Preception (UCR diminution) in normal and neurotic subjects

Biological Psychology 5 (1977) 15-22 © North-Holland Publishing Company

PRECEPTION (UCR DIMINUTION) IN NORMAL AND NEUROTIC SUBJECTS J.F. ORLEBEKE and L.J.P. VAN DOORNEN Department o f Experimental Psychology, Free University, De Boelelaan 1115, Amsterdam, The Netherlands Accepted for publication 28 October 1976

Three groups of subjects, viz. low trait anxious (LA), high trait anxious (HA) and neurotic patients (PAT) received a series of warned and unwarned unpleasant auditory stimuli. The expectation that the warned stimuli would evoke smaller accelerative heart rate responses than the unwarned ones was not confirmed. On the contrary, the responses to the warned stimuli were larger than to the unwarned stimuli. Evidence was provided for the idea that homeostatic mechanisms were, at least in part, responsible for this result, though the possibility that even homeostatic heart rate changes can have psychologically relevant effects on central structures was not excluded. Neither the responses during the IS1 nor the responses to the unpleasant stimuli (UCS) differed between groups although the response in the ISI was in the predicted direction, i.e. a stronger initial acceleration in the LA group as compared to the HA and PAT groups. It was further suggested that the difficulty separating homeostatic effects from changes in sensitivity of the organism makes the operationalization of preception in terms of UCR amplitude of heart rate questionable.

1. Introduction Lykken (1959) found that the amplitude o f the SCR to a painful electric shock was considerably reduced when the shock was preceded b y a warning signal. Since that publication several confirmations o f this 'preception-phenomenon' (as it has been labelled by Lykken) followed, some of which attempted to detect the laws to which the underlying mechanism seems to obey. Phasic heart rate acceleration (Lykken, Macindoe and Tellegen, 1972) and the p300 component of the vertex cortical evoked response (Lykken et al., 1972; Roth, 1973)appear to undergo the same reduction as the SCR. Lykken has proposed that these findings suggest the existence o f a neurophysiological mechanism which enables the organism to ' t u n e ' its afferent system selectively, i.e. the warning signal initiates a phasic inhibitory process, which reaches a maximum effect after one or two seconds (response reduction is maximal when ISI is about 1 or 2 sec). Not only can this preparatory tuning produce response reduction (negative preception), but also response enhancement (positive preception), which may occur when the second signal has a positive value for the subject. The experimental evidence for positive preception, however, is less 15

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convincing than that for negative preception. In the present study the term preception unless otherwise qualified, refers to the more frequent observed phenomenon of negative preception. Two important questions occupy the discussion in literature. First, is it necessary to make a distinction between preception and habituation, which is also a phenomenon of phasic response reduction? Secondly, is preception merely a consequence of effector fatigue (peripheral response interference)? In answer to the first question Lykken and Tellegen (1974) argue that predictability (= constant ISI) is a necessary condition for preception, but not for habituation. Preception could have an additional function in that it shortcircuits the slower process of habituation as a consequence of which the OR during early trials is attenuated before habituation would otherwise be complete. This resembles the so-called one-trial conditioning, where semantic labelling of the CS (= informing the subject about stimulus contingencies) immediately brings the CR at the maximum level. According to Lykken and Tellegen (1974) habituation is a typical first signal system process, whereas preception is a second signal system process, although the response mechanism may be the same. The problem of whether preception is a consequence of effector fatigue was examined in a critical experiment by Peeke and Grings (1968). Three groups of subjects were used, the first group receiving a constant ISI (between toneCS and shock UCS) of 5 sec, the second group a variable ISI between 0.6 and 11 sec and the third group random sequences of CS and UCS. Four trials had identical ISI's for the three groups and UCR's were compared only for those trials. UCR amplitude (SCR, Ac) was largest in the random ISI condition and smallest in the constant ISI condition. This indicates that the psychologically relevant variable predictability is the crucial variable and not effector fatigue. Preception should be considered a biological adaptive mechanism: the reduction of the effect of noxious or unpleasant stimulation can be considered to have survival value. It is possible that the absence of preception, or even the presence of positive preception when stimulation might cause damage, is a factor contributing to (mental) illness. Lykken, Macindoe and Tellegen (1972) have found some evidence for the fact that high anxious subjects (classified on the Activity Preference Questionnaire (APQ) of Lykken and Katzenmeyer) show a larger heart rate acceleration to shock than low anxious subjects both in a warned and unwarned condition. Heart rate acceleration to warned shocks, however, was considerably lower in low anxious subjects in comparison with high anxious subjects. Thus, in both groups preception was evident but it was stronger in low anxious than in high anxious subjects. A differential effect manifested itself also in the anticipatory heart rate acceleration (greater in low anxious subjects than in high anxious subjects). Cardiac acceleration might be an indication of (adaptive) defensive inhibition of (sensory) input (e.g. Lacey, 1972). The experiment of Lykken and Tellegen (1974) was replicated with three groups of subjects viz. low and high trait anxious subjects and a group of neurotic patients. The main argument for replication was that their results may not reflect unequi-

