Issues
Volume 165 Issue 4
Editorials Sudden infant death syndrome Susan M Beal (MJA 1996; 165: 179)Motor neurone disease and the life of motor neurones Garth A Nicholson (MJA 1996; 165: 180)Outpatient chemotherapy: there's no place like home - sometimes John R Zalcberg, Jim Siderov, Mark Petty (MJA 1996; 165: 182)Hyperparathyroidism: a management dilemma Solomon Posen (MJA 1996; 165: 183) Research Home chemotherapy for cancer patients: cost analysis and safety Raymond M Lowenthal, Anne Piaszczyk, Gillian E Arthur, Sue O'Malley (MJA 1996; 165: 184)Survey of haemolytic-uraemic syndrome in Queensland 1979-1995 Youichi Mizusawa, Lydia A Pitcher, John R Burke, Michael C Falk, Waichiro Mizushima (MJA 1996; 165: 188)Asthma and atopy in four rural Australian Aboriginal communities Antony J Veale, Jennifer K Peat, Euan R Tovey, Cheryl M Salome, John E Thompson, Ann J Woolcock (MJA 1996; 165: 192) Notable Cases Surgically proven primary hyperparathyroidism with a suppressed intact parathyroid hormone Paul Glendenning, Peter T Pullan, David Gulland, Anthony J Edis (MJA 1996; 165: 197) Position Statement Paediatric advanced life support The Australian Resuscitation Council Guidelines The Advanced Life Support Committee of the Australian Resuscitation Council Abstract - Article (MJA 1996; 165: 199) Viewpoint Trends in childhood disability Eve M Blair, Ruth E Shean (MJA 1996; 165: 206) Managing HIV HIV and the doctor's role in public health Ronald Penny, Don Grimes, Peter Baume (MJA 1996; 165: 209)HIV prevention in the community: sexual transmission David Bradford, Susan Kippax, Don Baxter (MJA 1996; 165: 210)Prospects for a preventive HIV vaccine Stephen J Kent, Robert L Clancy, Gordon L Ada (MJA 1996; 165: 212) MJA Practice Essentials - Dermatology Psoriasis Paul A Weller (MJA 1996; 165: 216) Review Anabolic steroids and the mind Brian Corrigan Abstract - Article (MJA 1996; 165: 222)
Position statement
Paediatric advanced life support
Position Statement Paediatric advanced life support The Australian Resuscitation Council Guidelines The Advanced Life Support Committee of the Australian Resuscitation Council MJA 1996; 165: 199-206 Basic cardiorespiratory resuscitation - Advanced life support - Techniques in paediatric advanced life support - Medications and fluids used in paediatric advanced life support - Management after resuscitation - Cessation of cardiopulmonary resuscitation - Contributors - References - Register to be notified of new articles by email - These guidelines by the Australian Resuscitation Council (ARC) provide brief step-by-step outlines of the management of common life-threatening emergencies in infants and children. The guidelines are similar, but not identical, to guidelines published by the American Heart Association 1 and the European Resuscitation Council. 2 An international liaison committee (including representation from the ARC) is attempting to resolve differences and will in due course publish common advisory statements. The current guidelines are specifically for advanced life support, but some essential techniques of basic life support are presented. Further details of basic life support for infants and children 3 and specific guidelines for resuscitation of asphyxiated newborn infants have been published. 4,5 Basic cardiorespiratory resuscitation Cardiorespiratory arrest should be suspected when the infant or child loses consciousness, appears pale or cyanosed, or is apnoeic or pulseless (see definitions in Box 1). Assess airway and breathing by observing movement of the chest and feeling for expired breath. Position the head and neck to maintain an open airway. Movement of the chest without expiration implies an obstructed airway. If the obstruction is not relieved by backward head tilt and chin lift or by forward jaw thrust, the pharynx should be inspected with a laryngoscope and cleared of any secretions, vomitus or blood with a sucker (Yankauer). Forceps (Magill) may be needed to extract a foreign body. If spontaneous ventilation is not immediately resumed, artificial ventilation is commenced with mouth-to-mask expired air, a self-inflating resuscitation bag or an oxygen-inflated bag and mask circuit. Supplemental 