Abstract
Inflation
To the befuddlement of physicists, the universe is expanding; in fact it is accelerating apart at an unbelievable rate. The precise explanation for this is still a matter for debate, but dark forces in the fabric of the universe are thought to be in play (Perlmutter et al., 1999; Riess et al., 1998). While the implications of this are profound, the timeframe involved means there is little chance of any direct impact on humankind as we know it. In contrast, another kind of expansion is affecting our lives here and now and also seems to have no end in sight: the diagnostic expansion of bipolarity.
A brief history of why polar, tri-polar and bipolar
Why polar?
In 1980, the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III) replaced manic-depressive illness with the term ‘bipolar disorder’ (APA, 1980). This was the first time that DSM recognised the unipolar–bipolar distinction as proposed by Leonhard many decades earlier. However, there was one subtle difference: Leonhard had used the terms ‘monopolar’ (unipolar) and ‘bipolar’ to describe recurrent affective disorders, but in DSM-III recurrence was given less importance as a discriminating feature of affective illnesses, and polarity therefore gained salience, even though, arguably, recurrence provides a better means of grouping mood disorders (Leonhard, 1957; Perris, 1966). Two additional factors appear likely to have contributed to the dominance of polarity. First, a change in polarity (such as the occurrence of mania in the context of previous depression) is a readily identified differentiator; second, the incredibly low threshold for defining ‘recurrence’ of depressive disorders in DSM (two or more episodes) meant that, in practice, everyone qualified as having recurrent depression, thereby rendering this descriptor meaningless (APA, 1994).
Tri- and bi-polar?
Bipolar II disorder was introduced in DSM-IV, after it was realised that not all presentations of mania qualified for bipolar I disorder and that manic symptoms of shorter duration were rather common (APA, 1994). Bipolar II disorder has recently been reified in DSM-5 following nearly two decades of interest in defining its occurrence and mapping its prevalence (APA, 2013). Alongside this process, however, many additional questions have been asked about the possible existence of other kinds of bipolar disorder. These questions arise because studies of bipolar II disorder have revealed that many individuals either experience sufficient manic symptoms, but for very short periods (fewer than 4 days), or have individual symptoms that meet the duration criteria but are too few in number to cross the threshold for diagnosis. A few of these myriad presentations have been captured in DSM-5, either as ‘other specified bipolar and related disorders’ or as ‘conditions for further study’ (APA, 2013). Another form of bipolarity that came to light during the DSM-IV era, termed ‘bipolar III disorder’, describes the occurrence of mania or hypomania in the context of antidepressant treatment (treatment-emergent mania) (Akiskal, 2007). It is thought to represent the unmasking of an underlying bipolar diathesis, although there is some debate as to whether treatment-induced manic symptoms are equivalent to spontaneous mania.
In this manner, bipolar disorder has been diversified and expanded and, whilst each step is explicable and apparently logical, the potential for bipolarity to permeate normalcy – facilitated by the recent changes in DSM-5 – is a grave concern.
Bipolar II has problems too
There is no doubt that, outside bipolar I disorder, there are clinical changes in mood, energy and activity that debilitate a considerable number of psychiatric patients. In other words, individuals with bipolar II disorder, if this is taken to mean ‘bipolarity that is not bipolar I disorder’, certainly exist and they are often very unwell. The practical difficulties that ensue are how best to define these syndromes, to understand their evolution and trajectory, and to determine optimal treatment. Careful revision of bipolar II disorder in DSM-5 could have assisted with these matters, but instead bipolar II has remained much the same, with profound ongoing consequences.
Already, three major problems plague bipolar II disorder: first, its diagnostic expansion to the point that it encroaches on normal experience; second, its frequent misdiagnosis because of overlap with other disorders; and, third, its treatment lacks differentiation from that of bipolar I disorder.
Blurred lines
The diagnostic boundaries of bipolar II disorder are known to be arbitrary, and hence its detection remains open to subjective interpretation of hypomanic symptomatology (Malhi et al., 2010). This inability to characterise the disorder, and in particular a failure to identify a pristine lower boundary, has advanced the conflation of bipolar II disorder with normalcy and contributed to its over-diagnosis, particularly in young people, where it has seemingly given rise to an epidemic.
