Movement Variability and Bradykinesia in Parkinson's Disease

Abstract

When making discrete aiming movements, patients with Parkinson's disease show greater inherent variability in the endpoints of their movements than do normal subjects. Endpoint variability can be reduced, by moving more slowly, by utilizing visual guidance, and by making small amplitude movements. The greater variability of patients is not a universal finding, but depends on the conditions of movement. For small movements the performance of patients equates to that of controls. For larger movements the results indicate that if sufficient time is available, patients can use visual guidance (if available) to reduce the variability of their movements to the level of normals. Patients can generate fast and/or large amplitude arm movements if required, but they are erratic if made in the dark or over a short duration. Their difficulty lies not so much in the magnitude of muscle force available to them, but rather in an inability to produce it consistently for any given movement attempted. Bradykinesia may in part result from this inherent variability in that parkinsonian patients, in order to maintain accuracy within acceptable limits, are forced to increase the duration of their movements to a level where they can make use of visual guidance. In any event, theoretical explanations for the movement disorder in Parkinson's disease advanced in the literature need to take some account of this increased variability of movement.

Why Don't We Move Faster? Parkinson's Disease, Movement Vigor, and Implicit Motivation

“…Our finding that PD patients had a normal speed-accuracy trade-off is consistent with some previous studies (Montgomery and Nuessen, 1990;Majsak et al, 1998) but contradicts others (Sheridan and Flowers, 1990;Phillips et al, 1994), which described a larger increase in endpoint variability when PD patients moved faster. One possible explanation is that patients in the previous studies made movements either in reaction-time mode (they were instructed to move when a tone sounded) or under external pacing.…”

“…An explanation offered for bradykinesia is that it is a compensatory response to increased endpoint variability, that is to say, compensation for a primary impairment in the speed-accuracy trade-off (Sheridan and Flowers, 1990;Phillips et al, 1994). We envisioned a second mechanism, supported by our results: for a given task, there is a shift in the balance between the perceived reward of arriving to the target quickly and the amount of effort or energy required to achieve the fast movement.…”

“…A cardinal feature of PD is generalized movement slowing (bradykinesia), which critically cannot be explained by an intrinsic limitation in execution (England and Schwab, 1961), but rather is a problem of scaling speed to movement distance (Hallett and Khoshbin, 1980;Berardelli et al, 2001). A proposed explanation for this scaling deficit is that bradykinesia is a compensatory response: patients slow down because of a loss of accuracy at normal speeds (Montgomery and Nuessen, 1990;Sheridan and Flowers, 1990;Phillips et al, 1994).…”

Loss of gait control assessed by cognitive-motor dual-tasks: pros and cons in detecting people at risk of developing Alzheimer’s and Parkinson’s diseases

“…They are characterized by (i) decreases in gait speed, stride length, and arm swing amplitude (Lewek et al 2010;Volpe et al 2017) and (ii) increases in cadence, double support time, arm swing amplitude, swing time asymmetry (Yogev et al 2007), and variability in stride time and swing time (Baltadjieva et al 2006;Mirek et al 2007;Svehlík et al 2009;Lewek et al 2010;Volpe et al 2017). From a behavioral point of view, the gait showing results from the inability of PD patients to generate sufficient stride length and arm swing amplitude (i.e., gait hypokinesia) even though cadence control remains intact (Morris et al 1994;Hausdorff 2009), whereas the increased variability in temporal parameters from an alteration of the internal cueing mechanism needed to walk in a rhythmic fashion (Sheridan and Flowers 1990;Morris et al 1994;Ebersbach et al 1999;Schaafsma et al 2003). From a neuropathological point of view, the causes of these gait disorders may result from (i) dopaminergic striatal deficit (Wu et al 2015), (ii) excessive inhibition of the mesopontine locomotion center by the basal ganglia (Sterling et al 2015), and (iii) cortical cholinergic denervation (Bohnen et al 2013;Müller et al 2015).…”

Incoordination of a sequential motor task in Parkinson's disease

“…Bradykinesia tends to improve with antiparkinsonian drugs such as levodopa (Sheridan et al, 1987;Miller and DeLong, 1988;Sheridan and Flowers, 1990). A number of kinematic analysis studies of unconstrained arm movements in PD participants have been performed to understand the nature and mechanism of bradykinesia (Flash et al, 1992;Bennett, 1994, 1997;Gentilucci and Negrotti, 1999b).…”