Behor. Res. i-her. Vol. 28, No. 5. pp. 373-384, Printed in Great Britain. All rights rewwd

EYSENCK’S

1990 Copyright

0005-7967190 $3.00 + 0.00 g 1990 Pergamon Press plc

INCUBATION OF FEAR HYPOTHESIS: AN EXPERIMENTAL TEST MARCUSRICHARDS’* and IRENEMARTINS

‘Neurological Institute, College of Physicians and Surgeons, Columbia University, 710 West 168th Street, New York, NY 10032, U.S.A. and *Department of Psychology, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London SE5 8AF, England (Received

I2 January

1990)

Summary-The present experiment was designed to ttst Eysenck’s hypothesis that repeated exposure to an unreinforced CS of brief duration following acquisition of a classical aversive CR may lead to a progressive increase in the strength of that CR, provided that the UCS is intense and the CR has drive-like properties. Using a between-groups design, -normal human subjects were given identical classical acauisition trials, followed bv extinction trials where CS duration was either 2. 8 or 16 sec. The UCS was of ftxed high intensity. Dependent measures were tonic and phasic heart rate and skin conductance. No evidence of incubation was found as a function of CS duration. Nor was there any indication that CS duration differentially affected resistance to extinction. A small number of subjects showed evidence of incubation with heart rate measures during extinction. However, there was no indication that this enhancement was governed by the parameters suggested by Eysenck. UCR amplitude, which showed a positive correspondence with CS-bound activity throughout the trials, did not reliably predict incubation. Problems concerning both the definition and the demonstration of incubation are discussed.

INTRODUCTION

According to the conditioning model of neurosis, neurosis consists of fear maintained over time by repeated exposure to once-neutral stimuli that have been endowed with anxiogenic properties through association with a traumatic event. While this theory has existed in one form or another for most of the twentieth century, it has come under severe strain in recent years. Criticism has come not only from opponents of the entire approach, but also from conditioning theorists themselves. For example, many authors (e.g. Kimmel, 1979; Eysenck, 1979) have argued that classical conditioning cannot account for the persistence of fear implied by the’concept of neurosis, since classical CRs are easily extinguished in the laboratory. There have, however, been attempts to amend classical conditioning theory in order to maintain its status as a viable account of neurosis. Perhaps the most salient of these attempts is Eysenck’s incubation of fear hypothesis, which was developed not only to account for the persistence of fear but also to explain the increase in fear which may be observed in neurotics during the absence of further exposure to a traumatic event. In 1956, Razran formulated a theory of extinction emphasizing the importance of responseproduced physiological feedback. Extinction occurs, suggested Razran, as a result of the diminution of interoceptive and proprioceptive cues following the removal of the UCS. The consequent reduction in CR strength then itself becomes a CR to these declining cues. Importantly, Razran suggested that this process only occurs when the CR is smaller than the UCR. However, extinction may be slow or impossible if the CR is close in magnitude to the UCR since under this condition, the interoceptive and proprioceptive cues are less likely to attenuate. Eysenck (1968, 1979) extended this proposition by suggesting that under certain circumstances, feedback (referred to as Nocive Responses) from an aversive classical CR, including fear/anxiety and interoceptive cues, may cause that CR to become self-reinforcing following withdrawal of the UCS. Eysenck argues that the strength of a CR is the net result of two opposing forces, the inhibitory process of extinction, where removal of the UCS results in a decrement in CR strength, and incubation, which occurs when the self-reinforcing properties of the CR are sufficiently powerful to offset this inhibitory process, so that every unreinforced CS presentation causes an increase in CR strength. ‘To whom all correspondence should be addressed. BRT28,%.4

