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 cerebrovascular disease. Show all posts
Showing posts with label cerebrovascular disease. Show all posts

Monday, October 29, 2018

Mapping the collaterome for precision cerebrovascular health: Theranostics in the continuum of stroke and dementia

Lots of big words used but zero usefulness for stroke recovery.

Mapping the collaterome for precision cerebrovascular health: Theranostics in the continuum of stroke and dementia


First Published May 30, 2017 Research Article
Precision cerebrovascular health or individualized long-term preservation of the brain and associated blood vessels, is predicated on understanding, diagnosing, and tailoring therapies for people at risk of ischemic injury associated with stroke and vascular dementia. The associated imaging patterns are sculpted by the protective effect of the collaterome, the innate compensatory ability of the brain and vasculature to offset hypoperfusion when antegrade or normal arterial inflow pathways are compromised. Theranostics or rational and synchronous use of diagnostic studies in tandem with specific therapies to optimally guide patient outcomes in ischemic brain disorders may capitalize on the pivotal role of the collaterome. Understanding the functional impact of the collaterome across populations of individuals would advance translational science on the brain, while questions with immediate clinical implications may be prioritized. Big data and systematic analyses are necessary to develop normative standards, multimodal imaging atlases, and delineation of specific patterns to guide clinical management. Large-scale, systematic imaging analyses of the collaterome provide a platform for translational work on cerebral collateral circulation and hemodynamics and a theranostic framework with direct clinical implications. This article frames incipient research objectives to guide precision stroke medicine in coming years, building upon the collaterome concept in brain health.

Saturday, June 18, 2016

Effects of cilostazol on cognition and regional cerebral blood flow in patients with Alzheimer's disease and cerebrovascular disease: A pilot study

Since your doctor should be concerned about your chances of getting dementia/Alzheimers maybe this can be added to your stroke protocol against dementia. But I almost guarantee that your doctor knows nothing about preventing dementia or even that it is likely you will get it.










Good luck, because you will need it.
Your 33% dementia chance post-stroke from an Australian study?   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

Is your doctor even testing you for MCI post-stroke?
http://onlinelibrary.wiley.com/doi/10.1111/j.1447-0594.2012.00866.x/abstract;jsessionid=3065AD84D5893717785970A20BB2DAD8.f02t02?userIsAuthenticated=false&deniedAccessCustomisedMessage=
  1. Hirofumi Sakurai*,
  2. Haruo Hanyu,
  3. Tomohiko Sato,
  4. Kazumasa Kume,
  5. Kentaro Hirao,
  6. Hidekazu Kanetaka and
  7. Toshihiko Iwamoto
Version of Record online: 4 JUN 2012
DOI: 10.1111/j.1447-0594.2012.00866.x
Geriatrics & Gerontology International

Geriatrics & Gerontology International

Volume 13, Issue 1, pages 90–97, January 2013


How to Cite

Sakurai, H., Hanyu, H., Sato, T., Kume, K., Hirao, K., Kanetaka, H. and Iwamoto, T. (2013), Effects of cilostazol on cognition and regional cerebral blood flow in patients with Alzheimer's disease and cerebrovascular disease: A pilot study. Geriatrics & Gerontology International, 13: 90–97. doi: 10.1111/j.1447-0594.2012.00866.x

Author Information

  1. Department of Geriatric Medicine, Tokyo Medical University, Tokyo, Japan
*Dr Hirofumi Sakurai MD PhD, Department of Geriatric Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan. Email: sakurah@tokyo-med.ac.jp

Publication History

  1. Issue online: 3 JAN 2013
  2. Version of Record online: 4 JUN 2012
  3. Accepted for publication 12 March 2012.

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Keywords:

  • Alzheimer's disease;
  • cerebral blood flow;
  • cerebrovascular disease;
  • cilostazol;
  • cognition
Aim:  It remains unknown whether antiplatelet agents have a preventive effect on cognitive decline in patients with Alzheimer's disease (AD). We investigated the effects of cilostazol, an antiplatelet agent and cyclic adenosine monophosphate phosphodiesterase 3 inhibitor, on cognition and regional cerebral blood flow (rCBF) in elderly patients with AD and cerebrovascular disease (CVD).
Methods:  A total of 20 patients with AD and CVD were randomly assigned to a cilostazol group (n = 11, 100 mg daily) or control group (n = 9, aspirin 100 mg or clopidogrel 50 mg–75 mg daily) for 6 months.
Results:  The cilostazol group did not show any statistically significant changes in cognitive function test scores, whereas the control group showed statistically significant cognitive decline on the Alzheimer's Disease Assessment Scale-Cognitive Subscale (Japanese version), Revised Wechsler Memory Scale (logical memory-I) and Trail Making Test-A. Analysis of covariance of treatment effect revealed that the cilostazol group showed increased rCBF in the right anterior cingulate lobe compared with baseline, whereas the control group showed decreased rCBF in the left middle temporal gyrus compared with baseline.
Conclusion:  These findings suggest that cilostazol might have a preventive effect on cognitive decline in patients with AD and CVD. Geriatr Gerontol Int 2013; 13: 90–97.