Contribution of passive stiffness to ankle plantarflexor moment during gait after stroke.
OBJECTIVE
To measure the contribution of passive stiffness to the ankle plantarflexor moment during gait in subjects with hemiparesis early after stroke. The relationship of passive stiffness with gait speed was also examined.


METHODS
Cross-sectional, descriptive.


METHODS
A sample of convenience of 14 patients (54.7+/-10.9 yrs) with a hemiparesis for less than 5 months and 11 healthy controls (50.6+/-11.6 yrs).


METHODS
The contribution of passive stiffness to the plantarflexor moment during gait was obtained using moment-angle slope (stiffness) values. Total plantarflexor stiffness was measured during gait, and passive stiffness was measured during passive dorsiflexion imposed by an isokinetic dynamometer at velocities and ranges of movement matched with values recorded during the plantarflexor lengthening period of the stance phase. The contribution of passive stiffness was obtained by dividing the passive stiffness (dynamometer) by the total plantarflexor stiffness (gait).


RESULTS
On the paretic side, passive stiffness contributed more (16.8%; range 2.9% to 49.6%) to total plantarflexor stiffness during gait compared (p<.01) with both the nonparetic side (7.3%) and control values (5.9%). This increased contribution on the paretic side resulted from a large muscle-tendon passive stiffness, a decreased active muscle contribution, or both. Although in some patients the increased passive component led to the development of a total plantarflexor stiffness that was within normal values, it did not in others either because the active component was very small or because limited dorsiflexion during the stance phase prevented the passive component tension to develop. The contribution of passive stiffness was not significantly (p>.05) related to gait speed in both the patients and the controls.


CONCLUSIONS
The increased contribution of passive stiffness to total plantarflexor moment during gait likely acts as an adaptation for a defective muscle active component, helping ankle push-off at the end of the stance phase. Although this mechanism is effective in most of the patients, it cannot come into action if the dorsiflexion movement during the stance phase is prevented, for instance, by enhanced stretch reflexes.
Lamontagne
A
A
Rehabilitation Research Group, Rehabilitation Institute of Quebec, Canada.
Malouin
F
F
Richards
C L
CL
D000328:Adult; D000368:Aged; D000843:Ankle Joint / Q000503:physiopathology*; D003430:Cross-Sectional Studies; D005260:Female; D005528:Foot / Q000503:physiopathology; D005684:Gait; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000503:physiopathology; D010291:Paresis / Q000503:physiopathology*; D020521:Stroke / Q000503:physiopathology*