Darryl Bassett

Borderline personality disorder and bipolar affective disorder. Spectra or spectre? A review

Objective: Bipolar affective disorder and borderline personality disorder have long been considered to have significant similarities and comorbidity. This review endeavours to clarify the similarities and differences between these disorders, with an effort to determine whether they reflect different forms of the same illness or separate illness clusters. Method: The published literature relating to bipolar affective disorders, borderline personality disorders, and related areas of knowledge was reviewed using searches of several electronic databases (AMED, CINHAL, Embase, Ovid, ProQuest, MEDLINE, Web of Science, ScienceDirect) and published texts. These findings were combined with the personal clinical experience of the author, and information gathered from colleagues, to create a review of this topic. Results: Bipolar affective disorders and borderline personality disorders differ with respect to sense of self, disruption of relationships, family history of bipolar disorders, the benefits of medications, the extent of cognitive deficits, the form of affective dysregulation and mood cycling, the incidence of suicide and suicide attempts, the form of psychotic episodes, the incidence of early sexual abuse but not early trauma in general, the loss of brain substance, alterations in cortical activity, glucocorticoid receptor sensitivity, and mitochondrial dysfunction. They are similar with respect to non-specific features of affective dysregulation, the incidence of atypical depressive features, the incidence of self-mutilation, the incidence of transporter polymorphisms, possible genetic linkages, overall reduction in limbic modulation, reduction in the size of hippocampi and amygdala, and the incidence of sleep disruption. Conclusions: This review concludes that bipolar affective disorders and borderline personality disorder are separate disorders, but have significant elements in common.

A consensus statement for safety monitoring guidelines of treatments for major depressive disorder

Objective: This paper aims to present an overview of screening and safety considerations for the treatment of clinical depressive disorders and make recommendations for safety monitoring. Method: Data were sourced by a literature search using MEDLINE and a manual search of scientific journals to identify relevant articles. Draft guidelines were prepared and serially revised in an iterative manner until all co-authors gave final approval of content. Results: Screening and monitoring can detect medical causes of depression. Specific adverse effects associated with antidepressant treatments may be reduced or identified earlier by baseline screening and agent-specific monitoring after commencing treatment. Conclusion: The adoption of safety monitoring guidelines when treating clinical depression is likely to improve overall physical health status and treatment outcome. It is important to implement these guidelines in the routine management of clinical depression.

Stimulants for depression: On the up and up?:

The use of traditional psychostimulants (methylphenidate and dexamphetamine) and stimulant-like drugs (modafinil and armodafinil) for the treatment of depression is a growing concern given the lack of research evidence supporting their effectiveness. The current article describes the role of stimulants in treating depression – specifically their risks and benefits and their potential use alongside antidepressants. Clinically, the rapid amelioration of depressive symptoms with traditional psychostimulants is often dramatic but short-lived, and this suggests that they likely operate via different mechanisms to conventional antidepressants. More importantly, there is little evidence from randomised controlled trials supporting their efficacy in treating depression, although modafinil has been shown to be effective in reducing prominent depressive symptoms, such as fatigue. Research is urgently required to clarify psychostimulants’ mechanisms of action and to evaluate their long-term benefits and risks in the treatment of major and bipolar depression. Ultimately, specificity of action needs to be determined to inform the sophisticated clinical use of psychostimulants in the management of depression. Until then they should only be prescribed if absolutely necessary, and even then their prescription should be facilitatory and time limited unless it is for investigational purposes.

Defining melancholia: A core mood disorder

Gordon Parker, Darryl Bassett, Tim Outhred, Grace Morris, Amber Hamilton, Pritha Das, Bernhard T Baune, Michael Berk, Philip Boyce, Bill Lyndon, Roger Mulder, Ajeet B Singh, Gin S Malhi

Defining disorders with permeable borders: you say bipolar, I say borderline!

1Mood Assessment and Classification (MAC) Committee, Sydney, NSW, Australia 2Private Practice in Psychiatry and Division of Psychiatry, University of Western Australia, Perth, WA, Australia 3Department of Psychological Medicine, University of Otago – Christchurch, Christchurch, New Zealand 4Academic Department of Psychiatry, Northern Sydney Local Health District, St Leonards, NSW, Australia 5Sydney Medical School, Northern, University of Sydney, Sydney, NSW, Australia 6CADE Clinic, Royal North Shore Hospital, Northern Sydney Local Health District, St Leonards, NSW, Australia 7School of Medicine, IMPACT Strategic Research Centre, Deakin University, Barwon Health, Geelong, Vic., Australia 8Department of Psychiatry, Orygen Research Centre, Florey Institute for Neuroscience and Mental Health, University of Melbourne, Melbourne, Vic., Australia 9Discipline of Psychiatry, University of Adelaide, Adelaide, SA, Australia 10Discipline of Psychiatry, Sydney Medical School, Westmead Clinical School, University of Sydney, Sydney, NSW, Australia 11Mood Disorders Unit, Northside Clinic, Greenwich, NSW, Australia 12ECT Services, Northside Group Hospitals, Greenwich, NSW, Australia 13School of Psychiatry, University of New South Wales, Sydney, NSW, Australia 14Black Dog Institute, Sydney, NSW, Australia

Why the hype about subtype? Bipolar I, bipolar II--it's simply bipolar, through and through!

