Vestibular migraine mimicking acute unilateral vestibulopathy: a case report and mini review

1 Introduction

Vestibular migraine (VM) is one of the most common causes of recurrent episodic vertigo or dizziness. It may affect up to 1% of the general population (Lempert et al., 2022), yet it is often misdiagnosed, particularly in Emergency Department settings (ED) (Baron and Steenerson, 2025). Despite its high prevalence, the pathophysiological mechanisms remain to be fully elucidated. Recent studies have reinforced the existence of a complex trigeminovascular system in the pathophysiology of VM (Espinosa-Sanchez and Lopez-Escamez, 2015; Huang et al., 2020).

However, vestibular neuritis (VN), now subsumed under the category of Acute Unilateral Vestibulopathy (AUVP), is the epitome of a peripheral acute vestibular syndrome (Strupp et al., 2022). It is characterized by horizontal spontaneous nystagmus, and the head impulse test reveals an abrupt reduction in vestibular-ocular reflex (VOR) function on the affected side due to acute unilateral vestibular deafferentation (Halmagyi et al., 2010; Kattah et al., 2009).

Although patients show progressive improvement of symptoms in the days following AUVP through central compensation mechanisms, the recovery of the VOR is usually incomplete, gradual-developing over weeks to months-and occurs to a significant degree in approximately 50% of patients after 2 months when the initial gain is < 0.5 (Büki et al., 2017; Halmagyi et al., 2010).

This study presents a woman who reported experiencing recurrent episodes of dizziness and photophobia, triggered by the ingestion of sweets, sleep deprivation, and emotional overload. However, on the day following her outpatient consultation, she experienced a crisis in the ED, whose documented characteristics were consistent with AUVP. The patient was recruited to the ongoing “Validação do Protocolo Diagnóstico para o Paciente com Tontura Aguda nos Pronto-Atendimentos Brasileiros” study (Ethics Committee approval number 5.959.538). She also consented to individual publication of her data.

2 Case description

A 40-year-old woman, chiropractor, presented for an outpatient appointment reporting three distinct episodes of disabling imbalance that occurred over a 2-month period, each lasting 24 h, without triggers for change in body position or others. In all events, endovenous dimenhydrinate was necessary, and in the most recent episode oral flunarizine 10 mg/day was administered for a few days following the event. These crises were associated with vomiting, intense photophobia, and the presence of scintillating scotomas. The most recent episode occurred 2 weeks before the appointment. No history of trauma, recent infections, pattern changes of the menstrual cycle, new medication or substance abuse. In response to a query regarding the presence of additional symptoms, she denied the occurrence of headaches, cervical pain, diplopia, dark vision, sensory loss, or hearing complaints during the previous months.

Her medical history included the diagnosis of migraine with aura in early adolescence, whose symptoms improved over time with behavioral adjustments, primarily related to sleep and consumption of sweets. She denied motion sensitivity. The recurrence of migraine with visual aura was observed only in instances of her attempt to use oral contraceptives, a method which was rendered unfeasible due to the propensity of headaches. She also mentioned the treatment of Hashimoto's thyroiditis and a depressive disorder, currently without symptoms, with levothyroxine, and sertraline, respectively.

However, when asked about her current sleep habits, she said that she was going through emotional overload due to her child's school problems, and therefore she was experiencing sleep deprivation.

The findings from the general physical, neurological, neurotological, and otorhinolaryngological evaluations were normal at the consultation, including HINTS+ (Head-Impulse, Nystagmus, Test of Skew, plus testing of hearing), head shaking nystagmus test, saccades, and smooth pursuit assessments, as well as positional tests (with Frenzel's goggles).

Ultimately, the consultation concluded that the patient was experiencing episodic vestibular syndrome without triggers (Newman-Toker and Edlow, 2015), accompanied by significant photophobia and associated with dietary issues, hormonal changes, stress, and sleep deprivation. Considering the patient's sex, age, and normal bedside examination during the inter-crisis period, the initial diagnostic hypothesis was VM, although the patient has not experienced five crises, as recommended in the current consensus (Lempert et al., 2022). Video-oculography (VOG), video head impulse test (vHIT), audiometry, tympanometry, and Subjective Vertical Visual (SVV) test were requested, as well as blood tests including complete blood count, lipid profile, thyroid function tests, and glucose and insulin curve. Sleep and dietary advices were recommended, as well as going to the ED in case of a new crisis.

