Published Research - General Sleep and RLS (WED)

For everything and anything else not covered in the other RLS sections.
ViewsAskew
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Post by ViewsAskew »

Ann - Take what you need, leave the rest

Managing Your RLS

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ViewsAskew
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Post by ViewsAskew »

Holy Cow!!!!!

http://www.dailygalaxy.com/my_weblog/20 ... mutat.html

Thank goodness someone is making flies sleepless! They WILL resolve these problems, they WILL. These types of studies give me faith and make me almost giddy. Then again, I just had a thought that they might figure it out and find that to resolve it would be impossible or painful or harmful...OK I'm sobered again. Still hopeful, but everything is back in perspective

:wink:
Ann - Take what you need, leave the rest

Managing Your RLS

Opinions presented by Discussion Board Moderators are personal in nature and do not, in any way, represent the opinion of the RLS Foundation, and are not medical advice.

cornelia

Post by cornelia »

Thanks for posting this Ann. It's all so interesting and hopeful. And funny to read too.

Corrie

cornelia

Post by cornelia »

A 4th RLS gene has been found!


Nature Genetics
Published online: 27 July 2008 | doi:10.1038/ng.190


PTPRD (protein tyrosine phosphatase receptor type delta) is associated with restless legs syndrome
Barbara Schormair1,2,19, David Kemlink1,3,19, Darina Roeske4, Gertrud Eckstein1,3, Lan Xiong5, Peter Lichtner1,2, Stephan Ripke4, Claudia Trenkwalder6, Alexander Zimprich7, Karin Stiasny-Kolster8, Wolfgang Oertel8, Cornelius G Bachmann9, Walter Paulus9, Birgit Högl10, Birgit Frauscher10, Viola Gschliesser10, Werner Poewe10, Ines Peglau11, Pavel Vodicka12, Jana Vávrová3, Karel Sonka3, Sona Nevsimalova3, Jacques Montplaisir13,14, Gustavo Turecki15, Guy Rouleau5, Christian Gieger16, Thomas Illig16, H-Erich Wichmann16,17, Florian Holsboer4, Bertram Müller-Myhsok4, Thomas Meitinger1,2 & Juliane Winkelmann1,2,4,18


Top of pageWe identified association of restless legs syndrome (RLS) with PTPRD at 9p23–24 in 2,458 affected individuals and 4,749 controls from Germany, Austria, Czechia and Canada. Two independent SNPs in the 5' UTR of splice variants expressed predominantly in the central nervous system showed highly significant P values (rs4626664, Pnominal/ corrected = 5.91 10-10, odds ratio (OR) = 1.44; rs1975197, Pnominal/ corrected = 5.81 10-9, OR = 1.31). This work identifies PTPRD as the fourth genome-wide significant locus for RLS.

Corrie

ViewsAskew
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OK, it's not really research, but it's news about RLS and treatments.

http://www.revolutionhealth.com/blogs/s ... ps-r-15903

A device that helps restless legs?

Posted on 11:07AM (EDT) on 2008-09-12

Enhanced external counter pulsation (EECP) is used to treat angina (heart pain from inadequate circulation). This treatment involves a device that provides pressure to the legs in sort of a pumping fashion. For cardiac problems it enhances return of blood flow to the heart, which somehow improves small vessel blood flow to cardiac muscle. Over the years there have been a suggestion that this might help the symptoms of restless legs syndrome (RLS). It was noticed that some heart failure patients undergoing this treatment had improved RLS symptoms. In fact, a study in 2006 addressed the effect of EECP on RLS symptoms over the course of about one month. Taken as a group, the symptoms of RLS as measured by the International RLS rating scale significantly improved compared to before treatment. Some of the patients even had sustained improvement for 3 months. However, only 6 patients were studied.

Why would pressing on the legs help RLS? I don’t know, but there are several reasons to suspect that it might. First, many patients with RLS provide themselves a “counter-measure” to help the feeling. That is, many patients rub their legs or massage their legs, or even hit their legs when they are having RLS, and they find that it help. Also, walking (which always helps) increases blood return to the heart, because the contraction of the muscles squeezes the blood upwards. Also, some researchers think that patients with varicose veins are more likely to have RLS, and that treatment of varicose veins can help RLS.

RLS is a strange condition which can be triggered or caused by problems in several areas of the nervous system, including the brain, lower spine, and perhaps the nerves to the legs or the blood vessels of the legs. How these various areas are integrated to produce or relieve RLS is not yet clear, but it is not surprising that physical manipulation of some type in the legs might help.