Australian & New Zealand Journal of Psychiatry, 50(4) Bipolar disorder (BD) is frequently misdiagnosed and mismanaged because the ‘concept’ of BD II lacks definition, and prognostic value. Hypomania was first described and introduced into practice by Falret and Mendel in the 19th century. Despite long-standing recognition of the syndrome, a precise definition of hypomania has remained elusive. In 1976, upon observing less severe symptoms of mania that could be treated without hospitalization, Dunner et al. (1976) conceived BD II. Two decades later, BD II was formally installed in Diagnostic and Statistical Manual of Mental Disorders–Fourth Edition (DSM-IV), with the diagnosis contingent on the occurrence of hypomania in the context of a previous major depressive episode. In Diagnostic and Statistical Manual of Mental Disorders–Fifth Edition (DSM-5), increased activity/energy was added as a core feature of mania/hypomania, alongside elevated or irritable mood. In hypomania, these symptoms must last for a minimum of 4 consecutive days, contrasting with the 7-day criterion for a manic episode. In addition, hypomania requires an unequivocal change in functioning that is out of character for the individual. An interesting and critical distinction with mania, however, is that this change in function, while observable to others, is not severe enough in hypomania to cause marked impairment, necessitate hospitalization or present with psychotic symptoms. Thus, DSM-5 defines and distinguishes hypomania and mania on the basis of duration of symptoms and severity of illness (associated impairment). However, in practice, it is extremely difficult to distinguish between no, some or marked impairment, which necessarily cascades as a function of severity. In sum, the criteria for hypomania are fuzzy and, clinically, its distinction serves no purpose other than perhaps to obscure the inception of mania.

The limitations of using randomised controlled trials as a basis for developing treatment guidelines

Randomised controlled trials (RCTs) are considered the ‘gold standard’ by which novel psychotropic medications and psychological interventions are evaluated and consequently adopted into widespread clinical practice. However, there are some limitations to using RCTs as the basis for developing treatment guidelines. While RCTs allow researchers to determine whether a given medication or intervention is effective in a specific patient sample, for practicing clinicians it is more important to know whether it will work for their particular patient in their particular setting. This information cannot be garnered from an RCT. These inherent limitations are exacerbated by biases in design, recruitment, sample populations and data analysis that are inevitable in real-world studies. While trial registration and CONSORT have been implemented to correct and improve these issues, it is worrying that many trials fail to achieve such standards and yet their findings are used to inform clinical decision making. This perspective piece questions the assumptions of RCTs and highlights the widespread distortion of findings that currently undermine the credibility of this powerful design. It is recommended that the clinical guidelines include advice as to what should be considered good and relevant evidence and that external bodies continue to monitor RCTs to ensure that the outcomes published indeed reflect reality.

Is atypical depression simply a typical depression with unusual symptoms

The term ‘atypical depression’ (AD) was first used by West and Dally in 1959 to describe depressed patients who failed to respond to tricyclic antidepressants (TCAs) but responded to the monoamine oxidase inhibitor (MAOI), iproniazid. Subsequently, Klein and Davis described a condition they labelled hysteroid dysphoria consisting of a subgroup of depressed female patients who demonstrated ‘an extreme response to admiration, approval and personal rejection’ and who also had symptoms of hypersomnia and hyperphagia (for a review of the history, see Davidson, 2007; Parker et al., 2002). Much later, it was recognised that these patients were further characterised by the symptoms of mood reactivity, weight gain, reverse diurnal mood variation and profound energy loss – captured in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) as ‘feeling heavy, leaden, or weighted down, usually in the arms or legs; this is generally present for at least an hour a day but often lasts for many hours at a time’ and described as ‘leaden paralysis’. These clinical features have come to be known as ‘atypical’, contrasting them from the ‘typical’ features of appetite loss, weight loss, decreased sleep and morning worsening over-represented in melancholic depression. ‘Rejection sensitivity’ was subsequently included as a clinical feature of atypical depression. DSM-5 classifies atypical features as a specifier for depressive disorder, with the diagnostic criteria primarily of mood reactivity with two or more of the following: significant weight gain or increased appetite, hypersomnia, leaden paralysis and a long-standing pattern of interpersonal rejection Is atypical depression simply a typical depression with unusual symptoms?

