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Introduction: Persistent postural-perceptual dizziness (PPPD) and vestibular migraine (VM) share symptoms of visual vertigo and motion sickness that can be confusing for clinicians to distinguish. We compare the severity of these symptoms and dynamic subjective visual vertical (dSVV) in these two common vestibular conditions., Method: Twenty-nine patients with PPPD, 37 with VM, and 29 controls were surveyed for subjective symptoms using the visual vertigo analogue scale (VVAS) and motion sickness susceptibility questionnaire during childhood (MSA) and the past 10 years (MSB). dSVV is a measure of visual dependence measures perception of verticality against a rotating background (5 deg./s)., Results: VVAS revealed contextual differences for dizziness between those with PPPD and VM. Ratings of visual vertigo were most severe in PPPD, less in VM, and mild in controls (VVAS PPPD 27.1, VM 11.2, control 4.6, p < 0.001). MSA was more severe in VM than in PPPD or control (12.8 vs 7.6 vs 8.5, p = 0.01). MSB was more severe in VM than controls (MSB score 12.9 VS 8.1 p = 0.009) but was not different than PPPD (MSB score 10.0, p = 0.10). dSVV alignment was similar among the three groups (p = 0.83). Both VM and PPPD groups had greater simulator sickness than controls after completing the dSVV., Conclusions: Patients with PPPD report more visual vertigo than those with VM, but a history of motion sickness as a child is more common in VM. Additionally, the environmental context that induces visual vertigo is different between PPPD and VM., Competing Interests: Declaration of competing interest None of the authors have competing interests., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Objective: To find out if motion sickness susceptibility (MSS) of vestibular migraine (VM) patients and migraine only (MO) patients can be reliably detected with a single simple question: "Can you read while travelling in a car without getting motion sick?"., Method: Ninety-two definite VM and 58 MO patients and 74 healthy control (HC) subjects were asked about their MSS and about being able to read while riding in a car without becoming motion sick. A Motion Sickness Susceptibility Questionnaire (MSSQ-Short) including childhood (MSA), adulthood (MSB) and total (MST) parts was also administered to all participants. ROC curves of MSSQ-Short were prepared for "not being able to read in a car" as the gold standard., Results: Mean MSA scores were significantly higher in both VM and MO patients than in HCs (p < 0.001), but their scores were not significantly different (p = 0.171). Mean MSB and MST scores were significantly higher in VM than in MO patients (p < 0.001) and both VM and MO patients had significantly higher scores than HCs (p < 0.001). MSA scores were significantly higher than MSB scores in MO patients (p < 0.001). All sections of the questionnaire were associated with high area-under-curve values for MSS detected by the question about being able to read in a car without becoming motion sick., Conclusion: We propose that all migraine patients could have the same level of MSS in childhood but MO patients are able to compensate over years, but VM patients are not. A quick way to determine MSS is to ask about the ability to read without becoming motion sickness while riding a car., (Copyright © 2023 Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico-Facial. Published by Elsevier España S.L.U. All rights reserved.)

Background: Migraine and vestibular migraine are disorders associated with a heightened motion sensitivity that provoke symptoms of motion-induced nausea and motion sickness. VM affects ∼3% of adults in the USA and affects three-fold more women than men. Triptans (selective serotonin receptor agonists) relieve migraine pain but lack efficacy for vertigo. Murine models of photophobia and allodynia have used injections of calcitonin gene-related peptide (CGRP) or other migraine triggers, such as sodium nitroprusside (SNP), to induce migraine sensitivities in mice to touch and light. Yet, there is limited research on whether these triggers affect motion-induced nausea in mice, and whether migraine blockers can reduce these migraine symptoms. We hypothesized that systemic delivery of CGRP or SNP will increase motion sickness susceptibility and motion-induced nausea in mouse models, and that migraine blockers can block these changes induced by systemically delivered CGRP or SNP., Methods: We investigated two measures of motion sickness assessment [motion sickness index (MSI) scoring and motion-induced thermoregulation] after intraperitoneal injections of either CGRP or SNP in C57BL/6J mice. The drugs olcegepant, sumatriptan and rizatriptan were used to assess the efficacy of migraine blockers., Results: MSI measures were confounded by CGRP's effect on gastric distress. However, analysis of tail vasodilatations as a surrogate for motion-induced nausea was robust for both migraine triggers. Only olcegepant treatment rescued tail vasodilatations., Conclusions: These preclinical findings support the use of small molecule CGRP receptor antagonists for the treatment of motion-induced nausea of migraine, and show that triptan therapeutics are ineffective against motion-induced nausea of migraine. Trial Registration: Not Applicable., Competing Interests: Declaration of conflicting interestsThe authors declare that there are no potential conflicts of interest with respect to the research, authorship and/or publication of this article.

