Pain
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Review
Gender differences in pain modulation by diffuse noxious inhibitory controls: a systematic review.
Over the last decade, extensive research has demonstrated sex differences in pain perception and modulation. Several factors have been proposed to account for the differences observed between men and women, including pain modulation through diffuse noxious inhibitory controls (DNIC). Studies investigating sex differences in DNIC have shown mixed results, with some reporting decreased DNIC effect in women compared with men, while others found no difference in DNIC between the sexes. ⋯ The majority of studies using pain report as the outcome found significantly more efficient DNIC in males than females (mean female/male ratio=0.54). Studies evaluating pain thresholds and nociceptive flexion reflex indicated the opposite when simply averaged across studies; however, weighted analyses of threshold found more efficient DNIC in males. Gender differences in DNIC effect depend on both the experimental methodology and the modes of measurement of the effect.
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Due to maturation-related plasticity of the developing nociceptive system, neonatal nociceptive input, as induced by medical procedures in the neonatal intensive care unit (NICU), may cause long-term alterations in pain processing. Using functional magnetic resonance imaging, this study investigated the cerebral pain response in school-aged children and adolescents (11-16 yr) with experience in a NICU after preterm (
or=37 weeks gestational age, N=9) as compared to fullterm control children without early hospitalization (N=9). NICU children had been recruited retrospectively among former patients of the Children's University Hospital Mannheim. ⋯ This exaggerated brain response was pain-specific and was not observed during non-painful warmth stimulation. Preterms' continuous pain ratings revealed a tendency for increased sensitization within and a lack of habituation across trials. In highly vulnerable children such as preterms, neonatal nociceptive input may, aside from other neurodevelopmental consequences, persistently increase the gain within pain pathways. -
Somatosensory neurons detect environmental stimuli, converting external cues into neural activity that is relayed first to second-order neurons in the spinal cord. The detection of cold is proposed to be mediated by the ion channels TRPM8 and TRPA1. However, there is significant debate regarding the role of each channel in cold-evoked pain, complicating their potential as drug targets for conditions such as cold allodynia and hyperalgesia. ⋯ Furthermore, nocifensive behaviors to the cold-mimetic icilin are absent in TRPM8(-/-) and DKO mice, but are retained in TRPA1-nulls (TRPA1(-/-)). Finally, neural activity, measured by expression of the immediate-early gene c-fos, evoked by hindpaw stimulation with noxious cold, menthol, or icilin is reduced in TRPM8(-/-) and DKO mice, but not in TRPA1(-/-) animals. Thus our results show that noxious cold signaling is exclusive to TRPM8, mediating neural and behavioral responses to cold and cold-mimetics, and that TRPA1 is not required for acute cold pain in mammals.
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Complex regional pain syndrome (CRPS) is a syndrome that describes a broad spectrum of sensory, motor and autonomic-like features with unproven etiology. The International Association for the Study of Pain (IASP) diagnostic criteria of CRPS shows high sensitivity but poor specificity. Using statistical-pattern-recognition methods, American researchers have suggested a new set of criteria offering acceptable sensitivity and high specificity. ⋯ Our diagnostic criteria are not exactly the same as the American criteria, indicating a need for more regionally based CRPS diagnostic criteria. Different sets of CRPS diagnostic criteria could lead to dissimilar patients being diagnosed as CRPS, however, presenting problems for translation of therapeutic effects found in various studies. Therefore, we further recognize a need for a global set of common CRPS diagnostic criteria.
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Chronic stressful events induce biochemical, physiological and psychological changes, resulting in stress-related neuropsychiatric disorders, such as anxiety or depression. Using repeated social defeat as a stressful event model, we show that this preclinical paradigm induces a transient increase in the expression of the genes encoding the pro-inflammatory molecules iNOS and COX-2. We provide the first demonstration that chronic stress affects spinal plasticity through a mechanism involving local neuroinflammation. ⋯ The present study highlights the adverse effects of chronic stress on spinal neuroinflammation triggering sensory hypersensitivity. Exploration of this phenomenon points out the divergence between pain sensitivity and anxiety-induced hyperalgesia, which is in agreement with clinical observations. Altogether, these data open up new perspectives for clinical research devoted to the evaluation and treatment of pain in anxio-depressive patients.