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.

Wednesday, November 5, 2014

Efficacy of nitric oxide, with or without continuing antihypertensive treatment, for management of high blood pressure in acute stroke (ENOS): a partial-factorial randomised controlled trial

I can't tell from this whether NO is used at all. I plan on using NO for these reasons;
Which way does your doctor recommend you get your nitric oxide?
Does your doctor even know the benefits of nitric oxide for stroke?

Modulation of Adult Neurogenesis by the Nitric Oxide System

Efficacy of Nitric Oxide in Stroke' (ENOS) study 

Inhaled Nitric Oxide Protects Males But not Females from Neonatal Mouse Hypoxia–Ischemia Brain Injury 

 

  Regulation of Injury-Induced Neurogenesis by Nitric Oxide

 

 Nitric Oxide and the Biological Cascades Underlying Increased Neurogenesis, Enhanced Learning Ability, and Academic Ability as an Effect of Increased Bouts of Physical Activity

  Inhalation of nitric oxide could help improve blood flow to ischemic brain

  Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function

 

  Cerebrovascular protection by various nitric oxide donors in rats after experimental stroke

 

Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function

The latest here:

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2814%2961121-1/abstract?rss=yes 

The ENOS Trial Investigators

Summary

Background

High blood pressure is associated with poor outcome after stroke. Whether blood pressure should be lowered early after stroke, and whether to continue or temporarily withdraw existing antihypertensive drugs, is not known. We assessed outcomes after stroke in patients given drugs to lower their blood pressure.

Methods

In our multicentre, partial-factorial trial, we randomly assigned patients admitted to hospital with an acute ischaemic or haemorrhagic stroke and raised systolic blood pressure (systolic 140—220 mm Hg) to 7 days of transdermal glyceryl trinitrate (5 mg per day), started within 48 h of stroke onset, or to no glyceryl trinitrate (control group). A subset of patients who were taking antihypertensive drugs before their stroke were also randomly assigned to continue or stop taking these drugs. The primary outcome was function, assessed with the modified Rankin Scale at 90 days by observers masked to treatment assignment. This study is registered, number ISRCTN99414122.

Findings

Between July 20, 2001, and Oct 14, 2013, we enrolled 4011 patients. Mean blood pressure was 167 (SD 19) mm Hg/90 (13) mm Hg at baseline (median 26 h [16—37] after stroke onset), and was significantly reduced on day 1 in 2000 patients allocated to glyceryl trinitrate compared with 2011 controls (difference −7·0 [95% CI −8·5 to −5·6] mm Hg/—3·5 [—4·4 to −2·6] mm Hg; both p<0·0001), and on day 7 in 1053 patients allocated to continue antihypertensive drugs compared with 1044 patients randomised to stop them (difference −9·5 [95% CI −11·8 to −7·2] mm Hg/—5·0 [—6·4 to −3·7] mm Hg; both p<0·0001). Functional outcome at day 90 did not differ in either treatment comparison—the adjusted common odds ratio (OR) for worse outcome with glyceryl trinitrate versus no glyceryl trinitrate was 1·01 (95% CI 0·91—1·13; p=0·83), and with continue versus stop antihypertensive drugs OR was 1·05 (0·90—1·22; p=0·55).

Interpretation

In patients with acute stroke and high blood pressure, transdermal glyceryl trinitrate lowered blood pressure and had acceptable safety but did not improve functional outcome. We show no evidence to support continuing prestroke antihypertensive drugs in patients in the first few days after acute stroke.

 

No comments:

Post a Comment