Vestibular and postural findings in the motion sickness syndrome MOHAMED A. HAMID, PhD, DIC, Cleveland, Ohio
MOTION SICKNESS SYNDROME
Motion sickness has been a known medical entity since Hippocrates. Since the nineteenth century, several theories have been postulated to explain the underlying mechanisms of motion sickness, until a general acceptance has been established for the vestibularvisual sensory conflict theory. Most motion sickness studies have been predominantly in animal^.^.^ Studies of human beings investigated the incidence and symptoms in selective populations (e.g., Navy, Air Force, and airline passengers), and effects of anti-motion sickness medications. This study was designed to investigate vestibular and postural responses in subjects with motion sickness in an attempt to define the clinical motion sickness syndrome and its possible epidemiologic and genetic correlates. Subjects (N = 161; 57 women and 104 men) were presented, with the main complaint being motion intolerance, unsteadiness, and nausea of varying degree without hearing symptoms, incapacitating vertigo, or significant neurotologic findings. Subjects’ mean age was 45 years (range, 14 to 73 years). The majority reported motion sickness since early childhood and that at least one member of their immediate family currently has motion sickness. All subjects underwent ocular motility (DC EOG), vestibular (caloric and chair test), and dynamic posturography using standard test protocols. EOG results showed no saccadic or pursuit abnormalities. Positional nystagmus was present in 35% of subjects and only four subjects showed paroxysmal positioning nystagmus. Unilateral vestibular deficit was not observed. Hyperactive VOR gain (peak eye velocity/peak head velocity > 2 SD) was evident in 126 subjects (78%). VOR gain is controlled by the vestibulo-cerebellum. It can therefore be argued that subjects with motion sickness exhibit physiologic reduction in cerebellar‘3’
From the Section of Vestibular and Balance Disorders, Department of Otolaryngology, Cleveland Clinic Foundation. Presented at the Annual Meeting of the American Neurology Society, Palm Beach, Fla., April 27, 1990. Reprint requests: Mohamed A. Hamid, PhD, Section of Vestibular and Balance Disorders, Department of Otolaryngology, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44132. 23 I 1I25991
vestibular interaction by comparison to non-motion sickness subjects. Additionally, with a lesser cerebellar control, the VOR becomes “unstable”, leading to VOR asymmetry reflected by positional nystagmus. Dynamic posturography showed hip sway strategy in 92 (57%) and vestibular deficit pattern in 20 (12%) subjects. It appears that subjects with motion sickness subconsciously “select” hip sway strategy to minimize the magnitude of active head movements, and therefore minimize vestibular stimulation to avoid the unpleasant symptoms of motion sickness. Genetics in Motion Sickness
Although it was difficult to obtain a detailed family history, most subjects reported that at least one member of their parental or own family has motion sickness. No sex difference was apparent. It was difficult to construct meaningful pedigrees; however, data suggest a possible genetic component in motion sickness. Role of Vestibular Rehabilitation in Motion Sickness
Currently, management of motion sickness is limited to use of antimotion sickness medications, which are tailored to each individual subject. Vestibular rehabilitation was offered to all subjects, and 30 elected to undergo individualized programs aimed at improving hip sway strategy, eye-head coordination, and increasing sensory (vestibular-visual proprioceptive) redundancy. Subjects had an average of 1.5 visits, then continued on their own with the program. Symptoms were rated on a scale of I (no symptoms) to 10 (severe symptoms). Statistical analysis (Welch test) showed significant decrease in the mean symptoms after rehabilitation ( p = 0.5). SUMMARY
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 con135
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OtolaryngologyHead and Neck Surgery
136 HAMID
structed. Prospective studies are warranted to further establish the patterns of the motion sickness syndrome. REFERENCES
Motion Sickness, New york: Academic Reason JT, Press, 1975. 2. Crampton GH. Motion and space sickness. Florida: CRC Press, 1989. JJ.
3. Igarashi M, Himi T,Kulescz WB, Kobayashi K. Role of otolith
endorgans in the genesis of vestibular-visual conflict sickness (pitch) in the squirrel monkey (first report). Aviat Space Environ Med 1987;58:A207. 4. Wilpizeski CR, Lowry LD, Goldman WS. Motion-induced sickness following bilateral ablation of area postrema in squirrel monkeys. Laryngoscope 1986;96:1221.
