Spinning Through History: Evolution of the Concept of Vestibular Migraine. — TEI-tagged view

Yoon-Hee ChapersName (2023date). “Spinning Through History: Evolution of the Concept of Vestibular Migraine..” Otology & Neurotology Opentitle·j.

Object of study — the history of how migraineterm·dom and vestibular symptoms have been conceptualised

Research question — how ideas about vestibular migraineterm·dom developed and how they shape its treatment

Contribution — a history of the ideas behind vestibular migraineterm·dom, to show which have lasted and which should keep evolving

Full text — tagged

Spinning Through History: Evolution of the Concept of Vestibular Migraineterm·dom.

Abstract Vestibular migraineterm·dom represents a growing public health problem, imposing enormous societal burdens in the form of patient suffering, loss of productivity, and direct healthcare costs. This raises the question of how we developed our ideas about vestibular migraineterm·dom and how these ideas shape how we treat it.

This reviewterm·mth walks through the history of how our conceptualization of migraineterm·dom and vestibular symptoms evolved, starting with clinical observations in ancient times, inclusion under the umbrella of Meniere’s diseaseterm·dom, and then separation from Meniere’s diseaseterm·dom with its own identity. Tradition, clinical observations, and diagnostic criteriaterm·key developed by professional societies have played prominent roles in building our current concept of vestibular migraineterm·dom. A reviewterm·mth of the ideas that have shaped our current conception of vestibular migraineterm·dom may help us to see which ones have stood the test of time and which ones should continue to evolve. As in other disciplines, we study history in medicine to be inspired, warned, and sometimes, to be freed.

Keywords: Meniere’s diseaseterm·dom, migraineterm·dom, vertigoterm·dom, vestibular migraineterm·dom Cerebral congestionterm·dom was the predominant mechanism evoked for paroxysmal neurological symptoms, including vertigoterm·dom, until the mid-19th century.

In 1861, Prosper Meniere showed evidence for inner ear involvement in the generation of vertigoterm·dom, defying the cerebral congestionterm·dom theory.

Episodic vertigoterm·dom was originally conceptualized under the Meniere’s umbrella in the early 20th century then moved to under the migraineterm·dom umbrella in the early 21st century as vestibular migraineterm·dom.

The current diagnostic criteriaterm·key for vestibular migraineterm·dom were developed as a collaboration between the International Headache Society and the International Bárány Societyterm·key.

Vestibular migraineterm·dom has quickly become the most common diagnosis in specialty practices caring for patients with headaches and vestibular symptoms, now accounting for 25% of patients in headache clinics and up to 30% of patients in neurotology clinics ( 1 – 4 ). What this high prevalence of vestibular migraineterm·dom reflects is how common dizzinessterm·dom and vestibular symptoms are in people who are prone to headaches and how much the right framework for understanding their association is needed.

The current diagnostic criteriaterm·key for definite and probable vestibular migraineterm·dom jointly, that was created by the International Classification of Headache Disorders (ICHDterm·key) and the International Bárány Societyterm·key, were built off the criteria for migraineterm·dom headaches, a primary headache disorder ( 5 , 6 ) (Table 1 ). The presumption is that vestibular migraineterm·dom is itself a primary disorder without a structural cause. Yet, vestibular migraineterm·dom symptoms heavily overlap with those of Meniere’s diseaseterm·dom, a disorder of known structural inner ear dysfunction. Ambiguity in which category of disorders vestibular symptoms with headache should be placed has led to diagnostic and management unease, especially when there are subjective symptoms such as tinnitus but no objective abnormalities such as hearing loss.

