title: Sudden infant death syndrome: neonatal hypodynamia (reduced exercise level).
abstract: Sudden infant death syndrome (SIDS) has been described as a silent unexpected death during sleep. Infants with near-miss SIDS have shown a higher heart rate and diminished heart rate variability during sleep. Non-rapid-eye-movement (NREM) sleep rate variability was related to respiration. A decreased heart rate variability was also observed in infants with respiratory distress syndrome (RDS) or prenatal hypoxia. It was hypothesized that decreased heart rate variability and decreased body measurement during sleep were related to a decreased arousal response. Cardiac output is greater in the supine position. Acetylcholine slows the heart beat. Postural changes modify the acute baroreflex control of the heart rate. The cerebellum also contributes to the reflex anti-orthostatic (supine) cardiovascular response to postural change. Delayed myelination of various areas of the brain occurred in SIDS victims and it was suggested that the defect in central respiratory control could be a motor rather than a sensory problem, and that the search for abnormalities should be extended to regions in the cerebellum and pre-frontal-temporal-limbic systems. The cerebellum exercises control over motor neuron impulses from the cerebral cortex to lower structures. An extended period of neonatal decreased body movement has its counterpart in the astronaut exposed to the deconditioning effect of zero gravity. Hypodynamia induces hyperglycemia, insulin resistance, renal inositoluria and impaired nerve conduction. Myoinositol is 20 times higher in fetal-like tissue than in adults. The insecticide lindane (gammexane) is an inositol antagonist. Lindane administration to neonatal rats induced low levels of specific components of myelin proteins in oligodendrocytes in the brain. The activity of these specific enzymes was reduced in oligodendrocytes in the brain of SIDS victims. It is hypothesized that lindane administration to laboratory neonatal animals is a laboratory model for studying delayed development of the brain in SIDS.
authors.affiliation: Te Aroha, New Zealand.
authors.forename: G M
authors.initials: GM
authors.lastname: Reid
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D006801:Humans; D018476:Hypokinesia / Q000503:physiopathology*; D000860:Hypoxia / Q000196:embryology; D007223:Infant; D007231:Infant, Newborn; D008954:Models, Biological; D009043:Motor Activity; D009068:Movement; D005082:Physical Exertion; D012127:Respiratory Distress Syndrome, Newborn / Q000503:physiopathology; D012895:Sleep, REM / Q000502:physiology; D013398:Sudden Infant Death / Q000209:etiology / Q000517:prevention & control