Mechanisms of Post-stroke Stiff-Knee Gait: A Narrative Review.
Kellen T Krajewski, J Sebastián Correa Bs, Ricardo Siu and 2 others
PMID 39815400WHAT IT FOUND
Post-stroke stiff-knee gait is not simply quadriceps spasticity.
Possible mechanisms include reflexes, abnormal tone, poor coordination, and weak push-off, and current definitions and tests are imprecise.
Key findings
01Stiff-knee gait after stroke is a swing-phase knee flexion pattern, not a fixed clinical diagnosis, and there is no agreed quantitative criterion.
02Quadriceps hyperreflexia is a prominent proposed mechanism, but abnormal tone, motor incoordination, and reduced propulsion may also contribute.
03Spasticity-targeting treatments such as botulinum toxin and baclofen have mixed results and reported only a ~5° increase in knee flexion.
STILL TO COME
How it was doneWhat they foundWhat it means for PTs
Read the rest of this summary
You get three full summaries a month, free, and we do not ask for a card. Search, the TL;DRs and your library stay unlimited either way.
What it does not show
This is a narrative review, not a systematic review or trial, so it does not show that any treatment works. The paper says there is no agreed quantitative criterion for stiff-knee gait and definitions vary, so studies may not be measuring the same thing. Many cited findings are associations from small, heterogeneous samples, not causal proof. Muscle synergy composition and somatosensory function have not been measured directly in people with stiff-knee gait. The authors say clinical strength and spasticity tests are imprecise and largely subjective, and misdiagnosis is possible.
Declared interests
The authors declare no competing interests and no financial benefits.
The easy way to misread this
Do not conclude that stiff-knee gait after stroke is caused by quadriceps spasticity or that botulinum toxin and baclofen are proven to restore knee flexion. The paper says the reviewed treatments have mixed results and only a ~5° increase in knee flexion.