I'm seriously thinking of pulling back from my stroke blog for a while. It has completely consumed my life for the past 5 years and I'm not seeing much effect yet. Everything is pretty much laid out on how to fix the stroke medical system. Every single stroke hospital in the world should be doing the exact same thing I'm doing, analyzing stroke research and seeing where it applies in the stroke protocols or setting up research to answer the question of how to get translational effects out of the research. I'm superfluous There is no real intellectual challenge anymore in this. It is a management challenge and I've already proven in an earlier career that I hit the Peter Principle really hard when I was promoted to manager. Part of this is because I'm tired and I want to recover a couple hours for myself each night, maybe I'll finally catch up on sleep.
I will still post but probably put them up in a draft status until the weekend when I can blast them all out.
There is still lots to do:
1. I have 20-30 ebooks to write yet on stroke
2. I have to create content for the various URLs I own.
AFTERYOURSTROKE.COM
AFTERYOURSTROKE.INFO
AFTERYOURSTROKE.NET
AFTERYOURSTROKE.ORG
DEANREINKE.COM
DEANREINKE.INFO
DEANREINKE.NET
DEANREINKE.ORG
DEANSSTROKEMUSINGS.COM
STROKERESEARCHINSTITUTE.COM
STROKERESEARCHINSTITUTE.INFO
STROKERESEARCHINSTITUTE.NET
STROKERESEARCHINSTITUTE.ORG
STROKESURVIVORINSTITUTE.COM
STROKETRIBEBLOGS.COM
3. I have to start up a stroke research foundation.
4. I have to recover enough to start running again.
5. I have to start a stroke blog farm.
Part of this is because I want to start another blog:
Deans' Michigan musings - Michigan is in a world of hurt from all the disastrous policies that have been implemented. And I happen to think that if I apply myself I could solve these problems. Hopefully leading to another career in public policy.
http://www.jamesaltucher.com/2015/06/quitter/?
This
scientific commentary refers to ‘Perfusion computed tomography to
assist decision making for stroke thrombolysis’, by Bivard et al. (doi:10.1093/brain/awv071).
The
ischaemic penumbra, defined as severely hypoperfused, functionally
impaired yet salvageable tissue, has been established as the key target
for acute stroke therapy for more than three decades (Muir et al., 2006).
However, the penumbra has a limited lifespan and, unless reperfused
early, it progresses to become part of the irreversibly damaged tissue
referred to as the ‘core’. The core therefore grows over time,
incorporating first the most hypoperfused portions of the penumbra, and
then progressively less hypoperfused portions, until none remains. How
fast this process occurs varies greatly from subject to subject, mainly
because of variable pial collaterals and the occurrence of spontaneous
reperfusion (Fig. 1). On a mechanistic basis, reperfusion therapy—such
as with intravenous thrombolysis using recombinant tissue plasminogen
activator (rt-PA)—would be expected to be of no benefit, and potentially
harmful, in cases with large core or no penumbra (Marchal et al., 1993).