Last thing: A news report this week talks about a company that has patented and is now funding research into their device for RLS. I don’t know what the device is, but I look forward to hearing more about it, and I’m sure that the many people who suffer from RLS do too. Maybe then, even RLS patients can enjoy their sleep.

J. Steven Poceta MD is a licensed practitioner of neurology and sleep disorders who has been engaged by Revolution Health. No information in this blog is intended to diagnose or treat any condition. The opinions expressed here are Dr. Poceta’s own and do not necessarily reflect those of Revolution Health.
Ann - Take what you need, leave the rest

Managing Your RLS

Opinions presented by Discussion Board Moderators are personal in nature and do not, in any way, represent the opinion of the RLS Foundation, and are not medical advice.

cornelia

Post by cornelia »

Yes, that sounded so promising once. But dr Walters later did a double blind study with no promising results.

Corrie

ViewsAskew
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Post by ViewsAskew »

I remember that, Corrie. But, this company is making some kind of device...interesting to see if it helps anyone or just takes money out of our pockets.
Ann - Take what you need, leave the rest

Managing Your RLS

Opinions presented by Discussion Board Moderators are personal in nature and do not, in any way, represent the opinion of the RLS Foundation, and are not medical advice.

ViewsAskew
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Post by ViewsAskew »

It's nice to see that they are still studying RLS in interesting ways:

http://radiologybull.blogspot.com/2008/ ... ology.html

The original post was on Ovid.com

Astrakas, L G. ; Konitsiotis, S ; Margariti, P ; Tsouli, S ; Tzarouhi, L ; Argyropoulou, M I.
T2 relaxometry and fMRI of the brain in late-onset restless legs syndrome
Neurology. 71(12):911-916, September 16, 2008.
Abstract
Objective: To assess in patients with late-onset idiopathic restless legs syndrome (RLS) the brain iron content with magnetic resonance relaxometry, and brain activation during dorsiflexion and plantar flexion of both feet, using fMRI.Methods: The study was approved by the institutional review board, and informed consent was obtained. Twenty-five RLS patients (14 women, 11 men; age range 55-82 years; mean 66.5 +/- 8.9 years; disease duration 6.5 +/- 4.5 years) and 12 sex- and age-matched controls were studied. A T1-weighted high-resolution three-dimensional spoiled gradient echo sequence was used for structural imaging, a multislice spin echo [TAU]2-weighted sequence was used for T2 relaxometry, and a single-shot multislice gradient echo planar sequence was used for fMRI. The motor paradigm consisted of alternating periods of rest and movement, each 40 seconds in duration. Region of interest analysis was used on the T2 relaxometry maps. Statistical parametric mapping software was used for analysis of the functional data.Results: T2 relaxation time was significantly higher in patients than in controls in the substantia nigra pars compacta. Within-group analysis showed that both patients and controls activated the primary motor cortex, the primary somatosensory cortex, the somatosensory association cortex, and the middle cerebellar peduncles. Patients also activated the thalamus, putamen, middle frontal gyrus, and cingulate gyrus. Between-group analysis showed that patients had higher activation of the dorsolateral prefrontal cortex.Conclusion: Late-onset restless legs syndrome is associated with low iron content of the basal ganglia and increased activity of the dorsolateral prefrontal cortex
Ann - Take what you need, leave the rest

Managing Your RLS

Opinions presented by Discussion Board Moderators are personal in nature and do not, in any way, represent the opinion of the RLS Foundation, and are not medical advice.

ViewsAskew
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Post by ViewsAskew »

I am posting this although it's not really just RLS - it was actually about fibro. But since we have so many people with fibro who have RLS, I thought it might be helpful.

Efficacy of Waon therapy for fibromyalgia.

Intern Med. 2008;47(16):1473-6. Epub 2008 Aug 15.

Matsushita K, Masuda A, Tei C.

The First Department of Internal Medicine, Kagoshima University Hospital.

PMID: 18703857


OBJECTIVE: Fibromyalgia syndrome (FMS) is a chronic syndrome
characterized by widespread pain with tenderness in specific areas.
We examined the applicability of Waon therapy (soothing warmth
therapy) as a new method of pain treatment in patients with FMS.

