Can seizures and rhabdomyolysis be apotentially serious complication ofhyponatremia due to polydipsia?

Patrick Tolan, Denis O’Loughlin and John Botha, FrankstonHospital, Frankston, Australia:

We report the case of AB, a 41-year-old single femaleadmitted to the intensive care unit with seizures sec-ondary to severe hyponatremia, who subsequently devel-oped rhabdomyolysis.

She had a 10-year history of paranoid schizophrenia.At no time prior to this episode were problems withexcessive water intake or hyponatremia noted.

In the weeks prior to her admission with seizures shehad been receiving assertive community treatment with acase manager visiting daily and monitoring her medica-tion compliance. (Olanzapine 10 mg per day and sertra-line 50 mg per day.)

In the days prior to her admission she reported that sheconsumed about 10 glasses of water per day which shesaid was normal for her.

On the morning of her admission she was found at homeunconscious and unrouseable and had several generalisedtonic-clonic seizures. She was intubated by ambulancestaff and transferred to the emergency department.

On arrival in the emergency department her GlasgowComa Score was 3/15. She was hypothermic temperatureof 34.8°C, pulse 90 beats per minute and blood pressure120/70 mmHg. There were no focal neurological signs andwith the exception of bi-basal crepitations in the lung fieldsand a rash on both legs examination was unremarkable.

She had a low serum sodium 104 mmol/L (135–145 mmol/L) and a low urinary osmolarity. A head com-puterized tomography scan was normal.

The differential diagnoses made at initial assessmentwere a syndrome of inappropriate antidiuretic hormonesecretion or water intoxication secondary to psychogenicpolydipsia. A low urinary osmolarity, however, madeSIADH unlikely.

She was transferred to the intensive care departmenton artificial ventilation with the electrolyte imbalancecorrected over the following 48 h with hypertonic salineand diuresis.

Creatinine kinase (CK) was normal on admissionrising slowly to peak at 91 970 IU/L (1–170 IU/L) onday 5 although there were no other features of neuro-leptic malignant syndrome (i.e. no pyrexia, confusion,rigidity or autonomic instability). Creatinine kinase MBfraction troponin and electrocardiogram were all normal.Urinary myoglobin was strongly positive suggesting sig-nificant rhabdomyolysis. Despite neuroleptic malignantsyndrome being unlikely it was felt prudent to cease botholanzapine and sertraline.

During the following 4 days in hospital she remainedwell, the biochemical abnormalities correcting them-selves. She refused inpatient psychiatric admission fol-lowing discharge from the medical ward and did notsatisfy criteria for involuntary treatment at that time.She was discharged home for outpatient follow up on nopsychotropic medication and at the time of writing hadbeen re-admitted to hospital for a trial of clozapine.During this admission her serum sodium was within thenormal range.

If NMS is discounted as playing a role in this case thenthe cause of the rhabdomyolysis remains unclear. Pos-sibilities are rhabdomyolysis secondary to seizures ordilutional hyponatremia (DH).

In the literature there has been a number of reports ofrhabdomyolysis secondary to water intoxication. In onecase from Japan [1], a 44-year-old woman consumed 3 Lof water after drinking alcohol. She became stuporouswith sodium of 115 mEq/L and subsequently had a CK rise to 28 560 IU/L. In this case the occurrence ofrhabdomyolysis was attributed to water intoxication. Inanother case also from Japan [2], a 32-year-old womanwith schizophrenia had a sodium level of 102 mEq/L anddeveloped a CK of 39 900 on day 5 of admission. Thetiming of this rise would appear to coincide with that ofAB’s present case. Another case from Switzerland was a 42-year-old man with schizophrenia who developedseizures secondary to DH and rhabdomyolysis [3].

These cases indicate that seizures and rhabdomyolysiscan be a potentially serious complication of hypona-tremia due to polydipsia.

References1. Tomiyama J, Kametani H, Kumagai Y, Adachi Y, Tohri K. Water

intoxication and rhabdomyolysis. Japanese Journal of Medicine1990; 29:52–55.

2. Nagata T, Aoki M, Kato H, Mochizuki H, Tateyama M, ItoyamaY. A case of rhabdomyolysis with water intoxication confirmedby muscle biopsy. Brain and Nerve 2000; 52:53–57.

3. Wicki J, Rutschmann OT, Burri H, Vecchietti G, Desmeules J.Rhabdomyolysis after correction of hyponatremia due topsychogenic polydipsia possibly complicated by clozapine.Annals of Pharmacology 1998; 32:892–895.

Response to ‘Signal transmission, rather thanreception, is the underlying neurochemicalabnormality in schizophrenia’

Amiel C. Christie, Wollongong, Australia:I would like to take this opportunity of commenting on

Brian Dean’s most interesting review in this Journal [1].As reviewed by him, there would appear to be wide-

spread consensus that schizophrenia is essentially a

Correspondence

functional aberration of the chemical systems involved insignal transmission, be they presynaptic or postsynaptic.

However, he does not mention that antipsychotic drugsdo not produce beneficial effects almost immediately butmay take months [2], unlike other drugs, for examplepain relief by Aspirin or morphine, which act almostimmediately, if at all; and of course alcohol as many amotorist will attest. Although there are a number of pos-sible explanations for this delay, a likely possibility isthat neuroleptic drugs, of variable chemical composition,block the action of a toxic environmental factor damag-ing the neuronal synapse, as their beneficial effect is onlymanifested after recovery of the damage caused to thesignal transmission system by the now-blocked toxin.The mechanism of action of neuroleptic drugs could bea slow healing process involving weeks or months.

