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Journal of Vestibular Research xx (2021) x–xx 1

DOI:10.3233/VES-200005
IOS Press

1 Motion sickness diagnostic criteria:


2 Consensus document of the classification
committee of the Bárány society

f
3

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4 Yoon-Hee Chaa,1,∗ , John Goldingb,1 , Behrang Keshavarzc,1 , Joseph Furmand , Ji-Soo Kime ,
5 Jose A. Lopez-Escamezf,g,h , Måns Magnussoni , Bill J. Yatesj , Ben D. Lawsonk ,
Advisors: Jeffrey Staabl and Alexandre Bisdorffm,1

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6

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a Department of Neurology, University of Minnesota, Minneapolis, MN, USA
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b Psychology, School for Social Sciences, University of Westminster, London UK
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c Toronto Rehabilitation Institute – University Health Network, Toronto, ON, Canada; Department of Psychology,

10 Ryerson University, Toronto, ON, Canada

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d Department of Otolaryngology, University of Pittsburgh, Pittsburgh, PA, USA

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e Department of Neurology Seoul National University, Seoul, Republic of Korea

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f Department of Surgery, Division of Otolaryngology, Universidad de Granada, Granada, Spain

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g Otology and Neurotology Group CTS495, Department of Genomic Medicine, Centre for Genomics and Oncology

Research – Pfizer/Univ. de Granada/Junta de Andalucı́a (GENyO), PTS, Granada, Spain


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h Department of Otolaryngology, Instituto de Investigación Biosanitaria ibs. GRANADA Hospital Universitario

17 Virgen de las Nieves, Granada, Spain


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i Department of Otorhinolaryngology, Lund University, Lund, Sweden

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j Department of Otolaryngology, University of Pittsburgh, Pittsburgh, PA, USA

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k Naval Submarine Medical Research Laboratory, Naval Submarine Base New London, Groton CT, USA
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l Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA
m Department of Neurology, Centre Hospitalier Emile Mayrisch, L-4005 Esch-sur-Alzette, Luxembourg
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24
Received 11 August 2020
Accepted 8 February 2021

25 Abstract. We present diagnostic criteria for motion sickness, visually induced motion sickness (VIMS), motion sickness
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26 disorder (MSD), and VIMS disorder (VIMSD) to be included in the International Classification of Vestibular Disorders.
27 Motion sickness and VIMS are normal physiological responses that can be elicited in almost all people, but susceptibility
28 and severity can be high enough for the response to be considered a disorder in some cases. This report provides guidelines
29 for evaluating signs and symptoms caused by physical motion or visual motion and for diagnosing an individual as having a
30 response that is severe enough to constitute a disorder.
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31 The diagnostic criteria for motion sickness and VIMS include adverse reactions elicited during exposure to physical motion
32 or visual motion leading to observable signs or symptoms of greater than minimal severity in the following domains: nausea
33 and/or gastrointestinal disturbance, thermoregulatory disruption, alterations in arousal, dizziness and/or vertigo, headache
34 and/or ocular strain. These signs/symptoms occur during the motion exposure, build as the exposure is prolonged, and
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35 eventually stop after the motion ends. Motion sickness disorder and VIMSD are diagnosed when recurrent episodes of

1 Except for the first three authors and the last author, all authors

are listed alphabetically.


∗ Corresponding authors. Yoon-Hee Cha, Department of Neu-

rology, University of Minnesota, Minneapolis, MN, USA. E-mail:


[email protected].

ISSN 0957-4271/$35.00 © 2021 – IOS Press. All rights reserved.


2 Y.-H. Cha et al. / Motion sickness diagnostic criteria

36 motion sickness or VIMS are reliably triggered by the same or similar stimuli, severity does not significantly decrease after
37 repeated exposure, and signs/symptoms lead to activity modification, avoidance behavior, or aversive emotional responses.
38
Motion sickness/MSD and VIMS/VIMSD can occur separately or together. Severity of symptoms in reaction to physical
39
motion or visual motion stimuli varies widely and can change within an individual due to aging, adaptation, and comorbid
40
disorders. We discuss the main methods for measuring motion sickness symptoms, the situations conducive to motion sickness
41
and VIMS, and the individual traits associated with increased susceptibility. These additional considerations will improve
42
diagnosis by fostering accurate measurement and understanding of the situational and personal factors associated with MSD
43
and VIMSD.

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36 1. Introduction dramatically in the early 20th century due to the 76

unprecedented number of military troops being trans- 77

37 The Classification Committee of the Bárány So- ported by sea, air, and land. The initiation of space 78

38 ciety was charged with establishing standardized travel in the 1960s further spurred interest in motion 79

39 international clinical diagnostic criteria for motion si- sickness research, fostering some of the assessment 80

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40 ckness and visually induced motion sickness (VIMS) tools and countermeasures that are used today [6]. 81

41 and when these conditions constitute disorders. These Motion sickness that is mainly caused by stimu- 82

42 criteria were developed by an international group of lation of the visual system, often in the absence of 83

43 vestibular specialists, scientists, and therapists for the physical motion, has received increased recognition 84

Bárány Society in order to promote a common refer- recently [7, 8]. Symptoms of VIMS were reported as

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44 85

45 ence frame across disciplines involved in the care of early as the 19th century in the haunted swing amuse- 86

46 the general public and of individuals with high sus- ment ride and documented during adaptation to visual 87

47 ceptibility to motion sickness and VIMS. Though a rearrangement and subsequent readaptation to nor- 88

48 common phenomenon, sickness induced by physical mal vision [9–11]. These early reports noted symp- 89
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49 motion of the person or visual motion can adversely toms such as dizziness, nausea, and vertigo, each of 90

50 affect otherwise healthy individuals and decrease which is still featured today in the most widely-used 91

51 safety in situations that require high levels of concen- simulator sickness state questionnaire [12]. Modern 92

52 tration. The establishment of these criteria recognizes scientific studies of VIMS were first documented in 93

53 that motion sickness and VIMS, while being normal the 1950s in the laboratory and the military domains 94

physiologic responses, can have profound negative when optokinetic stimuli and flight simulators were
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54 95

55 effects when symptoms are severe, and can some- found to cause motion sickness-like symptoms (nau- 96

times be considered a motion sickness disorder sea, dizziness, vertigo/disorientation, blurred vision,
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56 97

57 (MSD) or visually induced motion sickness disorder headache, and drowsiness) [13–17]. Due to recent 98

58 (VIMSD). technological advancements, visual displays and 99

applications have become pervasive (surround the- 100

59 1.1. History aters, vehicle simulators, virtual reality, augmented 101


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reality), making VIMS a common phenomenon. 102

60 Descriptions of motion induced sickness date back


61 to 400 BCE, becoming more common as modes of 1.2. Theories 103

62 transportation advanced with time. Ancient Greek


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63 texts mention symptoms of seasickness such as nau- Motion sickness and VIMS are polysymptomatic 104

