Optic ataxia in patients with thalamic lesions.

Abstract

Lesions in the parietal cortex can strongly impair visually guided reach-grasping behaviour. A specific reaching deficit termed 'optic ataxia' (OA) occurs when eye and hand position are dissociated. OA has typically been studied in patients with lesions in the parietal cortex, neglecting potential thalamic contributions. Here, we examined 28 acute stroke patients (age 58.9 ± 12.6 years) with circumscribed thalamic lesions for the presence of OA. We leveraged MRI-based lesion-symptom mapping to address the contributions of specific thalamic nuclei to visually guided reaching deficits under foveal and peripheral viewing conditions. Based on the cortical literature, we hypothesized that lesions in thalamic nuclei with strong connections to the inferior and superior parietal cortex, such as the ventrolateral nucleus and pulvinar might lead to OA. In comparison with age-matched healthy subjects (n = 40, age 60.6 ± 9.1 years), we identified five thalamic patients with OA, most pronounced for reaches with the contralesional hand into the contralesional space. While motor and grasping deficits and OA occurred frequently together, they did not always co-occur, and visual attention deficits could not account for the OA either. Comparing the lesion maps of patients with and without OA, the critical lesion site for OA was not restricted to one circumscribed thalamic region within the Morel atlas. Instead, it encompassed several medial and lateral nuclei within and around the internal medullary laminar complex. Interestingly, this region matches the so-called central thalamus, a functionally defined thalamic region that is considered a 'higher-order' nucleus complex. It receives afferent inputs from the cerebellum and brainstem regions and connects to fronto-parietal regions involved in eye movement control. Taken together, our results suggest the critical importance of thalamic nuclei for the spatial transformation from eye- into body-centred coordinates.