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Effect of early onset otitis media on brainstem and cortical auditory processing

Effect of early onset otitis media on brainstem and cortical auditory processing Background: Otitis media (OM) leads to significant reduction in the hearing sensitivity. The reduced auditory input, if in the early years of life when the auditory neural system is still maturing, may adversely influence the structural as well as functional development of the system. Past research has reported abnormalities in both the structure and function of brainstem nuclei following auditory deprivation, but, it has not necessarily focused on children who had OM in their first year of life. It can also be said that if auditory processing is affected at the brainstem level because of early onset OM (reduced auditory input in the crucial periods of neural development), then, it may be said that auditory processing is also affected at the cortical level because it receives distorted input from the brainstem. Therefore, the purpose of this study was to document the effects of early onset OM on auditory processing, if any, at the brainstem as well as at cortical levels. A related purpose of the study was to investigate the persistence of the effects of early onset OM, if any, on auditory processing. Methods: A cross sectional approach and a standard group comparison design was used in the study. Thirty children, who had OM between 6 and 12 months of age and who were in the age range of 3.1 – 5.6 years participated in the study. Children with OM were divided into 3 groups based on their age. Click evoked auditory brainstem responses (ABRs) and late latency responses (LLRs) were recorded from these children, and the responses were compared with those from age and gender matched normal children without any history of OM. The data from the 2 groups was statistically analyzed through independent t test. Pearson's Product Moment correlation was computed to examine the relationship between results of ABR and LLR in children with early onset OM. Results: The mean central conduction time was significantly increased and the mean amplitude of wave I and III of ABRs was significantly reduced in children with early onset OM compared to normal children. Also, the latency of all LLR waves was significantly less in children with early onset OM than in normal children. However, significant differences in mean values of either ABR or LLR (latencies or interwave intervals as the case may be) were observed only in 3-year old children. There was a significant, but negative association between central conduction time and latency of LLRs. Conclusion: OM in the first year of life leads to negative effects on brainstem signal processing even if it has occurred only for a short duration (maximum of 3 months). In such a situation, auditory cortical structures probably show compensatory changes through central gain to offset the prolonged central conduction time. Although the results of the present study showed that the negative effects of early onset OM (occurring in the first year of life) on auditory processing disappeared by the time the children were 4.1 years, there is need for longitudinal studies on this to confirm the findings. Page 1 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 changes continue into adolescence [15]. The sensori Background Adequate sensory experience is critical to the developing motor region witnesses the earliest myelogenesis [16]. nervous system – for the expression as well as mainte- Waves I, II and V of auditory brainstem responses are nance of sensory functions even when such functions are readily discernible at birth [17], while the inter-peak inter- innately determined [1]. Development and maintenance vals II–III and IV–V continue to shorten during the first 2 of auditory sense is no exception. In other words, reduced years of life [18]. These intervals reflect trans-synaptic auditory input, early in life, may affect auditory process- transmission. Matschke, Stenzel, Plath, and Zilles [19], in ing later in life. Otitis media (OM) is a common condition a study of 39 human brains ranging in age from 29 weeks that results in hearing loss in early years of life. Sandeep of gestation to 70 years, demonstrated that myelination and Jayaram [2] have reported that OM occurring early in takes place in the first year of life which is necessary for life may lead to subtle difficulties in speech identification, functional maturation. It appears that normal auditory particularly under adverse listening conditions. Further- development is dependent on adequate stimulation dur- more, such negative effects may persist for 4 years or even ing this sensitive period of life. There is also evidence to more after an attack of OM. say that inter-peak intervals and central conduction time rd of the auditory brainstem responses shorten between 3 OM is the most prevalent disease during childhood, next trimester of pregnancy and first 2 years of life [20]. Matu- only to common cold. It is estimated that chronic OM ration of nerve cells in the upper nuclei as well as myelini- affects 65 million to 330 million people worldwide, and zation of small and large fibers in the auditory pathway 60% of them (39 million to 200 million) show clinically was the reason for the reduction in central conduction significant hearing impairment [3]. Incidence of OM is time. known to be higher in the first 3 years of life [4]. Jayaram [5], in an Indian population, reported that OM was the Synchronized encoding of transient acoustic information cause of conductive hearing loss in nearly 71% of the at the brainstem level leads to robust processing of audi- 1505 persons ranging in age from 1 – 80 years. Similar tory signals at the cortical level in the normal auditory sys- results have been reported also by Parsram and Jalvi [6]. tem. Dys-synchronized activity at the brainstem may result in temporally degraded responses. Degraded audi- Past research has demonstrated that early OM in children tory signals will not obviously result in the accurate influences auditory brainstem physiology [7]. Webster encoding of the temporal features of the signal at the audi- and Webster [7] reported a reduction in both the size and tory cortex. Wible, Nicol and Kraus [21] recorded ABR and number of neurons in the auditory brainstem in subjects LLR for speech sound/da/in children with language-based with OM. Past research has documented prolonged laten- learning problems and reported a good positive correla- cies for wave III and wave V [8-13], delayed wave III and tion between the results of ABR and LLR. Prolonged dura- prolonged III–V wave intervals [8], prolonged wave III–V tion of brainstem encoding of speech sound onset, interval [9] and, prolonged wave III–V and I–V intervals suggesting less precise timing of generation and/or trans- [10,11]. Anteby et al. [12] and Hafner, Anteby, Pratt et al. mission at inferior colliculus, was associated with weaker [14] reported significant increase in the III–V and I–V cortical activity. Wible et al reported 2 distinct group of interwave intervals for several OM groups (separated by subjects in whom auditory processing was different. The clinical state and history of treatment) compared with a first group of subjects demonstrated measures of auditory control group. Persistence of delayed waves has been signal processing at brainstem and cortical levels that were thought to be a reflection of the slowly recovering system proportionate to each other. The abnormal processing of than structural damage per se [9]. auditory signals in these subjects at the cortical level may primarily have been a result of corrupt 'input' to the tha- Delayed wave III and V, and prolonged interpeak intervals lamo-cortical circuitry which, in turn, was perhaps I–III and III–V are the most common findings reported in because of possibly degraded processing and/or transmis- past research on children with early onset OM. However, sion at the lateral lemniscus and/or inferior colliculus. A there seems to be very little common in the operational second group of children showed degraded processing at definition of early onset OM in the studies referred to the brainstem level, but robust processing of signals at the above. Early OM was OM occurring before 18 months in cortical level. However, as changes in LLRs are deter- Gunnarson and Finitzo [10], in infancy [9], before 12 mined, among other factors, by the integrity of underlying months of age [13], before 5.8 years of age at the least neural substrates at the peripheral, brainstem, and cortical [11], and before 2 years 4 months at the least in Chambers levels, it is logical to say that LLRs are influenced also by et al. [8]. the maturation and/or pathological status of the lower- level auditory processors. There is evidence to show that major changes in brain organization take place in the first year of life though Page 2 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Thus, cortical potentials are reported to be more sensitive b) Children in the age range of 4.1 to 4.6 years. The inter- than brainstem potentials in detecting subtle auditory val between OM and the time of testing was 3 to 4 years. processing deficits [22,23]. However, there are no studies which have recorded cortical potentials in children to c) Children in the age range of 5.1 to 5.6 years. The inter- study the effects of early onset OM. As there is some evi- val between OM and the time of testing was 4 to 5 years. dence to suggest that auditory processing is affected at the level of brainstem as a consequence of OM, it can be Grouping according to age was necessary to analyze the assumed that auditory cortex receives abnormal input persistence of the effects of early onset OM, if any, on from the brainstem which, in turn, results in abnormal auditory processing at brainstem and cortical levels. Sub- auditory processing at the cortical level also. Such effects jects included in the experimental group had normal would be more pronounced if OM, and thus the reduced results on otoscopic examination, pure tone audiometry auditory input, occurs before 2 years of chronological age testing (Orbiter 922 diagnostic audiometer) as well as as auditory brainstem and cortical structures show greater immittance evaluation (Grason Staddler Inc. Tympstar). development in the first year of a child's life. Most of the children