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.

Wednesday, May 27, 2015

Vinpocetine increases cerebral blood flow and oxygenation in stroke patients: a near infrared spectroscopy and transcranial Doppler study

Only 13 years old so I wonder if this is in use anywhere. I had not heard of this before except it seems to help in middle ear infections. Acute or hyperacute?
http://www.sciencedirect.com/science/article/pii/S092982660200006X
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Abstract

Objective: To investigate the effect of vinpocetine on cerebral blood flow (CBF) in the compromised circulation of a stroke affected hemisphere using transcranial Doppler (TCD) and near infrared spectroscopy (NIRS) methods.  
Methods: 43 patients with ischemic stroke were randomized into vinpocetine (VP) and placebo group in a double blind, placebo-controlled study of the effect of a single-dose i.v. infusion of vinpocetine on cerebral blood perfusion and oxygenation. In the VP group 20 mg VP in 500 ml saline, in the placebo group 500 ml saline alone were administered. The concentrations of oxy-, reduced- and total hemoglobin were measured by NIRS frontolaterally on the side of lesion while the mean cerebral blood flow velocity (CBFV), the pulsatility index (PI) and Doppler spectral intensity (DSI) were monitored by TCD in the middle cerebral artery on the same side. Values were averaged for the first 5 min prior to the infusion and for the last 5 min of infusion and they were compared between groups.  
Results: The concentration of all three chromophores increased during infusion in the VP group (mean dHbT=1.03, CI95=0.84, P=0.058; mean dHbO=0.92, CI95=0.91, P=0.071; mean dHb=0.10, CI95=0.21, P=0.297). The HbT and HbO showed a substantially smaller increase in the placebo group (mean dHbT=0.31, CI95=0.74, P=0.22; mean dHbO=0.57, CI95=0.80, P=0.094) while the Hb decreased (mean dHb=−0.26, CI95=0.29, P=0.05). Comparing to the placebo group Hb increased significantly in the VP group (P=0.027) while the increase of HbO and HbT did not reach the level of significance (P=0.29 and 0.11). DSI showed a significantly larger increase in the VP than in placebo group (dDSI=25.8 CI95=8.8 [VP]; dDSI=3.3, CI95=3.7 [Placebo], P<0.005). The CBFV and PI did not differ significantly between groups. (dVm=5.0±2.98 cm/s [VP], dVm=4.1±2.57 cm/s [Placebo], P=0.28; dPI=0.08 [VP], dPI=0.09 [Placebo]; P=0.47).  
Conclusion: VP increases cerebral perfusion and parenchymal oxygen extraction as well. The increased perfusion was indicated by NIRS and by TCD measurement of DSI while conventional velocity and pulsatility measurements failed to detect theses effects. NIRS is a sensitive, feasible method of measuring changes in regional blood flow and tissue oxygenation in the superficial cortex.

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