Screening for manic symptoms
As its progenitors emphasize,13 the Bipolarity Index supplements but does not replace DSM-IV. Clinicians must still screen for manic or hypomanic symptoms to assess the first dimension of the index. Examples of systematizing this screening in routine clinical care include the Digfast mnemonic (originated by Falk15), the Mood Disorders Questionnaire (MDQ),16 MDQ-Adolescent,17 the Bipolar Spectrum Diagnostic Scale (BSDS),18 and the Hypomania Checklist (HCL-32).19 These questionnaires are self-report instruments that take just a few moments to complete and are available in various forms on the Internet (Table 2).

While the MDQ may be best suited for a primary care practice (because of its quick and easy administration and interpretation), the BSDS and HCL-32 may be preferable in a psychiatric practice, because they have greater sensitivity for BDII18,20,21 (although potentially at the expense of lower specificity20). Zimmerman and colleagues22 argued that the sensitivity and specificity of the MDQ may be too low to justify its use as a screening instrument.

However, another recent analysis23 suggests that these instruments are sufficiently accurate when used to augment an educated clinician's hunch—which, according to the above data, should be based in part on an assessment of nonmanic bipolar markers. If the clinician's degree of suspicion is high, the predictive value of a positive MDQ or BSDS is between 85% and 90% (with one outlier study at 65%). Conversely, if the clinician's suspicion is low and the test is negative, the negative predictive value is over 90% (no outliers). Thus, these tests are particularly good for confirming a negative impression and acceptably strong for affirming a suspicion of BD, but their results must be evaluated with great caution when they run counter to an informed clinical hunch.23

What should be done when one's hunch and a screen for manic symptoms (eg, MDQ, BSDS, HCL-32, or DIGFAST) conflict? If clinical suspicion is high but the screening is negative, the clinician must consider that the patient lacks insight into his/her manic symptoms and thus, collateral information is needed. If clinical suspicion is low but the test is positive, there is a high risk of a false positive, following the categorical approachof DSM-IV. But is the test result still meaningful in some way? Does such a result indicate some form of subthreshold BD? Current research provides scant data to address this question (a biological marker of some sort could help here). In the meantime, the answer depends on how one conceptualizes bipolarity.

What are we modeling?
The Figure shows several different ways of thinking about the diagnosis of BD. With the categorical DSM approach there is no middle ground; a patient either has unipolar depression or 1 of 3 discrete levels of bipolarity. By contrast, the data on nonmanic bipolar markers suggest that patients can have many different degrees of bipolarity. If so, does bipolar propensity increase exponentially (Model B) or linearly (Model C)? This will probably remain unclear until we have a better understanding of the etiology of BD.

Could a patient even have some degree of bipolarity with no hypomania or mania at all, as indicated by the pair of asterisks in the Figure? This theory was proposed by Ghaemi and colleagues,11 who characterized bipolar spectrum disorder asmajor depression accompanied by multiple nonmanic bipolar markers. Family history of BD in a first-degree relative and antidepressant-induced hypomania are given particular weight. Although this concept was found useful in a small pilot study24 and is a logical extension when thinking in spectrum terms, it is not a validated entity. Do such patients have more adverse reactions to antidepressants than purely unipolar patients? The answer to this important question remains unknown.

Implications
At present, clinicians must prove that bipolarity is present by looking for manic symptoms. If none are found, the patient is presumed unipolar. If the search is conducted cursorily, or not at all, the diagnosis defaults to major depression; and if a medication is used, it will almost certainly be an antidepressant. Routine use of tools described herein could improve the accuracy of this rule-out process, especially in primary care.

However, at a conceptual level, bipolar depression might be a better default assumption when a patient presents with depression. With this approach, the burden of proof lies in demonstrating that manic markers, including all 5 dimensions of the Bipolarity Index, are notpresent. This might lower the incidence of antidepressant prescriptions for patients for whom antidepressants may worsen their condition. But what if only a few indicators of bipolarity are present? When should a clinician begin to be concerned about using an antidepressant? For now, physicians' approaches in this situation are likely to be determined primarily by their level of concern about antidepressant risks in patients with BD.25 For an example of a data-based and very concerned view, see the recent review by El-Mallakh and colleagues.26

Several investigators have presented data showing that antidepressant monotherapy in BDII can be associated with good outcomes, at least in the short term and for some patients.27,28 But clearly at some point along the continuum (Figure), antidepressants become, if not contraindicated, at least less than optimal initial therapy. Currently psychiatrists use DSM-IV criteria as a proxy indicator of which patients should receive mood stabilizers. (When the primary target is depression, we would presumably select from those that have demonstrated antidepressant efficacy.) However, this assumes that bipolarity is a step function, as shown for the DSM-IV model in the Figure. If B or C are better models, as appears to be the case, we should think more broadly about which patients can safely be given an antidepressant.

Do continuum models risk overpromotion of mood stabilizers for patients who do not have BD? This is an obvious and concerning logical extrapolation. Historically, we have protected patients from the risks of the medication treatments for BD and the stigma of the label by setting the bar high for making this diagnosis, especially in children. However, another way to protect patients would be to set the bar high for anypharmacological approach, given the data on the efficacy of such alternatives as psychotherapy, exercise, and light therapies. This approach would protect against both the Scylla of underdiagnosis and antidepressant exposure and the Charybdis of overdiagnosis and mood-stabilizer risks—as long as a more aggressive approach, where potentially necessary, is outlined in advance and ready for launch.
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