Descending
pain inhibition is an endogenous
pain control system thought to depend partially on the activation of bulbospinal monoaminergic pathways. Deficits in descending
pain inhibition have been reported in numerous human
chronic pain conditions, but there is currently no consensus regarding the neurochemical correlates responsible for this deficit. The aims of this study were to 1) assess the efficacy of descending
pain inhibition in
pain-free and
chronic pain subjects, 2) screen for changes in centrally (ie, cerebrospinal fluid) and peripherally (ie, plasma) acting monoamine concentrations, and 3) explore the relationship between descending
pain inhibition and monoamine
neurotransmitter concentrations. Our results clearly show a deficit in
pain inhibition, along with lower plasma
norepinephrine and
metanephrine concentrations in
chronic pain subjects, compared to
pain-free subjects. No differences were found in cerebrospinal fluid
neurotransmitter concentrations. Finally, our results revealed a positive relationship between blood-bound
norepinephrine and
metanephrine concentrations and the efficacy of descending
pain inhibition. Thus, basal monoamine levels in blood were related to descending
pain inhibition. This finding supports the emerging idea that individual differences in descending
pain inhibition may be linked to individual differences in peripheral processes, such as monoamines release in blood, which are possibly related to cardiovascular control.
PERSPECTIVES: This article presents psychophysical and neurochemical findings that indicate that the latent potential of descending
pain inhibitory responses is associated with differential activity in peripheral processes governed by monoamine
neurotransmitter release, bringing insights into the relationship between descending
pain inhibition and cardiovascular control in humans.