in the experimental group had A type tympanogram, and normal acoustic reflexes. Six of the 30 Therefore, the purpose of this study was to determine the children, 3 in the 3-year age group and 3 in the 4-year age effect of early onset OM (occurring in the first year of life) group, had no acoustic reflexes. These children were also on auditory brainstem and cortical potentials in an Indian included in the study as their hearing thresholds were the population. A second purpose was to see the persisting same as that of children with normal acoustic reflexes. nature of the effects of early onset OM. The high probabil- Results of otoscopic examination and audiological evalu- ity of OM, in Indian population, as a cause of conductive ations are shown in Table 2. Subjects included in the study hearing loss [5,6] necessitates such studies in the Indian had all been in the register of either All India Institute of context. Speech or Hearing, Mysore or the district hospital of the city of Mysore. Information on the early episodes of OM (between 6 and 12 months of age) was obtained from the Methods Participants records maintained at the institute or hospital or by fam- Thirty children aged 3.1 to 5.6 years and who had OM ily doctors. All the children belonged to the lower socio- between 6 and 12 months of their chronological age were economic strata of the society. Parents of these children included in the study. The selected children did not have had an annual income of around $ 1750 and had less than any attacks of OM after they crossed 1 year of age. Some 10 years of scholastic education. Children in the experi- of the characteristics of children in the experimental mental group were attending nursery classes or play groups are shown in Table 1. Children thus selected into homes in the area in which they were living. the study were sub grouped on the basis of age to form three experimental groups (10 children in each group) as There were 3 control groups with 10 normal children in follows: each group. The children in the control groups were matched for age, gender and socioeconomic status with a) Children in the age range of 3.1 to 3.6 years. The inter- those in the experimental groups. It was made sure that val between OM and the time of testing was 2 to 3 years. the children included in the control groups did not have a history of OM, or any other middle ear problem, by check- Table 1: Some characteristics of children in the experimental group Characteristics No. of children Gender 15 Males Females Number of episodes of otitis media 12 Single Multiple Duration of otitis media 12 < 1 month 3–6 months Ear affected 04 Unilateral Bilateral Page 3 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Table 2: Results of otoscopic examination and audiological evaluation Otoscopic examination Pure tone average (dBHL) Tympanogram Group Age Right Ear Left Ear Right Ear Left Ear Right Ear Left Ear Control 3 yrs Normal Normal 12.66 13.18 A A 4 yrs Normal Normal 11.84 12.18 A A 5 yrs Normal Normal 11.74 11.94 A A Experimental 3 yrs Normal Normal 12.93 12.53 A A 4 yrs Normal Normal 13.66 13.18 A A 5 yrs Normal Normal 11.22 12.28 A A Note. Pure tone average was average of thresholds at 500 Hz, 1 kHz, 2 kHz and 4 kHz. ing medical reports (if available with the family doctor), Data analysis or parental reports, or by an otoscopic examination. The Absolute peak latency, inter-peak intervals, inter aural children in the control group underwent the same tests as intervals, peak amplitude and V/I amplitude ratio of ABRs children in the experimental group and had essentially were measured for each child. The ABRs and LLRs were normal results on otoscopic examination, and pure tone checked for replicability by recording twice using the same as well as impedance audiometric testing. Besides, it was protocol. Only replicable waves were considered for anal- ensured that none of the children included in the study ysis. A representative replicable LLR recording is shown in had any auditory processing disorder as judged from their Figure 1. Prior to analysis of individual LLR waves, grand performance on a standard checklist for auditory process- averages of the waves were computed. This was done sep- ing disorder developed by Yathiraj & Mascarenhas [24]. arately for children of different age groups. The LLR in individual subjects were identified and measured with ref- Children in both the groups were native speakers of Kan- erence to the latency range in the grand average. Wave nada (a Dravidian language spoken by about 55 million latency and amplitudes of P1, N1, P2 and N2 were meas- people primarily in the state of Karnataka in Southern ured for each individual wave. Average baseline electrical India) and belonged to the same geographical location activity was calculated for each individual recording. (Mysore and the surrounding districts of Mysore). All chil- Amplitude, measured in the post stimulus electrical activ- dren included in the study were attending nursery or play ity, was corrected with reference to the average baseline homes in their respective residential areas. Children were amplitude of that particular individual recording. The included in the study only after a written consent from waves identified and the parameters measured reflect one of the parents which was obtained after the parents 100% agreement between the first author of the study and were explained the purpose of the study. An ethics com- two other audiologists working in the area of auditory mittee of the All India Institute of Speech and Hearing, evoked potentials (with more than 10 years experience in headed by a retired justice of the High court of Karnataka the field). has approved the research from the ethical angle in 2004. Results Test procedure Prior to comparison of the results of the control and the The protocol included recording ABRs as well as LLRs for experimental groups, the responses of the two ears were clicks. The subjects were seated in a comfortable, relaxed compared in each of the subject (experimental and con- position while being tested. As LLRs are reported to be trol) and age groups, using paired t test. Results showed affected by the state of arousal, subjects were encouraged no significant difference between the 2 ears in any of the not to sleep. A cartoon movie of the child's interest was subject groups, or in any of the age groups, either for ABR played to ensure that the children did not sleep. The elec- or LLR, or for any of the response parameters (latency or trode sites were cleaned using Neoprep cleaning gel. amplitude or interwave interval, or amplitude ratio). Recording was through silver chloride disc electrodes. All Therefore, data from the 2 ears were combined for further recordings were made only after ensuring low skin imped- statistical analysis. The right-left combined data was nor- ance. Protocol for recording evoked potentials is given in mally distributed as revealed by Kolmogorov-Smirnov test Table 3. The responses were recorded for right and left ear of normality. separately. Effect on ABRs Independent t test was used to compare the results of ABR between children with and with out early onset OM. The Page 4 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Table 3: Test protocol for recording auditory brainstem responses and late latency responses Parameter Auditory brainstem responses Late latency responses Stimuli Clicks Clicks Stimulus intensity 70 dBnHL 70 dBnHL Transducer TDH 39P headphones TDH 39P headphones Repetition rate 11.1/s 1.1/s Stimulus polarity Rarefaction Rarefaction Number of sweeps 1500 500 Filter setting 30–3000 Hz 1–30 Hz Analysis window -10 ms to +25 ms -50 ms to +350 ms Electrode montage Vertical montage Vertical montage Positive – Cz Positive – Cz, Negative – M , M Negative – M /M 1 2 1 2 Ground – Nasion Ground – Nasion Electrode impedance < 5 kOhms < 5 kOhms results of all the statistical analysis, with reference to ABRs, a) There was no significant difference between the control are given in Tables 4 to 6. The major results are summa- and the experimental groups in the mean absolute laten- rized below: cies of ABR in any of the three age groups (Table 4). b) The mean I–III and I–V intervals were significantly pro- longed in 3-year old children with early onset OM. This A Figure 1 representative late latency response recording depicting a good replicability A representative late latency response recording depicting a good replicability. Page 5 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Table 4: Mean latencies (in ms) of click evoked auditory pared to normal children of that age. Again, this effect was brainstem responses, standard deviations (SD) and the results of not seen in older children (4.1 years and above) (Table 6). t test Children with early onset OM, aged 4 years and above, did not differ from normal children with respect to any of Age Parameter Group Mean SD tp the amplitude parameters. 3 years Wave I Control 1.86 0.16 1.502 >0.05 Experimental 1.76 0.24 An analysis of ABR latencies of only children who had Wave III Control 3.78 0.10 1.836 >0.05 normal acoustic reflexes was made. Results are not given Experimental 3.84 0.13 here, but are available with the authors. The results are not Wave V Control 5.67 0.15 1.887 >0.05 different from that when children with no reflexes are Experimental 5.77 0.21 considered. 