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29 - Abnormalities of the Hippocampus in Sudden and Unexpected Death in Early Life

Published online by Cambridge University Press:  20 July 2018

Hannah C Kinney
Affiliation:
Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, USA
Robin L Haynes
Affiliation:
Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, USA
Dawna D Armstrong
Affiliation:
Retired Professor Pathology Baylor College of Medicine, Department of Pathology, Houston, USA
Richard D Goldstein
Affiliation:
Department of Psychosocial Oncology and Palliative Care, Dana-Farber Cancer Institute, Department of Medicine, Boston Children's Hospital and Harvard Medical School, Boston, USA
Jodhie R. Duncan
Affiliation:
University of Melbourne
Roger W. Byard
Affiliation:
University of Adelaide
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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.

Type
Chapter
Information
SIDS Sudden Infant and Early Childhood Death
The past, the present and the future
, pp. 661 - 688
Publisher: The University of Adelaide Press
Print publication year: 2018

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