Migraine-related vertigo: Diagnosis and treatment

A comprehensive review of the neurotologic manifestations of migraine is presented, focusing on the most recent publications regarding the epidemiology, clinical presentation, pathophysiology, diagnosis, and management of migraine-related vertigo (MV). A strong association exists between vertigo and migraine, with MV being the most common cause of spontaneous (nonpositional) episodic vertigo. Symptoms can be quite variable among patients and within individual patients over time, creating a diagnostic challenge. MV generally presents with attacks of spontaneous or positional vertigo lasting seconds to days with associated migrainous symptoms. Operational diagnostic criteria have been proposed but are not included in the most recent International Headache Society classification of migraine. Better elucidation of the neurologic linkages between the central vestibular pathways and migraine-related pathways and the discovery of ion channel defects underlying some causes of familial migraine, ataxia, and vertigo have furthered the understanding of MV pathophysiology. Treatment of MV currently parallels that of migraine headache, as proper studies of optimal MV management are just beginning.     

Headaches related to triptans therapy in patients of migrainous vertigo

Dizziness and vertigo are frequently reported by patients with migraine. In migrainous vertigo (MV), vertigo is causally related to migraine. Patients of MV usually have an attenuated or absent headache with their vertigo as compared with their usual headache of migraine. Here we report three female patients of MV in which administration of triptan was associated with induction (two patients) or exacerbation (one patient) of headache with disappearance of vertigo. We suggest that headache and vertigo of migraine may be inversely related to each other and suppression of one may induce or aggravate the other.     

Horizontal Direction‐Changing Positional Nystagmus and Vertigo: A Case of Vestibular Migraine Masquerading as Horizontal Canal BPPV

Episodic positional vertigo is typically due to benign paroxysmal positional vertigo (BPPV) but may also be a manifestation of vestibular migraine. Distinguishing vestibular migraine from BPPV is essential since the treatment of each disorder is markedly different. The 31‐month clinical course of a 41‐year‐old woman with vestibular migraine causing recurrent positional vertigo is described. During vestibular migraine attacks, she developed left‐beating nystagmus in the upright position with removal of fixation, and geotropic horizontal nystagmus during the supine roll test. Interictally, her exam demonstrated positional apogeotropic horizontal nystagmus with the supine roll test, more intense in the supine head left position. Her vestibular migraine was successfully controlled with topiramate and eletriptan.     

Benign paroxysmal vertigo of childhood: a long-term follow-up

We examined clinical aspects of Benign Paroxysmal Vertigo (BPV) in infancy and its most frequent differential diagnosis, in particular analogies and differences with forms of "migrainous vertigo" (MV) of later onset. During a long-term follow-up of 7 cases of BPV, diagnosed according to the Basser criteria, 5 of 7 BPV cases spontaneously resolved and 6 of 7 patients later developed migraine and other migraine-related symptoms. This course differs from that described for MV only in the age of onset of headache and in the chronological relationship with vertigo. The authors suggest that BPV can be interpreted as a migraine precursor and MV as a migraine equivalent.     

Migrainous Vertigo Responsive to Intravenous Methylprednisolone: Case Reports

Migrainous vertigo (MV) is a newer evolving concept in which vertigo is causally related to migraine. We report 4 patients with MV. Episodes of severe MV of more than 1-day duration were successfully terminated by intravenous methylprednisolone (IV MPS) in 2 patients. Two other patients who had attacks of MV almost daily also showed complete response to IV MPS.     

