Journal
NEUROLOGY
Volume 80, Issue 20, Pages 1850-1855Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e318292a31d
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Funding
- Michael J. Fox Foundation for Parkinson's Research, United States of America [P14104]
- Medical Research Council, United Kingdom (Clinical Sciences Center, Neurology Group core grant)
- MRC [MC_U120036861, G1100810] Funding Source: UKRI
- Medical Research Council [G1100810, MC_U120036861] Funding Source: researchfish
- Austrian Science Fund (FWF) [P14104] Funding Source: Austrian Science Fund (FWF)
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Objective: The underlying pathophysiology of tremor in Parkinson disease (PD) is unclear; however, it is known that tremor does not appear to be as responsive to dopaminergic medication as bradykinesia or rigidity. It is suggested that serotonergic dysfunction could have a role in tremor development. Methods: Using C-11-DASB PET, a marker of serotonin transporter binding, and clinical observations, we have investigated function of serotonergic terminals in 12 patients with tremor-predominant and 12 with akinetic-rigid PD. Findings were compared with those of 12 healthy controls. Results: Reductions of C-11-DASB in caudate, putamen, and raphe nuclei significantly correlated with tremor severity on posture and action, but not with resting tremor. The tremor-predominant group also showed reductions of C-11-DASB in other regions involved in motor circuitry, including the thalamus and Brodmann areas 4 and 10. Conclusions: Our findings support a role for serotonergic dysfunction in motor circuitries in the generation of postural tremor in PD.
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