100% oxygen should be added. Insertion of an oropharyngeal airway (Guedel) may facilitate ventilation. Assess the circulation by palpating the carotid, brachial or femoral pulse. Commence external cardiac compression (ECC) if a pulse is not palpable or it is: < 80 beats per minute (bpm) in a newborn or infant; < 60 bpm in a small child; < 40 bpm in a large child. Precede ECC with 2-5 slow breaths to reinflate the lungs. The patient should be placed on a firm surface, and compression directed to the lower sternum to a depth approximating a third of the anteroposterior diameter of the chest, or at a depth of 2-3 cm and rate of 100/min for a newborn or infant; depth of 3-4 cm and rate of 100/min for a small child; depth of 4-5 cm and rate of 80-100/min for a large child. ECC for a newborn or infant can be performed with two fingers, although a better technique is to encircle the chest with both hands, compressing the sternum anteriorly with the thumbs while stabilising the vertebral column posteriorly with the fingers. The rescuer's hands must encircle the chest freely and not restrict chest expansion. ECC for a small child can be performed with the heel of one hand and, for a large child or teenager, with two hands. A cycle should be 50% chest compression and 50% relaxation. Combine ECC and assisted ventilation in an infant or small child in a ratio of 5 : 1. For a large child or teenager in whom a two-handed technique of ECC is required, a single rescuer may achieve better circulation and ventilation with a ratio of compression to ventilation of 15 : 2. If a mask is used, breaths should be delivered between successive compressions to allow adequate expansion of the lungs, but if an endotracheal tube is used coordination is less crucial as effective ventilation can be given against the resistance imposed by ECC. For the asphyxiated newborn, ECC should be at a rate of 120/minute and ventilation at 40-60/min (i.e., in a ratio of 3 : 1). 5,6 Advanced life support Advanced life support implies a patent airway by endotracheal intubation, mechanical ventilation with oxygen, the treatment of cardiac arrhythmias, the treatment of the cause of cardiorespiratory arrest and of complications arising from its management. When several rescuers are in attendance, tracheal intubation and ventilation, display of the electrocardiograph (ECG) and access to the circulation should be attempted simultaneously. Thereafter treatment should be guided by the cardiac rhythm (see Flowchart in Box 2). Tracheal intubation is the first priority. This establishes and maintains a patent airway, facilitates mechanical ventilation with 100% oxygen, minimises pulmonary aspiration, enables suctioning of the trachea and provides a route for the administration of selected drugs. If intubation cannot be accomplished easily, ventilate and oxygenate the patient using a mask before reattempting intubation. Assess the cardiac rhythm by displaying the ECG via chest leads or the defibrillator paddles. Proceed with drug therapy or immediate direct current (DC) shock (Box 2), while maintaining ECC and mechanical ventilation with supplemental 100% oxygen. Secure access to the circulation with a peripheral intravenous (IV) cannula. If cannulation is difficult, do not waste time (more than 90 seconds) with repeated unsuccessful attempts -- instead use the intraosseous (IO) route or the (less effective) respiratory tract via the endotracheal tube (ETT). 7 All drugs and resuscitative fluids may be given via the IO route but only adrenaline, atropine and lignocaine may be given via the ETT. Central venous cannulation of the subclavian or internal jugular veins should not be attempted initially as it wastes time and is potentially hazardous. However, cannulation of an external jugular or femoral vein may be easily accomplished. Surgical cutdown onto a vein may be required. Intracardiac injection should not be attempted unless all alternative methods of access to the circulation are impossible. The doses of drugs, DC shock and fluid therapy are based on body weight, which may be estimated according to age if the weight is unknown: Newborn: 3.5 kg 1 year: 10 kg 1-9 years: (age in years x 2) + 8 kg 10 years and over: age in years x 3.3 kg. Doses may also be prescribed on the basis of height. 