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Depression and the Lifetime Reproductive Cycle

Premenstrual Dysphoric Disorder

The DSM-IV classifies premenstrual dysphoric disorder (PMDD) under research diagnostic criteria as depression not otherwise specified (Table below). Mood and anxiety symptoms can occur only during the premenstrual period, or preexisting symptoms can become worse at this time. Identifying and treating symptoms that have a significant effect on patients is important; dismissing them as "simple" premenstrual symptoms deprives women of potentially beneficial treatment.

PMDD is a severely distressing and debilitating condition that requires treatment. Between 3 and 5 percent of women meet the diagnostic criteria for this disorder, which presents with symptoms of depression and anxiety as well as cognitive and physical symptoms. The diagnosis of PMDD requires the presence of five of 11 symptoms, with at least one of the first four symptoms experienced during the last week of the luteal phase; in addition, remission of symptoms must occur within a few days of the onset of menstruation. The symptoms should not represent the exacerbation of preexisting anxiety, depression or personality disorder. Furthermore, duration, impairment and prospective diagnostic validation criteria must be met.

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The literature shows a lack of consensus regarding the pathophysiology of PMDD and its relationship to neuroendocrine, hormonal or serotoninergic mechanisms. Many investigators have concluded that women with this disorder have an abnormal response to normal gonadal steroids. Longitudinal studies indicate that women who experience PMDD have a greater risk of future depression during pregnancy, the postpartum period and the perimenopausal period, thereby suggesting a biochemical relationship between depression and the disorder.

Both nonpharmacologic and pharmacologic measures have been employed in the treatment of PMDD (Table below). Nonpharmacologic treatments such as aerobic exercise, caffeine restriction, complex carbohydrate consumption and moderation of alcohol intake have not been consistently beneficial in alleviating the symptoms of the disorder.

Pharmacologic treatments for PMDD have included progesterone, antidepressants and antianxiety drugs. Progesterone therapy has been relatively ineffective. Although tricyclic antidepressants have been beneficial, side effects limit their use. Serotonergic antidepressants appear to be effective in reducing symptoms. Clomipramine (Anafranil), a tricyclic antidepressant, may also be effective. Gonadotropin-releasing hormone (GnRH) agonists such as leuprolide (Lupron) have been effective; because GnRH agonists can cause menopausal symptoms, they should be used only in patients who are resistant to other forms of therapy. The results achieved with benzodiazepines, especially alprazolam (Xanax), have been mixed. The current literature indicates that if simpler, nonpharmacologic options are ineffective, selective serotonin selective reuptake inhibitors (SSRIs) may be used to treat patients with PMDD. The use of calcium supplementation to reduce symptoms has recently attracted interest.

Depression During Pregnancy

In the past, pregnancy was viewed as a period of well-being that made women feel biologically "complete" and that provided "protection" against psychiatric disorders. However, the prevalence rates for depression are now known to be similar in pregnant and nongravid women. Factors such as a history of depression or PMDD, younger age, limited social support, living alone, greater number of children, marital conflict and ambivalence about pregnancy increase the risk of depression during pregnancy and the postpartum period. A history of depression during the antenatal phase remains one of the strongest predictors of future depression during pregnancy and the puerperium.

Pharmacotherapy for depression during pregnancy requires an assessment of the risks and benefits of treatment for both mother and fetus. The risks of treatment should be compared with the risks of not treating depression, which may include suicide, poor maternal and fetal nutrition, an adverse neonatal obstetric outcome and the continuation of depression into the postpartum period. Untreated depression may also affect mother-child bonding and may be a cause of chronic depression and treatment resistance.

A prospective European study of 689 women exposed to therapeutic dosages of tricyclic and noncyclic antidepressants during the first trimester of pregnancy found no causal relationship between in utero exposure to these drugs and adverse pregnancy outcomes. Similar findings were reported for another study of 400 pregnant women with documented exposure to tricyclic antidepressants.

If simpler, nonpharmacologic options are ineffective, selective serotonin reuptake inhibitors may be used to treat premenstrual dysphoric disorder.

One study involving 228 pregnant women treated with fluoxetine during the first trimester found no increase in teratogenicity but did note perinatal neurobehavioral effects. Other investigators observed no effect on global intelligence quotient, language or behavioral development in preschool children exposed in utero to either tricyclic antidepressants or fluoxetine.

