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

Saturday, June 10, 2017

Association between total-Tau and brain atrophy one year after first-ever stroke

So what the fuck is the solution? I don't care how well you describe the problem, it is totally useless without a solution. Once again more followup needed which will never occur. Maybe some of these might help which your doctor knows nothing about. How fucking incompetent is your doctor and stroke hospital? Don't do these on your own

From June, 2013;

Low Diastolic Pressure Linked to Brain Atrophy

And this from November, 2012:

Relationship between Physical Activity and Brain Atrophy Progression.

And from September, 2014: 

Lack of sleep may shrink your brain

From June, 2013:

Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment

 

Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial

 

Study shows that IVIG could prevent brain atrophy, delay onset of Alzheimer's disease Oct. 2015

 


https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-017-0890-6
  • Hege Ihle-HansenEmail author,
  • Guri Hagberg,
  • Brynjar Fure,
  • Bente Thommessen,
  • Morten W. Fagerland,
  • Anne R. Øksengård,
  • Knut Engedal and
  • Per Selnes
BMC NeurologyBMC series – open, inclusive and trusted201717:107
DOI: 10.1186/s12883-017-0890-6
Received: 31 January 2017
Accepted: 29 May 2017
Published: 5 June 2017

Abstract

Background

Although the most serious consequence of neuronal ischemia is acute neuronal death, mounting evidence suggests similarities between stroke and neurodegenerative disease. Brain atrophy visualized on structural MRI and pathological cerebrospinal fluid (CSF) concentrations of microtubule-associated protein tau (T-tau) and phosphorylated microtubule-associated protein tau indicate neurofibrillary degeneration. We aimed to explore the association between CSF T-tau and brain atrophy 1 year post-stroke.

Methods

We included 210 patients with first-ever ischemic stroke or transitory ischemic attack without pre-existing cognitive impairment. After 12 months, subjects underwent MRI, and CSF biomarkers were assessed. Using SIENAX (part of FSL), ventricular CSF volume and total brain volume were estimated and normalized for subject head size. The association between T-tau as explanatory variable and ventricular and total brain volume as outcome variables were studied using linear regression.

Results

One hundred eighty-two patients completed the follow-up. Forty-four had a lumbar puncture. Of these, 31 had their MRI with identical scan parameters. Mean age was 70.2 years (SD 11.7). Ventricular volume on MRI was significantly associated with age, but not with gender. In the multiple regression model, there was a significant association between T-tau and both ventricular (beta 0.44, 95% CI 376.3, 394.9, p = 0.021) and global brain volume (beta −0.50, 95% CI −565.9, −78.3, p = 0.011). There was no significant association between CSF T-tau 1 year post-stroke and baseline volumes.

Conclusion

T-tau measured 1 year post-stroke is associated with measures of brain atrophy. The findings indicate that acute stroke may enhance or trigger tau-linked neurodegeneration with loss of neurons.

Trial registration

Clinicaltrials.gov NCT00506818, July 23, 2007.
Inclusion from February 2007, randomization and intervention from May 2007 and trial registration in July 2007.

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