Objective: To investigate the clinical features of patients with definite vestibular migraine (dVM)., Methods: A total of 91 patients with vestibular symptoms accompanied by migraines/migraine-like symptoms were enrolled and diagnosed according to the criteria of the Bárány Society and the International Headache Society. Baseline data were collected. Videonystagmography and immune-related laboratory tests were performed., Results: Among the 91 patients, 62 (68.1%) had dVM (11 men, 51 women). Among dVM patients, migraine occurred earlier than vestibular symptoms in 42 (67.7%) patients. Spontaneous vertigo occurred in 41 (66.1%) patients. Induced vertigo occurred in 21 (33.9%) patients. Motion sickness occurred in 33 (53.2%) patients. Central oculomotor dysfunction was observed in 11 (17.7%) patients. Caloric test revealed unilateral horizontal semicircular canal dysfunction in 12 (19.4%) patients. Severe intolerance during the test occurred in 44 (71.0%) patients with dVM. 12 (19.4%) patients showed abnormal immune-related indicators., Conclusion: dVM is more common in women. The onset of migraine precedes that of vestibular symptoms, which are often accompanied by photophobia and phonophobia. Motion sickness and severe caloric test intolerance can contribute to the diagnosis of dVM. Immunological indicators are abnormal in some patients with dVM, dVM may be secondary or an accompanying disorder, but the causal relationship needs further investigation., Level of Evidence: IV., (Copyright © 2022. Published by Elsevier Editora Ltda.)

Objective: To evaluate demographic and clinical features of vestibular migraine (VM) patients METHODS: Four hundred fifteen patients with VM were evaluated by using a structured questionnaire in addition to clinical examination., Results: The mean age of headache and vertigo onset was 25 years and 39 years, respectively. In 12.3%, benign paroxysmal positional vertigo (BPPV) was detected during the interictal period. Ten percent had hearing loss on audiometry, in 8.7% it was one-sided low-frequency sensory-neural hearing loss below 2000 Hz and the history was typical for Meniere's disease (MD) in addition to VM. Tinnitus was present in 94.4%, aural fullness in 83.4%, nausea in 72.2% and vomiting in 30.5% of patients with VM/MD. The prevalence of these symptoms was higher in patients with VM/MD than in pure VM. Median attack severity determined by visual analog scale measured in centimeters from 0 to 10 was 8 for headache and 7 for vertigo for the whole group. Severe headache was significantly correlated with age of ≤ 43 years (OR: 6.831, 95% CI: [4.10-11.63]; p < 0.001) and severe vertigo was significantly correlated with age ≥ 41 years (OR: 7.073, 95% CI: [4.55-10.98]; p < 0.001). Motion sickness was revealed from past medical history in 51.8%. Family history of migraine was present in 72.5% and the age of onset of both migraine headaches (p = 0.008) and vertigo attacks (p = 0.004) was lower in these patients., Conclusion: Younger patients suffered more severe headache attacks whereas vertigo attack severity was higher in the elderly. BPPV and MD were commonly associated with VM and VM/MD was accompanied by aural and autonomic features more frequently than pure VM. Previous history of motion sickness was detected in more than half of the whole group. Family history of migraine was associated with younger onset of migraine headaches and vertigo attacks., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Background: We assessed frequency of vestibular symptoms in Headache Clinic patients over 10 years., Methods: A descriptive study of 5111 consecutive patients with tension-type headache or migraine, analyzed for dizziness/ vertigo accompanying headache and for a lifetime history of motion-sickness, cyclic vomiting, recurrent abdominal pain or atopy. Migraine patients were re-grouped as those with vestibular symptoms (dizziness/vertigo or motion sickness) and those without and their data then re-analyzed., Results: There were 1880 migraine patients and 3231 tension-type headache patients. Significantly more migraine patients than tension-type headache patients experienced vestibular symptoms (p< 0.0001). The migraine with vestibular symptoms group was significantly younger (p< 0.05) had more aura, more phonophobia with migraine attacks (p< 0.0001). Menstruation and reported sleep problems impacted on headaches. While past history of cyclical vomiting, recurrent abdominal pain or atopy was about twice as common in migraine with aura and it was also more common in migraine with vestibular symptoms than migraine without vestibular symptoms., Conclusions: Vestibular symptoms are common in migraine patients. Migraine with vestibular symptoms might constitute a special group, one more likely to have had cyclic vomiting, recurrent abdominal pain or atopy.

