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ORIGINAL ARTICLE
Year : 2003  |  Volume : 5  |  Issue : 1  |  Page : 15-20

Auditory evoked potential evaluation of the higher auditory processing at late latency


Assistant Professor, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia

Date of Web Publication11-Jul-2020

Correspondence Address:
PhD. Audiology Khayria A Al-Abduljawad
Assistant Professor, King Saud University, P.O.Box. 271512 Riyadh 11352 Tel: 01 4455293
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-8491.289560

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  Abstract 


Aim: To examine the N1/P2 complex of the auditory evoked potential and its susceptibility to PPI and to compare the amplitudes of these responses and their suppression.
Material and Methods: Twenty healthy volunteers, ten males and ten females were entered in this study. Their mean age 21.5 years. Before entering the study their hearing thresholds at 0.5,1,2, and 4k HZ were measured, none of them were found to have thresholds above 20dB.
Results: The female subjects in this study showed slightly higher auditory evoked potential responses and lower response latencies than the males.
Conclusion: Our findings are consistent with sex differences. These are attributed to differences in skull dimensions, brain volume and conduction distances.

Keywords: late latency auditory evoked potential; N1/P2 complex; prepulse


How to cite this article:
Al-Abduljawad KA. Auditory evoked potential evaluation of the higher auditory processing at late latency. Saudi J Otorhinolaryngol Head Neck Surg 2003;5:15-20

How to cite this URL:
Al-Abduljawad KA. Auditory evoked potential evaluation of the higher auditory processing at late latency. Saudi J Otorhinolaryngol Head Neck Surg [serial online] 2003 [cited 2022 Dec 4];5:15-20. Available from: https://www.sjohns.org/text.asp?2003/5/1/15/289560




  Introduction Top


The auditory brain stem resonse (ABR) is considered as the auditory evoked potential (AEP) that is most widely used by audiologists. However, other kinds of AEPs also provide information not obtainable with the ABR, such as, latetatency auditory evoked potentials (LLAEPs), also known as cortical evoked potentials [1],[2]. These responses occur in the range of 100-300 ms after the stimulus and overlap wiyh the so called “endogenous” or “cognitive” potentials. The N1 and P2 peaks are affected by the level of behavioral arousal, and are suppressed by sedative durgs, for example benzodiazepines [3],[4], Prepulse inhibition (PPI) of the loud acoustic response is the suppression of the response that is normally evoked by an intense stimulus [5], The N1 and P2 potentials are negative and positive peaks occurring within the “late-latency” band of the auditory evoked response (approximately 100 and 200 ms after stimulus onset) [6]. The difference in potential between the two peaks is the amplitude of the N1/P2 complex, their amplitudes are often in the range of tens of microvolts, allowing adequate measurements of averaged potentials with as few as 20-50 sweeps [7]. In adults, N1 has a latency of about 100 ms, and P2 about 180-200 ms [8], much longer latencies being recorded in young children [9].The precise origins of the LLAEPs remain controversial. PPI of the loud acoustic response is the suppression of the response that is normally evoked by an intense stimulus (the pulse) by presentation of a weak stimulus (the prepulse) shortly before the pulse [10].The degree of suppression induced by the prepulse depends critically on the interval separating the prepulse and pulse. Some PPI have been found with interstimulus intervals as short as 15 ms [11]. However, intervals between 30 and 500 ms produce the most reliable inhibition [12],[13]. The degree of PPI is also intensity-dependent, relatively intense prepulses producing more profound inhibition than prepulses whose intensity is close to the threshold of detectability [14]. PPI is widely regarded as a prototype form of sensorimotor “gating” or “filtering”. For example [15], “prepulse inhibition appears to reflect a “hard-wired” centrally mediated behavioral gating”.The aims of this study were firstly to examin if the N1/P2 complex of the auditory evoked potential is susceptible to PPI. Secondly to copare the amplitudes of these reponses and their suppression by prepulses in male and femal subjects.


  Methods: Top


Subjects were shown an information leaflet explaining the nature and purpose of the experiment, and they gave their consent in writing to participate in the experiment.

