Aetiology
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Aanpak van slaapklachten en insomnie (slapeloosheid) bij volwassenen in de eerste lijnPublished by: Werkgroep Ontwikkeling Richtlijnen Eerste Lijn (Worel)Last published: 2018Prise en charge des problèmes de sommeil et de l’insomnie chez l’adulte en première lignePublished by: Groupe de Travail Développement de recommmandations de première ligneLast published: 2018It is generally accepted that insomnia is a disorder of hyperarousal.[18] One cognitive model suggests that rumination and worry about life stresses can disrupt sleep and the reaction to not sleeping, including alarm and worry over sleep, can lead to arousal, giving rise to acute episodes of insomnia, and creating difficulties with sleep onset and/or returning to sleep after waking.[19] Other precipitants of acute episodes of insomnia may be a change in sleep environment, increased light exposure, noise, excessively high or low ambient temperatures, or a poor mattress. Additionally, life changes or stressful life events adversely affect sleep. A recent death or sickness in close contacts, a new job or school, or upcoming deadlines can cause insomnia. Subsequently, once a person regularly experiences sleep difficulties, the disruption of sleep may persist due to perpetuating factors such as maladaptive cognition or behaviour, as well as anxiety relating to sleep difficulties or anticipated difficulty in daytime function.
The principal aetiological conceptualisation of insomnia is often called the '3P' model and comprises 3 groups of factors that explain the onset and maintenance of insomnia: predisposing, precipitating, and perpetuating.[20] Predisposing factors include conditions that confer vulnerability such as family history of insomnia and certain medical and psychiatric disorders that precede the onset of insomnia. Then, a precipitating factor such as a stressful life event or hospitalisation may trigger an episode of acute insomnia. Ultimately, perpetuating factors may prolong an episode of acute insomnia and lead to chronic insomnia; these factors include maladaptive behaviours and cognitions such as extending sleep opportunity to make up for lost sleep (in bed early, out of bed late, napping), worrying about whether sleep will occur, and concern over the adverse health and functional consequences of insufficient sleep.
Chronic insomnia can be comorbid with an underlying medical condition (e.g., COPD, cancer, congestive heart failure, Parkinson's disease), a psychiatric disorder (e.g., schizophrenia, depression, bipolar disorder, anxiety disorders, or attention deficit hyperactivity disorder), drug or alcohol use (or withdrawal), or environmental factors.[21][22][23] It may occur exclusively during an episode of illness, or may precede or follow it.
Psychiatric disorders, particularly anxiety and depression, are the most common comorbidities.[16][24][25] When insomnia is comorbid with depression, the insomnia often precedes the onset of affective symptoms, and it is among the most likely symptoms to persist once the affective symptoms of a depressive episode have been treated.[26] Insomnia is associated with a significantly increased risk of depression, and treating insomnia in non-depressed patients has been shown to prevent depression.[27][28][29] Certain antidepressants may contribute to sleep difficulties, although some medications have fewer sleep effects than others.[30] One meta-analysis of randomised controlled trials found that acetylcholinesterase inhibitors, dopamine agonists, and selective serotonin reuptake inhibitors were the classes of drug most likely to be associated with sleep disturbance.[31]
Patients with chronic medical conditions (e.g., cancer, congestive heart failure, chronic respiratory disorders, Parkinson's disease, chronic pain) have a higher prevalence of insomnia than the general population.[32][33][34][35] Pain disorders, in particular, have an especially strong correlation with insomnia.[13][36][37] Increased pain levels often precede sleep abnormalities, and sleep difficulties seem to exacerbate pain symptoms.[38]
Of note, the current diagnostic definitions, both DSM-5-TR and International Classification of Sleep Disorders-3-TR, no longer make distinguish between 'primary' and 'secondary' (or comorbid) insomnia because:[1][2]
there is considerable uncertainty about the direction of causality in secondary insomnia;
the treatment of the primary condition is often insufficient to resolve the insomnia; and
both primary and secondary insomnia share numerous characteristics, especially the aforementioned perpetuating factors, which need to be addressed in order to achieve remission.
