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Year : 2020  |  Volume : 13  |  Issue : 6  |  Page : 636-641  

Vestibular migraine: Our experiences at a tertiary care teaching hospital of Eastern India

1 Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha 'O' Anusandhan University (Deemed to be), Bhubaneswar, Odisha, India
2 Department of Community Medicine, IMS and SUM Hospital, Siksha 'O' Anusandhan University (Deemed to be), Bhubaneswar, Odisha, India

Date of Submission13-Jul-2019
Date of Decision09-Dec-2019
Date of Acceptance03-Mar-2020
Date of Web Publication6-Nov-2020

Correspondence Address:
Santosh Kumar Swain
Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha 'O' Anusandhan University(Deemed to be), Bhubaneswar, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mjdrdypu.mjdrdypu_201_19

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Introduction: The etiopathology and management of vestibular migraine (VM) are a puzzling dilemma among the clinician. The migraine and vertigo are important symptoms of VM. Objective: Clinical and audio-vestibular evaluation of VM patients. Materials and Methods: It is a prospective study which was conducted between June 2016 and May 2019. Patients attending vertigo clinic were thoroughly reviewed. The patients of VM were selected on the basis of criteria fulfilling the International classification of headache disorders, 3rd edition (beta version). Neuro-otological examinations with videonystagmography (VNG) and vestibular evoked myogenic potentials (VEMPs) tests were done in all cases those diagnosed for VM. Results: There were 51 VM patients out of 168 dizzy patients during the study period. Aural fullness (45.09%) was the most common aural symptom, followed by tinnitus and hearing loss. Phonophobia (82.35%) was the most common migrainous symptom. The relation between headache and menstrual period among female patients was significant. VNG was showing abnormality in 11.76% of cases during caloric test with the highest abnormality in positional test. In VEMPs, 32 patients (62.74%) had abnormal cervical VEMPs response, whereas abnormal ocular VEMPs response seen 38 patients (74.50%). Conclusion: VM is a leading cause of vertigo in the clinical practice and high percentage of patients presented with abnormalities in VNG and VEMPs during vestibular symptoms. Proper history taking and neuro-otological examination and vestibular investigations help for the early diagnosis and treatment.

Keywords: Dizziness, migraine, vertigo, vestibular evoked myogenic potentials, vestibular migraine

How to cite this article:
Swain SK, Behera IC, Sahoo L. Vestibular migraine: Our experiences at a tertiary care teaching hospital of Eastern India. Med J DY Patil Vidyapeeth 2020;13:636-41

How to cite this URL:
Swain SK, Behera IC, Sahoo L. Vestibular migraine: Our experiences at a tertiary care teaching hospital of Eastern India. Med J DY Patil Vidyapeeth [serial online] 2020 [cited 2021 Aug 4];13:636-41. Available from: https://www.mjdrdypv.org/text.asp?2020/13/6/636/300129

  Introduction Top

Vestibular migraine (VM) is a type of migraine causing vestibular symptoms along with features of typical migraine. It is found that 1% of the population suffers from VM which is the most common central cause for vertigo and the second most common cause of vertigo overall in clinical practice.[1] It is also called as migraine-associated vertigo, migraine-related vertigo (MRV), Migrainous vertigo, or basilar artery migraine.[2] VM was first described by Dieterich and Brandt in 1999[3] and it corresponds to a type of migraine where the main symptom is vestibular. VM is more prevalent in individuals without aura and predominantly affects female, at a ratio up to 5:1 (female/male).[4] VM is often confused with vestibular disorders, which are an important cause for dizziness complained by the patients. Patients of VM often have the vestibular symptoms ranging from severe vertigo to less specific symptoms such as dizziness, head motion intolerance, and unsteadiness. The internationally accepted criteria for the diagnosis of VM are based on recurrent attacks of vestibular symptoms of moderate severity, a history of migraine, a temporal association between migraine and vestibular symptoms and exclusion of other causes for vestibular symptoms. The duration of acute attack is between 5 min and 72 h.[2] Some patients of VM may be free from migraine attack for months to years.[5] Pathological nystagmus is often seen during the attack of VM patients. Vestibular tests often show abnormality such as vestibulo-ocular tests in VM patients. Abnormality in vestibulospinal pathway is also seen in VM patients as detected in cervical VEMPs (cVEMPs) testing.[6] This study is aimed to analyze the clinical presentations, investigations, and treatment of VM patients at a tertiary care teaching hospital of eastern India.

