Læknablaðið - 15.12.2012, Blaðsíða 31
Y F I R L I T
25. Johnson WH, Sunahara FA, Landolt JP. Importancc of the
vestibular system in visually induced nausea and self-
vection. J Vestib Res 1999; 9:83-7.
26. Graybiel A. Susceptibility to acute motion sickness in
blind persons. Aerosp Med 1970; 41: 650-3.
27. Treisman M. Motion sickness: an evolutionary hypothesis.
Science 1977; 197:493-5.
28. Money KE, Cheung BS. Another function of the inner ear:
facilitation of the emetic response to poisons. Aviat Space
Environ Med 1983; 54:208-11.
29. Eisenman LM. Motion sickness may be caused by a
neurohumoral action of acetylcholine. Med Hypotheses
2009; 73: 790-3.
30. Golding JF, Mueller AG, Gresty MA. A motion sickness
maximum around the 0.2 Hz frequency range of hori-
zontal translational oscillation. Aviat Space Environ Med
2001; 72:188-92.
31. Mills KL, Griffin MJ. Effect of seating, vision and direction
of horizontal oscillation on motion sickness. Aviat Space
Environ Med 2000; 71:996-1002.
32. Carriot J, Cian C, Paillard A, Denise P, Lackner JR.
Influence of multisensory graviceptive information on the
apparent zenith. Exp Brain Res 2011; 208: 569-79.
33. Reason JT. Motion sickness adaptation: a neural mismatch
model. J R Soc Med 1978; 71:819-29.
34. Dobie TG, May JG. Cognitive-behavioral management of
motion sickness. Aviat Space Environ Med 1994; 65: Cl-2.
35. Murray JB. Psychophysiological aspects of motion
sickness. Percept Mot Skills 1997; 85:1163-7.
36. Mills D. Motion sickness. Is it all in the mind? Aust Fam
Physician 1999; 28:1274,80.
37. Strickland BA, Hahn GL, Adler H. Studies on airsickness.
J Aviat Med 1950; 21:90-7.
38. Chinn HI. Motion sickness in the military sen'ice. Mil Surg
1951;108:20-9.
39. Grunfeld EA, Price C, Goadsby PJ, Gresty MA. Motion
sickness, migraine, and menstruation in mariners. Lancet
1998; 351:1106.
40. Wertheim AH. Working in a moving environment.
Ergonomics 1998; 41:1845-58.
41. Money KE. Motion sickness. Physiol Rev 1970; 50:1-39.
42. Bemard C. Introduction á L'etudee de la Médecine
Experimentale. Balliére, París 1865.
43. Wood CD, Stewart JJ, Wood MJ, Struve FA, Straumanis JJ,
Mims ME, et al. Habituation and motion sickness. J Clin
Pharmacol 1994; 34: 628-34.
44. Sjómaður NN. Skrifað á spássíu spumingablaðs, 2002.
45. Levy RA, Jones DR, Carlson EH. Biofeedback rehabilita-
tion of airsick aircrew. Aviat Space Environ Med 1981; 52:
118-21.
46. Banks RD, Salisbury DA, Ceresia PJ. The Canadian Forces
Airsickness Rehabilitation Program, 1981-1991. Aviat
Space Environ Med 1992; 63:1098-101.
47. Wood CD, Manno JE, Manno BR, Odenheimer RC,
Baimsfather LE. The effect of antimotion sickness dmgs
on habituation to motion. Aviat Space Environ Med 1986;
57:539-42.
48. Lackner JR, Graybiel A. Use of promethazine to hasten
adaptation to provocative motion. J Clin Pharmacol 1994;
34: 644-8.
49. Shupak A, Gordon CR. Motion sickness: advances in
pathogenesis, prediction, prevention, and treatment. Aviat
Space Environ Med 2006; 77:1213-23.
50. Uijtdehaage SH, Stem RM, Koch KL. Effects of scopolam-
ine on autonomic profiles underlying motion sickness
susceptibility. Aviat Space Environ Med 1993; 64:1-8.