Objective: We wanted to study otolith function by measuring the static subjective visual vertical (SVV) in migraine patients and in controls with and without kinetosis (motion sickness)., Methods and Material: Forty-seven patients with moderately severe migraine and 96 healthy controls were enrolled. Using a questionnaire, persons with kinetosis were identified. The SVV test was performed in a totally dark room. Subjects wore a stiffneck to stabilize the head in an erect position. They were required to adjust an infrared line to the gravitational vertical with a hand-held infrared remote controlled potentiometer., Results: The deviation of SVV in the group of migraine patients was not significantly different from that of controls, regardless of whether an aura was associated. SVV was not significantly influenced by the presence of dizziness/non specific vertigo or kinetosis., Conclusion: Patients with moderately severe migraine under prophylactic medication correctly estimate the visual verticality in the headache-free period. It is suggested that a deviation of SVV in a headache-free migraine patient may not be attributed to his migraine disorder as such regardless whether kinetosis is associated., (Copyright © 2011 Elsevier B.V. All rights reserved.)

The brainstem is a structurally complex region, containing numerous ascending and descending fibres that converge on centres that regulate bodily functions essential to life. Afferent input from the cranial tissues and the special senses is processed, in part, in brainstem nuclei. In addition, brainstem centres modulate the flow of pain messages and other forms of sensory information to higher regions of the brain, and influence the general excitability of these cortical regions. Thus, disruptions in brainstem processing might evoke a complex range of unpleasant symptoms, vegetative changes and neurovascular disturbances and that, together, form attacks of migraine. Migraine is linked with various co-morbid conditions, the most prominent being motion sickness. Symptoms such as nausea, dizziness and headache are common to motion sickness and migraine; moreover, migraine sufferers have a heightened vulnerability to motion sickness. As both maladies involve reflexes that relay in the brainstem, symptoms may share the same neural circuitry. In consequence, subclinical interictal persistence of disturbances in these brainstem pathways could not only increase vulnerability to recurrent attacks of migraine but also increase susceptibility to motion sickness. Mechanisms that mediate symptoms of motion sickness and migraine are explored in this paper. The physiology of motion sickness and migraine is discussed, and neurotransmitters that may be involved in the manifestation of symptoms are reviewed. Recent findings have shed light on the relationship between migraine and motion sickness, and provide insights into the generation of migraine attacks., ((c) 2010. Published by Elsevier Ltd. All rights reserved.)

