Science topic

Sleep Disorders - Science topic

Conditions characterized by disturbances of usual sleep patterns or behaviors. Sleep disorders may be divided into three major categories: DYSSOMNIAS (i.e. disorders characterized by insomnia or hypersomnia), PARASOMNIAS (abnormal sleep behaviors), and sleep disorders secondary to medical or psychiatric disorders. (From Thorpy, Sleep Disorders Medicine, 1994, p187)
Questions related to Sleep Disorders
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Insomnia is a form of sleep disorder. Having difficulty in sleeping may increase the symptoms of mental health problems. What are the common causes, effects and probable cure for insomnia? Sharing is caring. Thanks!!!
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Sleep problems such as insomnia are a common symptom of many mental illnesses, including anxiety, depression, schizophrenia, bipolar disorder and attention deficit hyperactivity disorder (ADHD).
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One of my students has proposed to work on prevalence of OSA in Indian population. On the basis of specific inventory we can identify a person with OSA. However, is there any objective procedure to validate the findings based on questionnaire/ inventory?
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The definitive diagnosis of OSA must be made by a physician. Sleep-related breathing disorders constitute a lot of disorders - one of which is sleep apnea. Sleep apnea again can be central sleep apnea (rare) or obstructive sleep apnea. Thus, only with proper history taking, screening questionnaires, clinical examination, proper referral (ENT) for tonsils and adenoids (in growing population) can further examination be undertaken. Patients with history of snoring, gasping respiration, nocturnal awakenings, etc. should be screened as these are common signs and symptoms with OSA.
An in-center sleep study is the gold standard PSG. A cheaper option is out of center sleep study (OCST). Home Study Apnea Testing (HSAT) is one type of OCST. HSAT does not typically include EEG.
The determination of the need for a sleep study, the interpretation of the results, and the diagnosis must be made by physician. An orthodontist can help in the treatment of OSA in collaboration with the physician. Other respiratory functional tests such as expiratory flow volume, inspiratory flow volume, acoustic rhinometry, rhinomanometry can be used to assess respiratory function as well.
I have attached the paper that shows the American Association of orthodontists stand on the team approach and the role of orthodontists for OSA. I have also attached my recent paper on the effect of expansion on airway and the future directions with this treatment methodology.
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Sleep study is mandatory for adult patients with sleep apnea. Is it the same for pediatric patient with sleep apnea?
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Polysomnography can be used to perform accurate diagnosis regarding the presence and severity of apnea in children. However, the other aids mentioned above such as tonsil size, behaviour issues, noctural enuresis, etc. can help to screen the patients.
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I am currently interested about normal flora of the body (microbes), which are also involved in many diseases and aging, how can we control our diet or normal flora to maintain our health, as obesity is also linked, timing of food we eat also linked to normal flora. Chronobiology is also emerging field so thinking of it is essential part of sleep disorders and other chronic diseases.
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Trillions of microbes live in close symbiosis with their host and have impacts on various aspects of host physiology as well as predisposition to the disease. The endogenous clock is a highly conserved timekeeper able to align organismal physiology to the daily cycle, thus maximizing survival and fitness. Circadian rhythms coordinate whole-body biological processes synchronizing cellular biochemical reactions, tissue function and finally controlling systemic homeostasis. Kindly check the following RG link:
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Hello. I working on a sleep project. Sleep is of paramount importance for resetting brain and body function. While newborns tend to sleep most of their day hours, geriatric population often suffers of lack of enough sleep. Most of the people will subjectively complain about their sleep, at least at one point in their life. While life requirements and schedule might play a major aspect in this, other sleep disorders should be ruled out. There is thus a need to use objective measures to better assess sleep quality and quantity. Can anyone please suggest the objective measures of sleep quality?
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Nice Contribution Dirk Cysarz
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Complimentary alternative treatments like meditation, yoga, herbal etc.
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Please see the following PDF attachments.
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Sleep problems can be seen in patients with Parkinson's disease. Can it be about serotonin?
In mice, ablation of the raphe and no production serotonin increases wakefulness and impairs the homeostatic response to sleep deprivation.(DOI:https://doi.org/10.1016/j.neuron.2019.05.038)
Even in the absence of depression, the CSF levels of 5-I-HAA of patients with Parkinson’s disease are lower than those of age-matched controls.
( DOI: 10.1176/jnp.2.1.88 )
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Thank you for great articles. They gave me a new perspective about PD.
I want to suggest an article: Serotonergic dysregulation is linked to sleep problems in Parkinson's disease (doi:10.1016/j.nicl.2018.03.001)
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I am working towards this sleep disorder paper in artificial neural network i am in need of more medical dataset to done the result effectively kindly share the link related to sleeping disorder medical dataset kindly do the needful and thankyou
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I am wondering if anyone has used Empatica E4 for collecting bio-signals from participants. Is this any good? compared to say more established systems like Biopac ? 
Thanks!
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I would not recommend using Empatica E4 to calculate HRV. We have compared PPG (as used in E4) versus ECG and it overly sensitive to any motion for the data to be usable.
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there are side effects in child ?
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Lactium is safe, and it does not induce any side effect.
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The majority of individuals with depression experience sleep disturbances. Depression is also over-represented among populations with a variety of sleep disorders. Although sleep disturbances are typical features of depression, such symptoms sometimes appear prior to an episode of depression.
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Sleep disturbance can be viewed as an independent variable of depression. Sleep and mental health are interrelated. Recent studies indicate that problems sleeping can contribute to the formation of depression and vice versa. Please, see
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Sleep is biological function, its repetitive routine of day and night, its time of sleeping, quality of sleeping, ageing and chronic diseases like depression affect more of that, how can we manage insomnia or sleep disorder with physiological or pharmacological manners, this is very important issue in the world, reviews and articles related to general physiology and its control,
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There are tons of research papers, reviews, and books available online as well in pubmed.
You can also refer my book as well:
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Our program is called reSTART Life, PLLC and we've been around since 2009. First in the country and still the leader. We've seen some amazing cases. Perhaps you would like to do some of your research with our clients? They are almost universally sleep deprived when they arrive and they can take a long time to get regulated again.
If you would like to chat my best email is hilarie.cash@restartlife.com.
