencephalograph, and muscle activity. All the elec trodes sites were then showed to the subject. The electrodes that I will be attaching to these loca tions on your body are quite harm less and will not cause you any pain or discomfort. The paste that is used to attach these electrodes, except for GSR and respiration, is this white cream of essentially a salt base. This paste is quite harmless and will wash off with soap and water. I shall clean all the paste after the session is over. This paste allows for better conductivity of your physiological responses. The dark paste for the GSR electrode is a saline zinc sul fate solution, but since I shall be using this gauze between your skin and the electrode, it will not leave any marks on your skin. I shall attach the GSR electrodes to your palms with a rubber band, and I would like you to tell me its degree of comfortness, so that too much pressure will not be exerted to your hands. I shall clean the GSR electrode site with distilled water, and all the other electrode locations with alcohol. This glass probe which I will position under your nostril will sense your respir ation (breathing).”
This instruction was given only in session one of Phase I
and not in any of the following sessions. Any instruction
pertinent to the session and the phase were then given.
Phase I (Training). After the subject was seated in the
cushioned chair and electrodes were attached, the experi
menter explained the basic paradigm of the session. The
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Ill
subject was shown a diagram of the session, (Appendix C)
and given the following instruction, simultaneously:
"The purpose of this session is to find our whether it is possible for you to control your GSR. As you will notice on this diagram the session is conducted in five minute increments of training and rest periods. There are total of six such periods, three training and three rest periods in the sequence presented in this diagram. Remember, during the train ing periods, whenever you emit a spon taneous GSR you will automatically receive a flash of the green light. Spontaneous GSR occurs without your knowledge. However, by letting you know when they do occur it should be possible for you to increase (sup press) them. We cannot tell you how this is done, but to aid you, whenever you emit a spontaneous GSR you will automatically receive a flash of the green light. Try to increase these in number. After this training period is finished the blue light will come on for a brief period, designating that the rest period has started. All you have to do during this period is to relax. After the rest period is over the next training period starts. This procedure sequences are conducted and the T-R period sequences are conducted and the session is over. So, all you have to do is to make yourself comfortable in this chair and follow the following instruction. Please try to keep your movements to a minimum, but do not move around a great deal. These recording devices are very sensitive and tend to be distrupted if you move. After I leave the room, there will be approximately a 10-15 minute rest period during which I will adjust
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 112
the machines. When you see the blue light come on the first training period starts, and the session will be conducted as above. Do you have any questions?"
Those questions which pertain to the instructions
were answered by reading that part of the instructions. The
instructions were repeated until the subject acknowledged
that he understood them completely. Any other question
that pertained to the experiment beyond the scope of the
instruction was answered by saying that since the experimenter
did not want to influence his behavior, they would be answered
when the experiment was over. These instructions were
also repeated at the beginning of each of the following
sessions in Phase I.
The overhead lights were then extinguished and the
door to the experimental room closed, placing subject in
total darkness. The experimenter then adjourned to the
adjacent equipment room. Following a calibration period,
a 10-min baseline recording period was conducted. The
last minute of the baseline was selected for base level
period. At the end of this period the non-contingent light
designated to the subject the start of the first training
period.
The subjects in the increase and decrease group
received a brief (.1-sec) flash of the green light when
ever the GSR changed 500 ohm or more in the appropriate
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 113
direction. Contingent reinforcements were presented by
the experimenter as quickly as possible after the pen had
reached the response magnitude criterion value. Those
responses beginning one to three sec after reinforcement
delivery were defined as elicited GSR and were neither
counted for reinforced. In addition, since erratic breath
ing (such as a sudden deep breath), and movements can some
times precede a GSR and act as confounding somatic responses
caused the experimenter to ignore those responses and not
reinforce them. Furthermore, any GSR occuring while EMG
activity increased were not reinforced and were not counted.
These responses were defined as elicited GSRs, and the
experimenter was not interested in conditioning these res
ponses. The subjects movement, erratic breathing, were
not on polygraph by the experimenter.
After the training period all subjects received a
5-min rest period, beginning and ending of which was signaled
by the non-contingent light. No reinforcement was presented
during this period.
This sequence of T-R was repeated thru consecutive
times in each session, for a total of three training (T)
and three rest (R) periods. After the session was over,
the electrodes were removed and an interview was conducted.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 114
Interview. Each subject was asked if he had the impression
at any time during the session that the reinforcement was
contingent upon "something he might have done." If a
negative reply was given, the experimenter told subject the
contingent light had been controlled by his behavior during
the experimental session, and during the next session try
to determine this behavior in order to achieve a better
GSR control. Subjects were also asked if they could deter
mine in which training period they were most successful in
controlling their GSR. The subjects were then thanked and
asked not to discuss the experiment with anyone.
Each session in phase one, including the attachment
of the sensors, instructions and the response-contingency
questionnaire, lasted about an hour (Appendix C). Phase
I lasted for six consecutive days.
Phase II (Testing). Phase II session began immediately
after Phase I for all subjects for three consecutive days.
This phase was explained to subjects as a testing phase
during which the subjects’ skill in controlling their GSR
was to be tested in presence of the phobic stimulus. The
procedure for preparing electrodes and the subjects was
the same as in Phase I.
After electrodes were attached, the subjects
were shown the basic paradigm of the session (Appendix D)
and were instructed that:
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. "By now, you have achieved cer tain amount of skill in controlling your GSR. During the next three ses sions, we would like to test your skill in the presence of a stimulus, namely a snake phobic stimulus. As you can note in the diagram in front of you, the procedure for conducting the session is exactly the same as the sessions in Phase I, with the exception that during those periods which you were trained to control your GSR, we will be presenting you with the snake. What we would like you to do is to control your GSR ac cording to the direction you were trained increase/decrease. That is we would like you to try to increase (decrease) your GSR while the snake is in the room. Basically, this is what will happen. After I leave the room, I would like you to make yourself comfortable in the chair while I am adjusting the machine in the next room. This period is the same as the pervious session, that is, it will last about 10-15 minutes. After, I have adjust the recorders, I will clear the room and bring in the snake which is secured in a glass cage and will place the cage on this table which is 8 feet away from you. Since the cage is completely secured, the snake will not be able to escape from the cage. You must have your eyes closed while I am transferring the snake in the room, and keep them closed after I leave the room, until I signal you with the blue light that the testing period is started. After the test ing period starts, open your eyes and start to control your GSR in the direction you were trained (i.e., increase or decrease). You will not recieve the reinforcement (the green light) at any time that you increase (decrease) your GSR.
owner. Further reproduction prohibited without permission. 116
After this.testing period is over, you will recieve the blue light signal designating that the rest period has begun. Close your eyes. At this time I shall come in and remove the case from the room, after which you can open your eyes and rest for the remainder of this period. Approximately 45-30 sec before the rest period is over, I shall come in again and bring the cage in. Again, you must have your eyes closed while I am transfer ring the snake into the room, and have them closed till you receive the light signal designating that the rest period is over and the next testing period starts during which you try to control your GSR. There will be a total of three testing and three rest periods of 5-min intervals. So that the dur ation of the session is the same as the sessions in Phase I” .
These instructions were repeated as many times as necessary
till the subjects acknowleged that he understood the pro
cedure. Only those questions pertinent to the instructions
were answered. Before leaving the room the experimenter,
then, instructed the subjects:
"So all you have to do is to make yourself comfortable in this chair and follow the instructions. Please try to keep your movements to minimum. These recording machines are quite sensitive and tend to be disrupted if you move, as I have told you previously. Remember to have your eyes closed while I am transferring the snake in and out of the room."
The overhead light was then turned off, and the door to the
experimental room closed, placing subject in total darkness.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 117
The experimenter then adjourned to the equipment room.
Following an initial brief period during which calibration
of sensitivity of all physiological variables were ensued,
a 10-min period was conducted in order to obtain a baseline
for the base level period. At the end of this period the
experimenter transferred the snake in the cage into the
room and placed it 8 feet away front of subject. He then
exited from the experimental room and entered the equipment
room. By signaling with the non-contingent light the start
of the first testing period started. The end of 5-min
testing intervals was signaled by the non-contingent light
and the experimenter entered the experimental room and
removed the snake, and again from 45-30 sec before the
rest period was over the snake was transferred into the
experimental room. The experimenter did not make any com
munication with subject during these stimulus-transportations,
except to tell him to close his eyes or open them as designated
in the procedure. This insured that subject would be aware
of closing his eyes, in particular during transportation
of the snake. The Test-Rest sequence was repeated three
consecutive times for each session, rendering a total of
three test and three rest periods.
After the experimental session was over the electrodes
were removed and subject was given the Fear Thermometer scale,
for purpose of self-rating of his fear during the total ses-
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 118
sion. Subject was then thanked, and asked not to discuss
the session with anyone.
The next two sessions in Phase II were conducted
in the same exact procedure as in session 1 of this phase
except that the distance of the snake to subject was reduced
by increments of three feet, rendering distances of 5-It
for session 2, and 2-ft for session 3, respectively. This
procedure was explained in the instruction to subject for
each session.
During Phase II, all subjects were asked whether
they did want to participate in the sessions, after the
instructions were given. This facet of the procedure was
deemed by the experimenter to be most important for phobic
subjects, since the noxious stimulus would be present during
these sessions.
Post-Treatment. This session was conducted approximately
7-10 days after the last session in Phase II was concluded.
The procedure was exactly the same as the Pre-treatment ses
sion, for conducting the BAT of Fear Thermometer scale. In
this session subjects were also given a comprehensive
questionnaire on the experimental procedure and their
behavior during the experiment (Appendix H).
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER 7
Results
All data on the polygram was visually scored for
each subject. The ploygram measurements in terms of milli
meters of pen displacement were converted to physical units
of SRRs in microhms. Heart rate and respiration were count
ed in terms of beats per minute and inhalation exhalation
cycles per minute, respectively.
Statistical analysis— Biomedical Computer Data
Program, BMD, (Dixon, 1972)— for the body of the data con
sisted of a 5-factor analysis of variance with repeated
measure on one factor, namely, treatment. A Newman-Keuls
multiple comparison was performed on the significant results
where specified.
Skin Resistance Response
The basic dependent measure was the number of
responses emitted per minute of training (or testing) and
rest periods for Phase I and Phase II. A response was
counted only if its magnitude was equal or greater than
500 microhms in increase or decrease direction for appropriately
direction-designated groups. No response was counted if
it appeared within 3 seconds after presentation of a light
stimulus (i.e., was elicited by the light). These criteria
119
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 120
applied to all of the subjects.
The basic response frequency measure was subjected
to a 100 x n/T+I/R+1 transformation used by Fowler and Kimmel
(1962), and Kimmel (1963). Specifically, skin resistance
response for the training, testing, and rest periods were
first transformed to 'f T+l to overcome the skewness of its
frequency distribution, and to reduce the influence of
extreme values. Then, the transformed measure for each
minute of training, testing, and rest periods was expressed
as percentages of the average transformed measure of one
minute of rest just preceeding the first training (or
testing) periods, the latter value serving as a base, or
initial value. This was performed separately for each
subject. In order to reduce variability, each subject's
transformed relative frequency was averaged over each 5
minute of the training (or testing) and rest periods.
Tables 1 through 8 represent the average transformed fre
quency response for each subject.
Figures 1 through 4 describe the changes in this
measure of relative response frequency during the 9 days
of experimental sessions for each of the four groups. Each
experimental session is represented in three-5 min blocks
of training and rest and testing and rest, yielding 27
blocks for the 9 experimental days.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 121
Tables 1-8. Hie transformed relative frequencies of SRRs not associated with EMGs or respiration irreqularities for each day of Phase I and Phase II, in 5-min blocks of Training & Rest and Testing & Best. Each table represents one individual subject's scores which comprise the groups as follows: Tables 1 & 2: Phobic Increase group; Tables 3 & 4: Phobic Decrease group; Tables 5 & 6: Non phobic Increase group; and Tables 7 & 8: Nonphobic Decrease group.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 122 50. 00 50. 62. 29 62. 6 4 61. 29 67. 69. 27 69. Rest Test 90. 96 90. 107. 53 107. Training Rest 90. 96 90. Rest 110. 71 37 110. 126. 8905 108. 130. 20 95. 17 137. 92. 772 0 92. 55 27 6. 105. 13 111. 89. 68 89. 42 62. 60 85. 102. 42 102. 102. 51 102. 107. 12 107. 96 70. 74 75. Test Training Rest Table 1 Table Rest 83. 42 83. 82 93. 64 91. 78 78. 86. 92 86. 69. 27 69. 86. 18 86. 94. 64 94. Rest 111. 41 111. 116. 56 116. 84 56 145. 84 137. 165. 70 173. 1 1 1 Transformed Skin Resistance Response Frequencies Response Resistance Skin Transformed Test 185. 81 185. Training 12 62 76 107. 121. 334 109. 81 98. 627 93. 520 84. 440 124. 751 82. 45 80. 87 89. 51 62. 838 107. 992 142. One Two Phases Days
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 00 00 00 64 0 71 70. 7 6.56 7 0.00 100. 100. 114. 100. 0.00 100. Rest 70. 71 70. 71 70. 144. 72 144. 134. 64 134. 100. 147. 64 147. 235.45 Training Rest 70. 71 70. 63 98. 81. 0 6 0 61 81. 132. Rest 100.0028 108. 108. 28 108. 108. 28 108. Rest Test 100. 00 100. 114. 64 36 114. 192. 86. 92 86. 71 70. 98. 63 98. 137. 21 28 137. 108. 108. 28 108. 145. 68 145. Training Table 2 Table 70. 71 70. 71 70. 70. 71 70. 57 167. Rest 108. 28 108. 100.0092 122. 116. 48 116. 100. 00 100. 232.49 Rest Test Transformed Skin Resistance Response Frequencies Response Resistance Skin Transformed 120.00 64 114. 156. 48 156. 113. 37 113. 132. 96 40 132. 139. 238.74 103. 13 103. 128. 98 128. 194. 99 00 194. 100. 229.91 Test Training 6 1 2 5 3 4 8 7 9 Days One Two Phases
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Rest 108. 28 108. 92 122. 100. 00 100. Test 88. 28 88. 90 86. 70. 71 70. 71 70. 116. 56 116. 00 100. 100. 00 100. 28 00 108. 100. 28 108. 92 142. 108. 28 108. Training Rest 76. 56 76. 84. 85 84. Rest Rest 108. 28 108. 114. 04 114. 71 70. 14 56 94. 56 116. 116. 100. 00 100. 100. 00 28 100. 108. 100. 00 100. 108. 28 108. 104. 49 104. Test Table 3 Table 9 6. 5 6 5 6. 9 92 86. Rest Training Rest 100. 00 100. 00 100. 70. 71 70. 7 6. 5 6 5 776. 92. 7 56 76. 71 70. 71 70. Transformed Skin Resistance Response Frequencies Response Resistance Skin Transformed 100. 00 00 100. 100. 00 13 100. 133. 124. 85 56 124. 116. 108. 28 28 108. 108. 00 00 100. 100. 00 28 100. 108. 116. 56 28 116. 108. 108. 28 108. Test 6 2 5 3 1 4 7 9 8 Days Training One Two Phases
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced
Table 4 co H <+■< T3 _v: OS es P-c •r—i 1- 0 G co O s-> £ 0 CO cn o 0 G 0 0 a c CO 0 s-, cu 3 0 0 o o 0 cr c CO cu Q .c E OS • H H a: •H • C£ • •H •4-* 4-J 0 co 0 >, 01 0 0 0 h o CO C p c o> co 0 0 CO C o o c p 0 c t C p 0 w to H H H *—H »~ 1 o CD o CD c^. ^H LO r^ co CsJ CO Oo CO — CO f—H CO 00 . # • . . . - CO r-H CD CD CD ID CD* CD >- ■ I i CD LO LO i »“H o o o CO ^H CO CO o * fH p*H —H D
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 127 76. 56 76. 70. 71 70. 100.00 108. 28 108. 100. 00 100. Rest Rest 84. 85 84. 7 6. 5 6 5 6. 7 116. 56 116. 28 108. 114. 64 114. 00 100. 64 114. 139.49 92 142. 28 108. 108. 28 108. 133. 00 133. 00 100. Training 70. 71 70. Rest Rest Test 108. 28 108. 100. 00 100. 00 100. 122. 92 122. 1 2006 81. 2800 100. 56 76. 56 95. 9.00 194. 36 139. 116. 00 100. 0.28108. 00 100. 116.5600 100. Test Table 6 28 28 00 00 70. 71 Rest Rest Training 0.00 100. 108. Transformed Skin Resistance Response Frequencies Response Resistance Skin Transformed 70. 71 70. 131. 20 131. 20 131. 108. 194. 08 194. 00 100. 129. 61 120. 71 70. 133. 00 133. 00 100. 100. 00 100. 100. 114. 64 114. 48 149. 100. Test Training 6 2 3 5 1 7 8 4 9 One Two Phases Days
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced
Table 7 co '+-< 73 dk OS E OC C •H c M O u s 0 Si 0 0 cn C O CD CD cn a O 0) >1 h to C cn CD C? 3 cu c o CD CO l ; . H Q OC CL. s: E E OC OS *H •H cn c > o 0 0 0 (0 >1 to CO to ro s-. c ro - s 0 w c h CO c Cn 0 cn h CO CD CO CD m c 00 CO CO CD CD CO CO CO CD CO C LO CD CO CM CO o CM m CD CO CO CD m c 00 CD CD C CM CD LO CD CD m c co CM CD CM CO CM CO LO m O 0 c o CD CD CO CO CD CO CM C o CO CO CO CO Cm CO 00 CD CM CO CO CO CM CO m CD CD O CD CD CM CO o CO CM CO CO CO o LO CM CO CD CM CM
CO CO CO O CO CD CO CO CD 0 0 LO CM o O CO CD CO CO CO O CO G) CD CO LO l cm in CO CO CO CO CD CM CO CO CM CM "sT CM CO O E 0C H OC E 4-> OC +-» 0 to 0 to 0 w 0 w 0 w h CD to h O O o c CO CD CM CO CO CM *- c CO 0 0 LO CO o C LO CO CO CO CO CM D C O D C . ^ r ID CO CD f—i CD CM LO o cm CD CO LO 00 CD CD O CD CO m co o CO o c CO LO cm CM CD CD CO CD LO LO CO CM LO CM LO 129 70. 71 70. 70. 71 70. Rest Rest 100. 00 100. 100. 00 100. 108. 28 108. 100. 00 100. 00 100. Test 7 6. 5 6 5 6. 7 81.06 56 76. 108. 28 108. 108. 28 108. 100. 00 100. 85 124. 100. 00 100. 116. 56 116. Training Rest Rest 116. 56 20 116. 131. 100. 00 100. 1 81. 06 81. 56 76. 06 81. 76. 56 76. 63 98. 108. 28 28 108. 108. 100. 00 100. 108. 28 92 108. 122. 122. 92 139.. 49 92 122. 139.. 100. 00 28 100. 108. Test Training Table 8 Table Rest 76. 56 76. 76. 56 76. 71 70. 77 92. 82. 42 82. 112. 77 112. 100. 00 100. 129.28 100. 00 100. 28 108.
