Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 

 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 1  |  Issue : 1  |  Page : 3-11

Central auditory plasticity indexed by mismatch negativity


Department of Otolaryngology, Audiology Unit, Head and Neck Surgery, Tanta University Hospitals, Tanta, Egypt

Date of Submission03-Feb-2014
Date of Acceptance15-Feb-2014
Date of Web Publication28-Jul-2014

Correspondence Address:
Takwa A Gabr
Audiology Unit, Department of Otolaryngology, Head and Neck Surgery, Tanta University Hospitals, Tanta
Egypt
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2314-8667.137558

Rights and Permissions
  Abstract 

Introduction
Unilateral hearing loss (UHL) represents a particular model for investigating the functional auditory plasticity in humans. Normally, monaural stimulation produces a normal pattern of a contralateral dominance. With UHL, this pattern changes.
Objective
The aim of the study was to investigate the effects of UHL side and age at onset on auditory processing.
Design
Mismatch negativity (MMN) was recorded in response to speech and tone stimuli.
Study sample
This study included two groups: the control (50 bilateral normal hearing) and study (206 UHL patients) groups. This group was further classified according to UHL side and age at UHL onset.
Results
In controls, higher speech-evoked MMN amplitude was recorded in the right ear. The study group showed impaired speech-evoked MMN in either left or right UHL patients, especially in early onset UHL patients. Tone-evoked MMN was not affected in controls or UHL patients.
Conclusion
Cortical reorganization induced by UHL occurs mainly in patients with left-side affection. Speech processing is affected in UHL irrespective of the affected side, especially in early onset patients.

Keywords: auditory plasticity, cortical reorganization, mismatch negativity, unilateral hearing loss


How to cite this article:
Elshintinawy AH, Kolkaila E, Gabr TA. Central auditory plasticity indexed by mismatch negativity. Adv Arab Acad Audio-Vestibul J 2014;1:3-11

How to cite this URL:
Elshintinawy AH, Kolkaila E, Gabr TA. Central auditory plasticity indexed by mismatch negativity. Adv Arab Acad Audio-Vestibul J [serial online] 2014 [cited 2017 Dec 11];1:3-11. Available from: http://www.aaj.eg.net/text.asp?2014/1/1/3/137558


  Introduction Top


Central auditory pathways do not develop normally in the absence of acoustic stimulation as shown in animal and human studies [1]. Any significant reduction in sensory input will induce anatomic and physiologic alterations of the auditory pathways. These alterations occur in response to both monaural and binaural deprivation [2]. The sensory maps in the mature central auditory system can reorganize in response to long period of hearing loss or reintroduction of sensory input through hearing aids or cochlear implantation [3].

In normal hearing individuals, the cortical activation pattern is characterized by shorter and larger neurophysiological responses over the hemisphere contralateral to the stimulated ear in response to monaural stimulation [4,5]. This activation pattern is due to the contralateral auditory pathway dominance as it contains a greater number of nerve fibers than the ipsilateral one with more direct activation of the contralateral auditory cortex [6].

Unilateral hearing loss (UHL) represents a particular model for investigating the functional auditory plasticity in humans. In mammals, a number of changes in the neural projection pathways have been described following unilateral deafening in the auditory brainstem, midbrain, and primary auditory cortex [7].

Several studies showed that UHL is followed by functional reorganization of the frequency maps in the auditory cortex with alteration of the neural responses and binaural interactions at various levels in the auditory pathway. This occurs in both the developing [8] and the mature auditory system [9]. There is an assumption that the developing human brain is particularly sensitive to auditory deprivation. Thus, the presence of a normal acoustic environment during sensitive periods in early childhood is mandatory to ensure normal hearing and speech development [10].

Plastic changes of the central auditory system can be studied by mismatch negativity (MMN). It is an evoked potential elicited by a sequence of repeated stimuli in which an 'odd' or 'rare' stimulus occurs on a low percentage (˜10-15%) of presentations. MMN is an objective and sensitive measure of processes associated with auditory discrimination of both simple and complex signals. Hence, MMN appears to index automatic attention-independent discrimination of an acoustic difference, rather than simply a detection of an acoustic event [11-14]. In addition, it can be used as an indicator of neurophysiologic changes in the central auditory nervous system resulting from learning and auditory experience [15].

In more than 90% of the population, cortical processes of spoken language perception and production are asymmetrically presented in the left hemisphere of the brain. Thus, cortical activation changes following UHL may be different for left versus right ear UHL [16,17]. Studying the effect of UHL using MMN will be addressed in this study.


