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Speech identification and cortical potentials in individuals with auditory neuropathy

Speech identification and cortical potentials in individuals with auditory neuropathy Background: Present study investigated the relationship between speech identification scores in quiet and parameters of cortical potentials (latency of P1, N1, and P2; and amplitude of N1/P2) in individuals with auditory neuropathy. Methods: Ten individuals with auditory neuropathy (five males and five females) and ten individuals with normal hearing in the age range of 12 to 39 yr participated in the study. Speech identification ability was assessed for bi-syllabic words and cortical potentials were recorded for click stimuli. Results: Results revealed that in individuals with auditory neuropathy, speech identification scores were significantly poorer than that of individuals with normal hearing. Individuals with auditory neuropathy were further classified into two groups, Good Performers and Poor Performers based on their speech identification scores. It was observed that the mean amplitude of N1/P2 of Poor Performers was significantly lower than that of Good Performers and those with normal hearing. There was no significant effect of group on the latency of the peaks. Speech identification scores showed a good correlation with the amplitude of cortical potentials (N1/P2 complex) but did not show a significant correlation with the latency of cortical potentials. Conclusion: Results of the present study suggests that measuring the cortical potentials may offer a means for predicting perceptual skills in individuals with auditory neuropathy. neuropathy are suggestive of a retro-cochlear pathology, Background Auditory neuropathy is one of the hearing disorders in the exact site of pathology and patho-physiological mech- which cochlear amplification is normal but neural trans- anism leading to auditory neuropathy is not known. Two mission in afferent pathway is disordered. The integrity of physiological explanations proposed for the neurophysio- cochlear function in this population is provided by the logical manifestations observed include dys-synchronized presence of evoked oto-acoustic emissions and/or coch- spikes discharge and/or reduced spike of the auditory lear microphonics (CM), and the abnormal neural trans- nerves [1,2]. mission or dys-synchrony is indicated by the absence of auditory brainstem responses and middle ear muscle Hearing sensitivity in individuals with auditory neuropa- reflexes. Although the audiological findings in auditory thy may range from normal hearing to profound hearing Page 1 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 impairment [3]. A majority of individuals with auditory present study was undertaken to study the relationship neuropathy have low frequency hearing loss with dispro- between speech perception ability in quiet and parame- portionately poor speech recognition scores for the degree ters of cortical potentials in individuals with auditory neu- of hearing loss [3]. Speech identification ability in indi- ropathy. viduals with auditory neuropathy varies considerably among patients but approximately 60 to 70% of individ- Methods I. Participants uals have identification scores well below the estimated identification scores from their pure-tone thresholds Ten individuals with auditory neuropathy and ten indi- [3,4]. viduals with normal hearing participated in the present study. Out of ten individuals with normal hearing, five Starr et al. [5] attempted to record click evoked cortical were males and five were females with ages ranging from potentials (P1, N1 and P2) in four of ten adults subjects 12 to 39 yr with a mean of 22 yr. The individuals with nor- with auditory neuropathy. The responses to supra-thresh- mal hearing had pure-tone sensitivity of less than 15 dB old click stimuli were recordable in three of four subjects. HL at octave frequencies from 250 Hz to 8000 Hz. These They further observed that the subject with absent cortical individuals were volunteers from local college and potentials had poorer speech identification score than schools. other three subjects. Kraus et al. [6] subsequently pre- sented a case report showing cortical evoked potentials in Participants with auditory neuropathy were recruited a teenager with auditory neuropathy, whose identification from the clients registered at the Audiology clinic of the score in quiet was 100%, whereas in adverse conditions, All India Institute of Speech and Hearing, Mysore, India. the identification scores were very poor. As the cortical Table 1 shows the audiological profile of the ten partici- potentials were normal in this client, they hypothesized pants (5 males and 5 females) with auditory neuropathy. that speech perception in quiet was not significantly The age of the participants ranged from 12 to 39 yr with a affected by poor synchronization at the brainstem level if mean of 20.7 yr. The pure-tone average (average of pure synchronization is preserved at the cortical level. Results tone thresholds at 500, 1000, 2000, 4000 and 8000 Hz) of some of the investigations carried out later support this ranged from 10 to 48 dB HL. A majority of the participants hypothesis. Rance et al. [7] observed better speech identi- had symmetrical hearing loss in both the ears. The audio- fication scores in children with auditory neuropathy who metric configuration was rising pattern in a majority of had normal cortical potentials when compared to those the participants. All the participants had present TEOAEs with abnormal cortical potentials. Vanaja and Manjula [8] and absent middle ear acoustic reflexes (both ipsilateral reported that individuals who have higher amplitude in and contralateral) and the auditory brainstem responses. cortical potentials had better speech identification scores None of participants had any family history or any other and also benefitted more with a hearing aid than those medical complications. All the participants were native with lesser amplitude. speakers of Kannada, a Dravidian language spoken in a southern state of India. Thus, limited information available in literature shows that auditory neuropathy individuals having poor identi- fication scores in quiet have abnormal or absent cortical potentials suggesting that integrity of processing at corti- cal level is important for speech understanding. The Table 1: Audiological profile of individuals with auditory neuropathy S.No Age/Sex Pure-tone Average (dB HL) Pure-tone Average (dB HL) ABR in both ears OAE in both ears Acoustic reflex in both ears Right ear Left ear AN1 12 ys/M 26.00 31.00 Absent Present Absent AN2 20 ys/F 31.00 34.00 Absent Present Absent AN3 15 ys/F 30.00 36.00 Absent Present Absent AN4 39 ys/F 33.00 39.00 Absent Present Absent AN5 12 ys/M 44.00 43.00 Absent Present Absent AN6 24 ys/M 31.00 38.00 Absent Present Absent AN7 27 yr/F 42.00 31.00 Absent Present Absent AN8 20 yr/M 48.00 46.00 Absent Present Absent AN9 18 yrs/M 19.00 10.00 Absent Present Absent AN10 20 yrs/M 43.00 39.00 Absent Present Absent Page 2 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 II. Data Collection Results a. Assessment of speech