|Year : 2021 | Volume
| Issue : 3 | Page : 179-183
Santosh Kumar Swain1, Sampada Munjal1, Suryakanta Pradhan2
1 Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University (Deemed to Be), Bhubaneswar, Odisha, India
2 Department of Otorhinolaryngology, Apollo Hospital, Bhubaneswar, Odisha, India
|Date of Submission||14-Jan-2019|
|Date of Decision||28-Mar-2021|
|Date of Acceptance||05-May-2021|
|Date of Web Publication||07-Jul-2021|
Santosh Kumar Swain
Department of Otorhinolaryngology, IMS and SUM Hospital, Siksha “O” Anusandhan University (Deemed to Be), Bhubaneswar, Odisha
Source of Support: None, Conflict of Interest: None
Vestibular migraine (VM) is a distinct clinical entity which accounts for major vestibular symptoms among the adult and children. It is now accepted as a major cause for episodic vertigo. The pathophysiology for VM is not completely understood and is always a puzzling dilemma. Patients often present with vertigo, headache, photophobia, and phonophobia. The clinical examinations and laboratory investigations are usually within normal limit. The diagnosis of VM is often challenging as there are no confirmatory tests available. The treatment is often similar to the migraine headache. The present-day recommendation is to use the same prophylactic medications used for migraine including beta-blockers, antidepressants, and anticonvulsants. It is always a challenging disease for clinician and often creates a puzzle for diagnosis and treatment. Proper diagnosis and treatment of VM need a thorough understanding of the current literatures which are discussed details in this review article.
Keywords: Migraine, migraine-related vertigo, vertigo, vestibular migraine
|How to cite this article:|
Swain SK, Munjal S, Pradhan S. Vestibular migraine. Apollo Med 2021;18:179-83
| Introduction|| |
Dizziness is a common clinical symptom in daily medical practice. Patient presenting migraine along with vertigo or dizziness is called as vestibular migraine (VM). It is also called as migraine-associated vertigo (MAV), migraine-related vertigo (MRV), migrainous vertigo, or basilar artery migraine. VM is a type of migraine results in vestibular symptoms in addition to the typical symptoms of migraine. VM was first described by Dieterich and Brandt in 1999 and it corresponds to a type of migraine where main symptom is vestibular. VM is more prevalent in individuals without aura and predominantly affects female, at a ratio up to 5:1 (F/M). It is documented that 1% of the population suffers with VM which accounts for most common central cause of episodic vertigo and second most common cause of vertigo in total. VM is often confused with vestibular disorders which are important cause for dizziness complained by the patients. The most common vestibular disorders which manifest in dizziness are benign paroxysmal positional vertigo, VM, Meniere's disease, and vestibular neuritis in decreasing order of frequency. VM represents the second most common cause for vertigo after benign paroxysmal positional vertigo.
| Methods|| |
A literature search was done using PubMed (MEDLINE), Scopus, and Google Scholar. The search was conducted between the years 1980 and 2018 using the keywords VM, MRV, and MAV. Articles were selected on the basis of pathophysiology, epidemiology, clinical presentations, diagnosis, and treatment. A total of 38 articles were selected and the comprehensive search was summarized in this review article.
VM is more commonly seen than other vestibular disorders. Vertigo and migraine are common clinical entity which affects 7% and 14% of the general population, respectively. The simultaneous occurrence of vertigo and migraine would be 1% if occurring at random. However, a present epidemiological study document that 3.2% of the populations have both vertigo and migraine. It affects female about three times more common than male. It has been reported lifetime prevalence of migraine of 16%, a lifetime prevalence of vertigo of 7%, and a comorbidity of 3.2% rather than 1.1% expected chance of individual. One study documented that VM has a 1-year prevalence of 0.89% and accounts for approximately 10% of patients seen for vertigo and approximately 10% of patients seen for migraine. In one study, the 1-year prevalence of VM in female aged 40–54 years is 5%.
The basic pathophysiology for migraine 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. The vasodilatation effect of parasympathetic stimuli on trigeminovascular reflex may be augmented by neurokinin A, calcitonin gene-related peptide, and substance P released from sensory terminals of trigeminal nerve. Vestibular pathways often contribute to both peripheral and central migraine mechanism. 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. Alternatively, there is direct connection from 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 such as vasospasm-induced ischemia of the inner ear and plasma extravasations during migraine attack may lead to permanent injury to vestibule and cochlea., The clinical presentations of these patients are often similar to vestibular dysfunction. Furthermore, 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.
