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Panic Disorder |
Overcoming Anxiety (Home) > Panic Disorder > Areas of Controversy and Debate Areas of Controversy and DebateSince the introduction of the DSM-III, the nosological position of PD has been controversial. Two main positions have arisen and given rise to a long-lasting debate. Most North American psychiatrists consider the panic attack to be the central feature of the disorder. Panic is seen as a pathological, primary phenomenon, central to the origin of the disorder. Its association with agoraphobia is interpreted as the avoidance behaviour being a secondary or a derived phenomenon, both aetiopathogenetically and chronologically . This position considers the panic attack as a predominantly biological event, qualitatively distinct from the others forms of anxiety. Moreover, the American view of PD is that repeated, sudden and spontaneous panic attacks are only seen in panic disorder. Panic attacks seen in other conditions are not spontaneous. Since agoraphobia is only considered a consequence of panic, this position denies its existence without panic. Several studies support this view. The fact that panic attacks could be experimentally provoked in predisposed subjects by a series of chemical challenges reinforced the hypothesis of a biological origin of PD. The possibility of provoking anxiety in normal subjects and increasing panic attacks in panic patients by the use of yohimbine or isoproterenol point to an important role for the noradrenergic system in PD. Consistent with this hypothesis is the observation that drugs preventing spontaneous panic attacks appear to reduce the locus coeruleus firing rate , whereas the panicogenic stimuli usually increase this firing. In favour of the American view are also electroencephalographic data, which show that night panics occur outside rapid eye movement phases of sleep. Changes in EEG and cerebral blood flow, anatomical abnormalities in the mesiotemporal region on magnetic resonance imaging, hyposensitivity to benzodiazepines and neurological soft signs have all been reported in PD. As a confirmation of some biological abnormality, Nutt et al. demonstrated that flumazenil is anxiogenic in patients with PD: possible explanations of this finding are that in PD there is a relative deficiency of an anxiolytic ligand, or that the set point of the benzodiazepine receptor is shifted in the inverse agonist direction. Not all these findings may be unequivocally interpreted as in favour of the biological view. The response to a chemical challenge, for instance, can be seen as the intrapsychic dramatisation of bodily sensations, rather than as a specific substance response. The fact that the various chemical challenges do not share any common mechanisms could be explained on this basis. In addition, the broad range of drugs effective for panic could suggest a low biological specificity. Moreover, the specificity of the response of panic anxiety to tricicylic antidepressants has not been confirmed in other trials, where other forms of anxiety, e.g., GAD, proved to respond to these drugs. Many European psychiatrists contend that the single panic attack is an aspecific phenomenon, which can be found in many other conditions: somatic illness, depression, alcohol abuse, borderline states, acute psychosis, etc. Isolated panic attacks are also frequent in normal subjects. This position therefore contends that panic per se is neither specific nor pathological. Panic becomes pathological when its occurrence is combined with specific premorbid vulnerability factors. Preconstitutive aspects of panic must exist either as a peculiar cognitive pattern or as a vulnerability to environmental events. The European position maintains that a phobic attitude precedes the development of panic and that specific temperamental features are necessary in order for PD to occur. There are findings that seem to support this position. All community epidemiological studies report the presence of a consistent rate of subjects affected by agoraphobia without panic attacks. Patients affected by PD were reported to show prodromal symptoms before the onset of the disorder. The presence of personological-temperamental traits predisposing to agoraphobia is also supported by empirical verification. As often happens with biological data, however, all these findings may lend themselves to different interpretation. For instance, the abnormal response to life events could be due to impairment of the cerebral neuroendocrine systems that should cope with stress. Recent findings report that patients with PD show a blunted adrenocorticotropic hormone response to corticotropin-releasing hormone (CRH) in association with basal hypercortisolism
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