ICHD-3 and Barany Society Criteria for Vestibular Migraineterm·dom Adding to the complexity is that vestibular migraineterm·dom criteria allow for a variety of symptoms, including spontaneous vertigoterm·dom of either self or visual surround motion, positional vertigoterm·dom, visually-induced vertigoterm·dom, head motion-induced vertigoterm·dom, and head motion-induced dizzinessterm·dom with nausea. Allowable symptoms can last from 5 minutes to 72 hours, representing a wide parameter space ( 5 ). Understanding how we developed our current ideas of vestibular migraineterm·dom may be useful in deciding which paradigms for vestibular symptoms and headaches are the most salient for treatment and perhaps even prevention of new cases. To that end, this reviewterm·mth will describe the evolution of our current concept of vestibular migraineterm·dom. Of note, while the International Classification of Vestibular Disorders developed by the Bárány Societyterm·key defined dizzinessterm·dom and vertigoterm·dom to be distinct symptoms (dizzinessterm·dom as spatial disorientation and vertigoterm·dom as an illusion of motion), for the purpose of this reviewterm·mth, they will be used interchangeably as vestibular symptoms have historically been referred to by either word ( 7 ).

PREVALENCE AND BURDEN Neuhauser et al. ( 9 ) in Germany first developed criteria for “migrainous vertigoterm·dom,” a term that evolved into vestibular migraineterm·dom. They found that 7% of patients in their dizzinessterm·dom clinics and 9% of patients in their headache clinics met the criteria for migrainous vertigoterm·dom ( 8 ). They estimated the population 1 year and lifetime prevalence of migraineterm·dom assessed by telephone interview of 4869 people as 0.89% and 0.98%, respectively.

The most recent assessment of vestibular migraineterm·dom in the United States puts the prevalence number even higher at 2.7%, of which 75.8% are female ( 10 ). In this study, Formeister used 2008 census data and retroactively applied the 2012 Bárány Societyterm·key criteria for vestibular migraineterm·dom to a sample of 21,871 people who had completed a 210-item Balance and Dizzinessterm·dom Supplement based on 74,236 total respondents ( 10 ). The risk factors for vestibular migraineterm·dom were found to be age <40 years, female sex, anxiety, depression, and prior head trauma. Extrapolation of the prevalence estimates from this study to the 2023 census would yield over 9 million people suffering from vestibular migraineterm·dom in the United States ( 11 ).

Despite the large numbers, the overall burden of vestibular migraineterm·dom may be underreported. It has only been in recent years that there has been the development of a handicap inventory created specifically for vestibular migraineterm·dom (VM-PATHI: Vestibular Migraineterm·dom Patient Assessment Tool and Handicap Inventory) that directly queries the experience of patients with combined headache and vestibular symptoms ( 12 , 13 ). A growing number of studies have shown that the risk of falls and nonvestibular symptoms such as cognitive dysfunction and chronic fatigue are significantly higher in patients with vestibular migraineterm·dom than in those without ( 14 – 16 ). The complexity of symptoms in vestibular migraineterm·dom explains the high annual cost of caring for these patients, estimated at $11,371 compared to $9,579 for Meniere’s diseaseterm·dom and $8,247 for Benign paroxysmal positional vertigoterm·dom ( 17 ). Considering the chronicity of vestibular migraineterm·dom and the young age of onset, these values represent a significant national economic and public health burden.

THE CEREBRAL CONGESTIONterm·dom MODEL OF VERTIGOterm·dom The connection between headache and vertigoterm·dom was made at least as far back as Hippocrates (BCE 470-360). “ … south winds relax the body, make the tissues moist, reduce acuity of hearing, and produce headaches and vertigoterm·dom .” Aphorisms Sect 3:17 ( 18 ). Hippocrates’, “four humors,” model of human illness (blood, black bile, yellow bile, and phlegm), was continued by Galen of Pergamum (CE 129–200), the chief authority on medicine and biology until the 19th century credited for creating the term “hemicrania” from which the word “migraineterm·dom,” derives. In his work, De locis affectis , (“On the affected parts”), he attributed kephalalgiaterm·dom (headache) to the retention of yellow bile in the stomach, the headache being relieved with vomiting. Skotomaterm·dom referred to one of several forms of vertigoterm·dom that leads to impaired and sometimes darkened vision ( 19 ).

