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Titolo:
Cochlear ischemia induced by circulating iron particles under magnetic control: An animal model for sudden hearing loss
Autore:
Schweinfurth, JM; Cacace, AT;
Indirizzi:
Albany Med Coll, Albany, NY 12208 USA Albany Med Coll Albany NY USA 12208Albany Med Coll, Albany, NY 12208 USA
Titolo Testata:
AMERICAN JOURNAL OF OTOLOGY
fascicolo: 5, volume: 21, anno: 2000,
pagine: 636 - 640
SICI:
0192-9763(200009)21:5<636:CIIBCI>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACOUSTIC-DISTORTION PRODUCTS; OTOACOUSTIC EMISSIONS; CLINICAL-APPLICATIONS; HUMAN-BEINGS; BLOOD-FLOW;
Keywords:
sudden hearing loss; cochlear ischemia; otoacoustic emissions; embolization; magnetic iron particles;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Schweinfurth, JM S-2100 MCN, Nashville, TN 37212 USA S-2100 MCN NashvilleTN USA 37212 ashville, TN 37212 USA
Citazione:
J.M. Schweinfurth e A.T. Cacace, "Cochlear ischemia induced by circulating iron particles under magnetic control: An animal model for sudden hearing loss", AM J OTOL, 21(5), 2000, pp. 636-640

Abstract

Purpose: To correlate the absence of distortion-product otoacoustic emissions observed in sudden hearing loss (SHL) with a possible thromboembolic vascular cause, using an animal model. Background: Distortion-product otoacoustic emissions (DPOAEs) are sensitive to cochlear disorders and are absent in cochlear injury. In a previous study, the authors showed that 75% of patients with SHL who have no measurable emissions do not recover hearing. The underlying cause of the loss of emissions is unknown, but it may be secondary to cochlear ischemia. Methods: Six New Zealand white rabbits underwent unilateral cochlear embolization through the use of circulating iron particles under magnetic control. Cochlear function was monitored through DPOAE recordings of the experimental and control ears. Results: In all animals, a rapid decrease in emissions was noted, which fluctuated but returned to baseline within 2 hours to 3 weeks after embolization, leaving no measurable residual defects. The DPOAEs were suppressed by 5 to 19 dB within 10 minutes of injection of iron solution and magnet placement. The lowest emissions were obtained at 30 minutes and again at 120 minutes, which were 12 to 37 dB below preembolization levels. Two animals returned to baseline DPOAE levels at 1 to 3 weeks, with no identifiable residual deficits. Conclusion: It is likely that the loss of emissions seen in the present study is related to cochlear ischemia. The early suppression of DPOAEs in therabbit cochlea. after embolization may parallel that in SHL patients with absence of DPOAEs on presentation.

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Documento generato il 04/12/20 alle ore 19:11:15