Objective: To investigate the relationship between striatal dopamine transporter binding and rest tremor.

Background: In vivo dopamine transporter imaging is a useful tool for distinguishing nigrostriatal degenerative conditions (e.g. Parkinson’s disease) from other, non-progressive causes of tremor. However, while many of the motoric features of Parkinson’s disease (e.g. bradykinesia, rigidity, hypomimia) correlate well with reduced striatal dopamine transporter binding, the same relationship has not been demonstrated for tremor.(1) This poses a paradox, given the tendency for Parkinsonian tremor to preponderate on the side that is worst affected by bradykinesia and rigidity,(2) to respond to levodopa, and to correlate with imaging markers of contralateral striatal dopaminergic function in animal studies.(3)

Method: Participants with upper limb tremor were recruited for the study. Participants  underwent standardised clinical assessment, structured and videotaped clinical examination, tremor neurophysiology study of both upper limbs using accelerometry and surface EMG, and Technetium-99m TRODAT-1 brain SPECT imaging. Normalised striatal uptake values were calculated. Tremor EMG and accelerometry time series were processed with Fourier transformation to identify peak tremor power within a window of 3-10 Hz.

Results: 27 participants were recruited. Multiple regression analysis of tremor power in a limb sEMG or accelerometry channel versus contralateral striatal uptake failed to yield any significant associations. However, analysis of the difference or ratio between left and right tremor power for each participant yielded associations between excess rest tremor in a limb and reduced dopamine transporter binding in the contralateral striatum (as compared with the ipsilateral striatum). No such association was found for postural or kinetic tremor.

Conclusion: These data suggest a relationship between rest tremor and a contralateral reduction in striatal dopamine binding. Use of quantitative neurophysiology techniques and side-to-side comparison of data for each participant may allow the demonstration of clinico-pathophysiological relationships in tremor that have remained occult to previous studies.

References: 1. Helmich RC, Hallett M, Deuschl G, Toni I, Bloem BR. Cerebral causes and consequences of parkinsonian resting tremor: a tale of two circuits? Brain. 2012;135(Pt 11):3206-26. 2. Toth C, Rajput M, Rajput AH. Anomalies of asymmetry of clinical signs in parkinsonism. Movement disorders : official journal of the Movement Disorder Society. 2004;19(2):151-7. 3. Eberling JL, Pivirotto P, Bringas J, Bankiewicz KS. Tremor is associated with PET measures of nigrostriatal dopamine function in MPTP-lesioned monkeys. Exp Neurol. 2000;165(2):342-6.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/asymmetrical-striatal-dopamine-transporter-binding-correlates-with-excess-contralateral-rest-tremor/