Vestibular migraine (VM) is the most common cause of spontaneous episodic vestibular syndrome with a lifetime prevalence of approximately 1% (1). VM occurs in patients with a current or previous history of migraines and recurrent episodes of vestibular symptoms accompanied by migraine features. Treatment of VM is usually directed to the underlying condition by identifying and avoiding dietary triggers and prescribing prophylactic antimigraine medications (2). Antimigraine medications are considered when VM episodes are frequent, severe, or not well controlled by acute therapies; therapies should also be individualized based on comorbidities, potential side effects, and contraindications (2). Several studies have reported reduced or absent vestibular evoked myogenic potential (VEMP) responses in patients with VM indicating a dysfunction of the vestibulo-collic reflex (3–5). The pathophysiology of VM appears to be closely related to vestibular abnormalities, especially in the vestibulospinal pathways. Despite the increasing number of studies related to VM, most reports have focused on the characteristics of the disease, including the results of neurological tests (3–5). Treatment and prognosis related to vestibular abnormalities have not yet been fully documented. It is important to understand the prognostic factors to predict the disease course, properly counsel patients with VM, and conduct appropriate therapeutic planning. In our current study, we evaluated the response to medications in patients with VM with recurrent vertigo attacks for more than 1 month and determined the association between treatment responsiveness and abnormal vestibular results, including v-HIT (video-head impulse test), cervical and ocular vestibular evoked myogenic potentials (c- and o-VEMPs), and posturography measurements.

A retrospective chart review conducted from March 2020 to September 2022 identified 25 patients diagnosed with VM. The diagnosis of VM was based on the recent criteria for VM (4), which are as follows: (a) at least five episodes with vestibular symptoms of moderate or severe intensity, lasting 5 min to 72 h; (b) current or previous history of migraine with or without aura according to the International Classification of Headache Disorders criteria; and (c) one or more migraine features with at least 50% of vestibular episodes: 1. Headache with at least two of the following characteristics: one-sided location, pulsating quality, and moderate or severe pain intensity aggravated by routine physical activity; 2. Photophobia and phonophobia, 3. visual aura; and (d) not better accounted for by another vestibular or International Classification of Headache Disorders diagnosis. Other diseases that may cause recurrent vertigo, such as central origin or Meniere’s disease, and a previous history of otologic diseases or head trauma, were excluded from this study. There were 25 patients (24 females and one male). The average age was 44.2 ± 12.2 years.

Several questionnaires, including the Dizziness Handicap Inventory (DHI), Tinnitus Handicap Inventory (THI), and Hospital Anxiety and Depression Scale (HADS) were administered at the initial visit. Patients underwent pure-tone audiometry (PTA), c- and o-VEMP, v-HIT, and posturography during the interictal period, which was usually performed within one week of the first visit to the clinic.

Overall, after treatment, most of the patients had improved dizziness and headache, and the CGI-s was 2.7 ± 1.3. Twelve and 13 participants had GR and PR, respectively. Participant characteristics based on treatment responses are shown in Table 2. There were no statistically significant differences between the two groups (n.s). Tinnitus was present and absent in 17 and 8 patients, respectively. The treatment differences between patients with and without tinnitus are summarized in Figure 1. The score of THI was 21.0 ± 18.1 in patients with tinnitus. There were no statistically significant intergroup differences in treatment outcomes between the two groups.

The disease duration ranged from 1 month to 480 months. The average was 75.2 ± 105.7 months. The CGI-s was 1.77 ± 0.8 and 3.2 ± 1.3 in patients who suffered less than 12 months and more than 12 months, respectively. A statistically significant difference was observed between the two groups (p < 0.001) (Figure 2).

Regarding the semicircular canal function, there were eight normal and 17 abnormal VHITs. There were no statistically significant differences between the GR and PR groups as shown in Table 3.

Concerning c-VEMP, patients with GR were significantly small AR with respect to PR [19.2 ± 12.8 and 62.5 ± 42.5, respectively, (p < 0.01)]. There were 17 cases of normal c-VEMP and 8 cases of abnormal c-VEMP. Group A was defined as normal c-VEMP, and Group B was defined as abnormal c-VEMP. The patients of Group A had better prognosis (CGI-s = 2.3 ± 1.3 and 3.5 ± 1.1 respectively) (Figure 3), with 9 abnormal VHIT and 8 normal VHIT participants. There were eight abnormal VHIT cases in group B. Statistically significant differences were observed between the two groups concerning the VHIT results (p < 0.05). Participants had 8 normal VHIT, and 17 had an abnormal VHIT. Concerning treatment outcome, CGI-s of normal VHIT and abnormal VHIT were 2.2 ± 1.2 and 2.9 ± 1.4, respectively. There were no statistically significant differences between the two groups (Figure 3).

oVEMP 500 Hz results and prognosis are summarized in Figure 4. There were five normal, six unilateral, and 14 bilateral no responses in 500hz o-VEMP. CGI-s of normal, unilateral, and bilateral no responses were 1.4 ± 0.5, 2.8 ± 1.3, and 3.1 ± 1.2, respectively. There was a statistically significant difference between normal and bilateral no responses (p < 0.05).

