PubMed · 9572257
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P Flachenecker, K Reiners. 1998. Autonomic nervous system testing.. https://doi.org/10.1002/(sici)1097-4598(199805)21%3A5%3C680%3A%3Aaid-mus25%3E3.0.co%3B2-y
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The incidence of sudden infant death syndrome (SIDS) has dropped significantly in most countries following the development of education campaigns on the avoidance of risk factors for SIDS. However, questions have been raised about the physiological mechanism responsible for the effects of these environmental risk factors. Since 1985, a series of prospective, multicentric studies have been developed to address these questions; over 20,000 infants were recorded during one night in a sleep laboratory and among these, 40 infants eventually died of SIDS. In this review, the following methods were employed: sleep recordings and analysis, monitoring procedure, data analysis of sleep stages, cardiorespiratory and oxygen saturation, scoring of arousals, spectral analysis of the heart rate and the determination of arousal thresholds, and statistical analysis and the results including sleep apneas, arousals and heart rate and autonomic controls in both future SIDS victims and normal infants were introduced separately. In addition, the physiological effect of prenatal risk factors (maternal smoking during gestation) and postnatal risk factors (administration of sedative drugs, prone sleeping position, ambient temperature, sleeping with the face covered by a bed sheet, pacifiers and breastfeeding) in normal infants were analyzed. In conclusion, the physiological studies undertaken on the basis of epidemiological findings provide some clues about the physiological mechanisms linked with SIDS. Although the description of the mechanisms responsible for SIDS is still far from complete, it appears to involve both arousal responses and cardiac autonomic controls during sleep-wake processes.
BACKGROUND: Little is known about the autonomic control of the native sinus node (NSN) after heart transplantation because its electrical activity is difficult to detect with skin electrodes. METHODS AND RESULTS: The intracardiac electrogram of the NSN and the donor heart electrocardiogram were measured simultaneously. A total of 351 recordings of 107 heart transplant patients (age 53.6+/-12.3 years) were obtained up to 1 year after transplantation. In a subgroup of 41 patients, consecutive recordings were made. Eleven recordings of heart failure patients (age 56.2+/-6.5 years) awaiting cardiac transplantation were used as controls. To examine a relationship between autonomic indices of the NSN and hemodynamics of the donor heart, intracardiac pressures and cardiac output were recorded in the same session. Heart rate variability (HRV) parameters in time and frequency domain of the NSN showed a significant increase starting at 6 months after transplantation, whereas heart rate of the NSN tended to decrease. Heart rate and HRV parameters remained constant over the first year in the donor heart. Higher values of low-frequency and high-frequency powers in the NSN were associated with lower values of right ventricular, pulmonary artery, and mean atrial pressure and cardiac output. Recordings of patients with rejection could not be distinguished from those without rejection based on the spectral content of HRV of either the NSN or the donor heart. CONCLUSIONS: These data suggest a restoration of autonomic modulation of the NSN. This restoration is associated with hemodynamic improvement of the donor heart.
A 51-year-old man presenting with paroxysmal attacks of unilateral sweating for 1 year was studied. Clinical and laboratory findings made the diagnosis of Shapiro or Harlequin syndrome unlikely. The onset of the sweating "crisis" was immediately followed by a progressive decrease in rectal and skin temperature, lasting for about 2 hours. This indicated that hypothermia was related to an abnormal downward shift of the thermoregulatory set point and a delayed effect of mechanisms blocking heat dissipation.