  Aims Top


The present study was designed to investigate whether left and right UHL has differential effects on the auditory processing of speech and tone stimuli through MMN recording. The effect of UHL onset [whether it occurred before or after the age at which full Arabic language development (8 years) occurs] on auditory processing was also studied.


  Patients and methods Top


This study included 206 participants. They were chosen from the patients attending the Audiology Unit at Tanta University Hospitals as well as from the volunteers. They were divided into two groups: control group and study group.

Control group

A total of 50 normal hearing individuals with no history of otological complaints were included in the control group and their age range was 18-45 years. All individuals had bilateral normal peripheral hearing thresholds in the frequency range of 250-8000 Hz as well as normal middle ear function. Individuals of this group were tested in both right and left ears.

Study group

A total of 156 patients with profound UHL were included in the study group. Their age range was 18-45 years. This group was divided into two subgroups: left ear in right unilateral hearing loss (RHL-L) including 78 patients and right ear in left unilateral hearing loss (LHL-R) including 78 patients. In UHL patients, bone conduction hearing thresholds on the deaf side were greater than 70 dBHL at all tested frequencies (500-4000 Hz).

For both subgroups, the hearing threshold in the intact ear was better than 25 dBHL (in the frequency range of 250-8000 Hz). The exclusion criteria were: age above 45 years, hearing loss even at single frequency in both ears of the control group or in the healthy ear of the study group, history of otological, psychological, neurological, or language disorders, history of systemic disease (such as diabetes or hypertension) or cardiovascular diseases, and patients with prolonged noise exposure, acoustic trauma, or previous ototoxic medication. Patients with a suspected retrocochlear lesion were excluded from the study.

To study the age at onset of UHL on auditory processing, a cutoff of 8 years was chosen because it is the age at which full Arabic language development occurs [18]. Hence, the study groups were further divided into: RHL-L less than 8 and LHL-R less than 8 (patients with UHL onset before 8 years) and RHL-L more than 8 and LHL-R more than 8 (patients with UHL onset after 8 years).

The study was conducted at the Audiology Unit of the Otolaryngology, Head and Neck Surgery Department, Tanta University Hospitals. Consents were obtained from all patients after explaining the test procedure as well as the aims of the study. All patients were subjected to full history taking, otological examination, basic audiological evaluation, and MMN using two types of stimuli: speech consonant vowel syllables (/da/ as standard and /ga/ as deviant) [Table 1] and tone stimuli (1000 Hz as standard and 2000 Hz as deviant with 150 ms duration for both tones). Both types of stimuli were presented in an oddball paradigm at 50 dBSL (re-pure tone audiometry average at 500, 1000, 2000, and 4000 Hz in the healthy ear).

The repetition rates were 1/s and 0.7/s for speech and tone stimuli, respectively. Band-pass filtering of EEG activity was 1-30 Hz. Time window of recording started at -50 ms up to 400 ms. The probability of deviant stimuli was 15% for both stimuli. During test acquisition, every participant was instructed to lie down calmly on a comfortable coach. They were engaged in reading a selected magazine or newspaper and were instructed not to concentrate on the presented stimuli.
Table 1 Specifications of /da/ and /ga/ speech stimuli used in this study

Click here to view


Electrode montage differed according to the patient tested. In patients with RHL-L, three disposable electrodes were used fixed as the following: one high frontal Fz (positive electrode), one low frontal Fpz (ground electrode), and one on the left mastoid bone (negative electrode). In LHL-R, the electrode montage was high frontal Fz (positive electrode), low frontal Fpz (ground electrode), and on the right mastoid bone (negative electrode). In bilateral normal hearing individuals, four electrodes were fixed as the following: high frontal Fz (positive electrode), low frontal Fpz (ground electrode), and the last two electrodes were placed on the left and right mastoids (as reference electrode) depending on the recording side.

After finishing the test, offline manipulation of data was performed starting with identification of N100 as the negativity occurring in the latency range of 80-120 ms after stimulus presentation. MMN was identified as the most prominent negativity that follows N100 in the range of 150-250 ms. Detection of MMN is based on the determination of two bases where the difference waveform should cross the zero level after the response. The first base is identified at the point of first negative deflection from zero line and the second base is identified at the point of the return to positivity. Response is determined by comparing it to 50 ms baseline recording before stimulus presentation. MMN latency, amplitude, duration, and area were calculated.

