TY - JOUR
T1 - Acute bilateral superior branch vestibular neuropathy
AU - Yacovino, Dario A.
AU - Finlay, John B.
AU - Jaimes, Valentina N.Urbina
AU - Verdecchia, Daniel H.
AU - Schubert, Michael C.
N1 - Publisher Copyright:
© 2018 Yacovino, Finlay, Urbina Jaimes, Verdecchia and Schubert.
PY - 2018/5/17
Y1 - 2018/5/17
N2 - The rapid onset of a bilateral vestibular hypofunction (BVH) is often attributed to vestibular ototoxicity. However, without any prior exposure to ototoxins, the idiopathic form of BVH is most common. Although sequential bilateral vestibular neuritis (VN) is described as a cause of BVH, clinical evidence for simultaneous and acute onset bilateral VN is unknown. We describe a patient with an acute onset of severe gait ataxia and oscillopsia with features compatible with acute BVH putatively due to a bilateral VN, which we serially evaluated with clinical and laboratory vestibular function testing over the course of 1 year. Initially, bilateral superior and horizontal semicircular canals and bilateral utricles were impaired, consistent with damage to both superior branches of each vestibular nerve. Hearing was spared. Only modest results were obtained following 6 months of vestibular rehabilitation. At a 1-year follow-up, only the utricular function of one side recovered. This case is the first evidence supporting an acute presentation of bilateral VN as a cause for BVH, which would not have been observed without critical assessment of each of the 10 vestibular end organs.
AB - The rapid onset of a bilateral vestibular hypofunction (BVH) is often attributed to vestibular ototoxicity. However, without any prior exposure to ototoxins, the idiopathic form of BVH is most common. Although sequential bilateral vestibular neuritis (VN) is described as a cause of BVH, clinical evidence for simultaneous and acute onset bilateral VN is unknown. We describe a patient with an acute onset of severe gait ataxia and oscillopsia with features compatible with acute BVH putatively due to a bilateral VN, which we serially evaluated with clinical and laboratory vestibular function testing over the course of 1 year. Initially, bilateral superior and horizontal semicircular canals and bilateral utricles were impaired, consistent with damage to both superior branches of each vestibular nerve. Hearing was spared. Only modest results were obtained following 6 months of vestibular rehabilitation. At a 1-year follow-up, only the utricular function of one side recovered. This case is the first evidence supporting an acute presentation of bilateral VN as a cause for BVH, which would not have been observed without critical assessment of each of the 10 vestibular end organs.
KW - Acute gait ataxia
KW - Bilateral vestibular hypofunction
KW - Head impulse test
KW - Vestibular neuritis
KW - Vestibulo-ocular reflex
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U2 - 10.3389/fneur.2018.00353
DO - 10.3389/fneur.2018.00353
M3 - Article
C2 - 29867751
AN - SCOPUS:85046997583
SN - 1664-2295
VL - 9
JO - Frontiers in Neurology
JF - Frontiers in Neurology
IS - MAY
M1 - 353
ER -