Mental health

Panic disorder and coronary artery spasm Whatever the causative mechanism, prolonged chest pain during panic attacks requires investigation MJA 1998; 168: 376-377 The three cases reported by Mansour et al1 in this issue of the Journal add to the evidence for increased risk of adverse cardiovascular events in people with severe anxiety. The existing evidence derives from both prospective epidemiological studies2,3 and controlled longitudinal clinical studies.4 In the latter, mortality was related to severity of emotional arousal; panic disorder patients were at greater risk of sudden cardiac death than patients with lesser forms of anxiety, such as generalised anxiety disorder. Two of the cases reported by Mansour et al (Patients 1 and 3) showed a close temporal association between panic attacks and ischaemic chest pain. In the absence of severe obstructive coronary disease, might the ischaemia be due to coronary artery spasm? Patient 1 presented with severe chest pain accompanying episodes of panic. An electrocardiogram (ECG) showed mild tachycardia and ST-segment depression, but no cardiac enzymes were released, and the coronary angiogram was normal. With subsequent panic attacks, the patient continued to experience anginal pain, which resolved completely after prescription of amlodipine (a potent dihydropyridine calcium antagonist known to prevent epicardial coronary spasm). Patient 3 had long-standing panic disorder and mild hypertension. He had acute ischaemic chest pain during a panic attack; cardiac enzyme levels were raised, and infarction was diagnosed. Angiography showed no underlying atherosclerosis. Angina-like chest pain occurred during subsequent panic attacks, but once again resolved completely after amlodipine therapy. The other patient (Patient 2) experienced an infarct associated with exercise rather than with an acute panic attack. Coronary angiography during the acute stage showed that the infarct-related artery was occluded, while the other coronary arteries were normal. The patient had a nine-year history of panic disorder, and previous panic attacks had been accompanied by chest pain. However, no chest pain occurred during post-infarction panic attacks, and there was no temporal relationship between panic attacks and the major ischaemic episode. Although coronary artery spasm is one of the plausible mechanisms for the cardiac ischaemia, none of these patients had convincing evidence of spasm during panic attacks. Spasm of an epicardial coronary artery usually results in ST-segment elevation, which accompanies transmural ischaemia. A definitive diagnosis of coronary spasm requires demonstration of ST-segment elevation, or spasm at angiography, during spontaneous angina or after provocation with ergonovine, acetylcholine or hyperventilation. In Patient 1, the ECG during chest pain showed ST-segment depression, while in Patient 3 no ECG changes were seen. While coronary spasm with ST-segment depression or even no ST changes has been reported, this is very uncommon. In Patient 1, the presence of tachycardia along with ST-segment depression raises the possibility of Syndrome X (angina-like chest pain with ST-segment depression, no demonstrable myocardial ischaemia and normal coronary arteries,5 which is not to be confused with the endocrinological Syndrome X, or insulin resistance metabolic syndrome6 ). Another possible explanation is the coronary "slow flow" phenomenon, which may be caused by microvascular spasm, although slow flow was not mentioned in the angiography report. Nevertheless, the complete resolution of angina in Patients 1 and 3 after treatment with amlodipine provides circumstantial evidence that spasm was involved. Radionuclide studies shed some light on a possible link between mental stress and coronary vasoconstriction. Subjects exposed to minor experimental stress have been shown to develop significantly reduced coronary perfusion and ischaemic abnormalities of left ventricular wall motion. These abnormalities are due to coronary vasoconstriction, but are limited to subjects with at least minor degrees of underlying coronary artery disease, and are more pronounced when this disease is more severe. Subjects with normal arteries do not show such changes.7 Similarly, coronary spasm in the setting of emotional problems was described in nine women with normal or near-normal arteries,8 but it was likely that most had at least minor atherosclerosis (ie, <25% narrowing). In two of the patients reported by Mansour et al, coronary vessels were normal (and possibly also in Patient 2 before occlusion), so induction of spasm or vasoconstriction with ischaemia seems inconsistent with the experimental studies. However, angiographically "normal" arteries may harbour minor atherosclerotic lesions that do not encroach on the lumen. In addition, the severe and overwhelming emotional stress and arousal typical of panic, which these patients doubtless experienced, contrasts with the relatively minor tasks with minimal emotional responses to which the experimental subjects were exposed. The coronary vascular responses to severe and minor stress may be quite different. For example, extreme rage induced myocardial infarction in dogs, although after a critical stenosis had been created in a coronary artery.9 Severe emotional arousal deserves further investigation. Wilkinson et al showed that patients with panic disorder have dramatic increases in epinephrine secretion and cardiac epinephrine spillover during panic, but that baseline levels and responses to mild experimental stress differ little from those of control subjects.10 Cardiac perfusion and functional studies during panic would be of interest, but would require panic attacks to be artificially induced in the laboratory. The absence of ECG changes in Patient 3, despite severe chest pain and significantly raised cardiac enzyme levels, raises an important issue about myocardial ischaemia. In the radionuclide studies mentioned above, significant decreases in perfusion or abnormalities in wall motion often occurred without ischaemic pain or ECG changes. Ischaemia can be electrocardiographically "silent", particularly in certain vascular distributions, such as that of the left circumflex coronary artery. Nevertheless, it must be unusual that ischaemia sufficient to produce necrosis should produce no ECG changes. These cases should raise clinician awareness of the potential association between severe anxiety and myocardial ischaemia, so that patients with chest discomfort and panic disorder are appropriately investigated. All patients with severe panic accompanied by prolonged chest pain should have cardiac enzyme levels measured, irrespective of ECG findings. While epicardial coronary artery spasm is a plausible explanation, further investigations are needed into the mechanisms of ischaemia in panic disorder. S Ben Freedman Professor, and Head, Department of Cardiology Concord Repatriation General Hospital, University of Sydney, NSW Christopher C Tennant Professor and Head, Department of Academic Psychiatry Royal North Shore Hospital, University of Sydney, Sydney, NSW Mansour VM, Dominic JC, Jennings GL, et al. Panic disorder: coronary spasm as a basis for cardiac risk? Med J Aust 1997; 168: 390-392. Kawachi I, Sparrow D, Vokonas PS, Weiss ST. Symptoms of anxiety and risk of coronary heart disease. Circulation 1994; 90: 2225-2229. Kawachi I, Colditz GA, Ascherio A, et al. Prospective study of phobic anxiety and risk of coronary heart disease in men. Circulation 1994; 89: 1992-1997. Coryell W, Noyes R, Clancy J. Excess mortality in panic disorder. A comparison with primary unipolar depression. Arch Gen Psychiatry 1982; 39: 701-703. Cannon RO. Does coronary endothelial dysfunction cause myocardial ischemia in the absence of obstructive coronary artery disease? Circulation 1997; 96: 3251-3254. Alford FP. Syndrome X (insulin resistance metabolic syndrome): a deadly quartet or an awesome foursome? Med J Aust 1996; 164: 4-5. Tennant C. Experimental stress and cardiac function. J Psychosom Res 1996; 40: 569-583. Bashour T, Hakim O, Cheng TO. Coronary spastic angina in middle-aged women: a psychosomatic disorder? Am Heart J 1983; 106: 609-613. Verrier RL, Hagestad EL, Lown B. Delayed myocardial ischemia induced by anger. Circulation 1987; 75: 249-254. Wilkinson DJC, Thompson JM, Lambert GW, et al. Sympathetic activity in patients with panic disorders at rest, under laboratory mental stress and during panic attacks. Arch Gen Psychiatry 1998. In press. Reprints: Professor S Ben Freedman, Department of Cardiology, Concord Repatriation General Hospital, Hospital Road, Concord, Sydney, 2137. - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Christopher C Tennant

Panic disorder: coronary spasm as a basis for cardiac risk? Virginia M Mansour, Dominic J C Wilkinson, Garry L Jennings, Rosemary G Schwarz, Jane M Thompson and Murray D Esler For editorial comment see Freedman & Tennant Patients with panic disorder often complain of angina-like chest pain during panic attacks, but this is not usually considered life-threatening. We describe three patients with panic disorder and documented cardiac ischaemia during episodes of chest pain. In two, it progressed to myocardial infarction. As none had atherosclerosis evident at coronary angiography, the mechanism was presumed to be coronary artery spasm. These cases illustrate that pain typical of angina during panic attacks may have an organic cause. (MJA 1998: 168; 390-392) Introduction - Case records - Discussion - Acknowledgement - References - Authors' details - - ©MJA1998 Introduction Panic disorder is characterised by unpredictable and overwhelming feelings of fear accompanied by various symptoms of sympathetic nervous system arousal, such as sweating, palpitations, diarrhoea, and tremor.1 Often, angina-like chest pain is also present, but detailed cardiac "workup" in patients with panic disorder typically shows no abnormalities. Thus, although panic disorder is distressing and disabling, it has not been thought life-threatening. However, recent well conducted, prospective epidemiological studies show substantially increased risk of myocardial infarction and sudden death in patients with panic disorder (three- to six-fold increase).2,3 These patients sit at the crossroads of cardiology and neuropsychiatry, and provide a clinical model for investigation of the relationship between stress and heart disease. The mechanism by which cardiac risk is increased in panic disorder is not known, but has been thought to involve activation of the sympathetic nerves of the heart, predisposing to ventricular arrhythmias. We present three patients with panic disorder and chest pain whose cases suggest coronary artery spasm as a pos sible mechanism. Case records All three patients met the diagnostic criteria for panic disorder of the Diagnostic and statistical manual of mental disorders (4th edition),4 and all were non-smokers. Patient 1 A 34-year-old woman presented to a hospital casualty department in November 1996 with severe chest pain radiating to her left arm and shortness of breath after having taken cocaine. She also complained of palpitations, dizziness, tremor, and an overwhelming sense of doom and fear. She had taken cocaine occasionally over the previous two years without panic symptoms. An electrocardiogram (ECG) showed inferolateral ST-segment depression suggesting ischaemia. The pain eased with sublingual nitroglycerine and intramuscular morphine. A thallium exercise stress test two weeks later gave normal results. The patient presented again a month later with recurrent episodes of severe chest pain accompanying panic attack symptoms. She had stopped using cocaine after the first panic attack. An ECG taken during persisting pain again showed inferolateral ST-segment depression (Figure 1, below). Serum creatine kinase (CK) levels were normal. Coronary angiography during subsequent hospital admission (when the patient was free of pain) showed a normal coronary arterial tree (Figure 1). The patient was prescribed the selective serotonin reuptake inhibitor paroxetine (20 mg, increasing to 40 mg, daily), low dose aspirin (100 mg daily) and alprazolam (0.5 mg daily). Over two months' follow-up, panic attacks were less frequent, but chest pain recurred with each. After the addition of the slow calcium-channel blocker amlodipine (5 mg daily), her infrequent panic attacks were pain-free. Patient 2 A 42-year-old woman suffered anteroseptal infarction in November 1996 after exercise. Although she had no antecedent panic attack, she had a nine-year history of panic disorder, with panic attacks commonly associated with chest pain. She had been jogging as usual that morning without any symptoms, and presented later in the day with chest tightness and left-arm pain. A 12-lead ECG (Figure 2, below) showed anteroseptal ST-segment elevation consistent with acute myocardial infarction. Acute coronary angiography (Figure 2) showed total occlusion of the left anterior descending coronary artery in its mid portion. Treatment with balloon angioplasty and abciximab (an inhibitor of platelet aggregation) achieved complete recanalisation, and the pain resolved. No atherosclerosis was evident in the coronary arterial tree. Although a vasodilator was not given during angiography, the treating cardiologist described the angiogram as indicating development of fresh thrombus at a site of spasm in an otherwise normal coronary artery. Low dose aspirin and amlodipine (5 mg daily) were prescribed. The patient had further panic attacks (without chest pain) until paroxetine (20 mg daily) was also prescribed. Patient 3 A 46-year-old man presented to a casualty department in October 1996 with severe chest pain during a panic attack. He had long-standing panic disorder and a 15-year history of mild essential hypertension treated by propranolol (40 mg daily). His ECG was normal in the casualty department, and he was not admitted. The chest pain failed to resolve over the next 10 hours and he attended his family doctor, who found a raised serum CK level and arranged urgent hospital admission. His serum CK level rose progressively in hospital, peaking at 518 U/L (normal range [NR], 0-130 U/L), with CK MB isoenzyme level 66 U/L (NR, 0-10 U/L), leading to a diagnosis of myocardial infarction. Coronary angiography 14 days later, when the patient was free of pain, gave normal results, with no evidence of atherosclerosis. Over the ensuing eight months, the patient had increasingly frequent panic attacks accompanied by angina-like pain. He was prescribed paroxetine (20 mg, increasing to 40 mg, daily) and alprazolam (0.5 mg daily). Although the panic attacks became less frequent when the daily paroxetine dose was increased to 40 mg, chest pain persisted until amlodipine (5 mg daily) and aspirin (100 mg daily) were added to the regimen. Discussion These three patients with panic disorder had otherwise inexplicable episodes of cardiac ischaemia. In all three, the panic attacks were typically accompanied by chest pain. In two, the documented ischaemic events (angina with ST-segment depression in one and myocardial infarction in the other) occurred during a panic attack. In the third, while myocardial infarction was associated with exercise rather than a panic attack, there was a long prior history of panic attacks with chest pain. None of the three had atherosclerosis evident on coronary angiography, and two were women with no classical cardiac risk factors. Coronary artery spasm was thought to be the underlying mechanism of the ischaemia in all three cases. In some circumstances, patients with primary cardiac arrhythmias can be misdiagnosed as having panic disorder.5 Similarly, it might perhaps be argued that our patients had variant angina, with the anxiety disorder developing after a period of misdiagnosis of the cause of the chest pain, so that the myocardial ischaemia was a cause rather than a consequence of the panic disorder. However, in Patients 2 and 3 the diagnosis of panic disorder antedated the development of chest pain during panic attacks, while in Patient 1 angina-like pain was a feature of the first and of most subsequent panic attacks. The mechanism by which coronary spasm develops in panic disorder is not clear. Cigarette smoking can underlie coronary spasm, but our three patients were non-smokers. Hyperventilation, often a concomitant of a panic attack, can precipitate coronary spasm in the presence of atheroma6 and even in coronary arteries free of atherosclerosis.7 Patients who had spontaneous panic attacks in the research laboratory have shown a substantial increase in adrenaline secretion and sympathetic nervous system activity. 8 However, adrenaline typically increases, rather than decreases, coronary blood flow by means of b -adrenergic coronary vasodilatation.9 Similarly, sympathetic nervous system stimulation usually causes coronary vasodilatation and increases flow, partly through the attendant metabolic myocardial stimulation, but also through direct effects on the vasculature.9 In some circumstances, disorders of coronary vasomotion have been linked to dysfunction of the vascular endothelium. Endothelial function was not assessed in our patients, but such tests would be relevant for future prospective studies given that the mechanism of presumed spasm remains elusive. We suspect that coronary spasm is not uncommon during panic attacks, particularly in patients with typical angina-like pain, and that panic disorder may be an undetected cause of otherwise inexplicable coronary heart disease, especially in premenopausal women, who are otherwise at low cardiac risk. It may possibly overlap clinically with "Syndrome X", a poorly understood condition in which recurrent myocardial ischaemia occurs despite the presence of structurally normal coronary arteries. This condition, not to be confused with the endocrinological Syndrome X (insulin metabolic resistance syndrome),11 seems to result, not from coronary spasm, but from reduced myocardial flow reserve caused by a functional abnormality in the cardiac microcirculation.10 Formal testing involving measurements of coronary blood flow under conditions which increase it reflexly, such as exercise, would be needed to exclude this syndrome. An understanding of the mechanism of coronary spasm in panic disorder would facilitate therapeutic intervention. At present, we treat patients with panic disorder and clinical evidence of coronary spasm with drugs and other measures aimed at preventing or minimising their panic attacks,1 a slow calcium-channel blocker as a non-specific antispasm measure, and low dose aspirin as prophylaxis against coronary thrombosis during spasm. It is difficult to know how far to pursue cardiac testing in patients with panic disorder. As we believe their level of cardiac risk is low overall, we recommend selective investigation of those with typical angina-like pain during panic attacks. Capturing ECG evidence of myocardial ischaemia during a panic attack, either during clinic or emergency department attendance or on Holter monitoring, is of central clinical relevance. While it is important to exclude the presence of fixed coronary artery stenosis (which may coexist, particularly in older patients), standard provocative ischaemia testing is not entirely satisfactory; exercise or vasodilator pharmacological challenges are inappropriate for behaviourally induced ischaemia. Panic attacks can be induced in some patients by breathing a mixture of carbon dioxide (10%-15%) and oxygen.12 ECG or thallium stress testing using this stimulus as a challenge is worth future research evaluation. Panic disorder may provide a useful clinical model for studying the possible link between stress and heart disease. A direct relationship between mental stress and sudden death has been seen in special circumstances, such as inherited long-QT-interval syndromes, in which there is electrical instability of the heart muscle.13 In addition, rates of non-traumatic sudden death were markedly increased in people with underlying coronary disease during the 1994 Los Angeles earthquake.14 However, research on stress and heart disease has been hampered by disagreement over what constitutes stress and how to measure it. In panic disorder, the episodes of recurring, often inexplicable, anxiety can be regarded as repeated mental stress reactions. The study of cardiac risk during panic attacks may be a valid method for testing the general proposition that the clinical endpoints of ischaemic heart disease can be "triggered" by stressful events. Acknowledgement This work was supported by a Project Grant from the National Heart Foundation of Australia and an Institute Grant to the Baker Medical Research Institute from the National Health and Medical Research Council of Australia. The contributions of Dr David Prior and Sister Leonie Johnston in the research cardiac catheter laboratory are gratefully acknowledged. The authors also wish to thank Dr Emmanuel G Manolas for provision, through the Epworth Hospital, of clinical and angiographic findings on his patient. References Agras WS. The diagnosis and treatment of panic disorder. Annu Rev Med 1993; 44: 39-51. Kawachi I, Colditz GA, Ascherio A, et al. Prospective study of phobic anxiety and risk of coronary heart disease in men. Circulation 1994; 89: 1992-1997. Kawachi I, Sparrow D, Vokonas PS, Weiss ST. Symptoms of anxiety and risk of coronary heart disease. Circulation 1994; 90: 2225-2229. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994: 394-403. Lessmeier TJ, Gamperling D, Johnson-Liddon V, et al. Unrecognized paroxysmal supraventricular tachycardia. Potential for misdiagnosis as panic disorder. Arch Intern Med 1997; 157: 537-543. Girotti LA, Crosatto JR, Messuti H, et al. The hyperventilation test as a method for developing successful therapy in Prinzmetal angina. Am J Cardiol 1982; 49: 834-841. Yasue H, Nagao M, Omote S, et al. Coronary arterial spasm and Prinzmetal's variant form of angina induced by hyperventilation and Tris-buffer infusion. Circulation 1978; 58: 56-62. Wilkinson DJC, Thompson JM, Lambert GW, et al. Sympathetic activity in patients with panic disorder at rest, under laboratory mental stress and during panic attacks. Arch Gen Psychiatry 1998. In press. Hjemdahl P. Physiology of the autonomic nervous system as related to cardio vascular function: implications for stress research. In: Byrne DG, Rosenman RH, editors. Anxiety and the heart. New York: Hemisphere Publishing, 1990: 95-158. Fragasso G, Rossetti E, Dosio F, et al. High prevalence of the thallium-201 reverse redistribution phenomenon in patients with Syndrome X. Eur Heart J 1996; 17: 1482-1461. Alford FP. Syndrome X (insulin resistance metabolic syndrome): a deadly quartet or an awesome foursome? Med J Aust 1996; 164: 4-5. Battaglia M, Perna G. The 35% CO 2 challenge in panic disorder: optimization by receiver operating characteristics (ROC) analysis. J Psychiatr Res 1995; 29: 111-119. Zipes DP. The long QT interval syndrome. A rosetta stone for sympathetically mediated ventricular tachyarrhythmias. Circulation 1991; 84: 1414-1419. Leor J, Poole WK, Kloner RA. Sudden cardiac death triggered by an earthquake. N Engl J Med 1996; 334: 413-419. (Received 28 Aug 1997, accepted 21 Jan 1998) Authors' details Baker Medical Research Institute, Melbourne, VIC. Virginia M Mansour, MB BS, Clinical Research Associate; Jane M Thompson, MB BS, Clinical Research Associate; Murray D Esler, PhD, FRACP, Associate Director. Melbourne University, Melbourne, VIC. Dominic J C Wilkinson, BMedSci, Medical Student. Alfred Hospital Heart Centre, Melbourne, VIC. Garry L Jennings, MD, FRACP, Director. Medical Advisory Committee, The Melbourne Clinic, Melbourne, VIC. Rosemary G Schwarz, FRANZCP, Chair. Reprints: Professor M D Esler, Human Neurotransmitter Research Laboratory, Baker Medical Research Institute, PO Box 348, Prahran, VIC 3181. E-mail: Esler AT Baker.edu.au Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Virginia M Mansour · Garry L Jennings · Rosemary G Schwarz · Jane M Thompson · Murray D Esler