4 years Wave I Control 1.80 0.10 0.611 >0.05 Experimental 1.83 0.13 Wave III Control 3.80 0.12 1.265 >0.05 Effect on LLRs Experimental 3.86 0.15 The results of all the measurements made, and statistical Wave V Control 5.68 0.16 1.928 >0.05 analysis, with reference to LLRs, are given in Tables 5 and Experimental 5.79 0.20 6. The major results are summarized below: 5 years Wave I Control 1.80 0.19 0.104 >0.05 Experimental 1.81 0.11 a) The mean latencies of P1, N1, P2 and N2 were signifi- Wave III Control 3.77 0.20 1.282 >0.05 Experimental 3.71 0.12 cantly shorter in children with early onset OM compared Wave V Control 5.68 0.25 1.086 >0.05 to normal children. However, shorter latencies were noted Experimental 5.61 0.13 only with 3-year old children (Table 7 & Figure 2). b) The mean amplitude of LLR was not significantly differ- effect was not seen in children aged 4.1 years and more ent between children with and without early onset OM in (Table 5). any age group (Table 8). c) The mean amplitudes of wave I and III were signifi- cantly lower in 3-year old experimental children com- Table 5: Mean inter-wave intervals and inter-aural intervals (in ms) of click evoked auditory brainstem responses, standard deviations (SD) and the results of t test Age Parameter Group Mean SD tp 3 years I–III interval Control 1.92 0.09 3.333 <0.01 Experimental 2.04 0.12 III–V interval Control 1.89 0.09 1.047 >0.05 Experimental 1.93 0.15 I–V interval Control 3.81 0.13 3.102 <0.01 Experimental 3.97 0.18 Inter-aural interval Control 0.13 0.15 0.230 >0.05 Experimental 0.22 0.15 4 years I–III interval Control 2.00 0.99 0.923 >0.05 Experimental 2.03 0.12 III–V interval Control 1.88 0.13 1.362 >0.05 Experimental 1.93 0.13 I–V interval Control 3.88 0.16 1.553 >0.05 Experimental 3.96 0.19 Inter-aural interval Control 0.13 0.12 0.891 >0.05 Experimental 0.08 0.07 5 years I–III interval Control 1.90 0.11 2.027 >0.05 Experimental 1.97 0.11 III–V interval Control 1.91 0.11 0.043 >0.05 Experimental 1.90 0.11 I–V interval Control 3.88 0.17 1.554 >0.05 Experimental 3.80 0.12 Inter-aural interval Control 0.13 0.14 0.426 >0.05 Experimental 0.11 0.06 Page 6 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Table 6: Mean amplitudes (in μV) of click evoked auditory brainstem responses, standard deviations (SD) and the results of t test Age Parameter Group Mean SD tp 3 years Wave I Control 0.41 0.13 2.751 <0.01 Experimental 0.30 0.13 Wave III Control 0.30 0.10 2.619 <0.05 Experimental 0.20 0.14 Wave V Control 0.59 0.17 1.986 >0.05 Experimental 0.50 0.17 V/I amplitude ratio Control 1.61 0.51 0.131 >0.05 Experimental 2.08 1.25 4 years Wave I Control 0.56 0.32 0.409 >0.05 Experimental 0.31 0.21 Wave III Control 0.43 0.17 1.121 >0.05 Experimental 0.30 0.17 Wave V Control 0.54 0.15 0.516 >0.05 Experimental 0.50 0.26 V/I amplitude ratio Control 1.77 2.25 0.769 >0.05 Experimental 1.85 0.95 5 years Wave I Control 0.29 0.16 0.044 >0.05 Experimental 0.31 0.18 Wave III Control 0.26 0.14 0.165 >0.05 Experimental 0.34 0.30 Wave V Control 0.65 0.22 0.609 >0.05 Experimental 0.49 0.22 V/I amplitude ratio Control 2.38 1.99 0.326 >0.05 Experimental 2.88 2.13 Table 7: Mean latencies (in ms) of click evoked late latency responses, standard deviations (SD) and the results of t test Age Parameter Group Mean SD tp 3 years P1 Control 95.40 16.98 3.013 <0.01 Experimental 81.30 12.22 N1 Control 168.40 32.10 3.908 <0.01 Experimental 134.60 21.57 P2 Control 235.90 36.67 5.008 <0.01 Experimental 183.55 28.98 N2 Control 296.80 38.38 3.695 <0.01 Experimental 256.85 29.40 4 years P1 Control 79.38 16.40 0.893 >0.05 Experimental 84.05 17.69 N1 Control 147.61 36.61 0.152 >0.05 Experimental 149.20 27.40 P2 Control 205.55 49.03 0.185 >0.05 Experimental 208.45 47.14 N2 Control 259.27 44.72 0.699 >0.05 Experimental 270.30 51.64 5 years P1 Control 70.40 13.70 0.580 >0.05 Experimental 72.95 14.11 N1 Control 120.68 31.36 0.367 >0.05 Experimental 123.95 23.91 P2 Control 154.30 36.84 0.840 >0.05 Experimental 163.10 28.98 N2 Control 217.90 34.87 0.683 >0.05 Experimental 211.80 19.46 Page 7 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Gr Figure 2 and average late latency response waves Grand average late latency response waves. Note. Clear N1 and P2 were not evident in the grand average late latency responses, but these two peaks were clearly seen in most of the individual recordings. Correlation between ABR and LLR results among others], and increased III–V and I–V interwave A Pearson's Product Moment correlation was computed intervals [[14], among others], the present study found between interpeak intervals (I – III & I – V) of ABRs and only an increase in I–III and I–V interpeak intervals in 3- latency of LLR waves (P1, N1, P2 & N2) for 3-year old chil- year old children who had OM in their first year of life. dren in the experimental group (Table 9). The purpose Any comparison of the results of the present study with was to understand the relationship, or bearing that a sig- that of past research, however, should take into consider- nificantly longer interval (I–III & I–V) has on the timely ation the difference in the method of the studies particu- occurrence of P1, N1, P2 and N2. In other words, whether larly in subject selection and characterization of 'early longer interwave intervals (ABR) would, in turn, lead to onset OM'. delayed onset of LLRs. The results are depicted in Figures 3, 4, 5, 6, 7 and 8. There is no ready explanation for the results obtained in the present study, in particular the increased I–III and I–V interwave interval. An inspection of the mean absolute Discussion The results of the present study indicated that early onset latencies shows that there was a relative decrease in the OM and the consequent reduced auditory input influ- latency of wave I coupled with an increase in the latency ences auditory processing both at the lower brainstem and of wave V in 3-year old children with early onset OM cortical levels in subsequent years. The results of the resulting in a significant prolongation of I–V interval. present study on ABR are only in partial agreement with Physiologically, prolonged interwave intervals reflect results reported in the past. While past research has slowing down of the central conduction time in lower reported prolonged latencies of wave III and V [[13], brainstem. Page 8 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Table 8: Mean amplitudes of click evoked late latency responses The mean amplitude of wave I and III was significantly (in μV), standard deviations (SD) and the results of t test lower in children with OM compared to normal children, but only in the 3 year age group. Physiologically, either a Age Parameter Group Mean SD tP decrease in the number of nerve fibers firing in response to auditory stimulus or the fibres not firing in synchrony 3 years P1 Control 2.10 2.51 0.520 >0.05 Experimental 1.64 3.02 can result in decreased amplitude. Based on the results of N1 Control -1.83 3.01 0.869 >0.05 the present study on latency and amplitude, it is suggested Experimental -1.05 2.83 that it is the auditory nerve and cochlear nuclei that are P2 Control 2.15 1.88 1.404 >0.05 more susceptible to changes following early onset OM, Experimental 1.04 3.00 but this is something to be investigated through morpho- N2 Control -2.56 2.91 1.129 >0.05 Experimental -3.65 3.22 logical studies. 4 years P1 Control 0.94 1.10 0.799 >0.05 Experimental 1.46 2.54 LLR peaks occurred earlier in children with early onset N1 Control -2.44 1.52 2.121 >0.05 OM than in normal children. Again, the results were sig- Experimental -1.35 1.92 nificant only in the case of 3 year old children. This was P2 Control 0.49 1.48 1.579 >0.05 true for all 4 waves of LLR. There are no studies which Experimental 1.33 1.76 N2 Control -1.89 1.96 0.953 >0.05 have studied cortical potentials in children with early Experimental -2.63 2.69 onset OM, and therefore, no comparisons are possible. 5 years P1 Control 1.26 0.88 1.794 >0.05 However, the results of the present study do not agree Experimental 1.74 0.78 with results from studies which have investigated children N1 Control -0.94 1.51 0.559 >0.05 with auditory processing deficits [25-27]. It had been Experimental -1.19 1.38 hypothesized in the present study that abnormal auditory P2 Control 0.58 1.91 2.130 >0.05 Experimental -0.53 1.95 processing at the level of brainstem may lead to deviant N2 Control -2.47 1.46 0.805 >0.05 signal processing at the cortical level. But, the results of Experimental -2.13 1.26 correlation between I–III and I–V intervals with the latency of LLRs showed an inverse relationship between 110 280 Observed 160 Observed Linear Linear 50 140 1.7 1.8 1.9 2.0 2.1 2.2 2.3 1.7 1.8 1.9 2.0 2.1 2.2 2.3 I-III Interval (ms) I-III Interval (ms) 120 220 Observed Observed Linear 160 Linear 1.7 1.8 1.9 2.0 2.1 2.2 2.3 1.7 1.8 1.9 2.0 2.1 2.2 2.3 I-III Interval (ms) I-III Interval (ms) A scatter plot of in 3 Figure 3 year-old childr the enrelationship between I–III intervals of auditory brainstem responses and latency of late latency responses A scatter plot of the relationship between I–III intervals of auditory brainstem responses and latency of late latency responses in 3 year-old children. Page 9 of 13 (page number not for citation purposes) N 1 L atency (m s) P1 Latency (ms) N 2 L a te nc y (m s) P2 Latency (ms) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 160 Observed Observed Linear 140 Linear 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 I-V Interval (ms) I-V Interval (ms) Observed Observed Linear 160 Linear 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 I-V Interval (ms) I-V Interval (ms) Scatter plot r Figure 4 esponses in showing t 3 year-old chi he relation ldren ship between I–V intervals of auditory brainstem responses and latency of late latency Scatter plot showing the relationship between I–V intervals of auditory brainstem responses and latency of late latency responses in 3 year-old children. 120 300 60 Observed Observed 50 Linear 140 Linear 1.7 1.8 1.9 2.0 2.1 2.2 2.3 1.7 1.8 1.9 2.0 2.1 2.2 2.3 I-III Interval (ms) I-III Interval (ms) Observed Observed Linear 100 Linear 100 1.7 1.8 1.9 2.0 2.1 2.2 2.3 1.7 1.8 1.9 2.0 2.1 2.2 2.3 I-III Interval (ms) I-III Interval (ms) Scatter plot showing the relationship res Figure 5 ponses in 4 year-old children between I–III intervals of auditory brainstem responses and latency of late latency Scatter plot showing the relationship between I–III intervals of auditory brainstem responses and latency of late latency responses in 4 year-old children. Page 10 of 13 (page number not for citation purposes) N 1 L atency (m s) P1 Latency (m s) N1 Latency (ms) P1 Latency (ms) N2 Latency (m s) P2 Latency (ms) P2 Latency (ms) N 2 L a te nc y (m s ) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 120 300 Observed Observed Linear Linear 50 140 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 I-V Interval (ms) I-V Interval (ms) 200 400 Observed Observed 100 Linear 100 Linear 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 I-V Interval (ms) I-V Interval (ms) Scatter plot r Figure 6 esponses in showing t 4 year-old chi he relation ldren ship between I–V intervals of auditory brainstem responses and latency of late latency Scatter plot showing the relationship between I–V intervals of auditory brainstem responses and latency of late latency responses in 4 year-old children. 