Mismatch Negativity in children with Phonological Disorders

Introduction Mismatch negativity (MMN) represents a negative component of event-related potentials, which is mentioned by guidelines as an important tool to provide measurable data regarding the functionality of the auditory system in acoustic processing. However, the literature still lacks reliable data that can support the clinical use of this potential in the complementary diagnosis of central auditory processing (CAP) disorder (CAPD).Objectives To analyze whether MMN assessment might be associated with the CAP behavioral test battery, as well as to assess the effects of auditory ability deficits on MMN responses in the pediatric population.Methods In total, 45 age-matched children participated in the study. They were submitted to the CAP behavior assessment and to MMN. The children were tested with a combination of speech contrast consisting of acoustic syllables [da] versus [ta], governed by the oddball paradigm.Results Mismatch negativity did not show a direct association with a single test but with the combination of the four tests used as a behavioral test battery to identify CAPD. The results also indicated that the auditory ability deficits influenced the measurement of MMN latency (p = 0.003*), but not the amplitude (p = 0.857) or the area (p = 0.577).Conclusion Mismatch negativity was shown to be statistically associated with the battery of tests used to identify deficits in auditory abilities in the studied sample rather than with a single behavioral test. The deficits in auditory abilities were observed in the MMN latency. Mismatch negativity can be used to assess children with CAPD.

<p class="abstract"><strong>Background:</strong> Cochlear implant provides a great opportunity for children with severe to profound sensorineural hearing loss to restore normal hearing. Identifying mismatch negativity (MMN) in cochlear implant recipients helps to assess the role of central auditory structures in processing speech stimuli in those patients. The objective of the present study is to evaluate tone and speech discrimination in cochlear implanted children using mismatch negativity test.</p><p class="abstract"><strong>Methods:</strong> MMN was recorded in 35 children. They were divided into two groups. Control group consisted of 15 normal hearing children, their age ranged from 3-11 years. Study group consisted of 20 children fitted with unilateral CI, and their age matched the control group. Two oddball paradigms were used; the first was tone bursts (1000 Hz as standard stimulus and 1050 Hz as deviant stimulus). The second was synthesized speech stimuli (/da/ as standard stimulus and /ga/ as deviant one). Both paradigms were presented at 75dB SPL.</p><p class="abstract"><strong>Results:</strong> All cochlear implanted children included showed MMN on using both oddball paradigms. Comparing results of both groups revealed statistically significant differences in MMN latency and amplitude. There was a significant positive correlation between MMN latencies and the implantation age as well as the duration of hearing loss before implantation.</p><p><strong>Conclusions:</strong> MMN provides an objective tool to assess the auditory discrimination abilities in cochlear implanted children which may help in their rehabilitation and also in the optimum setting of their devices.</p>

This study examined how discriminability and prototypicality of nonnative phones modulate the amplitude of the Mismatch Negativity (MMN) event-related brain potential. We hypothesized that if a frequently occurring (standard) stimulus is not prototypical to a listener, a weaker predictive memory trace will be formed and a smaller MMN will be generated for a phonetic deviant, regardless of the discriminability between the standard and deviant stimuli. The MMN amplitudes of Japanese speakers hearing the English vowels /æ/ and /ɑ/ as standard stimuli and /ʌ/ as a deviant stimulus in an oddball paradigm were measured. Although the English /æ/-/ʌ/ contrast was more discriminable than the English /ɑ/-/ʌ/ contrast for Japanese speakers, when Japanese speakers heard the /æ/ standard stimulus (i.e., less prototypical as Japanese /a/) and the /ʌ/ deviant stimulus, their MMN amplitude was smaller than the one elicited when they heard /ɑ/ as a standard stimulus (i.e., more prototypical as Japanese /a/) and /ʌ/ as a deviant stimulus. The prototypicality of the standard stimuli in listeners’ phonological representations modulates the MMN amplitude more robustly than does the discriminability between standard and deviant stimuli.