identification ability Speech identification ability Stimuli Speech identification scores in individuals with normal Speech Identification Test in Kannada developed by Van- hearing ranged from 95% to 100% with a mean of 96% in dana [9] was used to assess open set speech identification both eras whereas in individuals with auditory neuropa- abilities. This test consists of 50 bi-syllabic meaningful thy identification scores in both eras ranged from 0 to words of Kannada. Validity and reliability of this test has 90% with a mean of 42.1% in the right ear and 41.2% in been established on native speakers of Kannada [9]. the left ear. Among the individuals with auditory neurop- athy, AN-3 had 0% identification in both eras. Figure 1 Procedure shows the individual data for speech identification scores The participants listened to speech tokens individually in in individuals with auditory neuropathy. Paired sample a double-walled, acoustically treated room where the "t" test revealed no significant difference (auditory neu- ambient levels were within permissible limits [10]. The ropathy: t = 0.1, p = 0.88; Normal: t = 0.05, p = 0.9) speech stimuli were presented through supra-aural head- between the ears for identification scores in both groups. phones (TDH – 39) of a calibrated [11] diagnostic audi- Hence, the data from the two ears were merged for further ometer (Madson OB-922). The stimuli were presented at statistical analysis. 40 dB SL (re: Speech Recognition Threshold) monaurally and the participants were asked to repeat the speech The mean speech identification scores for subjects in the token. The speech recognition scores were calculated by normal hearing group was 96% with a standard deviation counting the number of words correctly repeated. of 2.5% whereas the mean scores of individuals with audi- tory neuropathy was 42% with a standard deviation of b. Cortical evoked potentials 25.4%. An Independent Sample't' test revealed a signifi- The participants were seated comfortably in a reclining cant difference between the mean speech identification chair and the cortical evoked potentials were acquired scores of the two groups (t = 5.77, p < 0.01). using the Intelligent Hearing Smart EP system. The responses were picked up from a disc electrode placed on Pearson product-moment correlation was performed the midline site, Cz, with reference to an electrode placed between behavioral threshold and speech identification on the ipsilateral mastoid. The common electrode was scores in individuals with auditory neuropathy. Figure 2 placed at Fpz. It was ensured that the impedance at each shows the scatter plot between pure-tone average and electrode site was less than 5 k ohms and the inter-elec- speech identification scores. Pearson correlation coeffi- trode impedance was less than 2 k ohms. The participants were instructed not to pay attention to the stimuli while recording. The cortical potentials were recorded for each ear sepa- rately with click stimuli presented through insert-ear- phones (ER-3A) at a repetition rate of 1.1/sec at 80 dB nHL. Stimulus level used to elicit the cortical waveforms were supra-threshold for all participants. The EEG acquired was amplified 50,000 times and digitally filtered using a band pass filter of 1–30 Hz. The EEG was epoched using a window of 550 ms, including a 50 ms pre-stimu- lus baseline. Epochs greater than 45 μV were rejected. The EEG responses for 200 stimuli were averaged. The latency of P1, N1, P2, N2, and the amplitude of N1/P2 were meas- ured. The amplitude of N1/P2 was measured with peak- to-peak. Recordings were repeated twice to check for replicability. Only those peaks, which were replicable, were considered as a response. Three experienced audiologists independ- Speech id neuropathy Figure 1entification scores of the individuals with auditory ently analyzed the waveforms to identify and mark the Speech identification scores of the individuals with peaks in cortical potentials. It was considered as a auditory neuropathy. In the figure, X indicates of 0% iden- tification scores. response only if all the three audiologists identified the cortical potentials at the same latency. Page 3 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 cient revealed that there was no significant correlation auditory neuropathy but there was no significant differ- between speech identification scores and pure-tone aver- ence for the latency of N2 peak. The "t" value and the level age in individuals with auditory neuropathy (r = -0.37, p of significance are also shown in Table 2. The N1/P2 = 0.6). amplitude of the participants with auditory neuropathy did not differ significantly from that of normal hearing Cortical potentials individuals. However, the mean values of the amplitude Cortical evoked potentials were present and symmetrical for the participants with auditory neuropathy were in all the individuals with normal hearing. Cortical poten- slightly lower and the variability was greater when com- tials were present and symmetrical in all the individuals pared to those observed in normal subjects. with auditory neuropathy, except one participant (AN3). The responses were absent in a 15 year old participant As there was more variability in measures of individuals with a pure-tone average of 30 dB HL. Therefore, the age with AN, the data of the participants with auditory neu- and threshold cannot be the contributing factors for the ropathy were further divided into two groups based on absence of responses in this participant. their speech identification scores. Group I included "Good Performers" whose speech identification score was Paired Sample" t" test was performed to compare between more than 50% and Group II included "Poor Performers" two ears for latency of cortical potentials (P1, N1, P2 and whose speech identification score was less than or equal N2) and amplitude of N1/P2. The results revealed no sig- to 50%. The mean and standard deviation of latency and nificant difference between the two ears. For further anal- amplitude (N1/P2) cortical potentials for the two groups ysis, data of right ear and left ear were combined. The are presented in Table 3. It can be noted that the ampli- mean and standard deviation of latencies of P1, N1, P2, tude of Poor Performers was lower than that of Good Per- N2 in individuals with normal hearing and those with formers. Results of Kruskal Wallis test revealed that there auditory neuropathy are presented in Table 2. From the is a significant effect of group on the amplitude (p < 0.01) table it can be noted that the latencies in subjects with of N1/P2 peak. Mann-Whitney test was performed to auditory neuropathy were delayed by 20 – 50 ms for P1, assess the paired comparison between the groups. Results 40–80 ms for N1 and 30–80 ms for P2 when compared to revealed that the mean amplitude of Poor Performers was individuals with normal hearing. significantly lower than that of Good Performers (p < 0.01) and normal hearing subjects (p < 0.01). However, Independent sample "t"test was performed independently mean amplitude of Good Performers was not significantly for latency of cortical potentials (P1, N1, P2 and N2) and different from that of normal hearing subjects (p > 