Peter Parry

Aripiprazole in the Maintenance Treatment of Bipolar Disorder: A Critical Review of the Evidence and Its Dissemination into the Scientific Literature

A systematic search of the literature reveals limited evidence to support use of aripiprazole, a second-generation antipsychotic medication, in maintenance therapy of bipolar disorder, despite widespread use.

Pediatric Bipolar Disorder in an Era of “Mindless Psychiatry”

Objective: Pediatric bipolar disorder (PBD) reflects shifts in conceptualizing bipolar disorder among children and adolescents since the mid-1990s. Since then, PBD diagnoses, predominantly in the United States, have increased dramatically, and the diagnosis has attracted significant controversy. During the same period, psychiatric theory and practice has become increasingly biological. The aim of this paper is to examine the rise of PBD in terms of wider systemic influences. Method: In the context of literature referring to paradigm shifts in psychiatry, we reviewed the psychiatric literature, media cases, and information made available by investigative committees and journalists. Results: Social historians and prominent psychiatrists describe a paradigm shift in psychiatry over recent decades: from an era of “brainless psychiatry,” when an emphasis on psychodynamic and family factors predominated to the exclusion of biological factors, to a current era of “mindless psychiatry” that emphasizes neurobiological explanations for emotional and behavioral problems with limited regard for contextual meaning. Associated with this has been a tendency within psychiatry and society to neglect trauma and attachment insecurity as etiological factors; the “atheoretical” (but by default biomedical) premise of the Diagnostic and Statistical Manual of Mental Disorders (3rd and 4th eds.); the influence of the pharmaceutical industry in research, continuing medical education, and direct-to-consumer advertising; and inequality in the U.S. health system that favors “diagnostic upcoding.” Harm from overmedicating children is now a cause of public concern. Conclusion: It can be argued that PBD as a widespread diagnosis, particularly in the United States, reflects multiple factors associated with a paradigm shift within psychiatry rather than recognition of a previously overlooked common disorder.

Pre-Pubertal Paediatric Bipolar Disorder: A Controversy from America

Objective: The aim of this paper was to explore the rapid rise in the diagnosis of bipolar disorder (BD) in the paediatric, particularly pre-pubertal, age group, in the USA over the past decade and to look at associated controversies. Conclusions: There has been a very marked rise in the diagnosis of BD among pre-pubertal children, and to a lesser extent adolescents, in the USA since the mid 1990s. The rise appears to have been driven by a reconceptualizing of clusters of emotional and behavioural symptoms in the paediatric age group by some academic child psychiatry departments, most notably in St Louis, Boston and Cincinnati. There is controversy in both the academic literature and public media centring on diagnostic methods, epidemiological studies, adverse effects of medication including media-reported fatalities, and pharmaceutical company influence. With some exceptions, the traditional view of BD as being very rare prior to puberty and uncommon in adolescence appears accepted beyond the USA, though whether this is changing is as yet uncertain, and thus there are implications for Australian and New Zealand child and adolescent psychiatry.

Detached from attachment: neurobiology and phenomenology have a human face

Although at first glance melancholia and grief share some characteristics, the layperson of a century ago would have little difficulty distinguishing them. Paradoxically, the same layperson today might be confused, intuitively recognising a difference, yet forced perhaps to see both as forms of depression. Both have biological correlates and psychological parameters, but classical melancholia is immediately recognisable to an experienced clinician largely as a ‘biological disorder’, and grief, perhaps, as a relational process: a consequence of having been ‘attached’. Current diagnostic systems focus largely on reliable measurement of objective criteria in the present, despite widespread doubts about the validity of such an approach, and considerable interest in the doctrines of multicausality and equifinality. Meyer’s earlier psychobiology stressed the importance of understanding a person’s psychopathology and presenting phenomenology through their life story. We would argue that a failure to appreciate the functional significance of phenomenology, and the current and developmental context in which it developed, risks generating erroneous conclusions about the nature of the problem and potentially inappropriate treatment. Various theories are available in which to couch such an argument. Our emphasis is on attachment theory, which will be summarised briefly before reviewing some ambiguous clinical situations that can be informed by this understanding. Overview of attachment theory

