Partial arousal deficiency in SIDS victims and noradrenergic neuronal plasticity.

Sudden infant death syndrome (SIDS) victims had exhibited during sleep a reduction in cortical arousals despite an increase in subcortical activation. Arousal deficiency in SIDS victims was partial. We could suggest the latent existence of inadequate noradrenergic neuronal plasticity as the background of this partial arousal deficiency of SIDS victims.

Association between sleep apnea and reactive astrocytes in brainstems of victims of SIDS and in control infants.

Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age; 27 infants died from sudden infant death syndrome (SIDS), 5 from congenital cardiac abnormalities, 2 from infected pulmonary dysplasia, 2 from septic shock with multi-organ failure, 1 with a prolonged seizure, and another with prolonged neonatal hypoxemia. The frequency and duration of sleep apneas recorded some 3-12 weeks prior to the infants' death were analyzed. Brainstem material was retrospectively collected from these 33 infants and studied in an attempt to elucidate the relationship between sleep apnea and hypoxic gliosis. The findings were compared between the SIDS victims and the control infants. Brainstem materials were immunohistochemically studied for quantitization of reactive astrocytes using an anti-glial fibrillary acidic protein (GFAP) antibody. The pathological materials were collected within 24h of death. This study focuses on the association between respiratory characteristics and pathology. Physiological and pathological data in the arousal pathway of the brainstem were linked for each infant and variant-covariant analyses were carried out using physiological data as dependent variables and pathological data and categorical data to evaluate the association with SIDS or non-SIDS as independent variables. The study failed to statistically support an association between hypoxic loads, reflected by the GFAP-positive reactive astrocytes in brainstems, the classification of being SIDS or non-SIDS infants, and the characteristics of sleep apnea.

From physiology to pathology: arousal deficiency theory in sudden infant death syndrome (SIDS)--with reference to apoptosis and neuronal plasticity.

Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age (including 26 infant victims of sudden infant death syndrome (SIDS), 5 with congenital cardiac abnormalities, 2 from infected pulmonary dysplasia, 2 from septic shock with multi-organ failure, 1 with a prolonged seizure, 1 from prolonged neonatal hypoxemia, 1 from meningitis and brain infarction). The frequency and duration of sleep apneas recorded some 3-12 weeks before the infants' death were analyzed. Brainstem material from these 38 infants was studied in an attempt to elucidate the relationship between sleep apnea and neuronal pathological changes in the arousal pathway. Immunohistochemical analyses included the evaluation of growth-associated phosphoprotein 43 (GAP43) as a marker for synaptic plasticity. The terminal-deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method was used to identify apoptosis. The positive pathological reactions were quantitatively analyzed. The pathological and physiological data were linked for each infant. Akaike Information Criterion (AIC) statistics was calculated to elucidate the relationship between the physiological and the pathological data in the SIDS victims. The findings illustrated the possibility of an organic fragility within the arousal pathway, particularly in the midbrain periaqueductal gray matter, which is associated with the "visceral alerting response". This autonomic response occurs within an acetylcholine afferent system and pedunculopontine tegmental nucleus (PPTN). The finding is, in future SIDS infants, associated with repetitive sleep apnea.