Learning subjective health complaints

Transcription

1 Scandinavian Journal of Psychology, 2002, 43, Blackwell Science Ltd Learning subjective health complaints OMER VAN DEN BERGH, WINNIE WINTERS, STEPHAN DEVRIESE and ILSE VAN DIEST Department of Psychology, University of Leuven, Belgium Van den Bergh, O., Winters, W., Devriese, S. & Van Diest, I. (2002). Learning subjective health complaints. Scandinavian Journal of Psychology, 43, Symptom episodes often show a spatio-temporal structure, that is, they occur in a specific context for a certain duration. Repeated experiences may therefore be construed as associative learning trials, in which context elements are turned into predictive cues, triggering anticipatory processes conducive to subjective health complaints. A series of experiments, using inhalations of air enriched with CO 2 and external (odors) or internal (mental images) stimuli as cues, is discussed to show that subjective health complaints may occur upon presenting the cue alone. Learned symptoms may be unrelated to bodily responses and easily generalize to new related cues. Better learning occurs to cues with a negative affective valence and in participants scoring high for negative affectivity. Our findings are relevant to the understanding of medically unexplained ( functional ) syndromes and the poor relationship between objective and subjective health indicators in general. Key words: Health complaints, conditioning, MCS, CO 2 inhalation, hyperventilation. Omer Van den Bergh, Department of Psychology, University of Leuven, Tiensestraat 102, B-3000 Leuven, Belgium. Omer.Vandenbergh@psy.kuleuven.ac.be SUBJECTIVE HEALTH COMPLAINTS AND OBJECTIVE HEALTH INDICATORS Most people assume that subjective symptoms are a direct and linear expression of some dysfunction in the body. We easily tend to forget that subjective health symptoms are by definition psychological events: bodily signals have to be sensed, perceived, appreciated, interpreted, put into language, and expressed. Thus, signals from bodily dysfunction are but one, yet an extremely important, source of information, but psychological processes related to each of these information processing steps can seriously influence and bias subjective health symptoms (Pennebaker, 1982). No wonder correlations between subjective symptoms and objective signs of pathology can vary anywhere from zero to almost perfect. Medically unexplained symptoms account for some 20% of the consultations in primary care and for 25 35% of the new referrals of medical outpatients (Hamilton, Campos & Creed, 1996; Peveler, Kilkenny & Kinmonth, 1997; Van Hemert, Hengeveld, Bolk, Rooijmans & Vanderbroucke, 1993). A substantial proportion of them are related to socalled functional syndromes, such as chronic fatigue syndrome (CFS), fibromyalgia, multiple chemical sensitivity (MCS) and the like (Wessely, Nimnuan & Sharpe, 1999). The existence of medically unexplained symptoms and syndromes promotes two extreme positions. One is that some specific explanatory mechanism of dysfunction in the body must exist that has yet to be discovered. The other assumes that such symptoms are mainly the result of perceptualcognitive processes, amplifying (relatively minor) bodily sensations resulting from stress and anxiety. Several investigators hold positions between these extremes, but common to both views is a static model, that is, symptoms of a particular illness are considered as invariantly determined by the same set of processes. The perspective we take here is a dynamic one, implying that the relative importance of several mechanisms determining a particular set of symptoms may change over time within an individual. The occurrence of symptom episodes often shows a spatiotemporal structure. For example, an asthmatic patient may repeatedly experience dyspnea and wheezing in specific environmental conditions but not in others; an agoraphobic patient may feel shortness of breath and palpitations due to stress-induced hyperventilation in the supermarket, but not at home; a patient may occasionally have to undergo a distressing medical investigation in a specific hospital setting and feels relief a few hours later at home. In all these cases, symptom episodes have a certain duration and are experienced within a specific environmental context. This allows for prediction and anticipation, which may affect perceptualcognitive processing of somatic sensations during subsequent episodes. Several cognitive-perceptual models of symptom perception (Cioffi, 1991; Lang, Cuthbert & Melamed, 1986; Leventhal, 1986; Leventhal & Leventhal, 1993; Pennebaker, 1982) assume (a) that somatic events may become represented in memory; (b) that subsequent experiences, sharing common elements with the represented information, may activate this memory information automatically; and (c) that this information helps to structure and bias the actual experience (Van den Bergh, Stegen & Van de Woestijne, 1998). In addition, anticipation may also have consequences at the physiological level: Pavlov s dog started to salivate upon perceiving a predictive cue for food. Several systems in the body are indeed sensitive to learning, such as the autonomic, immune, and endocrine systems (Ax, Published by Blackwell Publishers, 108 Cowley Road, Oxford OX4 1JF, UK and 350 Main Street, Malden, MA 02148, USA. ISSN

