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Welcome to InSPIRE Lab!

Integrating Sensorimotor Plasticity Interventions & Recovery

The purpose of this lab is to study neural mechanisms underlying the control of movement and posture in persons with neuromotor deficits such as stroke and spinal cord injury. We conduct clinical studies to improve our knowledge of the neural structure and functions contributing to motor impairments and critically examine therapeutic interventions that may restore function. These goals motivate our ongoing research projects, which are described below.

 

Neural plasticity following CNS injury

Effects of intermittent hypoxia on neuromotor excitability in human spinal cord injury
Neural plasticity is a significant contributor to motor recovery following spinal cord injury. In animal models of SCI, intermittent hypoxia induces neural plasticity, strengthening synapses onto respiratory motor neurons by a mechanism known as long-term facilitation. Results from our work will be valuable in identifying novel strategies to control spinal neuron excitability and for improving voluntary control of movement in persons with incomplete spinal injury.


 

Neural regulation of multijoint coordination

Quantify neural contributions to multijoint coordination
Our lab looks to quantify how central nervous system injury alters the regulation of multijoint arm mechanics during voluntary muscle activation and to quantify the neural contributions to this discoordination. We use feature extraction algorithms to quantify the extent of these alterations and to determine if they contribute to the impaired muscle coupling at the shoulder and elbow that impose significant constraints on functional arm use.

Quantifying altered limb impedance after CNS injury
Endpoint impedance represents a measure of the mechanical interface a limb presents to its environment and is therefore thought to play a crucial role in the control of posture and movement. Limb mechanics can be quantified using estimates of endpoint impedance, which describes the dynamic relationship between externally imposed displacements of the limb and the forces required to effect those displacements. Previous studies have demonstrated that the patterns of muscle activation that can be achieved following stroke are highly constrained during maximum voluntary activations. If these patterns also contribute to impaired coordination during submaximal activations, we would expect the regulation of limb mechanics to also be constrained in this population.

Regulation of reflex function after CNS injury
Stretch reflexes are known to be altered following stroke. To date, however, most studies have focused on the spinal components of the reflex, thought to be mediated through short latency, spinal pathways. These pathways contribute to impairments such as spasticity and tremor, but the relationship between spasticity and stroke-related disabilities is not clear. A few studies also have examined longer-latency responses, which are known to be attenuated, decreasing its potential efficacy in tasks that require enhanced limb stability. These previous studies have been conducted only during interactions with a stiff environment. This project is investigating if stroke subjects retain the capacity to modulate these responses during interactions with compliant loads.

 
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