Clinical PsychologyReviau, Vol. 11, pp. 155-173, 1991 0272-7358/91 $3.00 + .

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Printed in the USA. All rights reserved. Copyright 0 1991 Pergamon Press plc

NEO-CONDITIONING AND THE

CLASSICAL THEORY OF FEAR
ACQUISITION

S. Rachman

University of British Columbia

ABSTRACT. The strengths and weaknesses of the classical theory of fear acquisition are set
out and then reconsidered in light of the radical revision of conditioning theory. It now
appears that conditioning can take place even when the CS and UCS are not contiguous.
Hence, most of the objections to the classical theory, based on the assumption that conditioning
requires contiguity of CS and UCS, can be removed.
The implications of the neo-conditioning perspective are considered, and it is argued that
the considerable advantages of the new view are however qualified because of an absence of
limits. Unqualified acceptance of a neo-conditioning explanation of fear acquisition would
lead us to expect far more fear than is observed. It is concluded that conditioning is best
construed as one of three pathways to fear.

The first modern theory of the causes of fear, based on the concept of
conditioning, had a central role in the development of behavior therapy. By 1978,
however, the conditioning theory appeared to be played out (Rachman, 1978). So
many weaknesses”had emerged that clinicians and researchers lost interest in the
theory, and turned instead to cognitive explanations. Important new ideas about
conditioning processes, described here as the neo-conditioning perspective, have
now renewed the subject and a radical revision of the concept of conditioning is
under way. “Conditioning theory has undergone a major revision,” (Dickinson,
1987, p. 57). It appears that “even the simplest forms of conditioning. . .involve
cognitive processes, that learning can occur without reinforcement. . .strict conti-
guity between the response or stimulus and the reinforcer is neither necessary nor
sufficient for conditioning” (p. 57-58). The purpose of this article is to explain the

The advice and suggestions of the Editor and an anonymous reviewer are gratefully
acknowledged.
Correspondence should be addressed to S. Rachman, Department of Psychology,
University of British Columbia, Vancouver, BC, Canada.

155
156 S. Kachman

classical theory and its flaws, and to consider the implications of the changing ideas
on conditioning for the classical theory. The new ideas may not presage the
emergence of a fully articulated revision of the theory, but will at very least add to
our knowledge and understanding of fear.

THE CLASSICAL THEORY

The conditioning theory of fear acquisition was influential and for many years
tacitly accepted, even though there was relatively little debate about its merits. The
theory constituted a welcome advance: it was useful in its own right, spawned
clinical applications, and incorporated other theories, especially those which
attempt to explain avoidance behavior. One version of the theory originated in the
important work of Mowrer. “The position here taken is that anxiety is a learned
response, occurring to signals (conditioned stimuli) that are premonitory of (i.e.,
have in the past been followed by) situations of injury or pain [unconditioned
stimuli]” (Mowrer, 1939, p. 565). He went on to argue that fear “may effectively
motivate human beings” and that the reduction of fear “may serve powerfully to
reinforce behavior that brings about such a state of relief or security.” Mowrer’s
thinking owed most to the writings of Pavlov, Freud, James, and Watson, and the
developments of Mowrer’s theory followed in the same tradition, amply encour-
aged by the results of research on the experimental induction of fears in animals.
As it illustrates the main features, and flaws, of conditioning theory, this discussion
will deal mainly with a version of the theory with which I have been associated
(Eysenck SC Rachman, 1965; Rachman 8c Costello, 1961; Wolpe & Rachman, 1960).
The major features of the theory are as follows. It is postulated that fears are
acquired, by a process of conditioning. “Neurotic reactions, like all others, are
learned reactions and must obey the laws of learning,” (original emphasis, Eysenck,
1960 p. 5). Neutral stimuli that are associated with a pain-producing or fear-
producing state of affairs, develop fearful qualities; they become conditioned fear
stimuli. The strength of the fear is determined by the number of repetitions of the
association between the pain/fear experienced and the stimuli, and by the intensity
of the fear or pain experienced in the presence of the stimuli. Stimuli resembling
the fear-evoking ones also acquire fearful properties, they become secondary
conditioned stimuli. The likelihood of fear developing is increased by confine-
ment, by exposure to high-intensity pain and/or fear situations, and by frequent
repetitions of the association between the new conditioned stimulus and the
pain/fear. It was proposed further that once objects or situations acquire fear-
provoking qualities, they develop motivating properties. A secondary fear-drive
emerges. Behavior which successfully reduces fear (e.g., avoidance) will increase in
strength.
Wolpe’s (1958) explanation of fear-conditioning did not include an account of
individual differences in vulnerability, but Eysenck attached considerable impor-
tance to such differences. It was postulated that (neurotic) introverts condition
easily and hence are more likely to develop excessive fears (Eysenck & Rach-
man, 1965).

THE EVIDENCE

Supporting evidence was drawn from six sources: research on the induction of
fear in animals, the development of anxiety states in combat soldiers, experiments
 Fear Acquisition 157

