Articles: hyperalgesia.
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J Orthop Sports Phys Ther · Nov 2010
Specific mechanical pain hypersensitivity over peripheral nerve trunks in women with either unilateral epicondylalgia or carpal tunnel syndrome.
Case-control study with blinded examiner. ⋯ Bilateral mechanical nerve pain hypersensitivity is related to specific and particular nerve trunks in women with either unilateral LE or CTS. Our results suggest the presence of central and peripheral sensitization mechanisms in individuals with either LE or CTS.
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Co-existing algogenic conditions in two internal organs in the same patient may mutually enhance pain symptoms (viscero-visceral hyperalgesia). The present study assessed this phenomenon in different models of visceral interaction. ⋯ In patients' subgroups, symptoms were also re-assessed after treatment of each condition or after no treatment. (a) CAD+Gs presented more numerous/intense angina/biliary episodes and more referred muscle chest/abdominal hyperalgesia than CAD or Gs; cardiac revascularization or cholecystectomy also reduced biliary or cardiac symptoms, respectively (0.001
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Excessive cervical facet capsular ligament stretch has been implicated as a cause of whiplash-associated disorders following rear-end impacts, but the pathophysiological mechanisms that produce chronic pain in these cases remain unclear. Using a rat model of C6-C7 cervical facet joint capsule stretch that produces sustained mechanical hyperalgesia, the presence of neuronal hyperexcitability was characterized 7 days after joint loading. Extracellular recordings of spinal dorsal horn neuronal activity between C6 and C8 (117 neurons) were obtained from anesthetized rats, with both painful and non-painful behavioral outcomes established by the magnitude of capsule stretch. ⋯ The proportion of cells in the deep laminae that responded as wide dynamic range neurons also was increased in the painful group relative to non-painful or sham groups (p<0.0348). These findings suggest that excessive facet capsule stretch, while not producing visible tearing, can produce functional plasticity of dorsal horn neuronal activity. The increase in neuronal firing across a range of stimulus magnitudes observed at day 7 post-injury provides the first direct evidence of neuronal modulation in the spinal cord following facet joint loading, and suggests that facet-mediated chronic pain following whiplash injury is driven, at least in part, by central sensitization.
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Painful neuropathy is a common complication of diabetes. Particularly in the early stage of diabetic neuropathy, patients are characterized by burning feet, hyperalgesia to heat, and mechanical stimuli, as if residual nociceptors were sensitized. Such symptoms are barely explained by common pathophysiological concepts of diabetic neuropathy. ⋯ Diabetic C-fibers show exaggerated sensitivity to hyperglycemic hypoxia with and without additional acidosis, conditions that are thought to mimic ischemic episodes in diabetic nerves. Ongoing C-fiber discharge is known to induce spinal sensitization. Together with altered receptor and ion channel expressions this may contribute to painful episodes in diabetic neuropathy.
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Central sensitisation is associated with chronic pain in whiplash patients. Predicting which patients will develop central sensitisation is difficult but patient expectations of recovery predict a variety of outcomes in whiplash patients. ⋯ Whiplash patients who expect 'never to get better' or 'don't know' have a much higher likelihood of developing at least one sign of central sensitisation 3 months after their collision.