Recovery, or at least partial recovery, of the patient’sclinical condition would never occur without such asynaptic recovery process. Of course the immune systemalso may be involved, thus explaining the variable degreeof recovery, for, as pointed out by Kane [3], ‘Overallless than 50% of people diagnosed with schizophreniashow a substantial clinical improvement after an averagefollow-up of 5–6 years. Although estimates vary as tothe proportion of patients who make a good functionalrecovery it is safe to say that these are in the minority’.Such a response to therapy can hardly be considered analtogether satisfactory outcome; nevertheless, recoveryor partial recovery can occur.

It would appear to have been overlooked that certaintoxic agents can cause delusions and hallucinations pre-sumably by damaging similar areas in the brain, in par-ticular the limbic system including the hippocampus, forexample, as in organic lead poisoning due to petrol con-taining tetra-ethyl lead and organic tin [4], and alsomycotoxins [5].

The multiplicity of symptoms in schizophrenia can beexplained by the particular site of synaptic action of thetoxin. Such zones in the brain could well be initiallydamaged by supplementary factors such as foetal anoxia,perinatal brain damage accompanying obstetric compli-cations and other risk factors and antecedents of schizo-phrenia [6].

However, the primary toxic factor, if single, wouldhave to be universal to explain the worldwide occurrenceof schizophrenia. There do appear to be relatively minimalgeographical variations in incidence, except that schizo-phrenia is rare in native communities unexposed to thedevelopments of modern civilization (including dietarycomponents) [7].

However, it is suggested by the writer [8] that thepotato, with its variable steroidal glycoalkaloid α-solamine-containing content, may be responsible as such

glycoalkaloids are known to have toxic effects, in par-ticular plasma membrane damage, and also teratogenicaction in certain animals, but this is not as yet con-clusively proven in humans. However, in an initial trialit would be prudent to exclude other edible steroidal glycoalkaloid-containing members of the solanaceaefamily namely egg-plant, tomatoes, capsicum and peppersas they also contain similar glycoalkaloids. In thisrespect an analogy can be drawn with coeliac diseasewhere not only wheat gluten but other gluten-containingfoods may also be pathogenic.

Thus the aetiology of schizophrenia can be fullyaccounted for by ingestion of a synapse-damaging toxininterfering with signal transmission ingested in the foodand accentuated by genetic predisposition in many cases,again as in coeliac disease, but with a greater genetic sus-ceptibility. Furthermore, this toxin would be enhanced inits action on the limbic and prefrontal systems in particu-lar when they have already been partly damaged byobstetric complications, especially anoxia.

In conclusion, it is suggested that the potato and pos-sibly other glycoalkaloid-containing members of thesolanaceae family mentioned above are worthy of furtherinvestigation in the aetiology of this baffling disease.

References1. Dean B. Signal transmission, rather than reception, is the

underlying neurochemical abnormality in schizophrenia.Australian and New Zealand Journal of Psychiatry 2000; 34:560–569.

2. Kety SS. Missing Links. In: Wynne LC, Cromwell RL,Matthysse S, eds. The nature of schizophrenia. New York: Wiley,1978:148–157.

3. Kane JM. Schizophrenia: how far have we come? CurrentOpinion in Psychiatry 1999; 12:17–18.

4. Verity MA. Toxic disorders. In: Graham DI, Lantos PI, eds.Greenfields neuropathology. Vol. 1. 6th edn. New York: OxfordUniversity Press, 1997:755–797.

5. Campbell GD, Daynes GW. Schizophrenia – a mycotoxicelement? [Note ] Nutrient Health 1995; 10:173–175.

6. Jablensky A. Schizophrenia: epidemiology. Current Opinion inPsychiatry 1999; 12:19–28.

7. Torrey EF. Prevalence studies in schizophrenia. British Journalof Psychiatry 1987; 150:598–608.

8. Christie AC. Schizophrenia: is the potato the environmentalculprit? Medical Hypotheses 1999; 53:80–86.

Reply to Dr Christie

Brian Dean, The Rebecca L. Cooper Research Laboratories,The Mental Health Research Institute of Victoria, Melbourne,Australia:

In a recent review, I proposed the hypothesis thatschizophrenia may be due to abnormalities in presynap-tic function [1]. It is now generally accepted that thereis a genetic susceptibility to schizophrenia [2] but that

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the onset of symptoms is, in some way, precipitated by environmental stressors [3]. In commenting on thehypothesis I have proposed, Dr Christie has suggestedthat a stressor that may be involved in precipitatingschizophrenia is the ingestion of glycoalkaloids, com-pounds that may be toxic to the human brain. In partic-ular, Dr Christie has suggested that the ingestion of thesolanaceous glycoalkaloids in the potato are a promi-nent cause of schizophrenia [4]. Moreover, Dr Christiehas proposed that the consumption of potatoes world-wide could account for the uniform incidence of schizo-phrenia in different communities. Given the dearth ofknowledge on possible environmental factors, such ahypothesis deserves further consideration.

