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PubMed · 3268030

Cochleostomy. Long term results.

E Ried
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Abstract

The original technique of the operation of cochleostomy is described. It should be considered as conservative operation, since it produces an "ostomy" of the cochlear promontory bone, joining the spiral ligament and mucosa of middle ear, without opening of the Cochlea. There is no risk of iatrogenic anacusis. The follow up of 178 cases with more than 10 years after surgery is described. The results are significantly better than endolymphatic sac surgery.

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CochleaFollow-Up StudiesHumansMeniere DiseaseOstomyPostoperative ComplicationsJournal Article

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E Ried. 1988. Cochleostomy. Long term results.. https://pubmed.ncbi.nlm.nih.gov/3268030/

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PubMed2006

A model of peripherally developing hearing loss and tinnitus based on the role of hypoxia and ischemia.

The incidence of sensorineural hearing loss often caused by direct damage to the cochlear hair cells is by far more frequent and more serious than disorders affecting the external ear or the middle ear. Mechanisms that are discussed to be relevant for the genesis of tinnitus and acquired hearing impairment are hair cell loss, signal transduction disturbances in the region of the outer and inner hair cells and the spiral ganglion, impairment of cochlear blood flow, mechanical disturbance, and hypoxia and ischemia. The present model surveys the possible cellular and molecular biological causes of peripherally developing hearing loss and tinnitus. In particular, the paper discusses the roles of hypoxia and ischemia in the cochlea and in the etiology of the neurosensory types of tinnitus. Peripheral origins of hearing disturbances and tinnitus may be: (a) damage to the stereocilia and the tip links, (b) dysfunction of potassium channels or (c) modification of the glutamate release. Moreover, the hypoxia inducible factor-1 may have an important role to play as a key transcription factor in the cells' adaptation to hypoxia and ischemia. An impairment of the cochlear blood flow may be induced by the expression of target genes like nitrogen monoxide synthase and endothelin-1 resulting in tinnitus. The paper discusses consequences resulting from the present model for the medical treatment of peripherally developing tinnitus and hearing loss.

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