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.

Sunday, August 11, 2013

Neural and Muscular Determinants of Dorsiflexor Weakness in Chronic Stroke Survivors

Meaningless to me but your doctor will know all about it and tell you in the next week.
http://journals.humankinetics.com/mc-current-issue/mc-volume-17-issue-3-july/neural-and-muscular-determinants-of-dorsiflexor-weakness-in-chronic-stroke-survivors
Few examined the contribution of neural and muscular deficits to weakness in the same stroke subject. We determined maximal voluntary contraction (MVC) and 50 Hz torques, activation (twitch interpolation), electromyographic (EMG) amplitude and antagonist coactivation, and muscle volume using magnetic resonance imaging (MRI) of the dorsiflexors bilaterally in 7 chronic stroke subjects (40–67 y). Recordings of MVC and 50 Hz torque were also done in 7 control subjects (24–69 y) without stroke. The MVC torque was smaller in the contralesional than ipsilesilesional limb (29.8 ± 21.3 Nm vs. 42.5 ± 12.0 Nm, p = .04), and was associated with deficits in activation (r2 = .77) and EMG amplitude (r2 = .71). Antagonist coactivation percentage was not significantly different between limbs. Muscle volume, 50 Hz torque, and specific torque (50Hz torque/muscle volume) were also not different between sides. The concept that atrophy is commonplace after stroke is not supported by the results. Our findings indicate that dorsiflexor weakness in mobile stroke survivors is not explained by atrophy or reduced torque generating capacity suggesting an important role for central factors.
Keywords: muscle function, special needs populations, strength, isometric

Authors: Cliff S. Klein, Geoffrey A. Power, Dina Brooks, Charles L. Rice
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