Introduction
Insomnia is a sleep disorder characterized by the inability to obtain an adequate amount or quality of sleep (the difficulty can be in falling asleep, remaining asleep, or both).
While the term is sometimes used to describe a disorder demonstrated by polysomnographic evidence of disturbed sleep, insomnia is often practically defined as a positive response to either of two questions: "Do you experience difficulty sleeping?" or "Do you have difficulty falling or staying asleep?"
Epidemiology
Many population-based studies. have been carried on about insomnia - a general consensus had developed from such researches that approximately 20-30% of a variety of adult samples drawn from different countries report one or more of the symptoms of insomnia (difficulty initiating sleep, difficulty maintaining sleep, waking up too early, and in some cases, nonrestorative or poor quality of sleep). This disturb appeared to be more frequent among women than men (30.7% vs. 19.5%), and to be increased by age (mean values around 7% among individuals between 18 and 24 years of age, and 45% among individuals over 65 years of age)
Yet the application in the latest years of more stringent diagnostic criteria (which include: perceived daytime impairment or distress as a function of the insomnia symptoms, symptoms persistance for at least 1 month and not only in presence of other sleep disorders, mental disorders, or direct physiological effects of a substance or medical condition), has highly reduced the current prevalence, now estimated around 10%.
(N.B.: Heritability is a factor to be carefully considered in the epidemiologic description of this disturb; as an exemple, in a classic twin study., >1,000 monozygotic twins and >800 dizygotic twins were examined in terms of insomnia and sleepiness, and genetic influence was estimated at 57% (yet of course the particular genetic contributions in this matter remain to be identified, as do many other aspects).
Risk Factors
The most clearly identified risk factors are age and gender: prevalence increases in women and older adults (see Epidemiology above).
Most relevant contributor to insomnia onsetting is also the presence of coexisting medical conditions, such as chronic diseases (dyspnea, gastroesophageal reflux disease, neurodegenerative diseases, pain conditions) and psychiatric disorders (most frequent of which is depression - insomnia itself is a diagnostic symptom for depressive disorders).
Other factors to be considered are particular habits (i.e. night working, …) and menses and menopause regarding women.
(It is important to recognize that these factors do not cause insomnia, but rather they can be triggering factors of insomnia in predisposed individuals.)
Pathological Mechanisms
The insomnia patients usually exhibit significantly higher values in many parameters which are to indicate the general body activity, such as metabolic rates (measured at intervals across the 24-hour day by oxygen consumption (VO2)) and heart rate.
Moreover, chronic activation of the stress response system is evidenced in insomnia patients:
- Several studies have found high cortisol levels in poor sleepers.
As we know, cortisol is produced by the zona fasciculata of the adrenal gland in response to the ACTH signalling.
It has a daily circadian secretion, yet it is found to be increased in stress condition.
Its many targets are different and spread throughout the body; very important are its immunosoppressory action (inhibits the release of pyrogenic substances in the body, and downregulates the exposition of Interleukine-2 receptors (IL-2R) on the Th (CD4+) cells, thereby preventing their activation)
and its role in sustaining gluconeogenesis and glycogenolysis in order to increase blood glucose levels and raise the amount of molecules readily available for the catabolic enzymes.
- Urinary catecholamines have been correlated with stage 1 sleep percentage and wake time after sleep onset: which is to say, the higher the cathecolamine blood (and urinary) levels are, the longer insomniac patients will remain in sleep stage 1 and the more frequent and long will be their waking phases. The cathecolamine effects on the body are well known (most important of them being the ones on heart and vases, mediated by alpha and beta receptors).
- As a last confirm of the aroused activity of the body during insomnia, positron emission tomography (PET) has been used to assess cerebral glucose metabolism in patients.42
Compared to healthy subjects, patients with insomnia exhibited greater cerebral glucose metabolism during waking and non-rapid eye movement (REM) sleep states. Furthermore, the insomnia patients demonstrated smaller reductions in relative metabolism from waking to non-REM sleep in wake-promoting regions of the brain.
Consequences
Due to its chronicity, insomnia is associated with substantial impairments in an individual's quality of life. Research has shown that among the daytime consequences of insomnia, the increased occurrence of accidents poses the greatest health risk. Insomniacs are 2.5 to 4.5 times more likely than controls to have an accident. In a sample of 8,625 community respondents in France, Léger et al.. reported that 8% of insomniacs and 1% of non-insomniacs had an industrial accident in the past 12 months. Work productivity is also compromised among insomniacs due to work-related problems (i.e., higher rates of absenteeism, decreased concentration, and difficulty performing duties).
Treatment
Pharmacological and non-pharmacological terapies are both often used (and often mixed of course) in the treatment of insomnia.
Among the first are sedatives such as benzodiazepines (molecules binding to GABA-A receptors) and non.benzodiazepines; being their prescription and use still very frequent, the many collateral effects and doubts about their real effectiveness are shifting the focus on less harsh therapies. In fact it is now known that drugs like the aforementioned are able to increase sleeping time and decrease the difficulty in falling asleep, but they do so enhancing the light, non-restorative, stages of sleep and reducing the length of the R.E.M. phases (the therapy might be not only uneffective, but even harmful). Besides benzodiazepines and similar usually lead to tolerance and physical dependence.
Non-pharmacological methods include actions such as attention to sleep hygiene, stimulus control, behavioral interventions, sleep-restriction therapy, paradoxical intention, patient education and relaxation therapy. Hypnosis may be used too, but only in short-term terapy programs, as it causes tolerance development. The listed activities have proved quite useful in reducing the disease effects.
It is obviously necessary to try and act upon not only insomnia itself, but on the collateral disorders that accompany it too: an extremely interesting theory and study is the one that concerns the sleep deprivation as a therapeutic tool for depression, added to the somministration of drugs like Modafinil (stimulates the production and releasing of excitatory neurotransmitters such as serotonin, norepinephrine, dopamine, etc).