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vocally the preception phenomenon. As it is necessary, when using SCR as a response measure, to exclude an influence like effector fatigue, it is also necessary when using HR as a response measure to be aware of other factors (like homeostasis) that may influence heart rate responses.

2. Method 2.1. Subjects

From 70 female sophomores 10 extremely anxious subjects and 10 extremely stable subjects were selected. For this selection a double criterion was used: High anxious (HA) subjects were defined as both high (upper 25%) on neuroticism (measured with a Dutch scale equivalent to the Maudsley Personality Inventory)and high (upper 25%) on debilitating anxiety (measured with a Dutch scale comparable with the better known TAQ of Mandler and Sarason, 1952). Stable subjects were defined as scoring in the lower quartile of both variables. (The correlation between these two anxiety measures is about 0.50.) A third group of 15 subjects consisted of neurotic patients (PAT), 10 females and 5 males, randomly selected from a group of out-patients with free floating anxiety symptoms, who were in group therapy in our department. The 5 male subjects were added to the design because " of secondary interest in sex differences: however, as can be seen, this variable was not varied systematically and is therefore analyzed separately for the PAT group only. To diminish medication effects, patients were asked to stop medication for 24 hours preceding the experiment. Although several subjects were ~ot able to do so we did not exclude these subjects, supposing that nevertheless the patients would be relatively more anxious than the other groups. 2.2. Apparatus

Heart rate (ECG) was measured with a Beckman dynograph recorder, type 411. In addition, the output of the ECG amplifier was fed to a Bell and Howell magnetic recorder (VR 3200) for later automatic processing of R - R intervals. ECG was recorded from a lead 1 configuration, using Siemens electrodes. Subjects were seated in a soundproof room. 2.3. Procedure

All subjects received 2 blocks of stimuli; blocks were separated by 5min rest. The blocks consisted of ten 100 dB 1000 Hz tones of 2 sec duration, half of which were preceded by a 60 dB white noise warning signal of I sec. The ISI was 5 sec and the intertrial interval varied from 30 to 50 sec. The position of the 5 warning signals in each block was determined at random for every subject, so that the first trial was

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a warned one for some subjects and a non-warned one for others. From the ECG the R - R interval periods were determined with computer-aid and converted to bpm. Both the heart rate response in the ISI (variables: groups (3), warned-nonwarned = W/NW (2) and seconds (5)) and to the UCS (variables: groups (3), warned-nonwarned = W/NW (2) and seconds (8)) were analyzed on a second-tosecond basis.

3. Results Only the first block of 10 stimuli was analyzed. In the second block the UCR was too much habituated in most subjects to define any response reduction by the supposed preception mechanism. 3.1. S e x differences

The PAT group consisted of 10 females and 5 males. In an ANOVA, where sex (2), seconds (8) and warned/non-warned (2) were the variables, no significant main effect of sex, nor any significant interaction effect with sex was found. We therefore decided to regard the patients as one group of 15 subjects. 3.2. Interval response