on the induction of fear in a small number of children, clinical observations,

incidental findings from the use of aversion therapy, and a few experiments on the
effects of traumatic stimulation. The role of individual vulnerability was supported
by evidence of ease of conditioning in introverts, and by psychometric analyses of
samples of neurotic patients. Reference will also be made to evidence that has
accumulated since the theory was formulated.
The strongest and most systematic evidence was drawn from a multitude of
experiments on laboratory animals. Evidently, it is easy to generate fear reactions
in animals by exposing them to a conjunction of neutral and aversive stimuli,
usually electric shock. The acquired fear reactions (usually inferred from the
emergence of avoidance behavior, physiological disturbances, and disruptive
behavior, or by some combination of these three indexes) can be produced readily
by employing conventional conditioning procedures. There is little doubt about
the facility with which fear reactions can be conditioned, at least in animals that are
tested under laboratory constraints.
Observations of people under combat conditions show that intense fear can
result from traumatic stimulation. Flanagan (1948) reported that the overwhelm-
ing majority of combat air crew experienced fear during their missions and
although these reactions were relatively transient, they sometimes presaged the
development of combat fatigue that included strong elements of fear. A minority
of air crew developed significant and lasting fears. The form and content of these
fears, their tendency to generalize, and the conditions under which they arose are
consistent with the conditioning theory.
The development of conditioned nausea reactions is commonly observed in
patients receiving chemotherapy (Burish & Carey, 1986; Cella, Pratt, & Holland,
1986). The factors that influence conditioning processes in other circumstances
(e.g., UCs strength in laboratory studies), are similarly influential in the emergence
of the persisting reactions of nausea. In their review of numerous reports,
covering roughly 1700 adult patients, Burish and Carey (1986) calculated that 32%
reported anticipatory nausea and/or vomiting. The figures for anticipatory anxiety
probably are even larger (e.g., 80% of 60 patients in the Cella et al. study). The
nausea/vomiting lasted for more than two years in most of their cases (Cella et al.,
1986). Bearing in mind the caution that conditioning of nausea or disgust does not
necessarily imply that fear responses are conditionable, we can turn to the clinical
accounts of fear acquisition.
In clinical practice, it is not uncommon for patients to give an account of the
development of their fears that can be construed in conditioning terms. Sometimes
they can date the onset of the fear to a specific conditioning experience. Every one
of 34 cases of dental phobia reported having had a traumatic dental experience,
such as fearing suffocation from an anaesthetic mask, on at least one occasion in
childhood (Lautch, 1971). However, these 34 people were found to be generally
neurotic and 10 comparison subjects who had experienced comparable traumatic
incidents with dentists during their childhood showed little sign of dental fear.
In a study of people who are frightened of dogs, Di Nardo et al. (1988) found
that nearly two-thirds had experienced a conditioning event in which a dog
featured, and in over half of these instances the animal had inflicted pain.
However, two-thirds of a comparable group of subjects who were not frightened
of dogs reported that they too had experienced a potentially conditioning event,
and that in half of the instances the animal had inflicted pain. These reports
provide some support for the theory, but also illustrate the fact that conditioning
158 S. Rachman

experiences, even those of a painful nature, do not necessarily give rise to fear.
Here, as in other instances, there was less fear than an unqualified conditioning
theory would lead us to predict. Presumably those people who experienced
conditioning events, even painful ones, but failed to acquire a fear, placed a
different interpretation on the event than did those who became frightened. Di
Nardo and his colleagues (1988) note that all of their fearful subjects “believed that
fear and physical harm were likely consequences of an encounter with a dog, while
very few non-fearful subjects had such expectations. . .an exaggerated expectation
of harm appears to be a factor in the maintenance of the fear.”
The role which subjects or phobic patients attribute to direct and indirect
experiences in generating their fears, differs with the content of the fear. In their
analysis of 183 patients with clinically significant phobias, classified into six
different groups of fear, Ost and Hugdahl (1981) found a range of attributions.
For example, 88% of the agoraphobic patients attributed the onset of their phobia
to a conditioning experience, but only 50% of the patients who were frightened of
animals attributed the onset of their fear to such an experience. Among those who
feared animals, 40% traced the origin to indirect experiences, but this was
uncommon among the agoraphobics. The percentages of patients who attributed
greatest importance to direct experiences, which in this analysis coincides with
conditioning onset, were as follows, in ascending order: blood phobics, animal
phobics, social phobics, dental phobics, claustrophobics, and agoraphobics.
Across all groups, there was a strong tendency to attribute the onset of the
phobia to direct conditioning experiences and three times as many patients made
this attribution rather than one involving indirect acquisition. Interesting as they
are, these figures cannot be taken at face value because they are compiled from the
patients’ recollection of the onset of their phobia, and their interpretation of those
events. Information of this kind is open to some distortion as the result of
forgetting and the operation of biases in interpreting past events. Ost and
Hugdahl’s (1985) finding that the overwhelming majority of agoraphobic patients
ascribe the onset of their fears to conditioning experiences has to be reconciled
with contrary evidence reported by Mathews, Gelder, and Johnston (198 1) who
found little evidence of conditioning onsets in their patients. They criticized the
conditioning theory and pointed out that the agoraphobics whom they studied
“cannot as a rule recall either any event that provoked intense fear or any repeated
fearful event that occurred in the circumstances they subsequently came to avoid”
(p. 43). Ost and Hugdahl argue that thefirst (original emphasis) episode of anxiety
can be identified in only a minority of cases, but go on to point out that “after the
first occurrence the anxiety attack reappears in the situations that are avoided, and
this certainly serves as a repeated fearful event. .nearly half (46%) of the patients
described a rapid onset” and early development of the phobia so that, “within two
weeks from the first anxiety attack, they had a fully developed agoraphobia” (Ost
& Hugdahl, 1985, p. 629). It emerges from this apparent conflict of evidence that
a good deal depends on the definition of the conditioning event, and these
discrepancies are unlikely to be resolved until a standard criterion is applied in
deciding whether or not an event is regarded as a conditioning experience
(Rachman, 1989).
The classical demonstration by Watson and Rayner (1920) of the deliberate
genesis of fear in a young child had a considerable influence on early theorists, but
attempts to reproduce these findings had little success (e.g., Bregman, 1934;
Valentine, 1946). The most systematic collection of information on the induction
 Fear Acquisition 159

