Using neuro-cognitive modelling to link attention deficits to structural and functional brain changes

‘Visual attention’ is an emerging property of interconnected neural networks, in which the interconnections are biased to promote targets over distracting stimuli. It has been shown that efficiency of the attention system is lost after many kinds of brain damage, with each presumably effecting different aspects of basic visual attention functions. Yet, our understanding of these processes is limited by the methodological shortcomings of classical neuropsychological assessment. The overarching goal of the current thesis was to overcome these constrains and thereby extend the link between attention deficits and underlying brain changes. The here used approach incorporates parametric measurement of visual attention derived from the computational Theory of Visual Attention (TVA, Bundesen, 1990) and modern magnetic resonance imaging techniques. Project 1 of the current thesis applied a combined TVA–neuroimaging analysis in a neurodevelopmental model (preterm birth) to relate attention deficits with changes in functional connectivity networks. We found that pre- versus full-term born adults show a selective reduction of visual short-term memory capacity. The remarkable changes we observed in attention-related large-scale brain networks of the occipital and posterior parietal cortices were most pronounced in those preterm born individuals with the most preserved attention functions. This finding was interpreted as evidence for a compensatory reorganization of functional connectivity in order to ameliorate the advert consequences of preterm birth on visual short-term memory. Project 2 of this thesis applied a combined TVA-neuroimaging analysis in a neurodegenerative model (posterior cortical atrophy) to relate attention deficits with structural changes in grey and white matter morphometry. Compared to healthy control participants, patients with posterior cortical atrophy suffered from a selective disturbance of visual processing speed. The individual rate of processing speed slowing was a valid predictor for the severity of simultanagnosia, the core symptom in this clinical condition. We further found wide-spread atrophy in occipital as well as parietal and to a smaller degree in temporal brain areas. White matter degeneration in the superior parietal lobe, rather than atrophy of any grey matter cluster, was significantly associated with patients’ impaired processing speed. Based on these results we propose that disruption of white matter pathways especially within the superior parietal lobe leads to reduced processing speed which then results in the overt clinical symptoms of simultanagnosia. Altogether, projects of the current thesis expanded the link between specific attention deficits and underlying brain damage by using neuro-cognitive modelling. We demonstrated that parametric measurements of attention facilitate, in the role of intermediate cognitive constructs, the mapping between etiological factors and behavioral outcomes. Identifying predictable behavior-brain relationships in attention disorders may offer new perspectives for diagnosis and treatment. The clinical application of an integrated TVA-neuroimaging analysis could additionally compliment insights from healthy participants toward understanding the principles of normal visual attention as well as identifying their neuronal basis.