Psychophysiological aspects of systematic desensitization: Some outstanding issues

Bchav. Res. & Therapy, 1971. Vol. 9, pp. 65 to 77. Pergamon Press. Printed in England

PSYCHOPHYSIOLOGICAL ASPECTS OF SYSTEMATIC DESENSITIZATION: SOME OUTSTANDING ISSUES* LAWRENCE F. VAN EGEREN Department

of Psychiatry, Duke University Medical Center, Durham, North Carolina, U.S.A. (Received 3 August 1970)

Summary-Nine psychophysiological propositions generated by systematic desensitization theory were examined in the light of recent research. Four propositions were substantially contirmed, four partially con6rrned and one was not confirmed. Facts reviewed did no agree with the prediction from desensitization theory that less threatening stimuli decondition faster than more threatening stimuli. With the exception noted above, desensitization theory was generally supported. A scheme for distinguishing four types of autonomic response change (habituation, reciprocal inhibition, counterconditioning and extinction) was presented.

desensitization is the method for reducing phobic anxiety developed originally by Wolpe (1958). The essential elements of the method are that ordered phobic scenes are presented repeatedly to the patient’s imagination while he is in a deeply relaxed state.? This set of operations is believed to lead to synaptic changes in neural circuitry mediating phobias and to a reduction in intensity of phobic behavior and phobic anxiety (Wolpe, 1966). The four elements also contain the source of many fundamentally important psychophysiological propositions. Desensitization treatment as customarily practiced was originally supported by classical neurophysiology and the early conception of habituation of spinal reflexes; according to Sherrington (1906, p. 220), “ . . . a spinal reflex under continuous excitation or frequent repetition becomes weaker and may cease altogether . . . . spinal reflexes fade out sooner under a weak stimulus than under a strong one”. Sherrington’s view of habituation can be generalized to higher nervous system functions. When supraspinal neural units are excited repeatedly by weak stimuli the neural response tends to decay exponentially (Thompson and Spencer, 1966). The key to quick adaptation of most nervous system responses has been monotonous repetition of weak stimuli. If anxiety is defined broadly as sympatheticdominated autonomic nervous system activity (Wolpe, 1966), monotonous repetition of weak phobic stimuli would appear to be a rational way of reducing it, in that its operations are those producing rapid habituation of most neural responses. Use of the hierarchical order of presenting phobic stimuli and muscle relaxation in desensitization would help satisfy the conditions of weak stimuli and mild nervous system response for maximum (rapid) habituation. The theme of this paper is that while a number of psychophysiological studies (Geer, 1966 ; Grings and Uno, 1968 ; Grossberg and Wilson, 1968 ; Lader, Gelder and Marks, 1967 ; Lang, in press; Lang, Melamed and Hart, in press ; Paul, 1969 ; Van Egeren, Feather SYSTEMATIC

* This research was supported by National Institute of Mental Health, Grant MH 0839445. t We shall ignore for the moment that Wolpe sometimes uses counterconditioning agents other than relaxation. 65

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LAWRENCE F. VAN EG@ZEN

and Hein, in press) partially support desensitization theory as originally conceived, the precise physiological mechanisms of change are largely unknown and are unlikely to be identical with mechanisms for physiological habituation. Desensitization appears to involve, physiologically, a set of loosely integrated reflexes, each potentially subject to different sources of autonomic regulation and types, and perhaps mechanisms, of change. The need to expand the traditional conditioned stimulus (phobic situation)-conditioned response (excessive sympathetic reaction) model will be suggested. A CLARIFICATION

OF LANGUAGE

As Lader and Mathews (1968) have pointed out, terminology in desensitization has been confusing. Four terms (reciprocal inhibition, habituation, counterconditioning and extinction) particularly need clarification, and such clarification is relevant to a physiological analysis. Two dimensions of response plasticity which are important in neurophysiology and systematic desensitization are the permanence of the alteration in function and whether that alteration was aided by antagonistic inhibition. We suggest that the four predominant types of response plasticity in desensitization can be ordered on a surface formed by these two dimensions (Fig. 1). This system embodies a two-way distinction between response changes which are (a) enduring (extinction, counterconditioning) or temporary (reciprocal inhibition, habituation) and (b) occurred in the presence (reciprocal inhibition, counterconditioning) or absence (habituation, extinction) of (presumed, operationally controlled) antagonistic inhibition. It is assumed that antagonistic inhibition and stability of change are finite continuous, rather than discrete, dimensions and that reciprocal inhibition, habituation, counterconditioning and extinction are change phenomena lying at their extrema.

