Deans' stroke musings: Neurovascular Mechanisms of Ischemia Tolerance Against Brain Injury

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.

Saturday, November 9, 2013

Neurovascular Mechanisms of Ischemia Tolerance Against Brain Injury

More proof that preconditioning neuronal stressors help prevent ishemic injury. That brings up the interesting possibility that maybe TIAs should all have this preconditioning to reduce ischemic damage. Don't listen to me, no medical training.
http://link.springer.com/chapter/10.1007/978-1-4614-8690-9_10

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Abstract

Traumatic brain injury (TBI) can result in secondary ischemia. This secondary ischemic insult is implicated in post-TBI pathophysiology. Pharmacological intervention to elevate cerebral blood flow can improve outcomes following TBI. The brain and other organ systems have an innate ability to induce protection against ischemic injury, limiting the severity of the ischemia-induced damage. This “self” protection can be initiated by exposing the brain to a stimulus before ischemia called “preconditioning,” such as exposure to a mild episode(s) of ischemia, hypoxia, anesthesia, or pharmacologically induced mild cell stressors. Current efforts to reduce ischemia-induced brain damage have been the focus in determining the mechanisms of preconditioning-induced ischemia tolerance as findings may help lower cerebral ischemia-induced brain damage in at-risk patients including TBI patients. Different preconditioning paradigms have been shown to lower TBI-induced damage. Although not all of the mechanisms of preconditioning are confirmed in models of TBI, basic mechanisms of preconditioning applies here as ischemia is a major part of TBI. Ischemic preconditioning, in part, confers protection by modulating regulators of cerebral blood flow, increase angiogenesis, and prevent cerebral ischemia-induced increase in blood–brain barrier permeability. This chapter highlights preconditioning-induced changes in components of the neurovascular system involved in ischemia tolerance. Understanding of these pathways may aid in the development of novel therapies to protect the brain from TBI-induced secondary ischemic insult.