Functional and structural plasticity following spinal cord injury: contributions to chronic central neuropathic pain

Chronic neuropathic pain is highly prevalent in patients with spinal cord injury (SCI) but treatment options are very limited. Despite the characterization of structural changes in the spinal pain matrix in animal models of SCI, the causal relationship between these changes and pain remains unknown. This proposal aims to address in mouse SCI models and in SCI patients the structural changes underlying chronic central neuropathic pain.

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Sensory deprivation as trigger for neuropathic pain following
spinal cord injury. Central paresis leading to immobilization results
in altered sensory input. Inadequate sensory stimulation may result in maladaptive
plasticity, which can induce neuropathic pain.
Sensorimotor activity providing appropriate sensory input might
prevent and reverse this process.

Taking advantage of transgenic animals to specifically label, silence or activate subpopulations of spinal and sensory neurons, the contribution of neuronal subpopulations to aberrant plasticity and pain-related behaviors will be identified. Parallel studies in SCI patients will use neurological, neurophysiological and MRI imaging to examine similar parameters. In addition, studies in SCI mouse models and SCI patients will address the central question whether and how sensorimotor activation (rehabilitation and exercise) versus deprivation (immobilization) modulate spinal structural plasticity and neuropathic pain.

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