Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Thursday, May 4, 2017

Dalfampridine Improves Cognitive Impairment in Multiple Sclerosis

Would this help post-stroke? It seemed to fail in walking post-stroke. Since I have never been able to find out if stroke demyelinates nerves in the brain, that answer may tell us whether this would work for stroke. So ask your doctor that question, 'Does stroke demyelinate nerves in the brain?'  A neurologist I saw once tried to tell me that was the case but I think he was just blowing smoke out his ass, trying to pull the stunt that I(the doctor) know more than you, so just shut up about questions.

Acorda ditches dalfampridine poststroke walking studies

Ask your doctor for help in getting this clinically tested in stroke patients, you shouldn't have to ask, it should already be part of their goals and objectives. Assuming the stroke department head is competent and actually wants to solve all the problems in stroke.

Dalfampridine Improves Cognitive Impairment in Multiple Sclerosis

By Alex Morrisson
BOSTON -- May 2, 2017 -- Treatment with dalfampridine appears to improve cognitive impairment and some cognitive functioning tasks among patients diagnosed with multiple sclerosis (MS), according to clinical trial results presented at the 2017 Annual Meeting of the American Academy of Neurology (AAN).
“Dalfampridine should be considered as an effective treatment option for cognitive impairment in multiple sclerosis,” said lead author Laura De Giglio, MD, PhD, Sapienza University, Rome, Italy, speaking here on April 26.
Dr. De Giglio and colleagues randomised subjects in a 2:1 fashion to receive either 10-mg dalfampridine twice daily or placebo for 12 weeks.
Baseline score in the Symbol Digit Modalities Test (SDMT) was a mean of 30 seconds. The primary endpoint of the study was the improvement of processing speed measured with SDMT. Four weeks after the end of treatment, evaluable patients treated with dalfampridine (n = 70) achieved a scoring increase of 9.89 seconds on the Symbol Digit Modalities Test (SDMT) compared with evaluable patients on placebo (n = 37) who achieved a scoring increase of 4.89 seconds (P = .001).
In all, 76.1% of subjects treated with dalfampridine achieved at least a 20% improvement in the SDMT compared with 41.4% of the subjects receiving placebo (P = .001).
On a variety of secondary measures, subjects taking dalfampridine also showed some improvement on spatial memory, cognitive fatigue, and the overall Multiple Sclerosis Functional Composite.
Most subjects were in their mid-to-late 40s; about 60% were female. Subjects had a diagnosis of multiple sclerosis for about 15 years.
“Thirty-five to sixty percent of multiple sclerosis patients are believed to have some cognitive dysfunction, but results of treatment for this aspect of the disease have been limited or inconsistent,” noted Dr. De Giglio.
Dalfampridine, approved in the United States to improve walking difficulty in patients with MS, is a selective neuronal potassium-channel blocker that is designed to improve conduction of action potential in demyelinated nerve fibers. The drug is believed to increase the release of neurotransmitters in synapses and at the neuromuscular junctions.
Funding for this study was provided by Biogen, Cambridge, Massachusetts.
[Presentation title: Dalfampridine Improves Cognitive Impairment in Multiple Sclerosis (MS): Results From a Randomised, Double-blind, Placebo-controlled Trial.]

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