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 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:

Tuesday, May 15, 2018

F72. Contralesional brain activity in acute ischemic stroke

I can't see any use of this. Describes what is happening but gives no interventions to accomplish that to help survivor recovery. The point of stroke research is to help patients recover. The president of that great stroke association should be forcefully communicating that to all stroke researchers.  But we have fucking failures of stroke associations instead.


The non-injured, contralateral hemisphere is increasingly acknowledged in recovery from acute ischemic stroke. We estimate the value of conventional EEG recordings for identification of contralateral hemisphere involvement in relation to functional recovery.


We analyzed two-minute epochs from 21 electrode EEG registrations from 18 patients with acute hemispheric ischemic stroke and compared with 18 age-matched controls. Outcome was dichotomized as good (mRS 0–2) or poor (mRS 3–5 or death) at three months. Effects of the infarct on the ipsi- and contralateral hemispheres were analyzed by the delta/alpha ratio (DAR) and two measures of functional connectivity (magnitude squared coherence (MSC) and weighted phase lag index (WPLI)).


DAR was higher in patients than in controls, both in the ipsilateral and in the contralateral hemisphere (median 4.5 ± 6.7 ipsilateral and 2.4 ± 2.0 contralateral vs. 0.5 ± 0.5 in the control group, P < 0.001), indicating robust EEG changes in both lesioned and non-lesioned hemisphere. MSC and WPLI in the alpha and beta frequency bands were lower in patients than in controls in both hemispheres, indicating clear disturbances of functional connectivity (P < 0.05). In the poor outcome group, contralateral MSC and WPLI were lower than in the good outcome group, although these differences did not reach statistical significance.


Short conventional EEG measurements show robust changes of brain activity and functional connectivity in both ipsilateral and contralateral hemisphere of patients with acute ischemic stroke. Changes of remote functional connectivity tend to interact with functional recovery. Associations between contralateral functional connectivity measures and incidence of apathy and depression are currently analyzed and will be presented.
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