Appendix A

Simmons, Rita G.; Phillips, Jeffrey B.; Lojewski, Renee A.; Wang, Zuwei; Boyd, Jason; Putcha, Lakshmi

doi:10.3357/asem.2668.2010

Cited by 21 publications

(4 citation statements)

References 6 publications

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“…With incremental exposure, people also can develop context specific adaptations so that, for example, they can move between a rotating artificial gravity environment and a stationary environment without either sensory motor control or motion sickness problems (Graybiel and Knepton 1978a, b; Lackner and DiZio 2000a, b, 2006). Drugs such as promethazine and scopolamine provide protective benefit (Bar et al 2009; Davis et al 1993; Graybiel and Lackner 1987; Gordon et al 2001; Klocker et al 2001; Nachum et al 2001, 2006; Simmons et al 2010). These drugs are central nervous system depressants and induce drowsiness so that they are often used in combination with dexedrine and ephedrine, respectively.…”

Section: How Can Motion Sickness Be Avoided or Attenuated?mentioning

confidence: 99%

Motion sickness: more than nausea and vomiting

2014

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Motion sickness is a complex syndrome that includes many features besides nausea and vomiting. This review describes some of these factors and points out that under normal circumstances, many cases of motion sickness go unrecognized. Motion sickness can occur during exposure to physical motion, visual motion, and virtual motion, and only those without a functioning vestibular system are fully immune. The range of vulnerability in the normal population varies about 10,000 to 1. Sleep deprivation can also enhance susceptibility. Systematic studies conducted in parabolic flight have identified velocity storage of semicircular canal signals—velocity integration—as being a key factor in both space motion sickness and terrestrial motion sickness. Adaptation procedures that have been developed to increase resistance to motion sickness reduce this time constant. A fully adequate theory of motion sickness is not presently available. Limitations of two popular theories, the evolutionary and the ecological, are described. A sensory conflict theory can explain many but not all aspects of motion sickness elicitation. However, extending the theory to include conflicts related to visceral afferent feedback elicited by voluntary and passive body motion greatly expands its explanatory range. Future goals should include determining why some conflicts are provocative and others are not but instead lead to perceptual reinterpretations of ongoing body motion. The contribution of visceral afferents in relation to vestibular and cerebellar signals in evoking sickness also deserves further exploration. Substantial progress is being made in identifying the physiological mechanisms underlying the evocation of nausea, vomiting, and anxiety, and a comprehensive understanding of motion sickness may soon be attainable. Adequate anti-motion sickness drugs without adverse side effects are not yet available.

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Section: How Can Motion Sickness Be Avoided or Attenuated?mentioning

confidence: 99%

Motion sickness: more than nausea and vomiting

2014

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“…Furthermore scopolamine nasal spray [77,78] was found to be an effective and safe treatment in motion sickness, with a fast onset within 30 min after administration.…”

Section: Prevention and Treatment Of Motion Sicknessmentioning

confidence: 99%

Neuronal Mechanisms and the Treatment of Motion Sickness

Schmäl¹

2013

Pharmacology

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The aim of this review is to provide an overview of the physiological basis, clinical picture and treatment options for motion sickness. Motion sickness is a well-known nausea and vomiting syndrome in otherwise healthy people. The physical signs of motion sickness occur in both humans and animals during travel by sea, automobile or airplane and in space. Furthermore, some other special situations, such as simulators, the cinema and video games, have been described as causing pseudomotion sickness. Children between 2 and 12 years old are most susceptible to motion sickness, and women are more frequently affected than men. Predisposing factors include menstruation, pregnancy, migraines and possibly a side difference in the mass of otoconia in the vestibular organs. Therapy is directed towards decreasing conflicting sensory input, accelerating the process of adaptation and controlling nausea and vomiting. To control these vegetative symptoms, scopolamine and antihistamines are the most effective drugs.

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“…The benefits of IN administration include greater acceptance by patients, particularly children, and the access that the IN route provides to the CNS, thus avoiding first pass clearance by the liver and potential toxicity to non-target organs. Recent successes include use of IN-administered midazolam for the treatment of status epilepticus in children and young adults (McMullan et al, 2010); IN scopolamine for motion sickness (Simmons et al, 2010), and IN insulin has been shown to improve cognition in early Alzheimer’s disease (Benedict et al, 2004). …”

Section: Introductionmentioning

confidence: 99%

Manipulation of olfactory tight junctions using papaverine to enhance intranasal delivery of gemcitabine to the brain

et al. 2013

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Context Delivery of drugs from the nasal cavity to the brain is becoming more widely accepted, due to the non-invasive nature of this route and the ability to circumvent the blood brain barrier (BBB). Objective Because of similarities in the proteins comprising the olfactory epithelial tight junction (TJ) proteins and those of the BBB, we sought to determine whether papaverine (PV), which is known to reversibly enhance BBB permeability, could increase the delivery of intranasally administered gemcitabine to the central nervous system in rats. Experimental methods Included intranasal administration of gemcitabine, fluorescein isothiocyanate-dextran beads and PV, histopathology, immunostaining, RT-PCR, western blot analysis, immunofluorescence localization, spectrofluorometric analysis, in vivo brain microdialysis, HPLC analysis and in vitro gemcitabine recovery. Results and discussion PV transiently decreased the levels and altered immunolocalization of the TJ protein phosphorylated-occludin in the olfactory epithelium, while causing an approximately four-fold increase in gemcitabine concentration reaching the brain. The enhanced delivery was not accompanied by nasal epithelial damage or toxicity to distant organs. Conclusions The ability to transiently and safely increase drug delivery from the nose to the brain represents a non-invasive way to improve treatment of patients with brain disorders.

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Appendix A

Cited by 21 publications

References 6 publications

Motion sickness: more than nausea and vomiting

Motion sickness: more than nausea and vomiting

Neuronal Mechanisms and the Treatment of Motion Sickness

Manipulation of olfactory tight junctions using papaverine to enhance intranasal delivery of gemcitabine to the brain

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