8,9 Drug doses according to the 50th percentiles of weight and height for age are given in Box 3. Asystole or severe bradycardia If the cardiac rate is unresponsive to ventilation with 100% oxygen, asystole or pulseless severe bradycardia ( < 80 bpm in an infant, < 60 bpm in a small child, < 40 bpm in a large child or teenager) should be treated with adrenaline (10 µg/kg IV or IO, or 100 µg/kg via the ETT). The subsequent dose of adrenaline by any route is up to 100 µg/kg. If sinus rhythm cannot be restored, sodium bicarbonate (1 mmol/kg IV or IO) and/or atropine (20 µg/kg IV, IO or ETT), with additional doses of adrenaline, may be successful. If facilities are available, cardiac pacing (via the oesophageal, transcutaneous, transvenous or epicardial routes) may be effective. Ventricular fibrillation and pulseless ventricular tachycardia The only effective treatment of ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) is DC shock. If the onset of VF is recent or is observed, a precordial thump may be given (although its efficacy has not been proven) and defibrillation should be attempted before any other treatment. The initial DC shock treatment of VF or pulseless VT is 2 J/kg, increasing to a maximum of 4 J/kg 10,11 in a series of three shocks. If sinus rhythm does not occur, give adrenaline (10 µg/kg IV or IO, or 100 µg/kg ETT) and a further three shocks of 4 J/kg. Persistent or refractory VF or VT may be treated with lignocaine (1 mg/kg IV, IO or ETT) followed by another series of up to three shocks of 4 J/kg. If the VF or VT remains refractory, alternative agents (bretylium tosylate 5 mg/kg, sodium bicarbonate 1 mmol/kg, magnesium sulfate 0.05-0.1 mmol/kg) may be tried, in combination with adrenaline (100 µg/kg IV, IO or ETT) and a series of three shocks of 4 J/kg. However, no drug has been conclusively proven to improve the efficacy of DC shock. Electromechanical dissociation (pulseless electrical activity) Electromechanical dissociation exists if pulses are absent despite relatively normal coordinated electrical activity on the ECG. It may be due to poor intrinsic myocardial contractility or secondary to a number of remediable causes, including hypoxaemia, hypovolaemia, severe acidosis, tension pneumothorax, pericardial tamponade, hyperkalaemia, hypocalcaemia, poisoning with a calcium channel blocker or hypothermia. It may also be due to massive pulmonary embolism. Treatment is with adrenaline, 10 µg/kg IV or IO or 100 µg/kg ETT initially, with subsequent doses up to 100 µg/kg by any route. If the electromechanical dissociation is persistent, consider hypovolaemia or severe acidosis and give a bolus of crystalloid or colloid fluid (20 mL/kg IV or IO) and/or sodium bicarbonate (1 mmol/kg). An underlying cause should be sought by clinical examination and investigations, including a chest x-ray, 12-lead ECG and echocardiograph if possible. Supraventricular tachycardia Supraventricular tachycardia (SVT) may cause severe hypotension or pulselessness. Synchronised DC shock (0.5-1 J/kg) should be given immediately to a pulseless patient. If blood pressure is adequate, vagal stimulation or drug therapy may be used. Adenosine is the drug of first choice. Alternatives are digoxin, a beta-blocker or a calcium channel blocker. Calcium channel blockers should not be used to treat SVT in infants because their negative inotropic effect may be fatal. Techniques in Paediatric advanced life support are given in Box 4. Medications and fluids used in paediatric advanced life support are summarised in Box 5. Management after resuscitation The cause of cardiorespiratory arrest should be sought and specifically treated. Complications of the resuscitation procedure should also be sought, especially if secondary deterioration occurs. This includes a chest x-ray to check the position of the endotracheal tube, to exclude pneumothorax, lung collapse or aspiration and to check the cardiac silhouette, and a blood sample for estimation of the haemoglobin level, pH, gas tensions and electrolyte and glucose concentrations. Supportive therapy