0.01). amplitude (N1/P2). Results revealed a statistically signifi- cant difference between the latencies of P1, N1, and P2 Kruskal Wallis test performed to study the effect of group peaks in individuals with normal hearing and those with on the latency of cortical potentials revealed that there was a significant effect of group on the latency (p < 0.01) for all the components except for N2. Mann-Whitney test was performed to assess the paired comparison between the groups. Results revealed that both in Good Performers and Poor Performers, the mean latency for all the peaks except N2 differed significantly from that of normal hear- ing subjects but there was no significant difference for latency for all the peaks between Good Performers and Poor Performers (p < 0.01). Pearson product-moment correlation was carried out to study the correlation of the peak latency of P1, N1, P2, N2 and the amplitude of N1/P2 with the behavioral thresh- olds (pure-tone average) and speech identification scores. It can be observed from Table 4 that the latency of cortical potentials did not show a significant correlation with the pure tone average or with speech identification scores. However, the amplitude of N1/P2 showed a significant Relationship tion scores of individuals Figure 2 between the pure-to with auditory neuropathy ne threshold and identifica- correlation with speech identification scores. Relation Relationship between the pure-tone threshold and between N1/P2 amplitude and speech identification identification scores of individuals with auditory neu- ropathy. scores is depicted in the scatter plot along with regression curve in Figure 3. Page 4 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 Table 2: Mean, SD, and "t" value of latencies and amplitude cortical potentials in individuals with normal hearing and auditory neuropathy Participants Latencies (m sec) Amplitude N1/P2 (μV) P1 N1 P2 N2 AN 76 (20) 124(31) 185(43) 243(50) 4.4(2.4) Normal 50 (8.1) 85(9) 142(12) 218(13) 6.2(1.3) "t" Value 4.1* 2.8* 3.05* 1.6 - 0.82 "p" Value 0.001 0.001 0.001 0.057 0.05 * Significant at p < 0.01 Inspection of individuals data revealed that two partici- in individuals with auditory neuropathy. Other factors pants had normal latencies with reduced amplitudes and impair the speech understanding capability in these indi- their speech identification scores were poor (AN4, AN6), viduals. whereas two participants who had normal latencies with good amplitude (AN2 and AN7) had better speech identi- One of the possible contributors for their poor speech fication scores. Five subjects who had prolonged latencies identification score is disrupted neural synchrony, which with normal amplitude also showed good speech identifi- impairs the listener's ability to processes the dynamic cation scores. Figure 4 shows the waveforms of individu- nature of speech signals. It has been reported that dis- als with auditory neuropathy and those with normal rupted neural synchrony impairs the ability to use enve- hearing. lope cues in speech and also impair the ability to perceive rapid change of spectral shapes in the speech stimuli [2,4,14]. Discussion Speech identification in individuals with auditory neuropathy Cortical potentials in individuals with auditory neuropathy In the present study, speech identification scores in indi- Latencies of cortical potentials in individuals with audi- viduals with auditory neuropathy were significantly lower tory neuropathy were significantly prolonged when com- than that observed for participants with normal hearing. pared to normal hearing listeners. Though not statistically Further, the correlation analysis revealed that speech iden- significant, the mean amplitude of the cortical potentials tification scores for individuals with auditory neuropathy was lower than that observed in participants with normal were disproportionate to their pure-tone threshold. This is hearing and the variability was high in individuals with best illustrated by comparing the speech identification auditory neuropathy. Latencies and amplitude variations scores in individuals with auditory neuropathy to those in individuals with auditory neuropathy may not be due expected by degree of hearing loss for patients with coch- to increased pure-tone threshold, as there was no correla- lear hearing loss [12]. In the present study, in 72% of indi- tion between pure-tone thresholds and cortical potentials viduals, the speech identification scores were lower when (latency and amplitude), suggesting that the latency and compared to those reported by Vanaja and Jayaram [12] amplitude of cortical potentials were not affected by the for ears with sensorineural hearing loss. Sininger and Oba hearing thresholds of the participants in the present study. [3] observed that speech identification scores for 69% of Oates, Kurtzberg, and Satpells [15] reported that the laten- their patients with auditory neuropathy were lower than cies and amplitude of P1/N1/P2 were not significantly that reported for patients with cochlear pathology by Yel- affected in subjects with cochlear hearing loss of less than lin et al. [13]. These results suggest that speech identifica- moderate degree. Cortical potentials were absent in AN3 tion scores do not depend upon the pure-tone thresholds who had pure-tone threshold of 30 dB HL whereas it was Table 3: Mean and SD of latencies and amplitude cortical potentials for the two groups of auditory neuropathy and individuals with normal hearing Participants Latency (msec) Amplitude P1 N1 P2 N2 N1/P2 (μV) Normal 50 (8.1) 85(9) 142(12) 218(13) 6.2(1.3) Good Performers 84(16.8) 133(30.8) 186(53.8) 227(26.2) 6.0(1.5) Poor Performers 78(20.2) 125(27.6) 184(27.4) 231(18.2) 2.6(1.3) Page 5 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 literature [5,8,17]. No clear-cut explanation can be pro- vided for the variability observed in latencies of cortical potentials. The variability in latencies observed across individuals with auditory neuropathy in the present study may have been related to the underlining patho-physiol- ogy. That is prolonged latencies may be due to the dys- synchronous firing [18-20,14] whereas normal latencies may be due to the reduced numbers of fibers [1,14]. The magnitude of reduction in amplitude in either of patho- physiology depends upon the severity of the condition [14,21]. Further investigation correlating cortical poten- tials with neurological findings need to be carried out to confirm this. Relation between speech identification scores and cortical potentials In the present study individuals who had cortical poten- Scatter plot tud r Figure 3 opa e of thy cortical pote between speech identification ntials in individuals wi scores and ampli- th auditory neu- Scatter plot between speech identification scores tials with better amplitude had better speech identifica- and amplitude of cortical potentials in individuals tion scores than those with absent/abnormal amplitude with auditory neuropathy. in cortical potentials. Participant AN3 in the present study had absent cortical potentials and very poor speech iden- tification scores. Similar results have been reported by ear- lier investigators [7,5,17]. These results suggest that it