Warmly,
H
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Sounds interesting. I'd like to know.
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What is the relationship between sleep disorder, daily health and heart disease?
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Hi
I recomend you to read the works of Smolenski, Hermida and Portaluppi about blood presure and circdain rhythms. They did some very intresting works.
Amit
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Hello everyone.
From a pathophysiologic point of view, how long is it reasonable to look back in the nasal flow signal of OSA patients to see whether a desaturation episode is related to a previous nasal flow reduction? The delay amount might depend on specific patient's characteristics. In that case, are there phenotypes of patients with obstructive sleep apnoeas that take such delay variability into account?
Thank you in advance.
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Hello Matteo,
Here is the study that might be helpful:
Ng AS, Wong TK, Gohel MD, Yu WW, Chung JW, Fan KL. Using pulse oximetry level to indicate the occurrence of sleep apnoea events. Stud Health Technol Inform. 2006;122:672-5.
In brief, this research on ten people ( all men, mean age 45 /SD 8.9, body mass index 27/SD 3.3, apnea/hypopnea index 47/SD 15) attempted to select pulse oximetry (SpO2) level as an alternative parameter to indicate the occurrence of sleep apnoea. Time differences were compared between the "onset of nasal airflow cessation" and the "onset of three percent oxygen desaturation from the baseline" during sleep apnoea events. The results of this study showed there was around a twenty second delay after the onset of the cessation of nasal airflow. The paper provides results for each individual patient: the lowest time, in second (mean/SD) is 19.5/5.8, and the highest is 27.3/7.74.
These researchers concluded that the SpO2 level is not immediately sensitive to the occurrence of sleep apnea, where the time delay may be caused by: i) time utilized by the devise to process the signal, ii) time needed to carry deoxygenated blood to the finger, or iii) the desaturating of SpO2 level, which is affected by the last sleep apnea event and during the occurrence of repetitive events.
Hope this helps. Best wishes with your study,
Tatyana
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I am a firm believer in the potential benefits of ACT for a range of difficulties.
Do people have information about ACT for sleep?
Does anyone have clinical experience of using ACT-related interventions and a sense of how successful the interventions were?
Thanks!
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I've only read one study that looks at ACT for insomnia: https://www.karger.com/Article/Abstract/365173
I've used mostly CBT-I for sleep, but I imagine the mindfulness component of ACT would work quite well as would cognitive defusion for people who are kept up by thoughts... the only thing is that sleep hygiene and behavioral changes aren't inherent in the model but you could probably blend the behavioral components of CBT-I and ACT for sleep... would be an interesting interventions.
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Hi! Melatonine is indicated in Europe for sleep disorders in patients > 65 years old .
The secretion of melatonin is regulated by light. Apparently, the following mechanism is observed: absence of light => increase of NE => action on beta1 and alpa-adrenergic receptors of the pineal gland = > activation of N-acetyltransferase => synthesis and release of melatonin (Touitou Y., 2005).
My question is this: When we give the patient melatonin tablets (or a melatonin agonist as the agomelatine), should we be concerned about a potential inhibitory feedback on endogenous melatonin secretion (as is the case for corticosteroids and inhibition of the hyphalamic-pituitary axis): Do we have info about the regulation of this key enzyme, the N-acetyltransferase, by melatonine ? Do cells of pineal gland express melatonin receptors ?
Thank you in advance for your reply :) !
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No, there is no classical negative feedback at all. However, exogenous melatonin might advance or delay the endogenous pineal melatonin production accordingly to the intake time. See work by Alfred Lewy defining dim light melatonin onset and melatonin phase response curve. Alternatively, please, read our review recently published in Endocrine Review.
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Dear fellow researchers,
for a study focusing on sleep disorders, we aimed to recruite a healthy sample via social media to serve as control group for a sample of patients with sleep disorders.
However, the prevalence of self-reported sleep disorders was exceptionally high in this self-selected "healthy" control Group (>60%). We hypothesize that subjects who experience sleeping disorders might have been more likely to be interested in a study focusing on sleeping disorders comapred to the general population, thereby inducing a systematic sampling bias.
Are there any studies which have systematically focused on this question?
Many thanks and kind regards, Simone
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Hello Simone,
your question is great. I came across one study recently reporting that only 4.3 percent of people in developed countries, regardless of age, reported no health problems. The likelihood of having any disease increased with age: 64 percent of children under age 5 had a health problem and almost 100 percent of elderly adults.
Sleep and wakefulness states are interrelated, and disorders of wakefulness expect to be manifested in disorders of sleep and vice versa. I cannot recall any study that estimated any sleep problem prevalence higher than 35 percent, across ages. This raises a question how readily people disclose problems with sleep, and whether or not long- term Sleep difficulties impact perception and ability to recognize sleep problems.
Best wishes with your study,
Tatyana
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I noticed that most study on sleep (including sleep deprivation and rebound) use a photoperiod of LD 12:12. In this way, for sleep deprivation, they usually choose to deprive 6, 12, 24h. Is that like a convention we should follow?
For me I want to raise them under different photoperiod, like longday and shortday photoperiod (e.g. LD 11:13, 15:9..). I am not sure whether it is OK. Thanks for your kind and useful answer!
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If you systematically change the photoperiod from 12:12 to another photoperiod in certain small increments that can be a useful way to ascertain the impacts of gradual shifts in the day length. Just because certain photoperiods (e.g., 6:18, 24:0, etc.) have been used should not limit you from looking at others. Having said that, you may find it beneficial to include at least one photoperiod that has been included in other studies for comparison purposes. But ultimately, it depends upon your specific hypothesis you want to test.
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I am working on modeling the relationship of the above mentioned variables with Psychological Well-being. I need references and any concrete arguments. How can i model the relationship of these variables with Psychological well-being?
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I am researching the feelings that drivers have experienced in the face of events they encounter while driving. I use heart rate for this work. Is it possible to detect irritability, stress, excitement, sleepiness by heart rate, or should I also take another signal? Do these heart rates have upper and lower limits for these feelings? Could you help me with the subject?
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its not possibile with heart rate. but IBI data can do your work
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Does it matter lowest concentration of oxygen in the air we breathe indoors in big cities and that people in the countryside are often outdoors.
