Abstract
Noxious stimulation of the skin with either chemical, electrical or heat stimuli leads to the development of primary hyperalgesia at the site of injury, and to secondary hyperalgesia in normal skin surrounding the injury. Secondary hyperalgesia is inducible in most individuals and is attributed to central neuronal sensitization. Some individuals develop large areas of secondary hyperalgesia (high-sensitization responders), while others develop small areas (low-sensitization responders). The magnitude of each area is reproducible within individuals, and can be regarded as a phenotypic characteristic. To study differences in the propensity to develop central sensitization we examined differences in brain activity and anatomy according to individual phenotypical expression of secondary hyperalgesia by magnetic resonance imaging. Forty healthy volunteers received a first-degree burn-injury (47°C, 7 min, 9 cm2) on the non-dominant lower-leg. Areas of secondary hyperalgesia were assessed 100 min after the injury. We measured neuronal activation by recording blood-oxygen-level-dependent-signals (BOLD-signals) during mechanical noxious stimulation before burn injury and in both primary and secondary hyperalgesia areas after burn-injury. In addition, T1-weighted images were used to measure differences in gray-matter density in cortical and subcortical regions of the brain. We found significant differences in neuronal activity between high- and low-sensitization responders at baseline (before application of the burn-injury) (p < 0.05). After the burn-injury, we found significant differences between responders during noxious stimulation of both primary (p < 0.01) and secondary hyperalgesia (p ≤ 0.04) skin areas. A decreased volume of the right (p = 0.001) and left caudate nucleus (p = 0.01) was detected in high-sensitization responders in comparison to low-sensitization responders. These findings suggest that brain-structure and neuronal activation to noxious stimulation differs according to secondary hyperalgesia phenotype. This indicates differences in central sensitization according to phenotype, which may have predictive value on the susceptibility to development of high-intensity acute and persistent pain.
Highlights
Injury-induced sensitization of the central nervous system is a condition that is believed to play an important role in the development and maintenance of pain
The magnitude of secondary hyperalgesia areas varies widely between individuals, the intra-individual variability is low, i.e., individuals will continue to develop areas of similar magnitude when exposed to the same noxious stimulus [7]
A total of 55 volunteers were screened for magnitude of secondary hyperalgesia areas
Summary
Injury-induced sensitization of the central nervous system is a condition that is believed to play an important role in the development and maintenance of pain. During sensitization the central nervous system is regulated into a state of high reactivity in which sensory inputs from both injured and non-injured adjacent areas produce augmented responses [1,2,3]. One important question is whether some individuals develop more central sensitization than others and if such individuals are predisposed to higher levels of acute and chronic pain experience. The proneness to develop secondary hyperalgesia has been used to study differences in central sensitization [7]. The magnitude of secondary hyperalgesia areas varies widely between individuals, the intra-individual variability is low, i.e., individuals will continue to develop areas of similar magnitude when exposed to the same noxious stimulus [7]. Development of secondary hyperalgesia seems to be a phenotypic characteristic [7]
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