Migrainous Vertigo: Results of Caloric Testing and Stabilometric Findings

Background.— Association between migraine and vertigo has been widely studied during the last years. A central or peripheral vestibular damage may occur in patients with migrainous vertigo. Despite much evidence, at present the International Headache Society classification does not include a specific category for migrainous vertigo. Objectives.— To assess the prevalence of central and peripheral vestibular disorders and postural abnormalities in patients diagnosed as affected by definite migrainous vertigo according to Neuhauser. Methods.— Thirty patients with migraine and acute vertigo lasting from minutes to hours underwent a full otoneurological screening for spontaneous, positional, and positioning nystagmus with head‐shaking and head‐thrust (Halmagyi) tests, an audiometric examination, and videonystagmography with bithermal stimulation according to Freyss. Videonystagmographic findings were compared with those of 15 migraineurs without lifetime vertigo (group M). Next day, a static posturography was performed; posturographic results have been compared with those of a second control group of 30 healthy patients matched for age and sex (group C). Results.— In total, 14 subjects with migrainous vertigo showed otovestibular disorders; 6 subjects showed impaired vestibulo‐oculomotor reflexes (20%). Five more patients had bilateral increased responses (16.6%). Five patients showed signs of central brainstem or cerebellar disorders for altered pursuit or saccades or positional direction changing nystagmus. Stabilometric results returned higher values of Length and Surface above all when testing was performed in eyes closed conditions compared with the normal control group. The subgroup of 14 subjects with migrainous vertigo and vestibular abnormalities performed poorly in stabilometric exams and seemed to rely more on visual cues in balance control than the subgroup of 16 subjects with migrainous vertigo but without abnormalities. Discussion.— Our results indicate that vestibular functional damage may occur in all vestibular pathways; central and peripheral signs are equally represented. Our data are not inconsistent with the hypothesis that a vestibulo‐spinal dysfunction is the causal factor for the posturographic results. Moreover, the Visual Romberg Index is significant for increased visual cue dependence in migraineurs.     

Association of benign recurrent vertigo and migraine in 208 patients

The aim of this study was to determine the association of benign recurrent vertigo (BRV) and migraine, using standardized questionnaire-based interview of 208 patients with BRV recruited through a University Neurotology clinic. Of 208 patients with BRV, 180 (87%) met the International Classification of Headache Disorders 2004 criteria for migraine: 112 migraine with aura (62%) and 68 without aura (38%). Twenty-eight (13%) did not meet criteria for migraine. Among patients with migraine, 70% experienced headache, one or more auras, photophobia, or auditory symptoms with some or all of their vertigo attacks, meeting the criteria for definite migrainous vertigo. Thirty per cent never experienced migraine symptoms concurrent with vertigo attacks. These met criteria for probable migrainous vertigo. Among patients without migraine, 21% experienced either photophobia or auditory symptoms with some or all of their vertigo attacks; 79% experienced only isolated vertigo. The age of onset and duration of vertigo attacks did not differ significantly between patients with (34 ± 1.2 years) and patients without migraine (31 ± 3.0 years). In patients with migraine, the age of onset of migraine headache preceded the onset of vertigo attacks by an average of 14 years and aura preceded vertigo by 8 years. The most frequent duration of vertigo attacks was between 1 h and 1 day. Benign recurrent vertigo is highly associated with migraine, but a high proportion of patients with BRV and migraine never have migraine symptoms during their vertigo attacks. Other features such as age of onset and duration of vertigo are similar between patients with or without migraine.     

Vertigo, Motion Sickness and Migraine

SYNOPSIS
The frequency of vestibular symptoms in 104 headache patients during the headache-free phase was studied. The group was comprised of 84 patients with migraine (24 classical and 60 common) 12 with tension and 8 with cluster headache. Fifty-four headache-free subjects served as controls. All the participants filled out a vestibular symptom questionnaire.
Patients with classical migraine reported significantly more vestibular symptoms than the controls. Specifically they had more dizzy spells (r = 0.002) and vertigo episodes (r = 0.01) not associated with the headache. They also had more frequent motion sickness spells. Of the classical migraine patients reporting motion sickness 87% experienced it at least once in 6 weeks compared to only 11% of the controls. Classical migraine patients also probably have an especially "sensitive" vestibular system, as evidenced by increased tendency to visual vertigo (r = 0.005) and significantly increased dizziness when they themselves were spinning.
The common migraine patients showed a tendency to vestibular impairment that was not statistically significant. Recent findings of vestibular function abnormalities in this group may suggest an evolving dysfunction that is not yet symptomatic. Patients with tension and cluster headache did not differ from the controls in all the vestibular symptoms studied.
In summary, our findings indicate clearly a vestibular impairment in classical migraine. The relation to "benign recurrent vertigo," problems in the relationship of the occurrence of motion sickness to migraine and the possible mechanism causing the vestibular dysfunction are discussed.     