Borderline personality disorder and polycystic ovary syndrome

Australian & New Zealand Journal of Psychiatry, 50(4) environment, facing a new life in a foreign city. He then elaborated a story of a young boy living there alone, after his immediate family had all passed away from a disease. The chopped down wood was used to build a farmhouse. His grandfather remained and cared for him, until he grew old and passed away. He was able to talk about how the boy felt sad and alone, although he derived some comfort from the farm animals. This session was very useful in terms of allowing the patient to talk about his emotions in an indirect and less confronting manner. Because he enjoyed the session, rapport was built, and he felt comfortable to talk freely. In a second case, a 7-year-old boy presented with oppositional behaviour and tantrums at school and at home following the recent separation of his parents. During his play sessions, he chose to play with Lego blocks and created an elaborate army where he was the general with a base camp, soldiers, planes and tanks. Each session was characterised by an intense battle against the approaching enemy fought on multiple battle-fronts with ground and aerial attacks. His soldiers would frequently launch rescue missions for kidnapped soldiers. After every session, his army always won without any casualties. Despite his denial of a connection to his family battles, he was able to say ‘I’m like my dad’. His behaviour improved after this. These sessions provided him with an opportunity to use his imagination to process the conflict associated with the separation of his parents in a non-threatening way. This experience allowed him to explore and be the master of his play environment. In the real world, he did not have any control over his real-life situation, but within the playroom, he was imbued with a sense of control to make positive changes in his inner world. In both cases, the children experienced a therapeutic intervention, while the registrars learnt and experienced the value of therapeutic play for children.

Tinkering at the margins: A response to Chanen

To the Editors, In his commentary “Tinkering at the margins”,1 Chanen maintains that the distinction between borderline personality disorder (BPD) and bipolar disorder (BD) can be readily determined in “daytoday clinical practice” using current diagnostic criteria. It is common, however, for it to be argued that their differentiation is difficult. We suggest that there are two reasons for such differentiation difficulties. Firstly, there is a need to proceed beyond clinical syndrome criteria and enrich them with condition correlates. For example, in recent studies and reviews, samples of those with a BPD were able to be differentiated at levels in excess of 90% from those with a BP condition by a small set of variables including (i) female gender, (ii) childhood sexual abuse, (iii) depersonalization in childhood, (iv) sensitivity to criticism, (v) relationship difficulties, (vi) absence of a bipolar family history and (vi) a higher rate of deliberate selfharm and suicidal attempts.2 It was also noted that the mood states in those with BPD are marked more by anger than by euphoria, that the depressive episodes tend to be nonmelancholic as against the likelihood of melancholic episodes in those with a BP condition, that there is a greater likelihood of a family history of impulse disorders in those with a BPD, and that those with a BPD evolve into the disorder in adolescence and adulthood rather than showing the “trend break” generally evidenced by those with a bipolar condition (i.e. a new state of categorical mood swings commencing rather than evolving). The second reason for differentiation difficulties is that we, as clinicians, tend to operate to a rule of parsimony (i.e. which condition is “the diagnosis”?), while studies have identified that 10%20% of those with BP or BPD also have the other condition. In our paper “Defining permeable borders: you say bipolar, I say borderline!” we were, however, attempting more to clarify the interface between BPD and BD, rather than to identify those characteristics of these disorders that were unmistakably different. For example, it is clinically relatively easy to distinguish severe mania in BD from the highly aroused emotive states of BPD. Our intention was to explore the boundaries of these disorders in an attempt to identify their differences and similarities. With this in mind, the constructs of “projective identification” and “noxious sense of self” are meaningful because they offer fundamental differences in these disorders which are reflected in clinical presentations. While Chanen is correct that sexual and other forms of abuse occur in association with BD, the prominence of such abuse in BPD is so pervasive that many observers have suggested BPD would be better considered a form of complex posttraumatic stress disorder. Chanen mentions the similarities of psychosis in BPD to a number of other psychiatric disorders. We agree that some elements of psychosis (auditory hallucinations) in BPD are similar to those observed in other disorders; however, the scientific evidence regarding the characteristics of psychosis in BPD is still lacking in clarity and is generally different in form and content from that seen in BD.3 In addition, we agree that there is insufficient scientific evidence that antipsychotic medications are often of limited efficacy in the psychosis associated with BPD, but our clinical experience and that of many others supports this contention. Studies of the life history of BPD support our contention that the prognosis for BPD is generally better than that for BD. It is true that patients with BPD are often left with residual difficulties in interpersonal interactions, but their emotional dysregulation and quality of life tend to improve with advancing age. In conclusion, we suggest that Chanen has overinterpreted the content of our paper – which sought, in essence, to clarify the interface between two complex groups of disorders.