Hyperarousal Theory of Primary Insomnia
Idiopathic or primary insomnia (PI) is largely an exclusionary diagnosis where psychiatric and medical causes of poor sleep have been ruled out. Substantial evidence has accumulated over the last two decades that PI reflects a predisposition to physiological hyperarousal. Measures of physiological activation which have been found to distinguish PI sufferers from normal sleepers are summarized in a recent review and include:
- Elevated heart rate and sympathetic nervous system activation during sleep and wake periods
- Increased risk for hypertension
- Increased ACTH and cortisol secretion
- Decreased nocturnal melatonin secretion
- Increased whole-body metabolic rate both during sleep and the daytime
- Elevated global brain metabolism both in sleep and awake based on functional neuro-imaging
- Smaller sleep-related decline in metabolism in brain regions controlling general and emotional arousal
Spectral EEG measures
- Increased nighttime high frequency (beta) EEG activity
Multiple Sleep Latency Testing
- Decreased ability to fall asleep on the MSLT (a laboratory sleep study involving daytime nap opportunities).
Such consistent findings across diverse physiological systems support elevated physiological arousal in PI. Genetic twin studies showing a strong heritability for insomnia lend additional support. Furthermore, recent studies indicate that the daytime dysphoria experienced in PI is related to the hyperarousal and not secondary to the sleep disturbance per se.
Understanding the nature of PI can often reduce the stress and anxiety such patients typically experience about their sleep and allow them to partner more effectively with the physician in identifying which measures – cognitive/behavioral therapy, exercise, medications & relaxation techniques – are most helpful.
Sarah S. Mosko, PhD Peter A. Fotinakes, MD
Sleep Medicine Specialist Medical Director
1 Bonnet MH and Arand, DL. Hyperarousal and insomnia: State of the science. Sleep Med. Rev. 2010:14;9-15.