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.
Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,116 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
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.
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