Comorbidity and misdiagnosis
The second problem, namely that of overlapping diagnoses, is both a conceptual problem and one of dependence on phenomenology for arriving at diagnoses. Clinical presentations of bipolar II disorder clearly ‘overlap’ with anxiety states, substance abuse and personality traits – all of which are usually captured diagnostically as comorbidities. This makes the demarcation of bipolar II disorder extremely difficult (Malhi et al., 2012). For example, it is often difficult to distinguish whether irritability and distractibility are features of bipolar II disorder or a consequence of heightened anxiety. Similarly, impulsivity and hedonic changes are common sequelae of substance abuse, which also generates a myriad of symptoms that can obfuscate bipolar phenomenology further. In a similar vein, personality traits and affective dysregulation mimic bipolar mood changes, making disambiguation based solely on phenomenology near impossible (Bassett, 2012; Coulston et al., 2012).
For these reasons, the creation of bipolar II disorder has more than doubled the problem of bipolarity, and it is important to note that this has not come at the expense of lowering the threshold for morbidity. Although technically bipolar II disorder causes less impairment than bipolar I disorder (hypomania versus mania), because manic symptoms are present for a shorter period of time and are less severe (no psychotic symptoms, for example (APA, 2013)), evidence suggests that the morbidity of depression in bipolar II disorder is equal to, if not greater than, that exacted by bipolar I disorder (Judd et al., 2002, 2003). Furthermore, subsyndromal symptoms are more common in bipolar II disorder and last longer (Judd et al., 2002, 2003).
Lack of therapeutic specificity
Interestingly, in terms of overall course, bipolar II disorder is possibly more similar to recurrent unipolar depression than it is to bipolar I disorder. However, despite this, the medications used to treat bipolar II disorder are virtually identical to those used for bipolar I disorder, and this is the third unsolved problem. In other words, bipolar II disorder has been unable to achieve sufficient therapeutic specificity. This is partly because all ‘bipolar medications’, with the notable exception of lithium, have actually been developed for other disorders. This is quite remarkable. The paradigm employed for the development of medications for the treatment of bipolar disorder has been to ‘adopt’ medications originally developed for different indications and to trial them in bipolar I disorder patients. Notably, medications trialled in one phase of acute bipolar illness (usually mania) have often been subsequently used informally across other phases of the disorder without much further investigation of putative benefits. As such, antidepressants have migrated from major depression, anticonvulsants from the treatment of epilepsy, and neuroleptics from the treatment of psychoses. This may explain why therapeutic subtyping within bipolar disorder has received little attention, and why in practice the management of bipolar II and bipolar I disorders is much the same. One problem this causes is that medications used in bipolar I disorder are often administered similarly in bipolar II disorder, despite a lack of evidence, and often in combinations for which there is virtually no evidence. Such extrapolation of practice and ‘evidence’ from bipolar I disorder to guide treatment in bipolar II disorder is widespread, undermines therapeutic differentiation of the two subtypes and renders diagnostic separation meaningless.
Try before you buy
Of the many potential drivers of the expansion of bipolar disorder, there are two that warrant specific consideration. First, academics and consumers have argued for better recognition and treatment of bipolar disorder, citing studies suggesting delayed diagnosis (mainly of bipolar I disorder) and the relative lack of efficacy of antidepressants in depression (Malhi, 2012). Second, the diagnosis of bipolar disorder has been championed by Pharma and seen as a target for expansion and investment, and as an opportunity for expanding the use of existing agents, particularly atypical antipsychotics. A combination of these two forces has propelled the diagnosis of bipolar disorder to a point where it is widely recognised and diagnosed and almost always treated with medications. And yet it remains poorly defined, with likely diminishing interest in identifying specific treatments.
Curiously, in certain circumstances, bipolar disorder may be seen as desirable (Chan and Sireling, 2010). From both a clinician’s and a patient’s perspective this label can be easier to assign, and to accept, respectively, than that of schizophrenia, although in some cases the distinction is difficult and the actual clinical features may be more indicative of a psychotic process.
