Mental health

Ethics Ethical issues in placebo-controlled trials in Alzheimer's disease Robert D Goldney and Brian F Stoffell MJA 2000; 173: 147-148 The use of placebos and the dubiousness of patients' ability to give informed consent give rise to various ethical concerns The use of placebos in clinical drug trials is the most conclusive method of elucidating the effectiveness of new medications. However, it has long been recognised that there are significant ethical issues with such trials, as some patients will be given no specific therapy.1,2Few would argue against the use of placebos in drug trials when there are no effective treatments available. However, there comes a time in the treatment of most illnesses when one or other treatment is recognised as effective. It is then that ethical questions arise in the use of placebos in evaluating other new treatments for the same condition. For example, it is difficult to justify the use of placebos in trialling new medications for treating depression. Gold standards such as tricyclic antidepressants, or the now well-established selective serotonin reuptake inhibitors, are generally used as benchmarks in studies examining the efficacy of new antidepressants. How well established do new treatments have to be before they themselves become the standard against which other new drugs should be investigated rather than subjecting patients to the risk of having no treatment at all? This situation is addressed in Section 12.4 of the recently published National Health and Medical Research Council (NHMRC) Statement on ethical conduct in research involving humans,3 which states: "The use of a placebo alone or the incorporation of a non-treatment control group is ethically unacceptable in a controlled trial where: (a) other available treatment has already been clearly shown to be effective; and (b) there is risk of significant harm in the absence of treatment. If there is genuine uncertainty about the net clinical benefit of a treatment, a placebo controlled trial or a trial with a no-treatment arm may be considered." This is clearly relevant in the emergence of approved treatments for Alzheimer's disease, for which new agents are now available.4 The two drugs available in Australia, tacrine and donepezil, have proven effective in double-blind randomised-controlled trials.5,6 This level of evidence (E2 or Level II)7 was considered sufficient for these drugs to have been approved for marketing by the Commonwealth Therapeutic Goods Administration. That being so, one would assume that at least criterion (a) above has been met. Criterion (b) above could be assumed if one accepts that Alzheimer's disease is a progressive condition. This would be significant if one were proposing a prolonged trial to demonstrate the efficacy of a medication, even if an established drug may only halt the process of decline. This has, for example, become relevant in the initial treatment of schizophrenia. One study showed more severe negative and positive symptoms in schizophrenia associated with a delay in the initiation of treatment, not attributable to poorer premorbid functioning actually delaying the commencement of treatment.8 Another study showed that cortical volume deficits were progressive, but that after treatment they appeared to be static or even partly reversible.9 The analogy between these findings for schizophrenia and the situation with Alzheimer's disease is compelling. The role of plaques containing amyloid beta-peptide (Abeta) in Alzheimer's disease has been elucidated, and there is now evidence of a correlation between elevated levels of Abeta plaques and cognitive decline.10 As the cholinesterase inhibitors tacrine and donepezil influence the formation of Abeta plaques,11 these drugs may be truly disease modifying. Naturally, such findings add to the debate about the wisdom of using placebo controls when a treatment is available. These issues in relation to Alzheimer's disease have been discussed recently in the international literature.12-18 Knopman et al noted that "the design of clinical trials must evolve as new therapies become available", and stated that "there is now a compelling case for alternatives to trials that include a treatment arm with no active therapy".14 In similar vein, Kawas et al concluded that "As new and more effective treatments emerge, the ethical framework for placebo use in AD (Alzheimer's Disease) studies will require frequent re-examination".17 This is of particular relevance to Alzheimer's disease, as the question arises as to whether or not the patients themselves are able to give informed consent. This is also addressed in the NHMRC Statement on ethical conduct in research involving humans,3 under Sections 5.2 and 5.3, which state: "Consent to participation in research by a person with an intellectual or mental impairment must be obtained from: (a) the person with the intellectual or mental impairment whenever the person is of sufficient competence and, where the impairment is temporary or recurrent, at a time when the impairment does not prevent the person giving or refusing consent; or failing that (b) the person's guardian, or an authority or other organisation or person having that responsibility at law. A Human Research Ethics Committee (HREC) must not approve, and consent cannot be given for, research which is contrary to the best interests of the person with the intellectual or mental impairment." The task of ethics committees is particularly onerous in light of these recommendations. The very fact that drugs have been approved by the Therapeutic Goods Administration must again be seen as compelling in terms of there being a treatment available which should be provided for patients in their potential best interests. However, although tacrine and donepezil have been approved for marketing, they are expensive and as yet not subsidised by the Pharmaceutical Benefits Scheme. This raises the question of whether or not it is ethical for those who will not be able to afford to continue with the treatment to be placed in a trial merely in the hope that they may be given the active drug and gain some temporary benefit. It is doubtful whether this is an ethically acceptable argument for allowing participation in such trials, especially as proxies will usually be giving consent, and their legitimate concern for the patient may give this "opportunity for an expensive therapy" too much moral weight. Institutional ethics committees will be increasingly confronted with these challenges in the coming years. It behoves all such committees to carefully consider these points, bearing in mind that there may also be changes in community attitudes about these issues. Robert D Goldney MD, Professor of Psychiatry, University of Adelaide The Adelaide Clinic, Gilberton, SA rgoldneyATmedicine.adelaide.edu.au Brian F Stoffell PhD, Director of Medical Ethics Flinders Medical Centre Flinders University of South Australia, Adelaide SA Reprints: Professor R D Goldney, The Adelaide Clinic, 33 Park Terrace, Gilberton, SA 5081 Haegerstam G, Huitfeldt B, Nilsson BS, et al. Placebo in clinical drug trials -- a multidisciplinary review. Methods Find Exp Clin Pharmacol 1982; 4: 261-278. Klerman GL. Scientific and ethical considerations in the use of placebo controls in clinical trials in psychopharmacology. Psychopharmacol Bull 1986; 22: 25-29. National Health and Medical Research Council. National statement on ethical conduct in research involving humans. Canberra: NHMRC, 1999. Brodaty H, Sachdev P. Drugs for the prevention and treatment of Alzheimer's disease. Med J Aust 1997; 167: 447-452. Knapp MJ, Knopman DS, Solomon PH, et al. A 30-week randomised controlled trial of high-dose tacrine in patients with Alzheimer's disease. JAMA 1994; 271: 985-991. Rogers SL, Farlow MR, Doody RS, et al. A 24-week, double-blind, placebo-controlled trial of donepezil in patients with Alzheimer's disease. Donepezil Study Group. Neurology 1998; 50: 136-145. National Health and Medical Research Council. A guide to the development, implementation and evaluation of clinical practice guidelines. Canberra: NHMRC, 1999. Haas GL, Garratt LS, Sweeney JA. Delay to first antipsychotic medication in schizophrenia: impact on symptomatology and clinical course of illness. Psychiatr Res 1998; 32: 151-159. Keshavan MS, Haas GL, Kahn CE, et al. Superior temporal gyrus and the course of early schizophrenia: progressive, static, or reversible? Psychiatr Res 1998; 32: 161-167. Naslund J, Haroutunian V, Mohs R, et al. Correlation between elevated levels of amyloid beta-peptide in the brain and cognitive decline. JAMA 2000; 283: 1571-1577. Emilien G, Beyreuther K, Masters CL, Maloteaux JM. Prospects for pharmacological intervention in Alzheimer disease. Arch Neurol 2000; 57: 454-459. Mariani L, Ventresca GP. Is the placebo still ethically acceptable and scientifically useful in clinical drug experimentation? Clin Ther 1996; 147: 595-598. Whitehouse PJ. Future prospects for Alzheimer's disease therapy: ethical and policy issues for the international community. Acta Neurol Scand Suppl 1996; 165: 145-149. Knopman D, Kahn J, Miles S. Clinical research designs for emerging treatments for Alzheimer disease: moving beyond placebo-controlled trials. Arch Neurol 1998; 55: 1425-1429. Karlawish JH, Whitehouse PJ. Is the placebo control obsolete in a world after donepezil and vitamin E? Arch Neurol 1998; 55: 1420-1424. Fry ST. Ethical issues in Alzheimer disease research. Alzheimer Dis Assoc Disord 1999; 13 (Suppl 1): S54-S58. Kawas CH, Clark CM, Farlow MR, et al. Clinical trials in Alzheimer disease: debate on the use of placebo controls. Alzheimer Dis Assoc Disord 1999; 13: 124-129. Whitehouse PJ, Arizaga R, Brodaty H, et al. Placebos in clinical trials in Alzheimer disease: an international discussion. Alzheimer Dis Assoc Disord 1999; 13: 121-123. Make a comment

Robert D Goldney · Brian F Stoffell

Clinical Practice An approach to managing depression in general practice Ian B Hickie MJA 2000; 173: 106-110 Long term management of patients with depression: an essential skill for all general practitioners Abstract - Early detection - Diagnostic pragmatism - Risk assessment - Engaging and empowering - Choosing an antidepressant - Beyond drug therapy - Conclusion - Authors' details - - More articles on Allied health Abstract Detection of depression in primary care can be enhanced by use of self-report assessment forms. With the new classes of antidepressants, there is the opportunity to choose specific drug classes for different types of depressive disorders. Depression is frequently a relapsing illness. Treatment goals should include long term reduction of vulnerability factors. An active therapeutic partnership can be facilitated by providing accurate detailed information early in the course of the illness. Behavioural therapies, which focus on modification of the sleep-wake cycle, activity planning and reduction of substance abuse, are essential. Structured problem solving is the most accessible form of cognitive intervention that general practitioners can readily provide. More complex cognitive therapies are usually provided by mental health professionals or general practitioners with extensive training. Although major depression is common in primary care, general practitioners (GPs) may still find it difficult to detect and treat depression unless they have a high index of suspicion and additional mental health training.1-3 A range of patient, doctor and practice organisation factors contribute to this difficulty.1-4 Patient factors include comorbid medical disorders, presentation of somatic rather than psychological symptoms, poor understanding of mental health and fear of stigma. Examples of practitioner factors are inadequate training and reluctance to provide psychological treatments, whereas practice organisation factors include too little time, too little remuneration, too little mental health specialist support, lack of use of screening tools, and lack of access to independent educational materials. However, improvement in the quality of mental health care provided by GPs is now firmly on the national agenda.4High quality mental health care consists not only of informed prescribing, but also of early detection, provision of sound information, use of effective non-pharmacological techniques and reduction in factors which will lead to long term vulnerability to recurrent depression. A range of initiatives are under way nationally to improve mental health practice in primary care. In this article, elements derived from SPHERE: A National Depression Project are described to highlight one coordinated approach to the educational, training and practice support infrastructure needed to make such initiatives sustainable.5 Early detection in primary care GPs are ideally placed to detect depression early in its course. While patients frequently present with other urgent medical problems or unexplained physical symptoms,2,6 primary care contacts are ideal for mental health screening. Although much mental health training focuses on improving interview and assessment skills, simple screening instruments are time-efficient and engage patients actively in the therapeutic process. As with other screening procedures, such tests are not diagnostic. Instead, they highlight those patients who require specific assessment by the practitioner. Patients usually welcome the opportunity to reveal their difficulties in this way. Good examples of such instruments include the 12-item General Health Questionnaire (GHQ),7 the Prime-MD,8 and the 34-item Somatic and Psychological HEalth REport (SPHERE).5 SPHERE can be used to produce an output that compares the severity of the patient's physical and mental symptoms with a national practice sample. Currently, the SPHERE Project promotes a simple screening device (Box 1), which emphasises that depression is a syndrome with major effects on thoughts, feelings, behaviours and bodily function. Diagnostic pragmatism Formal psychiatric classification systems have become extremely complex and lack validity in primary care.3 However, for GPs to make use of the available evidence on treatment efficacy, certain grades of depression need to be recognised. British and European psychiatry has emphasised the importance of identifying "endogenous" or "melancholic" disorders, as they respond preferentially to antidepressant drugs. The depressed phase of bipolar disorder (manic depressive illness) also fits this category. Recent Australian research has re-emphasised this concept,9 highlighting the need to recognise observed (not patient-reported) psychomotor slowing, or agitation, as hallmarks of the disorder. Melancholia is relatively rare in primary care (as distinct from specialist and hospital-based practice). In primary care, non-melancholic depressive disorders (either primary, concurrent with anxiety or secondary to medical illness) are common and disabling.1,2,10,11 Key risk factors include premorbid anxiety, family history of anxiety, depression and substance abuse, medical ill-health, dysfunctional intimate relationships, and social adversity. Increasing sophistication of genetic,12 biochemical and psychosocial research has led to a new conceptualisation of these disorders, with greater emphasis on the interaction between long term (genetic and past experiential) vulnerabilities and current life stressors. That is, depression rarely occurs "out of the blue", and patients who have had major episodes are at high risk of relapse.13 Further, in this model, patients with non-melancholic disorders have their own individual biology (genetically determined arousability or nervousness) that may be treated pharmacologically or non-pharmacologically. Diagnostically, it is important to recognise not only the overt depressive disorder but also whether it is accompanied by a specific anxiety disorder (eg, panic attacks or agoraphobia) that requires additional attention. The recognition of premorbid anxiety, substance abuse and/or significant personality dysfunction completes this diagnostic phase. Risk assessment One of the most important tasks in primary care is the assessment of risk of various forms of self-harm. Prevention of suicide should not be seen as the primary goal; nevertheless, research has highlighted the high risks of self-harm in both younger and older men, with the latter frequently contacting family doctors before making serious suicide attempts.14 Other risk factors, such as social isolation, substance abuse and access to lethal means, need to be noted and appropriate risk-reduction strategies implemented (eg, involvement of family, frequent appointments, emergency contact procedures, reduction of alcohol, removal of lethal means). GPs can underrate the degree of both short- and longer-term risk,15 and may need to engage others (eg, family, other primary care practitioners, or mental health specialists) more actively in collaborative long term risk reduction. A necessary emphasis is the assessment of a range of risk-taking strategies (eg, deliberately driving fast or recklessly) and forms of self-harm other than overt suicide attempts (eg, prolonged substance abuse, neglect of other medical problems). Engaging and empowering the patient The community has little specific knowledge about depression, and patients hold generally negative views about antidepressant drug therapy.16 The key to overcoming these negative stereotypes is the provision of independent and sophisticated information. Most patients wish to make active choices about treatment and, increasingly, to receive alternative opinions, but few practitioners have the materials they need to facilitate such discussions. Furthermore, some are reluctant to provide detailed information that may apparently contradict their therapeutic choices. Provision of accurate information early in the course of illness facilitates active engagement and helps create the framework for long term treatment adherence.17 While these concepts are now routine for disorders such as diabetes and asthma, they are yet to become routine even among mental health specialists who treat severe and/or relapsing depression. Choosing an antidepressant The new classes of antidepressants differ substantially in their benefits and side-effects. Rather than prescribing the same antidepressant (or the same class) to every patient with depression, there is the chance to choose specific classes for different types of depressive disorders. Pharmacological therapy should be accompanied by appropriate means for recording benefits and side-effects and placing drug therapy within an overall treatment framework. One also needs a "road-map" for initiating rational prescribing (Box 2). Currently, there is a general paucity of comparative evidence to influence choices of antidepressant compounds (both within and across classes). Internationally, this has meant a reliance on panels of experts rather than systematic reviews of published studies. In the course of designing the SPHERE Project, we relied strongly on the clinical opinion of experts and a survey of practitioners.18,19 Subsequent studies20,21 and professional group recommendations22 are largely consistent with these views. Consequently, we still recommend some specific starting points for antidepressant therapy. These include: Selective serotonin reuptake inhibitors (SSRIs) are particularly helpful for those with moderately depressed mood, premorbid anxiety and/or panic disorder, agoraphobia and/or obsessive-compulsive disorder.23,24 They are also "first-line" agents for depression in the context of other medical illnesses, adolescents, and older patients.19,22 Generally, these drugs are very similar and good reasons for choosing one over another are limited. When selecting an SSRI, factors to consider are drug interactions (cytochrome P-450 enzyme systems), severity of withdrawal syndromes, and tendency to cause initial agitation. Patients with principal complaints of fatigue and/or sleep disturbance, without severe mood disturbance, may require different strategies. Fatigue without obvious mood disturbance responds poorly to SSRIs,25 and SSRIs may be associated with worsening sleep patterns in the first few weeks of therapy.26 Some of these patients may benefit from the use of other antidepressant classes. Preliminary evidence suggests the usefulness of moclobemide in patients with fatigue,27 and nefazodone in patients with fatigue and sleep disturbance.28 Patients who do not respond to a course of SSRIs may instead respond to serotonin and noradrenaline reuptake inhibitors (SNRIs).20 Whether to use SNRIs as first-line agents in primary care is debatable, but psychiatrists do not generally recommend them in this setting19 because of their side-effects and more complex dosing schedule. They are strongly favoured for use in specialist practice where patients have generally failed one or more courses of the first-line agents or have more severe illnesses. Patients with melancholia, psychotic depression, treatment-resistant depression and/or other very severe mood disorders may do less well with SSRIs and may benefit from commencing therapy with SNRIs20 or tricyclic antidepressants (TCAs).29 Some particular patient groups (eg, those with chronic pain) still respond preferentially to TCAs.19 Beyond drug therapy A great deal of educational effort has been invested (largely by the pharmaceutical industry) in increasing doctor recognition of major depression and provision of safer pharmacological therapy. Unfortunate consequences of this drive may be the perception that these agents are more efficacious than the older agents or that non-pharmacological strategies are no longer relevant.30 Although initial drug therapy can assist patients to get "out of the hole", ongoing maintenance therapy (Box 3) is also critical. Maintenance therapy needs to be thought of in terms of How long should this patient stay on the drug? and What other non-pharmacological strategies are necessary for this patient?. One of the clear (and somewhat unexpected) benefits of the SSRIs is their capacity to reduce ongoing "trait" anxiety in those who have been life-long worriers.23 That is, they appear to modify a personality style that is otherwise at high risk of recurrence of depression. In general, patients should continue effective drug therapy for at least 6 to 12 months after they recover from a major depressive episode. If patients have had several previous depressive episodes, and have responded to drug therapy, then they should consider longer periods (2 to 5 years) of prophylactic antidepressant therapy.22 The effective non-pharmacological therapies are generally lumped together as "cognitive-behavioural" approaches. This describes a range of potential interventions that commence with essential behavioural elements (eg, education, treatment adherence monitoring, sleep-wake cycle and activity planning, modification of substance use; see Box 4)31 and then move to more cognitive approaches (eg, structured problem solving, formal cognitive therapy). While debate continues as to the extent of benefit from these approaches,32 it is generally accepted that they form the basis of most non-pharmacological interventions.22,33 There is an ongoing issue of practitioner competency, as such treatments are not necessarily effective if provided by clinicians with limited training.34 For all patients, keeping a daily diary is an essential part of the behavioural approach. A very good analogy for patients with depression is that of diabetes. Whatever drug therapy may be required, major lifestyle modifications are also needed. The more effective the non-drug therapy, then the greater the chance that the patients will be able to withdraw drug therapy. Many doctors provide lifestyle advice, but fail to encapsulate it within other critical features of the behavioural approach, such as explaining the rationale, self-monitoring, reviewing the effects of modified behaviour, and identifying obstacles to implementation. Behavioural management of anxiety (eg, general stress, panic attacks, avoidant behaviour, social anxiety) needs to be considered in those with high premorbid anxiety or ongoing anxiety phenomena. This may include general stress management (including physical exercise), slow-breathing techniques, progressive muscle relaxation, and staged confrontation of feared situations (exposure therapy). In general, patients with significant anxiety disorders do best when they receive cognitive as well as behavioural approaches. Structured problem solving Many untrained professionals confuse effective psychological interventions (eg, structured problem solving, interpersonal therapy, cognitive therapy) with non-specific support and advice. Although the latter may help reduce the risk of self-harm, they do little to resolve major depression. The most accessible form of psychological intervention for primary care practitioners is structured problem solving.35 This creates a framework for the patient to re-engage with practical approaches to perceived problems and learn new cognitive skills (Box 5). The key factor is not whether the patient's preferred solution is ultimately successful (which tends to be the doctor's main preoccupation), but whether the patient learns a more general approach to coping with ongoing life stressors. By focusing initially on a style of behavioural analysis that describes specific rather than general problems, and then ranks them in terms of likely difficulty, the patient is forced to move from a position of general hopelessness (eg, "There's nothing I can do", "Everything fails in the end") to more specific problems (eg, "I don't have a job"). Identifying specific problems allows the generation of option lists (eg, "Ask family", "Register with Centrelink", "Change industries"). Once a reasonable option list has been generated, the patient then evaluates the potential interventions. That is, the patient is being forced to engage in the style of rational thinking that people without depression take for granted. By contrast, patients with depression tend to think in global terms, generate few solutions, fail to evaluate their actions, and avoid implementation of realistic options. This approach is well suited to general practice as it can be learnt quickly, requires little ongoing supervision, and can be broken down into manageable time frames (eg, three to six sessions of 15 to 30 minutes each). As with other cognitive approaches, it engages the patient as an active partner and formally prohibits practitioners from simply offering their own behavioural analyses and/or preferred solutions. It may also prove to be a useful means for recruiting additional input from other key people (eg, spouse or parent), as they may be encouraged to generate additional options or assist with implementation. As many depressed patients find themselves in dysfunctional intimate relationships,36 this change of focus may also assist to re-engage those who have found interactions with the depressed person non-rewarding or aversive. Cognitive and interpersonal therapies These more formal psychological therapies are suited to patients with repeated episodes of depression, chronic depression, or clear evidence of repeating patterns of self-defeating thoughts, avoidant behaviours, or dysfunctional intimate relationships.33,37 These treatments can be difficult to provide in primary care, as they require considerable therapist training, ongoing supervision and monitoring of clinical skills, and modification of the practice environment (typically 12 to 16 sessions of 45 minutes' duration). However, GPs have indicated a willingness to learn key aspects of these skills and implement them in their practice.38 Widespread provision of these treatments will require more radical training and financing. These may be in the form of more "shared" and better-structured care with secondary mental health specialists systems,39 or through the development of a large group of GPs with these specialised skills. Conclusion Most GPs can now provide reasonable antidepressant therapy for patients they identify as having depression. Improved quality of practice depends on greater identification (particularly in those with concurrent medical illness), better quality of initial psychoeducation and behavioural management, and initiation of psychological strategies designed to improve treatment adherence and reduce long term vulnerability. Acknowledgements: The assistance of Tracey Davenport and Joanne Gander with the preparation of this manuscript was greatly appreciated. Disclosure statement: SPHERE: A National Depression Project was supported in 1998 and 1999 by Bristol-Myers Squibb Pharmaceuticals, manufacturers of Serzone (nefazodone). Evaluation of the SPHERE Project is currently supported by the New South Wales Health and Mental Health Branch of the Commonwealth Department of Health and Aged Care. Australian Divisions of General Practice provide financial support for SPHERE training programs in local districts. A trial of Aurorix (moclobemide) in patients with chronic fatigue was supported by Roche Pharmaceuticals. Pfizer, manufacturers of Zoloft (sertraline), plan to support a SPHERE education module (Depression in the Medically Ill) in 2000. Representatives of the SPHERE Project have provided educational sessions for employees of Wyeth Pharmaceuticals, manufacturers of Efexor (venlafaxine). References Thompson C, Kinmonth AL, Stevens L, et al. Effects of a clinical-practice guideline and practice-based education on detection and outcome of depression in primary care: Hampshire Depression Project randomised controlled trial. Lancet 2000; 355: 185-191. Simon GE, Von Korff M, Piccinelli M, et al. An international study of the relation between somatic symptoms and depression. N Engl J Med 1999; 341: 1329-1335. Hickie I. Primary care psychiatry is not specialist psychiatry in general practice. Med J Aust 1999; 170: 171-173. Primary care psychiatry -- the last frontier. A report of the Joint Consultative Committee. Canberra: Royal Australian College of General Practitioners and Royal Australian and New Zealand College of Psychiatrists, 1997. Hickie I, Hadzi-Pavlovic D, Scott E, et al. SPHERE: A National Depression Project. Australas Psychiatry 1998; 6: 248-250. Simon G, Ormel J, Von Korff M, Barlow W. Health care costs associated with depressive and anxiety disorders in primary care. Am J Psychiatry 1995; 152: 352-357. Goldberg D, Williams P. A user's guide to the General Health Questionnaire. Windsor, Berkshire: NFER-NELSON Publishing Company, 1988. Spitzer RL, Williams JB, Kroenke K, et al. Utility of a new procedure for diagnosing mental disorders in primary care. The PRIME-MD 1000 study. JAMA 1994; 272: 1749-1756. Parker G, Hadzi-Pavlovic D, editors. Melancholia: a disorder of movement and mood. New York: Cambridge University Press, 1996. Ustun TB, Sartorius N, editors. Mental illness in general health care: an international study. Chichester: John Wiley and Sons, 1995. Katon W, Von Korff M, Lin E, et al. Population-based care of depression: effective disease management strategies to decrease prevalence. Gen Hosp Psychiatry 1997; 19: 169-178. Kendler KS, Neale MC, Kessler RC, et al. Major depression and generalised anxiety disorder: same genes, (partly) different environments? Arch Gen Psychiatry 1992; 49: 716-722. Frank E, Kupfer DJ, Perel JM, et al. Three-year outcomes for maintenance therapies in recurrent depression. Arch Gen Psychiatry 1990; 47: 1093-1099. Stoppe G, Sandholzer H, Huppertz C, et al. Family physicians and the risk of suicide in the depressed elderly. J Affect Disord 1999; 54: 193-198. Milton J, Ferguson B, Mills T. Risk assessment and suicide prevention in primary care. Crisis 1999; 20: 171-177. Jorm AF, Korten AE, Jacomb PA, et al. "Mental health literacy": a survey of the public's ability to recognise mental disorders and their beliefs about the effectiveness of treatment. Med J Aust 1997; 166: 182-186. Kemp R, Kirov G, Everitt B, et al. Randomised controlled trial of compliance therapy: 18-month follow-up. Br J Psychiatry 1998; 172: 413-419. Hickie IB, Scott ES, Davenport TA. Enhancing the evidence base for clinical psychiatry: are practice surveys a useful tool? Med J Aust 1999; 171: 315-318. Hickie IB, Scott ES, Davenport TA. Are antidepressants all the same? Surveying the opinions of Australian psychiatrists. Aust N Z J Psychiatry 1999; 33: 642-649. Poirier M-F, Boyer P. Venlafaxine and paroxetine in treatment-resistant depression: double-blind, randomised comparison. Br J Psychiatry 1999; 175: 12-16. Boyd IW. Venlafaxine withdrawal reactions. Med J Aust 1998; 169: 91-92. American Psychiatric Association. Practice guideline for the treatment of patients with major depression. 2nd ed. Washington, DC: APA, 2000. Boerner RJ, Moller HJ. The importance of new antidepressants in the treatment of anxiety/depressive disorders. Pharmacopsychiatry 1999; 32: 119-126. Bakker A, van Dyck R, Spinhoven P, van Balkom AJ. Paroxetine, clomipramine, and cognitive therapy in the treatment of panic disorder. J Clin Psychiatry 1999; 60: 831-838. Vercoulen JHHM, Swanink CMA, Zitman FG, et al. Randomised, double-blind, placebo-controlled study of fluoxetine in chronic fatigue syndrome. Lancet 1996; 347: 858-861. Sharpley AL, Williamson DJ, Attenburrow MEJ, et al. The effect of paroxetine and nefazodone on sleep: a placebo controlled trial. Psychopharmacology 1996; 126: 50-54. Hickie I, Wilson A, Bennett B, et al. A double-blind placebo control trial of moclobemide in patients with chronic fatigue syndrome. J Clin Psychiatry 2000; in press. Hickie I. Nefazodone for patients with chronic fatigue syndrome. Aust N Z J Psychiatry 1999; 33: 278-280. Boyce P, Judd F. The place for the tricyclic antidepressants in the treatment of depression. Aust N Z J Psychiatry 1999; 33: 323-327. Boyce P, Hickie I. A brave new world in managing depression -- or is it? Aust Fam Physician 1994; 23: 627-632. Hickie I, Davenport T. A behavioral approach based on reconstructing the sleep-wake cycle. Cognitive Behav Pract 2000; in press. King R. Evidence-based practice: where is the evidence? The case of cognitive behaviour therapy and depression. Aust Psychol 1998; 33: 83-88. Scott J. Treatment of chronic depression. N Engl J Med 2000; 342: 1518-1520. Roth A, Fonagy P. What works for whom? A critical review of psychotherapy research. New York: Guilford Press, 1996. D'Zurilla TJ. Problem-solving therapy: a social competence approach to clinical intervention. 2nd ed. New York: Springer Publishing Company, 1999. Hickie I, Parker G, Wilhelm K, Tennant C. Perceived interpersonal risk factors of non-endogenous depression. Psychol Med 1991; 21: 399-412. Keller MB, McCullough JP, Klein DN, et al. A comparison of nefazodone, the cognitive behavioral-analysis system of psychotherapy, and their combination for the treatment of chronic depression. N Engl J Med 2000; 342: 1462-1470. Morgan H, Sumich H, Hickie I, et al. A cognitive-behavioural therapy training program for general practitioners to manage depression. Australas Psychiatry 1999; 7: 141-145. Katon W, Robinson P, Von Korff M, et al. A multifaceted intervention to improve treatment of depression in primary care. Arch Gen Psychiatry 1996; 53: 924-932. Authors' details School of Psychiatry, University of New South Wales, Sydney, NSW. Ian B Hickie, MD, FRANZCP, Professor of Community Psychiatry. Reprints: Professor I B Hickie, Academic Department of Psychiatry, 7 Chapel Street, Kogarah, NSW 2217. i.hickieATunsw.edu.au Make a comment 1: SPHERE checklist for depressive disorders. (From Hickie I, Scott E, Morgan H, et al. A brief guide to depression management. Melbourne: Educational Health Solutions, 2000. Used with permission.) Back to text 2: A "road map" for initiating antidepressant therapy. The times between treatment changes are a guide only. Actual washout periods will depend on the dose and duration of treatment and the current severity of depression. *For fluoxetine allow 14 days' washout. SSRI = selective serotonin reuptake inhibitor. 5HT2 antagonist=serotonin 2 receptor antagonist. RIMMA = reversible inhibitor of monoamine oxidase. SNRI = serotonin and noradrenaline reputake inhibitor. TCA = tricyclic antidepressant. ECT = tricyclic antidepressant. ECT = electroconvulsive therapy. (From Hickie I, Scott E, Morgan H, et al. Treating depression and anxiety in general practice: a training manual. Sydney: Educational Health Solutions, 1998. Used with permission.) Back to text 3: The course of depressive disorders. (From Hickie I, Scott E, Morgan H, et al. A brief guide to depression management. Melbourne: Educational Health Solutions, 2000. Used with permission.)Back to text Click in box for larger imageBack to text 5: A practical guide to structured problem solving. (From Hickie I, Scott E, Morgan h, et al. A brief guide to depression management. Melbourne: Educational Health Solutions, 2000. Used with permission.)Back to text

Ian B Hickie

Editorial Evaluating policy and practice: what are the effects of early hospital discharge after childbirth? Large, specific, randomised trials are the only way to answer this question MJA 2000; 172: 524-525 Two years ago the Journal published an article which described early hospital discharge after birth as a major risk factor for postnatal depression.1 There was also a strongly worded editorial supporting that conclusion.2 In this issue the message is reversed, with the finding by Thompson and colleagues that there is no evidence of increased risk.3 This is no trivial disagreement. A quarter of a million women give birth in Australia each year, virtually all of them spending less time in hospital than their mothers did, with close to 40% having an "early discharge" by the definition used in both articles (within 72 hours of birth).4Depression is a distressing and disabling condition for those directly affected, and particularly so in women with a new baby, who have just taken on a 24-hour-a-day, seven-day-a-week job. The effects of maternal depression may flow on to other vulnerable family members. Doctors and midwives, hospitals, policymakers and the general public need to know whether early discharge is safe or not. One problem in answering this question is the paucity of evidence from randomised trials on length of hospital stay after childbirth. Not only are there relatively few trials, but those that have been published have rarely measured maternal health outcomes such as depression, breastfeeding duration, confidence, or breastfeeding problems. The limited evidence from trials shows either no difference in depression between women discharged early and late, or a lower proportion of women becoming depressed after early discharge.5,6 The article by Thompson and colleagues3 is the third Australian population-based study which has shown no relationship between early discharge and depression after birth.7-10 All three of these studies were large enough to detect a twofold increase in the odds of becoming depressed after early discharge, as was found in the Nepean hospital-based study published in the Journal two years ago.1 All three, and the Nepean study, used the Edinburgh Postnatal Depression Scale (EPDS) with the same cut point of a score of more than 12 for probable depression, though the Victorian studies measured the point prevalence with a single score of more than 12 at six or eight months after birth, the ACT group measured the period prevalence from eight through 16 and 24 weeks, and the Nepean group required two or more scores over 12, from six, through 12, 18 and 24 weeks, confirmed by a structured clinical interview to measure the period prevalence of major depression. The difference in findings between the Nepean study and the other three studies is surprising. Thompson and colleagues suggest that an important contributing factor might be the routine provision of a postnatal visit from a midwife and more practical help at home in the ACT than at Nepean.3 However, this was not the case in the 1993/94 Victorian Survey of Recent Mothers, which found that only 66% of women who went home within 48 hours of birth, and only 27% of those going home on the third or fourth day, had a home visit from a midwife8 -- findings much closer to those of the Nepean study. It is also unlikely that temporal factors explain the discrepancy in findings, as the Victorian survey took place at a very similar time to the Nepean study. Public knowledge and expectations about postnatal stay would have been similar in both study populations. In interpreting non-experimental descriptive and observational studies, the key problem is selection bias -- in what ways do women who leave hospital early differ from those who stay longer, and are these differences in themselves factors which have a bearing on women's chances of becoming depressed in the following months? Predictable factors associated with shorter postnatal stays include maternal age less than 25 years, multiparity, unassisted birth, birth at term, low medical risk, birth centre care, and not having private health insurance. Psychological predictors of depression were measured in both the ACT and Nepean studies; they were not significantly associated with length of stay. The six vignettes in the Box describe some groups of women who will be over-represented (A, C, D, E) and under-represented (B, F) among new mothers going home early, despite having uncomplicated vaginal births at term. Young women are often over-represented in group D8 and women from diverse overseas backgrounds in group E.11 As all these women "chose" their length of stay, these vignettes draw attention to problems with the notion of "choice" as a key determinant. Some choices are constrained by factors outside the woman's control, especially social isolation and absence of a partner or other social support, which are common associations of depression at this life stage. We also know that women are not necessarily free to choose their length of stay, as almost a quarter of those discharged early in both the ACT study,3 and in Victoria,8,9 thought their stay had been too short. The vignettes also remind us that the relative proportions of women from groups A, C and E in study populations could easily contribute to, or even explain, the differing associations between length of stay and subsequent depression reported from different studies. Given the inevitability of such selection biases, which are impossible to adjust for, if we really want to know whether shortening postnatal stay is safe and cost-effective, or whether domiciliary midwifery or other postnatal support improves outcomes for mothers and babies, there is no alternative but to test these policies in randomised trials. Judith M Lumley Director Centre for the Study of Mothers' and Children's Health La Trobe University, Melbourne, VIC Hickey AR, Boyce PM, Ellwood D, Morris-Yates AD. Early discharge and risk of postnatal depression. Med J Aust 1997; 167: 244-247. Buist A. Counting the costs of early discharge after childbirth. Med J Aust 1997; 167: 236-237. Thompson JF, Roberts CL, Currie MJ, Ellwood DA. Early discharge and postnatal depression: a prospective cohort study. Med J Aust 2000; 172: 532-536. Day P, Sullivan EA, Ford J, Lancaster P. Australia's Mothers and Babies 1997. (Perinatal Statistical Series No. 9). Sydney: AIHW National Perinatal Statistics Unit, 1997. (AIHW Cat. No. PER 12.) Waldenström U. Early and late discharge after hospital birth: fatigue and emotional reactions in the postpartum period. J Psychosom Obstet Gynaecol 1988; 8: 127-135. Carty EM, Bradley CF. A randomized, controlled evaluation of early postpartum hospital discharge. Birth 1990; 17: 199-204. Small R, Lumley J, Brown S. To stay or not to stay: are fears about shorter lengths of stay justified? Midwifery 1992; 8: 170-177. Brown S, Lumley J, Small R. Reasons to stay, reasons to go. Victorian women talk about early discharge. Melbourne: Centre for the Study of Mothers' and Children's Health, 1995: 27-54. Brown S, Lumley J. Reasons to stay, reasons to go: results of an Australian population-based survey. Birth 1997; 24: 148-158. Brown S, Lumley J, Small R. Early obstetric discharge: does it make a difference to health outcomes? Paediatr Perinat Epidemiol 1998; 12: 49-71. Yelland J, Small R, Lumley J, et al. Support, sensitivity, satisfaction: Filipino, Turkish and Vietnamese women's experiences of postnatal hospital stay. Midwifery 1998; 14: 144-154. Make a comment Examples of scenarios in which women select different lengths of stay Group Description Length of stay Maternal health outcomes A Healthy mother, healthy baby, good or excellent family support Chooses to go home at 24-48 hours to be with her family in a restful atmosphere and establish breastfeeding Likely to be good B Healthy mother, healthy baby, good or excellent family support Chooses to stay in hospital for 5 or more days to establish breastfeeding, recover from the birth and have a good rest Likely to be good C Mother with major responsibilities at home and little or no family support Goes home as soon as she can ? D Mother who dislikes life in hospital Leaves as soon as she can, even despite strong advice to stay ? E Mother who does not find the hospital able to provide her with enough support and is unable to get enough rest there Leaves much earlier than she had planned to Possibly poor F Mother who has had a long, exhausting labour; baby who is difficult to feed; slow establishment of breastfeeding; mother loses self-confidence Stays much longer than she had planned to Possibly poor Back to text