_____ Transformed Skin Resistance Response Frequencies Response Resistance Skin Transformed 56 76. 70. 71 70. 70. 71 70. Test 108. 28 108. 100. 00 56 100. 116. 120.00 100.0056 116. 108. 28 108. 6 2 1 5 3 4 828 9 108. 7 Two One Phases Days Training Rest
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 130
The data was subjected to a repeated measure analy
sis of variance of a 5-factor design. The first interest
was the comparison between training and rest periods for
all groups and the comparison between the phobic and non
phobic and direction designated groups. Therefore, Phase I,
comprising of six days of training, was analyzed separately.
It was expected beforehand that the effects of reinforcement
would be observable in one or more of the two possible
ways. The first possibility was that the increase groups
of either phobic or nonphobic characteristics would produce
an increase in the rate of unelicited SRRs, and that the
decrease designated groups of either phobic or nonphobic
characteristics would produce a corresponding decrease in
the rate of emission of SRRs; both anticipated changes were
expected to be noticeable in the comparison of the groups
during reinforcement. The second possibility was that the
increases and decrease groups would respond differently
to the termination of reinforcement, i.e., during rest
periods.
The analysis of variance for Phase I indicated a
five-way interaction between group x treatment x days x
periods x T-R (training-rest). Table 25 is a summary of
all the main and interaction effects which were significant.
These were treatment (F=9-52, df=l/4, p^.05)» T-R periods
(P=l4.73j df=l/4, p^.025), treatment x T-R periods
(F=66.64, df=l/4, p^.005), treatment x periods (F=5-97,
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 131
df=2/8, -^.05), period x T-R periods (F=6.28, df=2/8, p
0 0 2 5 ) , and group x days x periods x T-R periods (F=2.77s
df=10.40, p ^ . 025), and group x treatment x days x periods
x T-R periods (F=2.68, df=10/40, p<.025).
Insert Table 25 about here
It should be mentioned that ’periods’ in all these
analyses represent a combination of training (or testing)
and rest periods- Thus each session would yield three such
periods. Whereas, T-R periods represent either training
(testing) or rest periods separately. Thus each session
would yield six such periods.
Figure 1 shows that for phobic increase group for
Phase I, the SRR frequency for training periods was usually
higher than the rest periods, and significantly different.
However, the response frequency although oscillating has
a general decline mode. This is represented by the indica
tion that for days 5 and 6 the SRR average frequency is
below the operant level.
Insert Figure 1 about here
Figure 2 indicates the general response frequency
for phobic decrease group. The SRR frequency for the
training periods is usually lower than the rest periods
and below the operant level, whereas the rest periods
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 132 P .005 .05 .05 F 9.52 5.97 6.28 .025 2.77 .025 2.68 .025 MS 317.98 100.91 303.59 109.48 293.73 1145.58 4685.00 14.73 .025 21191.90 66.64 1 10908.25 1 4 1 2 603.42 8 2 729.68 8 116.14 10 10 40 TABLE 25 TABLE x T-Rx AND REST PERIODS OF PHASE I (DAYS 1-6) PHASE (DAYS I OF PERIODS REST AND Source df Treatment x T-R x Treatment T-R (Training-Rest) Error Treatment Error 4 Error Treatment x Period x Treatment Period x T-R x Period Error ANALYSIS OF VARIANCE OF SRR TRANSFORMED RESPONSE FREQUENCIES DURING TRAINING DURING FREQUENCIES RESPONSE TRANSFORMED SRR OF VARIANCE OF ANALYSIS Group x Treatment x Day x Period x Day x Treatment x Group Group x Day x Period x T-Rx Period x Day x Group Error
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 133
CM oO
in co co co
CO 05 oo CM rH CM
CO CM TS«H OQ
S2
O m +J a u cS o Sh pq
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Figure 1. Relative frequency of SRRs not associated with EMGs or respiration irregularities in Phobic Increase group (PI), in 5-min blocks of Training (Phase), Testing (Phase II), and Rest (both phases) periods over 9 days.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 135
r-~ - CM ■ lO m ■ co CM o o O o o o o o O o O O O O s- O CT> CO vO m co CM o CT\ 00 I-'- vO in CM i—I (i +h/i +l x ooi) (%) ^Couanbsjy; asuodss^ psuuojsxiBJj, Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 136 response rate is above the operant level. Again, oscill ation of the response rate exists for this group for training and rest periods. Also, for day 6 there is significant difference between training and rest periods, for periods 2 and 3- Insert Figure 2 about here Figure 3 represents the average frequency of SRRs for nonphobic increase group. The result for this group is very clear cut, from the fact that no interaction exists for this group between training and rest periods across the six experimental days. The SRRs for the training periods is always above the operant level, whereas the rest periods are either above the operant level (days 1, 2, and 5)> or below the operant level (days 3, 4, and 6). Also, except for four periods, there is significant difference between all the training and rest periods. Insert Figure 3 about here Figure 4 indicates that the rate of responding for nonphobic decrease group is usually below the operant level, in particular for training periods. The rest periods' response rate are only above the operant level for some of the periods in days 4 and 5- Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Figure 2. Relative frequency of SRRs not associated with EMGs or respiration irregularities in Phobic Decrease group (PD), in 5-min blocks of Training of (Phase I), Testing (Phase II), and Rest (both phases) periods over 9 days. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 200 T(raining) i T(esting) 190 ^ M R(est) ! ^ __ R(est) 180 170 160 150 140 130 120 110 V •L 100 \ it 90 ■>*--- 80 70 60 50 9 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 u> Phase I (min) Phase II (min) oo Figure 2 Figure 3. Relative frequency of SRRs not associated with EMSs or respiration irregularities in Nonphobic Increase group (NPI), in 5- min blocks of Training (Phase I), Testing (Phase II), and Rest (both phases) periods over 9 days. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 200 o » T(raining) T(esting) R(est) 190 a R(est) 180 170 160 150 140 130 120 110 \ 100 to / A\ 90 / \ X c 80 70 60 50 ■ « » * - ■ * ‘ 1 ■ «- 123456789 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 ; (min) Phase II (min) Phase hi o Figure 3 i4i Insert Figure 4 about here In order to determine the main effect that was most responsible for interaction of the main effects the following procedure was adopted in collapsing of the data. The average transformed frequency SRRs were averaged for each day. Each average transformed frequency rate for the rest periods was substracted from its corresponding training period, i.e., T^-R^. Then all the new frequency rates were averaged across the session, i.e., (T-^-R-^) + ( ^ 2 ^ 2 ^ + (T^-R^/S- Analysis of variance indicated that only the treatment main effect was highly significant (F=66.65)s df=l/4, p.002). No other main effect or interaction was significant. Newman-Keuls multiple range test yielded a significant difference between either directions, and also between directions and the operant level (p^.01). The second main interest for this experiment was the rate of responding for the days when the phobic stimulus was present, specifically, Phase II. To compare the effect of the phobic stimulus on the different phobic and nonphobic groups during testing and rest periods, the following trans formation was applied to the SRR data of each subject. First, a Z-score was obtained for all the subject's scores using only the first six days for obtaining average mean. This mean was calculated separately for training and rest periods. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 1^2 Figure 4. Relative frequency of SRRs not associated with EMGs or respiration irregularities in Nonphobic Decrease (NFD) group, in 5- min blocks of Training (Phase I), Testing (Phase II), and Rest (both phases) periods over 9 days. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 200 190 180 170 160 150 140 130 120 110 190 90 80 / h 70 60 50 ■ •■■I— , I ■«■ » » » » 1 » I I « » I l I l I I ■■ -I- 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 J=r Phase I (min) Phase II (min) OJ Figure 4 144 Then using these means Z-scores were obtained for each of the training and rest, and each of the testing and rest periods. This was done separately for each subject. The rational was in order to take the effectiveness of the training out of responding rate during testing and thus be able to compare the subject’s voluntary control over his/her autonomic responding. The question here is whether subjects were controlling their own autonomic response or were there other factors involved? Analysis of variance for Phase II, that is, days 7, 8, and 9, indicated no main effects, but a period x period x T-R interaction effect (F=6.46, df=2/8, p < .025)3 and a group x treatment x days x period x T-R (P= 3 -993 df=4/l6, p^.02). Table 27 represents a summary of the significant results for these interactions. Insert Table 27 about here Figure 1 indicates the phobic increase group had a high rate of SRR rate during the test periods, and the rest periods are also higher than the rest periods during Phase I. Note that these figures (i.e., 1 through 4) are not adjusted Z-scores of SRRs but the primary transformation. However, the shape of the graph for Z-scores is quite sim ilar. The graphs indicate that the phobic groups had higher Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. TABLE 27 ANALYSIS OF VARIANCE OF SRR TRANSFORMED RESPCNSE FREQUENCIES DURING TESTING AND REST PERIODS OF PHASE II (DAYS 7-9) Source df MS F P Group x Period x T-R (Testing-Rest) 2 0.7781 6.46 .025 Error 8 0.1204 Group x Day x Treatment x Period 4 0.5422 3.99 .02 x T-R Error 16 0.1357 146 rate of SRR than the nonphobic groups. However, this difference is only significant for the phobic increase group, in particular for day 9 when a general increase is indicated across the session. The phobic decrease group has a general trend of increase in SRR rate from days 7 to 9j but this is not significant. For days 7 and 8 the rate of SRR during test ing period is less than the rest periods, except for the third testing period of day 8. Day 9 shows a higher rate of SRRs for testing than the rest periods, but this dif ference is not significant. The graph for nonphobic increase group shows that the rate of responding is rather constant across days but yet the testing periods indicate a higher rate of responding than the rest periods. The responding rate is higher than the operant level for all these days for the testing periods and slightly higher for the rest periods of days 8 and 9- The nonphobic decrease group shows a lower rate of responding for the testing periods, in general, than the rest periods. In addition virtually all the periods are below the operant level. Again, the data were collapsed over the T-R periods across sessions, as previously, in order to determine the main effect which was most responsible for the 5-way inter action. However, analysis of variance indicated no signi- Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 147 ficant main effect or significant interaction effect. In order to determine the effect of the hierarchy (change in the distance) of the phobic stimulus on the subject, each day of the testing was contrasted with days 5 and 6, when the phobic stimulus was not presented. Analysis of variance for days 5, 6, and 7 yielded no significance. For days 5> 6 and 8 there were no main effect significance, but a period x T-R significant inter action (F=ll. 32, df=2/8, p<.04), and a day x period x T-R significant interaction (F=6.593 df=2/8, p < ’.02). Analysis of variance for days 5, 6 and 9 indicated no main effect but a significant interaction for period x T-R effect (F=l8.49, df=2/8, p<.001), and a significant interaction for group x treatment x day x period x T-R effect (F=3.58, df=4/l6, p^.03). However, an analysis of variance for collapsed data for days 5* 6, and 9 did not yield any significance for any of the main effects of interactions. Heart Rate The heart rate records were analyzed by computing the number of beats per minute for each minute of the experimental sessions. Each minute interval was substracted from the number of beats per minute of the last minute of the operant level (initial value) of heart beat just prior to the first training period or testing period. This was Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. -fcr CO P .004 .02 F 11.32 MS 1.283 0.747 6.59 0.113 2 2 8 df TABLE 28 TRANSFORMED Z-SCORE RESPONSEFREQUENSIES DURING VARIANCE OF SRR SRR OF VARIANCE Source OF T-RPERIODS FOR DAYS 5, 6 &8 OF THE SECONDHIERACHY LEVEL ANALYSIS PeriodxT-R Treatment xPeriod x T-R Erro Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. VO P .001 .03 3.58 18.49 MSF 1.657 0.612 0.170 2 8 0.089 df 16 TABLE 29 xT-R Source T-RPERIODS FOR DAYS 5, 6 &8 OF THE THIRD HIERARCHY LEVEL ANALYSISOF VARIANCE OF TRANSFORMED SRR Z-SOORE RESPONSEFREQUENCIES DURING PeriodxT-R Error Groupx Treatment xDay xPeriod 4 Error Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 150 done separately for each subject. In order to reduce vari ability, each subjectTs transformed frequency was averaged over each 5 minutes of training, testing, and rest periods. Tables 9 through 16 represent these average transformed frequency beats per minute for all subjects for the nine days of experimental sessions. These average transformed frequencies of heart rate were then transformed to Z-scores. The procedure for this transformation is the same as for the Z-score transformation procedure performed for SRRs (see above). Analysis of variance of the repeated measure for Phase I for heart rate indicated no main effects significance, but a group x period interaction significance (F=6.69s df=2/8, p<^.025)j and a highly significant treatment x day x T-R interaction (P=4.973 df=5/10, p 30 represents a summary of the significant results. Insert Table 30 about here The group x period interaction indicates a general overall increase from period 1 to period 3 for the phobic groups, while the reverse is true for the nonphobic groups. However, the treatment x days x T-R interaction indicates that those subjects in SRR increase designated direction had a general increase of heart rate over days, while the reverse is true for decrease designated groups. Figures Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 151 Tables 9-16. The transformed frequencies of Heart Rate for each day of Phase I and Phase II, in 5-min blocks of Training & Rest and Testing & Rest. Each table represents one individual subject's scores which comprise the groups as follows: Tables 9 & 10: Phobic Increase group; Tables 11 & 12: Phobic Decrease group;Tables 13 & 14: Non phobic Increase group; and Tables 15 & 16: Nonphobic Decrease group. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced T a b l e 9 Adjusted Heart Rate Frequencies 1 1 i CL, Q : x (0 w 0 w (0 w Training } Rest T r a i n i n g J R e s t Training » Rest i i ! i i ! 1 1.2 ! 5.0 5.0 ! -0.8 1. 6 i -1. 4 I i • 3.2 { 3 . 