

So, genetic variations in ion channels and membrane transporters which regulate fluid homeostasis could explain the relationship between migraine and MD. Migraine, per se, may provoke episodic vertigo, and VM has a prevalence of about 1 % of the population. Įpidemiological studies report that around 56 % of MD patients also refer migrainous headaches in both disorders, a familial predisposition has been postulated.

Moreover, the association with migraine, episodic vertigo and MD, frequently observed clustered in families, including identical twins, supports the heritability of VM.

VM shows a transient vestibular dysfunction, and it presents overlapping symptoms with Meniere’s disease (MD) during the attacks. Vestibular migraineĭefinite vestibular migraine (VM) is defined by the occurrence of episodic vestibular symptoms and a history of migraine, demonstrating a temporal association between vestibular and migraine symptoms in at least 50 % of the attacks. These genes involve a large variety of functions such as ocular and brain development, insulin resistance, otolith biogenesis or iron homeostasis. The top ten genes involved in these regions include PVR元, GPD2, ACO1, AUTS2, GPR26, UBE2E2, CBLN4, BLOC1S5, LINGO2 and CPNE4. A genome-wide association study performed in 80494 individuals has identified 35 common single-nucleotide variants at genome-wide significant level. The condition has been associated with postoperative vomiting, altitude sickness, morning sickness and migraine. Its symptoms include dizziness, nausea, vomiting, pallor and headache. It is the most common vestibular condition affecting 30 % of the population. Motion sickness refers to autonomic signs and symptoms occurring during movement, and maybe elicited by self-motion or motion of the environment. By using whole exome sequencing and combining bioinformatics tools, novel variants in DTNA and FAM136A genes have been identified in familial Meniere’s disease, and this genomic strategy will facilitate the discovery of the genetic basis of familial vestibular disorders. However, the most relevant finding during the past years is the familial clustering observed in Meniere’s disease.

Some Mendelian sensorineural hearing loss also exhibits vestibular dysfunction, including DFNA9, DFNA11, DFNA15 and DFNA28. The clinical heterogeneity observed in different relatives of the same families suggests a variable penetrance and the interaction of several genes in each family. We present recent advances in the genetics of vestibular disorders with familial aggregation. Bilateral vestibular hypofunction is a rare condition, and some of patients also present cerebellar ataxia and neuropathy. Both are related to migraine and show a familial trend. The two most common vestibular disorders are motion sickness and vestibular migraine, affecting 30 and 1–2 % of the population respectively.