Does altitude affect the progression of Multiple Sclerosis, or the frequency relapses for patients with relapsing-remitting MS? - ResearchGate. Available from: https://www.researchgate.net/post/Does_altitude_affect_the_progression_of_Multiple_Sclerosis_or_the_frequency_relapses_for_patients_with_relapsing-remitting_MS [accessed Feb 2, 2016].
Tatyana Mollayeva · 32.58 · 55.43 · University of Toronto  said:
Hello, The acute lesions in MS consist of predominately T-lymphocytes and macrophages which infiltrate white matter tissue. At these cites of inflammation, while the blood-brain barrier is disturbed, the vessel wall itself is still preserved.  Wolff  in his article “Cerebral blood flow and oxygen delivery at high altitude”, High Alt Med Biol. 2000;1(1):33-8)  discusses that  at the high altitudes the rise in cerebral blood flow is sufficient that oxygen delivery to brain remains constant as arterial oxygen falls. However, if we consider that in patients with MS the blood-brain barrier has been compromised, it makes sense that the oxyhemoglobin desaturation at the high altitude (even intermittent) may promote inflammation and myelin damage, which may manifest as a clinical relapse.  Another potential link may exist between sleep disordered breathing, frequently occurring at high altitude, and which associates with systemic vascular dysfunction, and relapse in MS.  A very relevant to the discussion work has been recently published:
Palomares JA, Tummala S, Wang DJ. Et al. Water exchange across the blood-brain barrier in obstructive sleep apnea: An MRI diffusion-weighted pseudo-continuous arterial spin labeling study. J Neuroimaging. 2015;25(6):900-5.
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As someone who specializes in Multiple Sclerosis, the answer is that there is no difference in the prevalance of MS between big cities and the country side. If there is any, it is due to the lack of facilities and specialists in the country side. Thanks.
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I'm trying to figure out how these two methods could potentially be combined together.
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John, thank you very much. These are all great articles. Lots of food for thought. Much appreciated!
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My row data has 2000 observations.
Sleeping hours fluctuate from 1h (min) and 15h(max) so I want to categorize them into categories, but I don’t know what is important to consider, taking into account min. and max. values are really extreme. I was thinking in two possibilities first (<6h, 6-8h and >8h) and second (<6h, 6-7h, 7-8h, 8-9h, >9h), but do I need to think about frequency? Does categories have to be homogeneous? I am using SAS.
N=2000
Sleeping hours mean=7h
Skewness=0.0638
Thanks
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Assume you enjoy the statistical approach: why not putting the data into quartiles, pentiles or more detailed into10 classes.
On the other hand your physiological/pathophysiological suggestion of <6h meets insomniacs and the elderly. 6-8 h meets normals and >8h youngsters,  depressives and hypersomniacs. I would prefer your second proposal with 5 classes - somehow a compromise between statistics and biology. SAS will do everything.
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I would like to examine the role of emotions regulation strategies for the context of stigma through subjective disease repressions and quality of life in patients with narcolepsy and cataplexy. For this purpose, I would like to use the questionnaire inventories to collect the subjectively perceived stigma caused by the disease narcolepsy and cataplexy.
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Turismo y Ocio.
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measure eeg and emg for atheletes
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You can have simulation models or real time data acquisition from any sports men working on treadmills and cycling.
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Some define "short sleepers " whom sleep 6 h and less per night and others use duration less than 7h of sleep. Long sleepers are defined as sleeping 9h and more in most epidemiology studies. At the same time National Sleep Foundation recommended sleep duration is 7-9h.
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Here are references of a few studies which may help you to define short and long sleepers for an epidemiologic study. They all show that sleep duration critically depends on factors like age, gender, economic situation, health status, and others.
Good luck,
Hartmut
Kripke DF, et al. Sleep complaints of postmonopausal women. Clin J Women's health 2001; 1:244-252.
Monk TH, et al. A sleep diry and questionnaire study of naturally short sleep. J Sleep Res 2001; 10:173-179.
Basner M; Fomberstein KM; Razavi FM; Banks S; William JH; Rosa RR; Dinges DF. American time use survey: sleep time and its rela­tionship to waking activities. SLEEP 2007;30(9):1085-1095.
Putilov AA (2013) Patterns of Association of Health Problems with Sleep-Wake Timing and Duration. J Sleep Disor: Treat Care 2013, 2:4 (doi:http://dx.doi.org/10.4172/2325-9639.1000120)
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I am designing an automatic diagnosis system for detecting some brain diseases like Epilepsy,Alzheimer's and sleep disorders like Insomnia,Narcolepsy. But the problem is the features I have extracted are giving values in the same range for two diseases. So individually if I detect a single disease for my test EEG signal then it is showing positive for two disease. How can we solve this problem. Can we design a single system for all diseases rather than one system for each diseas.
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Although probably not what you looking for, simple physiological variables might add clarity such as age, EMG, HRV, BMI, reaction time, ...  I think the approach of looking for a number of diseases and trying to access their probabilities and distinguish from healthy controls may prove fruitful. Also the diseases that you mention have co-morbidities.  The  disease descriptions are inherently symptomatic and not based upon brain/body structure (just because we do not have the diagnostic ability to do so).  The results that you are getting may be accurate.  It is just that the diseases overlap.  Ultimately, this is a combine sensor and big data problem.
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Hi. everyone.
I am going to start a project for immune changes by short sleep in human.
However, I have a question. How long it takes for your body to adapt to acute sleep deficiency? Do you know a paper about this?
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Hi Jong-Suk, I am not sure, that I understand exactly what you mean. There is no "adaptation" to acute sleep deficiency. There is simply a sleep deprivation, and as a consequence the homeostatic sleep drive increase. "Adaptation" would imply, that the body would not need anymore sleep. This is however not the case, it is still a eprivation which has an impact on many other functions.
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Dear Prof. Brand
Is it possible me and Mrs Keshavarsi participate in sleep in child psychiatric disorders project?
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Dear Prof. Brand
Thanks; for sleep project?
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Here is a question for those who work in the intersections between the arts and the sciences.
As someone who exhibits symptoms of and who has done blood work that shows the FASPS condition in my genes, I am wondering what the connection with creativity is--if any.  I am also artistic.  I write and do visual art.
