Absence of a common functional denominator of visual disturbances in cerebellar disease.

Several studies have demonstrated disturbances of visual perception in patients suffering from cerebellar disease. In an attempt to determine the cause of these visual disturbances and thereby the cerebellar contribution to vision, we designed two sets of experiments in which we tested (i) the possibility of a general magnocellular deficit in cerebellar disease and (ii) the alternative possibility of impaired spatial attention underlying visual disturbances in cerebellar patients. The first set of experiments consisted of a test of position discrimination, a parvocellular function and tests tapping different aspects of motion perception including speed discrimination, direction discrimination and the ability to extract a coherent motion signal embedded in noise. The second set of experiments compared the performance on two different classes of texture discrimination. The first one required fast and precise shifts of focal spatial attention ('serial search'), the second one, testing preattentive texture discrimination ('pop-out'), did not. In the first set of experiments cerebellar patients were impaired on the position discrimination task as well as several, albeit not all, tests of motion perception. The pattern of disturbances obtained was neither compatible with the notion of a selective magnocellular deficit nor the idea, originally put forward by Ivry and Diener (J Cogn Neurosci 1991; 3: 355-66) that visual deficits are secondary to an impaired measurement of time. In the second set of experiments, cerebellar patients showed normal performance on pop-out tasks and normal performance on all variants of the serial search task except for the one requiring comparison of a single element presented with a sample of the target in short-term memory. In summary, our results support the existence of visual disturbances in cerebellar disease, but provide evidence against a common, simple denominator such as a timing deficit, deficient cerebellar modulation of magnocellular circuitry, deficits of spatial attention or visual working memory.