Abstract
Simpler explanation for catatonia
Pridmore and Rybak described four patients with catatonic syndromes who were able to use a mobile telephone when they apparently could not speak to other relatives or staff in person [1]. This peculiarity ‘… can raise questions about the patient being selective or manipulative, and call the diagnosis into question’. However, they felt that there was no doubt as to the validity of the diagnoses, and I am sure they were correct. Although increasingly rare, the features of the catatonic state are indubitable.
In my view their observation does not raise doubts about the diagnosis but about the nested assumptions upon which the diagnosis depends. These are, of course, the assumptions of reductionist biological psychiatry; essentially, that the clinical features are reducible to a physical lesion at the neuronal or subneuronal level in the brain. This belief drives the biological program in psychiatry [2] but is without warrant [3]. Reconceptualizing catatonia in simpler, different terms does justice to the observed features without setting up impossible constraints. If the condition is seen as a self-perpetuating state of psychologically determined hyperarousal, then there is no problem with the notion that, if they feel safe, the patients can briefly override the clinical syndrome. In more technical terms, a programming error can always mimic a physical fault in a Turing universal computing machine, but not vice versa.
The authors hinted at this but did not seem to see its full significance: ‘The telephone … may allow communication … without the arousing effect of (people's) physical presence’. That says it all: catatonia is a psychologically determined condition, which helps explain why it is going out of fashion.
Ethnic differences in prevalence of bipolar disorder in Te Rau Hinengaro: the New Zealand Mental Health Survey
An interesting insight into the presentation of bipolar disorder in a non-representative sample of service users in New Zealand is provided by Mellsop et al. [1] using data from the CAOS study [2]. These authors show that for both manic and depressive presentations in bipolar patients, Health of the Nation Outcome Scale (HoNOS) ratings of overactivity/disruptive behaviour were higher for Maori than for Europeans. They argue that overactivity and disruptive behaviour may have been mistaken for symptoms of bipolar disorder in Te Rau Hinengaro, the New Zealand Mental health Survey (NZMHS) [3], resulting incorrectly in higher reported prevalence of bipolar disorder for Maori. We disagree.
We note first that unfortunately Mellsop et al. did not take into account age or sex, let alone socioeconomic status, so that it is unclear to what extent these may have confounded their ethnic comparisons. Because a number of forensic services were included, it seems likely that there were more young men among their Maori bipolar patients so the European/Maori difference may reflect age and sex differences, not ethnicity per se.
Mellsop et al. state that in the NZMHS lay interviewers were deciding on the presence or absence of phenomena without the contextual knowledge clinicians use. This shows a misunderstanding of the nature of fully structured interviews such as the Composite International Diagnostic Interview (CIDI) [4]. In order to allow the use of trained lay interviewers all questions are completely pre-specified. Interviewers do not rate, they record responses. If one group are diagnosed with a higher prevalence than another group this is because they have been more likely to report enough symptoms to meet criteria [5].
Mellsop et al. also contend that the clinician-derived diagnosis of bipolar disorder in the CAOS must be more accurate than a CIDI 3.0 diagnosis. They do not describe the procedure by which the diagnoses were derived by the clinicians in the CAOS, nor do they provide any evidence about the reliability and validity of the procedures to support their contention. It has been known for some time that diagnoses derived from unstructured clinician interview are problematic both in terms of reliability and validity [6]. Similarly, they provide no information about the reliability or validity of the HoNOS in their study. Mellsop et al. base their argument on their findings of ethnic differences in mean ratings on item 1 (overactive, aggressive, disruptive or agitated behaviour) of the HoNOS. In a review of the instrument, Pirkis et al. noted that although interrater reliability of item 1 is good to moderate, the test–retest reliability is poor [7].
There has been a clinical validation study for bipolar disorder in the US National Comorbidity Study Replication (NCS-R) [8]. In that study clinical reappraisal did not indicate overdiagnosis with the CIDI 3.0, which was unbiased compared to the clinician-administered Structured Clinical Interview for DSM-IV (SCID) for lifetime disorder.
There are now three sources of data on the prevalence of bipolar disorder in different ethnic groups in New Zealand. One is the NZMHS, a nationally representative community survey in which the 12 month prevalence was found to be 4.6% for Maori and 1.8% for Others (non-Maori, non-Pacific), although this difference was reduced after control for age and sex to 3.8% versus 1.8%, and further reduced to 3.4% versus 1.9% after additional control for education and income [3]. The second is hospitalization data, which shows that age- and sex-standardized inpatient discharge rates were 2.4-fold higher in Maori than in non-Maori [9]. The third is the CAOS that, as Mellsop et al. report, included only services that volunteered to participate, so that ‘Incidence and prevalence figures cannot be extrapolated from these findings and applied to the general population’ [2]. In CAOS apparently there were no ethnic differences in the rates of diagnosis of bipolar disorder. Because the services were not taken from any defined population base it is not clear how any rates could be calculated from the CAOS data. Does this claim mean merely that the percentage of service users with bipolar disorder did not differ by ethnicity? This could occur if Maori had higher rates of other disorders as well, as is shown in the hospitalization data for schizophrenia [9]. Under this scenario the percentage of hospitalised cases with a particular disorder can be equal for each ethnic group even though the community prevalence differs and even when the percentage of patients admitted differs across ethnic groups. In conclusion, the critical appraisal of Mellsop et al. of the NZMHS findings with respect to ethnic differences in bipolar disorder does not take into account the problem of confounding by age and gender, or the non-representative sample of the CAOS. Furthermore, the argument put by Mellsop et al. assumes that the lay person-administered CIDI 3.0 overestimates caseness compared to a clinician assessment, whereas the available evidence does not support this contention. There is much still to be learned about the presentation of bipolar disorder and the prevalence of symptoms across different groups in New Zealand, but we are not convinced that the Mellsop et al. study has provided an explanation of the ethnic differences found in the NZMHS.