  Materials and Methods Top

This study was done from June 2016 to May 2019, and the patient's details were evaluated those attended the Vertigo Clinic, Department of Otorhinolaryngology with complaints of dizziness. This study was approved by Institutional Ethics Committee (IEC) with reference number IMS/CRL/IEC/24/2016. Patients of VM were diagnosed as per the criteria of the International Classification of Headache Disorders, 3rd edition (beta version).[2] A detail neuro-otological examinations were done for all diagnosed VM cases at Vertigo clinic of our department. History and primary complaint of vertigo were analyzed thoroughly. The associated medical comorbidities of the patients were documented. All the female patients and the effects of symptoms during the menstruation period were also analyzed. Pure tone audiometry was done in all the patients. Videonystagmography (VNG) with bithermal caloric testing was done in all cases of VM. Along with vestibular office tests, vestibular evoked myogenic potentials (VEMPs) such as cVEMPs and ocular VEMPs (oVEMPs) were done in all confirmed cases of VM. The consent from patients and parents were taken for publications of the data. All the VM patients were treated with flunarizine for prophylaxis and cinnarizine for acute vestibular symptoms.

  Results Top

A total number of 168 patients were examined during June 2016–May 2019 for dizziness. Fifty-one patients (30.35%) fulfilled for the criteria of VM. Of the 51 patients of MRV, 22 were male (43.13%) and 29 were female (56.86%) with mean age of 43.52 years and median of 46 years. Thirty-seven patients of VM shown auditory symptoms with the most common symptom of aural fullness (45.09%) [Table 1]. Phonophobia was the most common migrainous symptom and was seen in 82.35% of cases of VM [Table 1]. Rotatory vertigo was the most common type of vertigo in our study patients [Table 1], and the duration of vertigo varies from second to days [Table 2] 28 (54.90%) patients showed associated medical comorbidities [Table 3]. The headache of VM patients was worsening during the menstrual period by most of the female patients in 79.31% of cases [Table 4] whereas vertigo was seen during the menstrual period of 51.72% cases [Table 4]. All 51 patients underwent pure tone audiometry, which was normal in 46 patients. VNG had shown abnormality in 11.76% cases during caloric test with the highest abnormality in positional test [Table 5]. The positional nystagmus was horizontal-torsional or vertical in direction. Nystagmus recorded in this study was direction fixed or direction changing with changing head position and it was abolished by fixation. Of 51 patients, 32 patients (62.74%) had abnormal cVEMPs response whereas abnormal oVEMPs response seen 38 patients (74.50%) [Table 6]. Abnormal responses of VEMPs were either absent, delayed or diminished amplitude. Abnormal VEMPs response was either unilateral or bilateral. Forty-six patients (90.19%) responded to the antimigrainous prophylaxis and antivertigo medications in case of acute attack.
Table 1: Auditory, migrainous, and vestibular symptoms among patients of vestibular migraine

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Table 2: Duration vertigo (vestibular symptom) among vestibular migraine patients

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Table 3: Comorbidities in patients of vestibular migraine

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Table 4: Correlation of headache, vertigo, and menstrual period among female patients of vestibular migraine

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Table 5: Videonystagmography findings among vestibular migraine patients

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Table 6: Abnormal vestibular evoked myogenic potentials among vestibular migraine patients

