Cases reported "Motion Sickness"

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1/12. Visual-vestibular habituation and balance training for motion sickness.

    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.
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2/12. vertigo in virtual reality with haptics: case report.

    A researcher was working with a desktop virtual environment system. The system was displaying vector fields of a cyclonic weather system, and the system incorporated a haptic display of the forces in the cyclonic field. As the subject viewed the rotating cyclone field, they would move a handle "through" the representation of the moving winds and "feel" the forces buffeting the handle as it moved. Stopping after using the system for about 10 min, the user experienced an immediate sensation of postural instability for several minutes. Several hours later, there was the onset of vertigo with head turns. This vertigo lasted several hours and was accompanied with nausea and motion illusions that exacerbated by head movements. Symptoms persisted mildly the next day and were still present the third and fourth day, but by then were only provoked by head movements. There were no accompanying symptoms or history to suggest an inner ear disorder. physical examination of inner ear and associated neurologic function was normal. No other users of this system have reported similar symptoms. This case suggests that some individuals may be susceptible to the interaction of displays with motion and movement forces and as a result experience motion illusions. Operators of such systems should be aware of this potential and minimize exposure if vertigo occurs.
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3/12. Neurotologic issues.

    Progress has been made in the diagnosis and treatment of inner ear disorders. Autoimmune inner ear disorders and Meniere's disease (MD), the prototype inner ear disease, are highlighted in this review of current knowledge and contemporary dietary, medical, surgical, and vestibular rehabilitation therapy. A number of other peripheral vestibular disorders are presented and contrasted with MD.
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4/12. Simulator sickness in an army simulator.

    Simulator sickness describes a symptom reported by aircrew during or after flight simulator training. Some features are common to motion sickness but others, which are unusual during real flight, are believed to result specifically from the simulator environment. This paper describes the results of a questionnaire study examining the incidence and factors influencing simulator sickness in any army training system. Case histories are described and conclusions drawn with respect to health and safety, training and the effect on flight operations. One hundred and fifteen aircrew were registered in the questionnaire study. Data were collected from a history questionnaire, a post-sortie report and a delayed report form. Sixty-nine per cent of aircrew gave a history of symptoms in the simulator and 59.9 per cent experienced at least one symptom during the study period although few symptoms were rated as being other than slight. Only 3.6 per cent of subjects reported symptoms of disequilibrium. Comparative analysis of the results was performed after scoring symptoms to produce a sickness rating. This showed: association between simulator-induced sickness and greater flying experience; adaptation to the simulator environment; a history of sea sickness may predict susceptibility to simulator sickness; and no association of crew role and simulator sickness. Although some authorities believe simulator sickness to be a potential flight safety hazard there was little evidence from this study. Guidelines for the prevention of the problem are presented now that many factors have been identified. A general policy to 'ground' aircrew for a period following simulator training is not necessary, but severe cases should be assessed individually.
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5/12. Transdermal scopolamine-induced psychosis.

    Transdermal scopolamine (Transderm-Scop) is being increasingly used for effective prophylaxis of motion sickness. It is reported to have a lower incidence of CNS side effects than orally administered scopolamine. Although uncommon, such side effects occur more often in the elderly, in those with preexisting psychiatric disease, and in patients concurrently taking other medications with anticholinergic activity. Correct diagnosis may be delayed by the occult location of the delivery system, delayed onset of symptoms, prolonged action, absence of peripheral manifestations, and negative toxicologic screening tests. Treatment is usually supportive. physostigmine should be reserved for the treatment of severe symptoms.
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6/12. Vision therapy as a treatment for motion sickness.

    A case of visually-induced motion sickness (VIMS) is presented. The patient underwent a program of dynamic adaptive vision therapy which relieved her symptoms of motion sickness. Symptoms of VIMS may include photophobia, an inability to read in a moving auto, and nausea, dizziness, headache, eye strain and anxiety following provocative visual stimuli. The neural mismatch theory is discussed.
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7/12. Remote cerebral hemisphere symptoms from surgically treated patients with posterior fossa brain tumors; vascular factors: a basis for a theory concerning space sickness.

