Neurological Sciences and Neurophysiology

: 2020  |  Volume : 37  |  Issue : 2  |  Page : 41--49

Vestibular migraine: Considered from both the vestibular and the migraine point of view

Gulden Akdal1, Pınar Özçelik2, Aynur Özge3,  
1 Department of Neurology, Faculty of Medicine, Dokuz Eylul University; Department of Neurosciences, Institute of Health Sciences, Dokuz Eylül University, İzmir, Turkey
2 Department of Neurosciences, Institute of Health Sciences, Dokuz Eylül University, İzmir, Turkey
3 Department of Neurology, Faculty of Medicine, Mersin University, Mersin, Turkey

Correspondence Address:
Gulden Akdal
Department of Neurology and Neuroscience, Faculty of Medicine, Dokuz Eylül University, Izmir


A temporal overlap between vestibular symptoms, such as vertigo and head movement intolerance, and migraine symptoms, such as headache, photophobia, and phonophobia, is a requisite diagnostic criterion for the diagnosis of vestibular migraine (VM). Diagnostic criteria for VM have been proposed by an International Vestibular Research Group (the Bárány Society) and a headache research group (International Headache Society); however, in practice, it is still acceptable to divide patients suspected of VM into “definite VM” and “probable VM” groups. Here, a neuro-otologist and a headache specialist consider VM from their own points of view using four real cases, two from a dizzy clinic and two from a headache clinic, with expert opinions and arguments according to the current literature. The management is summarized on the basis of mechanism and comorbidity and the importance of prophylactic medication.

How to cite this article:
Akdal G, Özçelik P, Özge A. Vestibular migraine: Considered from both the vestibular and the migraine point of view.Neurol Sci Neurophysiol 2020;37:41-49

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Akdal G, Özçelik P, Özge A. Vestibular migraine: Considered from both the vestibular and the migraine point of view. Neurol Sci Neurophysiol [serial online] 2020 [cited 2023 May 29 ];37:41-49
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Many patients who present with migraine headaches will, if asked, also mention a range of vestibular symptoms ranging from chronic motion sensitivity and motion sickness, to attacks of vertigo with or without headache.[1],[2],[3] Conversely, many patients who present with vertigo or other vestibular symptoms will, if asked, also mention a range of migrainous symptoms such as photophobia, visual aura, or hemicranial headache attacks.[4],[5] This link between migraine and vestibular symptoms first reported by Aretaeus of Cappadocia around 131 BCE was officially designated as “vestibular migraine (VM)” in 2013 AD.[6],[7] In the real world, a patient with vestibular (adjective) migraine (noun) might present to a neurologist complaining either of headaches or of vertigo attacks. In either case, it is important that both complaints are considered. Here, two clinical neurologists, a headache specialist (Özge), the other a vestibular specialist (Akdal) together consider VM and try to form a single conceptual framework on which to base the assessment, diagnosis, treatment, and management of VM patients.


Case 1

A 31-year-old female presented with headaches since childhood. In the last 10 years, they had been severe, throbbing unilateral headaches, changing sides, increasing, in frequency in the last 3 years, and peaking at more than 20 affected days in the last month. She had also been experiencing dizziness and vertigo attacks lasting from about 30 min to 3 h, in the last 3 years. Nausea, occasionally vomiting, photophobia, phonophobia, and osmophobia, could accompany both the headache and vertigo attacks. She had no hearing problem, but did have allergic rhinitis, polycystic ovary disease, cardiac atrial septal defect, and mitral valve prolapse. Neurological and vestibular examination, audiogram, video head impulse test (vHIT), brain magnetic resonance imaging (MRI) with contrast, and temporal bone computed tomography were all normal. The patient was prescribed topiramate (titrated up to 100 mg/day) and domperidone 10 mg/day. She kept a headache diary and reported almost 70% reduction in headache frequency and vertigo spells stopped over 6 months; with atopy management (local steroids plus antihistamine with attacks), this improved to almost 90%.

Comment (AÖ)

Migraine is not just a headache. It is also a part of functional disorders complex interaction and comorbidities more than by coincidence.[8] Management of VM needs attention to comorbid medical conditions such as hypertension (about 60%), dyslipidemia (20%), depression (12%), diabetes mellitus (7%), hypothyroidism (7%), and epilepsy (4%).[9] Integrated management of the patient is necessary, and this case emphasizes the importance of complete evaluation and management of the comorbidities. Preventive management over 6 months taking into account comorbidities and potential side effects of drugs was superior to attack management in this case.

