Articles: hyperalgesia.
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Comparative Study
Increased pain sensitivity to intraoral capsaicin in patients with atypical odontalgia.
To use 2 well-characterized stimuli, the intraoral capsaicin model and the "nociceptive-specific" electrode, to compare superficial nociceptive function between patients with atypical odontalgia (AO) and matched healthy controls. Furthermore, the authors aimed to describe the sensitivity, specificity, and positive predictive values (PPV) of the techniques if group differences could be established. ⋯ AO patients show increased sensitivity to intraoral capsaicin but normal sensitivity to "nociceptive-specific" electrical stimulation of the face in an area proximal to the painful site. The use of the intraoral pain-provocation test with capsaicin as a possible adjunct to the diagnostic workup is hampered by the only moderately good sensitivity and specificity.
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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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Promising recent developments in the therapeutic value of neuropeptide antagonists have generated renewed importance in understanding the functional role of neuropeptides in nociception and inflammation. To explore this relationship we examined behavioral changes and primary afferent neuronal plasticity following deep tissue inflammation. One hour following craniofacial muscle inflammation ipsilateral as well as contralateral head withdrawal thresholds and ipsi- and contralateral hindpaw withdrawal thresholds were lowered and remained reduced for 28 days. ⋯ Local injection of CGRP antagonist directly into the masseter muscle prior to CFA produced similar, but less pronounced, effects. These findings indicate that unilateral craniofacial muscle inflammation produces mechanical allodynia at distant sites and upregulates CGRP and SP in primary afferent neurons innervating deep tissues. These data further implicate CGRP and SP in deep tissue nociceptive mechanisms and suggest that peptide antagonists may have therapeutic potential for musculoskeletal pain.
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Controlled Clinical Trial
Retrospenial cortical deactivation during painful stimulation of fibromyalgic patients.
To study fibromyalgic pain this article contrasts positron emission tomographic measures of regional cerebral blood flow (rCBF) during externally induced acute pain and rest in eight fibromyalgia syndrome patients. An expected pattern of frontal and parietal cortical activation during acute pain as compared to rest was observed. However, reduced rCBF was additionally found in the retrosplenial cortex during acute pain as compared to rest. This may reflect that externally induced pain inhibits fibromyalgic pain and syndrome-related evaluative processes located in the retrosplenial cortex, and that fibromyalgic pain results from exaggerated attention to sub-noxious pain signaling, that is, secondary hyperalgesia.
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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).