Pain
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In previous studies, pain behaviors produced in the spinal nerve ligation rat model of neuropathic pain were partly reduced by surgical lumbar sympathectomy. However, systemic injection of phentolamine, an alpha-adrenoceptor blocker, was not effective in reducing pain behaviors, at least in the Sprague-Dawley strain of rats. This suggests that sympathectomy removes not only adrenoceptor function but also other factors that must contribute importantly to the generation of neuropathic pain behaviors. ⋯ This effect was observed in a subset of neuropathic rats, and the drug responses were consistent in repeated treatments within the animal group. Neither phentolamine nor suramin changed the mechanical sensitivity of neuropathic rats when given alone. The data suggest that the purinergic substance ATP is co-released with NE from sympathetic nerve terminals and these two are together involved, at least in part, in the maintenance of the sympathetically dependent component of pain behaviors in some neuropathic rats.
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Randomized Controlled Trial Clinical Trial
Delayed onset muscle soreness: effect of an ischaemic block upon mechanical allodynia in humans.
The current study, for which ethical approval was obtained, was designed to assess the extent to which the tenderness or mechanical allodynia observed in delayed onset muscle soreness (DOMS) might be mediated by large diameter myelinated nerve fibres. Healthy human volunteers were recruited and randomly allocated to one of three groups: Normal-Control, Ischaemic-Control, and Test-DOMS (total n=21; n=7 in each group). In the Normal-Control group, subjects attended on a single occasion for assessment of mechanical pain threshold (MPT) at standardized sites over the biceps brachii using a pressure algometer for a period of 20 min. ⋯ Results showed a significant (P<0.05; ANOVA) increase in MPT in the Test-DOMS group by the 20 min point, corresponding to a 'normalization' of MPT; loss of the ability to distinguish between sharp/blunt sensation accompanied such changes. Parallel increases in reported pain were seen in both groups undergoing ischaemic block, indicating that the procedure did not alter nociception. While not definitive, these results suggest that altered processing of activity in large diameter (myelinated) afferents might underlie the mechanical allodynia observed in DOMS; thus, this is an area which warrants further investigation.
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The most common complication of herpes zoster in immunocompetent patients is postherpetic neuralgia (PHN). Sympathetic blocks have been traditionally used for patients with herpes zoster and PHN with three different therapeutic goals: pain relief during acute herpes zoster, pain relief during PHN, and prevention of PHN by treating patients with acute zoster. The role of sympathetic blocks in herpes zoster and PHN remains controversial due to methodologic shortcomings in published studies and the limited current understanding of the role of the sympathetic nervous system in mediating pain. Current theories of the pathophysiology of PHN, the role of the sympathetic nervous system in herpes zoster and PHN, and published studies investigating use of sympathetic nerve blocks in herpes zoster and PHN are reviewed.
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Peripheral neuropathic pain is produced by multiple etiological factors that initiate a number of diverse mechanisms operating at different sites and at different times and expressed both within, and across different disease states. Unraveling the mechanisms involved requires laboratory animal models that replicate as far as possible, the different pathophysiological changes present in patients. It is unlikely that a single animal model will include the full range of neuropathic pain mechanisms. ⋯ The mechanical (von Frey and pinprick) sensitivity and thermal (hot and cold) responsiveness is increased in the ipsilateral sural and to a lesser extent saphenous territories, without any change in heat thermal thresholds. Crush injury of the tibial and common peroneal nerves produce similar early changes, which return, however to baseline at 7-9 weeks. The spared nerve injury model may provide, therefore, an additional resource for unraveling the mechanisms responsible for the production of neuropathic pain.
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Many lines of evidence implicate the somatosensory areas near the lateral sulcus (Sylvian fissure) in the cortical representation of pain. Anatomical tracing studies in the monkey show nociceptive projection pathways to the vicinity of the secondary somatosensory cortex in the parietal operculum, and to anterior parts of insular cortex deep inside the Sylvian fissure. Clinical observations demonstrate alterations in pain sensation following lesions in these two areas in human parasylvian cortex. ⋯ This anatomical separation may be one of the reasons why single unit recordings of nociceptive neurons are scarce within regions comprising low-threshold mechanoreceptive neurons. The functional significance (sensory-discriminative, affective-motivational, cognitive-evaluative) of the closely spaced parasylvian cortical areas in acute and chronic pain is only poorly understood. It is likely that some of these areas are involved in sensory-limbic projection pathways that may subserve the recognition of potentially tissue damaging stimuli as well as pain memory.