Judith M Lumley

Research Early discharge and postnatal depression: a prospective cohort study Jane F Thompson, Christine L Roberts, Marian J Currie and David A Ellwood MJA 2000; 172: 532-536 For editorial comment see Lumley Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' Details - - More articles on Psychiatry Abstract Objectives: To determine whether women discharged from hospital ≤ 72 hours after childbirth (early discharge) were at greater risk of developing symptoms of postnatal depression during the following six months than those discharged later (late discharge), their reasons for early discharge and their level of postnatal support. Design and setting: Population-based, prospective cohort study with questionnaires at Day 4, and at 8, 16 and 24 weeks postpartum, conducted at all birth sites in the Australian Capital Territory (ACT). Participants: Women resident in the ACT giving birth to a live baby from March to October 1997. Main outcome measure: A score > 12 on the Edinburgh Postnatal Depression Scale (EPDS). Results: 1295 (70%) women consented to participate; 1193 (92%) were retained in the study to 24 weeks and, of these, 1182 returned all four questionnaires. Of the 1266 women for whom length-of-stay data were available, 467 (37%) were discharged early and 799 (63%) were discharged late. There were no significant differences between the proportion of women discharged early who ever scored > 12 on the EPDS during the six postpartum months and those discharged late (17% v. 20%), even after controlling for other risk factors (adjusted OR, 0.67; 95% CI, 0.44-1.01). Of women discharged early, 93% had at least one postnatal visit at home from a midwife and 81% were "very satisfied" with the care provided. Most women (96%) reported they had someone to help in practical ways. Conclusions: Women discharged early after childbirth do not have an increased risk of developing symptoms of postnatal depression during the following six months. In Australia, and internationally, the length of time spent in hospital following childbirth has been steadily decreasing since the early 1980s. This has prompted concern about the consequences of early discharge for both mothers and babies.1,2 Postnatal depression (PND) is a common disorder with long-term consequences for both mother and infant.3,4 It has been associated with psychosocial and obstetric factors3,5-7 and possibly dissatisfaction with length of stay.8,9 The association with early discharge is not clear. A small randomised controlled trial of early discharge from Sweden10 reported no difference in depression, while in a similar Canadian study women discharged early were less likely to be depressed.11 In observational studies, women discharged early have been reported to be either equally8,9,12,13 or less likely14,15 to be depressed. A recent Australian study reported an increased risk of PND in women discharged early.16 However, this study made no detailed assessment of support available to women, a factor that may be critical to emotional wellbeing of new mothers.17Here, we aimed to investigate whether early discharge following childbirth was associated with an increased risk of PND, why women elect early discharge, and to examine the social support available to women after discharge from hospital. Methods Participants This population-based, prospective cohort study included women resident in the ACT, planning to reside there for at least six months, aged ≥ 16 years, who gave birth to a live baby between March and October 1997 in any of the ACT's two public hospitals (one included a birth centre), two private hospitals, or at home. Women were excluded if their baby was admitted to the neonatal intensive care unit or adopted, if critically ill themselves, unable to give informed consent or complete the questionnaires for other reasons, or participating in another study. Participants were compared with all women who gave birth in the ACT during 1997 using data from the ACT Maternal and Perinatal Data Collection.18 Procedure The study was approved by the ACT Department of Health & Community Care Research Ethics Committee, and the ethics committees of participating hospitals. Postnatal ward or domiciliary midwives gave information sheets to women in the first few days after giving birth. Participants gave written informed consent when completing the first questionnaire as close to Day 4 as possible. They were then mailed questionnaires at eight, 16, and 24 weeks postpartum. Questionnaires The first questionnaire covered sociodemographic characteristics of mother and partner, a nine-item personality scale identifying "vulnerable" and "resilient" personality dimensions;16 a maternity "blues" questionnaire;19 a subset of four items from the Medical Outcomes Study Social Support Scale;20 questions about availability of and satisfaction with practical support, emotional support from partner, and a single summary question assessing global satisfaction with partner scored on a five-point Likert scale. Three questions asked about the nature of women's past relationship with their parents in relation to warmth/care, overprotection/controlling and independent decision making, with responses on a four-point scale. Questions were also included about the mother's history of depression (at any time as well as during or after a pregnancy) and whether the infant was breastfed. In the second questionnaire, women were asked to indicate whether any of a list of 30 possible reasons for their actual length of stay applied to them and whether they thought their length of stay was too long, about right or too short. The third questionnaire included questions about the number of and satisfaction with domiciliary visits. Satisfaction was measured by quality of care, accessibility and convenience,21 and a single summary question assessing overall satisfaction with care. Postnatal depression Postnatal depression was assessed at eight, 16 and 24 weeks using the 10-item Edinburgh Postnatal Depression Scale (EPDS), a self-report measure of depression developed for use in the postpartum period.22-24 Women scoring above 12 are likely to be suffering from a depressive illness. Length of stay For comparability with previous Australian research,16 and in keeping with ACT definitions, early discharge was defined as discharge up to 72 hours after giving birth, and late discharge as more than 72 hours after giving birth. Power of study A sample size of 944 is sufficient to detect with 95% confidence and 80% power an increase in prevalence of PND in the early discharge group at eight, 16 or 24 weeks from 7% to 14%,16 assuming 30% are discharged early and an overall attrition rate of 25%. To allow for variations in these assumptions, we set a target sample size of 1200 women. Statistical analyses The prevalences of EPDS scores greater than 12 were compared between women discharged early and late by means of contingency tables and unconditional logistic regression. We used logistic regression to assess the effect of previously identified risk factors on the association between early discharge and high EPDS scores. Six separate models were fitted for women ever scoring > 12 during the six postpartum months; for those who scored > 12 at eight weeks, 16 weeks or 24 weeks; and for women who scored > 12 on either two occasions or all three occasions. Results are expressed as crude and adjusted odds ratios (OR) with 95% confidence intervals. Results Study population Of 1961 ACT residents asked to participate in the study, 105 were ineligible and 1295 (70%) of the remainder agreed to participate. After 24 weeks, 1193 (92%) remained in the study. Of the 1295 who agreed to participate, 869 (67%) gave birth in a public hospital, 411 (32%) in a private hospital, and 15 (1%) at home, of whom six were transferred to hospital. Compared with all women who gave birth in 1997, participants were slightly older, more likely to be married or in a defacto relationship, to have given birth in a private hospital, and to have been discharged late (Box 1). The 102 (8%) who were lost to follow-up differed from those who remained in that they were significantly (P ≤ 0.001) more likely to be aged < 25 years (32% v. 12%), unmarried (14% v. 4%), born in a non-English-speaking country (19% v. 9%), and public patients (74% v. 56%). They were not significantly more likely to be in the early discharge group (46% v. 36%), but were significantly (P ≤ 0.001) less likely to be in paid employment in the previous 12 months (56% v. 74%), to have a paid position to resume after maternity leave (43% v. 63%) and to have been educated beyond Year 11 (60% v. 82%). They did not differ with respect to the following factors known to be associated with PND: vulnerable personality, level of social support, past history of depression, dissatisfaction with relationship with partner, or dissatisfaction with past relationship with mother. Length of stay After excluding the nine women who gave birth at home and were not transferred to hospital, and the 20 with missing data, there were length-of-stay data for 1266 (98%) women, 467 (37%) with early and 799 (63%) with late discharge. The early discharge group was significantly (P ≤ 0.001) more likely to be aged < 25 years (21% v. 10%), public patients (80% v. 44%) or to have delivered in a public hospital (94% v. 52%), multiparous (61% v. 54%), and to have given birth at > 39 weeks' gestation (85% v. 75%). Women discharged early were also significantly (P ≤ 0.001) more likely to have had a spontaneous onset of labour (74% v. 55%), an unassisted vaginal birth (90% v. 56%) and to formula-feed their infant from birth (10% v. 5%). They were significantly (P ≤ 0.001) less likely to have been in paid employment in the past 12 months (68% v. 76%), to have a paid position to resume (55% v. 66%) and to have been educated beyond Year 11 (74% v. 84%). They were significantly (P ≤ 0.001) less likely to rate their length of stay as "about right" than women discharged late (72% v. 82%), and more likely to rate their length of stay as "too short" (23% v. 8%). There were no statistically significant differences in vulnerable personality (17% v. 16%), level of social support (median score, 7 for both groups), past history of depression (29% v. 29%), maternity blues score (median score, 4 v. 5), dissatisfaction with partner (8% v. 6%), and past relationship with mother (not warm/caring, 6% v. 5%; overprotective/controlling, 52% v. 52%; did not encourage independent decision-making, 20% v. 21%). Postnatal depression Of the 1252 (97%) women with complete data at eight weeks postpartum, 129 (10%) scored > 12 on the EPDS. At 16 weeks, 91 of 1219 (8%) and at 24 weeks 90 of 1187 (8%) scored > 12. The cumulative incidence of an EPDS score > 12 over the six months of follow-up was 224/1295 (17%). Among women with complete data, 37/1172 (3%) had EPDS scores > 12 on two occasions and 23/1172 (2%) on all three occasions. Length of stay and postnatal depression Women discharged early were not more likely to ever score > 12 on the EPDS during the six months of follow-up than women discharged late: 72/429 (17%) compared with 150/751 (20%). The association between length of postnatal stay and PND symptoms remained statistically non-significant after adjusting for other risk factors (Box 2). This finding was robust for other outcome measures (Box 3). For all outcomes there was a consistent trend towards a reduced risk of PND symptoms for women discharged early. Reasons for choosing early discharge Reasons were given by 447 women (96%). The most common reason was a preference to be at home with their partner or family (74%). Other reasons were feeling confident with their baby and preferring to be at home (73%); so the father could be more involved in baby care (47%); being unhappy in hospital and unable to sleep or rest (41%); greater privacy (41%); to rest or recover after the birth (40%); not liking hospitals (34%); to establish breastfeeding (33%); and to have time to focus on the baby (32%). Of the women discharged early, 15% said they did not feel they had a choice about length of stay, and 14% felt under pressure from midwives to leave early. Women discharged early who felt they had no choice about length of stay were not significantly more likely to ever score > 12 on the EPDS (17% v. 17%), and neither were those who felt pressured to leave early (21% v. 16%; P = 0.4). Early discharge and postnatal support All women discharged within three days were eligible for home visits from midwives. Data were available on the number and nature of these visits for 432 women discharged early (93%). Of these, 404 (94%) had at least one visit, and 176 (41%) were visited up to Day 7. The maximum number of visits in the first seven days was 12, and 107 women (27%) were visited at least once after seven days. Eighty-eight per cent of the women thought the number of visits was "just right", while 8% thought it "not enough" and 4% "too many". Overall, 81% of these women said they were "very satisfied" with the care provided at home, 15% "satisfied in some ways but not in others" and 4% "very dissatisfied". Some women discharged after 72 hours were also eligible for and received home visits. The participating public hospitals' policy was for home visiting to be available up to Day 3, but sometimes this extended beyond 72 hours depending on the time of birth. Home visits were also available in cases of special need, and community-based maternal and child health nurses and midwives also offer some home visiting. Of the women discharged late, 364 (47%) received at least one visit at home from a midwife. In addition to support provided by health professionals, 96% of women discharged early reported that they had someone to help in practical ways in the first eight weeks postpartum. For 92% this was a partner, and for 47% their mother. Other family members (22%), friends (20%) and mothers-in-law (19%) were the next most common sources of help. The help received was satisfactory for 90% of the respondents; however, 23% said that they would like to know more people who could be asked for help. There were no statistically significant differences between women discharged early or late in availability of and satisfaction with practical help. Discussion The postnatal stay has become shorter without being properly evaluated in randomised controlled trials (RCTs). As shorter stays have become standard practice, the window of opportunity for conducting an appropriate RCT may have been lost.25 The best alternatives are prospective studies with heterogeneous samples of sufficient size to detect clinically significant effects of short postnatal stays. We found that women resident in the ACT electing short postnatal stays were not at increased risk for developing symptoms of PND. Our finding is consistent with those from two Victorian surveys,8,13 but differs from that of a study in Sydney which found a significantly increased risk of PND during the first six months in mothers discharged within three days.16 There are several possible explanations for the discrepant results between this study and our own, including differences in the outcome measures, population characteristics, postnatal support and reasons for early discharge. The same assessment tool to identify possible cases was used in the Victorian,8,13 Sydney16 and ACT studies, but in the Sydney study a psychiatric interview was added to confirm the diagnosis of PND. The use of a psychiatric examination is unlikely to explain differences in the results, as high scores on the EPDS coincide closely with diagnoses of PND. A validation study in Australian women found the EPDS to be highly sensitive (100%) and specific (96%), with a positive predictive value of 70%.22 Differences in the characteristics of women discharged early may also contribute to the different outcomes observed. In both the Sydney and the ACT studies, women discharged early were more likely to be multiparous, to have a lower level of education and to formula feed their infants in the first week than women discharged late. However, the women discharged early in the Sydney study16 were more likely than those in our study to report a poor relationship with parents and to have a history of depression; these associations were controlled for in the statistical analyses in the Sydney study and so cannot fully explain their different findings. Low levels of social support have been identified as a risk factor for PND,5 and another possible explanation for the differences in findings is that the two populations differed in the extent, nature of and satisfaction with postnatal support provided to women through early discharge programs and non-professional contacts. The authors of the Sydney study reported that only half of the women who elected early discharge participated in an early discharge program with domiciliary midwifery care.26 In our study, 94% of the women discharged early had had at least one visit from a midwife at home and the level of satisfaction with this care was high. Also, only 4% of women discharged early said they had no one to provide practical support at home. An overwhelming majority reported that their partners assisted them and most were satisfied with the level of help. Early discharge was introduced partly to offer more choices in care in a climate of increasing consumer participation in decisions. However, economic imperatives to increase patient throughput may lead to increasing pressure on women to leave hospital earlier than they would otherwise choose. The Sydney study26 did not report reasons for early discharge. Reasons given by women for leaving ACT hospitals early were generally positive, although 15% felt they did not have a choice and 14% felt pressured to leave (not mutually exclusive reasons). Several things should be considered when interpreting the results of our study. Firstly, as the Sydney study found double the rate of PND after early discharge,16 we formed our null hypothesis (that early discharge makes no difference) in the expectation that it would be disproved. Instead, we found no evidence of a significant difference in the rate of PND; in fact, early discharge tended to a protective effect (but this was not statistically significant). Our study does not prove that there is not an increased rate of PND for early discharge. However, in this population, it is unlikely that the true risk for early discharge was double that for late discharge. Secondly, although only 70% of women approached participated in the study, the characteristics of women who did participate were similar in important respects to those of the source population. However, our findings may not be generalisable to populations with differing PND risk factors or early discharge programs. Lastly, the women in our study selected their length of postnatal stay. Although we have controlled for known determinants, confounding by unknown determinants for PND cannot be excluded. We found that women who selected early discharge from hospital after childbirth and received midwifery support at home, and who were well supported by other family members, were not more likely to experience depressive symptoms in the first six months after childbirth. Very few women in this study were discharged early without home support, so it was not possible to determine whether early discharge without support was associated with an increased risk of PND symptoms. It may be important to ensure that all women discharged early after childbirth, in particular those lacking other sources of support, receive additional help from the healthcare system. What constitutes adequate postnatal support could be examined by RCTs comparing different patterns of home visiting. Acknowledgements This work was supported by a project grant from The Canberra Hospital Private Practice Fund. Additional funding was provided by The Canberra Hospital Auxiliary, the Nurses' Board of the ACT, and the ACT Department of Health & Community Care. The assistance of the midwives in recruiting women for this study is gratefully acknowledged. Robyn Attewell provided statistical advice. We are especially grateful to the women of the ACT who so generously gave their time to complete this study. References Buist AE. Counting the costs of early discharge after childbirth [editorial]. Med J Aust 1997; 167: 236-237. Braveman P, Egerter S, Pearl M, et al. Problems associated with early discharge of newborn infants. Early discharge of newborns and mothers: a critical review of the literature [review]. Pediatrics 1995; 96: 716-726. Boyce PM, Stubbs JM. The importance of postnatal depression. Med J Aust 1994; 161: 471-472. Murray L, Cooper P. Effects of postnatal depression on infant development. Arch Dis Childhood 1997; 77: 99-101. O'Hara MW, Swain AM. Rates and risk 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. Warner R, Appleby L, Whitton A, Faragher B. Demographic and obstetric risk factors for postnatal psychiatric morbidity. Br J Psychiatry 1996; 168: 607-611. 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. Dowswell T, Piercy J, Hirst J, et al. Short postnatal hospital stay: implications for women and service providers. J Public Health Med 1997; 19: 132-136. Waldenström U. Early and late discharge after hospital birth: fatigue and emotional reactions in the postpartum period. J Psychosomatic Obstet Gynaecol 1988; 8: 127-135. Carty EM, Bradley CF. A randomized, controlled evaluation of early postpartum hospital discharge. Birth 1990; 17: 199-204. Beck CT, Reynolds MA, Rutowski P. Maternity blues and postpartum depression. J Obstet Gynecol Neonatal Nurs 1992; 21: 287-293. Brown S, Lumley J, Small R. Early obstetric discharge: does it make a difference to health outcomes? Paediatr Perinat Epidemiol 1998; 12: 49-71. Burnell J, McCarthy M, Chamberlain GVP, et al. Patient preference and postnatal hospital stay. J Obstet Gynaecol 1982; 3: 43-47. James ML, Hudson CN, Gebski VJ, et al. An evaluation of planned early postnatal transfer home with nursing support. Med J Aust 1987; 147: 434-438. Hickey AR, Boyce PM, Ellwood D, Morris-Yates AD. Early discharge and risk for postnatal depression. Med J Aust 1997; 167: 244-247. Barclay KM, Chamberlain ME, Homer CS, Barclay LM. Early discharge and risk for postnatal depression [letter]. Med J Aust 1998; 168: 419-420. Bourne M. Maternal and perinatal status, ACT, 1997 tables. Canberra: Clinical Epidemiology and Health Outcomes Centre, ACT Department of Health & Community Care, 1999. Kennerley H, Gath D. Maternity blues. 1. Detection and measurement by questionnaire. Br J Psychiatry 1989; 155: 356-362. Sherbourne CD, Stewart AL. The MOS social support survey. Soc Sci Med 1991; 32: 705-714. Kenney P, Cameron S, King M, et al. Evaluation of obstetric early discharge: client satisfaction. Centre for Health Economics Research & Evaluation. Discussion Paper Series No 10. 1992. Boyce P, Stubbs J, Todd A. The Edinburgh postnatal depression scale: validation for an Australian sample. Aust N Z J Psychiatry 1993; 27: 472-476. 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. Murray L, Carothers AD. The validation of the Edinburgh Postnatal Depression Scale on a community sample. Br J Psychiatry 1990; 157: 288-290. Thompson JF, Roberts CL, Ellwood DA. Early discharge after childbirth: Too late for a randomised trial? Birth 1999; 26: 192-195. Hickey AR, Boyce PM, Morris-Yates AD, Ellwood DA. Early discharge and risk for postnatal depression [letter]. Med J Aust 1998; 168: 420. (Received 7 Oct 1999, accepted 3 Apr 2000) Authors' Details The Canberra Hospital, Garran, ACT. Jane F Thompson, MSc, PhD, Senior Research Officer, Women's & Children's Health. Marian J Currie, BapplSc, GDPH, Midwife, Maternity and Gynaecology Outpatients and Fetal Medicine Unit. David A Ellwood, FRANZCOG, Dphil, Professor of Obstetrics and Gynaecology, The Canberra Clinical School. New South Wales Centre for Perinatal Health Services Research, Departments of Obstetrics and Gynaecology and Public Health and Community Medicine, School of Population Health Services Research, University of Sydney, NSW. Christine L Roberts, MB BS, MHP, Senior Lecturer. Reprints: Dr J F Thompson, Women's and Childrens Health, The Canberra Hospital, PO Box 11, Woden, ACT 2606. jane.thompsonATact.gov.au ©MJA 2000

Jane F Thompson · Christine L Roberts · Marian J Currie · David A Ellwood

Letter Rethinking the early childcare agenda MJA 1999; 171: 166-167 To the Editor: We are concerned that Cook's article1 lacks a balanced review of the literature on childcare, being biased in its portrayal of the possible negative effects without consideration of the likely positive ones. This could have detrimental consequences for the many children in formal childcare in Australia, their parents, and the staff and others involved in what is now an integral and vital component of Australian society. Cook's article also draws strongly on overseas studies, although childcare systems in Australia are likely to be different from those in other countries. Positive health outcomes for children attending childcare include the detection of vision and hearing problems, higher vaccination rates, appropriate nutrition, the detection of child abuse and neglect, primary health and dental care, psychosocial benefits, and opportunities for health promotion.2 The issue of socioemotional development, including attachment theory, has been debated in the literature. Cook cites Belsky, but Belsky has been noted as often citing research that did not take into account the specific characteristics and quality of care.3 It is probable that social and cognitive development are related to quality of care, and Caldwell's study suggests that childcare may provide better quality of care, at least for cognitive development, than home care.4 Thus, childcare does not appear to be consistently detrimental to cognitive and language development and may have a positive influence.4 The investigation of the influence of childcare on children's development is complex and should be considered in interpreting such research. Harvey,5 in an extensive longitudinal study, found that parental employment had "minimal effects on children's later functioning", and that increased early parental income could positively affect childhood development. We do agree with Cook that increased flexibility for working parents should be encouraged. Flexible options, such as parental leave and part-time work for parents of young children, are often advantageous. In addition to increasing work options for parents, it is important that we strive for high quality childcare, subsidised if necessary, so that all families have the choice of providing such care for their children. Linda M Slack-Smith Senior Lecturer, School of Oral Health Sciences 179 Wellington Street, Perth, WA 6000 lindasATcyllene.uwa.edu.au Anne W Read Senior Research Officer, Division of Psychosocial Research TVW Telethon Institute for Child Health Research, Perth Stephen R Zubrick Associate Professor, and Head, Division of Psychosocial Research TVW Telethon Institute for Child Health Research, Perth Cook P. Rethinking the early childcare agenda. Med J Aust 1999; 170: 29-31. Andersson B. Children's development related to day-care, type of family and other home factors. Eur Child Adolesc Psychiatry 1996; 5: 73-75. Melhuish E, Moss P. Current and future issues in policy and research. In: Melhuish E, Moss P, editors. Day care for young children. London: Tavistock/Routledge, 1991: 225. Caldwell B. Impact of day care on the child. Pediatrics 1993; 91(1 Pt 2): 225-228. Harvey E. Short-term and long-term effects of early parental employment on children of the National Longitudinal Survey of Youth. Dev Psychol 1999; 35: 445-459. In reply: A literature review was beyond my purpose, but I summarised findings of a major meta-analysis, and explained why psychological outcomes are of most concern. Benefits of childcare are often publicised, but risks, proven or probable, should not be concealed from parents and policy-makers.1 Notwithstanding the 1971 New South Wales child psychiatrists' memorandum,2 it became politically incorrect to express concerns about childcare. In social sciences, the now-discredited ideology of cultural determinism prevailed, denying the relevance of evolutionary biology to human behaviour, even mothering. A pro-childcare "spin" has pervaded research reports. Slack-Smith and colleagues' statement that "childcare does not appear to be consistently detrimental to cognitive and language development . . ." is a typical childcare-advocacy "straw man". The reply is: nobody said it was! Ochiltree's review3 seemed to me to have eight such statements within five paragraphs, and was so "unbalanced" that I wrote a book,1 to which I refer readers. It covers the points made by Slack-Smith et al, which cannot be answered in a few words. Childcare advocates seldom acknowledge that "high quality childcare" is not reliably achievable. They quote overseas studies when favourable, but, when not, they claim Australian childcare is of higher quality.3 But one carer to five infants is "nobody's definition of quality".4 I argue that the early childcare agenda is misconceived and needs rethinking. Qualitatively better outcomes should be achievable without the associated risks.1,5,6 Peter S Cook Child Psychiatrist (retired) PO Box 84, Repton, NSW 2454 Cook PS. Early child care -- infants and nations at risk. Melbourne: News Weekly Books, 1997. New South Wales Branch of the Child Psychiatry Section of the Australian and New Zealand College of Psychiatrists. Memorandum on some aspects of the welfare of children aged under three years whose mothers are in full-time employment. Med J Aust 1971; 1: 446-448. Ochiltree G. Effects of child care on young children: forty years of research. Melbourne: Australian Institute of Family Studies, 1994: 65-66. (Early Childhood Study Paper No. 5.) Hope D. Spare the non-maternal care and nurture the child. The Australian 1998; June 4. Cook PS. Home truths absent in early childcare debate: we need parent-friendly options [opinion]. The Australian 1999; March 24. Cook PS. The role of myth in childcare policy [letter]. The Australian 1999; April 14. ª 1999 Medical Journal of Australia.

Editorial Schizophrenia today Improvements in treatment need to be built upon and applied more widely and effectively MJA 2000; 172: 470-471 Schizophrenia Awareness Week (21-27 May) has been running in Australia since 1981. During the past 19 years some of the original goals of the week have been achieved largely thanks to the efforts of the State-based Schizophrenia Fellowships and the mental health advocacy and education organisation SANE Australia. These goals have included getting the word "schizophrenia" into the public domain, educating the community about the treatability of the disorder, and encouraging groups of carers to work together to provide mutual support and to lobby governments for enhanced services for people suffering from psychotic disorders. Today, treatment is much more likely to occur in the community, allowing patients to retain a much-valued independence (although loneliness and ennui often develop in the absence of appropriate social supports). Today, medication options are also wider, with clozapine having been used by nearly 10 000 Australians with treatment-resistant disorders (Clozaril Patient Monitoring System, Mental Health Research Institute, Melbourne, unpublished data), and other dopamine and serotonin antagonist drugs, such as risperidone and olanzapine, finding an important role because of their fewer extrapyramidal side effects and, probably, better neurocognitive outcomes.1,2 Our understanding of the biology of schizophrenia has progressed, despite the absence of a signature pathophysiology. This understanding has evolved in light of growing evidence that the disorder is associated with disturbances of neural connectivity and neurodevelopment, and abnormalities in dopaminergic, serotonergic, GABAergic and glutamatergic neurotransmission, involving particular brain regions, including the hippocampus, ventral striatum, and prefrontal cortex.3,4 Nonetheless, schizophrenia remains one of the most stigmatised of all disorders. That the term often conjures up sentiments of derision rather than compassion is well illustrated by a recent description of the Federal Government's actions towards certain UN committees as ". . . at times, sycophantic, abusive, schizophrenic and downright childish".5 The extensive and enduring impact of schizophrenia and related psychiatric disorders on the lives of affected Australians has been brought into sharp focus by a recent Commonwealth Government-sponsored National Survey of 980 individuals with psychotic disorders, more than 60% of whom had schizophrenia.6 It found that the average duration of symptoms was 15 years; 47% of participants were judged to be seriously impaired, 58% were socially withdrawn and 72% did not have a regular job. In addition, the prevalence of tobacco use (males 73%, females 56%), alcohol misuse or dependence (30%), and dependence on or misuse of street drugs (cannabis 25%; others, including heroin, 13%) was considerably higher than in the general population. However, a significant minority of patients -- approximately 25% -- have only one or two episodes of illness, do not continue to need mental health services, and have lower levels of symptoms, impairment and disability. Other data indicate that the rate of suicide among people with schizophrenia is approximately 10 times higher than that in the general population.7 One troubling response to data such as these has been a call -- based on a prediction that Australian mental health budgets are likely to remain relatively fixed -- for reduced emphasis on the treatment of psychotic disorders because of their chronicity and perceived intractability, and for transfer of resources to disorders such as anxiety and depression, which are associated with better responses to treatment.8 An alternative, and in our view far preferable, response is to concentrate on strategies which use what data we have to press for greater overall funding for mental health. There is a strong case for this, as mental illnesses account for 13% of Australia's health burden, third in importance after heart disease and cancer.9 Further, there are several sources of optimism that such strategies will be successful and that new funding is obtainable. For example, prior to 1993, mental health was almost exclusively the preserve of the States and Territories, with the Commonwealth contributing only to Medicare and pharmaceutical benefits. However, since the First National Mental Health Plan, in 1993, the Commonwealth Government has become a significant contributor to public sector psychiatric programs, allocating more than $595 million to them over the years 1993-2003. Also, the States and Territories increased their funding by more than 14% in real terms between the 1992/93 and 1996/97 financial years.10 Another cause for optimism is that, even with high-disability disorders like schizophrenia, there are many measures that meaningfully improve the quality of life of affected individuals, but which need to be better applied. These include early intervention,11 community-based rehabilitation programs, family psychoeducational programs, a greater but targeted use of the newer antipsychotic drugs,12 and good access to residential disability support services and public housing. General practitioners, especially those able to work in conjunction with specialist mental health teams, are in a position to play key roles in ensuring that their patients are offered such treatments and services. This is because people with psychotic disorders often attend GPs (eg, more than 80% had attended their GP in the 12 months before being interviewed in the National Survey,6 with a median of five attendances during that time). The Consultation Liaison in Primary Care Practice (CLIPP) Program13 is one of a number of successful models of collaboration between GPs and mental health services that provide substantial benefit to patients. Future improvements in the management of schizophrenia will require better communication and coordination between patients and carers, medical practitioners, mental health services, and non-government agencies. It will also require the development of new services, the refinement and strengthening of existing ones, especially in the psychosocial domain, the discovery of prognostic markers, and the introduction of novel pharmacotherapies. Fundamental and applied research will be essential to the successful achievement of many of these outcomes. David L Copolov Director, Mental Health Research Institute of Victoria, and Professor, Department of Psychiatry, University of Melbourne, and Professor, Department of Psychological Medicine, Monash University Bruce S Singh Cato Professor, and Head, Department of Psychiatry, University of Melbourne and Clinical Director, North West Mental Health Program Green MF, Marshall BD Jnr, Wirshing WC, et al. Does risperidone improve verbal working memory in treatment-resistant schizophrenia? Am J Psych 1997; 154: 799-804. Purdon SE, Jones BD, Stip E, et al. Neuropsychological change in early phase schizophrenia during 12 months of treatment with olanzapine, risperidone, or haloperidol. The Canadian Collaborative Group for research in schizophrenia. Arch Gen Psychiatry 2000; 57: 249-258. Harrison PJ. The neuropathology of schizophrenia. A critical review of the data and their interpretation. Brain 1999; 122: 593-624. Copolov DL, Velakoulis D, McGorry PD, et al. Neurobiological findings in early phase schizophrenia. Brain Res Brain Res Rev 2000; 31: 157-165. Lewis P. A McEnroe of a nation, but without the charm [letter]. The Melbourne Age 2000 3 April: 14. Jablensky A, McGrath J, Herrman H, et al. People living with psychotic illness: an Australian study 1997-98, an overview. Canberra: Mental Health Branch, Commonwealth Department of Health and Aged Care, October 1999. Harris EC, Barraclough B. Suicide as an outcome for mental disorders: a meta-analysis. Br J Psychiatry 1997; 170: 205-228. Andrews G. Efficacy, effectiveness and efficiency in mental health service delivery. A N Z J Psychiatry 1999; 33: 316-322. Mathers C, Vos T, Stevenson C. The burden of disease and injury in Australia. Canberra: Australian Institute of Health and Welfare, November 1999. National mental health report 1997: 5th annual report: changes in Australia's mental health services under the National Mental Health Strategy 1996/97. Canberra: Department of Health and Family Services, 1998. McGorry PD, Krstev H, Harrigan S. Early detection and treatment delay: implications for outcome in early psychosis. Curr Opin Psychiatry 2000; 13: 37-43. Lehman AF, Steinwachs DM and the Co-investigators of the PORT Project. At issue: translating research into practice: the schizophrenia patient outcomes research team (PORT) treatment recommendations. Schizophr Bull 1998; 24: 1-10. Meadows G. Establishing a collaborative service model for primary mental health care. Med J Aust 1998; 168: 162-165. Make a comment

David L Copolov · Bruce S Singh

Introduction Concern about cannabis use is not new: ordinances were passed in 8th-century Egypt prohibiting use of hemp drugs, transgressors being subject to tooth extraction!1 In the 19th century, controversy over widespread cannabis use led to the Indian Hemp Drugs Commission, a large-scale investigation into the health effects (both physical and mental) of cannabis use. The Commission's wide-ranging report found that the relationship between cannabis and "mental injury" was complex, and criticised many witnesses for their obvious bias.2 Social, moral and political agendas continue to influence both cannabis research and the "cannabis debate".3 Are there grounds for concern? Cannabis is now widely used by young people in Australia, mostly intermittently. However, 7% of 17-year-old girls and 11% of boys the same age use it at least weekly.4 Furthermore, the concentration of the primary psychoactive component of cannabis, δ-9-tetrahydrocannabinol, may have increased in recent years due to hydroponic cultivation and cross-breeding,5 although the evidence for this is patchy.3 The implications for the mental health of users are unclear; the more pressing issue may be the as yet unquantified impact of a declining age of initiation into cannabis use.6There are several potential psychological harms of cannabis use (Box). The link between cannabis and psychosis remains the most intriguing. Specifically, cannabis has been noted to cause psychotic-like symptoms during intoxication, to lead to a "cannabis psychosis", to increase the relative risk of schizophrenia, and to affect the clinical course of established schizophrenia.11 Population studies, such as the Epidemiologic Catchment Area study in the United States, confirm an association between cannabis use and psychotic symptoms. In this study, daily marijuana use over a year was associated with a 2.4-times greater risk of psychotic experiences, while any use was associated with a 1.3-times greater risk for self-reported psychotic experiences when compared with non-users. The relative risk for daily users remained significant after adjustment for other substance abuse and baseline psychiatric diagnoses.12 Is there a specific "cannabis psychosis?" The case for a specific acute "cannabis psychosis" is based largely on case reports and case series that link a history of cannabis use with a psychotic presentation. Two types of presentation are described: a "toxic psychosis", in which psychotic symptoms are associated with confusion. This generally occurs after ingestion of large amounts of cannabis in someone with no significant psychiatric history, and recovery is usually rapid with abstinence;13 and a functional psychosis occurring without confusion (exacerbation of schizophrenia, and schizophreniform psychoses). The case for a true functional psychosis caused by cannabis is more vexed than the case for a "toxic psychosis", with various authors describing a heterogeneous clinical picture, often with manic features.14 The better-designed studies suggest that it is, in fact, hard to delineate a specific functional cannabis psychosis. McGuire and colleagues examined all patients presenting with psychotic symptoms at two London hospitals, comparing those with positive and negative results on urinary cannabinoid screening.15 Using structured interviews, they found a similar spread of diagnoses and illness onset among case and control patients, with similar numbers of first admissions and symptom profiles. Cannabis and schizophrenia Does cannabis cause schizophrenia? Perhaps the more worrying question is whether cannabis causes chronic psychosis, particularly schizophrenia. The work of Andreasson and others examined this question in a cohort of male Swedish conscripts, followed up through a national psychiatric case register.16 They found that having used cannabis between one and 10 times at conscription increased the relative risk of schizophrenia to 1.3, the risk rising to 6.0 for those who had used cannabis on 50 or more occasions. However, this relative risk was reduced after adjustment for factors which independently contributed to the risk of schizophrenia. While this study provides some of the strongest evidence for a link between cannabis and psychosis, methodological concerns have been raised. These include the temporal gap between self-reported cannabis use at conscription and later schizophrenia, the potential confounding role of other substance use (particularly as amphetamines were a major drug of abuse during the study period), the adequacy of psychological assessment at conscription, and the reliability of self-reported drug use at conscription.3 Nevertheless, the association between cannabis use and schizophrenia is strengthened by studies which demonstrate that cannabis is widely used among people with schizophrenia. A recent study in Newcastle examined substance use in all outpatients with schizophrenia, finding 29.9% of subjects had some use of cannabis in their lifetime, with 7.7% and 28.3% of subjects having lifetime diagnoses of cannabis abuse and dependence, respectively.17Notably, alcohol was more commonly used than cannabis, while amphetamines were the third most commonly used substance. A number of hypotheses have been proposed to explain the prevalence of cannabis use in schizophrenia. Apart from the causation/precipitation role, it has been suggested that cannabis is used as self-medication for psychotic or dysphoric symptoms, or to ameliorate the side effects of antipsychotic drugs. Alternatively, the relationship may reflect the common peaks of onset of schizophrenia and cannabis use (particularly as prevalence samples are seldom compared with age- or sex-matched general population controls), or the role of underlying factors such as demographic differences. How might cannabis use affect established schizophrenia? Clinical intuition suggests that cannabis has an adverse effect on the clinical course, a view supported by some well-designed studies. Linszen and colleagues studied 93 subjects with schizophrenia prospectively over a year, finding a higher rate of relapse in the cannabis-users than in the non-users, with a differential risk of relapse according to level of cannabis use.18 This effect persisted after adjustment for age, sex, age at first hospital admission, and alcohol use. However, this study was limited by the failure to consider the role of polysubstance use, reliance on self-report alone, and the gross measure of compliance used. Data from the Epidemiologic Catchment Area study also support a relationship between an alcohol- or cannabis-use disorder and a higher risk for hospitalisation in those with schizophrenia over a year.19 However, in this study, substance use covaried with depressive rather than psychotic symptoms, suggesting a complex relationship between substance use and symptoms in schizophrenia. Confounding issues: The relationship between cannabis and psychosis is thus far from straightforward. Cannabis is rarely the only substance used. Other factors, such as personality, may confound the relationship. One study found higher rates of schizotypy in volunteer cannabis users, raising the possibility that the relationship between cannabis and psychosis is mediated by a premorbid "psychosis prone" personality.20 Mueser and colleagues have identified antisocial personality as a common factor underlying both schizophrenia and substance-use disorders.21 Methodological concerns, such as the failure to assess and control for use of other substances and reliance on the case-study method, make it difficult to draw firm conclusions in this area. A possible neurophysiological link Recent findings in neuroscience have lent credence to a link between cannabis and psychosis. An endogenous cannabinoid system has been identified, with one type of cannabinoid receptor (CB1) found in the hippocampus, associated cortical areas, cerebellum and basal ganglia.22 In rat brain, cannabinoid receptors have been shown to collocate with dopamine D1 receptors,23 and cannabis administration increases the activity of tyrosine hydroxylase (an enzyme linked to dopamine metabolism).24 These findings hint at the mechanism through which cannabis could lead to psychosis, by modulation of dopaminergic transmission. The discovery of cannabinoid receptors has also led to the discovery of endogenous cannabinoids, among them anandamide (from the Sanskrit word for "bliss"). Such discoveries have encouraged some researchers to speak of a "cannabinoid hypothesis" of schizophrenia, likening the cognitive deficits of schizophrenia to those induced temporarily by δ-9-tetrahydrocannabinol. Indeed, a recent study found higher levels of two endogenous cannabinoids in cerebrospinal fluid in 10 patients with schizophrenia compared with 11 non-psychotic control patients.25 The authors suggested this may represent the response of the cannabinoid system to dopamine imbalance, or may reflect an underlying pathogenic "hypercannabinergic" state. This intriguing result can be viewed as preliminary only, because of the small number of subjects and the paucity of information about possible confounding factors, particularly substance use. The role of cannabinoids is being investigated in other neurological conditions, including Huntington's chorea and Tourette's syndrome. Such theories, while appealing, remain purely speculative. A hundred years have passed since the Indian Hemp Drugs Commission. The research that has followed confirms an association between cannabis and psychosis, but the nature of the connection remains elusive. We clearly see a need for further carefully controlled, prospective clinical studies, as well as insights from neuroscience, to clarify whether the relationship is causal or, in fact, due to factors common to both cannabis and psychosis. However, in the meantime, we believe it is important to inform young people with psychosis of the possible impact of ongoing cannabis use on their symptoms, particularly on the risk of relapse. References Dhunjibhoy JE. A brief resume of the types of insanity commonly met with in India, with a full description of Indian "hemp insanity" peculiar to the country. J Ment Sci 1930; 76: 254-264. Mikuriya TH. Physical, mental and moral effects: The Indian Hemp Drugs Commission Report. Int J Addict 1968; 3: 253-270. Hall W, Solowij N, Lemon J. The health and psychological consequences of cannabis use. National Drug Strategy Monograph Series No. 25. Canberra: AGPS, 1994. Donnelly N, Hall W. Patterns of cannabis use in Australia. National Drug Strategy Monograph Series No. 27. Canberra: AGPS, 1994. Adams IB, Martin BR. Cannabis: pharmacology and toxicology in animals and humans. Addiction 1996; 91: 1585-1614. Greenfield SF, O'Leary G. Sex differences in marijuana use in the United States. Harv Rev Psychiatry 1999; 6: 297-303. Fergusson DM, Horwood LJ. Early onset cannabis use and psychosocial adjustment in young adults. Addiction 1997; 92: 279-296. Yamaguchi K, Kandel DB. Patterns of drug use from adolescence to adulthood. II. Sequences of progression. Am J Public Health 1984; 74: 668-672. Solowij N. Cannabis and cognitive functioning. Cambridge: Cambridge University Press, 1998. Thornicroft G. Cannabis and psychosis. Is there epidemiological evidence for an association? Br J Psychiatry 1990; 157: 25-33. Hall W. Cannabis use and psychosis. Drug Alcohol Rev 1998; 17: 433-444. Tien AY, Anthony JC. Epidemiological analysis of alcohol and drug use as risk factors for psychotic experiences. J Nerv Ment Dis 1990; 178: 473-480. Bernhardson G, Gunne L-M. Forty-six cases of psychosis in cannabis abusers. Int J Addict 1972; 7: 9-16. Thacore VR, Shukla SRP. Cannabis psychosis and paranoid schizophrenia. Arch Gen Psychiatry 1976; 33: 383-386. McGuire P, Jones R, Harvey I, et al. Cannabis and acute psychosis. Schizophr Res 1994; 13: 161-168. Andreasson S, Allebeck P, Engstrom A, Rydberg U. Cannabis and schizophrenia. Lancet 1987; 2: 1483-1486. Fowler IL, Carr VJ, Carter NT, Lewin TJ. Patterns of current and lifetime substance use in schizophrenia. Schizophr Bull 1998; 24: 443-455. Linszen DH, Dingemans PM, Lenior ME. Cannabis abuse and the course of recent onset schizophrenic disorders. Arch Gen Psychiatry 1994; 51: 273-279. Cuffel BJ, Chase P. Remission and relapse of substance use disorders in schizophrenia. Results from a one-year prospective study. J Nerv Ment Dis 1994; 182: 342-348. Williams JH, Wellman NA, Rawlins JNP. Cannabis use correlates with schizotypy in healthy people. Addiction 1996; 91: 869-877. Mueser KT, Rosenberg SD, Drake RE, et al. Conduct disorder, antisocial personality disorder and substance use disorders in schizophrenia and major affective disorders. J Stud Alcohol 1999; 60: 278-284. Herkenham M, Lynn AB, Little MD, et al. Cannabinoid receptor localization in brain. Proc Natl Acad Sci U S A 1990; 87: 1932-1936. Herkenham M. Cannabinoid receptor localization in brain: relationship to motor and reward systems. Ann N Y Acad Sci 1992; 654: 19-32. Hernandez ML, Garcia-Gil L, Berrendro F, et al. Æ-9-tetrahydrocannabinol increases activity of tyrosine hydroxylase in cultured fetal mesencephalic neurons. J Mol Neurosci 1997; 8: 83-91. Leweke FM, Giuffrida A, Wurster U, et al. Elevated endogenous cannabinoids in schizophrenia. Neuroreport 1999; 10: 1665-1669. Authors' details Manly Hospital, Sydney, NSW. Diana R McKay, FRANZCP, Psychiatrist. University of Sydney Academic Psychiatry, Royal North Shore Hospital, Sydney, NSW. Christopher C Tennant, MD, FRANZCP, Professor of Psychiatry. Potential psychological harms of cannabis use Cannabis has been associated with: early school leaving (the strength of the association lessening after adjusting for cannabis users' poor school performance before cannabis use);7possible progression to other illicit drug use;8an "amotivation" syndrome (now felt to represent chronic intoxication in heavy long-term users); dependence;3subtle impairments in information processing;9 and psychosis.10

