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Published on: August 8, 2019
Sleep onset and cardiovascular activity in primary insomnia
Massimiliano de Zambotti1, Naima Covassin, Giuliano De Min Tona
1Department of General Psychology, University of Padova, Italy. massimiliano.dezambotti@unipd.it
Insomnia is linked to constant sympathetic nervous system overactivity, even during sleep onset. Normal sleepers show a typical autonomic drop, but insomniacs exhibit sustained hyperarousal, supporting physiological hyperarousal theories of insomnia.
Area of Science:
- Cardiovascular Physiology
- Sleep Medicine
- Autonomic Nervous System Regulation
Background:
- Sleep onset involves a shift from sympathetic to parasympathetic dominance.
- Insomniacs often display cardiovascular and electroencephalographic hyperactivity during wakefulness and sleep.
- Evidence for hyperactivity during sleep onset in primary insomnia is limited.
Purpose of the Study:
- To compare cardiovascular and autonomic responses before and after sleep onset in primary insomnia patients and normal sleepers.
- To investigate autonomic nervous system activity during the transition from wakefulness to sleep in insomniacs.
Main Methods:
- Utilized impedance cardiography for non-invasive measurement of heart rate (HR), stroke volume (SV), and cardiac output (CO).
- Assessed pre-ejection period (PEP) as an indicator of sympathetic β-adrenergic activity.
- Estimated heart rate variability (HRV) using frequency domain measures (LF, HF) during polysomnography.
Main Results:
- Both groups showed decreased HR and CO and increased SV and HF (n.u.) after sleep onset.
- Normal sleepers exhibited increased PEP post-sleep onset, indicating parasympathetic dominance.
- Insomniacs had unchanged PEP and lower PEP compared to controls, suggesting sustained sympathetic hyperactivation.
Conclusions:
- Normal sleepers demonstrate a progressive autonomic drop during sleep onset.
- Insomniacs exhibit constant sympathetic hyperactivation, even during sleep onset.
- Findings support the physiological hyperarousal hypothesis as a cause of primary insomnia.
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