- Email: [email protected]
The logical requirements for explanations of systematic desensitization
BErlAVlOa THERAPY(1973) 4, 506-514
The Logical Requirements for Explanations of Systematic Desensitization1 IAN M. EVANS University of Hawaii Honolulu, Hawaii 96822 A number of explanations of systematic desensitization have been suggested, each claiming some supportive evidence. The purpose of this paper is not to evaluate this experimental support, but to examine the logical structure of the explanations themselves. Many prove to be no more than loose, metaphorical statements, or models incongruent with clinical desensitization. The extinction explanation seems to have some precision, so the sort of empirical validation it would require is considered in some detail. Extinction as a low-level model is also contrasted with reciprocal inhibition as a higherorder construct for explaining response decrement. It is concluded that greater attention should be given to the formal structure of explanatory propositions so they may more effectively guide relevant research and clinical practice. A f e w years ago E v a n s a n d Wilson (1968) a t t e m p t e d to clarify the confusion of terms s u r r o u n d i n g systematic desensitization. A l t h o u g h m u c h of this confusion seems to continue, the p u r p o s e of the present p a p e r is not to h a r p on terminological issues, b u t to consider the logical status of the various explanations of desensitization that h a v e b e e n proposed. T h e r e are t w o m a i n reasons for b e i n g interested in the logic of desensitization explanations. Firstly, the p r o c e d u r e epitomizes the strategy of a p p l y i n g experimental principles to clinical problems, so that f r o m the s t u d y of desensitization explanations there should e m e r g e metatheoretical issues relevant to other extensions of b e h a v i o r theory. Secondly, increased clarity of explanation is clinically important, most especially w h e n the conventional desensitization t e c h n i q u e has failed, or seems u n d u l y 1 1 am grateful to those graduate students of psychology at the University of Hawaii who read and discussed the manuscript at various stages of its development. This paper constitutes part of a program of research in anxiety control which is being generously supported by the University of Hawaii Research Council. Requests for reprints should be sent to the author at the Psychology Department, the University of Hawaii, 2430 Campus Road, Honolulu, HI 96822. 506 Copyright © 1973 by Academic Press, Inc. All rights of reproduction in any form reserved.
THE LOGIC OF SYSTEMATIC DESENSITIZATION
507
labored, as it is then necessary to have a logical explanatory model to guide further treatment. Much of what currently passes as explanation with reference to desensitization is actually no more than simple politicking--translating the observable phenomena into the construct language of a more general theoretical system (e.g., belief, arousal, reinforcement). While perfectly legitimate as a start, there is a growing acceptance that this activity constitutes rather than antedates an explanation. It is common, for example, for those with an operant bent to interpret desensitization in reinforcement language (Salzinger, 1969; Sherman & Baer, 1969) without specifying the contribution of the various procedural elements. In the absence of these coordinating definitions, such theoretical enterprises are best described as metaphorical rather than explanatory. Most of the cognitive positions on desensitization are equally imprecise. Murray and Jacobson (1971), for instance, state that the critical change is that the patient comes to believe he can cope with the situation of concern. This suggestion might have the beginnings of some interesting hypotheses if the terminology and the proposed sequence of changes were clarified. Until such time the public utterance of these vague notions is out of place--unless their purely pictorial purpose is made explicit. A somewhat more advanced stage has been reached by Wilkins ( 1971 ), who uses the cognitive metaphor to point to aspects of desensitization that might originally have been overlooked or underrated. Davison and Wilson (19'72) have argued that the empirical support for these aspects is less than satisfactory; even so, one wonders what explanatory significance the isolation of variables really has. The discovery of variables related to successful outcome is frequently reckoned to provide explanatory meat somehow juicier than that theretofore served. As one of many possible examples, consider Leitenberg, Agras, Barlow, and Oliveau's study (1969). The subjects who were told that the desensitization was therapy did better than those told they were participating in an experiment on imagination. The latter group showed only marginal change. The authors claimed, with scant regard for logic, that these findings "pose certain problems for reciprocal inhibition conceptions" (p. 113). There are really two objections here, one being that the effect of verbal statements used to interpret the procedure to the subjects has no bearing on reciprocal inhibition. The other objection is to the idea that these interpretive statements have, in themselves, some explanatory significance simply because they enhanced the effect to be explained. Although much of the desensitization research follows this general model of adding or subtracting elements, a guess will be hazarded that the isolation of significant procedural variables will further understanding
508
IAN M. EVANs
only ff their effects are clearly predicted by an explanatory theory (an example will be given later when the kind of prediction arising from the extinction explanation is considered). This is simply an expression of the old necessary-sufllcient distinction. Even if it were shown that a variable is necessary for desensitization to work, the theoretical implications may still be quite trivial. It goes without saying, for instance, that the subject must obey the instructions, attend the sessions, and so forth. By the same reasoning it is to be expected that subjects supposedly participating in an experiment would behave differently to subjects receiving treatment. One is reminded here of Spence's (1956) irritation over tests of his theory that went beyond the boundary conditions specified. A slightly different case of boundary violation occurs when suggested explanations refer to procedures dissimilar to conventional desensitization techniques. Goldfried (1971) has argued that desensitization may be explained as a procedure which teaches the client a general skill for actively reducing anxiety. It has been thought for some time that relaxation training produces broad benefits (Neufeld, 1951), and the enhanced control resulting from specifically induced relaxation might be of special value when one of the stimuli regulating the anxiety is the individual's fear that he might lose control (e.g., Goorney, 1970). As a supplement to desensitization many clinicians instruct their clients in the use of differential relaxation in situations usually eliciting tension. Sympathetic as one might be to Goldfried's idea, however, these general procedures are not part of classical desensitization and thus cannot explain its immediate effects. Any explanation of desensitization must, then, be compatible with both the established procedure and its effect, which leads to the consideration of models as explanatory devices. Failure to appreciate the logic of the model causes much of the confusion evident in explanations of desensitization based on learning theory. Habituation, counter conditioning, or extinction explanations represent no more than the suggestion of an analogy between the clinical procedure and the less complicated experimental procedures described by those labels. The minimum logical requirement for proposing such an analogy is simply similarity in both the procedures and their consequences. Failure to conform in the latter regard makes it possible to rule out Lader and Wing's habituation explanation (Lader & Wing, 1966). The experimental phenomenon called habituation is one in which the response to a repetitive stimulus gradually disappears, only to reappear after rest or stimulus change (Sokolov, 1963). Apparently the stimuli themselves need not be identical as long as there is a predictable sequence (Unger, 1964), so the hierarchical presentation in desensitization can just slip by on that point.
