Poststroke dorsiflexor weakness and paretic limb foot drop increase the risk of stumbling and falling and decrease overall functional mobility. It is of interest whether dorsiflexor muscle weakness is primarily neurological in origin or whether morphological differences also contribute to the impairment. Ten poststroke hemiparetic individuals were imaged bilaterally using noninvasive medical imaging techniques. Magnetic resonance imaging was used to identify changes in tibialis anterior muscle volume and muscle belly length. Ultrasonography was used to measure fascicle length and pennation angle in a neutral position. We found no clinically meaningful bilateral differences in any architectural parameter across all subjects, which indicates that these subjects have the muscular capacity to dorsiflex their foot. Therefore, poststroke dorsiflexor weakness is primarily neural in origin and likely due to muscle activation failure or increased spasticity of the plantar flexors. The current finding suggests that electrical stimulation methods or additional neuromuscular retraining may be more beneficial than targeting muscle strength (i.e., increasing muscle mass). 1. Introduction In the United States alone, about 795,000 people suffer from a new or recurrent stroke each year [1]. Stroke survivors often suffer from hemiparesis or muscle weakness on one side of the body. Foot drop commonly occurs from muscle weakness in the paretic leg and manifests itself as a decrease in dorsiflexion range of motion [2]. For many poststroke survivors, paretic limb foot drop increases the risk of stumbling and falling and decreases functional mobility [2]. It is unclear whether dorsiflexor weakness is solely due to neurological impairment following stroke or whether changes in the muscle architecture are additional contributing factors. Muscle fascicle length and pennation angle (i.e., the angle in which the fascicles insert themselves into the aponeuroses of the muscle) are two architectural parameters that can influence how a muscle generates force. Varying these two parameters can alter the functional ability of a muscle, including range of motion and total force production [3]. Therefore, changes in fascicle length or pennation angle may contribute to post-stroke dorsiflexor weakness [4]. Medical imaging techniques (e.g., ultrasonography and magnetic resonance imaging) are often used to study muscle architecture in vivo in healthy populations and patients with neurological disorders [5–11]. However, little is known about poststroke muscle architectural changes. In the
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