4 0.4 J 1.0 0.2 | 5.8 O C 0 1 o c 1. 8 | 1. 0 0.8 l 1.8 4.8 j 4. 6 I -2. 4 j -4. 6 -5. 4 ! -5. 2 -0.4 j -2.4 I o l 1. 4 ! 2.4 o.o ! l.o 0. 2 1 1. 8 l i I o l -1.4 ! 3.0 -0. 8 i 0. 6 -2.4 ! -1.4 i » l l l I 1 i l { Test S Rest Test 1 Rest Test i Rest i i i ------1 ...... ' ----- 1 ' ■ 1 O X O O (X> CO t o c O ^ o CO LO CO CM O C7> CO N £ o 5.0 { 8.2 4.6 { 8.0 1 1 1 l 10. 2 J 11. 6 11. 0 I 12. 8 i rs-* 6.6 | 0.0 5.2 i 5.0 i i i l - j ------...... • ...... Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced Table 10 K m OS Table 11 < T3 T3 ffi P *!“-> cs + +J 0 w 0 0 0 0 0 ffl s- cr 0 0 c o © w h j CP eh a x: es QC *H •ft -M w « 0 W 0 0 S-, 0 m 0 0 w W CD )- 0 c c o O O 0 0 CO 0 0 CO CO CO i— H Table 12 T3 < cs u* TJ X H r • +-> +J +-> 3 cn w CD o CD W cr 0 0 Si (0 CD CD 3 c (0 E H CL, Q OS H OS JO •rt CS -i— I cn cn c c D> 0 cn >* cn S-> o> 0 cn 0 0 0 h 0 s-. 0 c o> 0 CO u 0 c to O L CO CS| CO o CO O 3 0 I • • • • « • • • • • • • • o o * o o CO co to M O CO LO ^ 0 0 CM l o c 0 3 0 Ov 03 CO O o LO o H r CS] 1 • to 03 l*"< i—H to (O LO Cs] 3 0 • • • O L CO LO CO co OCO CO H r 03 CO CO o Table 13 os tu •H •a < 73 E ■M + 3 0 c o 0 cn Si s- 0 O' 3 0 0 0 0 0 0 j OS E OS H a: Q E +■> CL, X CD 0 c o> Si 0 h 0 a 0 i S c 0 0 O' 0 Ss c 0 0 h i S (0 0 0 0 0 LO LO LO 3 0 LO 3 0 o ■sr" 0 0 . o 3 0 LO » LO LO (M 3 c l ~ 1 i « • • • • • • • • • O o o O i 3 0 o 3 0 3 0 < ■ O 0 c o o . O OCO LO 3 0 OLO CO 3 0 t 1 O 3 0 LO o c 3 0 3 0 LO O OCO CO 3 0 CD CO LO CO CO CO o o CO o LO o OJ LO LO . CSC E DC H OS EH CD 0 0 0 cn 0 0 h 0 0 0 0 0 E LO 3 0 3 0 CO O o 3 0 3 0 3 0 co’ D 0 CV5 00 CD H i I fH C 0 h s h • • • • O CT> CO LO CO CO LO o o 3 0 • LO f O 3 0 » LO 3 0 4 I • Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced Table 14 < T3 TJ ffi OS ■'—i U-, + +J +-> •H w 3 CD CD s-. 0 to to 0 s_ cr 3 0 c o Table 15 Adjusted Heart Rate Frequencies 1 1 C Z J 1 cn cn © CO l . Days Training J Rest Training | Rest Training J Rest 1 1 1 1 1 1 < - r M O O LO LO CO CM -1.4 1 3.8 -1.4 j 1.0 -2. 0 j 0. 6 -3.4 j-2.4 -5. 8 ! -6. 0 -4.0 ! -6.4 0 1 G CD 1 -4.8 j-0.6 -6. 0 } -0. 4 -2. 2 i 1. 2 1 2.8 | 4.8 0.0 { 9.2 2.6 { 7.4 1 I 3.4 j 4.2 0.8 ' 3 . 2 1.8 | 9. 6 -0.6 • 2.4 -2. 8 1. 6 -3. 8 ' -1. 2 l l l 1 1 1 Test J Rest Test } Rest Test J Rest 1 1 1 1 — "l ■ 1 1 1 1 H cn n c . " t 0 g -6.8 J-7.4 -9. 0 ! -1. 6 -8. 6 J -1. 0 l 1 1 0. 2 j 7. 2 -0.2 J 4. 6 1. 6 ! 4. 6 1 1 cj) 1. 6 | 4. 8 0.0 I 3. 2 -0.6 | 1.8 1 1 1 1 ______J ______------— 1...... • 158 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced Table 16 PS •0 03 X C < •H +-> 0 0 0 0 0 3 cn 3 0 0 s- D* c o 0 CO —\ m Q H 0- OS .c H r • •rH H OS H PS UJ cn cn 0 0 G 3 0 S- 0 C Cn 0 cn i S Cn 0 0 cn Si 0 c Cn 0 cn CO o cm O CM CO OCM CO CO CM MCM CM — C CO CM .—i 1 • • • • • • • • • • • o CD CM CM CM CO CO CM • • • O 0 c O CM CO 0 0 CO 0 0 CO CO CO o 1 1 CO o o CM CD CM LO o '• co CO CO o O CO CO* O CM 0 0 o LO LO G> O LO LO I I I I LO CM CM CO CO CO CT> H r o 1 I I I CC H H OS H OS 4-> 4—> 0 cn cn 0 cn 0 to 0 cn 0 cn 0 o CO CO CO CD 0 0 CO CO o 1 1 I 1 • • • • • • • • • . • CO o CO CO o O v. fv —< r— o o LO 0 CD 00 r "1 o #— o CO o o O 1 t 160 P .025 .005 F 6.96 4.97 MS 4.163 0.597 1.569 0.315 df TABLE 30 TABLE Source DURING TRAINING AND REST PERIODS OF PHASE I (DAYS 1-6) (DAYS PHASE I OF PERIODS REST AND TRAINING DURING ANALYSIS OF VARIANCE OF HEART RATE TRANSFORMED Z-SCORE RESPONSE FREQUENCIES RESPONSE Z-SCORE TRANSFORMED RATE HEART OF VARIANCE OF ANALYSIS Group x Period Period x Group Error 2 8 Treatment x Day x T-R (Training-Rest) (Training-Rest) T-R x 5 Day x Treatment Error Error 20 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 161 5 through 8 represent the changes in heart rate frequency during the nine of the experimental sessions for each of the four groups. Each experimental session is represented in three 5 min blocks of training and rest, or testing and rest periods, yielding 27 blocks for the 9 days. Insert Figure 5-8 about here An inspection of the graphs indicates that the sig nificant interactions was due - to nonphobic groups, whereas, both phobic groups had a stable form of heart rate responding. Analysis of variance for days 7, 8 and 9, that is, Phase II, indicated no significance for any of the main effects or interactions. This result is suggestive that vasoconstriction or heart beat control was not employed by any of the subjects to control their SRRs for any of the days in Phase II, in presence of the phobic stimulus during the testing periods. However, it was necessary to compare the response frequency for each of these days with the training session, i.e., Phase I, when the phobic stimulus was absent. There fore, the same procedure as for the SRR analysis of variance was employed— namely, days 5 and 6 were contrasted with days 7, 8, and 9 in separate analyses. Analysis of variance for days 5> 8, and 7 indicated Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 162 Figure 5. Relative transformed z-score frequencies of Heart Rate in Phobic Increase group (PI), in 5-min blocks of Training (Phase I), Testing (Phase II), and Rest (both Phases) periods over 9 days Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 163 •5 £ CD Oh rH CD ♦H P=H •5 s CD Oh o o CO o rH CO (uttu/sTeaq) a^-ea Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Figure 6. Relative transformed z-score frequensies of Heart Rate in Phobic Decrease group (PD), in 5-min blocks of Training (Phase I), Testing (Phase II), and Rest (both Phases) periods over 9 days. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 165 (uTui/srpgaq) Bye# ^ re e ji Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 166 Figure 7. Relative transformed z-score frequencies of Heart Rate in Ncnphobic Increase group (NPI), in 5-min blocks of Training (Phase I), Ttesting (Phase II), and Rest (both Phases) periods over 9 days. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 167 in CD CO r-c3 1 ft o a 0 f-i ft s •H s CD ft CO o o CO o csj (irnzi/srBaq) aivg ^tbsh Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 168 Figure 8. Relative transformed z-score frequencies of Heart Rate in Nonphobic Decrease group (NPD), in 5-min blocks of Training (Phase I), Testing (Phase II), and Rest (both Phases) periods over 9 days. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced +3.0 ¥ o i a / a B q 9 (irau/sa'Bsq) rH o o + o - tbsh CM o I O CO I t> O O 169 •H Pu £ c £3 s Q) r* CD 00 ph §> f-iCD 17 0 a significant treatment main effect (F=15-52, df=l/4, p-^.025)5 and a significant treatment x day x period interaction (F=3.^0, df/16, p^..04), indicating that those in the increase groups had a higher rate of responding than those subjects in the decrease groups, and that, this increase was highest for day 7 for the increase group, and lowest for day 7 for the decrease groups. Insert Table 31 about here Analysis of variance for days 55 6, and 8 indicated a period x T-R interaction significance (F=4.59, df=2/8, P ^ * 05)3 and a group x treatment x period x T-R inter action significance (F=7-70, df=2/8, p^.025). These inter actions indicate that overall there was a higher responding for the rest periods, although this significance was evident only for the second rest periods, and the only nonphobic increase and phobic decrease groups showed this trend (P < .05)- Those subjects in the increase groups had a higher rate of responding for both testing and rest periods in contrast to the decrease groups. Insert Table 32 about here Analysis of variance for days 55 6, and 9 did not yield any significant main effects or any significant inter actions . Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 171 P F 3.40 .04 3.04 0.245 47.35 15.52 .025 1 4 4 0.837 16 TABLE 31 TABLE Source df MS DURIN3 T-R PERIODS OF THE FIRST HIERARCHY LEVEL (DAYS 5, 7) & 6 5, (DAYS LEVEL HIERARCHY FIRST THE OF PERIODS T-R DURIN3 ANALYSIS OF VARIANCE OF HEART RATE TRANSFORMED Z-SCORE RESPONSE FREQUENCIES RESPONSE Z-SCORE TRANSFORMED RATE HEART OF VARIANCE OF ANALYSIS Treatment Error Period x Day x Treatment Error Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. TABLE 32 ANALYSIS OF VARIANCE OF HEART HATE TRANSFORMED Z-SCORE RESPCNSE FREQUENCIES DURING T-R PERIODS OF THE SEOOND HIERARCHY LEVEL (DAYS 5, 6 & 8) Source df MS F P Period x T-R 2 0.272 4.59 .05 Group x Treatment x Period x T-R 2 0.456 7.70 .025 Error 8 0.059 173 Respiration Rates Table 17 through 24 represent the transformed res piration rates for all of the subjects. The procedure for transformation of the scores for this response was the same as the heart rate transformation, except that, of course number of inspiration-expirations per minute intervals were used. Note that these tables do not represent the Z-score transformations obtained. The Z-score transformation pro cedure for these scores was performed the same way as for SRRs and HRs. Figures 9 through 12 represent changes in respiration rate during the nine days of the experimental sessions (all Z-scores) for each of the subjects. As for HRs and SRRs, each experimental session for this response is represented in three 5 min blocks of training and rest, or testing and rest, yielding 27 blocks for the nine days of the experimental sessions. Analysis of variance for days of 1 to 6 of Phase I indicated no main effect significance, but several inter actions significance. Table 33 represents a summary of these interactions, namely, a group x day interaction (F= 3.65s df=5/20, p^.025)s a day x period interaction (F=2.11, df=10/40, p<\.05)s a group x T-R interaction (F=8.995 df=l/4, P^-05)s a treatment x T-R interaction (F=10.78, df=l/4, P'C*05)s a treatment x period x T-R interaction (F=5-69s Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 174 Tables 17-24. The transformed frequencies of Respiration Cycles for each day of Phase I and Phase II, in 5-min blocks of Training & Rest and Testing & Rest. Each table represents one individual subject's- scores which comprise the groups as follows: Tables 17 & 18: Phobic Increase group; Tables 19 & 20: Phobic Decrease group; Tables 21 & 22: Ncn- phobic Increase group; and Tables 23 & 24: Nonphobic Decrease group. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced Table 17 < ■o TD s o i D H • H • tU +-> *r—l 4-> 4—> w 3 0 CD 5- 5- cn a O C CO CD i-l fO 0 CD r e 3 CD C O CQ 1 I Q 1 C -C w , > w 0 to to M l , Training } Rest Training } Rest Training | Rest i i i i -1. 0 ! -3. 8 -3. 6 ! -4. 8 -3. 4 | -3. 8 I i i CM 0.0 ! 1. 6 - 0 . 2 J 1 . 0 0 . 8 | 0 . 6 o c i 0 1 i TpW in CD -0. 8 j -i. 4 -1.0 1 -1.0 -0. 6 ! -3. 6 1 - o . 4 ; i . o 0. 6 ! 0.2 1. 4 | - 1 . 2 l 1 .4 1 3 . 6 -0. 6 ! 3. 2 2 . 0 ! 1. 2 i -0.6 ! 0.0 - 1 . 0 - 1 . 2 -0. 8 • 0.2 I l • I i Test | Rest Test | Rest Test i Rest i i i i X O O ^ O (X5 CO CO ; ^ CO CO E O O CO CO CO o 3 CO 03 to O O o CO CO 0 ^ - 0 co c Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced Table 18 T3 OS H • os U* < t •rt •<—H +-> +-> +-> 0 0 o s-< tr 3 0 0 D. U 0 0 0 CD CQ 0 c 3 0 c o ? H os OS P H OS H H • •1—1 o- •G CP m c t3 0 0 s» G 0 c CP © 0 s- >, 0 0 0 0 u 0 c 0 0 0 0 o 03 O C O o 03 CO o t 3 0 ■ 3 0 I I 1 1 . « • • • • i CO o t o t o t CO N o CM I I O 0 c 00 o O C 0 0 C\l o o r-H CO ' o CO 1 CO o o * o 3 0 o o CO o o o I 1 CO o o CO o o o i— o u I . < O C CO 03 O C o t o t 3 0 CO o 3 0 o t I 1 1 H OS E-t OS OS H -M 0 0 0 H O C o o O C o O C CO o 3 0 3 0 3 0 £ o * O I • • • • • • • • • • • CO O C o o u 3 0 o O C O L o t 3 0 O C - o O C 1 O C CsJ o O C C<] LO CT5 i 176 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced Table 19 •a os U-, < •a OS **■4 • H • +J 4 + CD CD CD 0 a »-« s- 3 0 0 p o c CO 3 CD o CD CO f0 O' G * — H j l c H OS os H H -C OS 10 0 -1 1 Cn 0 0 0 10 C >1 0 0 c a> (0 0 0 <0 ra 0 0 , o o o o o ■sr o o to o o o o o 0 0 o • • • • • • • • • • • • a 03 CO 03 o o o *— M CO . t E O CD h O O 3 0 o O <3* 0 0 O o CO 0 o D C o O o I 1 1 • Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced Table 20 0 < ■0 os os PL, -<—4 •rH +-> +J 3 0 0 0 a o 0 Table 21 OS U* + 0 o c 0 0 i S 0 0 CD o CD 3 0 0 CO a u CT c co fO j OS H Q H OS bs E CL. JS 0 0 0 0 i S O 0 i S C 0> 0 0 0 0 0 0 C i S CO 0 0 c h 0 0 H r ■'3* oto to o H r 03 r- H CO 1 2 . 0 «-H OCO CO 03 1 4 r 4 1 r 03 H r to 30 03 03 03 03 03 1 2 . 4 O 0 0 o to to 03 H r CO CO 1 ■ • • 2 . 6 " 1 1" H ^ 03 LO O 03 1 4 . 6 to CO ■^r to to o CO CO O LO LO 1 - 0 . 2 to o H * 03 o co* to r“H to 1 I 1 OS H OS H 4—> i - 4 4-* ) a CD co 0 0 O03 0 CO 0 CO O0 CO 03 0 CO CO o ■^r CO to csj 03 E-H i 1 ■1 # o s , # # • « • o o CD CO ts CO o t to O CO CO • « • LO 03 O 3 0 1“ I o to 3 0 o o 3 0 I . • 179 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced Table 22 < •0 OS "O DS P 1 I -1— I 1 -I— H • +J +-> +-> 0 oi 0 0 01 a 0 s-. 0 0 0 G 0 0 O* 0 c o CD 01 h Q E cs EH OS E OS Qi •C Si C 01 0 01 Si C 01 0 0 !_ & >. 01 0 0 0 01 0 01 0 h 0 C 01 0 h CO o CO i r— o CM 'a* O CM o o o • ■ • • . a a • • • a , • • • • a CO* O CO 00 CO cm CO o CM O 0 G -H r- CD CO I ■ CO CM o CO o o CO a a • • CO 4 »“ CO o CM CO CO LO O o o CM CM CM CO CM OCM CO CM O CM CM LO CO CO O CM o CO CO CO E DS H DS E DS 0 Ol 0 Ol CD C/3 0 01 h 0 01 Table 23 < T3 a: T3 P-. H • •rH H • 4-> + 3 w CD (1) cn o. u O C (0 0 CO 0 f-40 o P c ( rj 1) j 1 1 1 Q C £ CO w ro 0 0(0 l 2 , Training i Rest Training i Rest Training j Rest i ...... -...... i 1 ^ -3.8 1 1.4 -4. 6 2. 4 -3.2 ' 0.4 I i M O O o t LO OO CM -1. 2 I 0. 8 -0. 4 1. 0 -6. 8 J -1. 6 o c 0 1 i 0.0 {-0.4 1. 4 -1. 0 -3. 8 S -0. 8 I -6.0 J-2.4 -5. 8 -3. 4 -7. 2 ( -6. 2 -4. 2 I 0. 2 -2. 6 -2. 0 -5.4 I -0. 2 l l 2. 4 ! -4. 0 -8. 4 | -3. 0 -7.8 ! -3.8 I « I l i i 1i i Test 1 Rest Test | Rest Test J Rest i i1 i ...... i ...... i— ' 1------1 o c h o* w o ^ ^ ^ E 0 CD 00 N I I I I O £ h -7.6 {-4.2 -5. 4 -5. 0 1 t 1 - 03 C-J V LO CV3 -2.6 } 1.0 -2. 8 -2. 2 i -7.6 {-2.4 -5. 2 -1.4 i i --- i Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced Table 24 Q E OS Oi E -G CC H os CO 0 0 >1 co i S Cn 0 CO 0 0 h 0 c i S G tjl 3 0 Q) CO 3 i S c en h 0 w to O 03 3 0 O o CO o 03 i I 1 • • • • m * o CO O MCO CM CO LO CO OCM LO OL CO LO LO C I 1 n • • • • • • . CO ] O G 0 o l 3CM 03 C^. CO LO I 1 # o CM o 3 0 o 00 Cvl LO CM I I- * CD CO 00 CO (M O rH o LO rH CM O CO LO I 1 • CD CN. cn CO CM LO 1 0 03 I I i 1 • -H E OS OS E OS E w 0 0 0 CO 0 h h 0 cn 0 CO h 0 CO EH LO CD o OLO LO O CO CO LO OLO LO <: l 1 • • • « # • o l OLO LO CO oo LO 03 o on co I i LO 0 0 to CO 00 O CO LO CM I I H CO U) P .025 .05 .05 .05 F 3.65 4.69 2.11 2.27 .05 10.78 1.115 4.000 0.0001530.000183 8.99 .05 0.237 0.365 0.829 0.772 14.634 1 5 8 df MS 10 10 20 40 TABLE 33 Source FREQUENCIES DURING T-R PERIODS OF PHASE I (DAYS 1-6) PHASE I (DAYS OF PERIODS T-R DURING FREQUENCIES ANALYSIS DF VARIANCE OF RESPIRATION CYCLE TRANSFORMED Z-SOORE RESPONSE Z-SOORE TRANSFORMED CYCLE OFRESPIRATION VARIANCE DF ANALYSIS Error 4 0.000017 Error Group x Day x Group Error Group x T-R x(Training-Rest) Group Group x Treatment x Day x Period x Day x Treatment x Group Error Treatment x T-Rx Treatment 1 Treatment x Period x T-Rx Period x Treatment Period x Day 2 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 184 df=2/8, P interaction (F=2.273 df=10/40, p<^.05)- Figure 9 to 12 indicated that in general response rate for nonphobic increase group and nonphobic decrease group had a slop of downward trend across the six days of Phase I, while response rate for phobic decrease group oscillated from day to day, with day 1 and day 6 having the same general slope around the grand mean. The phobic increase show an increase tendency of RRs across days. Insert Figures 9-12 about here However, the mean square error for between inter actions are so very small that it suggests idiosyncratic differences between all subjects; thus such high number of interactions. Analysis of variance of collapsed data for this variable indicated that the group main effect was signi ficant only (F=10.66, df=l/4, p^.05)3 demonstrating that idiosyncratic differences between subjects is responsible for this difference. Insert Table 34 about here Analysis of variance for days 7 through 93 that is, Phase II, did not indicate any significant main effects or inhibited via this response variable. