Anxiety And PainHow Have Psychological Theories Elucidated the Nature of Anxiety: With Particular Reference to Panic DisorderEverybody has had experience with anxiety. Indeed anxiety responses have been found in all species right down to the sea slug (Rapee, et al 1998). The concept of anxiety was for a long time bound up with the work of Sigmund Freud where it was more commonly known as neurosis. Freud’s concept of neuroses consisted of a number of conditions characterised by irrational and disproportionate fear. Through time it became apparent that the term was a) becoming to wide a term to be of any use in explanation and b) too intimately connected to psychoanalytic theory, of which many of its basic theoretical assumptions were being increasingly called into question. As successive versions of the Diagnostic and Statistical Manual (DSM) were created the term neurosis was eventually superseded by Anxiety disorder.The current version of the Manual (DSM-IV) recognises six specific categories of anxiety: phobias, panic disorder, generalised anxiety disorder, obsessive-compulsive disorder, posttraumatic stress disorder, and acute stress disorder. Obviously in an essay such as this it would be impossible to give an adequate account of psychological theories regarding all of these distinct anxiety categories. Instead this essay will focus in on one important diagnostic category, that of Panic Disorder (PD). PD is chosen as it is has such extremely debilitating effects on the patient and has also been shown to incur a large proportion of health care costs relative to other anxiety disorders (Rees, Richards, & Smith, 1998) of which more is said below. This being the case there has been much recent research conducted into elucidating the nature of the condition and this offers a good opportunity to explore the way psychological research can help us to come to an understanding of such conditions in general.The Greek God Pan used to delight in terrifying lone travellers and it is his name that is used for the psychiatric condition known as Panic Disorder, though it has gone under many names including Dacosta’s syndrome, soldiers heart, neurasthenia and anxiety hysteria (Baron-Cohen 1997). The condition is characterised by sudden and overwhelming dread. It is now widely recognised that the disorder is not merely an extreme form of ordinary fear but rather a condition with its own causes and treatments. The diagnostic criteria that defines PD in the DSM-IV include: a fear and discomfort that arises suddenly and mounts to high intensity in 10 minutes or less, along with several of the following symptoms: a palpitating or pounding heart, laboured breathing, sweating, trembling, chest pain, nausea, dizziness, numbness and tingling in the hands and
feet, chills, hot flushes, choking sensations, a feeling of unreality, or a fear of collapsing, dying or going insane. The diagnostic criteria corresponds well with individual accounts of panic attacks, for example here is an account of a female sufferer:"--It started 10 years ago. I was sitting in a seminar in a hotel and this thing came out of the clear blue. I felt like I was dying. For me panic attack is almost a violent experience. I feel like I’m going insane. It makes me feel like I’m losing control in a very extreme way. My heart pounds really ...
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feet, chills, hot flushes, choking sensations, a feeling of unreality, or a fear of collapsing, dying or going insane. The diagnostic criteria corresponds well with individual accounts of panic attacks, for example here is an account of a female sufferer:"--It started 10 years ago. I was sitting in a seminar in a hotel and this thing came out of the clear blue. I felt like I was dying. For me panic attack is almost a violent experience. I feel like I’m going insane. It makes me feel like I’m losing control in a very extreme way. My heart pounds really hard, things seem unreal, and there’s this very strong feeling of impending doom." (Rapee, 1998) Typical onset of symptoms begin around late twenties and early thirties. There is a 6-month prevalence of panic disorder in major U.S. cities of around 6 in 1000 for men and 10 in 1000 for women (Weissman, 1985; cited in Baker, 1989). Onset is also associated with stressful life experiences (Pollard, Pollard & Corn, 1989; cited in Davison & Neale, 1998). PD is known to occur through a variety of cultures though it often carries with it strong cultural characteristics, for example among the Eskimo people of west Greenland it can take the form of kayak angst where symptoms include intense fear, disorientation and fear of drowning (Davison & Neale, 1998)PD has a high comorbidity with other disorders, which can make diagnosis difficult. It often occurs with or can lead to agoraphobic disorder, especially for women (Hallam, 1985). It often co-exists with major depression (Breier et al, 1986; cited