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  Discussion Top

Dizziness is a common clinical symptom seen in daily clinical practice. Migraine is a chronic disorder, and its main symptom is headache usually unilateral and pulsatile in nature and associated with photophobia and phonophobia, nausea, and vomiting. The association between dizziness and migraine headache is known since long times, and its occurrence is three times more often than if it would by chance alone.[7] The basic pathophysiology for migraine and VM is trigeminovascular reflex. Trigeminovascular reflex is a parasympathetic reflex which can cause vasodilatation of the large intracranial vessels. The activation mediated by trigeminal nucleus caudalis and C1–C2 dorsal horn neurons cause vasodilatation of large intracranial vessels.[8] The vasodilatation effect of parasympathetic stimuli on trigeminovascular reflex may be augmented by neurokinin A, calcitonin gene-related peptide, and substancePreleased from sensory terminals of trigeminal nerve.[9] Vestibular pathways often contribute to both peripheral and central migraine mechanisms.[10] There are two possible mechanisms for explaining the vertigo in migraine. Short duration vertigo has been suggested to be a brainstem aura which may be accompanied by changes in blood flow.[11] Alternatively, there is a direct connection from the posterior parietal cortex to the vestibular nuclei which gives a direct access for cortical mechanisms toward underlying migraine aura to reach areas for vestibular information processing and reflex performance. Few studies documented that repeated circulation/vascular problems like vasospasm induced ischemia of the inner ear and plasma extravasations during migraine attack may lead to permanent injury to vestibule and cochlea.[12],[13] The clinical presentations of these patients often similar to vestibular dysfunction. In addition, the evidence of the ion-channel defect and calcium channel disturbances of the labyrinth and its central connections often give a promising hypothesis for the diagnosis and treatment of VM.[14] The vestibular symptoms resulting from migraine usually similar to those seen in inner ear lesions such as benign paroxysmal positional vertigo and episodic vertigo in Ménière's disease.[15] The patient often complaints episodic spinning, imbalance or rotating sensation or giddiness or light headness from few seconds to hours or days. The patient often presents with severe episodic pulsating headache. The patient has usually no hearing loss when associated with common and classical migraine. In 80% of cases of basilar migraine have sensorineural hearing loss and tinnitus which may mimics to the Ménière's syndrome. The central lesions which mimic to VM are transient ischemic accident, multiple sclerosis, vestibulo-basilar artery insufficiency, neurodegenerative disorders and familial ataxia syndrome.[16] The International Headache Society (IHS) has declared well-recognized criteria for the diagnosis of migraine [Table 7].[17] However, the vertigo is mentioned in this classification only in respect of basilar migraine and benign paroxysmal positional vertigo. Now, it is thought that the higher prevalence of VM is more than the chance of association. Migraine may be classified into (1) common migraine (migraine without aura) where the headache is often unilateral and pulsating. The headache is aggravated by photophobia (sensitivity to light), phonophobia (sensitivity to sound), and physical activity. All neurological tests are usually normal; (2) classical migraine (Migraine with aura) where are 2–3 episodes of headache which proceeded by reversible central nervous system problems such as ataxia, dysarthria, diplopia, one side numbness/weakness, vertigo, and tinnitus. This phase is called aura and neurological tests are within normal limit; (3) basilar migraine (type of classical migraine) where there are features of basilar and vertebral artery spasm. There are clinical symptoms of brain stem hypoxia such as dysarthria, diplopia, vertigo, tinnitus, hearing loss, low level of consciousness, and weakness/numbness of limb. The symptoms stay for few minutes to hours. The headache often originates at the occipital and cervical areas; (4) VM where vestibular symptoms are additional features due to vestibule-cochlear artery spasm along with classical migraine; (5) complicated migraine/migrainous infraction where there is a classical type of migraine but the neurological symptoms are not reversible within 1 week and magnetic resonance imaging (MRI) reveals zone of ischemic infraction of the brain. VM was jointly described by the Barany Society and the subcommittee of IHS.[18] It is seen in the appendix of the 3rd edition of HIS as the first step for new clinical entities.[2] The criteria for the diagnosis of VM which accepted internationally are based on recurrent vestibular symptoms and migraine symptoms of moderate-to-severe, a past history of migraine, a temporal association between migraine symptoms and vestibular symptoms. The duration of acute episodes is often limited between 5 min and 72 h. The clinicians should find the presence or absence of aural symptoms to differentiate between Ménière's disease and VM [Table 8]. VM is a multi-factorial chronic disease and common among genetically susceptible people. It is characterized by headache associated with phonophobia, photophobia, vertigo, nausea, and vomiting. VM affects around 18% females and 6% males presenting neuro-otological manifestations such as vertigo, hearing loss, tinnitus, and aural fullness during crisis. Many patients may present these symptoms in the absence of headache.[19] In this study, the most common otologic manifestation was aural fullness. The physical examination of the patients is often normal between the attacks. During the attack of MRV, patients often show a nystagmus that suggests neither peripheral nor central vestibular abnormality. During attack of VM, nonparoxysmal positional nystagmus is common.