MJA Practice Essentials, Mental Health: 7. Crisis management in the community Alan Rosen "Paradoxically, if you survive them, it's in the bad conditions that you learn most about yourself." -- Tim McCartney-Snape, mountaineer (quoted in The Weekend Australian, 18-19 May 1996) MJA 1997; 167: 633-638 Synopsis - Introduction - What is a crisis? - Types of crisis - Contention in the crisis literature - Stages of a crisis - When to intervene - Practical management of a crisis - Practical points in intervention - A crisis is different from an emergency - The place of crisis intervention in psychiatric services - Who should manage crises? - Gaps in services - Conclusion - Acknowledgements - References - Authors' details - Box 1: Stages of crisis - Box 2: The process of crisis assessment and intervention - Box 3: Useful crisis resources - Case history: Stages of crisis and "depathologising" - Case history: Crisis intervention early in the course of a psychiatric illness - - - ©MJA1997 Synopsis A psychological crisis is a brief, non-illness response to severe stress. When maladaptive responses to crisis are detected, crisis intervention is employed to achieve a more adaptive resolution and a more effective learning experience. Psychiatric services cannot provide the entire range of crisis interventions required in our society. As communities, we should be encouraged to "look after our own" partly through a network of formal and informal crisis support structures. These should be carefully distinguished from emergency services. General practitioners and others in a good position to do crisis intervention require higher levels of awareness of and training in its uses, with support from specialty services. Crises can precipitate or be a consequence of mental illness. There is strong evidence that more specialised 24-hour crisis response services are needed for individuals with mental illness and their families. Evidence is emerging for the importance of early detection and intervention for young people who may be developing signs of mental illness or suicidal intention for the first time, which may manifest as a life crisis. If there is a potential or existing mental illness, good outcomes are more likely to result from good teamwork between general practitioners, other clinicians and specialist mental health services. (MJA 1997; 167: 633-638) Introduction "Crisis" was first used as a specific term in psychiatry by Gerald Caplan1,2 after considering earlier evidence that survivors of severe trauma, such as those in Lindemann's study of the "Cocoanut Grove" nightclub fire in Boston in 1942, had much better outcomes if they received immediate psychiatric help.3 A "crisis" was seen as a brief non-illness response to severe stress, and "crisis intervention" emerged to detect maladaptive responses to crises and to convert them into effective coping and learning experiences. Caplan's concept of crisis was influenced by the theories of his time. It relied on concepts of disease rather than health, and on mechanistic theories from Freud and General Systems Theory regarding "homeostasis" and "equilibrium". But these limitations were far outweighed by Caplan's contribution in emphasising the importance of preventive care, achieving mastery of the crisis, the social, cultural and material "supplies" necessary to avoid or resolve a crisis, and his pioneering advocacy of a community mental health approach.1,2,4 What is a crisis? Caplan's1,2 classic definition of crisis is an upset in the person's steady state provoked when an individual finds an obstacle to important life goals. This obstacle seems insurmountable, at least for a good while, by use of customary methods of problem solving. A crisis is a period of transition in the life of the individual, family or group, presenting individuals with a turning point in their lives, which may be seen as a challenge or a threat, a "make or break" new possibility or risk, a gain or a loss, or both simultaneously. Most crises are part of the normal range of life experiences that most people can expect, and most people will recover from crisis without professional intervention. However, there are crises outside the bounds of a person's everyday experience or coping resources which may require expert help to achieve recovery. Types of crisis Developmental crises: These are the transitions between the stages of life that we all go through. These major times of transition are often marked by "rites of passage" at clearly defined moments (e.g., those surrounding being born, becoming adult, getting married, becoming an elder, or dying). They are crises because they can be periods of severe and prolonged stress, as described by Tyhurst, another pioneer in this field,5 particularly if there is insufficient guidance and support to prevent getting stuck while in transit.6 In small-scale cultures, there is a sense of continuity and retained value in transiting from before birth to beyond death (e.g., becoming an ancestral resource). In Western societies, rites of passage between these stages have become blurred, the extended kinship networks they depend upon for clear expression have become scattered, the cultural value ascribed to such transitions varies with occupational and economic status, and events surrounding birth and death tend to be experienced as clinical termini.6 Situational crises: Sometimes called "accidental crises", these are more culture- and situation-specific (e.g., loss of job, income and/or home, accident or burglary, or loss through separation or divorce). Complex crises: These are not part of our everyday experience or shared accumulated knowledge, so we find them harder to cope with. They include: Severe trauma , such as violent personal assault, natural or man-made disasters, often directly involving and affecting both individuals and their immediate and extended support network, observers and helpers. 3,7,8 Crises associated with severe mental illness , which can increase both the number of crises a person experiences and sensitivity to a crisis. Reciprocally, the stress of crises can precipitate episodes of mental illness in those who are already vulnerable. Post-traumatic stress syndromes similar to those resulting from a disaster have been reported in some individuals 9 after emergency treatment of acute episodes of mental illness. Developmental, situational and complex crises may overlap, and one may lead to the other (e.g., a train driver distracted by being in crisis may make an error, causing a disaster). Contention in the crisis literature Controversy still surrounds the concept of crisis. The term defies consistent definition, and "crisis theory" is just that: mainly theoretical speculation based on descriptive accounts, with the cultural and clinical concepts of crisis deriving from seemingly different fields of inquiry. A personal crisis is not a clinical disorder. However, a severe or protracted response to crisis may lead to one (e.g., major depression, or, more commonly, an "adjustment disorder",10 defined as the development of clinically significant emotional or behavioural symptoms in response to an identifiable psychosocial stressor). Adjustment disorder should be distinguished from bereavement and other non-pathological reactions to crises which do not lead to marked distress in excess of what is expected, and which do not cause significant or lasting impairment in social or occupational functioning. Stress is not a synonym for crisis11 as all people face stress as part of the human condition. By no means all stressful experiences produce crises and the same type of stressor may be linked to crises, or even clinical disorders, in some but not in others. In contrast to crisis theory, some crisis interventions have been subjected to rigorous empirical study, demonstrating their effectiveness with specific problems (e.g., individuals and families seriously affected by mental illness).12,13 Crisis intervention can no longer be seen as a unified strategy for care, as many divergent practices in different settings have developed since its origin, from walk-in clinics to mobile home intervention, but Waldron has identified a number of common features.14 These include rapid service, intense work in the short term, and a practical here-and-now therapeutic focus. Stages of a crisis Box 1 presents a summary of the main stages, from the pre-crisis steady state, to crisis disequilibrium, to re-establishment of a new steady state, hopefully at an equal or higher level of organisation.11 It is often reported that a crisis state lasts several weeks, usually subsiding within one to two months, if successful resolution occurs. (See also "Case history: Stages of crisis") When to intervene Primary prevention: Strategies aimed at preventing the development of psychiatric illness altogether may be appropriate for people experiencing developmental or situational crises who have limited personal, social or cultural resources. Bereavement counselling, telephone counselling services and "How to survive Christmas" seminars18 are examples of practical primary prevention interventions in the community. Critical incident counselling may be offered to survivors or witnesses of traumatic events and disasters to prevent emergence of protracted grief reactions or post-traumatic stress disorder (PTSD),8 although efficacy in preventing PTSD remains unclear. Secondary and tertiary prevention: Secondary prevention implies that a psychological disorder has already emerged, and aims at reducing the severity, duration or the risk of recurrent relapse. Tertiary prevention is aimed at reducing the disability attendant on a disorder that is already prolonged. Indications include: People with early or acute mental illness -- preventing suicide and promoting recovery for individuals whose constitutional vulnerability and life stressors may have tipped them into an episode of mental illness, which can be highly responsive to timely crisis intervention and appropriate treatment.9,10 So-called "chronic outpatient attenders" or "chronic crisis repeaters", unnecessarily pejorative terms highlighting the frustration and attitudes of clinical staff towards these individuals who make frequent demands on services. It is often more economical and effective to provide intensive intervention at times of acute crisis rather than continuing unchallenging support of a long term sickness role. Many of these individuals have been severely traumatised in childhood. Specific interventions to deal with the sequelae of past abuse are still being developed and researched. Patients with severe or prolonged psychiatric disorders presenting with an acute exacerbation that may be precipitated by or cause a situational crisis. Defusing stressors by prompt crisis management (in conjunction with timely treatment, continuity of care and psychosocial rehabilitation) may prevent the build-up of disturbing symptoms, repeated life-disrupting hospitalisations, or suicide.9,12,13,15,17 Practical management of a crisis Crisis management is the entire process of working through the crisis to the point of resolution (Box 2). It usually includes not only the activities of the individual in crisis but also the members of the person's social network.4 Not all crises require crisis intervention, which is that aspect of crisis management carried out by crisis workers (e.g., clinicians, counsellors, police or chaplains). Practical points in intervention: Intervention frequently involves a general practitioner and a community mental health team, possibly including a psychiatrist or inpatient unit. Negotiate early in the process to formally clarify who will coordinate it, and who will do which components of the assessment and intervention (whether general practitioner, mental health worker or psychiatrist). The hospital or community crisis service should carefully identify the general practitioner's needs, especially for prompt or extra support, while the general practitioner should respond promptly to the crisis worker's liaison calls. Include family or other social or cultural supports in both the assessment and the intervention if possible. Collaborate with the individual or family in crisis ("doing with" rather than "doing to") to promote their "ownership" of the crisis, and learning of new coping and communi cation skills. Allow tension -- allowing or even encouraging a tolerable degree of arousal, tension or dependence for a limited time is sometimes functional in promoting crisis resolution. The clinician's role in a crisis can sometimes involve undoing previous inappropriate or excessive clinical interventions (e.g., inappropriate diagnoses or types of treatment, or general overmedication causing unnecessary sedation and/or other side effects). When referring a person in crisis to a hospital psychiatric unit, ask for a crisis assessment rather than insisting on hospital admission, as home-based community management often results in a better outcome. Home visits, within defined parameters of safety, should be considered for accurate assessment and review, and more direct access to all participants in the crisis. A small list of the most important specific goals for the crisis intervention which are realistic and achievable within a limited time frame should be agreed in advance between all participants, with a copy to each, and with an interactive process and date for review. If acute inpatient psychiatric care is needed, the same mental health professional(s) who engaged with the person in the community should be involved in the inpatient team (if possible) to make the transition easier and to ensure consistency of the clinical management plan agreed with the individual and family. A crisis is different from an emergency An emergency is a life-threatening situation demanding an immediate response. A crisis is often not immediately life-threatening and the timing of the response should be such as to include all participants in the crisis and existing or potential personal supports. Appropriate personnel to respond to an emergency are Police, Ambulance, Fire or Hospital Emergency Departments and/or State Emergency Services. Appropriate people to call in a crisis include general practitioners, community mental health professionals, community services officers, or lay crisis response organisations. The appropriate type of early response in an emergency is life preserving: securing physical safety, removing the person from the source of danger, and defusing physical violence. In a crisis, the early response should be crisis assessment and support, defusing stress and interpersonal strife. The use of the terms "crisis intervention" and "emergency psychiatry" are often confused by clinicians, and used interchangeably in the names and descriptions of services.17 But what difference does it make to patients and their families when they feel distressed and just know they need help now?19 In fact, they benefit by more appropriate referrals and settings for intervention when these distinctions are clearly made, while professionals are able to deliver such services more safely and effectively when they know the difference between a crisis response and an emergency response. Sometimes there is an overlap between a crisis and an emergency. When there is any hint of a crisis turning into an emergency, it is considered a skill, not a failure, if a mental health professional or general practitioner chooses not to work alone and calls for expert advice, police assistance, or other emergency services. The place of crisis intervention in psychiatric services The evidence indicates that 24-hour home-visiting crisis response services should be integrated into local comprehensive services for people seriously affected by mental illnesses and their families. 9,12,13,15,20 The potential for new learning and personal growth in this population and their families has probably been vastly underestimated, often by the clinicians involved.17 Systematic interventions to promote such new learning out of "using the crisis" of acute psychiatric episodes are being developed to reverse the potentially erosive effects of early psychosis on self-esteem, identity and related maturational tasks.9,19 Family problem-solving techniques aimed at acquiring new coping techniques in crisis have been shown to prevent relapses.20,21The principles of effective crisis intervention are consistent with current good practice in mental health services, regardless of the phase of care. There is evidence that people severely affected by psychiatric illnesses are much more likely to cooperate with interventions which are tailored to their individual needs, and when they feel listened to, are consulted and offered choices regarding types of proposed interventions. Cooperation is further enhanced when they and their families are provided with sufficient information and explanation, when time is taken to negotiate intervention goals, when low-key and low-dose interventions are offered (at home on their own "turf", if possible, rather than ours) and when the traumatising effects of involuntary hospital admission and heavy sedation are avoided.6,9,12,13,22 Inpatient psychiatric care is sometimes essential but should be arranged on a voluntary basis if possible. (See also "Case history: Crisis intervention early in the course of a psychiatric illness") Who should manage crises? General practitioners, community workers, police, ministers of religion, counsellors, as well as mental health professionals, are all in a position to be involved in crisis intervention. General practitioners are particularly well placed to help people in crisis and their families. Should all crises be referred to psychiatric services? Emphatically no, although psychiatric services are most appropriate for people in crisis who have diagnosable psychiatric illnesses and who may be suicidal. Firstly, psychiatric services do not have the resources or mandate to handle all crises in the community. There are community services for domestic abuse, children at risk, and sexual assault crises, non-government and church organisations dealing with couple, family, existential and spiritual crises, and networks for bereavement and disaster counselling. Secondly, many people requiring help with crises do not wish to be seen by a psychiatric service or professional, which they may perceive as stigmatising, and therefore adding to their troubles. When the crisis is not complicated by significant psychiatric symptoms, it may be managed with significantly better outcome by a general practitioner who has the person's trust and does not need to label the person with a psychiatric diagnosis.23 Thirdly, some communal voluntary organisations run crisis hotlines (e.g., Lifeline) which may produce more timely referrals to clinical services, or care for people who would not present clinically . Whether they reduce the number of suicides is a more contentious issue. Peer-group and consumer-driven mutual support lines are developing further, via telephone "warm-lines", interactive radio, computer bulletin board chat-lines and the Internet. While these are a potential wellspring of support, they may make the caller feel more vulnerable through public exposure, and the recipients may feel helpless if their concern is ignored or abused by an anonymous caller. Arguably, basic training in crisis support and coping skills should be adopted as essential components of community and school education.14 Gaps in services There is still a lack of child and adolescent mobile crisis services operating extended hours to augment outpatient nine-to-five mental health services for these age groups. Adolescents are at a time of developmental transition and are particularly vulnerable to crisis. Early intervention services available on a 24-hour mobile basis which are specifically designed to deal with the crises and psychiatric problems of young people, their families and peers may help to reduce the exceptionally high youth suicide rates in Australia. Conclusion The National Mental Health Strategy24 has provided impetus to develop extended-hours mobile community psychiatric services integrated with local inpatient services in both urban and rural centres across Australia. Yet it is by no means possible, nor appropriate, for psychiatric services to provide the full range of crisis intervention services needed by our community. A broad network of formal and informal crisis support structures is required to enable us to more effectively "look after our own". Some useful crisis resources. Acknowledgements I thank Dr Kai Lin Lie, Dr Dorothy Kral, Dr Gary Walter, Mr Paul Clenaghan, Ms Vivienne Miller and Ms Sylvia Hands for advice on the text. References Caplan G. Principles of preventive psychiatry. London: Tavistock 1964. Caplan G. Support systems and community mental health. New York: Behavioural Publications, 1974. Lindemann F. Symptomatology and management of acute grief. Am J Psychiat 1944; 101: 141-148. Hoff LA. People in crisis: understanding and helping. 2nd ed. Menlo Park, California: Addison Wesley, 1984. Tyhurst JS. The role of transitional states -- including disaster -- in mental illness. Symposium on Preventive and Social Psychiatry, Walter Reed Army Institute of Research. Washington DC: US Government Printing Office, 1958. Rosen A. The stigmatized stand up: active involvement in our own mental health services . Mental Health Aust 1985; 4: 3-17. Rosen A. Review of Raphael B. When disaster strikes. ASW Impact 15-16 March 1988. Raphael B. When disaster strikes: a handbook for the caring professions. London: Hutchison, 1986. McGorry P, Rosen A, Carr V, Pantelis G. Innovations in the treatment of psychosis. In: Andrews G, editor. Specialization in Psychiatry. Geigy Psychiatric Symposium Proceedings 1994; XV. Diagnostic and statistical manual of mental disorders. 4th ed. (DSM-IV). Washington DC: American Psychiatric Association, 1994. Parad HJ, Parad LG. Crisis intervention: yesterday, today and tomorrow. In: Punukollu NR, editor. Recent advances in crisis intervention. Vol I. Thuddersfield: International Institute of Crisis Intervention, 1992. Hoult J, Rosen A, Reynolds I. Community orientated treatment compared to psychiatric hospital orientated treatment. Soc Sci Med 1984; 18: 1005-1010. Stein LI, Test MA. Alternative to mental hospital treatment. I. Conceptual model, treatment programme and clinical evaluation. Arch Gen Psychiatry 1980; 37: 392-397. Waldron J. Crisis intervention. Br J Hosp Med 1984; 31: 4283-4287. Scott RD. A family oriented psychiatric service to the London Borough of Barnet. Health Trends 1980; 12: 66-68. Bassuk E, Gerson S. Chronic crisis patients: a discrete clinical group. Am J Psychiat 1980; 137: 1513-1517. Szmuckler G. The place of crisis intervention in psychiatry. Aust N Z J Psychiatry 1987; 21: 24-34. Dunsmore J. "On surviving Christmas" Seminars. Sydney: Department of Health Promotion and Education, Royal North Shore Hospital, 1990, 1995. Phelan M, Strathdee G, Thornicroft G, editors. Emergency mental health services in the community. Cambridge: Cambridge University Press, 1995. (See chapters by Katschnig, Emergency mental health services; Birchwood et al, Using the crisis; Kingdon and Jenkins, Suicide prevention; Sutherby and Szmuckler, Safe community assessments of crisis). Falloon IRH, Fadden G. Integrated mental health care. Cambridge: Cambridge University Press, 1993. McFarlane WR, Lukens E, Link B, et al. Multiple-family groups and psychoeducation in the treatment of schizophrenia. Arch Gen Psychiat 1995; 52: 679-687. Hambridge J, Rosen A. Impact of a mobile community intensive case management team in surburban Sydney. Aust N Z J Psychiatry 1994; 28: 438-445. Goldberg D. A classification of psychological distress for use in primary care settings. Soc Sci Med 1992; 35: 189-193. National Mental Health Strategy, 3rd annual report. Canberra: Department of Health, Housing and Community Services, 1995. Authors' details Royal North Shore Hospital and Community Health Services, Sydney, NSW. Alan Rosen, FRANZCP, DPM, Director; Associate Professor, University of Wollongong; Clinical Senior Lecturer, University of Sydney. Reprints: Dr Alan Rosen, Royal North Shore Hospital and Community Health Services, St Leonards, NSW 2065. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Alan Rosen

