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PANIC DISORDER: FROM ARCADIA TO AMERICA…
Prof Dave Swingler
Fort England Hospital
The referral was as unusual as the case was typical. What scudded out of the facsimile machine was a single page from a popular magazine detailing the account of a patient with Panic Disorder. On it, the self-referred sufferer had vigorously underlined symptom clusters with which he identified, and highlighted sections telling of a similarly tortuous course through various medical examinations and physical investigations that had yielded no cause for these pernicious episodes of anxiety. Both the story subject and the patient-to-be had been told, repeatedly, that there was "nothing wrong" with them.
Subsequent clinical evaluation would confirm that he did indeed suffer from Panic Disorder (PD). The condition had emerged some twenty five years before when, the passenger of a crowded train, he had experienced a sudden onset - "out of the blue" - of somatic symptoms including palpitations, a sense of choking, difficulty breathing, sweating, shaking and chest discomfort. He had felt nauseous, wanted to vomit and, most distressing, felt he was "going mad" and about to die. He fled the train as these symptoms reached their zenith and they subsided within half an hour, after which he felt normal again. But life was not going to be normal again. The subject became increasingly concerned that this episode would recur and he worried about the implications of the experience - that he was indeed "mad" or would imminently die of a heart attack. These fears were confirmed when he had further, unpredictable attacks. His behaviour changed: he avoided public places in case a catastrophe would befall him and help would not be at hand.
Help was not at hand from formal medicine either. Despite countless specialist opinions and extensive, expensive, physical investigations, nothing could be found. The opinions were that nothing was wrong. But something clearly was: he dropped out of university, his marriage fell apart and his social life became increasingly restricted. After the diagnosis had been made and simple, limited investigations excluded common or overt confounders (such as hyperthyroidism or caffeine intoxication), the sufferer responded well to citalopram (Cipramil®), a selective serotonin reuptake inhibitor, in combination with cognitive-behaviour therapy.
The word "Panic" derives from Pan, the Greek god of flocks and herds. Legend has it that he would descend, "out of the blue", on Arcadia at noon to frighten the animals, shepherds and nymphs. One of the latter, Syrinx, froze out of terror and became a reed from which Pan purportedly cut his pipes, a paradoxical symbol of "bucolic calm". Panic as a medical entity (albeit not the word) entered the literature as early as 1866 and De Costa described a condition prevalent in American Civil War combatants as "irritable heart" in 1871. Simultaneously, Westphal recorded cases of "agoraphobia" - literally fear of the market place - while Benedict coined the term "Platzschwindel" for "place dizziness" encountered in Vienna. In an entirely different setting, early twentieth century Danish explorers found Greenland Eskimo hunters who suffered "kayak angst". While awaiting seals to hunt on a sunny day out on calm seas the afflicted would, out of the blue, have difficulty breathing, experience racing hearts and fear imminent death. The subjects would race back to land and flee into their igloos, some never emerging again.
Panic as a disorder gained credence in the Sixties when it was discovered that lactate infusions could induce panic attacks in vulnerable individuals. This was an important finding at a time when psychiatry was flirting with rapprochement with the medical mainstream after decades in a more psychological domain. The conceptual development of anxiety is illuminating. Freud and Breuer's 1895 Studies on Hysteria separated anxiety neurosis from neurasthenia, a differentiation echoed eighty years later by the Research Diagnostic Criteria (RDC) division of anxiety neurosis into two groups. This was formalised by the 3rd edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM III) in 1980 that differentiated Panic Disorder from Generalized Anxiety Disorder. Donald F Klein's simultaneous conceptualization of anticipatory anxiety as a consequence of panic attacks rather than their precursor, that agoraphobia follows both and that panic attacks responded to the tricyclic antidepressant imipramine and not to anxiolytic benzodiazepines, was later integrated into subsequent editions of DSM.
The pre-eminence of American thinking if shaping psychiatric nosology over the last two decades has attracted criticism that PD is a North American construct serving political and economic interests. It is, however, now clear that the condition is universal and consistent across geographical and cultural boundaries. Further, a comparative analysis of "kayak angst", koro (a Chinese anxiety syndrome involving the fear of penile retraction into the body resulting in death) and PD across the domains of symptoms, onset, intensity and duration, shows striking similarities.
Panic attacks are the generic building blocks of PD. They consist of a cluster of somatic symptoms involving autonomic drive phenomena in respiratory, cardio-vascular and nervous systems with associated cognitive experiences of derealisation/depersonalisation, a sense of impending doom and urges to escape with fear of loss of control or death. They typically commence suddenly, reach a crescendo within ten minutes and abate within half to one hour. Panic attacks are central but not limited to PD and must be differentiated from episodes of intense anxiety. They commonly occur in depression and can be induced by substance (including caffeine) intoxication. The feature of PD, apart from recurrent unexpected panic attacks, is the development of worry about implications of the attacks and secondary phobic avoidant behaviours. These include agoraphobia, the opposite of claustrophobia, when sufferers fear public situations from which escape may be difficult or embarrassing or where help will not be at hand in the event of a panic attack.