THE LOGIC OF SYSTEMATICDESENSITIZATION
509
It is the phenomenon of dishabituation that is so damaging. The evidence consistently shows a permanent decrement in anxiety following desensitization, thus the habituation model is not appropriate (cf. Van Egeren, 1970). Turning to the counter conditioning explanation, one finds that the analogy breaks down at the level of procedure rather than outcome. Counter conditioning involves the explicit reinforcement of a response other than that no longer being reinforced. In desensitization another response, deep muscle relaxation, is introduced, but it is not specifically associated with the feared stimulus, 2 nor is it specifically reinforced. Whether or not relaxation actually comes to be controlled by the CS will be dependent on the degree to which this control is deliberately fostered by the therapist. At present there are no reports of counter conditioning having been successfully achieved. If counter conditioning could be used effectively to reduce anxiety, the procedure would be beyond the boundaries originally prescribed by Wolpe (1958). Counter conditioning is, in any event, only a special case of extinction. Extinction involves the presentation of a controlling stimulus without reinforcement such that the probability of the controlled response gradually decreases. Desensitization matches this model quite closely, although not as closely as prolonged exposure, or certain varieties of implosion. So at this point criteria much stricter than superficial similarity become involved in judging the model. What is necessary is the establishment of a point-to-point similarity, or correspondence, between the clinical treatment and the learning phenomena thought to be analogous (Oppenheimer, 1956). In the present case this involves two steps. Firstly, as already suggested, analogies must be drawn between the variables in experimental extinction and the supposedly comparable manipulations in desensitization. Weiss (1968) has called this the specification of a dictionary of analogies, or the rules of correspondence. Secondly, the empirical sentences of desensitization should be congruent with the empirical sentences of extinction. Two examples may be given of the attempt to establish correspondence. Eysenck and Beech (1971) have noted that it would be important to know whether massed hierarchy items (which may be considered analogous to the independent variable of massed CS presentation) enhance desensitization's efficacy (analogous to resistance to extinction). They point out, quite rightly, that there are no studies of massing in the true It is convenient to refer to the stimulus that elicits anxiety as the conditioned stimulus (CS), implying only that it is this stimulus which controls the anxiety and not that the anxiety must inevitably have been established by a process of classical conditioningl This is an example of a correspondence rule, to be discussed presently.
510
t~N ~. Ew~rs
sense of reduced inter-trial intervals. Even ff instances were available, the results to be expected are not, unfortunately, very clear-cut. Pavlov's original observation that massed trials speeded extinction was true only of total time to criterion, not number of CS presentations to criterion (Gormezano & Moore, 1969). Other studies have yielded conflicting resuits, perhaps because initial decrement is more rapid under massed trials, but later decrement is more rapid under spaced (Howat & Grant, 1958). If this finding were to be confirmed in the laboratory and reconfirmed clinically, it would constitute a very powerful demonstration that the extinction analogy is appropriate. The second example may be drawn from another important feature of experimental extinction, spontaneous recovery. Between therapeutic sessions (in the rest period) there should be a resurgence of the anxiety if extinction is analogous. Surprisingly, considering its significance, spontaneous recovery has been mentioned only casually in the clinical literature (e.g., Kubany, Sloggett & Evans, 1971; Rachman, 1966). If it can be confirmed that there is a spontaneous recovery effect in desensitization, the extinction model would again be shown most fitting. It is through the systematic elaboration of the correspondence rules and the affirmation of point-to-point similarity that the extinction model for desensitization may be tested. Of course the analogy should be attempted in the inferential sense, not the biological; it would remain a moot point as to whether similar underlying features were involved or not. Perhaps the most productive way to view the analogy is in terms of reproducible behavioral processes. Zimmerman (1968) has provided a detailed argument for preferring reproducible processes to the low-order functional laws questioned earlier. Conceptualizing desensitization as an attempt to reproduce the behavioral decrement observed in the laboratory places an important emphasis on the quantification of relevant variables and their interaction. So far, desensitization research has not been methodologically suitable for determining the predicted empirical sentences. The outcome measure, as a start, should not be dichotomized into success or failure, but should be a continuous measure of anxiety level (response strength). The same is true of the independent variables. Consider the much-debated role of relaxation. If an extinction model were adopted, relaxation could possibly be interpreted as a drive variable--a new 'analogy for the dictionary. There is evidence that anxiety has a drive function for both autonomic and motor responses (Eysenck, 1964; Lader & Wing, 1966; Spence, 1958), so that the lower the drive the smaller will be the anxiety response elicited by a phobic stimulus. Studies comparing desensitization with deep relaxation to desensitization in the normal resting state, describe this arrange-