2 148 O. Van den Bergh et al. Scand J Psychol 43 (2002) 1990; Siegel & Kreutzer, 1997), and may become involved with subsequent symptom episodes. In other words, a first symptom episode may predominantly be determined by a bodily dysfunction, but the nature and the relative dominance of the determinants of these symptoms may change across subsequent episodes. In the present article, we will focus on learning processes that may intervene and modify the relationship between symptoms and physiological responses. MULTIPLE CHEMICAL SENSITIVITY: AN EXAMPLE The idea of learned symptoms is one of the suggested explanations for MCS or ideopathic environmental intolerance (IEI). This is a syndrome with a variety of complaints in different organ systems. Most frequent are the neuropsychological complaints: dizziness, difficulties concentrating, poor memory, but also tiredness, chest pain, shortness of breath, and mood changes occur (Sorg, 1999). MCS is often mentioned together with fibromyalgia and CFS, but at least one typical aspect distinguishes MCS from other syndromes: patients attribute their symptoms to chemical, often odorous substances in their environment. Therefore MCS is sometimes referred to as chemical AIDS (Miller, 1994). A reliable estimate of the prevalence of MCS is hard to give. Some studies report prevalences from 3% to 5% (Graveling, Pilkington, George, Butler & Tannahill, 1999) in the US. MCS is more prevalent among women and in patients with a comorbid psychiatric diagnosis. Currently, there is no widely accepted explanation for this syndrome and several hypotheses, physiological, and psychological, are being investigated (Graveling et al., 1999; Miller, 1994; Shusterman, 1992; Sorg, 1999). A particular (and often dismissed) hypothesis is associative or Pavlovian learning ( Van den Bergh, Devriese, Winters, Veulemans, Nemery, Eelen & Van de Woestijne, 2001). In many patients, MCS is triggered by a toxic accident, which can be considered an unconditioned stimulus (US). Odors and other environmental cues that were present during this accident may function as conditioned stimuli (CS), implying that subsequent exposures to these cues alone would be sufficient to elicit symptoms. In its simplest form, this hypothesis relies only on a similarity with a procedure and offers no real explanation (for example, it does not specify the mechanisms through which these cues would cause symptoms). Except for some clinical case stories consistent with this explanation, no convincing evidence existed. We therefore started an experimental program, trying to build a laboratory model for MCS. BUILDING A LABORATORY MODEL FOR MCS: CAN SYMPTOMS BE LEARNED? In order to investigate how determinants of symptoms may evolve across subsequent symptom episodes, we embedded Capnograph Air Odor nebulizer Subject Pneumotachograph Mask 7.5% CO 2 - enriched air Valve switching air & CO 2 enriched air 7.5% CO 2 21% O % N 2 Fig. 1. Schema of the experimental set-up for an odor CO 2 inhalation paradigm. Acquisition Pause Test Trials Baseline: Air CS+ trial: Odor 1 + CO 2 CS- trial: Odor 2 + Air Baseline: Air CS+ test: Odor 1 + Air CS- test: Odor 2 + Air Fig. 2. Schema of the experimental design. the experience of symptoms in a straightforward associative learning paradigm. Symptoms were induced using inhalations of air enriched with 7.5% CO 2 for 2 minutes. This gas has no odor or taste, meaning that it can be administered unobtrusively and only its somatic effects become apparent, such as fast breathing, smothering sensations, chest tightness, feelings of choking, pounding heart, sweating, hot flushes, lump in throat, headache, tension, and anxious feelings. The symptoms start after about 20 s of inhalation, are moderate in intensity, and disappear quickly after the trial. An odor serving as predictive cue was mixed with the CO 2 - enriched air. In control trials, another odor was mixed with regular room air (see Fig. 1). The participants received three breathing trials of each type in an acquisition phase. In a subsequent test phase, the same set of trials was presented but this time without CO 2. 1 Several physiological measures were taken during the trials (mainly respiratory parameters, sometimes heart rate) and the intensity of the subjective symptoms was measured after each trial (see Fig. 2). In a series of studies (see Van den Bergh et al., in press, for a review), we showed that participants easily learn to feel Air Measures Subjective complaints Respiratory physiology (f, Vt, Ve) Subjective complaints Respiratory physiology (f, Vt, Ve)