However, only 1 day after her outpatient consultation at the affiliated Dizziness Center, the patient arrived at the ED with a new event. This time, she experienced an intense spinning vertigo, distinct from the imbalance described in previous episodes, but also accompanied by nausea, vomiting, and severe photophobia. She avoided opening her eyes because of the intense light sensitivity. The event began as soon as she woke up that morning and she attributed it to eating chocolate cake the night before. After an initial clinical evaluation that included an EKG and blood tests measuring glucose levels and cardiac enzymes, the neurotology team was called. The same expert from the outpatient clinic assisted her in the ED (ACLN).

She presented with spontaneous horizontal left-beating nystagmus with a small upbeat vertical component. The nystagmus increased with leftward gaze and improved with rightward gaze and visual fixation. Positional testing did not elicit any nystagmus besides the spontaneous nystagmus. The head impulse test was positive to the right, and the cover test was normal. She consented to participate in an ongoing study, after which some tests were performed while the attack was still occurring. The vHIT revealed reduced right horizontal canal gain (0.31), accompanied by overt and covert catch-up saccades. In contrast, left horizontal canal gain was 0.83, without saccades (Figure 1a). Testing of the vertical canals was normal. VOG revealed spontaneous left-beating nystagmus at 31°/s (Figure 1b), while saccades, smooth pursuit, and optokinetic reflexes remained preserved. SVV was also normal (+1.3°). There were no additional findings in Audiometry, Tympanometry, or blood tests.

Due to the severity of the symptoms and vomiting, hospitalization was necessary. A few hours after receiving the first intravenous doses of dimenhydrinate (30 mg) and methylprednisolone (500 mg), implemented by the frontline physicians before the neurotologist arrived, the patient was asymptomatic, with no nystagmus and normal head impulse test findings (Leong et al., 2021). The patient was discharged, and on the second day post-crisis, she underwent magnetic resonance imaging (MRI) and cranial and cervical magnetic resonance angiography (MRA). These tests were part of the research protocol in which she agreed to participate, as well as a glucose and insulin curve. The following autoimmune laboratory tests were requested: erythrocyte Sedimentation Rate (ESR), C-Reactive Protein (CRP), Circulating Immune Complexes, Total Complement Activity (CH50), Complement C3, Complement C4, Rheumatoid Factor, Antinuclear Antibodies (ANA), HEp-2 Titer and Pattern, Anti-cardiolipin Antibodies (IgG and IgM), Lupus Anticoagulant, Anti-thyroglobulin and Anti-thyroid Peroxidase Antibodies. All results were normal, as were the complete blood count, MRI, MRA, thyroid hormone levels, and glucose-insulin curves. Three days after the event, she returned to the outpatient setting. A subsequent vestibular examination revealed that the findings had normalized. This included a right horizontal canal gain of 1.01 on vHIT (Figure 2), an absence of catch-up saccades, and no spontaneous or head-shaking-evoked nystagmus.

The patient has been followed up for 8 months since the reported event and remains asymptomatic without medication. She has successfully implemented lifestyle modifications, including sleep hygiene, avoidance of known dietary triggers, and improved stress management.

3 Discussion and review

There are several reasons that motivate us to share this case. One of them is the knowledge that the first scientific description that linked balance disorders with migraine was a detailed case study by Aretaeus of Cappadocia in 131 AD (Kayan and Hood, 1984). Another peculiarity of the present study was the possibility for the same neurotologist to evaluate the patient at three distinct times, within the same week: before, during, and after the crisis. This approach enabled the precise observation of the transient weakness of the right lateral semicircular canal during the crisis, followed by its remarkably rapid recovery.

During the first consultation, the patient reported experiencing dizziness crises associated with photophobia, which led us to suspect VM. Although the number of crises did not meet the current diagnostic criteria, the clinical characteristics and previous diagnosis made migraine the most likely etiology. However, during the crisis, the findings of the bedsides, VOG and vHIT strongly suggested AUVP, due to the signs of vestibular deafferentation on the right.

This was the patient's fourth attack in 2 months. Its clinical features were very similar to those of previous reported attacks. AUVP is most frequently linked to vestibular neuritis, particularly in the absence of cardiovascular risk factors (Newman-Toker and Edlow, 2015; Filippopulos et al., 2022). Furthermore, viral etiology generally leads to a longer duration of symptoms, a more gradual normalization of bedside eye movement findings, and recurrence is exceptional (Halmagyi et al., 2010; Kattah et al., 2009). Therefore, it was clear that the patient was not experiencing a fourth case of viral neuritis. Other etiological possibilities were considered.