64 sea, vomiting, faintness, difficulty concentrating, and syndromes driven by the interaction between a spe- 105

65 lack of initiative which are still considered valid today cific stimulus and individual susceptibility. While 106

66 [1]. Theories to explain such reactions to motion there is no single, universally accepted theory of 107
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67 evolved over the centuries from pre-scientific ideas to motion sickness or VIMS, several hypotheses exist 108

68 later explanations concerning the effects of inner ear concerning the evolutionary origins and immediate 109

69 overstimulation or disrupted multisensory integration etiology of motion sickness and VIMS [6, 7, 17–21]. 110

70 [1–3]. It has long been known that the vestibular The sensory conflict/neural mismatch hypothesis 111

71 organs are implicated in seasickness [4] and that peo- of motion sickness is the most cited explanation. 112

72 ple without vestibular function are not susceptible to It posits that motion sickness is caused by a con- 113

73 motion sickness, even during highly sickening sea flict between expected versus actual interactions 114

74 conditions [5]. Modern interest in the mechanisms, among visual, vestibular, and somatosensory inputs 115

75 treatment, and prevention of motion sickness grew [6, 18]. This conflict can be due to dissonance among 116
Y.-H. Cha et al. / Motion sickness diagnostic criteria 3

117 different sensory modalities, intra-vestibular mis- nausea and vomiting without conferring any func- 169

118 match between canal and otolith inputs, mismatch tional benefit to the individual [27, 28]. 170

119 between current multisensory input versus multise-


120 nsory calibrations acquired during past stimuli, and/
121 or a discrepancy between the perceived and actual 2. Approach 171

122 orientation of the gravitational upright [19–22].


123 Motion sickness has also been hypothesized to be 2.1. Committee organization 172

124 a by-product of the abnormal activation of vestibulo-

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125 autonomic pathways by physical or apparent motion Members of the Classification Committee of the 173

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126 to which the human nervous system is unable to or Bárány Society (CCBS) met in Berlin, Germany in 174

127 has not had sufficient time to adapt [23, 24]. These March 2017 and proposed the creation of a subcom- 175

128 theories predict that motion sickness will diminish mittee to develop criteria for motion sickness for 176

129 with repeated exposure if the challenging motions the International Classification of Vestibular Disor- 177

130 are sufficiently within one’s adaptive capacity and the ders (ICVD). They selected a Chairperson (YHC) 178

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131 internal model of expected sensory input recalibrates. to choose subcommittee members who represented a 179

132 The toxin hypothesis of motion sickness is a vari- broad range of subspeciality expertise and who came 180

133 ant of the sensory conflict theory which attempts to from three different continents. Subcommittee com- 181

134 explain the evolutionary origins of the characteristic munication occurred through email and subsequent 182

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135 symptoms of motion sickness (e.g., nausea, vomit- meetings. The CCBS met again to discuss its progress 183

136 ing) rather than the immediate cause of the motion before the 30th Bárány Society meeting in Uppsala, 184

137 sickness reaction during a given stimulus [25]. This Sweden in June 2018, and in Berlin, Germany in 185

138 hypothesis postulates that motion-induced vomiting November 2019. Diagnostic criteria were developed 186

139 is an accidental, modern (transportation-related) by- through discussions among subcommittee members. 187
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140 product of an ancient evolutionarily protective respo- Draft criteria were presented to the CCBS in Novem- 188

141 nse to the neural effects of various toxins which are ber 2019 and then modified based on comments. A 189

142 often associated with distortions of sensory input. revised draft was made available for comment by the 190

143 Thus, sensory integration disturbances and neural eff- Bárány Society membership in January 2020. Fur- 191

144 ects are produced by modern motion which are simi- ther comments and concerns were addressed before 192

lar to ancient responses triggered by poisoning (e.g., publication.


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145 193

146 from spoiled meat, toxic plants, animal venom, or


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147 even intoxicants such as fermented fruit) [17]. A sha- 2.2. Selection of symptoms for criteria 194

148 red susceptibility to triggering the emetic pathway


149 by different mechanisms is supported by the obser- The diagnostic criteria described in this report are 195

150 vation that individuals with high motion sickness sus- derived from a large body of studies that have cat- 196

151 ceptibility are more likely to suffer from nausea and egorized motion sickness symptoms and have con- 197
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152 vomiting from other causes, such as chemotherapy tributed to the development of well-validated motion 198

153 and actual toxins [26]. However, many tenets of the sickness metrics. The categorization of the symptoms 199

154 toxin hypothesis have been questioned and modified. of motion sickness and VIMS was initially driven 200

155 The direct evolutionary hypothesis posits that an- by military and space exploration needs to include 201
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156 cient physical or apparent motions existed that could pre-vomiting symptoms. Vomiting, while objective, 202

157 have contributed directly to the evolution of aversive is usually a late sign of motion sickness and is 203

158 reactions, without the need for accidental co-opting impractical for assessing escalating severity of mot- 204

159 of a poison response via the neural effects of modern ion sickness and VIMS. The identification of ear- 205
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160 transportation [17]. Nevertheless, the direct poison- lier symptoms broadened the spectrum of severity 206

161 ing hypothesis posits that the body’s poison response of motion sickness and led to recognition of when 207

162 system shaped some of the signature motion sickness interventions were needed to stop the progression of 208

163 symptoms that emerged during the direct evolution of sickness. By the 1940s, some of the most common 209

164 aversive reaction to certain ancient motions. symptoms beyond obvious vomiting or retching were 210

165 Finally, the possibility has been raised that motion agreed upon by multiple authors (e.g., cold sweating, 211

166 sickness is simply an unfortunate structural conse- pallor), leading to a full diagnostic checklist contain- 212

167 quence of the proximity of anatomical pathways that ing multiple motion sickness symptoms developed by 213

168 mediate vestibular signals with those that mediate the 1960s [29–31]. 214
4 Y.-H. Cha et al. / Motion sickness diagnostic criteria

215 The three most influential multi-symptom motion urge to vomit, retching, actual vomiting, epigastric/ 262

216 sickness state questionnaires include: 1) the Sim- stomach discomfort/awareness, change in salivation 263

217 ulator Sickness Questionnaire/Motion Sickness and/or appetite, burping, and a desire to move bowels. 264

218 Questionnaire (SSQ/MSQ) [12], 2) the Pensacola Thermoregulatory disruption can include sweating/ 265

219 Diagnostic Index (PDI) (most-cited in [32], and fully cold sweating, clamminess, flushing, warmth, and 266

220 matured in [31]), and 3) the Motion Sickness Assess- pallor. Alterations in arousal can include drowsiness, 267

221 ment Questionnaire (MSAQ) [33]. The complete 28- fatigue, tiredness, and difficulty concentrating. Dizzi- 268

222 item MSQ and the 16-items focused on simulator ness and/or vertigo can include these symptoms as 269

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223 sickness that make up the SSQ portion have been well as disorientation, faintness, and visual motion 270