is present in AN 4 whose pure-tone average of 48 dB HL. possible to have good speech perception in quiet if the This further, supports the notion that cortical potentials cortical responses are present even if the brainstem did not depend upon the pure-tone average in the present responses are abnormal. Good synchronization at the study. auditory nerve and brainstem level does not appear to be essential for understanding speech in quiet situations [6]. Cortical potentials mature and attain adult latency and Results of physiological studies indicate that brainstem morphology by the age of 9 years and there will not be any neurons process the fast modulations of the complex sig- significant changes in latency until age of 50 yr [16]. As nals, whereas auditory cortex processes the slowly varying the age range of the participants in the present study var- the amplitude modulations of the complex signal [22], ied from 12 to 39 yr, the latency variations observed may which plays an important role in auditory communica- not be due to maturational changes. It was hypothesized tion [23]. that probably the severity of the neural dys-synchrony rather than the hearing loss contributed for the variability There was also a high positive correlation between speech in the cortical evoked responses observed in the present identification and the amplitude of N1/P2. That is, indi- study. viduals with better speech identification scores showed greater N1/P2 amplitude than those with poorer speech An interesting observation in the present study was that, identification scores. However, no correlation was some of individuals with auditory neuropathy had abnor- observed between latencies of cortical potentials and mal latencies with normal amplitude, whereas some had speech identification scores. Similar findings were normal latencies with abnormal amplitude in cortical observed in adults [8] and children[7] with auditory neu- potentials. Similar results have also been reported in the ropathy using hearing aids. They reported that the cortical Table 4: Correlation coefficients (r) of behavioral thresholds with cortical potentials and word recognition scores with cortical potentials "r" value Latency (ms) N1/P2 P1 N1 P2 N2 amplitude (μV) Behavioral Threshold -0.46 -0.25 -0.2 -0.3 -0.16 Speech Identification score 0.45 0.52 0.3 -0.1 0.86* * Significant at p < 0.05 Page 6 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 als with auditory neuropathy, the procedure can be used to obtain important information regarding severity and management options for these participants. Authors' contributions VKN was involved in designing the study, data collection, analysis, interpretation of results and preparing the man- uscript. CSV was involved in designing the study, analysis interpretation of results, and preparing the manuscript. Acknowledgements We thank Dr. Vijayalakshmi Bsasavaraj, Director, All India Institute of Speech and Hearing, for permitting us to conduct the study. We express our sincere thanks to all the participants for their patient cooperation. References 1. Starr A, Michalewski HJ, Zeng FG, FujiKawa-Brooks S, Lithicum F, Kim CS, Winner D, Keats B: Pathology and physiology of AN with novel mutation in the MPZ gene (tyr145->ser). Brain 2003, 126:1604-1619. 2. Zeng FG, Kong YY, Michalewski HJ, Starr A: Perceptual conse- quences of disrupted auditory nerve activity. J Neurohysiol 2005, 93(6):3050-3063. 3. Sininger Y, Oba S: Patients with AN: who are they and what can they hear? In A new perspective on hearing disorders Edited by: Sinin- ger Y, Starr A. Sandigo: Singular-Thomson learning; 2001:15-35. 4. Zeng FG, Oba S, Grade S, Sininger Y, Starr A: Temporal and speech processing deficits in AN. Neuroreport 1999, Represen th Figure 4 e two groups tative samples of cortical potentials recorded from 10:3429-3435. Representative samples of cortical potentials 5. Starr A, Picton TW, Sininger S, Hood LJ, Berlin CI: Auditory Neu- ropathy. Brain 1996, 119:741-753. recorded from the two groups. a) Wave forms of indi- 6. Kraus N, Bradlow MA, Cunningham CJ, King CD, Koch DB, Nicol TG, viduals with normal hearing. b) Wave forms with normal Mcgee TJ, Stein LK, Wright BA: Consequences of neural asyn- latencies and normal amplitude obtained from an individual chrony: A case of AN. J Assoc Res Otolaryngol 2000, 01:33-45. with auditory neuropathy. c) Wave forms with prolonged 7. Rance G, Cone-Wession B, Shepherd RK, Dowell RC, King AM, Rick- ards FW, Clark GM: Speech perception and cortical event latencies obtained from an individual with auditory neuropa- related potentials in children with AN. Ear Hear 2002, thy. d) Wave forms with normal latency and reduced ampli- 25:34-46. tude obtained from an individuals with auditory neuropathy 8. Vanaja CS, Manjula P: LLR as a measure of benefit derived from e) No response obtained from an individual with auditory hearing devices with auditory dys-synchrony. In first conference on Auditory Neuropathy Edited by: Shivashanker N, Shashikala HR. Ban- neuropathy. galore: Department of Speech pathology and Audiology, National Institute of Mental Health and Neuro sciences; 2004:136-146. 9. Vandana : Speech identification test in Kannada. Unpublished independent project, University of Mysore, Mysore, India; 1998. potentials were present in individuals with auditory neu- 10. American National Standards Institute: Maximum permissible ropathy who had good speech identification scores and ambient noise for audiometric rooms. ANSI S3.1-1999. New York: American National Standards Institute. these individuals also benefited from a hearing aid. Thus, 11. American National Standards Institute: Specification for audiom- it can be concluded that the speech recognition scores eters. ANSI S3.6-1996. New York: American National Standards probably depend on the severity of the disorder rather Institute. 12. Vanaja CS, Jayaram M: Sensitivity and specificity of audiological than the underlining patho-physiology. tests. Unpublished Project Report, All India Institute of Speech and Hearing, Mysore, India; 2003. 13. Yellin MW, Jerger J, Fifer RC: Norms for disproportionate loss in Conclusion speech intelligibility. Ear Hear 1989, 10:231-234. Results of the present study support the previously 14. Rance G: Auditory Neuropathy/Dys-synchrony and it's Per- reported findings that speech perception ability cannot be ceptual Consequences. Trends Amplif 2005, 9:1-43. 15. Oates P, Kurtzberg D, Stapells DR: Effect of sensoryneural hear- reliably estimated from behavioral pure-tone audiogram ing loss on cortical event-related potentials behavioral meas- in individuals with auditory neuropathy. Cortical poten- ures of sound processing. Ear Hear 2002, 23:399-415. tial testing may, however, offer a means of predicting 16. Hall JW: Effect of nonpathologic subject characteristics. Edited by: Allyn & Bacon. Handbook of auditory evoked responses; speech understanding ability in individuals with auditory 1992:70-103. neuropathy. The presence and amplitude of cortical 17. Satya-Murthi S, Wolpaw JR, Cacace AT, Scharffer CA: Late auditory evoked potentials can occur without brain stem potentials. potentials showed a significant correlation with open set Electroencephalogr Clin Neurophysiol 1983, 56:304-307. speech perception abilities. The absence of cortical poten- 18. Hendler T, Squires NK, Moore JK, Coyle PK: Auditory evoked tials indicates extremely poor speech perception abilities. potentials in multiple sclerosis: correlation with magnetic resonance imaging. J Basic Clin Physiol Pharmacol 1996, 7:245-278. If these results are replicated in a larger group of individu- Page 7 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 19. Japaridze G, Shakarishvili R, Kevanishvili Z: Auditory brainstem, middle-latency, and slow cortical responses in multiple scle- rosis. Acta Neurol Scand 2002, 106:47-53. 