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.

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.

This study classified speech impairment in 200 patients with Parkinson's disease (PD) into five levels of overall severity and described the corresponding type (voice, articulation, fluency) and extent (rated on a five-point scale) of impairment for each level. From two-minute conversational speech samples, parameters of voice, fluency and articulation were assessed by two trained-raters. Voice was found to be the leading deficit, most frequently affected and impaired to a greater extent than other features in the initial stages. Articulatory and fluency deficits manifested later, articulatory impairment matching voice impairment in frequency and extent at the `Severe' stage. At the final stage of `Profound' impairment, articulation was the most frequently impaired feature at the lowest level of performance. This study illustrates the prominence of voice and articulatory speech motor control deficits, and draws parallels with deficits of motor set and motor set instability in skeletal controls of gait and handwriting.

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Freezing of gait (FOG) has been identified as one of the main contributors to gait disturbances in Parkinson's disease. While the pathophysiology remains enigmatic, several factors such as step length and the sequence effect (step to step reduction in amplitude) may lead to the occurrence of FOG. It was hypothesized that by reducing step length, FOG episodes would present more frequently if a significant sequence effect (measured as a regression slope) was co-existent in the subject. Twenty-six participants with Parkinson's disease were separated clinically into a freezing (PD + FOG, n = 16) and non-freezing (PD-FOG, n = 10) group, with 10 age-matched control participants. Testing involved walking trials where preferred step length was set at 100%, 75%, 50% and 25% of normalized step length. The number of FOG episodes increased in the 50% condition and further increased in the 25% condition compared to other conditions. The participants with FOG also demonstrated a larger average regression slope, with significant differences in the 75%, 50% and 25% conditions when compared to the PD-FOG and control groups. There were no significant differences when comparing the slope of the PD-FOG and control group, indicating the reduced step length and the sequence effect may have led to the occurrence of FOG. These findings support the possible dual requirement of a reduced step length and a successive step to step amplitude reduction to lead to FOG.

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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.

Festination and freezing of gait (FOG) are poorly understood gait disorders that cause disability and falls in people with Parkinson disease (PD). In PD, basal ganglia malfunction leads to motor set deficits (hypokinesia), while altered motor cue production leads to a sequence effect, whereby movements becomes progressively smaller as in festination. We suggest both factors may contribute to FOG. Disturbance of set maintenance by the basal ganglia in PD has previously been examined in gait, but limited systematic evaluation of the sequence effect exists. In this study, we investigated the step-to-step amplitude relationship in 10 PD subjects with clinical evidence of festination and FOG. Four conditions were examined: off levodopa, off with attentional strategies, off with visual cues, and on levodopa. Participants demonstrated a sequence effect (F = 6.24; P = 0.001), which was reversed only by use of visual cues. In contrast, medication, attentional strategies, and visual cues all improved hypokinesia. Variability was marked both within and between participants in all conditions. The variability of FOG is suggested to relate to a combination of factors, including the sequence effect and its variability, as well as the severity of hypokinesia and its response to medications.