Cognitive and Biological Approaches to Panic Disorder - Essay Example

The cognitive and biological approaches to Panic Disorder The cognitive and biological approaches to Panic Disorder Roehampton - School of Human and Life Sciences In partial fulfillment of the requirements for PSY010X719S & PSY020X720S Instructor's Name Date Abstract According to the DSM-IV, panic disorder is classified as an anxiety disorder consisting of repeated and unexpected panic attacks. Panic Disorder (PD) is a condition that is characterized by recurring sudden increases in anxiety accompanied by a variety of intense bodily symptoms. It is a distressing phenomenon that many people suffer from at some point in their lives. PD makes about 5% of psychiatric diseases (Horwath, 1993). There are many theories of the nature of PD. And still, in spite of this, many misunderstanding. The authors had been defending as cognitive as biological and biochemical theories of PD physiology. Donald Klein's biological view of PD as a medical disease and David Clark's cognitive view of panic as an escalation of physiological activation due to catastrophic misinterpretations of bodily symptoms was a main point of argues about PD nature. This paper will review the main theories and will compare them. The cognitive and biological approaches to Panic Disorder The common features of PD include a racing or pounding heartbeat; dizziness and lightheadedness; feeling that "I can't catch my breath"; chest pains or a "heaviness" in the chest; flushes or chills; tingling in the hands, feet, legs, arms; jumpiness, trembling, twitching muscles; sweaty palms, flushed face; terror; fear of losing control; fear of a stroke that will lead to disability; fear of dying; fear of going crazy, etc. Sometimes stomach disorders are seen (Lydiard, 1994).A panic attack typically lasts several long minutes and is one of the most distressing conditions a person can experience. In some cases, panic attacks have been known to last for longer periods of time or to recur very quickly over and over again. The aftermath of a panic attack is very painful. The greatest fear is that the panic attack will come back again and again, making life too miserable to bear (Warshaw,2000). Panic is not necessarily brought on by a recognizable circumstance, and it may remain a mystery to the person involved. At other times, excessive stress or other negative life conditions can trigger an attack (Katerndahl,2000). Much research was carried out to understanding the biological and psychological mechanisms of PD and to developing effective treatments. A working consensus has been reached regarding its clinical features (as laid down in DSM-IV) and guidelines for its psychological or pharmacological treatments are delineated in documents from the NIH and the American Psychiatric Association. A number of theories have been suggested and tested. The majority of them are based on biochemical or physiological markers. Still, the exact etiology has not been found. The aim of this paper is to review the main theories of PD and to discuss them. Classification of theories 1. The serotonergic model suggests an exaggerated postsynaptic receptor response to synaptic serotonin. Recent studies report subsensitivity of 5HT1A receptors. The 5HT system or one of its subsystems may play a role in the pathophysiology of panic disorder, the precise nature of which must be delineated by further investigation. 2. The catecholamine model postulates increased sensitivity to adrenergic CNS discharges, with hypersensitivity of presynaptic alpha-2 receptors. 3. Similarly, the locus ceruleus model explains that panic symptoms are due to increased local discharge resulting in adrenergic neuron stimulation, similar to the more general catecholamine theory. Locus ceruleus activity also affects the hypothalamic-pituitary-adrenal axis, which can respond abnormally to clonidine in patients with panic disorder. 4. The lactate model focuses on symptom production by postulated aberrant metabolic activity induced by lactate. 5. The false suffocation carbon dioxide hypothesis explains panic phenomena by hypersensitive brainstem receptors. 6. The GABA model postulates decreased inhibitory receptor sensitivity, with a resultant excitatory effect. 7. The neuroanatomic model suggests that panic attacks are mediated by a "fear network" in the brain that involves the amygdala, the hypothalamus, and the brainstem centers. 8. The genetic hypothesis has attempted to refer panic disorder to definable genetic loci, without success to date (Colin, 2006). None of the theories can fully describe the variety of clinical presentations of PD and answer to all the questions. Biomedical model The principle of the biomedical model is that mental illness is basically or at least in part a biological disease. It discusses that there are some pathological changes in the central or peripheral nervous system structure, metabolism or catabolism of some endogenous substances or that there is a malfunctioning biochemistry. The fact that pharmacological treatment with tricyclic antidepressants and MAO inhibitors is effective in panic attacks, strongly supports this theory (Hoffman, 1999; Johnson, 1995). One of the first scientists that described this theory was Klein D.F (1994). Klein D.F. hypothesized that a physiologic misinterpretation by a suffocation monitor misfires an evolved suffocation alarm system. This produces sudden respiratory distress followed swiftly by a brief hyperventilation, panic, and the urge to flee. Carbon dioxide hypersensitivity is seen as due to the deranged suffocation alarm monitor. Klein used phenomena of panic during relaxation and sleep, late luteal phase dysphoric disorder, pregnancy, childbirth, pulmonary disease, separation anxiety, and treatment to test and illuminate the suffocation false alarm theory (Klein, 1994). He indicated that spontaneous panic cannot be fear, but must represent some other malfunction and suggested that the spontaneous panic is a suffocation false alarm. A recent challenge to the theory from acetazolamide infusion is discussed. Developing a possible antecedent for the pathologically depressed threshold for the suffocation alarm, in the form of a phasic endorphinergic deficiency was presented. The Kleins theory was probed by different authors. The suffocation alarm theory predicts differential emotional responding to biological challenges that affect arterial partial pressure of carbon dioxide (PCO-sub-2). These PD patients should exhibit (a) lower fear and less likelihood of panic in response to biological challenges that lower PCO-sub-2 levels, and (b) increased fear and greater likelihood of panic in response to biological challenges that raise PCO-sub-2 levels (inhalation of 35% CO-sub-2 gas). The following indicators of the suffocation monitor were assessed: (a) severity of dyspnea symptoms, (b) frequency of dyspnea symptoms, (c) heightened respiration rate, and (d) lowered PCO-sub-2 levels (Shmidt, 2000). Ratings of