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January 1971


Author Affiliations

University of Oklahoma Medical Center 800 Northeast 13 St Oklahoma City 73104

Arch Otolaryngol. 1971;93(1):112. doi:10.1001/archotol.1971.00770060144030

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We wish to express our appreciation for Dr. Silverstein's comments on our article.

We agree with Dr. Silverstein's suggestion that there might be a rupture of Reissner's membrane when changes in the endolymphatic Na+ concentrations fail to return to normal and wish to draw attention to this possibility as expressed on page 6 of the article:

The endolymphatic Na+ concentration did not return to the control level after intense and prolonged acoustic stimulation. Damage to the cochlear membranes or disturbance of cochlear blood supply may be responsible for this phenomenon.

Some investigators (Suga F: Otologia Fukuoka8 (Suppl 3):187, 1962) have reported that extremely intense sound produces irreversible decreases in endolymphatic direct current potential, and the cause of this phenomenon may have a common mechanism with the irreversible increase in the endolymphatic sodium ion concentration after intense sound stimulation.

The point regarding histological control is well taken. We are continuing the

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