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.

Tuesday, February 11, 2014

Depressive disorder, coronary heart disease, and stroke: dose–response and reverse causation effects in the Whitehall II cohort study

Your doctor will need to explain this, reverse causation sounds good but what the hell do I know?
http://cpr.sagepub.com/content/early/2014/01/31/2047487314520785.full
  1. Eric J Brunner1
  2. Martin J Shipley1
  3. Annie R Britton1
  4. Stephen A Stansfeld2
  5. Peter U Heuschmann3
  6. Anthony G Rudd4
  7. Charles DA Wolfe4,5
  8. Archana Singh-Manoux1,6
  9. Mika Kivimaki1
  1. 1University College London, London, UK
  2. 2Barts and the London School of Medicine and Dentistry, London, UK
  3. 3Institute of Clinical Epidemiology and Biometry; Comprehensive Heart Failure Center, University of Würzburg, Würzburg, Germany
  4. 4King’s College London and Guy’s & St. Thomas’ NHS Foundation Trust, London, UK
  5. 5National Institute for Health Research Biomedical Research Centre, King's College London and Guy's and St Thomas' NHS Foundation Trust, London, UK
  6. 6INSERM, Villejuif, France
  1. Eric Brunner, Department of Epidemiology and Public Health, University College London, London, WC1E 6BT, UK Email: e.brunner@ucl.ac.uk
 
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Abstract

Background Systematic reviews examining associations of depressive disorder with coronary heart disease and stroke produce mixed results. Failure to consider reverse causation and dose–response patterns may have caused inconsistencies in evidence.
Design This prospective cohort study on depressive disorder, coronary heart disease, and stroke analysed reverse causation and dose–response effects using four 5-year and three 10-year observation cycles (total follow up 24 years) based on multiple repeat measures of exposure.
Methods Participants in the Whitehall II study (n  = 10,036, 31,395 person-observations, age at start 44.4 years) provided up to six repeat measures of depressive symptoms via the 30-item General Health Questionnaire (GHQ-30) and one measure via Center for Epidemiologic Studies Depression Scale (CES-D). The cohort was followed up for major coronary events (coronary death/nonfatal myocardial infarction) and stroke (stroke death/morbidity) through the national mortality register Hospital Episode Statistics, ECG-screening, medical records, and self-report questionnaires.
Results GHQ-30 caseness predicted stroke over 0–5 years (age-, sex- and ethnicity-adjusted HR 1.60, 95% CI 1.1–2.3) but not over 5–10 years (HR 0.94, 95% CI 0.6–1.4). Using the last 5-year observation cycle, cumulative GHQ-30 caseness was associated with incident coronary heart disease in a dose–response manner (1–2 times a case: HR 1.12, 95% CI 0.7–1.7; 3–4 times: HR 2.06, 95% CI 1.2–3.7), and CES-D caseness predicted coronary heart disease (HR 1.81, 95% CI 1.1–3.1).
Conclusions There was evidence of a dose–response effect of depressive symptoms on risk of coronary heart disease. In contrast, prospective associations of depressive symptoms with stroke appeared to arise wholly or partly through reverse causation.
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