Galenic principles were carried into the Middle East and systematized by the Persian scholar Ibn Sina (Latin, Avicenna, CE 980–1037). In the Canon of Medicine, Ibn Sina described vertigoterm·dom as, “a brain disorder but as principle symptom of melancholy with ‘trembling,’ ’fear,’ and noises in the ear,” and later, “the patient feels ill and uneasy, and suffers from impaired vision, dizzinessterm·dom, and migrainous headaches, with yawning and stretching…” ( 20 ).

The prevailing belief for more than 2 millennia after Hippocrates was that vertigoterm·dom was due to fluid imbalances, specifically “apoplectiform cerebral congestionterm·dom” caused by the overfilling of blood vessels in the brain. This process was summarized in the “Tractatus de Apoplexia” by Francisco Bayle in 1678 and formed the basis of disease paradigms well into the mid-19th century ( 21 , 22 ). Disorders such as vertigoterm·dom, strokes, and epilepsy were thought to be due to compressed vessels or blockage by phlegm and were thus treated with bloodletting, leeches, laxatives, and purgatives ( 19 , 20 ).

The cerebral congestionterm·dom theory formed the foundation of neurological care in the United States. It was the main theme of the first textbook on neurological disorders published in 1871 by William Hammond (CE 1828–1900) the Surgeon General during the Civil War who became the first specialist in neurology in the United States ( 23 – 25 ). In his book, he described “active cerebral congestionterm·dom,” from arterial compression resulting in vertigoterm·dom, “In some cases, headache constitutes the chief feature of the disorder and is almost constantly present. There are noises, such as roaring, rumbling, and ringing, in the ears…” Passive cerebral congestionterm·dom due to venous compression would lead to, “Vertigoterm·dom, pain, illusions, hallucinations, and delusions, are nevertheless generally present at one time or another. But, the stupor or tendency to somnolence is the most prominent feature…” ( 23 ).

THE INNER EAR INJURY MODEL OF VERTIGOterm·dom Two thousand years of assumptions about the origins of vertigoterm·dom would be uprooted by Prosper Meniere (CE 1799–1862). Meniere was a French physician who trained at the prestigious hospital Hôtel-Dieu with the surgeon Baron Guillaume Dupuytren (CE 1777–1835). He was well-known for his obstetrical surgical skills and for his writing. Despite having no background in otology, he was appointed as the head of the Hospital for Deaf Mutes in 1838 when the holder of that position, Jean Marc Gaspard Itard (CE 1775–1838) died ( 26 , 27 ). In this new role, Meniere observed that deaf patients, already accepted to have inner ear disease, often experienced vertigoterm·dom.

In January 1861, Meniere presented a paper to the Paris Imperial Academy of Medicine entitled “Sur une forme de surdité grave dépendant d‘une lesion de lòreille interne,” (“On a serious form of deafness dependent on a lesion of the inner ear”) ( 28 , 29 ). He described a patient who had experienced episodes of vertigoterm·dom, tinnitus, and hearing loss but had no evidence of cerebral disease. This not only questioned the cerebral congestionterm·dom theory but also the exuberant treatments that were based on this theory. The talk was not well-attended but became part of a lively debate when, the following week, Armand Trousseau (CE 1820–1910), Physician-in-Chief at Hôtel-Dieu, presented a paper questioning the prevailing belief that epilepsy was due to apoplectiform cerebral congestionterm·dom. Trousseau’s and Meniere’s claims raised skepticism and vehement opposition, resulting in a debate period that was truncated due to fruitlessness and exasperation ( 27 , 30 ).