Comment (GA)

The headaches seemed more dominant and distressing than the vertigo and dizziness which were accompanying symptoms of severe migraine attacks. VM generally develops in patients with a long history of migraine headaches.[4] The patient did not report vertigo, spontaneous or positional or head-motion intolerance. We cannot consider this patient as a definite VM patient according to the International Classification of Headache Disorders 3rd ed.ition (ICHD-3) criteria [Table 1], since we do not know the number of vertigo attacks, but this patient should be followed as VM and the vertigo attacks were reduced by treatment.[10]{Table 1}

Case 2

A 42-year-old female presented with severe vertigo attacks accompanied by unilateral headache. She described rare, severe, menstrual, unilateral headache attacks accompanied by nausea, and phonophobia, aggravated by routine physical activities, for the last 10 years. She was not given any specific medication. She had a sudden onset severe headache and vertigo 4 years before, was seen in an Emergency Room, and treated with vestibular suppressants and sedatives. A year later, she had another headache and vertigo attack which had similar features but was more severe and led to hospitalization for 10 days and took a month to resolve with vestibular suppressants and sedatives. The last episode of headache and vertigo was a year ago accompanied by severe neck pain and blurred vision lasting 15 min. Audiogram and vHIT were normal; she could not tolerate caloric testing. Brain and spine MRIs were normal. She developed a severe anxiety disorder because of these symptoms. It was difficult for her to go to shopping malls and use escalators. In the past, she had motion sickness and atopic rhinitis. Family history revealed several individuals with migraine and ischemic cerebrovascular disorders. Her prophylactic management with topiramate (titrated up to 100 mg/day), montelukast (20 mg/day for 2 months), and short-term flunarizine (10 mg/day for 3 months) produced more than 50% clinical improvement. After 3 bilateral lidocaine greater occipital nerve blocks over 3 months, there was 90% improvement not only in headache frequency but also in severity and duration of the attacks. She did not complain of vertigo disturbing daily living activities. She still experiences menstrual migraine attacks; prophylaxis given for these attacks made reduction 80% to the severity and duration of the attacks.

Comment (AÖ)

Chronic migraine affects the daily life of individuals, and with accompanying vertiginous symptoms, these problems become more prominent. It can be accounted for as a part of brainstem aura or a part of associated symptoms depending on the temporal course. VM affects women up to five times as often as men.[4],[11] Headache is often worse during menstrual periods. Vestibular symptoms typically occur several years after the disease onset, when headaches are less frequent or even absent.[9] The onset of vestibular symptoms replacing the headache is more commonly seen in perimenopausal women, as in this.[4] More randomized controlled clinical studies are required both on the effects of occipital nerve block in chronic migraine with vertigo symptoms and for other interventional procedures such as botulinum toxin injections.[12],[13]

Comment (GA)

This patient had 3 severe vertigo attacks which brought her to the emergency room. She was hospitalized in two episodes and she had imbalance and dizziness for a month in the last one. She had problems in shopping malls where there are a lot of visual inputs. She had discomfort with the moving scene on the escalator. Since VM is the second common cause of vertigo attacks, it should not be difficult for the emergency and family doctors to link the connection with vertigo and migraine and to make the diagnosis, but it is not the case in reality.[4] It seems that it is not easy for clinicians to diagnose VM and needless medical consultation rate is high among VM patients before the correct diagnosis is finally made.[14] VM patients have significantly higher prevalence of anxiety and depressive symptoms and can unexpectedly experience recurrent and intense vertigo attacks which may aggravate their stress.[15],[16],[17],[18] Consequently, anxiety and panic attacks can be triggered and lead to avoidance behavior.[18]

