© Springer International Publishing Switzerland 2015Stephen Wetmore and Allan Rubin (eds.)Vestibular Migraine10.1007/978-3-319-14550-1_3
3. Historical Perspective of Vestibular Migraine
Departments of Otolaryngology, Neurology, Bioengineering and Physical Therapy, University of Pittsburgh, Eye and Ear Institute Suite 500, 200 Lothrop Street, Pittsburgh, PA 15213, USA
Departments of Otolaryngology, Neurobiology, Communication Science & Disorders, and Bioengineering, University of Pittsburgh, Eye and Ear Institute, Suite 107, 200 Lothrop Street, Pittsburgh, PA 15213, USA
KeywordsVestibular migraineHeterocraniaMigraine equivalentMigraine-associated dizzinessMigraine-related dizzinessMigraine-related vestibulopathyMigrainous vertigoBenign paroxysmal vertigo of childhoodBenign recurrent vertigoBasilar-type migraineBasilar-artery migraineNeurogenic inflammationTrigeminocerebrovascular systemCortical spreading depression
3.1 History of Medicine Perspective
The accounts of vertigo and migraine-like disorders in the ancient literature are highly consistent with the current view that vestibular migraine is a migraine variant produced by the convergence of vestibular information within migraine circuits , in a manner similar to auditory, visual, and somesthetic information. In the Hippocratic corpus, vertigo was regarded as a disease of the head, which could be (1) a symptom of engorgement of the head with blood  or (2) comorbid with fever, a throbbing head, and thin urine, with the notation that vertigo sufferers with headache tend to show madness . Aretæus of Cappodocia (first century of the Common Era) includes vertigo (1) as a separate chronic disease, (2) as a symptom of a form of the Cephalæa, the heterocrania (migraine), and (3) as a prognostic in some individuals for melancholia, epilepsy, or mania . There is little doubt that Cephalæa includes migraine, from its later description as “… an extreme paine in the heed, that a man can nat abide no lyght nor no noyse, and the patient doth loue to be in darke places. And his heed he dothe thynke doth go in peces, and a pylowe is better for the pacient, than a cote of defence .” “Vertigo or giddiness” and “hemicrania or megrim” were presented in successive chapters in the works of Ambrose Paré, with similar etiologic descriptions . This association persisted into the early twentieth century. For example, Lectures I and II of Gowers’ Clinical Lectures on the Borderland of Epilepsy discussed vertigo [7, 8], followed by Lecture III on migraine . The first use of the term vestibular migraine by Boenheim was discussed within this framework of clinical similarities between vertigo, migraine, and epilepsy .
3.2 Modern Era Perspective of Vestibular Migraine
More than 50 years ago, Selby and Lance  published a paper regarding the clinical aspects of 500 patients with migraine and what was then called vascular headache. These authors noted that vertigo occurred in 33 % of these patients during headache. Although the pathophysiology of this symptom was uncertain, this large series of patients provided clear evidence for an association between vestibular symptoms and migraine and confirmed previous observations by Boenheim , Heveroch , Symonds , Richter , and Friedman et al.  of dizziness symptoms during headache. In 1961, Bickerstaff described the so-called basilar artery migraine, now known as “basilar-type migraine,” as a disorder in which vestibular symptoms, including vertigo, are often prominent . Sturzenegger and Meienberg reported that 63 % of such patients had vertigo . However, only a small percentage of patients who meet the current criteria for vestibular migraine also meet criteria for basilar artery migraine . Bickerstaff’s 1961 description firmly established vestibular symptoms as a component of the symptomatology of some patients with migraine headache.
The idea that vestibular symptoms could be a migraine equivalent independent of headache was suggested earlier by Heveroch , Symonds , Richter , and Levy and O’Leary . Vestibular symptoms independent of headache were not generally considered as a possible migrainous phenomenon. Fenichel’s 1967 paper  proposed that “benign paroxysmal vertigo of childhood,” described initially by Basser in 1964 , was a migraine variant seen in childhood. More than 10 years later, Slater’s 1979 paper  proposed a link between “benign recurrent vertigo” in adults and migraine. Kuritzky et al. described 84 patients with migraine  and found that vestibular symptoms and signs, such as vertigo and dizziness, were more common in migraine than in controls. These authors also found that vestibular laboratory abnormalities are common in patients with migraine . These authors noted that vestibular symptoms occurred both temporally associated with migraine headache and interictally, i.e., between headaches, thereby furthering the concept that vestibular symptoms can be a migraine equivalent.
