Articles: hyperalgesia.
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The use of opioids for the treatment of chronic pain has increased dramatically over the past decade. Whether these drugs provide considerable benefits in terms of pain reduction and improved function to balance the risks associated with their use, however, is unclear. Of particular importance to clinicians treating chronic musculoskeletal pain is opioid-induced hyperalgesia, the activation of pronociceptive pathways by exogenous opioids that results in central sensitization to pain. ⋯ Opioids also have powerful positive effects on the reward and reinforcing circuits of the brain that might lead to continued drug use, even if there is no abuse or misuse. The societal risk of increased opioid prescription is associated with increased nonmedical use, serious adverse events and death. Patients with chronic musculoskeletal pain should avoid the long-term use of opioids unless the benefits are determined to outweigh risks, in which case, the use of chronic opioids should be regularly re-evaluated.
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Previous studies have demonstrated that sex differences in pain responsivity can be detected using various models of experimentally induced pain. The present study employed the mechanical pressure test in order to examine potential differences in pain report among men, normally menstruating women (NMW), and women taking monophasic oral contraceptives (OCW). Testing occurred during 5 phases of the menstrual cycle (menstrual, follicular, ovulatory, luteal, and late luteal) and all participants completed 10 sessions (2 sessions per phase). Menstrual-cycle phase was estimated for OCW based on their first day of menses. Men were tested at time points that roughly corresponded to the intervals during which the different phases occurred in NMW. During the mechanical pressure test, 4 different weights were placed on the fingers, one at a time, and ratings of pain were recorded for 30 seconds. The statistical decision-making model and a forced-choice procedure were used to analyze the response data. Two variables, based on signal detection theory, were thus generated: P(A), a measure of sensory pain, and B, a measure of response bias. P(A) is believed to be a measure of pain sensitivity while B measures stoicism. NMW tended to report lower P(A) values, indicating reduced ability to discriminate among different stimulus intensities, during the menstrual and late luteal phases compared to the luteal phase. OCW reported lower B values, indicating less stoicism, during the menstrual compared to the follicular and ovulatory phases. Men tended to have significantly lower B values than OCW, but not NMW. These results demonstrate subtle menstrual-cycle effects in NMW and OCW. Sex differences were few, with more group differences and trends emerging between OCW and men, as opposed to men and NMW. ⋯ The lack of consistent differences between men and NMW underscores the subtle impact of sex and hormonal changes in pain report. In addition, the data obtained in NMW support the notion that changes in hormone levels during the menstrual cycle can lead to changes in pain responsivity as NMW had trends for better discrimination in menstrual phases when estradiol levels were highest.
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Neuropathic pain syndromes are characterised by the occurrence of spontaneous ongoing and stimulus-induced pain. Stimulus-induced pain (hyperalgesia and allodynia) may result from sensitisation processes in the peripheral (primary hyperalgesia) or central (secondary hyperalgesia) nervous system. The underlying pathophysiological mechanisms at the nociceptor itself and at spinal synapses have become better understood. ⋯ These mechanisms include reorganisation of cortical somatotopic maps in sensory or motor areas (highly relevant for phantom limb pain and CRPS), increased activity in primary nociceptive areas, recruitment of new cortical areas usually not activated by nociceptive stimuli and aberrant activity in brain areas normally involved in descending inhibitory pain networks. Moreover, there is evidence from PET studies for changes of excitatory and inhibitory transmitter systems. Finally, advanced methods of structural brain imaging (voxel-based morphometry, VBM) show significant structural changes suggesting that chronic pain syndromes may be associated with neurodegeneration.
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Our aim was to assess thermal sensitivity in both trigeminal and extra-trigeminal regions in patients with myofascial temporomandibular disorder (TMD) but without comorbid conditions as compared to age-matched controls. Twenty women (age 24 +/- 3 years) diagnosed with myofascial TMD according to the research diagnostic criteria for TMD and 20 healthy women (age 24 +/- 4 years) were included. Warm and cold detection thresholds (WDT and CDT, respectively) and heat and cold pain thresholds (HPT and CPT, respectively) were bilaterally assessed over the masseter and frontalis muscles (trigeminal regions) and the wrist (extra-trigeminal region). ⋯ CPT (P < 0.001) over the trigeminal area was positively correlated with both pain intensity and duration of pain symptoms: the longer the history of pain or the greater the pain intensity, the higher the CPT (i.e., the greater cold hyperalgesia) over the trigeminal region. Our findings revealed bilateral thermal hyperalgesia (lower HPT and higher CPT) but normal WDT and CDT in trigeminal and extra-trigeminal regions in women with myofascial TMD as compared to healthy controls. Bilateral heat/cold hyperalgesia in trigeminal and extra-trigeminal areas may reflect a dysfunction of thermal channels in myofascial TMD patients as result of some combination of peripheral sensitization, facilitation of central nociceptive processing and/or decreased descending inhibition.
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Intraplantar injection of bee venom (BV) produces persistent spontaneous nociception (PSN), hyperalgesia, and inflammatory swelling of the injected paw. The present study was designed to determine the roles of peripheral metabotropic glutamate receptors (mGluRs) in BV-induced nociception and inflammation. We determined the effects of the group I mGluR antagonist AIDA, the group II mGluR agonist ADPC, and the group III mGluR agonist L-AP4 on BV-induced PSN, mechanical hyperalgesia, and inflammatory swelling. Pretreatment with intraplantar injections of AIDA, ADPC or L-AP4 at different doses significantly inhibited BV-induced PSN over the 1-hour observational period. The inhibitory effects of ADPC and L-AP4 were completely abolished by pretreatment with the group II mGluR antagonist LY341495 and the group III mGluR antagonist MSOP, respectively. Pretreatment with ADPC prevented the BV-induced decrease in paw-withdrawal mechanical threshold (PWMT) in a dose-dependent manner, while pretreatment with AIDA or L-AP4 had no effect. The antihyperalgesic effect of ADPC was completely abolished by pretreatment with LY341495. Pretreatment with AIDA, ADPC or L-AP4 at different doses had no effect on the BV-induced increase in the paw volume (PV), a measurement of inflammatory swelling. All contralateral drug treatments at the highest doses had no effect on BV-induced PSN, decreases in PWMT or increases in PV, eliminating the possibility of drug-induced systemic effects. These data suggest that the activation of mGluRs in the periphery may play a differential role in BV-induced nociception and inflammation. ⋯ The present study demonstrated that the intraplantar injection of antagonists or agonists of different mGluRs produced differential effects on bee venom-induced persistent spontaneous nociception and mechanical hyperalgesia. However, no effects on inflammation were observed, suggesting that mGluRs in the periphery have differential roles. Thus, therapies specifically targeting metabotropic glutamate receptors may improve the treatment of patients with persistent spontaneous nociception and hyperalgesia.