THE LOGIC OF SYSTEMATIC DESENSITIZATION
511
merit as the presence or absence of relaxation. In fact, the comparison is between two arbitrarily selected points on a continuous scale. Extending this argument one step further, it may be that a given set of relaxation instructions will result in a position on the drive scale which will depend on individual differences in emotional reactivity (e.g., Neuroticism, Eysenck, 1967) and the presence of other drive stimuli (e.g., the problem of relaxing patients who are anxious when reclining in front of the therapist, or when outside their homes). Given that extinction under high drive is protracted, it is possible to predict that as the strength of the phasic response (anxiety) becomes greater, so the relative importance of the drive variable (tonic level of relaxation-tension) increases progressively. In practical terms, the importance of relaxation may prove to be dependent upon the strength of the phobic anxiety, the stability of the patient, and the degree of anxiety aroused in the treatment setting. The purpose of this speculation is to show how the extinction mode/ suggests quite complicated interactions between parameters. Learning principles tel1 us something about the importance of numerous variables in extinction that might be considered when exploring desensitization. In order to make the extinction interpretation convincing, parametric studies are called for, just as Weiss has so successfully used the principles of correspondence in explaining social behavior by learning models (Weiss, 1968; Weiss& Miller, 1971). It is not clear why this strategy has been missed in behavior therapy research--perhaps on account of the expounded virtues of technique-oriented factorial research designs (Paul, 1969). Even at the applied level it is the parametric studies that are going to be of crucial import---suggesting how to arrange all variables so that extinction will be most rapid, and what to adjust in the event that progress is slow. Furthermore, by knowing a good deal about interactions among variables in learning research, it should be possible to deduce similar but as yet unknown relationships in the clinical situation. In this way the simple analogy attains its explanatory power. Assuming the analogy between desensitization and extinction proves useful, the higher-order explanation of the former would be encompassed by the explanation of the latter. While intellectually desirable, there would be little to gain clinically from the explanation of extinction. Yet it is at this level that much of the debate has taken place--over the bugbear of desensitization explanations, reciprocal inhibition. Wolpe's (1958) theory of desensitization fits into this higher-order category, as he modified Hull's (1943) theory of extinction by introducing reciprocal inhibition as an additional construct. The best place to test this theory is in the controlled laboratory setting; this has not yet been done. Nevertheless,
512
IAN M. EVANS
the reciprocal inhibition construct has been criticized in the literature, hence the need to comment on its logical status. Wolpe's theory shares, understandably, the internal logical problems of the Hullian explanation of extinction. On the other hand Hull's is one of the few extant theories of extinction available. If Jones's (1958) revision were accepted, and reciprocal inhibition substituted for reactive inhibition, then physiological states supposedly antagonistic to anxiety (sexual arousal, anger, digestive activity, relaxation) would subtract from the anxiety drive, and the conditioned inhibition from the positive habit. There is a good deal of supportive evidence for the first of these components (Gellhorn, 1967). The second component seems to have caused the greatest confusion, probably because conditioned inhibition in Hullian theory is a within-response construct (as is habit), whereas it is often interpreted as a competing response. It is clearly difficult to show the operation of a negative habit tendency, but renewed interest in inhibitory tendencies has resulted in their recent empirical demonstration (Hearst, 1969; Rescorla & LoLordo, 1965). In the absence of critical tests of reciprocal inhibition there is little more to be said, except to reaffirm its historical importance. For although the theory has been a decided red-herring for contemporary experimentalists, in the hands of its originator it has been extremely productive. It is not the way of science to attempt the dismissal of this possible explanation by simple disputation (Wilson & Davison, 1971). In concluding, it should be emphasized that the purpose of this paper is not to defend or criticize or review the evidence for any particular explanation of desensitization. Rather, it is a plea for greater concern over the logical structure of any explanation proffered. More attention has been paid the extinction explanation than any of the others because the extinction model has some precision and deployability--characteristics which are absent in the other explanations. Another reason, however, for focussing on extinction is that as a model, or analogy, its logic seems to be frequently misunderstood. As a result, the experimental literature is difficult to assimilate and is clinically unconstrnctive, particularly when one attempts to modify the desensitization procedure for the individual patient. Careful research should be supported by precision and logic in theory if explanations are to emerge that will provide the clinician with a rationale for his activities--and a rational basis for improving them. REFERENCES DAVISON,G. C., & WILSON,G. T. Critique of "Desensitization: social and cognitive factors underlying the effectiveness of Wolpe's procedure." Psychological Bulletin, 1972, 78, 28--31,
