Pain
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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.
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Randomized Controlled Trial
The role of developmental factors in predicting young children's use of a self-report scale for pain.
Accurate pain assessment is the foundation for effective pain management in children. At present, there is no clear consensus regarding the age at which young children are able to appropriately use self-report scales for pain. This study examined young children's ability to use the Faces Pain Scale-Revised; (FPS-R; [Hicks CL, von Baeyer CL, Spafford PA, van Korlaar I, Goodenough B. ⋯ However, over half of the 6-year-olds demonstrated difficulties using the FPS-R in response to the vignettes. Child age was the only significant predictor of children's ability to use the scale in response to the vignettes. Thus, a substantial number of young children experienced difficulties using the FPS-R when rating pain in hypothetical vignettes, although the ability to use the scale did improve with age.
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Controlled Clinical Trial
Increased taste intensity perception exhibited by patients with chronic back pain.
There is overlap between brain regions involved in taste and pain perception, and cortical injuries may lead to increases as well as decreases in sensitivity to taste. Recently it was shown that chronic back pain (CBP) is associated with a specific pattern of brain atrophy. Since CBP is characterized by increased sensitivity to pain, we reasoned that the sense of taste might also be enhanced in CBP. ⋯ There was no difference between CBP and control subjects for visual grayness rating. On the other hand, CBP patients in comparison to control subjects rated gustatory stimuli as significantly more intense but no more or less pleasant and showed a trend towards a lower detection threshold (i.e. increased sensitivity). The selectivity of the taste disturbance suggests interaction between pain and taste at specific brain sites and provides further evidence that CBP involves specific brain abnormalities.
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Randomized Controlled Trial
A PET activation study of brush-evoked allodynia in patients with nerve injury pain.
Acute experimental brush-evoked allodynia induces a cortical activation pattern that differs from that typically seen during experimental nociceptive pain. In this study, we used positron emission tomography to measure changes in regional cerebral blood flow (rCBF) in patients with clinical allodynia. Nine patients with peripheral nerve injury were scanned during rest, brush-evoked allodynia, and brushing of normal contralateral skin. ⋯ A direct post hoc comparison of brush -and allodynia-induced rCBF changes showed that allodynia was associated with significantly stronger activations in orbitofrontal cortex and ipsilateral insula whereas non-painful brushing more strongly activated SI and BA 5/7. These findings indicate that activity in the cortical network involved in the sensory-discriminative processing of nociceptive pain is downregulated in neuropathic pain. Instead, there is an upregulation of activity in the orbitofrontal and insular cortices, which is probably due to the stronger emotional load of neuropathic pain and higher computational demands of processing a mixed sensation of brush and pain.
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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.