An ANOVA revealed only one significant effect, viz. W/NW by seconds (F = 2,93, p < 0.02, df 5,145). Fig. 1 gives the response in the ISI for each group, for the warned trials only. To be sure that there was no response effect in the NW condition, the main effect 'seconds' in the NW condition was tested separately with a one way ANOVA. This effect was not significant: F(4,155) = 0.12. It can thus be concluded that the significant interaction is caused by the interval response in the W-condition. Although groups did not differ significantly in this respect, fig. 1 gives an impression of the direction of the differences. A comparison with the study of Lykken et al. (1972) with regard to the effect of anxiety is not fully justified because we used a different type of test to measure anxiety. The pre-CS heart rate levels for the LA, HA and PAT groups were 81,2; 75,9 and 78,5 bpm respectively. The differences were not significant (one way ANOVA:/7(2,29) = 0.58). 3.3 Response to the UCS

The UCR (a phasic heart rate acceleration) is significantly larger if preceded by a warning signal in comparison with the unwarned condition (F = 3.86, p < 0.001, df = 7,203). In fig. 2 this differential effect can be seen.

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This effect is the same for the three experimental groups (i.e. the interaction: groups by secs by W/NW is not significant). The pre-UCS heart rate levels for the LA, HA and PAT groups were 80.9; 74.7 and 76.5 bpm respectively, q he differences were not significant (one way ANOVA:/7(2,29) = 0.72).

4. Discussion Preception was operationalized as a reduction of UCR amplitude when the UCS was preceded by a warning signal, compared with the UCR to a stimulus not preceded by a warning signal. This expectation was not confirmed. On the contrary, the warned UCS produced a significantly larger heart rate acceleration than the unwarned UCS. The methodological point to be made here is what the influence of different prestimulus levels in the two conditions could have been. In the warned condition the UCR was preceded by an anticipatory deceleration. Fig. 1 clearly shows this deceleration for all groups just before UCS onset, to such an extent that heart rate level is below pre-CS level. Thus the level of departure of the warned UCR is lower than that of the unwarned UCR. Therefore the warned UCR can have been affected

J.F. Orlebeke, L.J.P. van Doornen / Preception

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Fig. 2. Heart rate UCR (averaged over all three experimental groups) to warned and unwarned

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by homeostatic feedback, which brings heart rate back to its initial level after the anticipatory deceleration just before UCS onset. The warned UCR can thus be considered the summed result of this homeostatic effect and the 'true' response to the warned UCS. This interpretat!on is supported by the following post hoc analysis. Of all subjects two groups were distinguished: first, those who evidently over all trials showed a greater acceleration to the unwarned UCS in comparison with the warned UCS (N 1 =9), and second, those who evidently showed the reverse pattern (N2 = 13). For each individual subject the mean pre-UCS heart rate level was compared with the mean pre-CS level for the warned trials only. For the first group preUCS was less than 1 bpm below pre-CS level; for the second group pre-UCS level was more than 5 bpm below pre-CS level. The difference between the two groups is statistically significant (Mann-Whitney U = 18.5,p < 0.01). So a homeostatic influence seems to be relevant in interpretating our paradoxical finding. This interpretation is in accord with a similar suggestion made by Epstein, Boudreau and Kling (1975). Lykken et al. (1972) found negative preception of the phasic heart rate response using an identical fixed warning interval of 5 sec. Besides CS and UCS Lykken et al. presented an extra warning stimulus of 1 sec duration, 1 sec before UCS (electric