Undeterred, Meniere published a paper in September 1861 entitled, “Mémoire sur des lésions de l’orielle interne donnant lieu à des symptômes de congestion cérébrale apoplectiforme,’ (A Report on Lesions of the Inner Ear Giving Rise to Symptoms of Cerebral Congestionterm·dom of Apoplectic Type,”) in which he extended a report that he had previously made on a young patient who had experienced sudden hearing loss and vertigoterm·dom shortly before death and had been found to have a “bloody exudate,” in the inner ear ( 31 ). He concluded the paper with this statement, quite controversial for its time, “All the evidence indicates that the organic lesion which produces these disturbances of function is situated in the semicircular canals” ( 31 ).

Meniere died in 1862 from pneumonia before seeing the widespread acceptance of his ideas. By as early as 1872, however, the triad of vertigoterm·dom, tinnitus, and hearing loss became known as, “Maladie de Meniere” ( 32 ),. Although he had not used the word, “hemorrhage,” Meniere’s original description of the “bloody exudate,” led to the assumption that Meniere’s diseaseterm·dom was due to inner ear hemorrhage well into the 20th century ( 33 ). This idea would be challenged by Kyoshiro Yamakawa in Japan and the team of Charles Hallpike and Hugh Cairns in England, who independently reported in 1938 that endolymphatic hydropsterm·dom (without hemorrhage) characterized Meniere’s diseaseterm·dom ( 34 – 36 ). Work over the following century would introduce additional mechanisms, such as autoimmunity and genetic contributions to Meniere’s pathogenesis ( 37 ).

MIGRAINEterm·dom CRITERIA AND VESTIBULAR SYMPTOMS Shortly after the introduction of, “Maladie de Meniere,” Edward Liveing published his seminal work on migrainesterm·dom entitled, “On Megrim: Sick-Headaches,” which included prominent sections on dizzinessterm·dom ( 38 ). Among other manifestations, he described visually-induced dizzinessterm·dom, spinning vertigoterm·dom, orthostatic intolerance, and the phenomenon of vection in migrainesterm·dom.

Vestibular symptoms as a formal feature of migraineterm·dom were solidified in 1961 when Bickerstaff reported on patients who experienced vertigoterm·dom in the context of what he termed “basilar artery migraineterm·dom” ( 39 ). The idea of a basilar artery localization of vertigoterm·dom was carried forward in the 1988 publication of the International Classification of Headache Disorders-1 (ICHD-1term), which included vestibular symptoms in the context of, “basilar migraineterm·dom.” This was softened to “basilar-type migraineterm·dom,” in ICHD-2 in 2004 as there was a lack of evidence for basilar artery involvement in the pathogenesis of vestibular symptoms in migraineterm·dom. “Brainstem-type,” symptoms were subsequently categorized under “migraineterm·dom with brainstem aura,” in ICHD-3 beta in 2013 and in the final form in 2018 ( 6 , 40 , 41 ). ICHD-3 also introduced the diagnosis of “vestibular migraineterm·dom,” in Appendix A1.6.6.

There has been an understandable concern that the definition of migraineterm·dom with brainstem aura is overly broad and overestimates the true prevalence of auras that are actually referable to the brainstem and are not potentially some other disorder ( 42 ). With these new criteria, the boundaries between Meniere’s attacks with migraineterm·dom, migraineterm·dom with brainstem aura, and vestibular migraineterm·dom became somewhat blurry since Meniere’s attacks are frequently associated with migraineterm·dom headaches ( 43 , 44 ).

MENIERE’S CRITERIA AND VESTIBULAR SYMPTOMS The criteria for Meniere’s diseaseterm·dom similarly underwent an evolution, starting with the American Academy of Ophthalmology and Otolaryngology Committee on Hearing and Equilibrium proposal in 1972 of 3 categories of Meniere’s diseaseterm·dom: 1) Classic Meniere’s: vertigoterm·dom with unilateral tinnitus and hearing loss, 2) Vestibular Meniere’s: vertigoterm·dom without auditory symptoms, and 3) Cochlear Meniere’s: progressive but fluctuating hearing loss, tinnitus, and aural fullness without vertigoterm·dom ( 45 ).