INHIBITION

ANTAGONISTIC l

-

Counterconditionin:

Reciprocal Inhibition

1

I

b LONG-TERM

SHORT-TERM

;obituotion ANTAGONISTIC

Extinction INHIBITION

0

ABSENT

FIG. 1. Autonomic

inhibition,

change surface. Four types of autonomic response plasticity (reciprocal habituation, counterconditioning and extinction) are represented as extrema on two dimensions (permanence of change and antagonistic inhibition).

In classical neurophysiology (Sherrington, 1906) the term reciprocal inhibition was applied to momentary, readily reversible inhibition of one nerve process by another, e.g.

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inhibition between antagonistic skeletal muscles. Habituation (Harris, 1943; Thompson and Spencer, 1966) refers- to response reductions resulting from repetition of constant stimulating conditions and partial or complete recovery of response amplitude when these conditions are interrupted and then reapplied. Habituation is an important, widespread phenomenon in the nervous system, observable at various levels of the nerval axis. While relatively long-term habituation has been reported (Thorpe, 1956) and has not always been distinguished from extinction (Hernandez-Peon, 1960), there is sufficient reason, owing to differences in parametric characteristics and postulated differences in underlying mechanisms (Sokolov, 1963, orientation reaction; Sharpless and Jasper, 1956, EEG arousal reaction), to distinguish between short- term and long-term adaptation processes, even though the distinction is necessarily some-what arbitrary. One of the distinguishing characteristics of habituation is its reversibility, while extinction usually implies greater stability of the response change, i.e. a true demonstration of negative learning. Counterconditioning implies further that some relatively stable change in function depended upon the prior occurrence of some process which antagonistically inhibited the diminished reaction. It would be of considerable importance to be able to say that autonomic reactions during desensitization habituate (e.g. like the flexion reflex in cat). Because a great deal is known about habituation, the above identification could increase considerably our understanding of physiological changes, and perhaps some of the major mechanisms of action, in desensitization. The first step is to determine the types of changes that may occur in desensitization (e.g. Fig. 1) and to carefully study their characteristic parametric relations. These can then be compared with similar parametric features of physiological habituation (nine have been listed by Thompson and Spencer, 1966). It is important to bear in mind that habituation is only one of the major types of physiological change that may occur in desensitization. SOME CENTRAL QUESTIONS From a psychophysiological point of view traditional desensitization therapy has raised a number of fundamentally important propositions: 1. Subjective anxiety is coupled with sympathetic nervous system activity. Some form of visceral or activational theory of emotion is implied. 2. Hallucination (imagination) of a phobic situation is a sufficient input condition for sympathetic activation. 3. Strength of the sympathetic response is proportional to the strength of stimulating conditions. (Principle of stimulus strength.) 4. Repeated imagination of weak phobic scenes gives rise to a gradually diminishing sympathetic response to such scenes. (Principle of habituation.) 5. Autonomic reactions do not recover response strength “spontaneously” following stimulus repetition, i.e. response adaptations are relatively enduring. (Principle of extinction.) 6. Muscle relaxation weakens (reduces) the sympathetic response to phobic stimulation. (Principle of reciprocal inhibition.) 7. Extinction operations are more effective under muscle relaxation than non-relaxation. (Principle of counterconditioning.) 8. Rate of decrease in sympathetic response to a repeated phobic stimulus is inversely proportional to the affective strength of the stmiulus. 9. Reduction of sympathetic reactions to a phobic stimulus generalizes to other stimuli in the same anxiety theme (hierarchy). (Principle of generalization.)

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In desensitization theory anxiety is broadly defined as a continuous (learned) sympathetic pattern of autonomic reaction (proposition 1) (Wolpe, 1966). The phobic situation is the conditioned stimulus (CS) and hallucinatory representation of it is what we will refer to as the central conditioned stimulus (CCS) or phobic image. Repetition of CCS is thought to reduce the conditioned sympathetic anxiety response (CR) (propositions 2 and 4), provided that the latter is not too intense (propositions 3 and 8). The strength of response is controlled by using an ascending order of presenting phobic scenes (propositions 3 and 9) and deep muscle relaxation (propositions 6 and 7). EXAMINATION

