Postpartum depression refers to a nonpsychotic mood disorder that meets diagnostic criteria for major or minor depression. There is no specific diagnosis of “postpartum depression” listed in the Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV), although there is a “postpartum onset specifier.” According to the ASAf-TV specifier, an episode may only be termed postpartum onset if it occurs within the first 4 weeks after delivery; however, the term postpartum depression is often used to describe women who experience a depressive episode up to 1 year after delivery. There is no particular time during the first year postpartum when depressive episodes are most likely to occur. Depressive episodes occurring in the postpartum period can be quite persistent, and can last 6-9 months. Furthermore, women experiencing postpartum depressive episodes are at increased risks for future depressions both associated with and independent of childbirth.
Although there is much debate surrounding the issue, postpartum depression does not appear to differ significantly from depressions occurring at other times in a woman’s life. However, a fluctuating course and mood lability may be more commonly found in postpartum episodes. Symptoms can include the full range of symptomatology experienced with major depression (e.g., depressed mood, loss of interest in usual activities, irritability, fatigue, difficulty making decisions, sleep and appetite disturbances, and suicidal ideation). The prevalence of postpartum depression is estimated in the range of 10%—15% if both minor and major depressions are included and 5%-8% if only episodes meeting criteria for major depression are included.
Women commonly experience mild dysphoria during the first week postpartum; however, such mild mood disturbance may be suggestive of “postpartum blues” rather than the more severe and chronic diagnosis of postpartum depression. Prevalence estimates for postpartum blues range from 26% to 85%. Symptoms of postpartum blues begin within a few days of delivery and may last from a few hours to several days. Women with postpartum blues may be more likely to experience the following symptoms: dysphoric mood, mood lability, crying, anxiety, insomnia, lack of appetite, and irritability. Women experiencing the blues are at increased risk for postpartum depression, but there no other negative sequelae.
A more severe postpartum disorder than the blues or depression is postpartum psychosis. Psychosis is marked by gross impairment in the ability to function, usually due to hallucinations and/or delusions, although severely depressed mood or profound confusion may instead be responsible for the impairment. The general consensus in the literature is that postpartum psychoses are no different from psychoses occurring at other times in a woman’s life and that they often take the form of bipolar disorder. Postpartum psychotic episodes typically occur within the first 2-4 weeks after delivery. The first month postpartum has been shown to be a time of elevated risk for a psychotic episode (perhaps a 13-fold increase); however, postpartum psychosis is extremely rare, with prevalence estimated between 1 and 4 in 1,000 deliveries.
The predominant biological explanation for postpartum blues and depression is that levels of specific reproductive hormones and steroids (e.g., estrogen, progesterone, prolactin, Cortisol) are either too high or low after delivery or that the rate of change in levels of these hormones after delivery is too rapid. For example, some researchers believe that the large increase in levels of estrogen and progesterone during pregnancy, followed by the abrupt decrease after delivery, may be responsible for postpartum depression. Despite the intuitive attraction of these theories, there is very little evidence to support them. Neurotransmitter abnormalities are central to many theories of psychiatric disturbance, and postpartum depression is no exception. There is currently little information on the possible impact of neurotransmitters (e.g., norepinephrine, epinephrine, monoamine oxidase, adrenoceptors) on postpartum depression, and findings are mixed. Stronger evidence supports the notion that thyroid dysfunction during pregnancy or after delivery is related to postpartum depression. It is estimated that a small percentage (i.e., between 1% and 4%) of postpartum depression cases may be specifically due to thyroid dysfunction. It is important to note that hormonal factors may only be important for women who are otherwise vulnerable to mood disorders due to biological/genetic, psychological, or social/environmental factors.