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Figure 9. Relative transformed z-score frequencies of Respiration Cycles In Phobic Increase group (PI), in 5-min blocks of Training (Phase I), Testing (Phase II), and Rest (both Phase) periods over 9 days. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced +3.0 ¥ O O (uxui/saioAo) a^ey; i + X urq.'e.iTdsaji •r O O CM i O CO I « oa * CM OI CSI CM 00 186 CM O 00 in 00 o uo 00 CM •a ft E N 3 •H r** 0 UO M ft E _ c ' a -H ft 0 187 Figure 10. Relative transformed z-score frequencies of Respiration cycles in Phobic Decrease group (PD), in 5-min blocks of Training (Phase I), Testing (Phase II), and Rest (both Phases) periods over 9 days. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 188 (urm/saioAo) arey uotiT3.it dsay Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 189 Figure 11. Itelative transformed z-score frequencies of Respiration Cycles in Ncnphobic Increase group (NPI), in 5-min blocks of Training (Phase I), Testing (Phase II), and Rest (both Phases) periods over 9 days. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced +3.0 i + ¥ uu/aoo uoT^BJxdsaa (uxui/saioAo) O 03 I CO I 190 oa in 3 0 03 —! T— 00 03 O CD 00 03 CO ft ■5 ft r 3 0) E r* 3 0) -1 £ §> 2 Figure 12. Relative transformed z-score frequencies of Respiration Cycles in Nonphobic Decrease group (NPD), in 5-min blocks of Training (Phase I), Testing (Phase II), and Rest (both Phases) periods over 9 days. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 192 Phase II (min) Figure 12 Phase I (min) 1.0 2.0 2.0 -3.0 + - + +3.0 s O w Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. VO OJ P .0 5 F MS 0.0001333 0 .0 0 0 0 1 2 5 10.66 1 4 df TABLE 34 Source RESPONSEFREQUENCIES DURING TRAINING ANDREST PERIODS OFPHASE I ANALYSISOFVARIANCE OF RESPIRATION CYCLE 03LLAPSED TRANSFORMED Z-SCORE Group Error Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 194 Analysis of variance for days 5S 6 and 7 (the first testing day) indicated a group main effect significant (P=73-953 df=l/4, p <.001). No other interactions or main effects were significant. This highly significant main effect is due to the very small MS error variance, indicating that responding is due to highly idiosyncratic group behavior (see Table 35). The graphs of RRs demonstrate that Phobic Increase group had a higher responding rate for test periods in contrast to rest periods, whereas the nonphobic increase group had a very much lower response rate during testing period in contrast to rest periods. The response rate for the decrease groups is much more stable and virtually not different from days 5 and 6. Analysis of variance for days 5S 6 and 8 indicated a period main effect significance (F=5-08, df=2/8, p<(-05)5 a significant day x period interaction (F=3.28, df=4/l6, P^-05)j and a treatment x day x period interaction (F=3.23, df=4/l6, p^.05). This latter interaction suggests that there was a significant lower responding rate for day 7 than for the other two days, that is, days 5 and 8 being not significant from each other, which is true for all groups. Also, the general direction of within days response rate has a decreasing slope, indicating that as the session progressed response rate lowered. Again, the graphs show that it is the response rate of the increase groups which Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 195 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. TABLE 36 ANALYSIS OF VARIANCE OF RESPIRATION CYCLE TRANSFORMED Z-SOORE RESPONSE FREQUENCIES DURING T-R PERIODS OF THE SECOND HIERARCHY LEVEL Source df MS F p Period 2 2.004 5.08 .05 Error 8 0.394 Day x Period 4 0.463 3.28 .05 Treatment x Day x Period 4 0.455 3.23 .05 Error 16 0.140 197 P .01 F 5.46 63.90 .002 MS 44.321 df TABLE 37 Source FREQUENCIESDURING T-R PERIODS OF THE THIRD HIERARCHYLEVEL Error 8 0.536 GroupErrorPeriod 1 4 2 0.693 2.932 ANALYSISOF VARIANCE OF RESPIRATION CYCLE TRANSFORMED Z-SCORERESPONSE Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 198 is responsible for these significant effects. Finally, the analysis of variance for days 5, 6, and 9 indicated two main effects being highly significant, namely, group main effect (F=63-90, df=l/4, p^.002), and period main effect (F=5.46, df=2/8, p^.Ol). The period main effect demonstrates that overall within sessions there was a tendency for decreasing RRs across each session. The group main effect significance is more indicative of the differences between the phobic and nonphobic subjects in the increase direction. BAT and Fear Thermometer The results obtained from the behavioral avoidance test (BAT), BAT latency, and the fear thermometer are presented in Tables 38, 39, and 40 respectively. Insert Tables 38, 39, and 40 about here Analysis of variance for BAT yielded no acceptable significance level between or within phobic and nonphobic subjects (p^.05). Also, no interaction was significant. Analysis of variance for latency measure yielded a significant pre-treatment main effect between subjects (F=9.32, df=l/4, p<.04), indicating that all the subjects, in particular nonphobic groups, had a reaction to snake as a novel stimulus (Table 4l). Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 199 Table 38 The scores for the pre- and post-behavioral avoidance test (BAT) for all the subjects in the phobic and nonphobic groups. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 200 Table 38 BAT Scores Groups Subjects Pre Post Phobic 5 16 17 Increase 58 1 7 Phobic 49 16 16 Decrease 16 17 17 Non- 25 22 22 Phobic Increase 29 ' 22 22 Non- 53 22 22 Phobic Decrease 24 22 22 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 201 Table 39 Latency of approach (in seconds) to the phobic stimulus during the pre- and post-behavioral avoidance test (BAT) for all the subjexts in the phobic and nonphobic groups. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Table 39 BAT Latency (sec) Groups Subjects Pre- Post- Phobic 5 90 73 Increase 58 37.5 30 Phobic 49 25 30 Decrease 16 104 49 Non- 25 115 50 Jt'DODlC Increase 29 180 52 Non- 53 165 70 Phobic Decrease 24 45 35 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 203 Table 40 The self-rated fear scores on the fear thermometer scale for all the subjects in the phobic and non phobic groups during the pre- and post-behavioral avoidance test (BAT) and during Phase II. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 204 Table 40 Fear Thermometer Phase II Groups Subjects Pre- Post- Session 1 Session2. Session 3 Phobic 5 7 9 10 10 6 Increase 58 9 3.5 2.5 2 5.5 Phobic 49 8.5 1.5 7 8.5 7 Decrease 16 9 1 1 2 7 Non- 25 3.5 2.5 2 1.5 1.5 Pobic Increase 29 2 1 1 1 1 Non- 53 2 1 1 1 1 Phobic Decrease 24 1 1 1 1 1 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 205 M < K O .=r H o > • < ic a CQ I E-i co cm O on a • a OV Q 2 < 1 a K VO VO a CM VO CO CM CM o s • 2 CM O H c— on a vo ov 2 E-I CO Q CO a t— i CO E-i •=r a cc a a a 2 O 2 i—I -=r a CO 2 CQ < < < a q E-I S H o >-l > o < 2 a Eh < a a o m a a o 2 C < 0 CD H O 0 K Jh s < 2 a > O a 0 CO c a a 0 w o e a Sh CO a o a 0 2 CO 2 Sh >H Eh a a < 2 <=C Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Analysis of variance for fear thermometer yielded a significant betvreen group effect (?=ld. 0 8 3 df=l/43 p^ -0 indicating a higher fear report for phobic groups than nonphobics. No other interaction or main effect proved significant (Table 42). Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 207 Q ■=r 1 a i—! a a Oh o 2 M L 3 CM K CM MO CO CO CO O O Q 2 s • • O co .= r K H OO i—1 a co t—i E-I CO a a S CO OJ o S H a h a a a a i—! -=C" a E-i 03 E-I CO < c-i a a < a a a co 2 a m a a Eh a Q a o a o co 2 CO < 1—1 CD C a o •H < 3 r - > 3 40 O•H a CO o CO a 3 H 3 o co O 3 >H 3 3 a a a < 2 < Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. CHAPTER 8 DISCUSSION AND CONCLUSIONS The primary purpose of Phase I was to determine whether or not the electrodermal activity can be conditioned as an operant in either increase or decrease directions. The results supported the conclusion that the rate of emission of unelicited SRRs can be conditioned by operant training procedure. Furthermore, there was no difference between the phobic and nonphobic groups in the designated direction. The most noteworthy result found here is the fact that suppression of the electrodermal activity is pos sible. This is important for it takes a step towards Lang's (1969) hypothesis and reduced autonomic response can be used as a direct form of treatment for cure of phobia. Although the literature (see review) has attempted instru mental conditioning of electrodermal activity in an increase direction, there has not been any attempt to instrumentally reinforce subjects to supress their rate of responding. In the studies reviewed, the attempt had been to differentiate between contingent and noncontingent reinforcement groups, whereas, in the present study this procedure did not exist, i.e., all subjects were reinforced acording to their appro priate designation. 208 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 209 The results for this study, in particular, for increase operant SRRs, is in conflict with those of Stern's (1967) study, in that the flash of green light was shown to act as a positive reinforcer. Thus, at least one other laboratory has shown positive results with this type of reinforcer. This result also is in support of Greene and Wirth (1974) who found no apparent effect of the intensity of light as used for reinforcer. However, in contrast with their proposal in dismissing Stern’s (1967) results, this experiment indicates that not only the light intensity does not influence the rate of responding, but that the distance of reinforcing light stimulus does not influence instrumental conditioning of SRR’s as purposed by Greene and Wirth (1974). Another noteworthy result of this study is the contrast with Greene and Nielson (1966), whose study found that low autonomic perceivers increased SRR frequency for contingent points on a counter, emphasizing the inverse relationship between conditioning and awareness. Whereas, in the present study all subjects were highly aware of their autonomic reaction, at least in presence of phobic stimulus, and were also told the relationship of the reinforcer, that is, the light, and their SRR behavior, indicating that the Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 210 Inverse relationship does not necessarily hold true in instrumental conditioning of autonomic behavior. In parti cular, Greene and Neilson CIS66) advanced the hypothesis that high autonomic perceivers found the instructions dif ficult to follow, as they would "know" when they were or were not relaxing. This difficulty may have led to an over-emphasis upon "trying" to relax which interfered with conditioning process. In contrast to their study, the instruction to "relax” was never given in the present study, and this factor as an independent variable may have been the variable interfering in their study, whereas in the present study the word "comfortable" was employed in the instructing the subjects. Admittedly, a question of sematics is involved in this argument; however, for this experiment the word "relax" could not have been used for it would have possible acted as an instruction set for relaxation hypothesis of counterconditioning. The support given subjects through instructions this concerning the exact contingencies of the reinforce ment differentiates this study from animal and other human operant research. These instructions were thought to be justified in the light of a priori supposed difficulty in bringing the electrodermal activity under a degree of fine control. The interaction between such instructions and re inforcement procedures employed in producing positive results Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 211 Is an interesting problem. Simply instructing subjects to produce electrodermal responses without feedback does net lead to sustained modification of response rates (Crider et al, 1966; Stern and Kaplan, 1966). Moreover, Johnson and Schwartz (1967) found no difference between informed and non-informed groups in the amount of electrodermal response supression produced with contingent punishment. On the other hand, contingent reinforcement of electrodermal responses with only minimal instructions to subjects to stay alert produces successful conditioning (Fowler and Kimmel, 1962; Rice, 1966). The gradual development over sessions (Figures 1-4) also suggests a reinforcement or training, as opposed to a purely cognitive, interpretation of the phenomenon. This is not to say that some degree of cognitive involvement may not be concomitant of operant electrodermal conditioning. In post-sessions and post-experimental inter views and subjects of the present study reported a good deal of problem-solving activity. Although none claimed to be able to predict the exact occurrence of a feedback reinforcer, each had worked out an idiosyncratic mental activity to meet the demand of the various schedules. Idiosyncratic responding can also be proposed for the other two measures analyzed for this experiment. In particular, heart rate data for Phase I suggest that this Reproduced with permission of the copyright owner. Further reproduction prohibited without permission 212 response can be ruled out as an SRR modifier within this procedure. However, a conditioning of heart rate in con comitance with this procedure is possible. Of the studies on electrodermal conditioning the result for heart rate has only been analyzed in aversive or avoidance conditioning procedures employed (see Schell and Grings, 1971; Martin, Dean and Shean, 1968). These studies reported a decelera tion of heart rate during shock avoidance periods for con tingent subjects (Schell and Grings, 1971), whereas for Martin et al (1968) study, heart rate acceleration was observed during avoidance procedure of electrodermal increase conditioning. The result of heart rate for the present study showed that nonphobic subjects in the increase group had a general trend of heart rate increase across days, as opposed to nonphobic decrease group who had a general decrease direction across days. The above finding is also true for across periods within sessions. The same result is also suggestive for phobic increase and phobic decrease groups, though not as pronounced. Furthermore, in general, heart rate during periods for all subjects tended to follow the same directional trend as the cor responding training periods. Perhaps the results are more in accordance with those obtained by Lacey, Kagan, Lacey, Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 