[20] At the time of aura, spontaneous or positional nystagmus can be seen whereas the patient may not have any neurological deficits. There is often family history of headache is present. The triggering factors such as stress, mental, physical, menstrual period, contraceptive pills, smoking, exposure to light and sound, deprivation of sleep, fasting, and certain foods. Vertigo in the migraine patient may precede the headache and be a part of the migrainous aura. It is often difficult to understand whether migraine and vertigo are two different presentations of the same pathophysiology. The diagnosis of VM is often challenging as there are no established confirmatory tests available for the diagnosis. The new criteria for the diagnosis of VM need at least 5 episodes of vestibular symptoms ranging from moderate to severe intensity. These vestibular episodes varying in length, ranging from few seconds to days and most of fall between 5 min and 72 h.[21] Routine blood tests such as complete blood count, erythrocyte sedimentation rate, and C-reactive protein are usually done in all cases of VM. The accurate diagnosis of VM needs exclusion of the vestibular symptoms. For excluding the vestibular causes, the different vestibular testing, audiograms, and neuro-imaging are required. VEMP is a testing for vestibulocollic reflexes and peripheral vestibular hypersensitivity to noise which help in the diagnosis of VM. VEMPs have abnormal reporting in patients with VM but the findings are usually heterogeneous. These findings show reduced electromyography amplitudes, bilateral or unilateral loss of cVEMP responses, shifting of maximum VEMP response from 500 to 1000 Hz and increased latencies.[22] These findings of VEMP are not specific for VM. Approximately 38% of patients suffering from VM present with auditory symptoms such as hearing loss, tinnitus, and aural fullness.[23] The hearing loss in VM varies from mild to moderate degree without much progression. There is documentation of mild bilateral downward sloping hearing loss over many years among VM patients.[24] Caloric electronystagmography (ENG) may be needed to differentiate peripheral vestibular diseases from VM. There is reduced caloric response in peripheral vestibular hypofunction/loss, vestibular neuritis, and labyrinthitis.[25] Video head impulse test is also useful to differentiate these vestibular disorders from VM.[25] MRI brain or magnetic resonance angiography can rule out the central lesions for vertigo-like cerebrovascular diseases.[25] Swaying sensation rather than vertigo is described by the patients of cerebrovascular diseases along with neurologic findings such as diplopia, visual field loss, limb weakness, or sensory loss.[25] As per a recent study, there are changes of gray matter in VM in comparison to control group with increased gray matter volume of the left temporal lobe, frontal lobe, left thalamus and occipital lobe as well as reduced gray matter in the left cerebellum.[26] It needs further evaluation of MRI for the VM patients. VM patients often show abnormality in ENG with mild degree of caloric paresis. VEMPs (cVEMPs and oVEMPs) are myogenic potentials which are originated by two separate pathways and these are vestibulospinal reflex and vestibulo-ocular reflex, respectively. These two depend on the functional integrity of otolith organs, vestibular nerve, vestibular nuclei, and neuromuscular plates. Any abnormality in these structures may results in the affection of potential parameters. The treatment of VM includes avoid the triggering factors and prophylactic medications. Patients should document the triggering factors with the target of discerning triggers of their migraine. Although some trigger cannot be changed like weather changes, its identification can at least give some predictability to symptoms. If triggers are not found or avoidance of triggers is not possible, then VM can be treated by drugs. There are very few published randomized trials of medications for VM[27] so it treated similar to other migraine in routine clinical practice. Prophylactic medications are advised when attacks are frequent, i.e., attack more than three once a week or severe symptoms even making driving dangerous. Prophylactic medications are also given when there are long duration symptoms. The prophylactic medications used in VM are anticonvulsants, anti-hypertensive and antidepressants [Table 9]. Drugs from each group can be combined in refractory type of VM. It is always better to start very low dose of any chosen group. The medication is usually given over 2–4 weeks and stopped by either any significant side effects or attending the dose as shown in [Table 9] for a month.
Table 7: Diagnostic criteria of vestibular migraine (International Headache Society and Barany Society)

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Table 8: Clinical presentations between vestibular migraine and Ménière's disease

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Table 9: Medications in vestibular migraine patients

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  Conclusion Top

Accurate diagnosis of VM is often challenging situation for clinicians. The high prevalence of VM and its significant impact on quality of life need further understanding of the pathophysiology for better care of VM. The presence of two symptoms of vertigo and headache simultaneously does not represent a definite causal relationship. In VM, the profile of the patients is commonly young adult female or male and clinical presentations such as dizziness of variable duration and headache. Each episode of dizziness is usually rotational sensation and or sense of imbalance which lasts for minutes to hours. A high percentage of patients presented with abnormalities in VNG and VEMPs. Migraine prophylaxis is often helpful for the treatment of VM.

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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]


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