Eysenck's theory of incubation: A critical analysis

EYSENCK’S THEORY OF INCUBATION: A CRITICAL ANALYSIS PHILIP Department

J. BERSH*

of Psychology, Temple University, Philadelphia, PA 19122, U.S.A. (Received 22 May 1979)

Sumntary-Eyseuck’s theory of incubation is summarized. Arguments and evidence concerning its validity and potential value are presented.

In several recent papers, Eysenck (1967, 1968, 1976, 1979) has proposed a conditioning model of neurosis. The core of the model is the phenomenon of ‘incubation’, Eysenck’s term for an increase in the strength of a Pavlovian conditioned response (CR) produced by unreinforced presentations of the conditions stimulus (B)t. The present paper focuses upon incubation and Eysenck’s proposed theoretical basis for the phenomenon rather than upon his application of the theory to neurotic behavior. _ The proposition that Pavlovian extinction procedures lead to a progressive decline in the strength of the CR is, of course, supported by a vast amount of experimental evidence. An enhancement in CR strength as the result of cs in the absence of possible contamination by operant processes would obviously constitute a radical departure from traditional or current views of Pavlovian extinction. Such a phenomenon would be completeIy in~mp&tible with the Re~orla-Wader theory (1972), for example. An immediate question, therefore, is whether incubation is real. Eysenck (1979) has mustered a varied body of experimental and clinical evidence for the occurence of the phenomenon. However, most of the laboratory studies cited are less than convincing. Napalkov (1963) not only reported very strong incubation on the basis of a single conditioning trial with unconditioned stimuli (UC%) of apparently moderate intensity, but claimed powerful second, third and higher orders of conditioning. In view of the remarkable nature of these results, replication with suitable controls is clearly required. After all, Pavlov (1927) experienced considerable difficulty with second-order conditioning even when first-order conditioning included many reinforced trials. He was unable to obtain stable third-order conditioning. Unfortunately, Napalkov’s totally inadequate description of experimental conditions makes true replication impossible. The most impressive example of incubation with human subjects has been provided by Campbell, Sanderson and Laverty (1964), but their experiment was hardly clean, since experimental subjects were injected with atropine, while control subjects were not. Moreover, their controls for Pavlovian con~tioning were inadequate (cf. Rescorla, 1967). A number of experiments (Lichtenstein, 1950; Solomon and bone, 1953; Maatsch, 1959; Reynierse, 1966) have included response-reinforcer (operant) contingencies which might account for the data and, at a minimum, should be considered to have influenced the results. Rohrbaugh, Riccio and Arthur (1972) interpreted the enhancement they obtained as incubation, but could not rule out the possibility of adventitous operant conditioning. Rohrbaugh and Riccio (1970) reported inconclusive results in one experiment, while in a second experiment the contribution of unreinforced exposures to a CS+ for shock to the reported enhancement effect cannot be disentangled from the possible contribution of exposures to a CS - for shock. Less questionable laboratory evidence for incubation has been provided by the qualitative data and observations of Dykman, Mack and Ackerman (1965). Their experimental procedures incorporated Pavlovian paradigms with no l This paper was written while the author was Visiting Professor, Department Psychiatry. De Crespigny Park, London S.E.5. England. t Eysenck’s symbol for unreinforced presentations of the conditioned stimutus.