Subjects

Twenty healthy volunteers, 10 males and 10 females, participated in this study. Their age ranged between 19 and 24 years with a mean age of 21.5. They all had no history of hearing loss and their hearing thresholds were below 20dB. Their hearing thresholds were measured at 0.5 and 4 kHz befor they were entered in the study. Those with ear disease or diabetes, hypertension and hearing thresholds above 20dB were excluded from the study.

Tests and Apparatuses

All recordings were made while the subject was seated in an armchair. Acoustic stimuli were generated by an (GSI 17 clinical audiometer) and were presented to the subject binaurally. A background 70-dB 1-kHz tone was present throughout the recording period. The sound pulses consisted of 40- ms 1-kHz tones of intensities 115 dB or 85 dB.

Stimuli were delivered by the CED 1401+ computer, which also recorded the electrophysiological data. The period of recording started with a 180 s “adaptation” period in which the background sound was presented. Then a single 115-dB pulse was presented (responses to this initial pulse were discarded). The remainder of the recording period consisted of 60 trials separated by inter-trial intervals varying between 15 and 35 s (mean 25 s), The stimuli presented in the trials were (i) a single 40ms 115-dB pulse (Hi-pulse trials, n = 20);(ii) a single 40-ms 85-dB pulse (Lo-pulse trials, n = 20); (iii) a 40-ms, 85-dB pulse, followed, after 120 ms, by a 40-ms 115 dB pulse (prepulse/pulse trials, n =20). The order of occurrence of the three types of trials was randomized with the constraint that the same type of trial did not occur more than twice-in succession.

Procedure

Each subject participated in a single session. After arrival in the clinic, the subject rested for 15 minutes before entering the testing room. Hearing thresholds were first tested. Then the electrodes were attached and recording commenced as described above. The total period of recording was approximately 30 minutes.

Data analysis

The evoked potentials recorded in each type of trial were averaged across the 20 trials. The latencies and amplitudes of the following components of the evoked responses were determined (values in parentheses indicate the range of latencies to the peak of the wave following stimulus onset): N5 (81-140 ms), and P2 (141-240 ms); in each case, amplitude was measured from the prestimulus baseline. In addition, the amplitude of the N1/P2 complex was measured as the amplitude difference from the peak of the N1 wave to the peak of the P2 wave (10). The data derived from the Lo-pulse and Hi-pulse trials were compared between males and females using Studentis t-test. Percent PPI was calculated for each component of the response, by using the formula:

100. [AHi-pulse -Aprepulse /pulse] /AHi-pulse Where AHi-pulse and Aprepulse / pulse are the amplitudes of the mean responses to the 115-dB pulses in the Hi-pulse and prepulse / pulse trials.


  Results: Top


The amplitudes and latencies of the N1 and P2 potentials evoked by the 85 dB and 115 dB pulses, and the amplitude of the N1/P2 complex, in the male and female is shown in [Table 1]. N1 potential: in both sex groups, the more intense stimulus was associated with an N1 potential of greater amplitude and shorter latency than the less intense stimulus. The amplitudes of Nl responses to both stimuli were greater in the females than in the males, this difference being statistically significant in the case of the more intense stimulus [85 dB: t(18)=1.7, pX).l ; 115 dB: t(18)=3.5, p<0.01], [Figure 1],[Figure 2].The latencies of the Nl potentials were somewhat shorter in the females than in the males; however the gender differences were not statistically significant [85 dB: t(18)=1.9,p=0.07; 115 dB: t(18)=1.7, p>0.1] [Figure 1],[Figure 2]. Substantial prepulse inhibition of the Nl potential occurred in the prepulse/ pulse trials; however, there was considerable variability within groups, and there was considerable between the males and the females [t (18) = 1.2, p>0.1].
Figure 1: Amplitude and latency of acoustic response at 85dB trails left hand panel amplitude and right hand panel latency show no significant difference between males and females [85dB:t (18)=1.7p>0.1]

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Figure 2: Amplitude and latency of acoustic response at 115dB trails left hand panel amplitude show significant difference between males and females [115dB:t(18)=3.5p<0.1], and right hand panel latency show no significant defferense between males and females [t(18)=0.3p<0.1]