Initial evaluation of vertigo

Benign paroxysmal positional vertigo, acute vestibular neuronitis, and Meniere's disease cause most cases of vertigo; however, family physicians must consider other causes including cerebrovascular disease, migraine, psychological disease, perilymphatic fistulas, multiple sclerosis, and intracranial neoplasms. Once it is determined that a patient has vertigo, the next task is to determine whether the patient has a peripheral or central cause of vertigo. Knowing the typical clinical presentations of the various causes of vertigo aids in making this distinction. The history (i.e., timing and duration of symptoms, provoking factors, associated signs and symptoms) and physical examination (especially of the head and neck and neurologic systems, as well as special tests such as the Dix-Hallpike maneuver) provide important clues to the diagnosis. Associated neurologic signs and symptoms, such as nystagmus that does not lessen when the patient focuses, point to central (and often more serious) causes of vertigo, which require further work-up with selected laboratory and radiologic studies such as magnetic resonance imaging.     

Treatment of vertigo

Vertigo is the illusion of motion, usually rotational motion. As patients age, vertigo becomes an increasingly common presenting complaint. The most common causes of this condition are benign paroxysmal positional vertigo, acute vestibular neuronitis or labyrinthitis, Ménière's disease, migraine, and anxiety disorders. Less common causes include vertebrobasilar ischemia and retrocochlear tumors. The distinction between peripheral and central vertigo usually can be made clinically and guides management decisions. Most patients with vertigo do not require extensive diagnostic testing and can be treated in the primary care setting. Benign paroxysmal positional vertigo usually improves with a canalith repositioning procedure. Acute vestibular neuronitis or labyrinthitis improves with initial stabilizing measures and a vestibular suppressant medication, followed by vestibular rehabilitation exercises. Meniere's disease often responds to the combination of a low-salt diet and diuretics. Vertiginous migraine headaches generally improve with dietary changes, a tricyclic antidepressant, and a beta blocker or calcium channel blocker. Vertigo associated with anxiety usually responds to a selective serotonin reuptake inhibitor.     

Migrainous vertigo: clinical, oculographic and posturographic findings

Migrainous vertigo (MV) is accepted as a common cause of episodic vertigo. The peripheral or central vestibular localization of the deficit as well as the pathophysiology is unclear. This prospective study was designed to assess the clinical features of MV and to search for the localization of the vestibular pathology. Thirty-five patients with MV, 20 patients with migraine and 20 healthy volunteers were studied. Comprehensive neurotological tests were performed between attacks. None of the normal controls or the patients with migraine had ocular motor deficits or caloric test abnormalities. Three patients in the MV group showed saccadic pursuit (8.6%), in one of whom saccadic hypometria was also present. Caloric test results revealed unilateral caloric hypofunction in seven patients (20%). Static posturography results revealed increased sway velocity when the eyes were closed or the platform was distorted in patients with MV. These findings during the symptom-free period revealed that peripheral vestibular dysfunction was more common than a central deficit.     

