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:

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.
My back ground story is here:

Saturday, August 25, 2018

Electrical Brain Stimulation May Improve Post-Stroke Aphasia

May improve should never be allowed in stroke research. Either it improves it and is written up as a stroke protocol or it doesn't work and you plainly say that. This is totally fucking worthless when  stuff like this is even written.

They don't tell you what type of tDCS(anodal tDCS? cathodal tDCS? HD-tDCS?)

Electrical Brain Stimulation May Improve Post-Stroke Aphasia

Patients with long-term aphasia named more words with noninvasive technique

  • by Contributing Writer, MedPage Today
  • This article is a collaboration between MedPage Today® and:
    Medpage Today

Action Points

  • Anodal transcranial direct current stimulation (A-tDCS) applied to the injured left brain hemisphere improved speech function in stroke patients with long-term aphasia, in a small, randomized, double-blind study.
  • Note that A-tDCS is non-invasive, passing direct current through the scalp/skull to the brain, producing a subthreshold modulation of resting membrane potentials, thereby modifying the function of distributed brain networks.
Transcranial direct current stimulation appeared helpful in stroke patients with long-term aphasia and is worthy of further study, researchers said.
In a double-blind randomized clinical trial, stroke patients with long-term aphasia who had anodal transcranial direct current stimulation (A-tDCS) combined with speech therapy correctly named an average of 13.9 words, compared with 8.3 words for patients who had sham tDCS with speech therapy, reported Julius Fridriksson, PhD, of the University of South Carolina in Columbia, and colleagues in JAMA Neurology.
"Transcranial direct current stimulation applied to the injured hemisphere improves rehabilitation outcome in stroke patients with aphasia," Fridriksson told MedPage Today. "The improvements are long lasting -- at least 6 months following rehabilitation -- and may benefit a large group of patients."
Transcranial direct current stimulation uses an electrical current (1 to 2 mA) induced between two electrodes on the scalp. It is part of an emerging branch of stroke therapeutics that targets neural repair, aiming to improve outcomes by promoting neuroplasticity within surviving neural elements, observed Steven Cramer, MD, MMSc, of the University of California Irvine, in an accompanying editorial.
Neural repair therapies being studied include small molecules, growth factors, monoclonal antibodies, brain stimulation, and other treatments. Compared with systemic drugs, tDCS offers patients reduced toxicity, "given that trillions of cells outside the brain are not exposed," Cramer noted. "Transcranial direct current stimulation has the additional advantage that it is noninvasive, passing direct current through the scalp/skull to the brain, producing a subthreshold modulation of resting membrane potentials, and thereby modifying the function of distributed brain networks."
In this double-blinded randomized clinical trial, Fridriksson and colleagues used a futility design to test adjunctive A-tDCS at two outpatient sites. From August 2012 to March 2017, the researchers enrolled patients with long-term aphasia (over 6 months) from a previous left hemisphere stroke, following them for 6 months. Patients had outpatient speech therapy for 3 weeks -- 15 sessions of 45 minutes each -- with either A-tDCS (1 mA) or sham tDCS applied to preserved left temporal lobe regions.
Patients in the treatment and sham group were matched based on site, baseline age, type of aphasia, and aphasia severity. A total of 34 patients had adjunctive A-tDCS and 40 patients had sham therapy. In both groups, the average age was 60 years and 70% were men. The A-tDCS participants were 44 months from stroke onset; the sham participants were 40 months from onset. About 53% of patients in both groups had Broca aphasia.
The primary outcome was the ability to name common objects, assessed twice before and after therapy sessions. From baseline to 1-week post-treatment, the adjusted mean change was 13.9 words (SE 2.4, 95% CI 9.0-18.7) for A-tDCS combined with speech therapy and 8.2 words (SE 2.2, 95% CI 3.8-12.6) for sham tDCS combined with speech therapy. This represented an absolute increase of 5.7 words (SE 3.3, 95% CI -0.9 to 12.3) and a relative increase of 70% for active tDCS compared with sham. No serious adverse events were associated with A-tDCS.
In the futility design, the primary null hypothesis assumed adjunctive A-tDCS would lead to at least a 1.5-item greater improvement in correct naming compared with sham, while the alternative hypothesis assumed no difference between treatment and sham. The P value for the futility hypothesis was 0.90, meaning the null hypothesis could not be rejected and further study of adjunctive A-tDCS would not be futile.
"Our plan is to replicate the current findings in a similar trial to verify the effects of the current trial," Fridriksson said. A follow-up paper will describe how genetic differences are related to tDCS response, he added: "The genetic marker will better enable clinicians to select patients who are good candidates for tDCS administration during aphasia rehabilitation."
This study was not powered for superiority analyses and no conclusions about the effectiveness of A-tDCS can be drawn from it. The authors also pointed out that they "cannot definitively determine that the naming improvements translate to improvements in quality of life."
This research was funded by the National Institute on Deafness and Other Communication Disorders.
Fridriksson and the researchers reported no conflicts of interest.
Cramer serves as a consultant for Microtransponder, Dart NeuroScience LLC, Roche, Neurolutions Inc, Regenera, AbbVie, SanBio, and TRCare.
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