Postpartum depression is also associated with numerous psychosocial risk factors. Women at risk for postpartum depression are more likely to have a poor marital relationship and to believe that they are not receiving adequate social support from others. Those who experience postpartum depression are more likely to have lower incomes and to come from lower social classes. In addition, high-risk women commonly experience significant life stressors during pregnancy and have more difficult pregnancies and deliveries than low-risk women. Finally, women who have experienced prior depressive episodes and showed evidence of at least mild mood disturbances during pregnancy are more likely to experience a postpartum depressive episode.
Psychological characteristics have also been examined for their possible relationships with postpartum depression. Some researchers have reported that higher levels of “neurotic” personality characteristics in depressed versus nondepressed mothers, although others have contradicted this finding. Several studies have found a significant relationship between levels of depression/emotional distress during pregnancy and levels postdelivery. Attributional style (the types of causes women identify for life events) has been found to predict postpartum depression in some, but not all studies. Attitudes regarding self-control, measured during pregnancy, may be a significant predictor of women’s level of postpartum depression. Finally, family history of psychopathology has also inconsistently been found to be a predictor of postpartum depression.
Several long-term follow-up studies of women with postpartum depression have reported on the consequences of the disorder for the woman’s children. Postpartum depression has been shown to affect the interactions between a mother and her infant. Depressed mothers exhibit fewer positive facial expressions and less animated verbalizations. In turn, infants of depressed mothers exhibit less interest in interactions and show a preference for sad faces and vocalizations. Infants of depressed mothers have been characterized as less securely attached and as showing fewer exploratory behaviors. A number of studies have found that during the preschool years, mothers who experienced postpartum depression rate their children as having more behavioral problems. Additionally, a large body of research suggests that children of women who experienced a postpartum depression perform significantly worse on tests of cognitive abilities than children of mothers who were nondepressed postpartum. Findings suggest that children of postpartum depressed mothers may show deficits in their social and emotional development relative to their peers born to nondepressed mothers.
Postpartum depression has also been shown to negatively affect the spousal relationship. Postpartum depressed women report receiving less support than postpartum nondepressed women in close relationships; however, this perceived lack of social support is most striking within the spousal relationship. Husbands typically disagree with their wives’ perceptions, often leading to marital dissatisfaction, a risk factor for depression in both women and men. In addition, depressed women perceive their overall family life to be more negative than non-depressed women. In addition to marital dissatisfaction, living with a depressed spouse is also a risk factor for depression, so that spouses of postpartum depressed women themselves experience more depressed mood than spouses of nondepressed women.
Antidepressant medications are commonly prescribed for postpartum depression; however, there are almost no controlled studies of the efficacy of psychotropic medications with postpartum women. The literature does support the use of nortriptyline, fluoxetine, and sertraline as medical treatments for postpartum depression. Because there are no data from controlled studies regarding the safety of antidepressant medication with breastfeeding women, the use of these medications with breastfeeding women is controversial. Transdermal estrogen, which is a hormonal treatment, has been tested as a treatment for postpartum depression with some success. Pregnant women with a history of postpartum depression have also been treated preventatively with antidepressants. In general, the few studies conducted suggest the efficacy of preventative pharmacologic treatment for women at risk for postpartum depression.
The efficacy of psychotherapeutic approaches to acute treatment of postpartum depression is strongly supported in the literature. Given the paucity of pharmacologic research with postpartum women and the lack of risks to the infant associated with counseling, psychotherapy could be considered a first-line approach to treatment. Interpersonal psychotherapy, client-centered therapy, nondirective therapies, and cognitive-behavioral therapy have all been shown to be superior to no treatment or waiting-list control conditions. A number of studies have also assessed the efficacy of preventative psychological treatments for postpartum depression. Prevention efforts have largely focused on antenatal relaxation training and/or group psychoeducation sessions regarding expectations for the postpartum period. In general, the prevention efforts resulted in a decrease in postpartum emotional distress. The literature suggests that outcome for preventive efforts may be improved by selecting patients who are at high risk for depression and by using aggressive measures to encourage patient retention in treatment.
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