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Editorial
Thanks to Our Reviewers in 2005
Joel Paris, MD
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In Debate
Do Many Patients With Depression Suffer From Bipolar Disorder?
Jules Angst, MD
(PDF)

Does Almost Everybody Suffer From a Bipolar Disorder?
Scott B Patten, MD, FRCPC, PhD
(PDF)

Original Research Community Survey of Bipolar Disorder in Canada: Lifetime Prevalence and Illness Characteristics
Ayal Schaffer, John Cairney, Amy Cheung, Scott Veldhuizen, Anthony Levitt,
(PDF)

Correlates of Methylphenidate Use in Canadian Children: A Cross-Sectional Study
Alice Charach, Hongmei Cao, Russell Schachar, Teresa To
(PDF)

Polysomnographic and Symptomatological Analyses of Major Depressive Disorder Patients Treated With Mirtazapine
Jianhua Shen, Sharon A Chung, Leonid Kayumov, Henry Moller, Naheed Hossain, Xuehua Wang, Prativa Deb, Frank Sun, Xin Huang, Marta Novak, Darryl Appleton, Colin M Shapiro
(PDF)

Suicidality, Depression, and Mental Health Service Use in Canada
Anne E Rhodes, Jennifer Bethell, Susan J Bondy
(PDF)

Status of First-Episode Psychosis Patients Presenting for Routine Care in a Defined Catchment Area
Jennifer Payne, Ashok Malla, Ross Norman, Deborah Windell, Nicole Brown
(PDF)

Test Wisconsin chez les patients souffrant de schizophrénie, et leurs frères et soeurs
Youssef El Hamaoui, Meryem Elyazaji, Sakina Yaalaoui, Linda Rachidi, Mohamed Saoud, Thierry d’Amato, Driss Moussaoui, Jean Dalery, Omar Battas
(PDF)

Book Reviews
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Clinical Handbook of Psychotropic Drugs. 14th revised edition
Review by
Nicholas Delva

Marijuana and Madness
Review by
Nady el-Guebaly

Manual of Psychiatric Care for the Medically Ill
Review by
François M Mai

Guidebook on Helping Persons with Mental Retardation Mourn
Review by
Bruce D McCreary

Ethical Issues in Forensic Mental Health Research
Review by
Paul Fedoroff

Letters to the Editor
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Re: Listening to the Past: History, Psychiatry, and Anxiety

Reply: Listening to the Past: History, Psychiatry, and Anxiety

In Debate

Do Many Patients With Depression Suffer From Bipolar Disorder?

Jules Angst, MD¹

(Can J Psychiatry 2006:51:3–5)

Click here for author affiliations. 

It has long been believed that depression is much more common than BD, a conclusion based on epidemiologic data that show relatively low lifetime prevalence rates for BD (from 0.5% to 1.8%), compared with rates that are 5 to 10 times higher for MDD (between 4.6% and 17.1% or more). In ranking the burden of depression far higher than that of BD, the WHO reflects these findings. However, the prevailing view is very much open to question.

Given the wide variations in prevalence rates, it is perhaps wiser to rely on the proportion of subjects with BD among patients with MDEs. Contemporary studies carried out in psychiatric practice have diagnosed between 40% and 60% of all patients with MDEs as suffering from BD II (1), whereas the figures from epidemiologic studies are between 11% and 21%.

The enormous differences may be explained by the longer observation periods, diagnostic skills, and information from significant others available in clinical practice, as opposed to the single sessions, use of lay interviewers, and lack of contextual characteristics in epidemiologic studies. It is probably because of the context provided by teachers’ and parents’ reports that 3 epidemiologic studies of school-aged children and adolescents found a much higher proportion of BDs among subjects with MDDs (between 21.6% and 43.8%) than did studies of adults.

Indeed, many aspects of the debate about whether many patients with depression do in fact have BDs lead back to the question of accurate diagnosis and what stands in its way.

Depression is relatively easy to diagnose; conversely, BD is difficult to diagnose. Moreover, a systematic bias exists in favour of a diagnosis of depression: any loss or lack of information on hypomanic symptoms will result in depression being diagnosed. In this sense, unipolar depression is a negative diagnosis (that is, nonbipolar). We know from advocacy group studies that patients may experience up to 10 years’ delay before their hypomania is identified. The reasons for this tardy recognition of BDs in patients and for the overdiagnosis of depression at their expense may be summarized as follows:

1. Initial hypomanic symptoms are notoriously difficult to recognize. In up to two-thirds of cases, BDs begin in early adolescence, manifesting first as depression at an age when brief periods of overactivity or hypomania are hard to distinguish from normal liveliness or hyperactive behaviour.

2. Depression is distressing, and sufferers tend to seek treatment, whereas hypomania is rarely subjectively perceived as pathological, although it may create behavioural problems more troublesome to the people around them than to the subjects themselves. As a result, hypomanic symptoms are often not reported spontaneously and pass unnoticed by physicians. The use of new instruments for the self-assessment of hypomanic symptoms has been shown to increase the recognition rate of BD substantially. For instance, in the large French multicentre EPIDEP study in psychiatric practice, the rate of BDs found almost doubled, from 22% to 40% (2).