That sufferers are subjected to elaborate medical investigation is not surprising as crucial differential diagnoses include cardiac ischaemia, asthma, transient cerebral ischaemic attacks or stroke, central nervous system infections and migraine, a variety of endocrine perturbations including hyperthyroidism, and anaphylaxis. Psychoactive substance intoxication and withdrawal (stimulants being the commonest) are often overlooked. Panic attacks not part of PD can occur in multiple psychiatric contexts such as other anxiety disorders, depression and factitious disorders. They can also be the content of malingering for secondary gain in forensic or compensation settings. Judicious clinical skill is required to diagnose PD as many of its mimics can also be consequences of the condition. Major Depressive Disorder complication rates vary widely, with reports from 10%-65%. Associated features include substance abuse, other co-morbid anxiety disorders such as Social Phobia and Generalized Anxiety Disorder (15%-30%), Specific Phobia (2%-20%), Obsessive Compulsive Disorder (10%) and Post Traumatic Stress Disorder (at least 10%). Suicide remains a risk and marital, occupational and financial consequences can be crippling.
While panic attacks are common, the 1.5%-2.5% lifetime prevalence of PD is approximately double that of schizophrenia. PD sufferers are over-represented in mental health facilities (10%), ear-nose-and-throat, respiratory and neurology clinics (10%-30%) and especially cardiology clinics (60%). A genetic basis to the disorder is borne out by risk increasing with genetic proximity to the proband. Risk of 1st degree relatives developing PD is 4-8 times that of the general population and rockets to 20 times if the age of onset is before twenty years of age. Monozygotic twins have a higher risk than dizygotic ones. Females are more vulnerable to develop PD, especially the subgroup associated with agoraphobia.
Elucidation of the biological mechanisms of PD is hampered by deciding what is primary - it is uncertain whether or not research findings are those causing the disorder or its consequence. Theories include a notion of autonomic nervous system dysregulation with an increased "tone", slowed habituation and excessive response. Roles for the limbic system in anticipatory anxiety and the prefrontal cortex in phobic avoidance have also been mooted. Noradrenaline in the locus ceruleus, serotonin at the median raphe nucleus and gamma aminobutyric acid (GABA) are the primary neurotransmitters implicated. Studies of "panicogens" - chemical agents able to induce panic - are illuminating. Apart from metabolic challenges with lactate and bicarbonate and respiratory precipitants of hyper- and hypocapnia, several pharmacological probes have thrown new light into the murky recesses of scientific understanding of panic. Flumazenil (GABA antagonist), fenfluramine (serotonin agonist) yohimbine (alpha2 noradrenergic autoreceptor antagonist) and caffeine (adenosine antagonist) all have the ability to induce panic. The association of PD with mitral valve prolapse is controversial. Early studies suggesting a reciprocal association were negatively affected by selection bias. The contemporary view is that, although they share common features, they are not co-morbid conditions.
PD is a condition that is best "managed" rather than merely "treated". Explanation, education and reassurance are pre-requisites for effective drug and psychological interventions. Biological treatments include anti-depressant agents, especially those with serotonergic activity. Tricyclic moieties imipramine and clomipramine are effective and three selective serotonin reuptake inhibitors - paroxetine (Aropax®), citalopram (Cipramil®) and sertraline (Zoloft®) are registered for use in South Africa. As this is likely to be a class effect, fluoxetine and fluvoxamine (Luvox®) may also have off-label utility. Irreversible and modern reversible mono-amine oxidase inhibitors, as well as lithium carbonate and anti-convulsants carbamazepine and valproate, have been used.
Psychodynamic and cognitive psychotherapeutic models can be applied in individual, couple and family contexts. The former (adapted from Shear) is based on a neurophysiological vulnerability leading to a psychological vulnerability which, strained by biologically or psychologically meaningful life stress, precipitates neuropsychological activation. An intrusive negative affect chaperones the initial episode of panic. Cognitive therapies currently predominate. Clark's approach posits that a trigger stimulus is perceived as a threat and leads to apprehension with a physiological response and normal bodily sensations. In individuals with a catastrophic rather than benign "cognitive style", these bodily sensations are misinterpreted as life threatening which is, in itself, a trigger stimulus and a vicious cycle ensues.
Social interventions are effective but none moreso than a combined bio-psycho-social approach. Follow up studies suggest that, ten years post-treatment, the condition has resolved in one third of patients, some 50% have only mild symptoms while a fifth are unchanged or deteriorating.
Panic Disorder. A condition, the conceptualization of which has directed a more refined understanding of the spectrum of anxiety disorders. A condition that straddles the divide between physical medicine and psychiatry and which could serve as a vehicle for their integration. A condition that is frequently overlooked in general medical settings, and yet is eminently treatable with both biological and psychological modalities.
More Information:
Patients may wish to consult their clinical practitioners or, in South Africa, contact the Depression and Anxiety Support Group telephone +27-(0)11-7831474/6 or 8841797, facsimile 8847074, email
anxiety@iafrica.com. Clinicians are referred to an excellent book on the subject "Panic Disorder: Clinical Diagnosis, Management and Mechanisms" edited by DJ Nutt et al published by Martin Dunitz in 1999. ISBN 1-85317-686-9. Visit
www.dunitz.co.uk.
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