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What are the special circumstances which are hypothesized to cause this self-reinforcement to overcome extinction and lead to incubation? Eysenck posits three conditions: (a) that the CR be a drive, (b) that the original UCS be intense (in order that the CR/Nocive Responses may become sufficiently strong to gain superiority over the normal process of extinction) and (c) that the duration of the unreinforced CS be short (since CR strength declines over time). While it has been argued that Eysenck does not clearly specify the nature of a drive-like CR (Gray, 1979), it might be suggested that the CR be of relevance to an intense preparatory or consummatory response. Whether this would include appetitive responding is an empirical question. Concerning proposition (b), there are several studies that show a positive relationship between UCS intensity and conditioning performance (e.g. Annua & Kamin, 1961; Boring & Morrow, 1968; Nicholaichuk, Quesnel & Tait, 1982; Wickens, Allen & Hill, 1963; Wickens & Harding, 1965; Zeiner, 1968). However, none of these studies offer any evidence of incubation during extinction following conditioning with an intense UCS. A study by Campbell, Sanderson and Laverty (1964) provides an exception to this observation. These authors exposed human volunteers to an extremely intense UCS-an injection of succinylcholine chloride dihydrate which caused a temporary respiratory paralysis with an average duration exceeding 90 sec. Autonomic CR magnitude showed a tendency to increase over repeated test sessions. However, it should be noted that this study suffers from poor methodology; data were only analysed for three Ss in the paired group and for one S in each of two control groups. Furthermore, Ss in the paired group were administered atropine (to reduce salivation during paralysis), whereas Ss in the control groups were not. There are, however, several studies that provide tentative support for proposition (c), that incubation is likely with unreinforced CSs of short, rather than long duration. Some of these studies have been carried out on rats (e.g. Rohrbaugh & Riccio, 1970; Silvestri, Rohrbaugh & Riccio, 1970) and some have used humans Ss (e.g. Miller & Levis, 1971; Stone & Borkovec, 1975). These studies have found a tendency for brief unreinforced CS exposure to produce greater fear than long unreinforced CS exposures and--crucially-no unreinforced CS exposure. For example, Miller and Levis (1971) gave school girls who reported a fear of snakes an initial behavioural avoidance test to a live snake. They were then exposed to the snake for either 0, 15, 30 or 45 min. All Ss were then given a second avoidance test. Ss were considered improved if their retest scores were higher than their initial test scores (i.e. they were able to approach closer to the snake). While all groups showed an improvement, the least improvement was shown by Ss who received the 15 min exposure. While the above studies are encouraging to Eysenck’s hypothesis, they contain a major limitation. They all tested the effects of unreinforced CS duration using a single outcome measure (e.g. latency to drink or duration of time spent in a ‘safe’ chamber for rats, a behavioural avoidance test for humans). However, Eysenck’s hypothesis predicts a progressive increase in CR strength resulting from multiple unreinforced CS exposures. Yet studies employing repeated dependent measures have failed to demonstrate such an outcome (Rohrbaugh & Arthur, 1972; Sartory & Eysenck, 1976; Malloy, 1981; White & Wong, 1982). A recent study by Sandin and Chorot (1989) using human Ss, delivered 12 CSs (slides of a snake or spider) with a duration of 4, 8 or 30 set, following a single CS-UCS (tone) acquisition trial. These authors found maintenance of shortlatency cardiac acceleration with the 4-set CS, provided a UCS of high intensity was used. However, for the purpose of analysis, data for these extinction trials were collapsed into a single trial block. It is impossible, therefore, to observe the response trend over the individual extinction trials. In view of this, and since only two of the above studies using repeated outcome measures were carried out on human Ss, it is fair to state that the incubation hypothesis has not been adequately tested. The present experiment, therefore, aimed to continue this investigation in humans by incorporating multiple unreinforced CS exposures of varying duration and employing trend analysis of the responses to these CSs. In line with proposition (b) of Eysenck’s hypothesis and in view of the evidence cited above that UCS intensity contributes to conditioning performance, UCS intensity was fixed at a high level. UCS intensity was not, therefore, used as an experimental variable. However, the effect of the UCS was appraised by measuring the amplitude of the UCR to the initial UCS and using this as a within-S predictor of CS-bound performance.

