Pain
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This fMRI study investigates the influence of a rating procedure on BOLD signals in common pain-activated cortical brain regions. Painful and non-painful mechanical impact stimuli were applied to the left hand of healthy volunteers. Subjects performed ratings of the perceived intensity during every second stimulation period by operating a visual analogue scale with the right hand. ⋯ Only the responses in the S1 projection field of the stimulated hand following pain were not influenced by the rating procedure. Furthermore, activations in the right and left posterior insular cortex and in the left superior frontal gyrus showed an opposite pattern, namely a stronger BOLD signal during "non-rating". We concluded: (1) Cortical areas regularly activated by painful stimuli may also be activated by touch stimulation. (2) Enhancement of the BOLD contrast by a rating procedure is probably an effect of closer stimulus evaluation and attention focussing. (3) In contrast to most other cortical regions, the posterior insular cortex, which is crucial for the integration of interoceptive afferent input, shows stronger responses in the absence of ratings, which points to a unique role of this region in the processing of somato-visceral information.
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Randomized Controlled Trial Clinical Trial
A randomised double blind trial of the effect of pre-emptive epidural ketamine on persistent pain after lower limb amputation.
Persistent pain has been reported in up to 80% of patients after limb amputation. The mechanisms are not fully understood, but nerve injury during amputation is important, with evidence for the crucial involvement of the spinal N-methyl d-aspartate (NMDA) receptor in central changes. The study objective was to assess the effect of pre-emptively modulating sensory input with epidural ketamine (an NMDA antagonist) on post-amputation pain and sensory processing. ⋯ The intrathecal/epidural technique used, with peri-operative sensory attenuation, may have reduced ongoing sensitisation, reducing the overall incidence of persistent pain. The improved short-term analgesia and reduced mechanical sensitivity in Group K may reflect acute effects of ketamine on central sensitisation. Longer term effects on mood were detected in Group K that requires further study.
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A novel prognostic approach to defining chronic pain was developed in a US primary care low back pain population, using a combination of information about pain history, current status and likely prognosis. We tested whether this method was generalizable to a UK population. A prospective cohort of 426 patients who consulted with back pain at one of five UK general practices, and who returned follow-up information 1-year later were included. ⋯ The cut-points for probable and possible chronic pain developed in the US population (80% and 50% probability of future clinically significant back pain, respectively) were appropriate for the UK population, but the cut-point for classifying people at low risk (20% probability) was not replicated in the UK sample. The newly derived cut-points in the UK sample were similar; they remained the same for probable chronic pain, were slightly increased for possible chronic pain, and slightly reduced for those at intermediate or low risk. This method for defining chronic pain prospectively, using risk thresholds for future clinically significant pain, appears to be generalizable to a UK back pain population, particularly for identifying probable chronic pain, and may be generalizable to other primary care low back pain populations.
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Glial activation is a typical response of the central nervous system to nerve injury. In the current investigation, we characterized the temporal and spatial pattern of glial proliferation, one of the most conspicuous features of glial activation, in relation to nerve injury-induced neuropathic pain. Using bromodeoxyuridine (BrdU) as a mitotic marker, we analyzed cell proliferation in the spinal cord, identified the phenotype of dividing cells, traced their fate, and correlated these phenomena with behavioural assays of the neuropathic pain syndrome. ⋯ These newly generated cells continued to divide over time with the response peaking at day 14 post-injury. Microglia were always the predominant phenotype which made up over 60% of activated microglia derived from this newly generated cell population. There was a close temporal correlation between microglial proliferation in the spinal cord dorsal horn and the abnormal pain responses, suggesting a contribution of the new microglia to the genesis of the neuropathic pain symptoms.