of conditioned fear in humans was carried out by Ohman and his colleagues in
Sweden (Ohman, 1987). Stimulated by Seligman’s (1971) concept of prepared
fears, Ohman and his colleagues undertook a lengthy program of research to
discover whether people are “prepared” to acquire fears to particular stimuli.
They found that it is possible to produce conditioned fear responses in humans
under laboratory conditions, but the responses tend to be weak, transient, and
incomplete. They are incomplete in the sense that the evidence for conditioning is
confined largely to changes in electrodermal activity, and it has not been possible
to obtain dependable consistent evidence of conditioned heartrate responses.
(Electrodermal activity can be used to index fear, but heartrate is a preferable
measure [Cook, Melamed, Cuthbert, McNeil, & Lang, 1988; Cuthbert & Lang,
1989; Marks & Huson, 1973; Lang, Melamed, 8c Hart, 1970; Mathews, 1971;
Hugdahl, 1989; Ost, 1989; Prigatano & Johnson, 1974; Sartory, Rachman, &
Grey, 1977; Sartory, 19891). The conditioned responses were of small magnitude
and not readily evoked, and with few exceptions, the electrodermal responses were
extinguished within a few trials. Also, the conditioned responses were easily
altered or abolished by instructions (see the review by McNally, 1987).
Incidental observations arising out of the use of aversion therapy, a technique
explicitly based on the classical conditioning theory, provided some early support
for the theory (Rachman & Teasdale, 1969) and in recent years has been
supplemented by work carried out by Baker and others (1984). After undergoing
repeated associations between alcohol and chemically induced nausea, many
patients experience nausea when they taste or even smell alcohol. In a famous case
reported by Hammersley (1957), a successfully treated patient subsequently
changed his mind and decided that abstinence was not the lesser of two evils. He
embarked on a “de-conditioning” program and repeatedly drank himself through
many episodes of intense nausea until his conditioned reaction to alcohol subsided
and finally disappeared.
Hallam and Rachman (1976) described yet another reaction. An alcoholic
patient who had been given whisky to drink during (electrical) aversion therapy
accused the therapist of adding a chemical to the whisky to give it a bad taste. (This
is not an uncommon report even when no chemicals are used.) The same patient
went into a bar against advice during treatment, but on trying to raise a glass
of whisky to his mouth had a panic attack and returned to hospital in an an-
xious state.
Bancroft (1969) observed the development of intense anxiety reactions among
some of his patients, but was careful to point out that the large majority showed no
signs of conditioned fear reactions, regardless of the success or failure of the
treatment program. These incidental findings indicate that what appear to be
conditioned fear responses can develop during aversion therapy, but it does not
necessarily follow that they are causally relevant to the outcome of therapy.
Recent evidence on the effects of aversion therapy convincingly demonstrates
that “aversion therapy does indeed result in a conditioned response to the target
stimulus” (Baker et al. 1984, p. 405). This conclusion is drawn from investigations
in which varying types of aversive stimulus, chemical or electrical, were used. After
therapy, the subjects responded differently to the conditioned stimulus than they
did to the neutral stimulus, supporting the view that there is an “associative
process in aversion therapy” (p. 406). Evidence of conditioning was provided by
the psychophysiological responses to the target stimulus, negative evaluations of
the stimulus, sometimes plain dislike for the stimulus, and indirectly by the
160 S. Rachman

decreased use of the addictive substance. It is of particular interest that the

heartrate responses emerged as an “especially sensitive index of aversive condi-
tioning effects” (p. 408), and that no other variable predicted the outcome of
therapy.
The research by Baker and his colleagues demonstrates that it is possible to
develop methods for conditioning psychophysiological, cognitive, and behavioral
reactions to aversive stimuli, but as they point out, the results defy a “simple
conditioning hypothesis.” In any event, the question which is presently at issue
centers on the feasibility of conditioningfrar reactions. Here it should be remem-
bered that Hallam and others (1972) found comparable psychophysiological,
cognitive and behavioral changes in patients who had been treated by noncondition-
ing methods. It is necessary to bear in mind that even if successful, demonstrations
that aversive procedures can be followed by conditioned fear need not imply that
naturally acquired fears necessarily follow the same, conditioning path.
Another source of support for a conditioning theory of fear acquisition comes
from experiments in which subjects were given injections of scoline, which
produces a temporary suspension of breathing (Sanderson et al., 1963). Not
surprisingly, most of the subjects who underwent this harrowing experience
developed intense fears of the stimulus encountered in or connected with the
experimental setting. The intensity of their fears tended to increase even in the
absence of further unpleasant experiences (providing one of the few examples of
fear incubation).
The conditioning theory of fear acquisition does not require single trial or
traumatic onsets, but fears that arise in an acute manner are more readily
accommodated than those of uncertain onset. Even though acute onset fears are
more easily accommodated, partly I suspect because our conception of condi-
tioned fear is based largely on laboratory experiments in which the aversive
stimulus is often traumatic, we also have to account for fears that are produced by
experiences of a subtraumatic or even of a nontraumatic nature.
Fears that emerge in the absence of any identifiable learning experience present
difficulties for the theory. Hence, fears that develop gradually (e.g., social fears)
and cannot be traced to specific occurrences are a potential embarrassment. Even
more troublesome are those fears that arise even in the absence of any direct
contact with the fear stimulus.
Although the importance of the phenomenon of acquired food aversions was
not made evident until 1966, it sometimes is used to buttress the traditional
conditioning theory. More fittingly, the findings on food aversions served as a
prompt for critical thinking that led to a radical revision of the concept of
conditioning. Garcia and his colleagues (Garcia & Koelling, 1966; Garcia, Ervin, &
Koelling, 1966) were the first to demonstrate that strong and lasting aversive
reactions can be acquired with ease when the appropriate food stimulus is
associated with illness, even if the illness occurs many hours after eating. The
phenomenon was given the catch-name of “the sauce Bearnaise” effect by Selig-
man and Hager (1972), who elucidated the theoretical significance of the research.
Given that the genesis of food aversions is a form of conditioning, and if we also
agree to an equation between the acquisition of a taste aversion and the acquisition
of a fear, this phenomenon may provide a valuable means of collecting informa-
tion about the conditioning theory of fear acquisition. In Seligman’s use of these
findings, phobias are seen as instances of highly prepared learning, and as such
 Fear Acquisition 161

are “selective, highly resistant to extinction, probably non-cognitive, and can be