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Table 1: Parameters of components of the auditory evoked potential record in males and Females (M,n=10; F,n=10)

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P2 potential: the P2 potential also showed a greater amplitude and shorter latency following the more intense stimulus. The amplitudes of the P2 potentials tended to be somewhat greater in the females than in the males, the difference being of borderline statistical significance in the case of the more intense stimulus [85 dB: t(18)=l.4,P>0.1; 115 dB: t(I8)=2.1, P=0.05] [Figure 2]. There were no significant differences between the latencies of the P2 potential [85 dB: t (18) =0.1, P>0.1; U5dB: t(18) = 1.3, P>0.1]. PPI of the N1/P2 complex is shown in [Figure 3]. Consistent prepulse inhibition of the P2 potential occurred in the prepulse/pulse trials; there was no significant difference between the males and the females [t (18) « 1.2, p>0.1] [Figure 3].
Figure 3: Consistent PPI was seen in both groups, with no significant difference between males and females [t(18) = 0.3,P> 0.1]

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N1/P2 complex. The amplitude of the N1/P2 complex was markedly greater following the 115 dB stimulus than following the 85 dB stimulus, reflecting the intensity-dependence of both component waves. Females showed larger responses than males, the difference being statistically significant in the case of the 115dB stimulus [85 dB: t (18) =1.8, P>0.08; 115 dB: t (18) =3.4, P>0.01]. Consistent PPI was seen in both groups, with no significant difference between males and females [t (18) =0.3, P>0.1] [Figure 3].


  Discussion Top


In agreement with many previous experiments, the Nl and P2 peaks are affected by the level of behavioral arousal, and are suppressed by sedative drugs, e.g. benzodiazepines [3],[4].

The primary auditory cortex is evidently crucial, as the responses are disrupted when this area is damaged [16],[17]. However, there is also evidence that other cortical areas, including those responsible for interpretation of speech sounds (Wernicke’s area), may be involved [18],[19]. Thus, loud acoustic responses evoked by intense acoustic stimuli may be suppressed by weak auditory, visual or tactile stimuli [20], Several clinical studies have shown that schizophrenic patients have diminished suppression of a middle latency component of the auditory evoked response , the P50 potential as well as diminished PPI of their startle responesses, compared to healthy control subjects [21]. In agreement with previous reports [22],[23],[24] the results of this study showed reliable PPI of some late-latency components of the auditory evoked potential, the Nl and P2 potentials. The present results show that the combined measure of the N1 and P2 waves, the amplitude of the NI/P2 complex, can reveal robust prepulse inhibition. The use of this measure, rather than the separate amplitudes of the N1 and P2 potentials, has the advantage of avoiding the ambiguities that may result from changes in the prestimulus baseline [6]. This is in partial agreement with the findings of Schall et al. (1996), which, using a somewhat different paired stimulus procedure, observed PPI of the N1 and P3 (P300) potentials, but not the P2 [25]. These impairments have often been regarded as separate manifestations of a deficit in the central regulation of’sensory gating” [11],[26]. In conclusion, the present results confirm the simultaneous occurrence of prepulse inhibition of electrophysiological responses evoked by the same acoustic stimulus, and the N1/P2 complex of the auditory evoked potential. This view of PPI is supported by the finding that inhibition is apparent at the first presentation of the prepulse/ pulse combination; in other words, PPI is not a learned behavior [15]. However, it has recently been reported that when weak prepulses were used, modality-selective habituation of PPI could be observed [10], suggested that PPI is better viewed as a emarkeri for the operation of a selective attention process [26].

The female subjects in this sample showed somewhat larger auditory evoked potential responses and shorter response latencies than the males, the findings are consistent with sex differences that are known to occur in a number of evoked potentials in different modalities; such differences have been attributed to differences in skull dimensions, brain volume and conduction distances [27],[29],[29].

Acknowledgement

I would like to thank Mr. Ahmed Al-Qohtani for enabling me to do this study through his technical expertise help with the statistical analysis in this paper.



 
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    Figures

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