From shunned to shining: doctors, madness and psychiatry in Australian and New Zealand cinema Alan Rosen, Garry Walter, Tom Politis and Michael Shortland The histories of psychiatry and the cinema are eerily intertwined MJA 1997; 167: 640-644 Introduction - A psychiatrist's perspective - Films and psychiatric stigma - Conclusions - Acknowledgements - References - Authors' details - - - ©MJA1997 Introduction The motion picture industry has had a long-standing interest in doctors and medicine generally and with psychiatry in particular. Cinema's fascination with modern psychiatry has been intense, with the two fields emerging at about the same time -- movies were first demonstrated publicly by the Lumière brothers, Edison and others in 1895, the same year that Freud wrote Project for a scientific psychology, the prototype of his later theories.1 In 1924, the producer Samuel Goldwyn was keen to exploit the association between sex and psychoanalysis on screen and tried unsuccessfully to enlist Freud's help in making a film with an offer of $US100 000.2 Psychiatric professionals in films have been variously venerated, demonised and marginalised (classified by Schneider as, respectively, "Dr Wonderful", "Dr Evil" and "Dr Dippy"3). Hyler offers an even more elaborate and colourful classification for psychiatric patients in films: rebellious free spirit, homicidal maniac, female seductress, enlightened member of society, narcissistic parasite, and zoo specimen.4 Schneider contends that there has been a welcome shift over the years in the way film has treated madness and psychiatry, with oppressive psychiatrists and zombified victims giving way to more human encounters and ambiguous, even hopeful, outcomes.2 Arguably, however, the complete range of favourable and unfavourable stereotypes of psychiatrists and patients continues to appear -- 1991 saw the psychiatrists Dr Wonderful (Prince of Tides), Dr Evil (Silence of the Lambs ) and Dr Dippy (What about Bob?). Although the vast majority of "psychiatric" films are American (partly because the discipline is embedded in that country's culture), some of the most incisive movies, especially recently, have come from Australia and New Zealand. A chronology of antipodean films with psychiatric themes is shown in Box 1. While doctors and nurses have long been represented in antipodean films (e.g., Sister Kenny [1946]), the "psychiatric" film made its début only in 1974 with Between Wars. Michael Thornhill's first feature, a pioneer in the revival of Australian cinema, Between Wars traces the career of Dr Edward Trenbow (played by Corin Redgrave), who becomes a well-respected Sydney psychiatrist. In the 1920s, he takes up residence at Callan Park Asylum. The film touches on issues of psychoanalysis and physical treatments, such as fever treatment. In another 1974 release, 27A , a middle-aged "metho" drinker joins Alcoholics Anonymous and undergoes a psychiatric examination. As a consequence, he is committed to a hospital for the criminally insane, to be detained indefinitely under the notorious Section 27A of the Queensland Mental Health Act . Nevertheless, apart from these two films, the psychiatrist figure receives scant attention in the 1970s. When it appears, it is usually as either a peripheral character or a stereotype. The 1980s saw some clichéd psychiatric themes. For example, in An Indecent Obsession (1985) Sister Honour Langtree, in charge of a military hospital for psychiatric patients, transgresses boundaries by developing a sexual attraction for a new patient. Wrong World (1985) has the almost mandatory escape from a psychiatric hospital, and Contagion (1987) features a homicidal person with schizophrenia. The 1980s also saw the emergence of a film category which has been called "the company of eccentrics".5 Perversely non-conformist, it often foregrounded quirky protagonists and against-the-grain themes. For example, the hero in John Laurie's Stroker (1987) is "a kind of mad, Chelmsford psychologist", 5 and all the central characters in Bliss (1984) and Pandemonium (1987) seem in dire need of psychiatric evaluation. Some of Jane Campion's films also thrive on borderline heroines (e.g., the volatile Dawn in Sweetie [1989]). These eccentric personalities paved the way for the more stigmatised protagonists in the films of the next decade. An Angel at my Table (1990) depicts the life story of the award-winning novelist Janet Frame. The image of an apparently hopeless mental patient shimmers with that of a somewhat odd creative genius. Similarly, Heavenly Creatures (1994), about the relationship of two New Zealand girls who murder one of their mothers, provides a counterpoint between eccentricity and premeditated evil. Bad Boy Bubby (1994) also extends the "eccentric cinema's" preoccupation with idiosyncratic characters and offbeat themes. Except for the "soft" ending, it is totally uncompromising -- about an "uncivilised" innocent, Bubby, and his mother, who have been caught in an incestuous, symbiotic web for 35 years. On the return of his estranged father, Bubby is freed into a world which he cannot comprehend, a contemporary society which he views through an unsocialised, childlike perspective. Although there is no psychiatric intervention in Bad Boy Bubby and in other 1990s films such as The Piano (1993) and Once Were Warriors (1994), the relentless playing out of dark psychopathology might nevertheless be included in the "psychiatric" film category. Common to Australian and New Zealand "psychiatric" films in the 1990s is the more compassionate, sensitive handling of many types of intellectual and psychiatric disability,6 as illustrated by Domaradzki's Struck by Lightning and McKenzie's On the Waves of the Adriatic (named for the ancient Greek custom of casting mentally ill people adrift in boats on the Adriatic Sea). There is also a greater emphasis on more realistic, character-driven studies of madness -- Angel Baby, Cosi, Lilian's Story and Shine all strive for the narrative/dramatic depiction of alienated or troubled people for human interest. For example, Michael Rymer, the director of Angel Baby (about two people with psychoses, Harry and Kate, who fall in love), states that his film "is not about crazy people. It's about people who have an illness". 7 Cosi, based on Louis Nowra's play8 about a group of patients in an asylum who rehearse for and perform Mozart's Cos" fan tutte, has its American parallel in One Flew Over the Cuckoo's Nest (1975). We warm to many of the patients in both. Lilian's Story and Shine were inspired by real-life personalities supposedly driven mad by aggressive, possessive fathers. Lilian's Story is based loosely on the life of legendary eccentric Bea Miles, who recited Shakespeare for a dollar on the streets of Sydney and rode taxis for a sonnet. In Shine, Geoffrey Rush's portrayal of the pianist David Helfgott endears him to us, and the character ultimately triumphs in both his personal and professional life. Angel Baby, Cosi, Lilian's Story and Shine are not centrally critiques of institutions, but, rather, reinforcements of humanism and faith. The ambiguity of Angel Baby 's ending, in which we are unsure whether the hero suicides, is both tragic and potentially uplifting. Even so, we are left with a nagging feeling that this film missed its chance to instil hope because of the assumption that real-life mental illness must end in tragedy. Unfortunately, alongside the greater humanism and faith depicted in recent Australian and New Zealand "psychiatric" films, negative stereotypes about people with mental illness persist. These include the "homicidal maniac" (Doug, to staff member Lewis, in Cosi : "Hope you've made out your will, Lewis . . . you're mine"), "female seductress" (Cherry, in Cosi, also to Lewis: "I really like you", as she leans forward to kiss him), and the "zoo specimen" (Kate, in Angel Baby, resembles a feral animal as she hisses to frighten off shoppers at a mall). In addition, An Angel at my Table and Shine link madness with creative genius. While the general public may see this as instilling hope, or even as inspirational, people with mental illness may conclude that someone with a mental illness needs an exceptional creative talent to be accepted. A psychiatrist's perspective How accurately have films portrayed mental illness in terms of presentation, aetiology and treatment? From a psychiatrist's perspective, it is gratifying that the most recent Australian and New Zealand "psychiatric" films (Cosi, Angel Baby, Lilian's Story and Shine) have dealt with psychoses, which need better public understanding. However, better understanding is also needed for a range of stereotypically less bizarre disorders, such as depression and anxiety disorders, that are seemingly harder for film-makers to dramatise. Nevertheless, psychopathology has been displayed creatively and vividly in the recent films, including: auditory hallucinations (a tormented Harry clutching his head in Angel Baby); pressure of speech and flight of ideas (David Helgott, at a frantic pace in Shine : "I remember Margaret. She called me a pig. All very complicated; complicato in Israel, a battleground. A war zone, a war; what a bore it's a war . . . war"); delusions of reference (Kate, in Angel Baby, watching Wheel of Fortune on television, suggests that "Astral [on the television] sends me messages no-one else can understand"); poor social skills (Kate again, on first meeting Harry's family, flicks a whole chicken leg onto her dress and later suggests to Harry's sister-in-law, whom she has just met: "[Harry's the] best lay I've ever had . . . [he's got] a side manoeuvre from hell"); and lack of insight (Kate again: "I don't hang around with psychos -- I'm not psycho"; on the other hand, it could be seen as very sensible not to associate with stigmatised people if you wish to avoid being stigmatised yourself). The cinema imputes both genetic and environmental factors in the development of mental illness, consistent with current belief, but tends to emphasise environment. In Angel Baby, when Kate becomes pregnant she is advised by her doctor that "there's a chance that the child will inherit your illness". In contrast, Shine suggests that David's harsh upbringing contributed to his psychiatric illness, an oversimplification of the underlying themes and contribution of David's father. Nevertheless, while parenting practices are no longer thought to be instrumental in the later expression of psychoses, there is validity in the notion that stress can precipitate relapses and takes a toll on all family members. A range of treatments, both physical and psychological, have been portrayed. Lust and Revenge (1996) draws parallels between psychotherapists, religious gurus and market forces in the arts and, in the process, satirises all three. There is ambivalence about physical treatments. In Cosi, a patient about to perform in the opera reassures its director: "I'll be on top of it . . . I purposely didn't take my medication." In contrast, Kate, in Angel Baby, begs: "I want my Stelazine." However, psychotropic medication is also depicted as society's means of controlling undesirable behaviour and individuals, as attested by the comments of head nurse Errol Greer in Cosi : "The patients are on varying degrees of medication . . . don't let that worry you -- just worry about the ones who aren't." Electroconvulsive therapy (ECT) is represented neutrally in Shine but negatively in Cosi, where smoke billows from the ECT machine, and the patients are threatened: "Start making our sets [for the opera] or else it's back to shock treatment." Involuntary admission or sedation is also depicted. In Lilian's Story, the heroine is incarcerated for 20 years on the word of her sexually abusive father, and in Cosi the wrong person ("normal" Lewis) is injected with a tranquilliser without adequate assessment or consent. The community psychiatry movement has been discussed only briefly but disparagingly. Errol, in Cosi, states: "Half-way houses, community care . . . come on, the Government cuts the cost and chucks them [the patients] on the street." This negative misrepresentation of contemporary, integrated 24-hour community and hospital care can be partly explained by Nowra having drawn on his early work experiences in a psychiatric hospital in 1971. While this is made explicit in the introduction to the play, the film fudges the historical time frame so that the audience can easily assume this is current practice. Films and psychiatric stigma Recently, the National Mental Health Policy9 and the Burdekin Report10 have highlighted the need for attention to psychiatric stigma, and community surveys have revealed many public misconceptions about people with mental illness.11 Does the cinema influence psychiatric stigma, or is stigma so deeply ingrained in society that films cannot make a difference either way? Do film makers have a responsibility to teach or to change attitudes, or should we resign ourselves to the fact that films are essentially entertainment? Possible consequences of cinema depictions of mental illness and psychiatry (positive and negative) are shown in Box 2. Disturbing findings from the Glasgow Media Group12 show that public attitudes to mental illness are influenced more by media accounts of mental illness, which instil fear, rather than by direct contact with people with mental illness. Mindful that films and other media often depict people with mental illness as unpredictably violent, the Royal College of Psychiatrists organised a petition (signed by 3000 members) asking the media to alter their practices in the portrayal of mental illness and to develop guidelines.12 However, the response from producers and media managers was a deafening silence. So, is there any good news in film psychiatry? The relatively large number and appeal of recent "psychiatric" films from Australia and New Zealand is encouraging, as are the new messages of hope, resilience, rebellion, self-determination and triumph. In the most recent films, not only are people with mental illness portrayed as real characters capable of expressing the gamut of human emotions, but also a positive stereotype appears to have emerged -- the patient as hero or role model. The recognition of Janet Frame as a great writer in An Angel at my Table and David Helfgott's relationship with Gillian and celebrated return to the concert stage in Shine are a far cry from Kate in Angel Baby, who, sedated, make-up running and generally looking worse for wear, attracts the comment from her nurse: "She looks cute, doesn't she?". Moreover, An Angel at my Table and Shine show that mentally ill people can be examples for the community at large in how to persevere and transform adversity. Film makers and actors may assume that with the gradual improvements in psychiatric settings and treatments, which are becoming more sensitive to the individual, less intrusive and less disruptive to life, psychiatry will not offer sufficiently dramatic screen images. However, as Simon Champ, chair of the Australian Mental Health Consumer Network, pointed out (at a School on Psychiatry and the Cinema at the University of Sydney, New South Wales, in April 1997): "There is plenty enough drama available if you care to accurately tune into the subjective experience of an individual or family who has survived mental illness." Doctors, psychiatrists and other mental health professionals can help promote positive depictions of mental illness and psychiatry (see Box 3). Further, if there is some truth in the negative depictions of psychiatry in film, we can only hope that mental health professionals, rather than muttering darkly and dismissing the images, will reflect thoughtfully and use this as a stimulus to change their practice. Conclusions Ignored for so long, psychiatry and mental illness are now the subject of many films produced in Australia and New Zealand. These films should not be rejected simply as "quirky" or "harmless fun", but should be critically appraised to ascertain attitudes to patients, their families, their doctors and mental health professionals. Speaking in a Hippocratic vein, if a "psychiatric" film does no undeserved harm to these stakeholders and also entertains and has artistic merit, this is for the good. If the film is also accurate and informative, challenges prevailing attitudes and transforms your life, so much the better. Acknowledgements We thank Ronin Films, Roadshow Entertainment and REP Distribution for providing images from their films. We are also grateful to Karen Barfoot, Anne Deveson, Simon Champ and Julie Rigg. References Schneider I. Images of the mind: psychiatry in the commercial film. Am J Psychiatry 1977; 134: 613-620. Shortland M. Screen memories: towards a history of psychiatry and psychoanalysis in the movies. Br J Hist Sci 1987; 20: 421-452. Schneider I. The theory and practice of movie psychiatry. Am J Psychiatry 1987; 144: 996-1002. Hyler SE, Gabbard GO, Schneider I. Homicidal maniacs and narcissistic parasites: stigmatisation of mentally ill persons in the movies. Hosp Community Psychiatry 1991; 42: 1044-1048. Dermody S, Jacka E (editors). The imaginary industry: Australian film in the late 1980s. Sydney: Australian Film, Television and Radio School, 1988: 132-154. Hall S. Method in the madness. The Bulletin 1996 May 28: 80-81. Urban A. Angel baby. Cinema Papers 1995; 104: 12. Nowra L. Cosi. Sydney: Currency Press, 1992. Australian Health Ministers. National Mental Health Policy. Canberra: AGPS, 1992. Human Rights and Equal Opportunity Commission. Human rights and mental illness: report of the national inquiry into the human rights of people with mental illness. Canberra: AGPS, 1993. Commonwealth Department of Health and Family Services. Community attitudes to mental illness: qualitative research report. Canberra: AGPS, 1993. Philo G. Changing media representations of mental health. Psychiatr Bull 1997; 21: 171-172. Walter G, Rosen A. Psychiatric stigma and the role of the psychiatrist. Australas Psychiatry 1997; 5: 72-74. (Received 12 Sep, accepted 28 Oct, 1997) Authors' details Royal North Shore Hospital and Community Mental Health Services, Sydney, NSW. Alan Rosen, FRANZCP, MRCPsych, Director; Associate Professor, University of Wollongong; and Senior Clinical Lecturer, University of Sydney. Central Sydney Area Health Service, Sydney, NSW. Garry Walter, FRANZCP, Staff Specialist Psychiatrist and Inpatient Director, Rivendell Unit; and Clinical Lecturer, Department of Psychological Medicine, University of Sydney. WEA Film Study Group, Sydney, NSW. Tom Politis, President. University of Sydney, Sydney, NSW. Michael Shortland, PhD, Associate Professor of History of Science. Reprints: Dr G Walter, Psychiatric Stigma Study Group, Rivendell Unit, Hospital Road, Concord West, NSW 2138. - ©MJA 1997 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Alan Rosen · Garry Walter

A five-year-old boy drew this "monster". After his father and grandmother (and the family dog) died within a 12-month period, the child made many drawings of monsters, which his mother thought was not "normal". His mother, herself depressed, brought him to an art therapist when he began "hitting himself on the head". During art therapy sessions, the monster drawings were accepted and freely talked about. The self-injurious behaviour stopped after the boy's third individual session.