Different studies have documented the genetics of the VM. Case series documented a genetic risk factor prevalent in patients suffering with VM, but the risk factors cannot be attributed any particular genetic mutation. A study was done among 24 patients suffering from benign recurrent vertigo and 220 family members who underwent a structured clinical interview revealed 40% of the first-degree relatives suffering from the same type recurrent vertigo episodes whereas in contrast to 2% of unrelated spouses. One study reported that VM might be heterogenous or monogenic. There is no evidence of an association between sodium and calcium channel genes linked to familial hemiplegic migraine. There is a region on chromosome 11q which common in females among family with MRV. There is 12.0 MB interval on chromosome 5q35 which contains a disease gene for familial MRV. The pathophysiology for VM is still unclear.
VM is a variant of migraine resulting in vestibular symptoms like vertigo along with symptoms of migraine. 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 Meniere's disease. Patient often complaints episodic spinning, imbalance or rotating sensation, or giddiness or lightheadedness from few seconds to hours or days. Patient often presents with severe episodic pulsating headache. Patient has usually no hearing loss when associated with common and classical migraine. In 80% cases of basilar migraine have sensorineural hearing loss and tinnitus which may mimics to the Meniere's syndrome. The physical examinations of patients suffering from MRV are usually normal between two episodes. During episodic attack, the patients generally manifest a nystagmus either peripheral or central vestibular abnormality. Nonparoxysmal positional nystagmus is often seen during episodic attack of VM.
The peripheral vestibular lesions which mimic to VM are Meniere's disease, vestibular neuronitis, benign paroxysmal positional vertigo, and perilymph fistula. The central lesions which mimic to VM are transient ischemic accident, multiple sclerosis, Vertebrobasilar insufficiency insufficiency, neurodegenerative disorders, and familial ataxia syndrome. The International Headache Society(IHS) has declared well-recognized criteria for the diagnosis of migraine [Table 1]. However, the vertigo is mentioned in this classification only in respect of basilar migraine and benign paroxysmal positional vertigo. Now, it is though that the higher prevalence of VM is more than the chance of association.
|Table 1: Diagnostic criteria of vestibular migraine (International Headache Society and Barany Society)|
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Migraine may be classified into (1) common migraine (migraine without aura) - 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) - there 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 as aura and neurological tests are within normal limit; (3) basilar migraine (type of classical migraine) - 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 - vestibular symptoms are additional features due to vestibule-cochlear artery spasm along with classical migraine; and (5) complicated migraine/migrainous infraction - it 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 Barany Society and the Subcommittee of IHS. It is seen in the appendix of the 3rd edition of HIS as a first step for new clinical entities. 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, and 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 Meniere's disease and VM [Table 2]. VM is a multifactorial 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% female and 6% male 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. 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. Hearing loss is not a clinical feature of common and classical migraine but on 80% cases of basilar migraine have sensorineural type of hearing loss and/or tinnitus resembling to the Meniere's syndrome. At the time of aura, spontaneous or positional nystagmus can be seen whereas patient may not have any neurological deficits. 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.
|Table 2: Difference (clinical presentations) between vestibular migraine and Meniere's disease|
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The diagnosis of VM is often challenging as there are no established confirmatory tests available for the diagnosis. The clinical diagnosis of VM may be difficult as it shares features with many clinical conditions. There is no such international agreement for spectrum of clinical symptoms covered under this disease or what medical terminology should be used. The vestibular symptoms and headache in VM may not be temporarily associated, which often hide the association. 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. Diagnostic tests often show nonspecific abnormal results which are also seen in patients with migraine those do not experience vestibular symptoms. 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 neuroimaging are required. Vestibular-evoked myogenic potential (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 heterogenous. These findings show reduced electromyography amplitudes, bilateral or unilateral lose of cervical VEMP responses, shifting of maximum VEMP response from 500 to 1000 Hz, and increased latencies. 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. 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. Caloric electronystagmography may be needed to differentiate peripheral vestibular diseases from VM. There is reduced caloric response in peripheral vestibular hypofunction/loss, vestibular neuritis, and labyrinthitis. Video head impulse test is also useful to differentiate these vestibular disorders from VM. MRI brain or MR angiography can rule out the central lesions for vertigo like cerebrovascular diseases. 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. As per a recent study, there are changes of gray matter in VM in comparison to control group with increased gray matter volume of left temporal lobe, frontal lobe, left thalamus and occipital lobe as well as reduced gray matter in the left cerebellum. It needs further evaluation of MRI for the VM patients. Caloric hypoactivity, oculomotor abnormalities, and hearing loss are rarely seen in VM.
Physiological tests are not sufficient alone for diagnosis of the VM as these are inconsistent and patients have high incidence of VM without vestibular presentations. However, the physiological tests can be employed to rule out other vestibular lesions and to establish the extent of vestibular lesions if present. Approximately 10%–20% of the patients suffering from VM have unilateral decrease in vestibular function. Patients with MRV have higher postural sway than patients without VM. There is reduced amplitude in VEMPs in patients of VM.
