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
Dear Clinicians/Researchers working on sleep disorders,
We are working on the automated detection of sleep disorders using EEG. While we can get good accuracy with binary classifiers distinguishing normal subjects from any one particular sleep disorder, the obtained accuracy is very low, when we attempt multiclass classifiers, where the classifier is expected to identify a specific sleep disorder from the following list: insomnia, narcolepsy, REM behavior disorder, bruxism, nocturnal frontal lobe epilepsy, periodic leg movement syndrome, and sleep-disordered breathing. I would like to know from the clinicians (i) what features they look for in identifying the above disorders (differential diagnosis) (ii) is EEG a meaningful signal to use for this purpose. if not, what other signals could be used? (iii) how is a clinical diagnosis performed?
I shall be very grateful for any useful input in this direction.
What is the relationship between sleep disturbance and emotional divorce?
What is the relationship between emotional divorce and violence for wives?
What is the relationship between eating disorder and violence for abused wives?
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!!!
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?
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?
Sleep study is mandatory for adult patients with sleep apnea. Is it the same for pediatric patient with sleep apnea?
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.
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?
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 )
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
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.
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,
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 email@example.com.
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.
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?
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 :) !
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
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!
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?
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?
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.
Sleeping hours mean=7h
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.
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.
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.
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?
Dear Prof. Brand
Is it possible me and Mrs Keshavarsi participate in sleep in child psychiatric disorders project?
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."
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?
There are many studies on sleep microstructure and neurological disorders compared to psychiatric disorders in which disturbances of sleep are very common symptoms.
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.
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
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?
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.
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.
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!
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!
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.....
Structure function of sleep
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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?
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.
Does anyone know how to interpret the scores in the Fletcher and Luckett questionnaire, related to sleep disorders? Thank you
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!
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?
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.
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).
SWS promoting MHb-IPN-MRN circuit opposes
the theta promoting circuit, active wake and REM sleep.
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.
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!
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.
Hi, Ranjan Piyush asked this question some time ago. Now, I'm asking tha same thing again.
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.
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.
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?
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???
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.
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
Actually so many studies on partial and complete deprivation, which making confusion to know the real concept behind this.
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.