Dataset Information

Basal ganglia and kinematics modulation: insights from Parkinson's and Huntington's diseases.

ABSTRACT: Movement kinematic variables related to force production can be modulated to respond appropriately to different contexts. We previously showed that in a choice-reaction time and a predictable timed-response task, normal subjects perform reaching movements to the same targets with two different kinematic patterns, a marker of flexibility. Here, we used the two tasks to determine whether basal ganglia are involved in the selection and modulation of movement kinematics and therefore in flexible force production. We tested seventeen patients in the early stages of Parkinson's disease, eleven pre-symptomatic Huntington's disease carriers and sixteen age-matched normal controls with the above-mentioned motor tasks. In both patient groups, the difference in kinematics (movement duration, peak velocity and acceleration) between the two tasks was significantly reduced compared to controls, indicating a limited range of choices or flexibility. However, this reduction was skewed in opposite directions in the two disorders, with force production being generally higher in Huntington's carriers and lower in Parkinson's patients compared to controls. We conclude that basal ganglia are involved in adapting movement to different contexts and selecting the appropriate movement force. The opposite trends in Parkinson's and Huntington's disease suggest that such regulation might depend on the balance between the outputs of direct and indirect pathways.

SUBMITTER: Moisello C

PROVIDER: S-EPMC3167928 | biostudies-literature | 2011 Sep

REPOSITORIES: biostudies-literature

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Basal ganglia and kinematics modulation: insights from Parkinson's and Huntington's diseases.

Moisello Clara C Perfetti Bernardo B Marinelli Lucio L Sanguineti Vittorio V Bove Marco M Feigin Andrew A Di Rocco Alessandro A Eidelberg David D Ghilardi M F MF

Parkinsonism & related disorders 20110720 8

Movement kinematic variables related to force production can be modulated to respond appropriately to different contexts. We previously showed that in a choice-reaction time and a predictable timed-response task, normal subjects perform reaching movements to the same targets with two different kinematic patterns, a marker of flexibility. Here, we used the two tasks to determine whether basal ganglia are involved in the selection and modulation of movement kinematics and therefore in flexible for ...[more]

PMID: 21764625

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Project description:Huntington's disease is caused by a CAG repeat expansion in the Huntingtin gene (HTT), coding for polyglutamine in the Huntingtin protein, with longer CAG repeats causing earlier age of onset. The variable 'Age' × ('CAG'-L), where 'Age' is the current age of the individual, 'CAG' is the repeat length and L is a constant (reflecting an approximation of the threshold), termed the 'CAG Age Product' (CAP) enables the consideration of many individuals with different CAG repeat expansions at the same time for analysis of any variable and graphing using the CAG Age Product score as the X axis. Structural MRI studies have showed that progressive striatal atrophy begins many years prior to the onset of diagnosable motor Huntington's disease, confirmed by longitudinal multicentre studies on three continents, including PREDICT-HD, TRACK-HD and IMAGE-HD. However, previous studies have not clarified the relationship between striatal atrophy, atrophy of other basal ganglia structures, and atrophy of other brain regions. The present study has analysed all three longitudinal datasets together using a single image segmentation algorithm and combining data from a large number of subjects across a range of CAG Age Product score. In addition, we have used a strategy of normalizing regional atrophy to atrophy of the whole brain, in order to determine which regions may undergo preferential degeneration. This made possible the detailed characterization of regional brain atrophy in relation to CAG Age Product score. There is dramatic selective atrophy of regions involved in the basal ganglia circuit-caudate, putamen, nucleus accumbens, globus pallidus and substantia nigra. Most other regions of the brain appear to have slower but steady degeneration. These results support (but certainly do not prove) the hypothesis of circuit-based spread of pathology in Huntington's disease, possibly due to spread of mutant Htt protein, though other connection-based mechanisms are possible. Therapeutic targets related to prion-like spread of pathology or other mechanisms may be suggested. In addition, they have implications for current neurosurgical therapeutic approaches, since delivery of therapeutic agents solely to the caudate and putamen may miss other structures affected early, such as nucleus accumbens and output nuclei of the striatum, the substantia nigra and the globus pallidus.

Dataset Information

Basal ganglia and kinematics modulation: insights from Parkinson's and Huntington's diseases.

Publications

Basal ganglia and kinematics modulation: insights from Parkinson's and Huntington's diseases.

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