Diagnosis and management of vertigo

Vertigo is an illusion of rotation due to a disorder of the vestibular system, almost always peripheral. In the history it must be distinguished from pre-syncope, seizures and panic attacks. A single attack of acute, isolated spontaneous vertigo lasting a day or more is due either to vestibular neuritis or cerebellar infarction; distinguishing between the two requires mastery of the head impulse test. Recurrent vertigo is mostly due to benign paroxysmal positioning vertigo (BPPV), Meniere's disease or migraine. With a good history, a positional test, an audiogram and a caloric test, it is usually possible to distinguish between these. BPPV is the single most common cause of recurrent vertigo and can usually be cured immediately with a particle repositioning manoeuvre. Posterior circulation ischaemia very rarely causes isolated vertigo attacks and when it does the attacks are brief and frequent and the history is short.     

The point prevalence of dizziness or vertigo in migraine--and factors that influence presentation

Objective.— To ascertain and characterize the point prevalence of dizziness or vertigo in migraineurs presenting for routine appointments at a specialty headache clinic. Background.— Migraine, dizziness, and vertigo are all common in the general population, affecting 13%, 20‐30%, and 5‐10% respectively. Thereby, chance concurrence of migraine with either dizziness or vertigo would be expected in roughly 4% of the general population. It is the authors' clinical impression that severe attacks of migraine are far more commonly associated with these complaints than chance would predict. Methods.— This is a prospective, cross‐sectional study of 462 consecutive patients who presented for consultation at a specialty headache clinic over a 4‐month period of time. During routine check‐in procedures, patients were asked to report their headache pain on a 1‐10 Likert scale. Patients were also asked to report if they were currently experiencing dizziness or vertigo. Responses to these questions were recorded along with vital signs. Diagnosis of migraine with or without aura was made by headache medicine specialists in accordance with International Classification of Headache Disorders – second edition criteria. Chi‐square analysis was used to examine the prevalence of vertigo or dizziness in subjects with varying intensity of headache, and by history of aura. Results.— Of the 425 evaluable subjects, 28% experienced aura. Subjects' average age was 43.8 years (range 15 to 76 years); 89.5% were female. At the time of evaluation, 72.4% of subjects reported some degree of ongoing headache pain and 15.7% reported concurrent dizziness or vertigo. The prevalence of dizziness or vertigo was twice as high (24.5% vs 12.1%) in migraine with aura compared to migraine without aura (P < .01), and prevalence increased with age (P < .05). There was a strong correlation between migraine pain and subjective complaint of vertigo (P < .001). When migraine pain was present at an intensity of 7 or greater (on a scale of 1‐10), almost half of the subjects (47.5%) reported concomitant dizziness or vertigo. Conclusions.— Subjective complaints of dizziness or vertigo appear to be relatively common accompaniments of migraine, particularly migraine with aura, and prevalence increases with age. Disequilibrium symptoms have a strong and positive association with the severity of migraine pain. With co‐occurrence higher than expected by chance, the relationship either reflects comorbidity or these symptoms may be part of the migraine presentation. With a point prevalence of 15.7%, and factors that link expression both to the intensity of migraine pain and to migraine aura, the authors believe that the true relationship may prove to be the latter.     

Prevalence and impact of migrainous vertigo in mid-life women: a community-based study

We surveyed 1436 women aged 40-54 years in the community. Of these, 278 (19.4%) were diagnosed with migraine or probable migraine based on the International Classification of Headache Disorder criteria. The diagnoses of migrainous vertigo (MV) were modified from Neuhauser's criteria. Of the 278 women, 238 (85.6%) underwent an interview and 72 (30.3%) of those with migraine or probable migraine had MV. The 1-year prevalence of MV among mid-life women was 5.0% (95% CI, 4.0-6.3%). The MV subjects had a higher proportion of aura (23.6% vs 9.6%; OR, 2.9), nausea (76.4% vs 55.8%; OR, 2.6) and photophobia (61.1% vs 41.7%; OR, 2.2) compared with the migraine subjects without MV. The migrainous subjects with and without MV had similar Short-Form 36 (SF-36) scores. Our study showed that MV was common in mid-life women. Their health-related quality of life was similar in migrainous subjects with MV and those without MV.     