Case 3

A 17-year-old girl was presented with vertigo attacks lasting minutes to hours, at least 8 in the last 3 months. She had no tinnitus, aural fullness, or hearing loss. Between vertigo episodes, she experienced head motion intolerance. Vertigo attacks might have been triggered by stress, hunger, and irregular sleep. She also noticed headaches, some around the time of the vertigo attacks, predominantly unilateral and throbbing, associated with nausea, photophobia, and phonophobia. Her headaches could last for a day if she did not take analgesics. She experienced headaches at least once a month. Her mother remembered that when the girl was about 4 years old, she had some brief vertigo attacks accompanied by nausea and vomiting and diagnosed and treated by a pediatrician as probable epileptic seizures. Her mother did not think that the treatment helped; she thought the improvement was due to the more regular sleep habits. The patient had been susceptible to motion sickness since childhood, in cars and trains, unable to go boating or on fairground rides. She remembered that some attacks might have been after eating chocolate. Both her parents had migraine headaches with aura, since childhood. Neurological and vestibular examination was normal. We explained to the girl, and her mother, that her headaches and vertigo episodes were closely related and controlling headache triggers would also help her vertigo. She was shown a list of foods which might trigger headaches and vertigo. Regular sleep was recommended. A month later, she reported that she had experienced only had a mild self-motion vertigo, triggered by hunger; her head motion intolerance had decreased. She realized that avoiding carbonated drinks and food containing monosodium glutamate was also helpful.

Comment (GA)

This patient's headaches met the ICHD-3 criteria for VM [10] [Table 1]. MRI was not necessary because neither the patient's history nor physical examination suggested secondary causes of headache disorders. Her childhood vertigo attacks are typical “benign paroxysmal vertigo of childhood,” now considered to be a migraine equivalent, which can progress to VM.[19],[20] Spinning vertigo, head motion intolerance, illusion of self motion, room tilt illusion, and positional vertigo are manifestations of VM.[4],[21],[22] Motion sickness is also a common vestibular symptom in migraine;[23],[24] migraineurs with motion sickness could be more prone to VM than migraineurs without it.[2],[25],[26]

In this patient, the triggers for vertigo and migraine were clear, and after making her aware of the condition, she reorganized her life accordingly, especially her sleeping habits.

Comment (AÖ)

Headache attacks suggest migraine, but more attacks would be needed for definitive diagnosis (minimum 5 attacks for migraine without aura and 2 attacks for migraine with aura).[10] On the other hand, migraine with brainstem aura [27] should be kept in mind for future migraine attacks depending on associated headache phenotype. In order to differentiate brainstem aura (e.g., dysarthria and vertigo) from transient ischemic attacks, benign paroxysmal positional vertigo, etc., clinicians should note that aura symptoms often spread gradually over 5 or more minutes and resolve within 60 min of onset and are commonly associated with migraine type headache.[10] Perhaps the patient should be investigated for a patent foramen ovale not only to define comorbidity but also for potential future risk of strokes.[28]

Case 4

A 44-year-old female hospital neurology nurse presented during a severe attack of acute, isolated spontaneous vertigo which began at work. The day before, she had noted tinnitus and realized that moving to her left in bed caused a spinning sensation. She felt more comfortable lying on her right. She had a similar, milder attack nearly 20 years before and was diagnosed having probable Ménière's disease. She had also had migraine with aura since age 18. She was having her menstrual period when vertigo attack started. She had always considered herself a motion sick person: she never liked elevators and shopping malls always discomforted her. In the last 20 years, she experienced some other mild vertigo episodes, but did not seek medical help. On examination, she had 3rd-degree right-beating, spontaneous nystagmus [Figure 1], suppressed by vision. Her lateral canal vHIT was normal and she was too unwell to tolerate vertical head impulse testing. Subjective visual horizontal and pure tone audiogram were normal. She was given prochlorphenazine IM; the attack lasted almost 24 h. Later, magnesium tablets were given to be taken during menstrual periods. She has not had any more vertigo attacks for almost 3 years.{Figure 1}

Comment (GA)

