Pain
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The transient receptor potential vanilloid channel 1 (TRPV1) is a nociceptive transducer located on nociceptive neurons. TRPV1 channels located on peripheral neurons mainly transduce the sense of heat and are also activated by low pH or capsaicin. The role of centrally located TRPV1 channels is not fully understood. ⋯ The results show that olvanil dose-dependently inhibited spontaneous and stimulus-induced activity within the trigeminocervical complex, whereas it had no effect on CSD susceptibility. We further demonstrated that the inhibiting effect of olvanil is mediated by vanilloid and cannabinoid receptor systems, thereby using the synergistic effects this dual mechanism offers. Curiously, TRPV1 receptor agonism may have anti-nociceptive properties through central mechanisms that would be of considerable interest to elucidate.
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Review Case Reports
Cervical spinal cord injection of epidural corticosteroids: comprehensive longitudinal study including multiparametric magnetic resonance imaging.
Despite widespread use, the efficacy of epidural corticosteroid injections (ESI) for osteoarthritis-associated neck or radicular pain remains uncertain, so even rare serious complications enter into discussions about use. However, various factors impede investigation and publication of serious adverse events. To that end, we developed new magnetic resonance imaging (MRI) techniques for spinal cord white matter quantification and used the best available physiological tests to characterize a cervical spinal cord lesion caused by inadvertent intramedullary injection of Depo-Medrol. ⋯ However, only CMCT metrics detected objective correlates of her left hemiparesis and bilateral hyperreflexia. DTI and MT metrics may better distinguish between post-traumatic demyelination and axonal degeneration than conventional MRI. These tests should be considered to better characterize similar spinal cord injuries.
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Comparative Study
Predictors of postoperative movement and resting pain following total knee replacement.
This study determined preoperative predictors of movement and resting pain following total knee replacement (TKR). We hypothesized that younger patients with higher preoperative pain intensity, pain sensitivity, trait anxiety, pain catastrophizing, and depression would be more likely to experience higher postoperative movement pain than older patients with lower scores on these variables prior to surgery, and that predictors would be similar for resting pain. Demographics, analgesic intake, anxiety, depression, pain catastrophizing, resting pain, movement pain (ie, during active knee range of motion), and quantitative sensory tests were performed preoperatively on 215 participants scheduled for a unilateral TKR. ⋯ These results suggest that patients with higher preoperative pain and depression are more likely to have higher pain following TKR, and younger patients may have higher resting pain. Cutaneous pain sensitivity predicted movement pain but not resting pain, suggesting that mechanisms underlying movement pain are different from resting pain. Aggressive management of preoperative pain, pain sensitivity, and depression prior to surgery may facilitate postoperative recovery.
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Hypoglycemia is a physiological stress that leads to the release of stress hormones, such as catecholamines and glucocorticoids, and proinflammatory cytokines. These factors, in euglycemic animal models, are associated with stress-induced hyperalgesia. The primary aim of this study was to determine whether experimental hypoglycemia in humans would lead to a hyperalgesic state. ⋯ In contrast to prior euglycemia exposure, prior hypoglycemia exposure resulted in enhanced pain sensitivity to hot and cold stimuli as well as enhanced temporal summation to repeated heat-pain stimuli. These findings suggest that prior exposure to hypoglycemia causes a state of enhanced pain sensitivity that is consistent with stress-induced hyperalgesia. This human model may provide a framework for hypothesis testing and targeted, mechanism-based pharmacological interventions to delineate the molecular basis of hyperalgesia and pain susceptibility.