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224 cited more than any other motion sickness state que- illusions. Headache and/or ocular strain can include 271

225 stionnaires and are relevant to the development of head pain, head fullness, eyestrain, difficulty focus- 272

226 other motion sickness scales (e.g. MSAQ[33], Mis- ing, and blurred vision. Blurred vision can also occur 273

227 ery Scale [34]). In order to form a more manageable in the context of vertigo. The presence of a greater 274

228 and easily remembered set of criteria, however, the number of signs and/or symptoms allows greater 275

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229 major items of the MSQ/SSQ and the PDI have specificity that symptoms are due to motion sickness. 276

230 been grouped. Cross-referencing the most agreed-


NOTES: 277
231 upon symptoms across multiple formal motion
232 sickness/VIMS diagnostic categorization efforts pro- 1. A variety of physical motion stimuli can trig- 278

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233 duced the motion sickness/VIMS criteria below and ger motion sickness. While highly susceptible 279

234 detailed in Tables 1–3. people tend to be susceptible to multiple motion 280

stimuli, susceptibility to one type of stimulus 281

does not necessarily correlate with suscepti- 282

235 3. Diagnostic criteria bility to others for an entire group of people. 283
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Examples of sickening motion stimuli include: 284

236 3.1. Motion sickness and visually induced a. Water transportation, e.g., ships, boats, ra- 285

237 motion sickness fts, submarines, floating, snorkeling, scuba- 286

diving 287

238 Motion sickness is diagnosed when the sickness b. Air transportation, e.g., airplanes, helico- 288

inducing stimulus is physical motion of the person; pters, hang-gliding, parasailing, skydiving,
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239 289

240 visually induced motion sickness (VIMS) is diag- parabolic flight 290
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241 nosed when the stimulus is visual motion. An acute c. Land transportation, e.g., cars, trains, truc- 291

242 episode of motion sickness/VIMS is sickness induced ks, buses, off-road vehicles (including arm- 292

243 by physical motion/visual motion that meets Criteria ored vehicles), self-driving cars, and some 293

244 A through D: forms of animal-based transportation (e.g., 294

camels) 295
A. Physical motion of the person1 or visual mo-
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245
d. Amusement devices, e.g., amusement park 296
246 tion2 elicits sign(s) and/or symptom(s) in at
rides, playground motion devices, certain 297
247 least one of the following categories, experie-
swings or hammocks 298
248 nced at greater-than-minimal severity:
e. Swaying buildings, e.g., low frequency 299
249 1. Nausea and/or gastrointestinal disturbance3
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wind or tremor-induced sway, especially in 300


250 2. Thermoregulatory disruption4
tall buildings 301
251 3. Alterations in arousal5
f. Vestibular stimulation in laboratory sett- 302
252 4. Dizziness and/or vertigo6
ings, e.g., Coriolis cross-coupling, off- 303
5. Headache and/or ocular strain7
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253
vertical axis rotation (OVAR), horizontal 304
254 B. Sign(s)/Symptom(s) appear during motion and
or vertical low frequency linear oscillation, 305
255 build as exposure is prolonged8
and certain stimuli aboard human centri- 306
256 C. Sign(s)/Symptom(s) eventually stop after ces-
fuges 307
257 sation of motion9
g. Space travel, e.g., upon entering orbit or 308
258 D. Sign(s)/Symptom(s) are not better accounted
first returning to Earth 309
259 for by another disease or disorder10
2. Visual stimulation may be presented via vir- 310

260 COMMENTS:Nausea and/or gastrointestinal dis- tual/augmented reality devices, simulators, 311

261 turbance can include a feeling of sickness with an movies, computer monitors, dynamic video 312
Y.-H. Cha et al. / Motion sickness diagnostic criteria 5

313 games, or optokinetic drums. Even certain weighed heavily by clinicians but failing to 365

314 small mobile displays can be disturbing under recollect the presence of pallor is inconclusive. 366

315 certain conditions (e.g., display parallax whe- 5. Symptoms such as fatigue, drowsiness, or diff- 367

316 rein foreground and background move) or iculty concentrating are part of the full list of 28 368

317 when viewed while walking or riding in a vehi- SSQ/MSQ symptoms and are considered to be 369

318 cle. When visually-triggered motion sickness suggestive of the ‘sopite’ syndrome [39]. Sev- 370

319 also includes physical motion, e.g., motion- eral other symptoms related to poor mood or 371

320 based flight simulators, driving simulators, or reduced motivation have been inferred to be 372

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321 ship simulators, the contributions of both forms sopite-related during prolonged motion tests 373

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322 of stimuli should be noted. [39], and symptoms such as fuzzy/foggy- 374

323 3. Many of these symptoms and others in the cri- headed, lazy/unmotivated, and relaxed have 375

324 teria have been formally defined [12, 17]. been endorsed by research participants recol- 376

325 Stomach awareness and discomfort are com- lecting situations involving mild motion [17, 377

326 mon early gastric manifestations of motion 40]. Fatigue due to motion sickness should be 378

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327 sickness. The unpleasant sensations can incl- distinguishable from sleep deprivation, phys- 379

328 ude the esophageal or epigastric areas. Nausea ical exhaustion, or other disorders causing 380

329 may be mild or severe. Though the probability lethargy. 381

330 of vomiting is generally related to the severity 6. When due to motion sickness, these symptoms 382

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331 of nausea, vomiting may rarely occur at low should not be solely attributable to vestibu- 383

332 or negligible levels of nausea without much lar disorders, changes in atmospheric pressure, 384

333 warning in some situations, or in very suscep- postural hypotension, or visual cliffs [41]. Fee- 385

334 tible people [35]. Prolonged mild or moderate lings of vertigo or spinning can also be elicited 386

335 nausea can occasionally lead to an ‘avalanche’ without motion sickness during piloting an air- 387
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336 phenomenon in which symptoms rapidly esca- craft without good visual references or exp- 388

337 late to vomiting [36]. If vomiting occurs du- eriencing a visually induced illusion of self- 389

338 ring a severe stimulus, it generally happens motion. When an episode of vertigo leads to 390

339 within 60-minutes of the onset of other symp- overlapping symptoms with motion sickness, 391

340 toms, such as moderate or severe nausea [23, these symptoms are considered sequelae of the 392

37]. Vomiting is not as common with VIMS vertigo spell and not a separate motion sick-
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341 393

342 as with physical motion, partially because ness syndrome. However, clinicians should be 394
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343 affected individuals can close their eyes before aware of differences between the ICVD and 395

344 symptoms become severe. Nausea and related the motion sickness literature, the latter of wh- 396

345 symptoms should be distinguishable by the ich established its symptom definitions prior to 397

346 clinician from primary gastric disorders and the ICVD. The ICVD defines dizziness as dis- 398

347 anxiety. turbed or distorted orientation without a sense 399


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348 4. When due to motion sickness, sweating is gen- of motion [42], whereas in motion sickness 400