As someone who is not expert on the possible implica-tions of ingesting components of food on the functioningof the brain, my initial response to Dr Christie’s hypoth-esis can only be a somewhat superficial consideration.However, such a hypothesis immediately suggests cer-tain outcomes that would be testable using existing data.The first of these proposals would be that the incidenceof schizophrenia should be lower in a society where con-sumption of the potato is low. The second would be thateating potatoes should result in a significant increase inthe ingestion of glycoalkaloids. The need to significantlyincrease glycoalkaloids to precipitate a deleterious out-come is suggested because humans can rapidly clear thisclass of compounds after they have been ingested [5].

Significantly, the incidence of schizophrenia is notlower in Japan [6], where traditionally there is a lowconsumption of potatoes. In addition, it has been shownthat the alkaloids in a potato are mainly located in theskin [7]. As the majority of potatoes consumed have the skin removed this should significantly reduce thelevels of alkaloid ingestion. Moreover, it has been shownthat cooking the potato also significantly reduces thelevels of all alkaloids that remain in the peeled potato[8]. None of the above findings would seem to readilysupport the hypothesis that eating potatoes is likely toresult in a high intake of solanaceous glycoalkaloids andtherefore be a significant risk factor for schizophrenia. Ithas been suggested that the effects of glycoalkaloids may vary with human genotype [9]. It could therefore be argued that the full effects of ingesting glyco-alkaloids may only be apparent in those with a schizo-phrenic genotype, a hypothesis that could deserve furtherinvestigation.

As is the case with all hypotheses, considerable exper-imental data is required to finally prove the premise putforward. All of us are faced with the problem of gainingsuch experimental data in addressing the enigma that isschizophrenia. Therefore, in the same way I hope todevelop the hypothesis I proposed, I will look forward to

reading further of the data produced by Dr Christie inattempting to prove that eating potatoes is indeed an envi-ronmental factor which could precipitate schizophrenia.

References1. Dean B. Signal transmission, rather than reception, is the

underlying neurochemical abnormality in schizophrenia.Australian and New Zealand Journal of Psychiatry 2000;34:560–569.

2. Tienari P, Wynne LC, Moring J et al. Finnish adoptive familystudy: sample selection and adoptee DSM-III-R diagnoses. ActaPsychiatrica Scandinavia 2000; 101:433–443.

3. Tsuang M. Schizophrenia: genes and environment. BiologicalPsychiatry 2000; 47:210–220.

4. Christie AC. Schizophrenia: is the potato the environmentalculprit? Medical Hypotheses 1999; 53:80–86.

5. Hellenas KE, Nyman A, Slanina P, Loof L, Gabrielsson J.Determination of potato glycoalkaloids and their aglycone inblood serum by high-performance liquid chromatography.Application to pharmacokinetic studies in humans. Journal ofChromatography 1992; 573:69–78.

6. Nakane Y, Ohta Y, Radford MH. Epidemiological studies ofschizophrenia in Japan. Schizophrenia Bulletin 1992;18:75–84.

7. Sotelo A, Serrano B. High-performance liquid chromatographicdetermination of the glycoalkaloids alpha-solanine and alpha-chaconine in 12 commercial varieties of Mexican potato.Journal of Agriculture and Food Chemistry 2000;48:2472–2475.

8. Ponnampalam R, Mondy NI. Effect of cooking on the totalglycoalkaloid content of potatoes. Journal of Agriculture andFood Chemistry 1983; 31:493–495.

9. Krasowski MD, McGehee DS, Moss J. Natural inhibitors ofcholinesterases: implications for adverse drug reactions.Canadian Journal of Anaesthetics 1997; 44:525–534.

Can we justifiably draw epidemiologicalconclusions from small case studies?

Shailesh Kumar, Division of Psychiatry, Auckland MedicalSchool and Rees Tapsell, Waitemata Health, Auckland, NewZealand:

We refer to the paper by MacKirdie and Shepherd onCapgras syndrome [1]. The authors, from a small town inNew Zealand, have described five cases of Capgras syn-drome, three of which are Maori. On the basis of thesecase reports they suggest that Capgras syndrome may bemore common in New Zealand Maori. They go on tospeculate that this increased rate among Maori might bea result of genetic and cultural factors. They also discussthe association between Capgras syndrome and violence,the relevance of which, to these cases, is unclear. Thisarticle purports to describe a series of case reports, butthe authors describe the demographics of their catchmentarea and hospital admissions in a manner that implies anepidemiological study.

Conclusions such as ‘Capgras syndrome is possiblymore common in Maori of New Zealand’, should be

made only as a result of well-designed, methodologicallysound studies that have paid careful attention to samp-ling, measurement and analysis [2]. This was not the case in this study. The sampling method used, inwhich the first author ‘became aware’ of her cases, issubject to significant selection bias. The authors do not discuss other significant details of sampling, forexample, how many patients were screened, how manypatients were excluded. The population base from whichthe authors found their cases is not representative ofNew Zealand.

The measurement and analytical techniques used arealso open to bias and speculation. Clinical details pro-vided in the paper are scant, at best. The authors mentionthat organic factors are frequently associated with Cap-gras syndrome, but no details of how organicity wasinvestigated, or excluded, are given. In one case (casefour) the authors make the diagnosis of Capgras syn-drome because of spiritual substitution (a deceasednephew replacing the spirit of the patient’s son). This isin direct contrast to the traditional description of substi-tution by physical look-alikes in Capgras syndrome.

