There is increasing evidence that the cerebellum and the basal ganglia serve not only a role in motor control but also in visual perception. Patients with Parkinson's disease (PD) as well as patients with cerebellar lesions exhibit impairments of vision that are not fully explained by ocular motor deficits. It is less clear to which extent these visual deficits contribute to an impaired control of visually guided movements. This study examined whether a dysfunction of the cerebellum or the basal ganglia induces impairments in depth perception, which affect action. We employed an illusionary display, the Ames trapezoidal window, to determine the ability of PD patients (n=10) and patients with spinocerebellar ataxia (SCA) (n=6) to process depth cues when estimating object slant. Participants either pointed to the edges of the window (motor judgement) or verbally indicated the perceived orientation of the display (verbal judgement). To control for ocular and limb motor deficits, participants judged the slant of a non-illusionary display in a second task. Slant estimation of the non-illusionary window was not impaired in either patient group when compared to control subjects (all P>0.2). In contrast, SCA as well as PD patients exhibited significantly greater slant estimation errors than controls when pointing to the illusionary window (P=0.005). In addition, both patient groups made larger errors than controls in their verbal judgements during binocular viewing of the illusion (P=0.005), but not during monocular viewing (P>0.2). In sum, the present findings point towards a role for both the basal ganglia and cerebellum for the processing of visual information about depth. Since the deficits were seen both in the context of action and perception and were only partially reconciled by the availability of binocular depth cues, we conclude that basal ganglia as well as cerebellar disease may affect the visual perception of depth.
Bibliographical noteFunding Information:
Acknowledgments The study was supported by a grant of the Deutsche Forschungsgemeinschaft (DFG) to MM (DFG MA 2209/ 3-1), by grants from the National Institute of Health to CMG (NIH RO1 NS37211) and by grants from the Minnesota Medical Foundation and the College of Education and Human Development. We sincerely thank all patients, who came from several Midwestern states, for their participation. Our thanks are extended to Carly Salminen of the Sensorimotor Control Laboratory for her help in collecting and analysing the data.
- Basal ganglia
- Depth perception
- Parkinson's disease
- Spinocerebellar ataxia