5 research outputs found
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The association of attachment style, postpartum PTSD and depression with bonding- A longitudinal path analysis model, from childbirth to six months.
BACKGROUND: There is substantial evidence that postpartum depression (PPD) is associated with a poor mother-infant bond, however, fewer studies have examined the role of other postpartum psychopathologies such as birth-related PTSD or relevant trait variables such as adult attachment styles in the quality of the mother-infant bond.
METHODS: 210 postpartum women were sampled in a maternity ward of a tertiary health care center. Participants completed questionnaires at three-time points. Demographics questionnaire and the Adult Attachment style scale were administrated at 1-4 days postpartum, the City Birth Trauma Scale and the Edinburgh Postpartum Depression Scale two months postpartum and the Postpartum Bonding questionnaire at six months postpartum.
RESULTS: The associations between adult attachment styles and postpartum bonding were fully mediated by postpartum psychopathology. Avoidant attachment had indirect effects on bonding through general PTSD symptoms (Beta=0.05, p=.019) and PPD (Beta=0.06, p=.010). Anxious attachment also had indirect effects on bonding through general PTSD symptoms (Beta=0.04, p=.044) and PPD (Beta=0.10, p=.001). In contrast, birth-related PTSD symptoms were not associated with bonding. The model presented a good fit.
LIMITATIONS: Women sampled from one health-care center and self-report measures used.
CONCLUSIONS: Our results suggest that although birth-related PTSD symptoms may cause difficulties, importantly they may not be associated with bonding difficulties six months postpartum. Therefore, women could be reassured that their birth-related PTSD symptoms, may not impact on bonding. Consequently, if interventions are specifically aimed at improving the mother-infant bond, the general-related PTSD, PPD symptoms and insecure attachment styles should be the focus of treatment
Role of KCNQ2 and KCNQ3 genes in juvenile idiopathic epilepsy in Arabian foals
Juvenile idiopathic epilepsy (JIE) in Arabian foals resembles benign-familial neonatal convulsion (BFNC) syndrome, a rare idiopathic epilepsy of new-born humans. BFNC syndrome exhibits genetic heterogeneity, as has been hypothesised to occur in Arabian foals, and is known to be caused by mutations in the voltage-gated potassium channel subunit KCNQ2 and KCNQ3 genes. The close phenotypic characteristics of both Arabian foals and children suggest these epileptic syndromes are caused by the same genetic disorder. In horses, the KCNQ2 and KCNQ3 genes are located on the terminal region of chromosomes 22 and 9, respectively, essentially homologous to their location on chromosomes 20q13.3 and 8q24 in humans. Gene trees for the KCNQ2 and KCNQ3 genes between horses and other mammals, particularly humans and mice, were constructed and compared to widely accepted mammalian phylogenetic trees. The KCNQ2 gene tree exhibited close clustering between horses and humans, relative to horses and mice, in contrast to the evolutionary trees of other mammals. Distance values between the horse and human groups were lower as opposed to those found between the horse and mouse groups. The similarity between the horse and the human, especially for the KCNQ2 gene, where the majority of mutations causing BFNC have been found, supports the hypothesis of similar heritable and genetic patterns of the disease in both species and suggests that contrary to the classic mouse-model concept, humans may be a more suitable model for the study of JIE in Arabian foals