Dataset Information

Abnormal explicit but normal implicit sequence learning in premanifest and early Huntington's disease.

ABSTRACT: Learning may occur with or without awareness, as explicit (intentional) or implicit (incidental) learning. The caudate nucleus and the putamen, which are affected early in Huntington's disease (HD), are thought to be essential for motor sequence learning. However, the results of existing studies are inconsistent concerning presence/absence of deficits in implicit and explicit motor sequence learning in HD. We assessed implicit and explicit motor sequence learning using sequences of equivalent structure in 15 individuals with a positive HD genetic test (7 premanifest; 8 early stage disease) and 11 matched controls. The HD group showed evidence of normal implicit motor sequence learning, whereas explicit motor sequence learning was impaired in manifest and premanifest HD gene carriers, with progressive decline with progressive disease. Explicit sequence learning may be a useful cognitive biomarker for HD progression.

SUBMITTER: Schneider SA

PROVIDER: S-EPMC2997693 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature

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Abnormal explicit but normal implicit sequence learning in premanifest and early Huntington's disease.

Schneider Susanne A SA Wilkinson Leonora L Bhatia Kailash P KP Henley Susie M D SM Rothwell John C JC Tabrizi Sarah J SJ Jahanshahi Marjan M

Movement disorders : official journal of the Movement Disorder Society 20100701 10

Learning may occur with or without awareness, as explicit (intentional) or implicit (incidental) learning. The caudate nucleus and the putamen, which are affected early in Huntington's disease (HD), are thought to be essential for motor sequence learning. However, the results of existing studies are inconsistent concerning presence/absence of deficits in implicit and explicit motor sequence learning in HD. We assessed implicit and explicit motor sequence learning using sequences of equivalent st ...[more]

PMID: 20544716

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Project description:The initial stages of neurodegeneration are commonly marked by normal levels of cognitive and motor performance despite the presence of structural brain pathology. Compensation is widely assumed to account for this preserved behaviour, but despite the apparent simplicity of such a concept, it has proven incredibly difficult to demonstrate such a phenomenon and distinguish it from disease-related pathology. Recently, we developed a model of compensation whereby brain activation, behaviour and pathology, components key to understanding compensation, have specific longitudinal trajectories over three phases of progression. Here, we empirically validate our explicit mathematical model by testing for the presence of compensation over time in neurodegeneration. Huntington's disease is an ideal model for examining longitudinal compensation in neurodegeneration as it is both monogenic and fully penetrant, so disease progression and potential compensation can be monitored many years prior to diagnosis. We defined our conditions for compensation as non-linear longitudinal trajectories of brain activity and performance in the presence of linear neuronal degeneration and applied our model of compensation to a large longitudinal cohort of premanifest and early-stage Huntington's disease patients from the multisite Track-On HD study. Focusing on cognitive and motor networks, we integrated progressive volume loss, task and resting state functional MRI and cognitive and motor behaviour across three sequential phases of neurodegenerative disease progression, adjusted for genetic disease load. Multivariate linear mixed models were fitted and trajectories for each variable tested. Our conceptualization of compensation was partially realized across certain motor and cognitive networks at differing levels. We found several significant network trends that were more complex than that hypothesized in our model. These trends suggest changes to our theoretical model where the network effects are delayed relative to performance effects. There was evidence of compensation primarily in the prefrontal component of the cognitive network, with increased effective connectivity between the left and right dorsolateral prefrontal cortex. Having developed an operational model for the explicit testing of longitudinal compensation in neurodegeneration, it appears that general patterns of our framework are consistent with the empirical data. With the proposed modifications, our operational model of compensation can be used to test for both cross-sectional and longitudinal compensation in neurodegenerative disease with similar patterns to Huntington's disease.

Dataset Information

Abnormal explicit but normal implicit sequence learning in premanifest and early Huntington's disease.

Publications

Abnormal explicit but normal implicit sequence learning in premanifest and early Huntington's disease.

Similar Datasets

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