Traditionally, postpartum psychiatric disorder are classified as maternity blues, puerperal psychosis,

postnatal depression. Postpartum phenomenology is characterized by a range of emotions transient

mood lability, irritability, weepiness to marked agitation, delusions, confusion, and delirium.

Etiologi

PP can be defined as a psychiatric manifestation with abrupt onset after delivery, a phase characterized
by overwhelming major biopsychosocial changes. Causation of PP is generaly multifactorial.

Perubahan bioogis  masa awal postpartum dicirikan dengan penurunan kadar steroid gonad. Terdapat
penurunan kadar progesterone antara fase pertama dan fase kedua persalinan, dan kadar estrogen yang
drastic setelah pelepasan plasenta sebagai sumber estrogen. Estrogen umumnya mempengaruhi system
monoaminergic, khususnya serotonin dan dopamine; mempengaruhi gejala afektif dan gejala psikotik.

Faktor psikososial  kehamilan dan transisi menjadi ibu dapat memberikan banyak stressos psikososial
seorang wanita harus melakukan penyesuaian terhadap image tubuh, hubungannya dengan suami dan
anggota keluarganya, dan tanggung jawabnya serta tingkah lakunya.

Faktor risiko yang berhubungan dengan gangguan postpartum  primigravida, ibu yang tidak menikah,
operasi cesar, dan komplikasi perinatal dan prenatal, riwayat gangguan psikotik, riwayat ansietas atau
depresi, riwayat gangguan psikiatrik pada keluarga, khususnya ibu atau saudara perempuan yang
mengalami gangguan psikiatri postpartum, adanya kejadian yang membuat stress saat kehamilan dan
menjelang persalinan, riwayat pelecehan seksual, sifat kepribadian vulnerable dan isolasi
social/pasangan yang tidak suportif.

Patofisiologi postpartum depression

Patofisiologinya kompleks dan masih belum diketahui pasti, namun ada bukti yang menunjukan bahwa
depresi postpartum berhubungan dengan:

Hormon  there are many good reasons to suspect that reproductive hormones are etiologically
important in PPD as they play important roles in emotion processing, arousal, cognition, and
motivation. They also regulate various biological systems implicated in major depression, such as
thyroid function, lactogenic hormones, the hypothalamic–pituitary–adrenal axis, the immune system,
and genetic expression (4). More- over, brain imaging studies have shown that reproductive hormones
modulate the neurocircuitry involved in normal and abnormal affective states. This suggests that
changes in reproductive hormone concentrations are capable of provoking affective dysregulation,
especially in women with a genetic susceptibility. Several studies have shown that peripartum changes
in allopregnanolone, a major progesterone metabolite, may play a critical role in PPD (4, 45–47).
Allopregnanolone, a modulator of γ-aminobutyric acid (GABA) receptors, affects both anxiety and
depression. Recent research has shown that the sudden decrease in allopregnanolone levels after
childbirth may play an important role in triggering PPD through GABA receptors (4).

Genetics  Genetic factors have also been implicated in the pathophysiology of PPD (48, 49). Exciting
evidence of genetic contribution has emerged from family and twin studies suggesting that PPD clusters
in families (20). Candidate gene studies of PPD have identified several of the same polymorphisms found
in nonperinatal depression, such as Val66Met polymorphism of brain-derived neurotrophic factor (50).
Genome-wide linkage studies of more than 1,200 women found genetic variations on chromosome
1q21.3–q32.1 and 9p24.3–p22.3 and in Hemicentin-1 (HMCN1), which contains several estrogen-
binding sites. All appear to increase susceptibility to PPD (51). Estrogen-induced epigenetic DNA
methylation changes have also been implicated in PPD (49). An excellent systematic review of the
genetics involved in PPD has been published (48); these findings will require independent larger
confirmatory studies.

Immune function  The immune axis is regulated by estradiol, which fluctuates during the perinatal
period. Anti-inflammatory cytokines responsible for immunosuppression are elevated in pregnancy to
protect the fetus. However, following delivery, the immune system rapidly becomes pro inflammatory
and remains so for several weeks. Women with PPD, compared with those who are not depressed,
appear to have different gene expression that is functionally related to immunity (52). Studies of
several prenatal immune markers of PPD have reported contradictory findings, so the role of immune
function in PPD remains unclear