Stiff Knee Gait Disorders as Neuromechanical Consequences of Spastic Hemiplegia in Chronic Stroke.
botulinum toxin
gait
nerve block
spasticity
stroke
Journal
Toxins
ISSN: 2072-6651
Titre abrégé: Toxins (Basel)
Pays: Switzerland
ID NLM: 101530765
Informations de publication
Date de publication:
07 03 2023
07 03 2023
Historique:
received:
03
01
2023
revised:
06
02
2023
accepted:
06
03
2023
medline:
30
3
2023
entrez:
28
3
2023
pubmed:
29
3
2023
Statut:
epublish
Résumé
Stiff knee gait (SKG) is defined as decreased knee flexion during the swing phase. It is one of the most common gait disorders following stroke. Knee extensor spasticity is commonly accepted as the primary cause. Clinical management has focused on the reduction in knee extensor spasticity. Recent advances in understanding of post-stroke hemiplegic gait suggest that SKG can present as mechanical consequences between muscle spasticity, weakness, and their interactions with ground reactions during walking. Various underlying mechanisms are presented through sample cases in this article. They include ankle plantar flexor spasticity, knee extensor spasticity, knee flexor and extensor coactivation, and hip flexor spasticity. Careful and thorough clinical assessment is advised to determine the primary cause for each patient. Understanding of these various presentations of SKG is helpful to guide clinical assessment and select appropriate target muscles for interventions.
Identifiants
pubmed: 36977095
pii: toxins15030204
doi: 10.3390/toxins15030204
pmc: PMC10053067
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
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