It was observed, however, that while both vestibular Meniere’s and cochlear Meniere’s could evolve to become the full syndrome of classical Meniere’s, they could remain as isolated syndromes for decades ( 46 , 47 ). Thus, in 1985, the committee dropped the latter 2 categories and kept Classic Meniere’s ( 48 ).

In 1995, the classic Meniere’s diagnosis was divided into “Certain,” “Definite,” “Probable,” and “Possible,” subcategories. The diagnosis of “certain,” could only be made by histopathologic correlation, which presented practical problems as it required surgical removal of the inner ear. “Possible Meniere’s,” could be diagnosed based on, “episodic vertigoterm·dom of the Meniere’s type,” without the hearing loss. This opened the door for many episodic vestibular symptoms not otherwise defined to be placed under Meniere’s umbrella, including syndromes that would later be defined as vestibular migraineterm·dom ( 49 ).

In 2015, the International Bárány Societyterm·key and the American Academy of Otolaryngology-Head and Neck Surgery modified the criteria for Meniere’s diseaseterm·dom to include only the “Definite,” and “Probable,” categories. Both required at least 2 episodes of vertigoterm·dom, tinnitus, or aural fullness, but only “Definite,” Meniere’s required documented hearing loss ( 5 , 50 , 51 ). The diagnostic criteriaterm·key for vestibular migraineterm·dom had been published in 2012, with the stipulation that it should be diagnosed when “Not better accounted for by another vestibular or ICHDterm·key diagnosis” ( 5 ). Thus, “Probable Meniere’s,” and vestibular migraineterm·dom became separated by the presence of hearing loss, aural symptoms, duration of vertigoterm·dom, and the greater range of vestibular symptoms allowed in vestibular migraineterm·dom.

Of note, while vestibular dysfunction measured by caloric responses is generally reported to be higher in Meniere’s diseaseterm·dom (up to 58%) than vestibular migraineterm·dom (up to 25%), they overlap in range so much that peripheral vestibular dysfunction cannot be used as a criterion to distinguish between these diagnoses ( 44 , 52 – 54 ). The overlap is even greater when considering less specific signs of asymmetric vestibular tone, such as head-shaking nystagmus ( 54 ). These differences should be viewed in the context of the reported high baseline rate of peripheral vestibular dysfunction in patients with migraineterm·dom headaches who do not experience vertigoterm·dom ( 55 ).

THE MIGRAINEterm·dom−MENIERE’S CONNECTION The link between migraineterm·dom headaches and vertigoterm·dom is so strong that Meniere, who suffered from migraineterm·dom headaches himself, said this: “I do not hesitate to regard these migrainesterm·dom as dependent upon a lesion of the inner ear; they are accompanied by noises, by vertigoterm·dom, by gradual diminution of hearing, and most often their deafness resists all methods of treatment” ( 29 , 56 ). We can be reasonably sure that migraineterm·dom headaches do not originate in the inner ear but we do not yet know what common pathology affects both the inner ear and pain pathways in the migraineterm·dom cascade.

Studies through the years have examined the prevalence of migraineterm·dom in Meniere’s diseaseterm·dom and more specifically in recurrent vertigoterm·dom without hearing loss. Radtke et al found a higher rate of migraineterm·dom in Meniere’s patients (56%) than controls (25%) ( 57 ). Ghavami et al reported a 51% rate of migraineterm·dom in Meniere’s patients including 41% that also met the criteria for vestibular migraineterm·dom ( 58 ). Ray et al ( 59 ) reported a rate of 45% of migraineterm·dom in Meniere’s patients versus 9% in other vestibular disorders. ChapersName et al showed that patients with Meniere’s diseaseterm·dom and migraineterm·dom were more likely to be female, have an earlier age of onset of Meniere’s symptoms, have bilateral hearing loss, and have a positive family history of both migraineterm·dom headaches and vertigoterm·dom than patients with Meniere’s diseaseterm·dom alone ( 60 ). This was confirmed by Clemmens and Ruckenstein, who showed that patients with bilateral Meniere’s diseaseterm·dom were more likely to be female, be younger, and have a personal history of migrainesterm·dom than patients with unilateral Meniere’s diseaseterm·dom ( 61 ).

