Top Stroke Rehabil 2009;16(5):367–376 © 2009 Thomas Land Publishers, Inc. www.thomasland.com doi: 10.1310/tsr1605-367 367 W alking ability is commonly impaired following stroke due to muscle weakness, disordered movement control, and, in some individuals, elevated muscle tone or hypertonicity. 1,2 Hypertonicity limits muscle distensibility due to several mechanisms including spasticity, alterations in passive structures that increase stiffness, and alterations to the intrinsic properties of the muscle. 3–5 The relative contributions of the various mechanisms to hypertonicity can change over time, leading, in severe cases, to restrictions in joint mobility due to contracture. 6 In the stance phase of gait, plantar flexor hypertonicity can result in an absence of heel contact and limited ability of the body to rotate over the stance limb (reduced dorsiflexion), which may be accompanied by knee hyperextension. 1,2,7–9 Further, the ankle plantar flexors are a major contributor to the work of walking in healthy gait 9,10 ; after stroke, the ability to generate plantar flexor force and power is markedly reduced paired with poor plantar support. 2,11 It follows that interventions aimed at improving or normalizing plantar flexor tone and function could result in marked improvements in gait. Botulinum toxin A (BTX-A) produces neuromuscular blockade that reduces spasticity or reflex-mediated and intrinsic muscle stiffness in select muscles by blocking the release of acetylcholine at the neuromuscular junction. 12–14 BTX-A is reportedly a safe and cost-effective method of treating muscle overactivity 15,16 Several Alison C. Novak, MSc, is PhD candidate, Motor Performance Laboratory, School of Rehabilitation Therapy, Queen’s University, Kingston, Ontario, Canada. Sandra J. Olney, PhD, is Professor Emeritus, Motor Performance Laboratory, School of Rehabilitation Therapy, Queen’s University, Kingston, Ontario, Canada. Stephen Bagg, MD, MSc, is Associate Professor, Department of Physical Medicine and Rehabilitation, Queen’s University, and Providence Care, St. Mary’s of the Lake Hospital, Kingston, Ontario, Canada. Brenda Brouwer, PhD, is Professor, Motor Performance Laboratory, School of Rehabilitation Therapy, Queen’s University, Kingston, Ontario, Canada. Gait Changes Following Botulinum Toxin A Treatment in Stroke Alison C. Novak, Sandra J. Olney, Stephen Bagg, and Brenda Brouwer Purpose: To characterize the effects of botulinum toxin A treatment of spastic plantar flexors in stroke on joint mobility and gait kinematics and kinetics. Method: Nine patients with hemiparetic stroke presenting with ankle hypertonicity participated in this exploratory open-label case series study. Comprehensive gait analysis provided bilateral kinematic and kinetic information for the ankle, knee, and hip joints throughout the stance phase. Data were obtained at baseline, 2 weeks, and 10 weeks post botulinum toxin injection of the spastic plantar flexors. Results: Passive ankle range of motion increased post injection (p < .05). The amount of plantarflexion in late stance was significantly reduced (p < .05) while the maximum dorsiflexion increased in midstance at 10 weeks post treatment. The angular displacement profiles for the knee revealed that patients tended to display less hyperextension following treatment (p = .053). No significant changes in kinetic measures were found; however, case-by-case observations suggested that most patients experienced improvements in positive work production. Conclusions: The findings indicate that botulinum toxin treatment results in improved joint mobility and ankle kinematics and, in some patients, increases in positive work, suggesting better gait performance. Key words: cerebrovascular disorders, function, hemiplegia, kinematics, kinetics, mobility, muscle hypertonia, spasticity Grand Rounds Elliot J. Roth, MD, Editor