A link between vestibular abnormalities and migraine was confirmed by the landmark paper by Kayan and Hood in 1984 . They noted a high prevalence of vestibular problems in patients with migraine headache as compared with patients with tension-type headache. Although not the first paper that identified the link between migraine and vestibular symptoms, nearly every paper regarding vestibular migraine since 1984 cites the Kayan and Hood paper as establishing a link between vestibular abnormalities and migraine in adults. Harker, in 1987 , proposed a classification scheme for grading the likelihood of an etiological rather than chance association between vestibular symptoms and migraine using the terms definite, probable, and possible. Some years later, Parker  emphasized the concept that paroxysmal vertigo occurred in patients with migraine and that the key observation regarding the association between migraine and vestibular symptoms is the temporal relationship between dizziness and headache. Parker noted that this temporal relationship can be quite variable.
Cutrer and Baloh in 1992  were the first to introduce a series of papers that addressed the link between migraine and vestibular symptoms in patients who presented with dizziness rather than headache. Cutrer and Baloh coined the term “migraine-associated dizziness” to describe a small number of patients, i.e., 91 of 5,000 patients, who were seen for dizziness in a tertiary care setting, whose symptoms could not be attributed to an alternative disorder and who suffered from migraine. Sixty-nine percent of these patients had vertigo. There was a wide range of duration of symptoms with about half of the patient’s reporting dizziness symptoms lasting for more than 1 day. Further support for a link between migraine and vestibular symptoms was provided in 1993 by Aragones et al.  who reported a high prevalence (about 33 %) of migraine in a group of 72 patients with vertigo of uncertain cause. In 1997, Savundra et al. coined the term “migraine-associated vertigo” . These authors also noted a high prevalence (about 32 %) of migraine in a group of 363 patients with vertigo and advocated for migraine-associated vertigo to be considered a distinct diagnostic entity. In that same year, Cass et al.  described 100 patients out of a total population of 4,400 who had a condition they termed “migraine-related vestibulopathy.” These authors considered migraine-related vestibulopathy as a distinct diagnostic entity and described laboratory abnormalities in this group. The diagnosis of migraine-related vestibulopathy was based on a combination of migraine headache, space and motion discomfort , and no other better diagnosis. By this time, migraine-related dizziness was considered a diagnostic possibility in all patients with dizziness whose signs and symptoms could not be ascribed to another recognizable neurotologic syndrome.
Johnson, in 1998 , provided a retrospective description of the clinical findings in a group of 99 of 665 patients with migraine-related dizziness/migraine-related vertigo using the diagnostic criteria that patients needed to have both migraine and dizziness/vertigo without a better diagnosis. Johnson’s contribution was primarily to promote the idea that treatment of these patients for migraine yielded favorable outcomes. This finding suggested that migraine-related dizziness was a bona fide disorder for which there was efficacious treatment and motivated the medical community to establish migraine-related dizziness as a diagnostic entity because of the possibility of successful treatment. In 1999, Dieterich and Brandt  published a highly regarded paper that reintroduced the term “vestibular migraine,” a designation first used by Boenheim  in 1917. Dieterich and Brandt  highlighted the concept that vestibular migraine is distinct from basilar-type migraine and that objective vestibular abnormalities are commonly seen between episodes of dizziness. Shortly thereafter, in 2001, Neuhauser et al. , in a seminal paper, established diagnostic criteria for a condition they termed “migrainous vertigo,” which has subsequently been renamed “vestibular migraine.” Neuhauser et al.  found that the lifetime prevalence of vestibular migraine was 7 % in their population of 200 patients with dizziness. A follow-on paper some 10 years later confirmed the validity of the Neuhauser diagnostic criteria for vestibular migraine . Subsequent papers confirmed the clinical utility of considering a diagnosis of vestibular migraine. In 2002, Reploeg and Goebel  reported a 72 % rate of efficacy of anti-migrainous therapy in a group of 81 patients with vestibular migraine. In 2011, Strupp et al.  outlined detailed treatment options for vestibular migraine noting that “vestibular migraine is increasingly regarded as the most common central cause of recurrent attacks of vertigo.” The diagnostic criteria for vestibular migraine published in 2012 , which are based upon a consensus between the Barany Society and the International Headache Society, firmly established vestibular migraine as a diagnostic entity. Now that there is general agreement upon nomenclature and diagnostic criteria, the field can focus on studies of the pathophysiology and management of vestibular migraine.