Much work on this condition has been done by the neurobiologist Louis Ptacek.
Nature Magazine defines FASPS ("light lark" sleepers) as being subject to circadian rhythms.
       "Biological circadian clocks oscillate with an approximately 24-hour period, are ubiquitous, and presumably confer a selective advantage by anticipating the transitions between day and night. The circadian rhythms of sleep, melatonin secretion and body core temperature are thought to be generated by the suprachiasmatic nucleus of the hypothalamus, the anatomic locus of the mammalian circadian clock. Autosomal semi-dominant mutations in rodents with fast or slow biological clocks (that is, short or long endogenous period lengths; tau) are associated with phase-advanced or delayed sleep−wake rhythms, respectively. These models predict the existence of familial human circadian rhythm variants but none of the human circadian rhythm disorders are known to have a familial tendency. Although a slight 'morning lark' tendency is common, individuals with a large and disabling sleep phase-advance are rare. This disorder, advanced sleep-phase syndrome, is characterized by very early sleep onset and offset; only two cases are reported in young adults. Here we describe three kindreds with a profound phase advance of the sleep−wake, melatonin and temperature rhythms associated with a very short tau. The trait segregates as an autosomal dominant with high penetrance. These kindreds represent a well-characterized familial circadian rhythm variant in humans and provide a unique opportunity for genetic analysis of human circadian physiology."
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Article on Circadian pattern - may shed some light as to timing of energy levels.
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Dose amylase can be used as a indicator to assessment sleep quality?
I am analyzing some data collected from a sleep study. one of the indices is salivary amylase. i found some papers said consecration of salivary amylase related to sympathetic nerve activity. and consecration of salivary amylase is quite level in daytime but decline during sleep period. so i think if the value of salivary amylase is low before sleep and high after wake up in situation A, but no not changed in situation B. can i explain this result as: situation A provide people a better waking up than situation B?  
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thank you very much.
 the study is conducted in two rooms, one was constructed by natural material and another one was constructed by plastic.  we measured  salivary amylase before and after sleep in the two rooms respectively. no significant difference was found between the two rooms either before or after sleeping. and no significant difference was found between before and after sleeping in plastic room. but in natural material room,salivary amylase increased after sleep compared before sleep. because of the material that used for the two rooms were different. many factors must related. however, first of all, i simply want to know dose the increasing of salivary amylase in natural material room mean better sleep quality or worse compared to that in plastic room . 
sincerely
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Issues of diversity, view points according to age, race pertaining to narcolepsy with cataplexy
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Please, study some manuscripts in the Attachment. There are elementary answers in the articles.
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what treatment options are there for narcolepsy ? please attach references to articles.
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There are many studies on sleep microstructure and neurological disorders compared to psychiatric disorders in which disturbances of sleep are very common symptoms.
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Are you exploring M.E/ CFS and FMS?
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Seeking to investigate whether it is better to train with the 'lights on' in the early morning (05:30 ish) as opposed to a low light environment. Does training with light increase neural firing, strength, alertness...etc
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Hi,
It is an inter. topic. I think you will not be able to generalise it, because every person has its "own circadian rhythm" (inner day-night clock, early bird ...) which is entrainable very differently. Probably you should ask some specialists in the field of chronobiology.
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Hello all. I see that you are proposing to measure HRV before, during and after sleep. What is the reasoning behind that? Does it comes from your own data or do you have some reference paper that support this hypothesis?
Many Thanks,
Patrick
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Dear Tatiyana,
Many thanks for your insights and link to papers. I refer to the paper: Neuropattern: A new translational tool to detect and treat stress pathology I. Strategical consideration, where he authors explicitly state (p.484), "The standardized protocol contains a baseline measure under calm sitting conditions directly before bedtime, an over- night measure, and a final measure immediately after awakening, again under calm sitting conditions. The HRV measure after awakening is considered a response measure, as compared to the evening measure. Variability of inter-beat intervals is analyzed to estimate sympathetic and parasympathetic activities. HRV data were scaled on 1860 healthy subjects and corrected for effects of sex, age, and body mass index. Values in the lower and upper quartiles, as well as deviations of 20 percentiles between evening and morning measures are included for analysis."
So my question was precisely addressing this protocol (in Italic above): Why doing measures before and after sleep, and not only during sleep?
Many thanks for discussing this very interesting point.
Patrick
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Hello,
I would like to ask if do you think that changes in sleep spindle activity might be followed by cognitive disturbances in general? 
I know that increased spindle activity is connected with improvements in procedural and declarative memory, that occurrence of sleep spindles might be an outcome marker for patients in coma or following traumatic brain injuries. Nevertheless, I was thinking if is it reasonable to associate sleep spindles activity with cognitive performance in general.
Could you tell me if do  you think that sleep spindles might influence cognitive performance apart from memory consolidation, please?
I really appreciate any help you can provide.
Kind regards,
Adriana
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Dear Adriana! There are various and sometimes conflicting opinions on the subject. Please read manuscripts in the annex to my letter.
Vladimir
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We're currently designing a study on the use of technology in treating insomnia. As a part of this we've planned to use wearable technology (e.g., a fitbit) to track sleep patterns. We're looking for a good way to gather the sleep data in a timely manner that doesn't involve hand-entering everything. If we could find an app or method to securely transmit the sleep data on a weekly basis that would be amazing. We'd welcome any help or leads.
Thanks!!
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Evenson, K. R., Goto, M. M., & Furberg, R. D. (2015). Systematic review of the validity and reliability of consumer-wearable activity trackers. The International Journal of Behavioral Nutrition and Physical Activity, 12, 159. https://doi.org/10.1186/s12966-015-0314-1
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Hi, I'm interested in Dream research, Specially working on Lucid Dreams. But there is a problem. I Have no Idea where Can I get or produce dream research data. 
Any help will be appreciated. 
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DreamBank is a great choice.
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With references, if possible, please.
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Thank you very much, Dr. Kulchtsky
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Could you tell me if light stimulation might be an adequate treatment for sleep-related disorders?
For instance blue light influences melatonin production, what might be helpful to re-entrain the circadian rhythm. Do you know about some light treatment that is nowadays used clinically?
