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.

Tuesday, August 28, 2018

Amphetamine regimen does not improve post-stroke motor recovery

So explain this then.

Motor recovery and axonal plasticity with short-term amphetamine after stroke

They achieved full motor recovery in rats.

The negative research here: 

Amphetamine regimen does not improve post-stroke motor recovery

A pilot clinical trial exploring the benefit of d-amphetamine combined with physical therapy for stroke patients found no evidence that the regimen improved post-stroke motor recovery.
The results, which were published in the August 27, 2018 issue of JAMA Neurology, are "another step to better understand an approach that may or may not eventually lead to a new way of improving recovery," said Dr. Larry Goldstein, chairman of Neurology at the University of Kentucky and the study's lead author.
Amphetamines were first synthesized in 1887 by Romanian chemist Lazar Edeleanu, but it wasn't until the late 1920's that amphetamines were identified as a medically useful mood and energy booster. By World War II, soldiers were using amphetamines to combat fatigue and improve morale; the military routinely distributed the drug to pilots flying long missions. In the 1960's, however, the medical community's enthusiasm for the drug as a safe and popular remedy for depression and fatigue faded.
Two decades later, the question came full circle when Sciencepublished the results of a complex, placebo-controlled study demonstrating that rats with brain injuries who were given amphetamines in conjunction with physical therapy showed notable improvement in motor function. Other studies in cats and mice suggested similar improvements.
Since then, the scientific community has worked to extend these successes to humans and further define the parameters for optimal efficacy, e.g. dose, timing/frequency/intensity of physical therapy, but with inconsistent results.
Goldstein et al aimed to further inform the debate. Their study screened 1665 ischemic stroke patients in five rehabilitation hospitals or inpatient units. Sixty-four participants were randomized to receive either 10mg of d-amphetamine or placebo combined with a one-hour physical therapy session every four days for six sessions, in addition to standard rehabilitation. Treatment began between ten and 30 days after ischemic stroke.
The primary outcome was defined as a difference in the change in Fugl-Meyer Motor scores, an impairment index assessing motor function, balance, and sensation. The study also assessed changes in the NIH-Stroke Scale, Canadian Neurological Scale, Action Research Arm test, Rankin Score, Functional Independence Measure, Ambulation Speed and Endurance, Mini Mental State examination, Beck Depression Index and the Stroke Impact Scale as secondary measures. Participants were tested at baseline, the end of treatment and again at three months post-stroke.
Resulting data showed no overall treatment-related difference in Fugl-Meyer Motor scores between baseline and 3-month post-stroke in the two test groups (18.65+2.27 points with d-amphetamine vs. 20.83+2.94 points with placebo). The two groups were equally comparable on all secondary outcome measures as well, and there was no difference in subgroups based on stroke location or baseline severity.
Goldstein said the next step is to explore other dosing regimens, treatment intervals and times between stroke and beginning treatment -- all factors that are important based on animal studies.
"The concept of using amphetamines as part of a regimen for stroke recovery is biologically complex, and this pilot was specifically designed to explore some of that complexity," he said. "This data should help elucidate the parameters for continued study."

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