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.

Monday, June 25, 2018

Targeting Reperfusion Injury in the Age of Mechanical Thrombectomy

Hell, we still haven't targeted the reperfusion(neuronal cascade of death) injury after tPA administration. All because we have NO STROKE STRATEGY AND NO STROKE LEADERSHIP. Nothing is going to get solved until we get stroke survivors in charge.
http://stroke.ahajournals.org/content/49/7/1796?etoc=
Atsushi Mizuma, Midori A. Yenari
https://doi.org/10.1161/STROKEAHA.117.017286
Stroke. 2018;49:1796-1802
Originally published May 14, 2018

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  • stroke
  • tissue-type plasminogen activator

    • Pharmacological recanalization with r-tPA (recombinant tissue-type plasminogen activator) has been the mainstay for acute ischemic stroke (IS) treatment.1 Recent randomized controlled trials have additionally demonstrated the efficacy of mechanical thrombectomy (MT).2–4 Although the restoration of blood flow is a major goal in acute treatment, if this occurs too late, worse damage can ensue, compared with no revascularization.5 This worsening results because of the generation of excess reactive oxygen species (ROS) which leads to direct cellular damage and indirect damage through the triggering of inflammation. Inflammation causes the generation of damaging immune mediators, effector molecules, and more ROS.6 ROS can also lead to apoptosis/necrosis via DNA/RNA damage and lipid peroxidation. This cycle is known as reperfusion injury (R/I; Figure). Experimental studies have shown that durations of >2- to 3-hours transient middle cerebral artery occlusion (tMCAO) lead to worsened injury compared with permanent MCAO.7 At the clinical level, delayed revascularization can sometimes lead to worsened outcomes.8 Hyperintense acute reperfusion marker seen on magnetic resonance imaging in some patients with stroke has been associated with hemorrhagic transformation (HTf) and clinical worsening, suggesting the existence of R/I in humans.9 Hence, adjunctive treatments to recanalization to target R/I has the potential to improve current outcomes while reducing complications of r-tPA.
    Figure.
    Reperfusion injury is thought to occur when a sudden influx of oxygenated blood introduces reactive oxygen species (ROS) into critically damaged ischemic brain. Ischemically damaged mitochondria become unable to efficiently neutralize ROS. Elevated ROS can directly damage DNA, RNA, and cause lipid peroxidation. ROS lead to immune cell activation, including brain resident microglia. Ischemic brain may also elaborate damage-associated molecular patterns (DAMPs) that act on Toll-like receptors (TLR) present on the surface of microglia. TLR activation triggers immune …
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