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Feb 11

(No title)

Gobel, E.W., Blomeke, K., Zadikoff, C., Simuni, T., Weintraub, S., Reber, P.J. (in press).  Implicit perceptual-motor skill learning in Mild Cognitive Impairment and Parkinson’s disease.  Neuropsychology.

Abstract

Objective: Implicit skill learning is hypothesized to depend on nondeclarative memory that operates independent of the medial temporal lobe (MTL) memory system and instead depends on cortico-striatal circuits between the basal ganglia and cortical areas supporting motor function and planning.  Research with the Serial Reaction Time (SRT) task suggests that patients with memory-disorders due to MTL damage exhibit normal implicit sequence learning.  However, reports of intact learning rely on observations of no group differences, leading to speculation whether implicit sequence learning is fully intact in these patients.  Patients with Parkinson’s Disease (PD) often exhibit impaired sequence learning, but this impairment is not universally observed.

Method: Implicit perceptual-motor sequence learning was examined using the Serial Interception Sequence Learning (SISL) task in patients with amnestic Mild Cognitive Impairment (MCI; n=11) and patients with PD (n=15).  Sequence learning in SISL is resistant to explicit learning and individually adapted task difficulty controls for baseline performance differences.

Results: Patients with MCI exhibited robust sequence learning, equivalent to healthy older adults (n=20), supporting the hypothesis that the MTL does not contribute to learning in this task.  In contrast, the majority of patients with PD exhibited no sequence-specific learning in spite of matched overall task performance.  Two patients with PD exhibited performance indicative of an explicit compensatory strategy suggesting that impaired implicit learning may lead to greater reliance on explicit memory in some individuals.

Conclusion: The differences in learning between patient groups provides strong evidence in favor of implicit sequence learning depending solely on intact basal ganglia function with no contribution from the MTL memory system.

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