OF EVIDENCE

Some factual evidence bearing on each of the above propositions now exists and will be examined below. 1. Subjective anxiety and autonomic outjlo w Research on cognitive and autonomic determinants of emotion (Schachter and Singer, 1962), the effects of spinal cord injuries on felt-emotion (Hohmann, 1966) and the correlation of physiological reactions and reported distress (Basowitz, Persky, Korchin and Grinker, 1955) indicate that anxiety states and sympathetic activity are related, although the relationship is not as direct, simple or reliable as was once thought. There is evidence that there is no tight or necessary coupling of subjective anxiety with autonomic activity. (e.g. Maranon, 1924). Nonetheless, there may be a loose, conditional and important relationship between the two. One of the major difficulties in establishing a relationship between the experience of anxiety and autonomic activity, which was pointed out by Cannon (1927) in his classic critique of the James-Lange theory of emotion, is that visceral activation can occur in non-emotional states (for example, as a result of respiratory maneuvers, postural adjustments, mental concentration, etc.). These non-emotional increases in energy expenditure introduce “error” into the anxiety-autonomic activity relationship or “artifacts” into the polygraphic recording. The other type of “error” occurs when the person reports that he is highly anxious while he is physiologically quiescent. Four possible outcomes of the anxiety-autonomic relationship are shown in Fig. 2 with data from thirty phobic subjects in a desensitization experiment. From responses on 36 trials a frequency table was formed for each subject on the basis of whether an anxiety rating given at the end of each trial was above or below his median rating and physiological reactions during the trial were above or below median reactions for each of four (heart rate, respiratory rate, digital pulse amplitude and magnitude of skin conductance) measures. Summary tables for relaxed and non-relaxed subjects are presented separately (Fig. 2). In general, when non-relaxed subjects gave small autonomic reactions during the pre-. sence of phobic imagery they tended to report low rather than high anxiety (upper row).* * The relationship between anxiety and physiological response was tested by adding the upper-left (Iow-low) and lower-right (high-high) cell frequencies and subtracting from this sum the sum of the upperright (low-high) and lower-left (high-low) cell frequencies for each subject and each variable. Each subject then had four scores representing the difference between the number of “congruent” trials (anxiety rating and physiological response both high or both low) and the number of “incongruent” trials (anxiety rating high and physiological response low or vice versa) for each of four physiological responses. The difference of the means from zero were tested separately for each group, with the following results: r=2.88, ~~0.01, DPA; r=2.77, pcO.01. BR; r=2.71, pO.O5, DPA; t=1.26,p>0.05, RR; t=3.15,p<0.005, HR; r=2.09,pi0.05, SCM, for relaxed subjects (df=14 for all tests).

PSYCHOPHYSIOLOGICAL AR

NR

R

PR

ASPECTS OF SYSTEMATIC DESENSITIZATION AR

AR

69

AR

I I

pR$J :iQ DPA

RR

$k-& ; k3lY2. HR

SCM

FIG. 2. Frequency tables indicating the relationship between magnitude of anxiety ratings and magnitude of physiological reactions (digital pulse amplitude, DPA, respiratory rate, RR, heart rate, HR, skin conductance magnitude, SCM). Each table contains the frequency distribution into low (L) and high (H) response categories for 36 trials and 15 non-relaxed (NR) and 15 relaxed (R) subjects.

When they gave large autonomic reactions they more often rated their anxiety as high than low (lower row). With the exception of heart rate, the anxiety-autonomic relationship was much less clear in the relaxed subjects. This difference between the two groups appeared not to result from differences in level of autonomic response or anxiety rating (e.g. a restricted response range in the relaxed subjects). There is an interesting possibility that muscle relaxation partially uncouples anxiety reports and autonomic reactions, perhaps by altering the subject’s criterion for reporting anxiety or by diverting attention from viscerosensory influx during imagery to the task of maintaining a deeply relaxed state. Dr. Richard Chapman and I are currently attempting to explore the first possibility. It would be helpful to be able to apply signal detection theory (Tanner and Swets, 1954) in order to determine whether viscerosensory input has information which is utilized in some form by the anxiety report system. Experiments on voluntary control of autonomic outflow (e.g. Belmaker, Procter and Feather, in press) and operant conditioning of visceral activity (Miller, 1967) are pertinent to this question, in that they indicate something about the discriminative capacity of the viscerosensory system; but they do not tell us anything about the likelihood that the anxiety report system utilizes the viscerosensory information potentially avaiiable to it. The latter is the critical question. 2. Phobic imagery and autonomic reaction There is now considerable evidence that phobic imagery produces significantly greater sympathetic activation than is associated with neutral imagery (Grossberg and Wilson, 1968; Lang et al., in press; Van Egeren, Feather and Hein, in press). We have found a sympathetic reaction when the subject is told to prepare to imagine a phobic scene, a second increase in digital vasoconstriction when he is told which particular scene to imagine, a second cardiac acceleration when he begins to imagine the scene, and a partial return toward baseline of the cardiovascular variables during a thirty second imagery period (Van Egeren et al., in press). Much of the sympathetic response in a non-specific reaction to the signal to prepare to imagine a scene, regardless of affective content, which likely reflects orientation reflexes (Sokolov, 1963). Since the effects of these non-specific reflexes likely continue into the imagery period, it is necessary to use neutral control stimuli when studying the autonomic correlates of phobic imagery.