No increase in teratogenic risk was reported in another prospective study of in utero exposure to the SSRIs (fluvoxamine, paroxetine and sertraline). In addition to being safe for use in pregnancy, these agents have favorable side effect profiles and therefore may be considered first-line therapy for depression severe enough to justify the use of medication during pregnancy. This recommendation is not consistent with the pregnancy ratings from the U.S. Food and Drug Administration (Table 8). Note, however, that experts in the field of teratology consider these ratings inadequate for determining safety in pregnancy.

Interpersonal and cognitive-behavioral therapies may have a special advantage in pregnant patients with less severe depression. These techniques can be helpful in resolving interpersonal and psychosocial conflicts, resulting in a positive outcome without exposing the mother or fetus to drugs. Such treatments can enhance pregnancy outcome.

Electroconvulsive therapy has been used to treat depression in pregnancy for over 50 years. This technique has been reported to be relatively safe in pregnant women with severe, refractory depression.

Depression During the Postpartum Period
Between 30 and 75 percent of women experience mild postpartum "baby blues" lasting four to 10 days. This postpartum depression is characterized by labile mood, tearfulness, irritability, anxiety, and sleep and appetite disturbances. Patient education and reassurance are generally adequate treatment measures. If physical symptoms (Table 2) and depressed mood persist for two weeks, patients should be evaluated for postpartum major depression, particularly if they have a history of depression.

Postpartum major depression is relatively common, with a prevalence rate approximately the same as that for major depression in nonpregnant women. Symptoms usually begin during the third trimester and are similar to those for major depression. In the United Kingdom, the Edinburgh Postnatal Depression Scale, a 10-item self-rating scale, is often used to detect postpartum depression. The risk of postpartum depression is increased in women with pregravid depression, a history of PMDD during pregnancy, primiparous status, negative life events during pregnancy, an inadequate social support system and marital problems.

Nonpuerperal depression and puerperal depression are treated similarly unless the mother is breast-feeding.

Pharmacologic and nonpharmacologic techniques have been used in the treatment of postpartum major depression. Nonpuerperal and puerperal depression are treated similarly unless the mother is breast-feeding. Data regarding the excretion of antidepressants in breast milk are limited. The American Academy of Pediatrics Committee on Drugs concluded that "antidepressants are drugs whose effect on nursing infants is unknown but may be of concern." Based on some reports, antidepressants considered to have no adverse effects on breast-fed infants (Table 8) may be considered for use in women with postpartum depression. Electroconvulsive therapy may be of value in patients who have severe depression with psychosis and an increased risk of suicide.

Some investigators have found that estrogen therapy may be effective in patients with postpartum major depression. Double-blind studies are necessary before this therapy can be recommended for general use.

Although pharmacotherapies for depression carry some risks, untreated depression may lead to significant problems. If depression is not treated, poor self-care, poor nutrition and newborn neglect may adversely affect infant development and maternal-child bonding.

Depression During the Perimenopausal Period

Perimenopause has been viewed as a period of risk for depression. However, depressive disorders do not seem to cluster around this period of the reproductive cycle. Symptoms of menopausal depression often occur in conjunction with vasomotor instability as a result of declining ovarian function.

Depression during both nonmenopausal and menopausal phases is diagnosed and treated in a similar manner. Estrogen replacement alone can provide relief of vasomotor symptoms, and minor cognitive and mood symptoms. This therapy is also useful in preventing osteoporosis. However, hormone replacement therapy has limited benefit in the treatment of major depression unless patients receive concomitant antidepressant drug therapy and/or psychotherapy.

Depression Associated with Infertility, Miscarriage or Perinatal Loss

The grief reaction related to infertility, miscarriage or perinatal loss of an infant is usually self-limited. If this reaction persists beyond eight weeks and self-esteem is reduced, patients should be evaluated for an adjustment disorder with depressed mood or major depression. If diagnosed, these disorders should be treated.

Authors: SUBHASH C. BHATIA, M.D., and SHASHI K. BHATIA, M.D. Creighton University School of Medicine and University of Nebraska College of Medicine, Omaha, Nebraska

The authors thank William Burke, M.D., of the University of Nebraska and Creighton University, for his review of the manuscript.

The authors of this article provide continuing medical education with financial support from Abbott Laboratories, Bristol-Myers Squibb Company, Glaxo Wellcome Inc. and Eli Lilly and Company.

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