The current definition of Vascular Dizziness encompasses stroke, vertebrobasilar TIA (VBTIA), and isolated labyrinthine ischemia or hemorrhage (Kim J et al., 2022). VBTIA presents a diagnostic challenge due to the absence of a biomarker. They are more prevalent in elderly individuals and those with other cardiovascular risk factors, such as comorbidities and a vertebrobasilar anatomical configuration that favors ischaemia (Edlow et al., 2023; Cortese et al., 2025). Approximately 85% of VBTIA patients present symptoms associated with dizziness or vertigo, such as transient visual loss (30%), syncope (27.2%), diplopia (10.7%), and balance-related fall (9.7%). In more than 80% of patients, the crises last less than 60 min (Neto et al., 2024; Edlow and Bellolio, 2024).

However, despite its rapid improvement, this lady's case did not meet the description above. The only accompanying symptom was photophobia. There were no ischaemic events on MRI or MRA. In addition, with regard to her youth, there were no reports of smoking, drug abuse or conditions of hypercoagulability, which weakens the hypothesis of an ischaemic pathophysiological substrate (Otite et al., 2017; Supanc et al., 2014).

The previous diagnosis of Hashimoto thyroiditis raised the possibility of autoimmune inner ear disease (AIED). This could potentially explain the rapid reversal of vestibular function after corticosteroid use, which led us to request further serological autoimmune tests. For some, AIED is defined as a rapidly progressive, often fluctuating bilateral sensorineural hearing loss responds to immunosuppressive therapy (Girasoli et al., 2018). Vestibular disorders coexist in 50–63% of patients (Bovo et al., 2006; Shah et al., 2023). The prevalence in women and in the age group between 20 and 50 is higher. It may be associated in 15–30% of cases with a systemic autoimmune disease (Girasoli et al., 2018; Russo et al., 2018).

In a survey of 47 patients with Hashimoto's thyroiditis, Chiarella et al. (2014) demonstrated that vestibular alterations were present in 50% of the patients, and established a significant correlation between vestibular alterations and serum anti-thyroid peroxidase antibodies. The patient in this study exhibited normal levels of anti-thyroglobulin and anti-peroxidase antibodies, as well as other inflammatory markers, indicating that the autoimmune disease was not active. In a recent meta-analysis that included 120 studies on AIED secondary to systemic autoimmune diseases, only the Chiarella study provided data from patients with Hashimoto's thyroiditis, thereby highlighting the probable rarity of this association (Shah et al., 2023).

In addition, the diagnosis of AIED remains problematic due to the lack of widely accepted criteria. Moreover, current suspicions are based primarily on idiopathic sensorineural hearing loss rather than vestibular symptoms (García-Berrocal J et al., 2005), rendering this a less plausible diagnosis in our patient.

Evaluating a VM crisis in the ED can be challenging, especially for front-line physicians, due to the variety of possible findings (Rocha et al., 2023). Numerous studies have reported that there are no specific findings indicative of VM on physical examinations or laboratory tests. Conversely, others suggest the possibility of unilateral vestibular dysfunction in VM (Sohn, 2016; Furman J et al., 2005; Huang et al., 2020).

The vHIT has been a valuable tool for the VOR assessment in the ED setting (Newman-Toker et al., 2013; Kim et al., 2023). During the interictal period, reduced VOR gain and corrective saccades on vHIT were reported to show a similar frequency to controls (Salmito and Ganança, 2021). Some studies have reported the presence of unilateral canal weakness in 7.5–11% of VM cases (Kang et al., 2016; Blödow et al., 2014), reporting lateral canals gain of up to 0.4 in VM patients (ElSherif et al., 2018).

There is a particular lack of data on vHIT during an acute VM crisis, mainly with regard to characterizing VOR gain values and identifying differences between crisis and post-crisis findings. Nevertheless, some studies have found reduced gain in 11–21.7% of VM patients in the ED (Batinović et al., 2025; Young et al., 2021; Kang et al., 2016; Waissbluth et al., 2023; Koç and Akkiliç, 2022).