should be provided until there is recovery of function of vital organs. This may include oxygen therapy, mechanical ventilation, inotropic infusion and renal support for several days or longer. Recovery in infants and children is usually slow because cardiorespiratory arrest is often secondary to prolonged global hypoxaemia and ischaemia with prior damage of other organs. Particular care should be taken to ensure adequate cerebral perfusion with well oxygenated blood and adequate blood pressure. Cessation of cardiopulmonary resuscitation The decision to cease cardiopulmonary resuscitation should be based on a number of factors, including the patient's pre-arrest condition, response to resuscitation, remediable factors, likely outcome and the opinions of experienced medical personnel. References Emergency Cardiac Care Committee and Subcommittees of the American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. JAMA 1992; 268: 2171-2302. Paediatric Life Support Working Party of the European Resuscitation Council. Guidelines for paediatric life support. BMJ 1994; 308: 1349-1355. Manual Australian Resuscitation Council. Policy Statements. Policies 12.1-12.9, November 1995. (Located at the Royal Australasian College of Surgeons, Spring Street, Melbourne.) Emergency Cardiac Care Committee and Subcommittee of the American Heart Association. Guidelines for cardio resuscitation and emergency cardiac care. JAMA 1992; 268: 2276-2281. Roy RN, Betheras FR. The Melbourne chart -- a logical guide to neonatal resuscitation. Anaesth Intens Care 1990; 18: 348-357. The Advanced Life Support Committee of the Australian Resuscitation Council. Adult advanced life support. The Australian Resuscitation Council Guidelines. Med J Aust 1993; 159: 616-621. Tibballs J. Endotracheal and intraosseous drug administration for paediatric CPR. Aust Fam Physician 1992; 21: 1477-1480. Lubitz SL, Seidel JS, Chameides L, et al. A rapid method for estimating weight and resuscitation drug dosages from length in the pediatric age group. Ann Emerg Med 1988; 17: 576-581. Oakley P, Phillips B, Molyneux E, Mackway-Jones K. Updated standard reference chart. BMJ 1993; 306: 1613. Chameides L, Brown GE, Raye JR, et al. Guidelines for defibrillation in infants and children. Report of the American Heart Association Target Activity Group: cardiopulmonary resuscitation in the young. Circulation 1977; 56 (suppl): 502A-503A. Gutgesell HP, Tacker HA, Geddes LA, et al. Energy dose for ventricular defibrillation of children. Pediatrics 1976; 58: 898-901. Rogers FB. Technical note: a quick and simple method of obtaining venous access in traumatic exsanguination. J Trauma 1993; 34: 142-143. Hornchen U, Schuttler J, Stoeckel H, et al. Endobronchial instillation of epinephrine during cardiopulmonary resuscitation. Crit Care Med 1987; 15: 1037-1039. Jasani MS, Nadkarni VM, Finkelstein MS, et al. Effects of different techniques of endotracheal epinephrine administration in pediatric porcine hypoxic-hypercarbic cardiopulmonary arrest. Crit Care Med 1994; 22: 1174-1180. Patterson M, Boenning D, Klein B. High dose epinephrine in pediatric cardiopulmonary arrest (CPA). Pediatric Emerg Care 1994; 10: 310. Goetting MG, Paradis NA. High-dose epinephrine improves outcome from pediatric cardiac arrest. Ann Emerg Med 1991; 20: 22-26. Contributors This document was drafted and revised by Dr James Tibballs at the request of the Australian Resuscitation Council. Submissions were received from members of the Advanced Life Support Committee of the ARC and from Dr R Henning, Dr F Shann, Ms S Kinney (Melbourne); Dr A Duncan (Perth); Dr J McEniery, Dr G Delbridge, Dr B Lister (Brisbane); Dr B Wilkins, Dr R Choong, Dr B Duffy, Dr T Gratten-Smith, Dr I Alexander, Dr M Schindler, Dr J Gillis, Dr A O'Connell, Dr D Schell, Dr O Miller (Sydney); Dr S R Keeley, Dr A J Slater, Dr G M Shaw, Dr J Raftos (Adelaide); Dr E R Segedin (Auckland); Dr L Quan (Seattle); and Dr D Zideman (London). Members of the Advanced Life Support Committee: Dr M Allen (ARC South Australian Branch). Dr R A Capps (Australian Defence Force). A/Prof V Callanan (ARC Chairman; and Australian and New Zealand College of Anaesthetists). Ms J Dennett (Confederation of Australian Critical Care Nurses). Mr M Draheim (ARC Tasmanian Branch). Ms J Finn (Royal College of Nursing, Australia). Dr L Grigg (Cardiac Society of Australia and New Zealand; and National Heart Foundation). Mr A Hadj (Royal Australasian College of Surgeons). Mr J Hall (Institute of Ambulance Officers, Australia). Mr K Hambrecht (Co-opted member). Prof G A Harrison (Chairman, ARC Advanced life Support Committee; and Australian and New Zealand College of Anaesthetists). Dr I Jacobs (ARC Western Australian Branch). Mr O Juul (ARC New South Wales Branch). Mr S Leahy (Surf Lifesaving Association of Australia). Ms J Maclean (Royal Lifesaving Society, Australia). Dr P Morley (ARC Victorian Branch). Dr J O'Callaghan (Co-opted member). Dr A Phillips (Royal Australian College of General Practitioners). Mr C Smith (ARC Queensland Branch). Dr J Taylor (Co-opted member). Dr J Tibballs (Australian and New Zealand Intensive Care Society). Mrs E P Tyler (Australian Red Cross Society). Dr J Wassertheil (Australasian College for Emergency Medicine). Dr J Williamson (St John Ambulance Australia). No reprints will be available. Correspondence: Dr J Tibballs, Intensive Care Unit, Royal Children's Hospital, Flemington Road, Parkville, Melbourne, VIC 3052. ©MJA 1996 Home |
Review
Anabolic steroids and the mind
Anabolic steroids and the mind Brian Corrigan MJA 1996; 165: 222-226 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Introduction - Psychological effects - Withdrawal symptoms - Drug dependence - Other psychiatric changes - Acknowledgements - References - Authors' details Register to be notified of new articles by email - - ©MJA1996 Anabolic steroids were first used by weight lifters and others involved in pursuits of strength, but are now taken, often in large doses, by young men interested in enhancing their appearance. The severe psychogenic side effects of these high doses include aggressive and violent behaviour. Problems with drug withdrawal and drug dependence are also common in users of anabolic steroids and these drugs may also provoke psychiatric disorders. I review these complications, as reported in the past decade, and comment on two recent violent murders in Sydney in which anabolic steroid use was implicated. Introduction S ydney has recently witnessed two particularly brutal murders by users of anabolic steroids. One man with recent paranoid tendencies took a claw hammer and battered his wife to death, and then shot himself. In the second murder a man met a woman he knew at a nightclub and they went to the stairwell of a nearby hotel. In the man's words "something snapped" and he murdered the woman. Experienced police described it as the most brutal attack they had encountered. In both these murders the level of aggression and violence fits the descriptive term steroid rage ("roid rage"). The male hormone testosterone, derived mainly from the testes, is an anabolic and androgenic steroid responsible for the production and maintenance of the male physical features, 1 as well as the recognisable male psychological and behavioural attributes. 1-3 Numerous human and animal studies support the psychological and aggressive effects of testosterone use, and some reports correlate testosterone levels with aggressive behaviour and dominance. 2,3 Anabolic steroids are derived by chemical manipulation of the 19-carbon testosterone molecule. Despite well documented problems with their use, they are widely abused in the community for non-medical reasons, mostly by young men to enhance their appearance by "bulking up" (i.e., increasing their lean muscle mass without increasing fat). How common their use is in Australia is not known, but a recent survey in the United States concluded that there were at least three million users at any one time and at least one million former users. 4 Side effects can occur with all anabolic steroids. 5 The higher the dose the higher the risk is the general rule, and side effects can be sudden, severe and unpredictable, and include sudden death. 