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.

Showing posts with label RLS. Show all posts
Showing posts with label RLS. Show all posts

Wednesday, May 27, 2020

Sleep load index predicts recurrent stroke

WHOM is going to do the followup research, write the protocol AND distribute to all stroke hospitals? Since we have NO LEADERSHIP in stroke nothing will happen and YOU AS A STROKE SURVIVOR will bear the brunt of  this failure. Hope you are ok with such incompetence.   

Sleep load index predicts recurrent stroke

A sleep load index that considers multiple sleep-wake disorders (SWD) predicts subsequent cardiovascular events during the 2 years after a stroke, preliminary results in an ongoing study suggest.
The index, which combines sleep duration, breathing with sleep disorders, Restless Leg Syndrome (RLS), insomnia, and sleep duration, is a better predictor of new events than a single sleep disorder alone.
Dr. Simone B. Duss
With more evidence of its usefulness, "the sleep load index could be integrated into clinical routine," Simone B. Duss, PhD, Department of Neurology, University of Bern Hospital, Switzerland, said at a press conference.
The findings were presented online at the 2020 European Academy of Neurology (EAN) Congress, which moved to a virtual meeting due to the COVID-19 pandemic.
Sleep-wake disorders are very common in stroke patients and may pre-exist or appear de novo as a consequence of brain damage, Duss said.
"They may also be the result of medical, psychological or environmental challenges these patients face after a stroke," he added.
Clear evidence
There is "clear evidence" that breathing with sleep disorders is a risk factor for stroke and negatively affects the outcome of the stroke if left untreated, Duss said.
But for other SWDs like insomnia, RLS and long and short sleep duration, "the evidence is less convincing," he said. "However, some studies still suggest that they influence stroke risk and outcome."
Experts believe that sleep disturbances after a stroke lead to sleep fragmentation, as well as decreased slow-wave sleep and REM sleep.
"This negatively affects neuroprotective inflammatory processes and synaptic plasticity during the stroke recovery process," said Duss. "In the end, this results in worse outcomes for recurring events, but also for activities of daily living and mood."
The new analysis aimed to assess the impact of sleep-wake disturbances on recurrent events and outcomes after stroke or transient ischemic attack (TIA).
It included 438 patients with acute stroke (85%) or TIA (15%). The mean age of the study population was 65 years, and 64% were men.
The researchers used the National Institutes of Health Stroke Scale (NIHSS) to assess the severity of the stroke. On admission, the NIHSS mean score was 4. The majority of strokes (77.2%) were supratentorial.
About a fifth of stroke patients and a third of TIA patients had had a previous event.
The researchers used functional outcome scores to assess the clinical course of stroke or TIA. Furthermore, they regularly asked patients about the recurrence of cardiovascular events.
The researchers assessed breathing with sleep disturbances during the acute phase of stroke, therefore in the early days, using respirography.
They collected information on the presence of other sleep-wake disorders from questionnaires and clinical interviews at 1 month, 3 months, 1 year and 2 years after the event.
About 26% of the subjects showed severe sleep disordered breathing, "meaning they had more than 20 apnea-hypopnea events per hour," Duss said.
More than a quarter of patients reported subclinical insomnia symptoms (measured using the Insomnia Severity Index), and up to 10% reported severe insomnia symptoms corresponding to the clinical diagnosis of insomnia, he said.
About 9% of patients in the acute phase of stroke, and 6% in the most chronic phase, met the diagnostic criteria for RLS.
More "biased"
The results for sleep duration were relatively "biased," Duss said. More patients reported longer sleep duration (more than 9 hours) at 1 month than at month 3, and more reported shorter sleep duration (4.0 hours or less) at month 3 than at month 1.
The researchers created a sleep load index for the combined impact of the various sleep-wake disturbances.
They used this index as a predictor of subsequent cardiovascular events in the 3 months after an event. They used a composite outcome that included recurrent stroke or TIA, myocardial infarction, heart failure, and urgent revascularization, as well as new cardiovascular events, from 3 to 24 months.
Analysis showed that the average sleep load index was higher for stroke patients with a recurring event compared to stroke patients or TIA without a recurring event (Wilcoxon rank sum test; P = .0002 ).
A multiple logistic regression model with the presence or absence of a recurrent event as a result showed that the sleep load index is a significant predictor of recurrent events (odds ratio, 2.10; P = .001).
This was true even after controlling for age, sex, and baseline severity of stroke.
The baseline rate of apnea / hypopnea and sleep duration were also significant predictors of new events. However, it is important to note that the sleep load index remained a significant predictor of recurring events even after excluding the component of the apnea / hypopnea index, Duss said.
"Therefore, the predictive power of the sleep load index is not only driven by the apnea / hypopnea index at the start of a stroke."
Sleep and wake disturbances "should be evaluated and considered more carefully in comprehensive treatment approaches," not only in stroke patients, but in neurological patients in general, Duss said
He noted that these are preliminary observations from an ongoing study. The results should be confirmed and should be when the study ends, he said.
The researchers are also analyzing MRI data to assess whether certain brain injuries are associated with sleep disorders.
Commenting for Medscape Medical News, Jesse Dawson, MD, professor of stroke medicine, University of Glasgow, Scotland, said the clinical scoring system included in the study "will be of great help in the design and conduct of clinical trials "
Although he and other stroke experts are aware of the high prevalence of sleep disorders after a stroke, "we don't routinely look for them as we're not sure if the intervention is beneficial," Dawson said.
This new study "suggests that there is an association with adverse outcomes," he said.
The research was supported by grants from the Swiss National Science Foundation and the Swiss Heart Foundation. Duss and Dawson have disclosed no relevant financial relationships.
Congress of the European Academy of Neurology (EAN) 2020: Abstract # 2078. Presented online on May 24, 2020.
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. (tagsToTranslate) stroke (t) stroke (t) cva (stroke) (t) sleep apnea (t) sleep disorder (t) sleep (t) transient ischemic attack (t) aunt (t) recurrent stroke (t) restless legs syndrome (rls) (t) restless legs syndrome (t) rls (t) acute stroke (t) ischemic stroke (t) stroke rehabilitation

