ORIGINAL ARTICLE Differences in striatal dopamine transporter density between tremor dominant and non-tremor Parkinson’ s disease Valtteri Kaasinen & Maija Kinos & Juho Joutsa & Marko Seppänen & Tommi Noponen Received: 24 February 2014 /Accepted: 2 May 2014 # Springer-Verlag Berlin Heidelberg 2014 Abstract Purpose Parkinson’ s disease (PD) can manifest with a tremor- dominant or a non-tremor (akinetic-rigid) phenotype. Al- though the tremor-dominant subtype may show a better prog- nosis, there is limited information on the phenotypic differ- ences regarding the level of striatal dopamine transmission. The present study investigated striatal dopamine transporter (DAT) binding characteristics in a large sample of patients with and without tremor. Methods [ 123 I]FP-CIT SPECT scans of 231 patients with a clinical diagnosis of PD and abnormal FP-CIT binding (157 with tremor, 74 without tremor) and 230 control patients with normal FP-CIT binding (148 with tremor, 82 without tremor) were analysed using an automated region-of-interest analysis of the scans (BRASS). Specific striatal binding ratios were compared between phenotypes and groups using age, sex, and symptom duration, predominant side of symptoms, dopami- nergic medications and scanner as covariates. Results Patients with PD had 28.1 – 65.0 % lower binding in all striatal regions compared to controls (p <0.001). The mean FP-CIT caudate nucleus uptake and the left caudate nucleus uptake were higher in PD patients with tremor than in PD patients without tremor (mean 9.0 % higher, left 10.5 % higher; p <0.05), whereas there were no differences between tremor and non-tremor control patients. No significant effects of tremor on DAT binding were observed in the anterior or posterior putamen. Conclusion The motor phenotype is associated with the extent of caudate dopamine terminal loss in PD, as dopamine function is relatively more preserved in tremor patients. Symptom type is related to caudate dopamine function only in association with Parkinsonian dopaminergic degeneration, not in intact dopa- mine systems in patients with non-PD tremor. Keywords Dopamine transporter . Parkinson’ s disease . Tremor . SPECT Introduction Tremor is a symptom characterized by involuntary, rhythmic and sinusoidal alternating movements of one or more body parts [1]. It is one of the cardinal symptoms of Parkinson’ s disease (PD) but seems to differ from bradykinesia and rigid- ity both clinically and pathophysiologically [2, 3]. Several lines of evidence indicate that tremor is a marker of relatively benign PD [3]. Motor progression [4–6] and cognitive pro- gression [7] of tremor-dominant PD appear to be slower than progression of non-tremor PD, i.e. postural instability gait disorder (PIGD) or akinetic-rigid PD. The slower rate of progression in tremor-dominant PD is correlated with less severe nigral cell loss based on post-mortem examination [8]. Non-tremor PD patients show reduced brain activity in the prefrontal cortex and globus pallidus [9], more prominent grey matter atrophy in motor-related regions and decreased functional connectivity [10] compared to tremor-dominant patients. From a treatment-related perspective, non-tremor PD seems to be associated with an increased risk of levodopa-induced dyskinesias [11]. Although lower CSF concentrations of β-amyloid 1–42, T- tau, P-tau 181 and α-synuclein have been reported in patients V. Kaasinen (*) : M. Kinos : J. Joutsa Division of Clinical Neurosciences, University of Turku and Turku University Hospital, POB 52, 20521 Turku, Finland e-mail: valtteri.kaasinen@tyks.fi V. Kaasinen : M. Kinos : J. Joutsa : M. Seppänen Turku PET Centre, University of Turku and Turku University Hospital, Turku, Finland M. Seppänen : T. Noponen Department of Clinical Physiology and Nuclear Medicine, University of Turku and Turku University Hospital, Turku, Finland Eur J Nucl Med Mol Imaging DOI 10.1007/s00259-014-2796-5