acquired in one trial” (Seligman & Hager, 1972, p. 452).
The idea that food aversions and fear might be related receives some indirect
support from the elevated incidence of food aversions in neurotic subjects. Wallen
(1945) compared 240 normal adults with 95 people of comparable age who had
been rejected from the U.S. Navy on the grounds of neurotic disturbance. The
neurotic men reported four times as many food aversions as did other subjects. As
neurotics have more fears than non-neurotic people, it seems possible that they
have a sensitivity of some type that predisposes them to acquire fears and aversions
more easily than do other people. If the acquisition of food aversion is used to
support the conditioning theory of fear on the assumption that the underlying
process of conditioning is common to both, it will have to take into account the
unexpected temporal stretch of the taste aversion phenomenon, that is, the delay
that supervenes between tasting the food and the onset of nausea. Classical
conditioning is expedited by temporal proximity between stimuli; although there
are convincing examples of conditioned responses being established even when
there are prolonged delays, these tend to be exceptional. Experimentally induced
food aversions are easily, powerfully and rapidly established, even when there are
delays between the events. Therefore, if the food aversion phenomenon helps to
provide support for a new or revised conditioning theory of fear, the temporal
qualities of classical conditioning processes will have to be de-emphasized.
The evidence on individual vulnerability is documented by Eysenck (1967).
There is little doubt about the correlation between introversion and anxiety
disorders, but the putative causal connection was not resolved, especially as it
proved difficult to confirm that introverts always are more “conditionable” than
extroverts. The existence of individual differences in vulnerability to fear-acquisi-
tion is evident, and a fresh attack on the problem emphasizes differences in
sensitivity. Certainly there are high correlations between anxiety/injury sensitivity
and total scores on fear questionnaires (Reiss, Peterson, & Gursky, 1988). The
overlap between such sensitivity and Eysenck’s (1967) concept of “dysthymia”
(high introversion and high neuroticism) is likely to be significant.
According to Reiss and his colleagues (Reiss, Peterson, Gursky, 8c McNally,
1986; Reiss et al., 1988), individual differences in fearfulness are largely the
results of differences in anxiety and injury sensitivity. “It is more important to
know what a person thinks will happen as a consequence of experiencing anxiety
than it is to know how much anxiety a person is experiencing” (Reiss et al., 1988,
p. 341). Usefully, their approach offers a way of explaining individual differences
in fearfulness, and why many people tend to have collections of fears.

WEIGHING THE EVIDENCE

There appears to be strong evidence to support the idea that fears can be acquired
by a conditioning process. This conclusion is justified even though some of the
evidence is subject to contrary interpretations, or is inherently weak. The strongest
evidence, both in the sense of its replicability and completeness, comes from the
genesis of fear in laboratory animals. This voluminous and convincing evidence is
supported by some limited findings on the induction of fear reactions in adults,
but the stimuli were traumatic. The work on the induction of fear in children is
inconsistent, based on very small numbers, and all of the experiments have been
I62 S. Rachman

criticized for errors of contamination and confounding. Clinical observations

provide interesting supporting evidence, but unfortunately the quality of the
information is unsatisfactory, comprising as it almost always does a selected set of
observations rarely supported by external confirmatory evidence. It also suffers
from the fact that the subject or patient’s account of the genesis of the fear rests on
the assumption of an accurate memory and powers of recall. This is an unsatisfac-
tory basis for building a theory. Because it has greater immediacy and the
possibility of at least some external confirmation, the evidence on combat fears
and combat neuroses has something to recommend it. Very little of this informa-
tion was collected in a systematic manner, and it too suffers from selection bias,
incompleteness, and the interpretive gloss placed on the accounts by the reporting
psychologist or psychiatrist. Nevertheless, it is rich in interest and authentic in
quality (Rachman, 1990). Fortunately, military combat is an exceptional experi-
ence and for purposes of psychological theorizing, it is unwise to overemphasize
the significance of fears which are acquired in these unnatural circumstances. The
intriguing findings on the speedy development of food aversions may have
opened a door for the establishment of a more satisfactory theory of nonrational
fears. Given that fears can be produced by conditioning events, these events may
be implicated to a greater or lesser extent in different types of phobias.
Whatever its value, the theory is not a satisfactorily comprehensive account of
the genesis, or maintenance, of human fears. Even in its strongest form, the
conditioning theory of fear acquisition cannot encompass all of the observed fears.
There is more than one pathway to fear.

ARGUMENTS AGAINST ACCEPTANCE

There are eight arguments against acceptance of the conditioning theory of fear
acquisition as a comprehensive explanation (Rachman, 1978; 1990). People fail to
acquire fears in what should be fear-conditioning situations, such as air raids. It is
difficult to -produce stable conditioned fear reactions in human subjects, even
under controlled laboratory conditions. The conditioning theory rests on the
untenable equipotentiality premise. The distribution of fears in normal and
neurotic populations is difficult to reconcile with the conditioning theory. A
significant number of people with phobias recount histories that cannot be
accommodated by the theory. Fears can be acquired indirectly or vicariously. Fears
can be acquired even when the causal events are temporally separated.

1. Failures to Acquire Fear. It would seem that few experiences could be more
frightening than undergoing an air raid, but the great majority of people
endured air raids extraordinarily well during the second World War, con-
trary to the universal expectation of mass panic (Janis, 1951). Exposure to
repeated bombing did not produce significant increases in psychiatric disor-
ders. Short-lived fear reactions were common, but surprisingly few persistent
phobic reactions developed. Few of the civilians who were injured or
wounded developed a fear of the situation in which they received the injury
(Rachman, 1990).
The observations of comparative fearlessness despite repeated exposures
to intense trauma, uncontrollability, uncertainty, and even injury, are con-
trary to the conditioning theory of fear acquisition. People subjected to
repeated air raids should acquire multiple intense conditioned fear reactions
and these should be strengthened by repeated exposures. Recent evidence of
 Fear Acquisition 163

