Pain
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The perception of pain results from an interaction between nociceptive and antinociceptive mechanisms. A better understanding of the neural circuitry underlying these physiological interactions provides an important opportunity to develop better treatment strategies for and ultimately even prevent pain. Here, we investigated how repeated painful stimulation over several days is processed, perceived and finally modulated in the healthy human brain. ⋯ The decreased perception of pain over time is reflected in decreased BOLD responses to nociceptive stimuli in classical pain areas, including thalamus, insula, SII and the putamen. In contrast to this finding, we found that pain-related responses in the rACC, specifically the subgenual anterior cingulate cortex (sgACC), significantly increased over time. Given this area's predominant role in endogenous pain control, this response pattern suggests that habituation to pain is at least in part mediated by increased antinociceptive activity.
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The effects of differential aversive Pavlovian conditioning on the functional organization of primary somatosensory cortex (SI) were examined in 17 healthy participants. Neuroelectric source imaging from 60 electrodes was employed while nine subjects received an innocuous electric stimulus (conditioned stimulus, CS) to one finger (left or right) that was followed by painful electric shock to the lower back (unconditioned stimulus, US) and an innocuous stimulus to the other finger that was never followed by pain. Eight subjects received a presentation of the innocuous and painful stimuli with equal probability to both fingers (control group). ⋯ Intensity and unpleasantness ratings were altered in a more unspecific manner and did not differ between groups and stimulus conditions. The data suggest that SI contributes to memory processes in associative learning. Pavlovian conditioning of tactile responses might be important in the altered processing of painful stimuli in chronic pain patients where enhanced conditioning has been demonstrated.
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Many children and adolescents experience recurrent pain, but only a few become disabled by it. Research has established that higher pain intensity and worse depression seem to predict poorer functioning in this population. Parent and family variables have been minimally researched. ⋯ Pain intensity and depression predicted functional disability. However, social/adaptive functioning was associated with different variables, including parent factors, and school attendance showed no association with pain intensity or anxiety. The results emphasise the need to measure multiple domains of functioning, and show that the connections between pain, physical disability and adaptive functioning are looser than might be predicted.
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The use of unidimensional scales to measure pain intensity has been criticised because of the multidimensional nature of pain. We conducted multiple linear regression analyses to determine which dimensions of pain--sensory versus affective--predicted scores on unidimensional scales measuring pain intensity and emotions in 109 Italian women suffering from chronic, non-malignant musculoskeletal pain. We then compared the results with earlier findings in two groups of cancer patients suffering from acute post-operative pain and chronic cancer-related pain, respectively. ⋯ Therefore, in contrast to earlier findings in two different types of cancer patients, in subjects affected by chronic non-malignant musculoskeletal pain, the scores on unidimensional pain intensity scales mainly reflect sensory pain dimensions, supporting the discriminant validity of the NRS and VAS used. However, the patients had some difficulty in distinguishing between sensory and emotional information. For this reason, several unidimensional scales to rate pain intensity and emotions separately should be used to obtain a complete picture of the status and needs of any given patient.
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Complex regional pain syndrome (CRPS) may lead to movement disorders (MDs) in some patients. Reliable information on the nature, chronology and clinical determinants of MDs in CRPS patients is lacking but could provide better insight in to the underlying pathophysiological mechanism. We retrospectively evaluated the clinical and temporal characteristics of MDs in patients with CRPS. ⋯ The hazard of developing dystonia in subsequent extremities increased with the number of extremities affected by dystonia. We conclude that dystonia in CRPS shows highly variable onset latency and is associated with younger age at onset and increased risk of developing dystonia in other extremities. The delayed onset and progression of dystonia in CRPS may indicate the involvement of a different underlying mechanism, possibly associated with maladaptive neuroplasticity.