Jessica Rose, PhD,
Associate Professor, Department of Orthopedic Surgery
Dr. Rose is a Professor in the department of Orthopaedic Surgery at Stanford University and directs the Motion & Gait Analysis Lab at Lucile Packard Children’s Hospital at Stanford, a multidisciplinary diagnostic service for patients with walking disorders and upper limb movement deficits. Her research investigates neonatal neuroimaging and perinatal risk factors in relation to neurodevelopment and gait in preterm children and examines neuromuscular mechanisms underlying motor deficits in cerebral palsy. Previous research investigated energy cost of walking, muscle pathology, postural balance, and neuromuscular activation in cerebral palsy. Dr. Rose served on the NIH Taskforce on Childhood Motor Disorders, chaired the Research Committee of the American Academy for Cerebral Palsy and Developmental Medicine (AACPDM), and serves on the AACPDM Steering Committee to develop common data elements (CDE) for cerebral palsy. She is on the Board of Directors of the Society for Brain Mapping and Therapeutics (SBMT). Her research reinforced an appreciation for the potential transformative impact of neuromuscular electrical stimulation (NMES) to improve motor deficits in cerebral palsy. She leads a Research Network on multichannel NMES-assisted gait for children with cerebral palsy. Dr. Rose is co-editor of Human Walking 3rd Edition, (Rose J and Gamble JG, Eds, Lippincott, WilIiams, and Wilkins 2006) a multidisciplinary perspective on human walking and gait analysis.
Neuromuscular deficits and gait analysis in cerebral palsy: Applications for artificial walking technologies
Cerebral palsy is the most common childhood disability, affecting approximately 3/1000 children in the general population and 15% of very-low-birth-weight preterm children. Although the initial brain injury is non-progressive, musculoskeletal impairments and functional limitations are progressive. Flexed-knee gait, a common walking disorder in children with CP (Wren et al, 2005), limits mobility, causes fatigue, and typically worsens over time, with many children loosing independence in functional mobility as teenagers and adults (Bell et al, 2002; Hanna et al, 2009; Kerr et al, 2011, Rosenbaum et al, 2002). Spastic CP is characterized by short muscle-tendon length and interrelated neuromuscular deficits including muscle weakness, spasticity, and impaired selective motor control (Rose et al, 2010). Affected muscles in CP have reduced neuromuscular activation and inability to sufficiently recruit and drive motor-units at higher firing rates (Rose et al, 2005). Flexed-knee gait in CP can arise from short and spastic hip and knee flexors or weak hip and ankle extensors. In young children, flexed-knee causes abnormal mechanical loads across the hip and knee that contribute to bone deformities and a permanently flexed and rotated gait (Steele et al, 2011). To date, surgical and pharmaceutical treatment of gait deficits offer only partial improvement, thus, most ambulatory children with CP have difficulty walking. More effective treatments for gait deficits in CP are needed at an early age, when there is optimal neuronal plasticity, rapid musculoskeletal growth and a greater likelihood of preventing musculoskeletal deformities.
Emerging artificial walking technologies have potential to significantly improve gait in CP. Previous research suggests that neuromuscular electrical stimulation (NMES) applied during gait may normalize walking patterns and improve muscle physiology and strength in children with CP (Wright et al, 2012; Damiano et al, 2013). Multichannel NMES-assisted gait in children with CP was found to reduce need for orthopaedic surgery (Johnston et al, 2004). However, NMES systems designed to improve walking require further development to deliver optimal activation patterns using variable-frequency trains (Binder-Macleod, 2005; Lee, 2000), and feedback control for step initiated activation. A systematic approach to NMES-assisted gait for children with CP can utilize gait analysis and musculoskeletal modeling to identify NMES patterns for optimal neuroprosthetic affects that promote hip and knee extension during stance and sufficient knee excursion in swing. Alternating on-off NMES protocols apply a distributive learning model to enhance muscle memory and longer-term neurotherapeutic affects. Outcome assessment can include the Gait Deviation Index based on 3D kinematics (Schwartz & Rozulmalski, 2008). For children with CP, treatment with NMES may improve gait patterns and muscle physiology, reducing growth-related deformities and the need for surgery.