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2016 ; 263 Suppl 1
(ä): S90-6
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Vestibular paroxysmia: a treatable neurovascular cross-compression syndrome
#MMPMID27083889
Brandt T
; Strupp M
; Dieterich M
J Neurol
2016[Apr]; 263 Suppl 1
(ä): S90-6
PMID27083889
show ga
The leading symptoms of vestibular paroxysmia (VP) are recurrent, spontaneous,
short attacks of spinning or non-spinning vertigo that generally last less than
one minute and occur in a series of up to 30 or more per day. VP may manifest
when arteries in the cerebellar pontine angle cause a segmental, pressure-induced
dysfunction of the eighth nerve. The symptoms are usually triggered by direct
pulsatile compression with ephaptic discharges, less often by conduction blocks.
MR imaging reveals the neurovascular compression of the eighth nerve (3D
constructive interference in steady state and 3D time-of-flight sequences) in
more than 95% of cases. A loop of the anterior inferior cerebellar artery seems
to be most often involved, less so the posterior inferior cerebellar artery, the
vertebral artery, or a vein. The frequent attacks of vertigo respond to
carbamazepine or oxcarbazepine, even in low dosages (200-600 mg/d or 300-900
mg/d, respectively), which have been shown to also be effective in children.
Alternative drugs to try are lamotrigine, phenytoin, gabapentin, topiramate or
baclofen or other non-antiepileptic drugs used in trigeminal neuralgia. The
results of ongoing randomized placebo-controlled treatment studies, however, are
not yet available. Surgical microvascular decompression of the eighth nerve is
the "ultima ratio" for medically intractable cases or in exceptional cases of
non-vascular compression of the eighth nerve by a tumor or cyst. The
International Barany Society for Neuro-Otology is currently working on a
consensus document on the clinical criteria for establishing a diagnosis of VP as
a clinical entity.