Diana R McKay · Christopher C Tennant

Editorial The health of young Australians Mental disorders account for the major burden of disease in young people MJA 2000; 172: 150-151 Community views on youth health tend to be polarised and contradictory. On the one hand, adolescents are seen as having few overt health needs: mortality is low by comparison to that in older groups, and most young people, and their parents, rate their health as good. On the other hand, the emergence in recent decades of youth suicide, drug abuse and new infectious diseases (eg, HIV) has elicited strong and sometimes conflicting opinions about moral and social threats to young people's health. Individualism, a growth in permissiveness, and a decline in religious affiliations have all attracted debate. The recent report Australia's young people: their health and well-being 1999,1 from the Australian Institute of Health and Welfare (AIHW), provides some clarity. It follows an earlier report on child health2 and gives the first comprehensive national picture of the health of young Australians (see Box for key points). In general, Australian youth remain healthy, and retain a positive view of their health. Some health trends are positive: overall mortality in young people in the 1990s was at historically low levels (mostly due to the substantial reductions in motor vehicle deaths in the previous two decades); and rates of teenage pregnancy were low compared with those of other First World countries. However, new threats to youth health have emerged: Mental and behavioural disorders are increasingly recognised as affecting youth disproportionately and account for over half their disease burden. With the changing profile of infectious disease, newer bloodborne and sexually transmitted diseases have become prominent, with threefold higher notifications of both chlamydia and hepatitis C. The prevalence of syphilis has declined further, but gonorrhoea notifications have doubled. Shifts in young people's lifestyle carry implications for health later in life. Tobacco use remains obstinately high, with 40% of young adults continuing to smoke. Physical activity declines across the teens, so that fewer than a third of women aged 20-24 years take part in regular, moderate to vigorous physical exercise. Moreover, 22% of 15-24 year olds already have a body mass index in the overweight or obese range for adults. Some groups have disproportionately high levels of health problems. Low socioeconomic status is linked to higher death and hospitalisation rates, as well as to lower self-rating of health. Recent death rates for young Aboriginal and Torres Strait Islanders are close to three times higher in males and twice as high in females compared with rates for non-Indigenous youth. High levels of mental disorders and substance abuse are major contributors at one level, but the fundamental causes are more likely to be found in social and economic conditions, the loss of cultural identity and the disaffection of youth in many of these communities. The report's findings will inevitably prompt questions about current health provision for young Australians. At present, young people's primary care attendances, for example, are mostly for relatively minor respiratory conditions, musculoskeletal problems or acne. The conditions contributing to the disease burden in young people are less common reasons for general practice presentations, suggesting scope for the development of "youth-friendly" primary-care services capable of responding to youth health problems. With training in adolescent health care, general practitioners can both learn and retain the skills for responding to youth health needs,3 and such training could be linked to health education for young people about access, availability and use of health services. Health promotion has an even greater role. Health problems cluster not only in particular groups but also in individuals. For example, the young regular tobacco user is more likely to engage in heavy alcohol consumption and illicit drug use, have poorer mental health and an overall less healthy lifestyle.4 The clustering can mostly be traced back to common determinants of health in family, community, school and developmental backgrounds. Recent North American research has emphasised the protective influence of family and school attachment on problems ranging from deliberate self-harm and emotional distress to tobacco and illicit substance use, violence and early sexual activity.5 Such findings have been mirrored in recent Australian research.6,7 More importantly, preventive intervention targeting these social risk and protective factors is feasible and can be effective.8,9 Family and school-based interventions, both in adolescence and during childhood, have been shown to reduce adolescent problems as diverse as antisocial behaviour, substance abuse and sexually risky behaviour.9 Similarly, strategies based on community mobilisation, peer support, mentoring and legislative enforcement show promise in specific areas. Many gaps in our knowledge remain. Mental health problems loom large, but available data provide an incomplete picture of current need, changes over time and effectiveness of current health provision. Health profiles of groups with the greatest needs -- the young, the homeless and the disabled -- are incomplete, as are those of Aboriginal and Torres Strait Islanders. Much remains to be learned about health interventions and their effectiveness. Most importantly, data on the psychosocial processes that underpin youth health are not available. Health promotion should be guided not only by knowledge of the health problems of young people, but also by an understanding of relevant risk and protective factors. For mental health problems, these are likely to include parental care, the experience of psychosocial adversity, trauma and violence, victimisation, school failure and underemployment. This understanding is of value, not only in selecting the focus of health promotion, but in helping to ensure its continued relevance and sustainability. A recent report from the World Health Organization noted that most investment has gone into innovation rather than continuing programs, with only one in five youth health programs extending beyond five years.10 Sustainable preventive health programs for youth necessarily depend on effective cooperation with government sectors such as education, justice and employment, as well as non-governmental organisations involved with youth, younger children and their families. As the most comprehensive available account of the health of young Australians, the AIHW report will do much to inform the intersectoral dialogue that must underpin the setting of priorities and, in turn, the development of a rational advocacy. However, implementing effective responses to these priorities will require further work to build a more complete picture of the psychosocial determinants of the major health problems of young people. George C Patton Professor of Adolescent Health, Department of Paediatrics University of Melbourne Centre for Adolescent Health, Melbourne, VIC pattonATcryptic.rch.unimelb.edu.au Lynelle J Moon Senior Analyst, Population Health Unit Australian Institute of Health and Welfare, Canberra, ACT Reprints: Professor G C Patton, Department of Paediatrics, University of Melbourne, Centre for Adolescent Health, 2 Gatehouse Street, Parkville, VIC 3052. Moon L, Meyer P, Grau J. Australia's young people: their health and well-being. PHE19. Canberra: Australian Institute of Health and Welfare, 1999. Moon L, Rahman N, Bhatia K. Australia's children: their health and well-being. PHE7. Canberra: Australian Institute of Health and Welfare, 1998. Sanci LA, Coffey C, Veit FCM, et al. Evaluation of an educational intervention for general practitioners in adolescent health care: randomised controlled study. BMJ 2000; 320: 224-230. Hibbert M, Caust J, Patton G, et al. The health of young people in Victoria. Melbourne: Centre for Adolescent Health, 1996. Resnick MD, Bearman PS, Blum RW, et al. Protecting adolescents from harm: findings from the National Longitudinal Study on Adolescent Health. JAMA 1997; 278: 823-832. Glover S, Burns JBH, Patton GC. The Gatehouse Project: the scope of school based intervention for the prevention of adolescent depression. Family Matters 1998; 49: 11-16. Silburn SR, Zubrick SR, Garton AF, et al. Western Australian Child Health Survey: Family and Community Health. Perth: Australian Bureau of Statistics, 1996. (Catalogue No. 4304.5) National Crime Strategy (Homel R, editor). Pathways to prevention. Canberra: Attorney General's Department, 1999. Toumbourou JW, Patton GC, Sawyer S, et al. Guidelines to inform planning and purchasing of evidence-based practice: interventions for promoting health in the adolescent population. Melbourne: Department of Human Services, 1999. WHO/UNFPA/UNICEF Study Group. Programming for adolescent health and development. Geneva: World Health Organization, 1999. Make a comment Key points from the report Australia's young people: their health and well-being 19991 Young Australians remain in good health... Two-thirds of young people rated their own health as "excellent" or "very good" and getting better. Overall death rates for 12-24 year olds declined by 29% over the period 1979-1992 to 60/100000 (partly due to a 60% decline in motor vehicle accident deaths, 1979-1997), and have remained stable since then. but there are areas of concern... The major burden of disease (combined effect of mortality and disability) for this age group is from mental disorders. Injury is the leading cause of death for 12-24 year olds (40/100000 per year in 1997), with two-thirds of all deaths attributed to some form of injury, including accidents and suicide. Suicide (15.1/100000 per year) and drug-related deaths (4.2/100000 per year) have not followed the declines in most other causes of death, particularly for young men. In 1998, 25% of young people aged 14-19 years and 40% of those aged 20-24 years were regular or occasional smokers. While 54% of 15-24 year olds in 1995 were of acceptable weight, 22% were overweight or obese. The proportions of young people reporting exercising at a "vigorous" or "moderate" level for sport or recreation declined with age. and some groups are worse off. Recent death rates (1995-1997) for Aboriginal and Torres Strait Islander youth were 2.8 times higher for males (278/100000 per year) and 2.0 times higher for females (70/100000 per year) than those of their non-Indigenous counterparts (males, 101/100000 per year; females, 35/100000 per year). The 20% of males in the lowest socioeconomic group were 1.7 times more likely to die and 1.4 times more likely to be hospitalised than males in the highest group; for females, these ratios were 1.4 and 1.2, respectively. Twenty per cent of unemployed youth in 1995 assessed their health status as being fair or poor, compared with 9% of employed youth and 8% of students. Back to text

George C Patton · Lynelle J Moon

Editorial Mood disturbances and coronary heart disease: progress in the past decade Psychological factors are increasingly being identified as important contributors to the onset and course of coronary heart disease MJA 2000; 172: 151-152 Psychological conditions, such as life event stress, mood disturbance and personality disorders, are believed to be important risk factors for coronary heart disease (CHD).1-3 Building on the work of the past decade, growing evidence is emerging that mood disturbances can contribute substantially to CHD. This work has studied the effect of a range of emotional conditions, including hostility and anger, but we will focus here on anxiety and depressed mood. Anxiety Studies of patients with pre-existing CHD show that anxiety, independently of conventional risk factors, can be predictive of recurrent acute CHD events.4 Moreover, prospective studies of anxiety in normal populations show that there is an association between anxiety assessed at enlistment and subsequent CHD mortality over many years, even when conventional risk factors are controlled for -- the relative risks are significant, being of the order of 5-6 for sudden death and 2-3 for fatal acute myocardial infarction (AMI).5 Impressive data also come from prospective studies of panic disorder, which show that CHD mortality risk may be doubled in people with the disorder.6,7 There has been strong supportive psychophysiological evidence -- for example, in patients with pre-existing CHD undergoing ventriculography and exposed to trivial experimental stressful tasks, a significant but transient reduction (of up to 50%) in coronary muscle perfusion can occur.2,8 At the other end of the evidence hierarchy are the clinical case reports of patients with panic disorder, found to be free of CHD at angiography, who have had an acute AMI or ongoing angina following panic attacks.9 It has furthermore been shown that patients with panic disorder, while lacking any demonstrable peripheral elevation in serum catecholamine levels, nonetheless have significant release of adrenaline from the coronary sinus during panic attacks.10 This may in turn adversely affect coronary perfusion, cardiac rhythm, shear forces on atheromatous plaques, and platelet function.11 States of severe emotional arousal can also affect underlying pathophysiological risk factors for CHD, including platelet function and haemostasis.12,13 Longer-term effects of anxiety on cardiovascular pathophysiology are also possible; it has been shown that subjects with an exaggerated blood pressure response to mental stress may experience more rapid progression of carotid atherosclerosis.14 Depressed mood Depressed mood is emerging as an important risk factor for CHD. Depressed mood in CHD patients is associated with increased mortality.15 The increased risk is not trivial (relative risk > 3), being of the same order as other risk factors such as prior AMI and impaired left ventricular function after infarction. Even in long-term studies of normal CHD-free populations, depression at enlistment doubles the risk of subsequent acute coronary events16 and increases mortality risk.17 States resembling depression, such as "vital exhaustion" (characterised by fatigue, irritability and demoralisation),18 have been shown to be associated with acute myocardial events in normal populations even when conventional risk factors are controlled. Unlike the more acute effects of anxiety, the effects of depression are not immediate. Indeed, in one prospective study, mortality rates in women with depression did not begin to increase until after 16 months of follow-up.19 Thus, depression may well have a prolonged mode of action on CHD risk. One study found that one component of depression (ie, hopelessness) was associated with more rapid progression of atherosclerosis.20 The CHD risk of a person with chronic depression or dysphoric mood, either as an induced state or an enduring trait of "depressive" personality, needs further study. Personality Recently the "type D ('distressed') personality" has been described by Denollet et al as a result of finding significant differences in CHD outcome in those with certain personality traits. The type D personality is identified by two components: the continual experience of negative emotions, including depression, and the inhibition of social expression of these emotions. In a sample of patients undergoing cardiac rehabilitation, deaths from cardiac causes were increased fourfold in those with type D personality even after controlling for conventional risk factors.21 This suggests that type D personality (whether as a biological construct of temperament or a constellation of habitual behaviours) is a risk factor at least equivalent in importance to the other, "conventional" coronary heart disease prognostic factors. Implications It is possible that the association between mood and CHD risk is not causal, but that the two are linked by some common underlying genetic factor, perhaps associated with vascular disease in general. Weighted against this interpretation are the experimental findings showing the effect of emotions on cardiovascular pathophysiology. To explore the possibility of covariance, prospective aetiological and interventional studies are necessary to examine both mood state (which is episodic) and the personality-based predisposition (trait) to depression. Intervention studies are now in progress to assess whether antidepressants may reduce CHD events in those with depression following AMI.22 In the meantime, in patients with pre-existing CHD or those at increased risk of CHD, the identification and treatment of mood disorders, including anxiety and depression, is important for improving quality of life and for reducing the risk of CHD events and mortality. Christopher C Tennant Professor, Department of Academic Psychiatry Loyola McLean Lilly Psychiatry Research Training Fellow Department of Academic Psychiatry Royal North Shore Hospital, St Leonards, NSW tennantATmed.usyd.edu.au Hemingway H, Marmot M. Evidence-based cardiology: psychosocial factors in the aetiology and prognosis of coronary heart disease. Systematic review of prospective cohort studies. BMJ 1999; 318: 1460-1467. Rozanski A, Blumenthal JA, Kaplan J. Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation 1999; 99: 2192-2217. Tennant CC, Palmer KJ, Langeluddecke PM, et al. Life event stress and myocardial reinfarction: a prospective study. Eur Heart J 1994; 15: 472-478. Moser DK, Dracup K. Is anxiety early after myocardial infarction associated with subsequent ischemic and arrhythmic events? Psychosom Med 1996; 58: 395-401. Kawachi I, Gollditz G, 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, House JD. Mortality among outpatients with anxiety disorder. Am J Psychiatry 1986; 143: 508-510. Weissman MM, Markowitz JS, Ouellette R, et al. Panic disorder and cardiovascular/cerebrovascular problems: results from a community survey. Am J Psychiatry 1990; 147: 1504-1508. Tennant C. Experimental stress and cardiac function. J Psychosom Res 1996; 40(6): 569-583. Mansour VM, Wilkinson DJ, Jennings GL, et al. Panic disorder: coronary spasm as a basis for cardiac risk? Med J Aust 1998; 168: 390-392. Wilkinson DJ, 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; 55: 511-520. Deedwania PC. Hemodynamic changes as triggers of cardiovascular events. Cardiol Clin 1996; 14: 229-238. Grignani G, Pacchiarini L, Zucchella M, et al. Effect of mental stress on platelet function in normal subjects and in patients with coronary artery disease. Haemostasis 1992; 22: 138-146. Malkoff SB, Muldoon MF, Zeigler ZR, Manuck SB. Blood platelet responsivity to acute mental stress. Psychosom Med 1993; 55: 477-482. Kamarck TW, Everson SA, Kaplan GA, et al. Exaggerated blood pressure responses during mental stress are associated with enhanced carotid atherosclerosis in middle-aged Finnish men: findings from the Kuopio Ischaemic Heart Disease Study. Circulation 1997; 96: 3842-3848. Frasure-Smith N, Lesperance F, Talajic M. Depression and 18-month prognosis after myocardial infarction. Circulation 1995; 91: 999-1005. Ford DE, Mead LA, Chang PP, et al. Depression is a risk factor for coronary artery diease in men: the precursors study. Arch Intern Med 1998; 158: 1422-1426. Simonsick EM, Wallace RB, Blazer DG, Berkman LF. Depressive symptomatology and hypertension-associated morbidity and mortality in older adults. Psychosom Med 1995; 57: 427-435. Appels A, Otten F. Exhaustion as precursor of cardiac death. Br J Clin Psychol 1992; 31: 351-356. Whooley MA, Browner WS. Association between depressive symptoms and mortality in older women. Arch Intern Med 1998; 158: 2129-2135. Everson SA, Kaplan GA, Goldberg DE, et al. Hopelessness and 4-year progression of carotid atherosclerosis. The Kuopio Ischaemic Heart Disease Risk Factor Study. Arterioscler Thromb Vasc Biol 1997; 17: 1490-1495. Denollet J, Stanislas US, Stroobant N, et al. Personality as independent predictor of long-term mortality in patients with coronary heart disease. Lancet 1996; 347: 417-421. Shapiro PA, Lesperance F, Frasure-Smith N, et al. An open-label preliminary trial of sertraline for treatment of major depression after acute myocardial infarction (the SADHAT Trial). Sertraline Anti-Depressant Heart Attack Trial. Am Heart J 1999; 137: 1100-1106. Make a comment

Christopher C Tennant · Loyola McLean

The Weight Debate Obesity and virtue. Is staying lean a matter of ethics? Self-control of one's own weight might be described as a form of bioethics John N Burry MJA 1999; 171: 609-610 Article - References - Authors' details - - More articles on Ethics

John N Burry

Review Attention deficit hyperactivity disorder in adults: conceptual and clinical issues Julian N Trollor MJA 1999; 171: 421-425 Abstract - Introduction - Conceptual issues - Clinical assessment - Management - Monitoring progress - Conclusion - Acknowledgement - References - Authors' details - - More articles on Psychiatry Abstract Reports published over the past decade indicate that attention deficit hyperactivity disorder (ADHD) is a cause of significant psychological impairment in adults. The adulthood disorder occurs as a continuation of its childhood counterpart, with the full ADHD syndrome persisting into early adulthood in about a third of those with childhood ADHD. Despite advances in the understanding of the neurobiology of adult ADHD, the diagnosis is made clinically by establishing a retrospective childhood diagnosis, evaluating the current symptom profile and excluding alternative medical or psychiatric causes of symptoms. Adults with ADHD have high rates of comorbid psychiatric disorder and suffer significant relationship dysfunction, work and educational failure. There is emerging evidence for the effectiveness of specific treatments for adult ADHD, including stimulant medications and some antidepressants. Clinicians should be aware of this potentially treatable disorder in young adults presenting with psychological difficulties and a history of childhood ADHD symptoms. Introduction Attention deficit hyperactivity disorder (ADHD) is one of the most common disorders of childhood, affecting 3%-5% of school-age children.1 It was previously considered a diagnosis applicable only to children and adolescents, but studies of cohorts of ADHD children followed up prospectively have shown that the condition continues into adulthood in an appreciable proportion of patients.2-6 These studies have highlighted the poor psychosocial outcome of this patient population in adulthood, with high rates of educational failure, substance misuse disorders, personality disorders and other psychopathological disorders. Conceptual issues Definition The diagnosis of adult ADHD, as with most psychiatric disorders, is made on clinical grounds. Case identification is based on systematic assessment of symptom profile and exclusion of alternative psychiatric or medical causes. The Diagnostic and statistical manual of mental disorders, 4th edition1 (DSM-IV), reflects the recent conceptual shift in ADHD diagnosis by using wording applicable to adults as well as children (Box 1). Because some ADHD symptoms (eg, inattention, forgetfulness, motor restlessness) occur commonly in the community to a varying extent, it is difficult to decide where the boundary should be drawn between normal and pathological. This dilemma is partly answered in DSM-IV by allowing only those symptoms that are persistent and maladaptive to be counted toward diagnosis. In addition, impairment in at least two settings (eg, work, university, home or social life) is required before a diagnosis of ADHD can be made. Facility exists in DSM-IV for clinicians to specify "ADHD in partial remission" for patients in whom the full diagnostic criteria, although met in childhood, are no longer fulfilled. The clinical status of this less severely affected group awaits clarification. Relationship to childhood ADHD ADHD symptoms must have been present in childhood (although not necessarily recognised) for an adulthood diagnosis to be sustainable. Follow-up studies of childhood ADHD cohorts show considerable discrepancy in reported rates of retention of ADHD diagnosis by early adulthood. Such discrepancies are multifactorial and relate to different diagnostic and exclusion criteria used for study entry, variation in illness severity in original cohorts and differences in age at follow-up. Although up to two-thirds of patients may continue to have symptoms of ADHD as adults,4 only a third will satisfy full diagnostic criteria at age 18,2,3 with further age-dependent decline continuing into the mid 20s.5,6 Comorbidity in adult ADHD Rates of psychopathology among ADHD children in adulthood are high (2-2.5 times those of controls), with a particularly high risk for antisocial personality disorder (up to 10 times that of controls) and drug or alcohol misuse (4-5 times that of controls).4,7 ADHD adults have elevated rates of mood disorder (2-6 times),7,8 anxiety disorders (2-4 times),7,8 relationship dysfunction (2 times),7 and learning disorder7 compared with control populations. The high rate of comorbid psychopathology seen in adult ADHD may be in part a reflection of the impact of longstanding adaptive impairments on development, as well as shared familial, environmental and possibly genetic vulnerabilities. Theoretical and practical implications of comorbidity in adult ADHD have been reviewed in detail elsewhere.9 Pathophysiology Despite its proposed neurobiological basis and predominantly biological treatment, the precise pathophysiological mechanisms of adult ADHD remain obscure. A complete review of this area is beyond the scope of this article and has been provided elsewhere.10,11 Research has focused on a hypothesised functional deficit of monoamines, especially dopamine and noradrenaline. An understanding of the functional12 and structural13-15 neuroanatomy of ADHD is beginning to emerge, implicating dysfunctional prefrontal-striatal circuits in the pathogenesis of ADHD. Clinical assessment The need for a diagnostic hierarchy The key steps in the diagnostic assessment of adults presenting with possible ADHD are shown in the Figure. Many presenting for assessment readily identify with the symptoms of the disorder. However, up to half of those presenting to specialty clinics for assessment of possible ADHD do not have ADHD as the primary diagnosis.16 Thus, approach to this popular diagnosis demands a standardised and objective assessment. Nature and severity of current symptoms The symptoms of ADHD in adults are an extension of those seen in children. Patients may experience difficulty sustaining attention in a number of settings, particularly when performing demanding cognitive tasks. Hyperactivity manifests physically, but may also have a mental component (having accelerated or multiple simultaneous thoughts); however, hyperactivity is not essential for the diagnosis. Patients may manifest impulsive symptoms verbally (by making tactless comments or interrupting others), or may engage in impulsive high risk activities. Often patients have poor organisational skills and an exaggerated response to minor frustrations. A longitudinal assessment of the impact of symptoms should be consistent with impairment secondary to ADHD symptoms. Common experiences of the ADHD sufferer may include recurrent educational or occupational failure, relationship instability and poor ability to organise personal affairs. Establishing a retrospective childhood diagnosis of ADHD A sound retrospective diagnosis of probable ADHD in childhood should be considered as a central precursor to a diagnosis of ADHD in adulthood. A retrospective assessment of childhood symptoms should be made regardless of whether a past childhood diagnosis of ADHD has been made. A retrospective diagnosis is supported by consistent parental reports of symptoms of ADHD in one or more settings, as well as objective accounts of aberrant behaviour recorded in past school reports. Assessing other psychological and medical problems All patients should be asked about the presence of symptoms of common psychiatric and medical disorders (past and present) that can mimic ADHD (Box 2). This is particularly important when patients present for the first time at a relatively late age (eg, over 35 years). In some cases, diagnostic difficulty arises where superimposed symptoms of a second psychiatric disorder coexist with longstanding symptoms of ADHD. Chronic use of many illicit drugs (eg, cannabis, cocaine, amphetamines) and alcohol should be considered as a possible cause of the presenting cognitive and behavioural symptoms. Adult ADHD patients are at high risk of comorbid drug misuse and are more likely to report failed attempts to curtail their drug use.17,18 In patients in whom possible ADHD symptoms and drug misuse occur together, it is usually prudent to reassess for ADHD symptoms after treatment of the drug misuse. Recent (eg, within the past two or three months) or ongoing misuse of illicit substances is a relative contraindication to prescription of stimulant medication. A non-stimulant treatment may be offered to patients with significant ADHD symptoms who are unable to curtail illicit drug use. Adjunctive diagnostic tests Routine investigations: Routine blood tests (urea, electrolyte, creatinine levels, a full blood count, liver and thyroid function tests) are of use only when the presentation suggests an underlying medical disorder. Random urinary drug screening may be performed to monitor illicit drug use in selected patients. An electrocardiogram (EEG) is performed in older adults or those with a history or signs of cardiac disease, particularly when treatment with tricyclic antidepressants is being considered. Rating scales: Rating scales are a useful adjunct to clinical assessment, but do not provide a diagnostic test for adult ADHD. Scales have been developed for retrospective self-report of childhood symptoms (eg, Wender-Utah Rating Scale19) and retrospective parent report of childhood symptoms (eg, Conners Abbreviated Symptom Questionnaire20). Rating scales can also be used to evaluate the severity of current symptoms and to monitor treatment (eg, Patient's Behavior Checklist for ADHD Adults21). Neuropsychological testing: A range of neuropsychological deficits have been reported in children and adolescents with ADHD. Preliminary neuropsychological studies of adults22-27 have produced some conflicting findings, but, on the whole, are consistent with those in childhood, and provide some support for the validity of adult ADHD. The most commonly administered test in adults is a computerised test of sustained attention (Continuous Performance Task). At present, there is insufficient evidence to recommend detailed neuropsychological evaluation for ADHD adults on a routine basis. However, neuropsychological testing may be useful in patients in whom diagnosis is difficult, or when cognitive impairment secondary to another disorder is suspected (eg, those with previous head injury, alcohol-related cognitive deficits, or early dementias). Neurophysiological testing: Quantitative electroencephalograph (EEG) abnormalities, including decreased power of alpha and beta bandwidths in posterior leads and increased frontal theta, have been demonstrated in ADHD children and adolescents.28-30 Quantitative EEG findings have not yet been systematically studied in adults with ADHD and, at present, cannot be advocated for routine assessment. Studies of event-related potentials (ERPs) in children and adolescents with ADHD have found a number of abnormalities in the late positive potential (P3b) amplitude and latency,30-32 as well as abnormalities of the early negative potentials (N1 and N2).31,33,34 However, these findings are seen in a variety of other disorders (eg, autism, learning disability) and hence lack diagnostic specificity. There are few published studies of ERP findings in adults with ADHD, and thus at present their use is for research rather than diagnostic assessment. Functional neuroimaging: Positron emission tomography (PET) findings, including abnormality of glucose uptake in the premotor and frontal cortices12 and reduced [fluorine-18] fluorodopa ratios in the prefrontal cortex,35 support the hypothesis of prefrontal and dopaminergic deficits as central to the pathophysiology of adult ADHD, but do not have clinical application. Structural and functional neuroimaging studies may be appropriate in selected cases when another cause of cognitive and behavioural symptoms is suspected. Management Education Response to initial diagnosis is highly variable, with reactions ranging from relief at an explanation for the symptoms to grief over the "lost years" of the untreated disorder. Education regarding ADHD and its treatment is essential. Further information can be obtained by patients from popular books, ADHD support groups, and the Internet <http://www.nimh.nih.gov/publicat/adhdmenu.cfm> Pharmacotherapy There are only a few published reports examining the efficacy of pharmacotherapy for adult ADHD.36 Drug treatment is generally reserved for those with moderate or severe symptoms, or when more conservative measures have failed. Current evidence supports stimulant responsiveness across age groups,37 but there have only been six published double-blind placebo-controlled trials of psychostimulant use in adults. A review of these36 noted considerable variability in response rates to stimulants (range, 25%-78%; mean, 52%) and attributed this to multiple factors, including diagnostic and dose variation between studies. No convincing evidence has emerged that long term supervised prescription of stimulants leads to drug tolerance or misuse. Commonly used dose ranges for the two stimulants available in Australia are the same as those for ADHD children (0.3-1.0 mg/kg per day for methylphenidate, and 0.2-0.5 mg/kg per day for dextroamphetamine). The mechanisms of action of stimulant medication have been reviewed.38 Stimulants should not be taken together with other psychotropic drugs, unless recommended by an experienced clinician. Tricyclic antidepressants (TCAs) have been assessed as effective treatments for childhood and adolescent ADHD. Two studies of ADHD in adults39-40 support a role for desipramine, nortriptyline and imipramine at typical antidepressant dosages as second-line treatment for adult ADHD. However, initial treatment with TCAs should be considered in selected patients (those at risk of misuse of prescribed stimulants, and those with comorbid depression and anxiety). The newer antidepressants venlafaxine41-43 and bupropion44 have shown promise in open studies, but further evaluation is required. Serotonin reuptake inhibitors may be appropriate for those with comorbid anxiety, depression, obsessive-compulsive symptoms and severe impulsivity, but as yet there is no evidence of their value for the treatment of ADHD symptoms alone. The monoamine oxidase-B inhibitor L-deprenyl has been shown to reduce ADHD symptoms in a single trial in adults.45 Cognitive behavioural therapy Cognitive and behavioural strategies have yet to be systematically evaluated as independent treatments for adult ADHD. However, to overcome skill deficits commonly seen in ADHD, patients can be taught basic skills such as time management, organisational strategies, problem solving and anger management. Controversial treatments A number of controversial treatments are available for adult ADHD. Dietary supplementation, exclusion diets and herbal supplements have not been shown to be of benefit in adults. EEG biofeedback is an expensive treatment of growing popularity, but has yet to be properly evaluated. A case history of adult ADHD in a 22-year-old man is given in Box 3. Monitoring progress Patient response to treatment can be monitored at various levels: subjective feedback from patient and family; self- and observer-rating scales; educational progress; employer reports; and repeat neuropsychological assessment. No consensus guidelines exist regarding duration of treatment or adequate methods of monitoring progress. If stimulant treatment has been continued through late adolescence into adulthood, it is prudent to review the need for continuing treatment every 6-12 months. A medication-free period (eg, 4-6 weeks) may allow re-evaluation of symptom severity, thus helping to determine the need for ongoing treatment. For patients commencing stimulant medication for the first time as adults, there should be clear evidence of functional improvement over the first 3-6 months of treatment. Clear short-term functional improvement justifies continuing stimulant prescription over the next 12 months. Thereafter, a patient's progress should be reviewed as above. Those with persistence of the full adult ADHD profile may require medication until educational goals have been met, or until stable employment is obtained. This allows the patient to further develop the skills needed to compensate for persisting symptoms. A small group of patients with severe symptoms may require stimulant medication indefinitely. Conclusion There are published reports to support the continuation of ADHD into adulthood in about a third of patients with childhood ADHD. Symptoms of the disorder can be disabling, and considerable comorbid psychopathology may be present. With recognition and appropriate management of the disorder, considerable gains may be anticipated in most patients. As with any emergent condition, our current understanding of adult ADHD is incomplete, and limited published data are available. A systematic and evidence-based approach to diagnosis and management is therefore required, which should be revised as new developments occur. Acknowledgement The assistance of Professor Perminder Sachdev in reviewing a previous draft version of this article is gratefully acknowledged. References American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th edition. Washington, DC: American Psychiatric Association, 1994: 83-85. Gittleman R, Mannuzza S, Shenker R, Bonagura N. Hyperactive boys almost grown up: I. Psychiatric status. Arch Gen Psychiatry 1985; 42: 937-947. Mannuzza S, Klein RG, Bonagura N, et al. Hyperactive boys almost grown up: V. Replication of psychiatric status. Arch Gen Psychiatry 1991; 48: 77-83. Weiss G, Hechtman L, Milroy T, Perlman T. Psychiatric status of hyperactives as adults: a controlled prospective 15-year follow-up of 63 hyperactive children. J Am Acad Child Psychiatry 1985; 24: 211-220. Mannuzza S, Klein RG, Bessler A, et al. Adult outcome of hyperactive boys: educational achievement, occupational rank and psychiatric status. Arch Gen Psychiatry 1993; 50: 565-576. Mannuzza S, Klein RG, Bessler A, et al. Adult psychiatric status of hyperactive boys grown up. Am J Psychiatry 1998; 155: 493-498. Biederman J, Faraone SV, Spencer T, et al. Patterns of psychiatric comorbidity, cognition, and psychosocial functioning in adults with attention deficit hyperactivity disorder. Am J Psychiatry 1993; 150: 1792-1798. Biederman J, Newcorn J, Sprich S. Comorbidity of attention deficit hyperactivity disorder with conduct, depressive, anxiety and other disorders. Am J Psychiatry 1991; 148: 564-577. Horning M. Addressing comorbidity in adults with Attention Deficit Hyperactivity Disorder. J Clin Psychiatry 1998; 59 [Suppl 7]: 69-75. Castellanos FX. Toward a pathophysiology of attention deficit hyperactivity disorder. Clin Paediatr 1997; 36: 381-393. Faraone SV, Biederman J. Neurobiology of Attention-Deficit Hyperactivity Disorder. Biol Psychiatry 1998; 44: 951-958. Zametkin AJ, Nordahl TE, Gross M, et al. Cerebral glucose metabolism in adults with hyperactivity of childhood onset. N Engl J Med 1990; 323: 1361-1366. Castellanos FX, Giedd JN, Eckburg P, et al. Quantitative morphology of the caudate nucleus in attention deficit hyperactivity disorder. Am J Psychiatry 1994; 151: 1791-1796. Semrud-Clikeman M, Filipek PA, Biederman J, et al. Attention-deficit hyperactivity disorder: magnetic resonance imaging morphometric analysis of the corpus callosum. J Am Acad Child Adolesc Psychiatry 1994; 33: 875-881. Castellanos FX, Giedd JN, Marsh WL, et al. Quantitative brain magnetic resonance imaging in attention deficit hyperactivity disorder. Arch Gen Psychiatry 1996; 53: 607-616. Roy-Byrne P, Scheele L, Brinkley J, et al. Adult attention deficit hyperactivity disorder: assessment guidelines based on clinical presentation to a specialty clinic. Compr Psychiatry 1997; 38: 133-140. Goodwin DW, Schulsinger F, Hermansen L, et al. Alcoholism and the hyperactive child syndrome. J Nerv Ment Dis 1975; 160: 349-353. Carroll KM, Rounsaville BJ. History and significance of childhood attention deficit hyperactivity disorder in treatment-seeking cocaine abusers. Compr Psychiatry 1993; 34: 75-82. Ward MF, Wender PH, Reimherr FW. The Wender Utah Rating Scale: an aid in the retrospective diagnosis of childhood attention deficit hyperactivity disorder. Am J Psychiatry 1993; 150: 885-890. Goyette CH, Conners CK, Ulrich RF. Normative data on Revised Conners Parent and Teacher Rating Scales. J Abnorm Child Psychol 1978; 6: 221-236. Patient's Behaviour Checklist for ADHD Adults. In: Barkley RA, ed. Attention deficit hyperactivity disorder: a clinical workbook. New York: The Guilford Press, 1991: 43. Seidman LJ, Biederman J, Weber W, et al. Neuropsychological function in adults with attention deficit hyperactivity disorder. Biol Psychiatry 1998; 44: 260-268. Matochik JA, Rumsey JM, Zametkin AJ, et al. Neuropsychological correlates of familial attention deficit hyperactivity disorder in adults. Neuropsychiatry, Neuropsychol Behav Neurol 1996; 9: 186-191. Downey KK, Stelson FW, Pomerleau OF, Giordani B. Adult attention deficit hyperactivity disorder: psychological test profiles in a clinical population. J Nerv Ment Dis 1997; 185: 32-38. Lovejoy DW, Ball JD, Keats M, et al. Neuropsychological performance of adults with attention deficit hyperactivity disorder (ADHD): diagnostic classification estimates for measures of frontal lobe/executive functioning. J Int Neuropsychol Soc 1999; 5: 222-233. Corbett B, Stanczak DE. Neuropsychological performance of adults evidencing attention-deficit hyperactivity disorder. Arch Clin Neuropsychol 1999; 14: 373-387. Jenkins M, Cohen R, Malloy P, et al. Neuropsychological measures which discriminate among adults with residual symptoms of attention deficit disorder and other attentional complaints. Clin Neuropsychol 1998; 12: 74-83. Mann CA, Lubar JF, Zimmerman AW, et al. Quantitative analysis of EEG in boys with attention deficit hyperactivity disorder: a controlled study with clinical implications. Paediatr Neurol 1992; 8: 30-36. Chabot RJ, Merkin H, Wood LM. Sensitivity and specificity of QEEG in children with attentional deficits or specific developmental learning disorders. Clin Electroencephalogr 1996; 27: 26-34. Kuperman S, Johnson B, Arndt S, et al. Quantitative EEG differences in a nonclinical sample of children with ADHD and undifferentiated ADD. J Am Acad Child Adolesc Psychiatry 1996; 35: 1009-1017. Loiselle DL, Stamm JS, Maitinsky S, Whipple SC. Evoked potential and behavioral signs of attentive dysfunctions in hyperactive boys. Psychophysiology 1980; 17: 193-201. Holcomb PH, Ackerman PT, Dykman RA. Cognitive event-related potentials in children with attentional and reading deficits. Psychophysiology 1985; 22: 656-667. Satterfield JH, Schell AM, Nicholas T, Backs RW. Topographic study of auditory event-related potentials in normal boys and boys with attention deficit disorder with hyperactivity. Psychophysiology 1988; 25: 591-606. Klorman R, Brumaghim JT, Salzman LF, et al. Effects of methylphenidate on processing negativities in patients with attention-deficit hyperactivity disorder. Psychophysiology 1990; 27: 328-337. Ernst M, Zametkin AJ, Matochik JA, Cohen RM. Dopa decarboxylase activity in attention deficit hyperactivity disorder adults -- a [fluorine-18] fluorodopa positron emission tomographic study. J Neurosci 1998; 18: 5901-5907. Wilens TE, Biederman J, Spencer TJ, Prince J. Pharmacotherapy of adult attention deficit hyperactivity disorder: a review. J Clin Psychopharmacol 1995; 15: 270-279. Spencer T, Biederman J, Wilens T, et al. Pharmacotherapy of attention-deficit hyperactivity disorder across the life cycle. J Am Acad Child Adolesc Psychiatry 1996; 35: 409-432. Solanto M. Neuropsychopharmacological mechanisms of stimulant drug action in attention-deficit hyperactivity disorder: a review and integration. Behav Brain Res 1998; 94: 127-152. Wilens TE, Biederman J, Mick E, Spencer TJ. A systematic assessment of tricyclic antidepressants in the treatment of adult attention-deficit hyperactivity disorder. J Nerv Ment Dis 1995; 183: 48-50. Wilens TE, Biederman J, Prince J, et al. Six-week, double-blind, placebo-controlled study of desipramine for adult attention deficit hyperactivity disorder. Am J Psychiatry 1996; 153: 1147-1153. Adler LA, Resnick S, Kunz M, Devinsky O. Open-label trial of venlafaxine in adults with attention deficit disorder. Psychopharmacol Bull 1995; 31: 785-788. Hedges D, Reimherr FW, Rodgers A, et al. An open trial of venlafaxine in adult patients with attention deficit hyperactivity disorder. Psychopharmacol Bull 1995; 31: 779-783. Findling RL, Schwartz MA, Flannery DL, Manos MJ. Venlafaxine in adults with attention-deficit hyperactivity disorder: an open clinical trial. J Clin Psychiatry 1996; 57: 184-189. Wender PH, Reimherr FW. Buproprion treatment of attention deficit hyperactivity disorder in adults. Am J Psychiatry 1990; 147: 1018-1020. Wood DR, Reimherr FW, Wender PH. The use of l-deprenyl in the treatment of attention deficit disorder, residual type (ADD, RT). Psychopharmacol Bull 1983; 19: 627-629. (Received 4 Feb, accepted for publication 20 Jul, 1999) Authors' details Neuropsychiatric Institute, Prince of Wales Hospital, Sydney, NSW. Julian N Trollor, MB BS, FRANZCP, Staff Specialist; and Conjoint Lecturer, School of Psychiatry, University of New South Wales. Reprints will not be available from the author. Correspondence: Dr J N Trollor, Neuropsychiatric Institute, McNevin Dickson Building, Prince of Wales Hospital, Randwick, NSW 2031. J. TrollorATunsw.edu.au 1: Summary of DSM-IV criteria for attention deficit hyperactivity disorder1 (all criteria from A to D must be met) A: Six or more symptoms of either Inattention or Hyperactivity-impulsivity present for at least six months to a degree that is maladaptive and inconsistent with developmental level. Inattention Often: fails to give close attention to details or makes careless mistakes in schoolwork, work or other activities has difficulty sustaining attention in tasks or play activities does not seem to listen when spoken to directly does not follow through on instructions and fails to finish schoolwork, chores or duties in the workplace has difficulty organising tasks and activities avoids, dislikes or is reluctant to engage in tasks that require sustained mental effort loses things necessary for tasks or activities easily distracted by extraneous stimuli forgetful in daily activities Hyperactivity-impulsivity Often: fidgets with hands, feet or squirms in seat leaves seat in classroom or other situations in which remaining seated is expected runs about or climbs excessively in situations in which it is inappropriate (in adolescents or adults, may be limited to subjective feelings of restlessness) has difficulty playing or engaging in leisure activities quietly "on the go" or acts as if "driven by a motor" talks excessively blurts out answers before questions completed has difficulty awaiting turn interrupts or intrudes on others B: Some symptoms causing impairment were present before 7 years of age. C: Some impairment is present in two or more settings. D: Evidence of clinically significant impairment in social, academic or occupational functioning. Back to textBack to text 2: Differential diagnoses of adult attention deficit hyperactivity disorder Medical Past head injury or anoxia Sleep disorders (eg, sleep apnoea) Recent viral infection including HIV Long term medical illness (eg, renal or liver failure) Seizure disorder (eg, petit mal) Endocrine disorder (eg, hypothyroidism, hyperthyroidism, hypoglycaemia) Psychiatric Anxiety disorder Major depression Bipolar disorder (eg, chronic hypomania) Cyclothymia Antisocial and borderline personality disorders Effect of prescribed medications (eg, benzodiazepines, anticholinergic drugs, anticonvulsants) Other central nervous system disorder (eg, degenerative disorders) Substance misuse (alcohol, long term cocaine or amphetamine use, cannabis) Back to text Case history -- adult attention deficit hyperactivity disorder (ADHD) Presentation: A 22-year-old unemployed carpenter, referred by his general practitioner, reported difficulty concentrating when reading or listening to verbal instructions, and difficulty following through multistep tasks. He had lost numerous jobs because of poor organisational skills, failure to complete assigned tasks, and a tendency to become easily bored or frustrated in his work. He was disorganised in most aspects of managing his personal affairs. There was a history of experimenting with illicit substances, instability in interpersonal relationships, and low self-esteem. The patient's mother confirmed his account of untreated, moderately severe ADHD symptoms from school entry. Assessment: The patient was physically restless, easily distracted and verbally impulsive. There was no evidence of psychiatric or medical illness. Neuropsychological assessment revealed reduced arithmetic skills, reduced speed of information processing, impulsive responses and failure to maintain attention over time. A diagnosis of ADHD was made. Management: Combined psychological and pharmacological treatment was instituted. Over a series of 12 sessions, the patient was given information about ADHD, and participated in sessions to enhance organisational skills, impulse control and self-esteem. He was prescribed dextroamphetamine, 5 mg twice a day, and later the dose was increased to 5 mg three times a day. Both the patient and his family reported amelioration of his symptoms. He was able to successfully start a part-time job, and later returned to full-time employment as a carpenter. A trial without stimulant medication at 12 months led to appreciable exacerbation of symptoms, and dextroamphetamine was reinstituted. He has remained in stable employment over a follow-up period of 18 months and continues to take dextroamphetamine on work days only. Back to text

