Searching the puerperal trigger of bipolar disorder

Abstract

Childbirth has been considered a trigger of severe maternal mental illness since antiquity. In the 18th century, Esquirol and Marcé, among others, provided accounts of mania and melancholia in women admitted to psychiatric hospitals after childbirth. Paffenbarger reported an 18fold higher rate of hospital admission in the first month postpartum compared to pregnancy. More recently, populationbased studies from Scotland and Denmark have confirmed that women are at a particularly increased risk of hospitalization for bipolar disorder in the postpartum period. Approximately 37% of women with bipolar disorder have a relapse of psychosis, hypo/mania, depression and/or psychiatric hospitalization during the 12 months after delivery.1 There is a growing body of evidence suggesting that the postpartum period is associated with the first onset of hypo/manic episodes in some women with major depressive disorder.2 Women experiencing the onset of a variety of psychiatric disorders after childbirth are also at a greater risk of developing bipolar disorder compared to those who have nonpostpartum onset of these disorders. Similar to baby blues, elation and other hypomanic symptoms (generally referred to as “the highs”) are common in the postpartum period. In some cases, the highs may be an early manifestation of bipolar disorder as they are followed by episodes of postpartum depression. Studies from several countries have found that 9.6– 49.1% of women have hypomanic symptoms immediately after childbirth, however, not all of these women meet the DSM5 criteria of hypomanic episodes.3 The postpartum period also affects the phenotypic presentation of mania. A recent withinsubject study found that postpartum manic episodes are more likely to be characterized by mixed symptoms than manic episodes outside of the postpartum period. To sum, the postpartum period is associated with an increased risk of first onset or recurrence of psychosis, hypo/mania, or depression. In this Editorial, we extend these arguments and propose that in order to understand the nature of the puerperal trigger in women with bipolar disorder, it is necessary to study the role of all reproductive events rather than focusing solely on the postpartum period. Also, the study of autoimmune diseases such as rheumatoid arthritis or multiple sclerosis, in which female hormones appear to play a role in the exacerbation or onset of symptoms, may improve our understanding of the puerperal trigger of bipolar disorder. The precise nature of the puerperal trigger for bipolar disorder remains poorly understood; however, genetic, hormonal, circadian rhythm, and autoimmune factors are generally considered to play a causal role. A better understanding of the postpartum trigger is important as it may provide clues to the etiology of bipolar disorder and specific pathophysiological mechanisms in females, and will boost the development of specific interventions for the prevention or treatment of bipolar mood episodes across the life cycle. Moreover, a better understanding of the puerperal trigger may shed light on the relationship between bipolar disorder and comorbid psychiatric disorders (e.g. anxiety disorders, obsessivecompulsive disorder, and substance use disorder) that are also associated with increased risk of recurrence in the postpartum period. In his authoritative book Motherhood and Mental Health, Brockington argued that elucidation of the etiology of puerperal psychosis (usually considered a manifestation of bipolar disorder) requires an understanding of the nature of the trigger, the diathesis, and determinants of the polarity of the puerperal episode.4 He concluded that about half of the cases of puerperal psychosis have a specific trigger operating in pregnancy and the rest have onsets linked to other reproductive events. More recently, Jones suggested that the study of the putative etiological factors for puerperal psychosis could provide clues to the understanding of mental illness in general. Various reproductive events, including menarche, premenstruum, cessation of breastfeeding, abortion, and perimenopause affect the course of bipolar disorder. Women are at a high risk for onset of bipolar disorder around menarche as approximately 18% of women with bipolar disorder have the emergence of mood symptoms within one year of menarche. Primiparity appears to be associated with an increased risk of developing puerperal psychosis. The menstrual cycle may affect the course of bipolar disorder. Depending on the type of the study (prospective or retrospective), 44– 68% of women have menstrual cyclerelated mood changes. The menopausal transition is also a vulnerable time for the first onset or exacerbation of symptoms of bipolar disorder. There is a lack of clarity about the effect of pregnancy on the course of bipolar disorder, as some studies have suggested a neutral or positive effect, while others have reported an increased risk of recurrence of mood episodes. Evidence in support of elevated risk of recurrence during pregnancy comes mainly from studies of discontinuation of mood stabilizers around the time of conception. Some women experience the onset of mania or psychosis prior to delivery with worsening of symptoms in the postpartum period. A retrospective study by Grof and colleagues found pregnancy had a protective effect on the course of bipolar I disorder as there were fewer and briefer mood episodes during pregnancy than before or after. Also, the recurrence risk during pregnancy was markedly lower than in the comparison group. Populationbased