110 220 80 180 Observed Observed 50 Linear 140 Linear 1.6 1.7 1.8 1.9 2.0 2.1 2.2 1.6 1.7 1.8 1.9 2.0 2.1 2.2 I-III Interval (ms) I-III Interval (ms) Observed Observed Linear 180 Linear 1.6 1.7 1.8 1.9 2.0 2.1 2.2 1.6 1.7 1.8 1.9 2.0 2.1 2.2 I-III Interval (ms) I-III Interval (ms) Scatter p respo Figure 7 nses lot showing the relationship between I–III int in 5 year-old children ervals of auditory brainstem responses and latency of late latency Scatter plot showing the relationship between I–III intervals of auditory brainstem responses and latency of late latency responses in 5 year-old children. Page 11 of 13 (page number not for citation purposes) N1 L atency (m s) P1 Latency (ms) N1 L atency (m s) P1 Latency (ms) P2 Latency (ms) N 2 L atency (m s) N2 L atency (m s) P2 Latency (ms) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 110 220 80 180 Observed Observed 50 Linear 140 Linear 3.5 3.6 3.7 3.8 3.9 4.0 4.1 3.5 3.6 3.7 3.8 3.9 4.0 4.1 I-V Interval (ms) I-V Interval (ms) Observed Observed Linear 80 Linear 180 3.5 3.6 3.7 3.8 3.9 4.0 4.1 3.5 3.6 3.7 3.8 3.9 4.0 4.1 I-V Interval (ms) I-V Interval (ms) Scatter plot r Figure 8 esponses in showing t 5 year-old chi he relation ldren ship between I–V intervals of auditory brainstem responses and latency of late latency Scatter plot showing the relationship between I–V intervals of auditory brainstem responses and latency of late latency responses in 5 year-old children. the results of ABR and LLR, and the correlation was signif- The effect of early onset OM on ABRs (prolongation of icant only for the relationship between I–V interval and interpeak intervals I–III and I–V, decreased peak ampli- LLRs. In other words, children who had prolonged con- tude of wave I and III), and LLRs (decreased latency of P1, duction time showed earlier LLR and vice versa. This could N1, P2 & N2) were statistically significant only for chil- be due to the phenomena of central gain in which cortical dren aged 3.1 to 3.6 years (interval between onset of OM structures (increased cortical excitability) show compen- and testing was 2 to 3 years). These effects were not satory changes when there is abnormality in the lower observed in children aged 4.1 years and more. These structures [28]. The poor morphology of LLRs (Figure 1, results on ABR are not in agreement with those reported grand average of LLRs) is a further testimony of a 'differ- by Folsom et al [13], Lenhardt et al [9] or Gunnarson and ent' type of auditory processing at the cortical level as a Finitzo [10]. However, as has been repeatedly mentioned, sequel of early onset OM. the present study and those quoted above differ in their method, particularly subject selection. Also, the subjects of Gunnarson and Finitzo [10] seem to have had more Table 9: Correlation coefficients, and their significance, for the severe OM while the two subjects of Lenhardt et al [9] had relationship between interwave intervals of auditory brainstem responses and latency of late latency responses in 3 year-old persistent OM since infancy. On the other hand, the sub- children jects of the present study had only one or, at the most, two attacks, and in most cases, OM lasted for less than 3 Parameter rp months. Therefore, whether the severity of OM or the duration of OM are factors to be accounted while describ- I–III interval & P1 -0.15 >0.05 ing the long standing effects of OM needs to be investi- I–III interval & N1 -0.02 >0.05 I–III interval & P2 -0.32 >0.05 gated. I–III interval & N2 -0.36 >0.05 I–V interval & P1 -0.63 <0.01 However, making a statement to the effect that the nega- I–V interval & N1 -0.47 <0.05 tive effects of early onset OM on ABRs and LLRs persist till I–V interval & P2 -0.52 <0.05 the children are 3 years old and disappear thereafter may I–V interval & N2 -0.45 <0.05 not be logical. Such an interpretation is not appropriate Page 12 of 13 (page number not for citation purposes) N1 L atency (m s) P1 Latency (m s) P2 Latency (ms) N 2 L atency (m s) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 11. Hall JW, Grose JH: The effect of otitis media with effusion on based on the results of a cross sectional approach because the masking-level difference and the auditory brainstem there is no way to say that subjects aged 4.1 years and reponse. J Speech Hear Res 1993, 36:210-217. more in the present study experienced negative effects of 12. Anteby I, Hafner H, Pratt H, Uri N: Auditory brainstem evoked potentials in evaluating the central effects of middle ear effu- early onset OM (prolonged ABR interwave intervals and sion. Int J Pediatr Otorhinolaryngol 1986, 12:1-11. early LLRs) when they were 3.6 years or less. This calls for 13. Folsom RC, Weber BA, Thompson G: Auditory brainstem responses and children with early recurrent middle ear dis- longitudinal studies on the topic. ease. Ann Otorhinolaryngol 1983, 92:249-253. 14. Hafner H, Anteby I, Pratt H, Golsher M, Shenhav R, Joachims HZ: An interesting observation from this study was that the Auditory brainstem evoked potentials in evaluating the effi- cacy of surgical ventilation of the middle ear. Int J Pediatr early latency of LLRs seen in children aged 3.1 to 3.6 years Otorhinolaryngol 1986, 12:13-22. with OM was not evident in children aged 4 years and 15. Huttenlocher P: Synaptic density in human frontal cortex – more. Subject to the limitations of a cross sectional Developmental changes and effects of aging. Brain Res 1979, 163:195-205. approach to problems of this nature, it can be said that 16. Vaughan HG Jr, Kurtzberg D: Electrophysiologic indices of compensatory mechanism at the cortical level is indeed a human brain maturation and cognitive development. In Developmental Behavioral Neuroscience Edited by: Gunnar MR, Nelson true phenomenon because once the normal conduction CA. New Jersey: Erlbaum-Hilsdale; 1992:1-36. time was restored (4.1 years and more), LLRs occurred at 17. Picton TW, Taylor MJ, Durieux-Smith A: Brainstem auditory expected levels of latency. evoked potentials in pediatrics. In Electrodiagnosis in Clinical Med- icine Edited by: Aminoff M. New York: Churchill Livingstone; 1992:537-569. Competing interests 18. Ponton CW, Moore JK, Eggermont JJ: ABR generation by parallel pathways: Differential maturation of axonal conduction time The author(s) declare that they have no competing inter- and synaptic transmission. Ear Hear 1996, 17(5):411-417. ests. 19. Matschke RG, Stenzel C, Plath P, Zilles K: Maturational aspects of the human auditory pathway: anatomical and electrophysio- logical findings. ORL J Otorhinolaryngol Relat Spec 1994, 56(2):68-72. Authors' contributions 20. Inagaki M, Tomita Y, Takashima S, Ohtani K, Andoh G, Takeshita K: Both the authors have made substantial contribution to Functional and morphometrical maturation of the brain- conception and design, or acquisition of data, or analysis stem auditory pathway. Brain Dev 1987, 9(6):597-601. 21. Wible B, Nicol T, Kraus N: Correlation between brainstem and and interpretation of data, have been involved in drafting cortical auditory processes in normal and language-impaired the manuscript or revising it critically for important intel- children. Brain 2005, 128:417-423. 22. Jirsa RE, Clontz BC: Long latency auditory event related poten- lectual content and have given final approval of the ver- tials from children with auditory processing disorders. Ear sion to be published. Hear 1990, 11:222-232. 23. Jerger J, Musiek F: Report of the consensus conference on the diagnosis of auditory processing disorders in school-aged Acknowledgements children. J Am Acad Audiol 2000, 11(9):467-474. The authors would like to thank the All India Institute of Speech and Hear- 24. Yathiraj A, Mascarenhas K: Effect of auditory stimulation in cen- ing, Mysore, for providing all the assistance to complete this project. tral auditory processing in children with CAPD. Unpublished project, All India Institute of Speech and Hearing, Mysore; 2003. 25. Scatterfield JH, Schell AM, Backs RW, Hidaka KC: Cross sectional References and longitudinal study of age effects of electrophysiological 1. Knudsen EI: Experiences alters the spatial tuning of auditory measures in hyperactive and normal children. Biol Psychiatry units in the optic tectum during a sensitive period in the barn 1984, 19:973-990. owl. J Neurosci 1985, 5:3094-3109. 26. Leppanen T, Lyytinen H: Auditory event related potentials in 2. Sandeep M, Jayaram M: Effect of early otitis media on speech the study of developmental language related disorders. perception. Under editorial process . Audiol Neurootol 1997, 2:308-340. 3. WHO: Chronic suppurative otitis media. Burden of illness 27. Arehole S: A preliminary study of the relationship between and management options. 2004 [http://www.who.int/child-ado long latency response and learning disorder. Br J Audiol 1995, lescent-health/New_Publications/CHILD_HEALTH/ 29:295-298. ISBN_92_4_159158_7.pdf]. 28. Salvi RJ, Wang J, Ding D, Stecker N, Arnold S: Auditory depriva- 4. Teele D, Klein J, Rosner B: Epidemiology of otitis media in chil- tion of central auditory system resulting from selective inner dren. Ann Otorhinolaryngol 1980, 89:5-6. hair cell loss: Animal model of auditory neuropathy. Scand 5. Jayaram M: Assessment of etiological factors of conductive Audiol 1999, 51:1-12. hearing loss. WHO Project Report 1, Mysore; 2007. 6. Parsram K, Jalvi R: Assessment of etiological factors for con- ductive hearing Impairment in general population in Mum- bai (All age groups). NIHH-WHO project, Mumbai; 2007. 7. Webster DB, Webster M: Effects of neonatal conductive hear- ing loss on brainstem auditory nuclei. Ann Otol Rhinol Laryngol 1979, 88:684-688. 8. Chambers RD, Rowan LE, Matthies ML, Novak MA: Auditory Brain-stem Responses in Children with Previous Otitis Media. Arch Otolaryngol Head Neck Surg 1989, 115:452-457. 9. Lenhardt ML, Shaia FT, Abedi E: Brain-stem evoked response waveform variation associated with recurrent otitis media. Arch Otolaryngol 1985, 111:315-316. 10. Gunnarson AD, Finitzo T: Conductive hearing loss during infancy: effects on later auditory brainstem physiology. J Speech Lang Hear Res 1991, 34:1207-1215. Page 13 of 13 (page number not for citation purposes) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Behavioral and Brain Functions Springer Journals

Effect of early onset otitis media on brainstem and cortical auditory processing

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Springer Journals
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Copyright © 2008 by Maruthy and Mannarukrishnaiah; licensee BioMed Central Ltd.