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shock) onset. We have seen that the period just before onset is rather crucial because of the strong deceleration in the warned condition. Lykken et al. (1972) do not provide a rationale for the use of this second cue. They find less heart rate acceleration to the UCS in the warned condition in comparison with the unwarned condition. This attenuated acceleration is preceded by a considerable accelerative response to the CS. After such an acceleration, less acceleration or more deceleration is to be expected. Lykken et al. (1972) deny the possibility that their negative preception phenomenon might be a demonstration of the LIV, because pre-UCS heart rate level is not approaching a physiological limit. However, we prefer to maintain the LIV hypothesis. We have two arguments for this. First, Hord, Johnson and Lubin (1964) have demonstrated that LIV does hold for physiological levels considerably below some 'physiological limit'. Second, from a logical point of view we can argue that the reason why Lykken et al. found preception (pre-UCS level high) is the same reason why we did find the opposite (pre-UCS level low). It should be noted that there are two differences between our experimental procedure and that of Lykken et al. (1972) which might be - at least partly - responsible for the differences in results. The first procedural difference is the quality of the UCS: an electric shock (exp. of Lykken et al.) can produce a different response in comparison with a 100 dB tone, although both are aversive so that we expect that the difference is gradual and not essential. A second procedural difference concerns the second warning cue in the design of Lykken et al. which is omitted in our design. Although the function of this second cue is not explained by Lykken et al. (1972), one can say that the second cue enhances the predictability of the UCS and thus preception. But even if this is the case, we maintain our opinion that the most important determinant of the UCR is the pre-UCS level (though this level can biological or psychological be functional) and to a lesser extend predictability. It is hard to believe that the inhibitory preception process (cognitive in nature according to Lykken and Tellegen, 1974) will not be triggered by the Sl and only by $2 in the paradigm of Lykken et al. (1972). If we assume first, that changes in heart rate, even when they are reflecting homeostatic mechnisms, have a functional value with regard to input regulation (Epstein et al., 1975), and second, that input reduction (negative preception) is maximal when heart rate is higest, then we can say that negative preception can only manifest itself during the accelerative phase of the response in the ISI. The anticipatory response gives continuous information about changes in sensitivity: the minimum at about 2 or 3 sec (peak of acceleration) and the maximum during deceleration. We think that the warning signal can produce an anticipatory state which is for the benefit of the organism if the ISI does not surpass about 4 sec. Beyond that point the input is not reduced but enhanced: heart rate is, as we cited, relatively low after 5 sec. Although the response in the ISI did not differ significantly between groups, it

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was in the direction to be expected and in agreement with the difference found by Lykken et al. (1972). It is possible that the acceleration (in LN subjects) is underestimated as a consequence o f the too low sample rate o f the second-to-second technique o f analysis. Long inter-beat intervals have a higher probability o f being sampled than smaller ones, as a consequence of which fast accelerations are flattened. In conclusion, the relatively stronger acceleration to the UCS in the warned condition, in comparison with the unwarned one, can be interpreted in several ways (1) The normal acceleration to a 100 dB tone, with a homeostatic effect superimposed on it, and (2) The increased sensitivity o f the organism as a result o f the anticipatory deceleration (according to the above mentioned hypothesis) (3) Both a LIV effect and an increased sensitivity are responsible. Such considerations raise the methodological problem o f how preception is to be operationalized in terms o f UCR heart rate amplitude. The same line of thinking holds when the anticipatory response is an acceleration, as is the case in the experiment o f Lykken et al. (1972).

References Epstein, S. (1973). Expectancy and magnitude of reaction to a noxious UCS. Psychophysiology, 10,100-107. Epstein, S., Boudreau, L. and Kling, S. (1975). Magnitude of heart rate and electrodermal response as a function of stimulus input, motor output, and their interaction. Psychophysiology, 12, 15-24. Headrick, M.W. and Graham, F.K. (1969). Multiple component heart rate responses conditioned under paced respiration. Journal of Experimental Psychology, 79,486--494. Hord, D.J., Johnson, L.C. and Lubin, A. (1964). Differential effect of the law of initial value (LIV) on autonomic variables. Psychophysiology, 1, 79-87. Lacey, J.I. (1972). Some cardiovascular correlates of sensorimotor behavior: Examples of visceral afferent feedback. In: C.H. Hockman (Ed.), Limbic system mechanisms and autonomic function. Springfield, Illinois: C.C. Thomas, 175-196. Lykken, D.T. (1959). Preliminary observations concerning the preception phenomenon. Psychophysiological Measurements Newsletter, 5, 2-7. Lykken, D.T., Macindoe, J. and Tellegen, A. (1972). Preception: Autonomic response to shocks as a function of predictability in time and locus. Psychophysiology, 9,318-333. Lykken, D.T. and Tellegen, A. (1974). On the validity of the preception hypothesis. Phychophysiology, 11,125-132. Mandler, G. and Sarason, S. (1952). A study of anxiety and learning. Journal of Abnormal and Social Psychology, 47 166-173. Peeke, S.C. and Grings, W.W. (1968). Magnitude of CR as a function of variability in the CSUCS relationship. Journal of Experimental Psychology, 77, 64-49. Roth, W.T. 1973. Auditory evoked responses to unpredictable stimuli. Psychophysiology, 10, 125-138.