I will be most grateful if someone could give me some information!
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Dear Ta-wei Guu,
thank you for your answer! Do you think that light theraphy might be beneficial for people, who suffer from chronic fatigue syndrome, as well? Is it reasonable to apply a light therapy, just as a support to, for instance Cognitive Behavioral Therapy?
Kind regards
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I'm trying to figure out the most affordable but reliable set-up to do intracranial EEG recordings to examine sleep in fish, etc. If anyone can recommend amplifier brands/models, software, etc. that would be great! Are there amplifiers that talk directly to a computer to save the data on hard drive or is an interface between amplifier and computer always necessary? This is a new area for me and I don't want to buy equipment I don't need. Thanks!
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Dear Theresa, 
if you want to try telemetry you could contact Cara Hildreth at Macquarie, and or our representative Parimal Kacha at ADI Instrument reselling telemetry in Australia. Best Regards
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I am interested in the progression of events that link histamine producing foods to poor gut health, leaky gut, under methylation, pyroleia, sleep disorders, tinnitus and the skin itching. Then how a person can crave the very foods that are bad for them and appear to need less sleep eventually leading to mental health issues.....
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Thanks Bill, am interested in natural management of histamine excess not medication. In my experience all medication masks symptoms while creating a raft of new issues. 
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Structure function of sleep
Deleted research item The research item mentioned here has been deleted
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 Kindly find the attached article, for a detailed explanation regarding the first question. 
A good article for the second question can be found through this link : http://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-11-79
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I was reading about delayed sleep phase syndrome (DSPS), an disorder where the body's perception of time is dilated so that patient's circadian clock has a period longer than 24hrs. So I am wondering whether this change in time perception would have an effect on the rate of aging?
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Hi, Delayed sleep phase syndrome (DSPS) is characterised by sleep onset and wake time that are regular but delayed relative to the conventional sleep-wake time.  Disorder, in which a circadian pacemaker has no phase in relation to the 24 hour light-dark cycle, is free-running disorder (FRD). The FRD occurs most frequently in blind people. Irregular sleep-wake rhythm disorder (ISWR) does not have well defined sleep-wake cycle, and this disorder is often seen in age-related disorders (i.e., dementia, Alzheimer's).  Each of these disorders (DSPS, FRD, ISWR) are characterised by abnormal distribution of sleep and wake periods. Recent theories of the function of sleep state that there is a cellular need for sleep, triggered by changes accumulated during wakefulness. In the case of dysregulated sleep and wakefulness process, pathological changes at the cellular level are expected. Kind regards.
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I want to measure Effect of sleep deprivation on Mood ...
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The gold standard would be to conduct an in lab PSG-polysomnography or a level II/III device in the person's home.Failing that wrist actigraphy would be the next best option. This would allow you to have a validated objective measure of sleep. When looking at mood relating to sleep deprivation I would also consider assessing chronotype. You may also want to look at existing sleep disorders using the Insomnia Severity Index, Berlin and the Epworth Sleepiness Scale as suggested by Maria. The Profile of Moods Questionnaire is sometimes used in these type of studies http://www.brianmac.co.uk/poms.htm
Cheers Ian D
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Is there any evidence that intermittent photic stimulation can induce sleepiness?
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Thank you André.
I actually meant in humans :)
However, this review is really interesting, with a lot of answers and even more questions to be further investigated!
Best
Dario
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My special interest is to evaluate sleep quality in patients with chronic pain.
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Brain perfusion, as referred in this article, includes delivery of nutrients and removal of wastes, besides the usual non-stop gas transfer. From my observations on REM sleep (or the deprivation of REM sleep to be exact) and taichi (the extra slow moving type which can trick the brain that he/she is not moving to simulate REM sleep), I could only say that brain perfusion happens probably not more than 30 minutes for a 7-hour good sleep. For city folks who are under constant stress, they will get less because they would have less REM sleep. During day time, the situation gets worse if they don’t do enough short walks or equivalent exercises (Note: endurance exercises are not counted at all). I believe that many chronic diseases including Alzheimer’s, HIV, cancers, etc. would be difficult to heal once the patients become immobile and/or cannot sleep well. Their brain cells would deteriorate slowly due to malnutrition and waste accumulation. Downstream organs will also be affected slowly one by one.
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For starters, neurons require an almost non-stop supply of glucose (the brain's main source of energy) or they will stop functioning efficiently or die, as they have very limited internal stores of glycogen. This is supplied via the blood, which constantly delivers glucose to the brain - if the blood contains too little glucose (such as during hypoglycemia in diabetics using insulin), symptoms like confusion and hypoglycemia start to appear very soon. This alone is a decent indicator that 'perfusion' as you define it happens constantly and not just thirty minutes per sleep cycle.
You can also map glucose consumption using FDG-PET: 18F-FDG is injected into the bloodstream, gets transferred into cells in the brain, and gets phosphorylated just like normal glucose would during metabolism. Again, the fact that this radioactive isotope passes the blood-brain barrier constantly suggests that nutrient delivery is a continuous process, and the fact that it gets phosphorylated suggests that there is metabolism going on.
Furthermore, your definition of 'perfusion' is incorrect, as perfusion simply refers to the delivery of blood to an organ. 
Finally, I'd be interested to see some proof that nutrient delivery and waste removal does *not* happen continuously, because this is the first time I've heard of it. From where did you get this 30 minute number? Increased heart rate does not necessarily imply increased brain perfusion, by the way, as cerebral blood vessels may constrict. I would suggest having a look at the literature on these subjects. I do agree that regular excercise and moving away from your desk every now and then will do your brain a lot of good, though!
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Does anyone know how to interpret the scores in the Fletcher and Luckett questionnaire, related to sleep disorders? Thank you
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Hi Maria,
The Fletcher and Luckett’s sleep questionnaire consists of  25 items, 4-point Likert scale (0=never,1=rarely, 2=occasionally,3=often). Scoring is simple: summary score, divided by 25 to determine the total burden/level of symptoms. Interpretation is also simple: higher scores indicate higher burden/level of sleep disturbance.
Kind regards,
Tatyana
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Sleep is temporary physiological state of unconsciousness from which the person can be aroused ( awaken ) by sensory stimuli .
