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Effects of Cortical Lesions on Middle-Latency Auditory Evoked Responses (MLR)

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Effects of Cortical Lesions on Middle-Latency Auditory Evoked Responses (MLR) 108 Electroencephalographv and clinical N europh~ siologv , 1987, 66: 108-120 Elsevier Scientific Publishers Ireland, Ltd. EEG 03032 Effects of cortical lesions on middle-latency auditory evoked responses (MLR) Paul Kileny *, Daniel Paccioretti ** and A.F. Wilson ** * Department of Otola~'ngology, Head and Neck SurgetT, Universi(v of Michtgan Medical Center, Ann A rbor. MI 48109 ( U. S. A,), and ** Glenrose Rehabilitation Hospital, Edmonton, Alberta (Canadak (Accepted for publication: 9 June, 1986) Summary Middle-latency auditory evoked responses (MLRs) were recorded simultaneously at 3 or 4 electrode locations in the coronal plane in 5 normal subjects, 11 patients with temporal lobe lesions and in 5 patients with cortical lesions not involving the temporal lobes. In patients with unilateral temporal lobe lesions, the amplitude of Pa and hence that of the Na-Pa complex was reduced over the involved hemisphere but remained intact over the contralateral hemisphere. No MLR asymmetries were demonstrated in patients with cortical lesions that did not affect the temporal lobes or in 2 cases with unilateral anterior temporal lobectomy. The latency of wave V of the auditory brain-stem response was within normal limits in the majority of the patients studied regardless of the site of their cortical lesion. Key words: middle-latency auditory evoked responses; cortical lesions; CT scans; coronal distribution; ipsilateral, contralateral hemisphere The middle-latency components of the auditory EEG filter (Scherg 1982; Sprague and Thornton evoked response (MLR) occur within a latency 1982; Kileny 1983). Considerable distortion may range of 100 msec following the presentation of an be introduced by high-pass filtering when utilizing effective auditory stimulus. Geisler et al. (1957) relatively steep analogue filters. With a relatively were the first to describe the MLR as 'an early wide input filter setting (i.e., 5-1500 Hz), one can response with an onset latency of about 20 msec' simultaneously record both the early brain-stem characterized by a vertex-positive peak with a components of the auditory evoked response and latency of about 30 msec. While the scalp distribu- the MLR components (C)zdamar et al. 1982; tion of the MLR is widespread, it has been re- Kileny 1983). The most prominent, robust and ported to be most prominent over fronto-central stable component in adults is the vertex-positive regions (Picton et al. 1974; Ozdamar and Kraus peak usually labeled Pa (peak latency 25-30 msec). 1983). With monaural stimulation, the responses Controversy surrounds the identity of the gen- recorded between vertex (Cz) and ipsilateral or erator sources of the MLR. While there is some contralateral earlobes were reported to be sym- overlapping of myogenic and neurogenic activity metrical (Peters and Mendel 1974). The configura- during the 100 msec poststimulus latency range, tion of the recorded MLR depends upon the char- the MLR is basically a neurogenic auditory evoked acteristics (cut-off frequencies, filter slopes) of the response which remains unaffected following the administration of neuromuscular blocking agents (Harker et al. 1977; Kileny 1983; Kileny et al. Correspondence to: Dr. P. Kileny, Dept. of Otolaryngology, Head and Neck Surgery, University of Michigan Hospitals, A. 1983). Responses have been recorded from the Alfred Taubman Health Care Center, TC-1904-0312, 1500 E. exposed human cortex within the latency range Medical Center Drive, Ann Arbor, MI 48109-0312, U.S.A. associated with the scalp-recorded MLR (Heath 0013-4649/87/$03.50 ~ 1987 Elsevier Scientific Publishers Ireland, Ltd. MLR IN CORTICAL LESIONS 109 and Galbraith 1966; Celesia et al. 1968; Pulletti tients with confirmed temporal lobe lesions ex- and Celesia 1970). These have been considered to hibited reduced or absent Pa peaks over the be primary auditory responses and were elicited damaged hemisphere. They concluded that the by both ipsilateral and contralateral auditory vertex-recorded MLR reflects contributions from stimulation. Their cortical distribution was limited symmetrical bilateral generators. Under normal to the posterior part of the superior temporal circumstances, their electrical activity is summed gyrus and the parietal and frontal operculum. at the vertex. With a unilateral lesion the vertex Cortical sensory responses recorded in this latency response would be diminished due to a reduction range are as a rule considered to be mediated by of the contribution originating from the affected the specific lemniscal sensory pathways and side. specific thalamic nuclei (Brazier 1972). Picton et The present study was prompted by the results al. (1974) listed several possible neural generator reported by Kraus et al. (1982). While their study sources for the MLR: thalamus, association cortex was unique in that it consistently correlated well- in frontal, parietal and temporal lobes. defined MLR abnormalities with documented A recent study by Woods and Clayworth (1985) brain lesions in