Pain
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Review Meta Analysis
Effect of various kinds of cervical spinal surgery on clinical outcomes: A systematic review and meta-analysis.
The choice of a specific surgical technique should be based on its benefits and harms. Previous reviews have shown that the benefit of surgery over conservative care is not clearly demonstrated in patients with disorders of the cervical spine. Also, no additional benefit of fusion upon anterior decompression techniques could be found. ⋯ Unfortunately, in these studies the authors had a clear conflict of interest. The differences in benefits and harms between the various surgical techniques are small. The surgeon, patient, and health care provider can therefore make the choice of any surgical technique based on experience, preferences, or costs.
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The aim of this study was to assess the function of the thermo-nociceptive system in 25 patients with long-lasting, medium-to-severe refractory complex regional pain syndrome (CRPS)-1 using behavioral (detection rates and reaction times) and electrophysiological (event-related brain potentials) responses to brief (50 milliseconds) and intense (suprathreshold for Aδ-nociceptors) carbon dioxide laser stimuli delivered to the affected and contralateral limbs, and by comparing these responses to the responses obtained in the left and right limbs of age- and sex-matched healthy controls. Compared with healthy controls and compared with the contralateral limb, the detection rate of pricking pain related to the activation of Aδ-fibers was markedly reduced at the affected limb. Furthermore, reaction times were substantially prolonged (>100 milliseconds in 84% of patients and >300milliseconds in 50% of patients). ⋯ Taken together, our results show that in the majority of patients with chronic CRPS-1, thermo-nociceptive pathways are dysfunctional. A number of pathological mechanisms involving the peripheral nervous system and/or the central nervous system could explain our results. However, the primary or secondary nature of these observed changes remains an open question.
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The perception of pain is determined by a combination of genetic, neurobiological, cultural, and emotional factors. Recent studies have demonstrated an association between specific genotypes and pain perception. Particular focus has been given to the triallelic polymorphism in the promoter region of the serotonin transporter gene in relation to pain perception. ⋯ However, in participants with a high expression of the serotonin transporter protein, conditioning with negative pictures increased pain intensity and positive pictures decreased pain intensity when compared with neutral pictures. In contrast, there were no significant effects of the pictures on pain perception in participants with either intermediate or low expression of the protein. These results suggest that polymorphisms in the serotonin transporter gene play an important role in emotions modulation of muscle pain.
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Human association studies of common genetic polymorphisms have identified many loci that are associated with risk of complex diseases, although individual loci typically have small effects. However, by envisaging genetic associations in terms of cellular pathways, rather than any specific polymorphism, combined effects of many biologically relevant alleles can be detected. The effects are likely to be most apparent in investigations of phenotypically homogenous subtypes of complex diseases. ⋯ A risk index representing combined effects of 6 SNPs from the serotonergic pathway was associated with greater odds of localized TMD (odds ratio 2.7, P=1.3 E-09), and the result was reproduced in a replication case-control cohort study of 639 people (odds ratio 1.6, P=0.014). A risk index representing combined effects of 8 SNPs from the T-cell receptor pathway was associated with greater odds of TMD with widespread pain (P=1.9 E-08), although the result was not significant in the replication cohort. These findings illustrate potential for clinical classification of chronic pain based on distinct molecular profiles and genetic background.
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Scientific evidence support the notion that migraine pathophysiology involves inherited alteration of brain excitability, intracranial arterial dilatation, recurrent activation and sensitization of the trigeminovascular pathway, and consequential structural and functional changes in genetically susceptible individuals. Evidence of altered brain excitability emerged from clinical and preclinical investigation of sensory auras, ictal and interictal hypersensitivity to visual, auditory and olfactory stimulation, and reduced activation of descending inhibitory pain pathways. ⋯ Also, structural and functional alterations include the presence of subcortical white mater lesions, thickening of cortical areas involved in processing sensory information, and cortical neuroplastic changes induced by cortical spreading depression. Here, we review recent anatomical data on the trigeminovascular pathway and its activation by cortical spreading depression, a novel understanding of the neural substrate of migraine-type photophobia, and modulation of the trigeminovascular pathway by the brainstem, hypothalamus and cortex.