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MeSH Review

Motion Sickness

 
 
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Disease relevance of Motion Sickness

 

Psychiatry related information on Motion Sickness

 

High impact information on Motion Sickness

 

Chemical compound and disease context of Motion Sickness

  • Comparison with placebo indicated that transdermal scopolamine provided protection against motion sickness at a significance level of p = 0.0001 and oral dimenhydrinate at a level of p = 0.05 [16].
  • For motion sickness, control can be achieved with various antagonists of muscarinic or histamine H1-receptors [17].
  • Hyoscine (scopolamine) is a competitive inhibitor of the muscarinic receptors of acetylcholine and it has been shown to be one of the most effective agents for preventing motion sickness [18].
  • In the motion sickness procedure, the DeltaT(forearm-fingertip) response was significantly attenuated, indicating a blunted vasoconstrictor response, and rectal temperature decreased at a faster rate [19].
  • Marked difference across the motion sickness susceptibility spectrum in the condition on discharge of lithium and antidepressant treated patients was also found, when compared to other drug therapies, suggesting specific drug responses by the motion sick group [20].
 

Biological context of Motion Sickness

  • Collectively, these results indicate that LY228729 is potent 5-HT1A agonist with bioavailability properties sufficient for clinical evaluation and with efficacy in preclinical models of anxiety, sexual disorders and motion sickness [21].
 

Anatomical context of Motion Sickness

 

Gene context of Motion Sickness

  • This may include indirect effects via receptors in the signal cascade behind the 5-HT(3) receptor channel complex such as substance P receptors and muscarinic receptors; this needs further investigation since ginger is effective against motion sickness which is cured by some vanilloids and by anticholinergics such as scopolamine [27].
  • Peripheral release of ENDO and ACTH may follow release of AVP; however, given the extensive and complex functional interactions that exist between AVP and the opiate systems, it is not yet possible to define a clear role for ENDO in the etiology of motion sickness [28].
  • Higher post-stress levels of AVP (p < 0.04) and ACTH (p < 0.02) were correlated with greater resistance to motion sickness [28].
  • Increased secretion of growth hormone, prolactin, antidiuretic hormone, and cortisol induced by the stress of motion sickness [29].
  • Furthermore, increases in vasoactive intestinal peptide levels participate in motion sickness [30].
 

Analytical, diagnostic and therapeutic context of Motion Sickness

References

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  19. Motion sickness potentiates core cooling during immersion in humans. Mekjavic, I.B., Tipton, M.J., Gennser, M., Eiken, O. J. Physiol. (Lond.) (2001) [Pubmed]
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