gms | German Medical Science

64th Annual Meeting of the German Society of Neurosurgery (DGNC)

German Society of Neurosurgery (DGNC)

26 - 29 May 2013, Düsseldorf

Microvascular decompression of the vestibulocochlear nerve for long-standing unilateral pulsatile tinnitus

Meeting Abstract

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  • Ariyan Pirayesh Islamian - Klinik für Neurochirurgie, Medizinische Hochschule Hannover, Hannover
  • Götz Lütjens - Klinik für Neurochirurgie, Medizinische Hochschule Hannover, Hannover
  • Joachim K. Krauss - Klinik für Neurochirurgie, Medizinische Hochschule Hannover, Hannover

Deutsche Gesellschaft für Neurochirurgie. 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Düsseldorf, 26.-29.05.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. DocP 020

doi: 10.3205/13dgnc441, urn:nbn:de:0183-13dgnc4418

Published: May 21, 2013

© 2013 Islamian et al.
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Outline

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Objective: Pulsatile tinnitus (PT) usually suggests a vascular etiology ranging from dural arteriovenous fistulae (dAVF), intracranial aneurysms and vascular tumors of the temporal bone and cerebello-pontine angle (CPA). Vascular compression of the eighth cranial nerve (CN VIII) may be an additional cause of tinnitus. However, microvascular decompression (MVD) solely for relieving tinnitus yielded poor results compared to those achieved for trigeminal neuralgia, hemifacial spasm and glossopharyngeal neuralgia. This discrepancy is mainly attributable to the lack of sufficient diagnostic criteria for tinnitus caused by neurovascular compression (NVC) and inadequate patient selection. We report on a patient with a long-standing history of unilateral PT that subsided following MVD of CN VIII to illustrate exemplarily the key criteria for identifying patients suffering from tinnitus due to NVC.

Method: A 73-year-old man presented with a 20-year history of constant distressing unilateral PT. Physical examination was remarkable for a sensorineural hearing loss ipsilateral (–80 dB in 1-2 kHz hearing range), vertigo and a coexistent peripheral facial nerve palsy (House-Brackmann grade II). T2WI MRI demonstrated a vascular loop crossing CN VIII in the CPA. Vascular pathologies such as dAVF and aneurysms were ruled out by digital subtraction angiography. With the presumptive diagnosis of NVC syndrome the patient underwent MVD. Intraoperatively, CN VIII was found to be impinged in its cisternal segment by an AICA loop. The latter was mobilized away from the nerve and a small Teflon felt was inserted between the offending vessel and CN VIII.

Results: Postoperatively the patient reported about an immediate resolution of PT. The ipsilateral afunctional preoperative hearing ability had deteriorated to anacusis. On 4-month follow-up facial nerve palsy and anacusis were unaltered, vertigo was alleviated, PT had not recurred and the patient reported improved quality of life.

Conclusions: In the presence of associated vertigo, sensorineural hearing loss and/or coexistent symptoms pertaining to the facial nerve or even the trigeminal nerve, one must consider the possibility of an irritative mechanism of CN VIII in the CPA as an additional cause of unilateral PT. Depending on the severity of tinnitus, MVD of CN VIII may be justified as a treatment option. Surgery may be effective independent from symptom duration. Selecting appropriate surgical candidates is crucial.