213 and Moss (1963), who found that for tasks requiring "rejec tion" of the environment (increase group in this study), the heart rate accelerates, while for tasks requiring "acceptance" (decrease groups in this study), heart rate decelerates. It should be remembered that the experimental environment in this study was not aversive in any sense during Phase I, in view of the fact that the subject was to make himself/herself comfortable and the room was dark- all suggesting inducement of calmness and acceptance of the environment. However, another possibility exists for the effects obtained in the heart rate results and SRRs results, and that is the results obtained from the respiration data. In all the studies mentioned in chapter H for conditioning of the electrodermal activity the proposal of correlation between respiration activity and electrodermal activity as conditioning factor has been discounted. This is in the view of the fact that some studies reinforced electrodermal activity despite respiratory irregularities, and some only reinforced in the absence of respiratory irregularities (Rice, 1966), as the latter procedure was followed in the present study. However, for heart rate results there seems to be a general concordance with respiration activity. What can possibly be suggested is that the correspondence direc tion was followed by heart rate and respiration. But there Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 214 Is little reason to assume that results from one autonomic variable are necessarily general!sable to other autonomic events. Relevant to this line of reasoning are the typically low intercorrelation in autonomic activity (Lazarus, 1966; Martin, 1961), and the differential innervation of various autonomic events. Thus, the EDA is controlled solely by sympathetic, heart rate is controlled by both sympathetic and parasympathetic innervations. The second main interest, and the important one for this study, was the effect obtained for procedure in Phase II. That is, what effect training of an autonomic activity has on the fear response when a phobic stimulus is present. The result clearly are against the hypothesis put forward by Paul (1969), in that reduction of fear is not necessarily obtainable by voluntary control of an autonomic response. What the results, obtained in this study, suggest are at best inconclusive. However, the SRR results are in agreement with several studies which have used this response more as a mechanism which may underlie desensitization (Barlow et al, 1969; Paul, 1969; Agras, 1967)- The pro cedure in this study yielded results suggestive that the subjects were able to control their autonomic activity, namely SRR, in the presence of the phobic stimulus (snake), This result is most important for the phobic decrease group, Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 215 for whom, if one is to postulate upon the desentization procedure of lov; autonomic arousal for successful therapy, then one would expect a change in post-treatment behavioral avoidance score as a demonstration of cure. Barlow et al (1969) have suggested the above mentioned postulate, but one needs to remember that in their study EMG relaxation was used and skin resistance response was only recorded as a concomitant observable response in measure of success in therapy. The results of post-BAT for the phobic group in the present study showed no appreciable change in avoid ance, despite the verbal report of low anxiety during test ing sessions of Phase II. If Lang (1969) is correct in his proposition that low verbal report and low autonomic activity is a sign of cure of phobia, then the results of this study were contrary to his postulation. Perhaps the results ob tained support Paul (1969) who suggested that there is low concordance between verbal report, therapy success, and autonomic activity. This certainly is true for the phobic decrease group of the present study. Another possibility for rejection of the theory proposed by Lang is the result which is obtained for the phobic group in the increase direction. In particular the results from one subject (see Table 38) is in contrast to his hypothesis. While this subject had a high rate of SRRs and low verbal report of anxiety during Phase II, there Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 216 was a change in the approach score for the post-BAT— that is, an increase in degree of approach. This seems to be in support of flooding procedure (Stampfl & Levis, 1967) where although relaxation is not used in the desensitiza tion procedure, the patient shows an improvement in reduc tion of his/her fear. Thus extinction of fear occures despite the non-use of relaxation techniques. The result for the other subject in this phobic increase group on post-BAT also shows an increase in degree of approach, although very minimal. The finding of 3 RR rate for the phobic groups of either trained directions may suggest a support for Wolpe’s (1958) comments that under circumstances anxiety does not dissipate between images, but appears to summate. This is certainly true for both groups characterized as phobic, and is in agreement with Paul (1969) results in that there is a response increment within each session and as the hier archy level increases— that is, across days for Phase II. At the same time, this study supports the results of the studies reviewed, in that there is a higher responding rate to noxious stimuli than to those rated neutral (Gross- berg and Wilson, 1969; Wilson, 1966, 1967; Lomont and Edwards, 1967; Geer, 1966; and Barlow et al, 1969, 1970) But, as mentioned, only the nonphobic subjects show a de crease in response rate across session and days (see results). Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 217 The response increment for the phobic groups would suggest that there was a relatively high anxiety in the subject, or it may have depended on the frequent applica tion of high intensity stimulation. Since the phobic groups reported relatively low anxiety during Phase II, then the second suggestion needs to be considered. This condition has been described as that which distrupts the usual process of habituation to repeated stimuli and may lead to an up ward spiral of responses into panic (Lader and Mathews, 1963, 1970). The above condition is also the same condition pre vailing in flooding sessions, suggesting that if continued for long periods this upward spiral must be self-limiting and in the end will lead also to decrement in autonomic anxiety responses (Boulougouris et al, 1971)• Since the present study did not use prolonged presentation of phobic stimulus, and it was interspaced with rest periods, it can not be postulated that flooding could have been completely present as a procedure. Thus, accounting for incomplete cure of phobia for the phobic increase group subjects as it is evident on BAT results. The result of heart rate data also is in support of the assumption of high arousal level during stimulus presentation. Lang, Melamed, and Hart (1970) reported high correlation between heart rate responses and a com posite measure of behavioral and self-reported fear at the Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 218 end of the treatment. Subjects v;ho showed high heart rate responded most to treatment and also declined of this response to repeated presentation of phobic stimulus even showed a better treatment effect. The results of heart rate data for both phobic groups in the present study show a similar trend for Phase II as Lang et al’s (1970) study. If it can be concluded that the training of SRRs is an effective mode of procedure in desensitization of fear with the sup port of the heart rate data, it is not clear why the phobic decrease group did not improve in post-treatment assessment. Again, the extinction hypothesis seems to be the most objective theory in this case, and only effective for the phobic increase group. The result from the respiration data are in accord ance with previous studies (Rimm and Bottrell, 1969; Lang et al, 1970), who reported higher response rate during the fearful scenes. It can also be seen that the results of this response for the phobic subjects (and nonphobic) decrements as the presentation of the phobic stimulus increases (with the exception of the nonphobic decrease group). The failure of the study to demonstrate any clear cut training procedure for cure of phobia as hypothesized by Lang (1969) can be postulated towards a support for Wolpe's (1958) theory of desensitization procedure. Further Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 219 support can be drawn fro ip. Paul (1969) that there is low concordance between autonomic activity and outcome of therapy. However, one point needs to be mentioned before a conclusion can be drawn to reject Lang’s hypothesis. The assumption that verbal report of low anxiety in the presence of a phobic stimulus would be a further support in success of therapy procedure used in the present study. That is, at least those subjects trained to reduce their SRR activity in presence of the phobic stimulus should re-evaluate their fear of snakes. In considering this assumption the post-treatment interviews are important. The response of subjects during these interviews indicate that this assumption was probably not justified. All sub jects reported that their low rating on the fear thermometer during Phase II was most likely to be due to "not being able to see the snake because the room was dark." Thus, by devaluating the fearfulness in darkness, all of the subjects were able to respond during Phase II without re evaluating their actual fear of snakes. It is, therefore, possible that the present methodology is inadequate for testing the original question of interest. Certainly one cannot study how cognitivity re-evaluating a fear affects avoidance behavior without first inducing the appropriate re-evaluation. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 220 Clearly, modification in current methodology are required if an adequate test of the original problem is made. Perhaps additional instructional manipulation could help to ensure the necessary re-evaluation of fear response on the part of the subjects. It might be necessary for the experimenter to overtly interpret the meaning of the feedback training and tell the subject that he/she is less afraid of the snake than he/she thought. Using the specimens in clear view would make it difficult for subjects to respond by simply devaluating it. Whatever the alterations attempted, future studies should pilot their instructional set and feedback manipula tion and assess their effect in post-treatment interviews. In the meantime, the original model proposed by Lang (1969) is yet to receive empirical support. This conclusion is supported by the present study, the findings of Paul (1969)9 and the original weaknesses in the original Lang’s (1969) model. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Appendix A Behavior Avoidance Test 221 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 222 The purpose of this session is simply to find out h o w afraid of snakes you are, as you had indicated on a previous questionnaire. To do this, you are asked to enter the room and carry this check list with you. On this check list, you are to indicate your greatest degree of approach to the snake. At the end of the runway in the room there is a harmless yellow-black snake securely enclosed in a glass cage. Follow the check list, and perform those instructions which can be done calmly. You are completely free to refuse to do so, at any time, if you wish. 1. Standing outside the door of the testing room. 2. Entering the testing room. 3. Positioning oneself so that the snake can be seen, at the beginning of the runway, which is numbered. |T] 4. Approaching the cage. CH 10. 5. t u 11. m 6. s 12. Eg] 7. EJ 13. m 8. EJ 14. m 9. m 15. 13 16. Touching the glass container. 17. Removing the screen cover. 18. Passing the fingers over the upper rim of the container a n d a p proaching the snake. 19. Touching the surface of the snake, for a period of 10 seconds. 20. Grasping the snake in firm hold long enough for the snake to be picked up. 21. Lifting the snake long en o u g h so that all parts are not touching the container. 22. Holding the snake against one's chest for a period of 10 seconds. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Appendix B Basic Experimental Design The schematic of all sessions conducted for each subject 223 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. j Post- Pre Phase II assessment Phase I I assessment GSR Session 1 Session 2 Session 3 Training GSR GSR GSR 1 session (6 sessions' Testing Testing Testing 1 session o \ Phobic K Behavior Behavior Avoicance Stimulus Stimulus Stimulus Avoidance Test t Test Nonphobic 8 ft (f) 5 ft (f) 2 ft (t) INCREASE Phobic Behavior Behavior Avoidance Stimulus Stimulus Stimulus Avoidance Test 1 8 ft ( J ) 5 ft (|) 2 f t U ) Test Nonphobic DECREASE Appendix C The schematic paradigm of a session in Phase I conducted for all subjects for six days. (Replace Baseline with Equipment adjustment for the diagram shown to the subjects). Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. without prohibited reproduction Further owner. copyright the of permission with Reproduced *5 *3 £ cd Rest Start End o o CO a) w a 1 sec sec 1 sec298 Appendix D The schematic paradigm of a session in Phase II conducted for all subjects for 3 days, with distance of the phobic sub ject changing in increments of 3-ft, i.e., 8-ft, 5-ft, and 2-ft. (Replace Baseline with Equipment adjustment for the para digm shown to the subject). Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 228 Rest 5 min 5 in ulus End Stim Phobic 30_aec_ Testing Rest 238 sec 238 absent Rest Phobic stimulus stimulus Phobic Periods lus lus out out Start sec 1 Stim- Stim- 30 sec 30 Phobic Phobic Phase II Phase Rest Testing 5 min 5 min 5 min 5 min 5 5 min 5 Testing 10 min 10 Phobic stimulus present stimulus Phobic Baseline Testing tions » Instruc Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Appendix E Autonomic Perception Inventory 229 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 230 This questionnaire consists of seven questions relating to your body awareness when you are anxious. In answering than please mark on the scale of zero to ten, your awareness of the particular body function. If you mark zero, it means that you are never consciously aware of that particular function when you are anxious. If you mark always, it means that you are always aware of any changes that occur to the specific body function (for example, heart rate). You may, of course, mark on the scale anywhere in between these numbers according to your perception of these body changes when you are anxious. Please read carefully. 1. When you are anxious, how often are you aware of any changes in your heart action. never always j______!______i______t______i______i______i______;______t______i i 01 2 3 4 5 67 8 9 10 2. When you are anxious, how often are you aware of any changes in your respiration? never always J______I______t______I______t______1______I______I______I______1______t_ 01 2345678 9 10 3: When you are anxious, how often are you aware of any changes in your muscle tension? never always j______i______t______ii fit f i i 012345678 9 10 4. When you are anxious, how often are you aware of any changes in your perspiration (sweating)? never always 1 > 1______1 1 1______1111______l_ 0123456789 10 5. When you are anxious, how often are you aware of any changes in your blood pressure? never always _T.