Diagnosis and Management of Vestibular Migraine

The lack of a universally accepted definition for this complex entity has contributed to delayed diagnosis and and treatment for those with this disorder. In this article, we will review the clinical manifestation, diagnosis and management of VM, with a focus on assisting in the differentiation between other potential diagnoses.

Pathophysiology of VM

A clear pathophysiology of VM has not been elucidated. Although predominantly a sporadic disease, there have been reported cases of familial occurrence with an auto-somal dominant inheritance [11,13]. Bahmad and colleagues mapped the first locus for familial VM to 5q35 within a 4-generation family [13]. On the contrary, a larger study conducted by Lee et al found VM to be to genetically heterogeneous with a subset linking to chromosome 22q12 [14]. Genetic defects of voltage-gated calcium channels are identified as causal factors for familial hemiplegic migraine and episodic ataxia type 2. Both these disease entities present with vertigo and migraine headaches suggesting a defective gene within the same chromosomal region could indicate a direct genetic link to VM. However, no such gene has been identified.

General consensus is that the action of spreading cortical depression as it reaches the somatosensory cortex in the posterior insula and temporoparietal junction elucidates migraine aura in patients with short attacks. However, due to the heterogeneity of VM, canal paresis and complex conditional nystagmus during acute stages are not explained through cortical spreading. Eggers et al suggests that vertigo symptoms occur as ictal sensation rather than the spreading of sensory or motor cortical depression [15]. However, due to discrepancies within the literature it is apparent that further research needs to be conducted to fully understand the pathophysiology of VM.

Clinical Manifestations of VM

Symptoms

As many as 80% to 90% of patients with VM report unsteadiness or balance problems, of which 50% to 60% typically report episodic spontaneous vertigo [16], either internal vertigo (a false sensation of self-motion) or external vertigo (a false sensation that the visual surround is spinning or flowing) [17]. The duration of episodes is highly variable, whereby approximately 30% of patients have episodes lasting minutes, 30% have attacks lasting hours, 30% have attacks over several days, while the remaining 10% have attacks lasting seconds only [18]. It may be difficult to distinguish if vestibular symptoms lasting seconds are related to their head motion intolerance, also known as head motion–induced vertigo [17], which is another frequent symptom in VM. Head motion–induced vertigo bears many similarities to motion sickness.

The interindividual temporal association of headache and vertigo is highly variable in VM patients and is a reason many patients find this diagnostic construct difficult to accept. Approximately 30% of adult patients eventually diagnosed with VM initially present without headaches [8]. Vertigo is only regularly associated with headache in 25% to 50% of VM patients [2,7]. A minority of patients report headache and vertigo never occurring together [2]. A temporal pattern, presenting as aura, occurs only in approximately 10% of cases [19]; therefore, vestibular episodes of VM should not be regarded as migraine auras [18]. Patients typically have migraine manifesting earlier in life with the vestibular symptoms following [13,20], whereby the mean age at onset of migraine and diagnosis of VM are approximately 22 and 35 years, respectively [2]. Consistently across studies that measure quality of life scores, VM patients report higher subjective levels of disability compared to patients with other vestibular illnesses, despite having less objective abnormalities [21]. Approximately 85% of VM patients experienced vestibular symptoms for at least 1 year before consulting neurootology services [21]. It could be argued that hypersensitivity of percept to vestibular symptoms reflect the general finding of augmented perceptions to various external stimuli underlying migraine [22,23].