Three assumptions involved in the rationale for loudness tolerance modification were investigated: (1) that an abnormal loudness discomfort level (LDL) is modifiable by sub-LDL stimulation, (2) that a relationship exists between abnormal LDL and reduced speech discrimination ability, and (3) that an improved LDL will result in better speech discrimination than evidenced before such modification. Twenty subjects with functional evidence of bilateral cochlear hearing loss were divided into four group. Each of three groups received a different type of sound exposure and the other groups served as a control. LDLs were determined before, interjacent to, and after exposure. No significant changes in LDL were found for any of the experimental groups. The parabolic articulation function associated in the literature with monaural cochlear lesions was absent for all cases. Sub-LDL exposure to high intensity speech does not appear to be an effective modifier of an abnormal LDL. The rationale for loudness discomfort level modification therapy, namely to improve speech discrimination, appears to be unwarranted. Abnormal loudness discomfort improvement may involve adjustment problems more responsive to behavioral modification approaches.
Cortical activity patterns predict robust speech discrimination ability in noise
