Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Friday, May 12, 2017

Obstructive sleep apnea in acute stroke

You'll have to ask your doctor what bed–side somnography is. I got the finger pulse oximetry test which showed no oxygenation problems but an official night sleep study showed sleep apnea of 6.5 times an hour.
https://www.mdlinx.com/internal-medicine/medical-news-article/2016/05/10/apnea-emergency-department-ischemia-stroke-tumor/6644674/?
Stroke
Ifergane G, et al.
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The authors prospectively evaluated clinical characteristics and laboratory markers of inflammation and coagulability associated with obstructive sleep apnea (OSA) severity during the acute post stroke period. Use of bed–side somnography technology revealed that in an unselected sample of patients with acute ischemic stroke, almost 90% had sleep–disordered breathing with third having severe form of the disorder. Sleep–disordered breathing was associated with significantly increased levels of inflammatory biomarkers, providing possible pathophysiological explanation of OSA–associated stroke risk. These results warrant prospective screening of patients with stroke for the presence of sleep–disordered breathing and lay the rationale for an interventional trial.

Methods

  • Consecutive patients admitted to the department of Neurology after an acute ischemic stroke were evaluated during the first 48 hours of symptom onset using Watch peripheral arterial tonometry, a wrist-worn ambulatory sleep study device that utilizes peripheral arterial tonometry.
  • Morning blood samples of the patient were tested for tumor necrosis factor, interleukin-6, and plasminogen activator inhibitor-1 levels.

Results

  • A total of 43 patients with acute stroke were admitted during the study period, 22 (51%) of which have been found to have moderate sleep apnea (apnea hypopnea index [AHI]≥15), AHI≥5 was found in 86% of the patients, and severe OSA (AHI≥30) in 32.5%.
  • Patients with OSA (AHI≥15) did not differ from the rest in stroke severity or symptoms, yet they had higher prevalence of recurrent stroke and atrial fibrillation.
  • All 3 biomarkers levels were higher among patients with AHI≥15: tumor necrosis factor (6.39 versus 3.57 pg/mL), interleukin-6 (6.64 versus 3.14 pg/mL), and plasminogen activator inhibitor-1 (176.64 versus 98.48 pg/mL).
  • After the stratification of AHI into 3 groups (AHI<5, 5-14, and ≥15), the analysis showed that only the highest AHI group differed from the other 2 groups in biomarkers levels.

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