THE PATHOGENESIS OF GAIT HYPOKINESIA IN PARKINSONS-DISEASE

To identify the fundamental deficit in gait hypokinesia in Parkinson's disease (PD) we conducted a series of experiments that compared PD su bjects with age- and height-matched controls in their capacity to regu late either stride length, cadence (steps per minute) ol both paramete rs to three conditions. In the first condition the spatial and tempora l parameters of gait were documented for slow: normal and fast walking . The second condition compared parkinsonian gait with the walking pat tern of elderly controls whilst controlling for two movement speeds: f ast (control preferred) speed find slow (PD preferred) speed. In the t hird condition we examined the ability of PD subjects to regulate one parameter (e.g. stride length) when the other two parameters (e.g. vel ocity and cadence) were held at control values. A total of 34 PD subje cts and 34 matched controls were tested using a footswitch stride anal ysis system that measured the spatial and temporal parameters of gait for gait for a series of 10 m walking trials. Parkinsonian subjects ex hibited marked gait hypokinesia in each of the experiments. Although t hey retained the capacity to vary their gait velocity in a similar man ner to controls, their range of response was reduced. Within the lower velocity range, PD subjects could vary their speed of walking by adju sting cadence and to a lesser extent, stride length. However when the speed of walking was controlled the stride length was found to be shou ter and the cadence higher in PD subjects than in controls. Stride len gth could not be upgraded by internal control mechanisms in response t o a fixed cadence set for age and height-matched velocity. In contrast , cadence was readily modulated by external cues and by internal contr ol mechanisms when stride length was fired 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 r elative increase in cadence exhibited by PD subjects is a compensatory mechanism for the difficulty in regulating stride length. These findi ngs are discussed in the context of the hypothesized role of the basal ganglia in generating internal cues for the maintenance of the gait s equence and in relation to the structuring of movement rehabilitation strategies.