Auditory event related potentials in children with peripheral hearing loss

An auditory oddball paradigm in humans generates a long-duration cortical negative potential, often referred to as mismatch negativity. Similar negativity has been documented in monkeys and cats, but it is controversial whether mismatch negativity also exists in awake rodents. To this end, we recorded cortical and hippocampal evoked responses in rats during alert immobility under a typical passive oddball paradigm that yields mismatch negativity in humans. The standard stimulus was a 9 kHz tone and the deviant either 7 or 11 kHz tone in the first condition. We found no evidence of a sustained potential shift when comparing evoked responses to standard and deviant stimuli. Instead, we found repetition-induced attenuation of the P60 component of the combined evoked response in the cortex, but not in the hippocampus. The attenuation extended over three days of recording and disappeared after 20 intervening days of rest. Reversal of the standard and deviant tones resulted is a robust enhancement of the N40 component not only in the cortex but also in the hippocampus. Responses to standard and deviant stimuli were affected similarly. Finally, we tested the effect of scopolamine in this paradigm. Scopolamine attenuated cortical N40 and P60 as well as hippocampal P60 components, but had no specific effect on the deviant response. We conclude that in an oddball paradigm the rat demonstrates repetition-induced attenuation of mid-latency responses, which resembles attenuation of the N1-component of human auditory evoked potential, but no mismatch negativity.

Language impairments can have a devastating effect on the individual’s life. Brain damage such as stroke may cause varying degrees of impaired language. Even milder language problems, such as developmental dyslexia or specific language impairment, can have long-lasting detrimental effects on the individual’s life, affecting both success at school as well as motivation and even self-esteem. In recent years, the mismatch negativity (MMN) has been intensively applied to study the neural basis of language impairments. These studies have shown that the MMN, which reflects the early stages of cortical sound discrimination, is abnormal in a large variety of language impairments. Furthermore, a close relationship between the MMN and some language disorders is suggested by significant correlations between the MMN and language test results. Further support is provided by follow-up studies suggesting that the MMN parameters may predict future language problems in children and by investigations indicating that intervention programs with an ameliorating effect also concurrently change the MMN. However, when interpreting the implications of MMN results it is important to acknowledge that this response specifically reflects early stages of auditory discrimination and should, therefore, be combined with measures probing the further steps of auditory processing for a more complete picture of the underlying deficits of language. The current review addresses how the MMN can be used in determining auditory impairments in language disorders such as aphasia, dyslexia, autism spectrum, and specific language impairment.

Mismatch negativity to slight pitch changes outside strong attentional focus

Setting standards: Auditory MMN and P3a habituate differentially in a two-syllable oddball task.

