Acute and Chronic Insomnia: What Has Time and/or Hyperarousal Got to Do with It?

Abstract

Nearly one-third of the population reports new onset or acute insomnia in a given year. Similarly, it is estimated that approximately 10% of the population endorses sleep initiation and maintenance problems consistent with diagnostic criteria for chronic insomnia. For decades, acute and chronic insomnia have been considered variations of the same condition or disorder, only really differentiated in terms of chronicity of symptoms (days/weeks versus months). Whether or not acute and chronic insomnia are part of the same phenomena is an important question, one that has yet to be empirically evaluated. The goal of the present theoretical review was to summarize the definitions of acute and chronic insomnia and discuss the role that hyperarousal may have in explaining how the pathophysiology of acute and chronic insomnia is likely different (i.e., what biopsychological factors precipitate and/or perpetuate acute insomnia, chronic insomnia, or both?).

Cortico-autonomic local arousals and heightened somatosensory arousability during NREM sleep of mice in neuropathic pain

“…Still, pain-related pathological changes in brain and periphery continued to be present in sleep. This is consistent with a state of "hyperarousal" whereby high-frequency power components are disproportionately elevated during sleep that is normally dominated by low-frequency rhythms (van Someren, 2020;Vargas et al, 2020), and where heart rate also remains elevated. As such alterations could affect arousability, we asked when and where in the brain this abnormal activity appeared.…”

“…Such high-frequency electrical rhythms during sleep are part of a physiological state referred to as "hyperarousal" (Feige et al, 2013;van Someren, 2020;Vargas et al, 2020) that has been related to less restorative sleep (Moldofsky et al, 1975;Krystal & Edinger, 2008), to misperceiving sleep as wakefulness (Perlis et al, 2001b;Lecci et al, 2020), and to higher heart rates (Maes et al, 2014), all of which are key features of insomnia disorders in humans. Other studies applied various metrics and proposed more spontaneous arousals and/or easier wake-ups in response to sensory stimulation (Parrino et al, 2009;Forget et al, 2011;Wei et al, 2017;Feige et al, 2018).…”

The longitudinal association between the use of antihypertensive drugs and 24-hour sleep in nursing homes. Results from the randomized controlled COSMOS trial

“…Conversely, the signi cant association between sleep onset latency and high blood pressure, may be due to other mechanisms. It could have been expected that high blood pressure was related to a general higher level of arousal (25,26). Since blood pressure were not related to daytime sleepiness, this could be the case, but the decreased sleep onset latency does not con rm this hypothesis.…”

“…Sleep problems may share physiological mechanisms with high blood pressure. Problems with falling asleep, sleep fragmentation and waking up early have been related to a state of hyperarousal (25). Having these sleep problems in combination with hyperarousal has been associated with a signi cant risk of hypertension (26).…”

Does Insomnia Exist without Hyperarousal? What Else Can There Be?

“…In fact, one perspective offered by Vargas and al. [1] questions if hyperarousal has anything to do with either acute or chronic insomnia. By disentangling how the flight-or-fight response suggested for acute insomnia is different to the learned hyperarousal observed in chronic insomnia, this review sets the tone for the rest of the issue.…”