3 Scand J Psychol 43 (2002) Learning subjective health complaints 149 symptoms: perceiving the odor that had been associated with CO 2 -enriched air during the acquisition phase induced an elevated level of symptoms (Van den Bergh, Kempynck, Van de Woestijne, Baeyens & Eelen, 1995; Van den Bergh, Stegen & Van de Woestijne, 1997). However, this learning effect occurred only with a foul-smelling odor as a cue (e.g. ammonia or butyric acid) and not with a neutral to positive odor (e.g. niaouli, a volatile oily substance containing eucalyptus). Interestingly, for both types of odors, participants knew equally well which odor had been associated with the CO 2 -induced symptoms. This finding is important because it suggests that mere conscious awareness of the contingencies between specific odors and symptom episodes is not sufficient for the findings to occur. In addition, it excludes an interpretation in terms of demand effects. Learned symptoms closely resembled the symptoms induced by CO 2 inhalation: the learning effects were most pronounced for respiratory symptoms (fast breathing, smothering sensations, chest tightness, feelings of choking) and did not occur for a set of dummy symptoms (symptoms not elicited by inhaling CO 2 ). In some studies, participants also had learned to breathe differently upon perceiving the odor associated with CO 2, but this finding was less reliable across studies. However, both correlational analyses and experimental manipulations showed that the learned (respiratory) symptoms were not an expression of the altered respiratory behavior. For example, when a reaction time task was administered during the test phase, it wiped out differences in respiratory responses between conditions but not in conditioned symptoms ( Van den Bergh et al., 1998). Not only odors, but also thoughts can function as learned cues for symptoms (Stegen, De Bruyne, Rasschaert, Van de Woestijne & Van den Bergh, 1999). When odors were substituted by having the participants imagining themselves being stuck in an elevator or a sauna while experiencing shortness of breath and suffocation induced by unobtrusively breathing air enriched with CO 2, subsequent images of these situations alone produced elevated symptoms of the same type. This did not happen when neutral to positive scenes were imagined in association with CO 2 -induced symptoms, despite roughly equal awareness of the arranged contingencies. Learned symptoms were quite persistent: testing the learning effects immediately after acquisition or after a delay of one week did not affect the results (Devriese, Winters, Stegen, Van Diest, Veulemans, Nemery, Eelen, Van de Woestijne & Van den Bergh, 2000). However, applying an extinction procedure (presenting the odor a number of times without CO 2 ) readily eliminated the symptoms (Van den Bergh, Stegen, Van Diest, Raes, Stulens, Eelen, Veulemans, Van de Woestijne & Nemery, 1999). Symptoms learned in response to one odor easily spread to other, not previously presented odors, but only when these were also foul smelling (Devriese et al., 2000). Importantly, all these effects tended to be more pronounced in participants scoring high on negative affectivity (Devriese et al., 2000; Van den Bergh et al., 1998). This is a general tendency to experience and report a variety of negative mood states, including anxiety, anger, disgust, scorn, guilt, fearfulness, and depression (Costa & McCrae, 1987; Vassend, 1989; Watson & Pennebaker, 1989). Also psychosomatic patients showed stronger learning effects (Van den Bergh et al., 1997). In sum, this set of results provides strong evidence that symptoms initially elicited by a specific physiological process may subsequently be elicited by an associated mental or environmental cue. This is more likely when the cue itself is unpleasant or has a negative value and when the subject scores high on negative affectivity. The present operationalization with odors is particularly relevant for MCS, as the symptoms are typically triggered by odorous chemicals and the CO 2 inhalation may be considered a laboratory analog for a toxic exposure in real life. However, several indications suggest that the scope of the laboratory model may be broadened: because mental cues can also become conditioned signals if they have been accompanied by symptoms, the mere conviction of being in a chemically polluted environment may become a sufficient trigger for symptoms. Furthermore, assuming that stressinduced hyperventilation episodes can function as a US in a similar way as CO 2 inhalation, it may at once explain why a toxic exposure is not always found in a MCS patient and why there is a considerable symptom overlap between MCS and hyperventilation ( Van den Bergh et al., 2001). RELEVANCE FOR OTHER SUBJECTIVE HEALTH COMPLAINTS The foregoing set of results may be particularly relevant for MCS. However, the general principle, namely that the determinants of symptoms may change over time within an individual and/or across situations, is of course relevant for all kinds of diseases or health