|Dichotomies are useful for education, communication, and simplification. Unfortunately, simplicity is useful, but untrue—whereas complexity is true, but useless.|
|—Vieta and Suppes, 20081|
This essay begins an ongoing series on bipolar disorder focused on clinical utility. From the point of view of psychiatrists seeing patients every day, I’ll examine treatment options, such as N-acetyl-l-cysteine and supraphysiologic doses of thyroid hormone, that appeal to patients but are inadequately researched.
I'll look at common problems in differential diagnosis as well as at specific challenges, such as pregnancy, and big-picture issues, such as the effect of socioeconomic factors on outcomes. In each case, the goal is to bring insights from research—and sometimes from history, philosophy, and social sciences—to the daily practice of psychiatry.
Let us start with the dilemma posed by Vieta and Suppes.1 As elsewhere, controversies in psychiatry commonly revolve around dichotomizing a complex issue, eg, do antidepressants cause suicidality, or reduce the risk? Are antipsychotics just too risky for young children, or does delaying treatment worsen the long-term picture? Is your patient’s depression unipolar or bipolar in origin?
Turning complex issues into simple questions makes them easier to consider and sometimes easier for patients to understand (in less time). Moreover, treating patients often requires making judgments in the face of overwhelming complexity: Is this depression due to circumstance? Does the timing really suggest causality? Or is this an endogenous mood shift that suggests “cycling”? How can this be teased out in the face of his financial problems, his job loss, his relationship struggles, and the difficulties his children are experiencing?
Sometimes one must simplify in the name of action. Take, for example, a 30-year-old man who does not have access to cognitive-behavioral therapy, whose diagnosis could be generalized anxiety disorder (GAD) with a history of multiple episodes of MDD, but who may also be regarded as having bipolar II (BP-II)—depending on how you interpret his agitation, insomnia, distractibility, irritability, and impulsivity. Are you going to prescribe an antidepressant or a mood stabilizer? Temporizing and gathering more data, to gain more insight into this patient’s problem, is appealing; but he is suffering and wants help as soon as possible, preferably today.
However, in psychiatry, making things simple, as in the statement “you have generalized anxiety disorder,” is frequently an oversimplification. Comorbidity is the norm, not the exception. DSM diagnoses overlap to a tremendous degree, with the bipolar/GAD overlap one of the most striking, as shown in the Table. (The DSM-intercommittee conversation that didn’t happen: “You have all those on your list too?”)
Narrowing one’s focus to arrive at a formal diagnosis risks premature closure: what looks like “cycling,” suggesting bipolar disorder, could be the chaos of the patient’s life. Treatment with a mood stabilizer might have no benefit, but it may subject the patient to risks such as Stevens-Johnson syndrome (divalproex and carbamazepine as well as lamotrigine) or hypothyroidism (not just lithium; quetiapine also carries this risk to some degree2,3). On the other hand, patients frequently do not recognize subtle hypomanic symptoms and focus instead on the dysphoric aspects of insomnia, disorganized thought, and agitation (often referred to as anxiety). Starting treatment with an antidepressant could precipitate a mixed state, which may be a greater concern than precipitating a frank manic episode, because mixed states are associated with suicide.4
1. Vieta E, Suppes T. Bipolar II disorder: arguments for and against a distinct diagnostic entity. Bipolar Disord. 2008;10(1, pt 2):163-178.
2. Poutanen O, Iso-Koivisto E, Työläjärvi M, Leinonen E. Quetiapine-associated hypothyroidism in young female patients: a report of three cases. Pharmacopsychiatry. 2010;43:237-239.
3. Park YM, Kang SG, Lee BH, Lee HJ. Decreased thyroid function in Korean women with bipolar disorder receiving valproic acid [published correction appears in Gen Hosp Psychiatry. 2011;33:300]. Gen Hosp Psychiatry. 2011;33:200.e13-e15.
4. Valentí M, Pacchiarotti I, Rosa AR, et al. Bipolar mixed episodes and antidepressants: a cohort study of bipolar I disorder patients. Bipolar Disord. 2011;13:145-154.
5. Ghaemi SN. Treatment of rapid-cycling bipolar disorder: are antidepressants mood destabilizers? Am J Psychiatry. 2008;165:300-302.
6. El-Mallakh RS, Gao Y, Briscoe BT, Roberts RJ. Antidepressant-induced tardive dysphoria. Psychother Psychosom. 2011;80:57-59.
7. Frances A, Jones KD. Bipolar disorder type II revisited. Bipolar Disord. 2012;14:474-477.
8. Linehan MM. Dialectical behavior therapy for borderline personality disorder. Theory and method. Bull Menninger Clin. 1987;51:261-276.
9. Aliyev NA, Aliyev ZN. Valproate (depakine-chrono) in the acute treatment of outpatients with generalized anxiety disorder without psychiatric comorbidity: randomized, double-blind placebo-controlled study. Eur Psychiatry. 2008;23:109-114.
10. Roy-Byrne PP, Ward NG, Donnelly PJ. Valproate in anxiety and withdrawal syndromes. J Clin Psychiatry. 1989;50(suppl):44-48.
11. Bipolarity Index. http://www.psycheducation.org/depression/STEPBipolarityIndex.htm. Accessed October 8, 2012.
12. Hypomania/mania symptom checklist (HCL-32). http://www.psycheducation.org/depression/HCL-32ListOnly.pdf. Accessed October 8, 2012.