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Neurophysiologic characterization of Re-emergent tremor (RET) in Parkinson’s disease

G. Leodori, D. Belvisi, A. Fabbrini, M. de Bartolo, M. Costanzo, F. Undurraga, A. Conte, A. Berardelli (Bethesda, MD, USA)

Meeting: 2019 International Congress

Abstract Number: 1421

Keywords: Neurophysiology, Transcranial magnetic stimulation(TMS), Tremors: Pathophysiology

Session Information

Date: Tuesday, September 24, 2019

Session Title: Tremor

Session Time: 1:45pm-3:15pm

Location: Les Muses Terrace, Level 3

Objective: To investigate: 1) the contribution of primary motor cortex (M1) to the generation of re-emergent tremor (RET) and rest tremor by measuring the Cortico-muscular coherence (CMC) [1] and the TMS tremor-resetting index (RI) (2). 2) the pathophysiological mechanisms generating RET by measuring M1 excitability during RET latency by TMS-EEG coregistration (3).

Background: Patients with Parkinson’s disease (PD) may have a tremor that appears after a variable latency while maintaining a posture (re-emergent tremor). Re-emergent tremor (RET) and rest tremor share similar clinical features, but it is unknown whether they also share pathophysiological mechanisms (4).

Method: We enrolled 10 PD patients with rest tremor and RET. CMC between EMG signal recorded on the extensor digitorum communis and cortical activity recorded on C3/C4 was measured during RET and resting tremor. Single-pulse (sp) TMS was delivered on M1 during RET and resting tremor and TMS-induced perturbations on tremor bursts were measured for calculating the RI. TMS-evoked potentials (TEPs) generated by spTMS delivered below motor threshold on M1 were recorded with a 32-channel EEG during posture before the reappearance of tremor (RET latency).

Results: RET and resting tremor showed significant CMC at tremor frequency and double tremor frequency with no significant differences between each other. Single-pulse TMS on M1 induces significant reset of both RET and rest tremor, with a trend for a higher effect on RET. TMS during RET latency produced TEPs characterized by peaks P30, P60 and N100. During RET latency, P60 over M1 progressively increases in amplitude.

Conclusion: RET and rest tremor share common pathophysiological mechanisms in which M1 plays a role as a central oscillator. RET latency is accompanied by changes in M1 cortical excitability. We, therefore, conclude that cortical mechanisms within M1 play a role in the pathophysiology of RET.

References: [1] Halliday et al.; Coherence between low-frequency activation of the motor cortex and tremor in patients with essential tremor; The Lancet, 2000. [2] Lu M.K. et al.; Resetting tremor by single and paired transcranial magnetic stimulation in Parkinson’s disease and essential tremor; Clin Neurophysiol, 2015. [3] Tremblay et al.; Clinical utility and prospective of TMS–EEG; Clin Neurophysiol, 2019. [4] Belvisi et al.; Re-emergent tremor in Parkinson’s disease; Parkinsonism Relat Disord. 2017.

To cite this abstract in AMA style:

G. Leodori, D. Belvisi, A. Fabbrini, M. de Bartolo, M. Costanzo, F. Undurraga, A. Conte, A. Berardelli. Neurophysiologic characterization of Re-emergent tremor (RET) in Parkinson’s disease [abstract]. Mov Disord. 2019; 34 (suppl 2). https://www.mdsabstracts.org/abstract/neurophysiologic-characterization-of-re-emergent-tremor-ret-in-parkinsons-disease/. Accessed May 15, 2025.
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