civilian reactions to the warlike conditions of the Middle East (Saigh, 1984;
1988) and Northern Ireland (Cairns & Wilson, 1984) are consistent with the
findings from World War II. These findings run contrary to prediction.
Lesser examples of the failure to acquire fear include people who fail to
develop a fear of dogs despite having unpleasant experiences with them, and
even having been bitten (di Nardo et al., 1988). Dental fears are fairly
common, but large numbers of people fail to develop a fear of dental
treatment even though they have undergone uncomfortable and even pain-
ful experiences while confined in the dentist’s chair (e.g., Lautch, 1971;
Davey, 1988).
The apparent absence of a direct relationship between injury and subse-
quent fear runs contrary to conditioning theory. There should be a direct
connection between injury and fear, but there is not (Rachman, 1990).
2. The Conditioning of Human Fears. Many writers on the subject of electrical
aversion therapy appeared to assume that the successful administration of
treatment would result in the development of a mini-phobia - repeated
associations of the conditioned stimulus with an unpleasant electrical shock
would result in a conditioned fear response to the presentation of the
stimulus (Hallam & Rachman, 1976). To the contrary, Marks and Gelder
(1967) found that most of their patients reported indifference to the condi-
tioned stimuli employed in electrical aversion therapy, and it was rare to find
anyone who complained of fear after undergoing the course of treatment.
The same observation was described by Bancroft (1969), and by Hallam,
Rachman, and Falkowski (1972).
Hallam and Rachman failed to confirm the prediction that conditioned
fear reactions would develop as a result of aversion therapy and instead, “the
‘conditioned response’ did not resemble either in magnitude or direction the
cardiac responses of phobic patients who are presented with their phobic
stimulus, and nor did the subjects report anxiety or discomfort in the presence
of the conditioned stimulus” (1976, p. 194). We were equally unsuccessful in
our search for evidence of conditioned fear reactions developing in alcoholic
patients who undertook aversion therapy: “. . .when alcoholics who have
undergone aversion therapy are compared with alcoholics who have been
treated in other ways, there is no difference in their subjective anxiety
responses to alcoholic stimuli or in the peripheral autonomic responses that
usually accompany states of fear or anxiety. Subjective distaste for alcohol
seems to be the only specific consequence of aversion therapy” (p. 195).
Ohman (1987) and his colleagues had only limited success in generating
conditioned fear reactions in the laboratory; the absence of expected condi-
tioned responses, and the instability, incompleteness and weakness of those
that were produced do not provide significant support for the conditioning
theory (McNally, 1987).
3. The Equipotentiality Premise. The theory assumes that any stimulus can be
transformed into a fear signal; the choice of stimulus is a matter of indiffer-
ence. Seligman (1970, 1971) h as argued convincingly that this premise is
untenable, and hence its incorporation in the theory is a weakness.
4. The Distribution of Fears. The corollary of the equipotentiality premise is that
all stimuli have an equal chance of being transformed into fear signals.
However, this is not borne out by surveys of the distribution of fears, either
in a general population or in psychiatric samples (Rachman, 1990).
164 S. Rachman

Subject only to their prominence in the environment, many objects and

situations should have an equal probability of provoking fear. What we find
instead is that some fears are exceedingly common, and certainly much too
common for the theory. Other fears are far too rare. The fear of snakes is
common and the fear of lambs is rare; moreover a genuine fear of snakes is
often reported by people who have not had contact with the reptiles. (Even
more surprising is the absence of fears of motor cars, and the very small
incidence of fears of motor travel.) Consequently, one is forced to conclude
that the fear of snakes can be acquired even in the absence of direct contact
- and this significant concession opens three possibities. The fear of snakes
is innate, or it can be transmitted indirectly, or the fear of snakes is “lurking”
and will appear with only slight provocation. The last two of these three
possibilities are compatible.
5. Patient’s Reports of Fear Onset. It can be difficult to determine the origin of a
patient’s phobia, and there are phobias in which there was “no apparent
trauma to initiate the phobia” (Marks, 1969, p. 42). Goorney and O’Connor
(1971) encountered this problem of identifying a plausible precipitant in
their analysis of the excessive fears of RAF crews during peacetime. In a
study of 97 cases, they were able to attribute the fear to specific precipitants
such as accidents or frightening incidents in a quarter of the cases. In
one-third there was no discernible cause, and in the remainder, the precipi-
tants, such as a return to flying after a long abstention, were not of a
traumatic or conditioning type.
The absence of a plausible conditioning precipitant in a significant number
of phobic patients was demonstrated in the analysis by Ost (1985), referred to
earlier. Twenty-one percent of 183 phobic patients reportedly acquired their
phobia indirectly, and the remaining 14% were unable to recall the onset. In
an expansion of this study Ost (1987) found an association between the
manner in which the phobia was acquired and the age of onset. The
indirectly acquired phobias developed at an earlier age than the phobias with
a conditioning origin.
6. The Vicarious Acquisition of Fear. The significant advances made in our
understanding of the processes of observational learning and modelling
made it plain that we acquire much of our behavior, including emotional
responses, by vicarious experiences (Bandura, 1969, 1977). It began to seem
probable that “fears can be acquired either directly or vicariously, and that
stimuli are likely to develop fearful qualities if they are associated, directly or
vicariously, with painful or frightening experiences” (Rachman, 1978, pp.
189-190). It was conceded at the time that the evidence in support of
vicarious acquisition of fear in humans was indirect and largely anecdotal, but
progress has been made and the case for accepting that fears can be acquired
vicariously is now strong (Rachman, 1990).
7. Acquisition 61; Transmission of Verbal Information. It was also suggested in 1978
that fears might be acquired by the absorption of verbal information,
especially information that conveys a threat (Rachman, 1978, pp. 193-194).
(In order to avoid confusion with the growing tendency to describe condi-
tioning in terms of information processing, the third pathway has been
re-named - transmission of zlerbal information.) The social transmission of
intense fear, even panic, is well illustrated by recurrent epidemics of Koro in
 Fear Acquidion I65

Southeast Asia. Koro, derived from the Malay word for “head of a turtle”, is a
“condition of psychiatric panic characterized by complaints of genital shrink-
age coupled with fear of impending death” (Tseng, Kan-Ming, Hsu, Li-
Shuen, Li-Wah, Gui-Qian, & Da-Wei, 1988, p. 1538). Recent episodes of this
intense fear, involving hundreds or thousands of people, occurred in Singa-
pore (1967), Thailand (1976), Assam (1982), and China (1984/1985 and
1987), and mainly affected isolated, poorly educated people who are strongly
influenced by folk beliefs. In a survey of 232 victims of the 1984/1985
epidemic in China, Tseng et al. (1988) found evidence that at their height,
the episodes of Koro were characterized by panic (intense fear, palpitations,
tremor, perspiration, fear of impending death or other catastrophe). The
Singapore epidemic appears to have been set off by a verbal report that
eating vaccinated pigs can produce Koro, and the Thai epidemic by a report
that the Viet Cong had poisoned Thai food to produce impotence.
The accumulation of evidence on this proposition, that fears can be
acquired by verbal information, has been slower but no less plausible.
8. Acquisition by Remote Events. At present there is not sufficient information to
include the acquisition of fear by a temporally remote event as an additional
argument against acceptance of the theory, but convincing proof that fears
can be acquired even when the stimulus and response events are separated in
time, would oppose the original conditioning theory.