You have accessThe ASHA LeaderFeature1 Apr 2011Auditory Remediation for Patients With Landau-Kleffner Syndrome Annette HurleyPhD, CCC-A Annette Hurley Google Scholar More articles by this author , PhD, CCC-A https://doi.org/10.1044/leader.FTR5.16042011.5 SectionsAbout ToolsAdd to favorites ShareFacebookTwitterLinked In http://www.asha.org/Publications/leader/2011/110405/Auditory-Remediation-for-Patients-With-Landau-Kleffner-Syndrome.htm Landau-Kleffner syndrome (LKS) is a rare neurological disorder that affects children and is characterized by aphasia that can develop suddenly or over a period of time. Often the deterioration in language is rapid, but it also may decline over several months (Miller et al, 1984). Although there is a body of evidence to support medical treatment for LKS, there is limited information about the clinical management for the language disorder or acquired (central) auditory processing disorder [(C)APD]. The prognosis of a child with LKS is unpredictable due to variability in the time and amount of recovery and the severity of the disorder. Speech-language pathologists are often challenged with the task of maximizing language recovery. Treatment techniques have relied on visual aids such as graphic symbols and visual language systems, as well as cued speech (for a review of language treatment options, see Alpern, 2010). Thomas Gibson listens to dichotic sentences during his treatment session with SLP Kristen Beckner. It also is important for clinicians to recognize auditory processing deficits associated with the acquired (C)APD that results from LKS and to offer a deficit-specific remediation plan to improve the patient’s auditory processing ability. Previous reports of auditory processing deficits in LKS patients have cited difficulty listening in background noise or other degraded environments, challenges with auditory discrimination, and problems with dichotic listening tasks (Bamiou, Musiek, & Luxon, 2001). An assistive listening device such as an FM system may be useful to improve the signal-to-noise ratio. Speech-in-noise training may also improve the patient’s listening ability. Dichotic listening treatment is one type of direct remediation for (C)APD that takes advantage of the brain’s lifelong capacity for plasticity and adaptive reorganization (Musiek, Chermak, & Weihing, 2007). LKS patients have an abnormal electroencephalogram (EEG) typified by abnormal spike activity in the temporal and/or parietal regions (Deonna, Beaumanoir, Gaillard, & Assal, 1991). The abnormal EEG activity occurs predominantly in the left temporal lobe, but may be present in both temporal lobes (Deonna et al., 1991). From anatomical and physiologic dichotic listening modeling, it is reasonable that the only way to isolate the damaged auditory pathway is to force this auditory pathway to work by direct auditory stimulation—dichotic listening. In normal listening conditions, auditory information is conducted to the auditory cortex by both ipsilateral and contralateral auditory pathways; however, during controlled dichotic listening, the ipsilateral pathway is suppressed by the dominant contralateral pathway. This dominant contralateral model was first proposed by Kimura (1961), whose data led her to hypothesize that the contralateral pathway must have greater neuronal innervation that enables it to be dominant over the ipsilateral pathway. Early work in the 19th century noted that most aphasia is the result of lesions in the left cerebral hemisphere, leading to the conclusion that most people are left-hemisphere-dominant for expressive and receptive language. Further, a language-related auditory signal presented to the right ear travels from the dominant contralateral right auditory pathway directly to the left hemisphere. Conversely, a language-related auditory signal directed to the left ear is conducted to the right cortex, but must be transferred to the left hemisphere via corpus callosum in order for the person to repeat what was heard in the left ear. Thus, it is not surprising that there is a slight right-ear advantage for neurologically normal listeners when listening to dichotic tasks (Kimura, 1961; Lowe, Cullen, Berlin, Thompson, & Willett, 1970; Berlin, Lowe-Bell, Cullen & Thompson, 1973). When there is damage or a lesion in the auditory temporal lobe, the ear contralateral to the lesion will be affected in dichotic listening tasks, as the contralateral pathway is the dominant pathway. Because lesions often are found in the left temporal lobe in LKS patients, a right-ear deficit on dichotic testing is expected. Dichotic listening training is an innovative treatment for the remediation of the compromised central auditory pathway (Musiek et al., 2007). Dichotic interaural intensity difference (DIID) training uses dichotic listening tasks in which the signal intensity presented to the unimpaired pathway is first decreased and then slowly increased over time as the weaker, impaired pathway grows stronger. DIID training purports to target