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In low- and middle-income countries little is known about changes in
women's mental health status from the perinatal period to 15 months
postpartum or the factors associated with different trajectories.
To determine the incidence and rates of recovery from common mental
disorders (CMD) among rural Vietnamese women and the risk and protective
factors associated with these outcomes from the perinatal period to 15
months after giving birth.
In a population-based prospective study, a systematically recruited
cohort of women completed baseline assessments in either the last
trimester of pregnancy or 4–6 weeks after giving birth and were followed
up 15 months later. The common mental disorders of major depression,
generalised anxiety and panic disorder were assessed by
psychiatrist-administered Structured Clinical Interview for DSM-IV
Disorders at both baseline and follow-up.
A total of 211 women provided complete data in this study. The incidence
rate of CMD in the first postpartum year was 13% (95% CI 8–19), and 70%
(95% CI 59–80) of women who had perinatal CMD recovered within the first
postpartum year. Incidence was associated with having experienced
childhood maltreatment, experiencing the intimate partner as providing
little care, sensitivity, kindness or affection, and the chronic stress
of household poverty. Recovery was associated with higher quality of a
woman's relationships with her intimate partner and her own mother,
longer period of mandated rest following birth, and sharing of domestic
tasks and infant care.
Modifiable social factors, in particular the quality of a woman's closest
relationships with her partner and her own mother, and participation by
family members in domestic work and infant care, are closely related to
women's mental health in the first year after giving birth in
One of the most significant advances in pain research is the realization that neurons are not the only cell type involved in the etiology of chronic pain. This realization has caused a radical shift from the previous dogma that neuronal dysfunction alone accounts for pain pathologies to the current framework of thinking that takes into account all cell types within the central nervous system (CNS). This shift in thinking stems from growing evidence that glia can modulate the function and directly shape the cellular architecture of nociceptive networks in the CNS. Microglia, in particular, are increasingly recognized as active principal players that respond to changes in physiological homeostasis by extending their processes toward the site of neural damage, and by releasing specific factors that have profound consequences on neuronal function and that contribute to CNS pathologies caused by disease or injury. A key molecule that modulates microglia activity is ATP, an endogenous ligand of the P2 receptor family. Microglia expresses several P2 receptor subtypes, and of these the P2X4 receptor subtype has emerged as a core microglia–neuron signaling pathway: activation of this receptor drives the release of brain-derived neurotrophic factor (BDNF), a cellular substrate that causes disinhibition of pain-transmitting spinal lamina I neurons. Converging evidence points to BDNF from spinal microglia as being a critical microglia–neuron signaling molecule that gates aberrant nociceptive processing in the spinal cord. The present review highlights recent advances in our understanding of P2X4 receptor-mediated signaling and regulation of BDNF in microglia, as well as the implications for microglia–neuron interactions in the pathobiology of neuropathic pain.
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