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It cannot be answered in a one-liner as there are over 90 types of sleep disorders. People have to be evaluated by sleep specialists. For example, age, sex, when it started, did anything triggered?, duration of the illness, medication history, family history, lifestyle factors, associated medical or mental health-related issues, bmi, knowledge obtained from parents or bedpartner with regards to the health condition, etc. It needs to be differentially diagnosed to exclude other potentially overlapping disorder, which might contribute to the current condition. I hope you understand the complexities!
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There is a facebook group with almost 1500 people on it who have delayed sleep phase syndrome, and I've been told that most of them have no idea where to go for effective treatment.  I think many to most of these people have had sleep medicine doctors, but nothing they've suggested has helped.  Does anyone know of some experts with effective clinical treatment in this area where these patients are not being referred?  Thanks!
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I suffered long sleep latency and/or insomnia. I found that I had an abnormal erythrocyte transketolase indicating thiamine deficiency. High triglycerides and inflammatory markers also suggested sugar ingestion. I stopped sugar in all its forms and it took six months to get the lab indications back to normal. This did not completely solve the problem but I found that biofeedback did and I can now sleep normally with no assistance.
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Up until now non-restorative sleep (NRS) has been one of the cardinal symptoms of insomnia. However, it has come to my knowledge that in the new editions of ICSD and DSM-V this criteria has been exluded from diagnosis. Unfortunately have I missed the discusson that led to this. Do anyone know any studies discussing the symptom NRS in relation to insomnia diagnostic criteria?
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Thank you Robert. It was a very interesting article on the subject.
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Sleeping aids should only be used for a short-term treatment when other measures have failed, but there are not many protocols for the management of patients who have already been taking sleeping aids for months or years.
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I have found that two groups shake out in this process.
The gotta have a med group and the alt therapy group.  the CBT treatment is very helpful for the alt therapy group and if the dosing is only for HS then the CBT and wait it out will work.
The other grouping however will not be able to follow this plan as they are med dependent.  For this group using a sedating non-benzo to replace the benzo will usually work. If they were on the benzo for anxiety then they will likely need the new med to assist them with those symptoms.  For this group I have found sedating muscle relaxants useful for the non anxiety group and for the others adding hydroxizine will usually get them through.  These folks MUST want to stop the benzo however, if its not what they WANT to do then best of luck.  Nothing is likely to work.
This is not much different from the methods used for opiate taper and the anxiety that usually with it.
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Has someone similar or contradictory results ? I would be curious to discuss.
as my circuit-based findings show that LHb and LPO reciprocally inhibit each other. While LPO possibly activates RMTg. LHb might reciprocally inhibit also orexinergic lateral hypothalamus (LH).
in :
SWS promoting MHb-IPN-MRN circuit opposes
the theta promoting circuit, active wake and REM sleep.
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I just read that PPT stimulates STN during REM sleep (Fernández-Mendoza et al., 2009) enhancing the fast (15–35 Hz) subthalamic oscillatory activity. So is possible that the firing of REM-on subthalamic neurons then activates SNr and GPi, what causes activation of LHb in REM sleep. This REM (and preREM, shortly before REM) sleep stimulation of LHb helps to suppress dopamine and serotonin release during REM, so prevents switching into waking and SWS state, respectively. Prolonged LHb activation might finally lead to suppression of SUM and theta oscillations in the brain, as LHb projects to SUM, which I predict is suppressed by LHb. In addition the SNr inhibits PPT, although is not clear of just the wake-on PPT neurons (those PPT neurons stimulate VTA) or also the REM-on neurons of PPT.
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Is there any effect on the airway and development of obstructive sleep apnoea after surgically setting the mandible back with a bilateral sagittal split osteotomy? Is there any evidence?
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Thank you Dr. Kulchitsky. I will read the articles you have sent.
I feel the CBCT gives the volumeric actual size of the airway other than the 2 dimensions of the lateral ceph. So calculations could be more accurate. What do you think?
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After upgrading our computers in performance and operating system we are not able to use a provided software to score sleep stages in humans anymore. So we need a new software based on Windows 7.  If possible the software should provide to store the data in .txt-files or any other MS Office-readable files. Furthermore, it would be great if these files contain 2 distinct marks concerning scored sleep stage and arousals/movement times for each epoch.
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Sorry for the late reply. But thanks for your recommendations :-)
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Could you please suggest a short scale for screening sleep disorders?
We want to screen university students for sleep disorders before studying the relationship between their health-related quality of life and the quality of their sleep.
I would appreciate every suggestion!
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In our sleeping lab at Charité Medical University of Berlin we use the Pittsburgh sleep quality index (PSQI) for the assessment of the quality of sleep. A further interview and disorder-specific questionnaires (Restless Legs Syndrom - Diagnostic Index (RLS-DI), International RLS Severity Scale (IRLS), Epworth Sleepiness Scale (ESS), Insomnia Severity Index) would be necessary to assess the prevalence and the severity of disorders among participants. 
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In adult sleep surgery, the spectrum of treatment options tend to stop at the bridge between the tongue base and supraglottis, the hyoid. It is my experience that the angle and firm integrity of the epiglottis as well as the malcic qualities of the aryepiglottic folds contribute significantly to the airway obtruction in these patients.
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Please forgive this long delay in responding:
Dr. Blakey first: I don't have an Asthma Clinic. I am an Otolaryngology subspecialist in Laryngology Bronchoesophagology (LBE).  I see a lot of major airway disease much of it surgical. The malacic larynx and pharynx can complicate the OSA patient's care since they can have disease that doesn't present with typical features. For example, they can have very low BMI's. You look into their mouths and they have short taught pallets. I'm not sure how they would look like asthmatics, though. This is inhalation and usually only manifest disease when asleep or sedated. 
Dr. Denbar: The issue is that no matter how high the driving CPAP pressure is some tissues cannot be distended in these patients. For example, the retrodisplaced epiglottis can actually be forced closed by the airflow. These patients may be helped a little but are so uncomfortable with these 15 or 18 cm pressures that they either don't ever get their machines or stop using them quickly. If they have this distal disease treated surgically, they commonly either have the principle issue treated or at least the resistant part of their disease, qualifying for a much lower (and tolerable) pressure. 
