Detection of intracochlear and intracranial pressure changes with otoacoustic emissions: a gerbil model.

Increased intracranial pressure (ICP) is known to affect the phases and levels of lower-frequency distortion-product otoacoustic emissions (DPOAE) in a characteristic manner suggestive of an increase in the stiffness of the stapes system, likely in relation to an attendant increased intracochlear pressure (ICoP). DPOAEs may thus provide an easy non-invasive means of gaining access to the otherwise elusive ICoP. However, the mechanisms by which DPOAEs actually relate to ICoP are unclear and may involve changes in the stiffness of the annular ligament, stapedius muscle and even some indirect contributions of other parts of the middle ear such as the tensor tympani. A systematic study of the role of each middle-ear element on ICoP-to-DPOAE relationships as a function of frequency was undertaken in gerbils under direct control of ICP via an intracranial catheter (from 0 to 500 daPa). After the bulla was widely opened, the tendons of the stapedius and tensor tympani muscles were severed in turn. A standard electroacoustic analog model of the middle ear was used for predicting the forward and reverse middle-ear transfer-functions changes under different experimental manipulations and their consequences on DPOAEs. The observed DPOAE changes chiefly consisted in a phase-lead peaking around 2.15 kHz in closed-bulla, and 1.2 kHz in open-bulla conditions. It was proportional to ICP increase provided ICP exceeded a threshold of about 50 daPa. The profiles of DPOAE shifts matched those derived from the premise that ICoP mainly induced a change in the stiffness of the stapes system. The possible involvement of the stapedius muscle was ruled out by the absence of any effect of cutting its tendon so that the intrinsically non-linear stiffness of the annular ligament must have been the main factor. A relatively minor contribution from the tensor tympani was observed, possibly in relation to the detection of ICoP-induced displacement of the ossicular chain by neuromuscular spindles.