What the hell is the solution?
Don't do things only halfway.
http://ptjournal.apta.org/content/early/2014/02/26/ptj.20130322.abstract
- Marcela de Abreu Silva-Couto (marcela.deabreu@yahoo.com.br),
- Christiane L. Prado-Medeiros,
- Ana Beatriz Oliveira,
- Carolina Carmona Alcântara,
- Araci Teixeira Guimarães,
- Tania Fatima Salvini,
- Rosana Mattioli and
- Thiago Luiz Russo
+ Author Affiliations
Abstract
Background and Purpose
The muscle weakness that is exhibited post-stroke is due to a
multifactorial etiology involving central nervous system and
skeletal muscle changes. Insulin-like growth
factor I (IGF-1) and IGF binding protein 3 (IGFBP-3) have been described
as biomarkers
of neuromuscular performance in many conditions.
However, no information about these biomarkers is available for chronic
hemiparetic
subjects. Thus, the purpose of the present study
was to investigate possible factors involved to muscle weakness in
chronic
post-stroke subjects, such as serum IGF-1 and
IGFBP-3 concentrations, muscle volume and neuromuscular performance of
knee
flexors and extensors in chronic hemiparetic
post-stroke subjects.
Methods A
cross-sectional study was performed on 14 post-stroke subjects who were
paired with healthy controls. Mobility, functionality,
balance and quality of life were recorded as
outcome measures. The knee flexor and extensor muscle volumes and
neuromuscular
performance were measured by nuclear magnetic
resonance, dynamometry and electromyography. The serum concentrations of
IGF-1
and IGFBP-3 were quantified by ELISA.
Results The
hemiparetic group had low concentrations of serum IGF-1 (25%) and
IGFBP-3 (40%); reduced muscle volume in the vastus
medialis (32%), vastus intermedius (29%), biceps
femoris (16%), semitendinosus and semimembranosus (12%); reduced peak
torque,
power and work of the knee flexors and
extensors; and altered agonist and antagonist muscle activation compared
to controls.
Conclusions Low serum IGF-1 and IGFBP-3 concentrations, deficits in neuromuscular performance, selective muscle atrophy, and decreased
agonist muscle activation are presented in chronic post-stroke subjects.
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