Pain
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Cold allodynia is a common complaint in patients with peripheral neuropathies. However, cold sensitivity of the different types of sensory afferents present in injured nerves is poorly known. We recorded activity evoked by cold in intact sensory fibers of the skin-saphenous nerve preparation and in axotomized sensory fibers of approximately 21 days-old neuromas of the saphenous nerve of mice, in vitro. ⋯ In conclusion, the transducing capacity to cold stimuli is substantially recovered in neuromas. Furthermore, axotomized fibers maintain the 4-AP-sensitive, voltage-activated, transient potassium conductance that counteracts the depolarizing effects of cold in the majority of intact, cold-insensitive primary afferents. Our results indicate that injured nociceptors do not develop abnormal cold sensitivity, suggesting that other mechanisms underlie the cold-induced allodynia following peripheral nerve injury.
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Transcutaneous electrical nerve stimulation (TENS) reduces pain through central mechanisms involving spinal cord and brainstem sites. Since TENS acts through central mechanisms, we hypothesized that TENS will reduce chronic bilateral hyperalgesia produced by unilateral inflammation when applied either ipsilateral or contralateral to the site of muscle inflammation. Sprague-Dawley rats were injected with carrageenan in the left gastrocnemius muscle belly. ⋯ Either low or high frequency TENS applied to the gastrocnemius muscle ipsilateral to the site of inflammation significantly reversed mechanical hyperalgesia, both ipsilateral and contralateral to the site of inflammation. Low or high frequency TENS applied to the gastrocnemius muscle contralateral to the site of inflammation also significantly reduced mechanical hyperalgesia, both ipsilateral and contralateral to the site of inflammation. Since ipsilateral or contralateral TENS treatments were effective in reducing chronic bilateral hyperalgesia in this animal model, we suggest that TENS act through modulating descending influences from supraspinal sites such as rostral ventromedial medulla (RVM).
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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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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.