Articles: hyperalgesia.
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Brain research bulletin · Mar 2006
Down-regulation of GFRalpha-1 expression by antisense oligodeoxynucleotide attenuates electroacupuncture analgesia on heat hyperalgesia in a rat model of neuropathic pain.
Glial cell line-derived neurotrophic factor (GDNF) has been proved to play an important role in the modulation of nociceptive transmission especially during neuropathic pain. It was reported that electroacupuncture (EA) had potent analgesic effect on neuropathic pain and our previous studies indicated that EA could activate endogenous GDNF signaling system (GDNF and its receptor GFRalpha-1) in dorsal root ganglions (DRGs) of neuropathic pain rats. ⋯ The results showed that: (1) cumulative EA had potent analgesic effect on neuropathic pain in rats; (2) the expression of GFRalpha-1 in DRGs was down-regulated by intrathecal delivery of antisense ODN, but not by normal saline (NS) or mismatch ODN; (3) EA analgesia was significantly attenuated by antisense ODN treatment. The present study demonstrated that endogenous GDNF signaling system was involved in EA analgesia on neuropathic pain in rats, which would deepen our realization of the mechanism of EA analgesia.
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To investigate cerebral activations underlying touch-evoked pain (dynamic-mechanical allodynia) in patients with neuropathic pain. ⋯ Allodynic stimulation recruits a complex cortical network. Activations include not only nociceptive but also motor and cognitive processing. Using a covariance approach (i.e., implementation of rating-weighted predictors) facilitates the detection of a neuronal matrix involved in the encoding of allodynia. The pattern of cortical deactivation during allodynia may hint at a shift of activation from tonically active sensory systems, like visual and vestibular cortices, into somatosensory-related brain areas.
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Controlled Clinical Trial
The level of small nerve fiber dysfunction does not predict pain in diabetic Neuropathy: a study using quantitative sensory testing.
To determine whether small nerve fiber dysfunction predicts pain in diabetic neuropathy using quantitative sensory testing of thermal thresholds. ⋯ Quantitative sensory testing of small nerve fiber function is a useful test to detect the presence of neuropathy, and overall diabetic patients with neuropathic pain have more sensory loss. However, small nerve fiber abnormalities detected by quantitative sensory testing do not predict the presence of pain in diabetic neuropathy.
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Glial cell line-derived neurotrophic factor (GDNF) has been hypothesized to play an important role in the modulation of nociceptive signals especially during neuropathic pain. The present study examined the expression of GDNF and GFRalpha-1 (the high-affinity receptor of GDNF) in dorsal root ganglions (DRG) in a rat model of neuropathic pain induced by chronic constriction injury (CCI) to the sciatic nerve. ⋯ The present study demonstrated that endogenous GDNF and GFRalpha-1 might play an anti-hyperalgesic role in neuropathic pain of rats. In addition, we found a down-regulation of somatostatin (SOM) in DRG and spinal dorsal horn after expression of GFRalpha-1 was knocked down, which suggested the possible relationship between the anti-hyperalgesic effect of GDNF and GFRalpha-1 on neuropathic pain and endogenous SOM.
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A reduced rectal perceptual threshold has been reported in patients with irritable bowel syndrome (IBS), but this phenomenon may be induced by a comorbid psychological state. We evaluated the rectal pain threshold at baseline and after conditioning (repetitive rectal painful distention: RRD) in patients with IBS or functional abdominal pain syndrome (FAPS), which is an abdominal pain disorder, and in healthy controls, and determined whether rectal hypersensitivity is a reliable marker for IBS. ⋯ Rectal hypersensitivity induced by RRD may be a reliable marker for IBS. Conditioning-induced visceral hypersensitivity may play a pathophysiologic role in IBS.