Results of our previous studies have shown that the slow, shuffling gait of Parkinson's disease patients is due to an inability to generate appropriate stride length and that cadence control is intact and is used as a compensatory mechanism. The reason for the reduced stride length is unclear, although deficient internal cue production or inadequate contribution to cortical motor set by the basal ganglia are two possible explanations. In this study we have examined the latter possibility by comparing the long-lasting effects of visual cues in improving stride length with that of attentional strategies. Computerized stride analysis was used to measure the spatial (distance) and temporal (timing) parameters of the walking pattern in a total of 54 subjects in three separate studies. In each study Parkinson's disease subjects were trained for 20 min by repeated 10 m walks set at control stride length (determined from control subjects matched for age, sex and height), using either visual floor markers or a mental picture of the appropriate stride size. Following training, the gait patterns were monitored (i) every 15 min for 2 h; (ii) whilst interspersing secondary tasks of increasing levels of complexity; (iii) covertly, when subjects were unaware that measurement was taking place. The results demonstrated that training with both visual cues and attentional strategies could maintain normal gait for the maximum recording time of 2 h. Secondary tasks reduced stride length towards baseline values as did covert monitoring. The findings confirm that the ability to generate a normal stepping pattern is not lost in Parkinson's disease and that gait hypokinesia reflects a difficulty in activating the motor control system. Normal stride length can be elicited in Parkinson's disease using attentional strategies and visual cues. Both strategies appear to share the same mechanism of focusing attention on the stride length. The effect of attention appears to require constant vigilance to prevent reverting to more automatic control mechanisms.

To identify the fundaamentall 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 regualte 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 seconde 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 controllled, 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 regualation 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.

Background and Purpose. The Timed “Up & Go” Test (TUG) is used to measure the ability of patients to perform sequential locomotor tasks that incorporate walking and turning. This study investigated the retest reliability, interrater reliability, and sensitivity of TUG scores in detecting changes in mobility in subjects with idiopathic Parkinson disease (PD). Subjects. The performance of 12 people with PD was compared with that of 12 age-matched comparison subjects without PD. Methods. The subjects with PD completed 5 trials of the TUG after withdrawal of levodopa for 12 hours (“off” phase of the medication cycle) as well as an additional 5 trials 1 hour after levodopa was administered (“on” phase of the medication cycle). They were scored on the Modified Webster Scale at both sessions. The comparison subjects also performed 5 TUG trials. All trials were videotaped and timed by 2 experienced raters. The videotape was later rated by 3 experienced clinicians and 3 inexperienced clinicians. Results. For the subjects with PD, within-session performance was highly consistent, with correlations (r) ranging from .80 to .98 for the “off” phase and from .73 to .99 for the “on” phase. The performance of the comparison subjects across the 5 trials was also highly consistent (r=.90–.97). Comparisons showed differences between trials 1 and 2 on the TUG for both groups. Removal of data for trial 1 (the practice trial) further enhanced retest reliability. There was close agreement in TUG scores among raters despite different levels of experience (intraclass correlation coefficient [3,1]=.87–.99). Mean TUG scores were different between the “on” and “off” phases of the levodopa cycle and between subjects with PD and comparison subjects during the “on” phase. Conclusion and Discussion. Retest reliability and interrater reliability of the TUG measurements were high, and the measurements reflected changes in performance according to levodopa use. The TUG can also be used to detect differences in performance between people with PD and elderly people without PD.