The mechanisms of vestibular migraine and motion sickness remain unknown. The aims of this study were to determine interictal vestibular dysfunction in migraineurs according to associated dizziness/vertigo and motion sickness, and to find out whether impaired uvulonodular inhibition over the vestibular system underlies the vestibular symptoms and signs by measuring tilt suppression of the vestibulo-ocular reflex (VOR). One hundred and thirty-one patients with migraine [65 with vestibular migraine (MV), 41 with migrainous dizziness (MD), and 25 with migraine only (MO)] and 50 normal controls underwent evaluation of vestibular function. Motion sickness was assessed using the motion sickness susceptibility questionnaire (MSSQ) and subjective scale. Compared with normal controls and MO group, patients with MV/MD showed increased VOR time constant (TC) and greater suppression of the post-rotatory nystagmus with forward head tilt. The mean MSSQ score and subjective scale were highest in MV group, followed by MD, MO, and controls (p = 0.002, p < 0.001). Multiple linear regression model analyses revealed that motion sickness is an independent factor of TC prolongation (p = 0.024). Twenty-eight (21.4%) patients with migraine also showed perverted head shaking nystagmus and 12 (9.2%) had positional nystagmus. In view of the increased tilt suppression of the VOR, we speculate that dysfunction of the nodulus/uvula may not account for the prolonged TCs in MD/MV. Instead, innate hypersensitivity of the vestibular system may be an underlying mechanism of motion sickness and increased TC in MD/MV. The increased tilt suppression may be an adaptive cerebellar mechanism to suppress the hyperactive vestibular system in migraineurs.

The objective of this study was to evaluate, in patients with migraine and healthy volunteers, with and without a history of motion sickness, the degree of discomfort elicited by drifting striped patterns. Eighteen healthy volunteers (HV) and 30 migraine patients participated in the study. Discomfort was greater in migraine patients than in HV, and in individuals with a history of motion sickness than in those without, but the effect of history of migraine was independent of history of motion sickness. Generalized Estimating Equations models for binary correlated data revealed that these differences did not depend on levels of duty cycle, spatial and temporal frequencies. Visual discomfort in migraine patients was associated with worse performance. There was a significant correlation between median degree of discomfort across conditions and number of migraine attacks in the past month. Discomfort to drifting striped patterns may be related to central sensitization in migraine patients.

Background: Limited evidence suggests that rizatriptan given before vestibular stimulation reduces motion sickness in persons with migraine-related dizziness. The present study was designed to test whether rizatriptan is also effective in protecting against visually-induced motion sickness and to test whether rizatriptan blocks the augmentation of motion sickness by head pain., Material and Methods: Using randomized double-blind, placebo-controlled methodology, 10 females, 6 with migrainous vertigo (V+) and four without vertigo (V-) received 10 mg rizatriptan or placebo two hours prior to being stimulated by optokinetic stripes. Visual stimulation was coupled with three pain conditions: no pain (N), thermally-induced hand pain (H) and temple pain (T). Motion sickness and subjective discomfort were measured., Results: Motion sickness was less after pre-treatment with rizatriptan for 4 of 10 subjects and more for 5 of 10 subjects. Augmentation of motion sickness by head pain was seen in 6 of 10 subjects; this effect was blunted by rizatriptan in 4 of these 6 subjects. Subjective discomfort was significantly more noticeable in V+ subjects as compared with V- subjects., Conclusions: These pilot data suggest that rizatriptan does not consistently reduce visually-induced motion sickness in migraineurs. Rizatriptan may diminish motion sickness potentiation by cranial pain.

Motion sickness commonly occurs after exposure to actual motion, such as car or amusement park rides, or virtual motion, such as panoramic movies. Motion sickness symptoms may be disabling, significantly limiting business, travel and leisure activities. Motion sickness occurs in approximately 50% of migraine sufferers. Understanding motion sickness in migraine patients may improve understanding of the physiology of both conditions. Recent literature suggests important relationships between the trigeminal system and vestibular nuclei that may have implications for both motion sickness and migraine. Studies demonstrating an important relationship between serotonin receptors and motion sickness susceptibility in both rodents and humans suggest possible new motion sickness prevention therapies.

