Investigating the function of the ventral visual reading pathway and its involvement in acquired reading disorders

Abstract

This thesis investigated the role of the left ventral occipitotemporal (vOT) cortex and how damage to this area causes peripheral reading disorders. Functional magnetic resonance imaging (fMRI) studies in volunteers demonstrated that the left vOT is activated by written words over numbers or perceptually-matched baselines, irrespective of the word’s location on the visual field. Mixed results were observed for the comparison of words versus false font stimuli. This response profile suggests that the left vOT is preferentially activated by words or word-like stimuli, due to either: (1) bottom-up specialisation for processing familiar word-forms; (2) top-down task-dependent modulation, or (3) a combination of the two. Further studies are proposed to discriminate between these possibilities. Thirteen patients with left occipitotemporal damage participated in the rehabilitation and fMRI studies. The patients were impaired on word, text and letter reading. A structural analysis showed that damage to the left occipitotemporal white matter, in the vicinity of the inferior longitudinal fasciculus, was associated with slow word reading speed. The fMRI study showed that the patients had reduced activation of the bilateral posterior superior temporal sulci relative to controls. Activity in this area correlated with reading speed. The efficacy of intensive whole-word recognition training was tested. Immediately after the training, trained words were read faster than untrained words, but the effects did not persist until the follow-up assessment. Hence, damage to the left vOT white matter impairs rapid whole-word recognition and is resistant to rehabilitation. The final study investigated the role of spatial frequency (SF) in the lateralisation of vOT function. Lateralisation of high and low SF processing was demonstrated, concordant with the lateralisation for words and faces to the left and right vOT respectively. A perceptual basis for the organisation of vOT cortex might explain why left vOT damage is resistant to treatment