20. Mc Donald WI, Sears TA: The effect of experimental demyeli- nation on conduction in the central nerves system. Brain 1970, 91:583-595. 21. Rapin I, Gravel J: "Auditory neuropathy": Physiologic and path- ologic evidence calls for more diagnostic specificity. Int J Pedi- atr Otorhinolaryngol 2003, 67:707-728. 22. Giraud AL, Lorenzi C, Ashburner J, Wable J, Johnsrude I, Frackowiak R, Kleinschmidt R: Representation of the Temporal Envelope of Sounds in the Human Brain. J Neurophysiol 2000, 84:1588-1598. 23. Drullman R, Festen JM, Plomp R: Effect of temporal envelope smearing on speech reception. J Acoust Soc Am 1994, 95:1053-1064. Publish with Bio Med Central and every scientist can read your work free of charge "BioMed Central will be the most significant development for disseminating the results of biomedical researc h in our lifetime." Sir Paul Nurse, Cancer Research UK Your research papers will be: available free of charge to the entire biomedical community peer reviewed and published immediately upon acceptance cited in PubMed and archived on PubMed Central yours — you keep the copyright BioMedcentral Submit your manuscript here: http://www.biomedcentral.com/info/publishing_adv.asp Page 8 of 8 (page number not for citation purposes) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Behavioral and Brain Functions Springer Journals

Speech identification and cortical potentials in individuals with auditory neuropathy

Narne, Vijaya; Vanaja, CS
Behavioral and Brain Functions , Volume 4 (1) – Mar 31, 2008
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Springer Journals
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Copyright © 2008 by Narne and Vanaja; licensee BioMed Central Ltd.
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Biomedicine; Neurosciences; Neurology; Behavioral Therapy; Psychiatry
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1744-9081
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Abstract

Background: Present study investigated the relationship between speech identification scores in quiet and parameters of cortical potentials (latency of P1, N1, and P2; and amplitude of N1/P2) in individuals with auditory neuropathy. Methods: Ten individuals with auditory neuropathy (five males and five females) and ten individuals with normal hearing in the age range of 12 to 39 yr participated in the study. Speech identification ability was assessed for bi-syllabic words and cortical potentials were recorded for click stimuli. Results: Results revealed that in individuals with auditory neuropathy, speech identification scores were significantly poorer than that of individuals with normal hearing. Individuals with auditory neuropathy were further classified into two groups, Good Performers and Poor Performers based on their speech identification scores. It was observed that the mean amplitude of N1/P2 of Poor Performers was significantly lower than that of Good Performers and those with normal hearing. There was no significant effect of group on the latency of the peaks. Speech identification scores showed a good correlation with the amplitude of cortical potentials (N1/P2 complex) but did not show a significant correlation with the latency of cortical potentials. Conclusion: Results of the present study suggests that measuring the cortical potentials may offer a means for predicting perceptual skills in individuals with auditory neuropathy. neuropathy are suggestive of a retro-cochlear pathology, Background Auditory neuropathy is one of the hearing disorders in the exact site of pathology and patho-physiological mech- which cochlear amplification is normal but neural trans- anism leading to auditory neuropathy is not known. Two mission in afferent pathway is disordered. The integrity of physiological explanations proposed for the neurophysio- cochlear function in this population is provided by the logical manifestations observed include dys-synchronized presence of evoked oto-acoustic emissions and/or coch- spikes discharge and/or reduced spike of the auditory lear microphonics (CM), and the abnormal neural trans- nerves [1,2]. mission or dys-synchrony is indicated by the absence of auditory brainstem responses and middle ear muscle Hearing sensitivity in individuals with auditory neuropa- reflexes. Although the audiological findings in auditory thy may range from normal hearing to profound hearing Page 1 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 impairment [3]. A majority of individuals with auditory present study was undertaken to study the relationship neuropathy have low frequency hearing loss with dispro- between speech perception ability in quiet and parame- portionately poor speech recognition scores for the degree ters of cortical potentials in individuals with auditory neu- of hearing loss [3]. Speech identification ability in indi- ropathy. viduals with auditory neuropathy varies considerably among patients but approximately 60 to 70% of individ- Methods I. Participants uals have identification scores well below the estimated identification scores from their pure-tone thresholds Ten individuals with auditory neuropathy and ten indi- [3,4]. viduals with normal hearing participated in the present study. Out of ten individuals with normal hearing, five Starr et al. [5] attempted to record click evoked cortical were males and five were females with ages ranging from potentials (P1, N1 and P2) in four of ten adults subjects 12 to 39 yr with a mean of 22 yr. The individuals with nor- with auditory neuropathy. The responses to supra-thresh- mal hearing had pure-tone sensitivity of less than 15 dB old click stimuli were recordable in three of four subjects. HL at octave frequencies from 250 Hz to 8000 Hz. These They further observed that the subject with absent cortical individuals were volunteers from local college and potentials had poorer speech identification score than schools. other three subjects. Kraus et al. [6] subsequently pre- sented a case report showing cortical evoked potentials in Participants with auditory neuropathy were recruited a teenager with auditory neuropathy, whose identification from the clients registered at the Audiology clinic of the score in quiet was 100%, whereas in adverse conditions, All India Institute of Speech and Hearing, Mysore, India. the identification scores were very poor. As the cortical Table 1 shows the audiological profile of the ten partici- potentials were normal in this client, they hypothesized pants (5 males and 5 females) with auditory neuropathy. that speech perception in quiet was not significantly The