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.

Wednesday, July 17, 2013

Prevention of Post-Stroke Disuse Muscle Atrophy with a Free Radical Scavenger

What is your doctor going to do with this information?
http://www.karger.com/Article/FullText/346424

Abstract

In spite of appropriate treatment in the acute phase of stroke, quite a few patients with hemiparetic stroke become disabled and stay in a wheelchair or bedridden state in the chronic phase. In stroke patients, gait dysfunction results mainly from severe hemiparesis due to ischemic damage to the motor neuron tract and partly from disuse muscle atrophy in paretic and nonparetic legs. Disuse muscle atrophy occurs even in healthy subjects as early as 4 days after bed rest immobilization and progresses further correlating with the duration of immobilization. Although detailed mechanisms of disuse muscle atrophy remain unclear, free radical scavengers are known to play an important role in the development of disuse muscle atrophy. One of the neuroprotective agents, edaravone, a free radical scavenger, succeeded in proving clinical usefulness in a phase III clinical trial in Japan.

In this trial, stroke patients were administered edaravone for 14 days consecutively. The results of the edaravone trial are taken to indicate that long-term administration of a free radical scavenger may prevent disuse atrophy thereby improving functional outcome. We performed a randomized pilot study in hemiparetic stroke patients to test the validity of this view. Acute stroke patients were randomly allocated to two groups, one receiving edaravone for 3 days (short-term group) and the other for 10-14 days (long-term group). At 3 months after stroke, the grade of femoral muscle atrophy was significantly milder and the maximum walking speed was significantly faster in the long-term group than in the short-term group.

The study suggests that long-term administration of a free radical scavenger may prevent the development of leg disuse atrophy thereby ameliorating locomotor function. Attention should be paid to myoprotective drug therapy in acute stroke, since it may be easier and clinically more effective than neuroprotective therapy from the viewpoint of functional prognosis.

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