Subject
Biomedicine; Neurosciences; Neurology; Behavioral Therapy; Psychiatry
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1744-9081
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10.1186/1744-9081-4-17
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18384677
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Abstract

Background: Otitis media (OM) leads to significant reduction in the hearing sensitivity. The reduced auditory input, if in the early years of life when the auditory neural system is still maturing, may adversely influence the structural as well as functional development of the system. Past research has reported abnormalities in both the structure and function of brainstem nuclei following auditory deprivation, but, it has not necessarily focused on children who had OM in their first year of life. It can also be said that if auditory processing is affected at the brainstem level because of early onset OM (reduced auditory input in the crucial periods of neural development), then, it may be said that auditory processing is also affected at the cortical level because it receives distorted input from the brainstem. Therefore, the purpose of this study was to document the effects of early onset OM on auditory processing, if any, at the brainstem as well as at cortical levels. A related purpose of the study was to investigate the persistence of the effects of early onset OM, if any, on auditory processing. Methods: A cross sectional approach and a standard group comparison design was used in the study. Thirty children, who had OM between 6 and 12 months of age and who were in the age range of 3.1 – 5.6 years participated in the study. Children with OM were divided into 3 groups based on their age. Click evoked auditory brainstem responses (ABRs) and late latency responses (LLRs) were recorded from these children, and the responses were compared with those from age and gender matched normal children without any history of OM. The data from the 2 groups was statistically analyzed through independent t test. Pearson's Product Moment correlation was computed to examine the relationship between results of ABR and LLR in children with early onset OM. Results: The mean central conduction time was significantly increased and the mean amplitude of wave I and III of ABRs was significantly reduced in children with early onset OM compared to normal children. Also, the latency of all LLR waves was significantly less in children with early onset OM than in normal children. However, significant differences in mean values of either ABR or LLR (latencies or interwave intervals as the case may be) were observed only in 3-year old children. There was a significant, but negative association between central conduction time and latency of LLRs. Conclusion: OM in the first year of life leads to negative effects on brainstem signal processing even if it has occurred only for a short duration (maximum of 3 months). In such a situation, auditory cortical structures probably show compensatory changes through central gain to offset the prolonged central conduction time. Although the results of the present study showed that the negative effects of early onset OM (occurring in the first year of life) on auditory processing disappeared by the time the children were 4.1 years, there is need for longitudinal studies on this to confirm the findings. Page 1 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 changes continue into adolescence [15]. The sensori Background Adequate sensory experience is critical to the developing motor region witnesses the earliest myelogenesis [16]. nervous system – for the expression as well as mainte- Waves I, II and V of auditory brainstem responses are nance of sensory functions even when such functions are readily discernible at birth [17], while the inter-peak inter- innately determined [1]. Development and maintenance vals II–III and IV–V continue to shorten during the first 2 of auditory sense is no exception. In other words, reduced years of life [18]. These intervals reflect trans-synaptic auditory input, early in life, may affect auditory process- transmission. Matschke, Stenzel, Plath, and Zilles [19], in ing later in life. Otitis media (OM) is a common condition a study of 39 human brains ranging in age from 29 weeks that results in hearing loss in early years of life. Sandeep of gestation to 70 years, demonstrated that myelination and Jayaram [2] have reported that OM occurring early in takes place in the first year of life which is necessary for life may lead to subtle difficulties in speech identification, functional maturation. It appears that normal auditory particularly under adverse listening conditions. Further- development is dependent on adequate stimulation dur- more, such negative effects may persist for 4 years or even ing this sensitive period of life. There is also evidence to more after an attack of OM. say that inter-peak intervals and central conduction time rd of the auditory brainstem responses shorten between 3 OM is the most prevalent disease during childhood, next trimester of pregnancy and first 2 years of life [20]. Matu- only to common cold. It is estimated that chronic OM ration of nerve cells in the upper nuclei as well as myelini- affects 65 million to 330 million people worldwide, and zation of small and large fibers in the auditory pathway 60% of them (39 million to 200 million) show clinically was the reason for the reduction in central conduction significant hearing impairment [3]. Incidence of OM is time. known to be higher in the first 3 years of life [4]. Jayaram [5], in an Indian population, reported that OM was the Synchronized encoding of transient acoustic information cause of conductive hearing loss in nearly 71% of the at the brainstem level leads to robust processing of audi- 1505 persons ranging in age from 1 – 80 years. Similar tory signals at the cortical level in the normal auditory sys- results have been reported also by Parsram and Jalvi [6]. tem. Dys-synchronized activity at the brainstem may result in temporally degraded responses. Degraded audi- Past research has demonstrated that early OM in children tory signals will not obviously result in the accurate influences auditory brainstem physiology [7]. Webster encoding of the temporal features of the signal at the audi- and Webster [7] reported a reduction in both the size and tory cortex. Wible, Nicol and Kraus [21] recorded ABR and number of neurons in the auditory brainstem in subjects LLR for speech sound/da/in children with language-based with OM. Past research has documented prolonged laten- learning problems and reported a good positive correla- cies for wave III and wave V [8-13], delayed wave III and tion between the results of ABR and LLR. Prolonged dura- prolonged III–V wave intervals [8], prolonged wave III–V tion of brainstem encoding of speech sound onset, interval [9] and, prolonged wave III–V and I–V intervals suggesting less precise timing of generation and/or trans- [10,11]. Anteby et al. [12] and Hafner, Anteby, Pratt et al. mission at inferior colliculus, was associated with weaker [14] reported significant increase in the III–V and I–V cortical activity. Wible et al reported 2 distinct group of interwave intervals for several OM groups (separated by subjects in whom auditory processing was different. The clinical state and history of treatment) compared with a first group of subjects demonstrated measures of auditory control group. Persistence of delayed waves has been signal processing at brainstem and cortical levels that were thought to be a reflection of the slowly recovering system proportionate to each other. The abnormal processing of than structural damage per se [9]. auditory signals in these subjects at the cortical level may primarily have been a result of corrupt 'input' to the tha- Delayed wave III and V, and prolonged interpeak intervals lamo-cortical circuitry which, in turn, was perhaps I–III and III–V are the most common findings reported in because of possibly degraded processing and/or transmis- past research on children with early onset OM. However, sion at the lateral lemniscus and/or inferior colliculus. A there seems to be very little common in the operational second group of children showed degraded processing at definition of early onset OM in the studies referred to the brainstem level, but robust processing of signals at the above. Early OM was OM occurring before 18 months in cortical level. However, as changes in LLRs are deter- Gunnarson and Finitzo [10], in infancy [9], before 12 mined, among other factors, by the integrity of underlying months of age [13], before 5.8 years of age at the least neural substrates at the peripheral, brainstem, and cortical [11], and before 2 years 4 months at the least in Chambers levels, it is logical to say that LLRs are influenced also by et al. [8]. the maturation and/or pathological status of the lower- level auditory processors. There is evidence to show that major changes in brain organization take place in the first year of life though Page 2 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Thus, cortical potentials are reported to be more sensitive b) Children in the age range of 4.1 to 4.6 years. The inter- than brainstem potentials in detecting subtle auditory val between OM and the time of testing was 3 to 4 years. processing deficits [22,23]. However, there are no studies which have recorded cortical potentials in children to c) Children in the age range of 5.1 to 5.6 years. The inter- study the effects of early onset OM. As there is some evi- val between OM and the time of testing was 4 to 5 years. dence to suggest that auditory processing is affected at the level of brainstem as a consequence of OM, it can be Grouping according to age was necessary to analyze the assumed that auditory cortex receives abnormal input persistence of the effects of early onset OM, if any, on from the brainstem which, in turn, results in abnormal auditory processing at brainstem and cortical levels. Sub- auditory processing at the cortical level also. Such effects jects included in the experimental group had normal would be more pronounced if OM, and thus the reduced results on otoscopic examination, pure tone audiometry auditory input, occurs before 2 years of chronological age testing (Orbiter 922 diagnostic audiometer) as well as as auditory brainstem