3. The period for observing patients is often too short to identify BD, which is diagnosed on the basis of a lifetime occurrence of hypomania or mania. Every new episode of depression is associated with a certain risk of switching into bipolarity. Lifelong follow-up data of hospitalized patients with depression have shown a constant diagnostic conversion rate of 1.25% yearly, a figure that is compatible with rates observed in many shorter follow-up studies. This means that 50% of patients with severe depression may be expected to become patients with BD over 40 years of illness (3).

4. The current diagnostic criteria for bipolarity need to be revised. The DSM-IV concept of hypomania, especially its restriction to a minimum duration of 4 days, has been seriously questioned by international experts (4).

Moreover, the application of the DSM-IV definition of hypomania as a diagnostic specifier for MDD is probably too strict and insufficiently sensitive. DSM-IV symptom Criterion A, in particular, is problematic: by requiring the presence of elevated mood or irritability and neglecting symptoms of overactivity, the Criterion A excludes many cases from the diagnosis. It may well be that the modern terminological preference for “mood disorder” over “affective disorder” has led to changes in mood having unjustified priority over increased activity and energy.

To compensate for this emphasis on mood changes, overactivity was added to the stem questions for hypomania (5); since 1981, symptoms of overactivity have been used in the Zurich Cohort Study (6) both for the screening of hypomania and as diagnostic Criterion A.

We know that patients are much more aware of increased activity than of mood changes like euphoria or irritability, which are more obvious to their nearest and dearest. Irritability, moreover, is a nonspecific symptom occurring in many syndromes (such as depression, anxiety, neurasthenia and perimenstrual syndromes); it should probably only be listed as one of the symptoms of hypomania and removed from Criterion A.

To question the clinical validity of the diagnostic criteria in the prospective Zurich Cohort Study (6), we applied to subjects with MDEs a diagnostic specifier for bipolarity that was broadened stepwise as follows: 1) DSM-IV hypomania, 2) strict Zurich definition (that is, episode duration of 1 day or longer and 3/7 criterial symptoms plus social consequences), and 3) broad Zurich definition (that is, 2/7 symptoms). The 2 Zurich subgroups with BD II (diagnosed according to specifiers 2 and 3 above) did not differ significantly in their family history of mania or in temperamental traits of cyclothymia from patients with BD II meeting full DSM-IV criteria, but they differed markedly from patients with MDEs and from control subjects. In contrast, patients with unipolar depression did not differ from control subjects in their family history of mania. The proposed broad definition of bipolarity identified one-half of all patients with MDEs as having BDs (6).

5. Another cause of the failure to diagnose BD is the consequence of the hypothesis of “drug-induced hypomania.” The current view is that switches from depression to hypomania occur solely in patients with BDs and that they are not caused by the treatment. There is no proper statistical evidence that such switches occur more often with treatment than with placebo (7). We should not forget that switches from depression into hypomania or mania and vice versa are inherent in BDs and were originally termed “folie circulaire” by Jean-Pierre Falret, father of the BD concept.

Categorical and Dimensional Concepts

Our debate is predicated in part on a unipolar–bipolar categorical classification of affective disorders consolidated over the last 40 years. Following the establishment—between 1966 and 1969—of the dichotomy of unipolar depression and BD, the development continued with the concept of BD II (8). In addition, there is growing evidence from epidemiologic and clinical studies that we are dealing with a spectrum of mood disorders with fluid borders stretching from unipolar mania across 3 bipolar subgroups—mania plus mild depression (dysthymia, minor depression, or recurrent brief depression), mania plus MDE, and MDE plus hypomania—to unipolar depression.

This categorical classification is fully compatible with the dimensional view, for which convincing evidence is provided by simultaneous ratings and self-assessments of both depressive and hypomanic symptoms (9) and by the distribution of self-assessed hypomanic symptoms in the general population in the US (10) and the UK (11). The continuous distribution of both depressive and hypomanic symptoms in the population makes the distinction between normal and pathological difficult, just as with blood pressure and pulse rate.

We all experience normal swings of mood and activity, with highs (such as successes and falling in love) and lows (such as failure or bereavement). On the basis of epidemiologic data, we can assume the existence of a continuum from normal to pathological mood and activity changes characterized and defined by their duration, severity, and congruence or incongruence with the quality and intensity of life events.

Many genes may be involved in our vulnerability and capacity to manifest such changes of mood and activity. Molecular genetic data are compatible with dimensional concepts, suggesting more quantitative than qualitative differences between unipolar and bipolar disorders.

A final unanswered question: What is the role of hypomanic or cyclothymic temperaments in relation to the bipolar spectrum? The answer is associated with the Axis I and Axis II distinction and the controversy about categorical and dimensional classifications. Prospective follow-up and genetic studies may give us valid answers. Until those data are available, such patients may be considered as predisposed to develop BD.

Conclusions

More epidemiologic studies are needed that systematically vary the diagnostic criteria for bipolarity and test their validity. The proportion of patients with BD among those with MDEs is heavily underestimated: at least one-quarter or even one-half of patients with MDEs may have a BD. The current diagnostic criteria for bipolarity need revision: instead of the requirement of a formal hypomanic episode, a diagnostic specifier for bipolarity should be developed that is applicable to major and minor depressive syndromes. Both a categorical and a dimensional classification are necessary.

Note

A more extensive list of studies consulted in the preparation of this paper is available from the author.