complaints, including those that have a clear medical explanation. Indeed, also in real illnesses a substantial proportion of the symptoms are medically unexplained. In an asthmatic sample, between 27% and 31% of the patients show more symptoms than expected from objective indicators, while approximately 17 20% show fewer symptoms (Nguyen, Wilson & German, 1996; Teeter & Bleecker, 1998). In a recent study of our group, we investigated the influence of histamine-induced bronchoconstriction on symptom perception in newly diagnosed asthma patients. A standard test was administered, involving a sequence of aerosol inhalations of histamine acid phosphate in doubling concentrations starting from mg/ml up to a level sufficient to induce a 20% fall in forced expiratory volume in 1 s. All subscale scores of the Asthma Symptom Checklist (ASC; Kinsman, Luparello, O Bannion & Spector, 1973) increased significantly between pre- and post-histamine

4 150 O. Van den Bergh et al. Scand J Psychol 43 (2002) inhalation. On the next day, the participants returned for a second part of the test. In fact, they were subjected to the same test procedure as on the previous day, but instead they inhaled a series of aerosols with saline ( NaCl). Despite unaffected respiratory function, increases in subjective symptoms of airways obstruction (e.g. chest tightening and congestion, chest pain, feeling respiratory discomfort) were observed and this was more pronounced in participants scoring high on negative affectivity (Put, 2001; Put, Demedts, Van den Bergh, Demyttenaere & Verleden, 1999). Apparently, environmental cues have become triggers for subjective asthma symptoms. Also Rietveld, Kolk, Colland and Prins (1997) showed that the subjective complaint of dyspnea was more related to the perception of wheezing than to parameters of objective lung function. In addition, false auditory feedback of wheezing induced sensations of dyspnea. A history of co-occurrences of wheezing noises and dyspnea in asthmatics may have turned the auditory cues into conditioned stimuli. The present perspective may also shed light on the debate about the so-called hyperventilation syndrome. Stressinduced hyperventilation may cause hypocapnia (a decreased CO 2 pressure in the blood) and respiratory alkalosis (an increase in the blood ph) which may cause a wide variety of symptoms, such as tingling sensations, muscle spasm, pounding heart, hot flushes, irregular and rapid heartbeat. In addition, hypocapnia produces cerebral vasoconstriction and cerebral hypoxia, which depresses cortical functions in the awake state. Hypoxia is associated with headache and with subjective cognitive symptoms of dizziness, derealization, memory and concentration problems, disorientation, and fainting (see Gardner, 1996, for a review). Despite hypocapnia being a well known biological dysfunction and a likely source of symptoms, there is little direct correlation between hypocapnia and symptoms. For example, Wientjes and Grossman (1994) showed that only 4% of the hyperventilation symptoms in daily life were explained by end-tidal PCO 2, whereas 33% were explained by anxiety. In that experiment, end-tidal PCO 2 was measured in a laboratory setting, which may make the measure less valid for symptoms in daily life. Hornsveld, Garssen, Dop, van Spiegel and de Haes (1996), taking ambulatory transcutaneous measures of PCO 2 during real life symptom episodes, showed that the symptoms of hyperventilation were often not accompanied by a lowered PCO 2 and that a lowered PCO 2 often followed rather than preceded the occurrence of symptoms. These findings have been taken as evidence that hyperventilation is not the cause of the complaints typically ascribed to it, and, in fact, have led to propositions that the hyperventilation syndrome has no scientific ground and should be dismissed. However, conceiving of hyperventilation episodes as learning trials in which environmental and mental cues may become conditioned stimuli for symptoms may explain the loose relationship between hypocapnia and symptoms in this syndrome. Many other examples of poor correlations between objective indicators of pathology and subjective symptoms exist in different areas of medicine (see Watson & Pennebaker, 1989) and may in part be elucidated by our perspective. But how do learned symptoms come about, and what are the modulating mechanisms? CRITICAL FACTORS AND MECHANISM IN SYMPTOM LEARNING In our view, conditioning should not be considered a theoretical explanation in itself for symptom learning, but a scientifically sound procedure with which to unravel the critical conditions determining learning of symptoms. In our studies, two such critical conditions emerged and prompt further investigation. The first is that we consistently found conditioning only to stimuli with a negative affective valence (e.g. odors and mental images) but not to neutral positive stimuli. Selective associations between conditioned and unconditioned stimuli have been documented