349 erally a ‘cold’ sweat that can accompany other research, dizziness is not always defined or has 401

350 autonomic signs and symptoms. The sweating a definition that does not exclude illusions of 402

351 is ‘cold’ because it occurs in the absence of a self-motion. Similarly, the ICVD defines ver- 403
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352 rise in ambient temperature, not because it is tigo as, “a sensation of self-motion when no 404

353 always experienced as cold clamminess. In self-motion is occurring or the sensation of dis- 405

354 fact, it is often preceded by a sudden warm sen- torted self-motion during an otherwise normal 406

355 sation in the face, neck, and/or upper chest. head movement,” [42] whereas in motion sic- 407
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356 Sweating due to motion sickness in a warm kness research, vertigo usually means a loss of 408

357 environment should be distinguishable from orientation with respect to the vertical upright 409

358 ambient thermal causes (e.g., by suddenness [12]. The ICVD definition of internal vertigo 410

359 of onset). Pallor is almost always present in does not explicitly distinguish among illusions 411

360 some combination prior to vomiting [38]. How- of angular motion, linear motion, or tilt. App- 412

361 ever, an individual’s recollection concerning lying the ICVD definition of vertigo to the mot- 413

362 pallor depends upon others to mention it for ion sickness literature, vertigo certainly can be 414

363 the individual to observe it (e.g., in a mirror). induced by motion stimuli which elicit motion 415

364 Therefore, a recollection of pallor should be sickness. The most widely used laboratory 416
6 Y.-H. Cha et al. / Motion sickness diagnostic criteria

417 protocol for the controlled elicitation of se- should be distinguishable from visual overwork 469

418 vere motion sickness (Coriolis cross-coupling or ocular/visual disorders. Blurred vision may 470

419 during constant velocity rotation in the dark) also accompany vertigo, and not always imply 471

420 repeatedly elicits a temporary illusion of dis- ocular dysfunction, however. 472

421 torted self-tilt displacement (and an even gre- 8. Symptoms that start immediately with move- 473

422 ater illusion of self-velocity) during otherwise ment or are maximal at the onset of motion 474

423 normal head movements. Similarly, illusions should raise suspicion for a possible disorder 475

424 of velocity and displacement can be caused (vestibular for physical motion, ocular or vis- 476

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425 by high-speed turns, low-frequency horizontal ual-vestibular for visual motion), an anxiety 477

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426 linear oscillation, viewing large optokinetic reaction, or an aversively conditioned response 478

427 fields, decelerating after non-pendular centri- wherein past motion sickness has led to classi- 479

428 fugation, various flight illusions (e.g., leans, cal conditioning to the sight and smell of the 480

429 somatogravic, G-excess), and terrestrial rea- situation. Strong stimuli in very susceptible 481

430 daptation following spaceflight, most of which individuals may induce symptoms with very lit- 482

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431 can cause motion sickness [41, 43]. For these tle temporal delay. Continued exposure within 483

432 reasons, it is best for clinicians not to assume the individual’s adaptive capacity may also lead 484

433 that a report of frank vertigo is evidence against to habituation and eventual reduction of sick- 485

434 motion sickness having occurred in a person ness. 486

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435 without vestibular pathology. 9. Although some symptoms of motion sickness 487

436 Visually induced dizziness (VID) is recognized or VIMS may persist after termination of the 488

437 as a sense of spatial disorientation caused by stimulus, the onset of sickness symptoms must 489

438 moving or visually complex stimuli and is time- occur during the motion stimulus and not begin 490

439 locked to the stimulus, ie. the onset is imm- exclusively after the stimulus has ended. This 491
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440 ediate with the onset of the visual stimulus. distinguishes motion sickness from mal de 492

441 Dizziness in VIMS is phenomenologically débarquement syndrome, which only begins 493

442 indistinguishable from VID, but the onset will once the motion has ended and lasts for at least 494

443 often be delayed and build in intensity with 48-hours [46]. 495

444 continued exposure. While whole-field motion 10. Motion sickness and VIMS may co-occur and 496

is known to readily elicit an illusion of self- symptom severity may be exacerbated by the
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445 497

446 motion (called vection), this illusion is neither presence of ocular motility disorders, visual- 498
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447 necessary nor sufficient for VIMS to occur [17]. vestibular disorders, or vestibular disorders 499

448 Nevertheless, a large field moving in the roll such as vestibular migraine, vestibular neuri- 500

449 (x-axis) of the head can cause a compelling sen- tis, or persistent postural perceptual dizziness. 501

450 sation of self-motion consistent with vection In these situations, both a diagnosis of motion 502

451 [44]. sickness or VIMS and the contributing disorder 503


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452 7. Greater susceptibility to motion sickness and should be made. 504

453 VIMS occurs in individuals with migraine or


454 vestibular migraine (See section 4.5.1) but hea- 3.2. Motion sickness disorder and visually 505
455 daches triggered by motion are not necessarily induced motion sickness disorder 506
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456 migraine headaches [45]. Though motion sick-


457 ness and VIMS symptoms typically resolve Motion sickness disorder (MSD) is diagnosed 507
458 quickly after the motion stops, headache can when the sickness inducing stimulus is physical 508
459 persist until specifically treated. Headache may motion; visually induced motion sickness disorder
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509
460 be more common and occur more frequently (VIMSD) is diagnosed when the stimulus is visual 510
461 without nausea in VIMS than in motion sick- motion. MSD or VIMSD is diagnosed when Criteria 511
462 ness caused by physical motion. A secondary A through E are met: 512
463 symptom, head fullness, is relevant as well,
464 since it is a similar symptom that has emerged A. At least five episodes of motion sickness/VIMS 513

465 frequently in simulator or cybersickness stud- triggered by the same or similar motion 514

466 ies. Eyestrain/discomfort, difficulty focusing, stimuli1,2,3 515

467 and visual blurring are particularly common sy- B. Sign(s)/Symptom(s) are reliably triggered by 516

468 mptoms of VIMS [7, 8]. Eye/visual symptoms the same or similar motion stimuli4 517
Y.-H. Cha et al. / Motion sickness diagnostic criteria 7

518 C. Sign(s)/Symptom(s) severity does (do) not sig- susceptibility, aversive conditioning, and the 568

519 nificantly decrease after repeated exposure to individual’s ability to adapt. The repeated trig- 569

520 the same or similar motion stimuli5 gering of sickness to the same stimulus signifies 570

521 D. Sign(s)/Symptom(s) lead to one or more of the an inability to habituate and is a core feature 571

522 following behavioral or emotional responses6 of MSD and VIMSD. An exception is made 572

523 a. Activity modification to abort sickness for stimuli that are extremely severe and infre- 573

524 sign(s)/symptom(s) quent such as exposure to parabolic flight or 574

525 b. Avoidance of the motion stimulus that trig- very rough sea conditions. 575

