Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale
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Gabapentin's main clinical use is in the treatment of neuropathic pain where its binding to neuronal alpha-2/delta subunits of voltage-gated calcium channels (VGCCs) is critical to its mechanism of action. Over the past 10 years, there have been several reports of gabapentin also having anti-nausea and anti-emetic effects in conditions including postoperative nausea and vomiting (PONV), chemotherapy-induced nausea and vomiting (CINV), and hyperemesis gravidarum (HG). ⋯ These 12 studies provided a Grade A recommendation for gabapentin use in treating PONV, a Grade B recommendation for use in treating CINV, and a Grade C recommendation for use in treating HG. Further research is needed to confirm these initial promising results, which implicate the alpha-2/delta VGCC subunit as a novel therapeutic target in the treatment of several N/V-associated clinical conditions.
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Cyclic vomiting syndrome (CVS) is a chronic disorder characterized by episodic nausea and vomiting. A large proportion of patients use marijuana to control their symptoms. Several case reports implicate marijuana as a cause of intractable vomiting with compulsive hot water bathing considered pathognomonic of "cannabinoid hyperemesis." We sought to examine the relationship between marijuana use and CVS. ⋯ With marijuana use, patients noted the greatest improvement with stress levels, appetite and nausea. Marijuana users were more likely to be male and have associated anxiety. Hot showers were not pathognomonic of marijuana use though they were more likely to be associated with its use.
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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.
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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.