Sensorimotor deficits in patients with central nervous system lesions: Explanations based on the lambda model of motor control

Reflex and motor deficits such as spasticity, limitations in force regulati on, inappropriate agonist/antagonist coactivation and movement segmentation are common sequelae of central nervous system (CNS) lesions. However, the disturbed control mechanisms underlying such deficits are still unclear. Da ta are presented according to which sensorimotor deficits in the elbow of a dult stroke patients and children with cerebral palsy (CP) may be related t o limitations in the regulation of stretch reflex (SR) thresholds (lambda s ) for elbow flexors and extensors. The presence of sensorimotor deficits is discussed within the framework of the lambda model of motor control by the analysis of: (1) velocity-dependent stretch reflexes in elbow flexors and extensors in stroke and CP patients and (2) angular ranges in which recipro cal or coactivation patterns of elbow flexor and extensor activity occur du ring reflex and voluntary activation in stroke patients. At least one bound ary of the SR threshold range for both flexors and extensors was located wi thin the physiological range of the elbow joint in all children with CP. In hemiparetic adults, SR thresholds were found within the physiological rang e for flexors in all but one subject and for extensors in 1/3 of the subjec ts. In addition, in hemiparetic adults? the angular ranges in which either agonist or antagonist muscle activity could be generated were decreased in all but one subject suggesting a limitation in the range of regulation of c entral commands responsible for reciprocal coordination between muscles. He miparetic adults with the most severe motor deficits were unable to specify anticipatory coactivation in the arm muscles to stabilize final arm positi on after sudden unloading. Limitations in SR threshold regulation may be a basic mechanism underlying sensorimotor deficits in patients with spastic m ovement disorders such as stroke and CP. This may account for abnormal move ment patterns and decreases in voluntary ranges of motion, maximal torques and speeds of movement seen in these patients. It also may account for musc le weakness and spasticity in parts of the physiological range. (C) 2000 El sevier Science B.V. All rights reserved. PsycINFO classification: 3297; 233 0.