The Prognosis and posturography results are summarized in Figure 5. The ENV cm2 on the foam rubber during the eyes-closed condition was 15.7 ± 12.3 in GR and 13.5 ± 6.0 in PR. There was no statistically significant difference between the GR and GR (n.s.) (Figure 5).

In our study, most patients experienced improvements in headache and dizziness, as evaluated by the CGI-s at 4 weeks after treatment. These results are similar to those of a previous study (19), in which more than 70% of patients with VM experienced improvements in both headache and vertigo through a combination of lifestyle changes and prophylactic medications. They concluded that abnormal vestibular ratios on posturography and abnormal VEMP responses were frequent findings in patients with VM with recurrent attacks for more than 6 months and were indicators of a poor prognosis.

Vestibular examinations revealed 17 abnormal VHIT, eight abnormal c-VEMPs, and 20 abnormal o-VEMPs. Among them, o- and c-VEMP results were related to treatment outcomes.

We attempted to identify the predictive factors in terms of prognosis in our VM cases by dividing them into two subgroups according to treatment response and comparing the results of vestibular tests between these two groups. Although the VHIT results were not significantly different between groups, abnormal o- or c-VEMPs were indicators of poor treatment outcomes. Furthermore, patients with normal c-VEMP levels have significantly better treatment outcomes. The results of o and c-VEMP were significantly better in patients with GR than in those with PR. But there was no significant difference of the ENV between patients with GR and with PR. Usually, patients with bad result of o and c-VEMP show bad result of ENV. If we see the relation between the result of c- and o-VEMP, and posturography, bad result of o and c-VEMP show bad result of ENV as we expected. However not all the subjects in GR bad good results of c- and o-VEMP.

Two of the subjects in GR group had significantly bad resus of posturography as we can see the large standard deviation in the Figure 5. These two subjects were exceptionally good prognosis with but bad c-and o-VEMP results. This error is related the small number of the subjects.

These findings suggest that the prognoses of headache and vertigo in VM are closely related to abnormalities in the vestibulospinal pathways, which may play a role in the pathogenesis of this disorder.

In previous reports, vestibular tests have focused on the detection of abnormal vestibuloocular function in the lateral semicircular canal. The C-VEMP has been used as a clinical test for vestibulospinal function, particularly in the saccule and inferior vestibular nerve regions. It has been reported that the rate of absence of unilateral or bilateral c-VEMP response was present in 44% of patients with VM compared to 3% of healthy controls and that c-VEMP amplitudes were significantly reduced in VM compared to controls, suggesting that peripheral vestibular structures, such as the saccule and central vestibular structures, are affected, and the inner ear also seems to contribute to vertigo in VM (3, 20).

In the present study, 32% (8/25) of patients who underwent c-VEMP tests showed abnormal results, and patients with normal c-VEMP showed significantly better recovery. These results are similar to those of a previous study, in which 29% of patients with abnormal c-VEMP had poor recovery compared to those with normal c-VEMP (19).

An important question that arises from the current study and findings of previous reports is the role of vestibular abnormalities in VM. There are many hypotheses concerning how migraines may result in audiovestibular symptoms. Audiovestibular symptoms can arise from trigeminal neurogenic inflammation of the labyrinth, resulting in local plasma extravasation or vasospasm of the internal auditory artery (21). The reciprocal connections between the inferior, medial, and lateral vestibular nuclei and the trigeminal nucleus caudalis suggest that vestibular and trigeminal information processing may be altered concurrently during migraine attacks and that vestibular signals may directly influence the trigeminovascular reflex pathways (22). However, it was reported that comorbid conditions (Meniere’s disease, benign paroxysmal positional vertigo, chronic subjective dizziness) are important contributors to vestibular symptoms and that induced vertigo can act as a migraine trigger in patients with migraine (23–25).

The present study had several limitations. First, the number of the subjects were too small to reach the conclusion. We should confirm the results with further study. Second, we used CGI-S for the scale. The best scale in this study would be a comparison of pre and post DHI score. However, since our study is retrospective chart review based on the medical record on daily practice, post DHI was not obtained. We usually recorded the CGI-S in daily practice, we used this scale for clinical evaluation. Third, we defined four weeks for the evaluation of treatment results, which may be brief. Evaluating the optimal medications for VM requires a double-blind, placebo-controlled, randomized study because of the complex nature of this condition. Forth, we cannot tell whether interictal test abnormalities reflect underlying deficits in the periphery or central mechanisms or vulnerabilities that can trigger subsequent attacks. Forth, an abnormality in the o-and c-VEMP tests does not indicate an abnormality of the vestibule, and the motor and central nervous systems can also influence the results. Despite these drawbacks, we evaluated the effectiveness of the current treatment strategy for VM and identified factors associated with the prognosis of this disorder using the same treatment strategy. Further studies with larger populations are needed to establish this exact relationship.

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

The studies involving humans were approved by Research Ethics Committee, Tokai University School of Medicine. The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study.

FG: Writing – original draft, Writing – review & editing. KW: Writing – review & editing. SK: Writing – review & editing. KO: Writing – review & editing.