Insomnia is an important public health issue because it has a significant negative impact on individuals' physical and social performance, ability to work and quality of life. Insomnia is defined by difficulty falling asleep, difficulty remaining asleep, early morning awakening and/or non-restorative sleep, associated with daytime consequences. These can include complaints of fatigue, somatic symptoms (e.g. reduced pain threshold), impaired cognition (e.g. reduced concentration and memory) and affective symptoms such as irritability, low mood and anxiety. Patients also often display behaviours such as help-seeking, self-treatment and limitation/restriction of daytime activities.
Insomnia has traditionally been viewed and treated as a symptom rather than a disease, and practitioners are generally taught that insomnia should be resolved through the treatment of underlying pathophysiological factors. Insomnia can be classified based on different features, including duration, comorbidity, symptom severity and presentation (sleep onset, sleep maintenance and end-of-sleep characteristics). Acute insomnia is defined if sleep problems last for between 1 and 3 nights per week, with no one episode lasting longer than several weeks. Whereas chronic insomnia is defined if there is difficulty initiating or maintaining sleep or non-restorative sleep persists for greater than 3 nights per week for 1 month or more.
Role of Dopamine in Sleep Disorders
Dopamine is a neurotransmitter from the catecholamine family that is considered to be a key neurological substrate of reward, and has traditionally been the target of pharmaceutical therapies for movement disorders, psychotic disorders, and to a lesser extent depression. Evidence also indicates, however, that dopamine is integral to the promotion and maintenance of arousal states (that is, wake-sleep states). Following the observation that dopamine is associated with arousal in animal models, human neuroimaging models, genetic models, and sleep-related movement disorders, it is intriguing to question whether dopamine may contribute to arousal-related sleep dysfunction in other sleep disorders with less well established pathophysiological basis, such as insomnia. To date, this hypothesis requires further validation, requiring rigorous empirical evaluation. This being so, it suffice to say, that the putative role for dopamine in insomnia rests primarily on documented associations of dopamine with arousal and other arousal disorders.
Vulnerability to Insomnia - The Role of Familial Aggregation
Although an underlying vulnerability to acute sleep disturbance and the subsequent development of chronic insomnia has been proposed by several investigators, relatively little data regarding specific factors that might predispose individuals to insomnia have been identified. In a recent study, researchers from the Sleep Disorders and Research centre in Detroit, sought to determine the degree of familial aggregation in vulnerability to stress-related sleep disturbance among siblings. The researchers identified that a potential genetic component to a predisposition towards insomnia may exist. The robust positive correlation found for vulnerability between siblings in the foregoing study is consistent with previous studies that have identified a genetic component to insomnia. Moreover, there is also preliminary evidence that at least one component of the predisposition to insomnia may include a pre-morbid vulnerability to stress-related sleep disruption.
Insomnia and Biological indicators
Inadequate and fragmented sleep disrupts the normal diurnal rhythm across regulatory systems and interfere with restorative qualities of sleep. Such disruptions put demands on regulatory systems to maintain homeostasis under adverse conditions i.e. allostasis. This is thought to cause gradual deterioration across systems, as there is an accumulation of wear and tear and the absence of adequate restoration, termed allostatic load.
Evidence of allostatic load is seen in changes to physiological set points for biological indicators within each system, including elevated LDL and triglycerides, poor glucose regulation, and increased inflammatory activity. Epidemiological evidence links poor quality and inadequate quantity of sleep to increased allostatic load and other diseases related to allostatic load such as diabetes, hypertension, metabolic syndrome and cardiovascular disease.
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