Julian N Trollor

Research Australian suicide trends 1964-1997: youth and beyond? Christopher H Cantor, Kerryn Neulinger and Diego De Leo MJA 1999; 171: 137-141 Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Psychiatry Abstract Objective: To examine Australian suicide rates across all ages, and compare Australian rates with those of other Western nations. Design: Australian Bureau of Statistics data were used to examine Australian suicide trends, 1964-1997, by age and sex. For comparison, suicide rates of 22 other Western nations, 1990-1994, were obtained from the World Health Organization. Results: Australian suicide rates for males 15-24 years and 25-34 years rose from 1964-1997. Comparable rates for females showed no significant change. Suicide rates for several of the older age and sex groups declined over this period. Comparison with suicide rates of other Western nations showed that, while Australian youth suicide rates are relatively high, this is not the case for older age groups. Australian suicide rates are higher than those in the European nations of origin of our major migrant groups, but similar to those of other Western nations also recently colonised by Europeans (Canada, the United States and New Zealand). Conclusions: Priorities for suicide prevention in Australia are correctly concentrated on youth, but the targeted age range should be extended to include men aged 25-34 years. A comprehensive policy should also not neglect the needs of other age groups. Further epidemiological study of national and international data may suggest new approaches to suicide prevention. Introduction It is well known that there is a high suicide rate in Australian males aged 15-24 years, and previous and present governments have instituted committees to address youth suicide rates.1 There have been only sporadic reports of suicide rates in other age groups,2 including suggestions of high rates in elderly people.2,3We present suicide rates and trends across all ages, placing them in context by comparing them with rates from other Western nations. The national focus on youth suicide to the relative exclusion of older age groups is examined in the light of these data. Methods Australian suicide and population data for 1964-1997 were obtained from the Australian Bureau of Statistics (ABS) and annual suicide rates (per 100 000 estimated mean resident population) were calculated (see Appendix). These were plotted by 10-year age groups and sex over time. Change over time was examined by comparing the suicide rate in 1964-1966 (rates were averaged to smooth out random fluctuations within one-year periods) with the suicide rate in 1995-1997; 95% confidence intervals were calculated for these two time periods to assess the significance of change. Variations in suicide rate trends over this 34-year period were assessed by calculating the series autocorrelation suicide rates and the values of Pearson's correlation coefficient. Years of potential life lost (YPLL) were calculated for 10-year age and sex groups for the most recent year (1997). The formula used was adapted from that used by the Australian Bureau of Statistics4 in order to incorporate age groups (Box 1). The Australian population at 30 June 1991 was chosen as the standard population, as suggested by the Australian Bureau of Statistics. International data were obtained from the World Health Organization (WHO)5-8 and Lester and Yang.9 Mean suicide rates were calculated for 23 Western countries (including Australia), averaged over 1990-1994, for 10-year age and sex groups. These 10-year age and sex rates were then ranked to compare Australia with other nations. Results Figures 1-8 show suicide rates over time for sex and 10-year age groups, as well as all ages combined. Males Suicide rates overall and for those aged 15-24 and 25-34 years increased significantly over time (1964-1966 to 1995-1997). The rise in suicide rates from 1973-1997 for men aged 25-34 years was of similar magnitude to the rise for those aged 15-24 years (Figures 2 and 3). Suicide rates in the older age groups (35 to 75 years and over) declined (for men aged 35-44 years and 75 years and over these declines were not statistically significant). Significant autocorrelations (P < 0.01) were found in each age group and for all ages combined. Females Suicide rates overall and for each age group from 25 to 75 years and over declined significantly (1964-1966 to 1995-1997). There was no change in suicide rates for females aged 15-24 years. Significant autocorrelations (P < 0.01) were found for all ages combined and for most age groups (the exceptions were those aged 15-24 years and 75 and over). Years of potential life lost by suicide in 1997 are shown in Box 2. Boxes 3a and 3b list the mean suicide rates (per 100 000 population) by age group and sex for 23 Western nations, including Australia. Discussion The priority accorded to youth suicide prevention by successive Australian governments is supported by our data. In the last three decades, when overall suicide rates were falling, the suicide rate of males 15-24 years more than doubled. Suggestions of a plateauing of this rate since 1989 are not supported by the latest figures for 1997, although it is premature to draw conclusions either way. (It should also be noted that at the time of submission of this article there were significant concerns about the validity of the 1997 suicide rate figures. For example, major rises in rates in New South Wales and Victoria were absent from Queensland -- the next most populous State -- suggesting the possibility of interstate data collection influences.) From a policy perspective, the most important finding is that suicide rate increases since 1973 for men aged 25-34 years have paralleled those of 15-24 year olds, with even less evidence of a recent plateau. Despite having shorter life expectancies, the toll in potential years of life lost (in 1997) was greatest for 25-34 year olds. These years are also the peak years for early parenthood, making the likelihood of there being bereaved offspring greater than in the younger group. These findings suggest that priority initiatives for youth suicide prevention should be extended to those aged 15-34 years, if not further (the high level of potential years of life lost continues to 44 years). The Federal Government's recently announced National Suicide Prevention Policy provides for ages beyond youth, by recognising that rising rates are not confined to the age group 15-24 years and that high suicide rates in the elderly should not be overlooked. It is unclear whether or to what extent the suicide phenomenon in boys and young men might be a cohort effect -- a "damaged" generation. The later commencement of the rise in suicide rate in men aged 25-34 years and the, as yet, absence in this age group of the possible 1990s plateau could be seen as consistent with this. Rates in females aged 15-24 years showed no convincing rise. It has previously been noted that suicide rates in females aged 15-19 years rose modestly between 1960 and 1989, while rates for those aged 20-24 years showed no overall change over this period.10 However, much of the rise in females aged 15-19 years was in the early 1960s, predating the rise in rates of 15-19-year-old males, but coinciding with a general, transient rise in suicide rates in females of all ages. Perhaps the most important observation regarding young females in the present study is that their suicide rates remained relatively static at a time when rates for most other female age groups declined. Suicide rates in children under 15 years of age have not significantly altered over time, although the small numbers involved do not lend confidence to rate estimates. The recording of suicide in children under the age of 10 years is affected by the different criteria used by the Australian Bureau of Statistics for determining suicide: it is considered that children have a limited ability to form an intent to suicide. Hence, more explicit evidence of suicidal intent is required,11 usually a coroner having stated explicitly that suicide was the cause of death. As most State and Territory Coroners' Acts discourage if not prohibit such findings (for all ages), such explicit statements are unlikely.11 Beyond 35 years in women, and 45 years in men, and up to 75 years and over for both sexes, Australian suicide trends are striking. In both sexes there have been major declines, and for much of the period these declining male and female rates have been parallel, quite unlike the trends for 15-24 year olds. It is unclear whether these declining rates have as yet plateaued. Even if this were not the case, it is inevitable that these declining rates will shortly level out and increase again (from the trends over the complete period a number of these age rates would reach zero in the early decades of the next century). In the early 1960s, suicide rates, particularly in women and in older age groups, rose in association with an epidemic of barbiturate poisoning, subsequently to fall in the late 1960s, reaching rates in the early 1970s similar to those before this epidemic.12,13 The causal factors determining the subsequent decline in rates of those between 35 and 74 years are yet to be determined. It is possible that such determination might yield valuable clues as to the causes and possible methods of preventing suicide in young people. International comparisons should be interpreted conservatively, as variations in data collection systems will account for some of the variations. With these reservations in mind, among 23 Western nations, Australian suicide rates for 15-24 year olds ranked fourth for males and eighth for females (Boxes 3a and 3b). Australian rates for both sexes between the ages of 35 and 74 years, as well as declining, compared favourably internationally (ranking in the middle of or below those of other Western nations). Although Australian suicide rates for those over 75 years were not declining, they nevertheless again compared favourably from an international perspective. Whereas the Australian suicide rate for 15-24-year-old males was over half that of the highest-placed nation (Finland), the corresponding ratio for males 75 years and over was about one-sixth. For females, these comparisons were even more marked. Nevertheless, a comprehensive policy should not overlook the needs of men over 75 years, especially as, in Australia, suicide rates in this age group surpass those of all other age groups. The Western nations with lower suicide rates include those that provided most of the early immigrants to Australia: Greece, Italy (except in the elderly), the United Kingdom and Ireland. The highest suicide rates were in mainland Western Europe (especially Hungary) and Scandinavia (especially Finland). Some of these nations, for example Denmark, have profiles radically different from that of Australia, with lower youth suicide rates but much higher rates in those over 35 years of age. Canada and, to a lesser extent, the United States and New Zealand are the nations with suicide rate profiles most similar to Australia's. All four of these nations have common characteristics of European migration, a comparatively short history (apart from their indigenous populations), geographical isolation, climatic extremes and more.10 They serve as potentially valuable nations to study shared characteristics that may affect suicide rates. Studies have yet to provide explanations for these similarities and differences which have often been overlooked, largely as a consequence of the worldwide lack of epidemiological mental health data. While differences in prevalence of psychiatric disorders are potentially relevant, the magnitude of the different international rates suggests other factors may operate. Hungary and Finland share common cultural origins and high suicide rates. It has been suggested that Finland's high suicide rates in young men may relate to cultural expectations that men should be tough and resilient14 -- a suggestion that might be equally relevant in Australia, New Zealand, the United States and Canada. It is possible that a better understanding of cultural influences and how to positively modify them might be relevant to suicide prevention. Acknowledgements The study was funded by Griffith University and Queensland Health through their co-funding of the Australian Institute for Suicide Research and Prevention. We thank the Australian Bureau of Statistics for providing information on suicide and population numbers. References Commonwealth Department of Health and Family Services. Youth suicide in Australia: a background monograph. 2nd edition. Canberra: AGPS, 1997. Snowdon J. Suicide rates and methods in different age groups: Australian data and perceptions. Int J Geriat Psychiatry 1997; 12: 253-258. Hassan R, Carr J. Changing patterns of suicide in Australia. Aust N Z J Psychiatry 1989; 23: 226-234. Australian Bureau of Statistics. Causes of death, Australia, 1996: 73. (Catalogue No. 3303.0.) World Health Organization. World Health Statistics Annual 1992. Geneva: WHO, 1993. World Health Organization. World Health Statistics Annual 1993. Geneva: WHO, 1994. World Health Organization. World Health Statistics Annual 1994. Geneva: WHO, 1995. World Health Organization. World Health Statistics Annual 1995. Geneva: WHO, 1996. Lester D, Yang B. Suicide and homicide in the twentieth century: Changes over time. Commack, NY: Nova Science, 1998: 165-204. Cantor CH, Leenaars AA, Lester D, et al. Suicide trends in eight predominantly English-speaking countries 1960-1989. Soc Psychiatry Psychiatr Epidemiol 1996; 31: 364-373. Cantor CH, Neulinger K, Roth J, Spinks D. The epidemiology of suicide and attempted suicide among young Australians: a report to the National Health and Medical Research Council: Australian Institute for Suicide Research and Prevention. In press. Oliver G, Hetzel BS. An analysis of recent trends in suicide rates in Australia. Int J Epidemiol 1973; 2: 91-101. Whitlock FA. Suicide in Brisbane, 1956-1973: The drug-death epidemic. Med J Aust 1975; 1: 737-743. Retterstol N. Suicide in the Nordic countries. Psychopathology 1992; 25: 254-265. (Received 14 Jan, accepted 7 Jun, 1999) Authors' details Australian Institute for Suicide Research and Prevention, Griffith University, Nathan, QLD. Christopher H Cantor, FRANZCP, MRCPsych, Senior Research Psychiatrist; Kerryn Neulinger, BBehSc, GradDipPsych, Research Assistant; Diego De Leo, MD, PhD, Director. Reprints will not be available from the authors. Correspondence: Dr C H Cantor, Australian Institute for Suicide Research and Prevention, Griffith University, Nathan, QLD 4111. Email: C. CantorATmailbox.gu.edu.au Back to textBack to text Back to text 3a: Mean male suicide rates (per 100000 population) for 23 Western countries by 10-year age groups, 1990-199415-24 yearsFinland 41.4 New Zealand 39.0 Switzerland 25.8 Australia 25.7 Canada 25.2 Norway 24.9 Austria 24.3 USA 21.9 Hungary 20.1 Scotland 19.0 Ireland 18.3 N Ireland 17.6Belgium 15.7 France 15.3 Germany 14.0 Sweden 13.4 Denmark 13.0 Engl/Wales 11.1 Netherlands 9.3 Spain 7.0 Italy 6.1 Portugal 5.8 Greece 4.0 25-34 yearsFinland 60.7 Hungary 54.4 Switzerland 32.7 New Zealand 32.0 France 32.0 Belgium 30.5 Austria 30.3 Australia 29.0 Canada 29.0 Ireland 27.1 Denmark 26.4 Norway 26.1Scotland 26.1 USA 24.6 Sweden 23.9 N Ireland 22.4 Germany 21.3 Engl/Wales 16.3 Netherlands 15.9 Portugal 13.2 Spain 10.6 Italy 10.3 Greece 5.635-44 yearsHungary 82.0 Finland 67.8 France 40.1 Denmark 38.1 Austria 37.2 Belgium 35.6 Switzerland 33.0 Sweden 29.3 Canada 27.3 Norway 26.9 Scotland 26.2 Germany 26.0Australia 25.2 New Zealand 23.9 USA 23.5 Ireland 22.9 Netherlands 17.7 Engl/Wales 17.4 N Ireland 15.5 Portugal 11.8 Italy 10.6 Spain 9.4 Greece 5.945-54 yearsHungary 95.1 Finland 64.1 Denmark 47.5 Austria 41.5 France 40.1 Switzerland 39.8 Belgium 36.2 Sweden 31.9 Germany 31.1 Norway 28.8 Canada 25.6 Scotland 24.2Australia 24.2 New Zealand 24.2 USA 23.1 Ireland 19.6 Netherlands 16.7 Engl/Wales 16.2 N Ireland 15.1 Portugal 14.6 Italy 12.6 Spain 11.9 Greece 6.755-64 yearsHungary 84.6 Finland 57.3 Austria 46.7 Denmark 42.6 Switzerland 41.9 belgium 38.9 France 38.1 Germany 32.2 Sweden 30.7 Norway 28.8 Ireland 25.9 USA 25.0 Canada 24.2 New Zealand 23.2 Australia 22.9 Portugal 21.5 Netherlands 18.6 Scotland 18.1 N Ireland 17.4 Spain 17.4 Italy 17.1 Engl/Wales 12.8 Greece 7.865-74 yearsHungary 92.5 Austria 61.1 Belgium 50.4 Switzerland 47.4 France 47.1 Denmark 46.4 Finland 45.9 Germany 35.9 Sweden 33.7 USA 30.9 Norway 30.7 Portugal 30.1 Australia 24.4 Spain 23.2 Italy 22.9 Canada 22.1 New Zealand 21.2 Netherlands 19.7 Ireland 18.3 Scotland 14.3 N Ireland 12.8 Engl/Wales 11.9 Greece 10.175+ yearsHungary 183.0 Austria 118.0 France 103.0 Belgium 98.6 Switzerland 89.8Germany 86.1 Denmark 74.9 Finland 71.9 Portugal 59.1 USA 55.4Sweden 51.9 Spain 47.8 Italy 44.3 Netherlands 35.4 Australia 32.8 Norway 31.8 New Zealand 29.8 Canada 28.9 Engl/Wales 17.1 Scotland 16.0Greece 15.8 Ireland 13.8 N Ireland 13.3Back to text Appendix: Identifying suicide deaths in Australia11 Coding deaths as suicide relies on an interaction between the Australian Bureau of Statistics (ABS) and State and Territory coroners and government medical officers. The six States and two Territories of Australia each have different Coroners' Acts. Most States and Territories discourage coroners from making formal pronouncements about suicide. Western Australia and New South Wales are the only States that routinely use suicide verdicts. ABS receives information from coroners that is generally sufficient for coding in most cases. Deaths that were in reality suicides, but were not deemed as such by coroners or the ABS, will most likely be coded as undetermined deaths or accidents, and involve similar causes as suicide deaths (eg, poisoning). There has been a rise in both undetermined and accidental deaths in recent years. However, the impact of these uncertainties is unlikely to be sufficient to greatly alter our overall study findings. Back to text 3b: Mean female suicide rates (per 100000 population) for 23 Western countries by 10-year age groups, 1990-199415-24 yearsFinland 7.5 Austria 6.2 Hungary 6.2 New Zealand 6.2 Sweden 5.9 Switzerland 5.8 Norway 5.5 Australia 5.1 Belgium 5.1 Canada 4.9 France 4.5 USA 3.8Netherlands 3.7 Scotland 3.7 Germany 3.5 Denmark 3.3 Ireland 2.5 N Ireland 2.4 Portugal 2.2 Engl/Wales 2.1 Italy 1.8 Spain 1.7 Greece 0.725-34 yearsFinland 12.0 Belgium 11.8 Hungary 11.6 Sweden 10.1 Switzerland 9.0 France 9.0 Scotland 8.3 Austria 8.0 Denmark 7.7 New Zealand 7.3 Netherlands 7.2 Norway 7.1Ireland 6.7 Australia 6.6 Canada 6.4 Germany 5.7 Germany 5.7 N Ireland 3.9 Portugal 3.5 Engl/Wales 3.5 Italy 2.9 Spain 2.6 Greece 1.435-44 yearsHungary 20.3 Finland 17.4 Denmark 15.7 Belgium 14.5 Switzerland 13.5 France 13.0 Austria 12.1 Sweden 11.8 Norway 9.8 Netherlands 9.6 Canada 8.1 Germany 7.7New Zealand 6.9 Scotland 6.8 N Ireland 6.8 Australia 6.6 USA 6.6 Ireland 4.8 Engl/Wales 3.9 Italy 3.9 Portugal 3.8 Spain 3.0 Greece 1.3 45-54 yearsHungary 26.5 Denmark 25.5 Finland 20.4 Belgium 18.2 Austria 17.1 Switzerland 16.7 France 16.5 Sweden 15.0 Germany 12.1 Norway 11.5 Netherlands 9.5 N Ireland 9.4New Zealand 8.9 Canada 8.1 USA 7.3 Scotland 7.2 Australia 7.0 Ireland 6.8 Portugal 5.0 Italy 4.9 Engl/Wales 4.7 Spain 3.9 Greece 2.355-64 yearsDenmark 28.5 Hungary 28.0 Belgium 17.9 France 17.6 Finland 17.5 Austria 17.4 Switzerland 17.0 Sweden 15.4 Germany 12.9 Norway 12.0 Netherlands 10.9 New Zealand 7.7Ireland 7.7 Australia 6.9 USA 6.8 Italy 6.8 Scotland 6.7 Canada 6.4 Portugal 6.2 Spain 6.0 N Ireland 4.8 Engl/Wales 4.7 Greece 2.4 65-74 yearsHungary 37.6 Denmark 31.5 Belgium 23.5 Switzerland 19.8 Austria 18.5 France 17.9 Germany 16.7 Sweden 13.5 Finland 13.3 Norway 12.4 Netherlands 10.4 Spain 8.8Portugal 8.1 Italy 8.0 New Zealand 6.6 Australia 6.6 Ireland 6.4 Scotland 6.4 USA 6.2 Canada 6.1 Engl/Wales 5.2 N Ireland 3.9 Greece 2.875+ yearsHungary 67.3 Denmark 30.2 Austria 28.5 Germany 26.4 France 25.3Belgium 24.2 Switzerland 23.0 Sweden 14.2 Portugal 12.2 Netherlands 12.1Spain 11.9 Finland 9.6 Italy 9.3 Norway 9.2 Australia 8.0Scotland 6.0 USA 6.0 Engl/Wales 5.9 Canada 4.7 New Zealand 4.3 Greece 3.4 Ireland 3.0 N Ireland 2.5Back to text

Christopher H Cantor · Kerryn Neulinger

Health Care Establishing a collaborative service model for primary mental health care A collaborative project between general practitioners and mental health services, which links a consultation-liaison model with shared care, was piloted with success. This article provides a broad overview of the service model and the stages in its development. Graham N Meadows MJA 1998; 168: 162-165 Introduction - History of the CLIPP service - Activity of the service - Benefits and costs - Summary and prospects - Acknowledgements - References - Authors' details - - More articles on Psychiatry Introduction Improving collaboration between mental health services and general practitioners in caring for people with serious mental illness is an aim of Commonwealth Government policy.1,2 Recent documents examining the psychiatry workforce have also recommended stronger links between specialist and generalist services in this area.3-5 Mental health care needs may often be more appropriately met by general practitioners than by long term specialist care. This will be true for many patients with anxiety disorders and depression, but also for selected patients with psychotic disorders. General practitioner involvement with people with continuing mental illness may also provide an opportunity to address unmet physical health needs,6 and may ultimately have an impact on the high rates of physical morbidity and mortality associated with major mental disorder.7Various models of consultation-liaison links between psychiatric services and GPs have been described in reports from the United Kingdom.8-11 Although this area of activity in Britain was described as "the silent growth of a new service" in 1984,12 a more recent review noted that many such schemes had not proceeded beyond pilot phase. This review stressed the need for further evaluations, including cost-benefit evaluation, in response to this situation.13 In Australia, a pilot scheme in Newcastle, New South Wales, providing consultation-liaison attachments to GPs was initially reported positively,14 but a later viewpoint paper alluded to less encouraging aspects, and the project did not move beyond pilot phase.15 A recent survey of psychiatrists in South Australia suggests considerable enthusiasm for collaboration in consultation-liaison models,16 but revealed little actual activity in this area. The Consultation Liaison in Primary Care Psychiatry (CLIPP) service model developed in the Northwest Melbourne Area Mental Health Service promotes collaboration between GPs and public mental health services in managing psychiatric problems. CLIPP is now established, with recurrent funding from State public mental health services, and is being extended into another area mental health service. This article describes the CLIPP model and the activity involved in ensuring its continuation beyond the pilot phase. History of the CLIPP service In 1993, Health and Community Services Victoria received Federal Government National Mental Health Initiative funding expressly for promoting shared care initiatives in mental health. Early in 1994, staff of the Northwest Melbourne Area Mental Health Service and local GPs (represented by the Division of General Practice) proposed a pilot project, for which they were granted $97 000 over two years. These funds supported a half-time psychiatric nurse case manager for 18 months and most of the cost of a half-time psychologist project officer for two years. The area mental health service contributed about four half-day sessions per week of psychiatrist time. Consultation-liaison attachments, although they are well liked and help to improve GP confidence, have been criticised as doing little to enhance GPs' involvement with the care of the seriously mentally ill.15 Shared care arrangements for specific patients with serious mental disorder may result in GPs feeling that public mental health services are not helping them with the types of problems they see most frequently. We aimed to counter these problems by combining the two approaches. Consultation-liaison attachments were set up first. General practitioners were recruited by mail through the Division. Interested GPs were followed up with personal visits by project staff, then with fortnightly visits by a psychiatrist to each practice (similar to the British "liaison-attachment" model9). Details of the consultation-liaison attachment system are shown in Box 1. Three months after setting up these attachments, shared care was initiated by asking participating GPs to accept patients referred from the area mental health service. At this point, the number of psychiatrist consultation appointments for patients referred by GPs was generally reduced to two each session to allow time for discussion of the shared care patients referred from the area health service. Operation of the shared care system is described in Box 2. During 1995, consultation-liaison attachments were set up with seven group practices of between two and 12 GPs. By late 1995, all of these practices were accepting patients transferred from the area mental heath service. The CLIPP service was recognised by a National Mental Health Achievement Award in 1996, in the category of prevention and health promotion. The project was reported to Health and Community Services Victoria, with an account of the development, and a cost-benefit analysis supported by work carried out in the area mental health service.17 Activity of the service During its first two years, CLIPP provided care to over 220 patients through the clinical consultation-liaison service, patients having been referred by 31 of the 40 GPs from the seven participating group practices. It has facilitated the transfer of over 90 clients from the area mental health service into shared care with 28 GPs, including GPs from each participating practice. Box 3 lists the clinical diagnoses of the patients in these two groups. The most common single impediment to the transfer of care to GPs -- affecting about 15 patients -- is drug costs. Some regimens are free to patients under area mental health service care, but prohibitively expensive (under the Pharmaceutical Benefits Scheme) for others. A change to a rebated alternative drug may sometimes remove this impediment, but is not always clinically appropriate. One partial solution would be for a GP to see patients every two to four weeks for clinical monitoring, while the psychiatrist sees them around six-monthly, prescribing through the area mental health service pharmacy. Among patients transferred to GPs, telephone follow-up by area mental health service staff has found that 90% report being satisfied with their management. One year after transfer to GP care, 60% felt their physical health care had improved with the increased GP input. In some 20% of cases, review of GP case notes showed that newly identified physical health problems had been treated. Two patients whose care was transferred to GPs died of natural causes. No other cases have so far been lost to follow-up. An unexpected referral route developed during the pilot phase of the service, with public community mental health services making one or two referrals a month to GPs working with CLIPP. This is appropriate for patients who present directly to these specialist services, but whose needs could be as well, or better, met in this augmented primary care model. Benefits and costs The pilot project was reported to Human Services Victoria in June 1996. While the clinical service had been running for little over a year, and was hardly ready for summative evaluation, the following benefits could be claimed on the basis of a combination of qualitative and quantitative data. The model: provides a large number of courses of GP care, with (through consultation-liaison attachments) specialist assessment and supervision; provides a valued educational opportunity for interested GPs; complements general practice care with systematic monitoring and community outreach (provided by the area mental health service) when necessary. This augments the capacity of GPs to provide care to individuals with continuing mental disorder; allows area mental health care to be provided locally and with more flexibility; shows high levels of consumer acceptability; and promotes the physical health of clients transferred to GPs. A detailed cost-effectiveness report of the project is in press.18 Costing analyses included projecting estimates of the activity of the service forward up to two years, and examining the projected cost effectiveness that could be reasonably expected from the service over that time. A simplified version of this analysis can be rendered as follows. The total cost of the CLIPP service was compared with the cost of providing care through area mental health services for the 110 patients in CLIPP who would otherwise have been cared for in the area mental health service. This group comprised 90 patients transferred from the area mental health service to GPs, 10 patients seen in the consultation-liaison attachments who would otherwise have had their care transferred to the area mental health service, and 10 patients diverted from triage at the area mental health service to GPs. Two patterns of area mental health service care that would otherwise have been required for the patients transferred into shared care through CLIPP were identified. These were 1-25 community service contacts per year, and 25-50 such contacts per year. The median cost per case for area mental health service care was estimated to be $623 and $2261 per annum, respectively.17 The 110 patients transferred to the CLIPP service were estimated to have originated from these two groups in a ratio of 4:1 (88 patients at $623 and 22 patients at $2261 per annum). From these estimates, the annual costs of mental health service care for the 110 patients transferred to GPs within CLIPP is $104 566. By comparison, the total cost of the CLIPP program (including the cost of staff initally funded through the Commonwealth Government grant, and psychiatrists whose time was committed from area mental health service budgets) was estimated at within $1000 of this sum. Hence, the model can be argued to be cost neutral for the area mental health service, but with the advantages to patients described earlier. The evaluation report was positively received by Human Services Victoria. In late 1996, commitment was made to continue funding for the project through the Western Region of Human Services Victoria, and extended to developing another project along similar lines in a nearby area of metropolitan Melbourne. Further development of the service is now an active process of participation between Western Region as purchasers and the Western Health Care Network as providers, with the support of academic staff from the University of Melbourne. Summary and prospects It has been previously shown that GP consultation-liaison services can be implemented in Australia.14 In the CLIPP model, the strengths of the relationships established through consultation-liaison links have been harnessed in support of effective shared care. Combining these two activities means that a cost-effectiveness case can be presented which is more convincing than that for a consultation-liaison service alone. Experience of this development suggests that, if such schemes are to continue, they need to meet the needs and expectations of all stakeholders with purchaser and provider roles -- GPs, patients, case managers, psychiatrists, and mental health service managers. Current plans for further development of the CLIPP model include use of computer-based reminder systems to support GPs in managing transferred patients, and providing periodic group education sessions for participating GPs. Over the next three years, CLIPP will provide the setting for a Commonwealth Department of Health and Family Services examination of process and outcome in shared care (General Practice Evaluation Program Grant 518). The new study uses a quasi-experimental design to compare processes and outcomes of care in the shared care setting with those in a community mental health service. Further systematic analysis of the consultation-liaison service is under way. This will include description of GP referral patterns, management suggestions from psychiatrists, determinants of outcomes, and a further cost-benefit analysis. I believe CLIPP to be a very useful model for improving collaboration between GPs and psychiatric services. It has allowed a diverse group of practitioners to work together in ways that transcend funding and organisational barriers in the interests of sensible arrangements for the delivery of health care. Acknowledgements Human Services Victoria for funding through Western Metropolitan Region budgets, particularly Mr John Hedditch for support in expansion of the service. The Commonwealth Government for funding through Mental Health Initiative funding and General Practice Divisional resources; also, Dr Philip Hegerty of the Northwest Division, Dr Bob Long, and the many other GPs involved. The project team from the Northwest Area mental health services: Dr Lynette Joubert, Mr Guy Dobson, Dr Carol Harvey, Dr Rajeev Kumar, Dr Philip Price, and Dr Michael Wong. Western Health Care Network management staff, particularly Mr George Shaw, for support. Mr Paul Mcrone, health economist at the Institute of Psychiatry, London, for assistance with cost-benefit analyses. References Australian Health Ministers' Advisory Council. National mental health plan. Canberra: AGPS, April 1992. Commonwealth Department of Human Services and Health. Better health outcomes for Australians: national goals, targets and strategies for better health outcomes into the next century. Canberra: AGPS, 1994. Solomon S and Associates, Buckingham B and Associates, Epstein M. Report of consultancy for the mental health workforce committee on medical workforce financing arrangements. Melbourne: The Associates, 1993. McKay B and Associates. Proposals for change final report: optimum supply and effective use of psychiatrists. Canberra: Bernie McKay and Associates, 1996. McKay B and Associates. Issues and options supplementary paper: optimum supply and effective use of psychiatrists: Canberra: Bernie McKay and Associates, 1996. Brugha TS, Wing JK, Smith BL. Physical health of the long term mentally ill in the community. Is there unmet need? Br J Psychiatry 1988; 155: 777-781. Allebeck P. Schizophrenia: a life shortening disease. Schizophrenia Bull 1989; 15: 81-89. Strathdee G, King M. The interface between primary and secondary psychiatric care. In: Williams P, Wilkinson G, Rawmsley K, editors. The scope of epidemiological psychiatry: Essays in honour of Michael Shepherd. London: Routledge, 1989: 420-433. Creed F, Marks B. Liaison psychiatry in general practice: a comparison of the liaison-attachment scheme and shifted outpatient models. J R Coll Gen Pract 1989; 39: 514-517. Strathdee G, McDonald E. Innovations: establishing psychiatric attachments to general practice: a six stage plan. Psychiatr Bull 1992; 154: 72-76. Strathdee G. Psychiatrists in primary care: the general practitioner viewpoint. Fam Pract 1988; 5: 111-115. Strathdee G, Williams P. A survey of psychiatrists in primary care: the silent growth of a new service. J R Coll Gen Pract 1984; 34: 615-618. Gask L, Sibbald B, Creed F. Evaluating models of working at the interface between mental health services and primary care. Br J Psychiatry 1997; 170: 6-11. Carr VJ, Donovan P. Psychiatry in general practice: a pilot scheme using the liaison-attachment model. Med J Aust 1992; 156: 379-382. Carr VJ, Reid ALA. Seeking solutions for mental health problems in general practice. Med J Aust 1996; 165: 435-436. Barber R, Williams AS. Psychiatrists working in primary care: a survey of general practitioners' attitude. Aust N Z J Psychiatry 1996; 30: 278-286. Meadows G, Gielewski H, Falconer B, et al. The pattern of care model: a tool for planning community mental health services. Psychiatr Serv 1997; 48: 218-223. Meadows G, Joubert L, Mcrone P, Dobson G. Consultation, collaboration and cost effectiveness: reflections on four years of shared care in Melbourne. In: Ellis P, editor. Community care -- working together. Proceedings of the Geigy Psychiatric Symposium; 1997 Dec 3-5; Wellington, New Zealand. Sydney: Novartis. In press. Received 1 Sep, accepted 22 Dec, 1997 Authors' details Department of Psychiatry, University of Melbourne, Royal Park Hospital, Melbourne, VIC. Graham N Meadows, MRCP(UK), FRANZCP, Senior Lecturer. Reprints: Dr G N Meadows, Department of Psychiatry, University of Melbourne, Royal Park Hospital, Private Bag 3, PO Parkville, VIC 3052. E-mail: g.meadowsATmedicine.unimelb.edu.au 1: Format for consultation-liaison attachments in the CLIPP project Psychiatrists provide consultation services for any patient referred by GPs. This service is provided at the general practice clinic. For group practices, visits are usually fortnightly, and 2-3 patients are seen per consultation Specific forms, which include a global impression rating by the GPs, are used to document the consultancy request from the GPs and responses by psychiatrists; follow-up forms are completed by GPs after three months, and include a repeat of the previous global impression rating and a change score. These forms are complemented by face-to-face discussion between GPs and psychiatrists during the fortnightly consultation at the GP's clinic, during which any patient can be discussed, including those not seen personally by the psychiatrist. Psychiatrist consultations are generally specifically intended to leave continuing care of each patient with the GP. General practitioners have been remunerated at the hourly rate for "Divisional activities by GPs" through a Divisional seeding grant for time spent in discussion with psychiatrists. The Royal Australian College of General Practitioners recognises this activity as continuing medical education, and awards two CME points per hour, or one point per patient referred. Back to text 2: Format for shared care in the CLIPP project Case managers within the area mental health service identify candidate patients -- typically clinically stable, without recent relapse, with fair to good insight, and with some social support. Patients are referred to the CLIPP nurse, who prepares the transfer. A concise summary of diagnosis, history, and treatment adherence is prepared from the case notes. Impediments to transfer are identified and acted upon where possible; the outcome of this action is recorded. The CLIPP nurse drafts a management plan and arranges a first CLIPP appointment, at which the GP, psychiatrist and patient discuss the draft and establish the plan for continuing management. The GP takes over the primary responsibility for the care of the patient. A patient registration and tracking system maintained by area mental health service staff supports the GP in maintaining continuity of care and provides information about satisfaction and other quality assurance. As part of this tracking system, an administrator maintains an electronic diary of due dates for review of each patient. Clinical staff then review patients three-monthly by telephone contact with the patient and by checking the GP's case notes for continued contact. Management plans usually also recommend that psychiatrists review patients every 6-12 months. Back to text 3: Diagnoses of CLIPP service patients, by origin of referralBroad diagnostic category*Consultation- liaison referralsReferrals from mental health service to GPsDepression and dysthymia105 12Adjustment disorder40--Anxiety disorders281Problems related to substance abuse11--Schizophrenia856No diagnosis8Bipolar disorder711Eating disorder4--Pain disorder3 --Axis ii (personality disorder) diagnosis only2--Delusional disorder12Somatoform disorder1--Dementia of Alzheimer type1--Dissociative fugue1--Medication-induced movement disorder1--Schizoaffective disorder--10Brief psychosis--1Totals22193* From Diagnostic and statistical manual of mental disorders, fourth edition. Washington, DC: American Psychiatric Association, 1994. Back to text

Graham N Meadows

Editorial Meeting the challenge of adolescent mental health For about one in five teenagers, emotional difficulties are more than a passing phase MJA 1997; 166: 399-400 Since the turn of the century, when the prominent American psychologist G Stanley Hall first described adolescence as a discrete developmental phase, emotional turmoil has been a part of popular conceptions of youth.1 Emotional and behavioural difficulties that would elicit concern at other times in life have been viewed as part of growing up, with an assumption that the adoption of adult social roles in the early twenties would bring emotional control and a "maturing out" of adolescent difficulties. In this context an apparent long neglect of adolescent mental health seems understandable. Views on adolescence and adolescent mental health have recently shifted. Puberty undoubtedly brings adjustments to physical maturity, changing roles within families and with peers, and the emergence of a more independent lifestyle. Most young people negotiate these changes without upheaval. By and large, they also avoid extremes in early experimentation with alcohol and recreational drugs, dieting and sexual activity.2 Given this more sanguine perspective on adolescent development, emerging concerns about adolescent mental health seem at first sight unwarranted. However, around one in five adolescents do pass through a more prolonged phase of emotional difficulties in which experiences of depression and anxiety are common.3 There is evidence that such difficulties have become commoner. Surveys of adults in several Western countries suggest that cohorts since World War II have higher rates of adolescent-onset psychiatric problems. North American studies, for example, have indicated up to a tenfold rise in rates of adolescent depression in more recently born groups.4 As a consequence, the late teens and early twenties appear to be the period of peak incidence for depression.5 Adolescent mental health has assumed importance for other reasons. One derives from the continuities between adolescent and adult psychopathology. Prospective studies indicate that adolescent depression, far from subsiding in early adulthood, substantially elevates the risk of a later disorder.6 A second reason lies in links between mental health and other indices of adolescent health status. Trends in health-damaging behaviour parallel those in adolescent mental health problems. The age of onset of alcohol and substance abuse and sexual risk behaviours has fallen, so that they have joined eating disorders and deliberate self-harm as adolescent health concerns. These parallel trends have prompted questions about possible causal links between adolescent mental health and behavioural problems. Such a link is probably clearest for suicidal behaviour, in which depressive symptoms are the strongest risk factors for both fatal and non-fatal self-harm.7,8 Risks for suicidal behaviour increase with the level of depressive symptoms. For the most part, adolescent suicidal behaviour does not result from a clear intent to kill oneself. Rather, it is best understood as a maladaptive reaction to the distress, negative self-evaluation and high levels of interpersonal conflict that commonly accompany depression.9 The implications for intervention are great. Self-harming adolescents commonly experience depressive symptoms but many will fall short of meeting criteria for depressive disorder. Preventive and clinical intervention efforts should therefore be broad-based and not restricted to those with a florid mental disorder. For this reason, "population-based" interventions aimed at promoting well-being and reducing depressive symptoms across a whole population, rather than focusing on those at highest risk, seem an attractive but neglected avenue for the prevention of suicidal behaviour.10 Adolescent psychopathology has been linked to other health-damaging behaviours.11,12 Depressive and anxiety symptoms are associated with adolescent alcohol and substance abuse, and their presence predicts progression to dependent patterns of consumption.13 Extreme weight control behaviours,14 adolescent smoking15 and early teenage pregnancy16 are among other behaviours associated with psychological disorders. Clarification of the underlying risk processes may offer strategies for intervention. Self-medication to relieve emotional distress may explain associations with smoking, alcohol and substance abuse, and points to a need to learn alternative means of dealing with emotional distress.15 Susceptibility to peer influences may be another explanation. Loss of self-confidence and social anxiety, which commonly accompany depression, may bring a greater readiness to adopt peer attitudes and behaviours as a means of engaging with a social group. In some instances, where psychopathology and health-damaging behaviour share a common origin, intervention may best focus on antecedent familial or social circumstances. Whatever the risk process, successful interventions for adolescent mental health problems are likely to bring other health benefits. The emerging importance of adolescent mental health carries implications for adolescent health care and health promotion. Within psychiatry this has been recognised in calls for a greater emphasis on the management of adolescent onset disorders.17 However, psychiatric services can deal only with a minority of adolescents with common disorders such as depression and anxiety, so responsibility for early recognition and treatment rests more broadly. General practitioners are likely to play a major role. This has been recognised in the National Health and Medical Research Council guidelines for the treatment of adolescent depression, which are accompanied by guidelines for the general practitioner in the psychological and medical management of adolescent depression.18 These skills are likely to play a central role in dealing with adolescent behavioural problems such as substance abuse, and, when dealing with associated emotional problems, may do much to prevent progression to dependent patterns of use. Meeting the challenge of adolescent mental health must ultimately extend to preventive action. Interventions to support families, schools, youth and community organisations in the creation of social environments which promote mental health and well-being should bring gains in adolescent mental health, which in turn are likely to bring diverse health benefits. George C Patton Associate Professor in Adolescent Psychiatry Centre for Adolescent Health, Department of Paediatrics University of Melbourne, VIC Hall GS. Adolescence: Its psychology and its relations to physiology, anthropology, sociology, sex, crime, religion and education. London: Sidney Appleton, 1905. Hibbert M, Caust J, Patton G, et al. The health of young people in Victoria. Melbourne: Centre for Adolescent Health, 1996. Offer D, Schonert-Reichl KA. Debunking the myths of adolescence: findings from recent research. J Am Acad Child Adolesc Psychiatry 1992; 31: 1003-1014. Burke KC, Burke JD Jr, Rae DS, Regier DA. Comparing age at onset of major depression and other psychiatric disorders by birth cohorts in five US community populations. Arch Gen Psychiatry 1991; 48: 789-795. 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. Harrington R. The natural history and treatment of child and adolescent affective /disorders. J Child Psychol Psychiat 1992; 33: 1287-1302. Patton GC, Harris R, Carlin JB, et al. Adolescent suicidal behaviours: a population based study of risk. Psychol Med 1997; 27. In press. Brent DA. Depression and suicide in children and adolescents. Pediatrics Rev 1993; 14: 380-388. Kienhorst I, de Wilde EJ, Diekstra RFW, Wolters WHG. Adolescents' image of their suicide attempt. J Am Acad Child Adolesc Psychiatry 1995; 34: 623-628. Rose G. The strategy of preventive medicine. Oxford: Oxford University Press; 1992. Fergusson DM, Horwood LJ, Lynskey MT. The comorbidities of adolescent problem behaviours: A latent class model. J Abnormal Child Psychol 1994; 22: 339-353. Feehan M, McGee R, Raja SN, Williams SM. DSM-III-R disorders in New Zealand 18-year-olds. Aust N Z J Psychiatry 1994; 28: 87-99. Jones P, Rodgers B, Murray R, Marmot M. Child developmental risk factors for adult schizophrenia in the British 1946 birth cohort. Lancet 1994; 344: 1398-1402. Patton GC, Carlin JB, Shao Q, et al. Adolescent dieting: health weight control or borderline eating disorder? J Child Psychol Psychiatry 1997; 38: 299-306. Patton GC, Hibbert MH, Rosier MJ, et al. Is smoking associated with depression and anxiety in teenagers? Am J Pub Health 1996; 86: 225-300. Kovacs M, Krol RS, Voti L. Early psychopathology and risk for teenage pregnancy among clinically referred girls. J Am Acad Child Adolesc Psychiatry 1994; 33: 106-114. McGorry P. The Centre for Young People's Mental Health: blending epidemiology and developmental psychiatry. Australasian Psychiatry 1996; 4: 243-247. Quality of Care and Health Outcomes Committee. Clinical practice guidelines: depression in young people. Canberra: NHMRC, 1997. © 1999 Medical Journal of Australia.