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Hi, Ranjan Piyush asked this question some time ago. Now, I'm asking tha same thing again.
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Thank you!
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Multiple sleep latency tests report SOREM, and sleep latency. I kindly inquire information on the latter. Specifically, I am interested how sleep latencies in multiple tests are distributed, and whether the distribution shows an exponential tail or a "fat" tail at large latencies.
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I have checked the data. There were 25 individuals without truncated MSLT events among 96 individuals recorded . Not very much but perhaps enough to give a rough picture? I have now sent the results of these 25 subjects for your consideration as an excel table to you by e-mail. (Found your e-mail address in Max Planck Institute for the Physics of complex Systems' web pages).
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In schizophrenia studies, dysfunction in thalamocortical dysfunction is proposed to be evident in aberrant sleep spindles and ERP measures of corollary discharge mechanism. Are there other similar measures linking sleep and ERP measures.
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In my PhD study I tried to find a correlation between the sleep spindle density measure with the N100-P200 ERP complex suppression during a 'corollary discharge' task. But the preliminary findings did not find any significant correlation.
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Epidemiological studies have reported relationship between short sleep duration and obesity. However, most of them have evaluated the sleep duration through the question How many hours do you usually sleep in a week day?.
can we  assume a chronic exposure to short sleep?
could we evaluate the time to exposure in a general question?
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 Thank you very much for yours answers...i am going to keep thinking about!
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The benzodiazepines and zolpidem are fine if used as a p.r.n., but I find most patients at some point end up having weeks or months require p.r.n.'s, after which they are dependent on these drugs.
Alternative, all off label, include trazadone, gabapentin, mirtazapine, quetiapine...and most recently Lyrica...
What evidence is there for ANY of the above and, since it is "new kid on the block," Lyrica???
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Dear Lewis,
It is very important clinical question. In my daily work i suggest to psychiatrists and GPs to introduce Lyrica, especially in patients with polypharmacy and addiction to benzodiazepines. I will put my opinion:
+ for LYRICA
- no need for benzodiazepines and antipsychotics (quetiapine is used often for this purpose in Europe)
- no extra drug-drug interactions (Lyrica has this positive effect)
- no problem with liver injuries and enzymes inductions (especially appropriate in patients with long term addiction)
- mild effect (SMD=0,5-0,6) for general anxiety disorder, which is usually present in psychiatric patients
- pain comorbidity and diabetes and seizures
- no fast up and down regulation of  receptors (mechanism of action), which is seen after the tolerance is established in patients treated on quetiapine
- no metabolic ADE, which is usually seen in H1 blockers (e. g. mirtazapine, quetipine)
- different mechanism of action (no GABA action (few), no H1 action)
- for LYRICA
- relative few data on positive effect (however there are few drugs which have positive effects on sleeping but are used often, e. g. quetiepine).
- high sedative effect, which is dose dependent usually
- bad adherence on drug (many capsules per day)
- kidney failure and dosage adjustment
- problem in switching in bipolar disorder (especially mania, which is less often seen in Neurontin)
- expensive drug
If I sum up Lyrica can reduce polypharmacy, because the number of drugs can be reduced by adding Lyrica, because drug has multiple indications. As clinical pharmacist specialist from psychiatry I often suggest Lyrica.
Regards,
Matej
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I can't support this with any direct citations, but I'm beginning to wonder if type 2 Narcolepsy may have an entirely different etiology than type 1. For example, we don't typically see in type 2 N the wholesale destruction of orexin neurons like we do in type 1. So obviously a substantial population of orexin neurons are there, but something is seems to be blocking or countering orexinergic transmission. Although the presentation of symptoms appears similar with the major difference being the presence of cataplexy in type 1 N, anecdotal evidence derived from sustained conversation with narcoleptics reveals that persons with type 2 N often don't experience the full cluster of symptoms classically associated with N, with many experiencing only EDS.
The question I'm most curious about is whether or not the actions of dynorphin, neurotensin, NARP. VGLUT2 and DLK-1 (did I miss any?) all of which are co-localized on orexin neurons, are also affected in type 2 (obviously in type 1 where the neuron is gone, they are no longer expressed).  Perhaps in type 2 N some other process such as GABAergic inhibition of orexin transmission is the culprit and not the autoimmune reaction presumed to result in the cluster of symptoms called type 1 N?  In which case everything else should be working?
Do you know of any research that has compared the difference in TOTAL neuroprotein etc. expression between type 1, type 2 and healthy controls to determine what the effect is of the loss of all of those neurochemicals? 
For example, there was an article in the press today showing that Ox modulates HT-5's regulation of respiration.  In type 1 N the dysmodulation should be more apparent than it is in type 2 N.  Is it?  That kind of thing.
I would think this avenue of inquiry is especially important  for those working on Ox receptor agonists.  For folks with type 1 N, would that be enough?  The neurons are gone so those other things still aren't going to be produced.  Does that matter?
ANy light anyone can shed on this would be appreciated.
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Thanks, Roger, I haven't seen that yet but I'll go look for it.
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some patients with OSA may have other co-morbid diseases including congestive heart failure or chronic renal failure, do these diseases with associated dyspnoea and difficulty in breathing frequent carousals and paroxysmal nocturnal dyspnoea (PND) alter the reading of the test, i.e. control of these conditions before PSG may give a different or better result
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The conditions you have mentioned are influent in the result of PSG in two ways: Central apnea and variation of respiratory control ( see respiratory frive, loop gain ). The influence isn't about the difficult in breathing but in the control of ventilatory drive
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I mean are there any effects on sleep in patients with Alzheimers with melatonin?
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See these two recent reviews:
Sleep and Alzheimer's disease.
Peter-Derex L, Yammine P, Bastuji H, Croisile B.
Sleep Med Rev. 2015 Feb;19:29-38. doi: 10.1016/j.smrv.2014.03.007.
Pharmacotherapies for sleep disturbances in Alzheimer's disease.
McCleery J, Cohen DA, Sharpley AL.
Cochrane Database Syst Rev. 2014 Mar 21;3:CD009178. doi: 10.1002/14651858.CD009178.pub2.
