In order to give a contribution to the genesis of the EOAEs, we have recorded echos in 24 subjects with unilateral sudden deafness (I. group); 20 ears with Menière disease (II. group); 22 ears with progressive sensorineural hearing loss (III. group) and 10 normally hearing young subjects as control group. The results have shown that the EOAEs were present in 100% (I. group), 84.6% (II. group) and 86.3% (III. group) in response to the tone-burst; while the echos were present only in the 57.1% (I. group), 38.4% (II. group) and 45.4% (III. group) in response to the click, although the audiometric threshold mean were greater than 45 dB HL for 2-4 KHz and 1 KHz in the three experimental groups except for 2-4 KHz in the subjects with Menière disease (37.5 dB HL). The properties of EOAEs (detection and saturation threshold, dynamic range and duration) depended on the degree of hearing loss. Our results seem to corroborate the hypothesis that EOAEs could be also produced by a passive intracochlear mechanism attributable to the travelling wave of the basilar membrane provoked by the perilymph. In the normal ear this passive mechanism could be superimposed by an active mechanism, linked to the contractile activity of the outer hair cells with a consequent increase in amplitude of the EOAEs for the same stimulus intensity.