This is more on delayed loss of nerve cells, I would prefer they call it the neuronal cascade of death.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=120237&CultureCode=en
Several weeks after mild brain ischemia, mice display a
depressive-like syndrome characterized by increased anxiety, inactivity
and “cheerlessness”. These symptoms of depression following a stroke are
associated with the delayed loss of nerve cells in the brain’s reward
regions. This is the major finding of a study published in the current
issue of Biological Psychiatry.
Scientists at Charité –
Universitätsmedizin Berlin collaborating with researchers from Bochum,
Magdeburg and Boston were able to show that delayed treatment of
laboratory mice with cipramil, an antidepressant of the selective
serotonin reuptake inhibitor (SSRI) family, not only prevented the
development of depression, but also attenuated the subacute degeneration
of nerve cells in the brain’s reward system after stroke. At the same
time, the area in the brain directly affected by the stroke turned out
to be smaller in those mice which had received the antidepressant.
“These results indicate that antidepressants from the SSRI group protect
nerve cells. This effect can also be harnessed even when medication is
started days after the stroke,” explains psychiatrist Prof. Golo
Kronenberg, who works on the subject of “Depression after Stroke” at the
Center for Stroke Research Berlin (CSB) at Charité.
Poststroke
depression is of great clinical relevance. Not only do symptoms of
depression occur frequently after stroke, they also negatively impact
stroke outcome with increased morbidity and mortality and worse
functional outcome. The neurobiological mechanisms underlying the
development of depression after a stroke have hardly been examined on
the molecular or cellular levels. Conversely, the effects of commonly
prescribed antidepressants on stroke outcome have only sparsely been
investigated.
“These results may be of considerable clinical
significance because until now it was assumed that the window for
effective treatment options after a stroke is limited to a few hours.
However, this study shows that a treatment even when started several
days after the stroke may still prove effective,” says Prof. Matthias
Endres, the Director of the Department of Neurology at Charité.
Based
on these experimental findings, the phenomenon of delayed nerve cell
loss will also be studied in human stroke patients using neuroimaging.
Furthermore, within the framework of the Clinic for Affective Disorders
that is currently being set up at the Experimental and Clinical Research
Center (ECRC) in Berlin-Buch, special consultation hours for patients
suffering from poststroke depression will be scheduled.
http://www.charite.de
This is so blindingly obvious and so easy to test. MRI or PET scans daily until the dead area no longer increases in size. Then we will know the timeframes for therapeutic intervention.
Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 28,972 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.
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