______I______»______I______1 1 1 1 1 1 1 0123456789 10 6. When you are anxious, how often are you aware of any changes in your body temperature? never always 11111111111 01 2 3 4 5 67 8 9 10 7. When you feel anxious, how often are you aware of any changes in your gastro (stomach)-intestinal organs? never always j______i______»______t______i______i______j______i______» i i 0123456789 10 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Appendix F Fear Thermometer Scale 231 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. During the avoidance test which you just participated in some degree of fear probably existed which you experienced. Rate this amount of fear w h i c h you experienced on the scale below. Note that the scale is numbered from 1 to 10. Number one (1) represents. . . and ten (10) represents high. 10 9 8 7 6 5 4 3 2 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Appendix G Daily Recording Table 233 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Subject Control Experimental Increase Decrease Date Phase one Session___ Phase two Session ___ Subject came in at ______Within past twenty four hours: Amount of sleep during previous night Nap? Meals Time Size Breakfast Lunch Dinner Snack Drug intake Alcohol______Minor Illnesses_____ Subject's behavior 30 min. prior to the appointment: Any food, drinking, & smoking Quiet, non-active way Within college In moderate temperature Lavaratory _ Temperature Subject's______Roan______relative humidity Frequency Fil-Pola- Ch.______Leads L H Sensit. ter rity Changes Checks EEG Occipital r - EEG Occipital 1 - EKG - Respiration - GSR - EMG forearm r - EM? forearm 1 - Notes: Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. Appendix H Comprehensive Questionnaire for all Subjects 235 Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 236 Subject # Date These questions pertain to your experience throughout the present ex periment which you have participated in. Please read carefully and try to an s w e r directly and sincerely. 1) H o w did y o u learn about this research? from a friend, from the ex perimenter, or in some other wa y (explain). 2) W h y did you decide to volunteer as a subject? Were you interested in the topic of the research (explain), in helping the experimenter, or in reward? Did you volunteer because you were asked by the ex perimenter, or for some other reason? 3) Did you have any doubts or resistance in taking part in the research (please explain) ? 4) H o w much were you interested in biofeedback at the moment you vol unteered for the experiment? Please try to quantify it on a scale ranging from 0 to 10 0 ■ 10* and please explain your interest. 5) H o w m u c h wo u l d you score your interest for biofeedback n o w that you have participated in this experiment. Please use the same scale 0■ ■ » - « ■ ■ « « « « 10» and explain Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 237 6) In what measure did your interest in the topic of research was satis fied by your participation, score overall and explain 0■ . » ■ » ■ « ■ ■ » * ■ —»10 7) Please explain and describe this research to a third person that does not k n o w anything about it 8) What was the purpose of the first six sessions? 9) What was the purpose of the second part of the experiment? Can you give rationale as to w h y the distance of the stimulus (the snake ) was changed? 10) Were the information and answers which you received during the study satisfactory or did you have the impression that some informa tion w a s withheld or that y o u were lied to (please explain) ? Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 238 11) W h a t w a s your technique or me t h o d in controlling your Galvanic Skin Response (sweating) during the first phase of the experiment (first six sessions) ? 12) If you did not have any particular method in controlling your GSR, what did you try to do to achieve control? Or what did you do during the sessions that is, mentally and physically. 13) Did you employ the same technique during the second phase of the experiment or did you choose another method? If so, please explain. 14) At present do you feel you have (or can) control your G S R ? Please quantify on the scale below. 0 represents not at all and 10 complete control. 0 ■ - » » * ■ « • ■ ■ 10 » Please explain. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 15) H a v e y o u tried to use this control in an y other settings than this experiment? Or has any situation arisen for you to use this con trol? Explain how and under what circumstances. 16) Please explain w h y you would not use this learning experience of control in a n y situation. 17) D o you believe it to be unethical for a person to learn such control? Explain. 18) D o you feel that the experimenter expected too high rates of perfor mance from you? C a n you quantify the experimenter's expectancy on the scale below? 19) A certain amount of relationship will develop between any two or more persons in any type of settings. H o w would you rate the ef fect of the relationship between you and the experimenter on the study? That is, w o u l d you h a v e don e differently in controlling your GSR. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 240 20) D o y o u believe that having the sna k e in the r o o m during the second phase of the experiment improved your feeling towards this animal, or is it otherwise? 21) W h a t w o u l d y o u attribute your c h a n g e of indicated fear of the s nake? W a s it the repeated exposure or knowing that you were controlling your GSR? Please explain. 22) A s s u m i n g that y o u had none or little exposure to biofeedback prior to taking part in this experiment, could you briefly explain what you think about it now? 23) W h y do you think you were chosen for this experiment? and do y o u k n o w wh a t the criteria w e r e ? 24) W o u l d you volunteer for this type of experiment again if given the opportunity? 25) Did y o u take an y type of drugs or alcohol while participating in this experiment? If so, please explain the type of drug. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 2kl 26) Wer e you under any medication or under medical care or psycho logical care before and during the experiment? Please explain. 27) H o w comfortable were you in your relationship with the experimenter? not very » ■ » • ■ • • . .. i —i 1 m u c h m u c h Explain: 28) H o w much did you feel you could trust the experimenter? 0 10 ■ — i ...... i ■ Explain. 29) O n the basis of your immediate experience, what were the best features of this research? 30) W h a t were the worst features of this experiment? 31) H o w do you think this experiment can be improved? 32) Did y ou ever discuss this experiment with s o m e o n e else? Did the discussion y ou had with this person affect your degree of partici pation in the experiment? Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 242 33) Please make any comment which you feel to be important and that has not been covered by a question concerning your feelings and expectations in taking part in the experiment or about your relationship with the experimenter. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. BIBLIOGRAPHY 243 1. Agras, W. S., Transfer during systematic desensitiza- tion theraoy. Behavior Research and Therapy, 19c7, 5, 193-199*." 2. Aveling, F., & McDowall, R. J. S., The effect of the circulation on the electrical resistance of the skin. Journal of Physiology, London, 1925, 60, 316- 321 . 3. Ax, A. F., & Bamford, J. R., Validation of a psycho- physiological test of aptitude for learning of social motives. Psychophysiology, 1968, 5., 316-332. 4. Barber, T. X., & Hahn, K. W., Jr. Hypnotic induction and "relaxation": An experimental study. Archives of General Psychiatry, 1963, 8_, 295-300. 5. Barber, T. X., & Hahn, D. W. Jr., Experimental studies in "hypnotic" behavior: Physiological and subjective effects of imagined pain. Journal of Nervous and Mental Disease, 1964, 139, 416-425. 6. Barlow, D. H., Agras, W. S., Leitenberg, H., & Wincze, H. P., An experimental analysis of the effective ness of "shaping" in reducing maladaptive avoidance behavior: An analogue study. Behavior Research and Therapy, 1970, 8_, 165-173- 7. Barlow, D. H., Leitenberg, H., Agras, W. S., & Wincze, J. P., The transfer gap in systematic desensiti zation: An analogue study. Behavior Research and Therapy, 1969, 7., 191-196. t t 8. Bernard, C. Lecons sur les proprietes physiologiques et les alterations pathologique des liquides de 1 Torganisme. Paris: Balliere, 1859• Cited by H. D. Kimmel, Instrumental conditioning. In W. F. Prokasy & D. C. Raskin (Eds), Electrodermal activity in psychological research. New York: Academic, 1973- 9. Birk, L., Crider, A., Shapiro, D., & Tursky, B. Operant electrodermal conditioning under partial curarization. Journal of Comparative and Physiological Psychology, 1966, 62, 165-1S^ ------ 10. Blank, I. H. Further observation in factors which influence the water content of the stratum corneum. Journal of Investigative Dermatology, 1953, 21, 259-271. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 244 11. Blank, I. H., & Gould, E. Penetration of anionic surfactants (surface active agents) into skin: I. Penetration cf sodium laurate and sodium uodecyl sulfate into excised human skin. Journal of Investi gative Dermatology, 1959, 33., 327-336. T 12. Bloch, V. Nouveu aspects de la methode psychogalvanique ou electrodermographique (EDG) comme critere des tensions affectives. Annee Psychologique, Paris, 1952, _52, 329-362. Cited by R. Edelberg, Electrical activity of the skin. In N. S. Greenfield & R. A. Sternback (Eds.), Handbook of psychophysiology. New York: Holt, Rinehart & Wilson, 1972. I T 13. Block, V. Le controle central de l ’activite electrodermale. Journal de Physiologie, 1965, 57., Supplement 13, 1-132. Cited by R. Edelberg, Electrical activity of the skin. In N. S. Greenfield & R. A. Sternback (Eds.), Handbook of psychophysiology, New York: Holt, Rinehart & Wilson, 1972. 14. Boulougouris, J. C., Marks, I. M., & Masset, P. Superiority of flooding (implosion) to desensitization for re ducing pathological fear. Behavior Research and Therapy, 1971, 9., 7-16. 15- Broadhurst, P. L., & Bignami, G. Correlative effects of psychogenetic selection: A study of the Roman High and Low Avoidance Strains. Behavior Research and Therapy, 1965, 2., 273-280. 16. Brown, C. C. A proposed standard nomenclature for psychophysiological measures. Psychophysiology, 1967, 4, 260-264. 17- Buettner, K. J. K. Diffusion of water vapor through small areas of human skin in normal environment. Journal of Applied Physiology, 1959, 14.» 269-275- 18. Buettner, K. J. K., & Odland, G. F. Physical factor of the skin barrier layer and water diffusion into human skin. Federation Proceedings, 1957, 16., 18. (abstract) 19- Burch, N. F., & Greiner, T. H. A bioelectric scale of human alertness: Concurrent recording of the EEG and GSR. Psychiatric Research Report of the all American Psychiatric Association, IsRToT- 12^ 183-193• Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 245 20. Clark, D. F. The treatment of monosymptomic phobia by systematic desenciti zation. Behavior Research ana 21. Coffman, N., & Kimmel, H. D. Instrumental conditioning of the GSR: A comparison of light deprivation and monotony hypotheses. Journal of Experimental Psy chology, 1971, 89, 410-413. . 22. Costello, C. G. Dissimilarities between conditioned avoidance responses and phobias. Psychological Review, 1970, 77, 250-254. 23. Cowie, V. , 8c Slater, E. Psychiatric genetics. In G. W. T. H. Fleming (Ed.), Recent progress in psychiatry (Vol. III). London: Churchill, 1959- 24. Craig, K. D. Physiological arousal as a function of imagined, vicarious and direct stress experiences. Journal of Abnormal Psychology, 1968, 73., 513-520 . 25- Crider, A., Shapiro, D., 8c Tursky, B. Reinforcement of spontaneous electrodermal activity. Journal of Comparative and Physiological Psychology, 1966, 61, 20-27. 2 6 . Darrow, C. ¥. Sensory, secretory and electrical changes in the skin following bodily exitation. Journal of Experimental Psychology, 1927, 1£, 197-226. 27- Darrow, C. W. The galvanic skin-reflex and finger volume changes. American Journal of Physiology, 1929, 88, 219-229. 28. Darrow, C. VI. The galvanic skin reflex (sweating) and blood pressure as preparatory and facilitative functions. Psychological Bulletin, 1936, 33., 73-94. 29. Darrow, C. W. Neural mechanisms controlling the palmar galvanic reflex and palmar sweating. Archives of Neurology and Psychiatry, 1937, 37.3 641-663• Ca) 30. Darrow, C. W. The equation of the galvanic skin reflex curve: I. The dynamic of reaction in relation to exiation-background. Journal of General Psychology, 1937, 16, 285-309. (b) Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 2 46 31. Darrow, C. VJ. , & Freeman, G. L. Palmar skin-resistance changes contrasted with non-p&lmar changes, and rate of insensible weight less. Journal of Experimental Psychology, 1934 , H , 739-748. 32. Davidson, P. 0., & Hiebert, S. F. Relaxation training, relaxation instruction and repeated exposure to a stressor film. Journal of Abnormal Psychology, 1971, 78, 154-159- 33- Darrow, C. W., & Gullickson, G. R. The peripheral mechanism of the galvanic skin response. Psycho physiology, 1970, 6, 597-600. 34. Day, J. L., ix Lippitt, M. W., Jr. A long-term electrode system for electrocardiography and impedance pneumo graphy. Psychophysiology, 1964, JL, 174-182. 35* Dixon, W. J. (Ed.), BMP biomedical computer programs. Berkeley: University of California Press, 1974. 36. Donner, L., & Guerney, B. G., Jr. Automated group desensitization for test anxiety. Behaviour Re search and Therapy, 1969, 7, 1-13- 37- Duffy, E. Activation and behavior. New York: Wiley, 1962. 38. Edelberg, R. Development of an electrode for long term application in biological recording. NASA Manned Spacecraft Center, Contract Report NAS~~9-445, September 1963- (a) 39- Edelberg, R. Electrophysiologic characteristics and interpretation of skin potential. U. S. Air Force School of Aerospace Medicine, Tech. Doc. Rep. 63-95- 1963. (b) 40. Edelberg, R. Effect of vasoconstriction on galvanic skin response amplitude. Journal of Applied Physio logy, 1964, 19, 427-430. (iJ3 41. Edelberg, R. Impedance of galvanic skin response ampli tude and sweat production. Journal of Investigative Dermatology, 1964, 4_2, 443-448. (b). 42. Edelberg, R. Development of methodology for bioelectric monitoring of human subjects. NASA Manned Space craft Center, Contract Report NAS 9-2839, September 1965. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 247 43. Edelberg, R. Electrical properties of the skin. In C. C. Brown (Ed.), Methods in psychophysiology, Baltimore: Williams & Wilkins, 1967. 44. Edelberg, R. Electrical activity of the skin. In N. S. Greenfield & R. A. Sternback (Eds.), Hand book of psychophysiology. New York: Holt, R’nine- hart and Winston, Inc., 1972. Pp. 367-418. 45. Edelberg, R., Greiner, T., & Burch, N. R. Some membrane properties of the effector in the galvanic skin response. Journal of Applied Physiology, I960, 15, 691-696. 