European journal of pain : EJP
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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.
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It has been reported that the whisker pad (WP) area, which is innervated by the second branch of the trigeminal nerve, shows allodynia/hyperalgesia following transection of the mental nerve (MN: the third branch of the trigeminal nerve). However, the mechanisms of this extra-territorial pain induction still remain unclear. Glia and cytokines are known to facilitate perception of noxious input, raising a possibility that these non-neuronal elements are involved in the induction and spread of allodynia/hyperalgesia at non-injured skin territory. ⋯ Administration of a noncompetitive antagonist of NMDA receptors MK-801 (i.t., 5 μg/rat) reversed allodynia/hyperalgesia. IL-1 receptor type I (IL-1RI) was localized in Fos- and phospho NR1-immunoreactive neurons. These results suggest that IL-1beta in the Vc plays an important role in the development of extra-territorial tactile allodynia/hyperalgesia after MN transection.
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Randomized Controlled Trial
Oral nitric-oxide donor glyceryl-trinitrate induces sensitization in spinal cord pain processing in migraineurs: a double-blind, placebo-controlled, cross-over study.
Nitric-oxide donor glyceryl-trinitrate (GTN) modulates cerebral and spinal regions that are involved in migraine and pain processing. We hypothesized that in migraineurs, the susceptibility to develop a migraine attack after GTN administration should parallel with an high sensitivity to GTN-induced change in the pain processing at spinal level. We used the temporal summation threshold (TST) of the lower limb nociceptive withdrawal reflex (NWR) and the related pain sensation to study in parallel the time-course of the effect of the GTN administration on the pain processing at spinal level in migraine and healthy subjects. ⋯ In migraineurs, GTN administration was associated to a significant facilitation in temporal summation of pain (reduced TST and increased painful sensation) 60', 120' and 180' after drug intake when compared to baseline, to placebo condition and to controls after GTN intake. Furthermore, in migraineurs who developed migraine after GTN, a significant facilitation in temporal summation of pain was detected 60', 120' and 180' after drug intake when compared to patients without clinical response. In migraineurs the susceptibility to develop migraine attack after GTN administration seems to be a specific trait of a subgroup of patients linked to a supersensitivity of the pain system to GTN.
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Attachment theory has been proposed as a framework for understanding the development of chronic pain, with evidence supporting the overrepresentation of insecure attachment styles in chronic pain populations and links between insecure attachment and factors known to impact one's ability to cope with pain. The present study sought to extend two earlier studies exploring the relationships between adult attachment and communication of an acute pain experience, in anticipation of providing insight into individual differences in vulnerability in development of chronic pain. It was hypothesised that: (a) fearful attachment would be associated with perceptions of the pain as less intense, and (b) anxious attachment would be associated with lower pain thresholds. ⋯ In addition, dismissing attachment was also associated with less intense pain, as well as increased coldpressor endurance (tolerance) in the presence of a known assessor. These associations were retained after controlling for measures of neuroticism, negative affect, age, and social desirability. The results of this study are consistent with the proposition that fearful and dismissing individuals tend to mask their underlying distress caused by the pain experience, potentially leading to difficulties coping with pain over time.