Phenotypic and genetic analysis of a large family with migraine-associated vertigo

Objectives.— To describe a large multigenerational family with migraine‐associated vertigo (MAV) combining a detailed phenotypic and genetic analysis. Background.— Migraine‐associated vertigo is said to be highly prevalent in the general population and, like other migraine syndromes, its etiology is felt to have a strong genetic component. However, so far, there have been no reports of large families with MAV. Methods.— Detailed clinical study was conducted on a large multigenerational family with MAV. Genetic study using identical‐by‐descent analysis with dense single nucleotide polymorphism (SNP) arrays was performed to examine consistent inheritance pattern among the affecteds. Results.— Clinical features of MAV were variable although most had other migraine symptoms with at least some of their attacks. We did not find a region of the genome shared by all eight subjects with MAV indicating a polygenetic inheritance for MAV even in this single large family. Conclusions.— A region on 11q shared by most affected females may contain a susceptibility allele for MAV that is expressed exclusively or predominantly by women.     

Migraine: An Alternative in the Diagnosis of Unclassified Vertigo

SYNOPSIS
Vertigo and unsteadiness are frequent reasons for medical consultation. In some cases, these symptoms remain unclassified. The association of equilibrium disorders with migraine is often mentioned in literature.
Seventy-two cases of unclassified vertigo were studied in order to ascertain the prevalence of migraine in patients affected by recurring episodes of vertigo from undetermined causes, and attempting to establish a possible relationship with migraine. Characteristics of the vertigo and the headache, were evaluated by clinical history and examination, electronystagmogram (ENG), electroencephalogram (EEG), computerized tomography scanning (CT) and/or magnetic resonance imaging (MRI). In the group of patients studied 50% suffered from headache, and 32.8% fulfilled the diagnostic criteria of migraine. Results suggest that only a thorough clinical history would be able to give enough information to establish the diagnosis of migraine in these patients.
These observations imply an alternative diagnosis to be taken into account when a case of unclassified vertigo is evaluated.     

ICE CREAM HEADACHE AND ORTHOSTATIC SYMPTOMS IN PATIENTS WITH MIGRAINE

SYNOPSIS
Migraine is arbitrarily defined; biological markers for the condition are needed. Two stereotyped phenomena which may be manifestations of central vasomotor instability have been studied in migraineurs and in control subjects. These phenomena are (1) "ice cream headache", the brief frontal pain that results from cold food contacting the roof of the oropharynx and (2) the presence of vertigo, visual obscurations, and/or scintillating scotomata following rapid postural shifts of the head.
Hospitalized (non-neurologic) patients (60 women, 48 men) were interviewed regarding the presence, quality, and intensity of the two phenomena. A history of headache was then elicited in some detail. The headache histories were assessed by the usual arbitrary criteria for migraine; this was done by an independent observer without knowledge of the presence of ice cream headache or postural symptoms. In the non-headache, control population (49), 31% had experienced mild ice cream headache; in the migraine group (59), 93% had experienced ice cream headache (p<.001), usually (77%) as a moderate to severe discomfort. Half of the migraineurs took precautions when ingesting cold foods. Of the controls, 8% had brief vertigo or lightheadedness with rapid postural shifts; postural symptoms were present in 68% of the migraine group (p>.001), most of whom (75%) reported that scintillating scotomata accompanied vertigo. Both syndromes occurred more regularly and more prominently in the migraine population.     

Migraine aura without headache: benign, but a diagnosis of exclusion

Migraine aura without headache should be considered as a diagnosis in anyone who has recurrent episodes of transient symptoms, especially those that are visual or neurological or involve vertigo. Visual and neurological symptoms due to migraine are not unusual and most commonly occur in older persons with a history of migraine headaches. Migraine aura without headache should be diagnosed only when transient ischemic attack and seizure disorders have been excluded.     

