Children with dystonia do not improve their movement performance despite a lifetime of practice. Recent theoretical results suggest that this may be due to one of two types of failure of motor learning: Type 1: inability to recognize relevant errors, Type 2: inability to generate examples of correct behavior. We propose a set of experiments to demonstrate that failure of motor learning may contribute to poor motor control in children with dystonia. To test this hypothesis, 30 children with primary or secondary dystonia and 30 control children will use surface electromyographic activity of either 2 or 4 muscles to control the position of cursors on a computer screen. Type 1 failure can be induced artificially by obscuring visual information about muscle activity. Type 2 failure can be induced using a difficult task in which 4 muscles control 4 dimensions of movement through an unknown linear mixing transformation, and the children must discover exactly one specific pattern of activity.
In specific aim 1, we will demonstrate that both control children and children with dystonia show increased co-activation of muscles when information about muscle activity is obscured, as predicted by type 1 failure of motor learning.
In specific aim 2, we will demonstrate that both control children and children with dystonia are unable to learn a difficult task until a successful example is learned in a simplified version of the same task. A successful result of this study will show that failure of motor learning is necessary and sufficient to produce part of the motor deficits in childhood dystonia. It will also show strategies for improvement of dystonia. In particular, type 1 failure can be improved ifbio- feedback of an unobserved mode (in this case, co-contraction of biceps and triceps) is provided. Type 2 failure can be improved if the correct solution is presented to children in a simplified task, so that they can then remember and return to the correct solution at will. These experiments will demonstrate a potentially important contributor to motor symptoms in dystonia, and they will indicate specific new treatment opportunities.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS052236-06
Application #
7770904
Study Section
Motor Function, Speech and Rehabilitation Study Section (MFSR)
Program Officer
Chen, Daofen
Project Start
2006-07-15
Project End
2012-02-28
Budget Start
2010-03-01
Budget End
2012-02-28
Support Year
6
Fiscal Year
2010
Total Cost
$311,459
Indirect Cost
Name
University of Southern California
Department
Biomedical Engineering
Type
Schools of Engineering
DUNS #
072933393
City
Los Angeles
State
CA
Country
United States
Zip Code
90089
Bertucco, Matteo; Sanger, Terence D (2015) Current and emerging strategies for treatment of childhood dystonia. J Hand Ther 28:185-93; quiz 194
Young, Scott J; Bertucco, Matteo; Sanger, Terence D (2014) Cathodal transcranial direct current stimulation in children with dystonia: a sham-controlled study. J Child Neurol 29:232-9
Chu, Virginia Way Tong; Sternad, Dagmar; Sanger, Terence David (2013) Healthy and dystonic children compensate for changes in motor variability. J Neurophysiol 109:2169-78
Young, Scott J; Bertucco, Matteo; Sheehan-Stross, Rebecca et al. (2013) Cathodal transcranial direct current stimulation in children with dystonia: a pilot open-label trial. J Child Neurol 28:1238-44
Young, Scott J; van Doornik, Johan; Sanger, Terence D (2011) Finger muscle control in children with dystonia. Mov Disord 26:1290-6
Young, Scott J; van Doornik, Johan; Sanger, Terence D (2011) Visual feedback reduces co-contraction in children with dystonia. J Child Neurol 26:37-43
Ben-Pazi, Hilla; Ishihara, Abraham; Kukke, Sahana et al. (2010) Increasing viscosity and inertia using a robotically controlled pen improves handwriting in children. J Child Neurol 25:674-80
Sanger, Terence D (2008) Use of surface electromyography (EMG) in the diagnosis of childhood hypertonia: a pilot study. J Child Neurol 23:644-8