Being able to examine this patient in an acute attack showed peripheral vestibular type dysfunction. Most VM patients are seen by appointment, while well, in Dizzy Clinics. In a study of acute migrainous vertigo attacks, about 50% of patients developed spontaneous primary position nystagmus and 15% have peripheral type vestibular dysfunction.[29],[30] As in Case 3, this patient also considered herself a motion sick person, which is common among VM patients.[31] Avoiding elevators and shopping malls might be a result of her anxiety disorder, also common in VM patients.[16] If we did not consider her previous mild vertigo attacks, her clinical situation would meet the Neuhauser criteria for definite VM,[4] but not ICHD criteria which need 5 vertigo episodes for diagnosis [10] and considered by some to be too restrictive.[32],[33],[34],[35] Differential diagnosis of VM is Ménière's disease; the principal objective difference is a unilateral, fluctuating low-frequency hearing loss in Ménière's disease, in addition to the tinnitus and fullness in the same ear. Some patients with VM also have tinnitus, even unilateral tinnitus but should not have persistent fullness or any hearing loss.[34] Furthermore, patients with Ménière's disease eventually develop impaired caloric responses from the affected ear. However, between the attacks, early in Ménière's disease, there will be no objective audiovestibular abnormality. In a patient seen during vertigo attack, even when the vestibular abnormalities, are florid as in this case, Ménière's disease and VM can be indistinguishable.[36] Furthermore, some Ménière's disease patients also have migraine, which makes correct diagnosis of an attack even more difficult.[37],[38] The Classification Committee of the Bárány Society and other societies described the new definite and probable Ménière's disease criteria.[39] Ménière's disease is considered definite with 2 attacks of vertigo lasting 20 min to 12 h and a documented low to mid frequency sensory-neural hearing loss in one ear, before, during, or after one of the vertigo attacks and considered probable with 2 or more vertigo attacks lasting 20 min to 24 h and fluctuating hearing, tinnitus, or fullness in one ear but no documented hearing loss.[39] The patient could be diagnosed as probable Ménière's disease, too. When her history of migraine headaches, motion sickness, and anxiety is considered, it is best to follow her as VM. Probable Ménière's disease and VM overlap since VM patients have aura (hearing, tinnitus, or fullness) and criteria for Ménière's disease do not require a documented low to mid frequency hearing loss. Controlling migraine triggers such as hunger, sleep deprivation and adding magnesium supplements during periods helped both patients. There is no really good evidence for the efficacy of any of the medications used to prevent VM – generally the same medications as used for migraine headaches.[37] Whether or not a patient tries any of these medications is essentially her own choice: if the VM attacks are frequent and severe enough, she might then be prepared to take the risk albeit small risk, of side effects for the potential benefit or fewer and less severe VM attacks.

Comment (AÖ)

Menstrual migraine is a specific migraine variant in which attacks occur just before, just after, or during menstrual periods. These attacks can present as isolated migraine attacks or together with a known migraine subtypes. There are data about the correlation between migraine and menstrual period in patients with VM. The worsening of headache during the menstrual period, well known among women diagnosed with migraine (50%–60% of the cases), was also observed in the present case. There are also data about the correlation dizziness versus menstrual period, some controversial.[9],[40],[41] Throbbing quality of headache and definitive associated features (nausea, photophobia, and phonophobia) including dizziness and vertigo were significantly more frequent in women than men in migraine without aura.[42] The gender impact varied across age groups and significant changes were seen in female migraineurs after 30 years of age.[43] However, we need more data about the relationship between VM and hormonal changes including menstrual attacks.

 Clinical Features of Vestibular Migraine

Clinical manifestations of VM vary from head motion intolerance to positional or spontaneous vertigo or both, recurrent imbalance triggered by head movements.[4],[22],[44] The vertigo/dizziness can last from seconds to hours or days, with headache in some patients and never with headache in others.[4],[5] Vertigo attacks can start even after the headaches have stopped especially in perimenopausal females.[11] Some patients have difficulty going into shopping malls and visiting places with a lot of visual inputs. Auditory involvement is very rare in VM and might simply indicate comorbid Ménière's disease.[5],[38] Between attacks, some subclinical oculomotor abnormalities might be found, perhaps perverted head-shaking nystagmus and central positioning nystagmus.[5],[31],[45] Vestibular impairment shown with caloric or impulsive testing is rare.[5],[46],[47],[48],[49] During a VM attack spontaneous or positional nystagmus consistent with a central vestibular dysfunction was found in 50% of patients and with peripheral vestibular dysfunction in 15% patients; in the rest localization could not be made.[29] In a patient with suspected VM, obvious audiovestibular impairment suggests an alternative or additional diagnosis.

 Criteria for Diagnosis of Vestibular Migraine

The association of migraine and vertigo is not coincidental; there is a threefold in increase incidence of vertigo in migraineurs.[1] Neuhauser et al. suggested criteria for definite and possible “migrainous vertigo,”[4] although different names have also been used including “migraine-related dizziness,”[50],[51] “migraine-related vestibulopathy,”[51],[52] and “VM.”[5] There is now agreement to use the term “VM.”[22] VM is the second most common cause of vertigo after benign paroxysmal positional vertigo with a prevalence of 1%.[4] The Classification of Vestibular Disorders Committee of the Bárány Society and the Migraine Classification Subcommittee of the International Headache Society (IHS) negotiated the diagnostic criteria of VM. After their agreement, VM was included in the appendix of the third beta edition of the ICHD (ICHD-3b) as a disease entity (IHS), but only definite VM criteria were defined in the appendix. These new criteria, requiring 5 vertigo attacks, limit the diagnosis of VM, when compared with the Neuhauser criteria which needed only 2 definite vertigo attacks and also allowed the diagnosis of probable VM diagnosis.

