Objective: To examine the differences in brain activity between resting and re-emergent tremor in PD, as well as to investigate the relationship between neuronal oscillatory activity in PD tremor phenotype patients.

Background: Re-emergent tremor (RET) in PD is characterized as a continuation of resting tremor (RT) while maintaining a stable posture[1]. The pathophysiology of both RT and RET is linked to deficits in cerebello-cortical circuits and dopaminergic depletion[2]. However, it remains unclear how these two types of tremors differ functionally.

Method: Forty PD patients (25 males, mean age 66.78 ± 5.03 years) and 40 age- and sex-matched healthy controls were assessed. EEG and EMG signals were recorded while the participants extended their hands against gravity. Tremor was recorded in both L-dopa ON and OFF for PD patients and mimicked by healthy controls. Coherent sources of EEG-EMG were located using beamforming technique, and information flow between different sources was estimated using time-resolved partial-directed coherence. Cross-frequency coupling (CFC) was then used to analyse the association between tremor frequency and neuronal oscillatory activity.

Results: Under L-dopa administration, coherent sources revealed differences in brain activity between RT and RET in the premotor cortex and cerebellum of PD patients, which were like those observed in healthy controls. However, PD patients exhibited an additional source location in the primary sensorimotor cortex. Withdrawal of L-dopa led to coherent sources being observed in the SMA and STN. Furthermore, L-dopa was found to suppress the strength of connections between these coherent sources and modulate the tremor-associated beta and gamma frequency, leading to a decrease in beta power and an increase in gamma power. These results provide direct evidence of pathological beta and prokinetic gamma activity in tremor phenotype patients.

Conclusion: These findings point the primary sensorimotor cortex in PD patients differs between RT and RET, which may be triggered by peripheral sensory input, such as moving the limb from a resting position to an outstretched posture. Additionally, the study indicated that oscillatory neuronal responses to dopamine medication were present at both beta and gamma, highlighting a tremor-related phenotype cortical network that operates within the concept of pathological beta and prokinetic gamma oscillations.

References: [1] Belvisi, D., Conte, A., Bologna, M., Bloise, M.C., Suppa, A., Formica, A., Costanzo, M., Cardone, P., Fabbrini, G. and Berardelli, A., 2017. Re-emergent tremor in Parkinson’s disease. Parkinsonism & related disorders, 36, pp.41-46.
[2] Dirkx, M.F. and Bologna, M., 2022. The pathophysiology of Parkinson’s disease tremor. Journal of the Neurological Sciences, p.120196.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/differences-in-brain-activity-and-oscillatory-responses-in-resting-and-re-emergent-tremor-in-parkinsons-disease/