Mary J. Wood

Effects of Ginger on Motion Sickness Susceptibility and Gastric Function

This study was designed to evaluate the antimotion sickness activity of ginger root (Zingiber officinale) and to characterize the effects of ginger on gastric function. Twenty-eight human volunteers participated in the project. Subjects made timed head movements in a rotating chair until they reached an endpoint of motion sickness short of vomiting (malaise III or M-III). Each subject was tested with either ginger or scopolamine and a placebo. A substance was judged to possess antimotion sickness activity if it allowed a greater number of head movements compared to placebo control. Gastric emptying of a liquid was measured by nuclear medicine techniques in normal and motion sick subjects. Gastric electrical activity was monitored by cutaneous (surface) electrodes positioned over the abdominal area. Powder ginger (whole root, 500 or 1,000 mg) or fresh ginger root (1,000 mg) provided no protection against motion sickness. In contrast, subjects performed an average of 147.5 more head movements (p less than 0.01) after scopolamine (0.6 mg p.o.) than after placebo. The rate of gastric emptying was significantly (p less than 0.05) slowed when tested immediately after M-III but was inhibited less when tested 15 min after M-III. Powdered ginger (500 mg) had no effect on gastric emptying in normal or motion-sick subjects. Gastric motility was also changed during motion sickness. The frequency of the electrogastrogram (EGG) was increased after M-III (tachygastria) and the normal increase in EGG amplitude after liquid ingestion was reduced in motion sick subjects. Although powdered ginger (500 mg) partially inhibited tachygastria in motion sickness, it did not enhance the EGG amplitude in motion sick subjects. We conclude that ginger does not possess antimotion sickness activity, nor does it significantly alter gastric function during motion sickness.

Comparison of Efficacy of Ginger with Various Antimotion Sickness Drugs

UNLABELLED Ginger and several other medications were compared with scopolamine and d-amphetamine for effectiveness in prevention of motion sickness. METHODS Double-blind techniques were used. The subjects were given the medications two hours before they were rotated in a chair making head movements until a symptom total short of vomiting was reached. Standardized N.A.S.A. techniques were used for speed of rotation and end-point of motion sickness. RESULTS The three doses of ginger were all at the placebo level of efficacy. Amitriptyline, ethopropazine and trihexyphenidyl increased the tolerated head movements but the increase was not statistically significant. Significant levels of protection were produced by dimenhydrinate, promethazine, scopolamine and d-amphetamine. Protection was further increased by combination of these latter drugs with d-amphetamine. Efficacy was greatest as the dose was increased. CONCLUSIONS The medication of choice in this study was scopolamine 0.6 mg with d-amphetamine 10 mg. This combination provided good protection with acceptable side effects.

Habituation and Motion Sickness

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.

Effectiveness and Duration of Intramuscular Antimotion Sickness Medications

Motion sickness inhibits gastric motility, making the oral route ineffective for medications. The intramuscular route is an effective alternative. The rotating chair was used to produce the M 111 level of motion sickness on the Graybiel Symptom Scale. The intramuscular medications given 30 minutes before rotation were compared with placebo (saline, 1 mL) for effectiveness and duration in increasing the number of tolerated head movements. Average placebo number of head movements was 294. Promethazine 25 mg increased head movements by 78% (P < .05), with a duration of 12 hours. Scopolamine 0.2 mg increased head movements by 91% (P < .05), with a duration of 4 hours. The effect of caffeine 250 mg and ephedrine 25 mg was not significant. When combined with scopolamine, ephedrine produced an 32% additive effect. Scopolamine 0.08 mg, 0.1 mg, and 0.2 mg and also promethazine 12.5 mg and 25 mg were significant (P < .05). Promethazine appears to be the drug of choice for intramuscular use because of a longer duration and a high level of effectiveness. Scopolamine was of high effectiveness, but had a duration of 4 hours. It was eight times as potent by the intramuscular as by the oral route.

Effects of Motion Sickness and Antimotion Sickness Drugs on Gastric Function

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 (∼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 sick subjects, and (4) the normal stimulatory effect of liquid ingestion on gastric motility does not occur in motion sick subjects. Both motion sickness and parenterally administered antimotion sickness drugs are potential sources of inhibited GE in space.

Screening bone scintigraphy in the staging of locally advanced head and neck cancer

A retrospective determination of the yield from screening bone scintigraphy in detecting bone metastasis when used for disease staging of 93 asymptomatic patients with locally extensive head and neck cancer was undertaken. The bone scintigraphy findings were correlated with observations from other radioimaging studies done within 1 month of head and neck cancer diagnosis. Bone scintigraphy did not reveal a single case of bone metastasis outside the head and neck region. On the other hand, 3 cases (8%) of resectable and 2 cases (5%) of non-resectable bone metastasis located within the head and neck area were observed among the 40 patients with abnormal bone scintigraphy. Old rib fracture or degenerative disease was responsible for the increased radionuclide uptake in bony areas below the clavicle in less than half of the remaining 35 cases. We conclude that the routine use of bone scintigraphy for disease staging in asymptomatic patients with locally advanced head and neck cancer is not warranted because the positive yield is low.