Pain
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"Don't look and it won't hurt" is commonly heard advice when receiving an injection, which implies that observing needle pricks enhances pain perception. Throughout our lives, we repeatedly learn that sharp objects cause pain when penetrating our skin, but situational expectations, like information given by the clinician prior to an injection, may also influence how viewing needle pricks affects forthcoming pain. How both previous experiences and acute situational expectations related to viewing needle pricks modulate pain perception is unknown. ⋯ Intensity ratings of electrical stimuli were higher when a clip was associated with expectation of painful compared to nonpainful stimuli, suggesting that situational expectations about forthcoming pain bias perceived intensity. Unpleasantness ratings and pupil dilation responses were higher when participants viewed a needle prick, compared to when they viewed a Q-tip touch, suggesting that previous experiences with viewing needle pricks primarily act upon perceived unpleasantness. Thus, remote painful experiences with viewing needle pricks, together with information given prior to an injection, differentially shape the impact of viewing a needle prick on pain perception.
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The current study examined the prospective relationship between pain-related fear and altered motor behavior, as well as perceived interference, among 51 healthy participants following induction of delayed-onset muscle soreness (DOMS) to the trunk extensor muscles. Healthy participants without history of back pain completed standardized reaches to high and low targets at self-paced and rapid speeds before and after induction of acute low back pain using a DOMS paradigm. Pain-related fear was assessed prior to DOMS induction. ⋯ Pain-related fear scores were not predictive of lumbar flexion during baseline, but predicted reduced lumbar flexion during self- and fast-paced trials to low target locations once DOMS was induced. Pain-related fear was likewise predictive of perceived interference in life activities following DOMS induction. The findings suggest that initially pain-free individuals with high pain-related fear adopt avoidant spinal strategies during common reaching movements shortly after injury is sustained, which may comprise a risk factor for future pain and disability.
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We quantified the immune histiocytic Langerhans cells (LCs) in skin biopsy samples of patients with distal small fiber neuropathy (SFN). Patients were divided according to the presence or absence of neuropathic pain (burning pain) assessed by a visual analogue scale (VAS). We studied 13 diabetic patients (pain-DSFN), 7 nondiabetic patients (pain-SFN) who reported relevant neuropathic pain (VAS ≥ 3), and 6 nondiabetic patients without neuropathic pain (no-pain-SFN). ⋯ There was a negative correlation between the IENFD and the number of LCs (r(2)=-0.13, P=.03). No statistically significant differences were found among groups of subjects either for the co-localization or for the number of LCs that were PGP 9.5-immunoreactive (analysis of variance; P>.05). These results indicate that patients with neuropathic pain in the context of SFN, specially those who had diabetes (DSFN), had an increased number of LCs in the epidermis that may play a role in the generation or maintenance of neuropathic pain.
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N-Methyl-d-aspartate (NMDA) receptors are thought to play an important role in the processes of central sensitization and pathogenesis of neuropathic pain, particularly after spinal cord injury (SCI). NMDA antagonists effectively reduce neuropathic pain, but serious side effects prevent their use as therapeutic drugs. NMDA NR2B antagonists have been reported to effectively reduce inflammatory and neuropathic pain. ⋯ Increased expression of NR2B in the hemisection model was reduced by intrathecal ifenprodil. These results suggest that intrathecal NMDA NR2B antagonist increased the mechanical nociceptive threshold after SCI without motor depression. A selective subtype of NMDA receptor, such as NR2B, may be a more selective target for pain control because NMDA receptors play a crucial role in the development and maintenance of chronic pain.
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An abundance of animal research suggests that fear inhibits pain whereas anxiety increases it. Human studies on this topic are more scarce, and the existing evidence seems rather inconsistent. Therefore, we aimed to investigate the divergent effects of both negative emotional states-that is, pain-related fear and anxiety on pain sensitivity and unpleasantness. ⋯ Moreover, this sex-specific sensitization is partially mediated by (conditioned) fear of movement-related pain. Women also report increasingly more fear of pain over conditioning blocks, while men do not. These results might be interesting in the light of the overrepresentation of women in a number of clinical pain conditions as well as anxiety disorders.