THE LOGIC OF SYSTEMATIC DESENSITIZATION
513
EVANS, I., & WILSON, T. Note on the terminological confusion surrounding systematic desensitization. Psychological Reports, 1968, 22, 187-191. EYSENCK, H. J. (Ed.) Experiments in motivation. Oxford: Pergamon, 1964. EYSENCK, H. J. The biological basis of personality. Springfield, Ill.: Thomas, 1967. EYSENCK, H. J., & BEECH, R. Counterconditioning and related methods. In A. E. Bergin & S. L. Garfield ( Eds. ), Handbook of psychotherapy and behavior change: an empirical analysis. New York: Wiley, 1971. Pp. 543--611. GELI~IOnN, E. Principles of autonomic-somatic integrations: physiological basis and psychological and clinical implications. Minneapolis: University of Minnesota Press, 1967. GOLDFRIED, M. R. Systematic desensitization as training in self-control. Journal of Consulting and Clinical Psychology, 1971, 37, 228-234. GOORNEY, A. B. Treatment of aviation phobias by behaviour therapy. British Journal of Psychiatry, 1970, 117, 535-544. GOnMEZANO, I., & MOOnE, J. W. Classical conditioning: empirical relationships. In M. H. Marx (Ed.), Learning: Processes. London: Macmillan, 1969. Pp. 133-168. HEARST, E. Excitation, inhibition and discrimination learning. In N. J. Mackintosh & W. K. Honig (Eds.), Fundamental issues in associative learning. Halifax: Dalhousie University Press, 1969. Pp. 1--41. HOWAT, H. G., & GRANT, D. A. Influence of intertrial interval during extinction on spontaneous recovery of conditioned eyelid responses. Journal of Experimental Psychology, 1958, 56, 11-15. HULL, C. L. Principles of behavior. New York: Appleton-Century-Crofts, 1943. JONES, H. G. The status of inhibition in Hull's system: a theoretical revision. Psychological Review, 1958, 65, 179-182. KU~ANY, E. S., SLOC~ETT, B. B., & EVANS, I. M. A clinical research model for the practice of individual psychotherapy. Paper presented at the meeting of the Hawaii Psychological Association, Honolulu, May, 1971. LADEla, M. H., & WINe, L. Psychological measures, sedative drugs and morbid anxiety. Oxford: Oxford University Press, 1966. LEITENBEnC, H., AcnAs, W. S., BAnLOW, D. H., & OLIVEAtr, D. C. Contribution of selective positive reinforcement and therapeutic instructions to systematic desensitization therapy. Journal of Abnormal Psychology, 1969, 74, 113-118. MummY, E. J., & JACOBSON,L. I. The nature of learning in traditional and behavioral psychotherapy. In A. E. Bergin & S. L. Garfield (Eds.), Handbook of psychotherapy and behavior change: An empirical analysis. New York: Wiley, 1971. Pp. 709-747. NEtrEELD, W. Re]axation methods in U. S. Navy Air Schools. American ]ournal of Psychiatry, 1951, 108, 132-137. OPI~ENHEIMEI~, R. Analogy in science. American Psychologist, 1956, 11, 127-135. PatrL, G. L. Behavior modification research: design and tactics. In C. M. Franks (Ed.), Behavior therapy: Appraisal and status. New York: McGraw-Hill, 1969. Pp. 2962. RACHMAN, S. Studies in desensitization: III. Speed of generalization. Behaviour Research and Therapy, 1966, 4~ 7-15. RESCORLA, R. A., & LoLomJo, V. M. Inhibition of avoidance behavior. Journal of Comparative and Physiological Psychology, 1965, 59, 406--412. SALZlNGEa, K. The place of operant conditioning of verbal behavior in psychotherapy. In C. M. Franks (Ed.), Behavior therapy: Appraisal and status. New York: McGraw-Hill, 1969. Pp. 375--395.
514
~N
M. EV.~NS
SrmaMA~r, J. A., & BuR, D. M. Appraisal of operant therapy techniques with children and adults. In C. M. Franks (Ed.), Behavior therapy: Appraisal and status. New York: McGraw-Hill, 1969. Pp. 192-219. SOKOLOV, Y. N. Perception and the conditioned reflex. (Trans. by S. W. Waydenfeld) Oxford: Pergamon, 1963. SPENCE, K. W. Behavior theory and conditioning. New Haven: Yale University Press, 1956. SPENCE, K. W. A theory of emotionally based drive ( D ) and its relation to performance in simple learning situations. Ame~can Psychologist, 1958, 1 3 , 131141. UNGER, S. M. Habituation of the vasoconstrictive orienting reaction. Journal of Experimental Psychology, 1964, 67, 11-18. V.~'q ECERm'q, L. F. Psychophysiology of systematic desensitization: the habituation model. Journal of Behavior Therapy and Experimental Psychiatry, 1970, 1, 249255. WEiss, R. F. An extension of Hullian learning theory to persuasive communication. In A. G. Greenwald, T, Brock, & T. Ostrom (Eds.), Psychological foundations of attitudes. New York: Academic Press, 1968. WEiss, R. F., & Mmn~R, F. G. The drive theory of social facilitation. Psychological Review, 1971, 78, 44-57. WJr.~rlrqS, W. Desensitization: social and cognitive factors underlying the effectiveness of Wolpe's procedure. Psychological Bulletin, 1971, 76, 311-317. WmsoN, G. T., & DAwsoN, G. C. Processes of fear reduction in systematic desensitization: animal studies. Psychological Bulletin, 1971, 76, 1-14. WoLPv., J. Psychotherapy by reciprocal inhibition. Stanford: Stanford University Press, 1958. ZIMM~a~AN, D. W. Functional laws and reproducible processes in behavior. Psychological Record, 1963, 13, 163-173.