5 The most common group of side effects involve psychological and/or psychiatric changes. Being psychoactive substances, 3,6 anabolic steroids are expected to produce some degree of psychological change after they have been taken for some time. Indeed, these changes (which include an increase in self-confidence, energy and motivation), if they allow people to train harder, may well be one of the main factors explaining the mechanism of action of anabolic steroids. 7 Psychological effects One of the earliest papers on psychological effects reported the side effects of anabolic steroids in 32 weight-trained men; 8 56% had a subjective perception of increased irritability and aggression. This also applied to a smaller group of 10 weight-trained female athletes. 9 A more recent report compared 13 anabolic steroid users with 14 non-users and 18 former users. 10 Steroid users had more frequent episodes of anger, which were of greater intensity and duration, and a more hostile attitude towards others. In general, psychological changes need to be related to the dose and duration of anabolic steroid use (e.g., taking one or two 5 mg tablets would not produce any changes, but after taking an increasing dose for some days several psychological changes may occur). These changes will develop if anabolic steroids are taken for long enough (just how long could possibly depend upon individual tolerance). The psychological changes that occur can be arbitrarily divided into three groups, representing a continuum of effects from milder through to more severe changes, especially if continued high doses are taken. Early effects are seen as changes in mood and euphoria: there is an increase in confidence, energy and self-esteem, with enhanced motivation and enthusiasm. There is also diminished fatigue, sleeplessness and an ability to train through pain. Libido may be decreased, but is more often increased, sometimes markedly. 11 Irritability, anger, agitation and a "strange edgy feeling" are commonly reported. With larger doses or after taking anabolic steroids for a longer time, there is a loss of inhibition and a lack of judgement, with mood swings or grandiose ideas. Prolonged users become suspicious, quarrelsome, impulsive and more aggressive. 7 Severe effects manifest when these aggressive feelings increase to the extent that violent, hostile, antisocial behaviour develops, meriting the descriptive title, well known in the steroid-taking community, of "roid rages". These rages can result in property damage, self-injury (including reckless driving or crashing cars), assaults, marriage break-ups, domestic violence, 12 child abuse, 12 suicide 13 and attempted murder or murder. 14-20 Partners of anabolic steroid users are at particular risk of serious injury, and there is even a self-help group, Anabolic Steroid Wives Association, 21 to help provide them with support. One group of men who often take anabolic steroids in high doses are those working as security officers or nightclub bouncers; 22 under the influence of the drug they may be provoked into a rage and seriously injure people, and at least one person has been killed as a result. 22 How common these rages are is not known. There is often a great reluctance by anabolic steroid users to report them to doctors, but they may be reported at times by the family. Rages generally result from taking a high dose for a prolonged period; how high a dose and for how long are yet to be defined. In addition, not all people taking high doses develop steroid rages. On the other hand, there are a few reports of rages in those taking quite low doses. 17,23-25 Some common features have been noted in men having these rages. They are generally young, come from apparently caring families, have not previously taken drugs or been in trouble with the police, and do not have a history of being aggressive. They usually feel no remorse at all after the rage, however antisocial their behaviour. 