Effect of systemic monosodium glutamate (MSG) on headache and pericranial muscle sensitivity
Department of Clinical Oral Physiology, School of Dentistry, University of Aarhus, Aarhus, Denmark. Cephalalgia
(Impact Factor: 4.89).
04/2009; 30(1):68-76. DOI: 10.1111/j.1468-2982.2009.01881.x
We conducted a double-blinded, placebo-controlled, crossover study to investigate the occurrence of adverse effects such as headache as well as pain and mechanical sensitivity in pericranial muscles after oral administration of monosodium glutamate (MSG). In three sessions, 14 healthy men drank sugar-free soda that contained either MSG (75 or 150 mg/kg) or NaCl (24 mg/kg, placebo). Plasma glutamate level, pain, pressure pain thresholds and tolerance levels, blood pressure (BP), heart rate and reported adverse effects were assessed for 2 h. No muscle pain or robust changes in mechanical sensitivity were detected, but there was a significant increase in reports of headache and subjectively reported pericranial muscle tenderness after MSG. Systolic BP was elevated in the high MSG session compared with low MSG and placebo. These findings add new information to the concept of MSG headache and craniofacial pain sensitivity.
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Available from: Lene Baad-Hansen
- "Although the MSG was dissolved in sugar free lemon soda, which we have previously found masks the taste of MSG , the vast majority of subjects correctly identified the substance administered to them when asked at the end of each 5 days session. Considering the significant increase in adverse effects, which occurred during MSG ingestion, this result is understandable. "
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ABSTRACT: A single intake of monosodium glutamate (MSG) may cause headache and increased muscle sensitivity. We conducted a double-blinded, placebo-controlled, crossover study to examine the effect of repeated MSG intake on spontaneous pain, mechanical sensitivity of masticatory muscles, side effects, and blood pressure.
Fourteen healthy subjects participated in 5 daily sessions for one week of MSG intake (150 mg/kg) or placebo (24 mg/kg NaCl) (randomized, double-blinded). Spontaneous pain, pressure pain thresholds and tolerance levels for the masseter and temporalis muscles, side effects, and blood pressure were evaluated before and 15, 30, and 50 min after MSG intake. Whole saliva samples were taken before and 30 min after MSG intake to assess glutamate concentrations.
Headache occurred in 8/14 subjects during MSG and 2/14 during placebo (P = 0.041). Salivary glutamate concentrations on Day 5 were elevated significantly (P < 0.05). Pressure pain thresholds in masseter muscle were reduced by MSG on Day 2 and 5 (P < 0.05). Blood pressure was significantly elevated after MSG (P < 0.040).
In conclusion, MSG induced mechanical sensitization in masseter muscle and adverse effects such as headache and short-lasting blood pressure elevation for which tolerance did not develop over 5 days of MSG intake.
The Journal of Headache and Pain 01/2013; 14(1):2. DOI:10.1186/1129-2377-14-2 · 2.80 Impact Factor
Available from: Katharine M Woessner
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ABSTRACT: Monosodium glutamate (MSG) is a salt form of a nonessential amino acid commonly used as a food additive for its unique flavor-enhancing qualities. Since the first description of the “monosodium glutamate symptom complex,” originally described as the “Chinese Restaurant syndrome,” a number of anecdotal reports and small clinical studies of variable quality have attributed a variety of symptoms to the dietary ingestion of MSG. Descriptions of MSG-induced asthma, urticaria, angioedema, and rhinitis have prompted some to suggest that MSG should be an etiologic consideration in patients presenting with these conditions. This chapter presents a critical review of the available literature related to the possible role of MSG in the so-called “Chinese restaurant syndrome” and in eliciting asthmatic bronchospasm, urticaria, angioedema, rhinitis, and headache. Despite concerns raised by early reports, decades of research have failed to demonstrate a clear and consistent relationship between MSG ingestion and the development of these conditions.
Food Allergy: Adverse Reactions to Foods and Food Additives, Fourth Edition, 01/2009: pages 369 - 376; , ISBN: 9781444300062
Available from: Xudong Dong
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ABSTRACT: The mechanism by which intramuscular injection of BoNTA into the craniofacial muscles decreases migraine headaches is not known. In a blinded study, the effect of BoNTA on the mechanical and chemical responsiveness of individual temporalis muscle nociceptors and muscle neurogenic vasodilation was investigated in female rats. Mechanical threshold was measured for 3h following intramuscular injection of BoNTA or vehicle, and for 10 min after a subsequent injection of the algogen glutamate. Injection of BoNTA significantly increased the mechanical threshold of muscle nociceptors without altering the muscle surface temperature and blocked glutamate-induced mechanical sensitization and neurogenic vasodilation. None of these effects were reproduced by pancuronium-induced muscle paralysis. Western blot analysis of temporalis muscles indicated that BoNTA significantly decreased SNAP-25. Measurement of interstitial glutamate concentration with a glutamate biosensor indicated that BoNTA significantly reduced glutamate concentrations. The mechanical sensitivity of muscle nociceptors is modulated by glutamate concentration through activation of peripheral NMDA receptors. Immunohistochemical experiments were conducted and they indicated that half of the NMDA-expressing temporalis nerve fibers co-expressed substance P or CGRP. Additional electrophysiology experiments examined the effect of antagonists for NMDA, CGRP and NK1 receptors on glutamate-induced effects. Glutamate-induced mechanical sensitization was only blocked by the NMDA receptor antagonist, but muscle neurogenic vasodilation was attenuated by NMDA or CGRP receptor antagonists. These data suggest that injection of BoNTA into craniofacial muscles acts to decrease migraine headaches by rapidly decreasing the mechanical sensitivity of temporalis muscle nociceptors through inhibition of glutamate release and by attenuating the provoked release of CGRP from muscle nociceptors.
Pain 12/2010; 151(3):606-16. DOI:10.1016/j.pain.2010.07.029 · 5.21 Impact Factor
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