Messages, expressed or implied, that any given con-dition is common among the Maori population shouldnot be given from such flawed studies. We object to suchfallacious conclusions being drawn from a small seriesof case reports. They may further disadvantage Maori by reinforcing some of the misperceptions held by laypublic and even professionals [3]. To discuss the associ-ation of this syndrome with violence among an alreadydisadvantaged group, in such an irrelevant fashion is, inour view, irresponsible. Previous authors have reportedCapgras syndrome in different cultures [4,5] but haveshown the courtesy to these cultures of not ascribing itscausation to racial factors as MacKirdie and Sheppardhave. The only message that should be given from thisseries of case reports, is that Capgras syndrome trans-gresses cultural boundaries.

It was a disappointment to us and to many of our col-leagues to read such an article in our college Journalbecause it raises questions about the peer review and edi-torial processes. It was particularly disappointing to readthis article given the current emphasis on evidence-baseddecision making and methodological rigour in research.One is left to wonder whether this article was reviewedby somebody with an understanding of the Maori cultureand epidemiological methods when such wide-rangingconclusions were being drawn from a small series ofcase reports.

References1. McKirdie C, Shepherd D. Capgras syndrome possibly more

common among the Maori of New Zealand. Australian and NewZealand Journal of Psychiatry 2000; 34:865–868.

2. Boyle MH. Guidelines for evaluating prevalence studies.Evidence-based Mental Health 1998; 1:37–39.

3. Johnstone K. Read J. Psychiatrists’ recommendations forimproving bicultural training and Maori mental health services:a New Zealand survey. Australian and New Zealand Journal ofPsychiatry 2000; 34:135–145.

4. Chawla S, Buchan T, Galen N. Capgras syndrome: a case reportfrom Zimbabwe. British Journal of Psychiatry 1987;151:254–256.

5. Arturo Silva J, Jalali B, Leong GB. Delusion of exchangeddoubles in an immigrant: a new Capgras variant? InternationalJournal of Social Psychiatry 1987; 33:299–302.

Reply to Drs Kumar and Tapsell

Catherine Mackirdy, Tauranga Hospital, Tauranga, NewZealand:

Thank you for the opportunity to respond to Drs Kumarand Tapsell.

They begin, by asking the wrong question. To suggestsomething is possibly the case, is to hypothesise, not toconclude.

Their opening paragraph is baffling: they suggest thatonly three out of the five cases were Maori, when it isquite clearly stated in the article that all five cases, bothlooked and identified as Maori.

To go through their every sentence in this vein couldbe seen as ungracious, and be tedious for the readers. Iremain willing, however, to debate their views at length,if you would like me to do so.

Welcome managed care

Mat Gelman, Dandenong Hospital, Melbourne, Australia:William Sutton was a notoriously prolific bank robber.

A master con-man and impersonator, he was a sticklerfor stealing only from banks. A massive America-widemanhunt eventually found him. The head detective thenasked him why he’d stolen solely from banks. Suttonreplied ‘Because that’s where the money is’.

This, however, was in an era before managed care anddiversions in health dollars.

Professor Larkins College Oration [1] noted health tobe a human right ‘and it is a national disgrace to see [it]made less accessible when we gloat about our economicsuccess’.

To cite examples of these disgraces: a colleague’s pre-viously well father at 55 had a first episode of angina.He saw an eminent cardiologist who requested a nextday angiogram. A clerk at the health insurance fundblocked this. She said payment couldn’t be made forwhat she portrayed as a pre-existing condition. In plead-ing unsuccessfully for her father the registrar met with

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stonewalling statements such as that government regula-tions prevented any leeway.

Further unholy alliances and values have manifested inmore systemic contexts. Callous economically drivenvalues were introduced into two hospitals I worked in.One was to be decommissioned, the other shamefullydegraded. Both were highly regarded by patients andtheir families. They had continuity of high quality care,were remarkably humane and effective. In their devolu-tion psychopathic processes were prominent.

In retrospect what’s most worrying is that long-standingstaff, myself included, took largely philosophical attitudes.From my reading, ‘I’m alright Jack’ isn’t listed among thehealthiest defences.

Freud wrote of denial in our attitude to personal mor-tality, of the unconscious never accepting the reality ofone’s death.

By extension are we denying the death of the highestquality public health system? Not to mention the emerg-ing stealth victory of a callous and destructive ethos andits duplicitous practitioners.

It wasn’t so long ago I was a medical student. A proudexcellent health system seemed as safe as banks.

Reference1. Larkins R. Health and society in the 21st century. Australian and

New Zealand Journal of Psychiatry 2000; 34:715–718.

Our Journal’s wrapping

Andrew Firestone and Di Clifton, Department ofPsychological Medicine, Monash University, and JeremyAnderson, Centre for Clinical Effectiveness, MonashInstitute of Public Health, Melbourne, Australia:

We wish to add our voices to the several requestsalready published, for the jettisoning of wrap-aroundadvertising with our Journal. The medium is themessage, as a wise man said; and ‘Prescribe Drug X –that about wraps it up’ is not a message we wish ourCollege to endorse, nor even appear to endorse. It is nowonder a drug company is prepared to pay so much, toprivilege drug prescribing over all other aspects of psy-chiatry. Please finally heed your colleagues’ wishes inthis matter, and bring this embarrassment to an end.