The Logical Requirements for Explanations of Systematic Desensitization1 IAN M. EVANS University of Hawaii Honolulu, Hawaii 96822 A number of explanations of systematic desensitization have been suggested, each claiming some supportive evidence. The purpose of this paper is not to evaluate this experimental support, but to examine the logical structure of the explanations themselves. Many prove to be no more than loose, metaphorical statements, or models incongruent with clinical desensitization. The extinction explanation seems to have some precision, so the sort of empirical validation it would require is considered in some detail. Extinction as a low-level model is also contrasted with reciprocal inhibition as a higherorder construct for explaining response decrement. It is concluded that greater attention should be given to the formal structure of explanatory propositions so they may more effectively guide relevant research and clinical practice. A f e w years ago E v a n s a n d Wilson (1968) a t t e m p t e d to clarify the confusion of terms s u r r o u n d i n g systematic desensitization. A l t h o u g h m u c h of this confusion seems to continue, the p u r p o s e of the present p a p e r is not to h a r p on terminological issues, b u t to consider the logical status of the various explanations of desensitization that h a v e b e e n proposed. T h e r e are t w o m a i n reasons for b e i n g interested in the logic of desensitization explanations. Firstly, the p r o c e d u r e epitomizes the strategy of a p p l y i n g experimental principles to clinical problems, so that f r o m the s t u d y of desensitization explanations there should e m e r g e metatheoretical issues relevant to other extensions of b e h a v i o r theory. Secondly, increased clarity of explanation is clinically important, most especially w h e n the conventional desensitization t e c h n i q u e has failed, or seems u n d u l y 1 1 am grateful to those graduate students of psychology at the University of Hawaii who read and discussed the manuscript at various stages of its development. This paper constitutes part of a program of research in anxiety control which is being generously supported by the University of Hawaii Research Council. Requests for reprints should be sent to the author at the Psychology Department, the University of Hawaii, 2430 Campus Road, Honolulu, HI 96822. 506 Copyright © 1973 by Academic Press, Inc. All rights of reproduction in any form reserved.
THE LOGIC OF SYSTEMATIC DESENSITIZATION
507
labored, as it is then necessary to have a logical explanatory model to guide further treatment. Much of what currently passes as explanation with reference to desensitization is actually no more than simple politicking--translating the observable phenomena into the construct language of a more general theoretical system (e.g., belief, arousal, reinforcement). While perfectly legitimate as a start, there is a growing acceptance that this activity constitutes rather than antedates an explanation. It is common, for example, for those with an operant bent to interpret desensitization in reinforcement language (Salzinger, 1969; Sherman & Baer, 1969) without specifying the contribution of the various procedural elements. In the absence of these coordinating definitions, such theoretical enterprises are best described as metaphorical rather than explanatory. Most of the cognitive positions on desensitization are equally imprecise. Murray and Jacobson (1971), for instance, state that the critical change is that the patient comes to believe he can cope with the situation of concern. This suggestion might have the beginnings of some interesting hypotheses if the terminology and the proposed sequence of changes were clarified. Until such time the public utterance of these vague notions is out of place--unless their purely pictorial purpose is made explicit. A somewhat more advanced stage has been reached by Wilkins ( 1971 ), who uses the cognitive metaphor to point to aspects of desensitization that might originally have been overlooked or underrated. Davison and Wilson (19'72) have argued that the empirical support for these aspects is less than satisfactory; even so, one wonders what explanatory significance the isolation of variables really has. The discovery of variables related to successful outcome is frequently reckoned to provide explanatory meat somehow juicier than that theretofore served. As one of many possible examples, consider Leitenberg, Agras, Barlow, and Oliveau's study (1969). The subjects who were told that the desensitization was therapy did better than those told they were participating in an experiment on imagination. The latter group showed only marginal change. The authors claimed, with scant regard for logic, that these findings "pose certain problems for reciprocal inhibition conceptions" (p. 113). There are really two objections here, one being that the effect of verbal statements used to interpret the procedure to the subjects has no bearing on reciprocal inhibition. The other objection is to the idea that these interpretive statements have, in themselves, some explanatory significance simply because they enhanced the effect to be explained. Although much of the desensitization research follows this general model of adding or subtracting elements, a guess will be hazarded that the isolation of significant procedural variables will further understanding
508
IAN M. EVANs
only ff their effects are clearly predicted by an explanatory theory (an example will be given later when the kind of prediction arising from the extinction explanation is considered). This is simply an expression of the old necessary-sufllcient distinction. Even if it were shown that a variable is necessary for desensitization to work, the theoretical implications may still be quite trivial. It goes without saying, for instance, that the subject must obey the instructions, attend the sessions, and so forth. By the same reasoning it is to be expected that subjects supposedly participating in an experiment would behave differently to subjects receiving treatment. One is reminded here of Spence's (1956) irritation over tests of his theory that went beyond the boundary conditions specified. A slightly different case of boundary violation occurs when suggested explanations refer to procedures dissimilar to conventional desensitization techniques. Goldfried (1971) has argued that desensitization may be explained as a procedure which teaches the client a general skill for actively reducing anxiety. It has been thought for some time that relaxation training produces broad benefits (Neufeld, 1951), and the enhanced control resulting from specifically induced relaxation might be of special value when one of the stimuli regulating the anxiety is the individual's fear that he might lose control (e.g., Goorney, 1970). As a supplement to desensitization many clinicians instruct their clients in the use of differential relaxation in situations usually eliciting tension. Sympathetic as one might be to Goldfried's idea, however, these general procedures are not part of classical desensitization and thus cannot explain its immediate effects. Any explanation of desensitization must, then, be compatible with both the established procedure and its effect, which leads to the consideration of models as explanatory devices. Failure to appreciate the logic of the model causes much of the confusion evident in explanations of desensitization based on learning theory. Habituation, counter conditioning, or extinction explanations represent no more than the suggestion of an analogy between the clinical procedure and the less complicated experimental procedures described by those labels. The minimum logical requirement for proposing such an analogy is simply similarity in both the procedures and their consequences. Failure to conform in the latter regard makes it possible to rule out Lader and Wing's habituation explanation (Lader & Wing, 1966). The experimental phenomenon called habituation is one in which the response to a repetitive stimulus gradually disappears, only to reappear after rest or stimulus change (Sokolov, 1963). Apparently the stimuli themselves need not be identical as long as there is a predictable sequence (Unger, 1964), so the hierarchical presentation in desensitization can just slip by on that point.