in Davison & Neale, 1998) and/or alcoholism, which may function as a coping strategy, especially for males (Hallam, 1985).Research (Rees, Richards, & Smith, 1998) has shown that PD sufferers have more medical tests, use emergency services more and are more likely to be misdiagnosed than other anxiety groups i.e. social phobics. Sufferers have also been shown to incur health service costs 11 times higher than controls and 5 times higher than social phobics. This may be due to PD sufferers being misdiagnosed in the first place or simply unconvinced by a PD diagnosis in the face of intense feelings of bodily dysfunction, i.e. a perceived feeling of heart attack or choking etc (Rees, Richards, & Smith, 1998).The two prevalent psychological theories for PD are the cognitive model (Clark, 1986, cited in Baker, 1989) and the psychophysiological (PP) model (Ehlers, 1989, cited in Baker, 1989). Both models assume the PD arises as a result of a tendency to associate harmless bodily symptoms (Clark, 1986; cited in Windmann, 1998) or of "bodily and/or cognitive changes" (Ehlers, 1989; cited in Windmann, 1998) with threat of immanent attack. The models consider PD as quantitatively not qualitatively different from normal panic episodes (as opposed to the more medical models which view it as more of a qualitative difference, see Baker, 1989) on a number of different dimensions. Which include the nature of the triggering event (internal vs. external), the nature (somatic vs. psychic) and time factor (sudden vs. gradual) of the dominant symptoms and also the nature of the feared outcomes of the attacks (immediate bodily/mental catastrophes vs. long term negative events, (Margraf & Ehlers; cited in Baker 1989)).Both PP and cognitive models propose that the perception of threat based upon physical symptoms create a positive feedback loop which exacerbates the perceived feeling of panic which spirals up into a full-blown panic attack. The cognitive model refers to this process as ‘cognitive misinterpretation’ as sufferers erroneously take normal bodily sensations (such as increased heart rate) and catastrophically misinterpret them as signs of physical threats. The PP model extends this idea in that it also proposes that associated conditioning of fear responses can also provide panic provoking mechanisms (McNally, 1994; cited in Windmann, 1998). Any one of the features of the feedback loop could precipitate the panic attack, for instance physiological changes may occur due to activity, drug intake, situational stressors etc. The person perceives these changes though not necessarily accurately, for example heart rate may seem to increase when lying down due to a change in posture, which increases cardiac awareness, the person may associate these bodily perceptions with danger which in turn cause further anxiety which leads to more physiological changes and so-on. PP theories consider bodily sensations to be the initial precipitator of panic attacks and the PD sufferer to have characteristics that make him/her more likely to experience bodily symptoms that are likely to trigger the attack. Such attributes can include a tendency for subtle hyperventilation, ‘weak neurological signs, and cardiovascular events (Margraf & Ehlers; cited in Baker, 1989).PD has also been found to run in families (Crow et al, 1987; cited in Davison & Neale, 1998) which may reflect a genetic diathesis. Klein (1980, 1981; cited in Baker, 1989), proposes that PD is linked to separation anxiety responses in early childhood. As such PD in this model is seen as a regression phenomenon whereas more evolutionary based approaches see PD as a normal if exaggerated adult response that performs an adaptive function in our species history (Baron-Cohen, 1997).Problems with the PP model include a lack of explanatory power as anxiety is said to be the result of perception of anxiety, which is a circular argument (Lang, 1988; cited in Windmann, 1998) and scientific theories need to avoid confounding explanans and explananda in the same account of a phenomena. A second problem is that the temporal succession of the ‘presumed causes from the presumed consequences’ is difficult to empirically disentangle, as they are strongly interdependent (Windmann, 1998 p.490). A third problem of both cognitive and PP models is that they do not explain why some people misread bodily symptoms as catastrophic whilst others do not.Cognitive models usually imply that PD sufferers have an attentional bias towards threat cues and bodily sensations (Beck, Emery & Greenberg, 1985; cited in Windmann, 1998). PD patients have been shown to have shorter response latencies to presentations of threatening words (Asmundsun, Sandler, Wilson & Walker, 1992; cited in Windmann, 1998). However it is unclear whether a cognitive bias towards threat perception in PD sufferers is a cause or a consequence of the disorder (McNally, 1994; cited in Windmann, 1998).A new