Timing Control in Parkinson’s Disease

Internal generation and modulation of timing may be an important underlying yet unrecognized mechanism of many symptoms in Parkinson’s disease. It has been recently debated whether the basal ganglia or cerebellum might contribute to overall timing control during movement execution. As seen in basal ganglia disorders such as Parkinson’s disease (PD) and Huntington’s disease (HD), timing dysfunction is present and contributes to the ability to control everyday movements. In some cases, timing deficits may be associated with very debilitating movement impairments such as speech festination, balance control (falling) and freezing of gait. One interesting example is how the ‘shuffling gait’ that is typical of PD can be improved with visual step cues spaced appropriately apart, even when dopaminergic medications are withdrawn. While this is a well known fact, it is important to consider whether the observed improvements in stride length may be the result of a spatiotemporal trade-off (Morris et al., 2001; 1994b). That is, while a larger stride length can be achieved with the use of visual step cues, a subsequent timing deficit (i.e. gait rhythmicity becoming even slower) may also result. However, unlike spatial parameters of movement like step length, timing dysfunction is resistant to the typical dopaminergic treatments used in Parkinson’s disease (Blin et al., 1991). Thus, research has argued that spatiotemporal trade-off may be the result of a shift of focus to specific spatial components of movement (Georgiou et al., 1993; Zijlstra et al., 1998), while temporal control is simultaneously sacrificed. Alternatively, the inability to modulate timing during movement may be part of an underlying deficit in the ability to process interoceptive sources of feedback that guide the control of movement. If this were the case, then internal timing would be an important direction for therapeutic interventions which might have the potential to improve motor symptoms in PD. Within this chapter we will examine timing deficits in upper limb repetitive and coordinated movements and also timing during gait in PD. Further, to evaluate how attention and processing of sensory feedback may contribute to timing control, we will take a close look at new methodologies to investigate timing control during gait in Parkinson’s disease. Specifically we will evaluate the ability of individuals with PD (while “On” and “Off” their dopaminergic medication) to modulate spatial and temporal components of gait in self-paced, and temporally-cued conditions using an auditory stimulus, and further to determine whether this modulation is dependent on the dopaminergic system. The concept of evaluating timing error will also be introduced as a potential way to better understand