Objective: To determine whether susceptibility to motion sickness provoked by unexpected movement is associated with susceptibility to visually induced motion sickness in migraine sufferers., Background: Migraine sufferers are unusually susceptible to motion sickness, but the mechanism of this susceptibility is not well understood. Possibilities include vestibular dysfunction secondary to vasomotor disturbances during migraine attacks, hyperexcitability of brainstem circuits that produce symptoms of motion sickness and migraine, and heightened susceptibility to visual illusions of movement., Method: A motion sickness susceptibility questionnaire that listed common triggers of motion sickness was filled out by 42 migraine sufferers and 39 headache-free controls of similar age and sex distribution to migraine sufferers., Results: A greater proportion of migraine sufferers than controls reported that traveling in cars and buses, reading in the car, using playground equipment, watching wide-screen movies and movement simulators, induced motion sickness. However, visually induced motion sickness appeared to be independent of motion sickness to most movement-related stimuli in migraine sufferers., Conclusions: The lack of association between susceptibility to movement-induced and visually induced motion sickness implies that more than one mechanism increases susceptibility to motion sickness in migraine sufferers.

To determine whether motion sickness induced by optokinetic stimulation would trigger migraine-like attacks, 27 migraine sufferers and 23 controls attended the laboratory up to three times at intervals of at least 3 weeks. On one occasion subjects experienced up to 15 min of optokinetic stimulation, followed by three 30-s applications of ice to the temple at 4-min intervals. On another occasion, the ice applications preceded and accompanied optokinetic stimulation. On a third occasion, one hand was immersed in ice water for 30 s, three times at 4-min intervals before and during optokinetic stimulation. Subjects recorded headache activity in a diary over the course of the study. None of the controls experienced a migraine-like attack at any stage of the experiment. In migraine sufferers, the incidence of migraine-like attacks was greater than the expected daily incidence of 8% after sessions that involved painful stimulation of the temple during or after optokinetic stimulation (44% and 28% of the group, respectively) (P<0.001). In contrast, migraine-like attacks developed in only 13% of migraine sufferers after the session that involved immersing the hand in ice water during optokinetic stimulation (not significant). The development of nausea and headache during optokinetic stimulation increased the likelihood of migraine-like attacks afterwards. These findings indicate that motion sickness and head pain increase susceptibility to migrainous attacks in migraine sufferers, and suggest that the symptoms of migraine build upon each other in a vicious circle. Thus, targeting multiple symptoms should be more effective than targeting individual symptoms, both for preventing and treating attacks of migraine.

Both migraine and vertigo are common complaints. Although they may coincide by chance, there is growing evidence for a clinical entity of recurrent vestibular symptoms related to migraine. This syndrome implies a possible causal relationship although the pathophysiology of migraine-related vertigo has not been fully elucidated. A migrainous aseptic inflammation is thought to create a central sensitivity that spreads from the trigeminal to the vestibular system. Diagnostic criteria for migraine-related vertigo are proposed. Treatment is based on anti-vertiginous drugs for acute interventions and prophylactic measures as are taken for migraine headaches. Multicenter, prospective controlled studies are highly warranted.