age of the participants ranged from 12 to 39 yr with a affected by poor synchronization at the brainstem level if mean of 20.7 yr. The pure-tone average (average of pure synchronization is preserved at the cortical level. Results tone thresholds at 500, 1000, 2000, 4000 and 8000 Hz) of some of the investigations carried out later support this ranged from 10 to 48 dB HL. A majority of the participants hypothesis. Rance et al. [7] observed better speech identi- had symmetrical hearing loss in both the ears. The audio- fication scores in children with auditory neuropathy who metric configuration was rising pattern in a majority of had normal cortical potentials when compared to those the participants. All the participants had present TEOAEs with abnormal cortical potentials. Vanaja and Manjula [8] and absent middle ear acoustic reflexes (both ipsilateral reported that individuals who have higher amplitude in and contralateral) and the auditory brainstem responses. cortical potentials had better speech identification scores None of participants had any family history or any other and also benefitted more with a hearing aid than those medical complications. All the participants were native with lesser amplitude. speakers of Kannada, a Dravidian language spoken in a southern state of India. Thus, limited information available in literature shows that auditory neuropathy individuals having poor identi- fication scores in quiet have abnormal or absent cortical potentials suggesting that integrity of processing at corti- cal level is important for speech understanding. The Table 1: Audiological profile of individuals with auditory neuropathy S.No Age/Sex Pure-tone Average (dB HL) Pure-tone Average (dB HL) ABR in both ears OAE in both ears Acoustic reflex in both ears Right ear Left ear AN1 12 ys/M 26.00 31.00 Absent Present Absent AN2 20 ys/F 31.00 34.00 Absent Present Absent AN3 15 ys/F 30.00 36.00 Absent Present Absent AN4 39 ys/F 33.00 39.00 Absent Present Absent AN5 12 ys/M 44.00 43.00 Absent Present Absent AN6 24 ys/M 31.00 38.00 Absent Present Absent AN7 27 yr/F 42.00 31.00 Absent Present Absent AN8 20 yr/M 48.00 46.00 Absent Present Absent AN9 18 yrs/M 19.00 10.00 Absent Present Absent AN10 20 yrs/M 43.00 39.00 Absent Present Absent Page 2 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 II. Data Collection Results a. Assessment of speech identification ability Speech identification ability Stimuli Speech identification scores in individuals with normal Speech Identification Test in Kannada developed by Van- hearing ranged from 95% to 100% with a mean of 96% in dana [9] was used to assess open set speech identification both eras whereas in individuals with auditory neuropa- abilities. This test consists of 50 bi-syllabic meaningful thy identification scores in both eras ranged from 0 to words of Kannada. Validity and reliability of this test has 90% with a mean of 42.1% in the right ear and 41.2% in been established on native speakers of Kannada [9]. the left ear. Among the individuals with auditory neurop- athy, AN-3 had 0% identification in both eras. Figure 1 Procedure shows the individual data for speech identification scores The participants listened to speech tokens individually in in individuals with auditory neuropathy. Paired sample a double-walled, acoustically treated room where the "t" test revealed no significant difference (auditory neu- ambient levels were within permissible limits [10]. The ropathy: t = 0.1, p = 0.88; Normal: t = 0.05, p = 0.9) speech stimuli were presented through supra-aural head- between the ears for identification scores in both groups. phones (TDH – 39) of a calibrated [11] diagnostic audi- Hence, the data from the two ears were merged for further ometer (Madson OB-922). The stimuli were presented at statistical analysis. 40 dB SL (re: Speech Recognition Threshold) monaurally and the participants were asked to repeat the speech The mean speech identification scores for subjects in the token. The speech recognition scores were calculated by normal hearing group was 96% with a standard deviation counting the number of words correctly repeated. of 2.5% whereas the mean scores of individuals with audi- tory neuropathy was 42% with a standard deviation of b. Cortical evoked potentials 25.4%. An Independent Sample't' test revealed a signifi- The participants were seated comfortably in a reclining cant difference between the mean speech identification chair and the cortical evoked potentials were acquired scores of the two groups (t = 5.77, p < 0.01). using the Intelligent Hearing Smart EP system. The responses were picked up from a disc electrode placed on Pearson product-moment correlation was performed the midline site, Cz, with reference to an electrode placed between behavioral threshold and speech identification on the ipsilateral mastoid. The common electrode was scores in individuals with auditory neuropathy. Figure 2 placed at Fpz. It was ensured that the impedance at each shows the scatter plot between pure-tone average and electrode site was less than 5 k ohms and the inter-elec- speech identification scores. Pearson correlation coeffi- trode impedance was less than 2 k ohms. The participants were instructed not to pay attention to the stimuli while recording. The cortical potentials were recorded for each ear sepa- rately with click stimuli presented through insert-ear- phones (ER-3A) at a repetition rate of 1.1/sec at 80 dB nHL. Stimulus level used to elicit the cortical waveforms were supra-threshold for all participants. The EEG acquired was amplified 50,000 times and digitally filtered using a band pass filter of 1–30 Hz. The EEG was epoched using a window of 550 ms, including a 50 ms pre-stimu- lus baseline. Epochs greater than 45 μV were rejected. The EEG responses for 200 stimuli were averaged. The latency of P1, N1, P2, N2, and the amplitude of N1/P2 were meas- ured. The amplitude of N1/P2 was measured with peak- to-peak. Recordings were repeated twice to check for replicability. Only those peaks, which were replicable, were considered as a response. Three experienced audiologists independ- Speech id neuropathy Figure 1entification scores of the individuals with auditory ently analyzed the waveforms to identify and mark the Speech identification scores of the individuals with peaks in cortical potentials. It was considered as a auditory neuropathy. In the figure, X indicates of 0% iden- tification scores. response only if all the three audiologists identified the cortical potentials at the same latency. Page 3 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 cient revealed that there was no significant correlation auditory neuropathy but there was no significant differ- between speech identification scores and pure-tone aver- ence for the latency of N2 peak. The "t" value and the level age in individuals with auditory neuropathy (r = -0.37, p of significance are also shown in Table 2. The N1/P2 = 0.6). amplitude of the participants with auditory neuropathy did not differ significantly from that of normal hearing Cortical potentials individuals. However, the mean values of the amplitude Cortical evoked potentials were present and symmetrical for the participants with auditory