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526 gers sickness 6. The usual behavioral response to motion sick- 576

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527 c. Aversive anticipatory emotions prior to ness or VIMS is to avoid the sickness-inducing 577

528 exposure to the motion stimulus motion stimulus or to shorten the duration of 578

529 E. Sign(s)/Symptom(s) are not better accounted exposure, when possible. When neither is pos- 579

530 for by another disease or disorder7 sible, negative anticipatory emotions or con- 580

ditioned aversive responses (e.g., anticipatory 581


COMMENTS:

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531
nausea) may occur prior to exposure to the 582

532 1. Probable MSD/VIMSD can be diagnosed if two motion stimulus. 583

533 to four episodes have occurred. 7. An individual may be diagnosed with MSD, 584

534 2. On a population level and in the absence of cer- VIMSD, or both. 585

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535 tain disorders that impact vestibular function
536 (see Section 4.5) motion sickness susceptibility 3.3. Motion sickness susceptibility and severity 586

537 typically peaks during youth and adolescence


538 and declines with age. Defining whether the Intense interest in motion sickness and VIMS in the 587

539 symptoms refer to the ≤ 12-year range or the last century has led to the development of a number of 588
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540 > 12-year range will help in accurate commu- severity and susceptibility scales. Several scales used 589

541 nication of current status and in determination for research purposes are presented, with common 590

542 of prognostic variables. Based on a simplified elements listed to show the overlap in queried symp- 591

543 scoring system of the MSSQ, the Pearson cor- toms (per Criteria 3.1 A) (Table 1 for multi-symptom 592

544 relation between recollected childhood (Part A) checklists of severity state [12, 31–33] [40], Table 2 593

and adult motion sickness susceptibility (Part for single-answer severity state questionnaires [49,
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545 594

546 B) is r = 0.65 [47, 48]. 50] [51–53] and Table 3 for retrospective scales for 595
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trait susceptibility [47, 48, 54]. 596


547 NOTES:
The subcommittee recommends that each scale be 597

548 3. Susceptibility to motion sickness or VIMS from used based on its specific advantages to the research 598

549 one type of stimulus may not predict reactions question or clinical application, e.g. the Motion Sick- 599

550 to other types of stimuli. Therefore, motion ness Susceptibility Questionnaire (MSSQ-Short) 600
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551 sickness and VIMS to each motion stimulus form to retrospectively estimate general motion sick- 601

552 (e.g., airplanes, automobiles, boats, virtual real- ness trait susceptibility [48], the first 16 items of the 602

553 ity systems, simulators) should be considered Simulator Susceptibility Questionnaire (SSQ) for 603

554 separately (see Notes 1&2, Section 3.1) estimating state VIMS, and the full list of 28 SSQ/ 604
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555 4. The induction of motion sickness and VIMS can MSQ symptoms for estimating state motion sickness 605

556 be specific to a particular transportation situa- [12]. 606

557 tion, e.g., the individual may only feel sick on While motion sickness can be induced in nearly 607

558 small boats but not large ships, smaller propel- all people with a sufficiently strong stimulus, there 608
Un

559 lor aircraft but not large jetliners, etc. Similarly, are individuals at the extremes of the population dis- 609

560 the induction of VIMS may be specific to a tribution of susceptibility. The distribution curve of 610

561 particular head-mounted virtual reality display, recollections of past susceptibility is linear up to 611

562 simulator, or viewing screen. about the 75Th percentile of susceptibility and flattens 612

563 5. Susceptibility to motion sickness and VIMS out on the high end of scores, e.g., on the MSSQ-Short 613

564 usually declines with repeated exposures, with form, out of a total possible score of 54, a score of 614

565 the rate of adaptation being dependent upon 11 = 50th percentile, 19 = 75th percentile, 27 = 90th 615

566 many factors including the strength or pred- percentile, and 31 = 95th percentile, indicating that 616

567 ictability of the initial stimulus, inherent only a small proportion of people are severely 617
8
Table 1
Multi-Symptom Checklist Motion Sickness Severity Questionnaires
MAIN MULTISYMPTOM CHECKLISTS
Known as Pensacola Diagnostic Index/Pensacola Simulator Sickness Questionnaire/ Motion Sickness Assessment
Diagnostic Criteria/Modified Pensacola Motion Sickness Questionnaire [12] Questionnaire [33]
Diagnostic Criteria [31, 32, 40]
Shorthand PDI/PDC/MPDC SSQ/MSQ MSAQ
Year 1968/1970/2014 1993 2001
Main Stimuli Initially validated during: rotation room (free SSQ: initially validated in stationary

Un
Studied movement, Dial Test, automated Coriolis and moving flight simulators
cross-coupling), Active/voluntary
Coriolis cross-coupling

Y.-H. Cha et al. / Motion sickness diagnostic criteria


co
Also used in: low-frequency oscillation, z-axis Also used in: virtual reality, optokinetic drums, etc. Initially validated during: optokinetic drum;
recumbant rotation, simulators, spaceflight, SSQ/MSQ: developed mainly for sea sickness; Also used in Coriolis cross-coupling,
parabolic flight, optokinetic drums, Also used in various lab motions, spaceflight, etc driving simulator, different vessels at sea,

rre
virtual reality, etc. parabolic flight, virtual reality, etc.
Severity Level for Most symptoms originally scored none- None-slight-moderate-severe 1–9 (1 = not at all, 9 = severely)
Each Symptom minimal-minor-major.

cte
Multisymptom No formal subfactors, but the following Oculomotor (O) Gastrointestinal (G)
Cluster Names symptoms are grouped as one severity Disorientation (D) Central (C)
continuum in original PDI: epigastric Nausea (N) Peripheral (P)
awareness/discomfort, minimal, moderate,

Symptoms Queried

Nausea,
Gastrointestinal
major nausea, vomiting/retching

Nausea
d Below are 16 SSQ symptoms + 12

Au
more comprising the full SSQ/MSQ
Nausea (N,D) Nausea (G)
Queasy (G)
Distburbance Vomiting/Retching

Epigastric awareness; Epigastric discomfort tho


Vomiting (on full MSQ)

Stomach awareness (N) (but defined


As if may vomit (G)
Sick to stomach (G)

rP
(assessed separately but neither counted as discomfort short of nausea)
towards severity score in original PDI) Decreased/Increased appetite (two items on
full MSQ)

roo
Burping (N)
Desite to move bowels (on full MSQ)
Increased Salivation Increased salivation (N)
Decreased salivation (on full MSQ)

f
Thermoregulatory Cold sweating Sweating (N) Sweaty (P)
Disruption Clammy/Cold sweat (P)
Flushing/warmth Hot/warm (P)
Pallor
(Continued)
Y.-H. Cha et al. / Motion sickness diagnostic criteria 9

Uneasy (S) (under Sopite cluster but dictionary


susceptible to motion sickness, i.e. 90% of people 618

score 0–27 while 10% of people score 28–54 on the 619

defines similarly to general discomfort)


