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, February 25, 2024

Does Limited Dorsiflexion during Swing Phase in Hemiparesis Depend on Spasticity?

So you described a problem but failed to do ONE DAMN THING to solve it? That is pure incompetence! Stroke research should get survivors recovered!

 Does Limited Dorsiflexion during Swing Phase in Hemiparesis Depend on Spasticity?

Maria Vinti * , Mathias Blandeau * , Hélène Pillet , Wafa Skalli , Philippe Decq , Andrea Merlo ,
Jean-Michel Gracies , Nicolas Bayle , Mouna Ghédira , Emilie Hutin
Posted Date: 19 February 2024
doi: 10.20944/preprints202402.0932.v1
Maria Vinti PhD 1, *, Mathias Blandeau PhD 2, *, Hélène Pillet PhD 3, Wafa Skalli PhD 3,
Philippe Decq MD 3,4, Andrea Merlo PhD 5, Jean-Michel Gracies MD PhD 6,7,
Nicolas Bayle MD 6,7, Mouna Ghédira PhD 6,7 and Emilie Hutin PhD 6,7
1 Univ. Limoges, HAVAE, UR 20217, F-87000 Limoges, France
2 Univ. Polytechnic Hauts-de-France, CNRS, UMR 8201 LAMIH, F-59313, Valenciennes, France
3 Institut de Biomécanique Humaine Georges Charpak, Arts et Métiers Sciences et Technologies, Paris,
France
4 AP-HP, Service de Neurochirurgie, Hôpital Beaujon, Clichy, 92 France
5 LAM–Motion Analysis Laboratory, Neuromotor and Rehabilitation Department, Azienda USL-IRCCS di
Reggio Emilia, San Sebastiano Hospital, Correggio (RE), Italy
6 UR 7377 BIOTN, Université Paris-Est Créteil (UPEC), F-94000 Créteil, France
7 Laboratoire Analyse et Restauration du Mouvement, AP-HP, Service de Rééducation Neurolocomotrice,
Hôpitaux Universitaires Henri Mondor, F-94000 Créteil, France
* Correspondence: mariaconcetta.vinti@unilim.fr (M.V.); mathias.blandeau@uphf.fr (M.B.)

Abstract: 

Plantar flexors (PF) spasticity is known to poorly correlate with active dorsiflexion (DF)
impairment throughout the swing phase of hemiparetic gait. Spastic Cocontraction, instead,
stemming from descending pathways, potentially misdirect antagonist PF activity opposing DF
during swing. Electromyographic (EMG) recordings, while unable to differentiate between
reflex-based and descending origins, may offer valuable insights into this distinction by exploring
PF EMG activity after tibial nerve neurotomy (which eliminates PF spasticity). Eleven subjects with
hemiparesis walking at comfortable velocity and 11 controls walking at comfortable and slow
velocity, underwent kinematic and PF/DF EMG analysis. Five of the hemiparetic subjects
underwent tibial neurotomy >1 year prior. We evaluated spasticity at rest (Tardieu scale), maximal
ankle dorsiflexion, tibialis anterior agonist recruitment and gastrocnemius medialis and soleus
cocontraction coefficients during swing. At slow velocity, controls (0.80±0.12 m/s) moved at a
similar pace as hemiparetic subjects (0.73±0.37 m/s, NS). Hemiparetic subjects showed: (i) reduced
ankle DF across swing (ii) increased PF cocontraction, including before any DF (iii) higher
cocontraction despite absent spasticity in tibial neurotomy subjects (iv) higher tibialis anterior
recruitment. Increased PF cocontraction occurs in the absence of spasticity or ankle DF despite
higher agonist recruitment. Spastic cocontraction is a major factor limiting active DF at swing,
unlike spasticity.

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