In conclusion, the weaknesses of the classical theory are serious but not
necessarily fatal. One can either search for an entirely new theory to replace it, or
adopt a reformist view and formulate modifications and extensions of the theory.
At its best the theory can provide a partial explanation for the genesis of some
fears. However, it cannot explain how the common fears are acquired, nor can it
explain the observed distribution of fears, the uncertain point of onset of many
phobias, the indirect transmission of fears, the ready acquisition of prepared
phobias, and tha failure of fears to arise in circumstances predicted by the theory.
Fears acquired without direct contact with a fearful stimulus are an added
problem for the theory, and the acquisition of fears when the causal events are
temporally separated, is yet one more burden.
A satisfactorily comprehensive theory of fear acquisition must accommodate all
of that information plus the facts that fears can emerge gradually as well as
suddenly, that there are individual differences in susceptibility, and the probable
acquisition of fears of objects/situations which the person has never encountered.
It is also necessary to account for the acquisition of fears by events that are
temporally separated.

NEO-CONDITIONING

The traditional belief that contiguity of the conditioned stimulus (CS) and the
unconditioned stimulus (US) is necessary for the establishment of a conditioned
response, is mistaken. Recognition of the occurrence of noncontiguous condition-
ing removes, in one sweep, most of the objections to the conditioning theory of
fear acquisition. Conditioned responses can develop even when the conditioned
stimulus and the unconditioned event are separated in time. The most convincing
166 S. Rachman

examples of noncontiguous conditioning come from the literature on food

aversions. If animals eat a novel food and are made ill minutes or even hours later,
they form a strong aversion to the food. A single experience is sufficient to
establish a lasting conditioned aversion.
The troublesome fact that many people cannot trace the onset of their fears to
particular conditioning episodes can be absorbed by assuming that noncontiguous
conditioning may have taken place. The many failures to acquire fear despite
contiguous associations (e.g., dog bites not followed by fear) can be accounted for
by blocking, and other failures accounted for by the fact that the stimulus (e.g.,
dog collar) is not the cause of the significant event. Animals, and people, can learn
that a stimulus is irrelevant “as a predictor of anything of significance”, (Dickinson,
1987, p. 66). These objections to conditioning theory no longer seem fatal.
Rescorla (1988) observes that, “although conditioning can sometimes be slow, in
fact most modern conditioning preparations routinely show rapid learning. One
trial learning is not confined to flavor-aversion” (p. 154). Moreover, the associative
span of animals “is capable of bridging long temporal intervals” (Mackintosh,
1983, p. 172). However, the learning must be selective, otherwise the animals
would collect a “useless clutter of irrelevant associations” (p. 172). According to
Mackintosh, the “function of conditioning is to enable organisms to discover
probable causes of events of significance” (p. 172).
Additional evidence that conditioning processes are not bound by contiguity
comes from research on the blocking effect and on the consequences of random
control. A stimulus will not become a conditioned signal (CS) even if it is repeatedly
presented immediately before a US event, unless it is of some value. If the US
event is already well predicted by another stimulus, the addition of a second
stimulus is of no value and hence no conditioning occurs. The established CS
prevents (blocks) the development of a second CS. If the delivery of the electric
shock is already well predicted by a tone (CS), then introducing a visual stimulus
(CS?) in addition to the tone will be of no predictive value and will not develop into
a conditioned signal. The second stimulus is redundant and conditioning will not
develop even if the conditioned stimulus is repeatedly presented in contiguity with
the electric shock (US). The existing conditioned response is sufficient and blocks
the development of the redundant new signal.
The random control effect also demonstrates that mere contiguity is not
sufficient to produce conditioning. If a stimulus, say a bell, regularly precedes an
electric shock, then conditioning will occur; however, if the electric shock also is
delivered repeatedly in the absence of the bell stimulus, little conditioning will
develop. “Temporal contiguity, then, between a CS (or response) and a reinforcer
is neither necessary nor sufficient to ensure conditioning” (Mackintosh, 1983, p.
173). The stimulus will not turn into a conditioned stimulus unless it predicts the
reinforcer better than other stimuli. The new stimulus is uninformative, and
“conditioning occurs selectively to good predictors of reinforcement at the ex-
pense of worse predictors” (p. 173).
The new view of conditioning is not merely an exercise in discrediting the
classical explanation. Interesting new phenomena have been discovered, fresh
predictions are now possible, and new explanations of associative learning have
been but forward. Simple contiguity is insufficient; information is the key, and the
prevalent view is that conditioning involves learning about the relations between
events. Rescorla (1988, p. 153) argues that “Pavlovian conditioning is not a stupid
 Fear Acquisition 167