MSSQ scale [47]. Norms may be different depending 620

on the demographic traits of the population sampled, 621

which should be considered when working with non- 622

representative populations [55, 56]. 623

Though highly susceptible people tend to develop 624


Annoyed/irritated (S)

motion sickness to more than one kind of stimu- 625

f
Tired/fatigued (S)

lus, susceptibility to motion sickness in individuals

Lightheaded (C)
626

roo
of normal susceptibility is not a strong predictor of
Spinning (C)

Faintlike (C)
627
Drowsy (S)

Dizzy (C)

susceptibility to VIMS. Prediction could be partially 628

limited by large individual variability in symptom 629

type and progression [56]. Nausea and vomiting 630

are typically less common in VIMS, whereas ocu- 631

rP
lar motor issues (e.g., eyestrain, blurred vision) and 632

headache are more common in VIMS than in motion 633

sickness. Additionally, older adults are more suscep- 634

tible to VIMS but not to motion sickness than younger 635

tho
adults [7, 17, 57].
Visual illusions of movement (when not in

636

The frequency and severity of motion sickness 637

events can be mitigated by reducing exposure to 638


device or vehicle) (on full MSQ)

sickness-inducing stimuli (e.g., via avoidance or ce- 639


Difficulty concentrating (N,O)

eyes open/closed) Vertigo (D)

ssation), modifying behavior during exposure to 640


Drowsiness (on full MSQ)

Depression (on full MSQ)

General discomfort (N,O)


Dizziness (D) (two items:
Confusion (on full MSQ)

Au
Boredom (on full MSQ)

reduce the stimulus impact (e.g., limiting head move- 641


Difficulty focusing (O)
Blurred vision (O,D)
Fullness of head (D)

ments), taking medications prior to exposure, maxi- 642

mizing helpful Earth-referenced cues (e.g., via view 643


Headache (O)

of the outside world), or by engaging in measured


Eystrain (O)

644
Fatigue (O)

amounts of motion exposure in order to induce habit- 645

uation. Interventions which have been tried include


d

646

habituation exercises (eye-head motion and repeated 647


cte

exposure) [23], pharmacologic pretreatments (anti- 648

muscarinic, anti-histaminic, anti-cholinergic medica- 649

tions) [58], non-pharmacological treatments (music, 650

smells) [59], and behavioral techniques (breathing 651

exercises, meditation) [60]. It is common to hear 652


rre

about ginger or acupressure as motion sickness coun-


Dizziness (two items for eyes

653

termeasures, but the empirical evidence for these in- 654

terventions is mixed [61–65]. The effectiveness of 655

these methods varies widely, with the greatest benefit 656


co

derived from adaptation, medications, and modify- 657


open/closed)
Drowsiness

ing behavior during exposure. Habituation is often 658


Headache

stimulus-specific, however, and may not generalize 659

across motion situations. 660


Un

3.4. MSD and VIMSD impact 661

Motion sickness that is mild, easily avoidable, or 662

has no functional impact is common among indi- 663

viduals with normal vestibular function and should 664


Alterations

Headache/
in Arousal

Dizziness/

not be considered a disorder. However, motion sick- 665


General
Vertigo

Ocular

ness susceptibility that affects activities of daily 666

living such as meeting basic transportation needs or 667


10
Table 2
Single Answer Motion Sickness Severity Scales
MAIN SINGLE-ANSWER QUESTIONNAIRES
Known as Illness Rating Misery Scale Fast Motion
[49, 50] [51,52] Sickness Scale [53]
Shorthand IR MISC FMS
Year 1992/2004 2005/2011 2011
Main Stimuli Initially validated in:Low frequency Initially validated in: Motion Initially validated in: passive visual
Studied motion/cross-coupled motion/Car; simulator/head mounted display; simulations of driving and
Several other stimuli since Several other stimuli since rollercoasters; Several other stimuli since
Severity Levels 0 = no symptoms 0 = no problems 0 = no sickness
1 = any symptoms, however slight∗ 1 = uneasiness 20 = frank sickness

Un 2 = mild symptoms∗
3 = mild nausea
4 = mild to moderate nausea
2 = vague∗∗
3 = slight∗∗
4 = fairly∗∗

Y.-H. Cha et al. / Motion sickness diagnostic criteria


co
5 = moderate nausea but can continue 5 = severe∗∗
6 = moderate nausea and want to stop 6 = slight nausea

E.g., stomach awareness; 7 = fair(ly) nausea

rre
other unspecified symptoms 8 = severe nausea
9 = retching
10 = vomiting

cte
∗∗
Individual Symptoms Dizziness, warmth, headache, No individual symptoms tracked,
Implicitly Contributing stomach awareness, sweating, but subjects instructed to focus on
to Overall Score other unspecified symptoms nausea, stomach problems,

d
and general discomfort
While ignoring other symptoms
(e.g., fatigue, dizziness, oculomotor)
Nausea,
Gastrointestinal
Distburbance
Nausea

Au Nausea
Retching
Vomiting
(Nausea)

tho
Salivation (Frank sickness)
(Stomach problems)
Stomach awareness Stomach awareness
Burping
Thermoregulatory
Disruption
Alterations rP Sweating
Warm

roo
in Arousal Tiredness
Yawning

Dizziness/Vertigo Dizziness

Headache/Ocular

Other
∗ NOTE:
Headache
Blurred vision

Uneasiness
f
General discomfort
Golding & Kerguelen used a 1–7 scale, Griffin et al. used a 0–6 scale.
Y.-H. Cha et al. / Motion sickness diagnostic criteria 11

Table 3
Retrospective Motion Sickness Trait Susceptibility Scales
Known as Pensacola Motion History Motion Sickness
Questionnaire [54] Susceptibility Questionnaire
(Long/Short)[47, 48]
Shorthand MHQ MSSQ; MSSQ-S;
(54 items; later shortened to 18)
Year 1990 1998/2006
Motion type queried Physical motion Physical motion

f
Components Part A Child (<12yrs)

roo
Part B Adult (last 10 yrs)
Queries incidence of 12 symptoms in 14 situations. Queries episodes of feeling sick or
The 12 symptoms include: vomiting, nausea, nauseated during each of 9 situations
stomach awareness, increased salivation, (Long version also queries
dizziness, drowsiness, sweating, pallor, vertigo, amount of exposure)
awareness of breathing, headache, or other.

rP
668 fulfilling obligations to family, employers, or social 25% in young adults; it is a frequent problem in 14% 702

669 contacts can have physical and mental health con- of adults younger than 30 years old and 7% of adults 703

670 sequences. Even in otherwise healthy individuals, 61 years old or older [72–74]. The prevalence of 704

671 motion sickness can reduce work or school produc- VIMS ranges widely depending on the stimulus type 705

tho
672 tivity and decrease social engagement through direct and the visual content, with rates varying from 1% 706

