Insomnia impare daytime cognitive functions

Individuals with insomnia consistently report difficulties pertaining to their cognitive functioning (e.g., memory, concentration). However, objective measurements of their performance on neuropsychological tests have produced inconsistent findings.  Recently, Fortier-Brochu E conducted a meta-analysis to provide a quantitative summary of evidence regarding the magnitude of differences between individuals with primary insomnia and normal sleepers on a broad range of neuropsychological measures. They found significant impairments (p<0.05) of small to moderate magnitude were found in individuals with insomnia for tasks assessing episodic memory (ES=-0.51), problem solving (ES=-0.42), manipulation in working memory (ES=-0.42), and retention in working memory (ES=-0.22). No significant group differences were observed for tasks assessing general cognitive function, perceptual and psychomotor processes, procedural learning, verbal functions, different dimensions of attention (alertness, complex reaction time, speed of information processing, selective attention, sustained attention/vigilance) and some aspects of executive functioning (verbal fluency, cognitive flexibility). Therefore, they concluded that individuals with insomnia exhibit performance impairments for several cognitive functions, including working memory, episodic memory and some aspects of executive functioning.


Why sleep cause cardiovascular disease

Poor sleep is prospectively linked to all-cause and cardiovascular mortality. So why. Recently, Motivala from UCLA Semel Institute in USA found that sleep loss is associated with increase cytokines in sleep deprivation studies and in primary insomnia patients. He said bidirectional communication between the brain and the inmmune system is carried out through a complex network of autonomic nerves, endocrine hormones and cytokines. Disturbed sleep appears to perturb the functioning of this network and therefore contribute to elevations in inflammatory mediators linked to cardiovascular disease.


Sleep disorders in medical disease

Insomnia and hypersomnia are highly comorbid with medical conditions, such as chronic pain and diabetes, as well as with various cardiovascular, respiratory, gastrointestinal, urinary and neurological disorders. Restless legs syndrome and periodic leg movement syndrome have been associated with iron deficiency, kidney disease, diabetes, and neurological, autoimmune, cardiovascular and respiratory disorders. Rapid eye movement behaviour disorder has been described as an early manifestation of serious central nervous system diseases; thus, close neurological monitoring of patients referring with this complaint is indicated.

Therefore, identification and management of any sleep disorder in medical patients is important for optimizing the course and prognosis. Of equal importance is the search for undetected medical disorder in patients presenting with sleep disorders.


Psychological Flexibility is effective to treat Insomnia in Persons with Chronic Pain

Sleep disturbance is a common complaint in people with chronic pain, and is associated with a range of adverse outcomes including reports of greater pain and disability. Most of these people usually use pain killer to help them reduce insomnia. Recently, McCracken et al from King's college in UK found psychological flexibity, a process from acceptance and commitment therapy is helpful for the insomniac with chronic pain. They found the components of psychological flexibility, particularly acceptance of pain and values-based action is positive correlations with sleep quality. They said the psychological flexibity may be a new candidate to treat insomnia in persons with chronic pain.


Sleep and primary headaches

The relationship between sleep and primary headaches has been known for over a century, particularly for headaches occurring during the night or early morning. Migraine, tension-tyre headache, and cluster headache may cause sleep fragmentation, insomnia, and hypersomnia, causing considerable social and economical costs and several familial problems. By contrast, sleep disorders may themselves trigger headache attacks. Finally, headaches and sleep disorders can also be symptoms of other underlying pathologies. Despite this background, there is still no clarity about the mechanism that links these two entities and their interdependence remains to be defined. Patients with primary headache should undergo a careful assessment of sleep habits.

Placebo is effective to treat insomnia?

In clinical trial, sometime we may found placebo administration significantly decreased subjective sleep latency and increased subjective total sleep time. So is placebo effective to treat insomnia?

Recently, Ogawa et al from Kyoto University in Japan investigate the association between subjective sleep latency  fluctuation and the placebo response. They found higher fluctuation of subjective sleep latency was associated with a greater decrease in subjective sleep latency in placebo treatment. Multivariate analysis suggested that a wider standard deviation for daily subjective sleep latency and a higher weekly mean sSL were independent predictors of greater improvement in mean subjective sleep latency during the subsequent weeks of placebo treatment. Likewise, a wider standard deviation and lower mean of subjective total sleep time were independent predictors of greater improvement in mean subjective total sleep time  in the subsequent weeks.

So, placebo is effective to treat the insomniac with high fluctuation of subjective sleep latency and total sleep time.


cognitive-behaviour therapy for behavioural insomnia of school-aged children.

Chronic sleep problems can lead to the development of behavioural insomnia of Childhood - a sleep disorder involving problematic sleep-onset associations (i.e., parental presence), and resulting in impairments for children and family members.

Recently, Paine et al from Flinders University in Australia perform a controlled evaluation of cognitive-behaviour therapy (CBT) for behavioural insomnia. 42 children (M = 9.3 ± 1.9 yrs, range 7-13 yrs, 18f, 24m) were randomised to CBT (N = 21) or waitlist control (N = 21). CBT consisted of 6 sessions, and combined behavioural sleep medicine techniques (e.g., sleep restriction) with anxiety treatment techniques (e.g., cognitive restructuring). Compared to waitlist controls, children receiving CBT showed significant improvements in sleep latency, wake after sleep onset, and sleep efficiency (all p ≤ .003), but not total sleep time (p > .05). CBT was also associated with a reduction in problematic sleep associations (p ≤ .001), child-reported total and separation anxiety (both p ≤ .01), with all gains being maintained 6 months post-treatment.

This is the first controlled study to demonstrate that multi-component CBT can be effective for the sleep, insomnia, and anxiety symptoms of Behavioural Insomnia of Childhood in school-aged children.