process by which the organism willy-nilly forms associations between any two
stimuli that happen to co-occur.” Rather, the organism is better seen as “an
information seeker, using logical and perceptual relations among events. . .to form
a sophistocated representation of its world” (p. 154). Conditioning is not merely a
transfer of power from one stimulus to another.
Contrary to an assumption of the classical theory, stimuli are not equally likely to
develop conditioning properties; some are more easily turned into conditioned
signals than others. Pain is more readily associated with auditory and visual stimuli
than with gustatory stimuli, and gastric distress is more easily associated with taste
than with vision. People, certainly adults, do not come fresh to new stimuli; they
already have a history of associations with the available stimuli. These previous
associations influence the occurrence or nonoccurrence of conditioning. So for
example, we all have a history of (benign) associations with dog collars. No one,
not even people who have distressing experiences with dogs, evers learns to fear
collars, despite the contiguous presence of the dog collar during the unpleasant
events. Dog collars do not predict distress, and they do not become conditioned
elicitors of fear. Although many people who have distressing experiences with
dogs learn to fear them, comparable numbers of people who have had such
experiences fail to acquire the fear (di Nardo et al., 1987). Presumably, a previous
history of pleasant and friendly experiences with dogs produces conditioned
predictions of harmless exchanges, and these predictions are not overturned by
one or several unpleasant events. The history of the stimulus influences the
conditioning process. Food aversions develop most readily to novel foods (Re-
vusky, 1977). Familiar and especially well-liked familiar foods are relatively
immune to conditioned food aversions. Presumably, familiar and well-liked peo-
ple, places, and animals are also relatively immune to conditioned fears. A relative
fear-immunity to familiar stimuli and situations may underlie the success of Neal
Miller’s (1960) “toughening up” exercises as a way of preventing the development
of fear.
The new research proves that animals can be conditioned not only to discrete
stimuli but also to the relationships between stimuli, and supports Rescorla’s (1988)
claim that “conditioning involves the learning of relations among events that are
complexly represented” (p. 158).
We have come a long way from classical Pavlovian conditioning, and the
flexibility and range of conditioning is far greater than was previously supposed
(Davey, 1988; Mackintosh, 1983; Rescorla, 1980, 1988). Conditioning can occur
even when the stimuli are separated in time, and in space, and it can occur not
only to discrete stimuli but also to abstract relationships between two or more
stimuli. Conditioning is a highly flexible and functional process.

Fear Matching

The introduction of a matching procedure (Rachman 8c Levitt, 1985; Rachman 8~

Lopatka, 1986) into the study of the prediction and overprediction of fear arose
independently of the neo-conditioning research, but is easy to integrate into
neo-conditioning ideas (Rachman, 1990; Rachman & Bichard, 1988). Fearful
people tend to start out by overpredicting how much fear they will experience in
specified circumstances, and then learn to predict with increasing accuracy.
Rachman and Bichard (1988) were driven to speculate that “the tendency to
165 S. Rachman

become increasingly accurate with practice suggests to us that people may have a
preference for accurate prediction, and that there might even be a ‘drive’ towards
accurate prediction” (p. 310). This recalls Mackintosh’s (1983, p. 173) view that
conditioning occurs “selectively to good predictors of reinforcement”.
If the humble rat/pigeon of Rescorla’s (1988) research is to be regarded as an
“information seeker, using logical and perceptual relations among events. . .to
form a sophisticated representation of its world” (p. 184), and if these seekers after
information learn to predict with increasing accuracy, then they share a common
propensity with our fearful subjects (Rachman, 1990; Rachman & Bichard, 1988)
even including our necessarily short claustrophobic volunteers (the test closet was
very small).

Fear Summation

Recent research on the summation of fear, the increase in fear that occurs when a
person is presented simultaneously with two or more objects of fear, is also easy to
integrate into neo-conditioning concepts. It turns out that a summation of fear will
occur if the reaction to fear Stimulus A presented alone is then followed by the
single presentation of a stronger fear stimulus, B. If Stimulus A produces x fear,
and then B produces x+ fear, the simultaneous presentation of A + B will
produce a fear response greater than x (summation). However if the second fear
stimulus (B) is fully predicted by the first fear (A), then no summation will occur.
If A = fear x
and B = fear x-
then A + B will = fear x or even x-
If a fear is already well predicted by a particular stimulus or object, the addition
of other fearful stimuli is unlikely to lead to an increment in fear. These and other
examples of the relation between recent research on human fear and the
neo-conditioning concepts are elaborated in Rachman (1990).
Davey (1987) has made stimulating attempts to incorporate the ideas of neo-
conditioning into the theory of classical conditioning, and provided experimental
demonstrations of the revaluation effect. The strength of a conditioned response
can be altered by “post-conditioning UCS revaluations” (p. 107), and it is possible
that a revaluation of the CS can also modify the conditioned response. Alterations
in the UCS or the CS, even when they occur in isolation, can have an effect on an
existing conditioned response. (Note that “the organism does retain information
about the US independently of its association with the CS” (Rescorla, 1974, p. 105.))
The implications for conditioned fear responses are considerable. A revaluation of
the UCS (say the danger presented by dogs) could diminish/eliminate (or increase)
the existing conditioned fear of dogs. A revaluation of the significance of rapid
canine movement (say, frisky and friendly rather than hostile and aggressive) can
alter the conditioned fear of dogs. In Clark’s (1988) theory of panic, a revaluation
of the CS (a change in bodily sensations) can reduce panic frequency/intensity. A
revaluation of the significance of hyperventilation can reduce panic intensity.
Presumably, a revaluation of a previously benign object/person/situation as being
dangerous can promote a new fear. This brings us close to the third pathway to
fear, the verbal informational acquisition of fear.
Siddle and Remington (1987) have analysed the clinical relevance of latent
inhibition in the light of neo-conditioning. Pre-exposure to a potentially threaten-
 Fear Acqukition 169

ing stimulus, carried out in neutral or calm conditions, can inhibit the develop-
ment of a conditioned fear response. They quote the example of pre-exposure to
novel flavors (e.g., cranberry juice) as a means of inhibiting the development of a
flavor aversion. The success of modelling experiences as a method for inhibiting
the occurrence of fear during hospital treatment (e.g., Melamed, 1977) can be
reinterpreted as a form of latent inhibition. However, if the modelling preparation
for hospital treatment is a form of latent inhibition, it is curiously limited in its
effects; the modelling preparation works less well or not at all on second or
subsequent applications (Melamed and Siegel, 1980, p. 330), and has a limited
time span in younger children (Melamed, 1977, p. 53). Neal Miller’s (1960)
observations on the value of toughening-up exercises also can be interpreted as
operating through latent inhibition.
The work of Davey and Siddle, the prescient review by Reiss (1980), and the
research on evaluative conditioning (Levey & Martin, 1987) are all promising
developments.

