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, September 23, 2015

Prognostic Factors for Cognitive Decline After Intracerebral Hemorrhage - 37% occurrence rate

I'm sure that if the neuronal cascade of death was stopped that would significantly reduce that percentage. But that won't occur until we fire the current stroke medical leadership.
http://stroke.ahajournals.org/content/early/2015/08/13/STROKEAHA.115.010200.abstract?sid=70c1375f-6280-4c34-aa5b-28f4ef2bbd54
  1. Marije R. Benedictus, MSc,
  2. Anaïs Hochart, MD,
  3. Costanza Rossi, MD, PhD,
  4. Gregoire Boulouis, MD,
  5. Hilde Hénon, MD, PhD,
  6. Wiesje M. van der Flier, PhD and
  7. Charlotte Cordonnier, MD, PhD
+ Author Affiliations
  1. From the Alzheimer Center and Department of Neurology (M.R.B., W.M.v.d.F.) and Department of Epidemiology and Biostatistics (W.M.v.d.F.), Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands; and Department of Neurology, INSERM U 1171, CHRU, University of Lille, Lille, France (A.H., C.R., G.B., H.H., C.C.).
  1. Correspondence to Charlotte Cordonnier, MD, PhD, Department of Neurology, Stroke Unit, Hopital Roger Salengro, INSERM U 1171, CHRU, University of Lille, Lille, France. E-mail charlotte.cordonnier@chru-lille.fr

Abstract

Background and Purpose—Stroke and dementia are closely related, but no prospective study ever focused on poststroke cognitive decline in patients with intracerebral hemorrhage (ICH). We aimed to determine prognostic factors for cognitive decline in patients with ICH.
Methods—We prospectively included 167 consecutive ICH survivors without preexisting dementia from the Prognosis of Intra-Cerebral Hemorrhage (PITCH) cohort. Median follow-up was 4 years (interquartile range, 2.3–5.4). We explored factors associated with cognitive decline using linear mixed models. Cognitive decline was determined based on repeated mini-mental state examination. We investigated each prognostic factor separately in univariate models. Next, we constructed clinical and radiological multivariable models. In a sensitivity analysis, we excluded patients with preexisting cognitive impairment.
Results—Median age was 64 (interquartile range, 53–75) years, 69 (41%) patients were women, and median mini-mental state examination at 6 months was 27 (interquartile range, 23–29). Overall, 37% of the patients declined during follow-up. Factors associated with cognitive decline in univariate analyses were previous stroke or transient ischemic attack, preexisting cognitive impairment, microbleed presence, severity of white matter hyperintensities, and severity of cortical atrophy. In multivariable analyses, previous stroke or transient ischemic attack (β [SE], −0.55 [0.23]; P<0.05), preexisting cognitive impairment (β [SE], −0.56 [0.25]; P<0.01), and severity of cortical atrophy (β [SE], −0.50 [0.19]; P<0.01) remained independent prognostic factors. In patients without preexisting cognitive impairment (n=139), severity of cortical atrophy (β [SE], −0.38 [0.17]; P<0.05) was the only prognostic factor for future cognitive decline.
Conclusions—Prognostic factors for cognitive decline after ICH are already present when ICH occurs, suggesting a process of ongoing cognitive impairment instead of new-onset decline induced by the ICH itself.

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