Mood stabilizers in Asperger’s syndrome

Harpreet S. Duggal, Siddhartha Dutta and Vinod K. Sinha,Central Institute of Psychiatry, Ranchi, India:

Among the affective disorders associated withAsperger’s syndrome (AS), depression is the commonestwith syndromal mania and bipolar disorder being

anecdotally reported [1]. Little information is availableon the management of manic symptoms in AS. We reporta case of AS whose comorbid mania responded to a com-bination of two mood stabilisers.

S., a 22-year-old male, presented with a history of poorsocialization, circumscribed areas of interest, oddities ofspeech, repetitive patterns of behaviour and an awkwardgait since early childhood. Besides these symptoms, thepatient, since the age of 4 years, had displayed obstinacy,irritability, anger outbursts and talkativeness. Over theyears, violence towards animals, beating small childrenand family members, and increased appetite were addedto his repertoire of symptoms. Two months before con-sulting us, his symptoms worsened so that at presenta-tion he had hyperactivity, pressure of speech, elatedaffect and grandiose delusions.

The patient was a product of uneventful pregnancy anddelivery with normal developmental milestones. Familyhistory revealed affective illness in maternal grandmother.In view of this presentation, a diagnosis of Asperger’ssyndrome with comorbid manic psychosis was madeaccording to ICD-10.

At intake, the patient had a score of 37 on the YoungMania Rating Scale (YMRS). He underwent routineblood investigations, which were normal. Though hiselectroencephalogram and brain magnetic resonanceimaging were unremarkable, a detailed neuropsycho-logical testing using Luria Nebraska NeuropsychologicalBattery suggested temporo-parietal and right frontal lobedysfunction. Considering these observations, patient wasstarted on valproate along with risperidone at 4 mg/day.The valproate was gradually increased to a maximumtolerable dose of 2000 mg/day (25 mg/kg/day), whichwas continued for another 4 weeks without any effect. It was then decided to add lithium, which was increasedto 1200 mg/day with serum levels at 1 mEq/L. Within 2 weeks of this combination, the patient showed a dramatic response in his affective symptoms with thescore on YMRS coming down to 12, a drop of 67%.Significant improvement occurred in the domains of ele-vated mood, irritability, speech and biological functions.

There are reports associating bipolar disorder with AS[2–4]. Patients with AS with a family history of affectiveillness may show a propensity to develop antidepressant-induced hypomania [5]. However, not much literature isavailable on the treatment of either spontaneous or drug-induced affective disorders in AS. In the above-cited caseseries [5], three patients with AS who developed fluoxe-tine-induced hypomania were adequately treated with val-proate. This did not occur in our case as our patientresponded only after lithium was added. There is evidencesupporting the use of lithium on a long-term prophylacticbasis in autistic patients with manic-like symptoms [4].

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In conclusion, authors highlight that chronic maniamay be common in some subsets of patients with AS,which may be mistaken as a manifestation of the behav-ioural dysreguation and mood swings associated withautistic syndromes. Making a diagnosis of comorbidmania in these patients and treating it with mood stabilizers may, thus, be a more pragmatic approach. At the same time, some patients with AS, althoughasymptomatic, are vulnerable to antidepressant-inducedhypomania, especially those having family history ofaffective illness. Hence, caution needs to be exercisedwhile prescribing antidepressants to such patients. Con-current use of mood stabilisers can be explored as analternative in these cases. That some cases of AS maybe aetiologically related to bipolar disorders [3] mayexplain the response to mood stabilizers. Finally, neu-robiological correlates of vulnerability for developingmania, either spontaneous or drug-induced, and thepredictors of response to mood stabilizers in AS requirefurther elucidation.

References1. Wing L. Asperger’s syndrome: a clinical account. Psychological

Medicine 1981; 11:115–129.2. Gillberg C. Asperger’s syndrome and recurrent psychosis –

a case study. Journal of Autism and Developmental Disorders1985; 15:389–397.

3. DeLong R. Children with autistic spectrum disorder and a familyhistory of affective disorder. Developmental Medicine and ChildNeurology 1994; 36:674–687.

4. Wozniak J, Biederman J, Faraone SV et al. Mania in childrenwith pervasive developmental disorder revisited. Journal of theAmerican Academy of Child and Adolescent Psychiatry 1997;36:1552–1559.

5. Damose J, Stine J, Brody L. Medication-induced hypomania inAsperger’s disorder. Journal of the American Academy of Childand Adolescent Psychiatry 1998; 37:248–249.

Acute severe catatonia in a young woman withchronic schizophrenia responding toparenteral clonazepam

Rajeev Kumar, Department of Psychological Medicine,University of Sydney, Sydney, Australia:

Catatonia is defined as a behavioural neurological syn-drome of multiple aetiology characterized by mutism,negativism, rigidity and stupor [1]. Rosebush and col-leagues [2] found that 9% of patients admitted to an adultpsychiatric unit presented with catatonia. Specific treat-ment of the catatonic syndrome is important because themotor signs often mask psychiatric symptoms. The treat-ment of catatonia has involved three main modalities:benzodiazepines, electroconvulsive therapy (ECT) andantipsychotics. In an acutely catatonic patient it is oftenhazardous to administer antipsychotics because they

may worsen catatonic signs, have a delayed effect or mayworsen a developing neuroleptic malignant syndrome.Both benzodiazepines and ECT have been found to bevery effective in treating catatonia. It has been recom-mended that a short-term trial of a benzodiazepineshould be given before considering ECT [3]. Althoughlorazepam is the most widely studied drug in catatonia,it is not available in its intramuscular form in Australia.I wish to report a case of catatonia that responded toclonazepam.

