Forward and backward spatial recall in Parkinson's disease and matched controls: A 1-year follow-up study

Abstract

Patients with Parkinson's disease (PD) exhibit a domain-general visuospatial dysfunction; however, no previous study has examined changes over time in forward and backward spatial recall in PD against controls. To evaluate changes in short-term (STM) and working memory (WM) dysfunction in PD, the current study assessed performance on a computer-modified version of the Corsi Block-Tapping Test (forward and backward recall) at two-time points 1 year apart, while simultaneously exploring associations with potentially relevant demographic and clinical variables. We enrolled 38 patients with PD and 38 controls matched for age, sex, and Montreal Cognitive Assessment (MoCA) total scores. Linear mixed-effects models analyzed the primary measured variables (forward and backward scores). At baseline, the dysfunction effect sizes were as follows: forward recall (−0.45, 95% CI [−0.90, 0.01]) and backward recall (−0.26, 95% CI [−0.71, 0.19]). At follow-up, patients exhibited substantially greater difficulties in backward recall (−0.65, 95% CI [−1.18, −0.13]) compared to the baseline assessment, whereas the forward dysfunction effect size remained almost the same (−0.43, 95% CI [−0.94, 0.09]). Age (p = .005, f = 0.35) and total scores on MoCA (p = .017, f = 0.18), irrespective of group and recall condition, were significant predictors of spatial block scores. The pattern of dysfunction effect sizes indicates that, in contrast to forward recall, backward recall dysfunction in PD worsened 1-year after the baseline assessment, presumably reflecting the progression of PD-related visuospatial WM dysfunction.

Keywords:

• Corsi Block-Tapping Test
• neuropsychological tests
• short-term memory
• working memory

Acknowledgments

The authors thank Michael Yung and Sam Flannery for their contribution.

Disclosure statement

The authors report there are no competing interests to declare.

Additional information

Funding

This work was supported by the Neurological Foundation of New Zealand [grant number 1517-SPG] and a University of Otago Doctoral Scholarship.