46. Edelman, R. I. Effects of differential afferent feed back on instrumental GSR conditioning. Journal of Psychology, 1970, 74, 3-14. 47. Edelman, R. I. Dysensitization and physiological arousal. Journal of Personality and Social Psychology, 1971, 17, 259-266. 48. Efran, J. S., & Marcia, J. E. Treatment of fears by expectancy manipulation: an exploratory investi gation. Proceedings of the 75th Annual Convention of the American Psychological Association^ 1967, 2, 239-240. 49. Efran, J. S., & Marcia, J. E. Systematic desensitization and social learning. In J. B. Rotter, J. E. Chance & E. J. Phares (Eds.), Application of a social learn ing theory of personality. New York: Holt, 1972. Pp- 524-532. 50. Errera, P. Some historical aspects of the concept of phobia. The Psychiactric Quarterly, 1962, 36, 325-336. 51. Eysenck, H. J. (Ed). Behaviour therapy and the neuroses. New York: Pergamon Press, I960. t T t 52. Fere, C. Note sur les modification de la tensicjn electrique dans le corps humain. Comptes rendus des Seances de la societe de Biologie, 1888, 5, 23-33- Cited by R. Edelberg, Electrical activity of the skin. In N. S. Greenfield 8c R. A. Stermback (Eds.), Hand book of psychophysiology. New York: Holt, Rinehart 8c Wilson, 1972. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 248 53- Fisher, S. Body image and asymmetry of reactivity. Journal of Abnormal ar.d Social Psychology, 1958, GO, 283-285- 54. Flanagan, J. Galvanic skin response: Emotion or atten tion? Proceedings of the 75th Annual Convention of the American Psychological Association, 1967* 2, 7-8. 55- Flesch, P., Goldstone, S. B., & Urbach, P. Palmar pore patterns: their significance in absorption of dyes. Archiv fur Dermatologie and Syphilis, 1951, 6_3, 228-231. 56. Folkins, C. H., Lawson, K. D., Opton, E. M., & Lazarus, R. S. Desensitization and the experimental reduction of threat. Journal of Abnormal Psychology, 1968, 73, 100-113- 57. Fowler, R. L., & Kimmel, H. D. Operant conditioning of the GSR. Journal of Experimental Psychology, 1962, 63, 563-5^74 58. Freedman, D. Hereditary control of early social behavior. In B. M. Foss (Ed.), Determinants of infant behavior III. London: Methuen^ 1965• Pp^ 149-155• 59- Fujimori, B. Studies on the galvanic skin response using current and potential method. Japanese Journal of Physiology, 1955, 5, 394-405- 60. Gale, E. N., Hyman, E., & Ayer, W. A. Physiological measures during systematic desensitization: A report of two cases. Journal of Clinical Psychology, 1970, 26, 247-250. 61. Garlington, W. K., & Cotier, S. B. Systematic desensiti zation of test anxiety. Behavior Research and Therapy, 1968, 6, 247-256. 62. Gavalas, R. J. Operant reinforcement of an autonomic response: Two studies. Journal of Experimental Analysis of Behavior, 1967, 10.5 119-130. 63 . Geddas, L. A., Baker, L. E., & Moore, A. G. Optimum electrolytic chloriding of silver electrodes. Medical and Biological Engineering, 1969, 49-56. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 249 64. Geer, J. H. Fear and autonomic arousal. Journal of Abnormal Psychology , i960 , 7_1, 2 53-255- 65. Geer, J. H. , 1 Katkin, E. S. Treatment of insomnia using a variant of systematic desensitization. Journal of Abnormal Psychology, 1966, 7_1, 161-164. 66. Gildemeisterj M., & Ellinghaus, J. Zur Physiologie der Meschlichen Haut: III. Uber die Abhangigkeid des Galvanischen Hautreflexes von der Temperature der Haut. Pflugers Archiv die Gesamte Physiologie, 1923, 200, 262-277• Cited by R. Edelberg, Electrical activity of the skin. In N. S. Greenfield & R. A. Sternback (Eds), Handbook of psychophysiology. New York: Holt, Rinehart & Wilson, 1972. 67. Greene, W. A. 8c Nielsen, T. C. Operant conditioning of high and low autonomic perceivers. Psychonomic Science, 1966, 6_, 359-360. 68. Greene, W. A., & Wirth, H. G. Operant conditioning of the skin resistance response with different inten sities of high flashes. Bulletin of Psychonomic Society, 1974, 4, 177-179- 69- Grings, W. W., & Uno, T. Counterconditioning: Fear and relaxation. Psychophysiology, 1968, 4, 479-485. 70. Grossberg, J. M. The physiological effectiveness of brief training in differential muscle relaxation. (Technical Report No. 9)- La Jolla, California: Western Behavioral Sciences Institute, 1965- 71. Grossberg, J. M., 8c Wilson, H. K. Physiological changes accompanying the visualization of fearful and neutral situations. Journal of Personality and Social Psychology, 1968, 10^ 124-133• 72. Guthrie, E. R. The Psychology of Learning. (rev. ed.) New York: Harper, 1952. 73. Haimovici, H. Evidence for adrenergic sweating in man. Journal of Applied Physiology, 1950, 2, 512-521. 74. Hara, K. Uber die Hemmung der Schweiss-secretion die nach Reizung der hinteren Wurzel. Pflungers Archiv fur die Gesamte Physiologie, 1929, 221, 692-694. Cited by R. Edelberg, Electrical activity of the skin. In N. S. Greenfield 8c R. A. Sternbach (Eds.), Handbook of psychophysiology. New York: Holt, Rine hart & Wilson, 1972. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 250 75. Herrnstein, R. J. Method and theory in the study of avoidance. Psyc h o 1 o g i c a 1 Review, 19 69 , 49-69 • 76. Hyrley, H. J., & Shelley, VJ. 3. The role of the myo epithelium of the human apocrine sweat gland. Journal of Investigative Dermatology, 1954, 22, 143-155- 77- Hyman, E. T., & Gale, E. N. Galvanic skin response and reported anxiety during systematic desensitization. Journal of Consulting and Clinical Psychology, 1973s 40, 108-114. 78. Isamat, F. Galvanic skin responses from stimulation limbic cortex. Journal of Neurophysiology, 1961, 24, 176-181. 79* Jacobson, E. Progressive Relaxation. Chicago: Univer sity of Chicago Press, 1938. 80. Janz, G. J., & Taniguchi, H. The silver-silver halide electrodes. Chemical Reviews, 1953a 397-437. 81. Jasper, H. H. The ten twenty electrode system of the international federation. Electroencephalography and Clinical Neurophysiology, 1958, 10, 371-375. 82. Jeffress, L. A. Galvanic phenomena of the skin. Journal of Experimental Psychology. 1928, 11, 130-144. 83. Johnson, L. C., & Lubin, A. Spontaneous electrodermal activity during sleeping and waking. Psychophysiology, 1966, 3, 8-17. 84. Johnson, H. J., & Schwartz, G. E. Suppression of GSR activity through operant reinforcement. Journal of Experimental Psycholoyg, 19675 75.3 307-312. 85. Jones, M. C. The elimination of children’s fears. Journal of Experimental Psychology, 1924, 382-390. 86. Katkin, E. S. Relationship between manifest anxiety and two indices of autonomic response to stress. Journal of Personality and Social Psychology, 1965, 2, 324-333- Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 251 87- Katkin, E. S. The relationship between a measure of transitory anxiety and spontaneous autonomic activity. Journal of Abnormal Psychology, 1565, T i , 142-1 15. 88. Katkin, E. S., 1 McCubbin, R. J. Habituation of the orienting response as a function of individual differences in anxiety and autonomic ability. Journal of Abnormal Psychology, 1969, 7_45 54-60. 8 9 . Katkin, E. S., & Murray, E. N. Instrumental Conditioning of autonomically mediated behavior: theoretical and methodological issues. Psychological Bulletin, 1968, 70, 52-68. 90. Kimmel, E., & Kimmel, H. D. A replication of operant conditioning of the GSR. Journal of Experimental Psychology, 19635 §5_, 212-213. 91. Kimmel, H. D. Instrumental Conditioning. In W. P. Prokasy 8c D. C. Raskin (Eds.), Electrodermal activity in sychological research. New York, Academic, 1973- Pp. 255-282. 92. Kimmel, H. D., & Hill, P. A. Operant conditioning of the GSR. Psychological Reports, I960, J_, 555-562. 93- Kimmel, H. D., & Hill, F. A. Two electrodermal measures of response to stress. Journal of Comparative and Physiological Psychologyj 1961, 9^s 395-397. 94. Klingman, A. M. The biology of the stratum corneum. In W. Montagana & W. C. Lobitz (Eds), The epidermis. New York: Academic, 1964. 95- Kuno, Y. Human perspriation. Springfield, 111.: Charles C . Thomas, 1956. 9 6 . Lacey, J. I., Bateman, D. E., & Van Lehn, R. Autonomic response specificity: An experimental study. Psycho somatic Medicine, 1953, 15. s 8-21. 97- Lacey, J. I., Kagen, J., Lacey, B. C., & Moss, H. A. Situational determinants and behavioral correlates of autonomic response patterns. In P. Knapp (Ed.), Expression of the emotions in man. New York: Inter national Universities Press, 1963• Pp. 161-196. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 252 9 8 . Lader, M. H., Gelder, M. G., & Marks, I. M. Palmer skin conductance measures as predicators of response to desensitization. Journal of Psychosomatic Research. 1967, 11, 233-290. 99- Lader, M. H., & Mathews, A. M. A physiological model of phobic anxiety and desensitization. Behaviour Research and Therapy, 1968, 6_, 411-421. 100, Lader, M. H., & Mathews, A. M. Physiological changes during spontaneous panic attacks. Journal of Psychosomatic Research, 1970, _l4, 377-382 101. Lader, M. H., & Montagu, J. D. The psycho-galvanic reflex: A pharmacological study of the peripheral mechanism. Journal of Neurology, Neurosurgery, and Psychiatry, 1962, 2~4~ 126-133• 102. Landis, C. Varieties of ps.ychopathological experience. Edited by P. A. Mettler, New York: Holt, Rinehart & Wilson, 1964. 103. Landis, C., & De Wick, H. N. The electrical phenomena of the skin (psychogalvanic reflex). Psychological Bulletin, 1929, 26, 64-119 104. Lang, P. J. Fear reduction and fear behavior: Problems in treating a construct. In 3rd Conference in Research in Psychotherapy. Chicago, 111., 1966. 105- Lang, P. J. The mechanics of desensitization and the laboratory studies of human fear. In C. M. Franks (Ed.), Behavior therapy: Appraisal and status. New York! McGraw-Hill, 1969• Pp. 160-191• 106. Lang, P. J., Melamed, B. G., 8c Hart, J. A psychophysio- logical analysis of fear modification using an automatic desensitization procedure. Journal of Abnormal Psychology, 1970, 76_, 220-234. 107. Langworthy, 0. R., 8c Richter, C. P. The influence of efferent cerebral pathways upon the sympathetic nervous system. Brain, 1930, 53., 178-193- 108. Lazarus, R. S. Psychological stress and coping process. New York: McGraw-Hill, 1966. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission 253 109 • Lehrer, P. M. A laboratory analog of desensitization: Psychcpr'.vsiological effects of relaxation. Psycho- physiology, 1970, 6, 6 34. (Abstract) 110. Lobitz, W. C., & Mason, H. R. Chemistry of palmar sweat: VII. Discussion of studies on chloride, urea, glucose, uric acid, ammonia-nitrogen and creatinine. Archiv fur Dematologie and Syphillis, 1948, 57., 907,915 111. Lomont, J. P., & Edwards, J. E. The role of relaxation in systematic desensitization. Behaviour Research and Therapy, 1967, 5., 11-25- 112. Lykken, D. T. Properties of electrodes used in electro dermal measurement. Journal of Comparative and Physiological Psychology, 1959* 52, 629-634. 113. McDowall, R. J. S. The physiology of psycho-galvanic reflex. Quarterly Journal of Experimental Physiology, 1933j 24, 277-285. 114. Malmo, R. B. Activation: A neuropsychological dimension. Psychological Review, 1959, 66., 367-386. 115. Marchais, P., & Jason, M. De la hipothymie et du con- ditionnement dans la constitution des neuroses phobiques. Annales Medico-Psychologiques, 1962 120, 572-577. Cited by I. M. Marks, Fears and phobias. London: William Heineman, 1969. 116. Marcia, J. E., Rubin, B. M., & Efran, J. S. Systematic desensitization: Expectancy change or countercon ditioning? Journal of Abnormal Psychology, 1969, 74, 382-386. 117. Marks, I. M. Fears and phobias. London: William Heinemann, 1969- 118. Marks, I. M., & Gelder, M. G. Different onset ages in varieties of phobias. American Journal of Psy chiatry, 1966, 123, 218-221. 119. Marks, I. M., & Huson, J. Physiological aspects of neutral and phobic imagery: Further observations. British Journal of Psychiatry, 1973, 122, 567-572. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 254 120 . Martinj 3. The assessment of anxiety by physiological behavioral measures. ?svchclorical Bulletin, 1961, 58, 234-255- 121. Martin, I., & Venables, P. H. The contribution of sweat gland activity to measure palmar skin conductance and potential. Paper presented at the 4th Annual Meeting of the Society for Psychophysiological Research, Washington, D. C ., October 19647 122. Martin, R. B., Dean, S. J., & Shean, G. Selection attention and instrumental modification of the GSR. Psychophysiology, 1968, 4_, 460,467- 123. Mathews, A. M. Psychophysiological approaches to the investigation of desensitization and related pro cedures. Psychological Bulletin, 1971, 76., 73-91- 124. Mathews, A. M., & Gelder, M. G. Psychophysiological investigation of brief training. Journal of Psycho nomic Research, 1969, 13., 1-12. 125- Maulsby, R. L., & Edelberg, R. The interrelationship between the galvanic skin response, basal resistance and temperature. Journal of Comparative and Physio logical Psychology, I960, 53, 475-479. 126. May, J. R., & Johnson, H. J. Positive reinforcement and suppression of spontaneous GSR activity. Journal of Experimental Psychology, 1969, 8o_, 193-195- 127. Migler, B. & Wolpe, J. Automated self-desensitization: A case report. Behaviour Research and Therapy, 1967, 5, 133-135. 128. Miller, N. E. Learnable drives and rewards. In S . S. Stevens (Ed.), Handbook of experimental Psychology. London: Wiley, 1951- 129- Miller, N. E. Learning of visceral and glandular responses. Science, 1969, 163, 434-445- T 130. Miller, S,, & Konorski, J. Sur une forme particuliere des reflexes conditionels. Comptes Rendues Societe Biologique, Paris, 1928, ££, 1155-1177- 131- Milstead, J. R. Operant GSR conditioning using a within - S design. Psychonomic Science, 1968, 13., 215-216. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 255 Montagna, W. The structure and function of the skin. (2nd ed . ) . dev: York: Academic, 19 o2. 133- Montague, J. D. The psychogalvanic reflex: A com parison of a c skin resistance and skin potential changes. Journal of Neurology, Neurosurgery, and Psychiatry! 1953, 2l! 119-128. 134. Mowrer, 0. H. Preparatory set (expectancy) - a deter minant in motivation and learning. Psychological Review, 1938, 4_5, 62-91. 135. Mowrer, 0. H. On the dual nature of learning - A re interpretation of "conditioning" and "problem solving." Harvard Educational Review, 1947, 17., 102-148. 136. Murphree, 0. D., Dykman, R. A., & Peters, J. E. Objec tive measures of behaviour in two strains of the pointer dog. Paper to the Symposium on Higher Nervous Activity, IV, World Psychiatry Congress, Madrid, 19 66. 137. Neumann, E. Thermal Changes in palmar skin resistance patterns. Psychophysiology, 1968, _5, 103-111. 138. Nordquist, R. E., Olson, R. L., & Everett, M. A. The transport, uptake, and storage of ferretin in human eoidermis. Archives of Dermatology, 1966, 94., 482-490. 