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Tonic and phasic heart rate (HR) and skin conductance (SC) were chosen as dependent variables, because there is substantial evidence that these autonomic response systems either show a positive correspondence with subjective anxiety, or show an increase in activation under conditions that evoke anxiety. This is true of tonic HR (e.g. Lang, Melamed & Hart, 1970; Sartory, Rachman & Grey, 1977; Clark, 1986; York, Borkovec, Vasey & Stern, 1987), phasic HR acceleration (Hare & Blevings, 1975; Klorman & Ryan, 1980; Hodes, Cook & Lang, 1985), tonic electrodermal activity (Kimmel & Hill, 1961; Katkin, 1965; Miller & Shmavonian, 1965; Fenz & Drosejko, 1969; Mansueto & Desiderato, 1971; Szpiler & Epstein, 1976) and phasic electrodermal activity (Epstein & Fenz, 1962; Geer, 1966; Wilson, 1967; Lang et al., 1970). The measurement of these responses also addresses proposition (a) of Eysenck’s hypothesis, that the CR must have drive-like properties, since activity in all these autonomic systems is highly relevant to strong preparatory or consummatory behaviour. METHOD

Subjects Twenty-eight normal human volunteers (M = 13, F = 15) were recruited either by advertisement in a local listings magazine, or personally by E. Ages ranged from 17 to 40. Ss were allocated to one of three groups on a quasi-random basis, with the proviso that each group was roughly balanced for sex. Ss received modest remuneration. Design A between-groups design was employed, using a 3 x 20 (group x trials) factorial strucutre with multiple repeated measures. The trial series consisted of an acquisition and an extinction phase, the latter following immediately after the former. All groups received 4 identical delayed classical acquisition trials. The CS consisted of a sinusoidal tone of 8 set duration at a level of 60 dB. CS termination coincided with onset of the UCS. The latter consisted of a sinusoidal tone of 1 set duration at a level of 110 dB. Both CS and UCS were delivered at a frequency of 1 kHz, with an immediate rise-time. Following acquisition, all Ss received 20 extinction trials, the CSs being of identical level and frequency to those during acquisition. Ss in Group 1 received CSs of identical duration (8 set) to that received in acquisition. Ss in Group 2 received CSs of 2 set duration and those in Group 3 received CSs of 16 set duration. A fixed inter-trial interval of 60 set was used throughout. Hypotheses (I) Strong hypothesis. Ss receiving the shortest unreinforced CSs (Group 2) will show incubation, reflected in a growth of autonomic responding across extinction trials, Ss receiving an unreinforced CS duration identical to that in acquisition (Group 1) will show a ‘normal’ extinction decrement and Ss exposed to the longest unreinforced CSs (Group 3) will show rapid extinction relative to the other Ss. (2) Weak hypothesis. Ss receiving the shortest unreinforced CSs will show failure of extinction or will show maintained responding relative to the other Ss. Eysenck (1983) has suggested that a strong UCS may produce ceiling effects which may obscure incubation. Therefore, extinction failure/response persistence may be taken as support for the hypothesis. To which it might be added that even if putative incubation is not occurring behind the mask of a ceiling effect, persistence would still be an outcome of great interest. It should be accepted, however, that such a position represents a ‘step back from the claim of direct evidence’ for incubation (Bersh, 1983). Procedure All Ss were tested individually. They were seated in a sound-dampened room adjacent to the recording apparatus. After screening for medication and major illness, devices for recording electrodermal activity and heart rate were attached to S. S was instructed to relax and to remain comfortably still while stable traces were obtained. S was then informed that he/she would hear tones over headphones, some of which would be soft and some of which would be loud and that nothing was required other than to listen to the tones, to relax and to try to keep still, especially

