Vestibularisparoxysmie

Zusammenfassung

Die Vestibularisparoxysmie ist ein neurovaskuläres Kompressionssyndrom des achten Hirnnerven mit einer Pathogenese analog zur Trigminusneuralgie oder zum Hemispasmus facilis. Klinisch ist die Erkrankung durch bis zu hundert Mal pro Tag auftretende, kurze, monosymptomatische Schwindelattacken charakterisiert. Seltener können diese mit Ohrsymptomen (einseitiger Tinnitus, Taubheit/Druckgefühl im Bereich des Ohrs, einseitige Hörminderung) vergesellschaftet sein. Häufig treten die Attacken ohne Auslöser auf, können aber auch inkonstant durch bestimmte Kopfoder Körperpositionen provoziert werden. Die klinisch-neurologische Untersuchung zeigt im Intervall keine spezifischen Auffälligkeiten, allenfalls gibt es Hinweise auf ein leichtes vestibulo-cochleäres Defizit. Dieses lässt sich dann in den Zusatzuntersuchungen wie Elektronystagmogafie, Hörtests oder akustisch-evozierte Potenziale dokumentieren. Eine cranielle MRT mit stark T2-gewichteter “constructive interference in steady-state” (CISS)-Sequenz dient dem Nachweis des Gefäß-Nerv-Kontaktes und dem Ausschluss konkurrierender Pathologien. Die Therapie erfolgt mit Carbamazepin oder Oxcarbazepin, eine operative Dekompression bleibt Ausnahmefällen vorbehalten.

Summary

Vestibular paroxysmia is a syndrome of neurovascular cross-compression of the eighth cranial nerve. It is assumed to have a pathogenesis analogous to that of trigeminal neuralgia or hemifacial spasm. The disease is clinically characterized by monosymptomatic attacks of vertigo which can occur up to hundreds of times a day. These can sometimes be associated with symptoms stemming from the auditory system (tinnitus, tingling sensation/light pressure in or around the ear, unilateral reduced hearing).The attacks often occur without provoking factors, but are sometimes triggered by certain head or body positions. The clinical-neurological examination in the attack-free interval usually gives normal results; sometimes there can be signs of a subtle vestibulo-cochlear deficit. These can also be documented with auxiliary tests such as electronystagmography, audiometry, or acoustic evoked potentials. A cranial MRI with the strongly T2-weighted “constructive interference in steady-state” (CISS) sequence can be used to document neurovascular cross-compression and to exclude other pathologies. The therapy of choice is carbamazepine or oxcarbazepine. Operative decompression is reserved for exceptional cases.

Schlüsselwörter

Vestibularisparoxysmie - Carbamazepin - Oxcarbazepin - Gefäß-Nerv-Kontakt

Keywords

Vestibular paroxysmia - carbamazepine - oxcarbamazepine - neurovascular cross-compression

• Literatur

• 1 Arbusow V. et al. Alternating episodes of vestibular nerve excitation and failure. Neurology 1998; 51: 1480-1483.
• 2 Brandt T, Dieterich M. Vestibular paroxysmia: vascular compression of the eighth nerve?. Lancet 1994; 343: 798-799.
• 3 Buettner UW. et al. Brainstem auditory evoked potential abnormalities in vascular malformations of the posterior fossa. J Neurol 1983; 229: 247-254.
• 4 Casselman JW. et al. Magnetic resonance examination of the inner ear and cerebellopontine angle in patients with vertigo and/or abnormal findings at vestibular testing. Acta Otolaryngol Suppl 1994; 513: 15-27.
• 5 Cheshire WP. Trigeminal neuralgia: for one nerve a multitude of treatments. Expert Rev Neurother 2007; 07: 1565-1579.
• 6 He L, Wu B, Zhou M. Non-antiepileptic drugs for trigeminal neuralgia. Cochrane Database Syst Rev 2006; 03: CD004029.
• 7 Hüfner K. et al. Vestibular Paroxysmia – Diagostic features and medical treatment. Neurology 2008; 71: 1006-1014.
• 8 Jannetta PJ. Neurovascular cross-compression in patients with hyperactive dysfunction symptoms of the eighth cranial nerve. Surg Forum 1975; 26: 467-468.
• 9 Jannetta PJ, Moller MB, Moller AR. Disabling positional vertigo. N Engl J Med 1984; 310: 1700-1705.
• 10 Kalkanis SN. et al. Microvascular decompression surgery in the United States, 1996 to 2000: mortality rates, morbidity rates, and the effects of hospital and surgeon volumes. Neurosurgery 2003; 52: 1251-1261.
• 11 Kanashiro AM. et al. [Vestibular paroxysmia: clinical study and treatment of eight patients]. Arq Neuropsiquiatr 2005; 63: 643-647.
• 12 Lang J. [Anatomy, length and blood vessel relations of “central” and “peripheral” paths of intracisternal cranial nerves]. Zentralbl Neurochir 1982; 43: 217-258.
• 13 Lawden MC. et al. Repetitive paroxysmal nystagmus and vertigo. Neurology 1995; 45: 276-280.
• 14 Levine RA. Typewriter tinnitus: a carbamazepineresponsive syndrome related to auditory nerve vascular compression. ORL J Otorhinolaryngol Relat Spec 2006; 68: 43-46.
• 15 Majoie CB. et al. Trigeminal neuralgia: comparison of two MR imaging techniques in the demonstration of neurovascular contact. Radiology 1997; 204: 455-460.
• 16 Makins AE. et al. Is there a correlation between vascular loops and unilateral auditory symptoms?. Laryngoscope 1998; 108: 1739-1742.
• 17 Minor LB. et al. Hyperventilation-induced nystagmus in patients with vestibular schwannoma. Neurology 1999; 53: 2158-2168.
• 18 Moller MB. et al. Microvascular decompression of the eighth nerve in patients with disabling positional vertigo: selection criteria and operative results in 207 patients. Acta Neurochir (Wien) 1993; 125: 75-82.
• 19 Moller MB. et al. Diagnosis and surgical treatment of disabling positional vertigo. J Neurosurg 1986; 64: 21-28.
• 20 Niwa Y. et al. [Identification of offending vessels in trigeminal neuralgia and hemifacial spasm using SPGR-MRI and 3D-TOF-MRA]. Rinsho Shinkeigaku 1996; 36: 544-550.
• 21 Odkvist LM. et al. Macrovascular causes underlying otoneurological disturbances. Acta Otolaryngol 1995; 115: 145-148.
• 22 Ostermann PO, Westerberg CE. Paroxysmal attacks in multiple sclerosis. Brain 1975; 98: 189-202.
• 23 Ryu H. et al. Neurovascular compression syndrome of the eighth cranial nerve. Can the site of compression explain the symptoms? Acta Neurochir (Wien) 1999; 141: 495-501.
• 24 Straube A. et al. Recurrent attacks with skew deviation, torsional nystagmus, and contraction of the left frontalis muscle. Neurology 1994; 44: 177-178.