Effects of eating on vection-induced motion sickness, cardiac vagal tone, and gastric myoelectric activity.

Uijtdehaage SH, Stern RM, Koch KL.

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

This study investigated the effect of food ingestion on motion sickness severity and its physiological mechanisms. Forty-six fasted subjects were assigned either to a meal group or to a no-meal group. Electrogastrographic (EGG) indices (normal 3 cpm activity and abnormal 4-9 cpm tachyarrhythmia) and respiratory sinus arrhythmia (RSA) were measured before and after a meal and during a subsequent exposure to a rotating drum in which illusory self-motion was induced. The results indicated that food intake enhanced cardiac parasympathetic tone (RSA) and increased gastric 3 cpm activity. Postprandial effects on motion sickness severity remain equivocal due to group differences in RSA baseline levels. During drum rotation, dysrhythmic activity of the stomach (tachyarrhythmia) and vagal withdrawal were observed. Furthermore, high levels of vagal tone prior to drum rotation predicted a low incidence of motion sickness symptoms, and were associated positively with gastric 3 cpm activity and negatively with tachyarrhythmia. These data suggest that enhanced levels of parasympathetic activity can alleviate motion sickness symptoms by suppressing, in part, its dysrhythmic gastric underpinnings.

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Role of histamine in motion sickness in Suncus murinus.

Kaji T, Saito H, Ueno S, Yasuhara T, Nakajima T, Matsuki N.

Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.

The levels of histamine (HA) and tele-methylhistamine (t-MH) were determined in five brain regions of Suncus murinus (suncus) and the effects of motion stimulus or drugs influencing the turnover of these amines were studied to elucidate the role of histamine in motion sickness. Shaking the animals for 2 min increased HA contents in telencephalon and diencephalon without significantly changing the t-MH levels. alpha-Fluoromethylhistidine (alpha-FMH), which is presumed to deplete the neuronal HA, tended to raise the HA levels. alpha-FMH slightly alleviated the vomiting response to motion stimulus and suppressed the HA increase in diencephalon caused by shaking. Compound 48/80, which releases HA from mast cells, did not alter the control HA levels, but effectively prevented the motion sickness and completely suppressed the motion-induced rises in HA levels. These results provide further evidence that brain HA plays an important role in the development of motion sickness.

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Idaverine, an M2- vs. M3-selective muscarinic antagonist, does not prevent motion sickness in cats.

Lucot JB, van Charldorp KJ, Tulp MT.

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

In this study, the affinity profile of idaverine for the M1- (neuronal tissue), M2- (heart) and M3- (glandular tissue/nonvascular smooth muscle) muscarinic receptors was examined by means of radioligand binding and in vitro organ bath experiments in order to use the compound for the investigation of the muscarinic receptor subtype involved in motion sickness. In the profile study a comparison was made with the muscarinic antagonists atropine, pirenzepine (M1-selective) AF-DX 116 (M2-selective) and 4-DAMP (high affinity for M1- and M3-binding sites). The affinity of idaverine appeared to be equally high for the M1- and M2-binding sites. However, the affinity for the M1-binding sites should be interpreted cautiously since the Hill slope deviated from unity. Idaverine showed a 20-fold selectivity for the M2-binding sites over the M3-binding sites, whereas it showed a small selectivity (less than 5-fold) for the M2-receptors compared to the ileal and tracheal smooth muscle receptors. Thus idaverine appears to be M2 over M3 selective. However, in contrast to AF-DX 116, it is not clear whether idaverine is also M2 over M1 selective. In experiments with cats, idaverine failed to prevent motion sickness at doses from 0.03 to 3 mg/kg. These results are interpreted to implicate M3-receptors in the motion sickness suppressant effect of antimuscarinic drugs.

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8-OH-DPAT does not interfere with habituation to motion-induced emesis in cats.

Lucot JB, Crampton GH.

