Motor Control Principles, Technology, and Abnormal Movements
A major overall goal of my research is to alleviate symptoms of movement disorders through an understanding of how these conditions disrupt normal motor control. This understanding can guide the design of interventions based on physical activity and technology (such as wearable sensors) to reduce the impact of abnormal movements in daily life.
A symptom of a movement disorder, for example, is slowing of movements (bradykinesia) in Parkinson’s disease (PD). Understanding the motor control basis of bradykinesia means to first understand how movement speed is normally controlled, and then figure out how PD disrupts normal speed control mechanisms to cause movements to slow down.
We know that bradykinesia is not due to weakness. Although people with PD often feel weak, they do not have the same type of weakness as people with diseases of muscles. Therefore the type of interventions to improve movement speed should differ from those that are appropriate for people with muscle disease.
In order to move at normal speeds, our muscles must generate sufficient force. Muscle disease causes a reduction in muscle mass, so that the force generated by muscles is no longer adequate. Performing strength exercises makes sense for muscle disease: repeated muscle contractions cause an increase in muscle mass. Technological devices like braces also make sense: they provide a mechanical substitute to replace the force lost by the reduced muscle mass.
Motor control principles are thus at the basis of current interventions for symptoms of muscle disease. The normal motor control principle relevant to muscle disease is known as “recruitment”: normal force is generated by activating a sufficient amount of muscle mass. The motor control basis for the motor symptom is that weakness in muscle disease is that the loss of muscle mass reduces the force that a muscle can generate. Physical therapy and technological interventions can be said to be guided by motor control principles: strength exercises counter the loss of force by stimulating an increase in muscle mass, and braces replace the action of the weakened muscles through mechanical support.
People with muscle disease walk slowly. The motor control basis for their slowness is force reduction due to loss of muscle mass. Therapies based on understanding this motor control problem help them walk faster.
People with PD walk slowly. Why? What therapies can help people with PD walk faster? By analogy with the muscle disease example, we should first wonder what makes people without PD walk at normal speeds: what motor control principles guide normal speed selection? Then we must understand how PD disrupts these normal speed control mechanisms: what is the motor control basis of bradykinesia? We can then design interventions based on this understanding: what exercises, and what technological devices, can lead people with PD to walk faster?