From Otoacoustic Emission to Late Auditory Potentials P300: the Inhibitory Effect

From Otoacoustic Emission to Late Auditory Potentials P300: the Inhibitory Effect

Research Paper Acta Neurobiol Exp 2012, 72: 296–308 From otoacoustic emission to late auditory potentials P300: the inhibitory effect Eliane Schochat*, Carla Gentile Matas, Alessandra Giannella Samelli, and Renata Mota Mamede Carvallo School of Medicine, Sao Paulo University, Sao Paulo, Brazil, *Email: [email protected] This study verifies the effects of contralateral noise on otoacoustic emissions and auditory evoked potentials. Short, middle and late auditory evoked potentials as well as otoacoustic emissions with and without white noise were assessed. Twenty-five subjects, normal-hearing, both genders, aged 18 to 30 years, were tested . In general, latencies of the various auditory potentials were increased at noise conditions, whereas amplitudes were diminished at noise conditions for short, middle and late latency responses combined in the same subject. The amplitude of otoacoustic emission decreased significantly in the condition with contralateral noise in comparison to the condition without noise. Our results indicate that most subjects presented different responses between conditions (with and without noise) in all tests, thereby suggesting that the efferent system was acting at both caudal and rostral portions of the auditory system. Key words: efferent pathways, contralateral suppression, otoacoustic emissions, auditory evoked potentials Abbreviations INTRODUCTION (EOAE) Evoked Otoacoustic Emission; The auditory system consists of ascending and (MOC) medial olivocochlear; descending (corticofugal) systems. The functional role (AC) auditory cortex; of the efferent auditory system in humans has not yet (MGB) medial geniculate body; been completely established and is difficult to demon- (IC) inferior colliculus; strate. Some methods employed in animals to study (CAPD) Central Auditory Processing Disorder; descending auditory pathways are often invasive and (ABR) Auditory Brainstem Response; damaging to the auditory pathways, and consequently, (MLR) -Middle Latency Response; they are not applicable in humans (Khalfa et al. 2001, (LLR) Late Latency Response; Di Girolamo et al. 2007). (TEOAE) Transient Evoked Otoacoustic Emission; The rostral part of the efferent auditory pathway has (CAS) Contralateral Acoustic Stimulation; received little attention and the anatomy and physiol- (AEP) Auditory Evoked Potentials; ogy of this region are not totally known in humans. In (BIC) Binaural Interaction Components; animals, this portion of the efferent system has been (CAEP) - Cortical Auditory Evoked Potential better studied (Khalfa et al. 2001, Perrot et al. 2006). Neurons in the deep layers of the auditory cortex (AC) Correspondence should be addressed to E. Schochat project back to the medial geniculate body (MGB), Email: [email protected] inferior colliculus (IC) and subcollicular auditory Received 01 August 2011, accepted 06 June 2012 nuclei. Corticothalamic fibers project only to the ipsi- © 2012 by Polish Neuroscience Society - PTBUN, Nencki Institute of Experimental Biology From OAE to P300 297 lateral MGB and thalamic reticular nucleus. However, structures. The sound-evoked response of descending corticocollicular fibers project bilaterally to the IC. pathways has not been studied to any great extent, The corticofugal projections are bilateral to the subcol- which makes it difficult to estimate the contribution to licular nuclei. The central nucleus of the IC projects the Auditory Brainstem Response (ABR) from the not only to the MGB and the superior colliculus, but structures of these pathways (Moller 2007). Concerning also to medial olivocochlear (MOC) neurons, which Middle Latency Response (MLR) and Late Latency mostly project to contralateral cochlear outer hair cells Response (LLR), the identification of source contribu- (Rasmussen 1946, Andersen et al. 1980, Huffman and tion becomes more complicated as the chain of activity Henson 1990, Warr et al. 1997, Suga et al. 2002, Suga ascends the auditory pathway, but it is believed that and Ma 2003). later stages of processing can influence activity at ear- Studying the caudal portion of the efferent system in lier stages from the cochlea to the auditory cortex humans, many authors showed that there is a reduction (Hackett 2007). of the cochlear response due to an inhibitory effect Some authors verified the effects of contralateral induced by contralateral noise activation of the MOC masking on different sites of auditory pathways, using a non-invasive procedure by recording of evoked assessed by AEP. For this condition, Salo and coau- otoacoustic emissions (EOAE) suppression (Collet et thors (2003) verified a decrease of N1 amplitude and al. 1990, Veuillet et al. 1991, Berlin et al. 1993, De an increase