model by Beck & Clark (1997) proposes a multistage information processing model. In this model a proposed threat can be detected by an early warning system, which operates subconsciously, and is purely stimulus-driven. Processing done at this stage is "relatively undifferentiated" and classifies threats only on a rough perceptual basis. This system is argued to be evolutionary useful in that a person who is ‘weighted’ towards more responses to possible threats, even if some of these constitute false alarms will have a greater chance of survival. And it is these false alarms that are described as ‘cognitive misinterpretations’ in the clinical literature (Clark, 1986, 1988; cited in Windmann, 1998). However the false alarm rates have to be minused from the ‘hit rates’ to be able to come to a figure of optimum survival value (see Windmann & Krüger, in press).Windmann (1998) suggests that the revised Beck & Clark (1997) model can be combined with neurobiological perspectives to provide a new model of PD. It is suggested that a dysfunction in the amygdala and the ascending transmitter system can lead to false alarm perceptions of threat, causing irrational fear and anxiety. This theory represents a monistic approach that unites the previously antithetical medical and psychological approaches. The new theory sheds some light on previously problematical aspects of PD. Some of these include the observation of groundless respiratory manoeuvres that occur during a panic attack. This can be accounted for in the new theory as the amygdala is connected to the central nuclei of respiratory regulation. It is also possible to see why antidepressants and alcohol can have alleviative effects upon PD as these should also counteract the effects of the pre-attentive alarm system (Windmann, 1998). The theory is supported by other finding of the role the amygdala has in fear production (Gloor, 1992; cited in Windmann, 1998).An implication of the theory regards the assumption that anxiety reflects an enhanced propensity to give false alarm reports regardless of the stimulus (i.e. whether it is neutral or not). The implication being that PD sufferers should display an enhanced response bias to tasks requiring the discrimination between threatening and neutral stimuli (Windmann, 1998) Although the theory is based upon the assumption of a physical dysfunction, Windmann does not go on to suggest a drug based therapeutic approach. Firstly, the problem of systemic effects that psychoactive drugs have on the whole brain often lead to unavoidable side effects, and secondly the brain’s extreme plasticity, even in adulthood offer the possibility that cognitive therapies may be useful in re-organising the structure of neuronal connections which can facilitate coping stratagies for the PD sufferer.Much research is still being done into the problem of Panic Disorder. Until recently the psychological and medical approaches have tended to avoid each other. In psychology the more successful models have tended to stress the cognitive aspects of the disorder and have proven useful in providing therapies for helping sufferers re-evaluate the symptoms and enable them to cope to a certain extent with the debilitating effects of the disorder. Drug therapies can be effective in taking away the symptoms but often entail deleterious side effects and can also be addictive. The new monistic approach offered by Windmann (1998) seems to provide a conceptual framework for both the medical and psychological approaches to work together for a more encompassing understanding of the disorder. According to this model the underlying cause, whilst biological in nature, may well still benefit from being treated with psychological/cognitive methods. The theory’s multidisciplinary approach also avoids the crude physical/mental distinctions that have to a large extent hindered a better understanding of the disorder until this time. REFERENCESBaker, R. (1989) Panic Disorder: Theory Research and Therapy. Chichester, UK: John Wiley & Sons Ltd.Baron-Cohen, S. (1997) The Maladaptive Mind: Classical readings in Evolutionary Psychology. Hove, UK: Taylor & Francis.Davison, G.C. & Neale, J.M. (1998) Abnormal Psychology. New York: John Wiley & Sons.Hallam, R.S. (1985) Anxiety: Psychological Perspectives on Panic and Agoraphobia. London: Harcourt Brace Jovanovich.Rapee, R., Mattick, R. & Murrel, E. (1998) Cognitive mediation in the affective component of spontaneous panic attacks, Journal of behaviour therapy and Experimental Psychiatry, Vol. 17, pp.245-53.Rees, C.S., Richards, J.C. & Smith, L.M. (1998) Medical utilisation and cost in Panic Disorder: A comparison with Social Phobics. Journal of Anxiety Disorders, Vol. 12, No. 5 Sept-Oct 98, pp. 421-435.Windmann, S. (1998) Panic Disorder from a Monistic perspective: Integrating Neurobiological and Psychological Approaches. Journal of Anxiety Disorders, Vol. 12, No. 5 Sept-Oct 98, pp.486-507.
