Diagnosis and Management of Vestibular Migraine

Another prominent feature of VM is that patients report a syndrome of visually-induced dizziness termed visual vertigo (VV). This is a heterogeneous syndrome with strabismic, peripheral, and/or central vestibular aetiologies [24]. Patients with VV complain of discomfort, postural destabilisation, dizziness, imbalance and spatial disorientation in challenging visual environments. Examples of such environments include walking down supermarket aisles, observing moving objects (eg, disco lights, people walking, moving traffic) or moving surroundings during travelling, and the movement of the eyes in general [24–26]. Most patients report more than one visual trigger [24]. Visual vertigo can often be difficult to distinguish from oscillopsia in patients with bilateral vestibular failure. What is most surprising is that patients with VV have a similar handicap level yet report much more vestibular symptoms compared with patients with bilateral vestibular failure [25]. Postural reactions triggered by external visual motion are destabilising with respect to the earth-vertical and are normally suppressed by central re-weighting of sensory postural cues [24]. Surprisingly, premorbid levels of anxiety and childhood motion sickness do not appear to have a correlation with VV [25]. Even in normal subjects, certain complex visual stimuli can induce transient motion sickness–like symptoms, as shown in experimental visually induced self-vection [27]. The Situational Characteristics Questionnaire (SVQ) is a 19-question, symptom-based questionnaire that has been shown to be useful in quantifying features of VV and may be useful in gauging improvement following physical therapies [25,26].

Early in the disease course, hearing loss should prompt an alternative diagnosis. However, late onset cochlear symptoms have been reported in VM. A study found that after 9 years of follow-up, the number of patients with cochlear symptoms more than doubled [28].

Clinical Examination Findings

The importance of the clinical examination is to rule out peripheral vestibular dysfunction and perform positional testing to look for benign paroxysmal positional vertigo (BPPV) or central positional nystagmus. Nonetheless, positional nystagmus has been reported in up to 28% of cases, including definite central-type positional nystagmus reported in as many as 18% [28].

Audiometric Findings and Auditory Brainstem Responses

Normal audiometry both during and between attacks is one of the key clinical features that distinguishes VM from Meniere’s disease [29]. Auditory brainstem response (ABR) results are typically normal in about 65% of patients [29]. Abnormal ABR results are typically nonspecific, such as mild elongation of wave I, III and V latencies and less commonly, prolongation of the inter-peak latencies.

Findings on Vestibular Function Testing

Whilst there are some reported abnormalities in vestibular function testing in VM patients, such findings need to be interpreted with caution due to the small number of subjects, as well as the variation in case definition and cut-off values. Most importantly, very few papers studied patients in the acute phase, and in some studies it was not even specified. The majority of studies report that VM patients interictally have grossly normal peripheral vestibular function with occasional minor irregularities. Profound interictal abnormalities such as complete canal paresis are usually indicative of other diagnoses. In between acute attacks, patients with VM typically have normal gaze, saccadic parameters, ocular pursuit gains and optokinetic nystagmus (OKN) gains on electronystagmography (ENG) or videonystagmography (VNG) [3]. A minority had a low amplitude (< 4 degrees per second) persistent positional nystagmus. On rotation testing of the vestibo-ocular reflex there is reduction of the mean gains compared to headache-free controls. Most reports in the literature do support that the majority of VM patients have grossly normal bithermal caloric testing, although abnormalities including higher slow phase velocities and canal paresis (usually partial) are reported [29–31]. The observation that the artificial vestibular stimulation caused by the caloric test was followed by a migraine attack within 24 hours in 49% of patients with migraine is very interesting [30], and it remains to be tested whether this phenomenon has the potential to be of assistance in the diagnosis of VM. Both VM patients and migraineurs without vertigo have similar subtle cVEMP (Cervical vestibular-evoked myogenic potentials) abnormalities, namely decreased global amplitude and absence of habituation [31]. On computerized dynamic posturography (CDP), a test of sway, VM patients typically demonstrate a surface-dependent pattern based on their SOT analysis [3], suggesting that VM patients may have a substantial vestibulo-spinal abnormality leading to difficulties integrating multiple conflicting sensory inputs [32].