Article

The mechanism and time course of increased wrist joint stiffness
poststroke and clinically observed wrist flexion deformity is still not well
understood. The components contributing to increased joint stiffness are of
neural reflexive and peripheral tissue origin and quantified by reflexive torque
and muscle slack length and stiffness coefficient parameters. OBJECTIVE: To
investigate the time course of the components contributing to wrist joint
stiffness during the first 26 weeks poststroke in a group of patients, stratified
by prognosis and functional recovery of the upper extremity. METHODS: A total of
36 stroke patients were measured on 8 occasions within the first 26 weeks
poststroke using ramp-and-hold rotations applied to the wrist joint by a robot
manipulator. Neural reflexive and peripheral tissue components were estimated
using an electromyography-driven antagonistic wrist model. Outcome was compared
between groups cross-sectionally at 26 weeks poststroke and development over time
was analyzed longitudinally. RESULTS: At 26 weeks poststroke, patients with poor
recovery (Action Research Arm Test [ARAT] </=9 points) showed a higher predicted
reflexive torque of the flexors ( P < .001) and reduced predicted slack length (
P < .001) indicating shortened muscles contributing to higher peripheral tissue
stiffness ( P < .001), compared with patients with good recovery (ARAT >/=10
points). Significant differences in peripheral tissue stiffness between groups
could be identified around weeks 4 and 5; for neural reflexive stiffness, this
was the case around week 12. CONCLUSIONS: We found onset of peripheral tissue
stiffness to precede neural reflexive stiffness. Temporal identification of
components contributing to joint stiffness after stroke may prompt longitudinal
interventional studies to further evaluate and eventually prevent these phenomena.

Langue : ANGLAIS