The mental health of young people inAustralia: Report by the National Mental HealthStrategy

Pierre Beumont, Department of Psychological Medicine,The University of Sydney, Sydney, Australia:

The release by the National Mental Health Strategyof its report on the mental health of young people inAustralia is a disappointment to those health profes-sionals and consumers who have a particular interest ineating disorders. Although in the declaration of itsintentions [1], the Committee stated that the four dis-orders on which it would concentrate were depression,attention deficit, conduct disorder and eating disorder,eating disorders are not contained in the publishedreport [2]. When asked to explain this discrepancy, amember of the Committee stated that the data for eatingdisorders was insufficient to draw any conclusions,probably because of the deficiency of the instrumentused [Sawyer MG, pers comm., 2001]. Perhaps that isnot surprising for patients who are characteristically sosecretive about their behaviours as are those with eatingdisorders when the assessment consisted, as in thiscase, of an interview with parents and the use of asymptom check list that was not designed to includethese illnesses.

The report does contain information on the well-known risk behaviours for eating disorders, viz dietingand exercise to control weight and use of vomiting, lax-atives and ‘pills’ to lose weight (surely pathological). Itis of note that the first two risk behaviours mentionedrank first and third among all the risk factors for girls,and that the second most common risk behaviour, vizsmoking, is also a well-recognised means of suppressingappetite [2, p.38, Table 7.3]. It is also noted that thesebehaviours are markedly more prevalent among subjectswith very high levels of emotional and behavioural prob-lems [2, p.41, Fig. 7.5]. Unfortunately, the report doesnot examine the relation of these variables to socialdeprivation.

Although it is accepted that a survey of this kindcannot answer all needs, it is inaccurate to term it com-prehensive when disorders such as anxiety and eatingdisorders are not included. The report admits the exclu-sion of anxiety disorders compromises its usefulness. Itshould do the same in respect to eating disorders. Itwould be unfortunate if the report were to be interpretedas indicating eating disorders are rare in this age group,rather than difficult to recognise. The burden of diseasethat eating disorders imposes on Australians is very sig-nificant [3]. In fact, many eating disorder patients maybe included in the depression category. Depression isknown to be commonly associated with eating disorders,

and the suicide rate of anorexia nervosa patients is evenhigher than those with major depression [4].

References1. Sawyer MG, Kosky RJ, Graetz BW, Arney F, Zubrick SR,

Baghurst P. The national survey of mental health and wellbeing:the child and adolescent component. Australian and New Zealand Journal of Psychiatry 2000; 34:214–220.

2. Sawyer MG, Arney FM, Baghurst PA et al. The mental health of young people in Australia: child and adolescent componentof the national survey of mental health and wellbeing.Canberra: Commonwealth Department of Health and AgedCare, 2000.

3. Mathers CVT, Stevenson C. The burden of disease and injury inAustralia. Canberra: AIWH, 1999.

4. Harris EC, Barraclough B. Excess mortality of mental disorder.British Journal of Psychiatry 1998; 173:11–53.

Reply to Professor Beumont

Michael Sawyer, Research & Evaluation Unit, Women’s andChildren’s Hospital, The University of Adelaide, Adelaide,Australia:

Thank you for the opportunity to respond to the letterfrom Professor Beaumont. As noted in the report, theneed to limit the survey to four disorders was a disap-pointment for us all. Unfortunately, the funding availablenecessitated this approach. Given the opportunity, wecertainly would have focused on a broader range ofchildhood disorders using multiple informants.

We are currently undertaking further analysis of thedata obtained in the survey. This will include analyseswhich examine the relationship between mental healthproblems and social disadvantage experienced by chil-dren in the community.

Transsexualism – need it always be a DSM-IVdisorder

Chris Cantor, Noosa Heads, Queensland, Australia:Bower [1] provided a useful review of DSM-IV issues

to do with gender identity disorder (GID). One of theessential DSM-IV criteria [2] for inclusion is ‘The dis-turbance causes clinically significant distress or impair-ment in social, occupational, or other important areas offunctioning.’ The exclusive use of the GID categories fortranssexualism might unreasonably ‘pathologize’ theproblem. Clinicians using DSM-IV, in my experience,are prone to bending reality to fit DSM criteria. In itsdefense, the DSM-IV under ‘Additional conditions thatmay be a focus of clinical attention’ includes a diagnosis‘Identity problem’ [2]. It states that ‘This category can beused when the focus of clinical attention is uncertaintyabout multiple issues relating to identity such as long-term goals, career choice, friendship patterns, sexual

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orientation and behaviour, moral values, and group loy-alties.’ This, at least in theory, would allow a subgroup oftranssexuals not to be classed as disordered.