139- Page, H. A. The facilitation of experimental extinction by response prevention as a function of the acquisi tion of a new response. Journal of Comparative and Physiological Psychology, 1955, 48, 14-IF7 140. Paul, G. L. Outcome of systematic desensitization I: Background, procedures and uncontrolled reports of individual treatment. In C . M. Franks (Ed), Behavior therapy: Appraisal and status. New York: McGraw Hill, 19o9. Pp3 63-104. (IT) 141. Paul, G. L. Outcome of systematic desensitization II: Controlled investigation of individual treatment, technique variations and current status. In C. M. Francks (Ed.), Behavior therapy: Appraisal and status. New York: McGraw-Hill, 1969- Pp. 105-159- (b) Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 256 142. Paul, G. L., & Trimbel, R. W. Recorded vs. "live" relaxation training and hypnotic suggestion: Com parative effectiveness for reducing physiological arousal and inhibiting stress response. Behavior Therapy, 1970, 1, 285-302. 143- Peters, J. E., Murphree, 0. K., Dykman, R. A., & Reese, W. G., Genetically determined abnormal behavior in dogs. Paper to symposium on Higher Nervous Activity, IV, World Psychiatry Congress, Madrid, 1966. 144. Rachman, S. Phobias: Their nature and control. Springfield, 111.: Charles C. Thomas, 1968. 145. Rachman, S. Treatment by prolonged exposure to high intensity stimulation. Behaviour Research and Therapy, 1969, (7, 259-302. 146. Ramsay, R. ¥., Barends, J., Breuker, J., & Kruseman, A. Massed versus spaced desensitization of fear. Behavior Research and Therapy, 1966, 4_, 205-208. 147. Rappaport, H., 8: Katkin, E. S. Relationships among manifest anxiety, response to stress, and percep tion of autonomic activity. Journal of Consulting and Clinical Psychology, 1972, 39^ 404-414. 148. Rein, H. Die Elektrophysiologie der Haut. In J. Jasassohn (Ed.), Handbuck der Haut und Geschlechtskrankheiten, I_, 43-91. Berlin: J. Springer, 1929- Cited by S. Rothman, Physiology and biochemistry of the skin. Chicago: University of Chicago Press, 1954. 149- Rice, D. G. Operant conditioning and associated electromyogram responses. Journal of Experimental Psychology, 1966, 7JU 908-912. 150. Richter, C. P. A study of electric skin resistance and psycho-galvanic reflex in a case of unilateral sweating. Brain, 1927, 50_, 216-235- 151. Richter, C. P. Physiological factors involved in the electric resistance of the skin. American Journal of Physiology, 1929, 88., 596-615. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 257 152. Richter, C. P. Galvanic skin reflex from animals with P O hG "p, "1 . r. 7 ~ ^ p v~i "r Q Q P r ’o ih 'g r") ^ fh 1 ^ 0 ^ 0 • A. *’’’1 2 J C 2 . 7"l 153- Rickies, W. H., Jr., & Day, J. L. Electrodermal activity in non-palmar skin sites. Psychophysiology, 1968, 4, 421-435- 154. Rigal, J., Raymond, J., & Rournier, A. On agoraphobia appearing after intestinal amebiasis. Mechanism of conditioning. Annals of Medicops.ychology, 1962, 120, 262-267- 155- Rimm, D. C., & Bottrell, J. Four measures of visual imagination. Behaviour Research and Therapy, 1969, 7, 63-69. 156. Robinson, S., & Robinson, A. H. Chemical composition of sweat. Physiological Review, 1968, 4_, 421-435. 157. Robinson, C., & Suinn, R. M. Group desensitization of a phobia in massed sessions. Behaviour Research and Therapy, 1969, 7., 319-321. 158. Rothman, S. (Ed.) Physiology and biochemistry of the skin. Chicago: University of Chicago Press, w n 159- Rushmer, R. F., Buettner, K. J. K., Short, J. M., & Odland, G. F. The skin. Science, 1966, 154, 343-348. 160. Rutter, M., Tizard, J., & Whitmore, K. Education, health and behavior. London: Longman’s, 1968. 161. Schell, A. M., & Grings, W. W. Avoidance conditioning of the GSR: Nature of the response. Psychophysio logy, 1971, 7, 402-407. 162. Schlosberg, H. The relationship between success and the laws of conditioning. Psychological Review, 1937, 44, 379-394. 163. Schwartz, G. E., & Johnson, H. J. Affective visual stimuli as operant reinforcers of GSR. Journal of Experimental Psychology, 1969, 80., 28-32. 164. Schwartz, H. G. Reflex activity within the sympathetic nervous system. American Journal of Physiology, 1934, 109, 593-60T: Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 258 165. Schwartz, H. G. Effect of experimental lesions of the cortex on the "Psychogalvanic reflex" in the cat. Arc I lives cf Neurology and Psycrilatr.y, Chicago, 19 37, 38, 308-320. 166. Shapiro, D., & Crider, H. Operant electrodermal Con ditioning under multiple schedules of reinforcement. Psychophysiology, 1967, 4_, 168-175. 167- Shapiro, D., Crider, H. E., & Tursky, B. Differentiation of an autonomic response through operant reinforce ment. Psychonomic Science, 1964, 1, 147-148. 168. Shelley, W. B., & Hurley, H. J. The physiology of the human axillary apocrine sweat gland. Journal of Investigative Dermatology, 1953, 20_, 285-297- 169. Sherrington, C. S. The integrative action of the nervous system. New Haven, Connecticut: Yale University Press, 1906. 170. Shields, J. Monozygotic twins brought up apart and brought up together. Oxford University Press, 1962. 171. Shields, J., & Slater, E. Heredity and psychological abnormality. In H. J. Eysenck (Ed), Handbook of abnormal psychology. (1st ed.). London: Pitman Medical, i960. 172. Sidis, B., & Nelson, L. The nature of causation of galvanic phenomena. Psychological Review, 1910, 17, 98-146. 173- Silverman, A. J., Cohen, S. I., & Shmavonia, B. M. Investigation of psychophysiologic relationship with skin resistance measures. Journal of Psychosomatic Research, 1959, 4., 65-8 7 . 174. Skinner, B. F. The behavior of organisms. New York: Appleton, 193$"! 175- Sokolov, E. N. Perception and conditioned reflex. New York: Macmillan, 1963. 176. Soloman, R. L., & Wynne, L. C. Traumatic avoidance learning: The principles of anxiety conservation and partial irreversibility. Psychological Review, 1954, 61, 353-385. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 259 177- Sommer, R. Elektromotorische Wirkungen der Finger. Neurologlsches Zentralblath, ] 905, 2_4_, 290-295- Cited by R. Edelberg, Electrical activity of the skin. In E . S. Greenfield 1 E. A. Sternback (Eds.), Handbook of psychophysiology. New York: Holt, Rinehart & Wilson, 1972. 178. Stampfl, T. G., & Lewis, D. J., Essentials of implosive therapy: A learning theory based psychodynamic behavioral therapy. Journal of Abnormal Psychology, 1967, 72, 496-503- 179- Stengel, E., Classification of mental disorders. Bul letin of World Health Organization, 1959, 21, 601-663- 180. Stern, R. M. Operant conditioning of spontaneous GSRs: Negative results. Journal of Experimental Psychology, 1967, 15, 128-130. 181. Stern, R. M. , Boles, J., 8c Dionis, J. Operant condition ing of spontaneous GSRs: Two unsuccessful attempts (Technical Report No. 13)• Office of Naval Research, Indiana University, 1968. 182. Sternbach, R. A., & Tursky, B. Ethnic differences among housewives in psychological and skin potential responses to electric shock. Psychophysiology, 1965, 1, 241-246. 183- Suchi, T., 1950. Cited by Y. Kuno, Human prespiration. Springfield, 111.: Charles C. Thomas, 1956. 184. Suinn, R. M. Short term desensitization therapy. Behaviour Research and Therapy, 1970, 8_, 129-136. 185- Suinn, R. M., Edie, C., & Spinelli, R. R. Accelerated massed desensitization: Innovation in short-term treatment. Behavior Therapy, 1970, 1, 303-311- 186, Suinn, R. M. & Hall, R. Marathon desensitization groups: An innovative technique. Behaviour Research and Therapy, 1970, 8_, 97-98. 187- Sweeney, T. M., Downes, A. M. & Matoltsy, A. G. The effect of dimethylsufoxide on the epidermal water barrier. Journal of Investigative Dermatology, 1966, 46, 300-302. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 260 183. Szakall, A. Experimettelle Daten zur Klarung der Funk- tion der Vacserbarriere In der Epidermic dee leber/Jen :-:enoCnen . ^sciui o — o r ...• ^ ..c '/.*:vr; , 1 j ^ a, o , a ^ I . o^ oea by A. M. Klingman, The stratum corneum. In VJ. Mon tagna & VJ. C. Lobitz (Eds.), The epidermis, New York: Academic, 1964. 189 - Takahara, K. Variation of the insensible prespiration due to cooling and warming of the skin. Journal of Oriental Medicine, 1934. Cited by Y. Kuno, Human prespiration. Springfield, 111.: Charles C . Thomas, 1956. 190. Tarchanoff, J. Uber die galvanischen Erocheinienger an der Haut des Menschen bei Reizung der Sinnesorgane und bei verschiedenen Formen der psychisohen Tatigkeit. Pflugers Archiv fur die gesamte Physiologie, 1890, 46, 46-55. Cited by P. H. Venabels & M. J. Christie, Mechanisms, instrumentation, recording techniques, and quantification of responses. In W. F. Prokasy & D. C. Raskin (Eds.), Electrodermal activity in psychological research. New York: Academic, 1973. 191. Taylor, J. A. A personality scale of manifest anxiety. Journal of Abnormal and Social Psychology, 1953, 4, 285-290. 192. Van Egeren, L. F., Feather, B. W., & Hein, P. L. Desensitization of phobias: Some psychophysiological propositions. Psychophysiology, 1971, 8_, 213-228. 193. Van Twyver, H. B., 8c Kimmel, H. D. Operant conditioning of the GSR with concomitant measurement of two somatic variables. Journal of Exoerimental Psychology, 1966, 72, 481-486. 19^. Venables, P. H. The relationship between PGR scores and temperature and humidity. Quarterly Journal of Experimental Psychology, 1955, 12-l8. 195- Venables, P. H., & Christie, M. J. Mechanisms, instru mentation, recording techniques, and quantification of responses. In W. F. Prokasy and D. C. Raskin (Eds.), Electrodermal activity in psychological research. New York: Academic. 1973, Pp. 1-124. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 261 196. Venables, P. K., & Martin, I. Skin resistance and skin potential. In P. H. Venables u I. Martin (ids.), A Manual of Psychonbyslols~lcal Methods. Mcv: York: W i l e y , 1967. 197. Venables, P. H., & Sayer, E. On the measurement of the level of skin potential. British Journal of Psychology, 1963, 54, 251-260. 198. Veraguth, 0. Das psychogalvanische Reflex - phanomen. Barlin: S. Garger, 1909. Cited by R. Edelberg, Electrical activity of the skin. In N. S. Green field & R. A. Sternback (Eds.), Handbook of psycho- physiology. New York: Holt, Rinehart & Wilson, 1972. 199. Wall, P. & Davis, G. D. The cerebral cortical systems affecting autonomic function. Journal of Neurophy siology, 1951, ib, 507-517. 200. Wang, G. H. The galvanic skin reflex: A review of old and recent works from a physiologic point-of-view. American Journal of Physical Medicine, 19 57, 36, 295-320; 1958, 37, 35-57- 201. Wang, G. H. The neural control of sweating. Madison: University of Wisconsin Press, 1964. 202. Wang, G. H., & Lu, T. W. Galvanic skin reflex induced in the cat by stimulation of the motor area of the cerebral cortex. Chinese Journal of Physiology, 1930, 4_, 303-324. Cited by R. Edelberg, Electrical activity of the skin. In N. S. Greenfield & R. A. Sternback (Eds.), Handbook of psychophysiology. New York: Holt, Rinehart & Wilson, 1972. (a) 203. Wang, G. H., 8c Lu, T. W. On "inhibition" of the secre tion of sweat in the cat by stimulation of dorsal nerve-roots. Chinese Journal of Physiology, 1930, 4_, 175-182. Cited by R. Edelberg, Electrical activity of the skin. In N. S. Greenfield & R. A. Sternback (Eds.), Handbook of phychophysiology, New York: Holt, Rinehart & Wilson, 1972. ("b") 204. Wang, G. H., 8c Lu, T. V/. On the intensity of the GSR induced by stimulation of postgangiolonic sypathetic nerve fibers with single induction shocks. Chinese Journal of Physiology, 1930, 4_, 393-400. Cited by Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 262 R . Edelberg, Electrical activity of the skin. In M . S. Greenfield 1 R. A. Sternback (Eds.), Handbook of psychophysiology. Rev; York: Holt, Rinehart a Wilson, 1972. (c) 205- Wang, G. H., & Richter, C. P. Action currents from the pad of cat’s foot produced by stimulation of the tuber cinerium. Chinese Journal of Physiology, 1928, _2, 297-284. Cited by R. Edelberg, Electrical activity of the skin. In N. S. Greenfield & R. A. Sternback, (Eds.), Handbook of psychophysiology. New York: Holt, Rinehart & Wilson, 1972. 206. Waters, W. P., McDonald, D. G., & Koresko, R. L. Psychophysiological responses during analogue systematic desensitization and nonrelaxation control procedures. Behaviour Research and Therapy, 1972 10, 381-393- 207- Wenger, M. A., & Cullen, T. D. Some problems in psycho physiological research: III. The effects of uncon trolled variables. In R. Roessler & N. S. Greenfield (Eds.), Psychophysiological correlates of psychological disorder. Madison: University of Wisconsin Press, 1962. 208. Wenger, M. A., Engel, B. T., & Clemens, T. L. Studies of autonomic response patterns: Rationale and methods. Behavioral Science, 1957, 2_, 216-221. 209. Wickert, P. Psychological Research on Problems of Redistribution. Army Air Forces Aviation Psychology Program, Research Report No. 14, Washington D. C., 1947. 210. Wilcott, R. C. Palmar skin sweating vs. palmar skin resistance and skin potential. Journal of Compar ative and Physiological Psychology, 1962, 55s 327-332. 211. Wilcott, R. C. Effects of high environmental temperature on sweating and skin resistance. Journal of Compara tive and Physiological Psychology, 1963j 56, 778-782. 212. Wilcott, R. C. The partial independence of skin potential and skin resistance from sweating. Psychophysiology, 1964, 1, 55-66. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 263 213- Wilcott, R. C. A comparative study of skin potential, resistance, and sv'eatinu of cat's, food pad. Psycho— physloloyy, 1965, 2, 62-71- 214. Wilcott, R. C. Skin potential and skin resistence recording from the minimal restrained cat. Psychophysiology, 1969, 5, 727-729- 215- Wilson, G. D. An electrodermal technique for the study of phobias. New Zealand Medical Journal, 1966, 65, 696-698. 216. Wilson, G. D. GSR responses to fear-related stimuli, Perceptual and Motor Skills, 1967, 24_, 401-402. 217- Wing, L. Instructional Manual for Camberwell Register, M. R. C. Social Psychiatry Research Unit, Institute of Psychiatry, London, 1965• 218 . Wolpe, J. Psychotherapy by reciprocal inhibition. Stanford, California: Stanford University Press, 1958. 219- Wolpe, J. The systematic desensitization treatment of neurosis. Journal of Nervous and Mental Disease, 1961, 132, 182-203- 220. Wolpe, J. Isolation of a conditioning procedure as the crucial psychotherapeutic factor: A case study. Journal of Nervous and Mental Disease, 1962, 134, 316-329. 221. 'Wolpe, J. Quantitative relationships in systematic desensitization of phobias. American Journal of Psychiatry, 1963, 119, 1062-10684 222. Wolpe, J. The comparative clinical status of condition ing therapies and psychoanalysis. In J. Wolpe, A. Salter & L. J. Reyna (Eds.), The conditioning therapies: The challenge in psychotherapy. New York: Holt, 1964. Pp. 5-16'. 223- Wolpe, J. The behavioristic conception of neurosis: A reply to two critics. Psychological Review, 1971, 78, 341-343. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission. 264 224. Wolpe, J., & Flood, J. The effect of relaxation on the galvanic skin response to repeated phobic stimuli in ciic3no.11;”* cruer . i c u n n m o .■>’inc.v_i.cn v n c nc.c. and Experimental Psychiatry, 1970, 1, 195-200. 225- Wolpe, J., & Lang, P. J. A fear survey schedule for use in behaviour therapy. Behaviour Research and Therapy, 1964, 2 , 27-30- 226. Wolpe, J., & Rachman, S. Psychoanalytic "evidence". A critique based on Freud’s case of Little Hans. Journal of Nervous and Mental Disease, I960, 130> 135-148. 227. Yokota, T., Takahashi, T., Kondo, M ., & Fujimori, B. Studies on the diphasic wave form of the galvanic skin flex. Electroencephalograph and Clinical Neurophysiology, 1959a 11» 687-696. Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.