Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale
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The aims were to investigate (1) if temporomandibular disorders (TMD) patients with temporomandibular joint (TMJ) pain had different conditioned pain modulation (CPM) compared with healthy subjects and, (2) if clinical pain characteristics influenced CPM. Sixteen TMD pain patients and 16 age-matched healthy subjects were participated. A mechanical conditioning stimulus (CS) was applied to pericranial muscles provoking a pain intensity of 5/10 on a visual analogue scale. ⋯ In the patients, the relative PPT changes during CS were not significantly higher than baseline at TMJ (5.3 ± 3.8 %, P = 0.981) and masseter (-2.8 ± 4.8 %, P = 1.000) but significantly higher at forearm (12.3 ± 4.7 %, P = 0.039). No correlation was detected between TMD pain intensity and CPM effect (R = -0.261; P = 0.337) or between pain duration and CPM effect (R = -0.423; P = 0.103) at painful TMJ. These findings indicate that CPM is impaired in TMD pain patients especially at sites with chronic pain but not at pain-free sites and that the clinical pain characteristics do not influence CPM.
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Muscular fatigue effects have been shown to be compensated by the implementation of adaptive compensatory neuromuscular strategies, resulting in modifications of the initial motion coordination. However, no studies have focused on the efficiency of the feedforward motor commands when muscular fatigue occurs for the first time during a particular movement. This study included 18 healthy subjects who had to perform arm-raising movements in a standing posture at a maximal velocity before and after a fatiguing procedure involving focal muscles. ⋯ Following the fatiguing procedure, acceleration peaks of the arm movement decreased by ~27%. APAs scaled to this lower fatigue-related disturbance during the very first trial post-fatigue, suggesting that the Central Nervous System can predict unexperienced mechanical effects of muscle fatigue. It is suggested that these results are accounted for by prediction processes in which the central integration of the groups III and IV afferents leads to an update of the internal model by remapping the relationship between focal motor command magnitude and the actual mechanical output.
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Postoperative nausea and vomiting (PONV) continues to be a most common complication of surgery and anesthesia. It has been suggested that the inherited factors may play a significant role in the background sensitivity to both PONV and also chemotherapy-induced nausea and vomiting (CINV), including resistance to antiemetic prophylaxis and/or therapy. This notion could be best exemplified by occurrence of PONV in several generations of families and concordance of PONV in monozygotic twins. ⋯ The results of targeted genomic association studies indicate that other genes are also associated with PONV and CINV, including OPRM1, and ABCB1. In addition, genes such as DRD2 and CHRM3 genes have recently been associated with PONV. The new genome-wide association studies seem also to indicate that the background genomic sensitivity to PONV and CINV might be multifactorial and include several genomic pathways.
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Genetic variants, such as single-nucleotide polymorphisms (SNPs), of the μ-opioid receptor gene (OPRM1) might be associated with individual differences in opioid sensitivity, as well as with the incidence and severity of postoperative nausea and vomiting (PONV). The goal of the present study was to determine, in a cohort of Japanese surgical patients, genotypes and haplotypes of several SNPs in the OPRM1 gene, and their association with PONV during the early (first 24 h) postoperative period. We examined the incidence and severity of PONV, during the first 24 h after surgery, in 85 Japanese patients receiving intravenous patient-controlled analgesia fentanyl analgesia for postoperative pain control. ⋯ The severity of PONV in carriers of the GGGAACGC haplotype was significantly lower than in the carriers of the other haplotypes (P < 0.05). One intronic SNP, rs9397685, and haplotypes constructed from eight SNPs within the OPRM1 gene locus might be involved in the severity of PONV associated with general anesthesia and opioid administration. This novel finding, if validated and verified in larger and additional ethnic cohorts, might contribute to better knowledge of the contribution of the OPRM1 gene to PONV.
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Nausea is a noxious, uncomfortable feeling usually located in the epigastrium. The pathophysiology of nausea encompasses brain-gut and gut-brain interaction. Nausea is associated with myoelectrical dysrhythmias of the stomach, an objective marker in the periphery. The aims of this review were to describe (1) the physiology of normal 3 cycle per minute (cpm) gastric myoelectrical activity and (2) conditions where shifts from normal 3 cpm gastric rhythms to gastric dysrhythmias are associated with the onset of nausea. Illusory self-motion, infusion of drugs such as morphine and glucagon, and ingestion of water or nutrient loads are several of the multitude of stimuli that induce acute nausea and a variety of gastric dysrhythmias such as tachygastrias (3.75-10 cpm) and bradygastrias (1.0-2.5 cpm). In nausea of motion sickness, increased nausea severity correlates with increased plasma vasopressin and epinephrine levels. Gastric dysrhythmias are also present in chronic gastrointestinal neuromuscular disorders such as gastroparesis. When gastric dysrhythmias resolve after drug or device therapies, nausea resolves. The shift in state from comfort in the epigastrium area and normal 3 cpm gastric rhythm to symptoms of nausea and gastric dysrhythmias represents dynamic gut-brain and brain-gut interactions that can be tracked by changes in gastric rhythm. ⋯ (1) gastric dysrhythmias represent at least one peripheral mechanism underlying the symptom of nausea, and (2) gastric dysrhythmias are an objective biomarker for nausea and potential therapeutic targets for anti-nauseant therapies.