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

Experiments were performed to determine if suppression of motion-induced emesis (motion sickness) by 8-OH-DPAT altered the development or retention of habituation to the motion stimulus. Cats received 8-OH-DPAT followed by provocative motion on three consecutive treatment days. A drug-free test on the fourth day resulted in an incidence of emesis that was not different from that obtained on the fourth consecutive day of drug-free motion testing. Three consecutive days of treatment with 8-OH-DPAT without motion had no effect on the incidence of motion sickness on the fourth day. It was concluded that suppression of motion sickness by 8-OH-DPAT does not alter the acquisition or retention of habituation.

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Scopolamine blood levels following buccal versus ingested tablets.

Golding JF, Gosden E, Gerrell J.

Institute of Naval Medicine, Gosport, Hants, United Kingdom.

Speed of absorption and elimination of an antimotion sickness drug sets limits on the protection afforded. The aim of this experiment was to determine whether a well proven antimotion sickness drug--scopolamine (hyoscine)--could be absorbed more rapidly from buccal tablets than from the standard issue ingested tablets. Plasma scopolamine levels were measured using a radioreceptor assay of repeated blood samples from 10 volunteers, each of whom took buccal and standard ingested tablets (both 0.6 mg scopolamine hydrobromide) on two different occasions, and from a further 8 volunteers following ingestion of a pharmacy-prepared scopolamine capsule (0.6 mg scopolamine hydrobromide). There was no statistically significant speed advantage for the buccal tablet (mean time to peak levels approx 50 min). Individual variation in the speed of scopolamine absorption and rate of elimination (mean half-life approx 170 min) was great. This may account for failure of motion sickness protection in some individuals.

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Vestibular and postural findings in the motion sickness syndrome.

Hamid MA.

Department of Otolaryngology, Cleveland Clinic Foundation, OH 44132.

The motion sickness syndrome constitutes varying degrees of subjective motion intolerance and three objective findings: hyperactive VOR (79%), hip sway strategy (60%), and positional nystagmus (42%). It is present in subjects who have a strong history of motion sickness. Vestibular rehabilitation appears to help control symptoms. The study also suggests an inheritance pattern, but a structured pedigree could not be constructed. Prospective studies are warranted to further establish the patterns of the motion sickness syndrome.

Online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1900614&dopt=Abstract motion sickness




Why is the driver rarely motion sick? The role of controllability in motion sickness.

Rolnick A, Lubow RE.

Motion Sickness and Human Performance Laboratory, Israeli Naval Hyperbaric Institute, Haifa.

The central hypothesis of the work is that the dimension of control-no control plays an important role in motion sickness. Although it is generally agreed that having control over a moving vehicle greatly reduces the likelihood of motion sickness, few studies have addressed this issue directly, and the theoretical explanation for this phenomenon is not completely clear. In this study, we equated groups differing in controllability for head movement, vision, activity, and predictability, which have often been suggested in the literature as explanations for the driver's immunity to motion sickness. Twenty-two pairs of yoked subjects were exposed to nauseogenic rotation. One subject of each pair had control over the rotation and head movements, while the other was exposed passively to the same motion stimulus. Subjects who had control reported significantly fewer motion sickness symptoms and less of a decrement in their well-being, as compared to the yoked subject without control. The results are discussed in relation to Reason's sensory rearrangement theory and the concept of feed-forward mechanisms in motion perception.

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Altered sensorimotor control of the body as an etiological factor in space motion sickness.

Lackner JR, Graybiel A, DiZio PA.

Ashton Graybiel Spatial Orientation Laboratory, Brandeis University, Waltham, MA 02254-9110.

Exposure to nonterrestrial force levels affects the activity of gravitoinertial force sensitive receptors of the body, both of labyrinthine and nonlabyrinthine origin. It also disrupts the normal patterning of motor control of body orientation and movement. The patterns and levels of muscle innervation necessary to achieve particular body configurations and to bring about particular body movements are greatly affected by background force level and body orientation relative to the force vector. The present studies demonstrate that such altered sensorimotor control of head and body posture along with altered vestibulomotor control are evocative of motion sickness. This observation has explanatory significance both for space motion sickness and the re-entry disturbances that occur after prolonged spaceflight.

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