51. Nachum Z, Shupak A, Gordon CR. Transdermal
scopolamine for prevention of motion sickness : clinical
pharmacokinetics and therapeutic applications. Clin
Pharmacokinet 2006; 45: 543-66.
52. Takeda N, Morita M, Hasegawa S, Horii A, Kubo T,
Matsunaga T. Neuropharmacology of motion sickness and
emesis. A review. Acta Otolaryngol Suppl 1993; 501:10-5.
53. Hu S, Stritzel R, Chandler A, Stem RM. P6 acupressure
reduces symptoms of vection-induced motion sickness.
Aviat Space Environ Med 1995; 66: 631-4.
54. Bertolucci LE, DiDario B. Efficacy of a portable acusti-
mulation device in controlling seasickness. Aviat Space
Environ Med 1995; 66:1155-8.
55. Bmce DG, Golding JF, Hockenhull N, Pethybridge RJ.
Acupressure and motion sickness. Aviat Space Environ
Med 1990; 61: 361-5.
56. Mowrey DB, Clayson DE. Motion sickness, ginger, and
psychophysics. Lancet 1982; 1:655-7.
57. Stewart JJ, Wood MJ, Wood CD, Mims ME. Effects of gin-
ger on motion sickness susceptibility and gastric function.
Pharmacology 1991; 42:111-20.
58. Cowings PS, Toscano WB. Autogenic-feedback training
exercise is superior to promethazine for control of motion
sickness symptoms. J Clin Pharmacol 2000; 40:1154-65.
59. Harm DL. Physiology of motion sickness symptoms. CRC
Press Inc, Flórída 1990.
60. Jozsvai EE, Pigeau RA. The effect of autogenic training
and biofeedback on motion sickness tolerance. Aviat Space
Environ Med 1996; 67:963-8.
61. Jones DR, Levy RA, Gardner L, Marsh RW, Patterson
JC. Self-control of psychophysiologic response to motion
stress: using biofeedback to treat airsickness. Aviat Space
Environ Med 1985; 56:1152-7.
ENGLISH SUMMARY
Seasickness
Petersen H
The purpose of this paper is to provide an overview of the physiological
basis, clinical picture and treatment opportunities of motion sickness.
Motion sickness can occur when sensory inputs from body orientation
and movements in space contradict or differ from those predicted
from experience. In that case disturbing symptoms can occur when a
person is exposed to unfamiliar movement or perceived movement in
the environment. Best known is when this occurs at sea, referred to as
sea sickness. Despite progress in the technology and comfort of modern
sea transit and transportation (ships, planes and overland vehicles) a
great number of workers and travellers still experience motion sickness,
with its coexisting risks of accidents. A survey performed on lcelandic
seamen indicates that up to 80% experience seasickness when at sea
and up to 80% experience mal de debarquement. Bouts are characteri-
zed by an initial phase of mild discomfort followed by neurologic and
gastro-intestinal manifestations. The delay in onset depends on specific
circumstances and individual susceptibility. Signals from the vestibular
system are essential fortriggering motion sickness, where vestibuloau-
tonomic pathways that typically subserve homeostasis play the key role.
Attacks are precipitated by conflicting sensory, visual and vestibular
signals but the underlying mechanism is unclear. The neural pathways
that produce nausea and vomiting during motion sickness are presumed
to be similar to those that generate illness after ingestion of toxins.
Most medications used for prevention and treatment induce unwanted
sedation, that both reduce ability to cope with the situation and delay
the most wanted adaptation. Furthermore, no one drug is completely
effective or preventive under all conditions.
Key words: motion sickness, human, postural control, epidemiology.
Correspondence: Hannes Petersen, hpet@hi.is
'Faculty of Medicine, University of lceland, 2Department of Otorhinolaryngology Head and Neck Surgery, Landspítali, Reykjavík, lceland.
LÆKNAblaðið 2012/98 659