THE LOGIC OF SYSTEMATICDESENSITIZATION
509
It is the phenomenon of dishabituation that is so damaging. The evidence consistently shows a permanent decrement in anxiety following desensitization, thus the habituation model is not appropriate (cf. Van Egeren, 1970). Turning to the counter conditioning explanation, one finds that the analogy breaks down at the level of procedure rather than outcome. Counter conditioning involves the explicit reinforcement of a response other than that no longer being reinforced. In desensitization another response, deep muscle relaxation, is introduced, but it is not specifically associated with the feared stimulus, 2 nor is it specifically reinforced. Whether or not relaxation actually comes to be controlled by the CS will be dependent on the degree to which this control is deliberately fostered by the therapist. At present there are no reports of counter conditioning having been successfully achieved. If counter conditioning could be used effectively to reduce anxiety, the procedure would be beyond the boundaries originally prescribed by Wolpe (1958). Counter conditioning is, in any event, only a special case of extinction. Extinction involves the presentation of a controlling stimulus without reinforcement such that the probability of the controlled response gradually decreases. Desensitization matches this model quite closely, although not as closely as prolonged exposure, or certain varieties of implosion. So at this point criteria much stricter than superficial similarity become involved in judging the model. What is necessary is the establishment of a point-to-point similarity, or correspondence, between the clinical treatment and the learning phenomena thought to be analogous (Oppenheimer, 1956). In the present case this involves two steps. Firstly, as already suggested, analogies must be drawn between the variables in experimental extinction and the supposedly comparable manipulations in desensitization. Weiss (1968) has called this the specification of a dictionary of analogies, or the rules of correspondence. Secondly, the empirical sentences of desensitization should be congruent with the empirical sentences of extinction. Two examples may be given of the attempt to establish correspondence. Eysenck and Beech (1971) have noted that it would be important to know whether massed hierarchy items (which may be considered analogous to the independent variable of massed CS presentation) enhance desensitization's efficacy (analogous to resistance to extinction). They point out, quite rightly, that there are no studies of massing in the true It is convenient to refer to the stimulus that elicits anxiety as the conditioned stimulus (CS), implying only that it is this stimulus which controls the anxiety and not that the anxiety must inevitably have been established by a process of classical conditioningl This is an example of a correspondence rule, to be discussed presently.
510
t~N ~. Ew~rs
sense of reduced inter-trial intervals. Even ff instances were available, the results to be expected are not, unfortunately, very clear-cut. Pavlov's original observation that massed trials speeded extinction was true only of total time to criterion, not number of CS presentations to criterion (Gormezano & Moore, 1969). Other studies have yielded conflicting resuits, perhaps because initial decrement is more rapid under massed trials, but later decrement is more rapid under spaced (Howat & Grant, 1958). If this finding were to be confirmed in the laboratory and reconfirmed clinically, it would constitute a very powerful demonstration that the extinction analogy is appropriate. The second example may be drawn from another important feature of experimental extinction, spontaneous recovery. Between therapeutic sessions (in the rest period) there should be a resurgence of the anxiety if extinction is analogous. Surprisingly, considering its significance, spontaneous recovery has been mentioned only casually in the clinical literature (e.g., Kubany, Sloggett & Evans, 1971; Rachman, 1966). If it can be confirmed that there is a spontaneous recovery effect in desensitization, the extinction model would again be shown most fitting. It is through the systematic elaboration of the correspondence rules and the affirmation of point-to-point similarity that the extinction model for desensitization may be tested. Of course the analogy should be attempted in the inferential sense, not the biological; it would remain a moot point as to whether similar underlying features were involved or not. Perhaps the most productive way to view the analogy is in terms of reproducible behavioral processes. Zimmerman (1968) has provided a detailed argument for preferring reproducible processes to the low-order functional laws questioned earlier. Conceptualizing desensitization as an attempt to reproduce the behavioral decrement observed in the laboratory places an important emphasis on the quantification of relevant variables and their interaction. So far, desensitization research has not been methodologically suitable for determining the predicted empirical sentences. The outcome measure, as a start, should not be dichotomized into success or failure, but should be a continuous measure of anxiety level (response strength). The same is true of the independent variables. Consider the much-debated role of relaxation. If an extinction model were adopted, relaxation could possibly be interpreted as a drive variable--a new 'analogy for the dictionary. There is evidence that anxiety has a drive function for both autonomic and motor responses (Eysenck, 1964; Lader & Wing, 1966; Spence, 1958), so that the lower the drive the smaller will be the anxiety response elicited by a phobic stimulus. Studies comparing desensitization with deep relaxation to desensitization in the normal resting state, describe this arrange-