The dizzy patient

A patient's history usually contains key information regarding the type of dizziness and the best way to direct diagnostic workup. In dizziness with a vestibular cause (benign positional vertigo, vestibular neuritis, Meniere's disease, migraine, vertebrobasilar insufficiency), patients often describe their world as spinning, whirling, or tilting. Treatment should be directed at the underlying cause whenever possible, and various antivertiginous and antiemetic medications can be used to suppress symptoms. Initiation of a vestibular exercise program as soon as possible after injury helps ensure the best compensation possible.     

Vestibul?rer Schwindel als Symptom der Migr?ne

Zusammenfassung Epidemiologie: Migräne und Schwindel sind häufige Beschwerden, so dass sie zufällig bei einem Patienten zusammentreffen können. Darüber hinaus gibt es jedoch Schwindel, der durch einen Migränemechanismus verursacht wird; in Spezialambulanzen für Schwindel macht er 6-8% der Diagnose aus. Klinik: Der migräneassoziierte Schwindel ist eine vestibuläre Erkrankung und manifestiert sich mit spontanen und lageabhängigen Drehschwindelattacken oder Schwindel bei Kopfbewegungen. Er tritt häufig ohne Kopfschmerzen auf und variiert in seiner Dauer von Sekunden bis zu 3 Wochen. Diagnose: Für einen migräneassoziierten Schwindel sollten die folgenden Merkmale erfüllt sein: 1. Rezidivierende vestibuläre Symptome, 2. Migräne nach den Kriterien der Internationelen Kopfschmerzgesellschaft, 3. migränetypische Symptome während der Schwindelattacken wie Kopfschmerzen, Licht- oder Geräuschempfindlichkeit, Flimmerskotome oder andere Migräneauren, 4. Ausschluss anderer Ursachen. Pathophysiologie: Die genauen Mechanismen des migräneassoziierten Schwindels sind noch ungeklärt. In Analogie zu den pathophysiologischen Modellen der Migräne werden eine kortikale "Spreading Depression", lokale Perfusionsstörungen, Ausschüttung von spezifischen Neurotransmittern und eine paroxysmale Dysfunktion von Ionenkanälen diskutiert. Klinisch finden sich sowohl Hinweise für periphere als auch für zentrale vestibuläre Funktionsstörungen. Therapie: Zur Behandlung werden die Substanzen eingesetzt, die sich in der akuten und prophylaktischen Therapie von Migränekopfschmerzen als wirksam erwiesen haben. Kontrollierte Therapiestudien fehlen für den migräneassoziierten Schwindel bislang. Abstract Epidemiology: Since both migraine and vertigo are common complaints in clinical practice they may coincide in an indiviudial patient just by chance. There are, however, numerous patients with vestibular symptoms caused by migraine, accounting for 6-8% of diagnoses in specialized dizziness clinics. Clinical Manifestation:< Migraine-associated vertigo is a vestibular disorder which manifests istself with spontaneous or positional rotational vertigo or dizziness induced by head motion. The vertigo may occur without accompanying headache and may last from seconds to several weeks. Diagnosis: Migraine-associated vertigo can be diagnosed according to the following crtiteria: 1. recurrent vestibular symptoms, 2. migraine according to the criteria of the International Headache Society, 3. migrainous symptoms during the vertigo such as headache, photophobia, phonophobia, scintillating scotoma or other auras, 4. exclusion of other causes. Pathophysiology: The mechanism of migraine-associated vertigo is still obscure. Several hypotheses relating to the pathophysiology of migraine have been proposed: cortical speading depression, regional changes in brain perfusion, release of neurotransmitters and paroxysmal dysfunction of ion channels. Clinical findings suggest both central and peripheral vestibular involvement. Therapy: Treatment is based on the repertoire of acute and prophylactic medications that are used for migrainous headaches. Controlled studies on the treatment of migraine-associated vertigo are still lacking.