Abstract
There have been some significant advances in the treatment of bipolar disorder over the past few years with the refinement and development of psychosocial treatments and new indications for medications for the prevention of bipolar relapse. While there have been some advances in treatment, the recognition and diagnosis of bipolar disorder remains a clinical challenge, with both under and over diagnosis causing significant problems (Malhi and Berk, 2011). This month’s issue of the ANZJP, contains papers related to the theme of bipolar disorder. Specifically, they address issues related to diagnosis, treatment and risks associated with and the underpinnings of bipolar disorder.
The editorial by Professor Gin Malhi (2012) on bipolar antidepressant agents sets the scene for the insightful perspectives that follow. Professor Allan Young (2012) begins the debate with an interesting proposal that attempts to unify the clinical investigation of the mood disorders spectrum. Professor Michael Gitlin (2012) follows with a challenging article that contains more questions than answers but highlights the need for further research into the treatment of bipolar depression. Professor Nassir Ghaemi (2012) argues for science over opinion but advocates its use alongside clinical experience and cautions against the indiscriminate and widespread use of antidepressants in bipolar disorder. Finally, Professor Joseph Goldberg (2012) brings the discussion to a close and suggests that we adopt a broader and more rational view of the issue.
Goldney (2012) then formally ‘opens the batting’ with an historical review of the concepts of mania and melancholia in relation to bipolar disorder. A fascinating aspect of this is the fierce debate, in the early 19th century in France, as to who was the first to carve out a recurrent mood disorder (folie circulaire or folie à double-forme) from other forms of insanity. These early descriptions of recurrent mood disorders are often forgotten as they were superceded by Kraepelin’s classic description of manic depressive illness. Following Kraepelin’s description the concept has broadened further with the introduction of the unipolar-bipolar concept that prompted another debate about primacy, and the official designation of the illness as bipolar disorder in 1980 with the introduction of DSM-III. A fundamental change occurred when bipolar II became a specific diagnostic type in DSM-IV. Interestingly, in DSM-III bipolar II was considered as atypical bipolar disorder.
The boundaries of bipolar II disorder are even less clear because of reliance on the ephemeral clinical pictures of hypomania and depression rather than mania and melancholia (Malhi et al., 2010). This issue is addressed by Bassett (2012) who examines the overlap between borderline personality disorder and bipolar II disorder. This is a matter of considerable clinical importance and one that taxes all clinicians. Misidentification culminates in inappropriate psychological and psychopharmacological interventions being administered to the detriment of both patients and service providers (Boyce and Wilson, 2011). Providing an ongoing perspective, Bassett reviews the phenomenology of the mood changes in both conditions along with the areas of overlap and difference. This review will be invaluable to clinicians who regularly confront this diagnostic challenge.
Clearly, a biomarker or endophenotype closely associated with bipolar disorder would aid diagnosis, but these remain elusive. Ong et al., (2012) employed a sophisticated set of analyses to interrogate MRI images that enabled them to compare the shape of the caudate nucleus between those with bipolar 1 disorder and a healthy matched group. While there were no significant differences in overall volume, the shape of the left caudate among patients with bipolar disorder was significantly different when compared to that of controls. These subtle changes may be a function of alterations in brain circuitry in bipolar disorder. While this is a novel finding, it requires replication and its implications warrant further research. Another approach to identify endophenotypes is to examine cognitive processing as performed by Quinn et al., (2012) who were able to demonstrate significant differences between melancholic and non-melancholic patients. Unfortunately this finding did not translate to electrophysiological differences between the groups but this may be because the changes are subtle. However, it may be that cognitive functioning proves to be a useful endophenotype.
As clinicians, an important consideration in managing patients with mania is the risk of violent behaviour. In a ward setting interpersonal violence does arise during manic episodes. Interestingly, the rates of violent offending are not elevated in patients with mania as demonstrated in Neilssen et al.,’s (2012) study of violent offenders in NSW. This study reports findings that counter prevailing misconceptions, however, it does not mean to say we should not be concerned about risks associated with mania; they do exist, particularly in regard to their interpersonal behaviour. We also need to be alert to risk of harm to infants of women with bipolar disorder as psychosis following childbirth (most commonly bipolar disorder) is associated with infanticide (Kim et al., 2008).
While we have a large number of pharmacological interventions that we can use in bipolar disorder, the major issue is ensuring compliance. Non-adherence is one of the most common reasons why patients relapse. Crowe et al., (2012) review group interventions that have been designed to improve medication adherence in patients with bipolar disorder. The interventions they review are based upon family psychoeducation approaches. While the interventions showed delayed time to relapse, there was no clear advantage in improving adherence. What has not been studied is the critical role of good clinical care provided by a psychiatrist. As Crowe et al. suggest the psychiatrist’s role encompasses ‘involving patients as active partners in decision making rather than positioning them as passive recipients of medical orders’.
Over the past few years there has been considerable effort into public health approaches aimed at reducing the levels of common mental disorders. These include, education programmes and improving mental health literacy. Unfortunately, it seems as if this effort is not translating into reducing psychological morbidity as shown by Jorm and colleagues (2012). This study reviewed population based research that measured psychological distress from 1995 up to 2011 and found no reduction in the level of distress even though antidepressant use increased. The findings raise important questions concerning efficacy and specificity of our interventions. Perhaps we should be trying to reduce more tangible things such as financial hardship? In this vein, Butterworth et al. (2012), using data from the 2007 National Survey of Mental Health and Wellbeing, has shown that financial hardship was strongly associated with depression. They suggest that strategies to address this would be an appropriate way to tackle the increasing rates of depression.
In conclusion, this issue of the ANZJP will provide readers with a set of papers that will be thought provoking and provide clinical insights that will aid in improving clinical practice.