THE LOGIC OF SYSTEMATIC DESENSITIZATION
511
merit as the presence or absence of relaxation. In fact, the comparison is between two arbitrarily selected points on a continuous scale. Extending this argument one step further, it may be that a given set of relaxation instructions will result in a position on the drive scale which will depend on individual differences in emotional reactivity (e.g., Neuroticism, Eysenck, 1967) and the presence of other drive stimuli (e.g., the problem of relaxing patients who are anxious when reclining in front of the therapist, or when outside their homes). Given that extinction under high drive is protracted, it is possible to predict that as the strength of the phasic response (anxiety) becomes greater, so the relative importance of the drive variable (tonic level of relaxation-tension) increases progressively. In practical terms, the importance of relaxation may prove to be dependent upon the strength of the phobic anxiety, the stability of the patient, and the degree of anxiety aroused in the treatment setting. The purpose of this speculation is to show how the extinction mode/ suggests quite complicated interactions between parameters. Learning principles tel1 us something about the importance of numerous variables in extinction that might be considered when exploring desensitization. In order to make the extinction interpretation convincing, parametric studies are called for, just as Weiss has so successfully used the principles of correspondence in explaining social behavior by learning models (Weiss, 1968; Weiss& Miller, 1971). It is not clear why this strategy has been missed in behavior therapy research--perhaps on account of the expounded virtues of technique-oriented factorial research designs (Paul, 1969). Even at the applied level it is the parametric studies that are going to be of crucial import---suggesting how to arrange all variables so that extinction will be most rapid, and what to adjust in the event that progress is slow. Furthermore, by knowing a good deal about interactions among variables in learning research, it should be possible to deduce similar but as yet unknown relationships in the clinical situation. In this way the simple analogy attains its explanatory power. Assuming the analogy between desensitization and extinction proves useful, the higher-order explanation of the former would be encompassed by the explanation of the latter. While intellectually desirable, there would be little to gain clinically from the explanation of extinction. Yet it is at this level that much of the debate has taken place--over the bugbear of desensitization explanations, reciprocal inhibition. Wolpe's (1958) theory of desensitization fits into this higher-order category, as he modified Hull's (1943) theory of extinction by introducing reciprocal inhibition as an additional construct. The best place to test this theory is in the controlled laboratory setting; this has not yet been done. Nevertheless,
512
IAN M. EVANS
the reciprocal inhibition construct has been criticized in the literature, hence the need to comment on its logical status. Wolpe's theory shares, understandably, the internal logical problems of the Hullian explanation of extinction. On the other hand Hull's is one of the few extant theories of extinction available. If Jones's (1958) revision were accepted, and reciprocal inhibition substituted for reactive inhibition, then physiological states supposedly antagonistic to anxiety (sexual arousal, anger, digestive activity, relaxation) would subtract from the anxiety drive, and the conditioned inhibition from the positive habit. There is a good deal of supportive evidence for the first of these components (Gellhorn, 1967). The second component seems to have caused the greatest confusion, probably because conditioned inhibition in Hullian theory is a within-response construct (as is habit), whereas it is often interpreted as a competing response. It is clearly difficult to show the operation of a negative habit tendency, but renewed interest in inhibitory tendencies has resulted in their recent empirical demonstration (Hearst, 1969; Rescorla & LoLordo, 1965). In the absence of critical tests of reciprocal inhibition there is little more to be said, except to reaffirm its historical importance. For although the theory has been a decided red-herring for contemporary experimentalists, in the hands of its originator it has been extremely productive. It is not the way of science to attempt the dismissal of this possible explanation by simple disputation (Wilson & Davison, 1971). In concluding, it should be emphasized that the purpose of this paper is not to defend or criticize or review the evidence for any particular explanation of desensitization. Rather, it is a plea for greater concern over the logical structure of any explanation proffered. More attention has been paid the extinction explanation than any of the others because the extinction model has some precision and deployability--characteristics which are absent in the other explanations. Another reason, however, for focussing on extinction is that as a model, or analogy, its logic seems to be frequently misunderstood. As a result, the experimental literature is difficult to assimilate and is clinically unconstrnctive, particularly when one attempts to modify the desensitization procedure for the individual patient. Careful research should be supported by precision and logic in theory if explanations are to emerge that will provide the clinician with a rationale for his activities--and a rational basis for improving them. REFERENCES DAVISON,G. C., & WILSON,G. T. Critique of "Desensitization: social and cognitive factors underlying the effectiveness of Wolpe's procedure." Psychological Bulletin, 1972, 78, 28--31,
