Following stroke, gait is often characterized by reduced flexion of the paretic limb accompanied by prolonged knee extension during late stance and swing. This movement pattern has been attributed to two competing origins: inadequate flexor activation and/or inappropriate extensor activation via excessive quadriceps activity. Evidence has demonstrated the dual importance of hip angle and limb load receptors in modulating muscle activity during the late stance phase of gait. Following stroke, however, the processing of afferent information may be disrupted by abnormal descending commands, which alter muscle activation and movement patterns. The primary goal of this proposal is to characterize the importance of hip angle sensors and load receptors in modulating activation patterns post-stroke to determine their respective role in contributing to abnormal gait. The primary hypothesis is that hyperexcitable heteronymous stretch reflexes from hip flexors onto knee extensors play a critical role in the mistiming of extensor activity and thus in gait abnormalities. The proposed experiments involve a careful examination of muscle activation patterns in response to isolated joint movements during passive conditions as well as during perturbed walking. Although appropriate afferent inputs associated with limb load and hip position are thought to be necessary for retraining 'normal' walking patterns after stroke, there are no quantitative studies which examine the role of hip angle and limb load in modulating muscle activity after stroke. [unreadable] [unreadable]