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Actually so many studies on partial and complete deprivation, which making confusion to know the real concept behind this.  
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CORRECTION: Upon further review, I was mistaken in my earlier post! Michael Bonnet defines Partial Sleep Deprivation as "nonsleep stage-specific reduction in total sleep" ("Sleep Deprivation" in Principles and practice of sleep medicine; p. 61). Thus in her post above, Tatyana was correct that the sleep deprivation I referred to is called Selective Sleep Deprivation.
My apologies for my error :(
Best regards, Glenn.
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I want to know,  is there any standard protocol to classify  sleep deprivation, as mention above ?
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I don't think that there is a validated scale for sleep deprivation.  I have suggested a method for estimating the pre-accident level of sleep deprivation in chapter 8 of my ebook, Anatomy of A Fatigue-Related Accident (https://www.smashwords.com/books/search?query=anatomy+fatigue).  It is:
"A simplistic method for calculating cumulative sleep debt follows. Work backward in 24-hour segments from the time of the incident to the last time that the individual was fully “caught up” on their sleep. For example, they were caught up because they had slept at least eight hours per night for a week or so. Alternatively, work backward as far into the past as possible. For each 24-hour period, estimate the hours of sleep acquired. Subtract each estimate from eight hours (or, substitute another, known minimum sleep time for an individual, such as seven-and-a-half hours). When the person acquired too few hours of sleep, the difference will be positive. When they have acquired “recovery” sleep, the person will have slept more than eight hours and the difference will be negative. If the difference is negative, multiply it by two because we make up sleep faster than we lose it. Add all of the positive and negative values together to get the cumulative sleep debt.”
An example follows in the ebook.  A version of this method can also be used on a day-to-day and week-by week basis by a worker.  I suggested doing this in my "21 Tips" book (http://21bookseries.com/store/products/21-tips-for-beating-fatigue-and-improving-your-health-happiness-and-safety/).  It is:
"Estimating your sleep debt is pretty easy. Record the total number of hours that you sleep each day during a vacation. This includes the major nighttime sleep period plus any daytime naps. Most likely, you will experience “recovery sleep” during the first several days of the vacation. That is, you will be repaying the sleep debt that you carried into the beginning of the vacation.
Eventually, you will settle into a pattern of sleeping a relatively stable number of hours per 24 hours. The average of these relatively stable amounts is your natural sleep need. Then, when facing night work demands, keep track of how many hours less than this number you sleep per 24 hours. This difference is your sleep debt, and it adds up across days.
The rate at which you can repay this debt varies from person to person: you can repay it with recovery sleep at a ratio of about two to one to about four to one. That is, if you have a sleep debt of six hours, you may repay it adequately with one-and-a-half to three hours of extra sleep that is of good quality and occurs during the nighttime. By "extra," I mean in addition to your known sleep need."
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I am in the process of evaluating EEG/EMG data from mice to detect sleep stages. According to literature, the most systems used are Neuroscore and Sleepsign. Can anyone help to identify the best with pros and cons? Any feedback would be greatly appreciated. Thanks.
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Sleepsign is quite good.
Any automated scoring requires visual double check.
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Role of Opiod in treatment of sleep disorder.
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The sedative-hypnotic effect of opioids (e.g. morphine) in addition to analgesia, particularly as a pre- and/or postoperative medication may be viewed positively. However, varied as the sleep disorders are, opioids are never the mainstay drugs in their management. The sedative/hypnotic benzodiazepines and better still, the non benzodiazepines (that do not produce severe respiratory depression unless other agents also are ingested concurrently) are being used with considerable successes.  The antihistamine (diphenhydramine), the antidepressants and some miscellaneous agents are also in use with success in special circumstances. The role of opioids in treating and managing sleep disorders is therefore limited.
Collop MD, Nancy."The effect of obstructive sleep apnea on chronic medical disorder Cleveland Clinic Journal of Medicine. 2007 74:1.
Ivanenko A and Massey C (October 1, 2006). "Assessment and Management of Sleep Disorders in Children. Psychiatric Times 23 (11).
Voderholzer, Ulrich; Guilleminault, Christian (2012). "Sleep disorders". Neurobiology of Psychiatric Disorders. Handbook of Clinical Neurology 106. pp. 527–40
  
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Can treating OSA reduce insomnia burden?
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There are some interesting and encouraging answers above. I've seen and heard about OSA patients who simply had no normal sleep. They would obstruct, wake to breathe, start to go to sleep, obstruct, and so on through the night.
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We are planning to write a project with the objective to examine sleep-wake profile of the prisoners. I want to know if anyone can share his/her experience on similar or comparable studies on the prisoners?
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I have consulted on a project that has examined sleep in prisoners. Given the limitations in such a population, we used both retrospective (PSQI, PSQI-A, MAPI) and prospective (two-week sleep diary) tools. The prevalence of sleep disruption, as one might expect, is quite high (75%). Local conditions and access to prisoners will of course dictate much of what you can do and the ethics of doing a study on a vulnerable population must too take preeminence.
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I recently read a paper by Ford, DE and Kamerow, DB carrying out an epidemiological study into sleep disturbances and psychiatric disorders finding that a lot of individuals experiencing issues with mental health also had a degree of insomnia/hypersomnia (bad sleeping habits). However this study is from 1989 and I was curious if anyone has more up-to-date research with the same claims? Thank you. 
I have attached a link to the paper 
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Dear Alex, did you already try a literature search on this topic. There is sufficient evidence for the association between sleep disorders and psychiatric / mental disorders. Please find attached a list with recent publications. Kind regards
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May I request the members of this forum to kindly share any publications on sleep disorders in women. I am particularly interested in prevalence and correlates of Insomnia. There are many types of classified sleep disorders and some changes have been advised in nomenclature in ICSD-3 version issued in Feb 2014.
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Dear Aayam Gupta, an interesting question. In addition to the references mentioned above, you should look at the published outcome of the Somnia study of 14 000 UK households: Venn S, Meadows R, Arber S. (2013) 'Gender differences in approaches to self-management of poor sleep in later life'. Elsevier Social Science and Medicine, 79 (1), pp. 117-123. The paper is attached; You may see some related issues on my page too.Hope this helps. Best wishes