The patient was a 22-year-old single woman, who hadan 8-year history of chronic schizophrenia. She wasadmitted to the hospital following a severe catatonicepisode characterized by mutism and refusing to eat anddrink. The patient was evaluated medically and all inves-tigations including a computed tomography scan werenormal. She was commenced on intramuscular clon-azepam 1 mg, and 1–2 hours later some improvement inher mobility was seen. Significant reduction in the motorsigns of catatonia were seen a day later, and she startedeating and drinking. Olanzapine 10 mg daily was startedbecause of her continuing symptoms. Clonazepam 1 mgtwice daily was continued orally for 5 more days beforebeing reduced gradually. The disappearance of her cata-tonic symptoms unmasked her underlying florid psychoticsymptoms. She demonstrated agitation, persecutory andgrandiose delusions, continuous auditory hallucinationsand disturbance in her volition. The psychotic symptomsimproved gradually without any relapse of catatonicsymptoms and she was discharged home after 4 weeks,with a prescription of 10 mg/day olanzapine.

In a majority of patients benzodiazepines are clearlyeffective. Therefore, it is important to reserve the use ofECT as a second line of treatment in those patients whodo not show any response to benzodiazepines in the first24–48 h. Several studies from the USA note the efficacyof lorazepam in the treatment of catatonia. Clonazepamis a useful alternative. This case also illustrates the effi-cacy of an atypical antipsychotic, olanzapine, in treatingthe florid psychotic symptoms which emerged once themotor symptoms of catatonia disappeared. The fact thatclonazepam was stopped without re-emergence of cata-tonia suggests that olanzapine was useful in preventing afurther catatonic relapse.

References1. Taylor MA. Catatonia. A review of a behavioral neurological

syndrome. Neuropsychiatry, Neuropsychology, BehavioralNeurology 1990; 3:48–72.

2. Rosebush PI, Hildebrand AM, Furlong BG, Mazurek MF.Catatonic syndrome in a general psychiatric population. Journalof Clinical Psychiatry 1990; 51:357–362.

3. Bush G, Fink M, Petrides G, Dowling F, Frances A, Catatonia II.Treatment with lorazepam and ECT. Acta PsychiatricaScandinavica 1996; 93:137–143.

Suicide and attempted suicide in the army inItaly 1986 to 1998

Iginia Mancinelli, Simone Lazanio, Lorella Ceciarelli,Anna Comparelli and Roberto Tatarelli, Department ofPsychiatric Sciences and Psychological Medicine, ‘LaSapienza’ University, Rome, Italy:

The armed forces (army, air force, navy) in mostcountries appear to have a lower suicide risk than the general population of the same age bracket andgender [1,2].

In Italy in 1998 the suicide rate in the military popula-tion was 1.1 per 100 000 and 0.92 per 100 000 amongofficers and non-commissioned officers respectively; inthe general male population of 20–24 years of agesuicide rate was 9.8 per 100 000 in 1994.

In the Italian army from 1986 to 1998 there were 76suicides and 84 attempted suicides (AS).

The age of subjects ranges from 18 to 31; the mostfrequent age bracket for suicides and attempted sui-cides was 19–21 with percentages of total suicides of36% in 19-year-olds, 25.3% in 20-year-olds and 13.3%in 21-year-olds. The AS percentages of total suicideswere 42.9%, 21.4% and 16.6%, respectively in theseages (χ2 = 9.87, p < 0.5).

The most frequently involved ranks were ordinary sol-diers who constituted 88.2% of suicides and 95.2% ofAS, followed by non-commissioned officers and officers(χ2 = 2.75, p < 0.5).

With reference to the enlistment data, the period ofhighest suicide risk was during the first and sixth monthsafter enlistment when the percentage respectively (at the first and sixth months) of 14.1% is concentrated; asfor AS the highest risk period was the first month with a percentage of 40.7% of all AS (χ2 = 103.07, p < 0.5)(Fig. 1.).

Of the men who committed suicide, their behaviour onmilitary duty was rated good in 47.4%, average in27.6%, excellent in 18.4%, poor in 3.9%, bad in 2.6%.For the AS group it was: average in 69%, good in 14.3%,poor in 9.5%, bad in 5.9%, excellent in 1.2% (χ2 = 43.86,p < 0.5).

The most frequent methods of suicide used were fire-arms (51.3%) and hanging-strangulation-suffocation(26.3%); for AS they were self-poisoning (42.9%) and cutting or point-stabbing wrists and arms (36.9%) (χ2 = 104.42, p < 0.5).

We think that the lower prevalence of suicide in the military population as compared to the civilian one ismainly due to two factors: (i) screening procedures ofmilitary personnel which are aimed in particular atexcluding mentally disturbed conscripts; and (ii) a pos-sible ‘holding role’ carried out by military environment.

We would like to acknowledge that our data wereobtained from the clinical documentation received by theItalian Epidemiological Observatory with reference tosuicides. Statistics were generated using StatisticalPackage for Social Sciences (SPSS, Chicago, IL, USA).The research was performed in cooperation with theDirectorate General of Medical Corps with the autho-rization of the Italian Ministry of Defence.