Over time, the relevance of migraineterm·dom headaches in otherwise spontaneous attacks of vertigoterm·dom became clearer. In their 1984 paper entitled, “The Neurotological Manifestations of Migraineterm·dom,” Kayan and Hood ( 62 ) showed that while the general sense of “giddiness,” differed only slightly, episodes of actual vertigoterm·dom were over 3 times higher and motion sickness over 2.5 times higher in patients with migraineterm·dom headaches than those with tension headaches. Rassekh and Harker found that patients with classical Meniere’s diseaseterm·dom (with hearing loss) had a much lower rate of migraineterm·dom at 22% than patients with “vestibular Meniere’s,” (vertigoterm·dom without hearing loss) at 81% (63). Brantberg and Baloh’s study found a 51% rate of migraineterm·dom in benign recurrent vertigoterm·dom patients (vertigoterm·dom without hearing loss) but only 21% in classical Meniere’s patients ( 43 ). ChapersName et al ( 64 ) found a migraineterm·dom prevalence of 87% in patients with benign recurrent vertigoterm·dom when the latter was defined as at least 2 spells of spontaneous vertigoterm·dom.

Altogether, though the rate of migraineterm·dom in Meniere’s has varied owing to differences in criteria for migraineterm·dom and Meniere’s diseaseterm·dom over time, the prevalence of migraineterm·dom headaches in patients with recurrent vertigoterm·dom both with and without hearing loss has usually been shown to be much higher than the population baseline rate of migraineterm·dom, typically reported as about 6%–18% ( 43 , 64 , 65 ). However, the migraineterm·dom incidence in Meniere’s has also occasionally been reported to be near baseline population levels and even lower than controls, raising concerns about ascertainment bias and the effect of changing criteria affecting the categorization of overlapping features ( 63 , 66 ).

EVOLUTION OF TERMINOLOGY Descriptions of Meniere’s attacks before they were called by this name frequently mention headaches or head pressure during the triad of vertigoterm·dom, tinnitus, and hearing loss ( 67 ). Efforts to define an episodic vertigoterm·dom syndrome without hearing loss led to an outpouring of terms that were not the full Meniere’s triad ( 5 , 8 , 53 , 68 – 81 ). The evolution of these terms shows the gradual movement of episodic vertigoterm·dom spells away from under the umbrella of Meniere’s diseaseterm·dom (a structural inner ear disorder) to under the umbrella of migraineterm·dom (a primary headache disorder) ( Fig. 1 ).

Evolution of terminology for episodic vestibular syndromes between Pseudo-Meniere’s disease and vestibular migraineterm·dom. Note that terms were used concurrently with a large span of overlap. They are listed according to the earliest reference in the most cited papers.

MECHANISM AND TREATMENT A variety of mechanisms for vestibular migraineterm·dom have been invoked through the years, such as spreading depression in the brainstem, the release of Calcitonin gene-related peptide (CGRP), vascular processes (vasoconstriction, ischemia, and arteriovenous shunting), and secondary hydrops from damage to the inner ear ( 53 , 82 – 84 ). Widespread cortical vestibular projections may raise the chances that vestibular symptoms could be caused by a multitude of factors that affect cortical function ( 85 , 86 ). Those factors could be anything from sleep, diet, activity, sunlight, chemicals, visual stimulation, and even cognitive load.