The autism spectrum disorder ‘epidemic’: Need for biopsychosocial formulation

In DSM-IV autism spectrum disorder (ASD) was defined as a cluster of lifelong neurodevelopmental disorders consisting of autistic disorder, Asperger’s syndrome and pervasive developmental disorder not otherwise specified (PDD-NOS). ASDs can be disabling disorders and warrant multi-faceted assessments and interventions that are often required in some form across the lifespan. The prevalence of ASDs has climbed dramatically in recent years and an over-diagnosis ‘epidemic’ has been suggested (Frances and Batstra, 2013). Partly to reduce over-diagnosis, ASDs have been consolidated in DSM-5, such that the subtypes are no longer used but all are referred to as ASD and severity is specified. ASD in DSM-5 is characterised by deficits in social communication and social interaction plus restricted repetitive behaviours, interests and activities (RRBs). Subjects without RRBs can be given a new DSM-5 diagnosis: social communication disorder. However, the DSM-5 field trials suggest most individuals currently diagnosed with ASDs will still have ASD under the new criteria. This allayed the fears of some advocacy groups. We argue that there is an overdiagnosis ‘epidemic’ of ASDs, particularly in the paediatric population, and doubt that DSM-5 criteria will minimize this. The underlying drivers of this and similar over-diagnostic ‘epidemics’ is a combination of the descriptive symptom-focused and context-deficient nosology inherent in the DSM model combined with needs for services and other psychosocial gains associated with the use of diagnostic labels. A false ASD diagnosis can provide practical benefits such as financial and educational assistance, but it comes with side effects that may take years to be fully apparent.

Biologism in Psychiatry: A Young Man's Experience of Being Diagnosed with "Pediatric Bipolar Disorder"

Pediatric bipolar disorder is a diagnosis that arose in the mid 1990s in the USA and has mostly remained confined to that nation. In this article a young American man (under a pseudonym) describes his experience of having the diagnosis throughout his adolescent years. His story was conveyed via correspondence and a meeting with the author, an Australian child psychiatrist. The young American’s story reveals several issues that afflict contemporary psychiatry, particularly in the USA, where social and economic factors have contributed to the rise of a dominant biomedical paradigm—or “biologism”. This focus on the “bio” to the relative exclusion of the “psychosocial” in both diagnosis and treatment can have serious consequences as this young man’s story attests. The author explores aspects of his tale to analyze how the pediatric bipolar disorder “epidemic” arose and became emblematic of a dominant biologism. This narrative points to the need, depending on the service and country, to return to or retain/improve a balanced biopsychosocial perspective in child and adolescent mental health. Child psychiatry needs to advocate for health systems that support deeper listening to our patients. Then we can explore with them the full range of contextual factors that contribute to symptoms of individual and family distress.

Reification of the paediatric bipolar hypothesis in the USA

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Paediatric bipolar disorder: Reality or myth?:

Australian & New Zealand Journal of Psychiatry, 52(9) I was reminded of this campaign while attending the recent RANZCP International Congress. While introducing one of the keynote speakers, the introducer announced the first syllable of his first name, and then unsure how to pronounce the rest, went on to his last name. Then, the speaker after him also called him by his truncated first name. Late I met the Speaker and asked him how he felt about being called by an incorrect first name. I told him why I was asking. When I had first gone to the United Kingdom in the late 1990s to do my postgraduate training, I had been told that my name was too difficult to pronounce so I will have to come up with a simpler first name. I had replied, ‘If I can make an effort to pronounce your name correctly, I expect you to do the same’. The Speaker and I traded some funny, and some not so funny, stories about our experiences with our names. He basically told me that he had accepted that that is the way it is going to be, and there was nothing he could do about it. The most heartbreaking story he told me was that one long-term colleague mistook a paper as being authored by him just because he had never known his full first name, to which he had replied, ‘I know all of us look the same to you but please read the full name first next time’. I have coined a new term for this phenomenon which is ‘Nominal Colonialism’. It goes like this, ‘You are now in MY country mate. Do not expect me to waste time on learning to pronounce your foreign-sounding, unfamiliar name. Change it to something simple that I can say easily’. I just wonder if colleagues realize how unfair it is to coerce other colleagues into simplifying their names, or to keep calling them with wrong, truncated or altered names. Maybe the RANZCP can learn a thing or two about cultural diversity from Palmerston North Girls’ High School.

Can antipsychotic medication administered for paediatric emotional and behavioural disorders lead to brain atrophy