References1. Rothberg J, Rock N, Shaw J, Jones F. Suicide in United States

army personnel. 1933–84. Military Medicine 1988;153:61–64.

2. Schroderus M, Lönnqvist JK, Aro HM. Trends in suicide ratesamong military conscripts. Acta Psychiatrica Scandinavica1992; 86:233–235.

Response to ‘Better mental health services foryoung people: responsibility, partnerships andprojects’

Patrick McGorry, Melbourne, Australia:Birleson and colleagues [1] deserve support for

attempting to come to grips with the serious publichealth issue of the deteriorating mental health of ado-lescents and young adults. They highlight many of the problems and draw attention to the yawning blind spot concerning the lack of services for young adults.However, they adopt such an unnecessarily defensive,conservative tone that many of the positive proposalsthey advance lose force and credibility. This is perhapsunderstandable given the global predicament of childand adolescent psychiatry and the pressures upon publicsector adult psychiatry which are touched on by theauthors. I would like to encourage Birleson and his

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Figure 1. Time between enlistment date and suicide(––) and attempted suicide (– – –).

colleagues to overcome their defensiveness, join forceswith potential allies such as ourselves, and colleagues in other states and overseas who largely agree on thenature of the issues. We believe there are a number ofpossible solutions and are keen to develop and evaluatealternative responses. Models are always unproven untilthey are given a fair trial. In any event we do seemagreed that the existing system of child and adolescentmental health services (CAMHS) and adult mentalhealth services (AMHS) has proven inadequate to thetask of responding to the mental health needs of adoles-cents and young adults, and is in urgent need of furtherreform. While Birleson and his colleagues seem to bemaking valiant efforts to improve the quality of theirlocal systems, we would welcome dialogue with themon their experiences as well as progress within ourevolving model (they quote a 5-year old planning refer-ence in relation to our model: there has since beenextensive growth and evolution in clinical and researchspheres across the spectrum of youth mental health). Iwould also encourage Birleson and colleagues to lookbeyond the confines of Victoria. New South Wales hasdeveloped innovative mental health models linking themental health care of adolescents and young adults in model programs as well as more systematically. InCanada and in parts of Western Europe there are otherinnovative examples from which we can all learn.Birleson and colleagues could usefully expand their‘learning organization’ framework to draw on widerexperiences. While space prevents a full treatment here,a more comprehensive exposition of the issues relevantto the mental health of young people is available in apaper submitted to the Journal [McGorry P et al.: unpub-lished data].

While there is substantial agreement about many ofthe issues involved in improving the response for the12–25 age group with emerging mental disorders,Birleson and colleagues do understate the seriousness ofthe problem. There are two elements to this. First, thelevel of caseness doubles between the child and ado-lescent period (14%) and the young adult period (27%)as measured in the recent national mental health sur-veys. Rutter and Smith [2] demonstrated that the level ofpsychosocial morbidity has been rising in the 12–26 agerange. Analysis of data from the Victorian Burden ofDisease Study [3] reveals that, in disadvantaged localgovernment areas in particular, mental disorders are the number one cause of morbidity in young people.Furthermore, the peak period of onset of most adult-typedisorders is in the adolescent and young adult period [4].While primary prevention (a non-clinical activity) is bestfocused in childhood, the peak period for early detectionand intervention (a clinical activity) of most (not all)

disorders is adolescence. Birleson and colleagues incommon with many authors blur this key distinctionbetween prevention and early intervention. Epidemi-ologically, most of these disorders are actually new casesarising through the acquisition of new kinds of symp-toms, while the minority are the intensification of pre-existing symptoms from childhood. This has recentlybeen pointed out by Eaton [5].

Second, young people, especially young men, haveuniformly very poor access to mental health services.To overcome this barrier, whatever the structural rela-tionship between child and adolescent psychiatry, thecultural setting in which services are delivered to ado-lescents and young adults (12–25 years) needs radicalreform. The Victorian Youth Strategy [6] which focusesprecisely on this age range, points out that this hasbeen addressed by other service systems but not bymental health services. It does not require a totally sep-arate system of care, a straw man advanced by Birlesonthrough flexible quotes from our earlier thinking, but itdoes demand a response qualitatively different from thatcurrently available within child and adolescent psychi-atry. Can CAMHS mount such a response? Certainlynot without allies and a more appropriate vision. AsBirleson and colleagues convey, CAMHS is under-resourced, rather beleagured and under threat from pae-diatricians who have taken over large tracts of the fieldanyway. The gaze of CAMHS clinicians is inherentlyretrospective into childhood and insufficiently forward-looking into the developmental maelstrom of adoles-cence and early adulthood. Developmental issues do notevaporate on turning 18. Specialists in this latter phaseneed to be able to adjust their gaze flexibly in bothdirections and recognize the momentum of youngpeople is forwards not backwards.