Statistical analysis

Statistical analysis was performed using SPSS (version 15; SPSS Inc., Chicago, Illinois, USA) software. Unpaired sample t-test was used to compare the mean of age, pure tone audiometry thresholds in the control group, and the normal ears in the UHL group. Quantitative variables were tested for normality distribution by the Kolmogorov-Smirnov test. According to this test, the data are either of normal distribution (if the test was not significant) or nonparametric (if the test was significant). In normally distributed variables (MMN duration), Student's t-test was used for two group comparison, whereas in nonparametric variables (MMN latency, amplitude, and area), the Mann-Whitney U-test was used for the same purpose.

Both tests were used for comparing MMN response between right and left ears in the control group (REC and LEC). They were also used to compare MMN response in REC with LHL-R and also to compare MMN response in LEC with RHL-L. They were also used to study the effect of UHL age at onset (before or after 8 years) on MMN response.


  Results Top


This study included two groups: the control group including 50 healthy normal hearing patients (27 men and 23 women), with mean age of 26.68 ± 6.8 years and mean of pure tone threshold of 16.3 ± 2.5 and 13.8 ± 7.1 dB in the right and left ear, respectively, and the study group including 156 patients with UHL (78 right UHL and 78 left UHL). Their mean age was 26.9 ± 9.4 years in LHL-R and 24.5 ± 7.1 years in RHL-L [Table 2]. The etiology of UHL was idiopathic in 46%, postfebrile in 29% of patients, and traumatic in 25%.
Table 2 Mean of age, number of patients, and sex in the control and study subgroups

Click here to view


Comparing MMN response in the REC and LEC showed a significantly higher MMN amplitude (P < 0.05) in the right (1.32 ± 0.61 mv) than in the left ear (1.085 ± 0.53 mv) in response to speech. With respect to tone stimulation, similar MMN responses were recorded in both ears ([Table 3] and [Figure 1].
Figure 1: Mismatch negativity (MMN) latency in the right ear of controls (REC) and right ear in left unilateral hearing loss (LHL-R) patients; and in the LECs and left ear in right unilateral hearing loss (RHL-L) patients in response to speech and tone stimuli.

Click here to view
Table 3 Comparison of mean and SD of different mismatch negativity component in the right and left ears of the control group on using speech and tone stimuli

Click here to view


The effect of unilateral hearing loss side

MMN response in RHL-L and LHL-R patients of the study subgroups were compared with REC and LEC, respectively. On using speech, MMN was present in only 49 patients (out of 78 patients) in the LHL-R subgroup with significantly delayed latency (195.4 ± 34.9 ms) when compared with REC (179.22 ± 20.8 ms). In RHL-L subgroup, MMN was recorded in all patients with significantly delayed latency (208 ± 36.8 ms) when compared with LEC (178.3 ± 24.14 ms). However, on using tone stimuli, MMN responses were similar in both LHL-R and RHL-L, with no significant difference from the control group ([Table 4] and [Figure 1] and [Figure 2].
Figure 2: Mismatch negativity (MMN) latency in the right ear of controls (REC) and study subgroups (RES<8 years and RES>8 years); and in the left ear of controls (LEC) and study subgroups (LES<8 years and LES > 8 years), on using speech and tone stimuli

Click here to view
Table 4 Comparison of mean and SD of mismatch negativity latency in the right and left ears of control, left and right unilateral hearing loss subgroups, and between study subgroups on using speech and tone stimuli

Click here to view


The effect of unilateral hearing loss age at onset

To study the effect of age at onset of UHL, the study groups were further divided into the following subgroups:

(1) RHL-L less than 8 years: included 21 patients with age at onset of right UHL before 8 years.

(2) RHL-L more than 8 years: included 57 patients with age at onset of right UHL after 8 years.

(3) LHL-R less than 8 years: included 18 patients with age at onset of left UHL before 8 years.

(4) LHL-R more than 8 years: included 60 patients with age at onset of left UHL after 8 years.

On using speech

(1) In left UHL, MMN was elicited in 47.6 and 68.4% of the LHL-R less than 8 years and LHL-R more than 8 years subgroups, respectively, with delayed latencies (203.3 ± 34.9 ms in LHL-R < 8 years and 193.3 ± 34.9 ms in LHL-R > 8 years); however, it was significant only in LHL-R less than 8 years when compared with control (179.22 ± 20.8 ms). Both subgroups showed no significant difference when compared with each other (P > 0.05) ([Table 5] and [Figure 3].
Figure 3: Examples of mismatch negativity (MMN) latency in (a) left ear of controls (LEC) on using speech stimuli (b) right ear of controls (REC) on tone stimuli, (c) absent MMN in response to speech stimuli in right ear in left unilateral hearing loss (LHL-R).

