Table of Contents
Abstract
Insomnia and Stress impacts both neural development of central nervous structures, and they are involved in many clinical outcomes like sleep disorders, depression, cognitive impairment and other sleep disorders. Few authors investigated accurately relationship between implications of these two troubles above, and occurrence or complications of sleep quality. It has been showed that, the quality and the duration of sleep depended strongly on the lifestyle and the personal environment. Knowing that, insomnia and stress are a permanent part of our daily life, a complete exploration of their combined effects on our sleep quality and sleep duration may move forward the general approach of therapist about sleep impairment. Indeed, a complete evaluation should be made continuously on a brain to record all the waves fluctuations related to sleep. To our knowledge, none made a clear statement on the combined effects of insomnia and stress on the Sleep Impairment events. The aim of this study is to explore how insomnia and stress together affects sleep quality and sleeps duration (SD), in the general population is associated in simultaneous with sleep components, psychological stress, depression, and anxiety.
Introduction
Insomnia is a phenomenon which can appear at every stage of life, from youthness to elderly. Through the whole life, brain is particularly influenced by, social and psychological interplay between the body and his environment. This process strongly affects the development of both peripheral and central nervous system. Of course, the majority of brain disorders are caused by a failure in one or many of the neuronal circuitry or normal neurobiology. As a consequence of this dysfunction, insomnia appears and become pathologic or persistent, even without any medication, or external factors like stress or mental illness. A healthy lifestyle with physical activities may ensure a healthy brain, and an excellent shield against central nervous system failure and cognitive disabilities. (Clum et al., 2001; Kramer et al., 2003; Neylan et al., 1998; Wittmann et al., 2000; Zammit et al. 1999)
Types of Insomnia:
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- There are two types of insomnia: primary and secondary.
- Primary insomnia: This means your sleep problems aren’t linked to any other health condition or problem.
Secondary insomnia: This means you have trouble sleeping because of a health condition (like asthma, depression, arthritis, cancer, or heartburn); pain; medication; or substance use (like alcohol)
Acute insomnia is brief and often happens because of life circumstances (for example, when you can’t fall asleep the night before an exam or after receiving stressful or bad news). Many people may have experienced this type of passing sleep disruption, and it tends to resolve without any treatment.
Chronic insomnia is disrupted sleep that occurs at least three nights per week and lasts at least three months. Chronic insomnia disorders can have many causes. Changes in the environment, unhealthy sleep habits, shift work, other clinical disorders, and certain medications could lead to a long-term pattern of insufficient sleep. People with chronic insomnia may benefit from some form of treatment to help them get back to healthy sleep patterns. Chronic insomnia can be comorbid, meaning it is linked to another medical or psychiatric issue, although sometimes it’s difficult to understand this cause and effect relationship.
People with insomnia tend to have difficulty falling asleep (onset), staying asleep (maintenance), and/or they wake up too early in the morning. Treatment for insomnia can include behavioural, psychological, medical components or some combination thereof. You and your doctor will need to talk about your particular situation and history of insomnia, as well as its causes, to decide on the best treatment plan. (Franzen et al.,2009; Yoo et al., 2007),
Epidemiologic data reported that, central nervous connections are modulated by the game of stimuli-response, play continuously by both nature and human and these modulations increase the risk to develop neurodegenerative diseases as well as mood diseases, and also insomnia. Young adults (between eighteen years old until thirty years old) are because of that, more expose to the risk to develop anxiety and psychiatric disorders. Until now, no final therapy exists for mood disorders, but prevention of risk factors and promotions of good lifestyle are important because, insomnia and brain disorders are not easy to identify. Physical activity, non-usage of drugs and sleep quality may help to decrease insomnia for young adult’s population, compared with a midlife and elderly population. Many other studies focused on risk factors like sociodemographic pattern of economic fluctuations, obesity, usage of drugs or family history of previous traumatic events in life; known to increase mental disorders and associated psychopathologies. (Walker and van Der Helm, 2009)
Insomnia is characterised by subjective complaints about dissatisfaction with sleep quality or duration, difficulty falling asleep at bedtime, waking up in the middle of the night or too early in the morning, or non-restorative or poor quality sleep. Insomnia also includes subjective reports of daytime symptoms such as fatigue or low energy, difficulties with cognitive functions (e.g., attention, concentration, and memory), and mood disturbances (e.g., irritability, dysphoria), all of which can produce functional impairments and are often the primary concerns that prompt patients to seek treatment. Polysomnographic assessment can show objective sleep impairments (e.g., longer sleep latencies, reduced sleep time), but severity does not always match the patient’s complaint of poor sleep. The cortex is more active in people with insomnia than in good sleepers, both around sleep onset and during non-rapid eye movement sleep; this is consistent with the general state of hyper arousal in people with insomnia. For daytime symptoms, assessment of neurobehavioral performance with objective tests shows selective performance deficits (e.g., attention, memory) in individuals with primary insomnia. Nonetheless, most patients perceive their global functioning as greatly impaired. The patient’s appraisal of sleep and daytime functioning is crucial since a diagnosis of insomnia is based on clinical symptoms rather than on objective laboratory findings.