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the hand to which recording electrodes were attached. S was assured that the loud tones would not be dangerous in any way, but that should he/she wish to terminate the session at any time or need to communicate with E for any reason, a wall intercom was active. Finally, S was informed that the tones would continue for 15 or 20 min. Headphones were then placed on S, following which E left the test room and entered the recording room. The trial sequence was then initiated. At the end of the sequence, E returned to the test room, informed S that the experiment was over and removed the recording devices. S remained in the test room to complete a self-administered post-experimental questionnaire. This questionnaire required S to rate, on a scale of O-9, the unpleasantness of the UCS, with 0 being not at all, and 9 being extremely unpleasant. Ss were also required to rate, again on scale of O-9, their subjective feeling of wellbeing, with 0 representing feeling well prepared and able to defend against the UCS, and 9 indicating that Ss felt very vulnerable. Apparatus (a) Stimulus equipment. The CS was generated by a Dymar AF Signal Generator (Type 741) and the UCS was generated by an Advance Electronics LF oscillator (SG65A). Both were delivered binaurally via Taiyo Dynamic Stereo MD8035 headphones. The level was checked with a Dawes sound level meter. The stimulus schedule was automated and controlled by a Commodore (CBM 4032) microcomputer linked to a Commodore 8250 lp disk drive. (b) Response measurement. Electrodermal activity was recorded from the middle phalanges of the second and third fingers of S’s left hand, using custom-made bipolar silver/silver chloride electrodes. A purpose-made electrode paste was used which contained 0.05 M NaCl (isotonic with human sweat) in a base of methyl cellulose (Grey & Smith, 1984; see also Clements, 1989). The current used across the electrodes was 10 PA. HR was recorded using a digital photoplethysmograph attached to the index finger of S’s left hand. This was linked to a custom-made a.c. amplifier which expressed raw pulse. The output of this was fed into a cardiotachometer (Devices 4522) which provided an analogue measure of HR. (c) Recording equipment. All data were recorded onto Scotch (Type 3M) one-quarter inch magnetic tape using a 6-channel Bell and Howell VR3200 tape recorder, and were displayed on an Elema Schonander Mingograph 800 6-channel polygraph. All data were digitized via a Biodata Microlink A/D converter, then stored on magnetic disk for subsequent reduction. Data reduction

For all responses, the software package SARA (Law, Levey & Martin, 1980) was used for data reduction. While responses for the 4 acquisition trials were kept separate, those for the 20 extinction trials were averaged into 4 blocks of 4 trials for the purpose of analysis. In the case of SC, this was done after transformation of the raw response values. In all cases, the individual tonic and phasic responses were averaged after they were extracted from the individual trials. (a) SC measures. Values for tonic pre-stimulus skin resistance level (SRL) were obtained for each trial, the level being measured 6 set prior to CS onset. SRL was converted to skin conductance level (SCL) using a log reciprocal transformation, values being expressed in micromhos (Venables & Christie, 1980). Phasic skin conductance response (SCR) values for the acquisition trials were obtained by measuring the level at the first response onset occurring after CS onset and before UCR onset. The level was then measured at the largest deflection occurring up to and including UCR onset. For the extinction trials, the first response onset occurring at or up to 5 set after CS onset was measured. Then the largest deflection occurring prior to a 50% recovery point was measured, provided that the latter did not occur within the CS interval or within 5 set after CS offset. If a 50% recovery point was not observed within an overall 34 set window, the largest deflection within this total window was measured. Change scores were obtained by subjecting the raw levels to a reciprocal transformation, then subtracting the peak levels from the onset levels. The resulting change scores were then subjected to a further log transformation, i.e. change scores were expressed as log change reciprocal. (b) HR measures. The HR output of the cardiotachometer was digitized, with a sampling rate of 12.5 Hz and was converted to beats per minute (BPM) by the SARA software. Tonic pre-stimulus levels were obtained by calculating mean HR for the 6 set preceding each CS onset.

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In order to investigate phasic changes in HR activity, evoked HR response curves were obtained by averaging 10 post-stimulus seconds for each trial. These seconds were then converted into change scores by subtracting the pre-stimulus mean levels from each second. For each trial, criterion responses were extracted from the array of change scores using response parameter analysis (RPA, e.g. Barry, 1977). Numerous studies have shown that the HR CR typically shows a triphasic topography, the three features being termed D 1, A and D2 by Gatchell and Lang (1973). Dl consists of an initial deceleration 1-2 see post CS onset and is an OR to nonsignal stimuli (Bohlin & Kjeliberg, 1979). This is followed by A, an accelerative phase peaking within the first 5 set post CS onset. Several studies suggest that A is a defence response (e.g. Hare & Blevings, 1975; Klorman & Ryan, 1980; Hodes ef al., 1985) and thus of direct interest in the measurement of fear and fear conditioning in the present experiment. Finally, D2 is a secondary deceleration reaching a maximum at approximately the eighth second post CS onset. This response is sometimes regarded as the “principal” HR CR (e.g. Wilson, 1969). However, consideration of the data indicated that the D2 response was not prominent in the present case. It was therefore decided to focus on the A response as the principal index of fear-related phasic cardiac responding in the present experiment. For this response, the maximum accelerative point occurring between 3 and 5 set post CS onset was extracted for each acquisition and extinction trial. Selection of this window was guided both by previous research and by consideration of the present data. Finally, UCRs were obtained by subtracting the level at second 9 post CS onset (i.e. the level at UCS onset) from the highest point within the subsequent four second-by-second mean levels. RESULTS

