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      The basal ganglia in perceptual timing: Timing performance in Multiple System Atrophy and Huntington's disease


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          The timing of perceptual events depends on an anatomically and functionally connected network comprising basal ganglia, cerebellum, pre-frontal cortex and supplementary motor area. Recent studies demonstrate the cerebellum to be involved in absolute, duration-based timing, but not in relative timing based on a regular beat. Conversely, functional involvement of the striatum is observed in relative timing, but its role in absolute timing is unclear.

          This work tests the specific role of the basal ganglia in the perceptual timing of auditory events. It aims to distinguish the hypothesised unified model of time perception ( Teki, Grube, & Griffiths, 2012), in which the striatum is a mandatory component for all timing tasks, from a modular system in which they subserve relative timing, with absolute timing processed by the cerebellum.

          Test groups comprised individuals with Multiple System Atrophy, a disorder in which similar pathology can produce clinical deficits associated with dysfunction of the cerebellum (MSA-C, n=8) or striatum (MSA-P, n=10), and early symptomatic Huntington's disease (HD, n=14). Individuals with chronic autoimmune peripheral neuropathy ( n=11) acted as controls.

          Six adaptive tasks were carried out to assess perceptual thresholds for absolute timing through duration discrimination for sub- and supra-second time intervals, and relative timing through the detection of beat-based regularity and irregularity, detection of a delay within an isochronous sequence, and the discrimination of sequences with metrical structure.

          All three patient groups exhibited impairments in performance in comparison with the control group for all tasks, and severity of impairment was significantly correlated with disease progression. No differences were demonstrated between MSA-C and MSA-P, and the most severe impairments were observed in those with HD.

          The data support an obligatory role for the basal ganglia in all tested timing tasks, both absolute and relative, as predicted by the unified model. The results are not compatible with models of a brain timing network based upon independent modules.

          Graphical abstract

          Ninety five percent confidence intervals for mean group performance by task. Var: sub-second variable-interval discrimination. Sup: supra-second variable-interval discrimination. Pul: detection of regularity (pulse or beat) within an irregular sequence. Iso: detection of deviation from isochrony. Irr: detection of irregularity within a regular sequence. Met: detection of distortion of a sequence with strong metrical structure.


          • Patients with basal ganglia disease undertook a battery of perceptual timing tasks.

          • All patients displayed poorer performance than neurological control participants.

          • Performance in Huntington's disease was worse than Multiple System Atrophy.

          • Poorer performance was significantly correlated with disease progression.

          • These findings support the hypothesised unified model of time perception.

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          Most cited references73

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          What makes us tick? Functional and neural mechanisms of interval timing.

          Time is a fundamental dimension of life. It is crucial for decisions about quantity, speed of movement and rate of return, as well as for motor control in walking, speech, playing or appreciating music, and participating in sports. Traditionally, the way in which time is perceived, represented and estimated has been explained using a pacemaker-accumulator model that is not only straightforward, but also surprisingly powerful in explaining behavioural and biological data. However, recent advances have challenged this traditional view. It is now proposed that the brain represents time in a distributed manner and tells the time by detecting the coincidental activation of different neural populations.
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              Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson's disease. Pathophysiologic and clinical implications.

              Autografting of dopamine-producing adrenal medullary tissue to the striatal region of the brain is now being attempted in patients with Parkinson's disease. Since the success of this neurosurgical approach to dopamine-replacement therapy may depend on the selection of the most appropriate subregion of the striatum for implantation, we examined the pattern and degree of dopamine loss in striatum obtained at autopsy from eight patients with idiopathic Parkinson's disease. We found that in the putamen there was a nearly complete depletion of dopamine in all subdivisions, with the greatest reduction in the caudal portions (less than 1 percent of the dopamine remaining). In the caudate nucleus, the only subdivision with severe dopamine reduction was the most dorsal rostral part (4 percent of the dopamine remaining); the other subdivisions still had substantial levels of dopamine (up to approximately 40 percent of control levels). We propose that the motor deficits that are a constant and characteristic feature of idiopathic Parkinson's disease are for the most part a consequence of dopamine loss in the putamen, and that the dopamine-related caudate deficits (in "higher" cognitive functions) are, if present, less marked or restricted to discrete functions only. We conclude that the putamen--particularly its caudal portions--may be the most appropriate site for intrastriatal application of dopamine-producing autografts in patients with idiopathic Parkinson's disease.

                Author and article information

                Pergamon Press
                1 January 2014
                January 2014
                : 52
                : 100
                : 73-81
                [a ]Auditory Group, Institute of Neuroscience, Newcastle University, Newcastle-upon-Tyne, United Kingdom
                [b ]Institute for Ageing and Health, Newcastle University, Newcastle-upon-Tyne, United Kingdom
                [c ]Walkergate Park Centre For Neurorehabilitation and Neuropsychiatry, Newcastle-upon-Tyne, United Kingdom
                [d ]Department of Clinical Neurosciences, School of Clinical Medicine, Addenbrookes Hospital, Cambridge CB2 0SP
                Author notes
                [* ]Corresponding author. Tel.: +44 191 222 3445. thomascope@ 123456gmail.com
                © 2013 The Authors

                This document may be redistributed and reused, subject to certain conditions.

                : 23 April 2013
                : 26 September 2013
                : 27 September 2013

                beat,multiple system atrophy,perceptual timing,basal ganglia,huntington's disease
                beat, multiple system atrophy, perceptual timing, basal ganglia, huntington's disease


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