physiological and subjective responding, as well as panic, were obtained during both a hyperventilation and a 35% CO-sub-2 challenge. None of the classification methods predicted differential emotional responding to hyperventilation versus 35% CO-sub-2 challenge. To test this theory, McNally R.J. et al. (1995) conducted phenomenologic comparisons between attack patterns of patients with panic disorder and community subjects who had experienced unexpected panic. Effect size and multivariate analyses revealed that three cognitive symptoms best discriminated clinical from nonclinical panic (fears of dying, heart attack, and loss of control). These findings are consistent with cognitive theories of panic. Although lacking the discriminative power of cognitive symptoms, suffocation sensations had the largest effect size of any physiological symptom. Kleins theory also explains why women are tend to have PD more often. the physiological response to CO2 in female patients with panic disorder differed significantly across multiple indicators, including at-rest breathing rate and end-tidal CO2 (Papp et al., 1997). Female patients showed the greatest CO2 sensitivity, illustrated by their highest respiratory rate. These findings suggest that female patients with panic disorder may have a hypersensitive suffocation alarm and may efficiently compensate for hypoxia and hypercapnia. The other authors in contrary rejected Kleins theory. They conclude that there is neither empirical evidence nor compelling argument to support the assumptions or the proposed neurological mechanism of a "suffocation alarm", true or false, or a CO2 "suffocation monitor" (Ley, 1994). Response to sodium lactate infusions has been proposed as an experimental model and a biologic marker for panic attacks. Several authors have claimed that patients suffering from panic attacks, but not normal controls, "panic" in response to lactate. A careful review of methods and results of 13 studies, however, reveals serious methodologic problems, lack of specificity and sensitivity, and a failure to consider cognitive variables. When baseline differences are ruled out, the responses of patients and controls may not differ. So far, response to lactate cannot be interpreted as a model and marker for panic attacks and does not provide evidence for their underlying biologic distinctness from other types of anxiety (Margraf, 1996). Klein's model is more complex and comprehensive than the simple carbon dioxide hypersensitivity theory and many aspects of the panic disorder fit into its framework. However, if the false suffocation alarm was the main triggering mechanism of panic attacks in the first group of patients in whom dyspnea is predominant, this symptom would have to be the necessary, sufficient and initial manifestation of panic attack. Apparently, that does not correspond to the clinical reality. Therefore, false suffocation alarm might be one of the possible mechanisms but certainly not the only one. Cognitive theory All the cognitivo-behavioral theories provide plausible hypotheses of the etiology of PD, and certainly reflect the experience of people who suffer from it. After all, these models are based on clinical experience with PD patients. On the other hand, their truthfulness does not discredit the claim that these patients have also an abnormality in their neurobiology that is either the cause or a consequence of their life experiences. Clark's theory Clark's theory of catastrophic interpretations (1988) sees panic attacks as a result of maladaptive and faulty interpretation of bodily sensations. Physical sensations that would be processed as normal, not alarming, or not registered at all by healthy individuals, are perceived as more dangerous than they really are and interpreted as an imminent physical or mental catastrophe. For instance, palpitations would be interpreted as a heart attack. According to Clark, such catastrophic interpretations trigger the panic attack. This theory would provide a plausible explanation for panic attacks during relaxation, since bodily sensations are more apparent when the person is relaxed. However, it cannot account for panic attacks during the deep stages of sleep, even though some might argue that some kind of a cognitive filter remains active, screens out unimportant signals, and lets those of personal importance go through. Such mechanism can be exemplified by sleeping mother who wakes up when her baby cries while nothing else disturbs her. However, it is questionable whether the mother's reflex to her child's distress is really comparable to the processing required for cognitive interpretation of bodily sensations. Thus, this theory may provide us with a partial explanation for the panic attack trigger or else of the escalation of symptoms once started; however, we cannot assume that such trigger is the only stimulus responsible for panic attacks. Different authors continued to develop this theory. According to Beck et al., the symptoms of anxiety follow, in a chain reaction manner, the initial impression of dying. Having experienced a series of panic attacks, the patient elaborates a set of automatic thoughts, i.e. cognitive shortcuts that require little processing and jump directly to faulty conclusions which focus mostly on impeding danger, madness, harm or death. Therefore, Beck et al. advance that agoraphobia is an association that easily forms between panic attacks and certain places or circumstances, especially those often feared by small children, such as tunnel, heights, dark or large crowds. The patients then fear being far from home, avoid certain places and often need a safe companion to provide them with some sense of security while away. Ehlers et al. (1988) proposed a model that explains panic attacks as a result of selective focusing on panicogenic interoception. According to this model, PD patients pay excessive attention to their somatic sensations. They are thus more likely to notice, perceive and react to common interoceptive stimuli. Such sensations then trigger a panic attack. There is also a hereditary mechanism in PD. Clinical experience with patients revealed that PD seems to run in families. These findings led to epidemiological studies investigating the incidence of this disorder in families of the patients. Despite methodological differences and variations in the definitions of the disorder as well as the target population of the anxious patients, the results seem to be relatively consistent. However, even though there is an increased incidence of PD in the families of the patients suffering from PD, that does not necessarily mean that genetics are responsible for the transmission. A plausible alternative hypothesis is that parents or relatives who are anxious can pass the anxiety and the anxiety-provoking thinking patterns on their offsprings; in other words, a pathologically anxious atmosphere at home may provoke anxiety in other members of the family. 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