Auditory Middle Latency Responses (MLRs) in Patients with Cortical Lesions

Abstract

Auditory Middle Latency Responses (MLRs) and Auditory Brain Stem Responses (ABRs) Were Simultaneously Recorded in 24 Patients with Cortical Primarily Affecting the Temporal Lobes. Site of Lesion Was Documented by Computerized Tomography (CT) Scan and Behavioral Profiles Assessing Language and Other Higher Cortical Functions Were Obtained. in Patients with Normal ABRs and Either Left or Right Hemisphere Lesions, MLR Components Na and Pa Obtained at the Vertex Were of Normal Shape and Latency. Exceptions to This Occurred in 2 Patients: One with Bilateral Temporal Lobe Lesions, the Second with an Infraventricular Left Temporal Lobe Lesion Extending into the Thalamic Radiations. Although Na and Pa Shape and Latency Were for the Most Part Unaltered, Pa Amplitude Tended to Cluster at the Low End and Below Normal Values. MLR Recorded in the Coronal Plate Showed Pa Amplitude to Be Attenuated or Absent over the Damaged Temporal Lobe Relative to the Vertex or the Intact Hemisphere. This Finding Contrasts with Data from Normal Subjects Where Pa Amplitude is Largest at the Vertex and Essentially Symmetrical About the Temporal Lobes. Patients Showing an Atypical Amplitude Distribution Tended to Have Lesions Involving Auditory Cortex and Adjacent White Matter Projections. No Obvious Correlations between MLR Abnormalities and Behavioral Findings Regarding Receptive and Expressive Language Processes Were Found. Pa Appears to Be Affected by Temporal Lobe Lesions Involving Auditory Cortex and Thalamic Projections. Our Findings Support the Hypothesis that Pa is Bilaterally Generated by Two Symmetrical, Vertically Oriented Dipole Sources Located About the Temporal Lobes. © 1982.

Department(s)

Chemistry

International Standard Serial Number (ISSN)

0013-4694

Document Type

Article - Journal

Document Version

Citation

File Type

text

Language(s)

English

Rights

© 2023 Elsevier, All rights reserved.

Publication Date

01 Jan 1982

PubMed ID

6179755

Share

 
COinS