Dr Bower noted [1] that transsexual ‘tomboys’ areusually tolerated or even admired by their peers, livethrough a comparatively tension-free adolescence, andas adults, if they are gender disturbed, impress as stable,sensible individuals, able to deal effectively with theirproblem. This sounds as though he is referring to trans-sexuals whose problems might not qualify for the GIDtag.

Years ago with recreational heroin use it was erro-neously assumed that it always constituted a disorder, yetsubsequently we have learnt that a significant proportionof users lead otherwise normal lifestyles. This requiredrevision of some key assumptions. However, transsexu-alism is more complicated. While many heroin users seethemselves as having no problem, transsexuals know thatsomething is horribly wrong – their bodies do not matchtheir brains sexually. I would be interested in Dr Bower’scomments on the notion of non-disordered transsexual-ism and how common it may be.

References1. Bower H. The gender identity disorder in the DSM-IV

classification: a critical evaluation. Australian and New ZealandJournal of Psychiatry 2001; 35:1–8.

2. American Psychiatric Association. Diagnostic and statisticalmanual of mental disorders (DSM-IV). Washington: AmericanPsychiatric Association, 1994.

Reply to Dr Cantor

Herbert Bower, The Melbourne Clinic and Monash GenderDysphoria Team, Melbourne, Australia:

I would like to thank Dr Cantor for his interestingalthough at times somewhat opaque comments. I shallattempt to answer them seriatim.

First: The heading ‘Transsexualism, need it always bea DSM-IV disorder’. Transsexualism (or gender identitydisorder (GID)) affects approximately 1:50 000 peoplein the world, it is not a DSM-IV disorder but defined bymany classifications and text books of psychiatry with acommon and essential criterion – the strongly held beliefby the individual that his or her gender identity con-tradicts the presenting sexual anatomy.

Second: He accuses the use of GID categories of‘pathologizing’ the problem. I agree with his opinion andstrongly believe in a ‘unitary’ concept of transsexualism.Furthermore, I see it aetiologically as a biological dis-order (genetic and hormonal). The vast majority of patientsare psychiatrically normal, some, according to theirpersonality structure have responded to a childhood andadolescence trauma of discrepancy between belief,

anatomy and a hostile environment with an adjustmentdisorder. Dr Cantor would call them a ‘subgroup of trans-sexuals, not disordered’. I would prefer the term ‘psy-chiatrically normal but transsexuals’.

Third: The phrase ‘their bodies do not match theirbrains sexually’ used by Dr Cantor, sounds harsh and atthe same time lacks definition and I prefer the terminol-ogy used in my first paragraph.

In summary, his letter has raised important issues, notreferred to by me within the framework of a critical eval-uation of the DSM-IV.

While the aetiology of any disorder remains un-certain, arguments about criteria and definition arehealthy and attempts to classify, although time-bound,are essential.

Connection between lithium and muscularincoordination

David Grounds, The Melbourne Clinic, Melbourne,Australia:

In November 2000 I was referred a 21-year-old manwho had suffered two manic attacks, the first being inMarch 2000 and the second not long after – when herelapsed because of compliance problems. Since his dis-charge in May 2000, he had been taking lithium carbon-ate and olanzapine. His serum lithium levels were withinthe therapeutic range, being 0.9 mmol/L in September2000.

In addition to side-effects of tiredness, ‘flatness’, andweight gain, which could be accounted for by the olan-zapine medication, his main complaint was of inco-ordination in fast bowling. He is a keen cricketer andbelonged to one of the lower grades of a metropolitancricket club. He said that he had bowled more wides thanstraight balls since resuming cricket after his discharge.

There have been reports of disturbance of neuro-muscular function in patients taking lithium and I sus-pected that was the most likely cause. His serum lithiumwas 1.0 and I reduced the dose to effect a lithium levelof 0.6, which resulted in improvement, but he was stillbowling a couple of wides an over. Cessation of olanza-pine did not have any benefit and I then changed hismood stabiliser to Epilim (Sanofi; Sydney, Australia) atthe end of December. His bowling gradually improved,and 4 weeks later he was back playing in the team.

