Pain
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Randomized Controlled Trial
The effects of noxious heat, auditory stimulation, a cognitive task, and time on task on pain perception and performance accuracy in healthy volunteers: a new experimental model.
The effects of cognitive and competing sensory processing tasks on pain perception and as a function of time are only partially understood. To study these effects, we compared the simultaneous effects of noxious heat stimulation (HS), auditory stimulation (AS) (sinusoidally modulated speech-like signal, SMSLS), and a cognitive task (CT) (rate change detection of the SMSLS) on pain perception and task performance over repeated experimental runs. Sixty healthy paid volunteers were randomly assigned to four groups, one exposed to AS while performing the CT, one to HS (46 degrees C/6 min), one to AS and HS, and one to AS and HS while performing the CT. ⋯ Neither pain rating, nor rate of errors on the CT varied significantly across runs. These findings point to a significant influence of competing passive sensory processing on pain perception, with the cognitive task not necessarily adding to the perception of pain. Advantages and shortcomings of the present experimental model for future pain studies are discussed.
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Our aim was to asses the efficacy of deep brain stimulation in post-stroke neuropathic pain. Since 2000, 15 patients with post-stroke intractable neuropathic pain were treated with deep brain stimulation of the periventricular gray area (PVG), sensory thalamus (Ventroposterolateral nucleus-VPL) or both. ⋯ However, there is a wide variation between patients. This study demonstrates that it is an effective treatment in 70% of such patients.
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Controlled Clinical Trial
Neural correlates of individual differences in pain-related fear and anxiety.
Although individual differences in fear and anxiety modulate the pain response and may even cause more suffering than the initiating physical stimulus, little is known about the neural systems mediating this relationship. The present study provided the first examination of the neural correlates of individual differences in the tendency to (1) feel anxious about the potentially negative implications of physical sensations, as measured by the anxiety sensitivity index (ASI), and (2) fear various types of physical pain, as indexed by the fear of pain questionnaire (FPQ). ⋯ These functional relationships cannot be wholly explained by generalized anxiety (indexed by STAI-T scores), which did not significantly correlate with activation of any regions. The present findings may help clarify both the impact of individual differences in emotion on the neural correlates of pain, and the roles in anxiety, fear, and pain processing played by medial and orbitofrontal systems.
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Clinical Trial
The relationship of adult attachment to emotion, catastrophizing, control, threshold and tolerance, in experimentally-induced pain.
Although insecure attachment has been associated with a range of variables linked with problematic adjustment to chronic pain, the causal direction of these relationships remains unclear. Adult attachment style is, theoretically, developmentally antecedent to cognitions, emotions and behaviours (and might therefore be expected to contribute to maladjustment). It can also be argued, however, that the experience of chronic pain increases attachment insecurity. ⋯ Of particular interest were findings that attachment style moderated the effects of pain intensity on the tendency to catastrophize, such that insecurely attached individuals were more likely to catastrophize when reporting high pain intensity. This is the first study to link attachment with perceptions of pain in a pain-free sample. These findings cast anxious attachment as a vulnerability factor for chronic pain following acute episodes of pain, while secure attachment may provide more resilience.
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Randomized Controlled Trial
Chronobiological characteristics of painful diabetic neuropathy and postherpetic neuralgia: diurnal pain variation and effects of analgesic therapy.
Clinical impressions suggest that neuropathic pain is often worse at night and significantly impairs sleep. However, the temporal pattern of neuropathic pain during waking hours has not been clearly characterized. Using clinical trial data, we have evaluated the diurnal variation of pain intensity before and during analgesic treatment in patients with diabetic neuropathy (DN) and postherpetic neuralgia (PHN). ⋯ Neuropathic pain intensity progressively increases throughout the day and this temporal profile appears to be unaffected by treatment with gabapentin and/or morphine. Advancing our understanding of the chronobiology of neuropathic pain may shed new light on various neurohormonal and neurophysiologic influences and lead to the identification of novel therapeutic targets. Furthermore, recognizing diurnal pain patterns may guide treatment strategies such as the targeted timing of analgesic therapies.