![]() As such, the initiation of insomnia and its acute phase is thought to occur in response to life-event stress. The evolution to chronic insomnia is thought to be largely, if not wholly, mediated by perpetuating factors that are behavioral in nature, relating to how the individual manages their insomnia. An acute episode, in turn, may resolve, in tandem with the precipitating event, or evolve into chronic insomnia. These characteristics, in combination with precipitating events, such as life stressors that may be biopsychosocial in nature, serve to initiate an acute episode of insomnia. 23 – 25 Spielman's model suggests that predispositional characteristics exist making some individuals more prone to insomnia than others. 22įrom a theoretical standpoint, the most well-established conceptualization of the pathogenesis of insomnia comes from Spielman and colleagues. Moreover, these figures fit with the only epidemiological study that uses the DSM-5-defined criteria for acute insomnia (i.e., a 9.15% incidence over 3 months). Interestingly, the only study with a follow-up period that could track the progression from acute insomnia to chronic insomnia as it occurred (3 months) found that rates of chronic insomnia, in a sample of hospitalized individuals, almost doubled over the period, from 10% to 19%, 16 suggesting a 3-month incidence rate of approximately 9%. ![]() Furthermore, differing criteria have been used in each study to define episodes of both acute (poor sleep/brief insomnia) and chronic insomnia (ranging between ≥ 1 month to ≥ 1 year), making definitive conclusions about the transition to chronic insomnia difficult. As such, it would be difficult to reliably track the transitions between normal sleep, acute insomnia, and chronic insomnia, based upon the time between accounts, while also relying heavily on memory. For example, with regard to the timeframes between assessments, one study retrospectively assessed insomnia symptoms at six time points, the shortest follow-up being 2 years, 15, 18 one retrospectively assessed once at 5 years, 20 and two others 17, 21 annually one for 3 consecutive years and the other at one time point. 15 – 21 The primary limitations of these seminal studies pertain to (1) the clear delineation of what constitutes acute insomnia, (2) whether the index episode represents a first-onset or recurrence of insomnia, (3) the mode of assessment used (in most cases non-standard instruments and often single-item questions), (4) the timeframes used for assessments (in most cases either at annual or bi-annual intervals), and (5) the lack of objective sleep measures like polysomnography. ![]() While a wealth of theoretical perspectives and cross-sectional studies exist on the topic of the natural history of insomnia, there are only a handful of prospective longitudinal studies that provide data on this subject. 14 What is unknown, however, is where this increased risk for depression occurs in the natural history of insomnia, as all the aforementioned studies have examined this link within the timeframe of chronic insomnia. ![]() 13 To that end, a recent meta-analysis suggests that chronic insomnia confers a two-fold risk for developing depression. 6 – 10 It has been shown that insomnia often precedes the onset of depression 11 is present throughout its developmental course, 12 and treating insomnia in those with depression results in a reduction in depressive symptoms. 1 – 5 The most compelling case for insomnia being a risk factor for future morbidity is with regard to Major Depression. ![]() Understanding the full course of insomnia is not only important to the arena of preventative sleep medicine but is underscored by accumulating evidence suggesting insomnia, in its chronic form, is a risk factor for a range of psychiatric and physical morbidities. meeting full criteria for Insomnia Disorder but with duration less than three months) may still warrant clinical attention, little is actually known about the early phase of insomnia. Despite the DSM-5 suggesting insomnia in its acute or short-term form (i.e. ![]()
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