However, all this does not mean that the nexus withchild psychiatry should be broken or even weakened, northat a nexus with adult psychiatry should not be engi-neered. For example, our current service model is nestedwith both child and adult psychiatry and seeks to evolveever smoother interfaces with both. There will certainlybe other ways of achieving the same clinical objectives.We do, however, need to determine where the natural‘joints’ for service provision exist. With the dividing lineat 16 or 18 years we are sawing through bone. The epi-demiological data confirms this. So do the views of con-sumers and carers who are strident in their criticisms ofthe split in services at 18 years. There is a severe lack of continuity of care currently across this period and ahuge gap for those with non-psychotic disorders beyond18 years. Whatever the relationships with child andadult psychiatry, I believe that transitional zones wouldbe better developed around puberty and again in the

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mid-twenties. It is necessary to extend the current ado-lescent focus into young adulthood, and there is astrong case that this requires new expertise and a qual-itatively different approach from traditional child andadult psychiatry. As described, this is being beginning tobe addressed in other states and other countries. We aretackling this challenge in a systematic manner whichgoes beyond a ‘pilot’. This is a much larger task than the extension of the Early Psychosis Prevention andIntervention Centre (EPPIC) model. We do realize theearly intervention principle must be implemented dif-ferently in other disorders with different characteristicsand prevalences. We appeal to Birleson and his col-leagues not to seek to marginalize our endeavour, butrather to embrace it as similar in spirit to their ownefforts. All subspecialties defined by developmentalphase have had to make their case for a more distinctidentity. Old age psychiatry has been the most recentand has established itself securely in a short period oftime. The profession should recognize the need for adevelopmentally and epidemiologically based youthpsychiatry focus, the structure of which could be thesubject of further debate and conclusion. Youth psychi-atry should not become isolated; it should retain itslinks to child psychiatry and must be better linked toadult psychiatry, but it has to grow and find a moreindependent place. Perhaps it isn’t surprising that youthwould find it challenging to find its place, but time is onits side.

References1. Birleson P, Luk ESL, Mileshkin C. Better mental health services

for young people: responsibility, partnerships and projects.Australian and New Zealand Journal of Psychiatry 2001;35:36–44.

2. Rutter M, Smith DJ, eds. Psychosocial disorders in youngpeople: time trends and their causes. Chichester: Wiley, 1995.

3. Vos T, Begg S. Victorian Burden of Disease Study.http://www.dhs.vic.gov.au/phd/lgabod/index.htm. AccessedMarch 2000.

4. Patton G. An epidemiological case for a separate adolescentpsychiatry? Australian and New Zealand Journal of Psychiatry1996; 30:563–566.

5. Eaton WW. The sociology of mental disorders. 3rd edn.Westport, CT: Praeger, 2001.

6. Office for Youth. Victorian youth strategy. Discussion paper.Melbourne: Communications Division, Department ofEducation, Employment and Training, 2001.

Response to ‘Traumatic stress in the 21stcentury’

John Ellard, Sydney, Australia:In his article ‘Traumatic stress in the 21st century’ in

the December issue of the Journal, McFarlane states

‘The general reluctance to accept the importance of hor-rific and life-threatening adult experience as an impor-tant cause of psychopathology is somewhat perplexing’[1] and then cites an article I have written as an example[2]. Had he read it carefully he would have encounteredthe sentence ‘calamitous experiences can indubitablycause severe psychiatric disorder, which may be longlasting’. This is the exact opposite of the opinion attrib-uted to me.

I had 18 years of military experience, including twowars, and was involved in the assessment of psychiatriccasualties therefrom. Additionally, it was my unhappyexperience to interview some of the prisoners-of-warreturning from Japanese captivity. In World War II –apart from the demobilization – psychiatric disorder wasthe most common cause of separation from the services.No one with this background could possibly hold theview attributed to me.

The problem is that none of us immersed in the dis-turbing consequences of severe trauma while it wasgoing on (and after) encountered the neat tick-a-boxpresentation of posttraumatic stress disorder first to befound in DSM-III in 1980. Instead, we saw the wholerange of psychopathology: acute psychosis, severedepression, disabling anxiety, conversions, you nameit. In an article published in the Medical Journal ofAustralia, I gave references to some of the many mili-tary psychiatrists who described what they saw. Sincethen I have acquired the detailed report on the psychi-atric experiences of the Eighth Air Force [3]. This for-mation took very severe casualties over Germany fromJuly 1942 to July 1943. The two main syndromesobserved were severe anxiety, or disabling somaticcomplaints: ‘nausea and vomiting, headache and dizzi-ness, rapid heart and palpitations, weakness and easyfatiguability or any of the myriad somatic symptomsthat may be associated with an anxiety state’. The syn-drome of DSM-III (and -IV) PTSD does not get amention.

It is difficult to believe that those of us concerned withservice personnel who had experienced major trauma,and those of us who had shared some of those experi-ences, could not see what we were looking at and that asyndrome first described in 1980 could be a paradigmwhich escaped notice in two World Wars, Korea andVietnam.

As I point out in the article, with examples, each warfrom the American Civil War on has produced its own particular epidemic of one or more psychiatric syn-dromes and I believe that we should be cautious if wefind ourselves discovering the same syndrome whereverwe look, particularly if many other observers with a

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special interest in the matter failed to notice it over manydecades.

References1. McFarlane AC. Traumatic stress in the 21st century. Australian

and New Zealand Journal of Psychiatry 2000; 34:896–902.

2. Ellard JHT. The epidemic of post-traumatic stress disorder:a passing phase? Medical Journal of Australia 1997;166:84–87.

3. Hastings DW, Wright DG, Glueck CG. Psychiatric Experiencesof the Eighth Air Force: first year of combat. A Report Submittedto the Air Surgeon. New York: Josiah Macy Jr Foundation,1944:30–32.