the deficit ear specifically, thus activating brain regions that receive auditory sensory input on the side of the lesion. Previous investigations have shown behavioral and electrophysiological evidence of improvement of the central auditory nervous system after DIID training (Musiek, Baran, & Shinn, 2004; Hurley & Billiet, 2007; for a complete review of the DIID procedure, see Musiek et al., 2007). Improvement after auditory rehabilitative dichotic listening in dichotic scores and language scores also were shown in a group of children with language disorders. Until recently, dichotic listening programs could be completed only in a controlled laboratory environment; now dichotic stimuli are available on compact discs. Dichotic exercises directly stimulate areas of the cortex, which in turn forces the auditory pathways to these areas to exercise and recruit existing neuronal connections or build new neural connections and pathways. As the integrity of these areas pathways is improved, speech stimuli can reach the language processing temporal lobe more efficiently, resulting in improvement of dichotic skills. Dichotic Training: Case Studies Two patients participated in dichotic listening training. “Michael” participated in dichotic listening therapy for two clinic semesters. “Thomas” lives in another state and participated in dichotic listening therapy with his speech-language pathologist. In dichotic training, stimuli are presented at different interaural intensities with a higher intensity directed to the poorer (dichotic scoring) and lower intensity directed to better (dichotic scoring) ear. Initial presentation level is at a comfortable level to the poorer scoring ear, and a soft level to the better (dichotic scoring) ear. When the individual’s target ear’s score reaches >70%, the intensity level delivered to the poorer ear is increased by 1, 2, or 5 dB. This continues until there are equal intensities presented to both ears. Because of the limited amount of dichotic listening materials, available, new recordings of digits, words, sentences, CVs and short stories were created and used in the training sessions. Case One: Michael Michael was the product of a normal pregnancy and birth. All developmental milestones were developing appropriately until the age of three. At that time, Michael’s speech and language skills began to decline. Initially, this decline in speech and language was attributed to sibling jealousy as this decline coincided with the birth of a younger sibling. Michael was sent for a hearing evaluation which established normal peripheral hearing. As Michael had a history of otitis media, the lack of progression in speech and language was next related to his history of ear infections. Subsequently, autism and pervasive developmental disorder were also erroneously diagnosed. With the onset of seizure activity at the age of three and a half years, the diagnosis of LKS was made after a characteristic spiking EEG. Nocturnal seizure activity continued until Michael was eleven years old, even though anticonvulsants were prescribed. At age 11, Michael had his first normal EEG. Our involvement with Michael began when he was 12.5 years old, as he was a subject in a study examining pre and post behavioral and electrophysiological measures after Fast ForWord® training, provided by Michael’s local school system. Approximately four weeks after Michael completed the Fast ForWord® program, Dichotic listening therapy began weekly for a total of twenty one hour dichotic listening training sessions. Post-testing showed improvement in dichotic scores after dichotic listening training, as well as improvements in electrophysiologic responses (auditory late response). In addition, unsolicited parental reports were positive. Extended family member, as well as Michael’s teachers, commented that his speech was improving and that he was speaking in complete sentences and thoughts, rather than in a telegraphic-type speech. They also reported that he rarely used signs. This cannot be validated, as we did not measure pre and post mean length utterance. Case Two: Thomas Thomas was the product of a normal pregnancy and birth history was normal. Gross motor development milestones were achieved at appropriate times. At age 3, Thomas had a speech-language evaluation to address articulation concerns. This assessment yielded normal results. Sleep concerns were noted as early as age 3 ½; at age 5 ½, a tonsillectomy/ adenoidectomy was performed for sleep apnea. Early behavioral, attention, language and hearing were first noted when Thomas was in pre-school. A speech-language assessment at that time (age 6.25) indicated a severe receptive language delay. Language regression and concerns continued over the next few years. Thomas had an abnormal EEG at age 8 years, 2 months indicated bilateral abnormalities, but left temporal lobe activity greater on the left side. Approximately six months later, an EEG indicated abnormalities on the right side, as well. Thomas is currently