After the publication of ICHD-3b (2018) and which is ICHD-3 now, studies using the new VM criteria appeared. In Korea, VM was found in 10.3% of the first-visit migraineurs in neurology clinics and it was suggested that VM should be considered as a migraine subtype and broader diagnostic category should be applied, including probable VM.[33] In China, 17% of migraineurs in headache clinics were diagnosed on the new criteria as having VM.[34] A neurotology clinic study used the Bárány 2012 VM criteria [22] definite and probable and as well as a third group – “atypical VM”, in order to cover those patients not meeting the standard criteria but whose symptoms strongly suggested VM. All three groups benefitted from treatment.[35] Compared to the Neuhauser criteria, the ICHD 3 criteria restrict the diagnosis of VM which emphasizes the need for modifying and relaxing the ICHD 3 criteria.[32]

Criteria are needed for research studies, but they are excessively restrictive in clinical practice. Some include atypical VM group for the patients not fitting the new criteria and started treatment.[35] A clinician inexperienced about VM or a clinician who makes the diagnosis only according to criteria might not start any treatment and wait for the certain number of attacks to fulfill the number required by the criteria. In a patient with vertigo attacks, a detailed headache history should be taken. This is not easy because patients do not think that they have migraine and consider it just a red wine headache or menstruation headache, so it is helpful to explain the vertigo-migraine link to the patient. When needed the three items, ID migraine test should be used.[53] The clinician needs to ask about motion sickness, the most common vestibular symptom in patients with migraine.[23],[24],[25] Taking a family migraine history is important in evaluating vertigo patients. Current criteria do not include family history of migraine, but future criteria might.

Knowing which patients with migraine have the potential to develop VM may give clues for planning the diagnosis and treatment of these patients.[2] With this objective, patients with vertigo/dizziness or motion sickness were divided into two groups, “migraine with vestibular symptoms” and “migraine without vestibular symptoms” in two different studies.[2],[3] One study with headache outpatient data included more than 5000 headache patients; a population-based study of 5323 subjects showed that migraine with vestibular symptoms was different to migraine without vestibular symptoms in many clinical aspects.[2],[3] Patients with migraine, even those without a history of vertigo have minor, nonspecific but progressive imbalance.[54],[55] When a patient with migraine has a vertigo attack, he/she will be a candidate for VM. The diagnosis is in the history not the examination.

 Possible Pathophysiology of Vestibular Migraine

Pathophysiology of VM is complex; there is no clear explanation. Vasospasm of the internal auditory artery has been considered to explain peripheral vestibular findings.[56] In some cases, the nystagmus during attacks suggests central vestibular dysfunction.[29] Vertigo is the most common aura of basilar migraine, the equivalent of spreading depression which might also be the cause of short vertigo attacks in VM.[5] Migraine and vertigo are common complaints in familial hemiplegic migraine and episodic ataxia type 2 (EA2) paroxysmal disorders due to mutations in the calcium channel gene CACNA1A.[57] Ion channel disorders could be related with the pathophysiology of migraine; however, studies examining mutations on candidate genes have given negative results.[58],[59] A brain MRI volumetric study in chronic migraine patients showed cerebellar and brainstem atrophy, which is a possible cause of vestibulo cerebellar impairment, leading to imbalance in migraineurs.[60] Recent studies have looked at positron emission tomography (PET) and functional magnetic resonance (fMR) imaging in VM. : A PET study of ictal and inter-ictal VM patients showed increased metabolism in the temporo parieto insular cortex and in thalami and decreased metabolism in the occipital cortex, explained by reciprocal inhibition between the visual and vestibular systems.[61] In 12 VM patients without aura an fMRI study after cold caloric ear irrigation showed increased thalamic activation, which had a positive correlation with the frequency of migraine attacks.[62] Two studies mentioned here demonstrated the involvement of thalamus in VM patients. A voxel-based morphometric MRI study showed that gray matter (GM) volume reduced in the superior, inferior, and middle (MT/V5) temporal gyrus as well as in the mid cingulate, dorsolateral prefrontal, insula, parietal, and occipital cortex. A negative correlation of disease duration and GM volume was presented in areas associated with pain and vestibular processing. In addition, negative correlation between headache severity and prefrontal cortex volume was observed.[63]

 Treatment of Vestibular Migraine

Since the pathophysiology of VM is not clear, treatment is challenging; data from the treatment of migraine headaches guides treatment of VM.

