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Clinical Trial Controlled Clinical Trial
Deficits in the coordination of agonist and antagonist muscles in stroke patients: implications for normal motor control.
- M F Levin, R W Selles, M H Verheul, and O G Meijer.
- Rehabilitation Institute of Montreal and University of Montreal, Montreal, Canada. levinm@ere.umontreal.ca
- Brain Res. 2000 Jan 24; 853 (2): 352-69.
AbstractMovement impairments about a single joint in stroke patients may be related to deficits in the central regulation of stretch reflex (SR) thresholds of agonist and antagonist muscles. One boundary of the SR threshold range for elbow flexor and extensor muscles was measured in hemiparetic subjects by analysing electromyographic activity during stretching of relaxed muscles at seven different velocities. For each velocity, dynamic SR thresholds were measured as angles at which electromyographic activity appeared. These data were used to determine the sensitivity of the threshold to velocity and the static SR thresholds for flexors and extensors. In contrast to relaxed muscles in healthy subjects, static flexor and extensor thresholds lay within the physiological range in 11/12 and 4/12 subjects, respectively. This implies that, in the range between the static SR threshold and one of the physiological joint limits, relaxation of the muscle was impossible. Subjects then made slow movements against different loads to determine their ranges of active movement. Maximal flexor and extensor torques were lower in hemiparetic subjects throughout the angular range. In some subjects, ranges were found in which no active torque could be produced in either extensor or both muscle groups. These ranges were related to the boundary values of SR thresholds found during passive muscle stretch. The range in which reciprocally organized agonist and antagonist muscle activity could be generated was limited in all but one subject. When attempting to produce torque from positions outside their measured range of movement, excessive muscle coactivation occurred, typically producing no or paradoxical motion in the opposite direction. Results suggest a relationship between spasticity measured at rest and the movement deficit in stroke by demonstrating a link between motor deficits and control deficits in the central regulation of individual SR thresholds.
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