Separate analyses of variance (ANOVAs) were performed to compare the performance of each patient group to that of the control participants for each of the dependent variables. The factors in these analyses were tempo (500 and 900 msec)

and participant group. Based on preliminary analyses, we averaged the results over the two hands for the controls, PD patients, and two cerebellar degeneration patients. For the cerebellar patients with unilateral lesions, we compared performance with the impaired, ipsilesional hand to that of the control participants. We also ran a separate analysis in which we compared the performance of the ipsilesional and contralesional hands for the unilateral patients. Surprisingly, none of these within-subject comparisons were significant. These null results likely reflect two factors. First, the number of participants with unilateral cerebellar lesions was small (n = 5). Second, a couple of the patients showed little impairment on the task, consistent with their marked clinical recovery. Thus, our focus here is on the comparison of the patient groups to the controls.

As an overall measure of performance, we assessed the SD of the intervals (Figure 19.2a). This measure was significantly increased in the cerebellar group, F(1, 11) = 7.11, P = .022, but not in the PD group, F(1, 9) = .44, P = .52. The decomposition of the variance revealed that the SDs of the motor delays (Figure 19.2b) were not different between the control group and the two patient groups: F(1, 11) = .001, P = .981, for the cerebellar group; F(1, 9) = .10, P = .753, for the PD group. The effect of pace and the group by pace interaction were not significant in either comparison.

In contrast, the estimates for the SD of the clock intervals (Figure 19.2c) were significantly elevated for the cerebellar group, F(1, 11) = 7.43, P = .019. No such deficit was found for the PD patients, F(1, 9) = .443, P = .52. As expected from a linear increase of clock SD with interval length (Ivry and Hazeltine, 1995), the effect of pace on the clock SD was significant in both comparisons: F(1, 11) = 36.6, F(1, 9) = 110.8, P < .001. The group x pace interaction was not significant for either comparison: F(1, 11) = .5, F(1, 9) = 2.6. These results are congruent with the idea that the higher variability of the performance of cerebellar patients is due to deficits in a central timing mechanism.

One measure of the quality of error correction is the mean synchronization error (Figure 19.3). Similar to previous reports, the mean asynchrony for the control participants was negative, indicating that their taps anticipated the onset of the tones. The magnitude of this asynchrony was similar for the patients with cerebellar lesions and controls, F(1, 11) = .09, P = .77. The PD patients showed a greater negative asynchrony than the controls, F(1, 9) = 7.99, P = .02. That is, the responses of the PD patients preceded the tones to a greater extent than the responses of the controls. The effect of pace was significant in both the control/cerebellar ANOVA, F(1, 11) = 9.23, P = .011, and control/Parkinson's ANOVA, F(1, 9) = 6.4, P = .031. In both, the negative asynchrony was greater in the 900-msec condition than in the 500-msec condition. The group x pace interaction was not significant in either case.

The estimates for the error correction parameter a are shown in Figure 19.4. The analyses indicate that the estimates for the cerebellar patients were not different from those obtained for the controls, F(1, 11) = .67, P = .80. The error correction values were lower in the PD patients than in the controls, although this comparison did not reach significance, F(1, 9) = 3.73, P = .085. The error correction estimate increased in size from the faster to the slower pace, an effect that was significant o Q ΓΌ)

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