George C Patton

Clinical Practice The role of the general practitioner in the treatment of schizophrenia: specific issues This article provides practical guidelines for general practitioners in treating schizophrenia. Specific areas include pharmacological treatment, supportive therapy, depression and suicide, alcohol and drug abuse, sexuality, and physical health. Vaughan J Carr MJA 1997; 166: 143-146 Introduction - Drug therapy - Supportive therapy - Depression and suicide - Alcohol and drug abuse - Sexuality - Physical health - Conclusion - Acknowledgements - References - Authors' details - - More articles on Psychiatry This is the second in a two-part series. The first article was published in the MJA 20 January 1997 issue. Introduction This second paper in this series deals with more specific issues in the primary care treatment of patients with schizophrenia, and attempts to clarify the roles of general practitioners (GPs) and specialist services, highlighting the areas which may be especially well provided by GPs. Practical guidelines are provided in the Box. Drug therapy Systematic accounts of the drug treatment of schizophrenia are available,1,2 and only matters particularly relevant to GPs will be covered here. Antipsychotic drugs are still chosen mostly on the basis of side effects. Low potency drugs (e.g., chlorpromazine, thioridazine) are more likely to produce sedation, postural hypotension and anticholinergic side effects, while higher potency drugs (e.g., haloperidol, fluphenazine) tend to cause more extrapyramidal side effects, such as parkinsonism, acute dystonia and akathisia. Some newer drugs (e.g., risperidone) are said to be more benign in their side effect profile; further use and investigation may bear this out. Clozapine seems unique in having marked benefits for about one-third of otherwise "treatment resistant" patients; this drug is subject to stringent controls because of the associated risk of agranulocytosis. Antipsychotic drugs are only partially effective in controlling psychotic symptoms. Up to 30% of patients on maintenance drug treatment relapse within two years3 -- this is not entirely explained by poor compliance. A third or more of schizophrenic patients taking antipsychotic drugs continue to experience delusions and/or hallucinations, usually in attenuated form.4,5 Therefore, when psychotic symptoms persist after two or more antipsychotic drugs have been taken (separately), in adequate doses, for a cumulative total of 12 months, measures other than drug treatment are necessary. Firstly, factors that may be contributing to persistent symptoms (e.g., drug or alcohol abuse, relationship problems) should be identified and dealt with if possible, usually by a specialist. Secondly, where appropriate, effective non-pharmacological treatment strategies should be added to a suitable drug regimen. Several individual psychological (e.g., cognitive behaviour therapies) and family-oriented (e.g., training in problem-solving skills) interventions are available. These require specialist expertise, and GPs can be instrumental in locating appropriate providers of these treatments. With very few exceptions, only one antipsychotic drug should be used at a time. The dose should be the minimum required to maintain remission, and side effects should be absent or minimal. Excessive doses of antipsychotic drugs augment negative symptoms, impair cognitive function, mimic depression, undermine compliance by causing dysphoria and discomfort, produce higher rates of side effects that contribute to stigmatisation by rendering the patient more conspicuous, and can cause irreversible complications (e.g., tardive dyskinesia). Overmedication also interferes with rehabilitation. GPs can monitor antipsychotic drug use to ensure that doses are not unnecessarily high. Doses of haloperidol greater than 10 mg per day (or the equivalent) are not currently justified and approximately half this amount is now recommended, even less for first psychotic episodes. Adjunctive medication (e.g., lithium, carbamazepine) should only be used on specialist advice. There is no role for long term use of benzodiazepines, although they can be useful adjuncts in acute episodes, particularly when sedating a patient in an emergency. Long term use of anticholinergic drugs for the treatment of drug-induced parkinsonism should be avoided as they may mask the signs of tardive dyskinesia and impair cognitive function. The relapse signature: Patients and their families should be encouraged to monitor the patient's symptoms in association with GPs and specialist services. Each patient is said to have a unique relapse "signature"6 -- a sequential emergence of symptoms and signs which herald an impending relapse. There is often a "window" of 2-4 weeks in which such early warning signs appear,6 signalling the need to increase doses of antipsychotic drugs to prevent relapse. GPs should review with patients their typical sequence of warning signs so that they can correctly interpret them and make timely adjustments to the drug regimen. Non-compliance with medication is inevitable at some stage in most patients' treatment. It is said that 80% of patients are non-compliant with medication 40%-80% of the time.7 Reasons for this include medication side effects, complex dosing schedules, stigma, lack of knowledge or false beliefs about medication, and poor insight or denial of illness.7,8 Some patients reason that stopping medication will signify they are not ill.8 Some patients may prefer the psychotic state, either because of certain rewards from being ill (secondary gain) or difficulties in coping with normal expectations and responsibilities.8 Non-compliance may occasionally be an attempt to assert control or a manifestation of rebellion. Dealing with non-compliance requires a good working relationship, incorporating sound education about the illness and its management. Keeping dosing schedules simple and eliminating side effects are important strategies. Asking about medication and reasons for non-compliance in a non-judgemental way will encourage disclosure. One useful strategy is to assume episodic non-compliance and openly regard each occasion as a learning opportunity for the patient. Involving the patient in drug management, including allowing limited self-regulation of doses,8 together with self-monitoring of symptoms, will benefit the patient. Simply resorting to depot medications undermines the patient's collaborative role in health care. Arranging for medication to be taken under supervision, which is fraught with potential conflict, or seeking legal means of enforcing drug administration (e.g., community treatment orders), should only be a last resort. Supportive therapy GPs, preferably in conjunction with specialist services, can provide supportive therapeutic relationships which predict good outcomes in schizophrenia.9 In general, realistic goals should be set, which include protecting vulnerabilities, minimising stress and strengthening adaptive capabilities.8 Initial supportive techniques of reassurance, explanation and the opportunity for airing emotion can progressively incorporate education about the illness and its management, clarification of patients' "relapse signatures", the role of medication, and attention to daily living skills, social and occupational functioning. Counselling by GPs can help patients learn simple stress management techniques, anxiety control strategies and problem-solving skills for coping with non-psychotic (e.g., social) anxiety and depression linked to relationship problems or stressful life events. GPs should supplement self-monitoring of symptoms by examining patients' mental state at each appointment. This includes assessment of the status of psychotic symptoms and, although it is important not to dwell excessively on these, GPs should not avoid asking such questions as: Do your beliefs about . . . continue to trouble you?; or Have you been hearing voices in the past few weeks? Are you able to ignore them? What have you found helpful when they occur? Patients with schizophrenia learn three kinds of palliative coping techniques to deal with psychotic and other symptoms:10 cognitive control (e.g., reappraisal, self-instruction, acceptance, manipulation of attention); behavioural control or the generation and implementation of action alternatives (e.g., increased or decreased activity, diversion, withdrawal from stimulation, altered arousal); and social support recruitment. They can be helped to identify their usual coping techniques, modify and extend them. GPs can encourage patients to practise these by imagining they have a particular symptom and then implementing an identified coping strategy. Such rehearsal of coping skills may facilitate their successful transfer to everyday settings. Families of schizophrenic patients need support and GPs can provide education, aided by various leaflets and other publications on schizophrenia which are now readily available. GPs can also provide explanation, reassurance, advice and the opportunity to air emotional distress (especially anger, shame, sadness and guilt). Specialist services can provide various forms of more specific family counselling and education on schizophrenia. Schizophrenia is usually a prolonged illness of relapses and remissions, but the eventual outcome is better than was previously thought -- most patients make a good long-term social recovery (i.e., improved social relationships and self-care abilities).11 The early years are crucial in determining the patient's ultimate level of function and substantial gains may take years to become apparent. Depression and suicide Depressive symptoms are common in schizophrenia, especially during recovery after an acute psychotic episode (postpsychotic depressive disorder). However, it can be difficult to distinguish between the almost ubiquitous low level depressive symptoms in schizophrenia and a major depressive syndrome that will require specific treatment. The negative symptoms of schizophrenia and the effects of antipsychotic drugs can both mimic depression. Nevertheless, discerning clinicians can diagnose a major depressive episode. A specialist referral to help confirm the diagnosis may be required. Depressive disorders in schizophrenic patients can be treated as for similar conditions in other patients, including the use of antidepressant medication. The risk of such drugs triggering relapse of schizophrenic symptoms is small. Major risks include the risk of suicide by overdose, and appropriate precautions should be taken to guard against this. A course of antidepressant drugs at recommended daily doses can be added to the antipsychotic drug regimen for 6-12 months, together with whatever psychotherapeutic assistance is indicated. Between 10% and 13% of schizophrenic patients commit suicide,12 mostly during the first 10 years of the illness. There are no reliable guidelines for predicting and preventing suicide in these patients. The schizophrenic patient more likely to commit suicide is a young, single, unemployed, socially isolated man whose illness is marked by numerous exacerbations and hospital admissions for psychosis.12 He often has a past history of depression and/or attempted suicide, and perhaps a non-delusional, demoralising awareness of his deterioration, which is particularly acute if he has previously had some higher education and realises that his family's expectations and his own ambitions are unlikely to be fulfilled. Sensitive enquiry may reveal considerable underlying emotional distress with depressive symptoms, accompanied by feelings of hopelessness and inadequacy. If a GP recognises something like this pattern in a patient, then a thorough assessment should be undertaken and an urgent specialist referral should be made if the GP is concerned about the patient's risk of suicide. Alcohol and drug abuse In an Australian sample of 194 patients, we estimated that the six-month prevalence of alcohol or drug abuse or dependence in schizophrenic patients treated by community mental health services was 26.8% and the lifetime rate was 59.8% (unpublished data). Apart from tobacco and caffeine, the commonest substance abused was alcohol, followed by cannabis and amphetamines. Up to 74% smoked cigarettes and 40% smoked more than 40 cigarettes daily; 17% consumed more than 600 g of caffeine daily. Substance abuse in schizophrenia is increasing,13 is more common in young men with antisocial characteristics, and has been linked to poor compliance with treatment, increased hospital admissions, depression, suicide, assaultive behaviour, instability of accommodation and homelessness. In addition, alcohol and cannabis have both been associated with increased positive symptoms of schizophrenia.14,15Detecting substance abuse in schizophrenia is the first priority. GPs should use non-judgemental enquiry to become thoroughly familiar with the patient's current and past pattern of drug use, including tobacco, caffeine and alcohol, gauging the quantity, frequency and context of use. An undetected alcohol or drug problem should be suspected in patients who respond poorly to treatment. If necessary, a referral can be made to mental health services with special therapeutic programs for psychiatric and substance abuse comorbidity. If alcohol or drug abuse is detected in patients during remission, even when no immediate adverse consequences are apparent, the GP should first attempt to determine the patient's reasons for using those substances. The patient can then be informed in a matter-of-fact way about their detrimental effects on schizophrenia and general health, highlighting the extent to which alcohol, cannabis and amphetamines worsen psychotic symptoms and lead to relapse. The difficulty is that this information may not match the selective recollection of patients, who may even report certain benefits from using drugs. It is preferable not to argue, but to point out that all substances, including therapeutic agents, have a certain "margin of safety" between desired effects and adverse consequences, but that the "margin of safety" for some drugs is much narrower than others. Having indicated that complete abstinence is the safest course of action, a harm minimisation approach can be negotiated as a satisfactory compromise. A series of short-term achievable goals can be identified in sequence, including aiming to control levels of consumption (including issues of safe needle use, where relevant), then moving on to goals for reducing consumption, incorporating strategies for preventing relapse and parting from the alcohol and drug culture. Simultaneously, the GP can attend to factors that may be contributing to the patient's substance use, including resolution of interpersonal and practical problems (e.g., money, accommodation), with the help of other agencies if necessary, and encourage the development of additional coping skills and the pursuit of other interests. Sexuality There are very few systematically collected data about sexual functioning of schizophrenic patients. Their fertility rates are increasing,16 and schizophrenic women can be at increased risk of sexual exploitation and abuse.17 For patients with schizophrenia, sexual fulfilment contributes to self-esteem and well-being, and psychosexual function and capacity for intimacy are important prognostic factors. However, antipsychotic drugs can interfere with sexual activity and inappropriate sexual behaviours caused by the illness can lead to ostracism and loneliness. GPs should enquire about patients' relationships, sexual behaviours, sexual orientation, knowledge of sexuality and reproduction, need for contraception, and understanding of safe-sex practices. It can also be helpful to ascertain whether the patient experiences any sexual dysfunction, which is common,18 but not always due to medication, and ensure that the patient is informed about sexually transmitted diseases where necessary. Specific interventions may be appropriate. Physical health Patients with schizophrenia often have high rates of concurrent physical illness,19,20 especially cardiovascular and respiratory diseases.21 Among the risk factors for physical ill-health are smoking, alcohol and drug use, antipsychotic drugs, poor nutrition and hygiene, obesity, sedentary lifestyle, poverty and social isolation. Schizophrenic patients should be examined six-monthly for side effects and complications of antipsychotic drug use. Akathisia can be detected by observing the patient at rest, both seated and standing, and asking whether there are any subjective feelings of restlessness (especially in the legs)22 which may be present in the absence of objective signs. Observations of gait and posture will enable the characteristic tremor and bradykinesia of parkinsonism to be detected, while passive flexion and extension of the upper limbs will reveal cog-wheel rigidity.23 Examination for tardive dyskinesia can be conducted using the readily available Abnormal Involuntary Movement Scale (AIMS), which facilitates detection and quantification of the variety of orobuccal and choreoathetoid limb movements possible in this condition.24 Parkinsonism and akathisia should be dealt with by a reduction in the dose of antipsychotic drugs or by changing to a lower-potency drug. Anticholinergic agents should only be used in the short term for parkinsonism and are ineffective for akathisia; the latter can sometimes be controlled with propranolol. There is no effective treatment for tardive dyskinesia and decisions about its management should be made in consultation with a psychiatrist or other specialist. Patients over the age of 40 require an annual physical (and dental) examination, including measurement of blood pressure, examination of the cardiovascular and respiratory systems and skin, assessment of drug side effects, and urinalysis.25 This can also provide an opportunity for a systems review to help detect symptoms which patients may not report spontaneously. Thyroid function, full blood count and erythrocyte sedimentation rate should be determined. Vision and hearing can be checked, and a chest x-ray and electrocardiogram ordered25 if there is any indication of cardiovascular or respiratory disease. Breast examination and Pap smear in women should be performed as indicated for the general female population. Conclusion Although the long-term treatment of schizophrenia is multimodal and multidisciplinary, GPs are in a position to take an active, even central, role in the care of patients with this illness. Models of "shared care" for schizophrenia involving GPs as integral members of the treatment team are just beginning to be established. If they live up to their promise they will provide significant improvements in the comprehensive care of schizophrenic patients. To function effectively in this context most GPs will require some initial training and continuing education. Acknowledgements I am grateful to Associate Professor Patrick McGorry and Drs Peter Hopkins, Brian Masters, Steve Robinson and Tony Ryan for their comments on earlier drafts of this paper. References Keks NA, Kulkarni J, Copolov DL. Treatment of schizophrenia. Med J Aust 1989; 151: 462-467. Kane JM. Schizophrenia. N Engl J Med 1996; 334: 34-41. Davis J. Overview: maintenance therapy in psychiatry: I. Schizophrenia. Am J Psychiatry 1975; 132: 1237-1245. Silverstein ML, Harrow M. First-rank symptoms in the postacute schizophrenic: a follow-up study. Am J Psychiatry 1978; 135: 1481-1486. Johnstone EC, Owens DGC, Gold A, et al. Schizophrenic patients discharged from hospital: a follow-up study. Br J Psychiatry 1984; 145: 586-590. Birchwood M, Macmillan F, Smith J. Early intervention. In: Birchwood M, Tarrier N, editors. Innovations in the psychological management of schizophrenia. Assessment, treatment and services. Chichester: John Wiley & Sons, 1992: 115-145. Van Kammen DP, Marder SR. Dopamine receptor antagonists. In: Kaplan HI, Sadock BJ, editors. Comprehensive textbook of psychiatry. 6th ed. Baltimore: Williams & Wilkins, 1995: 1987-2022. Fenton WS, McGlashan TH. Schizophrenia: individual psychotherapy. In: Kaplan HI, Sadock BJ, editors. Comprehensive textbook of psychiatry. 6th ed. Baltimore: Williams & Wilkins, 1995: 1007-1018. Frank AF, Gunderson JG. The role of the therapeutic alliance in the treatment of schizophrenia: relationship to course and outcome. Arch Gen Psychiatry 1990; 47: 228-236. Carr V. Patients' techniques for coping with schizophrenia: an exploratory study. Br J Med Psychol 1988; 61: 339-352. Harding CM, Zubin J, Strauss JS. Chronicity in schizophrenia: fact, partial fact, or artifact? Hosp Community Psychiatry 1987; 38: 477-485. Caldwell CB, Gottesman II. Schizophrenics kill themselves too: a review of risk factors for suicide. Schizophr Bull 1990; 16: 571-589. Cuffel BJ. Prevalence estimates of substance abuse in schizophrenia and their correlates. J Nerv Ment Dis 1992; 180: 589-592. Duke PJ, Pantelis C, Barnes TRE. South Westminster Schizophrenia Survey: alcohol use and its relation to symptoms, tardive dyskinesia and illness onset. Br J Psychiatry 1994; 164: 630-636. Linszen DH, Dingemans PM, Lentor ME. Cannabis abuse and the course of recent-onset schizophrenic disorders. Arch Gen Psychiatry 1994; 51: 273-279. Lane A, Byrne M, Mulvany F, et al. Reproductive behaviour in schizophrenia relative to other mental disorders: evidence for increased fertility in men despite decreased marital rate. Acta Psychiatr Scand 1995; 91: 222-228. Darves-Bornoz JM, Lemperiere T, Degiovanni A, Gaillard P. Sexual victimization in women with schizophrenia and bipolar disorder. Soc Psychiatry Psychiatr Epidemiol 1995; 30: 78-84. Bhui K, Puffet A, Herriot P. A survey of sexual problems amongst psychiatric inpatients. Soc Psychiatry Psychiatr Epidemiol 1995; 30: 73-77. Brugha TS, Wing JK, Smith BL. Physical health of the long-term mentally ill in the community. Is there unmet need? Br J Psychiatry 1989; 155: 777-781. Honig A, Pop P, Tan ES, et al. Physical illness in chronic psychiatric patients from a community psychiatric unit. The implications for daily practice. Br J Psychiatry 1989; 155: 58-64. Vieweg V, Pandurangi A, Levenson J, Silverman J. Medical disorders in the schizophrenic patient. Int J Psychiatry Med 1995; 25: 137-172. Barnes TRE. A rating scale for drug-induced akathisia. Br J Psychiatry 1989; 154: 672-676. Simpson GM, Angus JWS. A rating scale for extrapyramidal side effects. Acta Psychiatr Scand 1970; 212 Suppl: 11-19. Kaplan HI, Sadock BJ, Grebb JA, editors. Kaplan and Sadock's synopsis of psychiatry: behavioural science, clinical psychiatry. 7th ed. Baltimore: Williams & Wilkins, 1994: 952. Burns T, Kendrick T. Schizophrenia. In: Pullen I, Wilkinson G, Gray DP, editors. Psychiatry in general practice today. London: The Royal College of Psychiatrists and the Royal College of General Practitioners, 1994: 194-208. Authors' details Discipline of Psychiatry, Faculty of Medicine and Health Sciences, The University of Newcastle, Newcastle, NSW. Vaughan J Carr, MD, FRANZCP, Professor of Psychiatry. Reprints: Professor V J Carr, Discipline of Psychiatry, Faculty of Medicine and Health Sciences, The University of Newcastle, Callaghan, NSW 2308. 1: Practical guidelines for specific aspects of primary care for patients with schizophrenia Pharmacological treatment Antipsychotic drugs should be chosen after considering their relative side effects. Use only one antipsychotic drug at a time When symptoms persist despite compliance, consider non-pharmacological strategies Use minimum dose required for maintaining remission and avoiding side effects Monitor symptoms: identify relapse signature Explore reasons for non-compliance and regard as a learning opportunity Encourage patient's role as a collaborator Supportive therapy Develop a supportive therapeutic relationship within which you: Set realistic goals Educate both patient and family Encourage symptom self-monitoring and coping skills Depression and suicide Depressive symptoms are common in schizophrenia. Treat as in other patients, with antidepressant drugs if necessary Consider risk of suicide Refer to specialist if necessary Alcohol and drug abuse Substance abuse is highly prevalent in schizophrenia, and has adverse effects on the course of the illness. Routinely enquire about substance use Strongly suspect if treatment response is poor Inform patient of adverse effects, and negotiate harm minimisation through short-term goals Refer to specialist if necessary Sexuality Normal sexual functioning can be affected by the illness and by antipsychotic medication. Discuss contraception Discuss safe sexual practices Try to ascertain any sexual dysfunction Physical health Schizophrenic patients have many risk factors for and high rates of concurrent physical disease. Examine six-monthly for side effects and complications of antipsychotic drugs Do a physical check annually for patients over 40 Back to text

Vaughan J Carr

In light of the emphasis on community care for schizophrenia and the increasing role likely to be played by general practitioners, this paper describes some of the general principles involved in the treatment of this disorder and provides a set of practical guidelines to assist general practitioners. Vaughan J Carr Introduction - Understanding the disorder - Symptoms - Early detection of psychosis - Diagnosis - Establishing a working relationship - Practice issues - Liaison with mental health agencies - Involuntary admissions - Conclusion - Acknowledgements - References - Authors' details - - More articles on Psychiatry This is part one of a two-part series. The second article appears in the MJA 3 February 1997 issue. Introduction Awareness of the importance of the general practitioner (GP) in the treatment of schizophrenia1-3 is growing. Factors contributing to this include continuing deinstitutionalisation (begun in the 1950s); the discovery in the 1960s and 1970s that GPs were the major providers of community psychiatric care;4,5 and the development of innovative community mental health service models in the 1980s,6,7 with recent efforts to integrate GPs into them.1,8Psychiatry texts suitable for assisting GPs in treating schizophrenic patients9,10 do not provide comprehensive practical guidelines for primary care. The two papers* in this series are intended to help fill this gap until specific primary care research provides more knowledge. Understanding the disorder Schizophrenia can be viewed in terms of a "vulnerability-stress" model,11 within which it manifests as a result of interactions between a biopsychological predisposition and environmental stress (see Figure). Vulnerability to schizophrenia is determined by premorbid risk factors, while environmental stressors are destabilising factors.12,13 For a given vulnerability-stress interaction, moderating influences may alter the illness threshold, thereby determining the occurrence of episodes of illness. Protective factors raise this threshold and perpetuating factors lower it. Treatment for schizophrenia is multimodal: antipsychotic medication and learned palliative coping techniques act on the underlying vulnerability; social support and instrumental coping (coping behaviours in relation to external rather than internal or disease-related events) help in adaptation to potentially stressful life events; and family interventions and rehabilitation strategies can augment protective factors or counter perpetuating influences. Symptoms Symptoms of schizophrenia are currently considered in three groups.14 These are: psychotic, or positive, symptoms (delusions and hallucinations); negative symptoms, representing loss of normal functions (flat affect, alogia, apathy, anhedonia-asociality and inattentiveness); and disorganisation symptoms (bizarre or disorganised behaviour, disjointed speech or formal thought disorder, incongruous affect). Schizophrenic patients often have other, traditionally non-schizophrenic, symptoms such as depression, anxiety, somatisation, phobias, obsessions, compulsions, and post-traumatic stress symptoms. Early detection of psychosis The longer psychotic symptoms go untreated, the worse the outcome.15-17 Therefore, early detection and treatment with antipsychotic drugs is crucial.17 Many patients who experience incipient psychotic symptoms consult their GP for some reason, placing the GP in a prime position to identify the problem early and make a prompt referral. There are two main facets to early detection: identifying individuals with prodromal symptoms before the emergence of frank psychosis; and recognising early or incipient psychotic symptoms.18,19Prodromal assessment: Schizophrenia cannot be diagnosed on the basis of prodromal symptoms alone because these are non-specific.20,21 They include impaired concentration, anxiety, depression, irritability, rebelliousness, social withdrawal, loss of interest or motivation, impaired function at school or work, deteriorating self-care, somatic complaints, restlessness, self-injury or suicide attempts, alcohol and drug abuse, emotional lability, and uncharacteristic aggression or poor impulse control. Also, it is important to note that the odd ideas or perceptions and peculiarities of speech or behaviour occurring in the prodromal stages of schizophrenia may also occur in normal adolescents.21 In schizophrenia, such phenomena may be present for two years or more, although usually not longer than 6-12 months, before the onset of psychotic symptoms.15,22 If such non-specific problems occur in an adolescent or young adult, they should be taken seriously, the possibility of schizophrenia kept in reasonable perspective, and the patient referred for psychiatric assessment with a letter detailing the main findings. While such an assessment in the prodromal phase may be inconclusive, it can be useful because, firstly, a positive encounter with a psychiatrist or mental health team establishes an important contact that can be resumed in the future. Secondly, the GP can provide ongoing support to the patient and family while diagnostic uncertainty prevails by acknowledging the problems identified and helping to implement any recommendations made by specialist services. Dismissing the problem ignores and invalidates the family's experience and may foster denial and thereby delay reassessment and hence eventual diagnosis and treatment. Thus, a useful short term measure may be a supportive counselling approach incorporating simple problem-solving strategies. Thirdly, it is important to monitor progress carefully in repeated clinical assessments, enlisting the cooperation of both patient and family, so that significant clinical change can be detected swiftly. Early psychotic symptoms: GPs are generally better able to detect psychiatric problems if they have good rapport with their patients, an interest in psychosocial problems, the ability to convey interest and concern, and good interviewing skills.23-25 The latter include appropriate eye contact, empathic responsiveness to cues of emotional distress, attentive posture, listening with few interruptions, an unhurried style, and the capacity to ask directive questions of a psychosocial nature. If indicated, GPs should ask, matter-of-factly and without embarrassment, a set of questions designed to elicit psychotic phenomena. For example: Do you hear noises or voices when there is no-one speaking or nothing to explain what you are hearing? What do they say? How many are there? Do they seem to be having a conversation among themselves about you?; or Do you have experiences that no-one else thinks are true, such as feeling you are under the control of some person or force that you can't explain, believing that the radio or TV are referring to you, thinking that others can read your mind, suspecting that someone is trying to hurt you?; or Is there some interference with your thinking such as thoughts being put into your head which are not your own, feeling that your thoughts are broadcast aloud so that other people can hear what you are thinking, feeling that thoughts are being taken out of your head against your will?. Patients experiencing their first early psychotic symptoms may deny or conceal such experiences. However, if asked these questions in the context of a confiding relationship, they may be able to acknowledge them for the first time. More harm is probably done if such symptoms persist undetected and untreated than would occur by asking about them in their absence. Having detected a possible new case of schizophrenia, referral to a psychiatrist or mental health service is imperative. While prolonged delays in the referral process are unacceptable, time should be taken to discuss the reasons for and purpose of the referral with the patient and efforts made to identify a psychiatrist or clinical service team suitable for the individual concerned. Diagnosis The diagnosis of schizophrenia is a specialist task. The current emphasis on detecting the earliest phase of onset of persistent psychotic symptoms -- for which antipsychotic drugs are indicated -- means that treatment may be initiated before a firm diagnosis can be made. Waiting for a confident diagnosis risks a poorer outcome. In general, psychiatric diagnoses are provisional hypotheses that may need revision as new information comes to light. Schizophrenia is particularly difficult to diagnose as there are several conditions that may mimic it and the pattern of psychotic symptoms tends to be relatively unstable early in the course of the illness.26-28For all these reasons, GPs should remain wary of a diagnosis of schizophrenia, even when long "established". If response to treatment is poor or the patient seems particularly sensitive to the adverse effects of treatment, a reappraisal of the diagnosis, including specialist reassessment, should be considered. Establishing a working relationship The cornerstone of successful treatment of schizophrenia is a good working relationship with the patient that embodies the principle of personal continuity of care over time.29,30 This is rarely possible in public mental health services and is not adequately provided by multidisciplinary teams. The GP, by providing long-term personal continuity of care,31 can fill this important gap in the patient's treatment even while the patient remains under the care of a community mental health team. If there is no well developed relationship between patient and GP before the onset of psychosis, one can be developed during the several 10-15-minute consultations per year which these patients tend to have with their GPs for renewal of prescriptions and other medical matters;6,32 the interview skills referred to previously are required. A trusting atmosphere can thus develop and be used as a basis for supportive therapy. Patients should be treated as autonomous adults, capable of mature decision-making and able to adopt a rational approach to the illness and its treatment. Fostering a collaborative partnership between patient and doctor for the joint management of the illness helps to counter the low self-esteem and lack of confidence that usually follows the experience of psychosis. Practice issues General practices should have a register or system for identifying the records of patients with schizophrenia31 to ensure regular reviews of patient progress, just as with diabetes or other chronic physical diseases. This also assists in auditing quality of care and patient outcomes. Management protocols for common problems in treating schizophrenia can be developed based on the case register. For example, missed appointments by schizophrenic patients are likely to portend relapse, deterioration in functioning, depression, suicidal preoccupations or an episode of drug or alcohol abuse. The management protocol could include having receptionist staff first notify the GP of a missed appointment, followed by telephone contact, home visit, or notifying the patient's community mental health team. It would also serve the patient's interests if the management protocol had the flexibility to handle unscheduled appointments -- frontal lobe impairments can make it difficult for schizophrenic patients to plan ahead or to appreciate the need to make appointments, and they may simply turn up unexpectedly. Also, in group practices, one GP should be identified as the primary care provider for a particular patient to facilitate the personal continuity of care. A standard record-keeping format with a checklist of items individually tailored for each patient may help to ensure that important clinical matters are not overlooked. Liaison with mental health agencies Close liaison between GPs and mental health services is crucial for the successful community treatment of schizophrenia by GPs. Well established lines of communication with the patient's psychiatrist or case manager are essential. Versions of the "shared care" model can provide practical support for GPs and facilitate their integration with mental health services in caring for schizophrenic patients. Divisions of general practice could be further encouraged to develop patterns of providing mental health care using innovative models of this kind. Involuntary admissions For acutely psychotic schizophrenic patients for whom involuntary hospitalisation may be indicated under the relevant mental health act, a coordinated approach involving the GP and the local mental health outreach team is the preferred option. If such a service is not available, the GP will first need to determine whether the patient's behaviour represents an immediate and substantial danger to others (e.g., presence of a weapon, demonstrably violent actions). In dangerous situations, GPs should first protect themselves and other people. The police should be involved if physical containment of the patient (including whatever restraint can be humanely applied using a minimum of force) is necessary. Only when the situation has been rendered reasonably safe should the GP venture to speak to the patient. If there is no immediate danger, the GP should approach the patient in a calm, non-threatening manner, avoiding confrontation, and conduct an interview in a safe place with whatever privacy is feasible, but with adequate assistance at hand.33 This can be provided by ambulance officers, medical or paramedical personnel and other responsible individuals. In either case, having interviewed the patient long enough to confirm, using whatever additional information is available from others, that the patient's condition meets the criteria for involuntary admission, then the GP should arrange that promptly according to the relevant mental health act. The patient should be informed of this and the legal status of the order explained simply and directly. Patients should be taken to hospital by ambulance (rather than police car) under appropriate supervision; this is both safer for patients, especially if sedated, and also underlines the medical nature of the problem. Police officers should accompany the patient in the ambulance if continued restraint is necessary. Transport by police vehicle should be avoided as it is invariably traumatising for the patient and conveys an entirely wrong message to the patient as to the nature of the situation. Sedating an involuntary patient in the community before transport to the hospital should be avoided if possible, as it may interfere with subsequent diagnostic assessment. However, sedation is clinically indicated (although the legality varies from State to State) for patients thought to be at high immediate risk of injuring themselves or others, who require restraint to enable transportation, or if transportation is likely to be of long duration.34 The patient may need to be restrained first or, alternatively, may accept medication on being confronted by the persuasive presence of enough people. Sedation can often be achieved by giving chlorpromazine (100 mg) or diazepam (10-20 mg) orally; severely agitated psychotic patients may require diazepam (10-20 mg, orally) together with haloperidol (5-10 mg, orally). Suitable parenteral medications include intramuscular injection of droperidol or haloperidol (5-10 mg) and/or midazolam (2.5-5 mg).34 If a high potency antipsychotic drug is administered parenterally, it should be accompanied by benztropine (2 mg, intramuscularly) to avoid serious acute dystonic reactions like laryngeal dystonia. Intramuscular injection of chlorpromazine is always contraindicated as it can cause an injection abscess, while that of diazepam is unsuitable because rates of absorption vary. Conclusion Today's GPs are well positioned to play a major role in the early detection of schizophrenia. Given the importance of early detection in successful treatment, the alert GP can have a considerable impact on the course of this illness. This contribution continues beyond the initial stages of the illness as GPs can help to optimise treatment and improve clinical outcome by providing personal continuity of care, maintaining close liaison with other mental health agencies, and making specific provision for schizophrenic patients using clinical practice registers and management protocols, as well as confidently handling emergencies. Practical recommendations are summarised in the Box. More specific issues will be covered in a subsequent article in the Journal. Acknowledgements I am grateful to Associate Professor Patrick McGorry and Drs Peter Hopkins, Brian Masters, Steve Robinson and Tony Ryan for their comments on earlier drafts of this paper. References Falloon IRH, Shanahan W, Laporta M, Krekorian HAR. Integrated family, general practice and mental health care in the management of schizophrenia. J R Soc Med 1990; 83: 225-228. Wilkinson G. The role of primary care physicians in the treatment of patients with long-term mental disorders. Int Rev Psychiatry 1991; 3: 35-42. Kendrick T, Burns T, Freeling P, Sibbald B. Provision of care to general practice patients with disabling long-term mental illness: a survey in 16 practices. Br J Gen Pract 1994; 40: 301-305. Shepherd M, Cooper B, Brown AC, Kalton G. Psychiatric illness in general practice. London: Oxford University Press, 1966. Goldberg DP, Kay C, Thompson L. Psychiatric morbidity in general practice and the community. Psychol Med 1976; 6: 565-569. Stein LI, Test MA. Alternative to mental hospital treatment. I. Conceptual model, treatment program, and clinical evaluation. Arch Gen Psychiatry 1980; 37: 392-397. Hoult J. Community treatment of the acutely mentally ill. Br J Psychiatry 1986; 149: 137-144. Jackson G, Gater R, Goldberg D, et al. A new community mental health team based in primary care: a description of the service and its effect on service use in the first year. Br J Psychiatry 1993; 162: 375-384. Goldberg D, Benjamin S, Creed F. Psychiatry in medical practice. 2nd ed. London: Routledge, 1994. Pullen I, Wilkinson G, Wright A, Gray DP, editors. Psychiatry in general practice today. London: The Royal College of Psychiatrists and the Royal College of General Practitioners, 1994. Zubin J, Spring B. Vulnerability: a new view of schizophrenia. J Abnorm Psychol 1977; 86: 103-126. McGlashan TH, Hoffman RE. Schizophrenia: psychodynamic to neurodynamic theories. In: Kaplan HI, Sadock BJ, editors. Comprehensive textbook of psychiatry. 6th ed. Baltimore: Williams & Wilkins, 1995: 957-968. Fenton WS, McGlashan TH. Schizophrenia: individual psychotherapy. In: Kaplan HI, Sadock BJ, editors. Comprehensive textbook of psychiatry. 6th ed. Baltimore: Williams & Wilkins, 1995: 1007-1018. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994. Loebel AD, Lieberman JA, Alvir JMJ, et al. Duration of psychosis and outcome in first-episode schizophrenia. Am J Psychiatry 1992; 149: 1183-1188. Johnstone EC, Crow TJ, Johnson AL, MacMillan JF. The Northwick Park study of first episode schizophrenia: I. Presentation of the illness and problems relating to admission. Br J Psychiatry 1986; 148: 115-120. Wyatt RJ. Neuroleptics and the natural course of schizophrenia. Schizophr Bull 1991; 17: 325-351. McGorry P, Kulkarni J. Prevention and preventively oriented clinical care in psychotic disorders. Aust J Psychopharm 1994; 7: 62-69. McGorry P, Rosen A, Carr V, Pantelis C. Innovations in the treatment of psychosis. In: Andrews G, editor. Specialization in psychiatry. Proceedings of the 1993 Geigy Symposium. Sydney: CIBA-Geigy, 1994: 157-232. Jackson HJ, McGorry PD, Dudgeon P. Prodromal symptoms of schizophrenia in first-episode psychosis: prevalence and specificity. Compr Psychiatry 1995; 36: 241-250. McGorry PD, McFarlane C, Patton GC, et al. The prevalence of prodromal features of schizophrenia in adolescence: a preliminary survey. Acta Psychiatr Scand 1995; 92: 241-249. Beiser M, Erickson D, Fleming JAE, Iacono WG. Establishing the onset of psychotic illness. Am J Psychiatry 1993; 150: 1349-1354. Marks J, Goldberg D, Hillier V. Determinants of the ability of general practitioners to manage common mental disorders. Psychol Med 1979; 9: 337-353. Goldberg D, Steele JJ, Johnson A, Smith C. Ability of primary care physicians to make accurate ratings of psychiatric symptoms. Arch Gen Psychiatry 1982; 39: 829-833. Goldberg DP, Jenkins L, Millar T, Faragher EB. The ability of trainee general practitioners to identify psychological distress among their patients. Psychol Med 1993; 23: 185-193. McGorry PD. Paradigm failure in functional psychosis: review and implications. Aust N Z J Psychiatry 1991; 25: 43-55. McGorry PD, Copolov DL, Singh BS. Functional psychosis: the case for a loosening of associations. Schizophr Res 1990; 3: 221-234. Stanton MW, Joyce PR. Stability of psychiatric diagnosis in New Zealand psychiatric hospitals. Aust N Z J Psychiatry 1993; 27: 2-8. McGlashan T. Intensive individual psychotherapy of schizophrenia: a review of techniques. Arch Gen Psychiatry 1983; 40: 909-920. McGlashan T, Keats CJ. Schizophrenia: treatment process and outcome. Washington: American Psychiatric Press, 1989. Burns T, Kendrick T. Schizophrenia. In: Pullen I, Wilkinson G, Wright A, Gray DP, editors. Psychiatry in general practice today. London: The Royal College of Psychiatrists and the Royal College of General Practitioners, 1994: 194-208. Melzer D, Hale AS, Burns T, et al. Community care for patients with schizophrenia one year after hospital discharge. BMJ 1991; 303: 1023-1026. Hyman SE. Manual of psychiatric emergencies. 2nd ed. Boston: Little Brown, 1988. Victorian Drug Usage Advisory Committee. Psychotropic drug guidelines. 3rd ed. Melbourne: Victorian Medical Postgraduate Foundation Therapeutics Committee, 1995. Discipline of Psychiatry, Faculty of Medicine and Health Sciences, The University of Newcastle, Newcastle, NSW. Vaughan J Carr, MD, FRANZCP, Professor of Psychiatry. Reprints: Professor V J Carr, Discipline of Psychiatry, Faculty of Medicine and Health Sciences, The University of Newcastle, Callaghan, NSW 2308. 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/> Vulnerability Premorbid risk factors Family history of schizophrenia Perinatal complications Attention deflicts Impaired arousal modulation impaired social competence coping deficits Moderating influences Protective factors Social support Family problem-solving skills Medication compliance Perpetuating factors Social impoverishment Critical or emotionally overinvolved family Unemployment Alcohol or drug abuse Stress Acute Life events Recent physical illness Psychoactive drugs Chronic Ongoing family conflict Poverty Academic or work pressures Vulnerability-stress model of schizophrenia. Back to text Practical recommendations for primary care management of schizophrenic patients Early detection of psychosis Be alert for: 1. Prodromal symptoms Refer patient for psychiatric assessment Monitor patient's progress Support and counsel patient and family 2. Incipient psychotic symptoms Ask psychological probe questions Refer promptly to a psychiatrist or mental health service Diagnosis Is a specialist task, but remains provisional. Therefore: Remain prepared to revise the diagnosis Consider specialist reassessment if there are problems with treatment Working relationship Is based on personal continuity of care. Therefore: Develop a trusting relationship with the patient Treat the patient as an autonomous adult Foster collaboration with the patient in managing the illness Practice issues As patients with schizophrenia have special needs: Maintain a patient register Develop management protocols for problems such as missed appointments, and include flexibility to allow for unexpected behaviour Liaison with mental health agencies Is essential for successful community treatment of schizophrenic patients. Therefore: Maintain communication with the patient's psychiatrist or case manager Involuntary admissions The medical nature of these circumstances needs to be emphasised. Therefore: Work with a mental health team if possible First ensure safety of self and others (involve police if necessary) Use a non-threatening, non-confrontational approach to the patient Determine whether criteria for involuntary admission are present Follow procedures of local mental health act Clearly explain and inform the patient of his or her legal status Ensure supervised transport to hospital (preferably by ambulance) Sedation may be clinically indicated Back to text

