The incidence and effects of motion sickness among medical attendants during transport.

Wright MS, Bose CL, Stiles AD.

Department of Pediatrics, University of North Carolina, Chapel Hill 27599-7596, USA.

Motion sickness is a common and often debilitating problem. The purpose of this study was to determine the incidence and effects of the motion sickness syndromes, the Nausea and Sopite Syndromes, among medical transport personnel. Members of the Transport Teams of the University of North Carolina Hospitals completed a questionnaire to identify a history of susceptibility to motion sickness. An additional questionnaire evaluated each individual for symptoms of motion sickness during transport. The Digit Span Test portion of the Mini-Mental Status Examination (DST-MMSE) was used to evaluate cognitive function after transport. Control data on each subject were obtained by testing during nontransport shifts. The Nausea Syndrome was observed during transport in 46% of subjects; 65% experienced symptoms consistent with the Sopite Syndrome. Pretransport surveys were predictive of the Nausea Syndrome, but not of the Sopite Syndrome. The Nausea Syndrome was related to subjective assessments of the severity of motion experienced; the Sopite Syndrome did not correlate with the severity of motion. The DST-MMSE scores after transport were significantly lower than scores during nontransport periods in 85% of personnel. We conclude that transport personnel are susceptible to motion sickness manifested by both the Nausea Syndrome and the Sopite Syndrome. The presence of motion sickness is associated with a significant decline in performance on tests of attention and concentration.

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The possible role of nystagmus in motion sickness: a hypothesis.

Ebenholtz SM, Cohen MM, Linder BJ.

Schnurmacher Institute for Vision Research, SUNNY College of Optometry, New York 10010.

An alternative hypothesis to that provided by conflict theory is formulated to account for motion sickness. The new approach is predicted on the oculocardiac reflex (i.e., bradycardia produced by extra-ocular muscle traction) (18) and empirical evidence that retrobulbar anesthesia significantly lowers the incidence of emesis after strabismus surgery (14). Eye muscle traction is presumed to elicit afferent signals that ultimately stimulate the vagus nerve (15). The same neuromotor sequence is presumed to occur during reflexive eye movements under vestibular control and during more complicated combinations of reflexive and voluntary eye movements. It is proposed that the blocking of afferent signals from extra-ocular muscle in an otherwise intact vestibulo-ocular system will eliminate the signs and symptoms of motion sickness normally produced in a provocative environment.

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Antiemetic effects of flesinoxan in cats: comparisons with 8-hydroxy-2-(di-n-propylamino)tetralin.

Lucot JB.

Department of Pharmacology, Wright State University, Dayton, OH 45435.

The antiemetic effects of flesinoxan were evaluated following s.c. administration in cats. Flesinoxan produced a dose-dependent suppression of motion sickness and also reduced xylazine-induced emesis at higher doses. Flesinoxan had a short latency to onset and may have a brief duration of action. It was slightly more potent that 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), in contrast to their relative potencies on most other in vivo measures. High doses of both agonists produced defensive behavior as a result of 5-HT1A receptor stimulation. (-)-Propranolol, which previously reduced 8-OH-DPAT suppression of feline motion sickness, failed to reduce the antiemetic effect of flesinoxan. The dose of 3 mg/kg of NAN-190 (1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]piperazine) produced a slight decrease in motion sickness and added to the suppression of motion sickness by low doses of flesinoxan via an uncertain mechanism. It also reduced the antiemetic effect of higher doses of flesinoxan. In contrast, NAN-190 produced additive antiemetic effects when combined with 8-OH-DPAT and little if any reduction. NAN-190 reduced the defensiveness produced by both flesinoxan and 8-OH-DPAT. Phentolamine and sulpiride reduced neither the antiemetic effect nor the defensive behavior produced by flesinoxan, thus ruling out a role for alpha-adrenoceptors and dopamine D2 receptors. Flesinoxan exerted a broad spectrum antiemetic effect by an action at 5-HT1A receptors as does 8-OH-DPAT, but differed in its response to putative 5-HT1A receptor antagonists.

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[Experimental studies of motion sickness on board of a research ship]

[Article in German]

Helling K, Westhofen M.

Klinik fur Hals-, Nasen-, Ohrenheilkunde, Universitats-Krankenhaus Hamburg-Eppendorf.

To date the incidence and treatment of motion sickness have not been satisfactorily elucidated. Discrepancies among individuals in tolerating strong velocities and accelerations are well-known. To prevent motion sickness evaluations of individual predispositions are important. There are several current theories on the nature of motion sickness. These include the mismatching of sensory inputs, a Coriolis force, non-physiological stimuli and modulation of vestibuloocular reflexes (VOR). The main influence of the vestibular organ in generating kinetosis is obvious. Analysis of the chief movements of a ship demonstrates that linear acceleration is the principle factor in stimulating the vestibular organ. The moving gravity vector causes an intense otolith stimulation. By this means VOR is temporarily shut down. This effect can also be used for documenting motion sickness. A battery of vestibular tests was performed on the military research ship "Planet" during a 2-week autumny voyage on the Atlantic Ocean. Spontaneous nystagmus, bithermal bilateral responses and rotatory testing (slow harmonic acceleration) results were recorded by electronystagmography. Findings before starting and during the voyage were compared. A group of 3 unexperienced volunteers and 9 professional seamen were investigated. All unexperienced volunteers suffered from sea sickness, while none of the professionals showed any symptoms. At the beginning of the voyage the gain in nystagmus in harmonic acceleration testing was significantly lower in the professionals than in the unexperienced volunteers. During the voyage all professionals showed nearly constant gain values. All unexperienced individuals showed a decrease in gain only during the time of acute symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

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Habituation and motion sickness.

