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.

Monday, March 6, 2017

Cognitive function decline in patients with acute stroke is not prevented by nimodipine

Then what the hell is the protocol to prevent cognitive decline? Keep after your doctor until you get a specific answer. This decline has been known for decades, has your doctor done one damn thing about finding a solution? Does s/he know about any of the following? Pure incompetence, stupidity, indifference or laziness?
Maybe these:

Exercise May Stave Off Cognitive Decline by 10 Years

Growth Factor in Brain Tied to Slower Mental Decline

Omega 3 fatty acid for the prevention of cognitive decline and dementia

probiotics and tryptophan may slow down social cognitive decline in aging. 

Study shows that IVIG could prevent brain atrophy, delay onset of Alzheimer's disease

Systematic review shows ‘smart drug’ modafinil does enhance cognition

Eating away at cognitive decline: MIND diet may slow brain from aging by 7.5 years

10 Ways to Rev Up Your Brain and Reduce the Risk of Cognitive Decline

You can compare these to mine.
Dementia prevention 19 ways

 

 

 

 

 

 

 


http://www.healio.com/cardiology/stroke/news/online/%7B74692799-b80b-48ad-a8ef-7b14e75fd3aa%7D/cognitive-function-decline-in-patients-with-acute-stroke-is-not-prevented-by-nimodipine?

The calcium antagonist nimodipine did not prevent the decline of cognitive function in patients with acute stroke and mild cognitive impairment, according to a study presented at the International Stroke Conference.
Huahuang Zheng , MD, from the Capital Medical University in Beijing, and colleagues conducted a randomized, double blind, placebo-controlled trial at 23 sites across China.
The study included patients between the ages of 30 and 80 years who had a Mini-Mental State Examination (MMSE) score greater than dementia threshold corrected based on educational year, Montreal Cognitive Assessment (MoCA) scores less than 26 for more than 12 educational years and Hachinski scores of 7 or more.
Patients were randomly assigned to receive either 30 mg nimodipine (n = 329) 3 times per day or placebo (n = 325).
The primary endpoint of the study was change in cognitive function as determined by MMSE and Alzheimer’s Disease Assessment Scale – cognitive subscale (ADAS–Cog).
Secondary endpoints included changes in score from baseline to 6 months of MoCA and frontal assessment battery.
Zheng said there was no significant difference between the groups in MMSE –3 (OR = 0.56; 95% CI, 0.27-1.26), MMSE 0 (OR = 0.76; 95% CI, 0.55-1.07) or ADAS-Cog 4 (OR = 0.93; 95% CI, 0.52-1.66). For the outcome of ADAS-Cog 0, 34.15% of those assigned nimodipine achieved that threshold vs. 46.74% of those assigned placebo (OR = 0.59; 95% CI, 0.42-0.83).
Key secondary endpoints did not differ between the nimodipine and placebo groups (MoCA: nimodipine group, 1.89; placebo group, 1.66; P = .35; frontal assessment battery: nimodipine group, 0.85; placebo group, 0.67; P = .32).
“Vascular mild cognitive impairment in acute ischemic stroke patients might not benefit from nimodipine in prevention of cognitive function decline when treated 1 week after onset of stroke,” Zheng said during the presentation. “However, nimodipine might have a marginal positive effect on some specific cognitive domains and did not increase risk of stroke and other adverse events.”– by Dave Quaile
Reference:
Zheng H, et al. LB7. Presented at: International Stroke Conference; Feb. 22-24, 2017; Houston.
Disclosure : The study was funded in part by Bayer HealthCare Pharmaceuticals China. Zheng reports receiving research grants from the National Key Technology Research and Development program of the Ministry of Science and Technology of China.
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