21 It has been suggested that there may be an underlying predisposition to this type of behaviour and that excessive drug use "pushes them over the edge"; however, nearly all the cases described in the literature fit the description above. The first two murder cases in which taking anabolic steroids was used as a defence (called the "dumbbell defence" by Newsweek ) were in the United States in 1988; both men were found guilty of murder. Some 20 murders associated with the use of anabolic steroids have been reported in America, 26 but the usual pleas of innocence due to temporary insanity have never been upheld there. Sydney's two cases are summarised in the Box. Withdrawal symptoms All types of steroid drugs, including corticosteroids, produce withdrawal symptoms. 2 Depression is almost invariably one of the symptoms in anabolic steroid users: they miss the feeling of elation induced by the drugs. Other symptoms relate to loss of the positive psychological effects and include listlessness; apathy; loss of appetite, libido and self-esteem; feelings of anxiety; difficulty in concentrating; and mood swings. Withdrawal can also be associated with violent behaviour and rages. Hence, rages may result from taking either a high steroid dose or stopping taking the drug. Severe symptoms of steroid withdrawal may not be a problem in athletes, possibly because they take anabolic steroids in certain well defined phases and because they reduce the dose gradually. Body builders or weight trainers, however, have greater problems with withdrawal. They lose their new improved body image as their recently enhanced musculature shrinks away, and are likely to be driven back to taking steroids again and to have great trouble stopping them in the future. 27 Drug dependence Another related problem is drug dependence; pharmacological, psychological and genetic factors may all have an effect. This problem was first described in 1988 in a 23-year-old body builder; 28 anabolic steroid dependence was later reviewed, 29 and two other case reports followed. 30,31 Brower et al. produced a series of papers on anabolic steroid dependency and its management. 32-37 They initially published a case in a 24-year-old weight trainer with drug dependence, depression and aggression, 32 and later reported eight steroid-using weight lifters (age range, 23-65 years) who showed evidence of dependence at interview according to criteria of the Diagnostic and statistical manual of mental disorders (DSM-III-R). 33 In a review of 49 male weight lifters, average age 24 years, 28 (57%) were considered to be drug dependent. 37 Mechanisms discussed were either that (i) anabolic steroids may affect endogenous opioid 28 or monoaminergic brain systems, or (ii) that dependence may result from social reinforcement and the pleasure of having a muscular body. However, users were more likely to have expressed dissatisfaction with their body size and so dependence was considered to be driven more by negative reinforcement (trying to avoid feeling small). The presence of more than three DSM-III-R criteria is considered consistent with drug dependence, and Brower et al. found anabolic steroid users may have up to six of these ( Box 2). 37 Other psychiatric changes Several psychiatric disorders have been reported in association with anabolic steroid use since the first case was described in 1980. 38,39 The full list includes schizophrenia, 38 hypomania and mania, 40 delirium, 41 depression, 42 suicide, 10,28,43 and paranoia. 44 In the first reported case of anabolic steroid-related psychiatric disorder, in 1980, a 17-year-old male body builder developed acute schizophrenia when taking methandienone; he recovered on stopping the drug, but relapsed when he took it again. 38 In 1992, Freinhar and Alvarez 40 noted that referring doctors "often" commented on mood changes accompanying anabolic steroid therapy, and described a 27-year-old body builder with hypomania who was taking oxandrolone. He recovered on withdrawal of the drug but had a second attack when taking oxymetholone. A toxic confusional state with choreiform movements occurred in another patient taking 200-300 mg a day of oxymetholone; the condition improved on drug withdrawal. 41 Perry et al. studied 20 weight lifters taking anabolic steroids and 20 controls using a self-administered questionnaire and an interview. 45 The questionnaire showed an increase in psychotic features in the users, including paranoid thoughts, depression, increased hostility and aggression. Pope and Katz in 1987 reported two cases of psychosis in anabolic steroid users, 46 and then, in 1988, 41 cases (39 men) with a wide range of psychiatric problems. 