Pain
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Comparative Study
Cognitive modulation of pain-related brain responses depends on behavioral strategy.
Interactions of pain and cognition have been studied in humans and animals previously, but the relationship between such behavioral interactions and brain activity is unknown. We aimed to show using functional MRI (fMRI) how a cognitively demanding task (Stroop) modulates pain-related brain activations and conversely, how pain modulates attention-related activity. Reaction time data indicated two types of pain responders: subjects in the A group had a faster Stroop reaction time when pain was concomitant to the attention task, while those in the P group had a slower Stroop performance during painful stimulation. fMRI data obtained during Stroop performance with and without noxious stimulation were subjected to region of interest analyses. ⋯ None of the areas showing attention-related responses, including bilateral dorsolateral prefrontal and posterior parietal cortices, were modulated by pain. These findings suggest that cortical regions associated with pain can be modulated by cognitive strategies. Furthermore, the distinction of behavioral subgroups may relate to cognitive coping strategies taken by patients with chronic pain.
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The present study investigated the effects of two attributes of the experimenter (gender and professional status) on the report and tolerance of pain in male and female subjects. 160 non-psychology students (80 male and 80 female, aged 17-59 years) participated in a cold-pressor task. Subjects were assigned to one of 8 groups: male (M) and female (F) experimenters tested male (m) and female (f) students. In each combination (Mm, Mf, Fm, Ff), the cold-pressor task was conducted by either one of two faculty members (high professional) or one of two students (low professional). ⋯ Further, a significant interaction of experimenter gender and subject gender on pain tolerance indicated that subjects also tolerated pain longer when they were tested by an experimenter of the opposite sex. Additionally, a significant main effect for experimenter gender showed higher pain intensities for subjects tested by female experimenters. The observation that pain responsivity is influenced by the professional status of the experimenter might have implications for the study of pain in general and should be addressed in more detail in future experiments.
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A neuropathic-like pain syndrome was produced in rats following prolonged hindpaw ischemia and reperfusion, creating an animal model of complex regional pain syndrome-Type I (CRPS-I; reflex sympathetic dystrophy) that we call chronic post-ischemia pain (CPIP). The method involves placing a tourniquet (a tight fitting O-ring) on one hindlimb of an anesthetized rat just proximal to the ankle joint for 3 h, and removing it to allow reperfusion prior to termination of the anesthesia. Rats exhibit hyperemia and edema/plasma extravasation of the ischemic hindpaw for a period of 2-4 h after reperfusion. ⋯ The rats also exhibit spontaneous pain behaviors (hindpaw shaking, licking and favoring), and spread of hyperalgesia/allodynia to the uninjured contralateral hindpaw. Light-microscopic examination of the tibial nerve taken from the region just proximal to the tourniquet reveals no signs of nerve damage. Consistent with the hypothesis that the generation of free radicals may be partly responsible for CRPS-I and CPIP, two free radical scavengers, N-acetyl-L-cysteine (NAC) and 4-hydroxy-2,2,6,6-tetramethylpiperydine-1-oxyl (Tempol), were able to reduce signs of mechanical allodynia in this model.