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of Psychology, Institute of

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PHILIP J. BERSH

apparent sources of operant reinforcement. Symptoms of ‘behavioral disturbance’ became progressively more frequent during extinction, and the authors concluded that extinction was more ‘upsetting’ than conditioning. Even here, however, there was little parallelism between autonomic and motor indicators, and, since the extinction phase lasted for a number of days, some incubation of the type reviewed by McAllister and McAllister (1967) may have occurred. The latter possibility also exists for the case of the dog, Schnapps, as described by Dykman and Gantt (1960). In general, then, experimental evidence for incubation due to CS is not substantial. At best, incubation must be regarded, in the words of Rohrbaugh and Riccio (1970) as an ‘exceptional outcome’ in the laboratory. The clinic appears to offer more frequent cases of enhancement of ‘anxiety/fear’ during treatments based upon exposure to ‘fearprovoking’ stimuli, but the circumstances do not readily permit a determination of the precise basis for the effect or a clear identification of the variables which influence its occurrence. Assuming that incubation through CS can be shown to be a reliable, reproducible phenomenon, how does Eysenck propose to account for its occurrence? A summary ‘of the major propositions of his theory follows: (1) Incubation through Cs is an outgrowth of Pavlovian ‘B’ conditioning (Grant, 1964). Pavlovian ‘B’ conditioning differs from Pavlovian ‘A’ conditioning in several important ways: (a) The UCS elicits the complete UCR. As a result, the CS serves as a partial substitute for the UCS, often eliciting major components of the UCR. (b) The CR (or CR-produced stimuli) has drive properties. In addition, the UCS in Pavlovian ‘B’ conditioning is aversive. Accordingly, the CS acquires aversive properties (e.g. it elicits conditioned ‘anxiety/fear’ responses). (2) Since ‘anxiety/fear’ is aversive in its own right, it may contribute to the total aversive effect of a reinforced trial (i.e. CR + UCR may be significantly more aversive than UCR alone). Thus, the occurrence of the CR (or its stimuli) may increase the overall CR strengthening effect of a reinforced trial or may compensate for such reinforcement-reducing processes as UCS habituation. (3) If the CR (or its stimuli) is sufficiently aversive, it provides reinforcement akin to, but presumably weaker than, that provided by the UCS. ,Therefore the CS, even when not reinforced by the UCS (the Pavlovian extinction operation), may supply its own reinforcement through its elicitation of the CR. (4) Each failure to reinforce the CS automatically leads to a decrement in the strength of the CR. (5) Since each CS involves both reinforcement through CR elicitation and intrinsic extinction, the net effect of such a trial depends upon the relative magnitude of these antagonistic processes. (6) A critical point of CR strength exists above which the net effect of CS is to strengthen the CR and below which the net effect of CS is to weaken the CR. This critical point remains essentially constant for a given individual, though long term changes in its value may occur (e.g. through aging). (7) Two variables are critical to the outcome of CS. These are the intensity of the UCS during prior conditioning and the duration of each cs. The former variable determines the strength (and, therefore, the reinforcement- potential) of the CR at the outset of CS. The latter variable determines whether a CS has a net reinforcement or extinction effect. The strength of the CR decreases- progressively during a m. If CR strength is above the critical point at the time of CS termination, the cs increases CR strength (i.e. incubation occurs). If CR strength is below the critical point at the time of cs termination, the CS produces a decrement in CR strength (i.e. extinction occurs). Furthermore, the net strengthening effect of CS increases with the degree to which CR strength exceeds the critical level at the time of CS termination, while the net weakening effect of cs increases with the degree to which CR strength falls below the

Eysenck’s theory of incubation: a critical analysis

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STRENGTk I OFCR

:RITICAL POINT

1

‘\

B

.

CURVE ‘\.

C

A I

CRITICAL GRATE

‘\

LURATiON

OF 6

EXPOSURE

Fig. 1. Theoretical curves of CR strength as a function of m duration. The critical point rep resents the level of strength above which a m produces an enhancement in CR strength (i.e. incubation) and below which a m produces a decrement in CR strength (i.e. extinction). The critical point determines a critical duration of CS. This figure is taken from Eysenck (1979).

critical level. Whenever the reinforcement process is stronger, incubation occurs. Initial CR strength and the critical point combine to establish a critical duration for an incubation effect of a. Figure 1, taken from Eysenck (1979), illustrates some of these assumptions and suggests the form of the function relating the decline in CR strength to the duration of a a. The following analysis refers to the above numbered not necessarily considered in order:

paragraphs,

which, however, are

(1) The elicitation by the UCS of the complete UCR is unnecessary for Pavlovian ‘B conditioning. For example Crisler (1930) obtained excellent and complete conditioning of salivation in cats with morphine injection as the UCS, even though the cats were prevented from salivating during conditioning by an atropine sulphate block. A particularly dramatic case has been provided by Schoenfeld, Kadden and McMillan 1974). They developed a technique for controlling heart rate in rhesus monkeys by implantation of a cardiac pacer. With the heart rate kept perfectly constant, they exposed the monkeys to paired presentations of a tone and an intense shock. After the pacer was removed, the CS elicited a weIl-formed cardiac rate CR. Further conditioning trials without the pacer resulted in no change in the form or ~pIitude of the CR. In addition, the CR was extremely resistant to extinction, with no difference in resistance evident between subjects conditioned with and without pacing. In neither of the examples cited was the complete UCR eliminated. However, the evidence suggests strongly that such elimination, if feasible, would not prevent conditioning. Indeed, Schoenfeld et al. (1974) concluded that “responding appears to be unnecessary for behavioral acquisition.. . within the Pavlovian paradigm. o. If so, this would seem to require an interpretation of such behavioral modification in terms of the temporal relationships among the stimuli alone, and in terms of central processes rather than the peripheral ones to which Pavlovian conditioning has sometimes been referred.” It is suggested that no drive properties need be attributed to the CR (or its stimuli) as the result of Pavlovian ‘B’ conditioning. Eysenck (1979) recognizes fully that presentation of the CS (after conditioning with an aversive UCS)