Wood CD, Stewart JJ, Wood MJ, Struve FA, Straumanis JJ, Mims ME, Patrick GY.

Department of Pharmacology, Louisiana State University School of Medicine, Shreveport 71130.

The vestibular, cerebellar, and reticular systems are central in importance, in motion sickness and habituation, to the effects of motion. Nuclear medicine single photon emission computed tomography (SPECT) studies of cerebral blood flow and power spectral electroencephalographic recordings during motion sickness were used to determine alterations in the central nervous system. The rotating chair with and without visual stimulation was used to study the rate of habituation and the effect of antimotion sickness medications on this rate. An increase of theta waves over the frontal cortex indicated a decreased activation of the higher centers during motion sickness. Motion sickness also produces an increase of blood flow in the central cerebellum that has connections to the reticular system. This increase in cerebellar activity is relayed to the reticular system whereby neural recruitment builds up to trigger the vomiting center, producing motion sickness. Habituation may be a conditioned compensatory activation of the reticular neurons that prevents this disruption of normal activation. The rate of habituation when motion sickness was prevented by scopolamine was slowed, indicating that, if the central nervous system is not challenged by disruption of normal activation, it does not produce the compensatory reactions that result in habituation.

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Effects of motion sickness and antimotion sickness drugs on gastric function.

Stewart JJ, Wood MJ, Wood CD, Mims ME.

Department of Pharmacology, Louisiana State University Medical Center, Shreveport 71130-3932.

This study examined the effects of motion sickness and antimotion sickness drugs on gastric emptying (GE). Drugs were tested in normal and motion sick subjects. To induce motion sickness, subjects performed head movements while seated in a rotating chair. Gastric emptying of liquid (300 mL) was determined by nuclear medicine techniques, whereas gastric electrical activity, the electrogastrogram (EGG), was monitored from surface (cutaneous) electrodes positioned over the abdominal area. Gastric emptying was severely inhibited at the peak of motion sickness symptoms, but returned to normal 15 minutes later when symptoms abated. In normal (non-motion sick) subjects intramuscular (IM) scopolamine (0.1 mg) and IM promethazine (25 mg) inhibited GE, whereas erythromycin ethylsuccinate (EES) suspension (200 mg) given orally increased GE. When administered to motion sick subjects, IM scopolamine and IM promethazine added slightly, but not significantly, to the inhibition of GE already present. Oral EES did not significantly alter GE in motion sick subjects. Although EGG frequency remained within normal limits (approximately 2.5-3.5 cpm) after liquid ingestion in both normal and motion sick subjects, EGG amplitude was differentially affected in the two groups. Electrogastrogram amplitude increased twofold to fourfold after liquid ingestion in normal, but not in motion sick subjects. The results suggest that (1) maximal inhibition of GE is coincident with peak motion sickness symptoms, (2) both IM scopolamine and IM promethazine inhibit GE in normal subjects, but do not add significantly to the inhibition of GE already established during motion sickness, (3) orally administered erythromycin enhances GE in normal, but not in motion sickness subjects, and (4) the normal stimulatory effect of liquid ingestion on gastric motility does not occur in motion sick subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

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Etiologic significance of arginine vasopressin in motion sickness.

Cheung BS, Kohl RL, Money KE, Kinter LB.

Defence and Civil Institute of Environmental Medicine, North York, Ontario, Canada.

There is abundant evidence implicating the role of arginine vasopressin in motion sickness. The effects of AVP analogs on motion sickness were investigated in squirrel monkeys. Two specific V1 antagonists (SK&F 100273 and SK&F 103561) and three mixed V1/V2 antagonists (SK&F 101926, SK&F 105494, and SK&F 104146-D) were tested on six highly susceptible monkeys. Intravenous injections of 200 ug of a V1 antagonist abolished emesis in all six monkeys, and few prodromal symptoms remained (latency to emesis > 120 minutes, P < .001). Mixed V1/V2 antagonists failed to abolish emesis in all monkeys. However, there was a slight increase in the latency to the first bout of emesis/retching with the mixed antagonists when compared with the baseline. The dose-response relationship and rate of onset of action of the V1 antagonists (SK&F 100273) were explored. Latency to the first bout of emesis/retching increased to about twice that of the baseline when half of the effective antiemetic dose was used. The efficacy demonstrated by the specific V1 antagonists indicates that V1 receptors may modulate emesis.

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Chinese hyper-susceptibility to vection-induced motion sickness.

Stern RM, Hu S, LeBlanc R, Koch KL.

Department of Psychology, Pennsylvania State University, University Park 16802.

Little is known about the factors that control individual differences in susceptible to motion sickness. A serendipitous observation in our laboratory that most Chinese subjects become motion sick prompted this study. We used a rotating optokinetic drum to provoke motion sickness and compared gastric responses and symptom reports of Chinese, European-American, and African-American subjects. There was no difference in the responses of European-American and African-American subjects; however, Chinese subjects showed significantly greater disturbances in gastric activity and reported significantly more severe symptoms. We suggest that this hyper-susceptibility presents a natural model for the study of physiological mechanisms of nausea and other symptoms of motion sickness.

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