Australian & New Zealand Journal of Psychiatry, 00(0) In recent years, there has been considerable debate in adult psychiatry as to whether antipsychotic medication can cause cerebral atrophy, based on the findings of animal and human studies. However, the possibility that antipsychotics might have long-lasting effects on the structure and function of the developing brain has been less widely discussed in child psychiatry, despite the rising prescription rates of antipsychotics among Australian children and adolescents. A recent survey of Australian paediatricians found that psychotropics were the most commonly prescribed class of medication in paediatric practice. Although stimulants were the most prescribed psychotropic medication, antipsychotics were prescribed to 5.6% of children with developmental-behavioural and mental health diagnoses (Efron et al., 2017). It is well recognised that children are more sensitive than adults to the side effects of second-generation antipsychotics (SGAs), such as obesity, diabetes and sedation. However, there are no published studies on the possible effects of antipsychotic exposure on the brain volumes of children and adolescents treated for non-psychotic disorders. At present, our only guides are studies of adult patients with psychotic disorders, and animal studies that indicate cerebral atrophy can occur in the brains of normal juvenile animals exposed to antipsychotics (Vernon et al., 2011). Evidence from animal studies indicates that antipsychotic induced cerebral atrophy might occur in adult and juvenile animals in the absence of any neurological disease process like schizophrenia. For example, macaque monkeys demonstrated significant total brain weight loss of approximately 10% after 17–27 months of exposure to haloperidol or olanzapine, compared to macaque monkeys receiving sham medication (DorphPeterson et al., 2005). All major brain regions were affected, but the most significant changes were noted in the frontal and parietal lobes. A juvenile rat study replicated these findings with significant decreases in whole brain volume loss of between 6–8% following just 8 weeks of exposure to either haloperidol or olanzapine, compared to sham medication (Vernon et al., 2011). Most of the volume loss was identified in the frontal cerebral cortex. Of note, the effect was of similar magnitude for both the first-generation antipsychotic, haloperidol and the SGA, olanzapine. It is well known that patients with schizophrenia experience progressive brain volume loss. These findings reinforced the hypothesis that schizophrenia is potentially a neurodegenerative illness. However, based on animal studies, it has also been postulated that some of the progressive brain volume loss seen in schizophrenia might be a direct effect of antipsychotic medication. In a landmark study, Ho et al. (2011) specifically investigated the potential for antipsychotic associated brain volume loss. This cohort study followed up 211 patients with first episode schizophrenia using sequential high-resolution magnetic resonance imaging (MRI) scanning (average of three scans) over an average of 7.2 years. The study found that greater intensity of antipsychotic treatment (doses and treatment length) was associated with a small but significant loss of total brain volume. This effect remained, even after controlling for illness duration, illness severity and substance abuse. In fact, illness severity had only a modest correlation with total brain volume loss. The authors commented that these

Paediatric bipolar disorder: What are the dangers of treating a hypothetical disorder as a real disease?

Amerio et al. (2016) have recently reviewed the treatment of children and adolescents (aged 4–17 years) diagnosed with both paediatric bipolar disorder (PBD) and obsessive–compulsive disorder (OCD). They report Osler’s view, ‘medicine should be treatment of diseases, not of symptoms’ (p. 594), and, on this basis, recommend treating PBD as the underlying disease, using adult mood stabilisers for children and adolescents. Osler’s view is highly relevant to PBD: Is PBD really a ‘disease’ or just a loose collection of common ‘symptoms’ such as irritability and mood lability that arise from many causes in childhood? PBD began as an interesting research question, investigated by child psychiatrists working in US universities during the 1990s. They wondered whether adult bipolar disorder (BD) could be detected early in life and treatment instituted from childhood. Subsequent US studies focused on symptom profiles among young children including offspring of adults diagnosed with BD. However, after many studies over two decades, it was found to be difficult to predict a low prevalence condition like adult BD from high prevalence childhood symptoms such as irritability and mood lability measured decades earlier (Malhi, 2016). By definition, it is challenging to predict relatively rare outcomes from variable collections of frequently occurring antecedents. While PBD remained an interesting research hypothesis in Ivy League universities, it presented few dangers. However, the concept was prematurely translated into clinical practice, resulting in the widespread off-label prescribing of a broad range of adult psychotropic medications for children and adolescents, especially in the United States (Malhi, 2016). For instance, Amerio et al. (2016) located seven clinical studies of PBD–OCD, which included the use of clozapine (for a 13-year-old boy), lithium (including a 4-year-old boy), lamotragine, divalproex sodium, olanzapine, risperidone, quetiapine, aripiprazole, clonazepam, clomipramine and escitalopram among others (Table 1: p. 595). The risks and benefits of these 11 medications have not been fully investigated with randomised controlled trials in children, but the original clinical studies reported a variety of side effects such as increased appetite, sedation, slurred speech, gait disturbance, low blood pressure, neurological symptoms, agitation, manic switch and suicidal intent. In Australia and New Zealand, child psychiatrists have been careful observers of the US PBD phenomenon with the vast majority choosing not to adopt the hypothesis into clinical practice (Parry et al., 2009). This caution was well founded, as it has proved impossible to diagnose PBD accurately, and adult medications present iatrogenic dangers for children.