However, Calic et al., described an interesting case series of 10 patients with a previous diagnosis of VM, who presented to the ED with acute vertigo lasting more than 24 h, spontaneous peripheral nystagmus, and an abnormal head impulse test (though still presumed to be of VM origin). The vHIT confirmed a reduction in horizontal canal gain on the affected side (0.61 ± 0.2), which was often accompanied by catch-up saccades. When the authors compared these patients with a control group with definite vestibular neuritis, the horizontal canal deficit in the VM cohort was, on average, less severe and the cumulative amplitude of refixation saccades was smaller, suggesting a milder degree of peripheral hypofunction. On follow-up, vHIT showed partial recovery of vestibular function (0.77 ± 0.2) (Calic et al., 2020). This description is very similar to that of the subject of the present study, whose catch-up saccades also lacked the typical configuration observed in classical AUVP (Figure 1).

Patients with migraine typically exhibit hypersensitivity to light, visual motion, sounds, odors, and self-motion. It is not clear whether such hyperexcitability is at the level of the peripheral vestibular system or the brainstem, or whether it could be related to the modulating effects of the cerebellum or cerebral hemispheres on the vestibular system (Furman J et al., 2005; Jeong S et al., 2010; King et al., 2014; Huang et al., 2020; Espinosa-Sanchez and Lopez-Escamez, 2015; Vass et al., 2001).

Trigeminovascular reflex activation can produce vasodilation of intracranial, dural and inner ear arteries, which activates trigeminal sensory afferents (Dieterich et al., 2016; Espinosa-Sanchez and Lopez-Escamez, 2015; Frank et al., 2023). The activated trigeminal afferents release neuropeptides (e.g., calcitonin gene-related peptide, substance P, and neurokinin A) that produce local extravasation. Koo and Balaban (2006) demonstrated this same mechanism in most portions of the murine ear. In the inner ear, the extravasation and vasodilation may produce neurogenic sterile inflammation in the ganglia and the intralabyrinthine portions of the eighth cranial nerve. Extravasation into the stria vascularis may also alter K+ cycling, with an impact on hair cell transduction (Koo and Balaban, 2006).

Another possibility is that inflammatory elements migrate from the subarachnoid space to the inner ear through the cochlear aqueduct and/or the internal auditory canal. A recent systematic review evaluated auditory function in specific neurological conditions. Compared to controls, patients with migraine, multiple sclerosis, and Parkinson's disease presented an increased risk of altered otoacoustic emissions, with a suggestion that inflammatory factors within the cerebrospinal fluid could enter the labyrinth through their connection with the perilymph (Di Stadio et al., 2023).

The mechanisms by which migraine would cause a transient VOR dysfunction are not known and at this stage can only be speculative. Along the lines above, one possibility is that the presence of neuropeptides in the inner ear may cause local inflammation sufficient to induce transient and mild unilateral vestibular dysfunction with different neurophysiological characteristics to that seen in patients with AUVP, which might also explain the different saccadic patterns.

This case study highlights the clinical challenges faced when making a diagnosis in a patient with acute vertigo. It further strengthens the need to consider migraine as a possible cause of this clinical presentation, even in the face of features that may point to a peripheral vestibular cause. Careful neurotological evaluation during and outside of crises can aid the diagnostic process and better inform treatment decisions, although defining atypical presentations of migraine will only be possible with specific and sensitive biomarkers of the disease.

4 Patient perspective

“I had three episodes of really bad dizziness, nausea, vomiting, and I couldn't handle any light. I had to go to the emergency room during the first two episodes because I couldn't stop vomiting. One of them made the doctors think it could be a stroke, but all the hospital tests came back normal. So, the last episode happened the day after a medical visit, and it might've been linked to stress and a slice of chocolate cake. After I got evaluated and treated, I didn't have any more episodes.”

Generative AI statement

The author(s) declared that generative AI was not used in the creation of this manuscript.

Any alternative text (alt text) provided alongside figures in this article has been generated by Frontiers with the support of artificial intelligence and reasonable efforts have been made to ensure accuracy, including review by the authors wherever possible. If you identify any issues, please contact us.

Publisher's note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Footnotes

Edited by: Andreas Zwergal, Ludwig Maximilian University of Munich, Germany

Reviewed by: Filipp Maximilian Filippopulos, LMU Munich University Hospital, Germany

Preetam Chappity, Launceston General Hospital (LGH), Australia