2 results
Pre-loss personal factors and prolonged grief disorder in bereaved mothers
- Richard D. Goldstein, Carter R. Petty, Sue E. Morris, Melanie Human, Hein Odendaal, Amy Elliott, Deb Tobacco, Jyoti Angal, Lucy Brink, Hannah C. Kinney, Holly G. Prigerson, for the PASS Network
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- Journal:
- Psychological Medicine / Volume 49 / Issue 14 / October 2019
- Published online by Cambridge University Press:
- 09 November 2018, pp. 2370-2378
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- Article
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Background
Identifying characteristics of individuals at greatest risk for prolonged grief disorder (PGD) can improve its detection and elucidate the etiology of the disorder. The Safe Passage Study, a study of women at high risk for sudden infant death syndrome (SIDS), prospectively examined the psychosocial functioning of women while monitoring their healthy pregnancies. Mothers whose infants died of SIDS were followed in bereavement.
MethodsPre-loss data were collected from 12 000 pregnant mothers and analyzed for their associations with grief symptoms and PGD in 50 mothers whose infants died from SIDS, from 2 to 48 months after their infant's death, focusing on pre-loss risk factors of anxiety, depression, alcohol use, maternal age, the presence of other living children in the home, and previous child loss.
ResultsThe presence of any four risk factors significantly predicted PGD for 24 months post-loss (p < 0.003); 2–3 risk factors predicted PGD for 12 months (p = 0.02). PGD rates increased in the second post-loss year, converging in all groups to approximately 40% by 3 years. Pre-loss depressive symptoms were significantly associated with PGD. Higher alcohol intake and older maternal age were consistently positively associated with PGD. Predicted risk scores showed good discrimination between PGD and no PGD 6–24 months after loss (C-statistic = 0.83).
ConclusionsA combination of personal risk factors predicted PGD in 2 years of bereavement. There is a convergence of risk groups to high rates at 2–3 years, marked by increased PGD rates in mothers at low risk. The risk factors showed different effects on PGD.
29 - Abnormalities of the Hippocampus in Sudden and Unexpected Death in Early Life
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- By Hannah C Kinney, Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, USA, Robin L Haynes, Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, USA, Dawna D Armstrong, Retired Professor Pathology Baylor College of Medicine, Department of Pathology, Houston, USA, Richard D Goldstein, Department of Psychosocial Oncology and Palliative Care, Dana-Farber Cancer Institute, Department of Medicine, Boston Children's Hospital and Harvard Medical School, Boston, USA
- Edited by Jodhie R. Duncan, University of Melbourne, Roger W. Byard, University of Adelaide
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- Book:
- SIDS Sudden Infant and Early Childhood Death
- Published by:
- The University of Adelaide Press
- Published online:
- 20 July 2018
- Print publication:
- 30 April 2018, pp 661-688
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- Chapter
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Summary
Introduction
The terrifying aspect of the sudden infant death syndrome (SIDS) is that it occurs in infants who seem healthy and then die without warning when put down to sleep. SIDS is not typically witnessed and it is surmized that death occurs during sleep, or during one of the many transitions to waking that occur during normal infant sleep-wake cycles (1). Multiple sleep-related mechanisms have been proposed to cause SIDS (1, 2). These mechanisms include suffocation/asphyxiation in the face-down sleep position, central and/or obstructive sleep apnea, impaired-state-dependent responses to hypoxia and/ or hypercarbia, inadequate autoresuscitation, defective autonomic regulation of blood pressure or thermal responses, and abnormal arousal to life-threatening challenges during sleep.
In this chapter, we review the hypothesis and the neuropathologic evidence that SIDS is precipitated by a dentate gyrus-related seizure or a limbic-related instability that involves the central homeostatic network (CHN). We begin with an overview of this hypothesis, and then review our neuropathologic evidence for an epileptiform hippocampal lesion in the brain of a subset of SIDS infants and young children (41-50% respectively) who died suddenly and unexpectedly (3-5). We then consider the putative mechanism whereby dentate lesions cause seizures, the role of the hippocampus as part of the CHN in stress responses (such as the face-down sleep position), and the potential interactions of brainstem serotonergic (5-HT) deficits and the hippocampus in the pathogenesis of sudden death in infants. We conclude with further directions for research into the role of the hippocampus in sudden and unexpected death in early life.
The Limbic Seizure-Related Hypothesis in SIDS
In 1986, Harper suggested that some SIDS deaths may be due to a fatal seizure during sleep that arises in forebrain-limbic-related circuits (6). This hypothesis arose from the recognition of the following inter-related phenomena: limbic regions are particularly susceptible to epileptogenesis; sleep states lower the threshold for seizure; and SIDS is linked to sleep and arousal. Sleep itself is thought to be a precarious state, in part because of the loss of the major “back-up” forebrain systems of waking which influence the final common pathways in the brainstem that mediate central cardiorespiratory function during sleep. Forebrain limbic regions, such as the hippocampus and amygdala, which are part of the CHN, modulate brainstem cardiorespiratory control in a manner influenced by the sleep-waking cycles.