Articles: hyperalgesia.
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Randomized Controlled Trial Comparative Study
Analgesic and antihyperalgesic properties of propofol in a human pain model.
Propofol (Disoprivan, AstraZeneca AG, Zug, Switzerland) has long been considered to be nonanalgesic. However, accumulating evidence shows that propofol possesses modulatory action on pain processing and perception. In this study, the authors investigated the modulatory effects of propofol and a formulation similar to the solvent of propofol (10% Intralipid; Fresenius Kabi, Stans, Switzerland) on pain perception and central sensitization in healthy volunteers. ⋯ Propofol showed short-lasting analgesic properties during its administration, whereas the solvent-like formulation 10% Intralipid had no effect on pain perception.
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To review mechanisms that might contribute to sensory disturbances and sympathetically-maintained pain in complex regional pain syndrome (CRPS). ⋯ Sympathetic neural activity might contribute to pain and sensory disturbances in CRPS by feeding into nociceptive circuits at the site of injury or elsewhere in the CRPS-affected limb, within the dorsal horn, or via thalamo-cortical projections.
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This study aimed at investigating in details the spatial characteristics of muscular hyperalgesia after development of delayed onset muscle soreness (DOMS) in the trapezius muscle. High density pressure pain mapping consisting of 36 pain pressure threshold (PPT) recording points were assessed over the trapezius muscle from 20 subjects. PPT were recorded before, immediately after and 24h after eccentric exercise/rest for the exercise group (N=10) and the control group (N=10). ⋯ The hyperalgesia was also mostly developed in the muscle belly sites (P<0.001), further enhancing its position as the most sensitive part of the muscle. The present results showed the topographical distribution of pressure pain sensitivity over the trapezius muscle and also that hyperalgesia developed in a heterogeneous manner over the trapezius muscle in response to eccentric exercise underlining sensory partitioning of the muscle. The technique of high density pressure pain topographical mappings can be helpful in characterizing muscle hyperalgesia and its heterogeneity.
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Previous studies on sensory function in persistent postherniotomy pain (PPP) have only identified pressure pain threshold to be significantly different from pain-free patients despite several patients reporting cutaneous pain and wind-up phenomena. However the limited number of patients studied hinders evaluation of potential subgroups for further investigation and/or treatment allocation. Thus we used a standardized QST protocol to evaluate sensory functions in PPP and pain-free control patients, to allow individual sensory characterization of pain patients from calculated Z-values. ⋯ A high incidence (26%) of pressure hyperalgesia was found in the contralateral groin, with a significant correlation (rho=0.58, p=0.002) to the hyperalgesic level on the painful side, again suggesting central nervous mechanisms in PPP. In conclusion, this study shows that a standardized trauma results in heterogeneous combinations of hypo- and hyperalgesia. Z-score evaluation of sensory function identifies subpopulations in PPP, which may be used in selecting surgical and/or pharmacological treatment strategies.
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Painful diabetic neuropathy may be due to impairments in descending modulation of nociceptive transmission at the spinal cord. In the present study, streptozotocin diabetic rats (STZ rats) with neuropathic symptoms (mechanical hypersensitivity) were used to perform a time-course evaluation of neuronal activity at the spinal dorsal horn and at the periaqueductal grey matter (PAG), a major brainstem area of pain modulation. The expression of Fos protein, a marker of nociceptive activation, progressively increased at the spinal dorsal horn at 4 and 10 weeks. ⋯ The present study shows that diabetic neuropathy is accompanied by a progressive increase of the spontaneous neuronal activity at the spinal cord. Changes in descending modulation of nociceptive transmission from the PAG are likely to occur during diabetic neuropathy, probably with exacerbation of facilitatory actions. The effects of gabapentin in reversing the behavioural signs of diabetic neuropathy and neuronal hyperactivity in the spinal cord and PAG reinforce the central causes of diabetic neuropathy and point to the central targets of the drug.