Abstract
BackgroundThe progressive deterioration of gait in Huntington’s disease (HD) leads to functional decline and loss of function. To understand the underlying mechanisms responsible for the gait changes in HD, we examined the automatic control of gait by measuring the relationship between stride length and cadence. The relationship is strongly linked in healthy adults during automatic gait but disrupted in pathological gait disorders, such as Parkinson’s disease (PD).MethodsThe stride length cadence relationship was compared between seventeen participants with HD, twenty with PD and twenty one healthy older adults (HOA). Participants had their gait recorded at self-selected preferred, very slow, slow, fast and very fast speeds. Linear regression analysis was used to determine the slope and intercept of the relationship which were compared between groups. The adjustment of stride length and cadence when changing gait speeds was measured and compared within and between groups.ResultsLinearity was strong in all but two participants with HD and one with PD. Slope did not differ between groups (p > 0.05) but intercept was lower in the HD and PD groups compared to HOA (p < 0.05). Stride length was shorter in the HD and PD groups compared to controls at preferred and most adjusted speed conditions (p < 0.05) but cadence did not differ between groups (p > 0.05) regardless of speed. The HD group adjusted stride length and cadence similar to HOA when changing speed. The range of cadence across speed conditions did not differ between groups.ConclusionScaling of stride length but not the regulation of cadence was found to be disrupted in participants with HD.
Highlights
The progressive deterioration of gait in Huntington’s disease (HD) leads to functional decline and loss of function
Variability of angular kinematic gait parameters was shown to be higher in HD and Parkinson’s disease (PD) compared to controls [9] with chorea possibly contributing to this variability in HD
We proposed the Stride length cadence relationship (SLCrel) would be altered in HD compared to controls and that changes in the relationship would be the same in HD to that found in PD
Summary
The progressive deterioration of gait in Huntington’s disease (HD) leads to functional decline and loss of function. To understand the underlying mechanisms responsible for the gait changes in HD, we examined the automatic control of gait by measuring the relationship between stride length and cadence. Huntington’s disease (HD) is an autosomal dominant inherited neurodegenerative disorder that presents with characteristic gait changes, including decreased walking speed, step initiation difficulties [1,2,3] and a variable stepping pattern [4,5,6]. Disruption to the regulation of step length, greater step to step variability and disturbed gait initiation have been reported to occur before clinical signs of HD appear [2,13] and worsen as disease severity progresses [2,10,13]. Variability of angular kinematic gait parameters was shown to be higher in HD and PD compared to controls [9] with chorea possibly contributing to this variability in HD
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