METHODS: Thirteen female FMS patients (mean age, 45.2+/-15.5 years
old; range, 25-75) who fulfilled the criteria of the American College
of Rheumatology participated in this study. Patients received Waon
therapy once per day for 2 or 5 days/week. The patients were placed
in the supine or sitting position in a far infrared-ray dry sauna
maintained at an even temperature of 60 degrees C for 15 minutes, and
then transferred to a room maintained at 26-27 degrees C where they
were covered with a blanket from the neck down to keep them warm for
30 minutes. Reductions in subjective pain and symptoms were
determined using the pain visual analog scale (VAS) and fibromyalgia
impact questionnaire (FIQ).

RESULTS: All patients experienced a significant reduction in pain by
about half after the first session of Waon therapy (11-70%), and the
effect of Waon therapy became stable (20-78%) after 10 treatments.
Pain VAS and FIQ symptom scores were significantly (p<0.01) decreased
after Waon therapy and remained low throughout the observation period.

CONCLUSION: Waon therapy is effective for the treatment of
fibromyalgia syndrome.
Ann - Take what you need, leave the rest

Managing Your RLS

Opinions presented by Discussion Board Moderators are personal in nature and do not, in any way, represent the opinion of the RLS Foundation, and are not medical advice.

ViewsAskew
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Post by ViewsAskew »

Huh...I don't think I posted anything about this, but it seems familiar to me. I do wish that one of the side effects of this disorders wasn't a fractured memory!

At any rate, this is quite intriguing...a medical device to treat RLS. It's just starting out, but I'm fascinated to know what they plan on doing!

Here is the company that is providing the funding.
Ann - Take what you need, leave the rest

Managing Your RLS

Opinions presented by Discussion Board Moderators are personal in nature and do not, in any way, represent the opinion of the RLS Foundation, and are not medical advice.

cornelia

Post by cornelia »

Well, I am very interested in what they will come up with.

Thanks Ann, for posting these links. I always read them with interest.

Corrie

ViewsAskew
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Post by ViewsAskew »

Thank you, Corrie. It's nice to know that other people benefit from my postings.
Ann - Take what you need, leave the rest

Managing Your RLS

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ViewsAskew
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Post by ViewsAskew »

Obesity and sleep disorders has been discussed a lot recently. This studyis very interesting in how they approached the topic. For me, it raised some interesting questions. Not sure I have answers, but I'm glad to have read it.

Copied from NAPS

Obesity, excessive daytime sleepiness (EDS), and self-reported short sleep duration appear to be on the rise, while there is evidence that obesity and these sleep disorders are strongly connected. In this paper, we review data that challenge the common belief that the sleep apnoea and sleep loss, frequently associated with obesity, are the primary determinants of obesity-related objective daytime sleepiness and subjective fatigue (tiredness without increased sleep propensity). Specifically, obesity is associated with objective and subjective EDS regardless of the presence of sleep apnoea. The association between obesity and EDS was confirmed in recent studies of large random samples of the general population or clinical samples, which showed that the primary determinants of subjective EDS were depression, metabolic disturbances, i.e. obesity/diabetes and insulin resistance, and lack of physical activity, and, secondarily, sleep apnoea or sleep loss. Paradoxically, within the obese, with or without sleep apnoea, those who slept objectively better at night are sleepier (objectively) during the day than those who slept worse. The distinguishing factor between those that slept better vs. those that slept worse appears to be level of emotional stress. Furthermore, many studies reported that obesity is associated with self-reported short sleep duration; however, it appears that short sleep duration is a marker of emotional stress rather than a reflection of true sleep loss. Based on these data, we propose that obesity-related deeper sleep and objective EDS are primarily related to metabolic disturbances, whereas obesity-related poorer sleep and subjective fatigue appear to be the result of psychological distress. Furthermore, based on data from studies in normal controls and patients with sleep disorders, it appears that the interaction of the hypothalamic-pituitary-adrenal (HPA) axis and pro-inflammatory cytokines determines the level of sleep/arousal within the 24-hour cycle, i.e. "eucortisolemia" or "hypocortisolemia" plus hypercytokinemia is associated with high sleep efficiency and objective sleepiness, whereas "hypercortisolemia" plus hypercytokinemia is associated with low sleep efficiency and fatigue. In conclusion, we propose that the above-reviewed data provide the basis for a meaningful phenotypic and pathophysiologic sub-typing of obesity. One subtype is associated with emotional distress, poor sleep, fatigue, HPA axis "hyperactivity," and hypercytokinemia while the other is associated with non-distress, better sleep but more sleepiness, HPA axis "normo or hypoactivity," and hypercytokinemia. This proposed sub-typing may lead to novel, preventive and therapeutic strategies for obesity and its associated sleep disturbances.
Ann - Take what you need, leave the rest