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In desensitization practice and research phobic scenes are ordinarily ranked by the subject from the least to the most threatening. Stimulus strength will here refer to the degree of threat to the subject of a phobic situation or scene. Heart rate and skin conductance reactions (Lang et al., in press) and digital vasomotor and skin conductance reactions (Van Egeren et al., in press) have been found to be a positive linear function of stimulus strength defined in the above way. These findings are in accord with observations by Sokolov (1963) and Davis, Buchwald and Frankmann (19.5’5)on amplitude parameters of wellcontrolled physical stimuli and various autonomic responses. 4. Repeated phobic imagery and autonomic reaction There is some evidence that when phobic scenes are imagined repeatediy there is a decrease in heart rate, digtial vasomotor and skin conductance reactions to them (Lang et al., in press; Van Egeren et al., in press). We have found this decrease to often be an exponential function of the number of stimulus presentations; a large decrease during the first two or three presentations, followed by a smaller rate of decrease and an occasional late increase. These adaptations are somtimes larger than occur to neutral stimuli and represent more than habituation of non-specific orientation reflexes. They are similar to adaptations to repetitive stimuli of physiological reflexes (Wendt, 1951), startle reflexes (Presser and Hunter, 1936), autonomic reactions to physical stimuli (Davis, Buchwald and Frankmann, 1955) and exploratory responses (Berlyne, 1950). 5. Spontaneous recovery of autonomic responses We found no evidence of spontaneous recovery of autonomic (heart rate, respiratory rate, digital vasomotor, frequency and magnitude of skin conductan~) responses over a one week period following desensitization operations (Van Egeren et al., in press). Recovery processes over a longer period of time need to be studied. 6. Afuscle relaxation and autonomic reaction Nervous system circuitry for somatovisceral reflexes (Everett, 1965) and research on posterior hypothalamus and muscle spindle response of anaimals (Gellhorn, 1967), the interaction of muscle tension and autonomic motor activity in conditioning (Obrist and Webb, 1967) and relative latencies of autonomic and muscle reactions (Davis et al., 1955) indicate that skeletal muscle and autonomic motor systems are intimately related. Some interesting detailed mechanisms of the cardiac accelerator effects of muscle tension have been studied (Belmaker, Proctor and Feather, in press; Donald, Lind, McNicol, Humphreys, Taylor and Staunton, 1967; Staunton, Taylor and Donald, 1964). These accelerator effects persist when the blood supply to the arm is occluded (Staunton et al., 1964), indicating that the effects do not depend upon blood-borne mediators; nerve endings embedded in muscle which are sensitive to some products of contraction have been implicated (Donald et al., 1967).

It has been difficult to demonstrate the inhibitory effects on autonomic activation of muscle relaxation in a desensitization setting (Rachman, 1968). Muscle relaxation has been shown to inhibit autonomic stress reactions (Paul, 1969) and to be no more helpful than resting quietly (Lehrer, 1969). Van Egeren et al., (in press) found that muscle relaxation reduced only skin conductance reactions and that its effects were a curvilinear function of degree of threat associated with the phobic stimulus; relaxation was most effective in inhibiting this reaction to moderately intense scenes.