    Three case histories of patients with large tumors in the posterior fossa who were operated on in a sitting position subsequently developed 1 or more symptoms referable to the temporoparietooccipital regions of the brain 24 to 48 hours postoperatively. Initially, it was believed that such symptoms were due to a stimulation of the association pathways causing firing of remote association areas (See Ch. 4). Subsequent studies of the rotation of blood vessels of the brain in the developing embryo and a review of the anatomical location of the arteries supplying the temporoparietooccipital region led to the conclusion that some compromise of the posterior cerebral artery was responsible for the symptoms. The symptomatology in these brain tumor patients was not unlike that seen in the cosmonauts and astronauts in space flight, designated as "motion sickness" in the space literature. A suggestion was made as to clarification of the definitions. This author advocated that the term "motion sickness" be confined to those symptoms of dizziness, nausea, and vomiting, due to involvement of the peripheral end organ, the inner ear. "Space sickness" might include these symptoms but also might have the addition of disorientation or the inversion of image in space and formed or unformed hallucinations. These relate to the temporoparietooccipital area, the midtemporal, and the occipital regions. In such instances, there must be central involvement or a stimulation of this interpretive cortex of the brain. The remote symptoms from the supratentorial cotex were believed to be due to hypoxia related to the posterior cerebral artery compromise, resulting in delayed "luxury perfusion" and the development of local lactic acidosis. Transaxial transmission of force with an uncal tentorial herniation causing compression of the posterior cerebral artery was suggested as a mechanism responsible for the vascular compression.
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8/12. Self-control desensitization with cue-controlled relaxation for treatment of a conditioned vomiting response to air travel.

    A 33 yr old female with a flying phobia which involved frequent conditioned vomiting and fainting was successfully treated by a combination of self-control desensitization and cue-controlled relaxation. A 12 and 18 month follow-up indicated that treatment effects were maintained. Implications are discussed of this procedure for the treatment of conditioned nausea and vomiting resulting from cancer chemotherapy.
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9/12. Prevention of motion sickness in flight maneuvers, aided by transfer of adaptation effects acquired in the laboratory: ten consecutive referrals.

    Ten flyers, grounded because of nausea and vomiting, were referred as potential candidates for adaptation to cross-coupled angular accelerations in a slow-rotation room; such adaptation has been shown to "transfer" to flight maneuvers. There was no opportunity to attempt treatment in two candidates. Among the remaining eight, five regained flight status (62.5%); follow-up periods of those five candidates ranged from 10 to 27 months. In one of the three remaining candidates, a satisfactory level of adaptation was achieved but more than 4 months elapsed before his assignment to a duty squadron. After becoming sick in his first flight (F-104), he submitted a request to be removed from duty involving flying. In the remaining two candidates, the rate of their acquisition of adaptation not only was very slow but also, after leveling off, actually declined. In other words, poor as well as good performance is demonstrable in the slow-rotation room.
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10/12. motion sickness: part III--a clinical study based on surgery of posterior fossa tumors.

    Three patients who had large, benign cerebellar tumors were operated upon in the sitting position and developed symptoms referable to the temporoparieto-occipital region of the brain 24-48 h postoperatively. They consisted of dizziness, nausea, vomiting, formed and unformed hallucinations, and inversion of image or disorientation in space, some of which were experienced by some of the astronauts and cosmonauts during space flight. Such findings are not due to stimulation of the cerebellum, the site of the lesion, but must come from the cerebral hemisphere. The symptoms were believed to be caused by "the luxury perfusion" of Lassen with the development of local lactic acidosis secondary to vascular insufficiency to the brain in the distribution of the posterior cerebral artery thus stimulating the temporoparieto-occipital region. This theory is suggested to some degree by the work of Endo et al. using CT scans, which showed the shifting of increased blood flow from the frontal region to the temporoparieto-occipital region following removal of a benign posterior fossa tumor. The mechanism for the compression of the posterior cerebral artery may be due to uncal herniation at the tentorium. The authors believe that it might be well to consider further testing in a vertical or oblique plane rather than only in a centrifugal horizontal one. This method would tend to cause uncal herniation more readily. Monitoring of such effects could be done with the colored CT scan.
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