Journal
BRAIN
Volume 132, Issue -, Pages 336-346Publisher
OXFORD UNIV PRESS
DOI: 10.1093/brain/awn309
Keywords
Parkinsons disease; hybrid fMRI; cognitive control dynamics; verbal working memory; Striatum
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Funding
- Swedish Medical Research Council
- Parkinson Foundation in Sweden
- Swedish Association of Persons with Neurological Disabilities
- University of Umea
- Foundation for Clinical Neuroscience at Umea University Hospital
- Neuroscience at Umea University Hospital
- Lions Clubs Sweden's foundation for research in age-related diseases
- Lions Clubs Sweden's foundation for research in age- related diseases
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Using hybrid-blocked/event-related fMRI and the 2-back task we aimed to decompose tonic and phasic temporal dynamics of basal ganglia response abnormalities in working memory associated with early untreated Parkinsons disease. In view of the tonic/phasic dopamine hypothesis, which posits a functional division between phasic D-2-dependent striatal updating processes and tonic D-1-dependent prefrontal context-maintenance processes, we predicted that newly diagnosed, drug-nave Parkinsons disease patients, with selective striatal dopamine deprivation, would demonstrate transient rather than sustained activation changes in the basal ganglia during 2-back performance. Task-related activation patterns within discrete basal ganglia structures were directly compared between patients and healthy elderly controls. The obtained results yielded uniquely transient underactivation foci in caudate nuclei, putamen and globus pallidus in Parkinsons disease patients, which indicates suboptimal phasic implementation of striatal D-2-dependent gating mechanisms during updating. Sustained underactivation was only seen in the anterior putamen, which may reflect initial signs of tonic control impairment. No significant changes were exhibited in prefrontal cortex. The present findings resonate well with the tonic/phasic dopamine account and suggest that basal ganglia under-recruitment associated with executive dysfunction in early Parkinsons disease might predominantly stem from deficiencies in phasic executive components subserved by striatum.
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