Paediatric bipolar disorder is a controversial diagnosis
The editorial ‘Growing evidence to support early intervention in early onset bipolar disorder’ (BD), by Mao and Findling in the August issue of the Journal is one of the first papers on paediatric bipolar disorder (PBD) in the Australasian psychiatric literature [1]. But Mao and Findling give no indication of the extent of controversy surrounding the diagnosis of PBD, in particular pre-pubertal PBD. For example, in contrast to the Australian and New Zealand Journal of Psychiatry editorial, the February 2007 editorial of the American Journal of Psychiatry noted: ‘Pediatric bipolar disorder is notoriously controversial, with the epicenter of the debate being whether the condition can be diagnosed in pre-pubertal children at all’ [2].
The Australasian literature needs to be informed of this debate because although research into whether antecedents of BD exist in young children is laudable, our concern is that the Aust N Z J Psychiatry editorial may inspire increased use of antipsychotics and mood stabilizers among children and adolescents before either diagnosis or benefits are clear and these children will run the risk of serious side-effects.
Mao and Findling do acknowledge that ‘many clinicians are still reluctant to treat children and adolescents … with symptoms suggestive of a BD diathesis’ and that it is a ‘challenge to accurately diagnose … PBD’. Nonetheless they appear to take as a given that BD, or at least ‘cyclotaxia’ (Findling's term) referring to subsyndromal affective symptoms, can be diagnosed in children as well as adolescents.
In the USA there is rising controversy in both the academic literature and the public media fuelled by a rapid rise in diagnosis. Recent research shows a 44-fold increase in diagnosis of BD in the under-20 age group between 1994–95 and 2002–03 [3]. Concern over use of antipsychotic and mood-stabilizer medication in very young children follows the highly publicized death of a 4-year-old girl who was diagnosed with BD at age 28 months [4]. A study of 118 paediatric psychiatric patients aged 5–18 years on atypical antipsychotics for at least 6 months found that 11 (9%) had tardive dyskinesia [5].
Also in contrast to the Aust N Z J Psychiatry editorial, the July 2007 issue of the Canadian Journal of Psychiatry carries an editorial entitled ‘Controversies in childhood bipolar disorders’ [6], and while one lead paper maintains that the construct is valid the other lead paper by Duffy questions the existence of pre-pubertal PBD [7]. Duffy notes that while there is evidence ‘in some cases of prodromal psychiatric disturbances’ in offspring of parents with well-characterized BD, that in longitudinal studies of these offspring ‘there have been no observations of diagnosable BD in children under the age of 12 years’.
Duffy goes on to critique the PBD research literature in the way others have. The research is mainly predicated on phenomenology and tends to ignore developmental, traumatic and family dynamic issues. A relationship-based approach to understanding young children's behaviour is essential for diagnosis.
Duffy's Canadian paper on the same issue comes to a rather different conclusion to the Mao and Findling paper. It is a sign of the times that readers increasingly look to disclosures when judging papers. Duffy discloses sponsorship from the Canadian Institutes of Health Research and no pharmaceutical company support. Mao and Findling list 21 pharmaceutical companies in their disclosures.
Growing evidence to support early intervention in early onset bipolar disorder?
Reading the Editorial ‘Growing evidence to support early intervention in early onset bipolar disorder’ by Mao and Findling in the August issue of the Journal [1], reminded us of the story of the Emperor's new clothes.
The views of Mao and Findling, given editorial status without any critical comment, appear to reflect a widespread view among psychiatrists that early intervention should be embraced even in the absence of evidence of benefit and in the face of clear evidence that some early interventions can be harmful.
The authors argue that because bipolar disorder (BD) appears to be associated with progressive worsening over time, treatment should begin early in the course of illness. This would be a reasonable argument if (i) those who will develop the illness are able to be identified; (ii) the intervention was helpful at the time it was administered; and (iii) the intervention improved the long-term course of the disorder. Nothing in the Mao and Findling paper persuaded us that any of these criteria had been satisfied.
First, BD as described by Mao and Findling appears to be ill-defined. Terms such as ‘cyclotaxia’, ‘bipolar disorder not otherwise specified’ and ‘youths with subsyndromal symptoms’ would describe a heterogeneous group of troubled young people of whom an uncertain proportion will develop BD.
Second, the only placebo-controlled trial quoted by Mao and Findling (their own) showed no difference between the active treatment (divalproex sodium) and placebo. Surely the correct conclusion from that study is that there is no evidence for effective pharmacological therapy for those identified as being at high risk for bipolar disorder. Instead the authors state that ‘regardless of whether or not these children will develop BP-I, these children deserve early and effective treatment’ although they do concede that they ‘may not necessarily require pharmacotherapeutic interventions’.
Third, no evidence was presented that early intervention does change the long-term outcome of the disorder.
The views of Mao and Findling appear to accord with the practice of a number of Australian psychiatrists and we frequently see children graduating to our adult service who have been diagnosed with ‘bipolar’ and are on multiple medications, many of which cause potentially serious side-effects particularly weight gain, diabetes, and tardive dyskinesia.
We are concerned that some of our colleagues seem so ready to diagnose BD in young people when the diagnosis is far from clear cut. Presumably they are motivated by the need for early intervention.
We are also concerned that the ‘growing evidence for early intervention in bipolar disorder’ seems so unconvincing and we are concerned that the Journal allows the publication of such an article as its editorial, without comment.