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Grings and Uno (1968) used a promising counterconditioning procedure to demonstrate that relaxation can reduce skin conductance and, perhaps also, vasomotor reactions to a compound fear-relaxation conditioned stimulus. 7. Muscle relaxation and extinction ofautonomic reactions There is slight evidence that relaxation hastens extinction of vasomotor and skin conductance responses to phobic imagery (Van Egeren et al., in press). Covariance adjustments for extinction of responses to ccenes with neutral affective content left the vasomotor results unchanged, suggesting that relaxation affected more than extinction of non-specific vasomotor reactions {e.g. orientation reflexes). 8. Stimulus strength and extinction of autonomic reactions The rate of extinction of autonomic reactions to repetitive physical stimuli has been found to be generally proportional to the strength of the stimuli (Davis, Buchwald and Frankmann, 1955; Sokolov, 1963). The same relationship for autonomic reactions and phobic stimuli differing in degree of threat to the subject appears to be curvilinear; extinction was found to be greatest for moderately threatening scenes and greater for most threatening than for least threatening scenes (Van Egeren, in press).

There has been little study of this principle in a de~nsitization setting. Van Egeren et al. (in press) found generalization of extinction of responses from presented to not yet presented stimuli of the same stimulus hierarchy for only one (number of skin conductance responses) of five autonomic measures studied. Research on semantic generalization in classical conditioning (Feather, 1965) gives rise to the expectation that transfer of extinction for elements of the same stimulus hierarchy will occur, but that expectation has not yet been satisfactorily confirmed in desensitization research, To summarize, it may be useful to categorize the nine central propositions listed earlier, on the basis of degree of certainty of confirmation by the evidence cited above, into: high (proposition 2), medium (propositions 3-5), low (propositions 1,6,7 and 9) and very little or no (proposition 8) co~ation. The principal of habituation (proposition 4) of a~tono~c reactions during desensitization, as the term “habituation” is often used (namely, to denote any adaptation of responses to a repetitive stimulus), received some confirmation. It should be noted, however, that physiological habituation denotes a specific pattern of parametric relations which are likely important for understanding its physiological basis. Autonomic reaction changes in systematic desensitization do not have the same pattern of parametric relations, and ipso facto we cannot assume that the habituatory process of the nervous system will someday account for all of the major autonomic adaptations taking place during desensitization operations. To consider such adaptations as habituatory in the strict sense, proposition 8 would need to be confirmed and proposition 5 fail con&mation.* The presence of shortterm changes in non-relaxed subjects would then be demonstrated. There is currently evidence for autonomic changes during desensitization arising from extinction and countercon~tioning. * The inverse relationship between the rate of habituation and stimulus strength is a characteristic feature of physiological habituation (Thompson and Spencer, 1966).

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In addition to indicating certain parametric characteristics of autonomic adaptations during desensitization operations, the above propositions and associated evidence bear on two important issues in desensitization therapy: (a) the use of muscle relaxation to inhibit anxiety and (b) the use of an ascending (hierarchical) order of presenting phobic items. Current evidence indicates that under the right conditions muscular relaxation can facilitate extinction of autonomic reactions to phobic stimuli, and that autonomic reactions are related to anxiety reports. However, the relationships are weak, and conditional on the presence of the “right conditions”. It is difficult to achieve and maintain a deep state of relaxation in an experimental, psychoph~iological setting. Relaxation training is usually brief, the subject does not have the motivation of the expectation of thera~utic gain to learn to relax well, and the environmental context, the attached recording transducers, etc. often do not favor deep physical relaxation. What effects relaxation has in an experimental setting (which are often slight) is perhaps a lower limit of its effects in a therapeutic setting. Propositions 3, 8 and 9 are related to use of a hierarchical order of phobic scenes. Proposition 8 was not confirmed. Contrary to prediction, autonomic reactions to moderately and intensely threatening phobic scenes tended to extinguish faster than tomildly threatening scenes. This fact alone suggests that it may be necessary only to extinguish reactions to the most, or moderately, frightening phobic situations (Stampfl and Levis, in press; Wolpin and Raines, 1966) rather than navigate an ascending order. It is risky to make practical r~o~endations from psychophysiolo~cal data alone. While the ascending order may not be necessary for reducing autonomic reactions, it may be necessary to reduce subjective anxiety and/or phobic behavior. ANXIETY