Downloaded from oto.sagepub.com at LAURENTIAN UNIV LIBRARY on June 5, 2016
MOTION SICKNESS SYNDROME
Motion sickness has been a known medical entity since Hippocrates. Since the nineteenth century, several theories have been postulated to explain the underlying mechanisms of motion sickness, until a general acceptance has been established for the vestibularvisual sensory conflict theory. Most motion sickness studies have been predominantly in animal^.^.^ Studies of human beings investigated the incidence and symptoms in selective populations (e.g., Navy, Air Force, and airline passengers), and effects of anti-motion sickness medications. This study was designed to investigate vestibular and postural responses in subjects with motion sickness in an attempt to define the clinical motion sickness syndrome and its possible epidemiologic and genetic correlates. Subjects (N = 161; 57 women and 104 men) were presented, with the main complaint being motion intolerance, unsteadiness, and nausea of varying degree without hearing symptoms, incapacitating vertigo, or significant neurotologic findings. Subjects’ mean age was 45 years (range, 14 to 73 years). The majority reported motion sickness since early childhood and that at least one member of their immediate family currently has motion sickness. All subjects underwent ocular motility (DC EOG), vestibular (caloric and chair test), and dynamic posturography using standard test protocols. EOG results showed no saccadic or pursuit abnormalities. Positional nystagmus was present in 35% of subjects and only four subjects showed paroxysmal positioning nystagmus. Unilateral vestibular deficit was not observed. Hyperactive VOR gain (peak eye velocity/peak head velocity > 2 SD) was evident in 126 subjects (78%). VOR gain is controlled by the vestibulo-cerebellum. It can therefore be argued that subjects with motion sickness exhibit physiologic reduction in cerebellar‘3’
From the Section of Vestibular and Balance Disorders, Department of Otolaryngology, Cleveland Clinic Foundation. Presented at the Annual Meeting of the American Neurology Society, Palm Beach, Fla., April 27, 1990. Reprint requests: Mohamed A. Hamid, PhD, Section of Vestibular and Balance Disorders, Department of Otolaryngology, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44132. 23 I 1I25991
vestibular interaction by comparison to non-motion sickness subjects. Additionally, with a lesser cerebellar control, the VOR becomes “unstable”, leading to VOR asymmetry reflected by positional nystagmus. Dynamic posturography showed hip sway strategy in 92 (57%) and vestibular deficit pattern in 20 (12%) subjects. It appears that subjects with motion sickness subconsciously “select” hip sway strategy to minimize the magnitude of active head movements, and therefore minimize vestibular stimulation to avoid the unpleasant symptoms of motion sickness. Genetics in Motion Sickness
Although it was difficult to obtain a detailed family history, most subjects reported that at least one member of their parental or own family has motion sickness. No sex difference was apparent. It was difficult to construct meaningful pedigrees; however, data suggest a possible genetic component in motion sickness. Role of Vestibular Rehabilitation in Motion Sickness
Currently, management of motion sickness is limited to use of antimotion sickness medications, which are tailored to each individual subject. Vestibular rehabilitation was offered to all subjects, and 30 elected to undergo individualized programs aimed at improving hip sway strategy, eye-head coordination, and increasing sensory (vestibular-visual proprioceptive) redundancy. Subjects had an average of 1.5 visits, then continued on their own with the program. Symptoms were rated on a scale of I (no symptoms) to 10 (severe symptoms). Statistical analysis (Welch test) showed significant decrease in the mean symptoms after rehabilitation ( p = 0.5). SUMMARY
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 con135
Downloaded from oto.sagepub.com at LAURENTIAN UNIV LIBRARY on June 5, 2016
OtolaryngologyHead and Neck Surgery
136 HAMID
structed. Prospective studies are warranted to further establish the patterns of the motion sickness syndrome. REFERENCES
Motion Sickness, New york: Academic Reason JT, Press, 1975. 2. Crampton GH. Motion and space sickness. Florida: CRC Press, 1989. JJ.
3. Igarashi M, Himi T,Kulescz WB, Kobayashi K. Role of otolith
endorgans in the genesis of vestibular-visual conflict sickness (pitch) in the squirrel monkey (first report). Aviat Space Environ Med 1987;58:A207. 4. Wilpizeski CR, Lowry LD, Goldman WS. Motion-induced sickness following bilateral ablation of area postrema in squirrel monkeys. Laryngoscope 1986;96:1221.
Downloaded from oto.sagepub.com at LAURENTIAN UNIV LIBRARY on June 5, 2016
