Parkinson's disease and the internal control of action: A single-case study

Studies of saccadic eye movements in Parkinson's disease (PD) patients have revealed an oculomotor deficit associated with memory-guided eye movements, Such patients show normal visually guided saccades to peripheral targets, but are often impaired when required to make a saccade to the remembered location of a visual target, This deficit is characterized by an impairment in the ability to generate an appropriately scaled primary saccade. Similar findings have recently been obtained using a skeletomotor analogue of the memory-guided saccade task. In that study we examined transport and grasp kinematics for visually guided and memory-guided prehension movements in a group of patients with PD, and demonstrated analogous deficits to those previously reported for memory-guided saccadic eye movements. While the patient group did not differ from their age-matched controls when executing visually guided prehension movements, they were clearly shown to be significantly impaired when executing memory-guided reaches. Furthermore, the results indicated that the deficits exhibited by the PD group on memory-guided reaches were confined solely to those markers associated with the transport component of the prehension movement, i.e. reduced movement velocity and increased deceleration time. This paper extends our previous work, and reports four experiments which examined the effects of PD upon the sensorimotor mechanisms used to control prehension movements, Specifically, we examine the transport and grasp kinematics of a 49-year-old female patient with idiopathic PD and her age- and gender-matched control subject, for reaches executed under the following viewing conditions: Binocular visual feedback; Monocular visual feedback; No visual feedback (Open-loop); and Memory-guided reaches.