Foot drop causes decreased mobility and functional disturbances in healthy walking patterns leading to limitations in activities in daily living and lng term disability. Functional electrical stimulation (FES) of the affected ankle dorsal flexors has been used to facilitate activation in individuals post stroke. The mechanisms and long-term effects of FES applied to the peroneal nerve are not well understood and the benefits of improving motor cortex excitability via afferent pathway demonstrated in neurologically normal subjects have not been fully explored in individuals with central neurologic disorders. Previous research evaluating the effect of FES treatment on re-gaining voluntarily control the ankle dorsiflexors or preventing foot drop is relatively small in individuals with stroke. This may be du to the indirect nature of FES effect on the corticospinal/descending pathway. As a rehabilitation therapy, although the use of FES for foot drop in chronic stroke appears promising it has not yet been demonstrated to be more effective than activity-based therapy widely used in physical therapy environment. Lack of motor ability hinders stroke patients with motor deficits from participating in repetitive high-intensity muscle contraction training (VOL, activity-based therapy), a potentially beneficial approach in restoring voluntary motor drive to the affected muscle to increase strength. Attempting ankle dorsiflexor contractions with maximal effort, even in the patients who are not able to translate the effort into strong muscle contractions (because of interruption of the motor pathway by stroke) may be helpful to eventually restore voluntary motor drive to the affected ankle dorsiflexor muscles but this has not been investigated in stroke. Furthermore, very little is known regarding the neural mechanisms that encourage motor functional gain in general and correction of foot drop in particular. The current study proposes to maximize potential beneficial effects of training on regaining voluntary motor drive to ankle dorsiflexor and its strength in order for patients to be able to voluntarily lift the foot during walking by combining FES (expected to enhance voluntary motor drive through afferent or ascending pathway) and repetitive maximal voluntary efforts (VOL) to activate the ankle dorsiflexors (expected to increase voluntary motor drive via efferent or descending pathway) (AIM 2). The effect of training on voluntary motor drive and its translation to muscle activities wll be examined (AIM 1). We hypothesize that the paired modalities (FES+VOL) will be superior to either of the two alone (FES or VOL) in regaining voluntary control of the ankle dorsiflexors and correcting foot drop, and this will be examined by comparing clinical outcomes and neurophysiological responses among the three training regimes (FES+VOL, FES alone and VOL alone). The study may bring a more effective therapy for treating foot drop than currently available remedies and improve current understanding of central and peripheral neural mechanisms behind the motor function gains.
This study is relevant to the nearly 7 million stroke survivors in the United States and the 5 million individuals worldwide disabled but the secondary complications of stroke. The results of proposed research have the potential to create a paradigm shift from compensation for motor deficits to rehabilitation and recovery in the treatment of foot drop secondary to stroke. Restoring function through neuroplasticity and motor gain are especially relevant to public health, as restoring voluntary function is essential to the independence and quality of life in individuals with chronic stroke. This research will generate more effective stroke rehabilitation therapies so that the prevalence of post-stroke disability may be decreased.
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