All responses were analysed by MANOVA, using polynomial trend analysis for repeated measures with group as a between S factor (3 levels) and trials as a within-S factor (4 levels each for the averaged acquisition and extinction trials). For all analysis, Hotelling’s test is reported. Acquisition and extinction trials were analysed separately. Acquisition trials were subjected to an overall group contrast in order to check whether any group differences during extinction might be the result of similar group differences arising during acquisition caused by sampling error. This overall group contrast was also used for the extinction trials--the outcome measures of principal interest in the present experiment. (1) HR measures (a) Tonic pre-stimulus levels. The initial pre-stimulus HR level was normally distributed. The pre-stimulus levels for each acquisition trial and each extinction trial block are shown graphically for the three groups in Fig. 1. An increase in level from trial 1 to trial 2 can be observed. However, with the exception of Group 3, this increase was not maintained across trials and gradually reached levels below that of the first pre-stimulus level during extinction. No group effect or group x trials interaction was found during acquisition. However, a linear trials effect was marginally significant [F(3,23) = 3.01, P = O.OSl] during this phase, indicating a gentle increase in tonic HR during acquisition. The analysis was then repeated on the extinction trial blocks. Again, no group effect or group x trials interaction was found. However, a trials effect emerged [F(3,23) = 4.32, P = 0.0151, the effect being significant at the linear level and indicating a systematic decrement in HR over the extinction trials. (6) HR A _phasic responses. HR A magnitude for each acquisition trial and each extinction trial block is shown graphically for the three groups in Fig. 2. A growth of this response over the four acquisition trials, followed by a decline during extinction, is evident. No group effect or group x trials interaction was found with this response during acquisition. A linear trials effect was highly significant, however, during this phase [F(3,23) = 4.99, P = 0.008], indicating a marked growth of this response during acquisition. The analysis was then repeated on the extinction trial blocks. A group effect approached significance fF(2,25) = 2.9, P = 0.0741. However, while Fig. 2 indicates an overall decline in HR A magnitude over the extinction trials, both the trials effect and the group x trials interaction were

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nonsi~~~cant, suggesting considerabie variability in the trend of this response during extinction. The possible significance of this wili be discussed below. (c) The initial HR UCR. A l-way ANOVA revealed no group difference with the initial HR UCR. The initial HR UCR was then covaried with the mean, linear, quadratic and cubic polynomial components of the HR repeated measures, using multivariate analysis of covariance. This was done in order to investigate the extent to which the initial I-IR UCR influenced and thus predicted the magnitude of the HR repeated measures. The between-S (group) factor was not incorporated into the analysis. The initial HR UCR covaried significantly with the A response during acquisition at both the mean level [F(1,26) = 9.97, P = 0.0041 and the cubic level [F( 1,26) = 9.99, P = 0,004] and with this response during extinction, again at both the mean level [F(1,2&) = 5.1, P = 0.033] and cubic level [F( 1,26) = 9.6, P = OBOS].In order to determine the direction of the covariation, the HR UCR was divided using a median split. The A responses for these resultant high and fow UCR groups are shown graphically in Fig. 3,

