Whether you encounter postpartum depression (PPD) in a patient you have been treating or in one referred by her obstetrician, early, aggressive treatment is essential. Although PPD shares some symptoms with major depressive disorder (MDD)—and may be a subtype of that disorder—it also has distinguishing characteristics, such as timing of symptom onset. Two screening tools facilitate diagnosis.
Women with PPD usually respond to pharmacotherapy, but antidepressants’ potential effects on a nursing mother’s newborn are important to consider.
HPA axis dysregulation
Although the precise cause of PPD remains unclear, a better understanding is emerging of the complicated interplay of estrogen and progesterone with the hypothalamic-pituitary-adrenal (HPA) axis and other neuroregulatory systems associated with depressive illness. Two lines of evidence implicate hormonal dysregulation:
* Despite normal reproductive hormone levels, women with PPD may have an abnormal response to changes in these levels.
* Abnormalities in HPA axis activity appear to be associated with reproductive endocrine-related mood disorders in vulnerable women, particularly during the transition from childbirth to the immediate postpartum period.
Not just ‘baby blues’: Clues to postpartum depression
Most women will have mild mood and anxiety symptoms in the first few days to weeks postpartum—often referred to as the ‘baby blues’—but these symptoms usually resolve spontaneously. More severe and persistent depressed mood and anxiety should arouse suspicion of postpartum depression (PPD).
Although not categorized as a distinct disorder in the DSM-IV-TR, PPD is diagnosed using DSM-IV-TR criteria for a major depressive episode, including feelings of being overwhelmed, guilt or worthlessness, tearfulness, appetite change, difficulty sleeping (even when the baby is sleeping), difficulty concentrating, and loss of interest or pleasure in activities.
PPD symptoms differ, however, in some important ways from those of nonpuerperal depression. Distinguishing characteristics of PPD are:
* severe worry, anxiety, and/or agitation
* fears of hurting the baby or oneself
* not having any interest in the baby.
PPD usually begins within the first month postpartum but may occur later; the first 3 months appear to be the most vulnerable period.
A radical transition. Dramatic hormonal changes occur in the transition from pregnancy to postpartum.6 The third trimester of pregnancy is characterized by:
* high estrogen and progesterone levels
* a hyperactive HPA axis (normal during pregnancy)
* high plasma cortisol level, stimulated in part by high levels of estrogen and progesterone.7,8
Estrogen and progesterone rapidly decline as a woman transitions to the postpartum period, and HPA axis activity is blunted because of suppressed hypothalamic corticotrophin-releasing hormone (CRH) secretion.
Differences in HPA reactivity. In a normal HPA axis, the delivery of CRH from the paraventricular nucleus of the hypothalamus triggers the stimulation of adrenocorticotropic hormone (ACTH) from the anterior pituitary and, consequently, cortisol from the adrenal cortex. This hormonal system is regulated by negative feedback mediated by cortisol receptors on the anterior pituitary, hypothalamus, and hippocampus, as well as ACTH receptors in the anterior pituitary and CRH autoreceptors in the hypothalamus.
A hallmark feature of the HPA axis in depression is altered response to stress and inability to maintain regulation:
* In MDD, HPA axis hyperactivity is one of the most robust biological findings. In general, women with MDD exhibit high baseline cortisol and an exaggerated response to the dexamethasone/corticotropin releasing hormone test.
* In contrast, women with PPD experience a more blunted ACTH response to CRH, which may reflect a hyporeactive HPA axis.
Nonetheless, Bloch et al observed an increased cortisol response to CRH in women with a history of PPD during high-dose gonadal steroid administration, which suggests either a trait vulnerability related to PPD onset or a consequence of an earlier depression.
It has been hypothesized that both increased cortisol and decreased cortisol (observed under conditions of sustained elevated gonadal steroid levels or withdrawal of gonadal steroids) may result in insufficient glucocorticoid signaling. Impaired glucocorticoid signaling may be the “final common pathway” leading to psychiatric disturbance in MDD and PPD.
Understanding the characteristics of HPA axis reactivity in women with PPD could improve early identification and, theoretically, prevention or immediate treatment for at-risk women. In addition to HPA axis dysregulation, disturbances in other endocrine systems may play a role in PPD. Women with antenatal total and free thyroxine concentrations in the lower euthyroid range may be at increased risk of developing postpartum depressive symptoms.
2 tools for rapid postpartum depression screening
Two well-validated, simple-to-administer postpartum depression (PPD) screening instruments are useful during the postnatal period:
* the Edinburgh Postnatal Depression Scale (EPDS), a 10-item self-report questionnaire that asks about mood, anxiety, guilt, and suicide ideation
* the Postpartum Depression Screening Scale (PDSS), a 35-item self-report questionnaire that asks about sleeping/eating disturbances, anxiety/insecurity, emotional lability, mental confusion, loss of self, guilt/shame, and suicide ideation.
If screening indicates a patient has PPD, her psychiatric history will influence your treatment selection. Pay particular attention to:
* past episodes of depression, hypomania, or mania
* severity and timing of those episodes
* treatment history, including documentation of response to antidepressants.
References
1. Munk-Olsen T, Laursen TM, Pedersen CB, et al. New parents and mental disorders: a population-based register study. JAMA 2006;296:2592–9.
2. Gaynes BN, Gavin N, Meltzer-Brody S, et al. Perinatal depression: prevalence, screening accuracy, and screening outcomes. Evid Rep Technol Assess (Summ) 2005;(119):1–8.
3. Cox JL, Holden JM, Sagovsk R. Detection of postnatal depression. Development of the 10-item Edinburgh Postnatal Depression Scale. Br J Psychiatry 1987;150:782–6.
4. Beck CT, Gable RK. Comparative analysis of the performance of the Postpartum Depression Screening Scale with two other depression instruments. Nurs Res 2001;50:242–50.
5. Bloch M, Schmidt PJ, Danaceau M, et al. Effects of gonadal steroids in women with a history of postpartum depression. Am J Psychiatry 2000;157(6):924–30.
6. Mastorakos G, Ilias I. Maternal and fetal hypothalamic-pituitary-adrenal axes during pregnancy and postpartum. Ann N Y Acad Sci 2003;997:136–49.
7. Noltern WE, Lindheimer MD, Rueckert PA, et al. Diurnal patterns and regulation of cortisol secretion in pregnancy. J Clin Endocrinology Metab 1980;51:466–72.
8. Bloch M, Daly RC, Rubinow DR. Endocrine factors in the etiology of postpartum depression. Compr Psychiatry 2003;44(3):234–46.
9. Magiakou MA, Mastorakos G, Rabin D. Hypothalamic-cortico-releasing hormone suppression during the postpartum period: implications for the increase in psychiatric manifestations at this time. J Clin Endocrinol Metab 1996;81:1912–7.
Samantha Meltzer-Brody, MD, MPH;
Assistant professor, Department of psychiatry, University of North Carolina at Chapel Hill
Jennifer Payne, MD;
Assistant professor, Department of psychiatry and behavioral sciences, Johns Hopkins University, Baltimore, MD
David Rubinow, MD
Assad Meymandi Professor, Chair of psychiatry, University of North Carolina at Chapel Hill