and cortical structures show greater immittance evaluation (Grason Staddler Inc. Tympstar). development in the first year of a child's life. Most of the children in the experimental group had A type tympanogram, and normal acoustic reflexes. Six of the 30 Therefore, the purpose of this study was to determine the children, 3 in the 3-year age group and 3 in the 4-year age effect of early onset OM (occurring in the first year of life) group, had no acoustic reflexes. These children were also on auditory brainstem and cortical potentials in an Indian included in the study as their hearing thresholds were the population. A second purpose was to see the persisting same as that of children with normal acoustic reflexes. nature of the effects of early onset OM. The high probabil- Results of otoscopic examination and audiological evalu- ity of OM, in Indian population, as a cause of conductive ations are shown in Table 2. Subjects included in the study hearing loss [5,6] necessitates such studies in the Indian had all been in the register of either All India Institute of context. Speech or Hearing, Mysore or the district hospital of the city of Mysore. Information on the early episodes of OM (between 6 and 12 months of age) was obtained from the Methods Participants records maintained at the institute or hospital or by fam- Thirty children aged 3.1 to 5.6 years and who had OM ily doctors. All the children belonged to the lower socio- between 6 and 12 months of their chronological age were economic strata of the society. Parents of these children included in the study. The selected children did not have had an annual income of around $ 1750 and had less than any attacks of OM after they crossed 1 year of age. Some 10 years of scholastic education. Children in the experi- of the characteristics of children in the experimental mental group were attending nursery classes or play groups are shown in Table 1. Children thus selected into homes in the area in which they were living. the study were sub grouped on the basis of age to form three experimental groups (10 children in each group) as There were 3 control groups with 10 normal children in follows: each group. The children in the control groups were matched for age, gender and socioeconomic status with a) Children in the age range of 3.1 to 3.6 years. The inter- those in the experimental groups. It was made sure that val between OM and the time of testing was 2 to 3 years. the children included in the control groups did not have a history of OM, or any other middle ear problem, by check- Table 1: Some characteristics of children in the experimental group Characteristics No. of children Gender 15 Males Females Number of episodes of otitis media 12 Single Multiple Duration of otitis media 12 < 1 month 3–6 months Ear affected 04 Unilateral Bilateral Page 3 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Table 2: Results of otoscopic examination and audiological evaluation Otoscopic examination Pure tone average (dBHL) Tympanogram Group Age Right Ear Left Ear Right Ear Left Ear Right Ear Left Ear Control 3 yrs Normal Normal 12.66 13.18 A A 4 yrs Normal Normal 11.84 12.18 A A 5 yrs Normal Normal 11.74 11.94 A A Experimental 3 yrs Normal Normal 12.93 12.53 A A 4 yrs Normal Normal 13.66 13.18 A A 5 yrs Normal Normal 11.22 12.28 A A Note. Pure tone average was average of thresholds at 500 Hz, 1 kHz, 2 kHz and 4 kHz. ing medical reports (if available with the family doctor), Data analysis or parental reports, or by an otoscopic examination. The Absolute peak latency, inter-peak intervals, inter aural children in the control group underwent the same tests as intervals, peak amplitude and V/I amplitude ratio of ABRs children in the experimental group and had essentially were measured for each child. The ABRs and LLRs were normal results on otoscopic examination, and pure tone checked for replicability by recording twice using the same as well as impedance audiometric testing. Besides, it was protocol. Only replicable waves were considered for anal- ensured that none of the children included in the study ysis. A representative replicable LLR recording is shown in had any auditory processing disorder as judged from their Figure 1. Prior to analysis of individual LLR waves, grand performance on a standard checklist for auditory process- averages of the waves were computed. This was done sep- ing disorder developed by Yathiraj & Mascarenhas [24]. arately for children of different age groups. The LLR in individual subjects were identified and measured with ref- Children in both the groups were native speakers of Kan- erence to the latency range in the grand average. Wave nada (a Dravidian language spoken by about 55 million latency and amplitudes of P1, N1, P2 and N2 were meas- people primarily in the state of Karnataka in Southern ured for each individual wave. Average baseline electrical India) and belonged to the same geographical location activity was calculated for each individual recording. (Mysore and the surrounding districts of Mysore). All chil- Amplitude, measured in the post stimulus electrical activ- dren included in the study were attending nursery or play ity, was corrected with reference to the average baseline homes in their respective residential areas. Children were amplitude of that particular individual recording. The included in the study only after a written consent from waves identified and the parameters measured reflect one of the parents which was obtained after the parents 100% agreement between the first author of the study and were explained the purpose of the study. An ethics com- two other audiologists working in the area of auditory mittee of the All India Institute of Speech and Hearing, evoked potentials (with more than 10 years experience in headed by a retired justice of the High court of Karnataka the field). has approved the research from the ethical angle in 2004. Results Test procedure Prior to comparison of the results of the control and the The protocol included recording ABRs as well as LLRs for experimental groups, the responses of the two ears were clicks. The subjects were seated in a comfortable, relaxed compared in each of the subject (experimental and con- position while being tested. As LLRs are reported to be trol) and age groups, using paired t test. Results showed affected by the state of arousal, subjects were encouraged no significant difference between the 2 ears in any of the not to sleep. A cartoon movie of the child's interest was subject groups, or in any of the age groups, either for ABR played to ensure that the children did not sleep. The elec- or LLR, or for any of the response parameters (latency or trode sites were cleaned using Neoprep cleaning gel. amplitude or interwave interval, or amplitude ratio). Recording was through silver chloride disc electrodes. All Therefore, data from the 2 ears were combined for further recordings were made only after ensuring low skin imped- statistical analysis. The right-left combined data was nor- ance. Protocol for recording evoked potentials is given in mally distributed as revealed by Kolmogorov-Smirnov test Table 3. The responses were recorded for right and left ear of normality. separately. Effect on ABRs Independent t test was used to compare the results of ABR between children with and with out early onset OM. The Page 4 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Table 3: Test protocol for recording auditory brainstem responses and late latency responses Parameter Auditory brainstem responses Late latency responses Stimuli Clicks Clicks Stimulus intensity 70 dBnHL 70 dBnHL Transducer TDH 39P headphones TDH 39P headphones Repetition rate 11.1/s 1.1/s Stimulus polarity Rarefaction Rarefaction Number of sweeps 1500 500 Filter setting 30–3000 Hz 1–30 Hz Analysis window -10 ms to +25 ms -50 ms to +350 ms Electrode montage Vertical montage Vertical montage Positive – Cz Positive – Cz, Negative – M , M Negative – M /M 1 2 1 2 Ground – Nasion Ground – Nasion Electrode impedance < 5 kOhms < 5 kOhms results of all the statistical analysis, with reference to ABRs, a) There was no significant difference between the control are given in Tables 4 to 6. The major results are summa- and the experimental groups in the mean absolute laten- rized below: cies of ABR in any of the three age groups (Table 4). b) The mean I–III and I–V intervals were significantly pro- longed in 3-year old children with early onset OM. This A Figure 1 representative late latency response recording depicting a good replicability A representative late latency response recording depicting a good replicability. Page 5 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Table 4: Mean latencies (in ms) of click evoked auditory pared to normal children of that age. Again, this effect was brainstem responses, standard deviations (SD) and the results of not seen in older children (4.1 years and above) (Table 6). t test Children with early onset OM, aged 4 years and above, did not differ from normal children with respect to any of Age Parameter Group Mean SD tp the amplitude parameters. 3 years Wave I Control 1.86 0.16 1.502 >0.05 Experimental 1.76 0.24 An analysis of ABR latencies of only children who had Wave III Control 3.78 0.10 1.836 >0.05 normal acoustic reflexes was made. Results are not given Experimental 3.84 0.13 here, but are available with the authors. The results are not Wave V Control 5.67 0.15 1.887 >0.05 different from that when children with no reflexes are Experimental 5.77 0.21 considered. 