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The A response shows a sharp rise in magnitude between the second and third acquisition trials with high UCR responders, followed by an equally sharp decline during extinction, although the significant covariation at the mean level indicated that this response remained at the higher level throughout this phase for these Ss. Low UCR responders, on the other hand, showed a more gentle response profile for HR A throughout the trials. (2) SC measures (a) SCL. Two Ss from Group 1 showed extreme outlying values for the initial SCL. These Ss were excluded from the analysis of all SC measures. Initial SCL values for the remaining Ss were normally distributed. SCL showed a gentle increase during acquisition, followed by an equally gentle decrement during extinction. MANOVA revealed no group effect or group x trials interaction with this measure during acquisition. However, a highly significant trials effect was observed [F(3,21) = 20.75, P c O.OOl], the effect being significant at the linear, quadratic and cubic levels, thus describing the increase in SCL during this phase. Similar results emerged when the analysis was repeated on the extinction trial blocks; only a trials effect was found [F(3,21) = 16.66, P < O.OOl],the effect being significant at the linear level and representing a decrement during this phase. (b) SCRs. The SCRs for each acquisition trial and each extinction trial block are shown graphically for the three groups in Fig. 4. No group or trials effects were found with this measure during acquisition. However, a significant group x trials interaction emerged during this phase [F(6,40) = 2.41, P = 0.0441, the effect being significant at the cubic level. Inspection of Fig. 4 suggests that this interaction was caused by the sharp increase in responding from trial 2 to trial 3 by Group 1, a trend which was absent in the other two groups. Since the experimental conditions were identical for all Ss during acquisition, this difference probably arose from a sampling error and is thus unlikely to constitute an experimental effect. The analysis was then repeated on the four extinction trial blocks. Neither the group effect nor the group x trials interaction were significant. However, like SCL, a highly significant trials effect was found [F(3,21) = 7.84, P = O.OOl],the effect being significant at the linear level and indicating a systematic reduction in SCR magnitude during extinction. (c) The initial SC UCR. A l-way ANOVA revealed no group difference with the initial SC UCR. This measure was then covaried with the mean, linear, quadratic and cubic polynomial components of the SC repeated measures using the same technique as that used with HR above. Positive covariations were found between the SC UCR and SCL during acquisition at both the mean and quadratic level [F(1,24) = 62.73, P < 0.001 and F(1,24) = 15.53, P = 0.001, respectively] and

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between the SC UCR and mean SCL during extinction [F( 1,24) = 40.86, P > O.OOl].SCL is shown broken down by high and low UCR responders in Fig. 5. As can be seen, high UCR responders had consistently higher SCL than low UCR responders. Positive covariations were also found between the SC UCR and mean SCR magnitude, during both acquisition [F(l,24) = 58.72, P < O.OOl]and extinction fF(1,24) = 29.37, P < O,OOl]. Again, high UCR responders had high SCR magnitude. (3) Subjective measures Groups means and SDS for the UCS unpleasantness rating were as follows: Group 1; 7.4 (2. IZ), Group 2; 8.4 (l-9>, Group 3; 7.14 (2.73). Group means and SDS for the subjective wellbeing measure were as follows: Group 1; 5. I (2.28), Group 2; 7.44 (1.74), Group 3; 5.71 (2.87). A l-way ANOVA revealed no group difference with the former, although a group difference with the latter approached significance [F(2.25) = 2.6, P = 0.0961, the feeling of vulnerability being highest in Group 2. 1.4

