Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Monday, September 5, 2016

Secondary neurodegeneration after stroke is exacerbated by stress: A new opportunity for preserving viable brain tissue

How is your doctor using this to update your hyperacute protocols? Why should I trust anything written here when they don't even know how many strokes there are a year.
Brain, Behavior, and Immunity, Volume 57, Issue null, Page e15
F. Walker, K. Jones, Z. Zhao, L.K. Ong, M. Kluge, K. Zalewska, S. Johnson, M. Nilsson


As our population ages stroke is becoming an ever more prevalent condition, afflicting tens of thousands of people(Totally wrong - millions yearly) every year. The initial stroke event results in a very significant loss of brain tissue at the site of infarction. Unfortunately, however, viable brain tissue continues to be lost after the primary infarction process is complete, in a process known as secondary neurodegeneration (SND)(neuronal cascade of death). SND involves the progressive death of brain regions that were connected to the original infarcted territories. To better understand SND we have developed a highly controllable model of SND. Specifically, we induce a small stroke within the somatosensory cortex with the assistance of a custom built intrinsic optical signal imaging tandem lens macroscope. This procedure initiates a tightly constrained SND process. We have identified that SND-linked neuroinflammatory disturbances spread out from the injury site, as indicated by significantly enhanced pro-inflammatory signalling (mRNA and protein levels), microglial morphology, neuronal loss (histology), and infiltration of peripheral immune cells (flow cytometry). We have identified that these events are significantly suppressed by chronic stress, or by corticosterone alone, which is in-turn associated with greater cell loss at sites of SND. Collectively, these results suggest that detailed monitoring of stress loads and stress reduction strategies may be warranted in patients recovering from stroke.

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