Click here to view
Table 5 Comparison of mean and SD of mismatch negativity latency in the right ear of controls, right ear in left unilateral hearing loss < 8 years, and right ear in left unilateral hearing loss > 8 years subgroups on using speech and tone

Click here to view


(2) In right UHL, MMN was elicited in all patients of RHL-L less than 8 years and RHL-L more than 8 years, with significantly delayed MMN latencies (201.78 ± 25.9 ms in RHL-L < 8 years and 209.9 ± 49.5 ms in RHL-L >8 years) when compared with LEC (178.3 ± 24.14 ms). Both subgroups showed no significant difference when compared with each other (P < 0.05) [Table 6].
Table 6 Comparison of mean and SD of mismatch negativity latency in the left ear of controls, left ear in right unilateral hearing loss < 8 years, and left ear in right unilateral hearing loss > 8 years subgroups on using speech and tone

Click here to view


(3) Left UHL versus right UHL: comparing LHL-R less than 8 years with RHL-L less than 8 years revealed no significant difference between both subgroups at any MMN parameter. However, comparing LHL-R more than 8 years with RHL-L more than 8 years showed only significantly delayed MMN latency in RHL-L more than 8 years (193.3 ± 34.9 in LHL-R > 8 years and 209.9 ± 49.5 in RHL-L > 8 years) [Table 7].
Table 7 Comparison of mismatch negativity latency between right ear in left unilateral hearing loss < 8 years and left ear in right unilateral hearing loss < 8 years and between right ear in left unilateral hearing loss > 8 years and left ear in right unilateral hearing loss > 8 years on using both speech and tone

Click here to view


On using tone

MMN was elicited in all patients of the study subgroups, with no significant difference from each other or from control [Table 5] and [Table 6] and [Figure 2].

Comparing mismatch negativity to speech and tone stimuli

MMN was elicited in all patients in response to tone. However, it was recorded in 68.45% of LHL-R more than 8 years patients and in 47.6% of LHL-R less than 8 patients, with significantly delayed latency in response to speech when compared with tone-evoked MMN. MMN was recorded in all patients of RHL-L less than 8 years and RHL-L more than 8 years, with delayed latency in comparison with tone stimulation, which was significant in RHL-L more than 8 years only. With respect to MMN amplitude, duration, and area, they had similar results among different subgroups and were not affected by the stimulus type or onset of UHL [Table 8] and [Figure 3].
Table 8 Comparison of mean and SD of speech and tone-evoked mismatch negativity latency in the study subgroups

Click here to view



  Discussion Top


Cortical reorganization following unilateral deafness has been reported using different techniques in adult humans. However, the influence of the side of deafness on auditory cortical plasticity remains unclear [19]. In a previous study, Jancke et al. [20] reported that monaural stimulation activates superior temporal gyrus on the contralateral side in normal hearing adult individuals. This asymmetric cortical response has been attributed to differences in anatomical organization. Crossing auditory pathways may have a greater number of fibers and faster transmission speed relative to ipsilateral pathways [19,21].

In this study, different MMN parameters were evaluated (latency, amplitude, duration, and area) to compare auditory processing in UHL patients in response to speech and tone stimuli taking UHL side and age at onset into consideration.

On using speech stimuli

Comparing the REC and LEC showed only a significantly higher MMN amplitude in the right ear (P < 0.05). This reflects the normal dominance of the contralateral ascending auditory pathway in bilateral normal hearing individuals [22]. This pathway carries speech stimuli from the right ear directly to the left hemisphere to be processed. These findings are consistent with those of Hanss et al. [19] who reported contralateral pathway dominance in bilateral normal hearing individuals. Hence, speech stimulus is carried to the left hemisphere, which is more specialized in speech processing, than to the right one to be processed [13].

In left UHL (LHL-R), MMN was elicited only in 62.8% of patients with significantly delayed latency when compared with controls. This could be explained by increased ipsilateral pathway strength in patients with UHL [23], by more symmetric ipsilateral and contralateral pathways ([24]), or by a significant reversal pattern in favor of the ipsilateral cortex activation in response to speech sound [19]. In this case, part of speech stimulus will be carried to the right cortex and then passed through the corpus callosum to the left one to be processed and another part will be carried directly to the left cortex. Hence, the absent MMN or delayed MMN latency in left UHL patients in the current study might be due to: first, vulnerability of speech to the effect of reduced audibility; second, speech degradation through transmission in the ipsilateral pathway or through the interhemispheric connection in their way to the left cortex [25,26]; and third, speech processing in the ipsilateral cortex (right cortex), which is not specialized in speech processing [19].