Treatments for vestibular migraineterm·dom have so far relied on those for migraineterm·dom headaches with the addition of vestibular rehabilitation. The most common medications used to treat vestibular migraineterm·dom include calcium channel blockers (verapamil and flunarizine), beta-blockers (metoprolol and propranolol), selective serotonin reuptake inhibitors (venlafaxine), tricyclic amines, and a variety of anticonvulsants (topiramate and lamotrigine) ( 87 ). There are suggestions that the more recent anti-CGRP medications can be effective ( 88 , 89 ). So far, there has been no support for any therapy being superior to any other, making the choice of treatment based on factors such as patient tolerance and comorbid conditions ( 87 , 88 , 90 – 92 ). Treatments are also made on a foundation of diet, exercise, and stress regulation as well as careful use of vestibular habituation exercises to lessen head motion sensitivity ( 13 , 87 , 93 ).

THE WORK AHEAD The Association for Migraineterm·dom Disorders met in October 2020 to discuss gaps in knowledge about vestibular migraineterm·dom. The 7 gaps are summarized as follows: 1) Lack of a universally accepted range of phenotypes, 2) Continued underdiagnosis, 3) Lack of objective markers, 4) Lack of understanding of the pathophysiologic mechanism, 5) Gender disparity in migraine-related phenotypes, 6) Lack of a methodical treatment plan, 7) Need for patient-reported outcome measures to assess the efficacy of treatment ( 94 ).

The evolution of migraine-related vestibular symptoms away from artery-centric terms such as “basilar migraineterm·dom,” and “basilar-type migraineterm·dom,” towards more general terms like “migraineterm·dom with brainstem aura,” and now vestibular migraineterm·dom, reflects the observation that vestibular migraineterm·dom cannot be adequately explained by arterial pathology ( 6 , 40 ). The developing negative data on arterial pathology was not replaced with a testable new model, however, but ended up treating vestibular migraineterm·dom as a primary disorder of no known structural cause ( 5 ). Currently, vestibular migraineterm·dom is diagnosed based on symptoms rather than mechanisms. If a pathological mechanism were to be found, it could produce a variety of symptoms, creating an iterative cycle of defining what vestibular migraineterm·dom really is. It could turn out to be like Meniere’s diseaseterm·dom, which has multiple contributing vulnerabilities and instigators.

There is now a growing literature indicating that cerebral venous congestion syndromes from both intracranial and extracranial etiologies cause a variety of neurological symptoms including headaches, vertigoterm·dom, disorientation, obtundation, visual loss, tinnitus, and autonomic dysregulation ( 95 , 96 ). Because the rarity of intracranial venous stenosis cannot explain the high prevalence of vestibular migraineterm·dom, it may be time to look at cases of extracranial venous stenosis. Emerging case series indicate that extracranial venous compression can be associated with any of the symptoms that are associated with intracranial venous compression but happening in areas of high freedom of motion such as the neck, and that associated symptoms can be relieved by decompressing the obstruction ( 97 – 99 ). Digital subtraction venography has shown that compression of the internal jugular vein in patients with Meniere’s diseaseterm·dom can be reversed with percutaneous transluminal venoplasty and relieve vertigoterm·dom ( 100 , 101 ).

As we evolve our paradigms on vestibular migraineterm·dom, progress may not be a straight line but more like an ascending spiral that allows us to see old ideas from new vantage points. In light of what modern tools have shown us about intravascular flow, could “humors,” outside the head cause intracranial pressure dysregulation due to vascular congestion as has been recently proposed for extracranial venous compression ( 102 – 104 )? Could atmospheric pressure effects like “south winds,” affect the pressure in the inner ear, similar to how the hair cells in the lateral lines in fish detect pressure on their bodies ( 105 )? Could it appear that migraineterm·dom emanates from the ear not because of a shared arterial supply between the trigeminal nerve and the inner ear but because of a shared venous drainage ( 106 , 107 )? While we stand on the shoulders of giants to see further, being mindful of where our big ideas came from can help us to look in the right direction.

FUNDING SOURCES The author received no financial support for the research, authorship, and/or publication of this article.

CONFLICTS OF INTEREST None declared.

DATA AVAILABILITY STATEMENT All data presented in this paper are accessible through the references. Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

REFERENCES Associated Data Data Availability Statement All data presented in this paper are accessible through the references. Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.