Vaughan J Carr

Viewpoint Primary care psychiatry is not specialist psychiatry in general practice Current psychiatric diagnostic systems are not useful for general practice Ian B Hickie MJA 1999; 170: 171-173 Introduction - Barriers to psychiatric treatment in primary care - Classification systems in specialist psychiatry - Primary care psychiatry - Psychological disorders present with somatic symptoms - Psychological assessment in primary care - Acknowledgements - References - Authors' details - - More articles on Psychiatry Introduction At least 30% of patients who present to primary care have psychiatric disorders, while another third have sufficient psychological symptoms to justify detailed psychological assessment.1 While patients who present to primary care represent a minority of those with psychological disorders in the Australian community,2 less than half receive a psychiatric diagnosis when seen by their general practitioner.3 Specific pharmacological treatment is provided to less than half of patients in whom a diagnosis is made.3The public health and personal costs of this situation are large,4 and persist despite the increasing willingness of general practitioners to treat psychological disorders,5 the increased availability of safe and effective pharmacological agents, and the fact that patients prefer to be assessed by their general practitioner rather than mental health specialists.6 Current public health initiatives are designed to increase the likelihood that persons at risk (especially men and younger people) will present for treatment and that general practitioners will receive increased support and training to provide such treatments.5 Barriers to psychiatric treatment in primary care A range of patient, doctor and service factors contribute to the ongoing problems of under-recognition and undertreatment of psychological disorders in primary care. Patient-related factors include the presentation of somatic rather than psychological symptoms,7,8 the co-occurrence of medical and psychological problems, and the stigma associated with psychological diagnoses and treatments.6 Doctor-related factors include inadequate interview and diagnostic skills,9,10 insufficient undergraduate and postgraduate training,5 insufficient time devoted to adequate diagnostic assessment,5 and a lack of acquisition of new knowledge relevant to provision of treatments. Service-related factors5 include insufficient remuneration for psychological interventions, insufficient support from specialist public and private mental health services, and inadequate access to non-medical mental health professionals. An important but little-discussed factor is the current lack of a useful psychiatric diagnostic system for use in primary care. General practitioners typically report that, although they recognise behavioural disturbance, the common symptom patterns and deviant behaviours presented do not fit readily within the patterns described by specialist psychiatry. Currently, psychiatric education highlights the problems of under-recognition and undertreatment, but does not concede that much of the morbidity detected is not classical "major depression" or one of the discrete anxiety disorders.11 Moreover, much of the treatment data that forms the "evidence-base" for current recommendations has not been obtained in patients from primary care settings.12 Inevitably, therefore, practice guidelines for primary care represent extrapolations from treatment trials conducted within the specialist sector with patients without concurrent medical morbidity.12 Classification systems in specialist psychiatry During the past two decades, specialist psychiatry has focused on the development of complex criteria-based diagnostic systems (eg, DSM-IV, ICD-10).11,13 While such systems have improved diagnostic reliability for psychiatric research, they have often been inappropriately transferred directly to clinical settings. In practice, the systems frequently result in multiple diagnoses for individual patients (now termed "psychiatric comorbidity"), as the borders between the different diagnostic categories are indistinct. For example, many patients with "major depression" will also meet criteria for other anxiety disorders, such as generalised anxiety disorder and panic disorder.14As the current systems were designed for patients who present primarily with psychiatric disorders, their application in general medical and primary care settings is problematic. Patients frequently do not meet criteria for any specific psychiatric diagnosis, or fall into one of the "waste-basket" categories such as 300.81 Undifferentiated Somatoform Disorder or 311 Depressive Disorder, Not Otherwise Specified. Much of the psychological morbidity encountered in general practice falls into the "not otherwise specified" categories, and the diagnostic systems have tended to reinforce the notion that such disorders are not worthy of further systematic study. This is despite their clear contribution to ongoing healthcare costs and disability.1 Primary care psychiatry In contrast with specialist psychiatry, the emerging discipline of "primary care psychiatry" deals with those issues which are pertinent to psychological assessment and intervention in the primary care sector.15 This focus is justified by the fact that most patients in this sector present an admixture of affective and somatoform symptoms,7,16 and are managed without referral to the specialist sector.2 When referring, there is a strong preference towards those patients with overt psychological syndromes (eg, major depression, panic disorder) and away from those patients with somatoform disorders (eg, chronic fatigue, chronic pain), as the latter are poorly recognised by the current classification systems.8,17 This is despite the considerable disability associated with such disorders and the likelihood that such patients will seek a variety of treatments, including non-specific pharmacological and alternative medicine interventions.8,17Additionally, general practitioners frequently assess psychological disorders which occur in the context of obvious life stressors (eg, marital separation, job loss, or financial hardship). The diagnostic systems typically describe such disorders as "adjustment disorders" and imply that such maladaptive behavioural responses are usually shortlived and associated with minor degrees of disability. DSM-IV specifically describes adjustment disorders as a "residual category". This approach substantially underestimates the impact of such presentations on primary care practitioners and the degree of risk and disability which may result. Psychological disorders present with somatic symptoms Few patients simply report the syndromes described in DSM-IV or ICD-10. Typically, patients report prolonged fatigue, sleep disturbance and musculoskeletal aches and pains in association with mood, anxiety and/or neurocognitive symptoms.7,16,18 Consequently, primary care psychiatry emphasises diagnostic categories that are more useful to general practitioners. The most important of these are "mixed anxiety and depression" and "neurasthenia" (ie, nervous exhaustion or chronic fatigue). Together, these disorders are largely discounted by specialist psychiatry, even though they describe common presentations. The psychiatrist's "bible", DSM-IV, deals particularly poorly with both these disorders. Mixed anxiety and depression is presented simply as a possible form of depressive disorder that may warrant further investigation. Neurasthenia/chronic fatigue is not recognised, although the symptom pattern is described obliquely within 300.81 Undifferentiated Somatoform Disorder. The most recent and comprehensive community study of psychiatric disorders in North America (published from 1994 onwards) chose not to record the prevalence or health impacts of somatoform disorders.19 In contrast, studies supported by the World Health Organization continue to demonstrate the frequency of neurasthenia and its relevance for primary care practitioners.1 Fortunately, the recent National Health and Wellbeing Survey,2 conducted in the second half of 1997, obtained data on these conditions in Australia. Pilot data from that study support this emphasis in terms of prevalence and associated disability.20 Longitudinal studies suggest that these disorders are often chronic and likely to remain prevalent in the primary care setting.21 Although such disorders are distinctly lacking from many educational initiatives in primary care, emerging literature can be used to guide primary care physicians.8,22 The relevant notions include not only descriptions of key symptom sets (eg, chronic fatigue, irritable bowel, chronic pain, fibromyalgia and chronic headache), but also more coherent approaches to identification of problem behaviours (eg, rejection of medical reassurance, inappropriate investigation). This results frequently in combined medical and psychological approaches to treatment (eg, non-steroidal anti-inflammatory drugs and behavioural treatment for fibromyalgia; antidepressant drug and sleep-wake cycle behavioural management of chronic fatigue). Psychological assessment in primary care Current educational initiatives in primary care often emphasise the importance of simplistic diagnostic checklists for disorders such as "major depression" or "panic disorder". A more rational educational and treatment approach is based on the following framework: The common somatic and psychological presentations of distress and the psychosocial environment within which such presentations occur must be recognised. Within the logistic constraints of general practice this process may be assisted either by relevant screening instruments7 and/or by improving interviewing techniques.9 Behavioural constructs (eg, depressed mood, panic attacks, psychomotor retardation, chronic fatigue, chronic pain, sleep disturbance, and suicidal ideation) that require specific treatments independent of the final diagnosis need to be recognised. The degree of immediate risk to self and others should be determined. An assessment of those comorbid medical factors (eg, co-prescription of antihypertensives) that will influence treatment choice needs to occur. Within this framework there is the potential to bring a much larger group of currently untreated patients, particularly those with somatoform or adjustment disorders, into the diagnostic and treatment process. For individual management to succeed, the practitioner needs then to use very specific knowledge with regard to the patient's current personal and social circumstances and past experiences. Further developments will depend on a growing awareness of the inadequacies of the current classification systems and an increased demand for relevant aetiological and treatment research within the primary care sector. As this process gains momentum so will the capacity to identify and treat more effectively the large number of patients who present to primary care. Acknowledgements This research in general practice settings is supported by a National Health and Medical Research Council Program Grant (No. 953208). The editorial assistance of Tracey Davenport was greatly appreciated. References Ustun TB, Sartorius N, editors. Mental illness in general health care: an international study. Chichester: John Wiley and Sons, 1995. Mental health and wellbeing: profile of adults, Australia. Canberra: Australian Bureau of Statistics, 1998. (Catalogue no. 4326.0.) Harris MF, Silove D, Kehag E, et al. Anxiety and depression in general practice patients: prevalence and management. Med J Aust 1996; 164: 526-529. Murray CJL, Lopez AD, editors. The Global Burden of Disease: a comprehensive assessment of mortality and disability from diseases, injuries and risk factors in 1990 and projected to 2020. Boston: Harvard University Press, 1996. A report of the Joint Consultative Committee. Primary care psychiatry -- the last frontier. Canberra: Royal Australian College of General Practitioners and Royal Australian and New Zealand College of Psychiatrists, 1997. Jorm AF, Korten AE, Jacomb PA, et al. "Mental health literacy": a survey of the public's ability to recognise mental disorders and their beliefs about the effectiveness of treatment. Med J Aust 1997; 166: 182-186. Hickie I, Hooker A, Hadzi-Pavlovic D, et al. Fatigue in selected primary care settings: sociodemographic and psychiatric correlates. Med J Aust 1996; 164: 585-588. Hickie IB, Scott EM, Davenport TA. Somatic distress: developing more integrated concepts. Curr Opin Psychiatry 1998; 11: 153-158. Goldberg DP, Jenkins L, Millar T, Faragher EB. The ability of trainee general practitioners to identify psychological distress among their patients. Psychol Med 1993; 23: 185-193. Tobin M, Hickie I, Urbanc A. Increasing general practitioner skills with patients with serious mental illness. Aust Health Rev 1997; 20: 55-67. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994. American Psychiatric Association. Practice guidelines for major depressive disorder in adults. Am J Psychiatry 1993; 150 Supl: 1-26. World Health Organization. The tenth revision of the International Classification of Diseases and related health problems (ICD-10). Geneva: World Health Organization, 1992. Blazer DG, Kessler RC, McGonagle KA, Swartz MS. The prevalence and distribution of major depression in a national community sample: the National Comorbidity Survey. Am J Psychiatry 1994; 151: 979-986. Sartorius N, Ustun TB, Costa e Silva JA, et al. An international study of psychological problems in primary care. Preliminary report from the World Health Organization Collaborative Project on 'Psychological Problems in General Health Care'. Arch Gen Psychiatry 1993; 50: 819-824. Goldberg D, Gater R. Implications of the World Health Organisation study of mental illness in general health care for training primary care staff. Br J Gen Pract 1996; 46: 483-485. Hickie I, Hadzi-Pavlovic D, Ricci C. Reviving the diagnosis of neurasthenia. Psychol Med 1997; 27: 989-994. Mason P, Wilkinson G. The prevalence of psychiatric morbidity: OPCS survey of psychiatric morbidity in Great Britain. Br J Psychiatry 1996; 168: 1-3. 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. Hickie I, Pols R, Koschera A, Davenport T. Why are somatoform disorders so poorly recognised and treated? In: Andrews G, editor. Unmet needs for psychiatric care. Darlinghurst, Sydney: World Health Organization Collaborating Centre for Mental Health and Substance Abuse. In press 1999. Merikangas K, Angst J. Neurasthenia in a longitudinal cohort study of young adults. Psychol Med 1994; 24: 1013-1024. Wessely S, Hotopf M, Sharpe M. Chronic fatigue and its syndromes. New York: Oxford University Press, 1998. Authors' details School of Psychiatry, University of New South Wales, Sydney, NSW. Ian B Hickie, MD, FRANZCP, Professor of Community Psychiatry. Reprints: Professor I B Hickie, Academic Department of Psychiatry, 7 Chapel Street, Kogarah, NSW 2217. Email: i.hickieATunsw.edu.au 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/>

Ian B Hickie

Review Vascular dementia: diagnosis, management and possible prevention There has been a recent upsurge of interest in the clinical features of and risk factors for vascular dementia, and consensus is emerging on its diagnostic characteristics. We discuss these features and risk factors and the main intervention strategies, both for treatment and prevention. Perminder S Sachdev, Henry Brodaty and Jeffrey C L Looi MJA 1999; 170: 81-85 Introduction - Definition - Epidemiology - Clinical-pathological correlates and pathogenesis - Clinical features and diagnosis - Prognosis - Prevention and treatment - Acknowledgements - References - Authors' details - - More articles on Geriatrics Introduction Developments in the past three decades have led to a radical rethinking of the association between cerebrovascular disease (CVD) and dementia, and set the stage for a reconceptualisation of dementia from vascular causes. We will review recent developments in the concept of vascular dementia (VaD), and discuss its importance as a common, and potentially preventable, form of dementia. Definition There are two obvious steps in the diagnosis of VaD -- diagnosis of dementia per se and establishment of its vascular aetiology. Dementia is defined as a multifaceted decline in cognitive functioning causing impaired functioning in daily life.1,2 Impairment of memory is generally regarded as a necessary aspect, but decline in one or more other cognitive domains (ie, language, praxis, gnosis, visuoconstructive function, frontal-executive functions) must also be demonstrated.1,2 VaD is diagnosed if significant CVD is present and is judged to be causally relevant to the cognitive impairment.1-4What constitutes significant vascular aetiology is not always easy to establish. Minor cerebrovascular pathology is common in healthy elderly people5 and in association with other dementias, notably Alzheimer's disease (AD).6 Recent studies using magnetic resonance imaging (MRI) of the brain have reported periventricular hyperintensities on T2-weighted images, arguably vascular in origin, in up to 93% of healthy elderly individuals,5 so guidelines for determining the significance of cerebral vascular lesions are needed. An early approach was to base the diagnosis on the score obtained on an ischaemia scale,7 which comprises a list of historical and clinical examination items known to discriminate multi-infarct dementia (MID) from AD. On a 13-item scale (maximum score 18), a score of seven or more suggested MID and four or less suggested AD.7 This approach has limitations as it is based on a concept that VaD is caused by multiple strokes (hence, MID), now recognised to be only one vascular pathway to dementia. In addition, it uses only some of the relevant clinical information, and it excludes neuroimaging from consideration. More recent efforts have attempted to address these deficiencies. According to the NINDS-AIREN criteria (developed at an international workshop involving 54 neurologists and neuroscientists),4 a diagnosis of probable VaD is made if dementia is associated with focal neurological signs and imaging evidence of CVD is present. On computed tomography (CT) or MRI this could comprise multiple or strategic single infarcts, multiple lacunae, extensive white matter lesions (WMLs), or combinations of these. Like other dementias, VaD requires histopathological confirmation and is a postmortem diagnosis. Some investigators have argued that the emphasis on dementia in patients with CVD may be inappropriate for several reasons: (i) the diagnosis of dementia is contentious in many patients because a qualitative judgement is involved; (ii) it imposes a categorical distinction on the continuous construct of cognitive impairment; and (iii) it is important to recognise cognitive impairment before it has reached the stage of dementia, especially if prevention strategies are to be introduced. Thus, the term "vascular cognitive impairment" has been proposed, in which "vascular" refers to all causes of ischaemic CVD, and "cognitive impairment" encompasses all levels of cognitive decline, which may fall well short of dementia.8 Epidemiology Prevalences of VaD have varied across studies because of methodological differences, but point to VaD being the second most common dementia after AD in Western societies. A quantitative integration of studies published between 1945 and 1985 suggested an overall prevalence of dementia of 5.6% in people older than 60 years.9 AD was more prevalent than MID by a relative factor of 1.05 to 1.43 in Western societies. VaD had an increasing prevalence with age (a doubling every 5.3 years). It also found an excess of VaD in men, and a cross-national effect, with AD being more common in Western countries and VaD being much more common in Japan, China and Russia.9 A Swedish study estimated the lifetime risk of VaD as 34.5% for men and 19.4% for women.10 In community-based studies, the incidence of VaD has ranged from 0.17 to 0.71 per 100 person-years.10,11 In a sample of hospitalised ischaemic stroke patients, the incidence of VaD was estimated to be 8.4 per 100 person-years.12 Dementia was diagnosed in 26.3% and 31.8% of patients, respectively, in two studies at three months after an acute stroke.12,13Risk factors for VaD (summarised in Box 1) are incompletely understood.14 As stroke is a major determinant of VaD, it is reasonable to expect that risk factors for stroke would also increase the risk of VaD. While hypertension increases the risk of VaD, high systolic blood pressure may serve a protective role once dementia has set in.15 In one study, although subjects with VaD were more likely to have been hypertensive in the past, they currently had lower blood pressure values and more orthostatic hypotension than stroke patients without dementia.13 Genetic factors for CVD, and consequently VaD, are not well understood. Exceptions are rare disorders such as cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy (CADASIL) and autosomal dominant hereditary cerebral haemorrhage with amyloidosis -- Dutch type. The role of apolipoprotein E polymorphism in VaD is unclear; there is conflicting evidence for a link with the e4 allele.14 Not all stroke patients develop dementia, suggesting the nature and extent of strokes and their interaction with host factors are important. Left hemisphere strokes are more likely to produce severe cognitive impairment, and the infarction of certain strategic areas may be crucial (eg, deep frontal white matter, dominant thalamus and angular gyrus).12,13 VaD may occur in the absence of strokes, and this is usually associated with periventricular WMLs or lacunae and silent infarcts.4 Clinical-pathological correlates and pathogenesis Brain parenchymal lesions of vascular origin may be produced through ischaemia, haemorrhage or oedema. VaD may therefore be caused by multiple mechanisms, individually or in combination (Box 2). The resulting neuropathology will vary according to the dominant mechanisms and will comprise combinations of multiple large infarcts, single strategic infarcts, lacunae and WMLs. Multiple large infarcts may result in summative damage to widespread regions causing a heterogeneous pattern of deficits, overwhelming compensatory mechanisms. Single infarcts, when strategically placed and large, may affect a critical cortical or subcortical region to disrupt multiple cognitive functions. Lacunae (or lacunar infarcts) are small cavities, up to 1.5 cm in diameter, that usually occur in the basal ganglia, thalamus, pons, internal capsule and deep white matter areas irrigated by the superficial and deep penetrating arteries and arterioles. WMLs are commonly seen on CT and especially on T2-weighted MRI. As they are present in otherwise healthy elderly individuals, their pathological significance has been greatly debated.5 When their severity was considered, periventricular WMLs were reported in VaD to be 11.6 times greater than in AD and 3.5 times greater than in healthy people, and subcortical WMLs were 2.6 and 13.5 times greater, respectively.16 A threshold effect has been suggested, with cognitive impairment resulting when WMLs reach a certain severity. WMLs must nevertheless be distinguished from Binswanger's disease,17 a rare clinicopathological entity characterised by slowly progressive dementia, usually beginning in the fifth or sixth decade, and associated with hypertension, psychiatric features, gait disturbance, parkinsonism, corticobulbar features and incontinence. The vascular pathology in VaD is varied; atherosclerosis, arteriosclerosis, lipohyalinosis, amyloid angiopathy, senile arteriolar sclerosis and other angiopathies have been described.4 Systemic causes of thromboembolism are important in some cases: inflammatory diseases (eg, systemic lupus erythematosus, polyarteritis nodosa, sarcoidosis), hyperviscosity syndromes (eg, polycythaemia vera, sickle cell anaemia) and embolic disorders (eg, atrial fibrillation, myocardial infarction with mural thrombus, congenital heart disease, as well as septic, air or fat emboli). VaD and Alzheimer-type changes not uncommonly co-occur, and 10%-20% of patients with dementia are classified clinically and pathologically as having both AD and VaD. VaD is known to promote the clinical expression of AD;6 the relationship between these two dementias needs further study. Clinical features and diagnosis The onset of VaD is often sudden, with a transient ischaemic attack (TIA) or a stroke, after which the clinical course may be static, remitting or progressive, often with a fluctuating or stepwise deterioration. Predominantly subcortical lesions may produce cognitive impairment of gradual onset and slow progression. Other features that distinguish VaD from AD are nocturnal confusion and wandering, relative preservation of emotional responsiveness and personality until the later stages of the disease, and the presence of depression, emotional lability, incontinence and somatic symptoms.4 A history of risk factors for CVD should alert the clinician to the possibility of VaD, and the presence of focal neurological symptoms (such as visual disturbances, brainstem abnormalities, sensory or motor symptoms) and signs (hemiparesis, visual field defects, pseudobulbar palsy, extrapyramidal signs) will provide further support. The cognitive deficits in VaD are multifocal and therefore more varied than generally seen in AD. Memory deficit may not be as marked; discrepancies between verbal and non-verbal memory performance are often notable. Other common elements are visuospatial dysfunction, dysphasia, cognitive slowing and impairment of executive function.4 Impairment in frontal lobe functioning is usually more severe for VaD than AD. Language impairment in patients with left hemispheric strokes may impede the assessment of abnormalities in other cognitive domains. Assessment of a patient with possible VaD should include establishment of the diagnosis of dementia; documentation of evidence for CVD; determination of the aetiological role of CVD; evaluation of functional status of the individual and his or her disability, and the interpersonal and community supports available; and determination of risk and protective factors that could be modified (Box 3). Absence of vascular lesions on CT and, in particular, MRI is strong evidence against vascular aetiology. As CVD is commonly present in otherwise healthy individuals, guidelines are available for the topography and severity of lesions to be considered significant.4 At least a quarter of all white matter would need to be involved for the lesions to be clearly significant (Figure). Prognosis While not totally consistent, longitudinal studies of VaD suggest mortality rates greater than for AD and rates of admission to nursing homes comparable in the two. One study reported a five-year mortality rate of 63.6% (compared with 31.8% for AD) and a nursing home admission rate of 31.8% (compared with 20.6% for AD).19 Cognitive impairment in patients with stroke has adverse functional consequences, independent of any physical impairments. The prognosis may be improved by better treatment and preventive strategies. Prevention and treatment The management of risk factors for VaD offers the opportunity to reduce its incidence significantly, or, if dementia has already been diagnosed, halt its progression and sometimes achieve partial improvement. Some strategies for primary prevention of VaD are listed in Box 4. One of the more established interventions is control of hypertension. Treatment of patients with diastolic blood pressure (BP) greater than 110 mmHg is universally accepted, and there is evidence that treatment of those with diastolic BP of 90-110 mmHg and systolic BP greater than 160 mmHg is beneficial.20 While antihypertensive drugs are often indicated, lifestyle changes which lower BP are advisable at all levels of BP. In controlling hypertension, avoidance of hypotension is strongly advocated, as poor autoregulation in VaD patients increases its deleterious effects on cerebral blood flow. The control of risk factors such as hyperlipidaemia and diabetes mellitus may also have a stabilising effect, although evidence is lacking.21 Other modifiable factors include cigarette smoking, excessive alcohol consumption, obesity, and lack of exercise. Non-atherogenic risk factors that may be modifiable include atrial fibrillation and carotid artery stenosis. Warfarin is clearly beneficial in reducing the risk of stroke in patients with atrial fibrillation, with aspirin being less effective.22 In those with a past TIA or non-haemorrhagic stroke, antiplatelet therapy is helpful in reducing the risk of further such events. The optimal dose of aspirin to be used is not known, and doses between 75 mg and 325 mg are recommended.22 For those "failing" aspirin therapy, other antiplatelet agents, such as ticlopidine, may be indicated. Current evidence is insufficient to recommend aspirin for the primary prevention of stroke and VaD in low-risk individuals; there may be a slight increase in the risk of haemorrhagic stroke with such treatment.23 In stroke or TIA patients with a severe carotid artery stenosis (> 70% occlusion), carotid endarterectomy is an effective procedure. The role of such surgery in the presence of moderate stenosis or for asymptomatic individuals is uncertain.23 Many drugs have been investigated for treating VaD, but with limited success, and no drug can be positively recommended at present. Vasodilators (eg, hydergine [co-dergocrine mesylate; Sandoz], other alkaloids and cyclandelate) have some positive effects, and modest gains in cognition have been reported with an orally active haemorheological agent (pentoxifylline).22 A related drug, propentofylline, may exert an additional neuroprotective effect and has shown some promise in clinical trials.24 Other drugs that have been tried include the vinca alkaloids, calcium channel antagonists, nootropics, and extracts of Ginkgo biloba, with no convincing successes.25 Some of the drugs that improve memory in some AD patients (eg, cholinergic drugs such as tacrine and donepezil) may find a role in VaD. Other drugs may serve a neuroprotective role (eg, propentofylline, calcium channel antagonists and N-methyl-D-aspartate receptor antagonists). The mainstay of treatment is preventive and supportive. Supportive measures should include rigorous treatment of psychiatric complications such as depression, measures to facilitate independence, community or institutional care, and support for the carer. Specific neuropsychological rehabilitative measures may have a role in particular cases. Self-help groups such as the Alzheimer's (and Related Disorders) Association and the Stroke Society play an important supportive and educational role. Acknowledgements The assistance of Barbara Brierley and Agata Wachala in literature search is gratefully acknowledged. References World Health Organization. The ICD-10 classification of mental and behavioural disorders. Diagnostic criteria for research. Geneva: World Health Organization, 1993. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington DC: American Psychiatric Association, 1994. Chui HC, Victoroff JI, Margolin MD, et al. Criteria for the diagnosis of ischemic vascular dementia proposed by the State of California Alzheimer's Disease Diagnostic and Treatment Centers. Neurology 1992; 42: 473-480. Roman GC, Tatemichi TK, Erkinjuntti T, et al. Vascular dementia: diagnostic criteria for research studies. Report of the NINDS-AIREN international workshop. Neurology 1993; 43: 250-260. Kertesz A, Black SE, Tokar G, et al. Periventricular and subcortical hyperintensities on magnetic resonance imaging. "Rims, caps and unidentified bright objects." Arch Neurol 1988; 45: 404-408. Snowdon DA, Greiner LH, Mortimer JA, et al. Brain infarction and the clinical expression of Alzheimer disease: the nun study. JAMA 1997; 277: 813-817. Hachinski VC, Iliff LD, Zilkha E, et al. Cerebral blood flow in dementia. Arch Neurol 1975; 32: 632-637. Hachinski VC, Bowler JV. Vascular dementia. Neurology 1993; 43: 2159-2160. Jorm AF, Korten AE, Henderson AS. The prevalence of dementia: a quantitative integration of the literature. Acta Psychiatr Scand 1987; 76: 465-479. Hagnell O, Franck A, Grasbeck A, et al. Vascular dementia in the Lundby study: 1. A prospective, epidemiological study of incidence and risk from 1957-1972. Neuropsychobiology 1992; 26: 43-49. Schoenberg BS, Kokmen E, Okazaki H. Alzheimer's disease and other dementing illnesses in a defined United States population: incidence rates and clinical features. Ann Neurol 1987; 22: 724-729. Tatemichi TK, Paik M, Bagiella E, et al. Risk of dementia in a hospitalized cohort: results of a longitudinal study. Neurology 1994; 44: 1885-1892. Pohjasvaara T, Erkinjuntti T, Ylikoski R, et al. Clinical determinants of poststroke dementia. Stroke 1998; 29: 75-81. Gorelick PB. Status of risk factors for dementia associated with stroke. Stroke 1997; 28: 459-463. Gorelick PB, Brody JA, Cohen DC, et al. Risk factors for dementia associated with multiple cerebral infarcts: a case-control analysis in predominantly African-American hospital-based patients. Arch Neurol 1993; 50: 714-720. Boone BK, Miller BL, Lesser IM, et al. Neuropathological correlates of white matter lesions in healthy elderly subjects: a threshold effect. Arch Neurol 1992; 49: 546-554. Binswanger O. Die abgrenzung der allgemeined progressiven paralyse, I-III. Berl Klin Wochenschr 1884; 48: 1103-1105, 1137-1139, 1180-1186. Folstein M, Folstein S, McHugh PR. Mini-Mental State: a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975; 12: 189-198. Brodaty H, McGilchrist C, Harris L, Peters KE. Time until institutionalization and death in patients with dementia: role of caregiver training and risk factors. Arch Neurol 1993; 50: 643-650. Lawrence M, Cruickshank K. Hypertension. In: Lawrence M, Neil A, Mant D, Fowler G, editors. Prevention of cardiovascular disease. Oxford: Oxford University Press, 1996; 18-34. Atkins D, Psaty BM, Koepsell TD, et al. Cholesterol reduction and the risk for stroke in men: a meta-analysis of randomized controlled trials. Ann Intern Med 1993; 119: 136-145. Black RS, Barclay LL, Nolan KA, et al. Pentoxifylline in cerebrovascular dementia. J Am Geriatr Soc 1992; 40: 237-244. Mant J. Prevention of stroke. In: Lawrence M, Neil A, Mant D, Fowler G, editors. Prevention of cardiovascular disease. Oxford: Oxford University Press, 1996; 162-174. Marcusson J, and European Propentofylline Study Group. HWA 285 for the treatment of dementia: results of a 12 months clinical trial. J Cerebr Blood Flow Metab 1995; 15 Suppl 1: S107. Wong AHC, Smith M, Boon HS. Herbal remedies in psychiatric practice [review]. Arch Gen Psychiatry 1998; 55: 1033-1044. (Received 21 Apr, accepted 30 Jul, 1998) Authors' details School of Psychiatry, University of New South Wales, NSW. Perminder S Sachdev, MD, PhD, Professor of Neuropsychiatry, and Neuropsychiatric Institute, The Prince Henry Hospital, NSW; Henry Brodaty, MD, FRANZCP, Professor of Psychogeriatrics, and Academic Department of Psychogeriatrics, The Prince Henry Hospital, NSW. Neuropsychiatric Institute, The Prince Henry Hospital, NSW. Jeffrey C L Looi, MB BS, NSW Institute of Psychiatry Fellow. Reprints will not be available from the authors. Correspondence: Dr P S Sachdev, NPI, The Prince Henry Hospital, Little Bay, NSW 2036. Email: P. SachdevATunsw.edu.au Two magnetic resonance imaging proton-density transaxial cuts from the brain of a hypertensive patient with vascular dementia. Note extensive involvement of white matter, which appears as hyperintense signals. The patient's computed tomography brain scan showed minor periventricular hypodensity. Back to text 1: Risk factors for vascular dementiaSociodemographicAgeIncreasing incidence with age, especially after 60 yearsRace/ethnicHigher rates in Asian and black populations15SexHigher rates in menEducationMay have a protective effect12-15Atherogenic12-15HypertensionMajor risk factorCoronary artery disease Increases stroke riskDiabetes mellitusRisk factor for strokeCigarette smokingRisk factor for strokeHypercholesterolaemiaRisk factor for strokeFibrinogen, obesityEvidence lackingOther cardiovascularAtrial fibrillationRisk of cerebral embolismMitral valve prolapseCerebral embolismPeripheral vascular disease Inconsistent evidenceOther factorsGeneticWeak; CADASIL an exceptionApolipoprotein E polymorphism Evidence inconsistentAnticardiolipin antibodies Evidence inconsistentAlcoholismEvidence inconsistentStroke-relatedNumber, volume, location of stroke12,13Strategic silent infarctsPre-existent atrophyPresence of abnormal periventricular signal on magnetic resonance imaging, or (especially) on computed tomographyCADASIL = cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy Back to text 2: Pathogenetic mechanisms of vascular dementiaI. Infarct (single or multiple)A. Arterial territory infarct Multiple infarcts Single strategic infarcts B. Watershed infarction C. Lacunar infarctionII. Non-infarction ischaemiaA. Subcortical leukoencephalopathy (Binswanger's) B. Laminar necrosis C. Granular atrophy D. Gliosis or sclerosisIII. HaemorrhageA. Subdural B. Subarachnoid C. Intracerebral Back to text 3: Clinical assessment for vascular dementia History should include onset, course and nature of cognitive deficits, and information from the carer or other person close to the patient on subtle personality and behavioural changes that may have been noticed. Full neuropsychological evaluation is required at some stage, although the Mini-Mental State Examination,18 supplemented by clock-drawing and clinical assessment of frontal lobe functioning, may be useful for screening. Assessment of functional losses. This may be aided by administration of scales for activities of daily living and instrumental activities of daily living, and assessment at home by an occupational therapist. Psychiatric evaluation is important, as depressive disorder is common in patients with cerebrovascular disease and depression may produce a syndrome resembling dementia. Anxiety disorders and psychotic symptoms may also occur in people with vascular dementia. General physical examination, including pulse irregularity, cardiovascular status, carotid bruits, fundus examination, peripheral vascular disease and hypertension (multiple blood pressure measurements). Examination for focal neurological signs, in particular gait abnormality, visual field defects, pseudobulbar palsy (dysarthria, dysphagia, spastic tongue, brisk jaw jerk), brisk reflexes, extensor-plantar responses and spasticity in the limbs. Routine investigations, including full blood count, erythrocyte sedimentation rate, blood glucose, serum cholesterol and triglyceride level, syphilis serology, electrocardiogram, and chest x-ray. Investigations are directed towards providing evidence for CVD and its risk factors. Structural brain imaging (computed tomography or magnetic resonance imaging) is essential to provide information on the extent, type and distribution of vascular lesions and to exclude other potential causes of dementia, such as subdural haematoma or tumour. Functional imaging, such as single photon emission tomography, positron emission tomography and functional magnetic resonance imaging, may provide further information on the functional significance of any observed lesions or detect abnormalities not apparent on structural imaging. Other specialised investigations may include echocardiography, carotid doppler, antinuclear antibodies, antiphospholipid antibodies, lupus anticoagulant, serum protein electrophoresis and cerebrospinal fluid examination. Back to text 4: Some strategies for primary prevention of vascular dementia Target high risk groups. These include elderly people; people with hypertension, diabetes, atrial fibrillation, or past transient ischaemic attack or stroke; and smokers. Treat hypertension optimally. Treat diabetes. Control hyperlipidaemia. Persuade patients to cease smoking and decrease alcohol intake. Prescribe anticoagulants for atrial fibrillation. Provide antiplatelet therapy for high risk patients. Perform carotid endarterectomy for severe (> 70%) carotid stenosis. Use dietary control for diabetes, obesity and hyperlipidaemia. Recommend lifestyle changes (eg, weight loss, exercise, reduce stress, decrease salt intake). Intervene early for stroke and transient ischaemic attacks with neuroprotective agents (eg, propentofylline, calcium channel antagonists, N-methyl-D-aspartate receptor antagonists, antioxidants). Provide intensive rehabilitation after stroke. Back to text