extensively (see Davey, 1995, for a review of the preparedness notion) and several explanations have been advanced. For example, negative odors may promote stronger expectations of an aversive US than a neutral positive cue ( US-expectation effect). Along this line of reasoning, we created a negative context prior to conditioning in the odor CO 2 paradigm by having participants read information typically found on MCS patient websites ( Winters, Devriese Van Diest, I., Nemery, B., Veulemans, H., Eelen, P. & Van den Bergh, submitted). The information described a MCS case story and warned against the ubiquitously present chemical pollution. In this study, learned symptoms were observed in response to both a negative (ammonia) and a neutral positive odor (niaouli) after only one conditioning trial, whereas no one-trial conditioning was observed in the no information condition. This suggests that it is not the affective valence of the odor per se that is important, but probably the affective quality of the informational context elicited by the odor and/or the US expectation induced by it. Taking this reasoning further, this result suggests that warnings and campaigns against environmental pollution may actually promote the development of MCS as a side-effect to beneficial effects for the environment. A second intriguing finding is that symptom learning is more likely to occur in participants scoring high on negative affectivity. This person characteristic may contribute in several ways. First, persons with high negative affectivity may exhibit an attentional and interpretational bias toward internal sensations, meaning that a symptom episode may impact stronger upon them either by producing stronger autonomic responses and/or by interpreting internal responses (URs) as more threatening (Stegen, Neujens, Crombez, Hermans, Van de Woestijne & Van den Bergh, 1998; Stegen, Van Diest, Van de Woestijne & Van den Bergh, 2000, 2001; Watson & Pennebaker, 1989). An elevated intensity of the experienced unconditioned stimulus

5 Scand J Psychol 43 (2002) Learning subjective health complaints 151 may lead to stronger responses to the conditioned stimuli. Second, negative affectivity may bias persons to develop more explicit expectancies toward an aversive US either by themselves or by being selectively more open to catastrophizing culturally transmitted information about a disease (e.g. in the case of MCS, about the presence and toxicity of environmental chemicals). Third, persons with negative affectivity may be more vulnerable to post-conditioning inflation, that is, after having formed an association between a CS and a US, worrying and catastrophizing about the US experience (e.g. I am going to have cancer after a toxic exposure; or I may have a brain tumor after a hyperventilatory event) may inflate the subjective experience of the US and produce stronger learned responses. These two examples of critical factors for symptom learning are related to psychological processes. However, associative learning may also induce bodily responses in several systems, such as the autonomic, endocrine, and immune systems. For some symptoms, critical factors may be related to the involvement of those systems, such as conditioned arousal and related muscle tension and respiratory changes. But even then, the mere correlation of learned responses in a bodily system and learned symptoms does not automatically imply causality. On several occasions, our CO 2 inhalation paradigm induced both learned respiratory responses and corresponding learned respiratory symptoms. Yet, an explicit experimental test showed that the learned symptoms did also occur without the learned respiratory behavior (Van den Bergh et al., 1998). CONCLUSION Anticipation based on experienced contingencies is a pervasive process affecting many functional systems in living organisms. In human beings, these systems may range from basic biological processes to higher-level perceptualcognitive processes. We discussed evidence to show that the experience of contingency relationships between external or internal cues and unobtrusively induced symptom episodes may cause symptoms to emerge upon perceiving the cues alone; in other words, symptoms can be learned. In the examples we discussed, it is likely that perceptual-cognitive processes were responsible for learned symptoms. However, learned responses in bodily systems may be involved in other examples. The present perspective implies that the processes underlying symptoms may change over time and that the relationship between objective indicators, initially thought to cause the symptoms, and subjective complaints may become loose. We believe that this dynamic approach may offer a new way to look at the relationship between symptoms and bodily responses in many diseases. Supported by grant G N (Fund for Scientific Research Flanders, Belgium) and grant OT-97/16 (Research Council of the University of Leuven). 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