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Poster C47, Friday, August 17, 10:30 am – 12:15 pm, Room 2000AB

Atypical neural responses associated with inaccurate speech production in children with speech sound disorders

Alycia Cummings1, Ying Wu2;1Idaho State University - Meridian, 2University of California San Diego

Introduction. It is presently unknown what underlying mechanisms might account for the problems that children with speech sound disorders (SSD) encounter during speech production. One possible explanation is that they have poorly specified phonological representations, which are the result of inaccurate speech sound perception. In this view, SSD treatment aimed at improving sound production might lead to changes in neurocognitive processing associated with sound perception as well, including enhanced sensitivity post-treatment to the phonological properties of treatment sounds. To explore this prediction, the present study analyzed modulations in electroencephalographic (EEG) power and event-related potentials (ERP) elicited by auditory presentation of syllables in children with SSD prior to, and after completion of, a speech treatment program. Syllables contained phonemes that the children could (/b d/) and could not (/ɹ l ʧ ɵ s k/) say, one of which was each child’s treated phoneme. EEG and ERP responses to the ba syllable and treated sound syllables were compared pre- and post-treatment. It was expected that speech treatment would lead to changes in patterns of brain response associated with cognitive effort and acoustic feature encoding in conjunction with post-treatment speech production improvements. Methods. Participants. Twenty children with speech sound disorders (SSD) (7 male; 3.83-6.58 years). Stimuli and Procedure. Two oddball stimulus sets, each containing four consonant-vowel (CV) syllables: one standard (ba/treated sound) and three deviants (ba/treated sound, da, one other CV) were presented. Sixty-six channels of continuous EEG were recorded at a sampling rate of 256 Hz. EEG Analyses. Source level contributions to channel EEG were decomposed using Adaptive Mixed Model Independent Component (AMICA) Analysis in EEGLAB. IC scalp topographies were clustered on the basis of dipole locations. Event-related spectral perturbations (ERSPs) were computed from activations of each IC in each cluster. ERSP theta band power (3-6 Hz) analyses focused on IC clusters localized approximately to right and left IFG. ERP P2 Amplitude Analyses. Nine electrodes were divided into three groups: (1) Left: F5, FC5, C5; (2) Central: Fz, FCz, Cz; and (3) Right: F6, FC6, C6. The P2 was measured from 100-200 ms. Results. ERSP Theta Band Power. Post-treatment, theta band oscillations to the treated sound decreased in ICs localized in and near the right IFG (F(1,8) = 8.133, p = 0.021, partial eta2 = .504). ERP P2 Amplitude. The P2 elicited by treated sounds decreased in amplitude from pre-to-post treatment while the P2 elicited by /b/ increased (F(1,19) = 4.767, p = 0.042, partial eta2 = .201). Discussion. In response to treated sounds prior to treatment, children with SSD exhibited greater theta responses in areas of cortex associated with the right IFG, suggesting that sounds the children could not say required more cognitive processing effort; theta activity decreased post-treatment. Decreased post-treatment P2 amplitudes indicated that more specified neuronal populations responded to acoustic features of treated sounds. Thus, one potential neural deficit in SSD could be impaired right hemisphere theta oscillatory networks, which could impact the integration of acoustic features that allow for accurate phoneme perception and phonological development (Goswami, 2011).

Topic Area: Language Disorders