Deans' stroke musings

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Tuesday, September 27, 2016

Spastic cocontraction of plantar flexors during swing phase of gait in chronic hemiparesis

No clue what use this is going to be in getting you to 100% recovery. Bet your doctor doesn't either. Lots of fucking data but no content.
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In spastic hemiparesis, quantify agonist recruitment of tibialis anterior and triceps surae spastic cocontraction during swing phase of gait.

Material/Patients and methods

Thirty-seven subjects with chronic hemiparesis (49 ± 14 years, mean ± SD; time since lesion, 8 ± 7 years) performed a 3D gait analysis, barefoot at comfortable speed (10 optoelectronic cameras, 6 dynamometric force plates, analysis of 9 cycles), with bilateral electromyography of tibialis anterior (TA), soleus (SO) and gastrocnemius medialis (GM). Speed, step length and maximal active dorsiflexion during swing were measured. Indices of agonist recruitment, IRATA, and spastic cocontraction, ICCSO and ICCGM, were calculated over 3 periods of swing phase (T1, [0–33%]; T2, [34–66%]; T3, [67–100%]), by the ratio of the RMS of the electromyogram in the period of interest over the RMS of the electromyogram of the same muscle over 100 ms around the maximal agonist isometric activity (measured on standing position by a maximal effort against resistance). IRA and ICC were compared between the 3 periods and between paretic and non paretic sides using repeated measures MANOVA (significant effect, P < 0.05).


Speed, 0.68 ± 0.26 m/s; paretic step length, 0.48 ± 0.12 m, non paretic, 0.43 ± 0.15 m; paretic maximal active dorsiflexion, −3 ± 8°, non paretic, 6 ± 4°.
On the paretic side: IRATA decreased between T1 and T2 (T1, 0.69 ± 0.59; T2, 0.48 ± 0.39, P = 2E-4) and then remained unchanged at T3 (0.47 ± 0.45; vs T1, P = 1E-4; vs T2, ns), while ICCSO and ICCGM increased at T3 only (ICCSO, T2, 0.25 ± 0.21; T3, 0.57 ± 0.50; P = 5E-8; ICCGM, T2, 0.39 ± 0.40; T3, 0.59 ± 0.50; P = 2E-4). On the non-paretic side, IRATA, ICCSO and ICCGM remained unchanged (IRATA, T1, 0.32 ± 0.20; T2, 0.23 ± 0.13; T3, 0.25 ± 0.10, ns; ICCSO, T1, 0.12 ± 0.12; T2, 0.13 ± 0.12; T3, 0.25 ± 0.18 ns; ICCGM, T1, 0.17 ± 0.31; T2, 0.19 ± 0.27; T3, 0.26 ± 0.25 ns). Side xperiod effect, P = 0.04.

Discussion - Conclusion

During comfortable gait in chronic hemiparesis, there is a decrease in tibialis anterior recruitment from mid-swing phase on and an increase in soleus and gastrocnemius spastic cocontraction at late swing were found.

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