Neuropathology of sudden infant death (syndrome): literature review and evidence of a probable apoptotic degenerative cause

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http://link.springer.de/link/service/journals/00381/contents/02/00629/

© Springer-Verlag 2002

Invited Paper

Neuropathology of sudden infant death (syndrome): literature review and evidence of a probable apoptotic degenerative cause

D. Larry Sparks1, 2 and John C. Hunsaker III2, 3, 4, Contact Information

(1) Laboratory for Neurodegenerative Disease Research, Sun Health Research Institute, Sun City, AZ 85351, USA
(2) Division of Medical Examiner's Services, Kentucky Justice Cabinet, OACME, CLF, 100 Sower Boulevard, Suite 202, Frankfort, KY 40601-8272, USA
(3) Department of Pathology and Laboratory Medicine, UKMC, Lexington, KY 40536-0298, USA
(4) Division of Forensic Pathology, University of Kentucky College of Medicine, 800 Rose Street, MS 117, Lexington, KY 40536-0298, USA

Abstract

Background. The agonizing enigma of sudden infant death syndrome (SIDS) endures. Contemporary research concentrates on the central nervous system (CNS) as the prime cause.

Review and discussion. What follows is a review of the neuropathology of SIDS. A persuasive, but as yet unproved, hypothesis is that the lethal pathophysiologic derangement or mechanism in SIDS involves dysfunction of sleep-related cardiorespiratory homeostatic controls or failure to arouse or both. Neuropathological investigation of SIDS continues to be closely linked to the study of specific anatomic structures and regions of the CNS. The structures in these regions underpin and regulate normal cardiorespiratory function. It follows that dysfunction of one or more of these loci probably precipitates SIDS. Under this large umbrella review we include histological, immunohistochemical, and biochemical markers in the cerebrospinal fluid (CSF), cerebrum, cerebellum, brain stem, pituitary gland, and pineal gland. With variable effect, these regions are deemed to mediate the functionality of cardiorespiratory activity and the diurnal rhythms of sleep/arousal. The following factors, which (a) are associated with altered electrochemical or neural transmission and biochemical changes in the CNS and (b) predispose to systemic derangements that most probably precipitate SIDS, are subjects of ongoing investigation: evidence of delayed development; ischemic insult; degenerative changes; and synaptic alterations.

Conclusion. On the basis of current data, we add to these theoretical constructs by postulating that apoptotic neurodegeneration constitutes the anatomic substrate accounting for the pathophysiologic mechanism and proximate cause of SIDS.

Keywords. Alz-50 immunopathology - Neurodegeneration - Apoptosis - Microscopic diagnosis of SIDS

Contact Information E-mail: dr.john.hunsaker@mail.state.ky.us
Phone: +1-502-5644545
Fax: +1-502-5641699

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