673 effects from being ill, avoidance of sickness-inducing [75] to 60% [76] to 80–95% [77, 78]. 707

674 activities, or sedation induced by motion or by phar-


675 macological motion sickness remedies [27, 66, 67]. 4.2. Demographics 708

676 Nausea, lethargy, and drowsiness can shift attention


Au
677 away from critical tasks, while vomiting can lead to 4.2.1. Age 709

678 dehydration or aspiration [39, 68]. Susceptibility to motion sickness changes with 710

679 Formal disability scales can be paired with existing age. Infants are resistant to motion sickness until 711

680 motion sickness or VIMS scales to quantify disabil- about age 2, at which point motion sickness sus- 712

681 ity due to MSD or VIMSD. As an example, the ceptibility rises between the ages of 7–12 years and 713

declines thereafter and throughout adulthood [19,


d

682 Sheehan Disability Scale quantifies impact on work, 714

683 family, or social function on a 10-point scale along 72, 79]. Susceptibility gradually continues to decline 715

with age but may increase in a small proportion


cte

684 with a query of loss of work time or productivity 716

685 due to symptoms [69]. Alternatively, a basic impact of individuals [27]. An increase in susceptibility to 717

686 assessment that queries whether work, social, fam- VIMS as a factor of age has been well-documented, 718

687 ily, or travel difficulties are experienced (Yes or No) with older adults reporting more VIMS than younger 719

688 due to symptoms can be used as a quick assessment, adults [55, 80, 81]. Prevalence estimates should con- 720
rre

689 e.g., the Social Work Impact of Dizziness short form sider that people might self-restrict their behavior and 721

690 adapted for motion sickness [70, 71]. avoid situations that provoke motion sickness if they 722

691 Even if motion sickness or VIMS does not cre- are aware of their elevated susceptibility. 723

692 ate a disability, it should be recognized as a clinical


co

693 entity that deserves medical attention. In most cases 4.2.2. Sex 724

694 , education, exposure minimization, avoidance of The evidence of sex differences in motion sickness 725

695 exacerbating behaviors, short-term use of anti-motion is mixed. Only 50% of the studies in the litera- 726

696 sickness medications, or simple habituation exercises ture have found women to be significantly more 727
Un

697 beforehand may be employed to reduce morbidity. susceptible to motion sickness [17], with estimates 728

varying among studies depending on stimulus type, 729

endpoint studied, age, ethnicity, and hormonal status 730

698 4. Motion sickness clinical features [47, 74, 82–86]. Sex differences in motion sickness 731

are seen more frequently in survey studies than in 732

699 4.1. Prevalence controlled laboratory studies and more commonly 733

in older studies than recent ones [17]. Even among 734

700 The prevalence of motion sickness in childhood authors positing a sex difference, the estimated effect 735

701 has been estimated at 35–43% prior to puberty and of sex is only about one-third that of age [87, 88]. 736
12 Y.-H. Cha et al. / Motion sickness diagnostic criteria

737 Secondary hormonal factors such as the use of oral UBE2E2, CBLN4, MUTED, LINGO2 and CPNE4 786

738 contraceptives, menstruation, pregnancy, and cortisol [74]. A genetic risk score using the number of risk 787

739 levels correlate with motion sickness susceptibility alleles found on each individual for these 35 vari- 788

740 in women, which further complicates the association ants could be used to anticipate motion sickness 789

741 [87, 89, 90]. susceptibility. These genes involve a wide variety of 790

742 Sex differences in VIMS have been observed in functions such as brain, eye, and ear development and 791

743 some studies [81, 91–93], but it remains unclear even insulin resistance. Some of these loci overlap 792

744 whether such observations are due to women being with genes in individuals who experience dizziness, 793

f
745 more open about reporting than men, are better at post-operative nausea and vomiting, altitude sick- 794

roo
746 introspecting than men, or have less experienced ness, morning sickness, indigestion to dairy, and 795

747 with motion than men, among several other con- headache after red wine [74]. 796

748 founding reasons [17, 92]. A meta-analysis failed


749 to detect any sex differences in VIMS due to vir- 4.4. Other modifying factors 797

750 tual reality (VR) usage [94] while another study [95]

rP
751 concluded that VIMS sex differences in VR may be Other modifying factors may include baseline 798

752 accounted for by a non-sex-specific variable such as autonomic tone, glucose levels, and aerobic fitness 799

753 difficulty in fitting the VR properly to people with [100–102]. It is difficult to predict how these nu- 800

754 smaller interpupillary distance. A variety of other fac- merous factors, in combination, ultimately impact 801

tho
755 tors unrelated to sex can affect occurrence of VIMS, susceptibility in an individual, however. 802

756 including technical manipulations such as the size of


757 the field-of-view, video game experience, and passive 4.5. Associated syndromes 803

758 restraints [96–98]. Overall, the case is weak for dif-


759 ferences in VIMS that are specific to biological male 4.5.1. Migraine 804
Au
760 vs. female birth category. Symptoms of migraine and motion sickness ove- 805

rlap in many respects, e.g., nausea, stomach aware- 806

761 4.2.3. Race and ethnicity ness, and headache [84, 103]. Motion sickness is 807

762 Studies that assessed motion sickness susceptibil- self-reported in at least 50% of migraine headache 808

763 ity by questionnaire, rotation of the body with head sufferers with motion sickness in childhood correlat- 809

pitching, and exposure to optokinetic drums have ing with eventual development of migraine headaches
d

764 810

765 reported heightened susceptibility in people of Asian in adolescence and adulthood [47, 104, 105]. These 811
cte

766 descent compared to European or African descent associations suggest that neural pathways for nausea 812

767 [82, 99]. These differences persist in American-born and emesis are particularly sensitive in individuals 813

768 children of Asian parents, supporting at least a partial with migraine [47]. Scalp tenderness and nausea dur- 814

769 heritable component to motion sickness susceptibil- ing optokinetic stimulation increase more for those 815

770 ity[99]. who experience migraine than for those who do not 816
rre

771 Further controlled studies of the ethnic, racial, or [106]. Motion sickness induced by OVAR is espe- 817

772 cultural components to motion sickness are needed. cially intense in individuals with migraine [45]. This 818

773 Generalizations concerning these features which type of motion sickness may be blunted by rizatrip- 819

774 could influence decisions about patient care or occu- tan, a migraine abortive medication [107, 108]. In 820
co

775 pational status should be treated with caution. contrast, VIMS does not appear to be mitigated by 821

pre-treatment with rizatriptan [109]. Individuals with 822

776 4.3. Genetic migraine headaches experience both motion sickness 823

and VIMS to a higher degree than those without 824


Un

777 Heritability for motion sickness (in women) shows migraine, but the correlation between motion sick- 825

778 a 0.69 concordance in monozygotic twins and 0.44 ness and VIMS in this group is weak [110]. 826

779 concordance in dizygotic twins for childhood motion


780 sickness, yielding a heritability estimate of 70% [72]. 4.5.2. Structural vestibular disorders 827