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DISCUSSION Concerning the strong hypothesis, was there any evidence of incubation, i.e. did Ss in the short unreinforced CS group show an increase in response magnitude relative to Ss in the other two groups? The answer would appear to be a clear-cut no. In neither modality was there any indication of enhancement of response magnitude in the short-or any other-reinforced CS group during extinction. Neither did there appear to be any support for the weak hypothesis. Thus there was no evidence that Ss in the short CS group showed increased resistance to extinction, greater response maintenance or even slower response decrements relative to the other Ss. In order to check whether incubation had occurred at all, the extinction responses of each individual S were examined post hoc. To provide a formal criterion, incubation was defined as a progressive increase in the magnitude of a response across all four extinction trial blocks (Criterion A). Only one S met this criterion (from group 2, with HR A). The criterion was then relaxed in order to take into account possible ceiling effects (cf. Eysenck, 1983). Accordingly, incubation was said to have occurred if a progressive increase in the magnitude of a response was observed over the first three extinction trial blocks, followed by little or no reduction in the magnitude of the response from that of the third trial block, in the final trial block (Criterion B). A further two Ss met this new criterion, both from Group 2 (with tonic HR). The incubation criterion was then eased further; a response trend was deemed to be an instance of incubation if an increase in the magnitude of a response was observed across the first two extinction trial blocks, followed by little or no reduction in the magnitude of that response from that of the second trial block, over the remaining two trial blocks (Criterion C). Three extra Ss met this new criterion, two from Group 1 (one with tonic HR and one with HR A) and one from Group 3 (with HR A). Note that all of the responses satisfying these experimental criteria were cardiac. In this context, it is worth recalling that HR A magnitude showed considerable variability during extinction. Obviously, the above numbers are too small to permit statistical analysis. A potential strategy for the future, therefore, would be to pursue this approach with a larger sample to permit a meaningful contingency analysis to be carried out. Important questions to be addressed concern the conditions under which these various response patterns occur-for example, whether changing any of the experimental parameters would alter the ratio of Ss meeting each incubation criterion. Such a strategy would acknowledge that whatever the experimental parameters, incubation may only occur in a relatively small number of Ss and, accordingly, that its occurrence may be obscured by powerful statistical techniques such as MANOVA. Other important questions concern the nature of such Ss-for example, their personality characteristics and/or clinical histories. Again, the exploratory approach used here may be able to pinpoint the answers with greater accuracy than the more conventional technique of correlating across an entire sample. While it might be unrealistic in the future to anticipate incubation as a common occurrence, it is still necessary to enquire why incubation failed to emerge as a group phenomenon in the present experiment. Such failure may have arisen, in part, from aspects of the experimental design. For example, it is possible that changing CS duration from acquisition to extinction (in the case of Groups 2 and 3) may have produced a generalization decrement, or may have conferred safety signal properties onto the CS, since this change in stimulus conditions was correlated with UCS withdrawal. While there was no direct evidence of an increased response decrement in Groups 2 and 3 relative to Group 1, such an effect may have prevented the emergence of incubation in Group 2. However, the alternative strategy of equating CS duration across acquisition and extinction is likely to cause differing rates of acquisition-a serious confounding effect. The short CS itself (Group 2) may also have interfered with one of the outcome measures-the HR A response-since the latency window used to score this response (3-5 set) began close to the offset of the 2 set CS. Inspection of Fig. 2 indicates that the magnitude of these responses was smallest for this group during extinction. It is possible that the significant maintenance of this response reported by Sandin and Chorot (1989) resulted from the avoidance of this problem by the use of a 4 set CS. However, this issue only concerns HR A; there is no reason to expect that the different CS durations directly interfered with the expression of any other response measured in the present experiment.