Perminder S Sachdev · Henry Brodaty

Alternative Medicine Hypericum perforatum (St John's wort) in depression: pest or blessing? Joseph M Rey and Garry Walter St John's wort (SJW) was introduced into Australia during the 1880s for medicinal purposes, but was subsequently declared a noxious weed. There is now a resurgence of interest in the therapeutic properties of this herb. In particular, use of SJW as an antidepressant has increased in recent months owing to reports of its effectiveness and safety. Nevertheless, the controlled trials available have limitations. Increasing use of SJW in the community poses a variety of questions. For example, should medical practitioners become more knowledgeable about the effects and interactions of alternative remedies? What are the ethical and medical implications of "antidepressant" prescribing by non-medical persons? Who is to fund further research and treatment studies? How can quality of SJW preparations be guaranteed? (MJA 1998; 169: 583-586) Introduction - Botany - Active constituents - Antidepressant? - Mechanism of action - "First, do no harm" - Other health claims - Preparations - Precautions - Implications - Acknowledgements - References - Authors' details - - More articles on Complementary medicine "What is a weed? A plant whose virtues have not been discovered" - Ralph Waldo Emerson, Fortune of the Republic. Introduction Although a considerable proportion of the Australian population uses herbal medicines regularly,1,2 most medical professionals distrust herbal remedies and know little about them.3 This scepticism may be related to the perception that many of the claims of herbalists are unproven or fanciful. One of the current health crazes in Europe and the United States concerns Hypericum perforatum, more commonly known as St John's wort (SJW). Used to treat a range of ailments for more than 2000 years, and said to have been prescribed by Hippocrates himself,4 it is the apparent value of SJW as an antidepressant that has captured most recent attention, and been the subject of a recent meta-analysis.5In the past year alone, 10 books extolling the antidepressant effects of SJW were published. The titles are eloquent enough, among them St John's wort: nature's blues buster6 and The natural Prozac program: how to use St John's wort, the antidepressant herb.7 There have also been many review articles published in botanical and herbal medicine journals.8 An article in Time9 in 1997 elevated the herb to superstar status in the United States, and sales of SJW in that country skyrocketed. In Germany, SJW is used more extensively than conventional antidepressants for treating depression.10 In Australia, SJW has been attracting increasing media attention. Undoubtedly, consumption of this herb will become more prevalent. Are assertions about the antidepressant effects of SJW justified? The fact that the National Institute of Mental Health (NIMH) in the United States recently funded a US$4 million trial gives some credence to the claims. The NIMH study is testing whether SJW is more effective than a placebo or a selective serotonin reuptake inhibitor in the treatment of depression. If SJW does reduce depressive feelings, should we recommend its use? Are the extracts from SJW safe for human consumption? In this article, we seek to answer these questions and to inform clinicians about this herbal treatment, particularly in relation to depression. Botany The genus Hypericum contains more than 300 species. Hypericum perforatum is the species most often used in herbal remedies. It is an upright bush, growing to a metre tall, with oblong, perforated leaves and bright yellow flowers (see Figures). The leaves are dotted with translucent glands. There are many explanations for the appellation "St John's wort" (wort means "plant" in Old English); one is that the plant was named after St John the Baptist because the flowers were said to bloom on the anniversary of his execution. SJW is native to Europe, Asia and Africa, but not Australia. It has been introduced to parts of Queensland, New South Wales, Victoria, South Australia and Tasmania. The original introduction has been traced to the Ovens Valley in Victoria during a gold boom in the 1880s, when a German woman imported seed of the plant and established it for medicinal purposes.11 It soon overran her garden and spread to the nearby racecourse, from where it attracted the local name of "racecourse weed". As the goldminers moved out seeking new fields, the plant went with them, mainly in chaff for their horses. SJW has been declared a noxious weed in most areas; however, in some quarters the attitude towards the herb has changed and it is beginning to be seen as a cash crop. Earlier this year, the St John's Wort Landholders' Association was launched in Bathurst, NSW, to encourage harvesting of the weed.12 Australia expects to provide up to 20 per cent of the 7000 tonnes of SJW used worldwide each year.12 Active constituents Many constituents with potential biological activity have been extracted from the flowers and leaves, the parts of the plant used for medicinal purposes.4,8 These include naphthodianthrones, flavonoids, phloroglucinols and xanthones. Hypericin, one of the naphthodianthrones, has traditionally been considered the main active ingredient, but it is not known whether it is the antidepressant compound. The amount of hypericin varies widely in different parts of the plant, under different growth conditions, and at different times of the year.4,8 Is St John's wort antidepressant? Most of the research on SJW has been performed in Germany and published in Continental journals. There have been numerous open trials of SJW in depression and 24 double-blind studies: eight randomised, double-blind studies comparing SJW to other active medications (desipramine,13 imipramine,14,15 amitryptiline,16,17 diazepam18,19 and maprotiline20) and 16 randomised, double-blind studies comparing SJW to placebo. In two studies13,21 SJW was used in combination with valerian. There have been no head-to-head trials with newer antidepressants. As noted, an NIMH study is currently comparing SJW with a selective serotonin reuptake inhibitor and a placebo. A meta-analysis assessing 23 of the double-blind trials was published recently,5 and will not be replicated in this article. In summary, most patients in the reports had mild to moderately severe depression. (In mild depression the patient is distressed by depressive symptoms but will probably be able to perform most activities; symptoms are more numerous and intense when depression is of moderate severity, and the patient is likely to have significant difficulty in continuing with ordinary activities.)22 Three trials included patients with severe depression. Most trials lasted four to eight weeks. Across all reports, 50%-80% of patients improved with SJW, a rate similar to that achieved with conventional antidepressants. Patients with mild to moderate depression fared best. Vorbach et al found SJW superior to imipramine (75 mg/day) in severe depression,15 but the dose of imipramine was inadequate. SJW was found to be as effective as phototherapy in patients with seasonal affective disorder.23 A field of St John's wort. Declared a noxious weed in most areas of Australia, St John's wort is now being seen as a cash crop. Inset: Details of the flower. Photos courtesy of NSW Agriculture. Linde et al concluded that these studies had significant limitations.5 Most of the trials were small and used heterogeneous patient groups. Classification of depression was not uniform and none of the studies lasted longer than 12 weeks. Dosages of antidepressant in the comparison trials were subtherapeutic or in the low therapeutic range. Mechanism of action Although the exact mechanism of action remains obscure, substances contained in SJW extracts have been found to interact with a number of neurotransmitter systems implicated in depression and in psychiatric illness generally. SJW inhibits uptake of serotonin, noradrenaline and dopamine. Crude extract of SJW has a potent affinity for g-aminobutyric acid (GABA) receptors and inhibits monoamine oxidase.24 Recently, it has been postulated that the antidepressant effect of SJW may be due to its effect on interleukin-6.25 It is also of interest that the plant has high concentrations of melatonin,26 increases nocturnal production of melatonin,4 and increases deep sleep.27 Melatonin is thought to play a role in the aetiology of seasonal affective disorder and sleep.28 "First, do no harm" The popular belief that "natural products are safe" has not always been vindicated, as the tragic experience with royal jelly revealed.29 However, SJW has not been associated with serious adverse events in humans and appears well tolerated. The rates of adverse events with placebo (4.8%) and SJW (4.1%) in placebo-controlled trials are comparable.5 Fewer than 2% of patients in studies have stopped taking SJW.30 In an open trial of 3250 patients taking hypericum, side effects were reported by 2.4% of subjects.30 The most commonly noted adverse events were gastrointestinal symptoms (0.6%), allergic reactions (0.5%), fatigue (0.4%) and restlessness (0.3%). Other adverse reactions reported were emotional vulnerability, pruritus, weight gain and dizziness.4 Severe phototoxicity has been reported in cattle and sheep grazing on the plant8 (the veterinary term is "hypericism"), but not in humans taking therapeutic (antidepressant) doses. However, photosensitivity does appear to be a common problem for AIDS patients treated with high doses of hypericum in studies of the antiviral properties of SJW.4During the past 25 years there have been three reports, all in the past few months, to the Australian Adverse Drug Reactions Advisory Committee (ADRAC) relating to SJW (Dr Patrick Purcell, Acting Head, ADRAC, personal communication). These comprised hyperaesthesia in a 38-year-old woman; a combination of dyspnoea, flushing, headache, hyperventilation, mydriasis, nausea, pain, palpitations, rhinitis and tremor in a 47-year-old woman; and a fall in cyclosporin levels to 25% of previous levels in a woman in her mid-twenties (enzyme induction?). The low rate of reports to ADRAC may be due to under-reporting, insufficient identifying information about many of the herbs reported, uncommon use (until recently), or a low actual rate of adverse effects.31 Other health claims SJW is being promoted as a treatment for a range of other ailments besides depression, including anxiety and "stress", sleep problems, nocturnal enuresis, bacterial and viral infections, respiratory conditions, peptic ulceration, inflammatory arthritis, cancer, and skin wounds.4 It is also said to increase libido, an application dating from the Middle Ages: Take the ash of starlizard, civet oil and St John's wort oil. Smeared on the toe of the left foot and on the loins, the ointment will serve to reinvigorate.32 Tradition further had it that the herb would be most effective for stimulating sexual desire when picked at night while the picker was naked!32 Preparations, dosage and administration SJW is available as tablets, capsules, drops and teas and is produced by many manufacturers. An oil form is available for external use but has no place in treating depression. The optimum adult dose of SJW for treating depression, based on available studies, appears to be 300 mg of plant extract orally three times daily. However, doses used varied considerably among studies, and there are no systematic studies on the minimum therapeutic dose. Furthermore, the amount of active substances might vary depending on factors such as the extraction process, season, and plant part used. As with prescription antidepressants, there is a lag in onset of action. If side effects are intolerable, or if at six weeks SJW is deemed to be ineffective, the patient can be weaned off SJW and another antidepressant considered. Unfortunately, there are no data about "washout periods" following discontinuation of SJW. A conservative approach is to wait two weeks after ceasing SJW before commencing another agent. Precautions Because SJW may potentiate monoamine oxidase inhibitors (MAOIs), its combination with these compounds is best avoided. At this stage, combining SJW with other antidepressants is strongly discouraged for the same reasons. To our knowledge, there are no reports of dietary interactions with SJW, similar to those found with MAOIs, and no empirical studies dealing with this issue. Uterotonic activity has been reported in animal experiments,33 and for this reason SJW is not recommended in pregnancy. SJW has not been evaluated in children and adolescents. Because of the potential risk of phototoxicity, it has been suggested that patients should be advised not to sunbathe (naturally or artificially) while taking SJW and not to concurrently use photosensitising drugs such as chlorpromazine or tetracyclines. Implications for practice, research and policy Over the past few years the physical treatment of depression has been bolstered by the emergence of a number of new classes of antidepressant (such as selective serotonin reuptake inhibitors, reversible inhibitors of monoamine oxidase type A, serotonin and noradrenaline reuptake inhibitors, and 5-HT2 antagonists). A variety of augmenting agents are available and electroconvulsive therapy retains a place for more severe cases. Cognitive-behaviour therapy is also effective. Nevertheless, not all patients benefit from "standard" treatments and some people experience troublesome side effects. Further, antidepressant drugs are yet to meet with uniform community acceptance. A recent national survey found that, for depression, conventional antidepressants were perceived as helpful by 29% of respondents and harmful by 42%.34 In contrast, the treatment category that included vitamins, minerals, tonics and herbal medicines was considered helpful by 57% of respondents and harmful by 3%. Clearly, there is scope for alternative antidepressants if they can be shown to be safe and effective. SJW is the best known of several herbs being touted as antidepressant.24 However, available evidence for SJW is insufficient at this stage. Indeed, one of the aims of treating depression, the prevention of suicide, could be compromised by using a treatment that is yet to be fully investigated. If SJW is to consolidate a place in the medical armamentarium, several issues relating to clinical practice, research and policy will need to be addressed: Acknowledgement by medical practitioners of the existence of an alternative treatment system. The presence of another therapeutic system cannot be ignored.3,34,35 We need to routinely ask our patients about their use of SJW and other herbal preparations. This is particularly important as concurrent use of SJW and other antidepressant drugs may be harmful. Quality control of SJW preparations. The Register of Therapeutic Goods currently categorises SJW and most herbal preparations as "listed drugs", which are subject to fewer checks than "registered drugs". Apart from having to satisfy less-rigorous efficacy and safety criteria compared with registered drugs, listed drugs lack standardised preparation and are more prone to contamination, substitution, adulteration, incorrect packaging, wrong dosage, and inappropriate labelling and advertising.31 For example, in the case of SJW there is presently no way of knowing that the correct species of Hypericum is used, that the plant is harvested at the right time of year, that appropriate plant parts are chosen, dried and stored properly, and that the extraction process is uniform. All of these are known to affect biological activity. Funding of further research. Several breakthroughs in therapeutics have resulted from the study of natural substances,24 and SJW also promises to be rewarding in this area. However, further research into SJW will need to be funded from outside the pharmaceutical industry, by the National Health and Medical Research Council or other institutions. Herbal treatments cannot be patented, so the financial incentives for research that drive the pharmaceutical market are limited. Determination of the antidepressant component. SJW has many biologically active components. Determination of which of these are antidepressant may, in turn, contribute to the development of more refined preparations of SJW and further antidepressants, as well as increase our knowledge about the aetiology of depression. New treatment studies. To date, duration of trials has ranged from two to 12 weeks. Longer-term studies should be done to assess long term effects and the effectiveness of SJW in preventing relapse. Patient populations need to be described better and therapeutic doses of comparison antidepressants need to be used. Evaluation of SJW in certain subgroups. SJW has mainly been studied in adults with mild to moderate depression. There is a need to evaluate the herb in severely depressed patients. There is also a growing realisation that major depression is not uncommon in young people. Adult data cannot necessarily be generalised to the young, as the experience with tricyclic antidepressants has shown.36 Trials with children and adolescents are therefore necessary. The current situation in which treatment of depression with SJW is initiated by non-medical persons is fraught with danger. Suicide risk has been mentioned already. Non-medical prescription and supervision may preclude patients from receiving antidepressant treatments of demonstrated effectiveness. This has ethical implications, particularly in the case of children.37 Also, medical conditions that mimic depression, some of them common (eg, hypothyroidism), may remain unidentified and untreated. On the other hand, access to an over-the-counter antidepressant might be useful for patients with subclinical depression who are unlikely to be treated otherwise.38 For these reasons, a wider debate about who should prescribe SJW may be necessary. We find ourselves in the midst of an era in which new, better-tolerated therapeutic agents are being regularly introduced. Paradoxically, patients are turning to herbal remedies. Time will tell whether, in Australia, SJW is allowed to blossom in medicine as a bona fide antidepressant, or whether it should be weeded out. Acknowledgements Con Spiliopoulos, Glenda Schaffer, Susie Freeman, Rachel Rees, Patrick Purcell and Helen Cameron are thanked for their assistance. References MacLennan AH, Wilson DH, Taylor AW. Prevalence and cost of alternative medicine in Australia. Lancet 1996; 347: 569-573. Kristoffersen SS, Atkin PA, Shenfield GM. Uptake of alternative medicine [letter]. Lancet 1996; 347: 972. Thompson A. As patients embrace herbal remedies, dearth of scientific evidence frustrates clinicians. Am J Health Syst Pharm 1997; 54: 2656, 2658, 2664. Chavez ML, Chavez ML. Saint John's wort. Hosp Pharm 1997; 32: 1621-1632. Linde K, Ramirez G, Mulrow CD, et al. St. John's wort for depression: an overview and meta-analysis of randomised clinical trials. BMJ 1996; 313: 253-258. Cass H. St John's wort: nature's blues buster. New York: Avery Publishing Group, 1998. Zuess J. The natural Prozac program: how to use St John's wort, the antide pressant herb. New York: Three Rivers Press, 1997. Wohlmuth H. St John's wort -- phytotherapy for depression. Botanical Pathways 1997; 2: 3-5. Nash M. Nature's Prozac? Time 1997; Sep 22: 80-81. De Smet PAG, Nolen WA. St John's wort as an antidepressant. BMJ 1996; 313: 241-242. Parsons WT. Noxious weeds of Victoria. Melbourne, Inkata Press, 1973. Crossweller A. Farmers to cash in by weeding out wort. Daily Telegraph (Sydney). 1998; July 6: 5. Steger W. Depressive verstimmungen. Z Allgemeinmed 1985; 61: 914-918. Werth W. Psychotonin M versus imipramin in der chirurgie. Der Kassenarzt 1989; 15: 64-68. Vorbach EU, Hubner WD, Arnoldt KH. Effectiveness and tolerance of the hypericum extract L1 160 in comparison with imipramine: randomised double blind study with 135 outpatients. J Geriatr Psychiatry Neurol 1994; 7 Suppl 1: S19-S23. Kniebel R, Burchard JM. Zur therapie depressive verstimmungen in der praxis. Z Allgemeinmed 1988; 64: 689-696. Bergmann R, Nubner J, Demling J. Behandlungen leichter bis mittelschwerer depressionen. Therapiewoche Neurologie/Psychiatrie 1993; 7: 235-240. Warnecke G. Beeinflussung klimakterischer depressionen. Z Allgemeinmed 1986; 62: 1111-1113. Panijel J. Die behandlung mittelschwerer angstustande. Therapiewoche 1985; 41: 4659-4668. Harrer G, Hubner WD, Podzuweit H. Effectiveness and tolerance of the hypericum extract L1 160 compared with maprotiline: a multi-centre double-blind study. J Geriatr Psychiatry Neurol 1994; 7 Suppl 1: S24-S28. Ditzler K, Gessner B, Schatton WFH, Willems M. Clinical trial on Neuropas versus placebo in patients with mild to moderate depressive symptoms: a placebo- controlled, randomised double-blind study. Complement Ther Med 1994; 2: 5-13. World Health Organization. The ICD-10 classification of mental and behavioral disorders. Clinical descriptions and diagnostic guidelines. Geneva: World Health Organization, 1992; 121-122. Martinez B. Hypericum in the treatment of seasonal affective disorder. J Geriatr Psychiatry Neurol 1994; 7 Suppl 1: S29-S33. Cott J. Natural product formulations available in Europe for psychotropic indications. Psychopharmacol Bull 1995; 31: 745-751. Thiele B, Brink I, Ploch M. Modulation of cytokine expression by Hypericum extract. J Geriatr Psychiatry Neurol 1994; 7 Suppl 1: S60-S62. Murch SJ, Simmons CB, Saxena PK. Melatonin in feverfew and other medicinal plants. Lancet 1997; 350: 1598-1599. Schulz H, Jobert M. Effects of hypericum extract on the sleep EEG in older volunteers. J Geriatr Psychiatry Neurol 1994; 7 Suppl 1: S39-S43. Wirz-Justice A. Biological rhythms in mood disorders. In: Bloom FE, Kupfer DJ, editors. Psychopharmacology: the fourth generation of progress. New York: Raven Press, 1995; 999-1018. Bullock RJ, Rohan A, Straatmans JA. Fatal royal-jelly induced asthma [letter]. Med J Aust 1994; 160: 44. Woelk H. Benefits and risks of the hypericum extract L1 160: drug monitoring study with 3250 patients. J Geriatr Psychiatry Neurol 1994; 7 Suppl 1: S34-S38. Drew AK, Myers SP. Safety issues in herbal medicine: implications for the health professions. Med J Aust 1997; 166: 538-541. Fletcher K. Themes for herbal gardens. Ringwood, Victoria: Viking, 1996; 16. Shiplochliev T. Extracts from a group of medical plants enhancing the uterine tonus. Vet Med Nauki 1981; 18: 94-98. Jorm AF, Korten AE, Jacomb PA, et al. Mental health literacy: a survey of the public's ability to recognise mental disorders and their beliefs about the effectiveness of treatment. Med J Aust 1997; 166: 182-186. Shenfield GM, Atkin PA, Kristoffersen SS. Alternative medicine: an expanding health industry. Med J Aust 1997; 166: 516-517. Hazell P, O'Connell D, Heathcote D, et al. Efficacy of tricyclic drugs in treating child and adolescent depression: a meta-analysis. BMJ 1995; 310: 897-890. Komesaroff PA. Use of complementary medicines: scientific and ethical issues. Med J Aust 1998; 169: 180-181. Cott JM, Fugh-Berman A. Is St John's wort (Hypericum perforatum) an effective antidepressant? J Nerv Ment Dis 1998; 186: 500-501. Authors' details Rivendell Unit, Concord West, NSW. Joseph M Rey, PhD, FRANZCP, Director, and Clinical Professor, Department of Psychological Medicine, University of Sydney; Garry Walter, FRANZCP, Inpatient Director, and Clinical Lecturer, Department of Psychological Medicine, University of Sydney. Reprints will not be available from the authors. Correspondence: Dr J M Rey, Rivendell Unit, Hospital Road, Concord West, NSW 2138. E-mail: jreyATmail.usyd.edu.au ©MJA 1998 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/>

Joseph M Rey · Garry Walter

Book Review Art brut The Cunningham Dax Collection: selected works of psychiatric art. Eric Cunningham Dax. Melbourne, Australia: Melbourne University Press 1998 (102 pp., $24.95). ISBN: 0 522 84768 4. For about half a century, the eminent Australian-based psychiatrist Eric Cunningham Dax AO has nurtured a collection of upward of nine thousand items of psychiatric art -- paintings, statues and embroideries executed by patients in the course of their treatment. The collection, currently housed in Melbourne, is one of only a handful in the world that classify items according to the patient's diagnosis for teaching, treatment and research purposes. Thanks to the sponsorship of the Gordon Darling Foundation, part of the collection is now accessible at all times and in all places via an inexpensive softcover volume of colour photographs of about 100 selected works, with succinct expert commentary and interpretation by Dax. A man feeling he is in hell tries to save himself by grasping at the roots of a tree, which he fails to reach. The artist killed himself a short time later. The three cardinal signs of a maniacal illness are elation, overactivity and a flight of ideas. This picture is unusual because a person who is acutely disturbed in this way rarely has the time or patience to complete a work. Here there are bright colours, many related ideas and symbols, an explosive jack-in-the-box and great activity. Ann Gregory Assistant Editor, MJA 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/>

Ann Gregory

- - More articles on Obstetrics & gynaecology and women's health Abstract Objectives: To review the evidence from all studies of adverse effects on infant outcome of psychotropic medications taken during pregnancy. Data sources: MEDLINE January 1976 - February 1998, EMBASE 1976 - February 1998, and bibliographies of retrieved articles. Study selection and data extraction: All studies focusing on adverse effects associated with psychotropic drug use during pregnancy, with a particular focus on prospective controlled studies. Outcome criteria: Congenital anomalies, perinatal complications and neurobehavioural sequelae. Data synthesis: 23 studies were identified, nine of which were prospective controlled studies: five involving antidepressants (tricyclic antidepressants [TCAs] and selective serotonin reuptake inhibitors [SSRIs]), one each involving lithium and carbamazepine, and two involving benzodiazepines. As statistical synthesis was not possible given the heterogeneity of outcome criteria, a qualitative review is provided. Neither the SSRIs nor the TCAs appear to cause major congenital anomalies, but both may be associated with a small increased risk of minor anomalies, prematurity and neonatal complications. Benzodiazepines, lithium, anticonvulsants and chlorpromazine do lead to an increased rate of congenital anomalies as well as neonatal problems. Studies of longer-term neurobehavioural sequelae of psychotropic medications are very limited, but at present do not indicate any adverse effects. Conclusions: While some psychotropes are associated with congenital anomalies and perinatal complications, mental illness per se may also be associated with an adverse outcome in the infant. Clearly, the risks to both mother and infant need to be carefully weighed and discussed with the parents. MJA 1998; 169: 428-431 Introduction Almost fifty per cent of pregnancies are unplanned,1 and up to 35% of pregnant women in western societies will be taking psychotropic medication.2 Most psychiatric disorders among women arise in the childbearing years, particularly in the Fperinatal period,3 and the effects of psychotropic medications on the fetus can present dilemmas in the treatment of pregnant women. One solution may be to cease therapy with these medications when pregnancy is contemplated or confirmed. However, women who stop taking medications during pregnancy experience high relapse rates.4 Suicidal behaviour, poor self-care, inadequate nutrition and poor antenatal clinic attendance, with a consequent lack of fetal monitoring, can all present risk to the fetus. Another aspect of mental illness during pregnancy is the possible direct effect of maternal illness per se on the fetus. Some studies have found an association between antenatal anxiety in women and increased obstetric complications such as prematurity, low birth weight,5 smaller head circumference and poorer scores on neonatal neurological examination.6 Women of low socioeconomic status who have depression have higher rates of premature and low birth-weight infants,7 while women with bipolar disorder who are not medicated also have higher rates of neonatal deaths and structural anomalies.8,9 One meta-analysis reports a higher incidence of obstetric complications in women with schizophrenia, regardless of whether the illness (and medications) began before or after delivery.10 This review examines the available evidence on the effects on the fetus of psychotropic medication used during pregnancy and provides some recommendations for treatment. Methods We searched MEDLINE (January 1976 - February 1998) using the following exploded medical subject headings (MeSH): "follow-up studies", "psychotropic drugs", "prenatal exposure", "adverse effects", "anticonvulsants", "pregnancy", "depressive disorder", "antidepressants", "infant" and "child development". A similar strategy was used in our EMBASE search (1976 - February 1998). Searches were limited to the English language. Studies that provide the highest level of evidence -- randomised controlled trials -- are not ethically acceptable in pregnancy. Thus we reviewed abstracts of articles for studies that met the following selection criteria: prospective controlled studies; retrospective studies; and case studies. This review is qualitative as the heterogeneity of outcome indicators means that data could not be analysed statistically. Outcome criteria Psychotropic drug use in pregnancy may be associated with three types of adverse outcome for the infant. Congenital anomalies: both major and minor physical anomalies (ie, those with and without cosmetic or functional importance) may occur with first-trimester exposure. The background incidence for each is 2%-4% and the cause is most often unknown.11 Perinatal complications: including poor obstetric outcome (eg, prematurity or low birth-weight) or syndromes related to drug use late in the third trimester, such as neonatal withdrawal or toxicity in the first few days after birth. Neurobehavioural sequelae: developmental delays, learning difficulties and neurological deficits resulting from drug exposure at any time in pregnancy. Results Of 23 studies identified, nine were prospective, non-randomised controlled studies. Five of these involved antidepressants (tricyclic antidepressants [TCAs]12,13and selective serotonin reuptake inhibitors [SSRIs]12-16), one involved lithium,17one carbamazepine,18 and two, benzodiazepines.1,19 These studies all controlled for maternal age and past obstetric history; some controlled for alcohol and smoking,12,13,15 but none controlled for other drugs. Summaries of the treatment of psychiatric disorders and use of psychotropic medications during pregnancy are shown in Boxes 1-4. Antidepressants Selective serotonin reuptake inhibitors (SSRIs): Fluoxetine was the first SSRI to be marketed and is the subject of most data currently available. Two prospective, controlled, but non-randomised, studies, have examined infant outcome in terms of congenital anomalies and perinatal complications after exposure to fluoxetine during pregnancy.12,14 Pastuzsak et al,12 found that rates of major anomalies and obstetric complications were no greater for women with depression taking fluoxetine, than for two control groups (women with depression exposed to tricyclic antidepressants, and non-depressed women not exposed to antidepressants, or other potential teratogens). Both groups with depression had increased rates of miscarriage and neonatal complications, including jaundice, hypotonia, cyanosis, apnoea and a number of minor physical anomalies (club feet, hydrocele, congenital hip dislocation and lacrimal stenosis). Chambers et al,14 found no increase in the rate of miscarriage and major anomalies, but among 97 infants examined for minor physical anomalies there was a significant increase in the number of infants with three or more such anomalies in the fluoxetine-exposed group. Infants of women exposed to fluoxetine in the third trimester had higher rates of prematurity, admission to special-care nurseries and poor neonatal adaptation than those exposed only in the first- and second-trimesters. In a prospective study of exposure to a variety of other SSRIs, Kulin et al found no increased rate of major congenital malformations, miscarriage, stillbirth or prematurity.15 Results from two non-controlled prospective studies of fluoxetine were conflicting. Goldstein, looking specifically at obstetric and neonatal complications with third-trimester exposure, reported a rate of neonatal complications comparable to that found in a general population survey, but almost double the normal rate of premature births,22 while McElhatton et al reported no increase in perinatal complications.23 Although the study of Chambers et al14 was far more methodologically sophisticated, its conclusions are still limited by its failure to control for use of other medication, smoking or alcohol. Given the lack of use of patients with depression as control subjects, none of these studies were able to separate any effect of depression per se from that of antidepressants on congenital anomalies or perinatal complications. In terms of neurobehavioural sequelae, a well-controlled study of children exposed to fluoxetine in utero and followed-up to the age of four, showed no increase in neurobehavioural deficits or developmental delays compared with non-exposed children of depressed mothers.13 Tricyclic antidepressants (TCAs): In terms of congenital anomalies and perinatal complications, a recent review of pooled results of 338 mothers indicated no increased risk of major structural anomalies with first-trimester exposure.20 Only two prospective studies have examined the potential teratogenic risk of tricyclics.12,23 Their findings were identical to those reported for fluoxetine. There have been some case reports of neonatal TCA withdrawal syndromes (irritabilty, jitteriness and convulsions)24 and anticholinergic effects (constipation and urinary retention).17 For neurobehavioural sequelae, the study of Nulman et al reported no increase in neurobehavioural deficits or developmental delays compared with non-exposed children.13 Other antidepressants (moclobemide, venlafaxine, nefazodone, mianserin, MAOIs): Heinonen et al cite a study of the use of MAOIs during pregnancy,25 reporting a higher rate of congenital anomalies in exposed infants. A report of 48 infants exposed to mianserin found one case of congenital anomaly.23 The lack of data on the newer antidepressants (moclobemide, venlafaxine, nefazodone) probably reflects their more recent entries onto the market. Benzodiazepines Pooled results from retrospective studies based on birth defect registry data on several hundred women indicate that the relative risk of cleft palate and lip is approximately 2-3-fold with first-trimester exposure to diazepam and 7-fold with alprazolam.20 While this increase in risk is statistically significant, the absolute risk remains small (having increased from 0.06% to 0.7%). The risk associated with other benzodiazepines has not been evaluated. Pastuszak et al prospectively examined 137 cases of benzodiazepine exposure in the first trimester and found no increase in congenital anomalies in the exposed group, but almost double the rate of miscarriages.1 Third-trimester exposure to benzodiazepines, especially to those with a long half-life, may lead to neonatal hypotonicity, failure to feed, apnoea and low Apgar scores.20 A small prospective study of 17 infants reported delays in developmental milestones at 18 months.19 However, a review of the literature on 550 infants followed-up to a maximum of four years of age, found no increase in neurobehavioural sequelae.26 Mood stabilisers Lithium: Initial reports from the Danish Register of Lithium Babies indicated significantly increased rates of cardiovascular malformations.27 A recent review of pooled data suggests a more modest risk of Ebstein's anomaly of the tricuspid valve (10-20 times that in the general population where it occurs in 1/20 000 cases).28 A prospective controlled study of 148 women, found a relative risk of 1.2 for all congenital anomalies and of 3.5 for cardiac anomalies in the babies exposed to lithium.29The "floppy baby" syndrome, in which the infant is hypotonic, cyanosed and suckles poorly is thought to be the result of lithium toxicity.30 Lithium has also been reported to affect neonatal thyroid function. A five-year follow-up of 60 children exposed to lithium in the second- and third-trimesters found no significant differences in developmental anomalies compared with non-exposed siblings.31 This was further supported by follow-up of 21 prospectively recruited infants, which found no difference in attainment of developmental milestones with the matched control group.32 Anticonvulsants: Carbamazepine and sodium valproate are effective mood stabilisers often used as alternatives to lithium for bipolar disorder.33 Data on the safety of using anticonvulsants during pregnancy derives from studies of women with epilepsy. Spina bifida occurs in 0.5%-1% of babies exposed to carbamazepine in the first trimester34 and in 1%-5% of those exposed to sodium valproate (compared with 0.03% in the general population).35 The risk may increase with higher serum levels and use of more than one anticonvulsant. Orofacial clefts and a number of minor malformations may also be associated with the use of these drugs. Withdrawal seizures in the infant have been reported with sodium valproate in a small case series.36 A recent small prospective controlled study of 36 infants indicates no developmental delays or cognitive impairment associated with carbamazepine use throughout pregnancy.18 Antipsychotics Among the typical (older) antipsychotics, pooled results of large retrospective and small prospective controlled studies of low dose chlorpromazine in weeks 4-10 indicate that its use in the first trimester may increase congenital anomalies by 0.4%.20 However, this increase in congenital anomalies was not seen with trifluoperazine.37 Two small retrospective studies of haloperidol exposure in utero also failed to show an increased rate of congenital malformations.38,39 Case reports, and one case series of chlorpromazine and other typical antipsychotics used in the third trimester, report neonatal restlessness, tremor, poor suckling, abnormal movements, jaundice and functional bowel obstruction.40 A five-year follow-up study showed no abnormalities in infants exposed to chlorpromazine in utero.41For the atypical (newer) antipsychotics (eg, clozapine, risperidone, olanzapine, zuclopenthixol) the only data currently available are from case reports, and so far there is no evidence of teratogenicity. There are no data available on neonatal complications or neurobehavioural sequelae. Conclusions The TCAs and SSRIs appear to be relatively safe in pregnancy, although they are possibly associated with increased rates of minor physical anomalies, prematurity, and neonatal complications. Chlorpromazine, long-acting benzodiazepines, lithium, and carbamazepine appear to be associated with major physical anomalies and poor neonatal adaptation. There is, however, some evidence to suggest that mental illness per se may be associated with an adverse outcome in the infant, while the risks to both mother and infant of a prolonged untreated episode of mental illness bear a considerable cost. The chain of causal events linking maternal illness and the use of medication to adverse outcomes in the offspring remains a complex issue. Before a decision concerning the use of psychotropic medication in pregnant women can be made, the risk-benefit ratio must be determined and discussed with the parents. References Pastuszak A, Koren G, Milich V, et al. Prospective assessment of pregnancy outcome following first-trimester exposure to benzodiazepines. In: Koren G, editor. Maternal and fetal toxicology. New York: Marcel Dekker, 1994: 77-88. Doering PL, Steward RB. The extent and character of drug consumption during pregnancy. JAMA 1978; 239: 843-846. Weissman MM, Olfson M. Depression in women: implications for health care research. Science 1995; 269: 799-801. Cohen LS, Rosenbaum JF. Psychotropic drug use during pregnancy: weighing the risks. J Clin Psychiatry 1998; 59 (Suppl 2): 18-28. Hedegaard M, Henriksen TB, Sabroe S, et al. Psychological distress in pregnancy and preterm delivery. Br J Psychiatry 1993; 307: 234-238. Lou HC, Hansen D, Nordenfoft M, et al. Prenatal stressors of human life affect fetal brain development. Dev Med Child Neurol 1994; 36: 826-832. Orr S, Miller C. Maternal depressive symptoms and the risk of poor pregnancy outcome: review of the literature and preliminary findings. Epidemiol Rev 1995; 17: 165-171. Kallen B, Tandberg A. Lithium and pregnancy: a cohort study on manic-depressive women. Acta Psychiatr Scand 1983; 68: 134-139. Kinney DK, Yurgelun-Todd DA, Levy DL, et al. Obstetrical complications in patients with bipolar disorder and their siblings. Psychiatry Res 1993; 48: 47-56. Sacker A, Done DJ, Crow TJ. Obstetric complications in children born to parents with schizophrenia: a meta-analysis of case-control studies Psychol Med 1996; 26: 279-287. Nelson K, Holmes LB. Malformations due to presumed spontaneous mutations in newborn infants. New Eng J Med 1989; 320: 19-23. Pastuszak A, Scick-Boschetto B, Zuber C, et al. Pregnancy outcome following first-trimester exposure to fluoxetine. JAMA 1993; 269: 2246-2248. Nulman I, Rovet J, Stewart DE, et al. Neurodevelopment of children exposed in utero to antidepressant drugs. New Engl J Med 1997; 336: 258-262. Chambers CD, Johnson KA, Dick LM, et al. Birth outcomes in pregnant women taking fluoxetine. New Engl J Med 1996; 335: 1010-1015. Kulin N, Pastuszak A, Sage S, et al. Pregnancy outcome following maternal use of new selective serotonin reuptake inhibitors: a prospective controlled multicentre study. JAMA 1998; 279: 609-610. Loebstein R, Koren G. Pregnancy outcome and neurodevelopment of children exposed in utero to psychoactive drugs: the Motherisk experience. J Psychiatry Neurosci 1997; 22: 192-196. Shearer WI, Schreiner RL, Marshall RE. Urinary retention in a neonate secondary to maternal ingestion of nortriptyline. J Paediatr 1972; 81: 570-572. Scolnik D, Nulman I, Rovet J, et al. The effects of phenytoin and carbamazepine monotherapy on infants' development. In: Koren G, editor. Maternal and fetal toxicology. A clinician guide. New York: Marcel Dekker, 1994: 45-58. Laegreid L, Hagberg G, Lundberg A. Neurodevelopment in late infancy after prenatal exposure to benzodiazepines: a prospective study. Neuropaediatr 1992; 23: 60-67. Altshuler LL, Cohen L, Szuba MP, et al. Pharmacologic management of psychiatric illness during pregnancy: Dilemmas and guidelines. Am J Psychiatry 1996; 153: 592-606. McNeil TF. A prospective study of postpartum psychosis in a high risk group: relationship to demographic and psychiatric history characteristics. Acta Psychiatr Scand 1987; 73: 35-43. Goldstein DJ. Effects of third trimester fluoxetine exposure on the newborn. Clin Psychopharmacol 1995; 15: 417-420. McElhatton PR, Garbis HM, Elefant E, et al. The outcome of pregnancy in 689 women exposed to therapeutic doses of antidepressants: a collaborative study of the European Network of Teratology Information Services. Reprod Toxicol 1996; 10: 285-294. Eggermont E. Withdrawal symptoms in neonates associated with maternal imipramine therapy. Lancet 1973; 2: 680. Heinonen OP, Slone D, Shapiro S. Birth defects and drugs in pregnancy. Littleton, Mass.: Publishing Services Group, 1977. McElhatton PR. The effect of benzodiazepine use during pregnancy and lactation. Reprod Toxicol 1994; 8: 461-475. Schou M, Goldfield MD, Weinstein MR, et al. Lithium and pregnancy, I. Report from the Register of Lithium Babies. BMJ 1973; 2: 135-136. Cohen LS, Friedman JM, Jefferson JW, et al. A reevaluation of risk of in utero exposure to lithium. JAMA 1994; 271: 146-150, correction; 271: 1485. Jacobson SJ, Jones K, Johnson K, et al. Prospective multicentre study of pregnancy outcome after lithium exposure during first trimester. Lancet 1992; 339: 530-533. Schou M, Amdisen A. Lithium and the placenta [letter]. Am J Obstet Gynecol 1995; 122: 541. Schou M. What happened to the lithium babies? A follow-up study of children born without malformations. Acta Psychiatr Scand 1976; 54: 193-197. Koren G, Pastuszak A, Jacobson S, et al. The safety of antidepressants in pregnancy. In: Koren G, editor. Maternal and fetal toxicology. A clinician guide. New York: Marcel Dekker, 1994: 59-76. Mitchell PB, Parker G. Treatment of bipolar disorder. Med J Aust 1991; 155: 488-492. Rosa F. Spina bifida in infants of women treated with carbamazepine during pregnancy. New Engl J Med 1991; 324: 674-677. Omtzigt JGC, Los FJ, Grobbee DE, et al. The risk of spina bifida aperta after first-trimester exposure to valproate in a prenatal cohort. Neurol 1992; 42 (suppl 5): 119-125. Thisted E, Ebbesen F. Malformations, withdrawal manifestations and hypoglycemia after exposure to valproate in utero. Arch Dis Childhood 1993; 69: 288-291. Rumeau-Rouquette C, Goujard J, Huel G. Possible teratogenicity effects of phenothiazines in human beings. Teratology 1997; 15: 57-64. Hanson JW, Oakley GP Jr. Haloperidol and limb deformity [letter]. JAMA 1975; 231: 26. Van Waes A, Van de Velde E. Safety evaluation of haloperidol in the treatment of hyperemesis gravidum. J Clin Pharmacol 1969; 9: 224-237. Auebach JG, Hans SL, Marcus J, et al. Maternal psychotropic medication and neonatal behaviour. Neurotoxicol Teratol 1992; 14: 399-406. Edlund MJ, Craig TJ. Antipsychotic drug use and birth defects: an epidemiologic reassessment. Compr Psychiatry 1984; 25: 32-38. (Received 16 Feb, accepted 8 Jul 1998) Authors' details Prince of Wales Hospital, Sydney, NSW. Marie-Paule V Austin, MB BS, FRANZCP, Staff Specialist in Liaison Psychiatry, and Conjoint Lecturer, School of Psychiatry, University of New South Wales; Philip B Mitchell, MD, FRANZCP, Administrative Director, Mood Disorders Unit, and Associate Professor, School of Psychiatry, University of New South Wales. Reprints will not be available from the authors. Correspondence: Dr M-P V Austin, Department of Liaison Psychiatry, Prince of Wales Hospital, Randwick, NSW 2031. E-mail: m.austinATunsw.edu.au 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/> 1: Treatment of depression in pregnancy If a pregnant woman is currently well, but has a history of relapse on withdrawal of medications, or if her current depressive episode is severe, the benefits of medications (direct for the mother and indirect for the infant) will usually outweigh the potential risks to the infant. It is good practice to use the minimum effective dosage and, if the mother does not plan to breast-feed, to halve the dose in the week before delivery to minimise any potential withdrawal in the infant. The infant should then be observed for withdrawal symptoms. The importance of general issues such as ceasing cigarette and alcohol intake, taking folate supplements and regular antenatal clinic attendance should be stressed to all expectant mothers. 2: Treatment of anxiety disorders in pregnancy Mothers taking a benzodiazepine regularly should be advised to taper the dose and to stop taking it before they become pregnant, and to use cognitive-behavioural management techniques and/or a small dose of a sedating tricyclic antidepressant (such as dothiepen) instead. Intermittent use of short-acting benzodiazepines is probably safe, and the long-acting diazepam used infrequently after the first trimester is probably not harmful. However, long-acting benzodiazepines (diazepam, clonazepam) should be avoided in the days before labour as they may compromise the infant's respiratory function during delivery. In mothers taking benzodiazepines on a long-term basis during pregnancy, and who do not plan to breast-feed, the medication should be slowly reduced before delivery to minimise neonatal withdrawal, and the infant will need to be observed for withdrawal symptoms. 3: Treatment of bipolar disorder in pregnancy First trimester Where possible, plan a drug-free first trimester by slowly tapering both lithium and anticonvulsants (to avoid acute relapse and withdrawal seizures, respectively) before conception. If the use of a mood stabiliser is unavoidable, lithium is a safer option. If first-trimester exposure has occured, an ultrasound scan and echocardiogram should be performed at 16-20 weeks to exclude cardiovascular, midline and other defects, and alpha-fetoprotein levels should be measured, as high levels are associated with congenital abnormalities. With inadvertent exposure to anticonvulsants, folate (which may reduce the risk of neural tube defects) should be given until the end of the first trimester.20 Antipsychotic medications may have to be used to achieve control of any disturbed behaviour in cases of manic relapse. Second- and third-trimesters When necessary, mood stabilisers may be recommenced in the second trimester. Lithium requirements will increase in the third trimester, but it is wise to reduce the dose by 25% just before delivery to avoid possible neonatal toxicity, and babies should be monitored for lithium toxicity for up to 10 days after birth. If the mother does not intend to breast-feed, it is best to reduce anticonvulsants before birth to minimise the risk of neonatal withdrawal symptoms. As women with bipolar disorder are at p articular risk of relapse postpartum (50%),21 therapy with mood stabilisers must be recommenced after the birth of the child. 4: Treatment of psychosis in pregnancy Chronic psychosis: depot antipsychotics are probably best avoided, given the potential for accumulation and toxicity in the neonate. For women with chronic psychosis, it is preferable to switch as early as possible to minimum effective doses of oral trifluoperazine or haloperidol and perform an ultrasound at 16-18 weeks to exclude the development of congenital abnormalities. Intensive case management and liaison with obstetric services is essential during this period as these women are at increased risk of relapse and poor antenatal care once they cease depot medication. Acute recurrent psychosis: should be managed as for bipolar disorder. Back to text

