Parietal and prefrontal control of distinct components of attention

Abstract

In this thesis, we investigate behavioural mechanisms and neural substrates of distinct components of endogenous spatial attention. Endogenous attention facilitates neural processing of the selected stimulus through one of two component mechanisms: either by influencing perceptual sensitivity, i.e., enhancing the quality of sensory information processing of the selected stimulus, or by altering decisional bias, i.e. by enhancing the weight afforded to selected sensory stimuli in the downstream decision process. It is unclear whether sensitivity and bias components of endogenous attention are under the control of common, shared or dissociated neural mechanisms. Moreover, it is unclear how key regions in the frontoparietal network contribute to sensitivity versus bias control. Here, we characterise how sensitivity and bias are co-modulated during endogenous visuospatial attention using a probabilistically cued, multialternative task (endogenous “Posner” cueing task), by analysing behaviour with a novel multidimensional signal detection model. We demonstrate – for the first time – that the model successfully decouples sensitivity and bias from human behavioural data in this attention task. Then, using transcranial magnetic stimulation (TMS), in conjunction with the aforementioned task and model paradigms, we provide novel evidence for the causal contributions of the right hemispheric PPC and FEF towards sensitivity and bias control during endogenous attention. In the first study, we tested whether the effects of endogenous cueing on sensitivity and bias could be decoupled using a probabilistically-cued, five-alternative change detection task tested with n=37 participants. Multi-alternative tasks, with more than two response options, cannot be correctly analysed using a conventional one-dimensional signal detection model. Consequently, we used a novel multidimensional signal detection model – the m-ADC model – that can decouple and accurately estimate sensitivity and bias parameters in such tasks. After confirming that the model fit human behavioural data successfully, we investigated how sensitivity and bias were each modulated by spatial cueing. We found that while bias was modulated in a graded manner according to the cue validity at each location, sensitivity followed an ‘all or none’ pattern of modulation – being highest at one location but not significantly different in the others. Cue related modulations of bias and sensitivity modulations did not covary. Further, decisional metrics such as reaction time, decision optimality and differential risk curvature were found to vary with bias, but not sensitivity. Overall, this study showed that endogenous attention modulates sensitivity and bias components of attention through dissociable behavioural mechanisms. In the second study, we probed the causal role of the human right hemispheric PPC (rPPC) in mediating the sensitivity versus bias components of endogenous attention. In a cohort of n=28 participants, we transiently inhibited activity in the rPPC with continuous theta burst stimulation (cTBS), following which they performed a spatially cued multialternative task similar to that employed in the first study. We analysed participants’ behavioural responses with the m-ADC model, and compared estimated parameters between the control (sham cTBS) and stimulation (rPPC cTBS) sessions. The results revealed a specific role for the rPPC in bias, but did not indicate stimulation induced sensitivity modulation. In particular, rPPC cTBS affected the voluntary reorientation of spatial bias towards the uncued location. The results show, for the first time, a specific role for rPPC in decisional bias modulation during endogenous attention. In the next study, we investigated the causal involvement of the human right hemispheric FEF (rFEF), in sensitivity and bias modulation during endogenous attention. As before, we inhibited the rFEF using cTBS and analysed its effect on sensitivity and bias parameters using the m-ADC task and model in n = 12 participants. The results suggested that the rFEF causally mediates the modulation of sensitivity rather than bias during endogenous attention. Specifically, rFEF cTBS increased sensitivity at the cued location but did not induce a significant modulation of bias. These results suggest a double dissociation between the rPPC and rFEF in terms of bias versus sensitivity modulation, respectively. In summary, the studies outlined in this thesis shed light on the mechanisms through which endogenous attention shapes sensory processing and decision-making. We find that the behavioural mechanisms and neural substrates of endogenous attention on sensitivity and bias changes are distinctive and dissociable. This opens up exciting future possibilities for precisely mapping specific attention-related neurophysiological processes in each brain region (rPPC, rFEF) to sensory or decisional functions, charting out the role of cortico-subcortical network interactions on sensitivity and bias and, ultimately, decoding how specific neural computations give rise to emergent cognitive phenomena, such as attention