managed medically for his abnormal nocturnal EEG. In July, 2009, Thomas was formally diagnosed with Landau-Kleffner Syndrome (LKS). Thomas began dichotic listening in October, 2009. He was seen at the LSU Health Sciences Center in July, 2010. Because of the geographical distance, Thomas has been working with his speech language pathologist on dichotic listening via recorded compact discs. Training began 20 minutes, twice per week, and is now listening weekly. Although we do not have comprehensive pre and post (C)APD test results, we have dichotic test scores from an assessment in July, 2009. Scores previously abnormal are now within normal limits. Reference Alpern C. A. (2010). Identification and Treatment of Landau-Kleffner Syndrome. ASHA Leader, September 21, 34–35. Google Scholar Bamiou D. E., Musiek F. M., & Luxon L. M. (2001). Aetiology and clinical presentations of auditory processing disorders—a review.Archives of Disease in Children, 85, 361–365. Google Scholar Berlin C. I., Lowe-Bell S. S., Culen J. K., & Thompson C. L. (1973). Dichotic speech perception: an interpretation of right-ear advantage and temporal offset effects.Journal of the Acoustical Society of America, 53, 699–709. Google Scholar Berlin C. I., Lowe-Bell S. S., Jannetta P. J., & Kline D. G. (1972). Central auditory deficits after temporal lobectomy.Archives of Otolaryngology, 96, 4–10. Google Scholar Deonna T., Beaumanoir A., Gaillard F., Assal G. (1977). Acquired aphasia in childhood with seizure disorder: a heterogeneous syndrome.Neuropadiatrie, 8, 263–273. Google Scholar Hurley A., & Billiet C. (2009). Dichotic interaural intensity difference (DIID) training; auditory remediation after CVA.Poster Presentation at the annual ASHA Convention, Chicago, IL. Google Scholar Kimura D. (1961). Cerebral dominance and the perception of verbal stimuli.Canadian Journal of Psychology, 15, 166–171. CrossrefGoogle Scholar Lowe S. S., Cullen J. K., Berlin C. I., Thompson C. L., & Willett M. E. (1970). Perception of simultaneous dichotic and monotic monosyllables.Journal of Speech and Hearing Research, 13, 812–822. LinkGoogle Scholar Miller J. F., Campbell T. F., Chapman R. S., & Weismer S. E. (1984). Language behavior in acquired childhood aphasia.In Holland A. (Ed.), Language disorders in childhood: Recent advances (pp. 57–99). San Diego: College Hill Press. Google Scholar Musiek F. E., Chermak G., & Weihing J. (2007). Auditory training.In In. Musiek F.E. and Chermak G. D. (Eds.), Handbook of (Central) Auditory Processing Disorder: Comprehensive Intervention, (Vol II, pp. 77-106). San Diego: Plural Publishing, 2007. Google Scholar Musiek F. E., Baran J. A., & Shinn J. (2004). Assessment and remediation of an auditory processing disorder associated with head trauma.Journal of the American Academy of Audiology, 15, 117–132. CrossrefGoogle Scholar Author Notes is an assistant professor in the Department of Communication Sciences at Louisiana State University Health Sciences Center in New Orleans, La. Contact her at [email protected]. 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There is a history of debate and controversy about the assessment and intervention of children diagnosed with auditory processing disorder (APD). Professionals in communication sciences and disorders view APD from different perspectives. Speech-language pathologists (SLPs) tend to view APD from the language and literacy perspective, or a top-down model, whereas audiologists tend to view APD from an auditory perception perspective, or a bottom-up model. Professionals who assess and treat children with APD need to bridge the gap and merge their different perspectives to plan effective intervention for children with APD. A panel of audiologists who demonstrated expertise in the area of Central Auditory Processing Disorders (CAPDs) developed The American Speech-Language-Hearing Association's (ASHA's) technical report on APDs (ASHA, 2005). This report was approved by ASHA's Executive board in 2005. In this report, central auditory processing refers to the efficiency and effectiveness by which the central nervous system uses auditory information. Central auditory processing includes the auditory mechanisms underlying the skills of sound localization and lateralization; auditory discrimination; auditory pattern recognition; temporal aspects of audition, including temporal integration, temporal discrimination, temporal ordering, and temporal masking; auditory performance in competing acoustic signals; and auditory performance with degraded acoustic signals (ASHA, 1996; Bellis, 2003; Chermak & Musiek, 1997; Jerger, 2009). A CAPD is a deficit in processing auditory input that is not due to higher-order language, cognitive, or related factors (Musiek, Bellis, & Chermak, 2005; Musiek & Chermak, 2007). However, children diagnosed with CAPD may experience difficulties in academic learning, speech, language, social skills, and literacy (e.g., encoding, decoding, reading comprehension, reading fluency, and written language).