Peter L Beagley

Early discharge and risk for postnatal depression Anthea R Hickey, Philip M Boyce, David Ellwood and Allen D Morris-Yates For editorial comment, see Buist Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - ©MJA1997 Abstract Objective: To determine whether early discharge ( < 72 hours) after childbirth increased the risk for women developing postnatal depression. Design: Prospective cohort design consisting of an initial interview, and six-weekly assessments for 24 weeks using a self-report questionnaire and the Edinburgh Postnatal Depression Scale (EPDS). Women discharged within 72 hours were compared with the remaining women. Setting: Tertiary referral hospital in western Sydney, New South Wales, 1993. Participants: All 749 women delivering over a three-month period were recruited. Of the 522 participants, 425 women completed the study. Main outcome measures: Women scoring > 13 on the EPDS on two or more occasions were considered potential "cases" of postnatal depression. The diagnosis was confirmed using the Structured Clinical Interview for DSM-III-R disorders (SCID). Results: Of the 153 women (36%) discharged early, 22 women (14.4%) developed postnatal depression over the study period compared with 20 of the 272 women (7.4%) who had standard length of stay. Women who were discharged within 72 hours had a significantly increased risk for developing postnatal depression (odds ratio [OR], 2.12; 95% confidence interval [CI], 1.07-4.21). This risk persisted when other sociodemographic, obstetric and psychosocial risk factors were controlled for in a logistic regression analysis (OR, 3.06; 95% CI, 1.22-7.69). Conclusion: Women planning early discharge after childbirth should be carefully assessed before discharge and follow-up should be rigorous. The potential to develop postnatal depression should be considered in all women choosing early discharge from hospital. MJA 1997; 167: 244-247 Introduction Over the past 20 years, technological advances have contributed to improved maternal and infant outcomes. In parallel, women have become more involved in their obstetric care: wanting to be more informed, be able to make choices and have childbirth demedicalised and "normalised". One initiative aimed at normalising the process has been early discharge programs, enabling women to return home earlier after childbirth than had been traditional. Women's desire for early discharge has fitted in well with the financial constraints put upon health care systems; reduced length of stay is seen as desirable because it reduces the cost of obstetric care. Postpartum studies have reported early-discharge programs to be a safe, cost-effective and satisfying alternative to the standard length of hospital stay among low-risk mothers and their infants.1-5 While these studies have shown that early discharge has no adverse physical effects, the only psychological effects examined have been women's satisfaction about making a choice or taking control of discharge rather than psychological morbidity.5,6 As postnatal depression is a common disorder which may have a long-term impact on the mother and her infant,7 the psychological outcome after childbirth is increasingly being recognised as important.8 Postnatal depression is associated with psychosocial factors, such as an excess of adverse life events, lack of social support, dysfunctional personality style and a past history of depression.8,9 Obstetric factors, such as emergency caesarean section, have also been implicated,10,11 but the impact of early discharge has not been extensively examined. The aim of our study was to investigate whether early discharge following childbirth had an effect on the development of postnatal depression in a heterogeneous sample of women. Methods Subjects All women who delivered at the Nepean Hospital, NSW, over a three-and-a-half-month period in 1993 were invited to participate in the study. Women were excluded from the study if their baby was stillborn, born with congenital abnormalities, adopted out, transferred to another hospital, or if the mother was diagnosed as suffering from puerperal psychosis. Early discharge was defined as discharge within 72 hours (the definition used at Nepean Hospital). Survey instruments Questionnaire: A self-report questionnaire was used to assess social and demographic circumstances. Socioeconomic status was determined according to a status-ranking list of occupations in Australia,12 using the women's partner's occupation (or her parents' occupation when this was not appropriate). A nine-item personality scale was included that identified different personality traits, scored on a 5-point Likert scale. Factor analysis of this personality scale identified "vulnerable" and "resilient" personality dimensions. The vulnerable personality dimension included being a worrier, nervy, timid and unassertive, sensitive, liable to emotional outbursts and needing to do things right. This scale is reliable (Cronbach α= 0.75), and is associated with increased risk for postnatal depression (Boyce P M, Hickey A R, Greenstock J A and Talley N J, Nepean Hospital, unpublished data). Interview: A semi-structured interview (conducted by A R H) was used to assess obstetric history, satisfaction with the labour, whether the delivery was congruent with expectations, the quality of the woman's social support, her personal and family psychiatric history, and the quality of her intimate relationships. We also obtained obstetric details from the labour ward computerised database. Edinburgh Postnatal Depression Scale (EPDS):13 The EPDS is a specifically designed measure of postnatal depression that has shown reliability and validity for the postpartum period.14-16 It consists of a 10-item self-report scale, with each item scored 0-3. A score of 13 or above is indicative of postnatal depression. It is not contaminated by symptoms (e.g., fatigue, weight loss, broken sleep) which may be reported by healthy nursing mothers. Tennant and Andrews life events scale:17,18 A self-report scale comprising 10 relevant life events (e.g., death of a family member or close friend, moving house, marriage); subjects were asked whether each event had happened to her over the past 12 months. A modified version of this scale was used in our study. Structured Clinical Interview for DSM-III-R (SCID):19 The SCID was administered to confirm postnatal depression "caseness". Postnatal depression was defined as meeting the criteria for major depression according to the Diagnostic and statistical manual of mental disorders, third edition, revised (DSM-III-R).20 Procedure The women were recruited immediately after delivery and asked if they would participate in a longitudinal study of postnatal depression. Women who agreed were given an initial semi-structured interview on the second or third day post partum, a self-report questionnaire and a baseline EPDS. The women were assessed a further four times -- at six, 12, 18 and 24 weeks post partum. At each interval, the women were posted the EPDS, a self-report questionnaire (consisting of questions on the baby's condition and feeding patterns as well as the quality of the women's relationship) and a stamped self-addressed envelope for returning the forms. Women who scored > 13 on the EPDS on two occasions (excluding their baseline EPDS score) were further interviewed using the SCID to determine postnatal depression "caseness". An equal number of women who scored < 13 on the EPDS were randomly selected and interviewed using the SCID. Statistical analysis Statistical analysis was performed using the SPSS computer program.21 Women were categorised as "cases" or "non-cases" of postnatal depression and into early and standard length of stay. Categorical data were analysed using odds ratios (OR), and chi-squared and t tests were used for comparing groups on dimensional data. A logistic regression analysis was used to determine whether length of stay remained a risk factor when controlling for other risk factors. Results Sample Of the 749 women who delivered during the three-and-a-half month period, 522 women (69.7%) agreed to participate in the study. Full data were available for 425 women (81.4%). The mean age of the sample was 26.9 years (standard deviation [SD], 5.0; range, 15-43), 367 women (86.4%) were married or in a de facto relationship, 58 women (13.6%) were single or separated, and 184 women (43.3%) were primiparous. The average period of formal education was 11.4 years (SD, 1.9; range, 9-15). Twenty-six women did not meet the inclusion criteria, 122 refused to participate in the study and 79 were unable to be contacted. There were no statistically significant differences in demographic and obstetric details between women who consented to participate and women who did not consent. The 97 women who withdrew from the study or had insufficient data were more likely to be younger (t = 5.91; P < 0.01), unemployed (chi-squared = 33.37; P < 0.01), single or separated (chi-squared = 59.46; P < 0.01) and have fewer years of formal education (t = 3.47; P < 0.01) compared with women who had full data. Forty-two women (9.9%) were categorised as having major depression, based upon scoring > 13 on the EPDS on two occasions and meeting DSM-III-R criteria for major depression. All of these women met "caseness" criteria for major depression on the SCID. None of the sample of women who screened negative (< 13) on the EPDS and were interviewed using the SCID met "caseness" criteria for major depression. Length of stay The average length of stay in hospital following delivery was 90.9 hours (SD, 43.1 hours; range, 16-307). Of the 425 participants in the study, 153 women (36%) were discharged within 72 hours (early-discharge group) and 272 women (64%) were discharged after 72 hours (standard-length-of-stay group). We compared sociodemographic and risk factors for the early-discharge and standard-length-of-stay groups of women. The early-discharge group were more likely to be multiparous (71.2% v. 48.5%; OR, 2.63; 95% confidence interval [CI], 1.69-4.10), have fewer years of formal education (11.01 years v. 11.5 years; t = 3.09; P < 0.01), to bottle feed in the first week post partum (20.9% v. 12.1%; OR, 1.91; 95% CI, 1.06-3.46), and report a poor relationship with parents (52.9% v. 40.1%; OR, 1.68; 95% CI, 1.11-2.56). They were also more likely to have a history of depression or postnatal depression, but this was not statistically significant (9.1% v. 4.4%; OR, 2.18; 95% CI, 0.92-5.19). The two groups did not differ with respect to age, marital or socioeconomic status, number of life events in the past year, or global satisfaction with their partner. Women in the early discharge group did not have a more vulnerable personality style and did not differ in baseline EPDS scores (5.1 v. 5.9; t = 0.24). Postnatal assessment The proportion of women who developed postnatal depression (as defined above) was higher among those discharged early than those discharged after three days. Three of the 13 women (23.1%) discharged within 24 hours, nine of the 58 women (15.5%) discharged between 24 and 48 hours, and 10 of the 82 women (12.2%) discharged between 48 to 72 hours developed postnatal depression. Of the 153 women discharged early (within 72 hours), 22 (14.4%) developed postnatal depression compared with 20 of the 272 women (7.4%) who had standard length of stay (OR, 2.12; 95% CI, 1.07-4.21). Of the 42 women who developed postnatal depression, 22 (52.4%) were discharged early. The possibility that the increased risk associated with early discharge could have arisen as a result of other, antecedent, risk factors for postnatal depression was examined using a hierarchical logistic regression,22 with postnatal depression as the dependent variable. Sociodemographic, historical, obstetric, and psychosocial factors (see below) were entered in the first step, baseline EPDS score in the second step and early discharge in the final step to see whether it would remain a risk factor after controlling for other risk factors. Sociodemographic factors: Age (5-yearly intervals), level of education (less or more than 10 years), social class (low or high socioeconomic status) and marital status (single, married or de facto relationship). Obstetric factors: Parity (multiparous or primiparous) and delivery type (spontaneous vaginal delivery, instrumental delivery or caesarean section). Psychosocial risk factors: Personality style (high or low vulnerability [extracted from the personality scale, with women scoring one standard deviation above the mean on the vulnerability component of the scale considered to be vulnerable]); quality of relationship with parents and in-laws (poor or good); satisfaction with relationship with partner (dissatisfied or satisfied); history of depression or postnatal depression; experience of none, one or two, or three or more life events over the previous 12 months; and whether they had had the desired-sex baby. When all sociodemographic, obstetric and psychosocial factors were entered, the model was highly significant (Box), with significantly increased risk for postnatal depression associated with dissatisfaction with partner relationship(s), reporting three or more life events in the past 12 months, and having a vulnerable personality. The model significantly improved (had better predictive power; chi-squared = 41.5; P < 0.0001) when baseline EPDS score was entered, and again when early discharge was entered. Early discharge increased the risk threefold (OR, 3.06; 95% CI, 1.22-7.69), after controlling for other risk factors. These results also support the more specific finding of early discharge, in which there was a 2.1-fold increased risk (95% CI, 1.07-4.21) of developing postnatal depression. Discussion Early discharge following childbirth is becoming more routine. It has been shown that neither maternal nor infant health is compromised by this practice; however, there is a paucity of research evaluating the psychological functioning of the mother following early discharge. We are aware of only one prospective study of the psychological morbidity associated with early discharge compared with customary length of stay in hospital. Beck et al.23 assessed depressive symptoms among 49 women at six and 12 weeks post partum using the Beck Depression Inventory (BDI).24 They found no significant difference between the early- versus standard-discharge groups on BDI scores. However, this study was confined to privately insured, primiparous women who had had uncomplicated pregnancy and labour. Therefore, their results have limited generalisability because most studies have identified that women opting for early discharge are more likely to be multiparous, older, have fewer years of formal education and lower socioeconomic status.25,26 While there have been no prospective studies on the psychological impact of early discharge in heterogeneous samples, one retrospective study found that women who reported that their postnatal hospital stay was too short were significantly more likely to have postnatal depression than those who reported the right length of stay.27 Our study shows that women discharged within three days of childbirth had an increased risk of developing postnatal depression. This increased risk is not the result of other well recognised risk factors for postnatal depression, such as experiencing life stresses, having a dysfunctional personality style, unsatisfactory interpersonal relationships28 or a history of depression. When these risk factors were controlled in a logistic regression analysis, early discharge was still a significant risk for postnatal depression, with an odds ratio of 3.06. Therefore, early discharge exerted an independent effect on the development of postnatal depression and was not simply a proxy for other, pre-existing, risk factors. We also found that one-third of the women who stayed in hospital for more than five days also experienced postnatal depression. However, they had all experienced complicated labours and some infants had been in neonatal intensive care for a prolonged period, which may have contributed to the higher rates of postnatal depression. Women discharged within three days of giving birth may be at an increased risk of postnatal depression because they have had insufficient time to recover from and work through the experience of childbirth. They may still be tired from the physical demands of childbirth and have to return to the stresses of everyday life, which includes looking after a household, their new baby and, in many cases, other children. This additional stress so soon after childbirth may increase the risk of depression. The "blues" are minor, transient depressive symptoms which generally arise on the third to fifth day post partum. Therefore, women on an early-discharge program leave hospital before the onset of the "blues". If they return to an environment where there is insufficient support, experiencing the "blues" may lead to depressive symptoms being perpetuated and contribute to the development of postnatal depression. Finally, women discharged early go home without having properly established breastfeeding, and therefore without the supervision and round-the-clock support of midwives to help them with the inevitable difficulties (e.g., breast engorgement, change in milk flow, unable to latch the baby correctly, leading to cracked, sore nipples) that arise after the milk "comes in" (generally on the third day). These difficulties can lead to an irritable baby and a tired, depressed mother. The association we found between early discharge and postnatal depression merely suggests causality. A prospective controlled study with women randomly assigned to early- or standard-discharge programs (controlling for parity, social support and past history) is needed to identify any causal link between early discharge and postnatal depression. The association between early discharge and postnatal depression has major public health implications. While health services are having to cut costs, early discharge may result in short-term cost savings. However, the consequences of postnatal depression could lead to escalating health care costs in the long term. Women entering an early-discharge program need a careful assessment, particularly those at risk for postnatal depression (e.g., poor family support or a history of depression). The possibility of postnatal depression should be kept in mind for all women who have been discharged early when they return for their postnatal check-ups. The EPDS could be used as a routine screen for such women. Finally, women with a history of postnatal depression should have counselling if they are considering early discharge and be advised that a longer hospital stay may reduce their risk of recurrent depression. References Yanover MJ, Jones D, Miller MD. Perinatal care of low-risk mothers and infants: Early discharge with home care. N Engl J Med 1976; 294: 702-705. Avery MD, Fournier LC, Jones PL, Sipovic CP. An early postpartum hospital discharge program: implementation and evaluation. J Obstet Gynecol Neonatal Nurs 1982; 11: 233-235. Burnell I, McCarthy M, Chamberlain GVP, et al. Patient preference and postnatal hospital stay. J Obstet Gynaecol 1982; 3: 43-47. Lemmer CM. Early discharge: outcomes of primiparas and their infants. J Obstet Gynecol Neonatal Nurs 1987; 16: 230-236. Hall WA, Carty EM. Managing the early discharge experience: taking control. J Adv Nurs 1993; 18: 574-582. Kenny P, King MT, Cameron S, Shiell A. Satisfaction with postnatal care -- the choice of home or hospital. Midwifery 1993; 9: 146-153. Murray L, Cooper PJ, Stein A. Postnatal depression and infant development. BMJ 1991; 302: 978-979. Boyce PM, Stubbs JM. The importance of postnatal depression [editorial]. Med J Aust 1994; 161: 471-472. O'Hara MW, Swain AM. Rates and risks of postpartum depression -- a meta-analysis. Int Rev Psychiatry 1996; 8: 37-54. Boyce PM, Todd AL. Increased risk of postnatal depression after emergency caesarean section. Med J Aust 1992; 157: 172-174. Murray L, Cartwright W. The role of obstetric factors in postpartum depression. J Reprod Infant Psychol 1993; 11: 215-219. Congalton AA, Cheshire FW. Status and prestige in Australia. Melbourne: Chesire Publishing Pty Ltd, 1969. Cox JL, Holden JM, Sagovsky R. Detection of postnatal depression: development of the 10-item Edinburgh Postnatal Depression Scale. Br J Psychiatry 1987; 150: 782-786. Harris B, Huckle P, Thomas R, et al. The use of rating scales to identify post-natal depression. Br J Psychiatry 1989; 154: 813-817. Murray L, Carothers AD. The validation of the Edinburgh Postnatal Depression Scale on a community sample. Br J Psychiatry 1990; 157: 288-290. Boyce PM, Stubbs JM, Todd AL. The Edinburgh Postnatal Depression Scale: validation for an Australian sample. Aust N Z J Psychiatry 1993; 27: 472-476. Tennant C, Andrews G. A scale to measure the cause of life events. Aust N Z J Psychiatry 1977; 11: 163-167. Brugha T, Bebbington P, Tennant C, Hurry J. The list of threatening experiences: a subset of 12 life event categories with considerable long-term contextual threat. Psychol Med 1985; 15: 189-194. Spitzer RL, Williams JBW, Gibbon M, First MB. Structured Clinical Interview for DSM-III-R: SCID user's guide for the structured clinical interview for DSM-III-R. Washington: American Psychiatric Press Inc, 1990. American Psychiatric Association. Diagnostic and statisitical manual of mental disorders, third edition revised (DSM-III-R). Washington DC: American Psychiatric Association, 1987. SPSS: Statistical package for the social sciences [computer program], release 6.1. Chicago, Ill: SPSS Inc, 1994. Fleiss JL, Williams JBW, Dubro AF. The logistic regression analysis of psychiatric data. J Psychiatr Res 1986; 20: 195-209. Beck CT, Reynolds MA, Rutowski P. Maternity blues and postpartum depression. J Obstet Gynecol Neonatal Nurs 1992; 21: 287-293. Beck AT, Ward CH, Mendelson M, et al. An inventory for measuring depression. Arch Gen Psychiatry 1961; 4: 561-571. Scott A. A cost analysis of early discharge and domiciliary visits versus standard hospital care for low-risk obstetric clients. Aust J Public Health 1994; 18: 96-100. Mitchell SD, Counsell AM, Geddis DC. Planned early discharge from New Zealand maternity hospitals. N Z Med J 1993; 106: 152-154. Astbury J, Brown S, Lumley J, Small R. Birth events, birth experiences and social differences in postnatal depression. Aust J Public Health 1994; 18: 176-184. O'Hara MW, Zekoski EM. Postpartum depression: a comprehensive review. In: Kumar R, Brockington IF, editors. Motherhood and mental illness 2: causes and consequences. London: Wright, 1988: 17-63. (Received 17 Feb, accepted 5 June 1997) Authors' details Department of Psychological Medicine, Nepean Hospital, Penrith, NSW. Anthea R Hickey, Psychologist, BPsych, MMedSc; Philip M Boyce, MD, FRANZCP, Professor of Psychiatry; Allen D Morris-Yates, BA(Hons), Senior Research Officer. Department of Obstetrics and Gynaecology, Canberra Hospital, ACT. David Ellwood, FRACOG, DPhil(Oxon), Professor of Obstetrics and Gynaecology. Reprints: Prof P M Boyce, Department of Psychological Medicine, Nepean Hospital, PO Box 63, Penrith, NSW 2751. E-mail: pboyceATmail.usyd.edu.au ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Anthea R Hickey · Philip M Boyce · David Ellwood · Allen D Morris-Yates