There is no doubt that if the vertigo attack is long or severe, vestibular suppressant treatment is suggested, but only for a few days not to delay vestibular compensation.[64] In small scale studies almotriptan, sumatriptan and zolmitriptan showed benefit in acute VM attacks and rizatriptan in the vestibular induced motion sickness of migraineurs, but larger scale studies are needed.[65],[66],[67],[68] Neuromodulation with external trigeminal or vagus nerve stimulation might be useful in acute VM attacks.[69],[70]

Migraine prophylaxis drugs commonly are used in VM. These include beta blockers (propranolol and metoprolol),[71],[72] calcium channel blockers (flunarizine, cinnarizine and verapamil),[73],[74],[75] antiepileptics (valproic acid, lamotrigine, and topiramate)[76],[77],[78] and antidepressant drugs (amitriptyline, nortriptiline and venlafaxine).[76],[77],[78],[79] In addition, acetazolamide, magnesium, and diet restrictions are also suggested.[77],[80],[81],[82] It is very difficult to compare the studies mentioned above, because the number of patients, final end points and outcomes were different in each study. All the drugs used in prophylactic treatment had side effects, which made some patients to stop treatment.[83],[84]

In 2016 the Cochrane Collaboration investigated studies published about prevention of VM attacks. In those studies where an interventional drug was tested against placebo or no treatment, none matched the Cochrane criteria.[85] In 2019, the first double-blind, placebo-controlled study with metoprolol in prophylactic treatment of VM was published and the authors stopped the study after 130 patients due poor accrual of the patients, not the side effect of the drug.[86] Interestingly, this study showed that both groups, drug and placebo, had less vertigo attacks in a 6 months period and metoprolol did not have any superiority to placebo. A 2017 study of children and adolescents using amitriptyline, topiramate and placebo did not show any superiority of the active drugs over placebo.[87]

The above finding is not astonishing. The first double-blind study in VM demonstrated that in migraine treatment, placebo effect should not be forgotten. A recent meta-analysis found that there was no superior drug for VM treatment.[42]

It is controversial when to start prophylactic treatment in VM. The general idea is to start treatment if the attack frequency decreases the quality of life. In our view, the first step in the treatment is explaining the vertigo and migraine relation to the patient, since VM is not well-known in primary care and the needless medical consultation rate is high among these patients.[88] It could be the first time that the patient heard about VM. The second step is to tell the patient that when the frequency of migraine attacks decreases, the vertigo and imbalance attacks will also decrease and to make the patient familiar with the migraine triggers such as fasting, sleep irregularities, and certain foods. Triggers can be detected using a headache and vertigo diary. Dietary trigger (e.g., caffeine, cheese, and red wine) avoidance has shown efficacy in migraine.[77],[82] For example, in our cases 3 and 4, this strategy controlled the VM episodes. Since VM attacks affect the quality of life in the most demanding and productive years of life, prophylaxis should be considered if triggers are not effectively controlled.[25],[74] In our opinion, VM prophylactic treatment should be tailored for every patient. Patients with hypertension might benefit from beta blockers and insomniacs from amitriptyline, depressives from venlafaxine, and the obese from topiramate. In addition, VM patients need to be informed about the importance of exercise. When necessary, vestibular rehabilitation should be suggested.


Patients with migraine can have many different vestibular symptoms – imbalance, motion-sickness, mal-de-debarquement, etc., even if they do not meet all current criteria for VMWhile patients with VM can present either with headaches or with balance problems that is with vertigo or with migraine, both sides of the story need to be considered, preferably by the same neurologistIn some cases, it is difficult to be sure if patients have VM or Ménière's disease even if they are examined during an acute attack. When the patient develops a unilateral low-frequency fluctuating hearing loss with tinnitus and fullness or a unilateral fluctuating caloric canal paresis, or both, the diagnosis of Ménière's disease is confirmed. VM and Ménière's disease occur together more often than by chance, so a patient can actually have bothThere is no specific treatment for VM; the same medications that are used for migraine headaches are also used for VM. It is also important to address the patient's lifestyle issues.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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