Mismatch negativity to change in spatial location of an auditory stimulus

A mismatch negativity event-related potential protocol was administered to dyslexic children and their respective controls to test whether a specific auditory deficit concerning phonetic processing or a lower level auditory processing deficit was present in developmental dyslexia. Three different contrast conditions were explored, including nonphonological sounds, contrasted in pitch and duration, and phonemes. Mismatch negativity amplitudes differed significantly between groups in the duration condition, whereas no differences were found in the frequency and phoneme conditions. Moreover, the dyslexic children had delayed mismatch negativity latencies in the three contrast conditions. Our results suggest a deficit in low-level auditory discrimination in dyslexic children, in particular when detecting stimulus duration, and support the rapid auditory processing theory of dyslexia.

This study investigated the magnetic mismatch field elicited by changes in streams of vowels or spectrally matched tones in children with autism spectrum disorder (ASD) relative to children with typical development to explore whether impaired sound discrimination may contribute to language impairments in autism spectrum disorder. Using magnetoencephalography, we recorded evoked neural activity to 300-Hz and 700-Hz tones (and /u/ and /a/ vowels) presented in an oddball paradigm with deviant stimuli (15%) occurring within a train of standards (85%). The magnetic mismatch field was robustly observed in both groups, but children with autism spectrum disorder demonstrated a significantly delayed magnetic mismatch field compared with typically developing peers. Difficulty parsing transient differences in sounds may lead to impaired acoustic or phonological representations and subsequent language impairment in autism spectrum disorder.

BackgroundMany young people with autism spectrum disorder (ASD) experience emotional and behavioural problems. However, the causes of these co-occurring difficulties are not well understood. Perceptual processing atypicalities are also often reported in individuals with ASD, but how these relate to co-occurring emotional and behavioural problems remains unclear, and few studies have used objective measurement of perceptual processing.MethodsEvent-related potentials (ERPs) were recorded in response to both standard and deviant stimuli (which varied in pitch) in an auditory oddball paradigm in adolescents (mean age of 13.56 years, SD = 1.12, range = 11.40–15.70) with ASD (n = 43) with a wide range of IQ (mean IQ of 84.14, SD = 24.24, range 27–129). Response to deviant as compared to standard stimuli (as indexed by the mismatch negativity (MMN)) and response to repeated presentations of standard stimuli (habituation) were measured. Multivariate regression tested the association between neural indices of perceptual processing and co-occurring emotional and behavioural problems.ResultsGreater sensitivity to changes in pitch in incoming auditory information (discrimination), as indexed by increased MMN amplitude, was associated with higher levels of parent-rated behaviour problems. MMN amplitude also showed a trend positive correlation with parent-rated sensory hyper-sensitivity. Conversely, greater habituation at the later N2 component was associated with higher levels of emotional problems. Upon more detailed analyses, this appeared to be driven by a selectively greater ERP response to the first (but not the second or third) standard stimuli that followed deviant stimuli. A similar pattern of association was found with other measures of anxiety. All results remained in covariation analyses controlling for age, sex and IQ, although the association between MMN amplitude and behaviour problems became non-significant when controlling for ASD severity.ConclusionsFindings suggest that alterations in mechanisms of perceptual processing and discrimination may be important for understanding co-occurring emotional and behavioural problems in young people with ASD.

Background: Auditory processing and language impairments are prominent in children with autism spectrum disorder (ASD). The present study integrated diffusion MR measures of white-matter microstructure and magnetoencephalography (MEG) measures of cortical dynamics to investigate associations between brain structure and function within auditory and language systems in ASD. Based on previous findings, abnormal structure-function relationships in auditory and language systems in ASD were hypothesized.Methods: Evaluable neuroimaging data was obtained from 44 typically developing (TD) children (mean age 10.4 ± 2.4 years) and 95 children with ASD (mean age 10.2 ± 2.6 years). Diffusion MR tractography was used to delineate and quantitatively assess the auditory radiation and arcuate fasciculus segments of the auditory and language systems. MEG was used to measure (1) superior temporal gyrus auditory evoked M100 latency in response to pure-tone stimuli as an indicator of auditory system conduction velocity, and (2) auditory vowel-contrast mismatch field (MMF) latency as a passive probe of early linguistic processes.Results: Atypical development of white matter and cortical function, along with atypical lateralization, were present in ASD. In both auditory and language systems, white matter integrity and cortical electrophysiology were found to be coupled in typically developing children, with white matter microstructural features contributing significantly to electrophysiological response latencies. However, in ASD, we observed uncoupled structure-function relationships in both auditory and language systems. Regression analyses in ASD indicated that factors other than white-matter microstructure additionally contribute to the latency of neural evoked responses and ultimately behavior. Results also indicated that whereas delayed M100 is a marker for ASD severity, MMF delay is more associated with language impairment.Conclusion: Present findings suggest atypical development of primary auditory as well as auditory language systems in ASD. Findings demonstrate the need for additional multimodal studies to better characterize the different structural features (white matter, gray matter, neurochemical concentration) that contribute to brain activity, both in typical development and in ASD. Finally, the neural latency measures were found to be of clinical significance, with M100 associated with overall ASD severity, and with MMF latency associated with language performance.