In March 2001 I had a further report from a patient. A 71-year-old married woman with recurrent depressionhad lithium added to her trimipramine regimen inJanuary 2000. Her serum levels since that time haveeither been 0.4 mmol/L or 0.5 mmol/L. She came for a follow-up consultation on the 6 March 2001 andinformed me that she had decided to cease the lithium

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because she was not able to serve properly when playingtennis, and believed this had only been a problem whileshe was on the lithium. To support her contention, 2 weeks after she ceased the lithium, her serving abilitywas back to normal.

My two patients made the connection between lithiumand their muscular incoordination, but some may not. Itwould be worthwhile for psychiatrists to keep in mindthis side-effect and to enquire about similar difficulties.

References1. Manocha M, Chokroverty S, Nora R. Peripheral and central

neural conduction: in patients on chronic lithium therapy. Muscle & nerve 1984; 7:575–576.

2. Waziri R, Davenport R. Lithium effects on neuromusculartransmission in: manic patients. Commun Psychopharmacol1979; 3:121–127.

Clozapine associated pericarditis and elevatedTroponin I

Stephen E Kay, James Doery and David Sholl, Departmentsof Clinical Biochemistry and Adolescent Psychiatry,Monash Medical Centre, Melbourne, Australia:

We refer to the recent correspondence by Reid et al.[1]. They describe a case of myocarditis due to clozapinein a young man who developed electrocardiographic(ECG) changes, but without changes in serum creatinekinase. We report a case of pericarditis associated withclozapine therapy, with ECG changes and serial eleva-tions in serum troponin I, a highly sensitive and specificmarker of myocardial injury.

A 16-year-old female with chronic, treatment resistantschizophrenia was seen in the emergency departmentfollowing a 2-week history of palpitations. One weekprior to presentation, she developed central and left-sided chest pain, which was sharp ‘like a knife’, pleuriticin quality, and relieved with paracetamol 1 g, orally. Thepatient also experienced shortness of breath waking herfrom sleep. Her chest pain worsened 2 days before pre-sentation. She had no history of cardiovascular disease,and was otherwise well. Clozapine, 25 mg daily orally,was commenced 3 weeks prior, and increased to 100 mgdaily over 2 weeks. She was also taking benztropinemesylate 2 mg daily orally, and diazepam 2 mg orally,when required for sedation.

On presentation, she had an oral temperature of 37°C;pulse rate of 124 beats/min, respirations of 24/min, andblood pressure of 124/59 mmHg. Physical examinationwas normal. An ECG showed p-mitrale in lead I, T-waveflattening in lead III, ST-segment elevation concave up-ward across all leads, and a biphasic P-wave in V1. Shewas admitted to the adolescent psychiatric unit for mon-itoring and analgesia, with a diagnosis of pericarditis

secondary to clozapine therapy. Her symptoms and ECGchanges resolved during admission. Clozapine was con-tinued with the informed consent of the patient, and closeconsultation with the laboratory and cardiology unit.

Blood tests initially revealed a rise in serum troponin Iof 1.89 µg/L (normal, < 0.4), decreasing the followingday to 0.29 µg/L (normal, < 0.4). Two weeks later, hertroponin I level was < 0.04 µg/L (normal, < 0.4), withcomplete symptom resolution. On commencement ofclozapine, 3 weeks prior to admission, her troponin I was0.34 µg/L (normal, < 0.4). Patients on clozapine at MonashMedical Centre are routinely monitored with troponin Ion commencement of therapy, and at 4-weekly intervals.Significant values in our laboratory for troponin I areacute coronary syndrome > 0.4 µg/L, and acute myo-cardial infarction > 1.5 µg/L. Serial creatine kinase, urea,creatinine, electrolytes, liver enzymes, and blood filmswere normal. Viral and bacterial serology was negative.Troponins were assayed on the Dimension RxL clinicalchemistry system (Dade Behring Inc., Newark, DE,19714. U.S.A.), and values were confirmed by re-assayat other Melbourne laboratories.

Clozapine is rarely associated with pericarditis [2],myocarditis and cardiomyopathy [3], or electrocardio-graph changes [4], but recent Australian data suggestsuch cardiac side-effects may be more common thanpreviously thought [1]. Greater monitoring of patientstaking clozapine would be expected to detect abnormal-ities in ECGs, but not necessarily creatine kinase. Themost recent and now preferred biological marker iscardiac troponin (I or T) [5,6]. Troponin I, unlike othercardiac markers, is a highly sensitive and nearly absol-utely specific indicator of myocardial damage, reflectingeven microscopic areas of myocardial necrosis [5,6].Unlike other cardiac markers, troponin I may be elevatedfor 7–10 days following acute myocardial injury [5,6].This is the first reported case of pericarditis due to cloza-pine, demonstrating elevations in troponin I, whichresolved despite continuation of therapy. This reportdemonstrates the usefulness of troponin I for detectingand monitoring cardiac side-effects in patients takingclozapine, and suggests that troponin I is the preferredmarker to monitor cardiac side-effects of clozapine.

