A method to differentiate the causes of stiff-knee gait in stroke patients

Abstract Stiff-knee gait (SKG) is a common abnormal gait pattern in patients after stroke characterized by insufficient knee flexion (KF) during swing. Overactivity of the rectus femoris (RF) is considered the primary cause of SKG. Inadequate push-off has been indicated as an additional cause in the...

Full description

Saved in:
Bibliographic Details
Published in:Gait & posture 2013-06, Vol.38 (2), p.165-169
Main Authors: Campanini, I, Merlo, A, Damiano, B
Format: Article
Language:English
Subjects:
Aged
Biomechanical Phenomena
Botulinum toxin
Case-Control Studies
Female
Gait - physiology
Gait Disorders, Neurologic - diagnosis
Gait Disorders, Neurologic - etiology
Gait Disorders, Neurologic - physiopathology
Humans
Knee Joint - physiopathology
Male
Middle Aged
Muscle Spasticity - diagnosis
Muscle Spasticity - etiology
Muscle Spasticity - physiopathology
Muscle, Skeletal - physiopathology
Orthopedics
Push-off
Quadriceps Muscle - physiopathology
Range of Motion, Articular - physiology
Retrospective Studies
Spasticity
Stiff knee gait
Stroke
Stroke - complications
Thigh
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract Stiff-knee gait (SKG) is a common abnormal gait pattern in patients after stroke characterized by insufficient knee flexion (KF) during swing. Overactivity of the rectus femoris (RF) is considered the primary cause of SKG. Inadequate push-off has been indicated as an additional cause in the recent literature, as KF depends on knee flexion velocity in preswing (KFV). We used the peak of vertical acceleration of the malleolus (PMVA) as a kinematic-based indirect measure of push-off and studied its relationship with KF and KFV in a sample of 20 healthy subjects walking fast ( v = 95 ± 5%height s−1 ), at self-selected speed ( v = 74 ± 5%height s−1 ), slow ( v = 54 ± 6%height s−1 ) and very slow ( v = 38 ± 5%height s−1 ) and in a sample of 52 stroke patients with SKG (age 60 ± 11, v = 20 ± 11%height s−1 ). In healthy subjects PMVA occurred before knee flexion acceleration ( p < 0.001) and hip flexion acceleration ( p < 0.001). KF appeared as a bottom-up mechanism driven by the ankle push-off. From a regression analysis, the PMVA-KFV cause–effect relationship resulted strictly linear, with R2 = 0.967, KFV = 0 + 7.1 × PMVA, P < 0.0001. Data from SKG patients were compared to this normal cause–effect model. For 44/52 patients the reduced KFV was combined with lack of push-off. Data from 8/52 patients only were statistically outside the 95%CI of the model, thus requiring for a braking mechanism to explain KFV reduction. In stroke adults of our sample the push-off impairment (85% of cases) and not the inappropriate knee extension moment produced by the thigh muscles was the primary cause of SKG. This result could explain the low average efficacy (
ISSN:0966-6362
1879-2219
DOI:10.1016/j.gaitpost.2013.05.003