Tuesday, December 13, 2016

Neurons paralyze us during REM sleep

I bet this also causes RLS - Restless Leg Syndrome, which was tested for in my sleep analysis. 
http://www.alphagalileo.org/ViewItem.aspx?ItemId=170863&CultureCode=en
During REM sleep, the brain inhibits the motor system, which makes the sleeper completely immobile. CNRS researchers working in the Centre de Recherche en Neurosciences de Lyon (CNRS/Université Claude Bernard Lyon 1/INSERM/Université Jean Monnet) have identified a population of neurons that is responsible for this transient muscle paralysis. The animal model created will shed light on the origin of some paradoxical sleep disorders, and more particularly the condition that prevents this paralysis. It will also be most useful in the study of Parkinson's disease, since these pathologies are related. This work was published on December 12, 2016 on the website of the journal Brain.

In spite of being in a deep sleep, the patients talk, move, kick and eventually fall out of bed. They are suffering from a parasomnia called REM Sleep Behavior Disorder1 (RBD). This disorder usually appears around the age of 50. Muscles are at rest during the REM sleep phase, but in these patients, there is no paralysis, although the reason for this is not known. The sleepers move abnormally, probably reflecting their dream activity.

A team from the Centre de Recherche en Neurosciences de Lyon (CNRS/INSERM/Université Claude Bernard Lyon 1/Université Jean Monnet) has taken one more step towards elucidating this pathology. The researchers identified neurons in the sublaterodorsal nucleus of the brain, ideally located to control motor system paralysis during REM sleep. In rats, they specifically targeted this neuron population, by adding genetically modified viral vectors2 to it. Once these are in the neural cells, they block the expression of a gene that allows synaptic glutamate secretion. Now incapable of releasing this excitatory neurotransmitter, the neurons can no longer communicate with their neighbors. They are disconnected from the cerebral network necessary for paralysis during REM sleep.

For 50 years, the scientific community has considered that these glutamate neurons generated REM itself. This team's experience invalidates this hypothesis: despite the absence of activity in this neuron circuit, the rats still experience this stage of sleep. They are fast asleep and disconnected from the outside world, with eyes closed. But these rats are no longer paralyzed. Their behavior is very reminiscent of the clinical profile of patients suffering from RBD. The glutamate neurons targeted in this study play an essential part in REM paralysis during sleep and are reportedly the first neurons affected in this neurological disease.

This research work goes beyond creating a new preclinical model that mimics this parasomnia. It may be of paramount importance in studying some neurodegenerative diseases. Recent clinical research has shown that patients diagnosed with RBD almost always develop the motor symptoms of Parkinson's disease, on average a decade later. The team is now attempting to develop an animal model that evolves from parasomnia into Parkinson's disease, in order to understand how neuron degeneration occurs.

The glutamate neurons of the sublaterodorsal nucleus emit a spontaneous red fluorescence indicating that the viral vectors used have been successfully added.
Notes
1REM sleep is also called paradoxical sleep.
2Provided by researchers at Tsukuba University in Japan

Attached files

  • The glutamate neurons of the sublaterodorsal nucleus emit a spontaneous red fluorescence indicating that the viral vectors used have been successfully added. © Sara Valencia Garcia / Patrice Fort, CNRS

  • In rats treated with viral vectors (C and D), neurons are still present (in brown) but are not longer capable of releasing glutamate (absence of black color). © Sara Valencia Garcia / Patrice Fort, CNRS