3.3 Origins of Current Diagnostic Criteria for Vestibular Migraine
With the acceptance of diagnostic criteria for vestibular migraine , there is some interest in reviewing the origins of these criteria. The term “vestibular migraine” was used initially by Boenheim in the early 1900s  in his description of patients with vertigo and migraine. As the association between vestibular symptoms and migraine was becoming recognized, various terms were used to describe what in retrospect was probably the same diagnostic entity, namely, what we now call vestibular migraine. The term “basilar artery migraine” was introduced by Bickerstaff in 1961  to describe a type of migraine that often was associated with vestibular symptoms. Sturzenegger and Meienberg in 1985  noted that 63 % of patients with confirmed basilar artery migraine complained of vertigo. The term “basilar-type migraine” replaced the term basilar artery migraine  and remains in usage to describe a type of migraine that may be associated with vestibular symptoms. However, few patients who meet diagnostic criteria for vestibular migraine also meet criteria for basilar-type migraine , which highlighted the need for a specific diagnostic entity that recognizes the large number of patients with migraine-related vestibular symptoms who lacked a diagnosis.
The terms “benign paroxysmal vertigo of childhood”  and “benign recurrent vertigo”  for adults also were used to denote a condition akin to vestibular migraine highlighting the episodic nature of the condition. Other terms such as “migraine-associated dizziness” , “migraine-associated vertigo” , “migraine-related vestibulopathy” , and “migrainous vertigo”  have each had their proponents. Dieterich and Brandt in 1999  reintroduced the term “vestibular migraine,” which is the nomenclature that is now agreed upon by both the Barany Society and the International Headache Society. Prior to the Neuhauser et al. 2001 seminal paper , there were no firm diagnostic criteria for vestibular migraine. For the most part, vestibular migraine was given different names and in its various forms, was considered a diagnosis of exclusion and was ascribed to patients without a definitive neurotologic diagnosis such as Meniere’s disease or BPPV, who suffered from migraine. The absence of strict diagnostic criteria resulted in a high degree of variability in estimates of incidence and prevalence and precluded reliable meta-analyses and treatment trials. Since 2001, most studies of vestibular migraine have used the Neuhauser et al. 2001  criteria, which were validated in a 2012 study that reassessed the initial cohort of patients regarding their current diagnosis . Brandt and Strupp in 2010  described treatment options for what is now considered an established diagnostic entity. The diagnostic criteria for vestibular migraine published in 2012  were minimally different from those proposed by Neuhauser et al. in 2001 . Importantly, these latest criteria were based on an international consensus of neurologists and otolaryngologists and were consistent with diagnostic criteria for migraine and its variants established by the International Headache Society . The establishment of diagnostic criteria for vestibular migraine should pave the way for future studies of the epidemiology, pathophysiology, and treatment of this now widely recognized, common, neurotologic disorder.
3.4 Pathophysiologic Perspective
The clinical evidence of comorbidity and advances in studies of migraine mechanisms suggested an overarching hypothesis that central vestibular pathways and the inner ear share the vascular, neurogenic inflammation and central neural mechanisms that have been implicated in the pathogenesis of migraine [43–47]. The development of this approach may be traced sequentially in review papers [1, 48–52]. Hence, vestibular migraine can be regarded as a migraine variant with vestibular manifestations.
The vascular theory of migraine was developed in the late 1930s by Harold Wolff [53, 54]. He proposed that preheadache phenomena (including vertigo) were the result of oligemia and/or transient ischemia from vasoconstriction. The headache pain, by contrast, was proposed to result from a rebound vasodilation and consequent activation of trigeminal nociceptors. Bickerstaff’s (1961)  concept of “basilar artery migraine” (or “basilar-type migraine”) was a logical extension of this model to involvement of vertebrobasilar perfusion of the vestibular nuclei, nerve, and inner ear. An expanded trigeminocerebrovascular system  concept provided a focus for exploring the link between vascular responsiveness and pain as a physiological consequence of activation of trigeminal ganglion innervation of cerebral and meningeal vasculature. Because the trigeminovascular system also innervates blood supply of the inner ear [56, 57], the concept was also consistent with a role in the known sensitivity to sound and vertigo in migraine.