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.