Periodic Reporting for period 4 - SENSOCOM (The tiny and the fast: the role of subcortical sensory structures in human communication)
Período documentado: 2020-07-01 hasta 2022-06-30
Communication is one of the most important functions for human social interactions. Yet there are many people who suffer from communication impairments, such as developmental dyslexia and autism spectrum disorders. Current neuroscience research typically associates cognitive functions including communication abilities with the cerebral cortex. However, several lines of research imply that dysfunction in tiny subcortical sensory structures can cause selective deficits in our ability to understand others when they talk to us – a process that is called speech recognition. Clearly, understanding of how the human brain recognises speech will improve our understanding of communication disorders and will enable the development of coping strategies and treatment paradigms. The goal of our project is to (i) investigate the role of subcortical sensory structures in speech recognition and (ii) specify how dysfunction in subcortical-cortical interaction is associated with speech recognition deficits in developmental dyslexia and autism spectrum disorders.
Investigating tiny subcortical sensory nuclei and their substructures in humans in vivo is technically extremely challenging. In the period covered by this report, we have developed ultra-high-resolution neuroimaging paradigms with which we are able to relate sensory subcortical responses to concrete speech recognition behaviour in neurotypical populations as well as people with developmental dyslexia and autism spectrum disorder. In addition we developed a cutting-edge multimodal approach including neurostimulation and computational modelling. Our projects are guided by the hypotheses derived from a novel model of cortico-subcortical interactions. For most projects data acquisition is ongoing or at the analysis stage. The already completed and published projects have produced two key results:
(i) We found that subcortical sensory nuclei (i.e. the sensory thalami) are involved not only when humans recognise auditory speech, but also when they recognise visual speech (i.e. when they understand what is said based on articulatory movements of the face). The amount of responses in the sensory thalami in both the auditory and the visual modality is related to speech recognition abilities. These findings imply that a full understanding of human speech recognition abilities needs to take dynamic corticothalamic interactions into account.
(ii) We found that developmental dyslexia is characterised by a reduction of white matter tracts that connect visual motion areas (V5/MT) to the visual sensory thalamus (lateral geniculate nucleus, LGN), but that white matter tracts between primary visual areas (V1) and LGN are intact. The specificity of the reduction to white matter tracts involved in visual motion processing is an important finding for two reasons: First it is a clear indication that developmental dyslexia is characterised not only by cerebral cortex dysfunction as proposed in most current developmental dyslexia models. Second, it gives first insight into the potential underlying mechanisms of the cortico-subcortical deficit.
(i) We found that subcortical sensory nuclei (i.e. the sensory thalami) are involved not only when humans recognise auditory speech, but also when they recognise visual speech (i.e. when they understand what is said based on articulatory movements of the face). The amount of responses in the sensory thalami in both the auditory and the visual modality is related to speech recognition abilities. These findings imply that a full understanding of human speech recognition abilities needs to take dynamic corticothalamic interactions into account.
(ii) We found that developmental dyslexia is characterised by a reduction of white matter tracts that connect visual motion areas (V5/MT) to the visual sensory thalamus (lateral geniculate nucleus, LGN), but that white matter tracts between primary visual areas (V1) and LGN are intact. The specificity of the reduction to white matter tracts involved in visual motion processing is an important finding for two reasons: First it is a clear indication that developmental dyslexia is characterised not only by cerebral cortex dysfunction as proposed in most current developmental dyslexia models. Second, it gives first insight into the potential underlying mechanisms of the cortico-subcortical deficit.
We have made substantial methodological progress in the localisation of subcortical sensory nuclei subdivisions and are now able to relate their responses to speech recognition behaviour. We expect that these paradigms will close the large gap between human neuroimaging experiments and animal neurophysiology and motivate cross-species experiments in conspecific communication. The novel computational neuroimaging approach for dynamic stimuli that we are currently developing will be a fundamental methodological advance for the field, because it can be used to directly test mechanistic predictions about ecologically valid auditory and visual perception in both neurotypical and clinical populations. Our work will provide a novel and refined model for cortical-subcortical interactions. I expect that these advances will yield not only fundamental insights into how the neurotypical human brain recognises speech, but also into the pathomechanism of two important communication deficits, developmental dyslexia and autism spectrum disorders.