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.

Monday, October 2, 2017

Spastic cocontraction of triceps surae increases with the tension applied during swing phase of gait in chronic hemiparesis

In conclusion, I see absolutely nothing here that helps survivors get recovered. You try to decipher the results paragraph. 

Spastic cocontraction of triceps surae increases with the tension applied during swing phase of gait in chronic hemiparesis










Objective

The present study aimed to quantify the impact of the tension applied on triceps surae during the swing phase of gait on its cocontraction in chronic hemiparesis.

Material/patients and methods

Forty-one subjects with chronic hemiparesis (50 ± 15 years; time since lesion, 7 ± 7 years; mean ± SD) completed a kinematic gait analysis, barefoot at comfortable speed (10 opto-electronic cameras, 6 dynamometric force plates, 27 ± 13 cycles analyzed/subject), with electromyography of soleus (so) and gastrocnemius medialis (gm) on the paretic side. The Coefficients of Spastic Cocontraction, CSCso and CSCgm, 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). In addition, a coefficient of lengthening of triceps surae, CLts, was computed over each period in the sagittal plane, from the ankle/knee displacements recorded during the period of interest divided by the total range of ankle/knee movements measured across all gait cycles. CSCso, CSCgm and CLts were compared between the 3 periods (ANOVA, significant effect P < 0.05). Exploration of individual correlations were performed with all gait cycles of each patient, using univariate regression analysis with CLts as predictor and coefficients of spastic cocontraction (CSCso and CSCgm) as dependent variables.

Results

Between T2 et T3, CSCso increased by 233 ± 54% (mean ± SEM, P < 1E-5) and CSCgm by 67 ± 10% (P = 0.0017). CLts increased by 23 ± 7% in T2 (P = 0.009) and 52 ± 12% in T3 (P < 1E-5). CLts was positively correlated with CSCso in 63% of cases (n = 25, r = 0.63 ± 0.04, P < 0.1) and with CSCgm in 53% of cases (n = 21, r = 0.60 ± 0.04, P < 0.1).

Discussion – conclusion

In chronic hemiparesis, tension (lengthening) applied on triceps surae is associated with the increase of its spastic cocontraction during swing phase of gait at comfortable speed.

No comments:

Post a Comment