neuropathy were in all the individuals with normal hearing. Cortical poten- slightly lower and the variability was greater when com- tials were present and symmetrical in all the individuals pared to those observed in normal subjects. with auditory neuropathy, except one participant (AN3). The responses were absent in a 15 year old participant As there was more variability in measures of individuals with a pure-tone average of 30 dB HL. Therefore, the age with AN, the data of the participants with auditory neu- and threshold cannot be the contributing factors for the ropathy were further divided into two groups based on absence of responses in this participant. their speech identification scores. Group I included "Good Performers" whose speech identification score was Paired Sample" t" test was performed to compare between more than 50% and Group II included "Poor Performers" two ears for latency of cortical potentials (P1, N1, P2 and whose speech identification score was less than or equal N2) and amplitude of N1/P2. The results revealed no sig- to 50%. The mean and standard deviation of latency and nificant difference between the two ears. For further anal- amplitude (N1/P2) cortical potentials for the two groups ysis, data of right ear and left ear were combined. The are presented in Table 3. It can be noted that the ampli- mean and standard deviation of latencies of P1, N1, P2, tude of Poor Performers was lower than that of Good Per- N2 in individuals with normal hearing and those with formers. Results of Kruskal Wallis test revealed that there auditory neuropathy are presented in Table 2. From the is a significant effect of group on the amplitude (p < 0.01) table it can be noted that the latencies in subjects with of N1/P2 peak. Mann-Whitney test was performed to auditory neuropathy were delayed by 20 – 50 ms for P1, assess the paired comparison between the groups. Results 40–80 ms for N1 and 30–80 ms for P2 when compared to revealed that the mean amplitude of Poor Performers was individuals with normal hearing. significantly lower than that of Good Performers (p < 0.01) and normal hearing subjects (p < 0.01). However, Independent sample "t"test was performed independently mean amplitude of Good Performers was not significantly for latency of cortical potentials (P1, N1, P2 and N2) and different from that of normal hearing subjects (p > 0.01). amplitude (N1/P2). Results revealed a statistically signifi- cant difference between the latencies of P1, N1, and P2 Kruskal Wallis test performed to study the effect of group peaks in individuals with normal hearing and those with on the latency of cortical potentials revealed that there was a significant effect of group on the latency (p < 0.01) for all the components except for N2. Mann-Whitney test was performed to assess the paired comparison between the groups. Results revealed that both in Good Performers and Poor Performers, the mean latency for all the peaks except N2 differed significantly from that of normal hear- ing subjects but there was no significant difference for latency for all the peaks between Good Performers and Poor Performers (p < 0.01). Pearson product-moment correlation was carried out to study the correlation of the peak latency of P1, N1, P2, N2 and the amplitude of N1/P2 with the behavioral thresh- olds (pure-tone average) and speech identification scores. It can be observed from Table 4 that the latency of cortical potentials did not show a significant correlation with the pure tone average or with speech identification scores. However, the amplitude of N1/P2 showed a significant Relationship tion scores of individuals Figure 2 between the pure-to with auditory neuropathy ne threshold and identifica- correlation with speech identification scores. Relation Relationship between the pure-tone threshold and between N1/P2 amplitude and speech identification identification scores of individuals with auditory neu- ropathy. scores is depicted in the scatter plot along with regression curve in Figure 3. Page 4 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 Table 2: Mean, SD, and "t" value of latencies and amplitude cortical potentials in individuals with normal hearing and auditory neuropathy Participants Latencies (m sec) Amplitude N1/P2 (μV) P1 N1 P2 N2 AN 76 (20) 124(31) 185(43) 243(50) 4.4(2.4) Normal 50 (8.1) 85(9) 142(12) 218(13) 6.2(1.3) "t" Value 4.1* 2.8* 3.05* 1.6 - 0.82 "p" Value 0.001 0.001 0.001 0.057 0.05 * Significant at p < 0.01 Inspection of individuals data revealed that two partici- in individuals with auditory neuropathy. Other factors pants had normal latencies with reduced amplitudes and impair the speech understanding capability in these indi- their speech identification scores were poor (AN4, AN6), viduals. whereas two participants who had normal latencies with good amplitude (AN2 and AN7) had better speech identi- One of the possible contributors for their poor speech fication scores. Five subjects who had prolonged latencies identification score is disrupted neural synchrony, which with normal amplitude also showed good speech identifi- impairs the listener's ability to processes the dynamic cation scores. Figure 4 shows the waveforms of individu- nature of speech signals. It has been reported that dis- als with auditory neuropathy and those with normal rupted neural synchrony impairs the ability to use enve- hearing. lope cues in speech and also impair the ability to perceive rapid change of spectral shapes in the speech stimuli [2,4,14]. Discussion Speech identification in individuals with auditory neuropathy Cortical potentials in individuals with auditory neuropathy In the present study, speech identification scores in indi- Latencies of cortical potentials in individuals with audi- viduals with auditory neuropathy were significantly lower tory neuropathy were significantly prolonged when com- than that observed for participants with normal hearing. pared to normal hearing listeners. Though not statistically Further, the correlation analysis revealed that speech iden- significant, the mean amplitude of the cortical potentials tification scores for individuals with auditory neuropathy was lower than that observed in participants with normal were disproportionate to their pure-tone threshold. This is hearing and the variability was high in individuals with best illustrated by comparing the speech identification auditory neuropathy. Latencies and amplitude variations scores in individuals with auditory neuropathy to those in individuals with auditory neuropathy may not be due expected by degree of hearing loss for patients with coch- to increased pure-tone threshold, as there was no correla- lear hearing loss [12]. In the present study, in 72% of indi- tion between pure-tone thresholds and cortical potentials viduals, the speech identification scores were lower when (latency and amplitude), suggesting that the latency and compared to those reported by Vanaja and Jayaram [12] amplitude of cortical potentials were not affected by the for ears with sensorineural hearing loss. Sininger and Oba hearing thresholds of the participants in the present study. [3] observed that speech identification scores for 69% of Oates, Kurtzberg, and Satpells [15] reported that the laten- their patients with auditory neuropathy were lower than cies and amplitude of P1/N1/P2 were not significantly that reported for patients with cochlear pathology by Yel- affected in subjects with cochlear hearing loss of less than lin et al. [13]. These results suggest that speech identifica- moderate degree. Cortical potentials were absent in AN3 tion scores do not depend upon the pure-tone thresholds who had pure-tone threshold of 30 dB HL whereas it was Table 3: Mean and SD of latencies and amplitude cortical potentials for the two groups of auditory neuropathy and individuals with normal hearing Participants Latency (msec) Amplitude P1 N1 P2 N2 N1/P2 (μV) Normal 50 (8.1) 85(9) 142(12) 218(13) 6.2(1.3) Good Performers 84(16.8) 133(30.8) 186(53.8) 227(26.2) 6.0(1.5) Poor Performers 78(20.2) 125(27.6) 184(27.4) 231(18.2) 2.6(1.3) Page 5 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 literature [5,8,17]. No clear-cut explanation can be pro- vided for the variability observed in latencies of cortical potentials. The variability in latencies observed across individuals with auditory neuropathy in the present study may have been related to the underlining patho-physiol- ogy. That is prolonged latencies may be due to the dys- synchronous firing [18-20,14] whereas normal latencies may be due to the reduced numbers of fibers [1,14]. The magnitude of reduction in amplitude in either of patho- physiology depends upon the severity of the condition [14,21]. Further investigation correlating cortical poten- tials with neurological findings need to be carried out to confirm this. Relation between speech identification scores and cortical potentials In the present study individuals who had cortical poten- Scatter plot tud r Figure 3 opa e of thy cortical pote between speech identification ntials in individuals wi scores and ampli- th auditory neu- Scatter plot between speech identification scores tials with better amplitude had better speech identifica- and amplitude of cortical potentials in individuals tion scores than those with absent/abnormal amplitude with auditory neuropathy. in cortical potentials. Participant AN3 in the present study had absent cortical potentials and very poor speech iden- tification scores. Similar results have been reported by ear- lier investigators [7,5,17]. These results suggest that it is present in AN 4 whose pure-tone average of 48 dB HL. possible to have good speech perception in quiet if the This further, supports the notion that cortical potentials cortical responses are present even if the brainstem did not depend upon the pure-tone average in the present responses are abnormal. Good synchronization at the study. auditory nerve and brainstem level does not appear to be essential for understanding speech in quiet situations [6]. Cortical potentials mature and attain adult latency and Results of physiological studies indicate that brainstem morphology by the age of 9 years and there will not be any neurons process the fast modulations of the complex sig- significant changes in latency until age of 50 yr [16]. As nals, whereas auditory cortex processes the slowly varying the age range of the participants in the present study var- the amplitude modulations of the complex signal [22], ied from 12 to 39 yr, the latency variations observed may which plays an important role in auditory communica- not be due to maturational changes. It was hypothesized tion [23]. that probably the severity of the neural dys-synchrony rather than the hearing loss contributed for the variability There was also a high positive correlation between speech in the cortical evoked responses observed in the present identification and the amplitude of N1/P2. That is, indi- study. viduals with better speech identification scores showed greater N1/P2 amplitude than those with poorer speech An interesting observation in the present study was that, identification scores. However, no correlation was some of individuals with auditory neuropathy had abnor- observed between latencies of cortical potentials and mal latencies with normal amplitude, whereas some had speech identification scores. Similar findings were normal latencies with abnormal amplitude in cortical observed in adults [8] and children[7] with auditory neu- potentials. Similar results have also been reported in the ropathy using hearing aids. They reported that the cortical Table 4: Correlation coefficients (r) of behavioral thresholds with cortical potentials and word recognition scores with cortical potentials "r" value Latency (ms) N1/P2 P1 N1 P2 N2 amplitude (μV) Behavioral Threshold -0.46 -0.25 -0.2 -0.3 -0.16 Speech Identification score 0.45 0.52 0.3 -0.1 0.86* * Significant at p < 0.05 Page 6 of 8 (page number not for citation purposes) Behavioral and Brain Functions 2008, 4:15 http://www.behavioralandbrainfunctions.com/content/4/1/15 als with auditory neuropathy, the procedure can be used to obtain important information regarding severity and management options for these participants. Authors' contributions VKN was involved in designing the study, data collection, analysis, interpretation of results and preparing the man- uscript. CSV was involved in designing the study, analysis interpretation of results, and preparing the manuscript. Acknowledgements We thank Dr. Vijayalakshmi Bsasavaraj, Director, All India Institute of Speech and Hearing, for permitting us to conduct the study. We express our sincere thanks to all the participants for their patient cooperation. References 1. Starr A, Michalewski HJ, Zeng FG, FujiKawa-Brooks S, Lithicum F, Kim CS, Winner D, Keats B: Pathology and physiology of AN with novel mutation in the MPZ gene (tyr145->ser). Brain 2003, 126:1604-1619. 2. Zeng FG, Kong YY, Michalewski HJ, Starr A: Perceptual conse- quences of disrupted auditory nerve activity. J Neurohysiol 2005, 93(6):3050-3063. 3. Sininger Y, Oba S: Patients with AN: who are they and what can they hear? In A new perspective on hearing disorders Edited by: Sinin- ger Y, Starr A. Sandigo: Singular-Thomson learning; 2001:15-35. 4. Zeng FG, Oba S, Grade S, Sininger Y, Starr A: Temporal and speech processing deficits in AN. 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Giraud AL, Lorenzi C, Ashburner J, Wable J, Johnsrude I, Frackowiak R, Kleinschmidt R: Representation of the Temporal Envelope of Sounds in the Human Brain. J Neurophysiol 2000, 84:1588-1598. 23. Drullman R, Festen JM, Plomp R: Effect of temporal envelope smearing on speech reception. J Acoust Soc Am 1994, 95:1053-1064. Publish with Bio Med Central and every scientist can read your work free of charge "BioMed Central will be the most significant development for disseminating the results of biomedical researc h in our lifetime." Sir Paul Nurse, Cancer Research UK Your research papers will be: available free of charge to the entire biomedical community peer reviewed and published immediately upon acceptance cited in PubMed and archived on PubMed Central yours — you keep the copyright BioMedcentral Submit your manuscript here: http://www.biomedcentral.com/info/publishing_adv.asp Page 8 of 8 (page number not for citation purposes)

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