The aim of this study was to determine whether trigeminal nerve discharge associated with painful stimulation of the temple would intensify symptoms of motion sickness in migraine sufferers. If so, this would support the notion that symptoms such as nausea and headache interact with each other during attacks of migraine. Symptoms of motion sickness were rated at 2 min intervals during 15 min of optokinetic stimulation in 27 migraine sufferers and 23 age- and sex-matched controls. To document changes in frontotemporal blood flow, pulse amplitude was monitored with photoelectric pulse transducers. To induce facial pain, ice was applied to the temple for 30 s, three times at 4 min intervals during optokinetic stimulation. On another occasion, pain was induced during optokinetic stimulation by immersing the non-dominant hand in 2 degrees C ice water for 30 s, three times at 4 min intervals. On a third occasion, measures were obtained during optokinetic stimulation alone. Migraine sufferers rated themselves as being generally more susceptible to motion sickness than controls. In addition, symptoms of motion sickness provoked by optokinetic stimulation were greater in migraine sufferers than in controls. Painful stimulation of the temple intensified nausea and headache during optokinetic stimulation, whereas painful stimulation of the hand did not. Since nausea also intensifies facial pain during motion sickness, nausea and headache may reinforce each other in a vicious circle. In the absence of painful stimulation, increases in pulse amplitude during optokinetic stimulation were greater in migraine sufferers than controls, possibly because the discomfort associated with motion sickness triggered extracranial vasodilatation in migraine sufferers as part of a fight-or-flight (defense) response. Extracranial vasodilatation did not differ between migraine sufferers and controls when ice was applied to the temple or hand during optokinetic stimulation, implying that the additional discomfort associated with painful stimulation of the head and hand evoked a defense response in controls. These findings suggest that a mechanism which boosts extracranial neurovascular reflexes to stress and which heightens symptoms of motion sickness, increases susceptibility to migraine.

Objective: To determine whether vomiting after mild head injury in children is related to migraine and to identify predictors of vomiting after head injury., Methods: A series of consecutive children admitted to the observation unit of an emergency department after mild head injury was identified by chart review. A telephone interview with the parents or child or both was then conducted by using a structured questionnaire., Results: Of 47 eligible children with acute head injury, 44 (94%) were contacted. The mean age at head injury was 7.4 years. Twenty-nine children (66%) vomited after the head injury. The likelihood of vomiting was increased if the child had a history of recurrent headache (p = 0.05). If the headaches were migrainous, the likelihood of vomiting increased further (p <0.002). All 15 children with a history of motion sickness vomited after the head injury. Family history of migraine, particularly maternal (n = 21), also predicted recurrent vomiting (p <0.001). If more than one of these predictive variables was present, the likelihood of vomiting was 100%., Conclusions: History of motion sickness, migraine headaches, and family history of migraine are highly predictive of vomiting after a mild head injury.

The incidence of motion sickness among 222 children in four diagnostic categories--migraine, nonmigraine headaches, seizure disorders, and learning disabilities--was compared. Motion sickness was found to be an associated feature in 45% of the cases of childhood migraine, in contrast to a 5% to 7% incidence in the other groups. Therefore, it is suggested that motion sickness be regarded as an additional reliable minor criterion in the diagnosis of childhood migraine. Hypotheses of common central and peripheral mechanisms underlying both conditions are offered.

Seven patients (all female, ranging in age from 5 to 53 years) had typical migraine and episodic unilateral mydriasis. These mydriatic episodes, usually occurring during the headache, lasted from 15 minutes to 24 hours and had occurred for three months to 35 years. Three patients had suffered from car sickness as children and there was a family history of migraine in six. Normal accommodation in five patients, normal responses to pilocarpine in two patients, and a return to normal or near-normal pupillary reaction in five patients with the cessation of headache made pharmacologic blockade unlikely. Although there are several possible neurogenic mechanisms, a parasympatholytic origin appears to be the most likely explanation for the mydriasis. Such episodes are generally benign.

The present study takes into consideration some of the symptoms comprised in the Periodic Syndrome. These include motion-sickness, cyclic vomiting, recurrent abdominal pains and paroxysmal vertigo. Particular consideration is given to the chronological and long-term aspects of such symptoms. Among 247 migraine sufferers in the pediatric age group, 173 subjects who complained of at least one of these symptoms were chosen. Results of the data show that motion-sickness is the first to manifest itself (mean age of onset 2 years), and has a tendency to continue into the headache period; cyclic vomiting appears in the third year of life, and terminates sooner than the other symptoms. At the mean age of five years abdominal pains start, and at seven, paroxysmal vertigo. Headache is the final symptom in this group. The sequentiality of such disturbances in each subject leads to the assumption that the Periodic Syndrome is the expression of a single disorder which manifests itself polymorphously as a rather precisely timed process.