References1. Reid P, McArthur M, Pridmore S. Clozapine rechallenge after

myocarditis. Australian and New Zealand Journal of Psychiatry2001; 35:249.

2. Catalano G, Catalano MC, Frankel-Wetter RL. Clozapineinduced polyserositis. Clinical Neuropharmacology 1997;20:352–356.

3. Kilian JG, Kerr K, Lawrence C, Celermajer DS. Myocarditis andcardiomyopathy associated with clozapine. Lancet 1999;354:1841–1845.

4. Ketch J, Herd A, Ludwig L. ST segment elevations withoutmyocardial infarction in a patient on clozapine. AmericanJournal of Emergency Medicine 1996; 14:111-112.

5. Alpert JS, Thygesen K, Antman E et al. Myocardial infarctionredefined: a consensus document of the joint European societyof cardiology/American college of cardiology committee for theredefinition of myocardial infarction. Journal of the AmericanCollege of Cardiology 2000; 36:959–969.

6. Apple FS, Wu AHB. Myocardial infarction redefined: role ofcardiac troponin testing. Clinical Chemistry 2001; 46:377–379.

Risperidone–induced Pisa syndrome

K. Jagadheesan, and S. Haque Nizamie, Central Institute ofPsychiatry, Kanke (PO), Ranchi, India:

Pisa syndrome is a rare dystonic reaction that occursduring treatment with typical antipsychotics [1]. Recently,this adversity has been noted in association with atypicalantipsychotics such as clozapine [2], sertindole [3] andolanzapine [4]. Although tardive dystonia has been noted[5], presently, Pisa syndrome, comprising all its features,during risperidone therapy has not been documented inthe literature. Herein we present a case of risperidone–induced Pisa syndrome.

A 24-year-old female with mental retardation, with afamily history of mental retardation (maternal cousin),was brought with an illness of 10 years duration beingcharacterised by inappropriate laughter, aggression, sus-piciousness and disorganised behaviour. Her first mentalstatus examination revealed irritable affect, delusions ofpersecution and reference and second person auditoryhallucinations. Except poorly developed secondary sexualcharacteristics, she had no other physical abnormality.With the diagnosis of mild mental retardation and un-specified psychosis, she was started on risperidone 2-mg/day and trihexyphenidyl 2-mg/day. After a fort-night, she developed symptoms which included tilting of her body towards backwards and to the left side andtremors and cogwheel rigidity of the extremities. Hence,trihexyphenidyl was increased to 4–6-mg/day. Althoughher psychosis responded to risperidone, because of thepersisting truncal tilting, it was discontinued and olanza-pine 5-mg/day was started. After 2 weeks of olanzapinetherapy, since there was some improvement in her motorabnormality and absence of psychotic symptoms, tri-hexyphenidyl was discontinued. However, a fortnightlater her truncal tilting worsened and she was restartedon trihexyphenidyl (4–6-mg/day). Her truncal abnormal-ity did not improve even after 4 weeks of trihexy-phenidyl addition and subsequently she was lost tofollow-up.

Pisa syndrome, an axial dystonia with flexion of thetrunk towards one side, appeared for the first time duringrisperidone therapy in this patient who had no exposureto typical antipsychotics. Also, these symptoms became

worse during olanzapine therapy following discontinua-tion of trihexyphenidyl. Notably, Pisa syndrome thatstarted with smaller doses of risperidone, which alsopersisted during olanzapine therapy, did not improvewith trihexyphenidyl. Similar to our patient, in an earlierstudy [6], a significant proportion of patients of Pisasyndrome had no improvement with anticholinergics.

Putative risk factors of Pisa syndrome include previoustreatment with classical antipsychotics, combined phar-macological treatment, female gender, old age and thepresence of an organic brain disorder [4]. In addition tothe female gender, our patient also had mental retarda-tion. The fact that Pisa syndrome of our patient did notimprove during treatment and consequently, patient waslost to follow-up suggest that the onset of Pisa syndromemay cause discontinuation of the responsible pharmaco-logical agents in spite of their therapeutic benefits.Thus, we suggest cautious use of risperidone and olan-zapine in the patients who are prone to this distressingsyndrome.

