To determine the influence of maternal smoking on autonomic nervous system in healthy infants, 36 infants were recorded polygraphically for one night. Their mothers were defined, according to their smoking frequency during pregnancy, as "nonsmokers" (no cigarettes smoked during pregnancy) or "smokers" (10 or more cigarettes per day). The infants had a median postnatal age of 10.5 wk (range 6 to 16 wk); 18 were born to nonsmokers, and 18 to smokers. During the whole night, spectral analyses of heart rate (HR) were evaluated as a function of sleep stages. Two major peaks were recognizable: a low-frequency component (LF) related to sympathetic and parasympathetic activities and a high-frequency component (HF) reflecting parasympathetic tonus. The ratio of LF/HF powers was calculated as an index of sympathovagal interaction. In REM sleep, "smokers" infants were characterized by significantly lower HF powers and normalized HF powers, and higher LF/HF ratios than "nonsmokers." The finding did not reach statistical significance in NREM sleep. In conclusion, maternal smoking induced changes in autonomic control and maturation in infants. These effects of cigarette smoke exposure can be added to those already reported and offer additional evidence for counseling mothers to stop smoking.
To evaluate changes in autonomic nervous system controls in response to obstructive events in future victims of sudden infant death syndrome (SIDS), we studied the polysomnographic sleep recordings of 18 future SIDS infants and those of 36 matched control infants. A heart rate autoregressive power spectral analysis was performed preceding and after the obstructive apneas. The low-frequency to high-frequency power ratio was computed to evaluate sympathovagal balance. Future SIDS victims had significantly more obstructive apneas (p = 0.001) and mixed apneas (p = 0.005) than control infants. Obstructive events occurred mainly during rapid eye movement sleep in the two populations (84.5% in future SIDS victims and 95.8% in control infants; p = NS). Comparing heart rate power spectral analysis before and after obstructive apneas in rapid eye movement sleep, high-frequency power values were significantly lower and low-frequency to high-frequency power ratios higher in future SIDS victims than in control infants. Compared with preapnea values, low-frequency to high-frequency power ratios significantly decreased after obstructive apneas in control infants (p < 0.001) but not in the future SIDS victims. When the obstructive apneas were divided according to duration, the findings were seen mainly for long apneas. In conclusion, future SIDS victims were characterized by different autonomic status and responses to obstructive apneas during sleep. These findings could be relevant to mechanisms implicated in some cases of SIDS.
We describe a family with an autosomal dominant form of retinal-cerebellar atrophy. There is an extreme variability in age of onset and severity of the clinical symptoms: some patients remain nearly asymptomatic throughout their entire life; others develop severe retinal and cerebellar symptoms after the age of 35 years; others suffer from a severe disorder with onset in adolescence and death during the third decade of life; in others the onset is in early childhood with prevalence of cerebellar symptoms. There is neither dementia nor epilepsy in any of the patients. Four out of five autopsies showed a severe retinal atrophy, and all five autopsies were also characterized by (1) a cerebellar atrophy affecting the spinocerebellar and olivocerebellar tracts, the cerebellar cortex and the efferent cerebellar pathways, (2) an involvement of the pyramidal pathways and of the motor neurons of brain stem and spinal cord, and (3) an atrophy of the subthalamic nucleus and to a much lesser extent of the pallidum, with also some damage to the substantia nigra. The posterior columns are much less affected except in one patient. In this family, we have excluded linkage with the two loci for spinocerebellar ataxia, i.e., SCA1 on chromosome 6p and SCA2 on chromosome 12q as well as with the locus for Machado-Joseph disease (MJD) on chromosome 14q. A genome-wide search is currently being performed to detect the disease locus responsible.
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