Current rheumatology reports
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Central changes in pain processing have been previously reported in patients with fibromyalgia syndrome. These changes include decreased thresholds to mechanical and thermal stimuli (allodynia) and central sensitization, both of which are fundamental to the generation of clinical pain. Therefore, psychophysical measures of central pain processing may be useful predictors of clinical pain intensity of fibromyalgia syndrome patients. ⋯ Particularly, the magnitude of wind-up after-sensations appeared to be one of the best predictors for clinical pain intensity of fibromyalgia syndrome patients (27%). Furthermore, the combination of tender point count, negative affect, and wind-up after-sensations accounted for approximately 50% of the variance in clinical pain intensity of fibromyalgia syndrome patients. Therefore, wind-up after-sensations, tender point count, and negative affect not only seem to represent relevant pain mechanisms but also strongly emphasize their importance for fibromyalgia syndrome pain.
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In this paper, the relationships between neural mechanisms of persistent pain and the neural representations of these conditions in the human and animal brain will be reviewed. Animal models of chronic pain, such as the sciatic nerve constrictive injuries, are accompanied by somatotopically organized increases in several pain-related areas of the brain. ⋯ This suggests that these somatic and visceral hyperalgesic states may be represented by increased activity in the same cerebral pathways and centers that are involved in nociceptive stimuli in normal individuals. Hyperalgesic states during clinically relevant pain are especially reflected in brain areas such as the anterior cingulate and prefrontal cortical regions.