References1. Ekbom K, Lindholm H, Ljungberg L. New dystonia syndrome

associated with butyrophenone therapy. Journal of Neurology1972; 202:94–103.

2. Kurtz G, Kapfhammer HP, Peuker B. Pisa syndrome underclozapine therapy. NERVENARZT 1993; 64:742–746.

3. Padberg F, Stubner S, Buch K, Hegerl U, Hampel H. Pisasyndrome during treatment with sertindole. British Journal ofPsychiatry 1998; 173:351–354.

4. Stubner S, Padberg F, Grohmann R et al. Pisa syndrome(Pleurothotonus). Report of a multicenter drug safetysurveillance project. Journal of Clinical Psychopharmacology2000; 61:569–574.

5. Fdhil H, Krebs MO, Beyle F, Vanelle JM, Olie JP. Tardivedystonia under risperidone treatment: a case of torticolis.Encephale 1998; 24:581–583.

6. Suzuki T, Hori T, Baba A et al. Clinical characteristics andpharmaceutical treatment of drug induced pleurothotonus (Pisa syndrome). Japanese Journal of Neuropsychopharmacology1997; 19:31–38.

A misleading and pejorative book

Saxby Pridmore and Iqbal Pasha, Hobart, Tasmania,Australia:

The human brain: a guided tour [1] was recently re-issued to coincide with a speaking tour of Australia bythe author. It contains (among others) the followingerrors of expression, clarity and fact:

1. Cerebrospinal fluid is ‘sampled from the lowerportion of the spinal cord’ [1, p.5].

2. ‘The brain has the consistency of a raw egg . . .’[1, p.6].

3. Phineas Gage lived ‘the rest of his life as a fair-ground freak, touring with the tamping iron still lodgedin his brain’ [1, p.23].

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4. ‘Until the 1960s frontal leucotomies were thetreatment of choice for a whole range of very intense andpersistent emotional responses’ [1, p.24].

5. ‘where this nerve leaves the retina and burrowsinto the brain is the “blind spot” . . .’ [1, p.57].

6. ‘Synaethesia tends to occur more in childhood,but can often be triggered in adults with psychotic dis-orders such as schizophrenia or by hallucinogenic drugs’[1, p.67].

7 ‘. . . it has been noted that the unconsciousness ofschizophrenics is frequently very similar to the illogicalbut very real consciousness of our dreams’ [1, p.74].

8. ‘In many regards amphetamine users resembleschizophrenics in that they are constantly at the mercy ofthe outside world, with no inner resources of mind toassess appropriately what is happening’ [1, p.113].

9. ‘Ecstasy is frequently referred to as a hallucinogenbecause it gives feelings of disembodiment as well as anoverriding feeling of elatedness’ [1, p.114].

10. Propranolol ‘does not itself gain access to thebrain’ [1, p.137].

11. ‘Patients recovering from . . . electric shock treat-ment (a radical therapy for severe depression) character-istically cannot remember what happened an hour or sobefore the event’ [1, p.159].

12. ‘A common and conspicuous feature of schizo-phrenia is excessive attention to the outside world, whichoften appears overly bright and buzzing without the

sobering perspective and exposition-basal interpretationof inner resources. Perhaps dreamers, schizophrenics,and non-humans share a similar type of consciousness,characterized by little memory for previous events, anddominated by generic facts and the immediacy of thehere and now’ [1, p.168].

13. Korsakoff’s syndrome patients have ‘loss ofmemory for everything that happened before being takeninto hospital’ [1, p.169].

14. ‘. . . patients suffering from disorders of the basalganglia such as Parkinson’s disease and Huntington’schorea have seemingly no problem explicitly remember-ing facts and events’ [1, p.174].

In the past it would have been argued that this bookwas written for the general market and no concern of theJournal. These days, however, we are more aware of ourduty to the general public. While The human brain: aguided tour [1] may be excellent in many regards andfrom the back cover it appears to have received rattlinggood reviews by the New Scientist and The Times, theclinical material is frequently wrong and pejorative.Psychiatrists should distance themselves from this publi-cation and warn patients and their relatives that it willmislead and may distress some readers.

References1. Greenfield S. The human brain: a guided tour. London: Phoenix,

1998.

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