4 years Wave I Control 1.80 0.10 0.611 >0.05 Experimental 1.83 0.13 Wave III Control 3.80 0.12 1.265 >0.05 Effect on LLRs Experimental 3.86 0.15 The results of all the measurements made, and statistical Wave V Control 5.68 0.16 1.928 >0.05 analysis, with reference to LLRs, are given in Tables 5 and Experimental 5.79 0.20 6. The major results are summarized below: 5 years Wave I Control 1.80 0.19 0.104 >0.05 Experimental 1.81 0.11 a) The mean latencies of P1, N1, P2 and N2 were signifi- Wave III Control 3.77 0.20 1.282 >0.05 Experimental 3.71 0.12 cantly shorter in children with early onset OM compared Wave V Control 5.68 0.25 1.086 >0.05 to normal children. However, shorter latencies were noted Experimental 5.61 0.13 only with 3-year old children (Table 7 & Figure 2). b) The mean amplitude of LLR was not significantly differ- effect was not seen in children aged 4.1 years and more ent between children with and without early onset OM in (Table 5). any age group (Table 8). c) The mean amplitudes of wave I and III were signifi- cantly lower in 3-year old experimental children com- Table 5: Mean inter-wave intervals and inter-aural intervals (in ms) of click evoked auditory brainstem responses, standard deviations (SD) and the results of t test Age Parameter Group Mean SD tp 3 years I–III interval Control 1.92 0.09 3.333 <0.01 Experimental 2.04 0.12 III–V interval Control 1.89 0.09 1.047 >0.05 Experimental 1.93 0.15 I–V interval Control 3.81 0.13 3.102 <0.01 Experimental 3.97 0.18 Inter-aural interval Control 0.13 0.15 0.230 >0.05 Experimental 0.22 0.15 4 years I–III interval Control 2.00 0.99 0.923 >0.05 Experimental 2.03 0.12 III–V interval Control 1.88 0.13 1.362 >0.05 Experimental 1.93 0.13 I–V interval Control 3.88 0.16 1.553 >0.05 Experimental 3.96 0.19 Inter-aural interval Control 0.13 0.12 0.891 >0.05 Experimental 0.08 0.07 5 years I–III interval Control 1.90 0.11 2.027 >0.05 Experimental 1.97 0.11 III–V interval Control 1.91 0.11 0.043 >0.05 Experimental 1.90 0.11 I–V interval Control 3.88 0.17 1.554 >0.05 Experimental 3.80 0.12 Inter-aural interval Control 0.13 0.14 0.426 >0.05 Experimental 0.11 0.06 Page 6 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Table 6: Mean amplitudes (in μV) of click evoked auditory brainstem responses, standard deviations (SD) and the results of t test Age Parameter Group Mean SD tp 3 years Wave I Control 0.41 0.13 2.751 <0.01 Experimental 0.30 0.13 Wave III Control 0.30 0.10 2.619 <0.05 Experimental 0.20 0.14 Wave V Control 0.59 0.17 1.986 >0.05 Experimental 0.50 0.17 V/I amplitude ratio Control 1.61 0.51 0.131 >0.05 Experimental 2.08 1.25 4 years Wave I Control 0.56 0.32 0.409 >0.05 Experimental 0.31 0.21 Wave III Control 0.43 0.17 1.121 >0.05 Experimental 0.30 0.17 Wave V Control 0.54 0.15 0.516 >0.05 Experimental 0.50 0.26 V/I amplitude ratio Control 1.77 2.25 0.769 >0.05 Experimental 1.85 0.95 5 years Wave I Control 0.29 0.16 0.044 >0.05 Experimental 0.31 0.18 Wave III Control 0.26 0.14 0.165 >0.05 Experimental 0.34 0.30 Wave V Control 0.65 0.22 0.609 >0.05 Experimental 0.49 0.22 V/I amplitude ratio Control 2.38 1.99 0.326 >0.05 Experimental 2.88 2.13 Table 7: Mean latencies (in ms) of click evoked late latency responses, standard deviations (SD) and the results of t test Age Parameter Group Mean SD tp 3 years P1 Control 95.40 16.98 3.013 <0.01 Experimental 81.30 12.22 N1 Control 168.40 32.10 3.908 <0.01 Experimental 134.60 21.57 P2 Control 235.90 36.67 5.008 <0.01 Experimental 183.55 28.98 N2 Control 296.80 38.38 3.695 <0.01 Experimental 256.85 29.40 4 years P1 Control 79.38 16.40 0.893 >0.05 Experimental 84.05 17.69 N1 Control 147.61 36.61 0.152 >0.05 Experimental 149.20 27.40 P2 Control 205.55 49.03 0.185 >0.05 Experimental 208.45 47.14 N2 Control 259.27 44.72 0.699 >0.05 Experimental 270.30 51.64 5 years P1 Control 70.40 13.70 0.580 >0.05 Experimental 72.95 14.11 N1 Control 120.68 31.36 0.367 >0.05 Experimental 123.95 23.91 P2 Control 154.30 36.84 0.840 >0.05 Experimental 163.10 28.98 N2 Control 217.90 34.87 0.683 >0.05 Experimental 211.80 19.46 Page 7 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Gr Figure 2 and average late latency response waves Grand average late latency response waves. Note. Clear N1 and P2 were not evident in the grand average late latency responses, but these two peaks were clearly seen in most of the individual recordings. Correlation between ABR and LLR results among others], and increased III–V and I–V interwave A Pearson's Product Moment correlation was computed intervals [[14], among others], the present study found between interpeak intervals (I – III & I – V) of ABRs and only an increase in I–III and I–V interpeak intervals in 3- latency of LLR waves (P1, N1, P2 & N2) for 3-year old chil- year old children who had OM in their first year of life. dren in the experimental group (Table 9). The purpose Any comparison of the results of the present study with was to understand the relationship, or bearing that a sig- that of past research, however, should take into consider- nificantly longer interval (I–III & I–V) has on the timely ation the difference in the method of the studies particu- occurrence of P1, N1, P2 and N2. In other words, whether larly in subject selection and characterization of 'early longer interwave intervals (ABR) would, in turn, lead to onset OM'. delayed onset of LLRs. The results are depicted in Figures 3, 4, 5, 6, 7 and 8. There is no ready explanation for the results obtained in the present study, in particular the increased I–III and I–V interwave interval. An inspection of the mean absolute Discussion The results of the present study indicated that early onset latencies shows that there was a relative decrease in the OM and the consequent reduced auditory input influ- latency of wave I coupled with an increase in the latency ences auditory processing both at the lower brainstem and of wave V in 3-year old children with early onset OM cortical levels in subsequent years. The results of the resulting in a significant prolongation of I–V interval. present study on ABR are only in partial agreement with Physiologically, prolonged interwave intervals reflect results reported in the past. While past research has slowing down of the central conduction time in lower reported prolonged latencies of wave III and V [[13], brainstem. Page 8 of 13 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 Table 8: Mean amplitudes of click evoked late latency responses The mean amplitude of wave I and III was significantly (in μV), standard deviations (SD) and the results of t test lower in children with OM compared to normal children, but only in the 3 year age group. Physiologically, either a Age Parameter Group Mean SD tP decrease in the number of nerve fibers firing in response to auditory stimulus or the fibres not firing in synchrony 3 years P1 Control 2.10 2.51 0.520 >0.05 Experimental 1.64 3.02 can result in decreased amplitude. Based on the results of N1 Control -1.83 3.01 0.869 >0.05 the present study on latency and amplitude, it is suggested Experimental -1.05 2.83 that it is the auditory nerve and cochlear nuclei that are P2 Control 2.15 1.88 1.404 >0.05 more susceptible to changes following early onset OM, Experimental 1.04 3.00 but this is something to be investigated through morpho- N2 Control -2.56 2.91 1.129 >0.05 Experimental -3.65 3.22 logical studies. 4 years P1 Control 0.94 1.10 0.799 >0.05 Experimental 1.46 2.54 LLR peaks occurred earlier in children with early onset N1 Control -2.44 1.52 2.121 >0.05 OM than in normal children. Again, the results were sig- Experimental -1.35 1.92 nificant only in the case of 3 year old children. This was P2 Control 0.49 1.48 1.579 >0.05 true for all 4 waves of LLR. There are no studies which Experimental 1.33 1.76 N2 Control -1.89 1.96 0.953 >0.05 have studied cortical potentials in children with early Experimental -2.63 2.69 onset OM, and therefore, no comparisons are possible. 5 years P1 Control 1.26 0.88 1.794 >0.05 However, the results of the present study do not agree Experimental 1.74 0.78 with results from studies which have investigated children N1 Control -0.94 1.51 0.559 >0.05 with auditory processing deficits [25-27]. It had been Experimental -1.19 1.38 hypothesized in the present study that abnormal auditory P2 Control 0.58 1.91 2.130 >0.05 Experimental -0.53 1.95 processing at the level of brainstem may lead to deviant N2 Control -2.47 1.46 0.805 >0.05 signal processing at the cortical level. But, the results of Experimental -2.13 1.26 correlation between I–III and I–V intervals with the latency of LLRs showed an inverse relationship between 110 280 Observed 160 Observed Linear Linear 50 140 1.7 1.8 1.9 2.0 2.1 2.2 2.3 1.7 1.8 1.9 2.0 2.1 2.2 2.3 I-III Interval (ms) I-III Interval (ms) 120 220 Observed Observed Linear 160 Linear 1.7 1.8 1.9 2.0 2.1 2.2 2.3 1.7 1.8 1.9 2.0 2.1 2.2 2.3 I-III Interval (ms) I-III Interval (ms) A scatter plot of in 3 Figure 3 year-old childr the enrelationship between I–III intervals of auditory brainstem responses and latency of late latency responses A scatter plot of the relationship between I–III intervals of auditory brainstem responses and latency of late latency responses in 3 year-old children. Page 9 of 13 (page number not for citation purposes) N 1 L atency (m s) P1 Latency (ms) N 2 L a te nc y (m s) P2 Latency (ms) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 160 Observed Observed Linear 140 Linear 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 I-V Interval (ms) I-V Interval (ms) Observed Observed Linear 160 Linear 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 I-V Interval (ms) I-V Interval (ms) Scatter plot r Figure 4 esponses in showing t 3 year-old chi he relation ldren ship between I–V intervals of auditory brainstem responses and latency of late latency Scatter plot showing the relationship between I–V intervals of auditory brainstem responses and latency of late latency responses in 3 year-old children. 120 300 60 Observed Observed 50 Linear 140 Linear 1.7 1.8 1.9 2.0 2.1 2.2 2.3 1.7 1.8 1.9 2.0 2.1 2.2 2.3 I-III Interval (ms) I-III Interval (ms) Observed Observed Linear 100 Linear 100 1.7 1.8 1.9 2.0 2.1 2.2 2.3 1.7 1.8 1.9 2.0 2.1 2.2 2.3 I-III Interval (ms) I-III Interval (ms) Scatter plot showing the relationship res Figure 5 ponses in 4 year-old children between I–III intervals of auditory brainstem responses and latency of late latency Scatter plot showing the relationship between I–III intervals of auditory brainstem responses and latency of late latency responses in 4 year-old children. Page 10 of 13 (page number not for citation purposes) N 1 L atency (m s) P1 Latency (m s) N1 Latency (ms) P1 Latency (ms) N2 Latency (m s) P2 Latency (ms) P2 Latency (ms) N 2 L a te nc y (m s ) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 120 300 Observed Observed Linear Linear 50 140 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 I-V Interval (ms) I-V Interval (ms) 200 400 Observed Observed 100 Linear 100 Linear 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 I-V Interval (ms) I-V Interval (ms) Scatter plot r Figure 6 esponses in showing t 4 year-old chi he relation ldren ship between I–V intervals of auditory brainstem responses and latency of late latency Scatter plot showing the relationship between I–V intervals of auditory brainstem responses and latency of late latency responses in 4 year-old children. 