Managing Your RLS

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Post by ViewsAskew »

More about sleep and obesity in general:

Copied from NAPS

Despite the early recognition of the strong association between obstructive sleep apnoea (OSA) and obesity, and OSA and cardiovascular problems, sleep apnoea has been treated as a "local abnormality" of the respiratory track rather than as a "systemic illness". In 1997, we first reported that the pro-inflammatory cytokines interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNFalpha) were elevated in patients with disorders of excessive daytime sleepiness (EDS) and proposed that these cytokines were mediators of daytime sleepiness. In subsequent studies, it was shown that IL-6, TNFalpha, and insulin levels were elevated in sleep apnoea independently of obesity and that visceral fat was the primary parameter linked with sleep apnoea. Further studies showed that women with the polycystic ovary syndrome (PCOS) were much more likely than controls to have sleep-disordered breathing (SDB) and daytime sleepiness, suggesting a pathogenetic role of insulin resistance in OSA. Additional accumulated evidence that supports the role of obesity and the associated metabolic aberrations in the pathogenesis of sleep apnoea and related symptoms include: obesity without sleep apnoea is associated with daytime sleepiness; the protective role of gonadal hormones as suggested by the increased prevalence of sleep apnoea in post-menopausal women and the significantly reduced risk for OSA in women on hormonal therapy; partial effects of continuous positive airway pressure (CPAP) in obese patients with apnoea on hypercytokinemia, insulin resistance indices, and visceral fat; and that the prevalence of the metabolic syndrome in the U.S. population from the Third National Health and Nutrition Examination Survey (1988-1994) parallels the prevalence of symptomatic sleep apnoea in general random samples. Furthermore, the beneficial effect of a cytokine antagonist on EDS and apnoea in obese, male apnoeics and that of exercise and weight loss on SDB and EDS in general random or clinical samples, supports the hypothesis that cytokines and insulin resistance are mediators of EDS and sleep apnoea in humans. Finally, our recent finding that in obese, hypothalamic CRH neuron is hypoactive, provides additional evidence on the potential central neural mechanisms for depressed ventilation and consequent development of sleep apnoea in obese individuals. In conclusion, accumulating evidence provides support to our thesis that obesity via inflammation, insulin resistance, visceral adiposity, and central neural mechanisms, e.g. hypofunctioning hypothalamic CRH, play a major role in the pathogenesis of sleep apnoea, sleepiness, and the associated cardiovascular co-morbidities.
Ann - Take what you need, leave the rest

Managing Your RLS

Opinions presented by Discussion Board Moderators are personal in nature and do not, in any way, represent the opinion of the RLS Foundation, and are not medical advice.

ViewsAskew
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Post by ViewsAskew »

More on iron in the brain. This study shows that iron is multiregional issue - it's not just low in the substantia nigra, the only area studied prior to this.

Copied from NAPS

Multiregional brain iron deficiency in restless legs syndrome.

GODAU J, KLOSE U, DI SANTO A, SCHWEITZER K, BERG D.
Mov Disord 2008;23(8):1184-7.
Hertie Institute for Clinical Brain Research and Center of Neurology, University of Tuebingen, Tuebingen, Germany. jana.godau@medizin.uni-tuebingen.de



Evidence for tissue iron deficiency in restless legs syndrome (RLS) is limited to the substantia nigra (SN). Using MRI, we assessed T2 values of various brain regions in 6 RLS patients and 19 controls and correlated them with sonographically assessed SN echogenicity. Both neuroimaging features are supposed to correlate with tissue iron content. Mean T2 values of all regions were higher in patients (2.9-7.8%), though significantly increased only in four regions; the mean T2 over all voxels was higher in patients (5.1%, P < 0.001) and correlated inversely with SN echogenicity (r = -0.61, P < 0.001). This indicates multiregional (global) brain iron deficiency in RLS and proposes SN echogenicity as a potential morphological marker for brain iron status. (c) 2008 Movement Disorder Society.
Ann - Take what you need, leave the rest

Managing Your RLS

Opinions presented by Discussion Board Moderators are personal in nature and do not, in any way, represent the opinion of the RLS Foundation, and are not medical advice.

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