Sometimes, insomnia only lasts a few days and goes away on its own, especially when the insomnia is tied to an obvious temporary cause, such as stress over an upcoming presentation, a painful breakup, or jet lag. Other times, insomnia is stubbornly persistent. Chronic insomnia is usually tied to an underlying mental or physical issue. Anxiety, stress, and depression are some of the most common causes of chronic insomnia. Having difficulty sleeping can also make anxiety, stress, and depression symptoms worse. Other common emotional and psychological causes include anger, worry, grief, bipolar disorder, and trauma. Treating these underlying problems is essential to resolving your insomnia.
Anxiety, stress, and depression are some of the most common causes of chronic insomnia. Having difficulty sleeping can also make anxiety, stress, and depression symptoms worse. Other common emotional and psychological causes include anger, worry, grief, bipolar disorder, and trauma. Treating these underlying problems is essential to resolving your insomnia.
Medical problems or illness: Many medical conditions and diseases can contribute to insomnia, including asthma, allergies, Parkinson’s disease, hyperthyroidism, acid reflux, kidney disease, and cancer. Chronic pain is also a common cause of insomnia.
Medications: Many prescription drugs can interfere with sleep, including antidepressants, stimulants for ADHD, corticosteroids, thyroid hormone, high blood pressure medications, and some contraceptives. Common over-the-counter culprits include cold and flu medications that contain alcohol, pain relievers that contain caffeine (Midol, Excedrin), diuretics, and slimming pills.
Sleep disorder: Insomnia is itself a sleep disorder, but it can also be a symptom of other sleep disorders, including sleep apnea, restless legs syndrome, and circadian rhythm disturbances tied to jet lag or late-night shift work.
In the last two decades, several models have been proposed to understand the etiology and path physiology of insomnia and most of them have emphasized the importance of the joint effect of stress and psychological factors in the pathogenesis of insomnia. The characteristic psychological profile of patients with insomnia, consisting of cognitive-emotional hyper arousal (i.e., obsessive, anxious, ruminative, and dysthymic personality traits) and emotion-oriented coping strategies, is thought to be present pre-morbidly and play a key role in the etiology of the disorder. Insomnia is associated with precipitating life events and cognitive-emotional arousal and is perceived by the patient as stressful on its own. Thus, insomnia should be expected to be associated with activation of the stress system. Stress has been associated with the activation of the hypothalamic-pituitary-adrenal (HPA) and the sympatho-adrenal-medullary axes, whereas corticotrophin-releasing hormone (CRH) and cortical (products of the hypothalamus and adrenals, respectively), and catecholamine (products of the sympathetic system) are known to cause arousal and sleeplessness to humans and animals. On the other hand, sleep and particularly deep sleep appears to have an “anti-stress” effect as it is associated with an inhibitory effect on the stress system including its main two components, the HPA axis and the sympathetic system.