110 220 80 180 Observed Observed 50 Linear 140 Linear 1.6 1.7 1.8 1.9 2.0 2.1 2.2 1.6 1.7 1.8 1.9 2.0 2.1 2.2 I-III Interval (ms) I-III Interval (ms) Observed Observed Linear 180 Linear 1.6 1.7 1.8 1.9 2.0 2.1 2.2 1.6 1.7 1.8 1.9 2.0 2.1 2.2 I-III Interval (ms) I-III Interval (ms) Scatter p respo Figure 7 nses lot showing the relationship between I–III int in 5 year-old children ervals of auditory brainstem responses and latency of late latency Scatter plot showing the relationship between I–III intervals of auditory brainstem responses and latency of late latency responses in 5 year-old children. Page 11 of 13 (page number not for citation purposes) N1 L atency (m s) P1 Latency (ms) N1 L atency (m s) P1 Latency (ms) P2 Latency (ms) N 2 L atency (m s) N2 L atency (m s) P2 Latency (ms) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 110 220 80 180 Observed Observed 50 Linear 140 Linear 3.5 3.6 3.7 3.8 3.9 4.0 4.1 3.5 3.6 3.7 3.8 3.9 4.0 4.1 I-V Interval (ms) I-V Interval (ms) Observed Observed Linear 80 Linear 180 3.5 3.6 3.7 3.8 3.9 4.0 4.1 3.5 3.6 3.7 3.8 3.9 4.0 4.1 I-V Interval (ms) I-V Interval (ms) Scatter plot r Figure 8 esponses in showing t 5 year-old chi he relation ldren ship between I–V intervals of auditory brainstem responses and latency of late latency Scatter plot showing the relationship between I–V intervals of auditory brainstem responses and latency of late latency responses in 5 year-old children. the results of ABR and LLR, and the correlation was signif- The effect of early onset OM on ABRs (prolongation of icant only for the relationship between I–V interval and interpeak intervals I–III and I–V, decreased peak ampli- LLRs. In other words, children who had prolonged con- tude of wave I and III), and LLRs (decreased latency of P1, duction time showed earlier LLR and vice versa. This could N1, P2 & N2) were statistically significant only for chil- be due to the phenomena of central gain in which cortical dren aged 3.1 to 3.6 years (interval between onset of OM structures (increased cortical excitability) show compen- and testing was 2 to 3 years). These effects were not satory changes when there is abnormality in the lower observed in children aged 4.1 years and more. These structures [28]. The poor morphology of LLRs (Figure 1, results on ABR are not in agreement with those reported grand average of LLRs) is a further testimony of a 'differ- by Folsom et al [13], Lenhardt et al [9] or Gunnarson and ent' type of auditory processing at the cortical level as a Finitzo [10]. However, as has been repeatedly mentioned, sequel of early onset OM. the present study and those quoted above differ in their method, particularly subject selection. Also, the subjects of Gunnarson and Finitzo [10] seem to have had more Table 9: Correlation coefficients, and their significance, for the severe OM while the two subjects of Lenhardt et al [9] had relationship between interwave intervals of auditory brainstem responses and latency of late latency responses in 3 year-old persistent OM since infancy. On the other hand, the sub- children jects of the present study had only one or, at the most, two attacks, and in most cases, OM lasted for less than 3 Parameter rp months. Therefore, whether the severity of OM or the duration of OM are factors to be accounted while describ- I–III interval & P1 -0.15 >0.05 ing the long standing effects of OM needs to be investi- I–III interval & N1 -0.02 >0.05 I–III interval & P2 -0.32 >0.05 gated. I–III interval & N2 -0.36 >0.05 I–V interval & P1 -0.63 <0.01 However, making a statement to the effect that the nega- I–V interval & N1 -0.47 <0.05 tive effects of early onset OM on ABRs and LLRs persist till I–V interval & P2 -0.52 <0.05 the children are 3 years old and disappear thereafter may I–V interval & N2 -0.45 <0.05 not be logical. Such an interpretation is not appropriate Page 12 of 13 (page number not for citation purposes) N1 L atency (m s) P1 Latency (m s) P2 Latency (ms) N 2 L atency (m s) Behavioral and Brain Functions 2008, 4:17 http://www.behavioralandbrainfunctions.com/content/4/1/17 11. Hall JW, Grose JH: The effect of otitis media with effusion on based on the results of a cross sectional approach because the masking-level difference and the auditory brainstem there is no way to say that subjects aged 4.1 years and reponse. J Speech Hear Res 1993, 36:210-217. more in the present study experienced negative effects of 12. Anteby I, Hafner H, Pratt H, Uri N: Auditory brainstem evoked potentials in evaluating the central effects of middle ear effu- early onset OM (prolonged ABR interwave intervals and sion. Int J Pediatr Otorhinolaryngol 1986, 12:1-11. early LLRs) when they were 3.6 years or less. This calls for 13. Folsom RC, Weber BA, Thompson G: Auditory brainstem responses and children with early recurrent middle ear dis- longitudinal studies on the topic. ease. Ann Otorhinolaryngol 1983, 92:249-253. 14. Hafner H, Anteby I, Pratt H, Golsher M, Shenhav R, Joachims HZ: An interesting observation from this study was that the Auditory brainstem evoked potentials in evaluating the effi- cacy of surgical ventilation of the middle ear. Int J Pediatr early latency of LLRs seen in children aged 3.1 to 3.6 years Otorhinolaryngol 1986, 12:13-22. with OM was not evident in children aged 4 years and 15. Huttenlocher P: Synaptic density in human frontal cortex – more. Subject to the limitations of a cross sectional Developmental changes and effects of aging. Brain Res 1979, 163:195-205. approach to problems of this nature, it can be said that 16. Vaughan HG Jr, Kurtzberg D: Electrophysiologic indices of compensatory mechanism at the cortical level is indeed a human brain maturation and cognitive development. In Developmental Behavioral Neuroscience Edited by: Gunnar MR, Nelson true phenomenon because once the normal conduction CA. New Jersey: Erlbaum-Hilsdale; 1992:1-36. time was restored (4.1 years and more), LLRs occurred at 17. Picton TW, Taylor MJ, Durieux-Smith A: Brainstem auditory expected levels of latency. evoked potentials in pediatrics. In Electrodiagnosis in Clinical Med- icine Edited by: Aminoff M. New York: Churchill Livingstone; 1992:537-569. Competing interests 18. Ponton CW, Moore JK, Eggermont JJ: ABR generation by parallel pathways: Differential maturation of axonal conduction time The author(s) declare that they have no competing inter- and synaptic transmission. Ear Hear 1996, 17(5):411-417. ests. 19. Matschke RG, Stenzel C, Plath P, Zilles K: Maturational aspects of the human auditory pathway: anatomical and electrophysio- logical findings. ORL J Otorhinolaryngol Relat Spec 1994, 56(2):68-72. Authors' contributions 20. Inagaki M, Tomita Y, Takashima S, Ohtani K, Andoh G, Takeshita K: Both the authors have made substantial contribution to Functional and morphometrical maturation of the brain- conception and design, or acquisition of data, or analysis stem auditory pathway. Brain Dev 1987, 9(6):597-601. 21. Wible B, Nicol T, Kraus N: Correlation between brainstem and and interpretation of data, have been involved in drafting cortical auditory processes in normal and language-impaired the manuscript or revising it critically for important intel- children. Brain 2005, 128:417-423. 22. Jirsa RE, Clontz BC: Long latency auditory event related poten- lectual content and have given final approval of the ver- tials from children with auditory processing disorders. Ear sion to be published. Hear 1990, 11:222-232. 23. Jerger J, Musiek F: Report of the consensus conference on the diagnosis of auditory processing disorders in school-aged Acknowledgements children. J Am Acad Audiol 2000, 11(9):467-474. The authors would like to thank the All India Institute of Speech and Hear- 24. Yathiraj A, Mascarenhas K: Effect of auditory stimulation in cen- ing, Mysore, for providing all the assistance to complete this project. tral auditory processing in children with CAPD. Unpublished project, All India Institute of Speech and Hearing, Mysore; 2003. 25. Scatterfield JH, Schell AM, Backs RW, Hidaka KC: Cross sectional References and longitudinal study of age effects of electrophysiological 1. Knudsen EI: Experiences alters the spatial tuning of auditory measures in hyperactive and normal children. Biol Psychiatry units in the optic tectum during a sensitive period in the barn 1984, 19:973-990. owl. J Neurosci 1985, 5:3094-3109. 26. Leppanen T, Lyytinen H: Auditory event related potentials in 2. Sandeep M, Jayaram M: Effect of early otitis media on speech the study of developmental language related disorders. perception. Under editorial process . Audiol Neurootol 1997, 2:308-340. 3. WHO: Chronic suppurative otitis media. Burden of illness 27. Arehole S: A preliminary study of the relationship between and management options. 2004 [http://www.who.int/child-ado long latency response and learning disorder. Br J Audiol 1995, lescent-health/New_Publications/CHILD_HEALTH/ 29:295-298. ISBN_92_4_159158_7.pdf]. 28. Salvi RJ, Wang J, Ding D, Stecker N, Arnold S: Auditory depriva- 4. Teele D, Klein J, Rosner B: Epidemiology of otitis media in chil- tion of central auditory system resulting from selective inner dren. Ann Otorhinolaryngol 1980, 89:5-6. hair cell loss: Animal model of auditory neuropathy. Scand 5. Jayaram M: Assessment of etiological factors of conductive Audiol 1999, 51:1-12. hearing loss. WHO Project Report 1, Mysore; 2007. 6. Parsram K, Jalvi R: Assessment of etiological factors for con- ductive hearing Impairment in general population in Mum- bai (All age groups). NIHH-WHO project, Mumbai; 2007. 7. Webster DB, Webster M: Effects of neonatal conductive hear- ing loss on brainstem auditory nuclei. Ann Otol Rhinol Laryngol 1979, 88:684-688. 8. Chambers RD, Rowan LE, Matthies ML, Novak MA: Auditory Brain-stem Responses in Children with Previous Otitis Media. Arch Otolaryngol Head Neck Surg 1989, 115:452-457. 9. Lenhardt ML, Shaia FT, Abedi E: Brain-stem evoked response waveform variation associated with recurrent otitis media. Arch Otolaryngol 1985, 111:315-316. 10. Gunnarson AD, Finitzo T: Conductive hearing loss during infancy: effects on later auditory brainstem physiology. J Speech Lang Hear Res 1991, 34:1207-1215. Page 13 of 13 (page number not for citation purposes)

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