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, June 11, 2013

Low Diastolic Pressure Linked to Brain Atrophy

So ask your doctor if your poor cognition is from this or are they working with Occams razor to immediately blame the stroke.
http://www.medpagetoday.com/Cardiology/Atherosclerosis/39745?
Shrinkage in subcortical regions of the brain was greater in patients with low baseline diastolic blood pressure in a prospective study, researchers said.
In 663 Dutch patients followed for a mean of 3.9 years (range 3.0 to 5.8), those with baseline diastolic pressure of 70 mm Hg or less showed a subcortical atrophy rate significantly higher than was seen in patients with baseline diastolic pressure greater than 90 mm Hg, according to Mirjam Geerlings, PhD, of the Julius Center for Health Sciences and Primary Care in Utrecht, the Netherlands, and colleagues.
The mean difference in subcortical volume loss during follow-up was 0.07%(95% CI 0.01%-0.14%) in those with low versus high baseline diastolic pressure, irrespective of later changes in diastolic pressure, the researchers reported online in JAMA Neurology.
A similar effect was seen with baseline mean arterial pressure, they added, with a difference in atrophy rate of 0.05% (95% CI 0.00%-0.10%) between patients with low versus high pressure values.
Geerlings and colleagues concluded that, although blood pressure lowering in general is beneficial in patients with higher pressures, the study findings suggest it can be overdone.
"Caution should be taken with further blood pressure lowering in patients who already have a low diastolic blood pressure," they wrote.
The findings emerged from a prospective cohort study called Secondary Manifestations of Arterial Disease-Magnetic Resonance, or SMART-MR, which recruited patients found to have cardiovascular disease for long-term follow-up starting in 2001. Patients underwent clinical and laboratory examinations along with MRI brain scans at baseline and again after a mean of 3.9 years.
Geerlings and colleagues were especially interested in brain atrophy rates because previous studies had yielded conflicting results, with some showing that high blood pressure predicted greater atrophy whereas others suggested an opposite effect.
Of the patients enrolled in the study and completing the follow-up evaluations, 97 had baseline diastolic pressure defined as low, 450 were in the normal range (71 to 90 mm Hg), and 116 had high diastolic pressure.
The distribution of other measured pressures -- systolic, mean arterial, and pulse pressures -- differed considerably. For example, 212 patients in the study had low mean arterial pressure at baseline, versus 225 in the normal range and 226 in the high range.
The relationships with brain volume changes over time also differed, with only mean arterial pressure showing the same pattern as was seen with diastolic pressure. There was no difference in rates of decline in ventricular fraction, for example, between groups stratified by baseline systolic pressure. Patients with high pulse pressure (greater than 70 mm Hg) showed greater ventricular atrophy than those with low pressure of less than 50 mm Hg (rate difference -0.07%, 95% CI -0.01% to -0.13%).
Only patients with coronary artery disease -- not those with cerebrovascular or peripheral artery disease -- showed significant associations between baseline blood pressure by any measure and subcortical brain atrophy, the researchers noted.
At the same time, however, patients with higher pressures at baseline tended to show lower rates of atrophy when, during the course of follow-up, pressures declined.
For instance, patients with normal baseline diastolic pressure whose diastolic pressure dropped during follow-up had subcortical atrophy rates lower by 0.07% (P<0.05) compared with patients with normal baseline diastolic pressure that increased during the study.
A similar relationship was seen with mean arterial pressure, with a mean difference in atrophy rate of 0.09% (P<0.05) for those with normal baseline values that declined during follow-up.
Geerlings and colleagues suggested that low blood pressure in patients with clear cardiovascular disease "could be a risk indicator of early vascular aging."
Another explanation could be that reduced blood pressure reflects decreased cardiac output and blood flow to the brain, the researchers wrote, which could lead to accelerated atrophy.
They suggested a specific mechanism linking blood pressure and brain atrophy, namely, "impaired cerebral autoregulation, making the brain more vulnerable for lower blood pressure levels."
Yet another potential explanation turns the causal direction around, they noted -- brain atrophy may somehow cause low blood pressure.
Limitations to the study included a degree of bias in patients completing follow-up, specifically, those missing the follow-up examinations tended to have been less healthy at baseline. Also, baseline blood pressure measurements were taken only once and were therefore subject to a "white coat" effect.
Finally, the researchers cautioned that the study involved only patients diagnosed with arterial disease, with limited applicability to other populations until more broadly based studies are undertaken.

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