Pain
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Randomized Controlled Trial
Stimulation of myofascial trigger points with ultrasound induces segmental antinociceptive effects: a randomized controlled study.
Musculoskeletal pain affects a significant proportion of the general population. The myofascial trigger point is recognized as a key factor in the pathophysiology of musculoskeletal pain. Ultrasound is commonly employed in the treatment and management of soft tissue pain and, in this study, we set out to investigate the segmental antinociceptive effect of ultrasound. ⋯ Following the ultrasound intervention, PPT readings were recorded at 1, 3, 5, 10 and 15 min intervals at both infraspinatus and gluteus medius trigger points; the difference between infraspinatus and gluteus medius PPT values, PPT seg, represents the segmental influence on the PPT. The ultrasound test group demonstrated statistically significant increases in PPT seg (decreased infraspinatus sensitivity) at 1, 3 and 5 min, when compared with PPT seg in the sham ultrasound group. These results establish that low-dose ultrasound evokes short-term segmental antinociceptive effects on trigger points which may have applications in the management of musculoskeletal pain.
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A prognostic approach to defining chronic pain has been proposed as an alternative to traditional definitions based on retrospective duration of pain. While this new approach performs well in low back pain (LBP), headache and orofacial pain, it is not known whether it translates to regional pain syndromes with an underlying pathological component, such as osteoarthritis (OA). We investigated the performance of this approach in a population-based cohort of older adults reporting knee pain, with a spectrum of radiographic knee OA. 676 adults (50 years+) attended a research clinic and were followed up at 18 months and 3 years. ⋯ The derived cut-points suggested a lower threshold for each of the risk groups than the previous LBP work. This prognostic approach to defining chronic pain appears to translate well to knee pain. Different cut-points for defining risk groups may be needed for different pain syndromes.
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Anxiety has been described as an important comorbidity in patients suffering from chronic pain. However, in animals the connection between persistent pain and anxiety has hardly been investigated. Therefore, in the current study it was assessed whether chronic pain also causes anxiety-like behaviour in animals and if it can be reversed by analgesic or anxiolytic drugs. ⋯ Morphine (3mg/kg; i.p.) and gabapentin (30 mg/kg; i.p.) significantly attenuated anxiety-like behaviour in the CCI lesioned rats: morphine increased entries into open arms from 3.0+/-0.4 to 7.7+/-1.4 (P=0.01), gabapentin elevated this value from 4.7+/-1 to 7.5+/-0.9 (P=0.02). These data suggest that rats subjected to neuropathic pain models develop anxiety-like behaviour which can be reversed by appropriate analgesic treatment. Morphine and gabapentin had no anxiolytic-like effect in sham treated animals, thus their effect on anxiety-like behaviour in the neuropathic pain model is likely indirect via their anti-nociceptive properties.
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Temporal summation of "second pain" (TSSP) is considered to be the result of C-fiber-evoked responses of dorsal horn neurons, termed 'windup'. TSSP is dependent on stimulus frequency (> or=0.33Hz) and is relevant for central sensitization and chronic pain. We have previously shown that compared to normal controls (NC), fibromyalgia (FM) subjects show abnormal TSSP, requiring lower stimulus intensities/frequencies to achieve similar TSSP. ⋯ In a second experiment, all aspects of individually adjusted TSSP heat pulses were kept the same except that the baseline temperature (BT) between heat pulses was surreptitiously alternated between 35 degrees C and 40 degrees C. These changes of BT resulted in significantly greater TSSP ratings of FM subjects compared to NC subjects, both at 35 degrees C and at 40 degrees C, but did not change their response to the first heat pulse of a stimulus train. These findings provide strong support for alterations of central pain sensitivity and not peripheral sensitization or rating bias as responsible for TSSP differences between NC and FM subjects.