AS A SYSTEMS CONCEPT

Anxiety is usually regarded as a state of a complex system having three major components: (a) experiential, (b) biological and (c) behavioral. Conceptually, it is a multidimensional concept; mathematically, it can be represented as a vector, rather than a scalar, quantity. A geometric interpretation for three autonomic measures is presented in Fig. 3. Three scores (e.g. heart rate, digital pulse amplitude and skin conductance) can be expressed as a single vector in a space of three dimensions. Three subjects on a single trial (or three trials of a single subject) may differ in amplitude (S 1 and S 2, Fig. 3) or direction (S 1 and S 3) of autonomic reaction. These two types of differences may indicate something quite different about the nature of the autonomic reaction. Utilizing a multivariate model, 8 of the 9 propositions listed above were examined for a system of autonomic responses (heart rate, respiratory rate, digital pulse amplitude, frequency and magnitude of skin conductance) through multivariate analyses of variance. Only propositions 2 and 3 were confirmed (Van Egeren et al., in press). Desensitization operations seldom produced a diffuse, undifferentiated response of the autonomic nervous system, or of that limited part of it being monitored. If anxiety is defined as a sympatheticdominated pattern of autonomic response (Wolpe, 1966), a multivariate model is advisable. When it was applied, it was seldom possible to make inferences to the autonomic system as a whole. Desensitization operations appeared to affect a set of Ioosely integrated autonomic responses having fairly distinctive p~ame~c characteristics and sources of regulation. Typically, an experimental operation shifted functioning of the system in direction, enough to reject one or two univariate hypotheses but not enough to reject the multivariate null hypothesis.

PSYCHOPHYSIOLOGICAL

ASPECTS OF SYSTEMATIC DESENSITIZATION

DPA

HR

73

SCF

DPA

SCF FIG. 3. Multidimensional anxiety space. The physiological component of anxiety is represented as a vector projection in a space of heart rate (KR), skin conductance frquency (SCF) and digital pulse amplitude (DPA) variables. The response pro&es of three subjects (upper insert) have been represented as three vectors for i~~tratio~. Changes in overall response amplitude lengthen the response vector; changes or d8erenw in dis~bution of autonomic outflow affect its direction in space.

POSSIBLE ELECTROCORTICAL CORRELATES There may be a variety of transient and steady-state shifts in brain waves during desensitization procedures. One type of change is illustrated in Fig. 4. The second signal initiates the onset of a 13 set imagery period. Concomitant with onset of imagery is complete alpha blocking, an increase in eye movements and no discernible change in forehead pulse amplitude. Early indications are that individuals will vary widely in degree of alpha blocking and increase in eye movement activity when imagery is initiated. Since these physiological parameters may reflect shifts in cortical excitability, stability of visual imagery and degree of mental concentration, all of which may in turn affect autonomic outflow, they are essential in the ~mprehensive study of the psychophysiolo~ of desensiti~tion. In addition to changes in spontaneous brain waves, desensitization procedures may be accompanied by slow-wave, steady-state shifts in scalp-recorded cortical voltage. This possibility is all the more important since Grey Walter’s (1964) discovery of the expectancy wave (E wave) or contingent negative variation (CM), best recorded in humans from the vertex of the head. A negative voltage recorded at this site, which is often ‘very resistant to habituation, appears when the individual is expecting and anticipating the appearance of some environmental event (Grey Walter, 1964). Cohen and Grey Walter (1966) showed that this vertex potential is related to the semantic characteristics of stimuli. Changes in the amplitude of the E wave may coincide with shifts in the historic meaning of the phobic stimulus and the phobic subject’s expectation of harm following successful desensitization therapy.

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F. VAN EGEREN

Fm. 4. Polygraphic recording of a subject showing the effects of visual imagery on spontaneous brain wave activity (desynchronization of electroencephalogram, EEG), eye movements (increase activity in ehctro-oculogram, EOG) and forehead blood volume (little change in forehead pulse amplitude, FPA). Upper deflection of the marker tracing (M) indicates presence of a warning tone; downward deflections indicate presence of tones signaling onset and offset of a 13-set imagery period,

