Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, February 19, 2015

Changes in chronotype after stroke: a pilot study

I have absolutely no idea what possible use this could be for survivors and their rehab, so punt it to your doctor.
http://journal.frontiersin.org/article/10.3389/fneur.2014.00287/full?
Thomas Kantermann1,2*, imageAndreas Meisel3,4, imageKatharina Fitzthum3,4, imageThomas Penzel5, imageIngo Fietze5 and imageLena Ulm3,4,6
  • 1Chronobiology Unit, Groningen Institute for Evolutionary Life Sciences, University of Groningen, Groningen, The Netherlands
  • 2Clinical Centre, Institute for Occupational, Social and Environmental Medicine, Ludwig-Maximilians University Munich, Munich, Germany
  • 3NeuroCure Clinical Research Center, Charité – Universitätsmedizin Berlin, Berlin, Germany
  • 4Department of Neurology, Center for Stroke Research Berlin, Charité – Universitätsmedizin Berlin, Berlin, Germany
  • 5Center of Sleep Medicine, Charité – Universitätsmedizin Berlin, Berlin, Germany
  • 6Centre for Clinical Research, The University of Queensland, Herston, QLD, Australia
This study aimed to elucidate associations between stroke onset and severity as well as chronotype (phase of entrainment) and internal time of stroke. Fifty-six first-ever ischemic stroke patients participated in a cross-sectional study assessing chronotype (mid-sleep on work-free days corrected for sleep deficit on workdays; MSFsc) by applying the Munich ChronoType Questionnaire (MCTQ). The MCTQ was completed twice, on average 68 ± 24 (SD) days post stroke and retrospectively for the time before stroke. To assess the impact of stroke in relation to internal time, InTstroke was calculated as MSFsc minus local time of stroke. Stroke severity was assessed via the standard clinical National Institute Health Stroke Scale (NIHSS) and modified Ranking Scale (mRS), both at hospital admission and discharge. Overall, most strokes occurred between noon and midnight. There was no significant association between MSFsc and stroke onset. MSFsc changed significantly after stroke, especially in patients with more severe strokes. Changes in MSFsc varied with InTstroke – the earlier the internal time of a stroke relative to MSFsc-before-stroke, the more MSFsc advanced after stroke. In addition, we provide first evidence that MSFsc changes varied between stroke locations. Larger trials are needed to confirm these findings.

Introduction

The onset of vascular events exhibits a circadian (about 24-h) pattern, with a prominent peak in the morning hours and a second, smaller peak in the early evening (14). This phenomenon is thought being caused by diurnal variations in underlying pathophysiological mechanisms, e.g., platelet aggregation, blood pressure, and catecholamine concentrations (3, 5). Several animal studies demonstrated that cerebrovascular events, in turn, also impact circadian rhythms and sleep architecture (69). Longer latencies to fall asleep, fragmented sleep, NREM sleep instability, and hypersomnia have also been described in stroke patients, indicating changes in sleep homeostasis and circadian rhythmicity after stroke (10, 11). Two studies with small sample sizes provided some evidence of altered timing in urinary melatonin as a marker of disturbed circadian rhythms in stroke patients (12, 13). However, knowledge on the interplay between sleep homeostasis, the circadian timing of sleep, and vascular events is still incomplete.
The circadian timing of sleep is regulated by an internal clock, which is synchronized (entrained) by light to the 24-h day (14, 15). The relation between external (local) and internal (circadian) time is called phase of entrainment (16) and people that differ in this trait are referred to as different chronotypes. Chronotype can easily be assessed with the Munich ChronoType Questionnaire [MCTQ; (16)] as the mid-point of sleep on work-free days (MSF), corrected for sleep deficit accumulated across the workweek (MSF sleep corrected; MSFsc). MSFsc as a measure for internal time allows calculating the internal time point of a physiological event (17, 18). Social jetlag (the difference between MSF and mid-sleep on workdays, MSW) is a surrogate measure for circadian rhythm disruption and has been linked to elevated heart rate in shift-workers (19), smoking (20), and depression (21). To date, no study has assessed phase of entrainment (chronotype) and social jetlag before and after stroke to compare the impact of stroke in relation to internal time.
The current study was the first to investigate associations between stroke onset and severity and internal time before and after stroke. We hypothesized that (a) there is a correlation between chronotype (MSFsc) and stroke onset, (b) experiencing a stroke results in chronotype changes, and (c) the impact of stroke varies with the internal time point a stroke happened.

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