Fri Jan 28
Speaker: Christopher Thompson (Dr. Hornby's group)
Title: Giving 110%: Generating supramaximal contractions in human incomplete spinal cord injury
Abstract: Spinal cord injury (SCI) is a debilitating disease process which results in profound impairments in an individual's ability to generate and control volitional force.
Impairments in volitional force generation are particularly devastating as the severity of impairments in force-generating capability, particularly of knee extensors, is a primary determinant of walking ability in individuals with motor incomplete SCI. In contrast to previous research indicating greater fatigue following SCI using electrically stimulated contractions, recently published data indicates individuals with motor incomplete SCI are able to generate supramaximal torque during repeated maximal volitional effort contractions, with little evidence of fatigue. As multiple sites spanning the neuromuscular system may contribute to this increase in volitional torque generation, our recent efforts have been directed towards understanding the mechanisms which underlie this phenomenon. This seminar will discuss one line of investigation which suggests spinal motoneuron excitability may contribute to supramaximal force generation. This work will provide an example of the limitations of human research and reinforce the importance of parallel animal research. Current efforts and future plans to further understand the mechanisms of supramaximal force generation in human incomplete SCI will be discussed.
Speaker: Matthieu Chardon (Dr. Rymer's group)
Title: Origins of hyperexcitability of the alpha motoneuron in stroke
Abstract: It is theorized that three mechanisms could be at the origins of spasticity in stroke at the alpha motoneuron level. We hypothesized that the alpha motoneuron is hyperexcitable and that the first mechanism - sustained depolarization - is likely to be the main contributor to spasticity in stroke.
We plan on testing this hypothesis by first measuring if the spastic motoneuron is hyperexcitable (Aim1). To do so we will first determine if the reflex threshold is lower in passive spastic muscles than in contralateral muscles. We will then estimate and compare excitatory post synaptic potentials (EPSPs) from the spastic and contralateral muscles using reconstructions derived from motor unit recordings (Aim2). If the EPSPs are similar than our hypothesis that the spastic motoneuron is hyperexcitable because it is depolarized will be confirmed. In order to complete this work we will need to develop a novel device that will be able to stimulate a single motoneuron pool. We have started to develop a computer controlled tendon tapping device. This device will be able to deliver position controlled tendon stretches thus guaranteeing a controlled input to the motoneuron poll. We will test the biceps brachii of 10 hemiparetic stroke survivors as our model. This work is significant for several reasons. The first is that a new device/technique will be developed for the clinical measurement of spasticity. Second, it may advance our understanding of the fundamental mechanisms underlying spasticity. This enhanced understanding may assist us in developing targeted therapies for 3.7 millions of stroke survivors suffering from spasticity in USA alone. Finally, when our study is completed as planned, we see the possibility for the tapper device to be utilized in other types of studies on spasticity.