Arousal deficiency theory in sudden infant death syndrome with reference to neuronal plasticity.
OBJECTIVE
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), five with congenital cardiac abnormalities, two from infected pulmonary dysplasia, two from septic shock with multi-organ failure, one with a prolonged seizure, one from prolonged neonatal hypoxemia and one from meningitis and brain infarction).


METHODS
The frequency and duration of sleep apnea events recorded some 3-12 weeks before the infants' deaths 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. The histochemical analyses included Bielschowsky staining and the immunohistochemical analyses included the evaluation of growth-associated phosphoprotein 43 (GAP43) and of synaptophysin as markers for synaptic plasticity. Neurofibrae with positive pathological reactions were quantitatively analyzed. Pathological and physiological data were linked for each infant.


RESULTS
The correlation between sleep apnea and neuronal plasticity in the arousal pathway of the SIDS victims was not seen in the control infants and the correlation between sleep apnea and neuronal plasticity in the arousal pathway found in the control infants was not seen in the SIDS victims.


CONCLUSIONS
These findings suggest that neuronal plasticity in the brainstem arousal pathway is related with SIDS.
Department of Legal Medicine, Tokyo Women's Medical University School of Medicine, 8-1 Kawada-cho, Shinjuku, Tokyo 162-8666, Japan. tsawagu@research.twmu.ac.jp
Toshiko
T
Sawaguchi
Ineko
I
Kato
Patricia
P
Franco
Hazim
H
Kadhim
Jose
J
Groswasser
Martine
M
Sottiaux
Hajime
H
Togari
Makio
M
Kobayashi
Hiroshi
H
Nishida
Akiko
A
Sawaguchi
Andre
A
Kahn