Dr. Rose serves on the Neurophysiology section of the NH Taskforce on Childhood Motor Disorders, is a member and Chaired the Research Committee of the American Academy for Cerebral Palsy and Developmental Medicine (AACPDM), serves on the Board of Directors of the Society for Brain Mapping and Therapeutics (SBMT), and leads the Research Network on Artificial Walking Technologies for multichannel NMES-assisted Gait for Children with CP. She is co-editor of the book, Human Walking 3rd Edition, (Rose J and Gamble JG, Editors, Lippincott, WilIiams and Wilkins, 2006) which offers a multidisciplinary perspective on human walking and gait analysis. She has served as course director of Anatomy of Movement (Ortho 222), a multidisciplinary course on musculoskeletal anatomy and clinical applications that offers perspectives from bioengineering, anthropology, and art history. She collaborates with professor Kazerooni of UC Berkely and US Bionics on development of a pediatric exoskeleton, which won the Robotics for Good international competition 2016.
Dr. Rose directs the Motion & Gait Analysis Lab at Lucile Packard Children's Hospital, a multidisciplinary diagnostic service for patients with gait and upper limb movement disorders. Dr. Rose's research investigates early brain and motor development in preterm children and the neuromuscular mechanisms underlying motor deficits in children with cerebral palsy (CP).
Previous research has investigated energy cost of walking, muscle pathology, postural balance, and neuromuscular activation in CP. Recent research investigates neonatal micro-structural brain development on diffusion tensor MRI in relation to motor function in preterm children. Initial research examined energetics of walking in CP and muscle pathophysiology in spastic CP (Rose et al, J Orthop Res, 1994). The histologic and morphometric study of spastic muscle in children with diplegia, revealed abnormal predominance of type 1 fibers and fiber size variability, suggesting reduced motor-unit firing rates associated with impaired descending motor signals. Neuromuscular activation and motor-unit firing characteristics were investigated with EMG decomposition techniques in spastic lower limb muscles in CP (Rose and McGill, Dev Med Child Neurol, 2005) and found maximal voluntary neuromuscular activation (maximal voluntary EMG/ M-wave amplitude) was substantially reduced, while motor-unit recruitment was found normal at low-moderate levels of contraction. Extrapolation to maximal levels of neuromuscular activation suggested maximal motor-unit firing rates were reduced to approximately 50% of control values. Four primary interrelated motor deficits of spastic CP: weakness, short muscle tendon unit, spasticity, and impaired selective motor control, were identified through these studies and through EMG studies of selective motor control. The EMG studies revealed obligatory muscle co-activation of gastrocnemius during quadriceps activation in spastic CP that contributes to gait deficits, in even mild CP (Rose et al, J Ped Orthop, 1999, Policy et al, J Ped Orthop, 2001). Postural balance was examined using force plate center-of pressure measures and found approximately 30% of children with spastic CP had balance impairment (Wolff et al, J Orthop Res, 1998, Rose et al, Dev Med Child Neurol, 2002).
Recent research examined neonatal micro-structural brain development on diffusion tensor MRI and motor function in very-low-birth-weight preterm children (Rose et al, Ped Res, 2005, Rose et al. Dev Med Child Neurol 2007; 2009). Related research investigated relations between cerebellar structure and postural balance in adults. Ongoing research examines early regional brain development and perinatal risk factors at near-term age in relation to later motor deficits. This research aims to develop a neonatal prognostic index for motor function to guide early, more effective intervention.