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, June 28, 2011

Nicotinergic impact on focal and non-focal neuroplasticity induced by non-invasive brain stimulation in non-smoking humans

I think this says nicotine in patch form helps with neuroplasticity. 32 pages in all.
http://repository.peerproject.eu:8080/jspui/bitstream/123456789/15484/1/PEER_stage2_10.1038%252Fnpp.2010.227.pdf
Abstract
Nicotine improves cognitive performance and modulates neuroplasticity in brain networks. The
neurophysiological mechanisms underlying nicotine-induced behavioral changes have been
sparsely studied, especially in humans. Global cholinergic activation focuses plasticity in
humans. However, the specific contribution of nicotinic receptors to these effects is unclear.
Henceforth, we explored the impact of nicotine on non-focal neuroplasticity induced by
transcranial direct current stimulation (tDCS) and focal, synapse-specific plasticity induced by
paired associative stimulation (PAS) in healthy non-smoking individuals. Forty eight subjects
participated in the study. Each subject received placebo and nicotine patches combined with one
of the stimulation protocols to the primary motor cortex in different sessions. Transcranial
magnetic stimulation (TMS) - elicited motor evoked potential (MEP) amplitudes were recorded
as a measure of corticospinal excitability until the evening of the second day following the
stimulation. Nicotine abolished or reduced both PAS- and tDCS-induced inhibitory
neuroplasticity. Non-focal facilitatory plasticity was also abolished, whereas focal facilitatory
plasticity was slightly prolonged by nicotine. Thus, nicotinergic influence on facilitatory, but not
inhibitory plasticity mimics that of global cholinergic enhancement. Therefore, activating
nicotinic receptors has clearly discernable effects from global cholinergic activation. These
nicotine-generated plasticity alterations might be important for the effects of the drug on
cognitive function.
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