A model for the management of self-poisoning Ian M Whyte, Andrew H Dawson, Nicholas A Buckley, Gregory L Carter and Catherine M Levey Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Service structure - Philosophy and strategies - Nursing perspective - Psychiatric perspective - Medical perspective - Outcomes and resource use - Discussion - Acknowledgements - References - Authors' details - ©MJA1997 Abstract Objective: To describe the development and activity of a multidisciplinary service to manage self-poisoning. Design: Descriptive, comparative study with prospective data collection. Setting: Regional toxicology treatment centre in the Hunter area of New South Wales (NSW) with primary and secondary referral service to 385 000 people and tertiary referral service to a further 100 000. Patients: All patients (1987-1995) with poisoning or envenomation presenting to the Hunter Area Toxicology Service (HATS). Main outcome measures: Average length of stay for HATS compared with national and NSW hospitals; mortality data for HATS compared with NSW. Results: Average length of stay for HATS was 0.53-1.22 days shorter than for all Australian hospitals, potentially saving 518 bed-days, valued at $468 000 per year. Average length of stay was 0.94-3.39 days shorter than for all NSW hospitals, saving 1470 bed-days at $1.4 million per year. Inpatient mortality (0.2%; 95% confidence interval, 0.0-1.1) was not significantly different from NSW (0.5%; 95% CI, 0.2-0.8). Standardised mortality ratios showed no greater all-cause suicide mortality. Conclusions: In our centralised model for managing self-poisoning, all toxicology patients in an area health service are diverted to one hospital, where all patients with deliberate self-poisoning are admitted under the one multidisciplinary team, and all receive psychiatric assessment. This model has substantially reduced bed stay, with considerable savings to the Hunter Area Health Service manifested as an increase in beds available for other purposes. MJA 1997; 167: 142-146 Introduction Estimates of admissions for deliberate self-poisoning vary from 1%1 up to 5%2 of public hospital admissions. More than 50% of these admissions occur between 6 pm and 2 am.3 Deliberate self-poisoning (including carbon monoxide) is the cause of death in 42% of suicides.4 With a few exceptions, deliberate self-poisoning is managed on an ad-hoc basis in Australian hospitals. Commonly, the patient is managed in the emergency department and, if required, admission occurs under the general physician of the day or under the specialty which best corresponds to the patient's toxicological problem. Other models include medical management for most patients occurring entirely within the emergency department/intensive care axis. In one centre, 30% of patients with deliberate self-poisoning were not formally admitted.5 In many centres, expertise in toxicology comes from outside the service providing the patient care (e.g., from Poisons Information Centres). In these models of management, not every patient with deliberate self-poisoning receives formal psychiatric assessment. Despite evidence that psychiatric intervention after parasuicide is worthwhile,6 psychiatric resources are commonly concentrated on those patients who require admission and those who have the most medically severe poisoning.7 However, significant suicidal risk is present for many patients with toxicologically "trivial" poisonings. Service structure In 1986 the Department of Clinical Pharmacology, then located at the Royal Newcastle Hospital, was requested to manage deliberate self-poisoning and other toxicology patients. The Hunter Area Toxicology Service (HATS) was established jointly by the Department of Clinical Toxicology and Pharmacology and the Department of Liaison Psychiatry in January 1987. The only increase in staff was one registrar position in clinical pharmacology. All deliberate self-poisoning patients are formally admitted under the HATS clinical toxicologist, who retains primary responsibility for care during the whole admission. A toxicology data collection form was developed which is also the formal admission record. The psychiatry team assess all patients with deliberate self-poisoning and, on request, other poisonings. Referral to the drug and alcohol service occurs as necessary. The patient is determined as medically fit for discharge by the toxicologist and the decision on appropriate discharge destination is made by the psychiatrist. Medical follow-up, when required, is the responsibility of the toxicologist. A relational database for collecting data on poisoned patients4 was written (by I M W) in late 1986. The complexity of this database has progressively increased and an extensive psychiatric component (written by G L C) became operational in January 1996. HATS was transferred to the Newcastle Mater Misericordiae Hospital in 1991 and took on an Area role (population, 385 000). All poisoning cases are transferred, either directly or after assessment at a closer hospital, to the Newcastle Mater Misericordiae Hospital unless they are too ill. If they are admitted to another hospital, they are admitted under the care of HATS. In practice, this relates to critically ill patients who are admitted to the intensive care unit at the presenting hospital under the care of the toxicologist from HATS, and discharged directly from that unit or transferred to the Newcastle Mater Misericordiae Hospital if they need more inpatient care after their intensive care stay. HATS provides a 24-hour telephone consulting service for the Upper and Lower Hunter Areas (population, 100 000) and a tertiary referral service when required. The clinical pathway for this managed care is shown in Figure 1. HATS medical management is provided by a full time equivalent clinical toxicologist (currently two clinical pharmacologists) and a registrar in clinical toxicology. The after hours service is provided by the two clinical pharmacologists with the addition of another clinical pharmacologist and a drug and alcohol specialist with an interest in toxicology. Every toxicology admission is seen by the medical team (at least once a day), seven days a week. HATS psychiatric care is provided by a psychiatrist, a psychiatry registrar and a clinical nurse consultant in psychiatry. An after hours service is provided by part of an area roster of psychiatry registrars and four to six "second on call" psychiatrists. Every deliberate self-poisoning admission is seen by the psychiatry team (at least once a day), seven days a week. Even when the patient is consciously or cognitively impaired, our practice is to begin the psychiatric assessment by obtaining a collateral history from family/friends and health care workers before proceeding with individual psychiatric assessment. If the patient presents with a toxicologically trivial poisoning after 5 pm or on weekends (which would allow discharge before the routine morning psychiatric review) then the psychiatric registrar on call will come in to do the assessment and decide on appropriate discharge destination. Philosophy and strategies HATS was established with the premise that deliberate self-poisoning is a presenting symptom for an underlying psychiatric disorder, personality disorder or psychosocial problem that requires assessment and intervention. A distinction is made between "drug overdose" (exposure to an amount of drug or toxin sufficient to cause harm) and the more inclusive term "deliberate self-poisoning", which also includes toxicologically trivial exposures. All admissions are formally discussed at a weekly multidisciplinary meeting where medical and psychiatric management is reviewed. When appropriate, individualised management plans are discussed for patients who have frequent presentations. Nursing perspective Nursing care of deliberate self-poisoning patients uses a combined medical and behavioural model. The staff recognise that patients with deliberate self-poisoning are entitled to a legitimate "sick role"8 and use a non-judgemental approach to patients and their relatives. Retention of patients for the full duration of treatment can be increased by emphasising the need for medical review and treating deliberate self-poisoning patients in a similar manner to other medical patients. In the acute phase of the admission, patients are kept in hospital pyjamas and their street clothes removed. Patients with catheters or intravenous cannulas often have these devices kept in situ until their mental state is assessed and their discharge destination is determined by the psychiatric team. The involvement of family and friends in helping to orientate and support the patient can lessen the nursing burden and improve compliance. Psychiatric perspective Psychiatric care of deliberate self-poisoning patients is aimed at maintaining the safety of the patient (and staff), enhancing compliance with decontamination and other medical treatment, psychological support, the initiation of treatment for specific indications (e.g., delirium, psychosis and relationship problems), and coordination of psychiatric follow-up. The incorporation of a psychiatry team in HATS allows for very early intervention in deliberate self-poisoning, in contrast to consulting the psychiatrist after completion of medical management. Medical perspective The primary aim in the treatment of poisoned patients is to reduce mortality and early and late morbidity. The secondary aim of treatment is to reduce hospital stay and use hospital resources efficiently. This is accomplished by an active education program9 focused on evidence-based management, good supportive care and actively discouraging punitive medical procedures. Outcomes and resource use The NSW Health Department Inpatient Statistics Collection uses average length of stay (with a minimum bed stay for a formal admission defined as one day). Examination of medical records data for patients with self-poisoning (ICD-9-CM10 codes E950-E959) admitted to the Royal Newcastle Hospital in 1985 and 1986 showed an average length of stay of 3.88 days. For 1987, when HATS began to operate, the average length of stay for this group of patients had decreased to 2.75 days and for 1988 to 1.4 days. In 1995 there were 736 admissions to HATS (see Box 1). The median (range) hospital stay is calculated because the data are not normally distributed. The lower quartile is at 10.5 hours and the upper quartile at 27.5 hours. The distribution of hospital stay for deliberate self-poisoning patients is shown in Figure 2. In 1994-1995, for all hospitals with an emergency department in the Greater Newcastle area, deliberate self-poisoning comprised 1.2% of medical admissions; most presented to Newcastle Mater Misericordiae Hospital, where they comprised 7.3% of medical admissions. Of the 520 deliberate self-poisoning admissions who received formal psychiatric assessment, 492 (94.6%) had had one or more formal diagnoses11 made of psychiatric disorder, personality disorder or other condition ("V" codes11). Average length of stay data for HATS compared with national data and all NSW public hospitals are shown in Boxes 2 and 3, respectively. Box 2 compares data derived from the HATS database for 1991-1994 with national data for 1992 (the most recent year available). Box 3 presents data from the NSW Health Department Inpatient Statistics Collection (1994-1995), and compares deliberate self-poisoning admissions to Newcastle Mater Misericordiae Hospital with the mean for all public hospitals in NSW. The data from Newcastle Mater Misericordiae Hospital in Box 3 are not derived from the HATS database, but rather from independent coding by the Medical Records Department of the Newcastle Mater Misericordiae Hospital according to ICD-9-CM.10 Both comparisons show a substantial reduction in bed stay for HATS. Since those patients not formally admitted at other hospitals are likely to be short stay presentations and thus not reported in the Inpatient Statistics Collection, we further analysed HATS data for 1993-1995. For all admissions average length of stay was 1.5 days; for all admissions with a hospital stay greater than 12 hours (72.6% of admissions) average length of stay was 1.69 days; for all admissions that required intensive care admission (16.8%), average length of stay was 2.59 days. There has been no evidence that reduced bed stay has compromised patient care, as mortality from deliberate self-poisoning during this period (1987-1995) has been 0.6% (24 deaths in 3856 deliberate self-poisoning admissions; 95% CI, 0.4-0.9). Most of these patients had an out-of-hospital cardiac arrest and death was inevitable on presentation.4 NSW Health Department data for 1992 (the most recent year for which death data are available) show 13 inpatient deaths in 2876 admissions in NSW (0.5%; 95% CI, 0.2-0.8). HATS data for 1992 show one inpatient death in 512 deliberate self-poisoning admissions (0.2%; 95% CI, 0.0-1.1). These proportions are not significantly different (chi-squared = 2.04; P = 0.36). Standardised mortality ratios for suicide in NSW show the Hunter Area has no greater all-cause suicide mortality.13 HATS' prospective data collection on all presentations in a defined population is a very powerful tool for observational research. We have been able to identify public health issues related to patterns of drug use,14,15 relative toxicity of drugs within classes16-18 and the impact of safety packaging of medications.19 The NSW Health Department, as part of its health outcomes strategy, has provided funds to HATS to develop the management model (and the database) so that it can be trialled at other centres in NSW. Discussion There are difficulties in comparing data collected by clinicians with a particular interest in a group of patients and national data derived from ICD-9 coding from all hospitals in Australia. The main difficulty is the potential for ascertainment bias. For example, it is possible the national data contain significant numbers of patients without true deliberate self-poisoning, who have a longer length of stay. This may make our comparisons less robust. However, the data for NMMH in Box 3 are the official data requested by the NSW Department of Health for inclusion in the NSW Inpatient Statistics Collection and are thus directly comparable to data from other NSW public hospitals. It could be argued that shorter length of stay in the Hunter is due to our policy of admitting all patients with deliberate self-poisoning regardless of severity. However, the greatest difference in average length of stay occurs in those patients with complications or comorbidities (Boxes 2 and 3), who require admission under any policy. Figure 2 shows that 90% of all our patients stay in hospital for less than 50 hours, which is less than the average length of stay for uncomplicated poisoning in NSW public hospitals (Box 3). In addition, HATS bed stay for all admissions (complicated and uncomplicated) after excluding those admitted for less than 12 hours (27.3% of presentations) is still shorter than the average length of stay for uncomplicated admissions to all NSW hospitals. The average length of stay for HATS admissions requiring intensive care is more than two days shorter than the average length of stay for all complicated admissions to NSW hospitals. The model of management of self-poisoning described in this article is, we believe, unique in Australia. The differences we have identified in this model are: all toxicology presentations in one Area Health Service are diverted (by ambulance services and emergency departments) to one hospital all deliberate self-poisoning presentations are admitted all admissions are to one team the team is multidisciplinary, with medical, psychiatric, drug and alcohol, and nursing participation all deliberate self-poisoning admissions receive psychiatric assessment a 24-hour service for management and advice is provided. We argue that all patients who present with deliberate self-poisoning should be admitted for several reasons: deliberate self-poisoning is a presenting symptom for another problem that requires assessment and intervention most deliberate self-poisoning admissions (94.6%) have a diagnosable psychiatric disorder, personality disorder or other psychiatric condition formal admission facilitates more efficient and effective assessment and management of both medical and psychiatric issues as more than half the presentations occur after hours, overnight admission is required to ensure adequate psychiatric assessment. This model has resulted in a substantial and significant reduction in bed stay, which increases beds available for other purposes in the Area. There are two ways of calculating the monetary cost if funding were on a diagnosis-related group (DRG) basis. The first is to multiply the bed-days saved by the DRG cost of a bed-day, as in Box 2 and Box 3. The second is to assume the saved beds will be occupied by patients attracting further DRG funding. Assigning a monetary value to this is not possible. It is clear, however, that based on DRG funding these saved bed-days are worth more to the Area than the cost of running the service. The reduction in bed stay has not been accompanied by a worsening in outcome, as defined by in-hospital mortality from deliberate self-poisoning or standardised mortality ratios for all-cause suicide. While the number of admissions to HATS in 1992 appears disproportionate, it is consistent with the proportion of admissions to other major hospitals1,2 and reflects our policy of admitting all patients who present with deliberate self-poisoning. It appears likely the Department of Health figures for admissions significantly underestimate the number of presentations for deliberate self-poisoning to NSW hospitals. If so, while the magnitude of the saving per admission may be uncertain, on a State-wide basis the potential savings from implementing our model are even greater. Without further data, determining the reasons for the shorter average length of stay is not possible, but anecdotal comparisons with other hospitals suggest the following possibilities: centralised, evidence-based management of specific poisonings resulting in earlier recognition of non-toxic or minimally toxic exposure more efficient gastrointestinal decontamination better management of significant toxic exposure more efficient use of psychiatric assessment, aftercare and discharge planning increased involvement of nursing staff in a multidisciplinary approach. Our current model of management has evolved using the skills and experience of those interested in poisoning in Newcastle. The only new position created was the registrar position in clinical pharmacology. We do not believe, however, that replicating the model or its outcomes is dependent on replicating our subspecialty mix. Nevertheless, the identification of a team to manage poisoning is crucial. In many health areas the emergency physicians may be the logical choice for such a team. This would require an extension of admitting rights into the general hospital or a collaborative venture with an identifiable medical team. A specific group of psychiatrists is also required. We believe that Area Health Services should consolidate acute toxicology services. A potential disadvantage of consolidation is loss of skills in the management of toxicological problems in other hospitals in the Area. This could be offset by making the service part of registrar and nursing training rotations. The advantages of consolidation include: individualising patient care continuity of care a better learning curve via greater experience training, education and research. The efficiencies of this model are a product of the reorganisation of largely existing resources to provide a multidisciplinary team approach to the management of poisoned patients. The provision of care is based on a philosophy that these patients are entitled to a legitimate sick role. The major stumbling block to establishing a similar dedicated service is in making the decision to reorganise existing services. As House et al. state, after reviewing services in the United Kingdom, "there is much to recommend in clinical diversity, but nothing to recommend [in] unplanned and incoordinated service provision".6 Acknowledgements We would like to acknowledge the support of nursing staff in the Intensive Care Unit, the Emergency Department and Ward 5E at the Newcastle Mater Misericordiae Hospital. The Hunter Area Toxicology Service has also received considerable support from the Mental Health Epidemiology Group (NSW Department of Health) and the Chief Executive Officer of the Hunter Area Health Service, Dr Timothy Smyth. Some of the later development of this service was supported by a NSW Health Department Health Outcomes grant and a grant from the Hunter Area Health Service. References Pond SM. Prescription for poisoning. Med J Aust 1995; 162: 174-175. McGrath J. A survey of deliberate self-poisoning. Med J Aust 1989; 150: 317-322. Buckley NA, Whyte IM, Dawson AH. There are days . . . and moons. Self-poisoning is not lunacy [letter]. Med J Aust 1993; 159: 786-789. Buckley NA, Whyte IM, Dawson AH, et al. Self-poisoning in Newcastle, 1987-1992. Med J Aust 1995; 162: 190-193. Davis AT, Kosky RJ. Attempted suicide in Adelaide and Perth: changing rates for males and females, 1971-1987. Med J Aust 1991; 154: 666-685. House A, Owens D, Storer D. Psycho-social intervention following attempted suicide: is there a case for better services? Int Rev Psychiatry 1992; 4: 15-22. Tengel E, Cook NG, Kreeger IS. Attempted suicide. London: Chapman & Hall, 1958. Parsons T. The social system. London: Routledge and Kegan Paul, 1951. Buckley NA, Dawson AH, Whyte IM. HyperTox -- a hypertext teaching program in toxicology. < http://www.ozemail.com.au/~ouad/toxi0002.html > > World Health Organisation: International Classification of Disease ICD-9. Clinical modification, 1978. Geneva: WHO, 1992. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994. Manual of resource items and their associated costs for use in submissions to the Pharmaceutical Benefits Advisory Committee involving economic analyses. Australian Government Publishing Service, Canberra, 1992. Stewart G, Chipps JA, Sayer G. Suicide mortality in NSW local government areas. NSW Public Health Bull 1995; 7: 1-10. Smith AJ, Whyte IM. New drugs for old: an issue for debate? Med J Aust 1988; 149: 581-582. Dawson AH, Whyte IM. Compound analgesics [letter]. Med J Aust 1990; 152: 334. Buckley NA, Dawson AH, Whyte IM, Henry DA. Greater toxicity in overdose of dothiepin than of other tricyclic antidepressants. Lancet 1994; 343: 159-162. Buckley NA, Dawson AH, Whyte IM, O'Connell DL. Relative toxicity of benzo diazepines in overdose. BMJ 1995; 310: 219-221. Buckley NA, Whyte IM, Dawson AH. Cardiotoxicity more common in thioridazine overdose than with other neuroleptics. J Toxicol Clin Toxicol 1995; 33: 199-204. Buckley NA, Newby DA, Dawson AH, Whyte IM. The effect of the introduction of safety packaging for carbamazepine on toxicity in overdose in adults. Pharmacoepidemiol Drug Safety 1995; 4: 351-354. (Received 26 Aug 1996, accepted 3 Apr 1997) Authors' details Newcastle Mater Misericordiae Hospital, Newcastle, NSW. Ian M Whyte, FRACP, Senior Staff Specialist and Director, Department of Clinical Toxicology and Pharmacology. Andrew H Dawson, FRCP, FRACP, Staff Specialist, Department of Clinical Toxicology and Pharmacology. Gregory L Carter, FRANZCP, Senior Staff Specialist, Department of Liaison Psychiatry. Catherine M Levey, RN, ICUCert, Clinical Nurse Specialist, Intensive Care Unit. Discipline of Clinical Pharmacology, University of Newcastle, Newcastle, NSW. Nicholas A Buckley, FRACP, Lecturer. Reprints: Dr I M Whyte, Department of Clinical Toxicology and Pharmacology, Newcastle Mater Misericordiae Hospital, Locked Bag 7, Hunter Regional Mail Centre, NSW 2310. E-mail: mdimw@cc.newcastle.edu.au ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Ian M Whyte · Andrew H Dawson · Nicholas A Buckley · Gregory L Carter · Cathterine M Levey