In right UHL (RHL-L), MMN was recorded in all patients, however, with significantly delayed latency when compared with controls. As Kholsa et al. [24] and Hine et al. [27] reported, patients with right UHL still preserve the normal contralateral pathway dominance. Hence, speech stimuli would be carried directly by the contralateral pathway from the left ear mainly to the right cortex. Then, stimuli pass through corpus callosum from the right to the left cortex to be processed. Hence, latency could be delayed because of interhemispheric transfer time [28].

On using tone stimuli

MMN revealed no significant difference between REC and LEC (P>0.05). This could be due to bilateral symmetrical pattern of activation in both hemispheres by nonspeech material of longer transitions (>40 ms) [29]. However, Binder et al. [30] reported that tone stimuli produce larger amplitude and more extensive activation in the right hemisphere. In UHL patients, MMN was recorded in all patients with no significant difference between the control group and either the LHL-R or RHL-L subgroups. This is not consistent with the study by some authors [7, 23, 24] who reported some modifications of the activation pattern over auditory areas in unilaterally deaf patients, which is dependent on the side of deafness. This also might indicate that simple sounds such as tones are less vulnerable to the effect of hearing loss.

Normal language development requires intact sensory channels, particularly hearing, precise motoric control of the vocal tract as well as normal intellectual function [31]. Arabic language development passes with different stages with respect to the phoneme acquisition and size of vocabulary, which ends by the age of 8 years. At that age, the child has full phonological maturation and full growth of vocabulary [18].

In left UHL, MMN was recorded in 47.6% of early onset patients (LHL-R < 8 years) with significantly delayed latency when compared with the REC. In late onset patients (LHL-R>8 years), MMN was recorded in 68.4% with no significant difference from controls. These results indicated that the earlier the age at onset of UHL, the more drastic its effect on speech processing, which is also vulnerable to the effect of reduced auditory inputs from one or both ears [32]. Patients with normal speech-evoked MMN showed the ability of the human cortex to alter its organization and regain its capacity for auditory processing even if it is deprived of its input late in life [33]. However, Scheffler et al. [7] reported that the earlier the age at onset of UHL, the stronger the compensatory mechanisms.

In right UHL, MMN was recorded in all patients with early onset UHL (RHL-L < 8 years) with significantly delayed latency when compared with the LECs. This is consistent with the study by Bess et al. [34] and Lieu [35] who found that children with early onset right UHL are at risk for language disorders when they were evaluated using speech in noise recognition and by sound localization skills as well as self-assessment questionnaire. Similarly, MMN was elicited in all patients with late onset of right UHL (RHL-L>8 years), with significantly delayed latency when compared with the LECs. This indicated that speech processing is impaired in patients with right UHL whether it occurred before or after complete development of language.

In early onset patients of UHL, MMN response was impaired in both right UHL (delayed MMN latency) and left UHL patients (absent or delayed MMN latency), indicating that speech processing is affected in early onset UHL regardless of the side of affection. This might be a result of reduced speech inputs to the auditory cortex before its full maturation, which, in turn, affect its processing as speech understanding requires highly developed cortex [36].

In late onset UHL, MMN was also absent in 31.6% of left UHL, with similar MMN response in rest of the patients compared with normal hearing individuals. This may indicate that left UHL patients had active plasticity, which explained why they were not significantly different from controls. This is in agreement with the study by Khosla et al. [24] and Hanss et al. [19] who suggested that auditory cortical plasticity mainly occurred in left-sided deafness. In right UHL, MMN response was recorded in all patients with significantly delayed latency when compared with late onset left UHL patients or with the control group. This suggested that plastic changes may not be active in late onset right UHL patients. However, Musiek [37] reported that even the mature brain is capable of undergoing fundamental reorganization at the cortical level.

MMN in response to tone stimuli showed that tone processing is not affected by the side or age at onset of UHL. Zatorre and Belin [38] reported that speech and tone are different in their temporal and spectral resolution as well as site of processing within the central auditory nervous system. Speech is processed in the left auditory cortex especially the core areas, whereas tone is processed in the right cortex mainly in the belt cortical areas. This hemispheric specialization may be related to asymmetries in myelination and spacing of cortical columns. Durrant and Lovring [36] and McGee and Kraus [39] reported that simple tone discrimination does not need full maturation of the auditory cortex, which continues for several years after birth until early adulthood. The authors also reported that the ability to discriminate one frequency of sound from another is most likely determined by the tuning functions of the primary auditory neurons. In contrast, processing of more complex stimuli such as speech requires adequate cortical maturation. The more complex the stimulus, the higher the level of processing in the auditory pathway [16]. Speech perception is essentially based on subtle differences in the timing of acoustic elements. The analysis of successive temporal changes in the acoustic signal requires special cortical mechanisms. This underlies the left hemispheric contribution to speech processing. However, analysis and coding of nonspeech stimuli is dependent on the right hemisphere [16,40].

