Cortical representations are plastic and are allocated based on the proportional use or disuse of a pathway. A steady stream of sensory input maintains the integrity of cortical networks; while in contrast, alterations in afferent activation promote sensorimotor reorganization. After an incomplete spinal cord injury (SCI), damage to the ascending and/or descending pathways induces widespread modifications to the sensorimotor system. Strengthening these spared sensorimotor pathways may be therapeutic by promoting functional recovery after injury.
Using a technique called transcranial magnetic stimulation (TMS), we show that the leg motor cortex is facilitated by peripheral sensory inputs via disinhibition and potentiation of excitatory intracortical circuits. Hence, in addition to its crucial role in sensory perception, excitation from peripheral sensory afferents can reinforce muscle activity by engaging, and possibly shaping, the activity of the human motor cortex. After SCI, the amount of excitation produced by afferent stimulation reaching the motor cortex is expectantly reduced and delayed. This reduction of sensory inflow to the motor cortex may contribute to our findings that cortical inhibition is down-regulated after SCI, and this compensation may aid in the recruitment of excitatory networks in the motor cortex as a result of the damage to its output neurons. By repeatedly pairing sensory inputs from a peripheral nerve in the leg with direct cortical activation by TMS, in an intervention called paired associative stimulation, we show that the motor system can be potentiated in both uninjured individuals and after SCI. In the uninjured subjects, we show that in order to produce associative facilitation, the time window required for coincident activation of the motor cortex by TMS and peripheral sensory inputs is not as narrow as previously thought (~100 vs. ~20 ms), likely due to the persistent activation of cortical neurons following activation by TMS. The potential to condition the nervous system with convergent afferent and cortical inputs suggests that paired associative stimulation may serve as a priming tool for motor plasticity and rehabilitation following SCI.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:AEU.10048/632 |
| Date | 11 1900 |
| Creators | Roy, Francois D. |
| Contributors | Gorassini, Monica A. (Biomedical Engineering; Centre for Neuroscience), Chan, K. Ming (Division of Physical Medicine and Rehabilitation; Centre for Neuroscience), Chen, Robert (Division of Neurology and Department of Medicine; University of Toronto), Collins, David F. (Physical Education and Recreation Faculty; Centre for Neuroscience), Jones, Kelvin E. (Physical Education and Recreation Faculty; Centre for Neuroscience), Stein, Richard B (Department of Physiology; Centre for Neuroscience) |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | English |
| Detected Language | English |
| Type | Thesis |
| Format | 4139313 bytes, application/pdf |
| Relation | Roy FD, Norton JA and Gorassini MA. Role of sustained excitability of the leg motor cortex after transcranial magnetic stimulation in associative plasticity. J Neurophysiol 98: 657-667, 2007., Roy FD and Gorassini MA. Peripheral sensory activation of cortical circuits in the leg motor cortex of man. J Physiol 586: 4091-4105, 2008., Roy FD. Suppression of EMG activity by subthreshold paired-pulse transcranial magnetic stimulation to the leg motor cortex. Exp Brain Res 193(3): 477-482, 2009., Jeffery DT, Norton JA, Roy FD, and Gorassini MA. Effects of transcranial direct current stimulation on the excitability of the leg motor cortex. Exp Brain Res 182: 281287, 2007., Poon DE, Roy FD, Gorassini MA, and Stein RB. Interaction of paired cortical and peripheral nerve stimulation on human motor neurons. Exp Brain Res 188: 13-21, 2008., Gorassini MA, Norton JA, Nevett-Duchcherer J, Roy FD, and Yang JF. Changes in locomotor muscle activity after treadmill training in subjects with incomplete spinal cord injury. J Neurophysiol 101(2):969-79, 2009. |
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