Autism spectrum disorder (ASD) is a serious neurodevelopmental
disorder, associated with autonomic dysregulation. However, the
pathomechanism leading to autonomic abnormalities is still unclear. The aim of this study was to assess autonomic nervous system (ANS) activity during baseline in homogenous group of autistic children using electrodermal activity (EDA), as an index of sympathetic activity and short
-term heart rate variability (HRV) reflecting predominantly cardiac vagal control. Fifteen ASD boys and 15 healthy age-matched boys at the age of 7-15 years were examined. The continuous EDA and ECG were recorded during resting phase in a supine position. Evaluated parameters: EDA amplitude (μS), RR interval, spectral power, peak frequency and power spectral density in low (LF-HRV: 0.04-0.15
Hz) and high-frequency (HF-HRV: 0.15-0.4 Hz) bands of HRV spectral analysis. In ASD group we found significantly shortened RR intervals
(729±20ms vs. 843±30 ms, p=0.005), lower mean EDA (0.66±0.13 μS vs. 1.66±0.42 μS, p=0.033), reduced spectral activity and power spectral density in HF-HRV compared to controls (2.93±0.12 ms2 vs. 3.38±0.10 ms2, p=0.01; 4.12±0.10 ms2/Hz vs. 4.56±0.11 ms2/Hz, p=0.008, respectively). We suggested that impairment in resting autonomic regulation associated with ASD could represent an important
pathomechanism leading to potential cardiovascular complications in ASD.
Spectral analysis of heart rate variability (HRV) during overnight polygraphic recording was performed in 11 healthy subjects. The total spectrum power, power of the VLF, LF and HF spectral bands and the mean R-R were evaluated. Compared to Stage 2 and Stage 4 non-REM sleep, the total spectrum power was significantly higher in REM sleep and its value gradually increased in the course of each REM cycle. The value of the VLF component (reflects slow regulatory mechanisms, e.g. the renin-angiotensin system, thermoregulation) was significantly higher in REM sleep than in Stage 2 and Stage 4 of non-REM sleep. The LF spectral component (linked to the sympathetic modulation) was significantly higher in REM sleep than in Stage 2 and Stage 4 non-REM sleep. On the contrary, a power of the HF spectral band (related to parasympathetic activity) was significantly higher in Stage 2 and Stage 4 non-REM than in REM sleep. The LF/HF ratio, which reflects the sympathovagal balance, had its maximal value during REM sleep and a minimal value in synchronous sleep. The LF/HF ratio significantly increased during 5-min segments of Stage 2 non-REM sleep immediately preceding REM sleep compared to 5-min segments of Stage 2 non-REM sleep preceding the slow-wave sleep. This expresses the sympathovagal shift to sympathetic predominance occurring before the onset of REM sleep. A significant lengthening of the R-R interval during subsequent cycles of Stage 2 non-REM sleep was documented, which is probably related to the shift of sympathovagal balance to a prevailing parasympathetic influence in the course of sleep. This finding corresponds to a trend of a gradual decrease of the LF/HF ratio in subsequent cycles of Stage 2 non-REM sleep.