Results of this study suggested that plastic changes related to tone processing are not affected by the age at which full Arabic language development occurs and are not dependent on the cortical maturation. This is consistent with the study by Syka [41] who reported that adult patients with UHL have plasticity, although not as much as that of young age patients. This also pointed to the presence of different patterns of plasticity, which depend on several factors. These factors include the type of the stimulus, duration of UHL, age of the patient, and the dominant pathway used to transmit auditory input to the auditory cortex (ipsilateral or contralateral).

The auditory system is greatly plastic and many compensatory mechanisms may occur after UHL. These plasticity mechanisms mainly involve the auditory cortex ipsilateral to the healthy ear. Such cortical changes are likely to be related to the modifications observed at subcortical levels in experimental animals. After unilateral cochlear ablation in adult gerbils, synaptic inhibition was predominantly decreased within the inferior colliculus ipsilateral to the healthy ear [42,43]. At the same time, there was an increased reported excitatory synaptogenesis within the ventral cochlear nucleus on the affected side - that is, the brainstem structure that projects mainly into the inferior colliculus ipsilateral to the healthy side [43].

In contrast, neurons from the affected side of the ventral cochlear nucleus projected inhibitory pathways on the opposite cochlear nucleus. Thus, there would be an active process of reorganization to compensate for the loss of sensory inputs on the deaf side; it may stem from bottom-up and top-down mechanisms [44]. Interestingly, the hemispheric differences in sound processing have been related to cytoarchitectural differences between the temporal lobes, the left temporal lobe showing more myelinated axons [45], with larger pyramidal cells, wider columns, and denser afferent innervations [46]. Even speculative, the anatomical and functional plastic changes occur between both hemispheres, with the right temporal lobe exhibiting a higher potency of remyelinization and afferentation than the left [19].


  Conclusion Top


Numerous studies have reported cortical reorganization following unilateral deafness in humans. Results of this study showed that cortical reorganization induced by UHL mainly occurs in patients with left-side affection. The current study also showed that speech processing is affected in UHL irrespective of the side of deafness, especially in early onset patients. Tone processing is not affected by side or age at onset of UHL. Hence, it can be concluded that plasticity is a much more complex process that depends on several factors. These factors include age of the patient, duration of UHL, the dominant hemisphere, the dominant pathway used to transmit auditory input to the auditory cortex (ipsilateral or contralateral), and the type of plastic changes that follow UHL. It also might include the type of the stimulus and the type of procedure used to study auditory plasticity.

Further investigations are needed to assess to what extent both asynchrony and asymmetry over the auditory areas could represent electrophysiological correlates of speech perception in unilaterally deaf and even normal hearing. Other model of electrophysiological test might be required to evaluate possible subcortical areas to auditory plasticity.

[TAG:2]Acknowledgements[/TAG:2]

 
  References Top

1.Sharma A, Dorman MF, Spahr AJ, Todd NW. Early cochlear implantation in children allows normal development of central auditory pathways. Ann Otol Rhinol Laryngol Suppl 2002; 189:38-41.  Back to cited text no. 1
    
2.Jen PHS, Sun XD. Influence of monaural plugging on postnatal development of auditory spatial sensitivity of inferior collicular neurons of the big brown bat, Eptesicus fuscus. Chin J Physiol 1990; 33:231-246.  Back to cited text no. 2
    
3.Sharma A, Dorman MF, Kral A. The influence of a sensitive period on central auditory development in children with unilateral and bilateral cochlear implants. Hear Res 2005; 203:134-143.  Back to cited text no. 3
    
4.Elberling C, Bak C, Kofoed B, Lebech J, Saermark K. Auditory magnetic fields from the human cortex. Influence of stimulus intensity. Scand Audiol 1981; 10:203-207.  Back to cited text no. 4
[PUBMED]    
5.Pantev C, Lutkenhoner B, Hoke M, Lehnertz K. Comparison between simultaneously recorded auditory-evoked magnetic fields and potentials elicited by ipsilateral, contralateral and binaural tone burst stimulation. Audiology 1986; 25:54-61.  Back to cited text no. 5
    
6.Zook JM, Casseday JH. Convergence of ascending pathways at the inferior colliculus of the mustache bat, Pteronotus parnellii. J Comp Neurol 1987; 261:347-361.  Back to cited text no. 6
[PUBMED]    
7.Scheffler K, Bilecen D, Schmid N, Tschopp K, Seelig J. Auditory cortical responses in hearing subjects and unilateral deaf patients as detected by functional magnetic resonance imaging. Cereb Cortex 1998; 8:156-163.  Back to cited text no. 7
    