The refreshing revival of interest in conditioning had widened our knowledge and
clarified some puzzles, but it is not free of problems. Phenomena that were
disallowed by the classical theory, such as the emergence of learned associations
between noncontiguous events, are now acceptable as forms of conditioning. This
enriched view of conditioning enables one to incorporate some of the phenomena
of fear and can shore up the heavily criticized classical theory, but at its present
stage the new view is still too liberal. It lacks limits, and there is little that it
disallows. At present, it is not possible to rule out a potentially fearful stimulus; it
is not possible to state in advance that a novel stimulus will or will not convey new
predictive information, such that the stimulus can become a fear CS. Offering
such tame stimuli as tissue paper, or lambs, or dog collars as nonpredictive is no
advance. No one would expect people to acquire fears of such stimuli. Further-
more, there are fearful stimuli that are nonpredictive. Many people have acquired
a fear of spiders, perhaps by a process of conditioning, even though the spider is
harmless and is known to be harmless. The spider is not followed by harm, and
insofar as the fear stimuli are said to be predictors of “probable causes of events of
significance” (Mackintosh, 1983, p. 172), this is a false predictor. Should we
therefore expect this predictor of harm to wane and disappear? (See for example,
Seligman’s paradox in Rachman, 1990). Many human fears are poor predictors of
harm or other aversive events but nevertheless persist. Unfortunately, these
examples do not bolster Rescorla’s (1988) hopeful view of organisms as “informa-
tion seekers. . . *(forming) a sophisticated representation of its world” (p. 154). The
many people who fear harmless spiders are, in this respect, less than sophisticated.
Fear can be acquired even when the signal (CS) and the aversive event (US) are
separated in time. In theory, almost any stimulus or past stimulus or event can
become a signal for fear, but in practice, people are found to have comparatively
few fears. The fears that we do acquire are confined to a handful of stimuli; fears
are not normally distributed. We no more have a clutter of irrelevant fears than we
do a “useless clutter of irrelevant associations” (Mackintosh, 1983, p. 1972).
Evidently, there are strict limits to the acquisition of fears by noncontiguous
events, but the revised view of conditioning has not yet progressed to the
170 S. Rachman

identification of these limits. Mackintosh’s (1983) idea that the function of

conditioning is to enable organisms to discover “probable causes of events of
significance” (p. 172), is a helpful starting point for a great deal of work.
Seligman’s (1971) theory of prepared phobias can provide a set of limits and is
compatible with the new view of conditioning, but it was not set out within that
perspective. At present, there are no laws of conditioning, or guidelines, to
provide a basis for limiting the possibilities of fear.
Pending further progress, it is preferable to pursue Seligman’s theory of
preparedness, and also to retain the “three pathways of fear” construal of how
fears are acquired. It is argued that fears can be acquired by (a) conditioning, (b)
vicarious transmission, and (c) by the transmission of verbal information (Rach-
man, 1978, 1990). Given that the three-pathways model and the revised model of
conditioning both deal with the way in which (fear) information is processed, it is
not unlikely that the two approaches to fear acquisition will begin to merge. It is
also worth drawing attention to a connection between the new view of conditioning
and cognitive explanations of the acquisition of fear. According to Clark’s (1988)
cognitive explanation of panic, the affected person’s misinterpretation of his/her
bodily sensations (trembling, palpitations, etc.) as signs of an impending catastro-
phe, cause the panic. The sensations predict an extremely aversive event. A strong
relationship between the sensations and an intense fear of catastrophe can be
established rapidly and lastingly. If this (conditioned?) relationship can be discon-
firmed (revalued?), the appearance of the sensations ceases to predict catastrophe
and the fear disappears. “The function of conditioning is to enable organisms to
discover probable causes of events of significance,” (Mackintosh, 1983, p. 172) and
in the case of panic disorder, the affected person makes an erroneous attribution
of the probable causes of an event of significance.
Several forms of abnormal behavior can be thought of as examples of “probable
causes” that are incorrectly interpreted, as in the case of panic disorder. Even
more interesting are those cases in which people recognize that their irrational
fears are indeed irrational-but the fear persists nevertheless. Perhaps the “prob-
able cause” here consists of the correct expectation that contact with the feared
object, say snake or spider, will indeed be followed by an unpleasant fearful
reaction. This expectation is correct-as is the person’s recognition that the
spider/snake is harmless.
However, repeated confirmations that the spider/snake does no harm should
promote the prediction of safety, and presumably begin to undermine the fear.
There is a further problem here, because if we argue that the fear stimulus (e.g.,
spider) correctly predicts the (aversive) response of fear, and persists for that
reason, most fears would be permanent. The stimulus predicts fear and fear is
indeed experienced; the prediction is confirmed. However, most fears decline
over time. Can the neo-conditioning perspective help us to classify those stimuli
that will be and those that will not be predictive and which fears will persist and
which ones decline?

Some Conclusions

The neo-conditioning perspective can help to make intelligible some of our

knowledge about how fears are acquired. The deletion of the requirement that the
conditioned stimulus and the aversive event must occur in temporal contiguity
 Fear Acquisition 171

removes a major objection to the conditioning theory of fear. In addition, new

information about fear (especially the summation of fear, and the overprediction
of fear) is compatible with the revised view (Rachman, 1990).
Some problems remain, and even a liberalized theory of conditioning cannot
account for fears that arise without alzy contact between the fear stimulus and the
aversive event. In these instances, the fear may be innate, or lurking, or symbolic.
The liberalized theory does not help to explain why fears fail to arise in
circumstances in which the conditioning theory would lead us to expect them (e.g.,
aerial bombing). Recourse to neo-conditioning phenomena, such as blocking, are
unlikely to succeed. What type of experience would block the development of a
fear of bombs? The neo-conditioning perspective will also need to explain why
apparently nonpredictive stimuli persistently evoke fear. The liberalized view
greatly expands the explanatory value of conditioning but does not provide the
basis for a comprehensive account of how fears are acquired. Fears can be
acquired by conditioning and by other processes. These other processes include
vicarious transmissions and transmissions of verbal information. To conclude,
conditioning is best construed as one of the three pathways to fear.

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