Marie-Paule V Austin · Philip B Mitchell

Eating disorders revisited. I: anorexia nervosa Peter N Gilchrist, David I Ben-Tovim, Phillipa J Hay, Ross S Kalucy and M Kay Walker MJA 1998; 169: 438-441 Synopsis - Introduction - Risk factors - Psychopathology - The role of the GP - Diagnosis - Treatment - References - Authors' details - - More articles on Psychiatry - ©MJA1998 Synopsis Anorexia nervosa is a serious psychiatric illness with a high morbidity and a significant lifetime mortality. Recurring themes in such patients centre on issues of self-worth and control. Treatment is difficult and prolonged, and may require hospitalisation. Therapy focuses on altering the misperceptions that patients have of themselves, both psychologically and physically. A multi-disciplinary team based in a specialised unit provides the treatment of choice, but if this is not available, a consistent, supportive relationship with an individual therapist familiar with the condition will be beneficial. Successful outcome should be based not simply on body weight but also on the resolution of anorexic thinking. Introduction Eating disorders have captured the public imagination. Images of severely emaciated young women suffering from anorexia nervosa appear often in glossy women's magazines and current affairs programs, while public disclosure of bulimia nervosa has become commonplace. This publicity tends to obscure the continuing puzzle created by these enduring, hard-to-treat, and sometimes fatal conditions. It is therefore timely to review the clinical dilemmas provided by eating disorders. Anorexia nervosa is not new,1 having first been described in the 17th century. The clinical presentation appears essentially unchanged since the first comprehensive accounts were produced in the late 19th century. Patients with anorexia nervosa are characterised by a relentless pursuit of thinness, resulting in weight loss and a refusal to maintain a normal body weight. This refusal has been described as a "normal weight phobia". Anorexia nervosa is not common. Worldwide, the true point prevalence is certainly no more than 0.5% of the female population over 15 years of age, and may be considerably less. Two studies of prevalence have been conducted in Australia: one reported a prevalence of 0.1% among a large group of schoolgirls,2 and the other reported a lifetime prevalence of 0.4% among a large group of twins.3 Evidence for changes in the incidence of anorexia nervosa is controversial. Reports of recent increased incidence in specific populations have been criticised on methodological grounds.4 Increased use of hospital services may reflect a change in the threshold for admission, as much as changing incidences.5 In our experience, demand for hospital services for these patients has not changed substantially. Anorexia nervosa can be fatal. Although death rates vary between studies and may be falling, a rule of thumb is that one patient per two hundred treated will die as a result of starvation or suicide during each treatment year. For patients who do survive, the burden of disability and distress remains considerable. Overall outcome varies between studies, but about 40% of patients make a good five-year recovery, 40% remain symptomatic but function reasonably well, and 20% remain severely symptomatic and are chronically disabled.6 Risk factors Sex: Anorexia nervosa occurs mainly, but not exclusively, among women; the female to male ratio is at least 10 to one. The origins of this sex difference remain unclear. However, as a society we are continually bombarded with images of impossibly slender young women. This, in part, explains the development of a "normative discontent" about physiologically unremarkable variations in body weight and shape.7 Dieting: Dieting is common in women in Australia and the first world, but only a small proportion of dieters develop anorexia nervosa. Why this proportion is so small remains unclear. However, normal dieting is almost certainly a trigger for the condition, and participation in occupations or sporting activities that require adherence to a strict diet is likely to place individuals at some risk.8,9 Other influences: Factors ranging from family communication characteristics such as blurring of boundaries and over identification, to personality styles such as perfectionism and obsessionality have been implicated as being of aetiological importance, but none have been validated with any scientific rigour.10 Psychopathology and clinical features The clinical features are deeply distressing for the observer; for the patient, the anorexic condition is a solution, but to what problem? The anorexic attitude is more understandable if being fat is seen as not being good enough, and being thinner is being better. In our view, the anorexic belief is: if my weight is right, then I am all right and if I am thinner then I must be a better person. Although the exact origins of such a state are unclear, patients commonly describe a pre-morbid sense of hopelessness, self-hatred and profound unworthiness. As weight loss occurs, individuals feel more disciplined and special. They can do something that their peers often talk about, but rarely succeed at: they can lose weight. In so doing they feel the ultimate triumph of control over their own bodies. Unfortunately, as self-control fails to influence the sense of self, and distress continues, the person displays a rigidity of outlook, and continues to pursue dietary perfection.11 The clinical picture that results is quite typical (Box 1). A change in eating patterns is one of the earliest signs of the disorder. Commonly, patients develop eating routines that have the effect of spreading out whatever enjoyment is to be had from eating, without losing control. Often these give the family and the patient the impression of an adequate dietary intake. Patients may dirty plates and eating utensils to maintain the facade of eating. Although the term "anorexia" implies loss of appetite, this is not correct. Anorexic patients are terrified of losing control of their appetite. Patients regularly describe a fear that meals will immediately be deposited as fat, so they must maintain control over food intake despite continuing hunger. Many abstain from food; others have eating binges followed by self-induced vomiting or purging. Vomiting and purging can also be seen in individuals whose food consumption is minimal. At one time, it was believed that anorexic patients had a distorted perception of themselves, as though they saw an expanded representation of themselves when they looked in the mirror. That view has not held up to scientific examination, but most people with anorexia nervosa do hold deeply negative attitudes towards their own bodies.12 They commonly feel that their hips and thighs are too large, and that their abdomen is too rounded and protuberant. The tenacity with which those feelings persist even in the face of profound emaciation is one of the most disconcerting and puzzling features of the condition. The clinical presentation and underlying problems are similar in men, although there may be a greater concern about health and fitness, rather than appearances.13 Patients with well-established anorexia nervosa are starving, and demonstrate various associated physiological changes (Box 2). These changes are non-specific consequences of the particular form of starvation seen in anorexia nervosa, and reverse with recovery. Anorexic patients may have changes in their menstrual patterns (oligo- or amenorrhoea) that may be concealed by the use of the contraceptive pill. Menses may cease before any substantial weight loss has occurred. Patients with anorexia nervosa are often depressed. There is debate whether the depression is solely related to the weight loss; more often a depressed mood or self-loathing precedes the decision to lose weight. Patients commonly describe a sense of hopelessness and acknowledge suicidal ideation. There may be a decrease in the level of enjoyment of life, although as they begin to lose weight, there may be increased physical activity. Whether this is a reflection of internal agitation or yet another way to burn off calories is not always clear. Patients often give a history of hyperventilation. Alcohol is used at times to decrease anxiety, and food intake is further reduced to compensate for the caloric intake. The role of the general practitioner General practitioners have an essential role in the early recognition and ongoing management of anorexia nervosa. Patients can present with anorexia nervosa at any age, but the onset of the disorder is most often in the mid-teenage years. Patients rarely present themselves for treatment; usually they are brought by family members who do not know what else to do. The family's concerns should be acknowledged, and the severity and potential chronicity of the illness be discussed even if there has not yet been a dramatic weight loss. For younger patients, the effects of starvation on physical development should be conveyed. Initial assessment is often difficult as patients may endeavour to conceal a degree of weight loss, be reluctant to be weighed, and try to minimise their difficulties. Information from other sources, such as family or school authorities, is usually necessary to complete the clinical picture. General practitioners are familiar with the dilemmas of caring for young people who seek to conceal information regarding their reasons for consulting from their families; when these issues relate to weight or diet, they are best seen as part of the illness. Families are commonly disrupted by the behaviour of the anorexic patient, and need support and advice. General practitioners can play a useful role in providing ongoing information and ensuring that families continue to maintain patients' safety despite entreaties by the patients that they will best recover by being left alone. Formal family therapy improves the outcome of adolescent patients still residing with their families, but does not change the outcome of older patients.14 In our experience, relationships that patients began when severely underweight often involve an element of rescue on behalf of the partner, who will then find actual recovery problematic. Anorexia nervosa is a serious condition and in our view specialised assessment, if only for diagnostic purposes, is indicated wherever possible. Further management can then be discussed with the specialist concerned. The therapeutic challenge presented by anorexic patients should never be underestimated. Diagnosis and investigations The diagnosis remains a clinical one. There are no specific investigations diagnostic of the disorder. The most widely used diagnostic criteria for defining anorexia nervosa are those in Box 3. With careful history-taking clinicians can elicit the degree of weight loss, which should be related to the pre-morbid weight. They should ask about the patient's heaviest, lightest and current weight, and the patient's own perceived ideal weight. Weight loss of more than 15% of average body weight is of considerable concern. Younger patients may show a failure to gain weight with developmental maturation, rather than loss of weight. Further enquiry should be made to determine if the weight loss has been voluntary, and to elicit any accompanying disturbances in body and self-related attitudes. While the diagnosis of anorexia nervosa is dependent on accurate history-taking, supporting observations may be made during physical examination and routine investigations (Boxes 2 and 4). The physical findings associated with starvation are quite variable, but the emergence of the biochemical indicators of starvation (Box 4) indicates a serious deterioration in the patient's health.16 Hormonal investigations are not warranted unless pituitary or ovarian dysfunction is seriously considered. Abnormal results such as hypokalaemia, a metabolic acidosis or alkalosis may suggest an eating disorder if the diagnosis was not previously considered. If the anorexic condition has been longstanding, bone densitometry may be useful to define the degree of bone loss and abnormalities. Treatment Treatment must be tailored to the needs of the patient and the severity of the illness. Denial of the severity or even the existence of a problem is extremely common, and the early phases of treatment are often difficult. Anorexia nervosa is a solution and an escape for the patient, so patients must have confidence that support will be available if they are to confront the varied internal and external conflicts that have precipitated the condition. These underlying problems are hard to deal with while patients have access to anorexia nervosa as a means of avoiding or resolving difficulties, so weight restoration and dietary normalisation remain the fundamental touchstones of treatment. However, they should only be one part of a comprehensive program of care, not a substitute for a long term approach. Referral to a specialised eating disorders service should always be contemplated, even for individuals whose weight loss is not yet marked. Referral is more urgent if amenorrhoea or weight loss of more than 10% has already occurred. If the general practitioner is experienced in the treatment of anorexia nervosa, this should continue, if possible, in conjunction with a specialised unit. Provision of such services varies between centres, however, and access may be particularly difficult for patients in country areas. Patients may become acutely medically unwell as a result of severe weight loss and dehydration, and may require resuscitation before any further treatment can be considered. Our unit has a close working relationship with our intensive care physicians, and severely unwell patients are admitted to the Intensive Care Unit for resuscitation before being transferred to our specialised eating disorders unit. The treatment of anorexia nervosa in our unit has evolved from long term inpatient programs with outpatient follow-up, to a predominantly outpatient strategy with hospital backup.17 Treatment begins on an outpatient basis, with inpatient care reserved for those individuals who fail to progress. The guiding principles of treatment are restoration of a normal weight range for height and age and the identification, and resolution, of the contributing family and personal problems. The hospital and staff should be portrayed as a resource that is available to the patient rather than as being able to provide a magical solution to the individual's problems. An eclectic approach is necessary, including individual and family therapy when warranted, dietary advice and, if considered appropriate, pharmacotherapy. A depressed mood may reflect an associated depressive illness and antidepressant medication can be of use. However, antidepressant medication is not recommended as a routine treatment. If a patient is highly agitated, especially when attempting to eat, then a major tranquilliser that does not have the disinhibiting effects of an anxiolytic agent may be useful, but should be instituted as part of the formal treatment program. Supervised weight gain, often involving bed rest, is still used for those who are unable to gain weight outside hospital. Prolonged hospitalisation is now limited to those who have failed in outpatient treatment or who have not benefited from brief admissions, except in young patients, where it is essential to gain weight to allow normal physical development. For patients who refuse active treatment, are treatment-resistant or live in isolated areas, general practitioners can provide an ongoing monitoring of patients' physical health. Insisting on admission to hospital is occasionally required if the patient is at physical risk, but should be avoided if possible. Such admissions should be in consultation with members of the ongoing treatment team. As a long term strategy, treatment orders have not proved helpful. Forced feeding, either naso-gastrically or intravenously, should only be used in life threatening medical situations, again, in conjunction with the treating team. References Kaufman MR, Heiman H. Evolution of psychosomatic concepts: anorexia nervosa. A paradigm. London: Hogarth Press, 1965. Ben-Tovim DI, Morton J. The epidemiology of anorexia nervosa in South Australia. Aust N Z J Psychiatry 1990; 24: 182-186. Wade T, Heath AC, Abraham S, et al. Assessing the prevalence of eating disorders in an Australian twin population. Aust N Z J Psychiatry 1996; 30: 845-851. Frombonne E. Anorexia nervosa. No evidence of an increase. Br J Psychiatry 1995; 166: 462-471. Halmi K. Changing rates of eating disorders: what does it mean? Am J Psychiat 1997; 152: 1256-1257. Herzog DB, Keller MB, Lavori PW. Outcome in anorexia nervosa and bulimia nervosa. A review of the literature. J Nerv Ment Dis 1988; 176: 131-143. Rodin J, Silberstein L, Striegel-Moore R. Women and weight: a normative discontent. Nebr Symp Motiv 1984; 31: 267-307. Richert AJ, Hummers JA. Patterns of physical activity in college students at possible risk for eating disorders. Int J Eating Disorders 1986; 5: 757-763. Gilchrist PN, Burke L. Eating disorders. In: Bloomfield J, Fricker PA, Fitch KD, editors. Textbook of science and medicine in sport. 2nd ed. London: Blackwell Science, 1995; 665-672. Strober M, Morrell W, Burroughs J, et al. A controlled family study of anorexia nervosa. J Psychiatr Res 1985; 19: 239-246. Vitousek KB, Daly J, Heiser C. Reconstructing the internal world of the eating- disordered individual: overcoming denial and distortion in self-report. Int J Eating Disorders 1991; 10: 647-666. Ben-Tovim DI, Walker MK. A quantitative study of body-related attitudes in patients with anorexia and bulimia nervosa. Psychol Med 1992; 22: 961-969. Carlat DJ, Camargo CA, Herzog DB. Eating disorders in males: a report of 135 patients. Am J Psychiat 1997; 154: 1127-1132. Russell GF, Szmukler GI, Dare C, Eisler I. An evaluation of family therapy in anorexia nervosa and bulimia nervosa. Arch Gen Psychiatry 1987; 44: 1047-1056. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Association, 1994. Sharp CW, Freeman CPL. The medical complications of anorexia nervosa. Br J Psychiatry 1993; 162: 452-462. Kalucy RS, Gilchrist PN, McFarlane CM, McFarlane AC. The evolution of a multi therapy orientation. In: Garner DM, Garfinkel PE, editors. Handbook of psychotherapy for anorexia nervosa and bulimia. New York: Guildford Press, 1984; 458-487. Authors' details Weight Disorder Unit, Flinders Medical Centre, Bedford Park, SA. Peter N Gilchrist, MB BS, FRANZCP, Clinical Director; David I Ben-Tovim, PhD, FRANZCP, Director of Research, and Associate Professor, Department of Psychiatry, Flinders University; M Kay Walker, BA(Hons), Research Officer. Department of Psychiatry, The University of Adelaide, Adelaide, SA. Phillipa J Hay, DPhil, FRANZCP, Senior Lecturer. Department of Psychiatry, Flinders University, Adelaide, SA. Ross S Kalucy, FRACP, FRANZCP, Professor. Reprints: Dr P N Gilchrist, Clinical Director, Weight Disorder Unit, Flinders Medical Centre, Bedford Park, SA 5042. - 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/>

Peter N Gilchrist · David I Ben-Tovim · Phillipa J Hay · Ross S Kalucy

General practice stress Winds of change buffet general practitioners MJA 1998; 169: 126-127 The long-running television series GP,1 with its changing cast of "general practitioners" and patients, nicely portrayed the enormous range and diversity of human problems which Australians expect their general practitioners (GPs) to help them solve. The series showed GPs to be ordinary humans, affected like the rest of the community by changing social and political pressures. In recent years, Australian GPs have felt particularly buffeted by their changing roles and feelings of being undervalued in comparison with their specialist colleagues. A national survey of GPs carried out in 19952 showed that, while about two-thirds were satisfied with their current role, 35 per cent indicated that they would leave general practice if they had somewhere else to go, with urban practitioners significantly more likely than their rural colleagues to report this view. The most common sources of dissatisfaction or frustration were a belief that the contribution of GPs is not appreciated by government, apprehensiveness about the changes and reforms in general practice, a belief that government was interfering in the ability to make clinical decisions, pressure to bulk bill patients, and the introduction of "blended" payments (remuneration through a mixture of fee-for-service and non-fee-for-service payments). In this issue of the Journal, Schattner and Coman3 report on a national sample of metropolitan GPs and their perceptions of stress in their work lives. One hundred and fifty-seven of the 296 respondents (53%) had considered leaving general practice because of occupational stress, and 32 (10.8%) claimed that they had experienced severe occupational stress in the past 12 months. Major work stressors (in terms of both frequency and severity) were time pressure to see patients, paperwork in general practice, and too much work to do in a limited time -- factors the authors define as linked to the context (ie, organisation and environment) rather than the content (ie, clinical duties) of general practice. Other frequent stressors were intrusion of work on family life, earning enough money, the pressure to bulk bill, the cost of practice overheads, phone interruptions during consultations, home visits during office hours, and unrealistic community expectations of the medical profession. There were complex relationships between frequency and severity of stressors -- for example, threat of litigation was ranked lowest for frequency but highest for severity. A third of respondents recorded General Health Questionnaire scores of 4 or more, and 12.8% recorded scores of 8 or more, suggesting that significant numbers of GPs are under real psychological strain. How serious is all of this? Should we be alarmed that those who are the first port of call for sick and stressed people are themselves often feeling stressed and unhappy? Or are GPs simply reflecting the fact that we are all being pushed by the pace of change and pressure to be more efficient and effective? Either way, policymakers would be unwise to ignore these findings. We are an affluent society and can afford a system in which GPs and their patients can spend relatively unpressured time together. The clinical decisions made at the first point of contact should not be made in the context of rapid throughput and time constraint. If our system is stressing the doctors, it is almost certainly also stressing their patients. So what are the solutions? The 1998-99 federal Budget4 contains a number of new initiatives in general practice which grew out of two major strategy reviews, the reports of which have recently been released: General practice. Changing the future through partnerships,5 and General practice education: the way forward.6 The Budget papers claim that these reviews mark a "watershed for general practice, providing a vision which will guide and support the work of the profession in the coming years". They argue that the achievement of this vision will depend to a large extent on building strong partnerships based on mutual trust between general practice, the community and government. The Report of the General Practice Strategy Review Group5 contained 174 recommendations, including a number relating to indexation of the GP benefits schedule, additional funding for rural workforce initiatives, incentives to promote microeconomic reform and practice amalgamations, support for expanded use of information technology, a new Practice Incentive Program to replace the unpopular Better Practice Program, and new funds for research. Most of the Review recommendations have been taken up by the Government, as outlined in the ministerial response to the Report, released on 10 June 1998.7 A report should also be available this year on the Relative Value Study, currently being undertaken under the auspices of the Department of Health and Family Services. This study is assessing the relative value of work (beginning with patient attendances) across craft groups within the medical profession, including an assessment of the relative cost structures of those activities. There are also some signs that GP leaders are talking to each other and that there is some mutual give-and-take by them with government. That, itself, is a healthy sign. Whether stress, dissatisfaction, and psychological strain for GPs working in their consulting rooms will diminish as a result of these and the many other changes on the horizon remains to be seen. Robert M Douglas Director Beverly M Sibthorpe Fellow, National Centre for Epidemiology and Population Health The Australian National University, Canberra, ACT GP [television series]. ABC Sydney: screened 1989 and 1994. Bailie R, Sibthorpe B, Douglas B, et al. Mixed feelings: satisfaction and disillusionment among Australian general practitioners. National Centre for Epidemiology and Population Health discussion paper number 12. ANU, Canberra: NCEPH, 1997. Schattner PL, Coman GJ. The stress of metropolitan general practice. Med J Aust 1998; 169: 133-137. Budget 1998-99 fact sheets. No. 4. Canberra: Department of Health and Family Services, 1998. General practice. Changing the future through partnerships. Report of the general practice strategy review group. Canberra: Commonwealth Department of Health and Family Services, 1998. General practice education: the way forward. Report of the ministerial review of general practice training. Canberra: Commonwealth Department of Health and Family Services, 1998. The Government's response to the reviews of general practice: general practice -- foundations for the future. Canberra: Commonwealth Department of Health and Family Services, 1998. - 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/>

Robert M Douglas · Beverly M Sibthorpe

Suicide among young Australians, 1964-1993: an interstate comparison of metropolitan and rural trends Michael J Dudley, Norman J Kelk, Tony M Florio, John P Howard and Brent G H Waters MJA 1998; 169: 77-80 See also Rosenman Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1998 Abstract Objectives: (i) To compare suicide rates in 15-24 year old men and women; and (ii) for 15-24 year old men, to investigate differences in suicide rates between metropolitan and rural areas, and changes in method-specific suicide rates and, in particular, firearm and hanging suicide rates in rural and metropolitan areas. Design: Retrospective analysis of Australian Bureau of Statistics (ABS) suicide data (1964-1993). Setting: All Australian States. Subjects: Young women and men aged 15-24 years who died by suicide. Results: Male youth suicide rates rose substantially over the 30 years in all Australian States, whereas female rates did not increase. Increases in suicide rates in young men in small rural towns consistently exceeded those in metropolitan areas in all Australian States. Metropolitan rates in 1964 were higher than those in small rural towns, but by 1993 the position was reversed. Medium-sized cities were the only areas where there was no consistent interstate trend. Differences were noted in suicide base rates in different States. High car exhaust suicide rates were noted in Western Australia, and high firearm suicide rates in Tasmania and Queensland. The ratio of firearm suicide rates in small rural areas to those in metropolitan areas rose in all mainland States, but the same ratio for hanging suicide rates changed little. Conclusions: All Australian States reflect national suicide trends in relation to sex and residential area. In some States, particular suicide methods predominate. A decreasing trend in overall firearm suicide rates in young men in all States from 1984 to 1993 conceals substantial increases in firearm suicide rates in small rural areas in all mainland States over the 30-year period. This, together with the marked rate ratio difference in firearm suicides between metropolitan and small rural areas, suggests that particular risk factors for suicide are operating in small rural areas. The fact that hanging rate ratios changed little suggests that more general factors in male youth suicide are also operating in all areas. A better understanding of similarities and differences in health risks faced by metropolitan and rural youth is required. Introduction Suicide rates for 15-24 year old Australian men have trebled since the early 1960s. However, these rate increases have not been uniform. In metropolitan areas they have doubled, but they have increased as much as 12-fold in towns with fewer than 4000 people. The rates for suicide with a firearm in 15-24 year old men have declined overall, and in metropolitan areas since the late 1980s, but they have continued to rise in rural areas. Rates of suicide by hanging have risen in all locations.1We aimed to answer questions about whether these national suicide trends are replicated at the State level. We wanted to know whether the trends for the larger States dominate the national picture, or whether the same fundamental trends are occurring in all States. Interstate analysis is also important, because health, education and welfare services are often organised and funded at a State level. Differences among the States have long been part of the Australian culture, and firearms legislation, in particular, is at present a State prerogative. In this article, we report suicide rates in young men and women (aged 15-24 years) in all Australian States and Territories, as well as suicide rates in young men by method of suicide, and by residential area, in all States, for 1964 to 1993. Methods Our methods are described in more detail elsewhere.1 Data on suicides and corresponding population data for subjects aged 15-24 years were sought from the Australian Bureau of Statistics (ABS) for the years 1964-1993. These data were de-identified, and an undertaking was given not to attempt to identify the subjects or to contact their families. Data concerning usual area of residence were available for all but 219 of 8537 people who had died by suicide. Subjects' usual place of residence was classified as: metropolitan areas of capital cities of each State; cities with populations >100 000; cities with populations >25 000; towns with populations >4000; or towns with populations <400. These cut-offs, chosen after consulting social geographical sources,2,3 approximate Australian urban groupings in order of size. Definitions of "metropolitan" and "rural" also follow guidelines given in these sources. Rates throughout are expressed as numbers of suicides per 100 000 of the at-risk population. Data were aggregated in 5-year epochs to enable longer-term trends to be discerned. Results Sex-specific suicide rates Suicide rates in 15-24 year old men rose substantially over the past 30 years in all Australian States and Territories, but rates in women of the same age did not (Figure 1). We will consider suicide rates in 15-24 year old men only in the remainder of the article. Method-specific suicide rates Considering the whole 30-year period, for 15-24 year old men, a clear trend exists, both nationally and for individual States, of a reduction in firearm suicide rates in the past 10-15 years, and of an increase in hanging suicide rates over the whole period at a substantially greater rate than the increase by all other methods. Car exhaust suicide rates also increased at a greater rate than the overall increase, especially in Western Australia, but to a lesser extent than suicide by hanging. Suicides by poisoning did not increase proportionally in any States or nationally. Hanging is now the most common method of youth suicide in most States, exceeding firearms as a means of suicide in all States except Queensland and Tasmania. In the most recent epoch, firearm suicide rates were highest in Tasmania and Queensland (Figure 2). Residence-specific suicide rates In all States, suicide rates in 15-24 year old men have increased substantially in metropolitan areas, but the greatest increases have been recorded for towns with a population under 4000. In 1964 in four States (New South Wales, Victoria, Queensland, Western Australia), metropolitan suicide rates exceeded those of small rural areas, but by 1993 the position was reversed (Figure 3). New South Wales Suicide rates in 15-24 year old men rose consistently in all residential categories except cities with over 25 000 people. Sydney's rates rose least (1.6-fold), smaller towns (population, <4000) rose the most (9.9-fold), and Newcastle- Wollongong (2.7-fold) and towns with populations over 4000 (3.8-fold) were intermediate. Victoria Suicide rates in 15-24 year old men rose in all residential areas. Melbourne's rates began from a low baseline, and in 1964 rate differences between Melbourne and smaller towns (population, <4000) were less marked than in NSW. Melbourne's rates rose least (4.2-fold), smaller towns with fewer than 4000 people the most (34.5-fold), and Geelong (5.7-fold) and larger towns (population, >4000) (5.5-fold) were intermediate. Queensland Suicide rates in 15-24 year old men in Brisbane trebled, and rates for the Gold Coast and Sunshine Coast, areas with a high population growth, which both now exceed 100 000 people, peaked in the mid 1970s, but then fell. Rates in cities (population, >25 000 and larger towns (population >4000) increased 1.7- and 1.9-fold, respectively, but in smaller towns (population, <4000) the increase was 31.6-fold. South Australia Differences in suicide rates in 15-24 year old men between metropolitan and small rural areas were less marked in States with lower populations. Adelaide's suicide rate for young men rose 2.7-fold, and in towns with populations under 4000 it rose 5.5-fold. Rates in larger towns (population, >4000) increased 1.8-fold. High rates in cities with populations >25 000 were based on small numbers. Western Australia Suicide rates in 15-24 year old men in Perth rose 2.5-fold and rates in smaller towns (population, <4000) rose 7.0-fold. Rates in larger towns (population, >4000) fluctuated, rising 3.2-fold overall. Tasmania Tasmania's suicide rates in 15-24 year old men have been consistently high. While Hobart's rates have more than doubled, rates in smaller towns (population, <4000) have risen 3.6-fold. Trends elsewhere were inconsistent, although high rates have been recorded. Firearm and hanging suicide rates for metropolitan and small rural areas Suicide with firearms or by hanging, the most common methods, account for between a half and two-thirds of suicides in 15-24 year old men in each State, so these have been analysed by place of residence. In all States the ratio of the firearms suicide rate in small rural areas to the firearms suicide rate in metropolitan areas rose substantially over the 30-year period. In contrast, this ratio for suicide rates by hanging remained much the same or rose minimally over the same period. Thus, the national trend for a reduction in firearm suicide rates conceals a continuing rise in firearm suicide rates in rural areas in all States. These increases were especially pronounced in Victoria and Queensland (41.5- and 36.7-fold respectively), while Tasmania's rates remained high throughout the period (Figure 4). Discussion National youth suicide trends according to sex of the subject are reflected in the rates of all the individual States: suicides in 15-24 year old men rose substantially, whereas those in 15-24 year old women did not change in the past 30 years. The disproportionate increase in suicide rates in young men in small rural areas nationally is also occurring consistently in all Australian States. Certain data limitations should be noted. Coroners often must exercise subjective judgements in determining verdicts, which may lead to possible systematic differences in rates between different States and over time; Errors may also arise from unstandardised methods of recording suicides, especially earlier in the study period;1 Population data may fluctuate in minor ways with changing residential area boundaries, notably with some towns being absorbed into larger cities; and The data do not allow inferences about particular local geographical areas (see for comparison National Injury Surveillance Unit data4). However, it is unlikely that changing coronial verdicts account for the magnitude or generality of the changes we noted. Cantor and Coory5 found that Queensland's provincial cities and rural towns of modest size had negligible rate increases compared with metropolitan and major urban areas from 1986 to 1991. They questioned whether there was a rural suicide problem in Queensland. Our study confirms their observations for Queensland cities with populations over 25 000, but notes a massive rate increase in towns with fewer than 4000 people, with substantial numbers supporting this finding. Further, the Queensland picture does not appear to be atypical. There are differences in suicide base rates in the various States. Whether Melbourne's low base rate in 1964 is coincidental, or a result of Victorian coroners showing less willingness to reach a verdict of suicide, requires further investigation. Tasmania's relative isolation, demographically stable population, and easy firearm access may explain its consistently high suicide rates. Suicide methods differ somewhat between States. The high rates for car exhaust suicides in Western Australia may reflect its relative isolation and this method's cultural acceptability. Carbon monoxide sensors, exhaust modifications and changes to catalytic converters may be effective prevention measures.6 High firearm suicide rates among 15-24 year old men in Tasmania and Queensland,7 rising metropolitan firearm suicide rates in those States, and rising rates in small towns (population, <4000) in all States, but especially Victoria and Queensland, probably relate to falling populations in small rural areas with stable or rising suicide numbers, the easy availability of firearms, and the more liberal firearm legislation in Tasmania and Queensland. Applying methods to prevent car exhaust suicide and reducing the availability of guns may reduce suicide rates by these two methods, and possibly total suicide rates.8 While rates for suicide by various methods may differ in different States, residential area trends for firearm and hanging suicides were pronounced in all States. A trend for overall firearm suicide rates to decrease in all States from 1984-1993 conceals substantial firearm rate increases in small rural areas in all mainland States over the 30-year period. Differences in rates between metropolitan and small rural areas, and the fact that the ratio of firearms suicide rates in small rural areas to those in metropolitan areas rose substantially in all mainland States, suggest that particular risk factors (directly and indirectly related to firearms) are operating in small rural areas. Restrictive legislation may differentially affect firearm suicides in metropolitan areas, where availability is lower.9 The rural economic downturn, the strain on small rural communities, and a major population exodus in all States from towns with fewer than 4000 people have meant added health burdens for those communities, with possibly specific risk factors.1 The fact that the equivalent ratio for hanging rates changed little suggests that more general factors are also operating across all areas in relation to suicide in young men. Particular States have local issues which require specific attention, but the fact that all Australian States reflect the national trends in youth suicide in relation to sex and residential area supports a national approach to youth suicide prevention. Effective national approaches will depend in part on acquiring a better understanding of the similarities and differences in health risks faced by metropolitan and rural youth.1 Acknowledgements Thanks are due to Caroline Haski and Margaret Alcock for their painstaking work as research assistants, and to the NSW Institute of Psychiatry, which partly funded this study. References Dudley M, Kelk N, Waters B, et al. Suicide among young rural Australians 1964-1993: a comparison with metropolitan trends. Soc Psychiatry Psychiatr Epidemiol 1997; 32: 251-260. Department of Primary Industries and Energy and Department of Human Services and Health. Rural, remote and metropolitan areas classification, 1991 Census edition. Canberra: AGPS, 1994. Holmes J. In: Jeans D, editor. Space and society. Chapters 2 and 3. Sydney: Sydney University Press, 1988: 24-74. Moller J. An atlas of injury death in Australia 1990-1992. Adelaide: National Injury Surveillance Unit, 1995. Also available online: <www.nisu.flinders.edu.au/data/atlas/atlas.html> Cantor C, Coory M. Is there a rural suicide problem? Aust J Public Health 1993; 17: 382-384. Australian Institute for Suicide Research and Prevention. Access to means of suicide by young Australians; a background report to the Commonwealth Department of Health and Family Services Youth Suicide Prevention Advisory Group. Brisbane: Australian Institute for Suicide Research and Prevention, 1996. Cantor C, Lewin T. Firearms and suicide in Australia. Aust N Z J Psychiatry 1990; 24: 500-509. Cantor C, Baume P. Access to methods of suicide: what impact? Aust N Z J Psychiatry 1998; 32: 8-14. Cantor C, Slater P. The impact of firearm control legislation on suicide in Queensland: preliminary findings. Med J Aust 1995; 162: 583-585. (Received 12 May 1997, accepted 17 Apr 1998) Authors' details University of New South Wales, Sydney, NSW. Michael J Dudley, MB BS, FRANZCP, Lecturer, School of Psychiatry. Norman J Kelk, PhD, Social Worker, School of Community Medicine. Prince of Wales Hospital, Sydney, NSW. Tony M Florio, MPsych, Clinical Psychologist. Macquarie University, Sydney, NSW. John P Howard, PhD, Clinical Psychologist. PO Box 474, Edgecliff, NSW. Brent G H Waters, MD, FRANZCP, Psychiatrist. Reprints will not be available from the authors. Correspondence: Dr M J Dudley, Department of Child and Adolescent Psychiatry, Sydney Children's Hospital, Randwick, NSW 2031. E-mail: m.dudleyATunsw.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/>

Michael J Dudley · Norman J Kelk · Tony M Florio · John P Howard

Preventing suicide: what will work and what will not Stephen J Rosenman Population, not individual, approaches to suicide prevention MJA 1998; 169: 100-102 See also Dudley et al Suicide is the second most common cause of death among young men in the Western world.1 The emotional impact of suicide, especially of young people, on the community has produced a "do something, do anything" flurry of preventive activity, directed mostly at identifying and intervening with people at high risk.2,3 Much of the activity is ineffective4 and some may even make things worse.5-7 Here, I argue that focusing on people at "high risk" squanders resources, and that we may have to abandon this approach to suicide prevention as an immediate health target. Can we identify and assist high-risk individuals? Focusing prevention on people at "high risk" of suicide appears efficient because it seems to concentrate on those most likely to benefit. But can we identify high-risk individuals? Dimensional risk factors, such as hypertension or depression, have a linear relationship to mortality; only an arbitrary cut-off separates high risk from low risk.8 For conditions with multiple risk factors, such as coronary heart disease and also suicide, each factor adds a little to the risk, but often only when it interacts with other factors. No single predictor or combination of predictors is present in every individual, and membership of the high-risk group changes from moment to moment. Half a bottle of whisky may create a high suicide risk within an hour. As we learn to specify risk more precisely, the identified high-risk group gets smaller and -- while the individual risk of each member increases -- as a group they contribute a diminishing proportion of all suicides. Many more suicides come from the very much larger low-risk population. In a hypothetical population of 100 000, we may identify 500 people with a high suicide risk of, say, 10% (the 10-year suicide risk in schizophrenia, for example) and the remaining 99 500 with a low risk of, say, 0.1% (the approximate 10-year suicide risk in the population). The high-risk group will produce 50 suicides, while 100 will come from the low-risk group -- prevention targeted at high-risk people will miss most of the suicides. Another problem appears once we identify high-risk individuals. They then need advice and treatment that is effective, available and acceptable to them. How do we measure effectiveness if we can count only the failures? If we look at population suicide rates, agencies such as telephone suicide crisis services seem ineffective.4 Intervention after suicide attempts has not only been of little effect,9 but is also irregular in its availability, and frequently ignored by those it is intended to benefit.10,11 Those deemed at high risk, such as those discharged from hospital after a suicide attempt, already receive intensive follow-up, and further improvements will show diminishing returns of people saved.12 However, the insuperable problem in the high-risk approach arises when we try to use common characteristics of history and personality to identify individuals at risk of events that are uncommon in statistical terms. For events as infrequent as suicide, even highly specific and sensitive predictions will have high error rates.13 Theoretically, suicide predictions with 99% specificity will predict 1000 suicides in a population of 100 000; but the current suicide rate of around 15 per 100 000 population means that, in a year, fewer than 20 will be correct predictions. In the real world, where 85% is "good" specificity, those who will ultimately die are hidden in a haystack of people "at risk". If a high-risk approach is ineffective, is any other strategy better? Newer approaches and paradigms for prevention in public health have not fully penetrated policymaking for mental disorders. William Haddon, a former Director of the United States National Highway Safety Bureau, propounded principles for injury prevention which widened the focus from the victim to the array of environmental interactions amenable to change (see below).14 More radically, Geoffrey Rose, an epidemiologist at the London School of Hygiene, switched the spotlight away from individuals at high risk of suicide and turned it onto whole populations.15 He argued that mortality falls more if we reduce the whole population's exposure to factors related to suicide than if we identify and treat high-risk people. Time to consider a population-based approach? The principle of the "population-based" approach is to apply preventive strategies to the whole population or subpopulation in order to shift the distribution of risk, so that at any time fewer people are over the threshold that leads to completed suicide16 (see Figure). We do not have to identify the individuals within the population to save them. This is demonstrated by the successful reduction in mortality from road trauma and from cardiovascular disease. These successes should now be models for suicide prevention. Road trauma deaths in Australia decreased after the apparently inexorable rise seen in the 1960s,17 and this decline clearly followed the introduction of measures that applied to the whole population. These measures -- seat belts, random breath tests for alcohol, speed-limit enforcement, and improvements to roads and cars -- succeeded where strategies to identify the "high-risk" individual -- the dangerous driver, "the nut holding the steering wheel" -- had failed or aggravated the problem. Each measure, ranging from those most proximate to the crash (seat belts, collapsible steering columns) through the antecedent conditions (alcohol, speed) to the most nebulous antecedents, such as public attitudes to road safety,18 contributed its bit to the sum of prevention, and mortality fell without anyone identifying a high-risk individual or tackling the chain of causes which explain an individual death. Indeed, by 1968, Haddon had already challenged myths of accident prevention: ". . . because drivers cause most accidents [we assume that] programs correspondingly must be concerned with drivers. In the real world there is no basis for making this assumption [which] leads to demonstrably false conclusions."19 The decline in cardiovascular disease mortality is not explained by the vigorous treatment of high-risk people. Established risk habits such as smoking and diet were strikingly resistant to change in high-risk individuals.20 More importantly, most cardiac deaths occur among the large numbers of lower-risk people. Overall cardiovascular mortality fell with the change in community-wide attitudes to cigarettes, diet, inactivity and stress.21 At first sight, suicide prevention in these terms seems much more difficult because the antecedents of suicide appear harder to discern and change. However, if we take what we do know about suicide risk and apply it to the population rather than to defining the individual at risk, reducing suicide may become feasible.4,12 How do we put a population-based approach into practice? Restricting access to the means of suicide (eg, by detoxification of domestic and vehicle exhaust gases, gun regulation, control of dangerous medication) will tackle the most proximate antecedents. Close antecedents susceptible to reduction include drug and alcohol abuse; the population load of mood disturbances, including clinical and subclinical depression;22-24 conduct disorders;22 and media modelling of suicide.25 The more remote antecedents in all age groups include socioeconomic deprivation26 and, to a surprisingly uncertain degree, unemployment.4,27 In younger populations, family breakdown and alienation, relationship losses, school failure and suspension may portend suicide,28 while in older populations loneliness and physical morbidity may do so.29 In Aboriginal populations, suicide is prefigured by substance abuse and high incarceration rates, which are problems for the whole community to address, not just the problems of high-risk individuals.30,31 What to do and where to start? Haddon and Baker14 assert that we should first do those things we can, rather than struggling with things we cannot define or alter. Attacks on access to means of suicide, such as firearms32 and car exhausts,33 are within our present reach. By a large margin, they will have the strongest and most immediate effect in reducing suicide rates,4 even though such measures may not strike at what might seem the most "important" emotional antecedents. The problem with social antecedents, such as alienation or drug abuse, is that they demand difficult social engineering. It is unpromising to try to reconstruct families after they have broken down. Reducing the incidence of family breakdown and other such antecedents in the community may not be easier, but may be more profitable34 in terms of prevention, and for this medical efforts must harmonise with other social and educational initiatives. Of course, these antecedent problems (and others such as mental illness) warrant action on their own merits, not just as targets in suicide prevention initiatives. We cannot comfortably assume that education campaigns will always help, and there are good arguments against tackling prevention through "suicide prevention" or "education" campaigns. In the past, school-based driver education in the United States was associated with unexpectedly higher road accidents and deaths.35 Suicide education campaigns in schools not only miss excluded students, but have also shown complex and possibly harmful effects on attitudes to suicide6,10 and on completed suicide.7 The final analysis Firstly, identifying and treating high-risk individuals is unlikely to result in lower suicide rates. The refinement of individual assessment has passed the point of diminishing returns, and the obsessive study of suicidal individuals will not uncover the Holy Grail of perfect prediction. Clearly, we will not stop doing our best for distressed and suicidal people, even though this will not reduce population suicide rates. But this is not prevention. Secondly, pessimism about suicide may not be justified, despite the rising rates. The turnaround in the rising road toll and in cardiovascular disease teaches what can be done. The lesson is that measures which reduce overall risk in the whole population will reduce the number of people above the fatal threshold, and we do not need to identify the high-risk people individually. Consequently, we may have to abandon the frontal assault on suicide. We cannot justify prevention campaigns driven by the suicidal risk of individuals, despite the intuitive and political appeal of such measures. Indeed, to the degree that they drive resources into ineffective strategies, current approaches to "suicide prevention" may impede suicide prevention. Instead, we must "bite the bullet" in restricting access to means of suicide, the most proximate factor. Beyond that, we need the diligent, unspectacular work in the population which mitigates those factors which lead, among other things, to suicide. For medicine, it is to treat the ill,36 whether or not they are suicidal, and, from a public health pulpit, to address the social ills which produce morbidity, whether or not they lead to suicide. References Pritchard C. New patterns of suicide by age and gender in the United Kingdom and the Western World 1974-1992; an indicator of social change? Soc Psychiatry Psychiatr Epidemiol 1996; 31: 227-234. CDC. From the Centers for Disease Control and Prevention. Suicide among children, adolescents and young adults -- United States 1980-1992. JAMA 1995; 274: 451-452. Commonwealth Department of Health and Family Services (Australia). Youth suicide in Australia: the National Youth Suicide Prevention Strategy. Canberra: Australian Government Printing Service, 1997. Gunnell D, Frankel S. Prevention of suicide: aspirations and evidence. BMJ 1994; 308: 1227-1233. Shaffer D, Garland A, Vieland V, et al. The impact of curriculum-based suicide prevention programs for teenagers. J Am Acad Child Adolesc Psychiatry 1191; 30: 588-596. Hazell P, King R. Arguments for and against teaching suicide prevention in schools. Aust N Z J Psychiatry 1996; 30: 633-642. Lester D. State initiatives in addressing youth suicide: evidence for their effectiveness. Soc Psychiatry Psychiatr Epidemiol 1992; 27: 75-77. Patton GC, Harris R, Carlin JB, et al. Adolescent suicidal behaviours: a population based study of risk. Psychol Med 1997; 27: 715-724. Deykin E, Chung-Chen H, Joshi N. Adolescent suicidal and self-destructive behaviours: results of an intervention study. J Adolesc Health Care 1986; 7: 88-95. Shaffer D, Garland A, Gould MS, et al. Preventing teenage suicide: A critical review. J Am Acad Child Adolesc Psychiatry 1988; 27: 675-687. Goldney RD. Out-patient follow-up of those who have attempted suicide: fact or fantasy? Aust N Z J Psychiatry 1975; 9: 111-113. Lewis G, Hawton K, Jones P. Strategies for preventing suicide. Br J Psychiatry 1997; 171: 351-354. Pokorny AD. Prediction of suicide in psychiatric patients. Arch Gen Psychiatry 1983; 40: 249-257. Haddon W, Baker SP. Injury control. In: Clark DW, McMahon B. Preventive and community medicine. Boston: Little Brown, 1981. Rose G. The strategy of preventive medicine. Oxford: Oxford University Press, 1985. Rose G. Mental disorder and the strategies of prevention. Psychol Med 1993; 23: 553-555. Federal Office of Road Safety (FORS). Trends in road safety. Monograph No 1. Canberra: FORS, 1997. Graham JD. Injuries from traffic accidents: Meeting the challenge. Annu Rev Public Health 1993; 14: 515-543. Haddon W. The changing approach to the epidemiology, prevention and amelioration of trauma: the transition to approaches etiologically rather than descriptively based. Am J Public Health 1968; 58: 1431-1438. Susser M. The tribulations of trials: Intervention in communities [editorial]. Am J Public Health 1995; 85: 156-158. Epstein FH. Cardiovascular disease epidemiology: a journey from the past into the future. Circulation 1996; 93: 1755-1764. Shaffer D, Gould MS, Fisher P, et al. Psychiatric diagnosis in child and adolescent suicide. Arch Gen Psychiatry 1996; 53: 339-348. Depression and suicide: are they preventable [editorial]? Lancet 1992; 340: 700-701. Brent DA, Perper JA, Goldstein CE, et al. Risk factors for adolescent suicide. Arch Gen Psychiatry 1988; 45: 581-585. Phillips DP, Carstensen MS. Clustering of teenage suicides after television news stories about suicide. New Engl J Med 1986; 315: 685-689. Gunnell DJ, Peters TJ, Kammerling RM, Brooks J. Relation between parasuicide, suicide psychiatric admissions and socioeconomic deprivation. BMJ 1995; 311: 226-230. Platt S. Unemployment and suicidal behaviour: a review of the literature. Soc Sci Med 1984: 19; 93-115. Gould MS, Fisher P, Parides M, et al. Psychosocial risk factors of child and adolescent completed suicide. Arch Gen Psychiatry 1996; 53: 1155-1162. Draper BM. Prevention of suicide in old age. Med J Aust 1995; 162: 533-534. Royal Commission into Aboriginal Deaths in Custody. National Report. Canberra: Australian Government Publishing Service, 1991. Hunter E. An examination of recent suicides in remote Australia: Further information from the Kimberley. Aust N Z J Psychiatry 1991; 25: 197-202. Kellerman AL, Rivara F, Somes G, et al. Suicide in the home in relation to gun ownership. New Engl J Med 1992; 327: 467-472. Rosenman SJ. Car exhaust suicide. Med J Aust 1997; 166: 288-289. Zigler EF, Taussig C, Black K. Early childhood intervention: a promising preventative for juvenile delinquency. Am J Psychol 1992; 47: 997-1006. Robertson LS. Crash involvement of teenaged drivers when driver education is eliminated from high school. Am J Public Health 1980; 70: 599-603. Wilkinson G. Can suicide be prevented? Better treatment of mental illness is more appropriate aim. BMJ 1994; 309: 860-861. Authors' details Canberra Psychiatry Group, and National Health and Medical Research Council Psychiatric Epidemiology Research Centre, Canberra, ACT Stephen J Rosenman, MD, FRANZCP, Psychiatrist. Reprints: Dr Stephen J Rosenman, GPO Box 610, Canberra, ACT 2601. E-mail: sjrATatrax.net.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/>

Stephen J Rosenman