Effets of Intensity Variations on Auditory Processing in Aphasia II. Different Intensities at Each Ear

A neurologic extinction model was applied to the auditory-processing disorders evidenced by 10 persons with aphasia. This model suggests that messages travel faster to the intact hemisphere, where they are more differentiated and articulated, than to the affected hemisphere. This leads to extinction and interference of the message. To overcome this extinction, the stimulus intensity was raised by 15 or 30 dB to one ear at a time. The stimuli were a cortical auditory-evoked response (AER) measure, a nonverbal intensity sequencing test (NVIST), a minimally varied phoneme-in-word discrimination and sequencing test (MVPT), and a semantic-syntactic level test (RTT). The results suggest that intensity can be traded for time in quantities large enough to overcome the extinction interference of auditory stimuli. Although some statistically significant results and meaningful trends toward improved performance were evident on the NVIST and the MVPT, a unilateral increase of stimulus intensity did not prove to be a potent mechanism for improving auditory comprehension. Sentence length material was not affected in either direction by selective amplification. The role of the left ear/right hemisphere as a facilitator of processing for linguistic and nonlinguistic material was suggested by the results of this study.     

Effects of intensity variations on auditory processing in aphasia. I. Equal intensities at each ear

Clinical observations have led several authors to suggest that talking louder improves auditory comprehension for the aphasic patient, while others suggest that it does nothing to help comprehension. To clarify these observations under experimental conditions, four measures of auditory processing (cortical-evoked responses, nonverbal intensity sequencing, phoneme in word discrimination and sequencing, and a semantic-syntactic measure of comprehension) were used in diotic presentation of stimuli to 10 aphasic subjects with left temporal lobe damage. The stimuli were presented at 70, 85, and 100 dB SPL. Results suggest that a simple diotic (true binaural) increase of stimulus intensity is not a potent variable for influencing auditory processing in patients with aphasia. Although a few subjects improved their performances on selected levels when stimulus intensity was increased, the performances of others decreased. Auditory-evoked response (AER) latencies and amplitudes generally were not significantly different between the damaged and intact hemispheres. The time-intensity trading function was demonstrated with the AER, particularly for the N2 component. The ear with the greatest advantage on dichotic listening was contralateral to the lesion and was contralateral to the hemisphere that had the shorter P1 latencies, longer N2 latencies, and smaller AER amplitudes.     

Effects of Electrolytic Lesions of the Superior Olivary Complex and Trapezoid Body on Brainstem Auditory-Evoked Potentials in the Guinea Pig: I. Vertex-Tragus Recordings

Brainstem auditory-evoked potentials (BAEP) were recorded between vertex and tragus in 22 guinea pigs, after destruction of the contralateral ear in order to produce monaural stimulation. Stimuli employed were 100 dB SPL clicks and tone bursts. Normative recordings showed five positive peaks, P₁-P₅ and four negative peaks, N₁-N₄. Electrolytic lesions were then made to the superior olivary complex (SOC) ipsilateral to the stimulation (6 animals), contralateral to the stimulation (8 animals), and trapezoid body (TB) (8 animals). In each group a statistical analysis of the results (amplitudes and latencies) was made (paired t test). After lesions to the ipsilateral SOC, there was an increase in the amplitude of P₁ and a decrease in P₃. After lesions to the contralateral SOC, there was a larger decrease in P₃, which disappeared in 2 guinea pigs which had a large lesion involving many TB fibers. After TB lesions, there was a decrease in the P₂-N₂ composite wave, disappearance of P₃ a decrease in P₄, and an increase in the latency of Pi and P₁-P₂ and P₂-P₄ intervals. After ipsilateral SOC lesions, which certainly involved the uncrossed olivocochlear efferent tract, the increase in P₁ suggested a disinhibition of the efferent fibers. The large decrease or the loss of P₃ after TB lesions and SOC lesions involving many TB fibers suggested that P₃ could be generated by the contralateral part of the TB fibers, in the vicinity of the contralateral SOC. These data are in agreement with the predominance of fiber tracts in the generation of BAEP.