Psychosocial disorders in young people: on the agenda but not on the mend Richard Eckersley Resolving psychosocial problems among young Australians will not be quick or easy and requires greater commitment from all sectors of the community Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". - - ©MJA1997 Psychosocial problems have featured prominently in the news and on political agendas in Australia in the past year. In the wake of the Port Arthur (Tasmania) massacre, governments tightened gun laws1 and acted on portrayals of violence in the electronic media.2 The Federal Government more than doubled funding for its National Youth Suicide Strategy, to $32 million over four years.3 The Victorian Government seemed poised on the brink of major drug law reform, then retreated; recently, it established a Youth Suicide Prevention Task Force and launched a new drug strategy.4-6 However, if we, as a society, really want to get to the heart of these problems, we will have to change fundamental aspects of our society and culture. Despite many years of political action, it is arguable that none of these issues has been adequately addressed, as the developments of the past year make clear. We are still losing the war against drugs. Crime remains a serious social problem. The epidemic of youth suicide continues. In 1950, the (age-adjusted) suicide rate for males aged 15-24 was 6.9 per 100 000 and, in 1995, 24.8 per 100 000; among females in this age group, the suicide rate in 1950 was 2.2 and, in 1995, 6.2 (Jerry Moller, Assistant Director, National Injury Surveillance Unit, Australian Institute of Health and Welfare, Adelaide, SA, 1996, personal communication) (Figure). These trends occurred, even though fewer suicide attempts today are fatal, par ticularly those involving poisoning.7 This is the method favoured by females,8 who attempt suicide at least as often as males.9-11 Although suicide is an uncommon event, new research is revealing the extent to which it is the tip of the iceberg of psychological distress and disturbance among young people. The research shows that this distress is not an aberrant personal response to life; nor is it confined to marginalised or dis advantaged young people (see Box). A similar situation exists in other Western nations. An international review of time trends in psychosocial disorders in young people concludes that there has been a "surprising and troubling" rise in these disorders since World War II in nearly all developed countries. The disorders include crime, drug abuse, depression, suicidal behaviour and suicide (only with eating disorders do the authors say the evidence for a rise in prevalence is inconclusive).13 This review says that, to a large extent, finding causal explanations of the increases "remains a project for the future"; it acknowledges causes could differ for different disorders, and even for the same disorder at different periods. However, it rejects several popular explanations for the trends, such as social disadvantage and inequality and unemployment (although these can be associated with disorder at an individual level). More likely explanations are: family conflict and breakup; increased expectations; and changes in adolescent transitions (in particular, the emergence of a youth culture that isolates young people from adults and increases peergroup influence; more tension between dependence and autonomy; and breakdowns in cohabiting relationships among young people).13 In assessing threats to the well-being of young people, the final report of a 10-year study in the United States says that: "Altogether, nearly half of American adolescents are at high or moderate risk of seriously damaging their life chances. The damage may be near-term and vivid, or it may be delayed, like a time bomb set in youth."14 The report notes that social and technological changes this century -- including more divorces and single-parent families, the erosion of neighbourhood networks, greater media and peer influence, and a lack of jobs -- mean that adolescents could lack "two crucial prerequisites" for healthy growth and development: "a close relationship with a dependable adult and the perception of meaningful opportunities in mainstream society."14 The situation may also reflect a growing failure of mod ern Western culture to provide an adequate framework of hope, moral values, and a sense of belonging and meaning in our lives, so weakening social cohesion and personal re silience.15-17 In investing so much meaning in the individual "self", we have left it dangerously exposed and isolated, because we have weakened the enduring personal, social and spiritual relationships that give deeper meaning and purpose to our lives. These broader sociocultural perspectives suggest that, while tragedies such as suicide arise from intensely personal circumstances, they also represent the extreme end of a spectrum of responses by many young people to modern life, ranging through degrees of depression, drug abuse, delinquency and suicidal ideation to a pervasive sense of alienation, disillusionment and demoralisation. Surveys of youth attitudes suggest that many young people are mistrustful, cynical and fatalistic; wary of commitment; outwardly confident but inwardly insecure; and alienated and disconnected from society.17,18 Young people believe that life should be fast-moving and fun; that they have to fend for themselves; that lifestyle options should be kept open; that governments are incapable of solving society's problems; and that they themselves are powerless to change social conditions. Linked to these attitudes is a widespread pessimism about the future of the nation and the world. A recent study found that more than half of a representative sample of 800 Australians aged 15 to 24 thought the twenty-first century was more likely to be a time of crisis and trouble than one of peace and prosperity.18,19 Only a third thought Australia's quality of life would be better in 2010 than it is now, while a third thought it would be worse. Pessimism increased with age. When it comes to their own lives, most young people are optimistic, but recent research suggests that even this personal optimism crumbles under the pressures young people face as they grow up and make their own way in the world.9,20 One study found that that at 15 youth were optimistic and positive, but by 25 many had become disillusioned and rudderless: "Youth seem unusually apathetic about the future. They are not negligent or ignorant of the challenges; they just feel powerless to do anything about it. It is a sense of being disenfranchised and disengaged, awaiting the outcome of events rather than anticipating a role in them."20 A recent international survey conducted by a consortium of advertising agencies identified a teen generation characterised by four moods -- alienated, cynical, experimental and savvy (Joanne Turner, MojoPartners, Sydney, personal communication). The survey found that Australian teens were not excited about much in life; that they expressed a lack of direction; and that they were uncertain and apprehensive about the future. Suicidal ideation and behaviour in young people is associated with factors such as hopelessness and feelings that they have little influence over their environment (i.e., that there is an external locus of control).10,21 More broadly, hope has recently been described as "a pervasive and significant correlate of health and disorder".22 Psychological well-being is also associated with feelings that life has meaning, with positive meaning being related to strong religious beliefs, values that transcend the self, membership in groups, dedication to a cause and clear life goals.23 We need to pay close attention to the way in which the broad sociocultural features of our society could be contributing to a lack of meaning and a lack of hopefulness, and hence to psychosocial problems, among young people. References Office of the Prime Minister. Media release and transcript of press conference [on guns] by the Prime Minister, the Hon John Howard. Canberra: 10 May 1996. Media release by the Federal Minister for Communications and the Arts, Senator The Hon. Richard Alston. Government to tighten controls on media violence. Canberra: Office of the Federal Minister for Communications and the Arts, 9 July 1996. Update on national youth suicide prevention programs. Canberra: Commonwealth Department of Health and Family Services. 13 March 1997. Drug laws fall short: Pennington. The Age (Melbourne), 12 June 1996: 1. Press release. Premier convenes suicide prevention taskforce. Melbourne: Office of the Premier of Victoria and the Minister for Health. 29 January 1997. "Vic acts on teen drugs." The Canberra Times , 8 January 1997: 12. Harrison J, Moller J. Learning from experience: towards prevention. In, Selby H, editor. The inquest handbook. Sydney: Federation Press (in press). Harrison J, Moller J, Dolinis J. Suicide in Australia: past trends and current patterns. Australian Injury Prevention Bulletin, Issue 5. Adelaide: National Injury Surveillance Unit, Australian Institute of Health and Welfare, February 1994. Zubrick SR, Silburn SR, Garton A, et al. Western Australian child health survey: developing health and well-being in the nineties. Perth: Australian Bureau of Statistics and the Institute for Child Health Research, 1995. Allison S, Pearce C, Martin G, et al. Parental influence, pessimism and adolescent suicidality. Arch Suicide Res 1996; 1: 229-242. Schweitzer R, Klayich M, McLean J. Suicidal ideation and behaviours among university students. Aust N Z J Psychiatry 1995; 29: 473-479. Rickwood D, d'Espaignet E. Psychological distress among older adolescents and young adults in Australia. Aust N Z J Public Health 1996; 20: 83-86 . Rutter M, Smith DJ, editors. Psychosocial disorders in young people -- time trends and their causes. Chichester: John Wiley and Sons, for Academia Europaea 1995: 782-808. Carnegie Council on Adolescent Development. Great transitions -- preparing adolescents for a new century. Concluding report. New York: Carnegie Corporation of New York, 1995: 10. Eckersley R. Youth and the challenge to change. Melbourne: Australian Commission for the Future, 1992. Eckersley R. Failing a generation: the impact of culture on the health and well-being of youth. J Paediatr Child Health 1993; 29 Suppl 1: S16-S19. Eckersley R. Values and visions: youth and the failure of modern western culture. Youth Studies Australia 1995; 14 (1): 13-21. Australian Science, Technology and Engineering Council (ASTEC). Having our say about the future -- young people's dreams and expectations of Australia in 2010 and the role of science and technology. Report of the ASTEC Youth Partnership Study 1996. Canberra: AGPS, 1996. First text citation to: Discussion paper, Appendix B. Eckersley R. Young people's perceptions of the future: what they mean and why they matter. pp 60-65. Second text citation to report as a whole. Eckersley R. Dreams and expectations: young people's views of the future. Youth Studies Australia 1996; 15 (3): 11-17 . A brief description of the youth futures program of the Australian Commission for the Future. Melbourne: Australian Commission for the Future, 1996. Pearce C, Martin G. Locus of control as an indicator of risk for suicidal behaviour among adolescents. Acta Psychiatr Scand 1993; 88: 409-414. Nunn KP. Personal hopefulness: a conceptual review of the relevance of the perceived future to psychiatry. Br J Med Psychol 1996; 69: 227-245. Zika S, Chamberlain K. The relation between meaning in life and psychological well-being. Br J Psychol 1992; 83: 133-145. Authors' details 23 Goble Street, Hughes, ACT. Richard Eckersley, BSc(Hons), MScSoc, Strategic Analyst and Science Writer. No reprints will be available from the author. Correspondence: Mr Richard Eckersley, 23 Goble Street, Hughes, ACT 2605. To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Richard Eckersley

Movement disorders with selective serotonin reuptake inhibitors Adverse Drug Reactions Advisory Committee MJA 1997; 166: 259 Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Orolingual dyskinesia - Cases - Akathisia - Case - Comment - References - - ©MJA1997 The selective serotonin reuptake inhibitors (SSRIs) are being prescribed increasingly for major depression. The Adverse Drug Reactions Advisory Committee (ADRAC) has received more than 1800 postmarketing reports of adverse reactions to the SSRIs (fluoxetine, paroxetine and sertraline), with the most common reactions reported being rashes, headache, anorexia, nausea, vomiting, diarrhoea, dizziness, agitation, tremor and increased sweating. Reports describing the movement disorders of orolingual dyskinesia and akathisia are reviewed here. Orolingual dyskinesia Marchioni et al. described orolingual movements (intermittent facial movements, initially involving the tongue and lips) in a 74-year-old woman who had taken fluoxetine for seven months. 1 ADRAC has received nine reports of orolingual dyskinesia (after excluding reports describing tardive dyskinesia or orolingual movements as part of a generalised dyskinesia) where an SSRI was the only suspected drug since 18 January 1993. Fluoxetine was the suspected drug in four reports, sertraline in three and paroxetine in two. The nine reports described seven women and two men aged 22-89 years (median, 51 years). These dyskinesias were variously described as abnormal involuntary orolingual-buccal movements, persistent repetitive jaw movements, involuntary chewing movements and involuntary facial movements. In eight of the nine patients, they started within one month of starting to take the SSRI; in the remaining patient the movements started five months after starting to take the SSRI. Six of the nine patients had recovered at the time of reporting. Cases A 29-year-old woman taking no other medications was prescribed paroxetine 20 mg daily for depression. Four hours after taking only one paroxetine tablet she developed persistent repetitive jaw movements with chattering of her teeth. The movements and chattering occurred markedly for two days, and continued to occur with cold or fatigue over the next two weeks before gradually settling. She took no tablets after the first one. In another case, a 22-year-old man taking no other medications was prescribed a 20 mg paroxetine tablet daily for depression. After taking paroxetine for four weeks he experienced involuntary facial movements, accompanied by disturbed speech and agitation. He immediately stopped taking the paroxetine and quickly and fully recovered. Akathisia Olivera described a 40-year-old woman who developed akathisia (a form of restlessness in which there is the inability to sit still, an urge to move about constantly and a feeling of muscular quivering) after three days of taking paroxetine 20 mg daily. 2 ADRAC has received nine reports of akathisia where an SSRI was the only suspected drug since 17 February 1993. Fluoxetine was the suspected drug in six reports, paroxetine in two and sertraline in one. These nine reports described seven women and two men aged 29-86 years (median, 54 years). The akathisia started within 33 days of commencing the SSRI in seven patients, and the onset was within two days of commencing the SSRI in two of these seven. However, in the remaining two patients, the akathisia started five and eight months after commencing the SSRI. Eight of the nine patients had recovered at the time of reporting. Case An 86-year-old woman was prescribed 20 mg paroxetine daily for depression. Her only other medication was 5 mg felodipine daily, which she had started taking 12 months previously. She developed akathisia after taking paroxetine for five months -- she was unable to keep still, with restless legs and a constant need to pace. After she stopped taking the paroxetine only, she recovered fully. Comment Although acute dystonia is well recognised as an early adverse reaction to SSRIs, orolingual dyskinesia might be mistakenly thought to only occur later as tardive dyskinesia. It is important for prescribers to be aware that movement disorders such as orolingual dyskinesia and akathisia can occur in patients of any age, and that their onset may vary considerably from immediately on starting treatment to after many months of treatment. Adverse Drug Reactions Advisory Committee, PO Box 100, Woden, ACT 2606. References Marchioni E, Perucca E, Soragna D, et al. Choreiform syndrome associated with fluoxetine treatment in a patient with deficient CYP2D6 activity. Neurology 1996; 46: 853. Olivera AA. A case of paroxetine-induced akathisia. Biol Psychiatry 1996; 39: 910. - - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

"Mental health literacy": a survey of the public's ability to recognise mental disorders and their beliefs about the effectiveness of treatment Anthony F Jorm, Ailsa E Korten, Patricia A Jacomb, Helen Christensen, Bryan Rodgers and Penelope Pollitt MJA 1997; 166: 182 Abstract - Introduction - Methods - Sample - Interview - Ethical approval - Results - Recognition - Choice and rating of available help - Prognosis - Discussion - References - Authors' details - ©MJA1997 Abstract Objectives: To assess the public's recognition of mental disorders and their beliefs about the effectiveness of various treatments ("mental health literacy"). Design: A cross-sectional survey, in 1995, with structured interviews using vignettes of a person with either depression or schizophrenia. Participants: A representative national sample of 2031 individuals aged 18 -74 years; 1010 participants were questioned about the depression vignette and 1021 about the schizophrenia vignette. Results: Most of the participants recognised the presence of some sort of mental disorder: 72% for the depression vignette (correctly labelled as depression by 39%) and 84% for the schizophrenia vignette (correctly labelled by 27%). When various people were rated as likely to be helpful or harmful for the person described in the vignette for depression, general practitioners (83%) and counsellors (74%) were most often rated as helpful, with psychiatrists (51%) and psychologists (49%) less so. Corresponding data for the schizophrenia vignette were: counsellors (81%), GPs (74%), psychiatrists (71%) and psychologists (62%). Many standard psychiatric treatments (antidepressants, antipsychotics, electroconvulsive therapy, admission to a psychiatric ward) were more often rated as harmful than helpful, and some non-standard treatments were rated highly (increased physical or social activity, relaxation and stress management, reading about people with similar problems). Vitamins and special diets were more often rated as helpful than were antidepressants and antipsychotics. Conclusion: If mental disorders are to be recognised early in the community and appropriate intervention sought, the level of mental health literacy needs to be raised. Further, public understanding of psychiatric treatments can be considerably improved. MJA 1997; 166: 182-186 Introduction "Health literacy" has been defined as the ability to gain access to, understand, and use information in ways which promote and maintain good health.1 By extension, we have coined the term "mental health literacy" to refer to knowledge and beliefs about mental disorders which aid their recognition, management or prevention. Mental health literacy includes the ability to recognise specific disorders; knowing how to seek mental health information; knowledge of risk factors and causes, of self-treatments, and of professional help available; and attitudes that promote recognition and appropriate help-seeking. The lifetime risk of developing a mental disorder is so high (nearly 50%)2 that almost the whole population will at some time have direct experience of such a disorder, either in themselves or in someone close. A high public level of mental health literacy would make early recognition of and appropriate intervention in these disorders more likely. Previous information on this topic is limited and is derived from national surveys on depression alone,3-5 or on depression and schizophrenia.6 Although these surveys found that most people believed depression to be treatable,3-5 most respondents had negative views about the effectiveness of medication for mental disorders. In contrast, counselling and psychotherapy were generally viewed more favourably.3,4,6 To assess the mental health literacy of the Australian population, we surveyed a representative national sample of adults on their knowledge of and beliefs about schizophrenia and depression. We report our findings on the ability of this population to recognise these disorders and their beliefs about the effectiveness of various treatments. Methods Sample The survey was carried out by the Australian Bureau of Statistics in August 1995 as part of its Population Survey Monitor.7 This is a household survey covering all private dwellings in urban and rural areas (excluding the sparsely settled areas) across all States and Territories. Selected households were initially sent a letter explaining that their dwelling had been selected for the survey. The letters gave advance notice that an interviewer would call to make an appointment. Interviewers made at least three call-backs in rural areas and at least five in urban areas before a dwelling was classified as "non-contact". Contact was made with a sample of 2531 households, with one person randomly sampled per household for a personal interview; 2164 persons agreed to participate (85%). Because a pilot study showed that people aged more than 75 years often had trouble understanding the interview, this age group was excluded, leaving a sample of 2031 respondents, aged 18-74. Fifty-six per cent of the sample was female and 74% Australian-born. The age distribution was: 21% aged 18-29, 25% aged 30-39, 22% aged 40-49, 16% aged 50-59, 11% aged 60-69 and 5% aged 70-74. The highest educational qualification was: secondary school certificate (51%), trade certificate/apprenticeship (11%), other certificate (17%), associate or undergraduate diploma (7%), bachelor's degree or higher (13%), still at school (1%). Weights were provided for each respondent, based on complex ratio estimation procedures, to adjust for probabilities of selection and to reduce non-response bias.7 Weighted percentages, which represent estimates of the whole of the Australian population aged 18-74, are presented here. Interview The interview was based on a vignette of a person suffering from a mental disorder. Half the sample were shown a vignette describing a person who met ICD-108 and DSM-IV9 criteria for major depression ( Box 1) and the others were shown a vignette of a person who met ICD-108 and DSM-IV9 criteria for schizophrenia ( Box 2). The sex of the person described was randomly assigned to be male (John) or female (Mary). After being shown the vignette and having it read out to them, respondents were asked two open-ended questions: "What would you say, if anything, is wrong with John/Mary?" and "How do you think John/Mary could best be helped?" The rest of the interview consisted of questions to determine the respondents' knowledge of and views about: Various people who could help (whether each category of person was likely to be helpful, harmful, or neither, for the person described); A range of possible treatments (whether each treatment was likely to be helpful, harmful, or neither, for the person described); Knowledge of likely prognosis; Knowledge of risk factors; and Beliefs associated with stigma and discrimination. Ethical approval Approval was obtained from the Ethics in Human Experimentation Committee of the Australian National University. Statistical analysis Using the chi-squared test, all estimates were compared according to recognition of a mental health problem. Only differences significant at the 0.01 level (P < 0.01) are reported below. Results Of the 2031 persons interviewed, 1010 were shown the depression vignette (508, John and 502, Mary) and 1021 were shown the schizophrenia vignette (514, John and 507, Mary). Recognition Figure 1 summarises responses to the question "What would you say, if anything, is wrong with John/Mary?", and shows those categories mentioned by at least 5% of the respondents (all responses were later categorised by the researchers). Multiple responses were allowed, and 30% of respondents gave at least two answers. For the depression vignette, 39% correctly identified depression and 22% mentioned stress. In all, 72% mentioned a category that could be regarded as being within the sphere of mental health. Eleven per cent mentioned items that we categorised as physical disorders (e.g., viruses, nutritional deficiencies, cancer), and half of these respondents did not mention a mental problem. A further 17% gave only answers that were extremely variable, but which we grouped as "personal or employment-related problems", "problems with not being active or sociable enough", and "other". Seven per cent of the sample responded with "don't know". For the schizophrenia vignette, although 84% mentioned at least one category in the sphere of mental health, only 27% recognised schizophrenia and a further 26% mentioned depression. Physical disorders were the only suggestion from 2% of the respondents, while 13% gave responses that described neither physical nor mental disorders (e.g., "has a problem"). There was less uncertainty with the schizophrenia vignette, however, in that only 4% responded with "don't know". Choice and rating of available help For the second open-ended question -- "How do you think John/Mary could best be helped?" -- 34% of the respondents (across both vignettes) made more than one suggestion. For the depression vignette, the most frequent response was "see a doctor" (44%), followed by "see a counsellor" (23%) and "talk over with family or friends" (20%). A psychiatrist was mentioned by 8%, while 5% answered "don't know". Responses for the schizophrenia vignette were: counsellor (31%), psychiatrist (28%), doctor (27%), family or friends (20%) and "don't know" (4%). The respondents were given a list of people who might potentially provide help and were asked to rate the various helpers by saying whether each would be helpful or harmful (Figure 2a). For the depression vignette, most of the respondents regarded GPs (83%), counsellors (74%), close friends (73%) and close family (70%) as helpful; around half the population rated telephone counselling services (53%), psychiatrists (51%) and psychologists (49%) as helpful. Fewer than 10% felt that any of the above groups would be harmful, although 43% believed it would be harmful for someone with depression to deal with it on their own. For the schizo phrenia vignette, most respondents regarded counsellors (81%), GPs (74%) and psychiatrists (71%) as helpful; a larger proportion of the population than for the depression vignette believed it would be harmful to try and deal with such problems alone (55%). Rating of pharmacological treatments Respondents were given a list of pharmacological treatments (Figure 2b) to rate as helpful or harmful. For the depression vignette, more of the respondents regarded each of the medications as harmful than helpful. The exception was the category vitamins, minerals, tonics or herbal medicines, which were regarded as helpful by 57% of respondents, and as harmful by 3%. Antidepressant medication was recognised as helpful by 29% and as harmful by 42% of respondents. For the schizophrenia vignette, antidepressants were regarded as helpful by 38% of respondents, followed by vitamins and minerals (34%) and antipsychotics (23%). The greatest percentage of "don't know" responses was for antipsychotics (about one-fifth of the respondents for both vignettes). Rating of non-pharmacological treatments When respondents were asked to rate non-pharmacological treatments (Figure 2c), most (for both the depression and the schizophrenia vignettes) regarded non-standard interventions (more physical or social activity; learn relaxation [including stress management, meditation or yoga courses]; reading about people with similar problems) as helpful and not harmful. On the other hand, most regarded admission to a psychiatric ward as harmful (depression, 62%; schizophrenia, 51%) and most regarded having electroconvulsive therapy (ECT) as harmful (depression, 72%; schizophrenia, 66%). For the depression vignette, psychotherapy was seen as helpful by 34% and harmful by 13%, compared with 55% helpful and 7% harmful for the schizophrenia vignette. The highest number of "don't know" responses was elicited for psychotherapy (16% for depression, 15% for schizophrenia) and for ECT (10% for depression and 14% for schizophrenia) (data not shown). As opinions about treatment might vary according to whether or not the respondent thought the person in the vignette had a mental health problem, the respondents were divided accordingly. The major difference in findings was that those who did not perceive a mental health problem were more likely to rate treatments as "neither helpful nor harmful" or to respond "don't know" . However, the rank ordering of treatments in terms of helpfulness was generally similar. Spearman rank correlation coefficients for the depression vignette were 0.82 (people), 0.90 (medicines) and 0.98 (treatments), and for the schizophrenia vignette they were 0.87 (people), 0.71 (medicines) and 0.98 (treatments). Prognosis All respondents were asked to give their views on prognosis with and without the professional help they thought most appropriate. For the depression vignette, 80% thought that there would be full recovery with help. If there was no help, 56% believed the person would get worse, and 5% that there would be full recovery. For the schizophrenia vignette, 69% believed that help would result in full recovery; if there was no help, 75% believed that the person would get worse, and 3% that there would be full recovery. Discussion Recognition of the presence of a mental disorder was high in our population sample, although only a minority gave the correct psychiatric label to their vignette. While it is not known whether there is any benefit to the public in being able to apply the correct psychiatric label, misidentifying a mental disorder as a physical one or as a problem unrelated to health may lead to inappropriate use or avoidance of health services. The major limitation in recognition is therefore seen in the 28% who thought the person described in the depression vignette did not have a mental disorder and the 16% who had the same opinion about the person in the schizophrenia vignette. When respondents were asked about the helpfulness of various people, GPs were rated very highly for both vignettes. Only half the respondents thought that a psychiatrist or psychologist would be helpful for the person in the depression vignette, a proportion less than that cited for GPs, counsellors, close friends, family, and telephone counselling. While psychiatrists and psychologists were rated as relatively more helpful for the person in the schizophrenia vignette, they were nevertheless less likely to be rated as helpful than counsellors or GPs. This suggests that public perceptions of mental health specialists need to be changed. Ratings given for the helpfulness of various treatments for depression are not consistent with the evidence of controlled trials, which have indicated that both antidepressant medication and psychotherapy are effective treatments. 10,11 Antidepressants were rated as helpful by 29% of our sample and as harmful by 42%, while psychotherapy was rated as helpful by 34% and harmful by 13%. Both were regarded as less helpful than treatments such as vitamins and minerals and special diets. The treatment with the highest negative rating was ECT. Although the patient described to the respondents could not be regarded as severely depressed enough to warrant ECT, 11 there is clearly a public perception that this treatment is harmful. The treatments that the public rated most highly were all non-standard in nature. These views may not be entirely misguided; there is evidence (e.g., from controlled trials) that physical exercise may have a positive effect on depression. 12 The findings were similar for the schizophrenia vignette. Although controlled trials show that antipsychotic medication is an effective treatment, 13 this was rated as helpful by 23% of the respondents and harmful by 34%; 20% did not offer an opinion. Similarly, admission to a psychiatric ward, which can be useful in the management of schizophrenia, 13 was rated as harmful by half the respondents. As with depression, non-standard interventions were the most likely to be rated as helpful. Despite these negative opinions of, or ignorance about, the helpfulness of many standard treatments, the public clearly sees the conditions described in the vignettes as treatable. The predominant belief that mental disorders are treatable has also been found in overseas surveys, 3,4 although a United States survey found that most respondents believed it possible to get better through one's own efforts. 5 There were some marked differences in responses to the depression and schizophrenia vignettes in terms of recognition, perceived helpfulness of treatments and prognosis. These differences show that the respondents did not see all mental disorders as the same and recognised that the condition described in the schizophrenia vignette required more vigorous intervention. Our results also indicate that the views of many members of the public diverge from those of health professionals, particularly mental health specialists. Such differences may lead to unwillingness to accept help from mental health professionals, or to a lack of adherence to advice given. Clearly, if mental disorders are to be recognised early and appropriate action taken, the level of mental health literacy in the population should be raised. There has been considerable interest in trying to improve the recognition and management of mental disorders in primary care, 10,14 but this knowledge needs to reach the consumers of services so that they can play a more effective role in the management of their own mental health. References Nutbeam D, Wise M, Bauman A, et al. Goals and targets for Australia's health in the year 2000 and beyond. Canberra: Australian Government Publishing Service, 1993. Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States: Results from the National Comorbidity Survey. Arch Gen Psychiatry 1994; 51: 8-19. McKeon P, Carrick S. Public attitudes to depression: a national survey. Ir J Psychol Med 1991; 8: 116-21. Sims A. The scar that is more than skin deep: the stigma of depression. Br J Gen Pract 1993; 43: 30-31. Regier DA, Hirschfeld RM, Goodwin FK, et al. The NIMH depression awareness, recognition, and treatment program: structure, aims, and scientific basis. Am J Psychiatry 1988; 145: 1351-1357. Angermeyer MC, Matschinger H. Public attitude towards psychiatric treatment. Acta Psychiatr Scand 1996; 94: 326-336. Australian Bureau of Statistics. Population survey monitor, August 1995 (No. 4103.0). Adelaide: ABS, 1995. World Health Organization. The ICD-10 classification of mental and behavioural disorders. Diagnostic criteria for research. Geneva: WHO, 1993. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed) (DSM-IV). Washington DC: APA, 1994. Depression Guideline Panel. Depression in primary care: Volume 2. Treatment of major depression. Clinical practice guideline, number 5. Rockville, MD: US Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1993. The Quality Assurance Project. A treatment outline for depressive disorders. Aust N Z J Psychiatry 1983; 17: 129-146. Byrne A, Byrne DG. The effect of exercise on depression, anxiety and other mood states: a review. J Psychosom Res 1993; 37: 565-574. The Quality Assurance Project. A treatment outline for the management of schizophrenia. Aust N Z J Psychiatry 1984; 18: 19-38. Ustun TB, Goldberg DP, Cooper JE, et al. A new classification for mental disorders with management guidelines for use in primary care: The ICD-10 PHC. Br J Gen Pract 1995; 45: 211-215. (Received 22 Feb 1996, accepted 4 Nov, 1996) Authors' details NHMRC Social Psychiatry Research Unit, The Australian National University, Canberra, ACT. Anthony F Jorm, PhD, DSc, Deputy Director; Ailsa E Korten, BSc, Research Officer; Patricia A Jacomb, MSc, Research Assistant; Helen Christensen, PhD, Fellow; Bryan Rodgers, PhD, Fellow; Penelope Pollitt, PhD, Research Fellow. No reprints will be available from the author. Correspondence: Dr A F Jorm, NHMRC Social Psychiatry Research Unit, The Australian National University, Canberra, ACT 0200. E-mail: Anthony. Jorm AT anu.edu.au - - - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Anthony F Jorm · Ailsa E Korten · Patricia A Jacomb · Helen Christensen · Bryan Rodgers · Penelope Pollitt

