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      Basal Ganglia Circuits Underlying the Pathophysiology of Levodopa-Induced Dyskinesia

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          Abstract

          Involuntary movements or dyskinesia, represent a debilitating complication of levodopa therapy for Parkinson's disease. Dyskinesia is, ultimately, experienced by the vast majority of the patients. Despite the importance of this problem, little was known about the cause of dyskinesia, a situation that has dramatically evolved in the last few years with a focus upon the molecular and signaling changes induced by chronic levodopa treatment. Departing from this, we here review the progress made in functional anatomy and neuroimaging that have had a tremendous impact on our understanding of the anatomo-functional organization of the basal ganglia in Parkinsonism and dyskinetic states, notably the demonstration that dyskinesia are linked to a pathological processing of limbic and cognitive information.

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          Most cited references 153

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          Parallel organization of functionally segregated circuits linking basal ganglia and cortex.

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            The functional anatomy of basal ganglia disorders.

            Basal ganglia disorders are a heterogeneous group of clinical syndromes with a common anatomic locus within the basal ganglia. To account for the variety of clinical manifestations associated with insults to various parts of the basal ganglia we propose a model in which specific types of basal ganglia disorders are associated with changes in the function of subpopulations of striatal projection neurons. This model is based on a synthesis of experimental animal and post-mortem human anatomic and neurochemical data. Hyperkinetic disorders, which are characterized by an excess of abnormal movements, are postulated to result from the selective impairment of striatal neurons projecting to the lateral globus pallidus. Hypokinetic disorders, such as Parkinson's disease, are hypothesized to result from a complex series of changes in the activity of striatal projection neuron subpopulations resulting in an increase in basal ganglia output. This model suggests that the activity of subpopulations of striatal projection neurons is differentially regulated by striatal afferents and that different striatal projection neuron subpopulations may mediate different aspects of motor control.
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              Non-motor symptoms of Parkinson's disease: diagnosis and management.

              The clinical diagnosis of Parkinson's disease rests on the identification of the characteristics related to dopamine deficiency that are a consequence of degeneration of the substantia nigra pars compacta. However, non-dopaminergic and non-motor symptoms are sometimes present before diagnosis and almost inevitably emerge with disease progression. Indeed, non-motor symptoms dominate the clinical picture of advanced Parkinson's disease and contribute to severe disability, impaired quality of life, and shortened life expectancy. By contrast with the dopaminergic symptoms of the disease, for which treatment is available, non-motor symptoms are often poorly recognised and inadequately treated. However, attention is now being focused on the recognition and quantitation of non-motor symptoms, which will form the basis of improved treatments. Some non-motor symptoms, including depression, constipation, pain, genitourinary problems, and sleep disorders, can be improved with available treatments. Other non-motor symptoms can be more refractory and need the introduction of novel non-dopaminergic drugs. Inevitably, the development of treatments that can slow or prevent the progression of Parkinson's disease and its multicentric neurodegeneration provides the best hope of curing non-motor symptoms.
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                Author and article information

                Journal
                Front Neuroanat
                Front. Neuroanat.
                Frontiers in Neuroanatomy
                Frontiers Research Foundation
                1662-5129
                13 August 2010
                14 September 2010
                2010
                : 4
                Affiliations
                1simpleCentre National de la Recherche Scientifique UMR 5227, Bordeaux Institute of Neuroscience, Université Victor-Segalen Bordeaux 2 Bordeaux, France
                Author notes

                Edited by: Jose L. Lanciego, University of Navarra, Spain

                Reviewed by: Jose L. Lanciego, University of Navarra, Spain; Marco Aurelio M. Freire, Federal University of Rio Grande do Norte, Brazil

                *Correspondence: Erwan Bezard, CNRS UMR 5227, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France. e-mail: erwan.bezard@ 123456u-bordeaux2.fr
                10.3389/fnana.2010.00131
                2947938
                20890450
                Copyright © 2010 Barroso-Chinea and Bezard.

                This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.

                Counts
                Figures: 0, Tables: 0, Equations: 0, References: 152, Pages: 9, Words: 9980
                Categories
                Neuroscience
                Review Article

                Neurosciences

                parkinson's disease, basal ganglia, abnormal involuntary movements, levodopa

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