47 This study was widely criticised because it was not a controlled, prospective trial and because of its selection of subjects. In 1994, they rectified this with a controlled study of 88 athletes who used anabolic steroids and 68 controls. 48 The Structured Clinical Interview for DSM-III-R was used for diagnosis; 25% showed evidence of drug dependence and 23% hypomania, mania or depression. Aggression or violence "often" accompanied hypomanic or manic episodes. The authors also suggested that steroid users are most vulnerable to major depressive episodes during the first three months after discontinuing anabolic steroid use. Depression has been mentioned previously in relation to drug withdrawal and dependence. Testosterone was formerly used to treat depression, but it is now known to cause it. 49 Suicide may also be a problem with either anabolic steroid drug dependence or after drug withdrawal (especially with sudden withdrawal). It is not often reported in medical journals, but may be reported in the press. Brower et al. reported a body builder who had suicidal thoughts of crashing his car, and warned of the dangers of anabolic steroids and suicide. 32 A different view of anabolic steroid complications was taken by Dimeft and Malone: 50 in 31 current users, 45 previous users and 88 non-users, they found psychiatric diagnoses to be more common in previous users, suggesting that psychiatric disorder may either predispose a person to, or result from, anabolic steroid use. There is one study which gives a contrary view. Bahrke et al., 51 using two valid psychometric inventories, studied 50 men (12 current steroid users, 14 previous users, and 24 non-users) and concluded that users taking an average daily dose of 45 mg showed minimal psychiatric effects. In conclusion, this brief review highlights some of the psychological problems encountered with anabolic steroid use. It does not appear that these problems are very common, but future research will show how much disability they cause. Acknowledgements I sincerely thank the librarians at Concord Hospital (Ms Kaye Lee) and Manly Hospital (Ms Diane James) for all their help, as well as Ms Kathleen Roach and Ms Nicki Vance at the Australian Sports Drug Agency. References Mooradian AD, Morley JE, Korenman SG. Biological actions of androgens. Endocr Rev 1987; 8: 1-28. Bahrke MS, Yesalis CE, Wright JE. Psychological and behavioural effects of endogenous testosterone levels and anabolic steroids among males. A review. Sports Med 1990; 10: 303-337. Hoberman JM, Yesalis CE. The history of synthetic testosterone. Sci Am 1995; Feb: 60-65. Yesalis CE, Kennedy NJ, Kopstein AN, Bahrke MS. Anabolic androgenic steroid use in the United States. JAMA 1993; 270: 1217-1221. Corrigan B. Drugs in sport. Sports Coach 1988; 12: 11-17. Parrott AC, Choi PY, Davies M. Anabolic steroid use by amateur athletes: effects upon psychological mood states. J Sports Med Phys Fitness 1994; 34: 292-298. Lombardo JA, Sickles RT. Medical and performance-enhancing effects of anabolic steroids. Psychiatr Ann 1992; 22: 19-23. Strauss RH, Wright JE, Finerman GAM. Side effects of anabolic steroids in weight-trained men. Physician Sportsmed 1983; 11: 86-96. Strauss RH, Ligget MT, Laaese RR. Anabolic steroid use perceived effects on weight-trained women athletes. JAMA 1985; 253: 2871-2873. Lefavi RG, Reeve TG, Newland MC. Relationship between anabolic steroid use and selected psychological parameters in male bodybuilders. J Sport Behav 1990; 13: 157-166. Moss HB, Panzak GL, Tarter RE. Sexual functioning of male anabolic steroid abusers. Arch Sex Behav 1993; 22: 1-12. Schulte HM, Hail M, Boyer M. Domestic violence associated with anabolic steroid abuse. Am J Psychiatry 1993; 150: 348. Brower KJ, Blow FC, Eliopulos GA, Beresford P. Anabolic androgenic steroids and suicide. Am J Psychiatry 1989; 146: 1075. Lubell A. Does steroid abuse cause or excuse violence? Physician Sportsmed 1989; 17: 177-185. 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Brian Corrigan
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