Depression, decisions and the desire to die All patients who request withdrawal of non-futile life-sustaining treatment should first undergo psychiatric assessment MJA 1996; 165: 411 Sadness and despair are normal responses to the news that one is gravely ill. However, as many as one in five seriously ill people go beyond this normal response to develop major depression.1-4Major depression is far more than a disorder of emotion; its effects on reason and the intellect may be just as profound. As it takes hold, it steadily infiltrates and infects its victim's every thought. Everything comes to be seen through a veil of despondency and despair. As time passes, sadness turns to emptiness and emptiness turns to pain. Increasingly, there seem fewer and fewer options. Often, toward the end, the patient can see no way out of the blackness and all hope is lost. Ten percent commit suicide. Some seriously ill people, like those with end-stage renal failure or potentially terminal cancer, require medical treatments to continue to live. In Australia, there is a legal right to refuse such treatment. The laws that bestow this right are based upon the principle of maximising autonomy, which asserts that competent adults should be allowed to make their own choices about their own lives, provided these choices do not cause harm to others. This principle assumes that the choices are not influenced by mental illness. However, one would expect that a patient with major depression might be more likely to refuse life-sustaining treatment, because of the cognitive effects of the depression. In this issue of the Journal, Hooper and colleagues (page 416) provide empirical evidence that depression does influence choice about life-sustaining treatment. They asked a cohort of elderly, depressed people to imagine which life-sustaining treatments they would reject in two hypothetical situations. They found that, on average, people rejected more life-sustaining treatments when they were depressed than when they had later recovered. Major depression is eminently treatable. If it can influence the seriously ill to refuse treatment, then some of those who do refuse treatment might be depressed and might change their minds if the depression were treated. Other recent studies have also shown a link between depression and a desire to die. Chochinov et al. found that 47% of terminally ill people who expressed a serious desire for death suffered from major depression.5 Emanuel et al. found that oncology patients who seriously considered and prepared for euthanasia or physician-assisted suicide were significantly more likely to be depressed.6 Taken together, these studies underline the importance of recognising and treating major depression before meeting a request to withdraw life-sustaining treatment. Unfortunately, the diagnosis of major depression in the gravely ill is very difficult. Low spirits are to be expected in serious illness, and many of the other features of major depression (such as weight loss and sleep disturbance) are also common in physical illnesses. The difficulty of diagnosis is reflected in studies that reveal that non-psychiatrically trained doctors miss up to half of cases of major depression in the medically ill.7-9 Life-sustaining treatments are often withdrawn in situations where their continuation would provide no tangible benefit to the patient. The decision to withhold these futile treatments will be based upon many factors besides patient preference. However, when a treatment is not futile, patient refusal is usually central to a decision to stop. A doctor caring for a patient in this situation has a duty to ensure that the refusal is not motivated by a major depression. Given the difficulties of accurate diagnosis, this duty is best fulfilled by asking a psychiatrist to review the patient. Advance directives ("living wills") are documents that allow their users to specify in advance which life-sustaining treatments they would accept if needed in the future. If an advance directive is made while a patient is depressed, it is unlikely to be a valid indication of that patient's future preferences. The same arguments outlined above apply. Advance directives made in the context of a serious illness should only be completed after psychiatric review. Without this review, doctors should be cautious about complying with the directive. The Northern Territory legislation that permits active voluntary euthanasia demands a psychiatric review before a patient can be assisted to die.10,11 This provision was included to provide patients with the best protection against the possibility of meeting a request driven by a treatable depression. Our duty to protect those with a desire to die extends far beyond those who request active euthanasia. Any patient who refuses life-sustaining treatment, and for whom such treatment would not be futile, should receive psychiatric review before that request is met. Christopher J RyanConsultation-Liaison Psychiatrist, Department of Psychiatry, Westmead Hospital, Sydney, NSW Bukberg J, Penman D, Holland JC. Depression in hospitalised cancer patients. Psychosom Med 1984; 46: 199-212. Maj M. Psychiatric aspects of HIV-1 infection and AIDS. Psychol Med 1990; 20: 547-563. Craven JL, Rodin GM, Johnson L, et al. The diagnosis of major depression in renal dialysis patients. Psychosom Med 1987; 49: 482-492. Clarke DM, Minas IH, Stuart GW. The prevalence of psychiatric morbidity in general hospital inpatients. Aust N Z J Psychiatry 1991; 25: 322-329. Chochinov HM, Wilson KG, Enns M, et al. Desire for death in the terminally ill. Am J Psych 1995; 152: 1185-1191. Emanuel EJ, Fairclough DL, Daniels ER, et al. Euthanasia and physician-assisted suicide: attitudes and experiences of oncology patients, oncologists and the public. Lancet 1996; 347: 1805-1810. Feldman E, Mayou R, Hawton K, et al. Psychiatric disorder in medical patients. QJM 1987; 63: 405-412. Nielson C, Williams TA. Depression in ambulatory medical patients: Prevalence by self-report questionnaire and recognition by nonpsychiatric physicians. Arch Gen Psychiatry 1980; 37: 999-1004. Clarke DM, Smith GC. Consultation-liaison psychiatry in general medical units. Aust N Z J Psychiatry 1995; 29: 424-432. Ryan CJ, Kaye M. Euthanasia in Australia. N Engl J Med 1996; 334: 1668-1669. Northern Territory Rights of the Terminally Ill Act. Legislative Assembly of the Northern Territory (Act No. 12 of 1995).

Christoper J Ryan

Major depression and refusal of life-sustaining medical treatment in the elderly Stuart C Hooper, Kevin J Vaughan, Christopher C Tennant and Janette M Perz MJA 1996; 165: 416-419 Abstract - Introduction - Methods - Patients and assessment - Follow-up - Statistical analyses - Results - Patients - Intensity of depression - Desire for life-sustaining treatment - Discussion - Acknowledgements - References - Authors' details Abstract Objective: To examine the effect of improvement or recovery from major depression in elderly patients on their desire for life-sustaining treatments. Design: Prospective case survey. Setting: Psychogeriatric Service of Hornsby Ku-ring-gai Hospital & Community Health Services and Ryde Hospital & Community Health Services (a community-based service serving an urban population with over 29 000 elderly people). Subjects: All patients referred with major depression (diagnosed by DSM-IV criteria) and no significant cognitive impairment between October 1994 and January 1995. Outcome measures: Number of life-sustaining treatments desired before and after treatment of depression in two hypothetical acute life-threatening illnesses (one with a good and the other with an uncertain prognosis), and intensity of depression on the Geriatric Depression Scale (GDS). Results: 22 subjects completed both stages of the study. Initial depression was severe in five, moderate in 16 and mild in one. GDS scores decreased in 18 subjects after treatment. Mean number of life-sustaining treatments desired by these patients increased significantly from 4.0 to 6.1 (out of seven possible treatments) in the "good prognosis" illness and from 6.4 to to 9.6 (out of 14) overall. The increase in the "uncertain prognosis" illness (2.3 to 3.4) was not significant. Conclusions: Moderate or severe major depression in the elderly is associated with a high degree of refusal of life-sustaining treatments. Treatment of the depression leads to increased acceptance of these treatments, particularly if prognosis is good. MJA 1996; 165: 416-419 Introduction Decisions about withdrawing or withholding life-sustaining medical treatments have become problematic in recent decades. Dramatic advances in medical technology enable many severely ill patients to remain alive, yet the decision to prolong life is tempered by the finite nature of resources, economic rationalism and the patient's quality of life. In the United States, it is estimated that decisions to limit medical treatment are made for about 70% of patients who die in hospital.1 In many cases, this is due to patient refusal of further medical treatment and is part of the strong shift towards respecting patients' autonomy and right to self-determination. In all Australian States, there is a common-law right for competent patients to refuse medical treatment, including life-sustaining treatment. In Victoria, South Australia and the Northern Territory, this right has received statutory recognition. In these States, legislation also permits competent individuals over 18 years to make advance directives ("living wills") specifying that in the event of a terminal illness the individual does not wish to be subjected to extraordinary life-prolonging measures.2 However, the potential influence of depressive illness on patients' refusal of life-sustaining treatment is often neglected. In the elderly (who are disproportionately represented among those who have life-sustaining treatment withheld or withdrawn), depression is often not recognised by primary care physicians.3-7 Misdiagnosis is especially likely in the elderly if symptoms are atypical (e.g., cognitive deficits [pseudo dementia], somatisation or anxiety). Further, with depression impairments in decision-making may be under-recognised, as the cognitive aspects of competence (which are emphasised by doctors and courts) may remain intact, while more subtle abilities (such as the ability to assign realistic values or meanings to the risks and benefits of prospective treatments)8,9 may be impaired. Depressed patients may undervalue potential positive outcomes and predict negative outcomes.9 These "affective" aspects of clinical competence are generally not considered as important as the "cognitive" aspects and can be more difficult to detect.10 The negative outlook disappears after recovery from depression, suggesting that it is specific to the illness phase and not a trait of depression-prone individuals.11,12 Case reports have highlighted patients who have initially refused, but later accepted, life-sustaining treatment after recovery from depression.9,15-18 Longitudinal studies of male Veterans Administration patients in the United States found that desire for life-sustaining treatment was not increased by recovery from major depression of mild to moderate severity,13,14 but was significantly increased if the major depression was severe.14 However, the extent to which results of these case reports and longitudinal studies can be generalised is uncertain. We therefore investigated the effect of recovery from major depression on preferences for life-sustaining treatments in a group of patients referred to an Australian community psychogeriatric service. Methods Our study was approved by the Ethics Committee of the Hornsby Ku-ring-gai Hospital & Community Health Services and Ryde Hospital & Community Health Services. Patients and assessment Subjects for the study were drawn from consecutive patients referred to the Psychogeriatric Service of Hornsby Ku-ring-gai Hospital between October 1994 and January 1995. The Psycho geriatric Service is a community-based service with inpatient facilities, serving an area with over 29 000 elderly people. Inclusion criteria: Diagnosis of DSM-IV major depression,19 made by clinical interview with the consultant psychiatrist and senior psychiatric registrar of the Psychogeriatric Service, according to DSM-IV criteria (Box 1). Severity of depression (mild, moderate, severe) was also assessed clinically with DSM-IV criteria; Mini-Mental State Examination score (MMSE) > 17.20 This was used to screen out patients with significant cognitive impairment; and Informed consent given. Intensity of depression was assessed with the Geriatric Depression Scale (GDS). This is a rating scale (not a diagnostic instrument) that provides a numerical index of intensity of depression and was designed exclusively for use in elderly patients. It contains 30 questions requiring a yes or no answer, which can be either self- or observer-administered. One-week test-retest reliability of 0.85 and criterion validity of 0.82 have been recorded.21,22 Desire for life-sustaining treatment was assessed by a questionnaire adapted from Lee and Ganzini,13 with simplification of the hypothetical scenarios. Patients were asked to "imagine that you developed a sudden life-threatening illness with an uncertain chance of recovery". They were then asked, "Would you want the following procedures should they be needed?". These comprised intravenous fluids with medication, nasogastric tube, blood transfusions, intensive care, kidney dialysis, mechanical ventilatory support, and cardiopulmonary resuscitation. The question was repeated for a similar illness with a good chance of complete recovery. Desire for life-sustaining treatment was quantified by assigning a point for each treatment desired. Follow-up After standard treatment for major depression (including pharmacological agents in all cases and electroconvulsive therapy in two), clinical assessments, GDS and questionnaires were repeated. At least six weeks was allowed before follow-up as the elderly may take longer to respond to antidepressant treatment. Recovery (remission) from major depression was diagnosed clinically at follow-up interview if patients no longer met the DSM-IV criteria for major depression. Statistical analyses The paired t test was used to compare initial and follow-up GDS scores. The Wilcoxon signed-rank test (a non-parametric test) was used to compare initial and follow-up scores for the life-sustaining treatment questionnaire, scoring 1 for any increase and 0 for any decrease and ignoring patients who did not change. The binomial distribution was consulted, with parameters 0.5 and the number of people who changed preferences. Results Patients Of 25 consecutive patients referred with major depression to the Psychogeriatric Service during the study period, 22 were included in the study. Two failed to meet the inclusion criteria (one did not give informed consent and the other did not score sufficiently on the MMSE) and a third died before follow-up. Demographic characteristics of the 22 who completed the study are shown in Box 2. A notable feature was the very high proportion of women in the group (82%). All but four of the patients were new referrals to the service and 10 (46%) were reporting their first depressive disorder. None had a history of previous prolonged psychiatric hospitalisations or previous suicide attempts. Twelve patients (55%) were treated in their homes, eight (36%) were treated predominantly in an inpatient psychiatric unit and two (9%) predominantly in a medical ward. Follow-up after a mean of 88.5 days (SD, 26.3) showed no significant changes in the number of medical illnesses or in demographic variables. Intensity of depression Severity of the depression was classed as moderate for 16 patients (73%), severe for five (23%) and mild for one (5%). Mean GDS score for the group was 24.4 (SD, 3.3) and decreased significantly on follow-up to 16.7 (SD, 8.0) ( P < 0.0005). Individual GDS scores decreased ("improved") in 18 patients, and 12 of these (55% of the total number) were diagnosed clinically as recovered from major depression, according to DSM-IV criteria. Desire for life-sustaining treatment Changes in desire for life-sustaining treatment among those whose depression improved or recovered are shown in Box 3. There were significant increases in the number of interventions desired overall and for the "good prognosis" illness among both the 12 patients who recovered from depression (according to DSM-IV criteria for remission) and the 18 whose GDS scores improved (including six who were not classed as recovered by DSM-IV criteria). There were also increases in the number of interventions desired for the "uncertain prognosis" illness, but the change was significant only in the "recovered" group. Of the 12 patients who recovered, nine had had major depression of moderate severity. The number of interventions desired among these nine also increased significantly overall ( P = 0.05) and for the "good prognosis" illness ( P = 0.04), but not for the "uncertain prognosis" illness. Discussion We found that remission of major depression in the elderly was associated with a significant increase in acceptance of life-sustaining treatments. This increase occurred for both moderate and severe forms of major depression. However, our study has limitations which should caution against drawing firm general conclusions. The main limitations are the relatively small sample size and the possibility of a gender bias caused by the high proportion of female patients. We also do not know the correlation between responses to hypothetical questionnaires and actual decisions when confronted with an "end of life" situation. However, indicating preferences to hypothetical scenarios is similar to executing a "living will" (also, in effect, hypothetical). The hypothetical scenarios examined only acute, not chronic, illnesses, and the findings of this study cannot necessarily be generalised to patients who have coexisting life-threatening medical conditions. In addition, the word "uncertain", used to describe prognosis in one of the scenarios, may have been ambiguous, as all prognoses are uncertain. It was chosen to enable comparison with Lee and Ganzini's studies,13,14 but "poor" or "unfavourable" would have been less ambiguous. A further limitation involved the diagnostic assessments, which did not use structured diagnostic instruments. Our results vary from those of other longitudinal studies.13,14 Ganzini et al.14 found that recovery from major depression was associated with change in preferences for life-sustaining treatments only if the depression was severe. Lee and Ganzini13,14 concluded that, in major depression of mild to moderate severity, "patients should not be discouraged from completing advance treatment directives and that choices by these patients to limit treatment should be respected". However, our finding of a significant increase in the number of life-sustaining treatments desired by nine patients who recovered from major depression of moderate severity suggests that doctors should be cautious about adopting such an approach in the elderly with moderate major depression. Differences between the results of our study and those of Ganzini et al.14 may have been caused by differences between samples and methods. Their sample had a higher proportion of men (81% versus 18% in our study) and their questionnaire about life-sustaining treatments was more complex, possibly affecting subject comprehension and reducing the sensitivity of the instrument. They used DSM-III-R criteria to diagnose major depression, but the differences between these criteria and the DSM-IV criteria that we used are minor. However, neither set of criteria precisely defines the boundaries between mild, moderate and severe forms of major depression, allowing the possibility of diagnostic bias in classifying severity. Further, in analysing their data, Ganzini et al.14 defined a clinically evident increase in preference for medical therapy as an increase in desire for a mean of three or more of the 14 possible interventions. A different cut-off (e.g., two or more of the 14 interventions) would have led to different results. In addition, we allowed a longer time before follow-up than Ganzini et al.14 (mean, 88.5 days versus 24.5 days), and, although we found that degree of recovery measured by GDS was no greater, it is possible that preferences for life-sustaining treatments may take longer to improve than depression. Another possibility is that the longer follow-up period in our study allowed factors other than changes in level of depression to affect preferences. These studies highlight the potential for depression to influence patient desire for life-sustaining treatments, suggesting that clinicians would be wise to take into account patients' mental state when assessing refusal of life-sustaining treatments. If doubt exists about a patient's decisional capacity, or whether major depression is present, psychiatric consultation is indicated. In the absence of an advance directive (completed before the onset of depression), severely depressed patients' wishes to forgo life-sustaining treatments should not be respected until an attempt is made to treat the depression. In contrast, it appears reasonable to respect the wishes of mildly depressed patients, whereas in moderate major depression consensus is lacking. It would be prudent (until further studies clarify this question) to err on the side of preserving life and to treat moderate major depression of moderate severity before respecting a refusal of life-sustaining treatments. Furthermore, patients with moderate or severe major depression who are planning to write advance directives should be encouraged not to do so until their depression has been treated. In our patients whose depression "improved", we found no significant increase in number of life-sustaining treatments desired for an illness with uncertain prognosis. Although the lack of significance may have been due to the small sample size, it suggests that the prognosis of the illness should also be considered in clinical settings. When prognosis is so poor that treatment becomes futile, refusal of life-sustaining treatments should be respected regardless of the presence of major depression, in accord with the ethical and legal principle that doctors are not required to administer futile treatments. The ethical dilemma presented by a depressed patient with dubious decisional capacity who refuses life-sustaining treatments has received little attention. The physician who complies faces the prospect that the patient's decision was biased by the depression and would have reversed on recovery. The physician who does not comply faces the possibility that the request was authentic and the patient's life has been prolonged against his or her wishes. In resolving the dilemma, careful consideration should be given to the severity of the depression, the prognosis of the illness and whether treatment would be deemed futile, and also to any previous directives made by the patient when their decisional capacity was clearly intact. Acknowledgements We acknowledge the generous support of Dr R Russell (Psychogeriatrician, Royal North Shore Hospital), and Dr W Jenneke (Staff Specialist Psychiatrist, Hornsby Ku-ring-gai Hospital). References Greco P, Shulman K, Lavizzo-Mourey R. The patient self-determination Act and the future of advance directives. Ann Intern Med 1991; 115: 639-643. CCH Australia. Death with dignity. Australian Health and Medical Law Reporter. Sydney: CCH Australia Ltd, 1995: paragraph 22-360. Regier D, Hirschfeld R, Goodwin F. The NIMH depression awareness, recognition, treatment program. Am J Psychiatry 1988; 145: 1351-1357. NIH Consensus Development Panel on Depression in Late Life. Diagnosis and treatment of depression in late life. JAMA 1992; 268: 1018-1024. Eisenberg L. Treating depression and anxiety in primary care -- closing the gap between knowledge and practice. N Engl J Med 1992; 16: 1080-1084. Nielson C, Williams T. Depression in ambulatory medical patients: prevalence by self report questionnaire and recognition by nonpsychiatric physicians. Arch Gen Psychiatry 1980; 37: 999-1004. Rapp S, Walsh D, Parisi S. Detecting depression in elderly medical inpatients. J Consult Clin Psychol 1988; 56: 509-513. Appelbaum P, Grisso T. Assessing patients' capacities to consent to treatment. N Engl J Med 1988; 319: 1635-1638. Gutheil T, Bursztajn H. Clinicians' guidelines for assessing and presenting subtle forms of patient incompetence in legal settings. Am J Psychiatry 1986; 143: 1020-1023. Bursztajn HJ, Harding HP, Gutheil TG, Brodsky A. Beyond cognition: the role of disordered affective states in impairing competence to consent to treatment. Bull Am Acad Psychiatry Law 1991; 19: 383-388. Chochinov HM, Wilson KG, Enns M, et al. Desire for death in the terminally ill. Am J Psychiatry 1995; 152: 1185-1191. Wilkinson IM, Blackburn I. Cognitive style in depressed and recovered depressed patients. Br J Clin Psychol 1981; 20: 283-292. Lee M, Ganzini L. The effect of recovery from depression on preferences for life-sustaining therapy in older patients. J Gerontol 1994; 49: M15-M21. Ganzini L, Lee M, Heintz R, et al. The effect of depression treatment on elderly patients' preferences for life-sustaining medical therapy. Am J Psychiatry 1994; 151: 1631-1636. Salzman C. ECT and ethical psychiatry. Am J Psychiatry 1977; 134: 1006-1009. Weitzel W, Purtilo R. Aggressive treatment of geriatric depression: what limits on intervention? Psychiatr Opin 1979; 160: 9-14. Swartz C, Stewart C. Melancholia and orders to restrict resuscitation. Hosp Community Psychiatry 1991; 42: 189-191. Baile F, DiMaggio J, Schapira D. The request for assistance in dying. Cancer 1993; 72: 2786-2791. American Psychiatric Association diagnostic and statistical manual of mental disorders (DSM-IV). 4th ed. Washington DC: APA, 1994. Folstein M, Folstein S, McHugh P. "Mini-Mental State": a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975; 12: 189-198. Yesavage J, Brink T, Rose T. Development and validation of a geriatric depression screening scale: a preliminary result. J Psychiatr Res 1983; 17: 37-49. Koenig HG, Meador KG, Cohen HF, Blazer DG. Self-rated depression scales and screening for major depression in older hospitalized patient with medical illness. J Am Geriatr Soc 1988; 36: 699-796. (Received 30 Oct 1995, accepted 3 Jun 1996) Authors' details Department of Mental Health, Hornsby Ku-Ring-Gai Hospital, Sydney, NSW. Stuart C Hooper, FRANZCP, Senior Psychiatric Registrar in Psychogeriatrics; now Consultant Psychiatrist, Sydney, NSW; Kevin J Vaughan, FRANZCP, Staff Specialist. Department of Academic Psychiatry, Royal North Shore Hospital, Sydney, NSW. Christopher C Tennant, FRANZCP, MD, Professor. Department of Psychology, Faculty of Arts and Social Sciences, University of Western Sydney, NSW. Janette M Perz, BA(Hons), Research Psychologist. No reprints will be available. Correspondence: Dr S C Hooper, 11 Clanalpine Street, Eastwood, NSW 2122.

