Responses of sympathetic outflow to skin during caloric stimulation in humans. (1/88)

We previously showed that caloric vestibular stimulation elicits increases in sympathetic outflow to muscle (MSNA) in humans. The present study was conducted to determine the effect of this stimulation on sympathetic outflow to skin (SSNA). The SSNA in the tibial and peroneal nerves and nystagmus was recorded in nine subjects when the external meatus was irrigated with 50 ml of cold (10 degrees C) or warm (44 degrees C) water. During nystagmus, the SSNA in tibial and peroneal nerves decreased to 50 +/- 4% (with baseline value set as 100%) and 61 +/- 4%, respectively. The degree of SSNA suppression in both nerves was proportional to the maximum slow-phase velocity of nystagmus. After nystagmus, the SSNA increased to 166 +/- 7 and 168 +/- 6%, respectively, and the degree of motion sickness symptoms was correlated with this SSNA increase. These results suggest that the SSNA response differs from the MSNA response during caloric vestibular stimulation and that the SSNA response elicited in the initial period of caloric vestibular stimulation is different from that observed during the period of motion sickness symptoms.  (+info)

Gastrointestinal motor and myoelectric correlates of motion sickness. (2/88)

The objectives of this study were to characterize the digestive tract motor and myoelectric responses associated with motion sickness. Twenty-two cats (1.5-3.0 kg) were chronically implanted with force transducers and electrodes on the stomach and small intestine. Motion sickness was activated by vertical oscillation (VO) at +/-0.5 g and identified as salivation, licking, or vomiting. Vomiting was initiated chemically by UK-14304 (2.5-15 microg/kg iv) or CuSO4 (10-50 mg ig). We found that VO caused vomiting (45% of trials), a decrease in gastrointestinal (GI) motility (69% of trials), salivation or licking (59% of trials), bradygastria (39% of trials), retrograde giant contraction (RGC, 43% of trials), giant migrating contraction (GMC, 5% of trials), and defecation (18% of trials). The decrease in GI motility occurred with (62% of trials) or without (69% of trials) vomiting. Motion sickness was accompanied by bradygastria (52% of trials) and decreased GI motility (70% of trials). Similar events occurred after CuSO4 and UK-14304, but the incidences of responses after CuSO4 were less frequent, except for vomiting, RGC, and GMC. UK-14304 never caused GMCs or defecation. The magnitude and velocity of the RGC were the same during all emetic stimuli, and RGCs never occurred without subsequent vomiting. Supradiaphragmatic vagotomy (n = 1) or atropine (n = 2, 10 or 50 microg/kg iv) blocked the RGC, but not vomiting, due to VO. We concluded that 1) oculovestibular stimulation causes digestive tract responses similar to other types of emetic stimuli, 2) decreased GI motility and bradygastria may be physiological correlates of the motion sickness, and 3) motion sickness may not be dependent on any specific GI motor or myoelectric response.  (+info)

Visual-vestibular habituation and balance training for motion sickness. (3/88)

BACKGROUND AND PURPOSE: This case report describes physical therapy for motion sickness in a 34-year-old woman. The purpose of the report is twofold: (1) to provide an overview of the literature regarding motion sickness syndrome, causal factors, and rationale for treatment and (2) to describe the evaluation and treatment of a patient with motion sickness. CASE DESCRIPTION AND OUTCOMES: The patient initially had moderate to severe visually induced motion sickness, which affected her functional abilities and prevented her from working. Following 10 weeks of a primarily home-based program of visual-vestibular habituation and balance training, her symptoms were alleviated and she could resume all work-related activities. DISCUSSION: Although motion sickness affects nearly one third of all people who travel by land, sea, or air, little documentation exists regarding prevention or management.  (+info)

Safety of air medical transportation after tissue plasminogen activator administration in acute ischemic stroke. (4/88)

BACKGROUND AND PURPOSE: We sought to determine the safety of air medical transport (AMT) of patients with acute ischemic stroke (AIS) immediately after or during administration of tissue plasminogen activator (tPA). Patients with AIS treated with tPA in nonuniversity hospitals frequently need transfer to tertiary care centers that can provide specialized care. AMT is a widely available mode of transport that is crucial in providing expedient and quality health care to critically ill patients while assuring high level of care during transportation. The safety of AMT of patients with AIS after or during administration of tPA has not been examined. METHODS: We performed retrospective chart review of 24 patients with AIS who were treated with intravenous tPA and transferred by helicopter to the Hospital of the University of Pennsylvania or the University of Cincinnati Hospital. The charts were reviewed for neurological complications, systemic complications, and adherence to the National Institutes of Neurological Disorders and Stroke (NINDS) protocol for AIS management. RESULTS: No major neurological or systemic complications occurred. Four patients had hypertension warranting treatment, 3 patients experienced motion sickness, 1 patient developed a transient confusional state, and 1 patient experienced minor systemic bleeding. Four NINDS protocol violations occurred, all related to blood pressure management. CONCLUSIONS: In this small series, AMT of AIS patients after thrombolysis was not associated with any major neurological or systemic complications. Flight crew education on the NINDS AIS protocol is essential in limiting the number of protocol violations. AMT of patients with AIS provides fast and safe access to tertiary centers that can provide state of the art stroke therapy.  (+info)

Comparison of the neurokinin-1 antagonist GR205171, alone and in combination with the 5-HT3 antagonist ondansetron, hyoscine and placebo in the prevention of motion-induced nausea in man. (5/88)