The management of VM needs treatment of vertigo attack and prophylactic treatment. The drugs used for prophylaxis are same as for migraine which includes beta-blockers, antidepressants, and anticonvulsants. There are two treatment options and these are prophylactic and abortive medications for migraine which can be used for the treatment of VM. One study documented 38% of VM responded to zolmitriptan versus 22% to placebo. The medications that are used for migraine prophylaxis can be used for the VM. These medications are propranolol, bisoprolol, flunarizine, and metoprolol., Serotonin has an important role in pathophysiology of migraine and also causes vestibular symptoms. Deprivation of tryptophan which is an amino acid used in serotonin synthesis resulting in heightened vertigo symptoms. Tricylic antidepressant which enhances central serotonin level may be useful in prophylactic treatment of VM particularly in patients with anxiety. GABA mimicking medications such as gabapentin are also helpful for the patients of VM.
| Conclusion|| |
Accurate diagnosis of VM is often challenging situation for clinicians. The pathophysiology for VM is always a puzzling dilemma for clinician. 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. There is always a challenge for the VM from both clinical and basic science aspect to enable appropriate and rational management of this disease. 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. Other clinical symptoms are photophobia, phonophobia, bilateral aural fullness, tinnitus, and otalgia. The majority of the VM patients have a past history of motion sickness. Videonystagmography (VNG) often shows positional nystagmus not localizing for a central or peripheral site of lesions. Migraine prophylaxis is often helpful for the treatment of VM.
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| References|| |
Dieterich M, Brandt T. Episodic vertigo related to migraine (90 cases): Vestibular migraine? J Neurol 1999;246:883-92.
Furman JM, Marcus DA, Balaban CD. Vestibular migraine: Clinical aspects and pathophysiology. Lancet Neurol 2013;12:706-15.
Maldonado Fernandez M, Birdi JS, Irving GJ, Murdin L, Kivekäs I, Strupp M. Pharmacological agents for the prevention of vestibular migraine. Cochrane Database Syst Rev 2015;6:1-35.
Strupp M, Brandt T. Peripheral vestibular disorders. Curr Opin Neurol 2013;26:81-9.
Lempert T, Neuhauser H. Epidemiology of vertigo, migraine and vestibular migraine. J Neurol 2009;256:333-8.
Cherchi M, Hain TC. Migraine-associated vertigo. Otolaryngol Clin North Am 2011;44:367-75, viii-ix.
Pagnini P, Vannucchi P, Giannoni B, Pecci R. Epigone migraine vertigo (EMV): A late migraine equivalent. Acta Otorhinolaryngol Ital 2014;34:62-70.
Neuhauser HK, Radtke A, von Brevern M, Feldmann M, Lezius F, Ziese T, et al
. Migrainous vertigo: Prevalence and impact on quality of life. Neurology 2006;67:1028-33.
Hsu LC, Wang SJ, Fuh JL. Prevalence and impact of migrainous vertigo in mid-life women: A community-based study. Cephalalgia 2011;31:77-83.
Goadsby PJ, Lipton RB, Ferrari MD. Migraine – Current understanding and treatment. N Engl J Med 2002;346:257-70.
May A, Goadsby PJ. The trigeminovascular system in humans: Pathophysiologic implications for primary headache syndromes of the neural influences on the cerebral circulation. J Cereb Blood Flow Metab 1999;19:115-27.
Furman JM, Marcus DA, Balaban CD. Migrainous vertigo: Development of a pathogenetic model and structured diagnostic interview. Curr Opin Neurol 2003;16:5-13.
Lee JW, Jung JY, Chung YS, Suh MW. Clinical manifestation and prognosis of vestibular migraine according to the vestibular function test results. Korean J Audiol 2013;17:18-22.
Parker W. Menière's disease. Etiologic considerations. Arch Otolaryngol Head Neck Surg 1995;121:377-82.
Radtke A, Lempert T, Gresty M, Brookes G, Bronstein A, Neuhauser H. Migraine and Meniere's disease: Is there a link? Neurology 2002;59:1700-4.
Kolkiela EA, Elsanadiky HH, Nour YA. A study of the correlation between migraine and vestibular vertigo. Egypt J Ear Nose Throat Allied Sci 2017;18:95-101.
Oh AK, Lee H, Jen JC, Corona S, Jacobson KM, Baloh RW. Familial benign recurrent vertigo. Am J Med Genet 2001;100:287-91.
