The pathogenesis of gait hypokinesia in Parkinson's disease

Abstract

To identify the fundamental deficit in gait hypokinesia in Parkinson's disease (PD) we conducted a series of experiments that compared PD subjects with age- and height-matched controls in their capacity to regulate either stride length, cadence (steps per minute) or both parameters to three conditions. In the first condition the spatial and temporal parameters of gait were documented for slow, normal and fast walking. The second condition compared parkinsonian gait with the walking pattern of elderly controls whilst controlling for two movement speeds: fast (control preferred) speed and slow (PD preferred) speed. In the third condition we examined the ability of PD subjects to regulate one parameter (e.g. stride length) when the other two parameters (e.g. velocity and cadence) were held at control values. A total of 34 PD subjects and 34 matched controls were tested using a footswitch stride analysis system that measured the spatial and temporal parameters of gait for a series of 10 m walking trials. Parkinsonian subjects exhibited marked gait hypokinesia in each of the experiments. Although they retained the capacity to vary their gait velocity in a similar manner to controls, their range of response was reduced. Within the lower velocity range, PD subjects could vary their speed of walking by adjusting cadence and, to a lesser extent, stride length. However, when the speed of walking was controlled, the stride length was found to be shorter and the cadence higher in PD subjects than in controls. Stride length could not be upgraded by internal control mechanisms in response to a fixed cadence set for age and height-matched velocity. In contrast, cadence was readily modulated by external cues and by internal control mechanisms when stride length was fixed to the values obtained for age- and height-matched controls. It was concluded that regulation of stride length is the fundamental problem in gait hypokinesia and the relative increase in cadence exhibited by PD subjects is a compensatory mechanism for the difficulty in regulating stride length. These findings are discussed in the context of the hypothesized role of the basal ganglia in generating internal cues for the maintenance of the gait sequence and in relation to the structuring of movement rehabilitation strategies.

Contributions of mild parkinsonian signs to gait performance in the elderly

“…Concerning the dopaminergic pathway, both bradykinesia and PIGD have been associated with [ 123 I]β-CIT SPECT binding in patients with PD (Pirker 2003). Additionally, gait akinesia in PD was mainly attributed to an inability to increase step length (Morris et al 1994). Interestingly, by comparing Alzheimer's disease patients with increased MPS and those with decreased MPS, Camicioli et al have previously shown that patients with more MPS showed impaired spatial and variability gait parameters (2006).…”

Agency, gait and self-consciousness

“…One relevant group to investigate both with respect to locomotion as well as the sense of agency and voluntary motor control are patients suffering from Parkinson's disease. Gait-impairments such as asymmetry or freezing-of-gait are well documented (Browner and Giladi, 2010;Morris et al, 1994), as is the underlying pathology (Agid and Blin, 1987;Alexander et al, 1986), but beyond the scope of the current review. Although initial work on agencyrelated processing in Parkinsonism has been published by Moore et al (2010b), further research is required to systematically link such findings to models of sensorimotor control, locomotion, and upperlimb and gait agency.…”

Quantitative Gait Analysis in Parkinson’s Disease: Comparison With a Healthy Control Group

“…2,10,[18][19][20] These studies also documented a tendency of longer duration in the double-support phase of the gait cycle and a normal cadence. In other studies, 21,22 a reduction of cadence values was reported.…”

“…Absence of dopamine in the basal ganglia circuit ultimately results in the loss of gait automaticity. Clinically, people with PD usually have the hallmark features of slowness (bradykinesia), 2 cessation of movement (akinesia), or freezing of gait. 3 As the disease advances, these gait disorders become more pronounced, disabling the patients and severely limiting their quality of life.…”

“…4 The reduction of stride length is considered the most prominent feature of PD gait and is often accompanied by lower walking speed and the tendency toward a longer duration in the double-support phase. 2,5,6 Other studies [7][8][9][10] have indicated that patients with PD are able to improve gait components, such as stride length and speed, if appropriate influences, like cues, are used.…”