THE LOGIC OF SYSTEMATIC DESENSITIZATION
513
EVANS, I., & WILSON, T. Note on the terminological confusion surrounding systematic desensitization. Psychological Reports, 1968, 22, 187-191. EYSENCK, H. J. (Ed.) Experiments in motivation. Oxford: Pergamon, 1964. EYSENCK, H. J. The biological basis of personality. Springfield, Ill.: Thomas, 1967. EYSENCK, H. J., & BEECH, R. Counterconditioning and related methods. In A. E. Bergin & S. L. Garfield ( Eds. ), Handbook of psychotherapy and behavior change: an empirical analysis. New York: Wiley, 1971. Pp. 543--611. GELI~IOnN, E. Principles of autonomic-somatic integrations: physiological basis and psychological and clinical implications. Minneapolis: University of Minnesota Press, 1967. GOLDFRIED, M. R. Systematic desensitization as training in self-control. Journal of Consulting and Clinical Psychology, 1971, 37, 228-234. GOORNEY, A. B. Treatment of aviation phobias by behaviour therapy. British Journal of Psychiatry, 1970, 117, 535-544. GOnMEZANO, I., & MOOnE, J. W. Classical conditioning: empirical relationships. In M. H. Marx (Ed.), Learning: Processes. London: Macmillan, 1969. Pp. 133-168. HEARST, E. Excitation, inhibition and discrimination learning. In N. J. Mackintosh & W. K. Honig (Eds.), Fundamental issues in associative learning. Halifax: Dalhousie University Press, 1969. Pp. 1--41. HOWAT, H. G., & GRANT, D. A. Influence of intertrial interval during extinction on spontaneous recovery of conditioned eyelid responses. Journal of Experimental Psychology, 1958, 56, 11-15. HULL, C. L. Principles of behavior. New York: Appleton-Century-Crofts, 1943. JONES, H. G. The status of inhibition in Hull's system: a theoretical revision. Psychological Review, 1958, 65, 179-182. KU~ANY, E. S., SLOC~ETT, B. B., & EVANS, I. M. A clinical research model for the practice of individual psychotherapy. Paper presented at the meeting of the Hawaii Psychological Association, Honolulu, May, 1971. LADEla, M. H., & WINe, L. Psychological measures, sedative drugs and morbid anxiety. Oxford: Oxford University Press, 1966. LEITENBEnC, H., AcnAs, W. S., BAnLOW, D. H., & OLIVEAtr, D. C. Contribution of selective positive reinforcement and therapeutic instructions to systematic desensitization therapy. Journal of Abnormal Psychology, 1969, 74, 113-118. MummY, E. J., & JACOBSON,L. I. The nature of learning in traditional and behavioral psychotherapy. In A. E. Bergin & S. L. Garfield (Eds.), Handbook of psychotherapy and behavior change: An empirical analysis. New York: Wiley, 1971. Pp. 709-747. NEtrEELD, W. Re]axation methods in U. S. Navy Air Schools. American ]ournal of Psychiatry, 1951, 108, 132-137. OPI~ENHEIMEI~, R. Analogy in science. American Psychologist, 1956, 11, 127-135. PatrL, G. L. Behavior modification research: design and tactics. In C. M. Franks (Ed.), Behavior therapy: Appraisal and status. New York: McGraw-Hill, 1969. Pp. 2962. RACHMAN, S. Studies in desensitization: III. Speed of generalization. Behaviour Research and Therapy, 1966, 4~ 7-15. RESCORLA, R. A., & LoLomJo, V. M. Inhibition of avoidance behavior. Journal of Comparative and Physiological Psychology, 1965, 59, 406--412. SALZlNGEa, K. The place of operant conditioning of verbal behavior in psychotherapy. In C. M. Franks (Ed.), Behavior therapy: Appraisal and status. New York: McGraw-Hill, 1969. Pp. 375--395.
514
~N
M. EV.~NS
SrmaMA~r, J. A., & BuR, D. M. Appraisal of operant therapy techniques with children and adults. In C. M. Franks (Ed.), Behavior therapy: Appraisal and status. New York: McGraw-Hill, 1969. Pp. 192-219. SOKOLOV, Y. N. Perception and the conditioned reflex. (Trans. by S. W. Waydenfeld) Oxford: Pergamon, 1963. SPENCE, K. W. Behavior theory and conditioning. New Haven: Yale University Press, 1956. SPENCE, K. W. A theory of emotionally based drive ( D ) and its relation to performance in simple learning situations. Ame~can Psychologist, 1958, 1 3 , 131141. UNGER, S. M. Habituation of the vasoconstrictive orienting reaction. Journal of Experimental Psychology, 1964, 67, 11-18. V.~'q ECERm'q, L. F. Psychophysiology of systematic desensitization: the habituation model. Journal of Behavior Therapy and Experimental Psychiatry, 1970, 1, 249255. WEiss, R. F. An extension of Hullian learning theory to persuasive communication. In A. G. Greenwald, T, Brock, & T. Ostrom (Eds.), Psychological foundations of attitudes. New York: Academic Press, 1968. WEiss, R. F., & Mmn~R, F. G. The drive theory of social facilitation. Psychological Review, 1971, 78, 44-57. WJr.~rlrqS, W. Desensitization: social and cognitive factors underlying the effectiveness of Wolpe's procedure. Psychological Bulletin, 1971, 76, 311-317. WmsoN, G. T., & DAwsoN, G. C. Processes of fear reduction in systematic desensitization: animal studies. Psychological Bulletin, 1971, 76, 1-14. WoLPv., J. Psychotherapy by reciprocal inhibition. Stanford: Stanford University Press, 1958. ZIMM~a~AN, D. W. Functional laws and reproducible processes in behavior. Psychological Record, 1963, 13, 163-173.