POSSIBLE MECHANISTS

OF ACTION

It is difficult, but important, to attempt to interpret findings from psychophysiological studies in search of possible insights into the mode of operation of desensitization therapy. The two most often cited accounts are the inhibition model (Wolpe, 1966) and the habituation model (Lader and Mathews, 1968). According to the inhibition model phobic anxiety is reduced by desensitization through relaxation-induced inhibition of the neural pathways which form the neuronal basis of phobias, i.e. by counterconditioning of somatosensoryvisceromotor phobic reflexes (Wolpe, 1966). According to the habituation model phobic anxiety is reduced by desensitization through a process of habituation (Lader and Mathews, 1968). The critical dependent variable is the rate of habituation (RH) of responses, which is assumed to be directly proportional to the difference between momen~a~ arousal levels and some critical arousal level above which habitation of reactions is slow or non-existent. Whatever raises the subject’s arousal level (e.g. intense phobic stimuli) lowers RH (i.e. stows habituation}; whatever lowers the subject’s arousal Ieve (e.g. muscle relaxation) speeds habituation. Desensitization therapy is effective because it creates conditions when habituation of anxiety reactions is maximal, i.e. the subject’s level of arousal is low. An implication of this model is that whatever ultimately explains habituatory processes of the nervous system will account for the mechanism of action of systematic desensitization as well (Lader and Mathews, 1968). As was alluded to earlier, desensitization and habituation appear to differ in two important parametric characteristics: (1) desensitized autonomic reactions do not recover response strength over a period of one week after stimulating conditions have been removed and (2) linear reductions in response strength resulting from repeating phobic stimuli tend

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ASPECTS OF SYSTEMATIC DESENSI’KIZATKW

75

ta be dire&y Fro~or~onal to (or a curvilinear function of) stimulus (affective) strength instead of inversely proportional as for habituated responses (Thompson and Spencer, I966). For this reason we hesitate to identify the process of desensitization with the process of habituation. In addition, we failed to find the rate of habituation inversely proportional to autonomic activity during rest or arousal levels, as predicted by the habituation model; on the contrary, we found rate of habituation of skin conductance activity directly proportional to skin conductance activity during rest (Van Egeren, in press).* Specific psychophysiological mechanisms associated with counterconditioning as discussed by Wolpe (1966) will likely become clearer as more is learned about the neurophysiological and neurochemical correlates of conditioning and extinction (Hyden, 1967; John, 1967). Some research on specific physiological mechanisms associated with reciprocal in~bition was cited earlier {e.g. Donald et af., 1967; Gellhorn, 1967; Staunton ef al_, 1964). Currently, it is not possible to account for the extinction of autonomic responses to threatening stimuli in terms of detailed mechanisms of action. The extinction process is not clear even for well-controlled physical stimuli (Davis, Buchwald and Frankmann, 1955). Certain cognitive mediating processes, such as stimulus satiation (Glanzer, 1953) and semantic satiation (Osgood, Suci and Tannenbaum, 1957), perhaps augmented by muscle relaxation, may be important.

CONCLUSIONS In order to understand desensitization therapy more completely it is well to study the effects of ideation on autonomic reactions. Utilization of controlled imagery is one approach. It has many di~~~~es, simply because so much is occurring at once. One is monitoring outflow to autonomic efIectors, each of which has multiple sources of regulation. Superimposed on non-specific background activity one hopes to observe the e&cts of phobic imagery. In point of time, autonomic responses can precede, accompany or follow mental imagery, in such manner as the latter is in partial functional control of the former, or vice versa; or the autonomic and cognitive systems may be simply correlative. The matter is complicated further by individual differences in mental sets, coping mechanisms and patterning of autonomic responses, Despite these problems, a number of lawful parameters of autonomic responses eljcited by phobic stimuli have been found. Some evidence exists that autonomic reactions are proportional to the affective intensity of phobic stimuli and that when phobic stimuli are repeated some responses extinguish and/or counteroondition. The effects of the interaction of stimulus strength with the speed of extinction and ~~nter~onditio~ng agrees less well with current de~nsiti~~on theory. Careful parametric analyses of autonomic reactions to threatening stimuli, such has characterized the analysis of autonomic components of orientation and defensive reffexes (Davis et al., 1955; SokoIov, 1963), may lead not only to more precise and accurate desensitization theory but to more eff&ctive and economical therapy as well. REFERENCES R. R. (1955) Anx&ty and Strm. McGraw-Hill, New York. B!mmmt R., PRocro~ E. and FEA~R B. (in press) Skeletal muscle tensian in operant heart rate conditioning. Psydwphyskdogy.

B~&c%vrrz H.,

PERSKY

H., Ko~cmm S. J. and Gamma

*&l&is researcha mmwhat different method for calculating habituation rates was employed tfian used in research cited by Lader and Mathews. The possible e&x& of this diEerence have been discussed elsewhere (van Egereq in press) and are believed to be sEg&t, that

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