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PHILIPJ. BERSH

constitutes the drive operation, but implies that the elicited CR constitutes the drive itself. Consider, however, the following hypothetical experiment. A CS is repeatedly paired with an intense aversive UCS. All autonomic components of the CR are then blocked by techniques like those used by Crisler (1930) and Schoenfeld er al. (1974). While the subject is under the influence of the block, termination of the CS is made contingent upon some operant. Would operant conditioning occur? Moreover could the subject be trained to avoid the aversive UCS? There is good reason to suggest an affirmative answer to both questions. Certainly much evidence can be cited to support the contention that avoidance behavior does not require the mediation of autonomic responses (e.g. Solomon and Wynne, 1953; Kamin, Brimer and Black, 1963; Gray, 1971; Seligman and Johnstone, 1973). Viewed this way, presentation of an aversive CS (without regard to its elicitation of autonomic CRs) is both the necessary and sufficient condition for an aversive drive. Such an operation fulfills the most basic attribute of a drive, namely that it creates a potential for reinforcement (e.g. Millenson, 1967). (2) If the CR adds significantly to the total aversive impact of a reinforced conditioning trial, its termination should materially reduce the total aversive impact of such a trial. Accordingly a response which terminated the eliciting stimulus for such a CR should be strengthened by negative reinforcement. However, Bolles, Stokes and Younger (1966) have found that a response which terminates the warning signal for shock, but does not avoid the shock, is not acquired unless the same response is permitted to terminate the shock (i.e. the UCS). (3) The view that a Pavlovian CR can supply its own reinforcement is novel, but quite reasonable. Similar views are not uncommon in operant conditioning. For example, Skinner’s (1938) treatment of operant chains assigns to response-produced stimuli the role of providing conditioned reinforcement for the maintenance of the link to which that response belongs. One version of two-process avoidance theory attributes the maintenance of avoidance responding to positive reinforcement by avoidanceresponse-produced stimuli, regarded as ‘safety signals’ (Gray, 197 1; Dinsmoor, 1977). None of the above criticisms is truly damaging to the theory, because none of the features criticized is essential to the theory. The heart of the - theory is the idea that, as the result of conditioning with an aversive UCS, a CS may elicit a CR (with its accompanying stimuli) sufficiently aversive to strengthen the CR despite the intrinsic weakening effect of withholding the UCS. The only requirement for incubation, then, is the elicitation by CS of such aversive CR’s. The occurrence of the UCR during prior conditioning, the contribution of the CR to the total aversive effect of a reinforced trial, and the subsequent drive status of the CR are logically -not relevant to the occurrence of incubation. A demonstration of incubation through CS under conditions where the major autonomic components of the CR are blocked would be required to rule out Eysenck’s form of incubation theory. A theory that characterizes ‘anxiety/fear’ as a central process (e.g. Rescorla and Solomon, 1967) would still be viable, but would encounter the usual difficulties created by the lack of independent measures of the hypothetical central state (e.g. Seligman and Johnstone, 1973). (7) It is clear that variables -other than UCS intensity will influence the strength of the CR at the outset of CS. Such variables [e.g. CS-UCS contingency (Rescorla, 1967), CS-UCS interval, schedule of reinforcement, etc.] must be incorporated into the theory. In addition, the theory fails to consider the possible role of the temporal distribution of CS. The assumed loss in CR strength as a function of the duration of a cs is supported primarily by clinical research data (e.g. Watson, Gaind and Marks, 1971; Stern and Marks, 1973). A direct laboratory demonstration in a strictly Pavlovian context has not been reported. In -any event, Eysenck’s assumptions concerning the joint influence of UCS intensity and CS duration upon CR strength in relation to a critical strength

Eysenck’s

theory of incubation:

a critical analysis

15

level, as pictured in Figure 1, have some provocative implications: (a) If a CS duration is determined empirically to produce an increment in CR strength (i.e. incubation), further CS at durations no greater than this value must generate a monotonically increasing CR strength -function. Presumably some upper limit of CR strength exists. At asymptote, further CS at durations no greater than this value must -maintain CR strength. Provided the critical strength level does not increase, such CS, - no mutter how numerous, can never result in a decrement in CR strength. (b) Since CS within the critical duration are assumed to produce an increment in CR strength, and since the critical duration- is assumed to covary with initial CR strength, it should be possible to lengthen the CS progressively while still generating a monotonically increasing CR strength function. Conversely, it should be - possible to extinguish the CR with progressively briefer CS, provided the initial CS exceeds the critical duration. (c) With total duration of CS exposure held constant and with all CS greater than the critical duration, extinction should be further advanced by exposing the subject to relatively few lengthy CS than by exposing the subject to more numerous, but brief I% The relative importance (to Pavlovian extinction) of number and duration of cs has not been explored directly. However, a parametric study by Schiff, Smith and Prochaska (1972) on the influence of these variables upon the facilitation of avoidance exinction by cs during avoidance response prevention provides indirect evidence for a reciprocal relation. They found that such facilitation was a function of total duration of CS without regard to the number of CS or the duration of each CS. On the other hand, some evidence from clinical research does suggest that ‘anxiety/ fear’ reduction covaries with the duration of individual exposures to phobic stimuli (Stern and Marks, 1973). Several implications of this aspect of Eysenck’s theory are completely at odds with the -. evidence. As indicated earlier, the strengthening or weakening effect of CS is assumed to vary with the degree- to which the CR is above or below the critical point at the time of termination. With CS duration held- constant at a value initially longer than the critical duration, for example, each CS would progressively weaken the CR. Thus on successive CS trials, initial CR strength would be less, so - that CR strength would fall further and further below the critical point by the time of CS termination. Accordingly, the size of the decrement in CR strength would grow with successive CS trials, yielding a positively decelerated extinction curve, or at least one that was positively decelerated until the occurrence of a floor effect as CR strength approached zero. It is well established, however, that the curve for Pavlovian extinction is negatively decelerated. Conversely, a constant cs duration, initially briefer than the critical duration, would progressively strengthen the CR, and, by the same logic, would generate a positively accelerated incubation curve, or at least one that was positively accelerated until the influence of a ceiling effect was sufficiently strong. The laboratory data presented by Eysenck (1979) to support the existence of an incubation effect show a negatively accelerated incubation curve (cf. Eysenck’s Figure 3). (5 and 6) Perhaps the most serious drawback of the theory is that it has little predictive power. Prediction of laboratory or clinical outcomes requires a precise (quantitative) specification both - of the critical point and of the way in which key variables (e.g. -UCS intensity, CS duration) determine the net strengthening or weakening effect of CS. Otherwise, all outcomes are susceptible to post-facto and circular interpretation. Clearly the theory has yet to advance to the necessary level of precision. A special problem is posed by the critical point, since the theory suggests that its value is determined in part by personality and other individual difference variables. This could necessitate a separate determination of the critical point for each subject. 8.11 T. I S/l--B

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PHILIP J. BERSH

CONCLUSIONS

Eysenck’s theory of incubation proposes a reasonable basis for an enhancement in the strength of a CR as the result of a. His assumption that a CR (with its accompanying stimuli) may be sufficiently aversive to provide reinforcement of the CS represents a more straightforward and supportable approach than that suggested by Quattelbaum (1970). The latter’s very dubious assumption is that operant (negative) reinforcement of an autonomic CR may occur as the result of CS, because, on such trials, the CR is not followed by (i.e. ‘avoids’) the aversive UCS. However, any theory of incubation must confront the fact that unmistakable evidence for such a phenomenon is very limited. Moreover, certain features of Eysenck’s theory are contraindicated by data. These include the assumptions that the UCS in Pavlovian ‘B’ conditioning must elicit the complere UCR and that the CR must act as a drive. Fortunately, neither of these assumptions is actually important to the theory. The most fundamental requirement is that- CS must elicit CR’s (with accompanying stimuli) which remain sufficiently aversive at CS termination to reinforce the CS despite the intrinsic weakening - effect of withholding the UCS. In other-. words, only the aversive status at the time of CS termination of the CR elicited by the CS IS critical. A more serious defect of the theory - involves its assumptions concerning CR strength as a function of UCS intensity and CS duration in relation to a critical level of strength - (see Figure 1). Such functions determine the net reinforcement or extinction effect of CS. These assumptions lead to the invalid deductions that extinction curves are positiuefy decelerated and incubation curves positioely accelerated. Most problematic for the theory is its lack of predictive power at its present stage of development. Since the outcome of cs is determined by antagonistic reinforcement and extinction processes, and since the theory does not permit a determination in advance of their relative strength, any laboratory or clinical result can be interpreted post-facto, but under the shadow of circularity. At best, the theory suggests qualitative guidelines for arranging conditions under which incubation may be more or less likely to occur. Accordingly, its potential for contribution to an understanding of ‘paradoxical’ failures of extinction, the etiology of neurosis or the effectiveness of therapeutic procedures must remain in doubt. REFERENCES BELLESR., STOKESL. and YOUNGER,M. (1966) Does CS termination

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a critical analysis

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