PT  - JOURNAL ARTICLE
AU  - Christoph Best
AU  - Joachim Gawehn
AU  - Heidrun H Krämer
AU  - Frank Thömke
AU  - Tugba Ibis
AU  - Wibke Müller-Forell
AU  - Marianne Dieterich
TI  - MRI and neurophysiology in vestibular paroxysmia: contradiction and correlation
AID  - 10.1136/jnnp-2013-305513
DP  - 2013 Dec 01
TA  - Journal of Neurology, Neurosurgery & Psychiatry
PG  - 1349--1356
VI  - 84
IP  - 12
4099  - http://jnnp.bmj.com/content/84/12/1349.short
4100  - http://jnnp.bmj.com/content/84/12/1349.full
SO  - J Neurol Neurosurg Psychiatry2013 Dec 01; 84
AB  - Background Vestibular paroxysmia (VP) is defined as neurovascular compression (NVC) syndrome of the eighth cranial nerve (N.VIII). The aim was to assess the sensitivity and specificity of MRI and the significance of audiovestibular testing in the diagnosis of VP. Methods 20 VP patients and, for control, 20 subjects with trigeminal neuralgia (TN) were included and underwent MRI (constructive interference in steady-state, time-of-flight MR angiography) for detection of a NVC between N.VIII and vessels. All VP patients received detailed audiovestibular testing. Results A NVC of N.VIII could be detected in all VP patients rendering a sensitivity of 100% and a specificity of 65% for the diagnosis of VP by MRI. Distance between brain stem and compressing vessels varied between 0.0 and 10.2 mm. In 15 cases, the compressing vessel was the anterior inferior cerebellar artery (75%, AICA), the posterior inferior cerebellar artery in one (5%, posterior inferior cerebellar artery (PICA)), a vein in two (10%) and the vertebral artery (10%, VA) in another two cases. Audiovestibular testing revealed normal results in five patients (25%), a clear unilateral loss of audiovestibular function in nine patients (45%) and audiovestibular results with coinstantaneous signs of reduced and increased function within the same nerve in six patients (30%). From the 20 TN patients 7, (35%) showed a NVC of the N.VIII (5 AICA, 1 PICA, 1 vein). Conclusions Only the combination of clinical examination, neurophysiological and imaging techniques is capable of (1) defining the affected side of a NVC and to (2) differentiate between a deficit syndrome and increased excitability in VP.