European journal of pain : EJP
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Pain Management Programmes (PMPs) are a multi-disciplinary approach to the management of chronic low back pain (CLBP). Notwithstanding evidence of effectiveness, successful take-up of programmes requires acceptability to patients. We used a discrete choice experiment to investigate patient preferences for alternative PMPs for managing CLBP in primary care. ⋯ Probability of take-up increases when PMPs better reflect patient preferences. Given preferences, resource constraints, and evidence on clinical outcomes of alternative configurations it is suggested more resource-intensive PMPs be reserved for those with the most severe and disabling pain and less intensive programmes delivered over a longer time period in smaller groups for those with less severe pain. These findings can inform future randomised trials to evaluate acceptable PMPs in primary care.
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The vast majority of human peripheral nerve injuries occur in the upper limb, whereas the most animal studies have been conducted using the hindlimb models of neuropathic pain, involving damages of the sciatic or lumbar spinal nerve(s). We attempted to develop a rat forelimb model of peripheral neuropathy by partial injury of the median and ulnar nerves. The halves of each nerve were transected by microscissors at about 5mm proximal from the elbow joint and behavioral signs of neuropathic pain, such as mechanical and cold allodynia, and heat hyperalgesia, were monitored up to 126 days following nerve injury. ⋯ These behaviors were significantly alleviated by administration of gabapentin (5 or 50mg/kg, i.p.) in a dose-dependent manner. Therefore, these abnormal sensitivities are interpreted as the signs of neuropathic pain following injury of the median and ulnar nerves. Our rat forelimb model of neuropathic pain may be useful for studying human neuropathic pain and screening for valuable drug candidates.
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Endogenous analgesia (EA) can be examined experimentally using a conditioned pain modulation (CPM) paradigm. While noxious conditioning stimulation intensities (CSIs) are mainly used, it has not been fully investigated in the same experimental design whether the experienced conditioning pain level affects CPM responses. The principal goal of the present study was to characterize CPM induction and magnitudes evoked by various conditioning pain levels. ⋯ Conditioning pain levels were correlated across all CSIs, as were CPM magnitudes (Ps ≤ 0.01). We conclude that among males, (i) once a CPM response is evoked by a required conditioning pain experience, its magnitude is not further affected by increasing conditioning pain and (ii) CPM magnitudes are inter-correlated, but unrelated to conditioning pain reports. These observations may suggest that CPM responses represent an intrinsic element of an individual's EA processes, which are not significantly affected by the experienced conditioning pain.
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Comparative Study
Postnatal expression of the homeobox gene Prrxl1 (Drg11) is increased in inflammatory but not neuropathic pain.
The paired-type homeodomain transcription factor Prrxl1 (also known as Drg11) is a key regulator of the differentiation and survival of dorsal root ganglia (DRG) and spinal nociceptive neurons in pre- and perinatal stages. Prrxl1(-/-) mice exhibit abnormalities in DRG-spinal projections, defects in superficial dorsal horn structure and neurochemistry, and reduced nociceptive behaviour in several pain tests. Although a low expression of Prrxl1 persists in dorsal root ganglia beyond embryonic development, no data exist on its role in adult life. ⋯ Interestingly, the expression of the mRNA splice variant Prrxl1b was unchanged in both pain conditions. Immunohistochemical studies showed an increase in the number of Prrxl1-positive neurons in the inflammatory pain model, which belonged both in the peptidergic and non-peptidergic categories. Our present results point to a role for Prrxl1 in sensitization of nociceptive neurons upon inflammatory pain.
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Eighteen patients with peripheral neuropathic pain (PNeP) and seven patients with central post-stroke pain (CPSP) all suffering from dynamic mechanical allodynia (DMA) in a limb were studied. From recent research it is reasonable to suggest that A-beta fibres constitute the peripheral substrate for DMA in patients with PNeP. The pathophysiological basis for DMA in patients with CPSP is unknown. ⋯ The rest of the patients lost DMA without transition to DMD. The transition or loss of DMA without transition occurred early and concurrently in time during the block and was paralleled by a continuous impairment of mainly A-beta fibre function. We therefore suggest DMA to be the hyperbole of DMD, the difference being the number of mechanoreceptive fibres having access to the nociceptive system.