Abstract
Central
sensitization is a condition that is usually associated with chronic pain, and
refers to a heightened level of spinal cord neuron excitability compared to
normal activation levels. In addition to this hyperexcitability resulting in a
disproportionately elevated pain response, the accompanying sensory receptor
field expansion can also increase
responsiveness to non- painful stimulation. Recent studies have examined the
role that autonomic nervous system dysfunction plays in the development of
central sensitization (1). These findings underscore the potentiality that
mediating autonomic output provides as an effective means of moderating central sensitization.
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