Sometimes the diagnosis of bipolar disorder is itself ‘trialled’. For example, mixed features that emerge in the context of depressive presentations (distractibility, agitation, irritability), which previously would have been regarded as superadded anxiety or agitated depression, may now be subsumed by bipolarity (Malhi, 2013). Indeed, recent research has suggested that up to a staggering 40% of patients with major depression may, from time to time, have what could be defined as ‘manic’ symptoms (Angst et al., 2010). In such cases, a diagnosis of bipolar disorder may be considered and ‘tested’ via a trial of ‘bipolar treatments’: a ‘try-polar’ approach.
From a patient’s perspective, a diagnosis of bipolar II disorder is certainly more attractive than that of schizophrenia. It may also be seen as preferable to being labelled as having a personality disorder. But in some cases it is simply a refuge from the consequences of bad behaviour or provides a more socially acceptable explanation for angry outbursts (Anand and Malhi, 2009).
In practice, a diagnosis of bipolar disorder is often invoked following treatment resistance or even poor response. In some cases of treatment-resistant depression, this is wholly appropriate because an incorrect paradigm has been used and a diagnosis of bipolar disorder has been missed. But in many instances it may be affording an opportunity to prescribe additional medications – outside their usual indication. ‘Trying’ bipolar is therefore linked to ‘buying bipolar’, in that, in many instances, medications can only be prescribed for a particular diagnosis, or reimbursement of costs to the patient is only possible, when medications are prescribed for a specific diagnosis. In these instances, a broader concept of bipolar disorder has perhaps been of benefit, but inadvertent consequences include over diagnosis, misdiagnosis and inappropriate treatment. The practice of ‘try-polar’ has also contributed to an increase in the need for ‘depolarisation’ – an au courant term used to describe the removal of an incorrect diagnosis of bipolar disorder (Malhi and Berk, 2011).
Conclusion
In summary, bipolar II disorder is a diagnosis that has multifarious problems.
There is concern over expansion of the diagnosis such that it intrudes into normal mood swings, which allows access to ‘bipolar medications’.
Psychiatrists have been encouraged to view bipolar II disorder as similar to bipolar I, rather than considering the similarities to recurrent depression, and again this has expanded the use of ‘bipolar medications’.
Other psychiatric conditions are often misdiagnosed as bipolar II and then the patient is medicated and managed with bipolar treatment strategies, often for long periods of time, until they are ‘depolarised’.
When there is diagnostic uncertainty (as is often the case in psychiatry) there is a tendency to ‘try’ the diagnosis and commence medication. This often produces non-specific calming effects, which then confirm the diagnosis and justify the initiation of treatment, further reinforcing the ‘try-polar’ paradigm.
For the foreseeable future, and at least until DSM-5 is revised, or the International Classification of Diseases (ICD) offers some novel advance, the difficulties created by the diagnosis of bipolar II disorder will have to be addressed by psychiatrists in their clinical practice. To do this, the tendency to deliquesce diagnostic boundaries so as to assign certain diagnostic labels in order to access particular treatments has to be tempered, and executed with caution, if at all; diagnoses of bipolar II disorder past and present need to be frequently reviewed and revised as necessary; and non-specific treatments should not be regarded as bipolar medications and used to confirm diagnostic hypotheses. There is no doubt that bipolarity extends beyond bipolar I disorder and that this moiety affects the lives of many individuals and therefore merits diagnosis and treatment; the key challenge is how to achieve this while avoiding mislabelling and mistreating those with other ailments, or with no illness at all.
Footnotes
Funding
This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
Declaration of interest
GSM has received research support from AstraZeneca, Eli Lilly, Organon, Pfizer, Servier and Wyeth. GSM has been a speaker for AstraZeneca, Eli Lilly, Janssen-Cilag, Lundbeck, Pfizer, Ranbaxy, Servier and Wyeth. He has been a consultant for AstraZeneca, Eli Lilly, Janssen-Cilag, Lundbeck and Servier.