ArticleCerebellum (London, England)2025
The Effect of Trial Numbers on Prism Adaptation: A Study of Pure Cerebellar Spinocerebellar Degeneration and Parkinson's Disease.
Article in Cerebellum (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPrism adaptation is used to study the cerebellar adaptive functions in neurological disorders. Previous papers reported that the number of prism exposure trials affected retention of the adaptation. However, it has not been studied how the trial number affects prism adaptation performances, especially its retention, in neurological disorders. Therefore, we aimed to investigate the relationship between exposure trial numbers and the acquisition of prism adaptation or the after-effects (AEs) (first and recovered) in patients with Parkinson's disease (PD), those with pure cerebellar-type spinocerebellar degeneration (SCD), and age-matched healthy volunteers (HVs).
methodsParticipants performed a finger-reaching task while wearing 20-D wedge-prism lenses, for 50 and 200 trials. The average of the errors in the last 10 prism exposure trials was considered an adaptation acquisition parameter. We also measured the first AE at the beginning of the post-exposure period and recovered AE by blocking visual feedback during the post-exposure period.
resultsIn the HVs, 200 trials enlarged the recovered AE compared to 50 trials, without any effects on adaptation acquisition or the first AE. In the SCD group, 200 trials normalized the reduced adaptation and first AE of 50 trials, with similar enlargement of the recovered AE. In the PD group, neither the adaptation acquisition nor first AE was affected by the trial number, but the recovered AE was larger than that of the HVs in 50 trials. No prism adaptation parameters correlated with any clinical severity scores.
conclusionsWe first showed that 200 trials compensate for reduced prism adaptation owing to cerebellar dysfunction compared to 50 trials. In PD, 50 trials induced an increase of the recovered AE, which may reflect the cerebellar circuit hyperfunction to compensate for the basal-ganglia dysfunction.
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