8.Harrison RV, Nagasawa A, Smith DW, Stanton S, Mount RJ. Reorganization of auditory cortex after neonatal high frequency cochlear hearing loss. Hear Res 1991; 54:11-19.  Back to cited text no. 8
    
9.Popelar J, Erre JP, Aran JM, Cazals Y. Plastic changes in ipsi-contralateral differences of auditory cortex and inferior colliculus evoked potentials after injury to one ear in the adult guinea pig. Hear Res 1994; 72:125-134.  Back to cited text no. 9
    
10.Tibussek D, Meister H, Walger M, Foerst A, Von WH. Hearing loss in early infancy affects maturation of the auditory pathway. Dev Med Child Neurol 2002; 44:123-129.  Back to cited text no. 10
    
11.Näätänen R, Lehtokoski A, Lennes M, Cheour M, Huotilainen M, Iivonen A, et al. Language-specific phoneme representations revealed by electric and magnetic brain responses. Nature 1997; 385:432-434.  Back to cited text no. 11
    
12.Näätänen R, Jacobsen T, Winkler I. Memory-based or afferent processes in mismatch negativity (MMN): a review of the evidence. Psychophysiology 2005; 42:25-32.  Back to cited text no. 12
    
13.Shtyrov Y, Kujala T, Palva S, Ilmoniemi RJ, Näätänen R. Discrimination of speech and of complex nonspeech sounds of different temporal structure in the left and right cerebral hemispheres. Neuroimage 2000; 12:657-663.  Back to cited text no. 13
    
14.Stapells DR, Kurtzberg D. Evoked potential assessment of auditory system integrity in infants. Clin Perinatol 1991; 18:497-518.  Back to cited text no. 14
    
15.Stapells DR. Event related potential indices of central auditory development in healthy children and in children with oral clefts [doctoral thesis]. Finland: Cognitive Brain Research, Department of Psychology, University of Helsinki; 2001.  Back to cited text no. 15
    
16.Zatorre RJ, Evans AC, Meyer E, Gjedde A. Lateralization of phonetic and pitch discrimination in speech processing. Science 1992; 256:846-849.  Back to cited text no. 16
    
17.Bilecen D, Seifritz E, Radu EW, Schmid N, Wetzel S, Probst R, Scheffler K. Cortical reorganization after acute unilateral hearing loss traced by fMRI. Neurology 2000; 54:765-767.  Back to cited text no. 17
    
18.Kotby MN. Diagnosis and management of communicatively handicapped child. Ain Shams Med J 1980; 31:303-317.  Back to cited text no. 18
    
19.Hanss J, Veuillet E, Adjout K, Besle J, Collet L, Thai-Van H. The effect of long-term unilateral deafness on the activation pattern in the auditory cortices of French-native speakers: influence of deafness side. BMC Neurosci 2009; 10:23.  Back to cited text no. 19
    
20.Jancke L, Wustenberg T, Schulze K, Heinze HJ. Asymmetric hemodynamic responses of the human auditory cortex to monaural and binaural stimulation. Hear Res 2002; 170:166-178.  Back to cited text no. 20
    
21.Majkowski J, Bochenek Z, Bochenek W, Knapik-Fijalkowska D, Kopec J. Latency of averaged evoked potentials to contralateral and ipsilateral auditory stimulation in normal subjects. Brain Res 1971; 25:416-419.  Back to cited text no. 21
    
22.Reite M, Teale P, Zimmerman J, Davis K, Whalen J. Source location of a 50 msec latency auditory evoked field component. Electroencephalogr Clin Neurophysiol 1988; 70:490-498.  Back to cited text no. 22
    
23.Ponton CW, Vasama JP, Tremblay K, Khosla D, Kwong B, Don M. Plasticity in the adult human central auditory system: evidence from late-onset profound unilateral deafness. Hear Res 2001; 154:32-44.  Back to cited text no. 23
    
24.Khosla D, Ponton CW, Eggermont JJ, Kwong B, Don M, Vasama JP. Differential ear effects of profound unilateral deafness on the adult human central auditory system. J Assoc Res Otolaryngol 2003; 4:235-249.  Back to cited text no. 24
    
25.Boatman D, Krauss G. Language lateralisation and early right ear deafness: was Wernicke right? J Neurol Neurosurg Psychiatry 2000; 69:538-554.  Back to cited text no. 25
    