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MARCUS ~XARDS

and IRES I~~~~~

Thirdly, it is possible that the delivery of multiple CS-only trials in a single session, with an IT1 of 1 min, may have constituted a massed procedure, thereby promoting efficient extinction in all groups. Jacobs and Blackbum (1987) have demonstrated incubation following a delay of 24 hr between acquisition and testing. However, the more significant a role that delays are found to play in promoting incubation, the less clear it is that the phenomenon can be explained by basic conditioning principles, despite Eysenck’s (1968) suggestion that ‘empty interval’ incubation might be governed by the same processes suggested by his theory. Finally, it is possible that the levels of fear produced in the present experiment were insufficient to evoke incubation in the first place. If true, this problem would rule out the use of the loud tone in paradigms designed to investigate conditioned fear, since UCS intensity (110 dB) was close to the upper limit tolerable in human research. What can be inferred from the subjective responses in the present experiment? The mean UCS unpleasantness rating was 7.7, thus tending toward the maximum value (9). Also, 59% of Ss gave the maximum rating. Furthermore, the mean vulnerability rating was 6.1, where the maximum value was 9. Again, 65% of Ss gave a rating of >5 (the median value) and 5 Ss gave the maximum rating. While these two subjective responses are not direct measures of anxiety, they do indirectly suggest that levels of distress were fairly high during the experiment. Whether they were sufficiently high to precipitate incubation remains a moot point. It is worth commenting, however, that an answer in the negative would effectively banish further exploration of incubation in humans from the laboratory on ethical grounds and would thus render the hypothesis ultimately untestable. As noted, UCS intensity was close to the upper limit tolerable for human research. Indeed, two Ss terminated the experiment in mid-session because they found the stimuli too distressing. In conclusion, while no guidelines have been laid down regarding the absolute levels of anxiety necessary to trigger incubation, indirect evidence suggests that levels of anxiety evoked in the present experiment were probably high in some Ss. In view of this, and in spite of the above design limitations, failure to observe incubation may ultimately reside in problems with the theory itself. Eysenck draws a distinction between the CR and the Nocive Response; “It is not (he suggests) the CR itself that acts as reinforcer, but rather the response-produced stimuli; not the autonomic, hormonal and muscular reactions themselves but rather the experience of fear/anxiety based upon them.” (Eysenck, 1968). This distinction corresponds to another-between fear and fear-of-fear (or first and second-order fear). For Eysenck, the crux of the matter is that fear-of-fear is itself aversive and thus has unconditional properties. It may therefore act as a UCS for further fear, which, via classical conditioning, may be sufficient to overcome the process of extinction. However, it is dimcult to see how this distinction operates in vivo. Consider an example provided by Eysenck (1968). Here, a man becomes impotent following the excessive intake of alcohol. CSs associated with this event subsequently evoke anxiety. This anxiety inhibits the sexual response causing a repetition of the impotence, which, in turn, triggers further anxiety. With such an example, fear of impotence may constitute the first order fear, but what or where is the fear of fear-of-impotence? In the present experiment, a distinction could be drawn between first-order fear/anxiety as a CR (as expressed, for example, by a HR increase) and a secondary fear based upon the aversiveness of this CR. But such a distinction seems arbitrary; why should autonomic responses and the subjective reactions to those responses not be considered as components of the same CR, each component suffering the same fate during extinction? Lyons (1979) has formalized this problem. If, he argues, first-order fear diminishes in the absence of the UCS, there is no reason to expect that the second-degree fear will not diminish in parallel, since the latter is based upon the former (this argument was in fact anticipated by Quattlebaum, 1970). There is evidence that panic-attack patients are over-sensitive to their somatic symptoms of anxiety (e.g. Ehlers, Margraf, Roth, Taylor & Birbaumer, 1988). However, it is not clear what distinguishes the panic-attack patient from the normal individual. The answer is unlikely to reside in the simple environmental parameters suggested by Eysenck. It seems reasonable, however, to look to individual differences for clues. From this perspective, the present experiment suggests that within-S reactivity plays an important part in the maintenance of autonomic responding. Specifically, Ss who showed high UCR amplitude also evidenced high

Eysenck’s incubation of fear hypothesis

383

levels of responsivity during both acquisition and extinction. Unconditional reactivity was not, however, shown to be a reliable predictor of incubation in the present experiment. Four out of the six Ss meeting the above incubation criteria fell into the upper UCR median in at least one UCR modality. Yet only two of these Ss showed a high initial HR UCR, the modality in which the instances of incubation were consistently found. In conclusion, while several studies have shown an elevation in fear resuhing from exposure to an unreinforced CS of brief duration following acquisition, there is little evidence that repeated brief unreinforced CS exposures will promote a progressive increase in CR strength. Nor is there any reliable evidence of such enhancement during extinction following acquisition with an intense UCS. The present study adds to these negative findings, although it provides evidence that an intense UCR can predict high levels of autonomic responsivity during repeated stimulation. Incubation itself, however, may be a more precarious phenomenon, although as Furedy, Riley and Fredrikson (1983) point out, the fact that it occurs at all is noteworthy. Indeed, Rohrbaugh and Riccio (1970) conclude that “enhancement is to be regarded as an exceptional outcome, yet one which should nonetheless be acknowledged”. The present study makes such an acknowledgement. However, it is fair to conclude that the factors governing the maintenance of incubation remain obscure and are likely to be more complex than those suggested by Eysenck’s hypothesis. Acknowledgement-The

first author is grateful to the Medical Research Council for financial support.

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