Stuart C Hooper · Kevin J Vaughan · Christoper C Tennant · Janette M Perz

Anabolic steroids and the mind Brian Corrigan MJA 1996; 165: 222-226 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Introduction - Psychological effects - Withdrawal symptoms - Drug dependence - Other psychiatric changes - Acknowledgements - References - Authors' details Register to be notified of new articles by email - - ©MJA1996 Anabolic steroids were first used by weight lifters and others involved in pursuits of strength, but are now taken, often in large doses, by young men interested in enhancing their appearance. The severe psychogenic side effects of these high doses include aggressive and violent behaviour. Problems with drug withdrawal and drug dependence are also common in users of anabolic steroids and these drugs may also provoke psychiatric disorders. I review these complications, as reported in the past decade, and comment on two recent violent murders in Sydney in which anabolic steroid use was implicated. Introduction S ydney has recently witnessed two particularly brutal murders by users of anabolic steroids. One man with recent paranoid tendencies took a claw hammer and battered his wife to death, and then shot himself. In the second murder a man met a woman he knew at a nightclub and they went to the stairwell of a nearby hotel. In the man's words "something snapped" and he murdered the woman. Experienced police described it as the most brutal attack they had encountered. In both these murders the level of aggression and violence fits the descriptive term steroid rage ("roid rage"). The male hormone testosterone, derived mainly from the testes, is an anabolic and androgenic steroid responsible for the production and maintenance of the male physical features, 1 as well as the recognisable male psychological and behavioural attributes. 1-3 Numerous human and animal studies support the psychological and aggressive effects of testosterone use, and some reports correlate testosterone levels with aggressive behaviour and dominance. 2,3 Anabolic steroids are derived by chemical manipulation of the 19-carbon testosterone molecule. Despite well documented problems with their use, they are widely abused in the community for non-medical reasons, mostly by young men to enhance their appearance by "bulking up" (i.e., increasing their lean muscle mass without increasing fat). How common their use is in Australia is not known, but a recent survey in the United States concluded that there were at least three million users at any one time and at least one million former users. 4 Side effects can occur with all anabolic steroids. 5 The higher the dose the higher the risk is the general rule, and side effects can be sudden, severe and unpredictable, and include sudden death. 5 The most common group of side effects involve psychological and/or psychiatric changes. Being psychoactive substances, 3,6 anabolic steroids are expected to produce some degree of psychological change after they have been taken for some time. Indeed, these changes (which include an increase in self-confidence, energy and motivation), if they allow people to train harder, may well be one of the main factors explaining the mechanism of action of anabolic steroids. 7 Psychological effects One of the earliest papers on psychological effects reported the side effects of anabolic steroids in 32 weight-trained men; 8 56% had a subjective perception of increased irritability and aggression. This also applied to a smaller group of 10 weight-trained female athletes. 9 A more recent report compared 13 anabolic steroid users with 14 non-users and 18 former users. 10 Steroid users had more frequent episodes of anger, which were of greater intensity and duration, and a more hostile attitude towards others. In general, psychological changes need to be related to the dose and duration of anabolic steroid use (e.g., taking one or two 5 mg tablets would not produce any changes, but after taking an increasing dose for some days several psychological changes may occur). These changes will develop if anabolic steroids are taken for long enough (just how long could possibly depend upon individual tolerance). The psychological changes that occur can be arbitrarily divided into three groups, representing a continuum of effects from milder through to more severe changes, especially if continued high doses are taken. Early effects are seen as changes in mood and euphoria: there is an increase in confidence, energy and self-esteem, with enhanced motivation and enthusiasm. There is also diminished fatigue, sleeplessness and an ability to train through pain. Libido may be decreased, but is more often increased, sometimes markedly. 11 Irritability, anger, agitation and a "strange edgy feeling" are commonly reported. With larger doses or after taking anabolic steroids for a longer time, there is a loss of inhibition and a lack of judgement, with mood swings or grandiose ideas. Prolonged users become suspicious, quarrelsome, impulsive and more aggressive. 7 Severe effects manifest when these aggressive feelings increase to the extent that violent, hostile, antisocial behaviour develops, meriting the descriptive title, well known in the steroid-taking community, of "roid rages". These rages can result in property damage, self-injury (including reckless driving or crashing cars), assaults, marriage break-ups, domestic violence, 12 child abuse, 12 suicide 13 and attempted murder or murder. 14-20 Partners of anabolic steroid users are at particular risk of serious injury, and there is even a self-help group, Anabolic Steroid Wives Association, 21 to help provide them with support. One group of men who often take anabolic steroids in high doses are those working as security officers or nightclub bouncers; 22 under the influence of the drug they may be provoked into a rage and seriously injure people, and at least one person has been killed as a result. 22 How common these rages are is not known. There is often a great reluctance by anabolic steroid users to report them to doctors, but they may be reported at times by the family. Rages generally result from taking a high dose for a prolonged period; how high a dose and for how long are yet to be defined. In addition, not all people taking high doses develop steroid rages. On the other hand, there are a few reports of rages in those taking quite low doses. 17,23-25 Some common features have been noted in men having these rages. They are generally young, come from apparently caring families, have not previously taken drugs or been in trouble with the police, and do not have a history of being aggressive. They usually feel no remorse at all after the rage, however antisocial their behaviour. 21 It has been suggested that there may be an underlying predisposition to this type of behaviour and that excessive drug use "pushes them over the edge"; however, nearly all the cases described in the literature fit the description above. The first two murder cases in which taking anabolic steroids was used as a defence (called the "dumbbell defence" by Newsweek ) were in the United States in 1988; both men were found guilty of murder. Some 20 murders associated with the use of anabolic steroids have been reported in America, 26 but the usual pleas of innocence due to temporary insanity have never been upheld there. Sydney's two cases are summarised in the Box. Withdrawal symptoms All types of steroid drugs, including corticosteroids, produce withdrawal symptoms. 2 Depression is almost invariably one of the symptoms in anabolic steroid users: they miss the feeling of elation induced by the drugs. Other symptoms relate to loss of the positive psychological effects and include listlessness; apathy; loss of appetite, libido and self-esteem; feelings of anxiety; difficulty in concentrating; and mood swings. Withdrawal can also be associated with violent behaviour and rages. Hence, rages may result from taking either a high steroid dose or stopping taking the drug. Severe symptoms of steroid withdrawal may not be a problem in athletes, possibly because they take anabolic steroids in certain well defined phases and because they reduce the dose gradually. Body builders or weight trainers, however, have greater problems with withdrawal. They lose their new improved body image as their recently enhanced musculature shrinks away, and are likely to be driven back to taking steroids again and to have great trouble stopping them in the future. 27 Drug dependence Another related problem is drug dependence; pharmacological, psychological and genetic factors may all have an effect. This problem was first described in 1988 in a 23-year-old body builder; 28 anabolic steroid dependence was later reviewed, 29 and two other case reports followed. 30,31 Brower et al. produced a series of papers on anabolic steroid dependency and its management. 32-37 They initially published a case in a 24-year-old weight trainer with drug dependence, depression and aggression, 32 and later reported eight steroid-using weight lifters (age range, 23-65 years) who showed evidence of dependence at interview according to criteria of the Diagnostic and statistical manual of mental disorders (DSM-III-R). 33 In a review of 49 male weight lifters, average age 24 years, 28 (57%) were considered to be drug dependent. 37 Mechanisms discussed were either that (i) anabolic steroids may affect endogenous opioid 28 or monoaminergic brain systems, or (ii) that dependence may result from social reinforcement and the pleasure of having a muscular body. However, users were more likely to have expressed dissatisfaction with their body size and so dependence was considered to be driven more by negative reinforcement (trying to avoid feeling small). The presence of more than three DSM-III-R criteria is considered consistent with drug dependence, and Brower et al. found anabolic steroid users may have up to six of these ( Box 2). 37 Other psychiatric changes Several psychiatric disorders have been reported in association with anabolic steroid use since the first case was described in 1980. 38,39 The full list includes schizophrenia, 38 hypomania and mania, 40 delirium, 41 depression, 42 suicide, 10,28,43 and paranoia. 44 In the first reported case of anabolic steroid-related psychiatric disorder, in 1980, a 17-year-old male body builder developed acute schizophrenia when taking methandienone; he recovered on stopping the drug, but relapsed when he took it again. 38 In 1992, Freinhar and Alvarez 40 noted that referring doctors "often" commented on mood changes accompanying anabolic steroid therapy, and described a 27-year-old body builder with hypomania who was taking oxandrolone. He recovered on withdrawal of the drug but had a second attack when taking oxymetholone. A toxic confusional state with choreiform movements occurred in another patient taking 200-300 mg a day of oxymetholone; the condition improved on drug withdrawal. 41 Perry et al. studied 20 weight lifters taking anabolic steroids and 20 controls using a self-administered questionnaire and an interview. 45 The questionnaire showed an increase in psychotic features in the users, including paranoid thoughts, depression, increased hostility and aggression. Pope and Katz in 1987 reported two cases of psychosis in anabolic steroid users, 46 and then, in 1988, 41 cases (39 men) with a wide range of psychiatric problems. 47 This study was widely criticised because it was not a controlled, prospective trial and because of its selection of subjects. In 1994, they rectified this with a controlled study of 88 athletes who used anabolic steroids and 68 controls. 48 The Structured Clinical Interview for DSM-III-R was used for diagnosis; 25% showed evidence of drug dependence and 23% hypomania, mania or depression. Aggression or violence "often" accompanied hypomanic or manic episodes. The authors also suggested that steroid users are most vulnerable to major depressive episodes during the first three months after discontinuing anabolic steroid use. Depression has been mentioned previously in relation to drug withdrawal and dependence. Testosterone was formerly used to treat depression, but it is now known to cause it. 49 Suicide may also be a problem with either anabolic steroid drug dependence or after drug withdrawal (especially with sudden withdrawal). It is not often reported in medical journals, but may be reported in the press. Brower et al. reported a body builder who had suicidal thoughts of crashing his car, and warned of the dangers of anabolic steroids and suicide. 32 A different view of anabolic steroid complications was taken by Dimeft and Malone: 50 in 31 current users, 45 previous users and 88 non-users, they found psychiatric diagnoses to be more common in previous users, suggesting that psychiatric disorder may either predispose a person to, or result from, anabolic steroid use. There is one study which gives a contrary view. Bahrke et al., 51 using two valid psychometric inventories, studied 50 men (12 current steroid users, 14 previous users, and 24 non-users) and concluded that users taking an average daily dose of 45 mg showed minimal psychiatric effects. In conclusion, this brief review highlights some of the psychological problems encountered with anabolic steroid use. It does not appear that these problems are very common, but future research will show how much disability they cause. 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Affective and psychotic symptoms associated with anabolic steroids use. Am J Psychiatry 1988; 145: 487-490. Pope HG, Katz DL. Psychiatric and medical effects of anabolic steroid use. A controlled study of 160 athletes. Arch Gen Psychiatry 1994; 51: 375-382. Alschule MD, Tillotson KJ. The use of testosterone in the treatment of depression. N Engl J Med 1948; 239: 1036-1038. Dimeft R, Malone D. Psychiatric disorders in weight lifters using anabolic steroids. Med Sci Sports Exerc 1991; 23: 18. Bahrke MS, Wright JE, Strauss RH, Catlin DH. Psychological moods and subjectively perceived behavioural and somatic changes accompanying anabolic steroid use. Am J Sports Med 1992; 20: 717-724. Author's details Institute of Sports Medicine, Concord Hospital, Sydney. Brian Corrigan , AM, FRACP, FACRM, Consultant Physician. Reprints: Dr B Corrigan, 1 Lookout Avenue, Dee Why, NSW 2099. - - To top of article - ©MJA1996 < URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Brian Corrigan