Pain can be modulated by different factors, such as sensory processing and plasticity. Evidence has shown that plasticity of primary sensorial neurons can induce neuroplasticity changes over the somatosensory networks, changing the subsequent responsiveness of those systems, in a state dependent manner. Moreover, the processing of nociceptor inputs from the afferent pathways can change the synaptic efficacy and excitability in the nociceptive pathways, which can ultimately induce changes in pain sensitivity. Therefore, it may be possible to centrally modify an individual´s pain perception in response to passive sensory experience, especially by sensory training. Median nerve stimulation (MNS) is a form of peripheral sensorial stimulation that is able to change the activity in the central nervous system (CNS). It is thought that the sensorial information driven by peripheral stimulation of the afferent pathways (i.e. spinothalamic and potentially the spinoreticular tracts) is relayed to the cortex through the thalamic nuclei. This type of sensorial stimulation has been thought to change brain activity based on a co-activation mechanism. The hypothesis underlying this assumption is that according to the Hebbian principle of plasticity, sensorial stimulation will induce a firing synchronization across the afferent neural pathway. Once it reaches the thalamic nuclei, sensorial information will then be relayed to the cortex by a pacemaker system that is able to generate and synchronize activity through thalamocortical circuitries. This co-activation mechanism hypothesis has been supported by neuroimaging data, in which activation of the primary and secondary somatosensory areas, as well as the insula, has been demonstrated following sensorial stimulation.
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