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

Abstract

Studies of saccadic eye movements in Parkinson's disease (PD) patients have revealed an ocuiomotor deficit associated with memory-gulded 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 findlngs have recently been obtained using a skeietomotor 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 prevlously 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 memoryguided reaches. Furthermore, the results indicated that the deficlts exhibited by the PD group on memoryguided reaches were confined solely to those markers associated with the transport component of the prehension movement, l.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.