of P2 amplitude, suggesting that these Ceulaer et al. 2001, James et al. 2002, Guinan 2006). effects were mediated by the efferent hearing system This mechanism provides an anti-masking effect and that further experiments to clarify the physiology that increases the discrimination of signal variation by of hearing should be performed. Similarly, Özdamar reducing the cochlear amplification of the response to and Bohórquez (2008) identified a significant altera- the noise. In addition, it supplies a feedback gain-con- tion in Pb wave of the MLR, suggesting that these trol system for moderate sound levels that mediates results were influenced by central mechanisms. selective attention and focuses attention during learn- Based on these assumptions, our hypothesis was ing (Galambos 1956, Harkrider and Smith 2005, that noise stimulates the efferent auditory system and Lilaonitkul and Guinan Jr 2009). that this stimulation could cause a modification of the On the other hand, in humans, the rostral part of the responses within the entire auditory system, including efferent auditory pathway is less understood, because the afferent auditory pathways. Thus, the aim of this direct clinical evaluation is difficult. However, there is study was to determine the effects of contralateral some evidence for cortical influence on cochlear white noise on transient evoked otoacoustic emissions micromechanical verified through EOAE. This effect and on short, middle and late auditory evoked poten- has been demonstrated in patients having undergone tials. surgical removal of Heschl’s gyrus (Khalfa et al. 2001), by electrical cortical stimulation in epileptic patients METHODS (Perrot et al. 2006) and by abnormal cortical function- ing resulting in impaired cortical feedback to the This study was carried out in the Auditory brainstem and to the MOC system in dyslexic children Investigation Laboratory with the approval of the Sao (Veuillet et al. 2007). Paulo University School of Medicine Ethics Committee The cortical influence on MOC system was also (Protocol no. 512/07). All participants provided writ- demonstrated in patients with (central) auditory pro- ten informed consent to participate in the study. cessing disorder (CAPD), who often have difficulty in Twenty-five subjects, both genders, took part in this understanding speech accompanied by noise (Wiehing study and the ages ranged between 18 and 30 years and Musiek 2008). Many patients with this kind of (mean 25.3 years). The inclusion criteria were the fol- disorder present abnormal efferent system functioning lowing: no hearing complaint, no middle ear com- that manifests as a reduced suppressive effect of EOAE plaint, and normal hearing in both ears. when compared to controls (Muchnik et al. 2004, An audiometric assessment was conducted on all par- Sanches and Carvallo 2006). ticipants. Following otoscopic inspection, tympanometry Auditory Evoked Potentials (AEP) are used to assess was carried out using a GSI 38 Auto Tymp (Grason- functioning and integrity of the auditory pathway Stadler Inc., Madison, WI) to document middle ear 298 E. Schochat et al. integrity and to help rule out conductive hearing loss. An ducted using only the response with limited frequency audiologic evaluation for pure-tone thresholds was car- range to only 4–6 kHz, as referenced by Hood and ried out with a GSI 61 Clinical Audiometer (Grason- colleagues and (1996). Stadler Inc., Madison, WI) using standard audiometric Electrophysiological evaluation was through inves- techniques in a sound-attenuated testing room to ensure tigation of the ABR, MLR, N1-P2 and the P300 with normal hearing (<20 dB from 250 to 8 000 Hz). and without contralateral white noise using a two- Following the OAE, the electrophysiologic tests channel electroneuromyograph (Biologic Traveler (ABR, MLR, LLR including N1, P2 and P300) were Electrodiagnostic Testing System; Biological Systems carried out in an electric and sound-attenuated testing Corp., Mundelein, IL, USA). The stimulus was 70 dB room. nHL and the noise was 60 dB nHL (Burkard and Transient Evoked Otoacoustic Emissions Hecox 1983, Burkard and Sims 2002, Özdamar and (TEOAEs) were recorded using an ILO 292 OAE Bohórquez 2008, Cone 2009) with a +10 dB signal-to- analyzer, version 5.61 (Otodynamics Ltd., Hatfield, noise ratio for all tests applied. The signal and the UK) using ILO insert phones. The TEOAEs were noise were delivered through TDH 39 earphones. The recorded in a linear mode with and without contral- individual was asked to remain with eyes closed dur- ateral acoustic stimulation (CAS). Under all condi- ing the recording of potentials, in order to control eye tions, the mean intensity of the clicks was 60–65 movement artifacts. SPL, and 200 sweeps were recorded for each ear For the ABR, a rate of 19 clicks per second with

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