humans, it did not address two revealed differences between the scalp distribu- important questions: tions and hemisphere-ear interactions of the Na (1) What, if any, are the effects of other local- and Pa components of the MLR in normal sub- ized cortical lesions not involving the temporal jects. While the Pa component exhibited the same lobes on the configuration of the MLR? baseline-to-peak absolute amplitude when re- (2) Is there an interaction between the site of corded over the ipsilateral and the contralateral lesion and the test-ear (right or left), i.e., is the hemisphere, the Na component exhibited reduced effect described by Kraus et al. (1982) more pro- latencies and increased amplitudes over the hemi- nounced when stimulating the ear ipsilateral to the sphere contralateral to the stimulated ear. lesion or when stimulating the ear contralateral to There have been conflicting reports in the liter- the lesion? ature concerning the effects of temporal lobe le- sions on the MLR. Parving et al. (1980) reported on a patient with auditory agnosia and docu- Materials and Methods mented bilateral temporal lobe lesions who ex- hibited normal MLRs. Ozdamar et al. (1982) re- Sixteen patients aged 21-71 years with a variety ported on a patient who also presented with bi- of cortical lesions (Table I) resulting mainly from lateral temporal lobe lesions, inconsistent aware- cerebrovascular accidents, 5 normal subjects and 2 ness of sound and impaired pure-tone hearing patients with right anterior lobectomies were in- sensitivity who presented with abnormal MLR cluded in this study. All patients were first as- wave forms: Pa was absent bilaterally. Based on sessed by conventional behavioral audiometry their respective results, the two groups of inves- techniques (pure-tones, speech and immittance). tigators arrived at opposite conclusions regarding They were also assessed by a speech-language the role of the primary auditory cortex in the pathologist and a psychologist to determine speech, generation of the MLR. language and cognitive skills. Table I lists the In a recent study, Kraus et al. (1982) reported following information on the 16 patients with on the effects of temporal lobe lesions on the cortical lesions: site of lesion determined from CT coronal scalp distribution of the MLR in 24 pa- scans, etiology, hearing status, the status of the tients. MLRs were recorded simultaneously at the auditory brain-stem response (ABR), speech-lan- vertex and over the right and the left hemispheres guage and cognitive function and the audiological slightly above the sylvian fissure in the coronal evaluations. plane. In contrast to normal subjects in whom the The evoked potential studies were performed amplitude of Pa was largest at the vertex and 2-4 weeks following the onset of the traumatic or symmetrical at the supra-sylvian electrodes, pa- vascular brain injury. Neuro-electrical activity was 110 P. KILENY ET AL. TABLE I Patient no. Age Sex Site of lesion Etiology Hearing ABR wave Speech-language and V latency cognitive function Patients with temporal lobe im,olvement 1 49 M (R) Fronto-temporal Trauma Mild mod. HF WNL Mild dysphonia, impaired Sensorineural memory Bilateral 2 70 F (L) Fronto-temporal Infarct Mild high freq. WNL Mild apraxia Sensorineural Bilateral 3 53 F (R) Fronto-temporal Infarct Mild-moderate WNL Mixed aphasia, Sensorineural decreased attention Bilateral 4 37 M (L) Fronto-temporal Infarct Mild-severe HF WNL Impaired expressive parietal Sensorineural language Bilateral 5 35 M (R) Temporal parietal Infarct Mild HF WNL Normal speech-language Sensorineural Bilateral 6 70 F (R) Temporal parietal Infarct Mild HF WNL Functional speech-language, Sensorineural impaired memory and attention 7 44 F (L) Temporal parietal Infarct Mild-moderate HF WNL Non-fluent aphasia, Sensorineural slow cognitive processing 8 62 M (L) Temporal parietal Infarct Mild-moderate HF WNL Severe receptive-expressive Sensorineural aphasia and dyspraxia 9 71 F (L) Deep temporal Infarct Mild-profound HF WNL Mild aphasia, impaired Sensorineural memory, attention and Bilateral cognitive insight 10 61 F (L) Fronto-temporal Infarct WNL WNL Moderate-severe verbal dyspraxia, impaired memory_ 11 56 M (L) Fronto-temporal Infarct Mild-moderate WNL Receptive and expressive HF sensorineural aphasia, impaired memory and cognitive insight Patients with lesions not affecting temporal lobes 1 21 M (L) Frontal Trauma Mild-moderate WNL Aphonia. anxiety HF sensorineural Bilateral 2 39 F (L) Fronto-parietal Infarct WNL WNL Apraxia and expressive aphasia 3 66 M (L) Posterior parietal Infarct Mild-severe Receptive and expressive Sensorineurat aphasia, impaired memory Bilateral and cognitive insight 4 67 M (L) Posterior parietal Infarct Mild-moderate WNL Mild apraxia Sensorineural Bilateral 5 17 M (L) Fronto-parietal Trauma WNL WNL Functional speech deficit recorded simultaneously at 3 or 4 scalp locations the sylvian fissure over the temporal lobe of the in the coronal plane as follows (10/20 electrode affected side (T3 and T4 respectively). All active system, Jasper 1958): vertex (Cz); right and left electrodes were referenced to common linked parietal electrodes just above the sylvian fissure earlobe electrodes.
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