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Altered processing of communication signals in the subcortical auditory sensory pathway in autism

Poster D59 in Poster Session D with Social Hour, Friday, October 7, 5:30 - 7:15 pm EDT, Millennium Hall

Stefanie Schelinski1,2, Alejandro Tabas1,2, Katharina von Kriegstein1,2; 1Technische Universität Dresden, 2Max Planck Institute for Human Cognitive and Brain Sciences

Human communication requires the fast and accurate processing of sensory signals, such as the voice. Traditionally, it is assumed that the cerebral cortex and limbic structures are specialised in processing speech, vocal identity, and emotional components of the sensory signal. Much less is known about the role of subcortical sensory pathway structures for communication and its impairments. For example, it is to-date unclear at which processing stage voice processing difficulties arise in autism. Here, we assessed the functional integrity of auditory pathway nuclei for processing voices in autism. We tested functioning of the auditory midbrain (inferior colliculus; IC) and thalamus (medial geniculate body; MGB) in three independent functional magnetic resonance imaging (fMRI) experiments in groups of adults with autism and pair-wise matched typically developed controls (matched on age, sex, handedness, and full-scale intelligence quotient (IQ)). We focused on two aspects of voice processing that are impaired in autism: voice identity perception, and recognising speech-in-noise. First, participants performed tasks on speaker identity and speech recognition (voice identity recognition experiment, n = 16 per group). Second, both groups passively listened to blocks of vocal and non-vocal sounds (vocal sound experiment, n = 16 per group). In the third experiment participants performed speech recognition tasks on speech that was either presented with or without noise (speech-in-noise recognition experiment, n = 17 per group). All participants had normal hearing (confirmed with pure tone audiometry) and did not take psychotropic medication. All participants in the autism group had previously received a formal clinical diagnosis and underwent additional clinical assessment including the ADOS and ADI-R. For the fMRI analysis we used a general linear model implemented in SPM12. We focused on four regions of interest (left and right IC and left and right MGB). We found reduced blood-oxygenation-level-dependent (BOLD) responses for the autism as compared to the typically developed control groups in the IC – the central midbrain structure of the auditory pathway (p < .0125 family wise error (FWE) corrected, and Bonferroni corrected for four ROIs). The right IC responded less in the autism as compared to the control group for voice identity, in contrast to speech recognition. The right IC also responded less in the autism as compared to the control group when passively listening to vocal in contrast to non-vocal sounds. Within the control group, the left and right IC responded more when recognising speech-in-noise as compared to when recognising speech without additional noise. In the autism group, this was only the case in the left, but not the right IC. The autism and the control group did not differ significantly in the average amount of head movements (all p values > 0.1 in all three experiments). Our results show that communication signal processing in autism is associated with reduced subcortical sensory functioning in the midbrain. The results highlight the importance of considering sensory processing alterations in explaining communication difficulties, which are at the core of autism.

Topic Areas: Disorders: Developmental, Speech Perception

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