While the majority of early studies reported no difference between subjectively defined “poor sleepers” and controls in the levels of cortical secretion, 22-24 later studies found that 24-h urinary free cortical, norepinephrine, and catecholamine metabolites levels were either increased in patients with insomnia with objective sleep disturbances as compared to controls or were correlated with PSG indices of sleep disturbance in insomnia patients. The few exceptions might be related to the fact that the objective sleep of patients with insomnia was very similar to that of controls or to lack of statistical power and controls not being carefully selected. In addition, it was shown that middle-aged healthy individuals were more vulnerable to the sleep disturbing effects of the stimulating hormones of the HPA axis, i.e., CRH, which may explain physiologically the increased prevalence of insomnia in older subjects. Furthermore, other studies have demonstrated that this type of insomnia is associated with increased nocturnal heart rate and impaired heart rate variability, increased overall oxygen consumption, a measure of whole-body metabolic rate and increased pupil size, indicative of sympathetic system activation, but not in insomnia defined only on subjective measures. Another paradox with patients with insomnia who typically complain that they are fatigued and sleepy during the day is that during the Multiple Sleep Latency Test (MSLT) they have either similar or increased daytime sleep latencies when compared to controls.
In fact, several studies have shown that, within patients with insomnia, those with shorter objective sleep duration show longer sleep latencies and are more alert in vigilance tests. This is in contrast to normal individuals who after sleep deprivation experience significantly reduced sleep latencies and decreased alertness in vigilance tests, i.e., physiological sleepiness. Thus, long latencies in the MSLT may represent a reliable marker of physiological hyper arousal in insomnia patients. Finally, evidence about the presence of central nervous system hyperarousal in insomnia comes from studies in human subjects using neuroimaging, and spectral, arousal, and event-related electroencephalography analyses as well as from studies on the neural circuitry of stress-induced insomnia in rats. Increased cortical arousal during sleep is present to a variable degree in all patients with insomnia and may explain why they perceive their sleep as wake and as non-restorative.
The most widely studied stressors in children and adolescents are exposure to violence, abuse (sexual, physical, emotional, or neglect), and divorce/marital conflict (Cicchetti 2005). McMahon et al. (2003) also provide an excellent review of the psychological consequences of such stressors. Psychological effects of maltreatment/abuse include the dysregulation of affect, provocative behaviours, the avoidance of intimacy, and disturbances in attachment (Haviland et al. 1995, Lowenthal 1998). Survivors of childhood sexual abuse have higher levels of both general distress and major psychological disturbances including personality disorders (Polusny & Follett 1995). Childhood abuse is also associated with negative views toward learning and poor school performance (Lowenthal 1998). Children of divorced parents have more reported antisocial behaviour, anxiety, and depression than their peers (Short 2002). Adult offspring of divorced parents report more current life stress, family conflict, and lack of friend support compared with those whose parents did not divorce (Short 2002). Exposure to nonresponsive environments has also been described as a stressor leading to learned helplessness (Peterson & Seligman 1984). Exposure to intense and chronic stressors during the developmental years has long-lasting neurobiological effects and puts one at increased risk for anxiety and mood disorders, aggressive dyscontrol problems, hypo-immune dysfunction, medical morbidity, structural changes in the CNS, and early death (Shaw 2003)
It is well known that first depressive episodes often develop following the occurrence of a major negative life event (Paykel 2001). Furthermore, there is evidence that stressful life events are causal for the onset of depression (see Hammen 2005, Kendler et al. 1999). A study of 13,006 patients in Denmark, with first psychiatric admissions diagnosed with depression, found more recent divorces, unemployment, and suicides by relatives compared with age- and gender-matched controls (Kessing et al. 2003). The diagnosis of a major medical illness often has been considered a severe life stressor and often is accompanied by high rates of depression (Cassem 1995). For example, a meta-analysis found that 24% of cancer patients are diagnosed with major depression (McDaniel et al. 1995).
Stressful life events often precede anxiety disorders as well (Faravelli & Pallanti 1989, FinlayJones & Brown 1981).Interestingly, long-term follow-up studies have shown that anxiety occurs more commonly before depression (Angst &Vollrath 1991, Breslau et al. 1995). In fact, in prospective studies, patients with anxiety are most likely to develop major depression after stressful life events occur (Brown et al. 1986).
