• Daryl J Wile, Katie Dinelle, Nasim Vafai, Jessamyn McKenzie, Joseph K Tsui, Paul Schaffer, Yu-Shin Ding, Matthew Farrer, Vesna Sossi, and A Jon Stoessl.
• University of British Columbia, Vancouver, BC, Canada.
• Mov. Disord. 2016 Mar 1; 31 (3): 405-9.

IntroductionThe basis for SWEDD is unclear, with most cases representing PD mimics but some later developing PD with a dopaminergic deficit.MethodsWe studied a patient initially diagnosed with SWEDD (based on (18)F-dopa PET) who developed unequivocal PD associated with a leucine-rich repeat kinase 2 p.G2019S mutation. Repeat multitracer PET was performed at 17 years' disease duration, including (+)[11C]dihydrotetrabenazine, [11C](N,N-dimethyl-2-(2-amino-4-cyanophenylthio) benzylamine (which binds the serotonin transporter), and (18)F-dopa.ResultsThe patient showed bilateral striatal dopaminergic denervation (right putamen 28% of age-matched normal, left putamen 33%). (18)F-dopa uptake was decreased, particularly on the left (mean 31% of normal vs. 45% on the more affected right side). Serotonin transporter binding was relatively preserved in the putamen (right mean 90% of normal, left 81%) and several cortical regions.ConclusionsSWEDD can occur in genetically determined PD and may, in some cases, be the result of compensatory nondopaminergic mechanisms operating in early disease.© 2015 International Parkinson and Movement Disorder Society.

24 keywords...

hide…