Pathophysiology
A converging theme of most pathophysiological models of insomnia is hyperarousal, a multidimensional construct involving not only physiological but also cognitive and emotional components.[39][40] In patients with insomnia, a number of physiological observations suggest a hyperactivated or hypermetabolic state. The whole-body metabolic rate is determined by assessment of oxygen consumption. Patients with insomnia exhibit significantly higher metabolic rates throughout the 24-hour day than healthy controls.[41][42] Heart rate variability provides a measure of sympathetic and parasympathetic nervous system activity; average heart rates were reported to be increased and variability decreased in all stages of sleep in patients with insomnia relative to healthy normal sleepers, but the evidence for impairment of heart rate variability in patients with insomnia has been questioned.[39][43][44]
Chronic activation of the stress response system in patients with insomnia is additional evidence of hyperarousal. High levels of 24-hour urinary free cortisol have been found in several studies of patients with insomnia.[39][45][46] Furthermore, urinary free cortisol levels have been positively correlated with total wake time, and urinary catecholamines have been correlated with wake time after sleep onset and stage 1 sleep. Plasma measures of cortisol and adrenocorticotrophic hormone (ACTH) have been evaluated in healthy normal sleepers and patients with insomnia.[45][46][47] These studies have produced somewhat mixed results but, overall, poor sleepers have higher plasma levels of cortisol and ACTH, suggesting an association between aberrant hypothalamic-pituitary-adrenal axis activation and the pathology of chronic insomnia.
Patients with insomnia display electroencephalogram (EEG) abnormalities indicative of pathological hyperarousal, including intrusion of wakefulness signatures such as sleep spindles and K complexes into deeper NREM stages of sleep.[39]
Patients experience cognitive arousal characterised by a tendency towards excessive worry and rumination especially during the pre-sleep period. Such cognitive arousal leads to emotional distress, which in turn mediates the relationship between cognitive and physiological arousal.[39]
Several endogenous molecules are involved in sleep-wake regulation. Wake-promoting substances include histamine, noradrenaline, dopamine, and the orexins (orexin 1 and 2; also called hypocretin), and sleep-promoting ones include gamma-aminobutyric acid (GABA), adenosine, serotonin, and melatonin.[48] These molecules are often the targets of pharmacological treatments of insomnia.
Consequences of chronic insomnia include:
Reduction in quality of life - in one study the extent of this was found to be similar to the reduction in quality of life seen in patients with chronic heart failure or depression.[49]
An increased risk of psychiatric disorders such as anxiety, depression, and suicidal ideation.[27][28][50]
Reduced performance at work and occupational accidents.[51][52][53]
Self-medication, and an increased risk of substance misuse.[15][54]
A possible increased risk of cardiovascular disease, diabetes, hypertension, and mortality, especially in short sleepers (≤6 hours on polysomnography or actigraphy), although other studies suggest that mortality is not increased in patients with frequent and ongoing insomnia.[55][56][57][58][59][60][61][62][63]
A possible increased risk of Alzheimer's disease.[64][65][66]
Other daytime dysfunction, including cognitive impairment. Results have been mixed, possibly owing to the nature of the assessments being performed, although impaired cognitive performance becomes a common concern in patients with chronic insomnia.[67][68]
Impaired driving performance.[71]
Unintentional injury and mortality.[72]
Classification
International Classification of Sleep Disorders, third edition, text revision (ICSD-3-TR)[2]
Chronic insomnia disorder
Short-term insomnia disorders
Other insomnia disorder
The current diagnostic definitions, both DSM-5-TR and ICSD-3-TR, specify the duration of at least 3 months for insomnia disorder, which thus serves as a cut-off to classify acute versus chronic insomnia. Although this 3-month criterion is based on consensus rather than research evidence, its clinical utility may stem from the observation that most clinical trials and clinical practices of cognitive behavioural therapy for insomnia (CBT-I), the widely recognised first-line treatment of insomnia, have targeted and successfully managed chronic insomnia lasting at least a couple of months. Furthermore, acute insomnia may be related to hyperarousal in response to stress, and chronic insomnia is usually characterised by conditioned wakefulness with maladaptive behaviours and cognitions.[3] However, emerging evidence, although still limited, indicates promising efficacy of CBT-I in treating insomnia lasting less than 3 months and preventing the progression of acute insomnia to chronic insomnia.[4][5][6] Based on this evidence and for other practical reasons, a clinician may manage acute insomnia in a similar way to chronic insomnia.[7]
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