AIMS: In man a neurokinin-1 (NK1) receptor antagonist has previously been shown to be ineffective in the prevention of motion-induced nausea. The antiemetic efficacy of NK1 receptor antagonists against chemotherapy-induced emesis is, however, enhanced when combined with a 5-HT3 receptor antagonist. Hence the efficacy of the NK1 antagonist GR205171 in combination with the 5-HT3 antagonist ondansetron (Zofrantrade mark) was assessed in motion-induced nausea. METHODS: GR205171 25 mg i.v., with and without concomitant administration of ondansetron 8 mg i.v., and hyoscine hydrobromide 0. 6 mg orally (positive control) were compared with placebo in a model of motion-induced nausea. The study was performed to a four-period, randomized, balanced, double-blind, crossover design in 16 healthy subjects. The end-point was the exposure to the motion stimulus required to produce moderate nausea in the subjects. RESULTS: The motion stimulus required to produce moderate nausea was significantly greater for the positive control than placebo (P < 0. 001). There was no significant difference between either GR205171 or GR205171 plus ondansetron and placebo (P = 0.648 and 0.342, respectively). CONCLUSIONS: The enhancement of NK1 receptor antagonist antiemetic activity through combination with a 5-HT3 receptor antagonist is not replicated in motion-induced nausea.  (+info)

The emetic and anti-emetic effects of the capsaicin analogue resiniferatoxin in Suncus murinus, the house musk shrew. (6/88)

1. In SUNCUS: murinus the ultrapotent capsaicin analogue resiniferatoxin (RTX) induced an emetic response in the dose range 1 - 1000 microg kg(-1), s.c. The latency was inversely related to dose and ranged from 41.2+/-4.4 min. (1 microg kg(-1), s.c.) to 2.7+/-0.6 min. (1000 microg kg(-1), s.c.). 2. The emetic response to RTX (10 or 100 microg kg(-1), s.c.) was blocked or markedly reduced by pre-treatment with RTX (100 microg kg(-1), s.c.), 8-OH-DPAT (100 microg kg(-1), s.c.), morphine (2 mg kg(-1), s.c.), neonatal capsaicin (100 mg kg(-1), s.c.) and the NK(1) receptor antagonist CP-99,994 (10 - 20 mg kg(-1), s.c.) but not by the 5-HT(3) receptor antagonist tropisetron (200 microg kg(-1), s.c.). 3. RTX (100 microg kg(-1), s.c.) induced c-fos-like immunoreactivity in the area postrema and parts of the nucleus tractus solitarius. This pattern is consistent with the proposal that the emetic effect is mediated via one or both of these structures and an involvement of substance P is discussed. 4. RTX (10 and 100 microg kg(-1), s.c.) had broad-spectrum antiemetic effects in Suncus as indicated by its ability to block or markedly reduce the emetic response to motion (1 Hz, 4 cm lateral, 10 min.), cisplatin (20 mg kg(-1), i.p.), intragastric copper sulphate (40 mg kg(-1), p.o.), nicotine (10 mg kg(-1), s.c.) and RTX (100 microg kg(-1), s.c.) itself. 5. It is proposed that the site of the anti-emetic effect is in the nucleus tractus solitarius and mechanisms involving the modulation of substance P release are discussed. 6. The general utility of SUNCUS: for investigations of vanilloid receptors is reviewed in the light of the exquisite sensitivity of the emetic reflex in this species to resiniferatoxin.  (+info)

A questionnaire for the assessment of the multiple dimensions of motion sickness. (7/88)

BACKGROUND: A limited number of attempts have been made to develop a questionnaire that assesses the experience of motion sickness. Further, many available questionnaires quantify motion sickness as a unidimensional construct. METHOD: Exploratory and confirmatory factor analyses of motion sickness descriptors were used to derive and verify four dimensions of motion sickness, which were defined as gastrointestinal, central, peripheral, and sopite-related. These dimensions of motion sickness were then used to construct a motion sickness assessment questionnaire (MSAQ) that was administered to individuals who were exposed to a rotating optokinetic drum. RESULTS: Total scores from the MSAQ correlated strongly with overall scores from the Pensacola Diagnostic Index (r = 0.81, p < 0.001) and the Nausea Profile (r = 0.92, p < 0.001). CONCLUSIONS: The MSAQ is a valid instrument for the assessment of motion sickness. In addition, the MSAQ may be used to assess motion sickness as a multidimensional rather than unidimensional construct.  (+info)

Gastric myoelectrical and autonomic cardiac reactivity to laboratory stressors. (8/88)

We evaluated the effects of two laboratory stressors (speech preparation and isometric handgrip) on gastric myoelectrical and autonomic cardiac activity, and the extent to which autonomic responses to these stressors and somatization predict reports of motion sickness during exposure to a rotating optokinetic drum. Both stressors prompted a decrease in preejection period (PEP) and respiratory sinus arrhythmia (RSA), and an increase in a dysrhythmic pattern of gastric myoelectrical activity, termed gastric tachyarrhythmia. Stressor-induced decreases in RSA and higher somatization scores predicted increased reports of motion sickness during drum rotation. These results demonstrate that laboratory stressors concurrently affect gastric myoelectrical activity and autonomic control of the heart, and that stressor-induced decreases in RSA and higher levels of somatization predict motion sickness susceptibility.  (+info)