781 A large genome-wide association study involving Loss of peripheral vestibular function significantly 828

782 80,494 individuals with carsickness found 35 sin- raises the threshold for motion sickness but the role 829

783 gle nucleotide variants at genome-wide significant of a functioning vestibulum for VIMS is less clear 830

784 levels. The top ten genes involved in these regions [45, 111–113]. Congruently, patients with chronic 831

785 included: PVRL3, GPD2, ACO1, AUTS2, GPR26, stable vestibular loss (unilateral and bilateral) report 832
Y.-H. Cha et al. / Motion sickness diagnostic criteria 13

833 less motion sickness on clinical motion sickness rat- not be the relevant marker of motion sickness suscep- 882

834 ings than healthy controls. In comparison, patients tibility, but rather the ability to modify the VOR in 883

835 with benign paroxysmal positional vertigo show a response to varying motion sickness-inducing stimuli 884

836 non-significant difference in motion sickness sus- [27, 88]. The relationship between motion sickness 885

837 ceptibility [79]. Patients with vestibular neuritis can susceptibility and adaptability of vestibular responses 886

838 experience either an increase or a decrease in motion has also been supported by lower cervical vestibular 887

839 sickness susceptibility after the onset of their disor- evoked myogenic potential (VEMPS) thresholds cor- 888

840 der, with increased susceptibility in uncompensated relating with the ability to habituate to seasickness; 889

f
841 cases [45, 57]. Two studies have shown that indi- this may be attributable to the wider potential range 890

roo
842 viduals with Ménière’s disease are more susceptible of adaptive responses to motion stimuli with lower 891

843 to motion sickness than healthy controls but are not VEMP thresholds [122]. 892

844 as susceptible as those with migraine or vestibular


845 migraine [114, 115]. There is no correlation between
846 the degree of caloric asymmetry in vestibular patients 6. Differential diagnosis 893

rP
847 and scores on a clinical motion sickness question-
848 naire. In contrast, patients with vestibular disorders Because motion sickness susceptibility in a healthy 894

849 without vestibular loss report higher degrees of mot- person generally declines with age, an adult present- 895

850 ion sickness than controls [45, 104]. About 10-min- ing with increasing susceptibility to motion should be 896

tho
851 utes of laboratory motion exposure has been shown evaluated for underlying causes of a lowered thresh- 897

852 to distinguish the susceptibility of individuals with old for motion sickness. This evaluation may include 898

853 different vestibular disorders (vestibular neuritis, an assessment for vestibular disorders, migraine, 899

854 bilateral vestibulopathy, vestibular migraine) [45]. endocrine abnormalities, ocular misalignment, and 900

other central nervous system disorders. Head motion- 901


Au
induced discomfort (when not undergoing passive 902

855 5. Motion sickness laboratory examinations whole-body motion) should be suspected as being 903

secondary to an uncompensated vestibular asymme- 904

856 Motion sickness may be induced in laboratory try and evaluated with vestibular laboratory testing, 905

857 settings with approximately 38% of the variabil- unless such discomfort is directly related to the after- 906

ity in motion sickness in operational settings being effects of prolonged adaptation to motion (e.g., return
d

858 907

859 explained by an individual’s response to provoca- to land after a voyage at sea). Similarly, abrupt 908
cte

860 tive laboratory motion tests [54]. Most of these changes in VIMS should prompt careful evaluations 909

861 established motion sickness tests are not used for for ocular and ocular motility problems. Clinicians 910

862 clinical diagnosis, however. Correlations between should be aware that head motion during certain 911

863 the MSSQ and laboratory-induced nausea by cross- types of uncompensated vestibular pathology or by 912

864 coupled stimulation have been reported to be between healthy persons during challenging motions or within 913
rre

865 0.14 and 0.58, with generally higher correlations seen unusual force environments (such as space) can each 914

866 for vertical translational oscillations than horizontal elicit similar symptoms of nausea, headache, dizzi- 915

867 oscillations [47]. Of the translational planes, motion ness, vertigo, oscillopsia, or visual blurring, so these 916

868 through the body-referenced X- or Y-axes (fore-aft or symptoms cannot be assumed to definitively dif- 917
co

869 side-to-side motion when upright, respectively) are ferentiate between vestibular pathology and motion 918

870 more provocative than the body-referenced Z-axis, sickness without further inquiry concerning when the 919

871 (up-down) but motion direction with respect to the symptoms appeared (e.g., relative to the last motion 920

872 gravity vector (e.g. vertical versus horizontal) is a experience), under what conditions they appeared 921
Un

873 less important factor [116]. (e.g., the type and duration of the motion experi- 922

874 An area of controversy is whether a smaller phase ence), and what additional symptoms were present 923

875 lead of the vestibulo-ocular reflex (VOR), which [43]. Finally, while a motion sickness disorder would 924

876 indicates enhanced velocity storage, is related patho- be more strongly suspected in a younger person scor- 925

877 physiologically to motion sickness susceptibility, as ing high on the MSSQ or a VIMS disorder in an 926

878 found in some laboratories [116–120] but not others older individual scoring high on the SSQ, individual 927

879 [88, 107]. The mixed findings may relate to the degree variability in motion sickness and VIMS susceptibil- 928

880 of habituation to the motion stimulus [121]. It has ity is high, so clinicians should be cautious not to 929

881 been proposed that the absolute value of the VOR may over-generalize from demographical findings.
14 Y.-H. Cha et al. / Motion sickness diagnostic criteria

930 7. Future directions protection under this title is not available for any work 977

of the U.S. Government.’ 978

931 The presentation of these criteria for motion si-


932 ckness acknowledges that there are still critical infor-
933 mation gaps to be filled in order to determine a clear
934 demarcation between motion sickness and VIMS as References 979

935 normal human responses to motion stimuli versus


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963 Acknowledgements and disclaimers a rotary visual field on susceptibles and nonsusceptibles 1018
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451–453. 1020
co

964 The working meetings for the International Cl- [14] R. Kennedy, G. Allgood, B. Van Hoy and M. Lilienthal, 1021

965 assification of Vestibular Disorders (ICVD) are finan- Motion sickness symptoms and postural changes follow- 1022

966 cially supported by the International Bárány Society ing flights in motion-based flight trainers, J Low Freq 1023
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Un

1025
968 association for neurological research. We thank zley and M.E. McCauley, Simulator sickness in U.S. Navy 1026

969 members of the Bárány Society for reviewing the flight simulators, Aviat Space Envir Md 60 (1988), 10–16. 1027

970 manuscript prior to publication. The views in this [16] D.R. Baltzley, R.S. Kennedy, K.S. Berbaum, M.G. Lilien- 1028
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973 Navy, Department of Defense, nor the U.S. Govern- [17] B.D. Lawson, Motion sickness symptomatology and 1032
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974 ment. This work was assisted by an employee of the
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