Radtke A, Neuhauser H, von Brevern M, Hottenrott T, Lempert T. Vestibular migraine-validity of clinical diagnostic criteria. Cephalalgia 2011;31:906-13.
Neuhauser H, Lempert T. Vestibular migraine. Neurol Clin 2009;27:379-91.
Cohen JM, Bigal ME, Newman LC. Migraine and vestibular symptoms-identifying clinical features that predict “vestibular migraine”. Headache 2011;51:1393-7.
Millen SJ, Schnurr CM, Schnurr BB. Vestibular migraine: Perspectives of otology versus neurology. Otol Neurotol 2011;32:330-7.
Cha YH, Lee H, Santell LS, Baloh RW. Association of benign recurrent vertigo and migraine in 208 patients. Cephalalgia 2009;29:550-5.
Udagatti VD, Dinesh Kumar R. Migraine related vertigo. Indian J Otolaryngol Head Neck Surg 2017;69:563-7.
International Headache Society Classification Subcommittee. International Classification of Headache Disorders, 2nd
edition. Cephalalgia 2004;24:1-160.
Lempert T, Olesen J, Furman J, Waterston J, Seemungal B, Carey J, et al
. Vestibular migraine: Diagnostic criteria. J Vestib Res 2012;22:167-72.
Zhang Y, Kong Q, Chen J, Li L, Wang D, Zhou J. International Classification of Headache Disorders 3rd edition beta-based field testing of vestibular migraine in China: Demographic, clinical characteristics, audiometric findings and diagnosis statues. Cephalalgia 2016;36:240-8.
Dash AK, Panda N, Khandelwal G, Lal V, Mann SS. Migraineand audiovestibular dysfunction: Is there a correlation? Am J Otolaryngol 2008;29:295-9.
Polensek SH, Tusa RJ. Nystagmus during attacks of vestibular migraine: An aid in diagnosis. Audiol Neurootol 2010;15:241-6.
O'Connell Ferster AP, Priesol AJ, Isildak H. The clinical manifestations of vestibular migraine: A review. Auris Nasus Larynx 2017;44:249-52.
Boldingh MI, Ljøstad U, Mygland A, Monstad P. Vestibular sensitivity in vestibular migraine: VEMPs and motion sickness susceptibility. Cephalalgia 2011;31:1211-9.
Neff BA, Staab JP, Eggers SD, Carlson ML, Schmitt WR, Van Abel KM, et al
. Auditory and vestibular symptoms and chronic subjective dizziness in patients with Ménière's disease, vestibular migraine, and Ménière's disease with concomitant vestibular migraine. Otol Neurotol 2012;33:1235-44.
Radtke A, von Brevern M, Neuhauser H, Hottenrott T, Lempert T. Vestibular migraine: Long-term follow-up of clinical symptoms and vestibulo-cochlear findings. Neurology 2012;79:1607-14.
Cohen JM, Escasena CA. Headache and dizziness: How to differentiate vestibular migraine from other conditions. Curr Pain Headache Rep 2015;19:31.
Casani AP, Sellari-Franceschini S, Napolitano A, Muscatello L, Dallan I. Otoneurologic dysfunctions in migraine patients with or without vertigo. Otol Neurotol 2009;30:961-7.
Celebisoy N, Gökçay F, Sirin H, Biçak N. Migrainous vertigo: Clinical, oculographic and posturographic findings. Cephalalgia 2008;28:72-7.
Messina R, Rocca MA, Colombo B, Teggi R, Falini A, Comi G, et al
. Structural brain abnormalities in patients with vestibular migraine. J Neurol 2017;264:295-303.
Bisdorff AR. Management of vestibular migraine. Ther Adv Neurol Disord 2011;4:183-91.
Neuhauser H, Radtke A, von Brevern M, Lempert T. Zolmitriptan for treatment of migrainous vertigo: A pilot randomized placebo-controlled trial. Neurology 2003;60:882-3.
Stolte B, Holle D, Naegel S, Diener HC, Obermann M. Vestibular migraine. Cephalalgia 2015;35:262-70.
Swain SK, Mohanty S, Sahu MC. Migraine-related vertigo in an elderly male. Apollo Med 2018;15:112-5. [Full text]
Drummond PD. Effect of tryptophan depletion on symptoms of motion sickness in migraineurs. Neurology 2005;65:620-2.
Fotuhi M, Glaun B, Quan SY, Sofare T. Vestibular migraine: A critical review of treatment trials. J Neurol 2009;256:711-6.
Brodsky JR, Cusick BA, Zhou G. Evaluation and management of vestibular migraine in children: Experience from a pediatric vestibular clinic. Eur J Paediatr Neurol 2016;20:85-92.
[Table 1], [Table 2]