26.Muller-Gass A, Marcoux A, Logan J, Campbell KB. The intensity of masking noise affects the mismatch negativity to speech sounds in human subjects. Neurosci Lett 2001; 299:197-200.  Back to cited text no. 26
    
27.Hine J, Thornton R, Davis A, Debener S. Does long-term unilateral deafness change auditory evoked potential asymmetries? Clin Neurophysiol 2008; 119:576-586.  Back to cited text no. 27
    
28.Sparks R, Goodglass H, Nickel B. Ipsilateral versus contralateral extinction in dichotic listening resulting from hemisphere lesions. Cortex 1970; 6:249-260.  Back to cited text no. 28
[PUBMED]    
29.Belin P, Zatorre RJ, Lafaille P, Ahad P, Pike B. Voice-selective areas in human auditory cortex. Nature 2000; 403:309-312.  Back to cited text no. 29
    
30.Binder JR, Frost JA, Hammeke TA, Bellgowan PSF, Springer JA, Kaufman JN, et al. Human temporal lobe activation by speech and nonspeech sounds. Cereb Cortex 2000; 10:512-528.  Back to cited text no. 30
    
31.Binder JR, Frost JA, Hammeke TA, Bellgowan PS, Springer JA, Kaufman JN et al. Language development: structure and function. USA: Dryden press Inc.; 1972.  Back to cited text no. 31
    
32.Willott JF. Physiological plasticity in the auditory system and its possible relevance to hearing aid use, deprivation effect and acclimatization. Ear Hear 1996; 17:66-77.  Back to cited text no. 32
    
33.Pantev C, Dinnesen A, Ross B, Wollbrink A, Knief A. Dynamics of auditory plasticity after cochlear implantation: a longitudinal study. Cereb Cortex 2006; 16:31-36.  Back to cited text no. 33
    
34.Bess FH, Tharpe AM, Gibler AM. Auditory performance of children with unilateral sensorineural hearing loss. Ear Hear 1986; 7:20-26.  Back to cited text no. 34
    
35.Lieu JE. Speech-language and educational consequences of unilateral hearing loss in children. Arch Otolaryngol Head Neck Surg 2004; 130:524-530.  Back to cited text no. 35
[PUBMED]    
36.Durrant JD, Lovring JH. Neurobiology of the auditory system. Bases of hearing science. Second edition. Chapter 6. Williams and Willkins: 1995;196-255.  Back to cited text no. 36
    
37.Musiek FE. Auditory plasticity: What is it, and why do clinicians need to know?. Hear J 2002; 55:70.  Back to cited text no. 37
    
38.Zatorre RJ, Belin P. Spectral and temporal processing in human auditory cortex. Cereb Cortex 2001; 11:946-953.  Back to cited text no. 38
    
39.McGee T, Kraus N. Auditory development reflected by middle latency response. Ear Hear 1996; 17:419-429.  Back to cited text no. 39
    
40.Johnsrude IS, Penhune VB, Zatorre RJ. Functional specificity in the right human auditory cortex for perceiving pitch direction. Brain 2000; 123:155-163.  Back to cited text no. 40
    
41.Syka J. Plastic changes in the central auditory system after hearing loss, restoration of function, and during learning. Physiol Rev 2002; 82:601-636.  Back to cited text no. 41
[PUBMED]    
42.Mossop JE, Wilson MJ, Caspary DM, Moore DR. Down-regulation of inhibition following unilateral deafening. Hear Res 2000; 147:183-187.  Back to cited text no. 42
    
43.Vale C, Juiz JM, Moore DR, Sanes DH. Unilateral cochlear ablation produces greater loss of inhibition in the contralateral inferior colliculus. Eur J Neurosci 2004; 20:2133-2140.  Back to cited text no. 43
    
44.Illing RB, Kraus KS, Meidinger MA. Reconnecting neuronal networks in the auditory brainstem following unilateral deafening. Hear Res 2005; 206:185-199.  Back to cited text no. 44
    
45.Anderson B, Southern BD, Powers RE. Anatomic asymmetries of the posterior superior temporal lobes: a postmortem study. Neuropsychiatry Neuropsychol Behav Neurol 1999; 12:247-254.  Back to cited text no. 45
    
46.Jongkees LB, Veer RA. Directional hearing capacity in hearing disorders. Acta Otolaryngol 1957; 48:465-474  Back to cited text no. 46
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
   Abstract
  Introduction
  Aims
  Patients and methods
  Results
  Discussion
  Conclusion
  Acknowledgements
   References
   Article Figures
   Article Tables

 Article Access Statistics
    Viewed1152    
    Printed34    
    Emailed0    
    PDF Downloaded123    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]