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, March 2, 2024

Remote ischemic conditioning for stroke: A critical systematic review

 This is totally useless! You didn't create a protocol on this that survivors can bring to their therapists! You've known about this for years and have DONE NOTHING USEFUL TO HELP SURVIVORS!

Remote ischemic conditioning for stroke: A critical systematic review

Abstract

Remote ischemic conditioning (RIC) is the application of brief periods of ischemia to an organ or tissue with the aim of inducing protection from ischemia in a distant organ. It was first developed as a cardioprotective strategy but has been increasingly investigated as a neuroprotective intervention. The mechanisms by which RIC achieves neuroprotection are incompletely understood. Preclinical studies focus on the hypothesis that RIC can protect the brain from ischemia reperfusion (IR) injury following the restoration of blood flow after occlusion of a large cerebral artery. However, increasingly, a role of chronic RIC (CRIC) is being investigated as a means of promoting recovery following an ischemic insult to the brain. The recent publication of two large, randomized control trials has provided promise that RIC could improve functional outcomes after acute ischemic stroke, and that there may be a role for CRIC in the prevention of recurrent stroke. Although less developed, there is also proof-of-concept to suggest that RIC may be used to reduce vasospasm after subarachnoid hemorrhage or improve cognitive outcomes in vascular dementia. As a cheap, well-tolerated and almost universally applicable intervention, the motivation for investigating possible benefit(You knew of the need, YET DID NOTHING TO HELP SURVIVORS!) of RIC in patients with cerebrovascular disease is great. In this review, we shall review the current evidence for RIC as applied to cerebrovascular disease.

Introduction

Remote ischemic conditioning (RIC) describes the technique of using non-lethal ischemic stimuli in one organ or tissue to protect against lethal ischemic events in a distant organ. Ischemic conditioning (IC) was first demonstrated using isolated dog hearts whereby brief periods of occlusion to the left circumflex artery were found to reduce infarct size when the same artery was subsequently occluded for 40 min, in comparison to non-conditioned hearts.1 Subsequently, it was shown that brief periods of ischemia applied to the circumflex artery protected against ischemia from a 1 h occlusion of the left anterior descending artery,2 suggesting that protection via IC is conveyed to a different part of an organ than that supplied by the conditioned artery. This concept was developed when brief periods of occlusion to the mesenteric artery reduced the size of myocardial infarction following prolonged occlusion of a coronary artery.3 While clearly an interesting phenomenon, it was difficult to imagine this technique translating into clinical practice, given the perceived danger of occluding blood supply to a major organ. However, cardioprotection was subsequently demonstrated using brief periods of ischemia to skeletal muscle.4 Thus, we arrive at the paradigm for RIC used today. Brief periods of non-lethal ischemia are applied to a limb, with the aim of inducing ischemic tolerance in a distant organ.
Several protocols exist for RIC. The stimulus can be given before, during, or after an ischemic event, referred to respectively as remote ischemic preconditioning (RIPreC), remote ischemic perconditioning (RIPerC), and remote ischemic postconditioning (RIPostC; see Figure 1). Ischemia is achieved by the inflation of a blood pressure cuff to supra-systolic pressures in one or multiple limbs. Most administration protocols involve four to five cycles of cuff inflation for 5 min. While early clinical studies predominantly used a single episode of RIC, given around the time of an ischemic event, increasingly, chronic RIC (CRIC) is used. This requires participants to carry out daily RIC as described above for several days, weeks, or even months.

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