The performance on learning tasks of patients in the early stages of Parkinson's disease

Canavan, A. G. M.; Passingham, Richard E.; Marsden, C. D.; Quinn, Niall; Wyke, Maria; Polkey, Charles E.

doi:10.1016/0028-3932(89)90167-x

Cited by 129 publications

(61 citation statements)

References 28 publications

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“…Dopamine has been shown to play a role in motivation (Fibiger and Phillips 1986;Robbins and Everitt 1996;Wise and Hoffman 1992;Wise 2004Wise , 2005, in the acquisition of appetitive conditioning tasks (Berridge and Robinson 1998;Everitt et al 1999;Ikemoto and Panksepp 1999), in many aspects of drug addiction (Berke and Hyman 2000;Di Chiara 2002;Everitt and Robbins 2005;Kelley and Berridge 2002;Koob 1992;Robinson and Berridge 2008;Wise 1996a, b) and is involved in disorders such as Parkinson disease (Canavan et al 1989;Voon et al 2010;Frank 2005;Knowlton et al 1996;Moustafa et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Computational models of reinforcement learning: the role of dopamine as a reward signal

2010

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Reinforcement learning is ubiquitous. Unlike other forms of learning, it involves the processing of fast yet content-poor feedback information to correct assumptions about the nature of a task or of a set of stimuli. This feedback information is often delivered as generic rewards or punishments, and has little to do with the stimulus features to be learned. How can such low-content feedback lead to such an efficient learning paradigm? Through a review of existing neuro-computational models of reinforcement learning, we suggest that the efficiency of this type of learning resides in the dynamic and synergistic cooperation of brain systems that use different levels of computations. The implementation of reward signals at the synaptic, cellular, network and system levels give the organism the necessary robustness, adaptability and processing speed required for evolutionary and behavioral success.

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Section: Introductionmentioning

confidence: 99%

Computational models of reinforcement learning: the role of dopamine as a reward signal

2010

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“…In Parkinson's disease, there is a profound loss of dopamine-containing neurons in the substantia nigra compacta (SNc), leading to dopamine depletion in the striatum. Studies have shown that the loss of dopamine that occurs in Parkinson's disease leads to a variety of learning and memory deficits, particularly on tasks that involve incremental, feedback-based learning of cue-outcome associations (Canavan et al, 1989;Cools, Barker, Sahakian, & Robbins, 2001a;Cools, Barker, Sahakian, & Robbins, 2001b;Gotham, Brown, & Marsden, 1998;Knowlton, Mangels, & Squire, 1996;Myers et al, 2003;Shohamy et al, 2004a;Shohamy, Myers, Onlaor, & Gluck, 2004b;Swainson et al, 2000;Vriezen & Moscovitch, 1990). By contrast, Parkinson's patients are generally not impaired on tasks which involve declarative, non-feedback-based learning, or tasks that require flexible use of knowledge (Knowlton et al, 1996;Myers et al, 2003;Shohamy et al, 2004a)-functions which are thought to rely on the medial temporal lobe (Eichenbaum, 2002;Gabrieli, 1998;Gluck & Myers, 1993;Robbins, 1996;Squire & Zola, 1996).…”

Section: Introductionmentioning

confidence: 99%

“…By contrast, less is known of the impact of L-dopa on learning and memory, and most studies reporting learning and memory impairments in Parkinson's disease have tested only medicated patients (e.g. Canavan et al, 1989;Knowlton et al, 1996;Myers et al, 2003;Shohamy et al, 2004aShohamy et al, , 2004b.…”

Section: Introductionmentioning

confidence: 99%

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l-dopa impairs learning, but spares generalization, in Parkinson's disease

et al. 2006

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In this study we examined the effect of dopaminergic modulation on learning and memory.Parkinson's patients were tested 'on' versus 'off' dopaminergic medication, using a two-phase learning and transfer task. We found that dopaminergic medication was associated with impaired learning of an incrementally acquired concurrent discrimination task, while patients withdrawn from dopaminergic medication performed as well as controls. In addition, we found a dissociation of the effect of medication within a single two-phase task: patients tested 'on' medication were not impaired at the ability to generalize based on learned information. The deficit among medicated patients appeared to be related specifically to the concurrent, incremental, feedback-based nature of the task: such a deficit was not found in a version of the task in which demands for concurrent error-processing learning were reduced. Taken together with a growing body of evidence emphasizing a role for midbrain dopamine in error-correcting, feedback-based learning processes, the present results suggest a framework for understanding previously conflicting results regarding the effect of medication on learning and memory in Parkinson's disease.

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“…Robbins son's disease (PD) (Yahr 1990). However, it is becoming increasingly clear that patients with PD may also exhibit cognitive deficits, not only in late-in-the-course demented patients (for review see Lees 1990), but even in unmedicated PD patients, relatively early in the course of the disease (Lees and Smith 1983;Sahakian et al 1988;Canavan et al 1989;Downes et al 1989;Cooper et al 1991). Many of the deficits seen are reminiscent of those occurring after frontal lobe damage.…”

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confidence: 99%

l-Dopa withdrawal in Parkinson's disease selectively impairs cognitive performance in tests sensitive to frontal lobe dysfunction

et al. 1992

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Abstract.A group of ten patients with idiopathic Parkinson's disease (PD) was tested on a series of automated tests of learning, memory, planning and attention whilst either on or off L-dopa medication. Controlled withdrawal of L-dopa interfered with aspects of performance on three of the tests that had previously been shown to be sensitive to frontal lobe dysfunction; a spatial working memory task, the Tower of London planning test, and a visual discrimination paradigm that also included intra-and extra-dimensional shift tests of selective attention. More specifically, errors were increased in the spatial working memory test, and both the accuracy and latency of thinking were impaired. Thinking time was significantly slowed following L-dopa withdrawal, even though the possible contaminating effects on motor slowing were fully controlled by a yoked control procedure. Nine out of ten patients reached a further stage of the visual discrimination, set-shifting paradigm when on, rather than off, L-dopa medication. Spatial span was also impaired off medication, but there were no effects of L-dopa withdrawal on tests of pattern and spatial recognition memory, simultaneous and delayed matching to sample or visuospatial conditional associative learning. Comparisons with a large control group confirmed previous findings that PD is associated with deficits on the majority of these tests. The results are discussed in terms of the fronto-striatal, dopamine dependent nature of some of the cognitive deficits found in PD, but the apparent dopamine-independent nature of deficits in other aspects of cognitive functioning, notably in tests of visual recognition memory and associative learning.

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The performance on learning tasks of patients in the early stages of Parkinson's disease

Cited by 129 publications

References 28 publications

Computational models of reinforcement learning: the role of dopamine as a reward signal

Computational models of reinforcement learning: the role of dopamine as a reward signal

l-dopa impairs learning, but spares generalization, in Parkinson's disease

l-Dopa withdrawal in Parkinson's disease selectively impairs cognitive performance in tests sensitive to frontal lobe dysfunction

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